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The Pronk Pops Show 898, May 23, 2017, Story 1: Suicide Bomber, 22-year-old Salman Abedi, Killed 22 and Wounded 119 In Radical Islamic Terrorist Attack in Manchester, England — Islamic State Claims Responsibility — President Trump Calls Them “Evil Losers” — Videos — Story 2: Budget Director Mulvaney Presents President Trump’s Fiscal Year 2018 U.S. Federal Budget — Dead On Arrival — Spending Addiction Disorder (SAD) Rampant in Congress — $500-$600 Billion Deficit in Fiscal Year 2018! — Videos — Story 3: Where is The Evidence of Collusion, Conspiracy, or Coordination Between Russians and Trump Campaign? and Where is The Evidence of Collusion, Conspiracy, or Coordination Between Foreign Governments and Clinton Campaign and Clinton Foundation? — Videos

Posted on May 23, 2017. Filed under: American History, Bombs, Breaking News, Congress, Countries, Crime, Culture, Defense Spending, Donald J. Trump, Donald J. Trump, Donald Trump, Elections, Employment, European History, Federal Government, Fourth Amendment, Freedom of Speech, Government, Government Dependency, Government Spending, Great Britain, Hate Speech, History, Homicide, House of Representatives, Human, Human Behavior, Independence, Islamic State, Language, Law, Life, Media, Medicare, Music, News, People, Philosophy, Photos, Politics, Polls, President Trump, Radio, Raymond Thomas Pronk, Second Amendment, Senate, Social Security, Spying, Success, Taxation, Taxes, Terror, Terrorism, United Kingdom, United States Constitution, United States of America, Videos, War, Wealth, Weapons, Welfare Spending, Wisdom | Tags: , , , , , , , , , , , , , , , , , , |

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The Pronk Pops Show Podcasts

Pronk Pops Show 898,  May 23, 2017

Pronk Pops Show 897,  May 22, 2017

Pronk Pops Show 896,  May 18, 2017

Pronk Pops Show 895,  May 17, 2017

Pronk Pops Show 894,  May 16, 2017

Pronk Pops Show 893,  May 15, 2017

Pronk Pops Show 892,  May 12, 2017

Pronk Pops Show 891,  May 11, 2017

Pronk Pops Show 890,  May 10, 2017

Pronk Pops Show 889,  May 9, 2017

Pronk Pops Show 888,  May 8, 2017

Pronk Pops Show 887,  May 5, 2017

Pronk Pops Show 886,  May 4, 2017

Pronk Pops Show 885,  May 3, 2017

Pronk Pops Show 884,  May 1, 2017

Pronk Pops Show 883 April 28, 2017

Pronk Pops Show 882: April 27, 2017

Pronk Pops Show 881: April 26, 2017

Pronk Pops Show 880: April 25, 2017

Pronk Pops Show 879: April 24, 2017

Pronk Pops Show 878: April 21, 2017

Pronk Pops Show 877: April 20, 2017

Pronk Pops Show 876: April 19, 2017

Pronk Pops Show 875: April 18, 2017

Pronk Pops Show 874: April 17, 2017

Pronk Pops Show 873: April 13, 2017

Pronk Pops Show 872: April 12, 2017

Pronk Pops Show 871: April 11, 2017

Pronk Pops Show 870: April 10, 2017

Pronk Pops Show 869: April 7, 2017

Pronk Pops Show 868: April 6, 2017

Pronk Pops Show 867: April 5, 2017

Pronk Pops Show 866: April 3, 2017

Pronk Pops Show 865: March 31, 2017

Pronk Pops Show 864: March 30, 2017

Pronk Pops Show 863: March 29, 2017

Pronk Pops Show 862: March 28, 2017

Pronk Pops Show 861: March 27, 2017

Pronk Pops Show 860: March 24, 2017

Pronk Pops Show 859: March 23, 2017

Pronk Pops Show 858: March 22, 2017

Pronk Pops Show 857: March 21, 2017

Pronk Pops Show 856: March 20, 2017

Pronk Pops Show 855: March 10, 2017

Pronk Pops Show 854: March 9, 2017

Pronk Pops Show 853: March 8, 2017

Pronk Pops Show 852: March 6, 2017

Pronk Pops Show 851: March 3, 2017

Pronk Pops Show 850: March 2, 2017

Pronk Pops Show 849: March 1, 2017

Pronk Pops Show 848: February 28, 2017

Pronk Pops Show 847: February 27, 2017

Pronk Pops Show 846: February 24, 2017

Pronk Pops Show 845: February 23, 2017

Pronk Pops Show 844: February 22, 2017

Pronk Pops Show 843: February 21, 2017

Pronk Pops Show 842: February 20, 2017

Pronk Pops Show 841: February 17, 2017

Pronk Pops Show 840: February 16, 2017

Pronk Pops Show 839: February 15, 2017

Pronk Pops Show 838: February 14, 2017

Pronk Pops Show 837: February 13, 2017

Pronk Pops Show 836: February 10, 2017

Pronk Pops Show 835: February 9, 2017

Pronk Pops Show 834: February 8, 2017

Pronk Pops Show 833: February 7, 2017

Pronk Pops Show 832: February 6, 2017

Pronk Pops Show 831: February 3, 2017

Pronk Pops Show 830: February 2, 2017

Image result for manchester england suicide bomber Suicide Bomber, 22-year-old Salman Abedi

This graphic shows where the explosion took place, in the foyer area, leading towards Victoria railway station Image result for trump budget proposal

Story 1:  Suicide Bomber, 22-year-old Salman Abedi,  Killed 22 and  Wounded 119 In Radical Islamic Terrorist Attack in Manchester, England — Islamic State Claims Responsibility — President Trump Calls Them “Evil Losers” — Videos

Image result for manchester england suicide bomberImage result for manchester england suicide bomber Suicide Bomber, 22-year-old Salman Abedi

Trump calls Manchester masterminds ‘evil losers’

U.K.’s Theresa May on Manchester Terror Attack

Lt. Col. Shaffer: Manchester terror attack is symbolic

Trump reacts to Manchester attack

Manchester police confirm identity of concert bomber

Published on May 23, 2017

The suicide bomber at an Ariana Grande concert has been identified as 22-year-old Salman Abedi, Manchester Police confirmed at a news conference Tuesday. Greater Manchester Chief Constable Ian Hopkins also said a 23-year-old man was arrested in connection with the attack. See the full news conference.

Who was behind the Manchester terror attack?

Manchester remains on edge following terror attack.

 

Manchester bomber identified: Latest in terror investigation

Last Updated May 23, 2017 3:03 PM EDT

LONDON — Police on Tuesday identified the man who blew himself up the previous night at an Ariana Grande concert in Manchester, England, as 22-year-old Salman Abedi. CBS News confirmed Abedi was known to British authorities prior to the attack.

In a generic statement posted online, the Islamic State of Iraq and Syria (ISIS) claimed responsibility for Abedi’s suicide bomb attack, which left 22 people dead, including children, at one of the entrances to the Manchester Arena.

Officials said one man was arrested Tuesday in southern Manchester in connection with the attack, and urged people to avoid the center of the city as raids continued at addresses around the city.

Police and British Prime Minister Theresa May made it clear the focus of the investigation was to determine whether the bomber “was acting alone, or was part of a wider group.”

ISIS issued its claim of responsibility in a brief, generic statement that did not identify the bomber and appeared to get some of the facts of the attack wrong. It claimed a “caliphate soldier managed to place a number of devices among a gathering of crusaders in Manchester, and detonated them.”

Officials say there was only one explosion, and there have been no indications that other devices were discovered at or near the arena.

U.S. intelligence sources told CBS News they were exercising caution on the early claim of responsibility from ISIS. Authorities are still looking into whether it was a killer who acted alone or who might have had some level of support from the terror network. U.S. intelligence officials were offering assistance in the investigation, as is standard practice in any case involving a close ally.

Dan Coats, the director of national intelligence, noted in Congress on Tuesday that ISIS frequently claims responsibility for terror attacks, and their claim has yet to be verified by U.S. officials.

Testifying in front of the Senate Armed Services Committee, Coats said the Manchester attack should serve as a reminder that the terrorist threat is “not going away and it needs significant attention.”

ISIS has repeatedly called for its supporters in the West to attack “soft targets” like sports events and concerts in any way possible.

Previous attacks in Europe and the U.S. have been claimed by individuals who support ISIS and have made contact with its members, but who were not directly supported or guided by the terror network.

Manchester police confirmed the arrest of a 23-year-old man in the southern Chorlton neighborhood of the city on Tuesday morning. The suspect taken into custody was not identified, but police said the arrest was linked to the bombing. Witnesses said the man was smiling as he was apprehended.

Police also confirmed that officers had conducted a controlled explosion at the scene of a separate raid connected to the arena attack in the Fallowfield neighborhood, in south Manchester.

According to British election rolls, Abedi was listed as living at the modest red brick semi-detached house in Fallowfield where police performed the controlled explosion.

Theo Brown, who lives near the Fallowfield address, told CBS News he heard a loud explosion and then saw about 50 law enforcement officers in the street.

The bomb wielded by Abedi was designed to kill and maim as many people as possible; many of the survivors suffered shrapnel wounds and ball bearings were found at the scene.

There was security at the concert, but the bomber apparently didn’t try to get into the venue, instead blowing himself up in an entrance foyer area as concert-goers flooded out of the arena. Prime Minister May said the attacker had deliberately chosen “his time and place to cause maximum carnage” in the young crowd.

http://www.cbsnews.com/news/ariana-grande-concert-manchester-arena-bombing-suspect-salman-abedi-isis-claim/

‘He was chanting Islamic prayers loudly in the street’: Neighbours of British-born suicide bomber – a keen Manchester United fan and son of airport security worker – tell of his ‘strange behaviour’ in the weeks before deadly attack

  • Manchester Arena concert suicide bomber has been named as Salman Abedi 
  • Terrorist was killed in the blast as he murdered 22 after Ariana Grande concert
  • Raids on address believed to be Abedi’s, where controlled explosion took place, and his brother Ismail’s address, where police arrested a 23-year-old man
  • Neighbours described Abedi as an abrasive, tall, skinny young man who was little known in the neighbourhood, and often seen in traditional Islamic clothing 
  • ISIS claimed today that one of its fanatics was responsible for the massacre
  • The ranting message threatened further attacks on ‘worshippers of the Cross’ 

The imam of the Mosque attended by Manchester Salman Abedi has revealed the suicide bomber looked at him ‘with hate’ when he gave a sermon criticising ISIS.

It comes as neighbours of the British-born Manchester United fan described his ‘strange behaviour’ in the weeks before he slaughtered 22 people.

The 22-year-old attacker, described as an abrasive, tall, skinny young man who was often seen in traditional Islamic clothing, was heard ‘chanting prayers loudly in the street’ outside his home in the south of the city.

Abedi is the third of four children by Libyan refugees who came to the UK to escape the Gaddafi regime.  They are believed to have lived in the Fallowfield area of south Manchester for at least ten years.

Last night, Abedi murdered and maimed concert goers as they left Manchester Arena after an Ariana Grande concert.

Armed police prepare to raid ‘home of Manchester suicide bomber’

This is the moment anti-terror police swooped to arrest a man over last night’s ISIS suicide bomb atrocity at Manchester Arena

Neighbours of British-born Manchester suicide bomber Salman Abedi have revealed his 'strange behaviour' in the weeks before he slaughtered 22 people

Neighbours of British-born Manchester suicide bomber Salman Abedi have revealed his ‘strange behaviour’ in the weeks before he slaughtered 22 people

A forensic investigator emerged from the house carrying a booklet called 'Know Your Chemicals'

A forensic investigator emerged from the house carrying a booklet called ‘Know Your Chemicals’

Mohammed Saeed, the imam of Didsbury Mosque and Islamic Centre (pictured), said Abedi had looked at him 'with hate' after he gave a sermon criticising ISIS

Mohammed Saeed, the imam of Didsbury Mosque and Islamic Centre (pictured), said Abedi had looked at him ‘with hate’ after he gave a sermon criticising ISIS

ISIS this morning claimed responsibility and threatened further attacks, saying ‘one of the caliphate’s soldiers placed bombs within a gathering of the Crusaders’.

Mohammed Saeed, the imam of Didsbury Mosque and Islamic Centre, said Abedi had looked at him ‘with hate’ after he gave a sermon criticising ISIS and Ansar al-Sharia in Libya in 2015.

He said the vast majority of people at the mosque were with him but a few signed a petition against him, reports the Guardian.

Mr Saeed said: ‘Salman showed me a face of hate after that sermon. He was showing me hatred.’

Forensic officers raid ‘home of Manchester suicide bomber’

Police were seen clutching a 'know your chemicals' manual as they carried out a raid at the property

Police were seen clutching a ‘know your chemicals’ manual as they carried out a raid at the property

He added that a friend was so worried for his safety that he got his adult children to sit beside Amedi in case he attacked the imam.

Police are trying to determine whether Abedi, a former Burnage Boys Academy pupil who appears to have been radicalised within the last couple of years, acted alone or was part of a wider terror cell.

There were unconfirmed reports that the whole family, apart from the two elder sons, recently returned to their native Libya.

It comes as dramatic pictures emerged showing anti-terror police swooping to arrest a 23-year-old man in Manchester over last night’s atrocity.

Abedi grew up in the Whalley Range area of the city, just yards from the school which hit the headlines in 2015 when twins and aspiring medical students, Zahra and Salma Halane, fled their homes and moved to Syria.

He is registered as having lived with his mother Samia Tabbal, father Ramadan, a former airport security worker, and a brother, Ismail, who was born in Westminster in 1993.

Separate pictures show raids at what is believed to have been Abedi’s home in Fallowfield, where a controlled explosion took place, and his brother Ismail’s address, where a 23-year-old man was arrested.

One neighbour claimed they heard Abedi chanting Islamic prayers at the home just weeks before the concert hall atrocity.

Police are urgently trying to work out whether Salman Abedi, who killed 22 last night as thousands of young people were leaving an Ariana Grande concert, was acting alone or whether he was 'part of a network'

Police are urgently trying to work out whether Salman Abedi, who killed 22 last night as thousands of young people were leaving an Ariana Grande concert, was acting alone or whether he was ‘part of a network’

A father carries away his daughter away following the suspected terror attack at the Ariana Grande concert 

A father carries away his daughter away following the suspected terror attack at the Ariana Grande concert

This was the scene inside the Manchester Arena last night after the suspected terror attack at the teen concert

This was the scene inside the Manchester Arena last night after the suspected terror attack at the teen concert

A major police operation is underway this morning to determine whether the suicide attacker who detonated a nail bomb at Manchester Arena last night was part of a terror cell

A major police operation is underway this morning to determine whether the suicide attacker who detonated a nail bomb at Manchester Arena last night was part of a terror cell

Forensic officers were seen emerging from the property carrying a police-issue booklet called ‘Know Your Chemicals’.

Lina Ahmed, 21, told MailOnline: ‘They are a Libyan family and they have been acting strangely.

‘A couple of months ago he [Salman] was chanting the first kalma [Islamic prayer] really loudly in the street. He was chanting in Arabic.

‘He was saying ‘There is only one God and the prophet Mohammed is his messenger’.’

Abedi’s former school friend Leon Hall told MailOnline he saw the killer last year and said he had grown a beard.

He also said the jihadist was a keen Manchester United fan.

Hall, 26, and Abedi lived close to each other in a row of run down terraced houses in the Moss Side area of Manchester.

They later ended up living next door to each other in a nearby street and went to the same school.

Hall said: ‘I saw him last year and he had a beard thing going on. We didn’t speak but just nodded to each other. I don’t remember seeing him with beard before.’

Hall said they grew up playing together on the street around their home.

‘He and I had a tussle many years ago when we were kids. It was over nothing, but he always had a bit of an attitude problem. I can’t say I really liked the man.’

A large police presence, including armed officers, was seen outside an address about a mile from the scene of the arrest

A large police presence, including armed officers, was seen outside an address about a mile from the scene of the arrest

Forensics wearing white suits were called to an address in Greater Manchester after a police operation

Forensics wearing white suits were called to an address in Greater Manchester after a police operation

Hall, who was sat outside his home with his sister, said Abedi was a Muslim.

Other family members at the house, who asked not to be named, confirmed that Abedi was a Muslim.

Hall said:’ I remember that he was a big Man Utd fan. I don’t think he went to the games but would follow them.’

Aerial shots showed police descending on a house in Fallowfield, Manchester as part of the investigation into the bombing massacre last night

Aerial shots showed police descending on a house in Fallowfield, Manchester as part of the investigation into the bombing massacre last night

Abedi, who lived in a housing association owned home about two miles from the scene of Monday night’s terror attack.

He later moved 400 yards away to another terraced home. The area is predominantly occupied by immigrants with many of the terraced homes housing newly arrived immigrants.

The current occupiers of the three-bedroom home where Abedi lived more than a decade ago said they had never met him or his family.

‘They were already gone when we moved in,’ said a woman clutching a small baby.

‘We do not know them and have never spoken to them.’

Abedi is understood to have attended Claremont Primary School a short distance from his home.

Officers are combing CCTV to determine whether the attacker carried out a ‘recce’ of the arena before detonating a nail bomb as thousands were leaving the concert.

The suicide attacker is said to have been ‘known’ to the authorities and anti-terrorist officers are going through hundreds of hours of CCTV footage trying to ‘pick him up’ during his journey to the arena.

Officers also believe that he will have carried out a ‘recce’ to the giant venue in recent days and a separate team are studying footage going back into the past week.

Footage shows officers arresting a 23-year-old man outside a Morrisons supermarket in Chorlton-Cum-Hardy, south Manchester this morning

Footage shows officers arresting a 23-year-old man outside a Morrisons supermarket in Chorlton-Cum-Hardy, south Manchester this morning

Police probing last night's terror attack said a 23-year-old man has been arrested outside a supermarket in south Manchester in connection with the arena massacre

Police probing last night’s terror attack said a 23-year-old man has been arrested outside a supermarket in south Manchester in connection with the arena massacre

Non-uniform anti-terror officers wearing masks to conceal their faces were seen emerging from a Black Mercedes before arresting a man outside a Morrison's in Chorlton

Non-uniform anti-terror officers wearing masks to conceal their faces were seen emerging from a Black Mercedes before arresting a man outside a Morrison’s in Chorlton

Forensic and bomb squad officers are studying the remains of the device recovered so far but initial indications are that the bombmaker had used a ‘level of sophistication’ suggesting he had received training and not made it from ‘a terror recipe’ on the Internet.

One security source told MailOnline: ‘It is unlikely that if the device was sophisticated that the suicide bomber made it – experience shows that organisations are reluctant to ‘waste’ the expertise of a bombmaker in an attack, preferring to keep him or her for another attack.

ISIS WARNS OF MORE ATTACKS

ISIS this morning claimed responsibility for the atrocity in a ranting statement that threatened further attacks on ‘worshippers of the Cross.

‘With Allah’s grace and support, a soldier of the Khilafah managed to place explosive devices in the midst of the gatherings of the Crusaders in the British city of Manchester,’ the statement said.

It added that the massacre was ‘revenge for Allah’s religion… in response to their transgressions against the lands of the Muslims.

‘The explosive devices were detonated in the shameless concert arena.

‘What comes next will be more severe on the worshipers of the Cross and their allies.’

‘It is therefore highly likely that this terrorist is part of a cell or had a support network and they are the priority.

‘Are there other devices, other terrorists out there and you can expect to see raids carried out in the next 48 hours linked to this.’

Detectives are also studying the bomber’s links to Syria or other jihadi hotbeds amid intelligence that he may have travelled abroad to the region.

At least 16 convicted or dead jihadi terrorists are known to have come from a small area of Manchester and several surveillance operations on suspects from the region have been on-going.

Possible links to ISIS-inspired cells involved in the Belgium, Paris and Stockholm attacks are also being examined.

Less than 24 hours after the atrocity ISIS claimed responsibility for the murders.

The extremists were quick to call the killer one of their soldiers, as has become the trend in the wake of many recent attacks in Europe.

According to the SITE Intel Group, which monitors jihadist groups, the ISIS statement described the explosion as having taken place at a ‘shameless concert arena’.

Casualties are stretchered out of the concert on Monday evening after a terror attack in the Ariana Grande concert

Casualties are stretchered out of the concert on Monday evening after a terror attack in the Ariana Grande concert

Police confirm 22 people are now confirmed dead after Manchester attack

They appeared to wrongly state that a number of explosive devices had been detonated, when police have said the attacker was carrying one bomb.

Part of the investigation into what happened is probing whether the killer was acting alone or as part of a network. ISIS has previously encouraged lone wolf attacks against Westerners.

Monday night’s carnage came as a result of a method described by some terror experts as more ‘sophisticated’ than other recent attacks in Europe.

The apparent suicide bombing tactic is markedly different from lone wolf Khalid Masood’s car and knife rampage in Westminster earlier this year.

Theresa May this morning said that police believe they know the identity of the attacker.

Children were among the 22 people killed as the explosion tore through fans leaving the pop concert at about 10.30pm last night.

Some 119 people were also injured in the blast caused by an improvised explosive device carried by the attacker, who was also killed.

Experts say the bomber employed a ‘sophisticated’ method of attack using a a device packed with nuts and bolts, so-called ‘dockyard confetti’, to cause maximum damage.

Former police officer and counter-terrorism expert Chris Phillips described the latest attack to hit the UK as ‘a step up’.

This distressing picture purportedly shows the inside of the arena after the suicide attack at the Ariana Grande concert - its veracity has been confirmed by the two witnesses

This distressing picture purportedly shows the inside of the arena after the suicide attack at the Ariana Grande concert – its veracity has been confirmed by the two witnesses

The identity of the attacker, who was also killed, is not yet known and the deadly blast is being treated as an act of terrorism

The identity of the attacker, who was also killed, is not yet known and the deadly blast is being treated as an act of terrorism

Eight-year-old Saffie Rose Roussos, from Preston, was killed when a suicide bomber let off a nail bomb at a packed pop concert last night

Another victim of the terror attack has been named locally as 18-year-old Georgina Callander. It is feared many children are among those killed, as well as parents who had accompanied their youngsters to the concert or were picking them up

Eight-year-old Saffie Rose Roussos (left), from Preston, and 18-year-old Georgina Callander (right) have been named as victims. It is feared many children are among those killed, as well as parents who had accompanied their youngsters to the concert or were picking them up

He told BBC Radio 4’s Today programme: ‘I think the point is that this was obviously a planned attack and that will involve people looking at the venue and seeing how the venue operates.

‘And also the fact that it sounds like this was a strapped on suicide belt and also from what we just heard, perhaps, with what we call dockyard confetti which is the little bits of nuts and bolts that are attached to the vest.

‘And those unfortunately are there deliberately to kill people and that’s the whole purpose of them. This does look like a step up and my worry, and I think the police’s worry now, is that this person probably wasn’t acting alone and there are other people that to be captured.’

Britain’s terrorist threat level stands at ‘severe,’ the second-highest rung on a five-point scale, meaning an attack is highly likely. Counter-terrorism police have said they are making on average an arrest every day in connection with suspected terrorism.

For the second time in two months, police and security services are embarking on a major terror investigation.

A Twitter account - which was unverified - posted this hours before the attack, warning of a terror attack 
The Twitter account also posted this picture of the ISIS flag with the hashtag 'Manchester Arena' 

A Twitter account – which was unverified – posted this four hours before the attack

Several ISIS-friendly accounts posted the hashtag #ManchesteArena and #ArianaGrande

Several ISIS-friendly accounts posted the hashtag #ManchesteArena and #ArianaGrande

None of the ISIS fan pages have claimed responsibility for last night's terror attack 

None of the ISIS fan pages have claimed responsibility for last night’s terror attack

The bomber is believed to have entered a foyer area of the venue through doors opened to allow young music fans to leave

The bomber is believed to have entered a foyer area of the venue through doors opened to allow young music fans to leave

As with the Westminster atrocity in March, in which five were killed, the most pressing question is whether the individual behind the Manchester blast was a so-called ‘lone wolf’ or part of a wider terror cell.

The working theory is that the perpetrator triggered the blast alone but the national police counter-terror network, assisted by MI5, are urgently piecing together his background to see whether he had any help in planning the outrage.

They will be looking to build a picture of the attacker’s movements both in recent weeks and months as well as immediately before the strike.

Another priority will be to establish whether any further linked attacks or copycat incidents are planned.

It is likely that the bomber’s communications will form a significant part of the inquiry, while investigators will also be checking if he was known to authorities in any way.

One area of focus will be examining the remnants of the device used in the attack as officers work to establish whether the perpetrator built it himself or had help.

As well as seeking to identify any potential accomplices in Britain, authorities will also be looking into the possibility of any link to international groups.

HOW BRITAIN HAS SUFFERED AT THE HANDS OF EXTREMISTS

After Britain as struck by terror again, here are some of the terrible events suffered by the country at the hands of extremists in recent years:

May 22, 2017: Twenty-two people – including children – are killed and around 59 injured during a terrorist bombing at a pop concert in Manchester.

It is thought a lone suicide bomber detonated an improvised explosive device as crowds of music fans, many of them youngsters, left the Manchester Arena following a performance by US artist Ariana Grande.

Concert-goers and witnesses have described the chaos after 'huge bomb-like bangs' went off in Manchester Arena following an Ariana Grande gig

Concert-goers and witnesses have described the chaos after ‘huge bomb-like bangs’ went off in Manchester Arena following an Ariana Grande gig

March 22, 2017: Five people are killed when an Islamist extremist launched a car and knife attack in central London.

Khalid Masood drove a hired car over Westminster Bridge, near the Houses of Parliament, mounted the pavement and hit pedestrians before crashing into railings outside the Palace of Westminster.

He stabbed Pc Keith Palmer, 48, to death and also killed US tourist Kurt Cochran, Romanian tourist Andreea Cristea, 31, plus Britons Aysha Frade, 44, and 75-year-old Leslie Rhodes. Masood was shot dead by police.

June 16, 2016: Labour MP Jo Cox is murdered outside her constituency office in Batley, West Yorkshire.

The mother-of-two, 41, was shot and stabbed multiple times by right-wing extremist Thomas Mair. He was later handed a whole-life prison sentence for her murder.

Fusilier Lee Rigby was murdered by Islamic extremists Michael Adebolajo and Michael Adebowale

Fusilier Lee Rigby was murdered by Islamic extremists Michael Adebolajo and Michael Adebowale

December 5, 2015: A lone attacker attempts to behead a passenger during an ISIS-inspired rampage in the ticket hall of Leytonstone Underground station in east London.

Somali-born Muhiddin Mire targeted strangers at random during the attack on December 5 2015 before slashing fellow passenger Lyle Zimmerman, 56, with a knife.

The schizophrenic was sent to Broadmoor Hospital after being given a life sentence with a minimum term of eight years for attempted murder.

May 22, 2013: Fusilier Lee Rigby is murdered by Islamic extremists Michael Adebolajo and Michael Adebowale.

The 25-year-old serviceman was walking near his barracks in Woolwich, south-eastLondon, when the pair rammed him with his car before attempting to hack off his head with knives.

The killers were jailed for life at the Old Bailey in February 2014.

June 30, 2007: Two men inspired by Islamist extremism ram a 4×4 laden with petrol and propane tanks into the main terminal of Glasgow Airport. One of the attackers died in the incident and five people were injured.

July 7, 2005: Four suicide bombers kill 52 and injure hundreds of others in blasts on the London Underground network and a bus.

Twenty-six died in the bombing at Russell Square on the Piccadilly line, six in the bombing at Edgware Road on the Circle line, seven in the bombing at Aldgate on the Circle line, and 13 in the bombing on a bus at Tavistock Square.

In the first hours after an attack on this scale investigators will be sifting through a number of theories as they work to settle on the most likely lines of inquiry.

There was no immediate claim of responsibility. Supporters of the ISIS, which holds territory in Iraq’s Mosul and around its de facto capital in the Syrian city of Raqqa, celebrated the blast online.

One wrote: ‘May they taste what the weak people in Mosul and (Raqqa) experience from their being bombed and burned,’ according to the U.S.-based SITE Intelligence Group.

Focus will now turn on why Manchester was selected as a target.

It comes two months after a 35-year-old man and a 32-year-old woman were arrested at an address in West Didsbury, Manchester on suspicion of preparation of terrorist acts.

The raids were linked to the Westminster attack that month in which Khalid Masood killed five and injured more than 50 by driving through crowds of tourists.

Earlier this year, Manchester-born jihadi Jamal Al-Harith was killed carrying out an ISIS suicide car bomb attack in Iraq.

Shortly after detonating the explosive-laden car near an army base, ISIS released a statement revealing al-Harith had been fighting for them under the name Abu Zakariya al-Britani.

Leaked ISIS documents later claimed he was recommended to the terror group by Raphael Hostey, a 24-year-old jihadi based in the northern city.

This graphic shows where the explosion took place, in the foyer area, leading towards Victoria railway station 

This graphic shows where the explosion took place, in the foyer area, leading towards Victoria railway station

Hostey is thought to have encouraged dozens of British Muslims to travel to Syria – including close friends Mohammad Azzam Javeed and Anil Khalil Raoufi – before being killed in a drone strike last May.

Last year, two British brothers from Manchester were killed fighting for ISIS in Syria.

Khalif Shariff, 21, and 18-year-old Abdulrahman are understood to have left their home in the city and travelled to the war-torn country in November 2014.

In 2015, Pakistani student Abid Naseer was convicted in a U.S. court of conspiring with al Qaeda to blow up the Arndale shopping centre in the centre of Manchester in April 2009.

In September, a Manchester florist was stunned after his image was used in an ISIS magazine.

Stephen Leyland, 64, was interviewed by counter-terrorism police after a photograph of him standing next to flowers was used in the Rumiyah publication.

The ranting 38-page magazine was one of many pieces of propaganda aimed at encouraging violence in the West.

It called for attacks on Britons and urged supporters of the terror group to take ‘even the blood of a merry Crusader citizen selling flowers to passersby’.

Two months later, fanatics urged lone-wolf attackers to ‘open the door to jihad’ in a video showing how to make a bomb and decapitate people.

Greater Manchester Police chief constable Ian Hopkins revealed the suicide bomber 'was carrying an improvised explosive device'

Greater Manchester Police chief constable Ian Hopkins revealed the suicide bomber ‘was carrying an improvised explosive device’

Forensics have been called in to examine the scene as police attempt to identify the attacker

Forensics have been called in to examine the scene as police attempt to identify the attacker

The instructional video, called ‘Explanation of How to Slaughter Disbelievers’, featured a balaclava-wearing terrorist in a kitchen explaining how to make bombs.

According to the terror monitoring group SITE, the bomb expert took viewers on a step-by-step guide on how to make deadly explosives.

Approximately 850 people from the UK have travelled to support or fight for jihadist organisations in Syria and Iraq, according to British authorities.

About half have since returned to the UK, with more than 100 people having been convicted foroffences relating to the conflict.

Former global terrorism operations director at MI6, Richard Barrett, said, while the attack was more sophisticated than recent ones, it does not automatically mean the person responsible was trained abroad to carry out the massacre.

He told Today: ‘I think people can build bombs, we have seen that in the past that it may be not that complicated to build a bomb which has an effect on the people immediately around you as this one certainly did.

‘Yeah, sure that’s a bit more sophisticated clearly than driving a car into people or stabbing them with a knife but I’m not sure that it requires somebody to go to Syria for example, to have training there to get that sort of expertise so I’m sure the police will be very interested indeed to look at whoever is responsible, what he has been doing over the last months.’

Witnesses reported hearing a 'huge bang' at the venue shortly after US singer Ariana Grande's gig finished

Witnesses reported hearing a ‘huge bang’ at the venue shortly after US singer Ariana Grande’s gig finished

A child was spotted clutching a balloon while wrapped in a foil wrap following the terror attack at the Manchester Arena

A child was spotted clutching a balloon while wrapped in a foil wrap following the terror attack at the Manchester Arena

Concert-goers helped injured people away from the gig last night. Witnesses describe the scene as 'like a warzone'

Concert-goers helped injured people away from the gig last night. Witnesses describe the scene as ‘like a warzone’

This photo shows the aftermath of the suicide bomb which ripped through the foyer of the venue killing parents and children

This photo shows the aftermath of the suicide bomb which ripped through the foyer of the venue killing parents and children

He said the security services face a ‘real challenge’ in monitoring potential threats and said investigations must involve ‘engagement’ with communities.

He said: ‘I think in terms of additional security it’s much more on that intelligence side, on engagement with the community, on trying to understand better why people do this sort of thing than it is on putting up more bollards or, as you say, moving the choke point of security just a bit further away.’

He described the attack, targeted at concert-goers including children, as ‘very, very cynical’.

He added: ‘That is why it is so important to understand, I think, whether this person was connected with other people, whether it was in some way directed by an organised group.

‘What was the intention behind it, in the broader strategic sense?’

The Manchester attack was the deadliest in Britain since four suicide bombers killed 52 London commuters on three subway trains and a bus in July 2005.

Pop concerts and nightclubs have been a terrorism target before. Almost 90 people were killed by gunmen inspired by ISIS at the Bataclan concert hall in Paris during a performance by Eagles of Death Metal in November 2015.

In Turkey, 39 people died when a gunman attacked New Year’s revelers at the Reina nightclub in Istanbul.

Manchester was hit by a huge Irish Republican Army bomb in 1996 that leveled a swath of the city center. More than 200 people were injured, though no one was killed.

http://www.dailymail.co.uk/news/article-4534224/Security-agents-know-Ariana-Grande-concert-bomber-s-name.html#ixzz4hwHwxSJE

Story 2: Budget Director Mulvaney Presents President Trump’s Fiscal Year 2018 U.S. Federal Budget —  Taxpayers First Budget — Videos

Image result for trump budget proposalImage result for Tax Payer first budgetImage result for Tax Payer first budgetImage result for Tax Payer first budgetImage result for trump budget proposal

Image result for trump budget proposal

Mulvaney: Trump’s Budget Puts Taxpayers First

Mulvaney Explains Trump Budget—Cuts For Poor, More For Military – Full Event

Trump’s new budget proposal: What’s in and what’s out

BREAKING Trump Just Cut Off Food Stamps For 2 MASSIVE Groups…Americans Are CHEERING! – News

Chuck Todd DESTROYS OMB DIR. MICK MULVANEY FOR TRUMP’S UNBALANCED BUDGET

Heritage Experts Analyze Trump’s Budget

May 23rd, 2017

Today, the Trump administration officially unveiled their first complete budget proposal called “A New Foundation for American Greatness.” Below is reaction from Heritage experts on the president’s plans:

Balancing the Budget

The president’s budget seeks to balance in no more than 10 years. This is a laudable and important goal that fiscal conservatives should keep their eye on. The budget does this in part with sensible mandatory spending reforms to Medicaid, welfare and disability programs. This budget proposal also follows the right approach on discretionary spending, by prioritizing national defense in a fiscally responsible way, with offsetting cuts to domestic programs that are redundant, improper, or otherwise wasteful. As is so often the case, however, the devil is in the details. Long-term budget solvency must include reforms to the largest entitlement programs: Medicare and Social Security. These programs alone consume 4 of every 10 federal dollars, and they are expanding. Moreover, this budget would rely on $2 trillion in economic feedback effects for deficit reduction, a figure that is highly uncertain. Greater spending cuts would have lent more fiscal credibility. Overall, this budget takes important strides toward cutting the federal government down to size.” —Romina Boccia, Deputy Director of the Thomas A. Roe Institute for Economic Policy Studies and the Grover M. Hermann fellow in federal budgetary affairs

Defense

“Though the White House is right to call for more, much-needed defense funding, $603 billion represents only a $16.8-billion increase from the Obama administration’s meager planned defense spending for 2018. A $603 billion budget for 2018 might be enough to stop the immediate deterioration and cuts in forces, but it will certainly not be enough to reverse the ravages already experienced. Perhaps the most heartening thing about this request is the administration’s follow-through on its expressed intent to repeal the defense budget caps set by the Budget Control Act of 2011, which have been both disruptive and destructive to military readiness.

The U.S. military—in both size and readiness—has shrunk to historically low levels, all while its budget has been held hostage to domestic policy whims.  Naysayers downplay the poor state of the military. But those who deny the existence of readiness problems are contradicted by the repeated testimony of dozens of senior uniformed and civilian military leaders. Those leaders uniformly agree that today’s military is desperately overtaxed and under-resourced. As the Heritage Foundation’s Index of U.S. Military Strength reports, today our armed forces would be severely challenged to execute our defense strategy with the current force.

The Heritage Foundation has proposed a 2018 funding level of $632 billion. It includes proposals for defense reform and savings to help restore our military’s strength and punch. Lawmakers finally need to demonstrate that they take the duty to provide for the common defense quite seriously. Lip service is not enough. We must begin to provide our men and women in uniform the equipment and resources they need to defend our country. Congress must hear and heed the Pentagon’s candid voice in the upcoming budget debates. And lawmakers must then act to begin rebuilding our depleted military now.” —Thomas Spoehr, Director of Heritage’s Center for National Defense

Transportation and Infrastructure

“The administration’s budget contains a number of laudable transportation and infrastructure proposals that reform wasteful or improper programs while empowering states and the private sector to meet the nation’s burgeoning transportation needs. Many of the reforms were recommended by the Heritage Foundation in its roadmap for $1.1 trillion in infrastructure investment and Blueprint for Balance, including: structural reform of our outdated Air Traffic Control system; reforming the wasteful Essential Air Service program; and auctioning off valuable spectrum for private use. Also encouraging is the proposal to reform the financing of the nation’s inland waterways infrastructure, which has long required modernization.

“However, many questions about the Administration’s signature infrastructure proposal remain. Worrisomely, the budget includes an additional $200 billion in spending as a placeholder for ‘private/public infrastructure investment’ with few details as to how the funds will be allocated. Details regarding the plan and whether they will be offset with meaningful cuts elsewhere will be crucial in evaluating the plan and ensuring a repeat of the 2009 stimulus boondoggle is avoided. In addition, the Budget includes a proposal to assume Highway Trust Fund spending levels fall to revenue levels—a savings of $15 billion to $20 billion per year. While limiting trust fund spending to revenues would be excellent policy, it is highly unlikely Congress will decide to rein in its overspending out of the Highway Trust Fund, which it has carried on for nearly 10 years. Simply assuming these savings will accrue without putting forward a substantive proposal to ensure that Congress stops its mismanagement of the trust fund would represent a nearly $100 billion budget gimmick and cannot be considered to have a real budgetary impact.

“While the Budget contains many worthwhile reforms, more details regarding the administration’s infrastructure proposal are required in order to form a comprehensive evaluation of the administration’s infrastructure agenda.” —Michael Sargent, Policy Analyst in Heritage’s Institute for Economic Freedom and Opportunity

Education

“The Trump administration’s full budget for education for FY 2018 would make some long-overdue cuts at the Department of Education, eyeing reductions in spending totaling $9.2 billion – a 13.6 percent cut in the agency’s current $68 billion annual budget. That type of reduction signals a serious commitment to reducing federal intervention in education – a necessary condition to make space for a restoration of state and local control.” —Lindsey Burke, Director of Heritage’s Center for Education Policy

Healthcare

“If enacted, the President’s budget would be a major down payment on federal entitlement reform. It cannot be overemphasized that analysts and economists, often of very different political persuasions, are united in their conviction that policymakers must take decisive steps to slow the growth of federal entitlement spending. By putting Medicaid on a budget—either through a fixed allotment to the states in the form of a block grant or a per capita cap—the Trump budget would give state officials much needed flexibility in managing the program and better target services to the poorest and most vulnerable of our citizens.” —Robert Moffit, Senior Fellow in Heritage’s Center for Health Policy Studies.

Tax Reform

“A month ago President Trump proposed a true tax cut for the American people. The President’s Budget assumes economic growth will make up the lost revenue, after including revenue reductions from Obamacare repeal. The budget proposal does not spell out exactly how the new tax code would accomplish this. The feasibility of the assumed three percent annual growth rate is highly dependent on the ultimate design of tax, regulatory, and other reforms – but we should continue to be optimistic that the economy is indeed able to sustain such growth. Regardless, updating the tax code while lowering tax rates for all Americans does not need to rely so heavily on economic growth. In combination with spending cuts, President Trump and Congress can provide tax and spending relief for the American people.” —Adam Michel, Policy Analyst in Heritage’s Thomas A. Roe Institute for Economic Policy Studies

Border Security 

“Given the intentional neglect towards border security that was a hallmark of the Obama administration, this additional funding that will improve physical security, as well as increase the technology, agents, officers, and equipment needed to actually enforce our immigration laws and secure the border, should be rapidly approved by Congress.”  —Hans von Spakovsky, Senior Legal Fellow in Heritage’s Edwin Meese III Center for Legal and Judicial Studies

GDP Projections

“The president’s budget includes very optimistic economic growth projections, which are a key ingredient in getting the debt under control and reaching budget balance by 2027. The growth projections have two flaws and one strength.

“The first flaw is that the Congressional Budget Office’s baseline—the rate of growth expected with no change to policy—is probably too optimistic to begin with. CBO has been forced to lower its future growth forecast every year since 2009. The second flaw is that the plan expects the president’s policies to sustain growth rates at the outer limit of pro-market optimism despite unfavorable demographics.

“The president’s economic projections do have a major data point in their favor: they represent a return toward the long-run trend in per capita GDP. That deviation from trend is partly to blame on the stultifying economic policies of the previous decade. Removing those constraints will be the first step in restoring the income growth to which Americans are long accustomed. With the right policies, 3 percent real GDP growth could be within the realm of the feasible. It would certainly be desirable.

“A restoration of growth will not, however, follow automatically from enacting the president’s agenda. A lot of other things have to go right as well as policy. So the president’s plan to eliminate the deficit and control the debt should not depend so much on things outside his control. Limiting the growth of entitlement spending would be a more certain path to balance than relying on historical forces.” —Salim Furth, Research Fellow in macroeconomics in Heritage’s Center for Data Analysis

http://www.heritage.org/budget-and-spending/commentary/heritage-experts-analyze-trumps-budget

Trump 2018 Budget Puts Tax Reform In Jeopardy

Federal taxes, spending, deficits, debt and politics.

The Trump fiscal 2018 budget that was released last night was a huge missed opportunity by the administration to switch from campaigning to governing. The Trump budget has next-to-no chance of being adopted or implemented by Congress, makes a government shutdown this fall far more likely and puts tax reform in serious jeopardy.

The Trump 2018 budget clearly is designed to appeal to no one but the Trump base. Not only does it make no effort to broaden interest in and support for the president’s program, but the budget’s extremely harsh spending cuts are almost certain to make opposition from both Democrats and moderate Republicans much, much easier.

This enhanced, enthusiastic and self-assured Democratic and Republican resistance to the Trump budget will greatly complicate congressional efforts to pass a fiscal 2018 budget resolution that were problematic even before the president submitted his plan.

Yes, the Trump budget will appeal to the House Freedom Caucus. Indeed, rather than having the work done in house, the White House seems to have outsourced its budget to the HFC and it’s budget philosophy.

But the HFC-preferred spending proposals that on the surface so appeal to the Trump base (let’s see how these voters feel when they realize how many of these cuts will affect them personally) will be eagerly opposed en masse by House Democrats. That will once again put GOP moderates — who after repeal and replace, the Comey firing and the president’s dwindling approval numbers are increasingly nervous about their reelection — in the position to determine whether the House can pass a budget resolution.

But if the Trump budget is any indication, it’s not clear that the White House or HFC will be willing to deal to comply with what the moderates will want.

Even if the House did manage to adopt a budget resolution with the extreme proposals in the Trump budget, that is almost certain to be opposed by enough Senate Republicans and all Senate Democrats to make passage in that house impossible. The Senate leadership then would have to choose between no budget resolution this year or developing a more restrained budget that its members could support.

No budget resolution would be a huge problem because it would prevent the use of the no filibuster reconciliation rules for tax reform (Reconciliation can only happen if a Congress adopts a budget resolution with reconciliation instructions). That may make a much more moderate budget resolution with far fewer (as in almost none) spending cuts the only way to move tax reform forward.

But that type of budget resolution would be a total repudiation of the Trump 2018 budget and yet another huge defeat for the White House. Although he won’t be able to veto the budget resolution to stop the legislative rout, Trump could retaliate by vetoing any fiscal 2018 appropriations that reflect Congress’s rejection of his spending priorities. Given that there’s not likely to be enough votes to override those vetoes, one, several or all federal agencies and departments could be forced to shut down this fall.

This situation would have been completely different had Trump chosen to govern rather than campaign and submitted a 2018 budget that reflected political realities instead of political arrogance. Had that happened, the budget would have been hailed as the start of a cooperative effort between the White House and Congress that showed Trump as a political and legislative force.

Instead, by the end of this week, the Trump 2018 budget is very likely to be nothing more than a political artifact that will have accomplished nothing.

https://www.forbes.com/sites/stancollender/2017/05/23/trump-2018-budget-puts-tax-reform-in-jeopardy/#5c49685e4e29

Story 3: Where is The Evidence of Collusion, Conspiracy, or Coordination Between Russians and Trump Campaign? and Where is The Evidence of Collusion, Conspiracy, or Coordination Between Foreign Governments and Clinton Campaign and Clinton Foundation? — Videos

Trey Gowdy Questions Former CIA Director John Brennan!

EVERY Trey Gowdy Question To John Brennan During Russia Interference Hearing 5/23/17

Brennan stopped short of describing Russia collusion

“Russians Have Purchased Influence from Democrats” – Newt Gingrich on Russian Democrat Connection

The Clinton Foundation Scandal Explained

Gingrich: Hillary Clinton can’t come to grips with reality

FOX’s James Rosen: FBI Sources Confirm ‘Public Corruption Case’ Against Clinton Foundation

Fox: FBI “Actively And Aggressively” Probing Clinton Foundation Corruption, “A Lot” Of Evidence

Woodward On Clinton Foundation “It’s Corrupt”

Clinton Foundation Scandal – Hillary Clinton Public Corruption – Andrew Napolitano – Stuart Varney

Published on Aug 10, 2016

Clinton Foundation Scandal – Hillary Clinton Public Corruption – Judge Andrew Napolitano – Stuart Varney

Foreign Donors Buying Political Influence Through The Clinton Global Initiative?

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Pronk Pops Show 830: February 2, 2017

Pronk Pops Show 829: February 1, 2017

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Story 1: President Trump: no collusion between me and my campaign and the Russians — Videos —

President Donald Trump: James Comey Is ‘A Showboat’ (Excerpt) | NBC Nightly News

President Trump Full Interview with Lester Holt NBC 5/11/17

Napolitano: Many FBI agents felt demeaned by Comey’s actions

Trump Interview With Lester Holt: President Asked Comey If He Was Under Investigation

President Donald Trump, in an exclusive interview Thursday with NBC News’ Lester Holt, called ousted FBI chief James Comey a “showboat” and revealed he asked Comey whether he was under investigation for alleged ties to Russia.

“I actually asked him” if I were under investigation, Trump said, noting that he spoke with Comey once over dinner and twice by phone.

“I said, if it’s possible would you let me know, ‘Am I under investigation?’ He said, ‘You are not under investigation.'”

“I know I’m not under investigation,” Trump told Holt during the 31-minute White House interview.

It would be highly unusual for someone who might be the focus of an FBI probe to ask whether he was under investigation and to be directly told by the FBI director that he was not.

Tune into NBC Nightly News at 6:30 p.m. ET to see more of Holt’s exclusive interview with Trump.

 

I Was Going to Fire Comey Anyway, Trump Tells Lester Holt in Interview 2:34

The president also reiterated his claim that he had been planning to fire Comey even before he received Deputy Attorney General Rod Rosenstein’s recommendation to do so.

“He’s a showboat, he’s grandstander, the FBI has been in turmoil,” Trump said of Comey in his wide-ranging interview with Holt. “You know that, I know that. Everybody knows that. You take a look at the FBI a year ago, it was in virtual turmoil, less than a year ago. It hasn’t recovered from that.”

Trump said he never tried to pressure Comey into dropping the FBI probe of the Trump campaign and insisted, “I want to find out if there was a problem in the election having to do with Russia.”

Asked by Holt if by firing Comey he was trying to send a “lay off” message to his successor, Trump said, “I’m not.”

“If Russia did anything, I want to know that,” he said.

But Trump also insisted there was no “collusion between me and my campaign and the Russians.”

“Also, the Russians did not affect the vote,” he said.

Holt’s interview with the president came as Washington was still reeling over Trump’s removal of Comey on Tuesday. And Trump’s revelation that he would have fired Comey even without Rosenstein’s input was not what his top officials had told reporters earlier this week.

White House Deputy Press Secretary Sarah Huckabee Sanders explained Thursday that she had spoken with the president on Tuesday night and didn’t ask him directly if he’d already made the decision to terminate Comey before seeing the Rosenstein memo, which she had earlier told reporters was the reason Trump ousted the FBI chief.

But Trump, in his talk with Holt, also contradicted Vice President Mike Pence’s account of how his boss came to his decision to fire Comey on the recommendation of Attorney General Jeff Sessions and Rosenstein.

When asked if Pence too had been kept in the dark, Sanders retorted “nobody was in the dark” and accused the media of creating a “false narrative.”

Play

 

WH: Trump Asking Comey About Investigation Not Inappropriate 0:37

On Wednesday, Trump claimed he canned Comey because “he was not doing a good job” and the White House on cited the FBI chief’s handling of the Hillary Clinton email investigation as the reason they were firing the veteran G-man.

The Democrats, many of whom believe that Comey’s intrusion into the election helped Trump win the presidency, immediately denounced the move and called for the appointment of a special prosecutor as New York Senator Charles Schumer suggested a “cover-up” was underway.

“The timing of Director Comey’s dismissal to me and many committee members on both sides of the aisle is especially troubling,” Senator Mark Warner, a Virginia Democrat, said Thursday at the opening of a Senate Intelligence Committee hearing.

“He was leading an active counterintelligence investigation into any links between the Trump campaign and the Russian government or its representatives, and whether there was any coordination between the campaign and Russia’s efforts to interfere in our election,” he said.

Asked whether he agreed that Comey was “showboat,” Senator Richard Burr (R-North Carolina) called him “one of the most ethical, upright, straightforward individuals I’ve had the opportunity to work with.”

“Sure there were FBI employees that disagreed with how he handled the Clinton email announcements,” Burr said. “The lion share of FBI employees respect the former director and it shows the professionalism that he brought to the role that he was in.”

http://www.nbcnews.com/news/us-news/trump-reveals-he-asked-comey-whether-he-was-under-investigation-n757821

Story 2: Democrats and Big Lie Media Having Nervous Breakdown Over President Trump Firing of Comey — Trump Derangement Syndrome Exposes Phony Hypocrites — ‘They’re coming to take me away’ — My Ding-A-Ling — Videos —

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Liberal Left SPIN Comey Firing by Trump! Political Hypocrisy & Media BIAS! GOWDY for FBI Director

Comey’s Firing Exposes Massive Hypocrisy

Trump defends firing Comey amid Democratic backlash

Maxine Waters Flips Her Wig After Confronted About Comey Flip-Flop

NBC Reporter Takes Maxine Waters to Task on Comey Hypocrisy

Sarah Huckabee Sanders Lists all the Democrats’ Flip-Flops on Comey

WHITE HOUSE Points Out Hypocrisy With Democrats And Firing Of James Comey (FNN)

Conway: Democrats trashed Comey then made him a martyr

Ari Fleischer: Hypocrisy from Democratic Party is appalling

Michelle Malkin: Hypocrisy over Comey firing is overwhelming

Gingrich: Liberals will move on to Martian conspiracies next

Acting FBI Director There Has Been No Effort To Impede The FBI’s Work To Date

Washington Post Rosenstein was asked to write up the justification for Comey’s firing by Trump

Trump Derangement Syndrome

Mark Levin: Schumer is undermining the Constitution

Dr. Gorka: Comey’s last testimony was the ‘last straw’

Democrats Hated James Comey Until Donald Trump Fired Him, And Now They Are His Defense Attorneys

“How The HELL Would You KNOW That??” Tucker Rips Journalist for Comey Hysteria

Napoleon XIV: ‘They’re coming to take me away’

Allan Sherman – Hello Muddah Hello Faddah (1963)

Chuck Berry – My Ding-A-Ling (1972)

CHUCK BERRY LYRICS

“My Ding-A-Ling”

When I was a little bitty boy
My grandmother bought me a cute little toy
Silver bells hanging on a string
She told me it was my ding-a-ling-a-ling, ohMy ding-a-ling, my ding-a-ling
I want you to play with my ding-a-ling
My ding-a-ling, my ding-a-ling
I want you to play with my ding-a-ling You know, then mama took me to Sunday school
They tried to teach me the golden rule
Everytime that choir would sing
Watch me playin’ with my ding-a-ling-a-ling, oh My ding-a-ling, my ding-a-ling
I want you to play with my ding-a-ling
My ding-a-ling, my ding-a-ling
I want you to play with my ding-a-ling Once I was climbing the garden wall
I slipped and had a terrible fall
I fell so hard, I heard bells ring
But held on to my ding-a-ling-a-ling, oh My ding-a-ling, my ding-a-ling
I want you to play with my ding-a-ling
My ding-a-ling, my ding-a-ling
I want you to play with my ding-a-lingOnce, I was swimmin’ ‘cross Turtle Creek
Man, them snappers all around my feet
Sure was hard swimmin’ ‘cross that thing
With both hands holdin’ my ding-a-ling-a-ling, ohMy ding-a-ling, my ding-a-ling
I want you to play with my ding-a-ling
My ding-a-ling, my ding-a-ling
I want you to play with my ding-a-lingThis little song, it ain’t so sad
The cutest little song you ever had
Those of you who will not sing
You must be playin’ with your own ding-a-lingMy ding-a-ling, my ding-a-ling
I want you to play with my ding-a-ling
My ding-a-ling, my ding-a-ling
I want you to play with my ding-a-lingYour own ding-a-ling, your own ding-a-ling
We saw you playin’ with your own ding-a-ling
My ding-a-ling, everybody sing
I wanna play with my ding-a-ling
I wanna play with my ding-a-ling

Inside Trump’s anger and impatience — and his sudden decision to fire Comey

Here’s what happened after Trump fired Comey

Democrats expressed outrage, Trump issued defiant tweets. (Video: Bastien Inzaurralde, Jayne Orenstein, Alice Li, Libby Casey, Priya Mathew/Photo: Jabin Botsford/The Washington Post)
Every time FBI Director James B. Comey appeared in public, an ever-watchful President Trump grew increasingly agitated that the topic was the one that he was most desperate to avoid: Russia.

Trump had long questioned Comey’s loyalty and judgment, and was infuriated by what he viewed as the director’s lack of action in recent weeks on leaks from within the federal government. By last weekend, he had made up his mind: Comey had to go.

At his golf course in Bedminster, N.J., Trump groused over Comey’s latest congressional testimony, which he thought was “strange,” and grew impatient with what he viewed as his sanctimony, according to White House officials. Comey, Trump figured, was using the Russia probe to become a martyr.

Back at work Monday morning in Washington, Trump told Vice President Pence and several senior aides — Reince Priebus, Stephen K. Bannon and Donald McGahn, among others — that he was ready to move on Comey. First, though, he wanted to talk with Attorney General Jeff Sessions, his trusted confidant, and Deputy Attorney General Rod J. Rosenstein, to whom Comey reported directly. Trump summoned the two of them to the White House for a meeting, according to a person close to the White House.

The president already had decided to fire Comey, according to this person. But in the meeting, several White House officials said Trump gave Sessions and Rosenstein a directive: to explain in writing the case against Comey.

The pair quickly fulfilled the boss’s orders, and the next day Trump fired Comey — a breathtaking move that thrust a White House already accustomed to chaos into a new level of tumult, one that has legal as well as political consequences.

Rosenstein threatened to resign after the narrative emerging from the White House on Tuesday evening cast him as a prime mover of the decision to fire Comey and that the president acted only on his recommendation, said the person close to the White House, who spoke on the condition of anonymity because of the sensitivity of the matter.

Justice Department officials declined to comment.

The stated rationale for Comey’s firing delivered Wednesday by principal deputy White House press secretary Sarah Huckabee Sanders was that he had committed “atrocities” in overseeing the FBI’s probe into Hillary Clinton’s use of a private email server as secretary of state, hurting morale in the bureau and compromising public trust.

“He wasn’t doing a good job,” Trump told reporters Wednesday. “Very simple. He wasn’t doing a good job.”

But the private accounts of more than 30 officials at the White House, the Justice Department, the FBI and on Capitol Hill, as well as Trump confidants and other senior Republicans, paint a conflicting narrative centered on the president’s brewing personal animus toward Comey. Many of those interviewed spoke on the condition of anonymity in order to candidly discuss internal deliberations.

Trump was angry that Comey would not support his baseless claim that President Barack Obama had his campaign offices wiretapped. Trump was frustrated when Comey revealed in Senate testimony the breadth of the counterintelligence investigation into Russia’s effort to sway the 2016 U.S. presidential election. And he fumed that Comey was giving too much attention to the Russia probe and not enough to investigating leaks to journalists.

The known actions that led to Comey’s dismissal raise as many questions as answers. Why was Sessions involved in discussions about the fate of the man leading the FBI’s Russia investigation, after having recused himself from the probe because he had falsely denied under oath his own past communications with the Russian ambassador?

Why had Trump discussed the Russia probe with the FBI director three times, as he claimed in his letter dismissing Comey, which could have been a violation of Justice Department policies that ongoing investigations generally are not to be discussed with White House officials?

And how much was the timing of Trump’s decision shaped by events spiraling out of his control — such as Monday’s testimony about Russian interference by former acting attorney general Sally Yates, or the fact that Comey last week requested more resources from the Justice Department to expand the FBI’s Russia probe?

In the weeks leading up to Comey’s firing, Trump administration officials had repeatedly urged the FBI to more aggressively pursue leak investigations, according to people familiar with the discussions. Administration officials sometimes sought to push the FBI to prioritize leak probes over the Russia interference case, and at other times urged the bureau to investigate disclosures of information that was not classified or highly sensitive and therefore did not constitute crimes, these people said.

Over time, administration officials grew increasingly dissatisfied with the FBI’s actions on that front. Comey’s appearances at congressional hearings caused even more tension between the White House and FBI, as Trump administration officials were angered that the director’s statements increased, rather than diminished, public attention on the Russia probe, officials said.

In his Tuesday letter dismissing Comey, Trump wrote: “I greatly appreciate you informing me, on three separate occasions, that I am not under investigation.” People familiar with the matter said that statement is not accurate, although they would not say how it was inaccurate. FBI officials declined to comment on the statement, and a White House official refused to discuss conversations between Trump and Comey.

‘Essentially declared war’

Within the Justice Department and the FBI, the firing of Comey has left raw anger, and some fear, according to multiple officials. Thomas O’Connor, the president of the FBI Agents Association, called Comey’s firing “a gut punch. We didn’t see it coming, and we don’t think Director Comey did anything that would lead to this.’’

Many employees said they were furious about the firing, saying the circumstances of his dismissal did more damage to the FBI’s independence than anything Comey did in his three-plus years in the job.

One intelligence official who works on Russian espionage matters said they were more determined than ever to pursue such cases. Another said Comey’s firing and the subsequent comments from the White House are attacks that won’t soon be forgotten. Trump had “essentially declared war on a lot of people at the FBI,” one official said. “I think there will be a concerted effort to respond over time in kind.”

While Trump and his aides sought to justify Comey’s firing, the now-canned FBI director, back from a work trip to Los Angeles, kept a low profile. He was observed puttering in his yard at his home in Northern Virginia on Wednesday.

In a message to FBI staff late Wednesday, Comey wrote: “I have long believed that a President can fire an FBI Director for any reason, or for no reason at all. I’m not going to spend time on the decision or the way it was executed. I hope you won’t either. It is done, and I will be fine, although I will miss you and the mission deeply.”

He added that “in times of turbulence, the American people should see the FBI as a rock of competence, honesty, and independence.”

Sam Nunberg, a former political adviser to Trump, said the FBI director misunderstood the president: “James Comey made the mistake of thinking that just because he announced the FBI was investigating possible collusion between the Russian government and the Trump campaign, he had unfettered job security. In my opinion, the president should have fired Comey the day he was sworn in.”

George Lombardi, a friend of the president and a frequent guest at his Mar-a-Lago Club, said: “This was a long time coming. There had been a lot of arguments back and forth in the White House and during the campaign, a lot of talk about what side of the fence [Comey] was on or if he was above political dirty tricks.”

Dating to the campaign, several men personally close to Trump deeply distrusted Comey and helped feed the candidate-turned-president’s suspicions of the FBI director, who declined to recommend charges against Clinton for what they all agreed was a criminal offense, according to several people familiar with the dynamic.

The men influencing Trump include Roger J. Stone, a self-proclaimed dirty trickster and longtime Trump confidant who himself has been linked to the FBI’s Russia investigation; former New York mayor Rudolph W. Giuliani, a Comey critic who has been known to kibbitz about the ousted FBI director with like-minded law enforcement figures; and Keith Schiller, a former New York police officer who functioned as Trump’s chief bodyguard and works in the West Wing as director of Oval Office operations.

“What Comey did to Hillary was disgraceful,” Stone said. “I’m glad Trump fired him over it.”

In fact, it was Schiller whom Trump tasked with hand-delivering a manila envelope containing the president’s termination letter to Comey’s office at FBI headquarters Tuesday afternoon. Trump’s aides did not appear to know that Comey would be out of the office, traveling on a recruiting trip in California, according to a White House official.

A chaotic response

Within the West Wing, there was little apparent dissent over the president’s decision to fire Comey, according to the accounts of several White House officials. McGahn, the White House counsel, and Priebus, the chief of staff, walked Trump through how the dismissal would work, with McGahn’s legal team taking the lead and coordinating with the Justice Department.

Ivanka Trump, the president’s daughter, and her husband, Jared Kushner — both of whom work in the White House — have frequently tried to blunt Trump’s riskier impulses but did not intervene to try to persuade him against firing Comey, according to two senior officials.

Trump kept a close hold on the process. White House press secretary Sean Spicer and communications director Michael Dubke were brought into the Oval Office and informed of the Comey decision just an hour before the news was announced. Other staffers in the West Wing found out about the FBI director’s firing when their cellphones buzzed with news alerts beginning around 5:40 p.m.

The media explosion was immediate and the political backlash was swift, with criticism pouring in not only from Democrats, but also from some Republicans. Trump and some of his advisers did not fully anticipate the ferocious reaction — in fact, some wrongly assumed many Democrats would support the move because they had been critical of Comey in the past — and were unprepared to contain the fallout.

When asked Tuesday night for an update on the unfolding situation, one top White House aide simply texted a reporter two fireworks emoji.

“I think the surprise of a great many in the White House was that as soon as this became a Trump decision, all of the Democrats who had long been calling for Comey’s ouster decided that this was now an awful decision,” Dubke said. “So there was a surprise at the politicization of Democrats on this so immediately and so universally.”

Trump’s team did not have a full-fledged communications strategy for how to announce and then explain the decision. As Trump, who had retired to the residence to eat dinner, sat in front of a television watching cable news coverage of Comey’s firing, he noticed another flaw: Nobody was defending him.

The president was irate, according to White House officials. Trump pinned much of the blame on Spicer and Dubke’s communications operation, wondering how there could be so many press staffers yet such negative coverage on cable news — although he, Priebus and others had afforded them almost no time to prepare.

“This is probably the most egregious example of press and communications incompetence since we’ve been here,” one West Wing official said. “It was an absolute disaster. And the president watched it unfold firsthand. He could see it.”

Former House speaker Newt Gingrich said Trump bears some responsibility for the turmoil because he kept the decision secret from some key aides.

“You can’t be the quarterback of the team if the rest of the team is not in the huddle,” Gingrich said. “The president has to learn to go a couple steps slower so that everyone can organize around him. When you don’t loop people in, you deprive yourself of all of the opportunities available to a president of the United States.”

For more than two hours after the news broke, Trump had no official spokesman, as his army of communications aides scrambled to craft a plan. By nightfall, Trump had ordered his talkers to talk; one adviser said the president wanted “his people” on the airwaves.

Counselor Kellyanne Conway ventured into what White House aides call “the lions’ den,” appearing on CNN both Tuesday night and Wednesday morning for combative interviews. “Especially on your network, you always want to talk about Russia, Russia, Russia,” Conway told CNN’s Chris Cuomo on Wednesday.

Spicer, meanwhile, threw together an impromptu news conference with reporters in the White House driveway, a few minutes before he taped a series of short television interviews inside the West Wing, where the lighting was better for the cameras. The press secretary stood alongside tall hedges in near darkness and agreed to answer questions with the cameras shuttered.

“Just turn the lights off,” Spicer ordered. “Turn the lights off. We’ll take care of this.”

Devlin Barrett, Jenna Johnson, Damian Paletta and Matt Zapotosky contributed to this report.

https://www.washingtonpost.com/politics/how-trumps-anger-and-impatience-prompted-him-to-fire-the-fbi-director/2017/05/10/d9642334-359c-11e7-b373-418f6849a004_story.html?utm_term=.59036046de08

 Story 3: Reporter/Journalist Jobs Declining Except in Washington D.C. — Videos 

Jim Spanfeller Considers the Decline and Fall of Journalism

Johnny Paycheck – Take This Job and Shove It

In the latest sign that Washington operates in an alternate economy, journalism jobs around the country dove 22 percent in the last 10 years, but they spiked a whopping 38 percent in the nation’s capital, according to a new economic study. What’s more, salaries for Washington journalists rose 7 percent while diving nationally.While 12,000 reporting jobs were eliminated in most markets in the last decade, the Washington journalism market expanded from 2,190 to 3,030. That is more than five journalists for every single House and Senate member.

In New York, by comparison, the drop was historic, from 5,330 jobs in 2005 to just 3,478 in 2015, said the study from Apartmentlist.com.

The study reviewed rents in major cities and showed how rents have spiked while the salaries of reporters hasn’t. That gap may be responsible for the shift by reporters, even award-winning journalists, to better paying public relations.

“Our analysis illustrated that reporter salaries are growing slower than rents in most metros. Nationwide, reporter salaries declined by 7 percent over the past decade while rents increased 9 percent. If this trend continues, publications will struggle to hire and retain talent,” said the report provided to Secrets.

The jobs number was a small part of the study, but a stunning one.

The highlights:

— The number of journalists in the U.S. fell 22 percent over the past decade. In D.C., the number of journalists increased 38 percent during the same period.

— Since 2005, journalists’ salaries fell 7 percent while rents rose 9 percent. In D.C., salaries grew 7 percent more than rents.

— In 2015, there were 3,030 reporters in the D.C. metro, compared with 2,190 ten years prior. Some smaller metros are left with as few as 40 journalists.

— Denver, Atlanta and Phoenix have seen the biggest growth in news jobs in mid-sized cities.

— The 50 state houses have just 1,592 reporters covering them, half of those in Washington.

The report concluded, “The decline in employment of reporters affects metros of all sizes and in all regions, but coverage in smaller metros is affected the most. Large national publications may need to play a role in adding coverage to smaller metros, perhaps sacrificing some depth in DC for greater breadth across the country. As with our teachers, society benefits when reporters can live and work in the communities that they serve, and an increased focus on local coverage can help reduce the divide between rural and urban Americans.”

Paul Bedard, the Washington Examiner’s “Washington Secrets” columnist, can be contacted at pbedard@washingtonexaminer.com

http://www.washingtonexaminer.com/study-media-jobs-salary-soar-38-in-dc-crash-22-nationally/article/2622763

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The Pronk Pops Show 792, November 8, 2016, Story 1:  It’s All Over Now — You Can’t Always Get What You Want and  — You Get What You Need– A Leader: President Elect Donald J. Trump — We Are The Champions — Another One Bites the Dust — Americans Love a Winner — Videos

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Pronk Pops Show 792: November 8, 2016

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Pronk Pops Show 781: October 21, 2016

Pronk Pops Show 780: October 20, 2016

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Pronk Pops Show 777: October 17, 2016

Pronk Pops Show 776: October 14, 2016

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Pronk Pops Show 774: October 12, 2016

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Pronk Pops Show 772: October 10, 2016

Pronk Pops Show 771: October 7, 2016

Pronk Pops Show 770: October 6, 2016

Pronk Pops Show 769: October 5, 2016 

Pronk Pops Show 768: October 3, 2016

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Pronk Pops Show 764: September 27, 2016

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Pronk Pops Show 762: September 23, 2016

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Pronk Pops Show 752: September 9, 2016

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Pronk Pops Show 750: September 7, 2016

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Pronk Pops Show 747: August 31, 2016

Pronk Pops Show 746: August 30, 2016

Pronk Pops Show 745: August 29, 2016

Pronk Pops Show 744: August 26, 2016

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Pronk Pops Show 741: August 23, 2016

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Pronk Pops Show 739: August 18, 2016

Pronk Pops Show 738: August 17, 2016

Pronk Pops Show 737: August 16, 2016

Pronk Pops Show 736: August 15, 2016

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Pronk Pops Show 733: August 9, 2016

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Story 1:  It’s All Over Now — You Can’t Always Get What You Want and  — You Get What You Need– A Leader:  President Elect Donald J. Trump — We Are The Champions — Another One Bites the Dust — Americans Love a Winner — Videos

Image result for images donald trump and freddie mercury we are the championsImage result for images donald trump you get what you need

Image result for cartoons wins is president of united states

Image result for cartoons on trump victory president elect

Image result for cartoons trump wins

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Image result for cartoons wins is president of united statesImage result for trump victory speechImage result for trump victory speechImage result for trump victory speechImage result for trump victory speechImage result for trump victory speech

The Green Papers: 2016 General Election

Donald John Trump, Sr. 290 59,587,143 47.51% American Independent,
Conservative,
Republican
51 (538) 538
Hillary Diane Rodham Clinton 228 59,790,479 47.67% Democratic,
Democratic-Farmer Labor,
Democratic-Nonpartisan League,
Women’s Equality,
Working Families
51 (538) 538

Gary Earl Johnson 4,048,436 3.23% (party left blank on ballot),
Independence,
Independent,
Libertarian
51 (538) 538

Jill E. Stein 1,208,917 0.96% By Petition,
D.C. Statehood Green,
Green,
Green Independent,
Green-Rainbow,
Independent,
Mountain,
Pacific Green,
Progressive,
Unaffiliated,
Write-in
45 (480) 3 (42) 522

    • 82 parties (or designations) running candidates for the Presidency

(Candidates may run under the banner of multiple parties. Hence, the number of parties may be greater than the number of candidates.)

Donald Trump’s acceptance speech after winning the 2016 Presidential election

Hillary Clinton FULL Concession Speech | Election 2016

LIVESTREAM: Election 2016 FULL Results Donald Trump WINS Florida, North Carolina, Ohio

LIVE Stream: Donald J. Trump Victory Party 11/8/16

Donald Trump wins Ohio, CNN projects

Donald Trump FULL SPEECH at FINAL Rally With Mike Pence

Queen – We Are The Champions (Official Video)

QUEEN LYRICS

“We Are The Champions”

I’ve paid my dues
Time after time.
I’ve done my sentence
But committed no crime.
And bad mistakes ‒
I’ve made a few.
I’ve had my share of sand kicked in my face
But I’ve come through.

(And I need just go on and on, and on, and on)

We are the champions, my friends,
And we’ll keep on fighting ’til the end.
We are the champions.
We are the champions.
No time for losers
‘Cause we are the champions of the world.

I’ve taken my bows
And my curtain calls.
You brought me fame and fortune, and everything that goes with it.
I thank you all.
But it’s been no bed of roses,
No pleasure cruise.
I consider it a challenge before the whole human race,
And I ain’t gonna lose.

(And I need just go on and on, and on, and on)

We are the champions, my friends,
And we’ll keep on fighting ’til the end.
We are the champions.
We are the champions.
No time for losers
‘Cause we are the champions of the world.

We are the champions, my friends,
And we’ll keep on fighting ’til the end.
We are the champions.
We are the champions.
No time for losers
‘Cause we are the champions.

Queen – Another One Bites the Dust (Official Video)

Another One Bites the Dust

Queen

Steve walks warily down the street,
With the brim pulled way down low
Ain’t no sound but the sound of his feet,
Machine guns ready to go
Are you ready,
Are you ready for this
Are you hanging on the edge of your seat
Out of the doorway the bullets rip
To the sound of the beat
Another one bites the dust
Another one bites the dust
And another one gone, and another one gone
Another one bites the dust
Hey, I’m gonna get you too
Another one bites the dust
How do you think I’m going to get along,
Without you, when you’re gone
You took me for everything that I had,
And kicked me out on my own
Are you happy, are you satisfied
How long can you stand the heat
Out of the doorway the bullets rip
To the sound of the beat
Another one bites the dust
Another one bites the dust
And another one gone, and another one gone
Another one bites the dust
Hey, I’m gonna get you too
Another one bites the dust
Another one bites the dust
Another one bites the dust
Another one bites the dust
Another one bites the dust
There are plenty of ways you can hurt a man
And bring him to the ground
You can beat him
You can cheat him
You can treat him bad and leave him
When he’s down
But I’m ready, yes I’m ready for you
I’m standing on my own two feet
Out of the doorway the bullets rip
Repeating the sound of the beat
Another one bites the dust
Another one bites the dust
And another one gone, and another one gone
Another one bites the dust
Hey, I’m gonna get you too
Another one bites the dust

Americans Love a Winner

The Rolling Stones – You Can’t Always Get What You Want (TV Show ’69)

The Rolling Stones – You Can’t Always Get What You Want (Live) – OFFICIAL

Rolling Stones – It’s All Over Now (stereo)

The Rolling Stones – Ruby Tuesday (Live) – Official 1991

The Beatles – I’m a Loser

Janis Joplin – Cry Baby (Live)

Queen’s Brian May Does Not Approve of Donald Trump’s Use of “We Are the Champions”

Queen's Brian May Does Not Approve of Donald Trump's Use of

In what some would consider some truly horrifying News of the World, Donald Trump celebrated winning the last wave of U.S. Republican primaries last night (June 7) by walking into a speech backed by Queen’s iconic victory anthem, “We Are the Champions.” Trouble is, the nomination has yet to be fully clinched — not to mention the fact that Queen are kind of bummed about having their old tune dragged into Trump’s campaign.

The musical moment happened last night at New York’s Trump National Golf Club, where the presumptive nominee thanked primary voters who pushed him to the top in New Jersey, New Mexico, South Dakota, Montana and California. Shortly after Trump was accompanied by Queen’s recording of “We Are the Champions,” from 1977’s News of the World, guitarist Brian May made an announcement through his personal webpage that he definitely didn’t give Drumpf the thumbs up to blast the track.

“I’ve had an avalanche of complaints – some of which you can see in our ‘Letters’ page – about Donald Trump using our ‘We Are The Champions’ track as his ‘theme’ song on USA TV,” May wrote.

May added that he was speaking for himself, not the rest of the surviving members of Queen, but further noted that the outfit have long distanced themselves from contributing music to political campaigns. Long story short, Trump shouldn’t have used the late Freddie Mercury’s rally cry on the epic anthem to boost his own cause.

“This is not an official Queen statement, but I can confirm that permission to use the track was neither sought nor given. We are taking advice on what steps we can take to ensure this use does not continue. Regardless of our views on Mr Trump’s platform, it has always been against our policy to allow Queen music to be used as a political campaigning tool. Our music embodies our own dreams and beliefs, but it is for all who care to listen and enjoy.”

Trump has been blasted for using songs without permission before. Last year, R.E.M. told the potential-POTUS to stop using their music in his “moronic charade of a campaign,” while Neil Young had also been involved in a back-and-forth beef over Trump using his “Rockin’ in the Free World.” They later reconciled, with Young allowing Trump to use the tune, despite being at odds with his personal politics.

http://exclaim.ca/music/article/queens_brian_may_doesnt_endorse_donald_trumps_use_of_we_are_the_champions

Rock Legends Pull the Plug on Trump Using ‘We Are The Champions’

 Brian May and Donald Trump

Brian May and Donald Trump | Photo: AFP-Reuters

Published 9 June 2016
Queen joins a long list of artists who have refused to allow Trump to use their music, including the Rolling Stones, Neil Young, R. E. M. and Adele.

The iconic British rock group Queen is trying to stop Donald Trump from using their hit song “We Are The Champions,” lead guitarist Brian May revealed Thursday

RELATED:
Adele is Really, Really Mad at Donald Trump and Here’s Why

The rock star said property tycoon Trump, the presumptive Republican nominee in the U.S. presidential elections, was using the song without permission.

May, 68, said he had received an “avalanche of complaints” about Trump using the anthem during a speech he gave Tuesday.

“Permission to use the track was neither sought nor given. We are taking advice on what steps we can take to ensure this use does not continue,” May wrote on his website.

“It has always been against our policy to allow Queen music to be used as a political campaigning tool.

“Our music embodies our own dreams and beliefs, but it is for all who care to listen and enjoy.”

“We Are The Champions” was written by the group’s late lead singer Freddie Mercury in 1977 and is an enduring celebratory anthem heard at sports events.


Queen join a long list of artists who have refused to allow Trump to use their music, including the Rolling Stones, Neil Young, R. E. M. and Adele.

REM’s Michael Stipe said, “Go fuck yourselves, the lot of you — you sad, attention-grabbing, power-hungry little men. Do not use our music or my voice for your moronic charade of a campaign,” after Trump played “It’s the End of the World as We Know It (and I Feel Fine)” at a rally.

Lawyers for Aerosmith singer Steven Tyler sent a cease and desist letter to Trump’s campaign, saying that his use of the song “Dream On” gives “the false impression that he is connected with, or endorses Mr. Trump’s presidential bid.”

http://www.telesurtv.net/english/news/Rock-Legends-Pull-the-Plug-on-Trump-Using-We-Are-The-Champions-20160609-0049.html

Donald Trump plays ‘You Can’t Always Get What You Want’ after RNC speech

Donald Trump closed the longest GOP presidential acceptance speech in recent times with the Rolling Stones’ “You Can’t Always Get What You Want.”

Trump has featured the track during his campaign, even drawing the ire of the Rolling Stones earlier this year. “The Rolling Stones have never given permission to the Trump campaign to use their songs and have requested that they cease all use immediately,” a spokesperson for the band said in a statement.

Those words, nor the irony of playing “You Can’t Always Get What You Want” during a Republican National Convention that was often quite divided – on Wednesday, for example, Sen. Ted Cruz (R-Texas) refused to endorse Trump from the stage and was summarily booed – was not lost on viewers. Social media exploded after Trump’s speech as the song played, with many mocking the Republican presidential nominee for the song choice.

http://www.ew.com/article/2016/07/22/donald-trump-you-cant-always-get-what-you-want

Several years ago, Rolling Stones’ frontman Mick Jagger disclosed his feelings about then-candidate Mick Romney on an Saturday Night Live episode. Jagger’s approval rating for Romney was a zero.

Adele’s staff recently pushed back when “Rolling in the Deep” and “Skyfall” were used without permission. When Neil Young complained about “Rockin’ in the Free World” being played at a GOP campaign, Trump shot back calling Young a phoney, as the rocker had asked for money to finance a music project. But apparently, raising funds and supporting a candidate are two separate issues for Neil, according to Time.

“I had gone to Donald’s office and asked him to finance my company. He wasn’t running for president at the time. And I thought maybe trying to rescue the art form of recorded sound would be a great thing for his legacy … So I thought I had a shot. It didn’t work out. But he was very gracious.”

The Republican candidate has also used songs by Elton John, added the Daily Beast. His publicist clarified the iconic Elton’s stance on the issue, but the musician clarified that it was nothing personal. He said he met Trump, who was nice to him, but said their political views greatly differ. John explained that he’s far from being a Republican and made a suggestion.

“Why not ask Ted f***ing Nugent? Or one of those f***king country stars? They’ll do it for you.

 http://www.inquisitr.com/2788458/rolling-stones-message-to-donald-trump-you-cant-always-get-what-you-want/#8XolCKDgFgje8AXd.99

 

Why Pollsters Disagree

A Commentary by Fran Coombs

The ultimate outsider is challenging the ultimate insider, and it’s driving the pollsters crazy.

Democrat Hillary Clinton – first lady of both the state of Arkansas and the United States, U.S. senator from New York, secretary of State and a regular in the global halls of power for more than 20 years. She knows what to say and how to say it. While many question what she has accomplished in any of those positions, there’s no doubt that she’s been there and done things. She represents the status quo, and for many Americans, there is comfort in that.

Republican Donald Trump – brash, brusque billionaire businessman from New York City, used to having his way and paying for it. He says what’s on his mind, often to the despair of his political advisors but to the delight of a usually hostile media. Trump thinks America’s going to hell and is ready to upset the applecart to turn things around. His outbursts – indeed, his entire candidacy – defy conventional political wisdom and have put him at odds with the leadership of his own party who question what he really has in mind. But he has millions of loyal followers across party lines that he has dubbed “a movement.”

Throw in allegations that Clinton is a liar and has mishandled classified information and charges that Trump, too, is a liar and a sexual harasser, and you have the most volatile presidential election in decades.

The polling industry is already struggling with the death of the landline telephone and trying to find new ways to compensate for that loss to achieve demographically balanced voter samples. Along comes the craziest election most of us have ever seen.

Consider that just a month ago, many pollsters were saying the election was already over and that Clinton had won. The three daily tracking polls – the Los Angeles Times, IBD/TIPP and Rasmussen Reports – consistently have shown a much tighter race. We’re the ones who add new voters to the existing mix every day and don’t just swoop in for a two- or three-day sample. But many in the media – perhaps most prominently the New York Times – began preparing for a second Clinton administration as if the voters had already spoken.

Yet despite the release of a damning 11-year-old video showing Trump making uncomfortably graphic comments about women, the race began tightening again, even among the pollsters who had previously declared it over. Then in mid-October, the FBI announced it was reopening the investigation of Clinton’s handling of classified information while secretary of State, and the race really began to close. One major pollster went from showing Clinton with a 12-point lead to a two-point race in just over a week. [The FBI on Sunday closed that case again, choosing to bring no charges against Clinton.]

At the same time, polling in the so-called battleground states was and continues to be all over the place. It’s not uncommon to see Clinton up by seven in a state in one poll, while another pollster shows Trump up by four in the same state. The Real Clear Politics averages meld all this together, but unlike in so many other years, there hasn’t been any consistent pattern among pollsters in most states for weeks.

What makes pollsters come up with different results? We can’t explain the formulas they use, but at Rasmussen Reports our demographics are based on historical trends in previous presidential elections, analysis of the new data we collect (we hear from 10,000 new likely U.S. voters every month) and our own political intuition.

With these factors, Rasmussen Reports’ final White House Watch daily tracking poll released yesterday showed Clinton with a 45% to 43% lead, with a +/- 2.5% margin of error.

Just a slight difference in any of these factors, though, explains the differences in polls. Using the same numbers, for example, if we create a model that shows slightly more GOP turnout among men and older voters, with two percent more whites voting Republican, it’s Trump 45%, Clinton 44%.

Those same numbers crunched through a model that shows a few more younger voters and more women turning out for the Democrats despite slightly less white turnout for Clinton still pushes her to a four-point lead.

Same numbers, slightly different formula, different results. It also highlights why turnout of their key demographic groups is so important to both major parties.

Then there’s the potential silent factor: Are voters even telling pollsters the truth? Seventeen percent (17%) of Likely Republican Voters are less likely this year to let others know how they intend to vote compared to previous presidential campaigns. Ten percent (10%) of Likely Democratic Voters say they are less likely to tell.

Make America Great Again vs. stay the course that President Obama has set. Today’s the showdown.

Fran Coombs is the managing editor of Rasmussen Reports.

http://www.rasmussenreports.com/public_content/politics/commentary_by_fran_coombs/why_pollsters_disagree

2016 US election results
Updated Nov 9, 2016 4:31 PM CST
Donald Trump won the presidency
Electoral vote
Popular vote
Clinton

228

Trump

279

59,795,906 votes59,589,136 votes

270 to win

 

Won

Leads

Swing states
All states
Clinton
Trump
Alabama

9 electoral votes
35%
718,084
63%
1,306,925
Alaska

3 electoral votes
38%
92,013
53%
129,786
Arizona

11 electoral votes
45%
888,374
50%
972,900
Arkansas

6 electoral votes
34%
378,729
60%
677,904
California

55 electoral votes
61%
5,481,885
33%
2,965,704
Colorado

9 electoral votes
47%
1,126,384
45%
1,075,770
Connecticut

7 electoral votes
54%
823,360
42%
637,919
Delaware

3 electoral votes
53%
235,581
42%
185,103
District of Columbia

3 electoral votes
93%
260,223
4%
11,553
Florida

29 electoral votes
48%
4,485,745
49%
4,605,515
Georgia

16 electoral votes
46%
1,837,300
51%
2,068,623
Hawaii

4 electoral votes
62%
266,827
30%
128,815
Idaho

4 electoral votes
28%
189,677
59%
407,199
Illinois

20 electoral votes
55%
2,977,498
39%
2,118,179
Indiana

11 electoral votes
38%
1,029,197
57%
1,555,020
Iowa

6 electoral votes
42%
650,790
52%
798,923
Kansas

6 electoral votes
36%
414,788
57%
656,009
Kentucky

8 electoral votes
33%
628,834
63%
1,202,942
Louisiana

8 electoral votes
38%
779,535
58%
1,178,004
Maine

4 electoral votes
48%
352,485
45%
332,591
Maryland

10 electoral votes
61%
1,497,951
35%
873,646
Massachusetts

11 electoral votes
61%
1,964,433
34%
1,082,521
Michigan

16 electoral votes
47%
2,267,373
48%
2,279,210
Minnesota

10 electoral votes
47%
1,363,755
45%
1,321,014
Mississippi

6 electoral votes
40%
462,250
58%
677,782
Missouri

10 electoral votes
38%
1,054,889
57%
1,585,753
Montana

3 electoral votes
36%
174,249
57%
273,696
Nebraska

5 electoral votes
34%
273,858
60%
485,819
Nevada

6 electoral votes
48%
537,753
46%
511,319
New Hampshire

4 electoral votes
48%
346,816
47%
345,379
New Jersey

14 electoral votes
55%
1,979,768
42%
1,516,915
New Mexico

5 electoral votes
48%
380,724
40%
315,875
New York

29 electoral votes
59%
4,143,541
37%
2,637,678
North Carolina

15 electoral votes
47%
2,162,074
51%
2,339,603
North Dakota

3 electoral votes
28%
93,526
64%
216,133
Ohio

18 electoral votes
44%
2,317,001
52%
2,771,984
Oklahoma

7 electoral votes
29%
419,788
65%
947,934
Oregon

7 electoral votes
52%
919,591
41%
725,090
Pennsylvania

20 electoral votes
48%
2,844,705
49%
2,912,941
Rhode Island

4 electoral votes
55%
225,445
40%
165,810
South Carolina

9 electoral votes
41%
849,469
55%
1,143,611
South Dakota

3 electoral votes
32%
117,442
62%
227,701
Tennessee

11 electoral votes
35%
867,110
61%
1,517,402
Texas

38 electoral votes
43%
3,852,923
53%
4,677,115
Utah

6 electoral votes
28%
222,858
47%
375,006
Vermont

3 electoral votes
61%
178,072
33%
95,027
Virginia

13 electoral votes
50%
1,916,845
45%
1,731,155
Washington

12 electoral votes
56%
1,118,772
38%
750,719
West Virginia

5 electoral votes
26%
187,457
69%
486,198
Wisconsin

10 electoral votes
47%
1,382,210
48%
1,409,467
Wyoming

3 electoral votes
22%
55,949
70%
174,248
Election insights
Check back for new insights as results are updated
Clinton won more counties whereless than 50% of the population is white
83.8%
Clinton
16.2%
Trump
Clinton won more counties where at least 45% of the population is African American
85.0%
Clinton
15.0%
Trump
Donald Trump won Wisconsin, which Mitt Romney lost in 2012
Donald Trump won Pennsylvania, which Mitt Romney lost in 2012
Donald Trump won Iowa, whichMitt Romney lost in 2012
Donald Trump won Florida, which Mitt Romney lost in 2012
Donald Trump won Ohio, whichMitt Romney lost in 2012
Sources: AP, Learn More

US election results: The maps and analysis that explain Donald Trump’s shock victory to become President

US election live results and maps
US election live results and maps in the race between Donald Trump and Hillary Clinton

Donald Trump has pledged to be a president “for all Americans” after being elected the 45th President of the United States, capturing crucial victories over Hillary Clinton in a remarkable show of strength.

The president-elect addressed supporters at his victory party in New York City after his Democratic rival Hillary Clinton called him to concede.

While Clinton had a higher share of the popular vote than Trump, the Republican was able to take a series of key battleground states including Florida, Ohio and North Carolina, before stunningly carrying Pennsylvania, a state that had not backed a Republican for president since 1988.

The celebrity businessman clinched victory after capturing Wisconsin’s 10 electoral votes, putting him over the 270 threshold that a candidate needed to secure to become President.

Mr Trump will govern with a Congress fully under Republican control. The GOP fended off a Democratic challenge in the Senate and the party also extended its grip on the House.

Donald Trump’s road to the White HousePlay!03:17

Presidential results maps

The electoral map is important. Each state is worth a certain number of electoral college votes, so it was essential that Trump and Clinton built a coalition of states to reach the magic number of 270.

A series of close Trump wins in crucial states in Florida, Ohio and North Carolina meant that he was able to gain the number of electoral votes he needed.

Our chart below sizes each state by their number of electoral college votes, showing how the big states have the power to tilt the election.

The key states in the election

Swing states with a lot of electoral votes to distribute, such as Florida and Ohio, have been targetted a lot by Clinton and Trump in recent weeks. How they end up voting would have a lot of influence on the final result.

States like Arizona, Florida, North Carolina, Ohio and Virginia have the power to swing the election. All but one of these five crucial states went to Trump.

  • 03:13HOW HILLARY CLINTON LOST THE US PRESIDENTIAL ELECTION
  • 02:00HOW THE WORLD REACTED TO DONALD TRUMP’S PRESIDENTIAL WIN
  • 13:27WATCH: HILLARY CLINTON’S CONCESSION 

Demographics were thought to be of importance here. Before electoral day, polling revealed a country divided down demographic lines. A country where men and whites tend to back Trump, while women and ethnic minorities flock to the Democrat’s candidate.

These demographic splits did come to light to a certain extent, but a key part in Clinton’s failure to claim certain states was the fact that ethnic minorities and women didn’t back her in the numbers initially expected.

Trump has triumphed in Ohio. This reliable bellwether state is worth a very handy 18 electoral college votes but it’s claim to fame is that it is the only one to have backed the successful presidential candidate in every election since 1964.

As such its result is seen as being very significant when determining the outcome of the race nationwide, with polling in Ohio was showing Trump marginally ahead of Clinton at the start of November. Situated on the Great Lakes, it is the seventh most populous state in the country.

Minority ethnic voters hold less sway here, with 83 per cent of the population being white according to the 2010 census compared to 72 per cent across the US as a whole.

Trump has won Florida’s vote for the 2016 presidency, marginally ahead of Clinton. Florida has been one of the hardest to call swing states in this election with the margins between the two candidates in recent polling being too close to call.

A week before the big day, polls were showing that Trump had taken a slight lead in the battle to take the state’s 29 electoral college votes. Florida is at once the oldest and one of the most racially diverse in America, and its voting in the past five presidential races has followed the result of the country as a whole.

Both candidates have had multiple campaign stops here in recent weeks. The state played a pivotal role in the 2000 election, when out of more than 5.8 million votes Bush beat Gore by 537 votes to claim all of its electoral college votes.

Clinton has triumphed in Virginia. Although not quite the boost that a state the size of Florida would give, Virginia’s 13 electoral college votes will be very handy addition for Clinton. Prior to Obama’s victory in 2008, Virginia had been a red state for the past forty years.

Nowadays, one in five of its people are black or African American, part of an increasingly moderate population based in its urban areas.

This shifting of demographics meant that the state was expected to stay Democrat this time around, with polls showing Clinton eight points clear of Trump at the end of October. Situated on the Atlantic coast, Virginia was the first colonial possession established in British America.

North Carolina’s voters have chosen Trump as their preferred presidential candidate. This result will be a blow for Clinton as North Carolina has been one of the toughest states to call in this election. Its 15 electoral college votes means that it is a valuable prize in the race to that all important 270 mark.

North Carolina was highly coveted this year with the candidates making multiple campaign stops there in the fortnight leading up to election day.

While Obama won it in 2008 with the assistance of demographic shifts and liberal urban areas, Romney managed to claim it for the Republicans in 2012 – the only swing state Obama lost in the last presidential election. This southeastern state is the ninth most populous in America and has a lower white population, at 64 per cent, than the average state.

Which states did Trump swing from Obama?

There are at least five states that swung from Obama in 2012 to Trump in 2016: Florida, Ohio, Wisconsin, Pennsylvania and Iowa. All of these were essential battlegrounds that both candidates canvassed hard.

Trump’s biggest victories

Trump’s most emphatic victory has come in the state of Wyoming where he won 174,248 votes – a 70.1 per cent share.

With most votes already counted Trump looks to have secured the votes of at least three in five voters in 10 states while Clinton can only boast the same vote share in five.

Congressional elections

The Senate and the House of Representatives, the two chambers that comprise America’s legislature, also have elections. Both of these chambers were in Republican hands prior to voting.

Senators are being elected in 34 states with the Republicans having a strong chance of holding onto their majority in the chamber.

The Republicans are on course to hold onto the Senate with a slightly reduced majority.

The House of Representatives is held more firmly in Republican hands with their majority of 59 looking very difficult to overturn even if Clinton had had a good day.

All 435 seats in the House were up for re-election with many having already called the result in favour of the republicans.

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The Pronk Pops Show 754, September 13, 2016, Story 1: Name That Malady — Parkinson’s Disease? Multiple sclerosis (MS)? A.L.S. ( Amyotrophic Lateral Sclerosis) or sometimes called Lou Gehrig’s disease? Power Palpitations? — Clue: Blue Sung Glasses! — Videos — Story 2: Clinton Will Power Through — Big Lie Media Lying and Spinning Away For Hillary–Send In The Clowns — There Here — Videos

Posted on September 13, 2016. Filed under: 2016 Presidential Campaign, 2016 Presidential Candidates, Addiction, American History, Blogroll, Breaking News, Bribery, Cartoons, College, Communications, Congress, Constitutional Law, Corruption, Countries, Crime, Culture, Diet, Disasters, Diseases, Donald J. Trump, Donald J. Trump, Donald Trump, Donald Trump, Drugs, Education, Elections, Empires, Employment, Exercise, Food, Foreign Policy, Government, Government Spending, Health, Health Care, High Crimes, Hillary Clinton, Hillary Clinton, Hillary Clinton, History, Homicide, House of Representatives, Human, Human Behavior, Illegal Immigration, Illegal Immigration, Immigration, Impeachment, Iran Nuclear Weapons Deal, Law, Legal Immigration, Life, Lying, Media, Medicare, Movies, Music, News, Philosophy, Photos, Politics, Polls, Progressives, Radio, Raymond Thomas Pronk, Resources, Scandals, Security, Senate, Unemployment, United States Constitution, United States of America, Videos, Violence, War, Wealth, Wisdom | Tags: , , , , , , , , , , , , , , , |

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Story 1: Name That Malady —  Parkinson’s Disease? Multiple sclerosis (MS)? A.L.S. ( Amyotrophic Lateral Sclerosis) or sometimes called Lou Gehrig’s disease? Power Palpitations? — Clue: Blue Sung Glasses! — Videos 

mal·a·dy
ˈmalədē/
noun
  1. a disease or ailment.
    “an incurable malady”
    synonyms: illness, sickness, disease, infection, ailment, disorder, complaint, indisposition, affliction,infirmity, syndrome;

    informalbug, virus
    “every time we visit Jerry, he has a new malady”

“Power tends to corrupt, and absolute power corrupts absolutely. .”

~John Emerich Edward Dalberg-Acton, 1st Baron Acton

Image result for cartoons hillary clinton health problems medical condition~

Hillary's dramatic collapse in New York on Sunday  is prompting new examination of her health ¿ as well as how her aides have closely guarded information

Image result for cartoons hillary clinton health problems medical condition

 

Image result for cartoons hillary clinton falling down

Image result for cartoons hillary clinton falling down

 

Image result for cartoons hillary clinton health problems medical condition

Image result for cartoons hillary clinton health problems medical condition

Image result for Hillary for President CartoonsImage result for cartoons hillary clinton health problems medical condition

 

Kids Singing About Disease

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Z1 F133 protective prism blue Seizure filter lens Vox Day Theodore Beale Drew Pinsky Ted Noel

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Bill Clinton weighs in on Hillary’s health

Dr. Drew: Hillary Has “Brain Damage”

Judy Collins Send in the Clowns

Isn’t it rich?
Are we a pair?
Me here at last on the ground,
You in mid-air..
Where are the clowns?

Isn’t it bliss?
Don’t you approve?
One who keeps tearing around,
One who can’t move…
Where are the clowns?
Send in the clowns.

Just when I’d stopped opening doors,
Finally knowing the one that I wanted was yours.
Making my entrance again with my usual flair
Sure of my lines…
No one is there.

Don’t you love farce?
My fault, I fear.
I thought that you’d want what I want…
Sorry, my dear!
And where are the clowns
Send in the clowns
Don’t bother, they’re here.

Isn’t it rich?
Isn’t it queer?
Losing my timing this late in my career.
And where are the clowns?
There ought to be clowns…
Well, maybe next year.

 

Three blood clots, a concussion, deep vein thrombosis: Hillary’s shielded medical history is no longer just for conspiracy theorists as her ‘penchant for privacy’ gets serious scrutiny

  • Clinton suffered her first blood clot in 1998 while she was First Lady and experienced a second incident in 2009
  • She suffered a concussion after falling in her home in 2013 near the end of her tenure as secretary of state
  • Her doctors say she has deep vein thrombosis, which can lead to clotting in leg veins
  • She suffered a blood clot in her brain in December 2011 and takes blood thinners to treat her condition
  • She has been diagnosed with hypothyroidism
  • Broke her elbow, as spokesman warned it would crimp her texting 
  • Clinton collapsed when she left a 9/11 ceremony early on Sunday. Her office finally revealed she has pneumonia
  • Campaign spokesman Brian Fallon says Clinton plans to release more medical records this week as criticism mounts

Hillary Clinton’s medical history – and her tendency to keep personal and medical information far from view – is coming in for new scrutiny following revelations that the candidate got diagnosed with pneumonia Friday in advance of her stumble in New York.

Clinton’s stumble, caught on camera Sunday after she had to leave Sept. 11th anniversary memorial services after about an hour and a half, was the latest in a line of health spats that have made it into the news during her career.

‘Antibiotics can take care of pneumonia. What’s the cure for an unhealthy penchant for privacy that repeatedly creates unnecessary problems?’ asked President Obama’s former message guru David Axelrod in a tweet Monday – a message promptly retweeted by Trump‘s campaign manager Kellyanne Conway.

Below is a compilation of Clinton’s ailments and health incidents that have entered the public record:

Clinton’s medical history – and her tendency to keep personal and medical information far from view – is coming in for new scrutiny following revelations that the candidate got diagnosed with pneumonia Friday

Hillary's dramatic collapse in New York on Sunday  is prompting new examination of her health ¿ as well as how her aides have closely guarded information

Hillary’s dramatic collapse in New York on Sunday  is prompting new examination of her health – as well as how her aides have closely guarded information

1998 Blood Clot

Clinton’s first known blood clot occurred in 1998, while she was still first lady.

Clinton experienced symptoms while attending a fundraiser for Sen. Charles Schumer of New York, who would soon become her Senate home-state colleague. Her right foot swelled up to the point where she couldn’t put on her shoe.

Clinton got quietly taken to the National Naval Medical Center in Bethesda for treatment at the time. She was found to have ‘a big clot’ blood clot behind her knee, Clinton wrote in her memoir, ‘Living History.’

She called it ‘the most significant health scare I’ve ever had,’ the Washington Post noted.

According to her physician, Mt. Kisco physician, Lisa Bardack, Clinton was advised at the time to take Lovenox, described as a short-acting blood thinner, when she took flights. The meds were discontinued when she went on Coumadin.

 

2009 Blood Clot 

 Clinton had a second blood clot incident in 2009. The episode was described by her doctor in a 2015 letter.

The doctor didn’t provide a detailed description of the event. Rather, she wrote that Clinton’s ‘past medical history is notable for a deep vein thrombosis in 1998, 2009 and a concussion in 2012.

Clinton takes a daily blood thinning medication for her deep vein thrombosis.

Clinton, a frequent flier whose staff catalogued her pursuit of the overall mileage record as secretary of state, may have exacerbated the problem through her extensive air travel.

Frequent jet travel can exacerbate blood clots, which is why some people make sure to walk around the cabin on long flights

Frequent jet travel can exacerbate blood clots, which is why some people make sure to walk around the cabin on long flights

2009 Elbow Fracture 

 Clinton had to work from home for a while after she fractured her elbow during a fall in 2009, CNN recounted. She fell at the State Department on the way to the White House, and went to George Washington University hospital for treatment.

She underwent a two-hour surgical procedure.

‘She is working from home. She is already taking some calls, and I’m sure starting to learn the limits of movement – how well you can text with one arm in a sling,’ quipped then spokesman P.J. Crowley at the time, in an early reference to Clinton’s communications habits.

Clinton was pictured wearing a sling emblazoned with the seal of the State Department when she returned to work. She also was photographed providing left-handed hand shake with a visiting Palestinian dignitary owing to her condition. She has showed no visible signs of lingering problems related to the injury.

HARD KNOCKS: Clinton got a fractured elbow in 2009, but still managed to negotiate with Hondouran leaders, and, according to her spokesman, text with one hand

HARD KNOCKS: Clinton got a fractured elbow in 2009, but still managed to negotiate with Hondouran leaders, and, according to her spokesman, text with one hand

2012 Blood Clot and Concussion 

Clinton got a bad stomach bug and fainted at her home in Washington in 2012, an event that led her to get a concussion. Information about what exactly had happened emerged only slowly over time.

As her doctor put it, ‘In December 2012, Mrs. Clinton suffered a stomach virus after traveling, became dehydrated, fainted and sustained a concussion.’

The then-secretary of state wasn’t seen in public between Dec. 7th and when she left the hospital in New York January 2, 2013.

Clinton experienced ‘double vision for a period of time and benefited from wearing glasses with a Fresnel Prism,’ a special corrective lens, her doctor wrote in a letter voluntarily released to the media in 2015 as part of Clinton’s presidential campaign. Her concussion ‘resolved within two months,’ Bardack wrote.

In 2014, Bill Clinton revealed that the injury ‘required six months of very serious work to get over.’ The former president called it a ‘terrible concussion’

Clinton was diagnosed with a blood clot in the brain, transverse sinus venous thrombosis, and began anticoagulation therapy, her doctor wrote.

Clinton had to work from home and postpone planned testimony before a House Benghazi committee.

Clinton leaves New York Presbyterian Hospital with husband Bill and daughter Chelsea on January 2, 2013. The secretary of state, had not been seen in public since Dec. 7

Clinton leaves New York Presbyterian Hospital with husband Bill and daughter Chelsea on January 2, 2013. The secretary of state, had not been seen in public since Dec. 7

Hypothyroidism

Clinton also suffers from Hypothyroidismrefers to an under-active thyroid gland, resulting in a lack of important hormones.

Clinton’s doctor identified the condition in her 2015 letter, but did not state for how long Clinton has suffered from the condition. She takes a medication called Armour Thyroid.

Allergies

Clinton suffers from ‘seasonal allergies,’ according to her physician. It isn’t known for how long she has suffered from allergies, although Clinton herself has cited her allergies when she has developed a cough – including on-stage during public events.

Her doctor states that Clinton is taking antihistamines, which treat the effects of allergies.

2016 Collapse and Pneumonia Diagnosis

Clinton had to leave a Sept. 11th service in New York early after spending 90 minutes at the ceremony. Her staff first cited heat and exhaustion, then ultimately revealed that Clinton had been diagnosed in pneumonia on Friday.

Clinton campaign spokesman Brian Fallon did not reveal what type of pneumonia Clinton has during a Monday interview on MSNBC, but said Clinton would be putting out more medical information.

‘She was put on antibiotics and advised to rest and modify her schedule,’ said Bardack in a statement released at the end of the day. While attending the event, ‘she became overheated and dehydrated. I have just examined her and she is now re-hydrated and recovering nicely.’

Hours after Clinton was taken away from the Sept. 11th ceremony, her office released a doctor’s statement. ‘Secretary Clinton has been experiencing a cough related to allergies. On Friday, during follow-up evaluation of her prolonged cough, she was diagnosed with pneumonia. She was put on antibiotics, and advised to rest and modify her schedule. While at this morning’s event, she became overheated and dehydrated. I have just examined her and she is now rehydrated and recovering nicely,’ Clinton’s doctor, Lisa Bardack, said in a written statement Sunday.’

‘There’s no other undisclosed condition. The pneumonia is the extent of it,’ Clinton campaign spokesman Brian Fallon told MSNBC.

Fallon also acknowledged: ‘I think in retrospect we could have handled it better in terms of providing more information more quickly.’

Campaign manager Robby Mook, speaking of the 90 minute delay before the press was told Clinton’s status after she left the New York event, said Monday: ‘We wish that that had been a lot shorter and that’s on us.’

Clinton herself tweeted Monday: ‘Thanks to everyone who’s reached out with well wishes! I’m feeling fine and getting better,’ signing the missive with the letter ‘H.’

Clinton had to shake with her left hand following her 2009 injury. She is pictured here with Palestinian Authority Salam Fayyad 

Clinton had to shake with her left hand following her 2009 injury. She is pictured here with Palestinian Authority Salam Fayyad

Clinton campaigned in New York in June along with aide Huma Abedin. She was diagnosed with pneumonia Friday, according to her office

Clinton campaigned in New York in June along with aide Huma Abedin. She was diagnosed with pneumonia Friday, according to her office

Clinton is 68 and would be 69 when she assumed office, second to Ronald Reagan in age taking office. Donald Trump is 70, and has released few details about his medical background.

‘She participates in a healthy lifestyle and has had a full medical evaluation, which reveals no evidence of additional medical issues or cardiovascular disease. Her cancer screening evaluations are all negative. She is in excellent physical condition and fit to serve as President of the United States,’ her doctor wrote.

The letter released by Clinton's physician details her 2012 concussion and double vision

The letter released by Clinton’s physician details her 2012 concussion and double vision

Clinton was a 'healthy-appearing female' during her last examination, according to Dr. Lisa Bardack

Clinton was a ‘healthy-appearing female’ during her last examination, according to Dr. Lisa Bardack

http://www.dailymail.co.uk/news/article-3786187/Three-blood-clots-concussion-deep-vein-thrombosis-Hillary-Clinton-s-shielded-medical-history-isn-t-just-conspiracy-theorists-penchant-privacy-gets-scrutiny.html#ixzz4KAAhLLNB

 

Parkinson’s disease

From Wikipedia, the free encyclopedia
“Parkinson’s” redirects here. For other uses, see Parkinson’s (disambiguation).
Parkinson’s disease
idiopathic or primary parkinsonism, hypokinetic rigid syndrome, paralysis agitans
Two sketches (one from the front and one from the right side) of a man, with an expressionless face. He is stooped forward and is presumably having difficulty walking.

Illustration of Parkinson’s disease by William Richard Gowers, which was first published in A Manual of Diseases of the Nervous System (1886)
Classification and external resources
Specialty Neurology
ICD10 G20, F02.3
ICD9-CM 332
OMIM 168600556500
DiseasesDB 9651
MedlinePlus 000755
eMedicine neuro/304neuro/635 in young
pmr/99 rehab
MeSH D010300
GeneReviews

Parkinson’s disease (PD) is a long term disorder of the central nervous system that mainly affects the motor system.[1] The symptoms generally come on slowly over time. Early in the disease, the most obvious are shaking, rigidity, slowness of movement, and difficulty with walking.[1]Thinking and behavioral problems may also occur.Dementia becomes common in the advanced stages of the disease. Depression and anxiety are also common occurring in more than a third of people with PD.[2] Other symptoms include sensory, sleep, and emotional problems.[1][2] The main motor symptoms are collectively called “parkinsonism“, or a “parkinsonian syndrome”.[3][4]

The cause of Parkinson’s disease is generally unknown, but believed to involve both genetic and environmental factors. Those with a family member affected are more likely to get the disease themselves[4] There is also an increased risk in people exposed to certain pesticides and among those who have had prior head injuries while there is a reduced risk in tobacco smokers and those who drink coffee or tea.[4][5] The motor symptoms of the disease result from the death of cells in the substantia nigra, a region of the midbrain. This results in not enough dopamine in these areas.[1] The reason for this cell death is poorly understood but involves the build-up ofproteins into Lewy bodies in the neurons.[4] Diagnosis of typical cases is mainly based on symptoms, with tests such as neuroimaging being used to rule out other diseases.[1]

There is no cure for Parkinson’s disease.[1] Initial treatments is typically with the antiparkinson medicationlevodopa, with dopamine agonists being used once levodopa becomes less effective. As the disease progresses and neurons continue to be lost, these medications become less effective while at the same time they produce acomplication marked by involuntary writhing movements.[2] Diet and some forms of rehabilitation have shown some effectiveness at improving symptoms.[6][7]Surgery to place the microelectrodes for deep brain stimulation has been used to reduce motor symptoms in severe cases where drugs are ineffective.[1] Evidence for treatments for the non-movement-related symptoms of PD, such as sleep disturbances and emotional problems, is less strong.[4]

In 2013 PD was present in 53 million people and resulted in about 103,000 deaths globally.[8][9] Parkinson’s disease typically occurs in people over the age of 60, of which about one percent are affected.[1][10] Males are more often affected than females.[4] When it is seen in people before the age of 40 or 50, it is called young onset PD.[11] The average life expectancy following diagnosis is between 7 and 14 years.[2] The disease is named after the English doctor James Parkinson, who published the first detailed description in An Essay on the Shaking Palsy, in 1817.[12][13] Public awareness campaigns include World Parkinson’s Day (on the birthday of James Parkinson, 11 April) and the use of a red tulip as the symbol of the disease.[14] People with parkinsonism who have increased the public’s awareness of the condition include actor Michael J. Fox, Olympic cyclist Davis Phinney, and late professional boxer Muhammad Ali.[15][16][17]

Classification

The term parkinsonism is used for a motor syndrome whose main symptoms are tremor at rest, stiffness, slowing of movement and postural instability. Parkinsonian syndromes can be divided into four subtypes, according to their origin:

  1. primary or idiopathic
  2. secondary or acquired
  3. hereditary parkinsonism, and
  4. Parkinson plus syndromes or multiple system degeneration.[18]

Parkinson’s disease is the most common form of parkinsonism and is usually defined as “primary” parkinsonism, meaning parkinsonism with no external identifiable cause.[19][20] In recent years several genes that are directly related to some cases of Parkinson’s disease have been discovered. As much as this conflicts with the definition of Parkinson’s disease as an idiopathic illness, genetic parkinsonism disorders with a similar clinical course to PD are generally included under the Parkinson’s disease label. The terms “familial Parkinson’s disease” and “sporadic Parkinson’s disease” can be used to differentiate genetic from truly idiopathic forms of the disease.[21]

Usually classified as a movement disorder, PD also gives rise to several non-motor types of symptoms such as sensory deficits,[22] cognitive difficulties, and sleep problems. Parkinson plus diseases are primary parkinsonisms which present additional features.[19] They include multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, and dementia with Lewy bodies.[19][23]

In terms of pathophysiology, PD is considered a synucleiopathy due to an abnormal accumulation of alpha-synuclein protein in the brain in the form of Lewy bodies, as opposed to other diseases such as Alzheimer’s disease where the brain accumulates tau protein in the form of neurofibrillary tangles.[24] Nevertheless, there is clinical and pathological overlap between tauopathies and synucleinopathies. The most typical symptom of Alzheimer’s disease, dementia, occurs in advanced stages of PD, while it is common to find neurofibrillary tangles in brains affected by PD.[24]

Dementia with Lewy bodies (DLB) is another synucleinopathy that has similarities with PD, and especially with the subset of PD cases with dementia. However, the relationship between PD and DLB is complex and still has to be clarified.[25] They may represent parts of a continuum or they may be separate diseases.[25]

Signs and symptoms

Black and white picture of a male with PD stooping forward as he walks. He is viewed from the left side and there is a chair behind him.

A man with Parkinson’s disease displaying a flexed walking posture pictured in 1892.[26]

French signature reads "Catherine Metzger 13 Octobre 1869"

Handwriting of a person affected by PD[27]

Parkinson’s disease affects movement, producing motor symptoms.[18] Non-motor symptoms, which include autonomic dysfunction, neuropsychiatric problems (mood, cognition, behavior or thought alterations), and sensory and sleep difficulties, are also common. Some of these non-motor symptoms are often present at the time of diagnosis and can precede motor symptoms.[18]

Motor

Further information: Parkinsonian gait

Four motor symptoms are considered cardinal in PD: tremor, rigidity, slowness of movement, and postural instability.[18]

Tremor is the most apparent and well-known symptom.[18] It is the most common; though around 30% of individuals with PD do not have tremor at disease onset, most develop it as the disease progresses.[18] It is usually a rest tremor: maximal when the limb is at rest and disappearing with voluntary movement and sleep.[18] It affects to a greater extent the most distal part of the limb and at onset typically appears in only a single arm or leg, becoming bilateral later.[18] Frequency of PD tremor is between 4 and 6 hertz (cycles per second). A feature of tremor is pill-rolling, the tendency of the index finger of the hand to get into contact with the thumb and perform together a circular movement.[18][28]The term derives from the similarity between the movement of people with PD and the earlier pharmaceutical technique of manually making pills.[28]

Hypokinesia (slowness of movement) is another characteristic feature of PD, and is associated with difficulties along the whole course of the movement process, from planning to initiation and finally execution of a movement.[18] Performance of sequential and simultaneous movement is hindered.[18] Bradykinesia is commonly a very disabling symptom in the early stages of the disease.[19] Initial manifestations are problems when performing daily tasks which require fine motor control such as writing, sewing or getting dressed.[18] Clinical evaluation is based on similar tasks such as alternating movements between both hands or both feet.[19] Bradykinesia is not equal for all movements or times. It is modified by the activity or emotional state of the subject, to the point that some people are barely able to walk yet can still ride a bicycle.[18] Generally people with PD have less difficulty when some sort of external cue is provided.[18][29]

Rigidity is stiffness and resistance to limb movement caused by increased muscle tone, an excessive and continuous contraction of muscles.[18] In parkinsonism the rigidity can be uniform (lead-pipe rigidity) or ratchety (cogwheel rigidity).[18][19][30][31] The combination of tremor and increased tone is considered to be at the origin of cogwheel rigidity.[32]Rigidity may be associated with joint pain; such pain being a frequent initial manifestation of the disease.[18] In early stages of Parkinson’s disease, rigidity is often asymmetrical and it tends to affect the neck and shoulder muscles prior to the muscles of the face and extremities.[33] With the progression of the disease, rigidity typically affects the whole body and reduces the ability to move.

Postural instability is typical in the late stages of the disease, leading to impaired balance and frequent falls,[34] and secondarily to bone fractures.[18] Instability is often absent in the initial stages, especially in younger people.[19] Up to 40% may experience falls and around 10% may have falls weekly, with the number of falls being related to the severity of PD.[18]

Other recognized motor signs and symptoms include gait and posture disturbances such as festination (rapid shuffling steps and a forward-flexed posture when walking),[18] speech and swallowing disturbances including voice disorders,[35]mask-like face expression or small handwriting, although the range of possible motor problems that can appear is large.[18]

Neuropsychiatric

Parkinson’s disease can cause neuropsychiatric disturbances which can range from mild to severe. This includes disorders of speech, cognition, mood, behaviour, and thought.[18]

Cognitive disturbances can occur in the early stages of the disease and sometimes prior to diagnosis, and increase in prevalence with duration of the disease.[18][36] The most common cognitive deficit in affected individuals is executive dysfunction, which can include problems with planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions, working memory, and selecting relevant sensory information.[36][37] Fluctuations in attention, impaired perception and estimation of time, slowed cognitive processing speed are among other cognitive difficulties.[36][37] Memory is affected, specifically in recalling learned information.[36] Nevertheless, improvement appears when recall is aided by cues.[36] Visuospatial difficulties are also part of the disease, seen for example when the individual is asked to perform tests of facial recognition and perception of the orientation of drawn lines.[36][37]

A person with PD has two to six times the risk of dementia compared to the general population.[18][36] The prevalence of dementia increases with duration of the disease.[36] Dementia is associated with a reducedquality of life in people with PD and their caregivers, increased mortality, and a higher probability of needing nursing home care.[36]

Behavior and mood alterations are more common in PD without cognitive impairment than in the general population, and are usually present in PD with dementia. The most frequent mood difficulties are depression,apathy and anxiety.[18] Establishing the diagnosis of depression is complicated by symptoms that often occur in Parkinson’s including dementia, decreased facial expression, decreased movement, a state of indifference, and quiet speech.[38]Impulse control behaviors such as medication overuse and craving, binge eating, hypersexuality, or pathological gambling can appear in PD and have been related to the medications used to manage the disease.[18][39]Psychotic symptoms—hallucinations or delusions—occur in 4% of people with PD, and it is assumed that the main precipitant of psychotic phenomena in Parkinson’s disease is dopaminergic excess secondary to treatment; it therefore becomes more common with increasing age and levodopa intake.[40][41]

Other

In addition to cognitive and motor symptoms, PD can impair other body functions.

Sleep problems are a feature of the disease and can be worsened by medications.[18] Symptoms can manifest as daytime drowsiness, disturbances in REM sleep, or insomnia.[18] A systematic review shows that sleep attacks occur in 13.0% of patients with Parkinson’s disease on dopaminergic medications.[42]

Alterations in the autonomic nervous system can lead to orthostatic hypotension (low blood pressure upon standing), oily skin and excessive sweating, urinary incontinence and altered sexual function.[18]Constipationand gastric dysmotility can be severe enough to cause discomfort and even endanger health.[6] PD is related to several eye and vision abnormalities such as decreased blink rate, dry eyes, deficient ocular pursuit(eye tracking) and saccadic movements (fast automatic movements of both eyes in the same direction), difficulties in directing gaze upward, and blurred or double vision.[18][43] Changes in perception may include an impaired sense of smell, sensation of pain and paresthesia (skin tingling and numbness).[18] All of these symptoms can occur years before diagnosis of the disease.[18]

Causes

Parkinson’s disease in most people is idiopathic (having no specific known cause). However, a small proportion of cases can be attributed to known genetic factors. Other factors have been associated with the risk of developing PD, but no causal relationships have been proven.

Environmental factors

U.S. Army helicopter spraying Agent Orange over Vietnamese agricultural land during the Vietnam war

A number of environmental factors have been associated with an increased risk of Parkinson’s including: pesticide exposure, head injuries, and living in the country or farming.[44][45] Rural environments and the drinking of well water may be risks as they are indirect measures of exposure to pesticides.[46][47]

Implicated agents include insecticides, primarily chlorpyrifos and organochlorines[48] and pesticides, such as rotenone or paraquat, and herbicides, such as Agent Orange andziram.[46][47][49][50]Heavy metals exposure has been proposed to be a risk factor, through possible accumulation in the substantia nigra; however, studies on the issue have been inconclusive.[46]

Genetics

Parkin crystal structure

PD traditionally has been considered a non-genetic disorder; however, around 15% of individuals with PD have a first-degree relative who has the disease.[19] At least 5% of people are now known to have forms of the disease that occur because of a mutation of one of several specific genes.[51]

Mutations in specific genes have been conclusively shown to cause PD. These genes code for alpha-synuclein (SNCA), parkin (PRKN), leucine-rich repeat kinase 2 (LRRK2 or dardarin), PTEN-induced putative kinase 1 (PINK1), DJ-1 and ATP13A2.[21][51] In most cases, people with these mutations will develop PD. With the exception of LRRK2, however, they account for only a small minority of cases of PD.[21] The most extensively studied PD-related genes are SNCA and LRRK2. Mutations in genes including SNCA, LRRK2 and glucocerebrosidase (GBA) have been found to be risk factors for sporadic PD. Mutations in GBA are known to cause Gaucher’s disease.[51]Genome-wide association studies, which search for mutated alleles with low penetrance in sporadic cases, have now yielded many positive results.[52]

The role of the SNCA gene is important in PD because the alpha-synuclein protein is the main component of Lewy bodies.[51]Missense mutations of the gene (in which a singlenucleotide is changed), and duplications and triplications of the locus containing it have been found in different groups with familial PD.[51] Missense mutations are rare.[51] On the other hand, multiplications of the SNCA locus account for around 2% of familial cases.[51] Multiplications have been found in asymptomatic carriers, which indicate that penetrance is incomplete or age-dependent.[51]

The LRRK2 gene (PARK8) encodes a protein called dardarin. The name dardarin was taken from a Basque word for tremor, because this gene was first identified in families from England and the north of Spain.[21]Mutations in LRRK2 are the most common known cause of familial and sporadic PD, accounting for approximately 5% of individuals with a family history of the disease and 3% of sporadic cases.[21][51] There are many mutations described in LRRK2, however unequivocal proof of causation only exists for a few.[51]

Several Parkinson-related genes are involved in the function of lysosomes, organelles that digest cellular waste products. It has been suggested that some forms of Parkinson may be caused by lysosome dysfunctions that reduce the ability of cells to break down alpha-synuclein.[53]

Pathology

Several brain cells stained in blue. The largest one, a neurone, with an approximately circular form, has a brown circular body inside it. The brown body is about 40% the diameter of the cell in which it appears.

A Lewy body (stained brown) in a brain cell of the substantia nigra in Parkinson’s disease. The brown colour is positive immunohistochemistrystaining for alpha-synuclein.

Anatomical

The basal ganglia, a group of brain structures innervated by the dopaminergic system, are the most seriously affected brain areas in PD.[54] The main pathologicalcharacteristic of PD is cell death in the substantia nigra and, more specifically, the ventral (front) part of the pars compacta, affecting up to 70% of the cells by the time death occurs.[21]

Macroscopic alterations can be noticed on cut surfaces of the brainstem, where neuronal loss can be inferred from a reduction of neuromelanin pigmentation in the substantia nigra and locus coeruleus.[55] The histopathology (microscopic anatomy) of the substantia nigra and several other brain regions shows neuronal loss and Lewy bodies in many of the remaining nerve cells. Neuronal loss is accompanied by death of astrocytes (star-shaped glial cells) and activation of the microglia (another type of glial cell). Lewy bodies are a key pathological feature of PD.[55]

Pathophysiology

Composite of three images, one in top row (referred to in caption as A), two in second row (referred to as B). Top shows a mid-line sagittal plane of the brainstem and cerebellum. There are three circles superimposed along the brainstem and an arrow linking them from bottom to top and continuing upward and forward towards the frontal lobes of the brain. A line of text accompanies each circle: lower is "1. Dorsal Motor X Nucleus", middle is "2. Gain Setting Nuclei" and upper is "3. Substantia Nigra/Amygdala". The fourth line of text above the others says "4. ...". The two images at the bottom of the composite are magnetic resonance imaging (MRI) scans, one sagittal and the other transverse, centred at the same brain coordinates (x=-1, y=-36, z=-49). A colored blob marking volume reduction covers most of the brainstem.

A. Schematic initial progression of Lewy body deposits in the first stages of Parkinson’s disease, as proposed by Braak and colleagues
B. Localization of the area of significant brain volume reduction in initial PD compared with a group of participants without the disease in a neuroimaging study, which concluded that brain stemdamage may be the first identifiable stage of PD neuropathology[56]

The primary symptoms of Parkinson’s disease result from greatly reduced activity of dopamine-secreting cells caused by cell death in the pars compacta region of thesubstantia nigra.[54]

There are five major pathways in the brain connecting other brain areas with the basal ganglia. These are known as the motor, oculo-motor, associative, limbic and orbitofrontalcircuits, with names indicating the main projection area of each circuit.[54] All of them are affected in PD, and their disruption explains many of the symptoms of the disease since these circuits are involved in a wide variety of functions including movement, attention and learning.[54] Scientifically, the motor circuit has been examined the most intensively.[54]

A particular conceptual model of the motor circuit and its alteration with PD has been of great influence since 1980, although some limitations have been pointed out which have led to modifications.[54] In this model, the basal ganglia normally exert a constant inhibitory influence on a wide range of motor systems, preventing them from becoming active at inappropriate times. When a decision is made to perform a particular action, inhibition is reduced for the required motor system, thereby releasing it for activation. Dopamine acts to facilitate this release of inhibition, so high levels of dopamine function tend to promote motor activity, while low levels of dopamine function, such as occur in PD, demand greater exertions of effort for any given movement. Thus, the net effect of dopamine depletion is to produce hypokinesia, an overall reduction in motor output.[54] Drugs that are used to treat PD, conversely, may produce excessive dopamine activity, allowing motor systems to be activated at inappropriate times and thereby producing dyskinesias.[54]

Brain cell death

There is speculation of several mechanisms by which the brain cells could be lost.[57] One mechanism consists of an abnormal accumulation of the protein alpha-synucleinbound to ubiquitin in the damaged cells. This insoluble protein accumulates inside neurones forming inclusions called Lewy bodies.[21][58] According to the Braak staging, a classification of the disease based on pathological findings, Lewy bodies first appear in the olfactory bulb, medulla oblongata and pontine tegmentum, with individuals at this stage being asymptomatic. As the disease progresses, Lewy bodies later develop in the substantia nigra, areas of the midbrain and basal forebrain, and in a last step theneocortex.[21] These brain sites are the main places of neuronal degeneration in PD; however, Lewy bodies may not cause cell death and they may be protective.[57][58] In people with dementia, a generalized presence of Lewy bodies is common in cortical areas. Neurofibrillary tangles and senile plaques, characteristic of Alzheimer’s disease, are not common unless the person is demented.[55]

Other cell-death mechanisms include proteosomal and lysosomal system dysfunction and reduced mitochondrial activity.[57] Iron accumulation in the substantia nigra is typically observed in conjunction with the protein inclusions. It may be related to oxidative stress, protein aggregation and neuronal death, but the mechanisms are not fully understood.[59]

Diagnosis

Sagittal PET scan at the level of the striatum. Hottest areas are the cortical grey matter and the striatum.

Fludeoxyglucose (18F) (FDG) PET scan of a healthy brain. Hotter areas reflect higher glucose uptake. A decreased activity in the basal ganglia can aid in diagnosing Parkinson’s disease.

A physician will diagnose Parkinson’s disease from the medical history and a neurological examination.[18] There is no lab test that will clearly identify the disease, but brain scans are sometimes used to rule out disorders that could give rise to similar symptoms. People may be given levodopa and resulting relief of motor impairment tends to confirm the diagnosis. The finding of Lewy bodies in the midbrain on autopsy is usually considered proof that the person had Parkinson’s disease. The progress of the illness over time may reveal it is not Parkinson’s disease, and some authorities recommend that the diagnosis should be periodically reviewed.[18][60]

Other causes that can secondarily produce a parkinsonian syndrome are Alzheimer’s disease, multiple cerebral infarction and drug-induced parkinsonism.[60]Parkinson plus syndromessuch as progressive supranuclear palsy and multiple system atrophy must be ruled out.[18] Anti-Parkinson’s medications are typically less effective at controlling symptoms in Parkinson plus syndromes.[18] Faster progression rates, early cognitive dysfunction or postural instability, minimal tremor or symmetry at onset may indicate a Parkinson plus disease rather than PD itself.[61] Genetic forms are usually classified as PD, although the terms familial Parkinson’s disease and familial parkinsonism are used for disease entities with an autosomal dominant or recessive pattern of inheritance.[19]

Medical organizations have created diagnostic criteria to ease and standardize the diagnostic process, especially in the early stages of the disease. The most widely known criteria come from the UK Parkinson’s Disease Society Brain Bank and the U.S. National Institute of Neurological Disorders and Stroke.[18] The PD Society Brain Bank criteria require slowness of movement (bradykinesia) plus either rigidity, resting tremor, or postural instability. Other possible causes of these symptoms need to be ruled out. Finally, three or more of the following features are required during onset or evolution: unilateral onset, tremor at rest, progression in time, asymmetry of motor symptoms, response to levodopa for at least five years, clinical course of at least ten years and appearance of dyskinesias induced by the intake of excessive levodopa.[18]Accuracy of diagnostic criteria evaluated at autopsy is 75–90%, with specialists such as neurologists having the highest rates.[18]

Computed tomography (CT) and conventional magnetic resonance imaging (MRI) brain scans of people with PD usually appear normal.[62] These techniques are nevertheless useful to rule out other diseases that can be secondary causes of parkinsonism, such as basal ganglia tumors, vascular pathology and hydrocephalus.[62] A specific technique of MRI, diffusion MRI, has been reported to be useful at discriminating between typical and atypical parkinsonism, although its exact diagnostic value is still under investigation.[62] Dopaminergic function in the basal ganglia can be measured with different PET and SPECTradiotracers. Examples are ioflupane (123I) (trade name DaTSCAN) and iometopane (Dopascan) for SPECT or fluorodeoxyglucose (18F)[62] and DTBZ[63] for PET. A pattern of reduced dopaminergic activity in the basal ganglia can aid in diagnosing PD.[62]

Prevention

Exercise in middle age reduces the risk of Parkinson’s disease later in life.[7]Caffeine also appears protective with a greater decrease in risk occurring with a larger intake of caffeinated beverages such as coffee.[64]Although tobacco smoke causes adverse health effects, decreases life expectancy and quality of life, it may reduce the risk of PD by a third when compared to non-smokers.[46] The basis for this effect is not known, but possibilities include an effect of nicotine as a dopamine stimulant.[46][65] Tobacco smoke contains compounds that act as MAO inhibitors that also might contribute to this effect.[66]

Antioxidants, such as vitamins C and D, have been proposed to protect against the disease but results of studies have been contradictory and no positive effect has been proven.[46] The results regarding fat and fatty acids have been contradictory, with various studies reporting protective effects, risk-increasing effects or no effects.[46] Also, there have been preliminary indications of a possible protective role of estrogens and anti-inflammatory drugs.[46]

Management

Pharmacological treatment of Parkinson’s disease

There is no cure for Parkinson’s disease, but medications, surgery, and multidisciplinary management can provide relief from the symptoms. The main families of drugs useful for treating motor symptoms are levodopa (usually combined with a dopa decarboxylase inhibitor or COMT inhibitor which does not cross the blood–brain barrier), dopamine agonists and MAO-B inhibitors.[67] The stage of the disease determines which group is most useful. Two stages are usually distinguished: an initial stage in which the individual with PD has already developed some disability for which he needs pharmacological treatment, then a second stage in which an individual develops motor complications related to levodopa usage.[67] Treatment in the initial stage aims for an optimal tradeoff between good symptom control and side-effects resulting from improvement of dopaminergic function. The start of levodopa (or L-DOPA) treatment may be delayed by using other medications such as MAO-B inhibitors and dopamine agonists, in the hope of delaying the onset of dyskinesias.[67] In the second stage the aim is to reduce symptoms while controlling fluctuations of the response to medication. Sudden withdrawals from medication or overuse have to be managed.[67] When medications are not enough to control symptoms, surgery, and deep brain stimulation can be of use.[68] In the final stages of the disease, palliative care is provided to improve quality of life.[69]

Levodopa

Levodopa has been the most widely used treatment for over 30 years.[67] L-DOPA is converted into dopamine in the dopaminergic neurons by dopa decarboxylase.[67] Since motor symptoms are produced by a lack of dopamine in the substantia nigra, the administration of L-DOPA temporarily diminishes the motor symptoms.[67]

Only 5–10% of L-DOPA crosses the blood–brain barrier. The remainder is often metabolized to dopamine elsewhere, causing a variety of side effects including nausea, dyskinesias and joint stiffness.[67]Carbidopaand benserazide are peripheral dopa decarboxylase inhibitors,[67] which help to prevent the metabolism of L-DOPA before it reaches the dopaminergic neurons, therefore reducing side effects and increasingbioavailability. They are generally given as combination preparations with levodopa.[67] Existing preparations are carbidopa/levodopa (co-careldopa) and benserazide/levodopa (co-beneldopa). Levodopa has been related to dopamine dysregulation syndrome, which is a compulsive overuse of the medication, and punding.[39] There are controlled release versions of levodopa in the form intravenous and intestinal infusions that spread out the effect of the medication. These slow-release levodopa preparations have not shown an increased control of motor symptoms or motor complications when compared to immediate release preparations.[67][70]

Tolcapone inhibits the COMT enzyme, which degrades dopamine, thereby prolonging the effects of levodopa.[67] It has been used to complement levodopa; however, its usefulness is limited by possible side effects such as liver damage.[67] A similarly effective drug, entacapone, has not been shown to cause significant alterations of liver function.[67] Licensed preparations of entacapone contain entacapone alone or in combination with carbidopa and levodopa.[67]

Levodopa preparations lead in the long term to the development of motor complications characterized by involuntary movements called dyskinesias and fluctuations in the response to medication.[67] When this occurs a person with PD can change from phases with good response to medication and few symptoms (“on” state), to phases with no response to medication and significant motor symptoms (“off” state).[67] For this reason, levodopa doses are kept as low as possible while maintaining functionality.[67] Delaying the initiation of therapy with levodopa by using alternatives (dopamine agonists and MAO-B inhibitors) is common practice.[67] A former strategy to reduce motor complications was to withdraw L-DOPA medication for some time. This is discouraged now since it can bring dangerous side effects such as neuroleptic malignant syndrome.[67] Most people with PD will eventually need levodopa and later develop motor side effects.[67]

Dopamine agonists

Several dopamine agonists that bind to dopaminergic post-synaptic receptors in the brain have similar effects to levodopa.[67] These were initially used for individuals experiencing on-off fluctuations and dyskinesias as a complementary therapy to levodopa; they are now mainly used on their own as an initial therapy for motor symptoms with the aim of delaying motor complications.[67][71] When used in late PD they are useful at reducing the off periods.[67] Dopamine agonists include bromocriptine, pergolide, pramipexole, ropinirole, piribedil, cabergoline, apomorphine and lisuride.

Dopamine agonists produce significant, although usually mild, side effects including drowsiness, hallucinations, insomnia, nausea, and constipation.[67] Sometimes side effects appear even at a minimal clinically effective dose, leading the physician to search for a different drug.[67] Compared with levodopa, dopamine agonists may delay motor complications of medication use but are less effective at controlling symptoms.[67]Nevertheless, they are usually effective enough to manage symptoms in the initial years.[19] They tend to be more expensive than levodopa.[19] Dyskinesias due to dopamine agonists are rare in younger people who have PD, but along with other side effects, become more common with age at onset.[19] Thus dopamine agonists are the preferred initial treatment for earlier onset, as opposed to levodopa in later onset.[19] Agonists have been related to impulse control disorders (such as compulsive sexual activity and eating, and pathological gambling and shopping) even more strongly than levodopa.[39]

Apomorphine, a non-orally administered dopamine agonist, may be used to reduce off periods and dyskinesia in late PD.[67] It is administered by intermittent injections or continuous subcutaneous infusions.[67] Since secondary effects such as confusion and hallucinations are common, individuals receiving apomorphine treatment should be closely monitored.[67] Two dopamine agonists that are administered through skin patches (lisuride and rotigotine) and are useful for people in the initial stages and possibly to control off states in those in the advanced state.[70]

MAO-B inhibitors

MAO-B inhibitors (safinamide, selegiline and rasagiline) increase the level of dopamine in the basal ganglia by blocking its metabolism. They inhibit monoamine oxidase B (MAO-B) which breaks down dopamine secreted by the dopaminergic neurons. The reduction in MAO-B activity results in increased L-DOPA in the striatum.[67] Like dopamine agonists, MAO-B inhibitors used as monotherapy improve motor symptoms and delay the need for levodopa in early disease, but produce more adverse effects and are less effective than levodopa. There are few studies of their effectiveness in the advanced stage, although results suggest that they are useful to reduce fluctuations between on and off periods.[67] An initial study indicated that selegiline in combination with levodopa increased the risk of death, but this was later disproven.[67]

Other drugs

Other drugs such as amantadine and anticholinergics may be useful as treatment of motor symptoms. However, the evidence supporting them lacks quality, so they are not first choice treatments.[67] In addition to motor symptoms, PD is accompanied by a diverse range of symptoms. A number of drugs have been used to treat some of these problems.[72] Examples are the use of quetiapine for psychosis, cholinesterase inhibitors for dementia, and modafinil for daytime sleepiness.[72][73] A 2010 meta-analysis found that non-steroidal anti-inflammatory drugs (apart from aspirin), have been associated with at least a 15 percent (higher in long-term and regular users) reduction of incidence of the development of Parkinson’s disease.[74]

Surgery

Placement of an electrode into the brain. The head is stabilised in a frame forstereotactic surgery.

Treating motor symptoms with surgery was once a common practice, but since the discovery of levodopa, the number of operations declined.[75] Studies in the past few decades have led to great improvements in surgical techniques, so that surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient.[75] Surgery for PD can be divided in two main groups: lesional and deep brain stimulation (DBS). Target areas for DBS or lesions include the thalamus, the globus pallidus or the subthalamic nucleus.[75]Deep brain stimulation (DBS) is the most commonly used surgical treatment, developed in the 1980s by Alim-Louis Benabid and others. It involves the implantation of a medical device called a neurostimulator which sends electrical impulses to specific parts of the brain. DBS is recommended for people who have PD with motor fluctuations and tremor inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe neuropsychiatric problems.[68] Other, less common, surgical therapies involve intentional formation of lesions to suppress overactivity of specific subcortical areas. For example, pallidotomy involves surgical destruction of the globus pallidus to control dyskinesia.[75]

Rehabilitation

Exercise programs are recommended in people with Parkinson’s disease.[7] There is some evidence that speech or mobility problems can improve with rehabilitation, although studies are scarce and of low quality.[76][77] Regular physical exercise with or without physiotherapy can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life.[77] When an exercise program is performed under the supervision of a physiotherapist, there are more improvements in motor symptoms, mental and emotional functions, daily living activities, and quality of life compared to a self-supervised exercise program at home.[78] In terms of improving flexibility and range of motion for people experiencing rigidity, generalized relaxation techniques such as gentle rocking have been found to decrease excessive muscle tension. Other effective techniques to promote relaxation include slow rotational movements of the extremities and trunk, rhythmic initiation, diaphragmatic breathing, and meditation techniques.[79] As for gait and addressing the challenges associated with the disease such as hypokinesia (slowness of movement), shuffling and decreased arm swing; physiotherapists have a variety of strategies to improve functional mobility and safety. Areas of interest with respect to gait during rehabilitation programs focus on but are not limited to improving gait speed, the base of support, stride length, trunk and arm swing movement. Strategies include utilizing assistive equipment (pole walking and treadmill walking), verbal cueing (manual, visual and auditory), exercises (marching and PNF patterns) and altering environments (surfaces, inputs, open vs. closed).[80] Strengthening exercises have shown improvements in strength and motor function for people with primary muscular weakness and weakness related to inactivity with mild to moderate Parkinson’s disease. However, reports show a significant interaction between strength and the time the medications was taken. Therefore, it is recommended that people with PD should perform exercises 45 minutes to one hour after medications when they are at their best.[81] Also, due to the forward flexed posture, and respiratory dysfunctions in advanced Parkinson’s disease, deep diaphragmatic breathing exercises are beneficial in improving chest wall mobility and vital capacity.[82] Exercise may improve constipation.[6]

One of the most widely practiced treatments for speech disorders associated with Parkinson’s disease is the Lee Silverman voice treatment (LSVT).[76][83] Speech therapy and specifically LSVT may improve speech.[76]Occupational therapy (OT) aims to promote health and quality of life by helping people with the disease to participate in as many of their daily living activities as possible.[76] There have been few studies on the effectiveness of OT and their quality is poor, although there is some indication that it may improve motor skills and quality of life for the duration of the therapy.[76][84]

Palliative care

Palliative care is specialized medical care for people with serious illnesses, including Parkinson’s. The goal of this speciality is to improve quality of life for both the person suffering from Parkinson’s and the family by providing relief from the symptoms, pain, and stress of illnesses.[85] As Parkinson’s is not a curable disease, all treatments are focused on slowing decline and improving quality of life, and are therefore palliative in nature.[86]

Palliative care should be involved earlier, rather than later in the disease course.[87][88] Palliative care specialists can help with physical symptoms, emotional factors such as loss of function and jobs, depression, fear, and existential concerns.[87][88][89]

Along with offering emotional support to both the patient and family, palliative care serves an important role in addressing goals of care. People with Parkinson’s may have many difficult decisions to make as the disease progresses such as wishes for feeding tube, non-invasive ventilator, and tracheostomy; wishes for or against cardiopulmonary resuscitation; and when to use hospice care.[86] Palliative care team members can help answer questions and guide people with Parkinson’s on these complex and emotional topics to help them make the best decision based on their own values.[88][90]

Other treatments

Muscles and nerves that control the digestive process may be affected by PD, resulting in constipation and gastroparesis (food remaining in the stomach for a longer period than normal).[6] A balanced diet, based on periodical nutritional assessments, is recommended and should be designed to avoid weight loss or gain and minimize consequences of gastrointestinal dysfunction.[6] As the disease advances, swallowing difficulties (dysphagia) may appear. In such cases it may be helpful to use thickening agents for liquid intake and an upright posture when eating, both measures reducing the risk of choking. Gastrostomy to deliver food directly into the stomach is possible in severe cases.[6]

Levodopa and proteins use the same transportation system in the intestine and the blood–brain barrier, thereby competing for access.[6] When they are taken together, this results in a reduced effectiveness of the drug.[6] Therefore, when levodopa is introduced, excessive protein consumption is discouraged and well balanced Mediterranean diet is recommended. In advanced stages, additional intake of low-protein products such as bread or pasta is recommended for similar reasons.[6] To minimize interaction with proteins, levodopa should be taken 30 minutes before meals.[6] At the same time, regimens for PD restrict proteins during breakfast and lunch, allowing protein intake in the evening.[6]

Repetitive transcranial magnetic stimulation temporarily improves levodopa-induced dyskinesias.[91] Its usefulness in PD is an open research topic,[92] although recent studies have shown no effect by rTMS.[93]Several nutrients have been proposed as possible treatments; however there is no evidence that vitamins or food additives improve symptoms.[94] There is no evidence to substantiate that acupuncture and practice of Qigong, or T’ai chi, have any effect on the course of the disease or symptoms. Further research on the viability of Tai chi for balance or motor skills are necessary.[95][96][97]Fava beans and velvet beans are natural sources of levodopa and are eaten by many people with PD. While they have shown some effectiveness in clinical trials,[98] their intake is not free of risks. Life-threatening adverse reactions have been described, such as the neuroleptic malignant syndrome.[99][100]

Prognosis

Global burden of Parkinson’s disease, measured in disability-adjusted life years per 100,000 inhabitants in 2004

  no data
  < 5
  5–12.5
  12.5–20
  20–27.5
  27.5–35
  35–42.5
  42.5–50
  50–57.5
  57.5–65
  65–72.5
  72.5–80
  > 80

PD invariably progresses with time. A severity rating method known as the Unified Parkinson’s Disease Rating Scale (UPDRS) is the most commonly used metric for clinical study. A modified version known as the MDS-UPDRS is also sometimes used. An older scaling method known as the Hoehn and Yahr scale (originally published in 1967), and a similar scale known as the Modified Hoehn and Yahr scale, have also been commonly used. The Hoehn and Yahr scale defines five basic stages of progression.

Motor symptoms, if not treated, advance aggressively in the early stages of the disease and more slowly later. Untreated, individuals are expected to lose independent ambulation after an average of eight years and be bedridden after ten years.[101] However, it is uncommon to find untreated people nowadays. Medication has improved the prognosis of motor symptoms, while at the same time it is a new source of disability because of the undesired effects of levodopa after years of use.[101] In people taking levodopa, the progression time of symptoms to a stage of high dependency from caregivers may be over 15 years.[101] However, it is hard to predict what course the disease will take for a given individual.[101] Age is the best predictor of disease progression.[57] The rate of motor decline is greater in those with less impairment at the time of diagnosis, while cognitive impairment is more frequent in those who are over 70 years of age at symptom onset.[57]

Since current therapies improve motor symptoms, disability at present is mainly related to non-motor features of the disease.[57] Nevertheless, the relationship between disease progression and disability is not linear. Disability is initially related to motor symptoms.[101] As the disease advances, disability is more related to motor symptoms that do not respond adequately to medication, such as swallowing/speech difficulties, and gait/balance problems; and also to motor complications, which appear in up to 50% of individuals after 5 years of levodopa usage.[101] Finally, after ten years most people with the disease have autonomic disturbances, sleep problems, mood alterations and cognitive decline.[101] All of these symptoms, especially cognitive decline, greatly increase disability.[57][101]

The life expectancy of people with PD is reduced.[101]Mortality ratios are around twice those of unaffected people.[101] Cognitive decline and dementia, old age at onset, a more advanced disease state and presence of swallowing problems are all mortality risk factors. On the other hand, a disease pattern mainly characterized by tremor as opposed to rigidity predicts an improved survival.[101] Death from aspiration pneumonia is twice as common in individuals with PD as in the healthy population.[101]

In 2013 PD resulted in about 103,000 deaths globally, up from 44,000 deaths in 1990.[8] The death rate increased from an average of 1.5 to 1.8 per 100,000 during that time.[8]

Epidemiology

Deaths from Parkinson disease per million persons in 2012

  0-1
  2-4
  5-6
  7-8
  9-10
  11-12
  13-17
  18-36
  37-62
  63-109

PD is the second most common neurodegenerative disorder after Alzheimer’s disease and affects approximately seven million people globally and one million people in the United States.[34][46] The proportion in a population at a given time is about 0.3% in industrialized countries. PD is more common in the elderly and rates rises from 1% in those over 60 years of age to 4% of the population over 80.[46] The mean age of onset is around 60 years, although 5–10% of cases, classified as young onset PD, begin between the ages of 20 and 50.[19] PD may be less prevalent in those of African and Asian ancestry, although this finding is disputed.[46] Some studies have proposed that it is more common in men than women, but others failed to detect any differences between the two sexes.[46] The number of new cases per year of PD is between 8 and 18 per 100,000 person–years.[46]

Many risk factors and protective factors have been proposed, sometimes in relation to theories concerning possible mechanisms of the disease, however, none have been conclusively related to PD by empirical evidence. When epidemiological studies have been carried out in order to test the relationship between a given factor and PD, they have often been flawed and their results have in some cases been contradictory.[46] The most frequently replicated relationships are an increased risk of PD in those exposed to pesticides, and a reduced risk in smokers.[46]

History

Jean-Martin Charcot, who made important contributions to the understanding of the disease and proposed its current name honoring James Parkinson

Several early sources, including an Egyptianpapyrus, an Ayurvedic medical treatise, the Bible, and Galen‘s writings, describe symptoms resembling those of PD.[102] After Galen there are no references unambiguously related to PD until the 17th century.[102] In the 17th and 18th centuries, several authors wrote about elements of the disease, including Sylvius,Gaubius, Hunter and Chomel.[102][103][104]

In 1817 an English doctor, James Parkinson, published his essay reporting six cases of paralysis agitans.[14]An Essay on the Shaking Palsy described the characteristic resting tremor, abnormal posture and gait, paralysis and diminished muscle strength, and the way that the disease progresses over time.[12][105] Early neurologists who made further additions to the knowledge of the disease include Trousseau, Gowers, Kinnier Wilson and Erb, and most notably Jean-Martin Charcot, whose studies between 1868 and 1881 were a landmark in the understanding of the disease.[14] Among other advances, he made the distinction between rigidity, weakness and bradykinesia.[14] He also championed the renaming of the disease in honor of James Parkinson.[14]

In 1912 Frederic Lewy described microscopic particles in affected brains, later named “Lewy bodies“.[14] In 1919 Konstantin Tretiakoff reported that the substantia nigra was the main cerebral structure affected, but this finding was not widely accepted until it was confirmed by further studies published by Rolf Hassler in 1938.[14] The underlying biochemical changes in the brain were identified in the 1950s, due largely to the work of Arvid Carlsson on the neurotransmitter dopamine and Oleh Hornykiewicz on its role on PD.[106] In 1997, alpha-synuclein was found to be the main component of Lewy bodies by Spillantini, Trojanowski, Goedert and others.[58]

Anticholinergics and surgery (lesioning of the corticospinal pathway or some of the basal ganglia structures) were the only treatments until the arrival of levodopa, which reduced their use dramatically.[103][107]Levodopa was first synthesized in 1911 by Casimir Funk, but it received little attention until the mid 20th century.[106] It entered clinical practice in 1967 and brought about a revolution in the management of PD.[106][108] By the late 1980s deep brain stimulation introduced by Alim-Louis Benabid and colleagues at Grenoble, France, emerged as a possible treatment.[109]

Society and culture

Cost

“Parkinson’s awareness” logo with red tulip symbol.

The costs of PD to society are high, but precise calculations are difficult due to methodological issues in research and differences between countries.[110] The annual cost in the UK is estimated to be between 449 million and 3.3 billion pounds, while the cost per patient per year in the U.S. is probably around $10,000 and the total burden around 23 billion dollars.[110] The largest share of direct cost comes from inpatient care and nursing homes, while the share coming from medication is substantially lower.[110] Indirect costs are high, due to reduced productivity and the burden on caregivers.[110] In addition to economic costs, PD reduces quality of life of those with the disease and their caregivers.[110]

Advocacy

11 April, the birthday of James Parkinson, has been designated as World Parkinson’s Day.[14] A red tulip was chosen by international organizations as the symbol of the disease in 2005: it represents the James Parkinson Tulip cultivar, registered in 1981 by a Dutch horticulturalist.[111] Advocacy organizations include the National Parkinson Foundation, which has provided more than $180 million in care, research and support services since 1982,[112]Parkinson’s Disease Foundation, which has distributed more than $115 million for research and nearly $50 million for education and advocacy programs since its founding in 1957 by William Black;[113][114] the American Parkinson Disease Association, founded in 1961;[115] and the European Parkinson’s Disease Association, founded in 1992.[116]

Notable cases

Muhammad Ali at theWorld Economic Forum inDavos, at the age of 64. He had shown signs of parkinsonism from the age of 38 until his death.

Actor Michael J. Fox has PD and has greatly increased the public awareness of the disease.[15] After diagnosis, Fox embraced his Parkinson’s in television roles, sometimes acting without medication, in order to further illustrate the effects of the condition. He has written two autobiographies in which his fight against the disease plays a major role,[117] and appeared before the United States Congress without medication to illustrate the effects of the disease.[117]The Michael J. Fox Foundation aims to develop a cure for Parkinson’s disease.[117] Fox received an honorary doctorate in medicine from Karolinska Institutet for his contributions to research in Parkinson’s disease.[118]

Professional cyclist and Olympic medalist Davis Phinney, who was diagnosed with young onset Parkinson’s at age 40, started the Davis Phinney Foundation in 2004 to support Parkinson’s research, focusing on quality of life for people with the disease.[16][119][120]

Muhammad Ali showed signs of Parkinson’s when he was 38, but was not diagnosed until he was 42, and has been called the “world’s most famous Parkinson’s patient”.[17] Whether he had PD or a parkinsonismrelated to boxing is unresolved.[121][122]

Research

There is little prospect of significant new PD treatments in the near future.[123] Currently active research directions include the search for new animal models of the disease and studies of the potential usefulness of gene therapy, stem cell transplants and neuroprotective agents.[57]

Animal models

PD is not known to occur naturally in any species other than humans, although animal models which show some features of the disease are used in research. The appearance of parkinsonian symptoms in a group of drug addicts in the early 1980s who consumed a contaminated batch of the synthetic opiateMPPP led to the discovery of the chemical MPTP as an agent that causes a parkinsonian syndrome in non-human primates as well as in humans.[124] Other predominant toxin-based models employ the insecticide rotenone, the herbicideparaquat and the fungicide maneb.[125] Models based on toxins are most commonly used in primates. Transgenic rodent models that replicate various aspects of PD have been developed.[126] Using the neurotoxin 6-hydroxydopamine, also known as 6-OHDA, it creates a model of Parkinson’s disease in rats by targeting and destroying dopaminergic neurons in the nigrostriatal pathway when injected into the substantia nigra.[127]

Gene therapy

Gene therapy typically involves the use of a non-infectious virus (i.e., a viral vector such as the adeno-associated virus) to shuttle genetic material into a part of the brain. The gene used leads to the production of anenzyme that helps to manage PD symptoms or protects the brain from further damage.[57][128] In 2010 there were four clinical trials using gene therapy in PD.[57] There have not been important adverse effects in these trials although the clinical usefulness of gene therapy is still unknown.[57] One of these reported positive results in 2011,[129] but the company filed for bankruptcy in March 2012.[130]

Neuroprotective treatments

Several chemical compounds such as GDNF (chemical structure pictured) have been proposed as neuroprotectors in PD, but their effectiveness has not been proven.

Investigations on neuroprotection are at the forefront of PD research. Several molecules have been proposed as potential treatments.[57] However, none of them have been conclusively demonstrated to reduce degeneration.[57] Agents currently under investigation include anti-apoptotics (omigapil, CEP-1347), antiglutamatergics, monoamine oxidase inhibitors (selegiline, rasagiline), promitochondrials (coenzyme Q10, creatine), calcium channel blockers (isradipine) and growth factors (GDNF).[57] Preclinical research also targets alpha-synuclein.[123] A vaccine that primes the human immune system to destroy alpha-synuclein, PD01A (developed by Austrian company, Affiris), has entered clinical trials in humans.[131]

Neural transplantation

Since early in the 1980s, fetal, porcine, carotid or retinal tissues have been used in cell transplants, in which dissociated cells are injected into the substantia nigra in the hope that they will incorporate themselves into the brain in a way that replaces the dopamine-producing cells that have been lost.[57] Although there was initial evidence ofmesencephalic dopamine-producing cell transplants being beneficial, double-blind trials to date indicate that cell transplants produce no long-term benefit.[57] An additional significant problem was the excess release of dopamine by the transplanted tissue, leading to dystonias.[132]Stem cell transplants are a recent research target, because stem cells are easy to manipulate and stem cells transplanted into the brains of rodents and monkeys have been found to survive and reduce behavioral abnormalities.[57][133]Nevertheless, use of fetal stem cells is controversial.[57] It has been proposed that effective treatments may be developed in a less controversial way by use of induced pluripotent stem cells taken from adults.[57]

https://en.wikipedia.org/wiki/Parkinson%27s_disease

Multiple sclerosis

From Wikipedia, the free encyclopedia
Multiple sclerosis
disseminated sclerosis, encephalomyelitis disseminata
MS Demyelinisation CD68 10xv2.jpg

Demyelination by MS. The CD68 colored tissue shows several macrophages in the area of the lesion. Original scale 1:100
Classification and external resources
Specialty Neurology
ICD10 G35
ICD9-CM 340
OMIM 126200
DiseasesDB 8412
MedlinePlus 000737
eMedicine neuro/228oph/179emerg/321pmr/82radio/461
Patient UK Multiple sclerosis
MeSH D009103
GeneReviews

Multiple sclerosis (MS) is a demyelinating disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged.[1] This damage disrupts the ability of parts of the nervous system to communicate, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems.[2][3][4] Specific symptoms can include double vision, blindness in one eye, muscle weakness, trouble with sensation, or trouble with coordination.[1] MS takes several forms, with new symptoms either occurring in isolated attacks (relapsing forms) or building up over time (progressive forms).[5] Between attacks, symptoms may disappear completely; however, permanent neurological problems often remain, especially as the disease advances.[5]

While the cause is not clear, the underlying mechanism is thought to be either destruction by the immune system or failure of the myelin-producing cells.[6] Proposed causes for this include genetics and environmental factors such as being triggered by a viral infection.[3][7] MS is usually diagnosed based on the presenting signs and symptoms and the results of supporting medical tests.[8]

There is no known cure for multiple sclerosis.[1] Treatments attempt to improve function after an attack and prevent new attacks.[3] Medications used to treat MS, while modestly effective, can have side effects and be poorly tolerated. Physical therapy can help with people’s ability to function.[1] Many people pursue alternative treatments, despite a lack of evidence.[9] The long-term outcome is difficult to predict, with good outcomes more often seen in women, those who develop the disease early in life, those with a relapsing course, and those who initially experienced few attacks.[10]Life expectancy is on average 5 to 10 years lower than that of an unaffected population.[2]

Multiple sclerosis is the most common autoimmune disorder affecting the central nervous system.[11] In 2013, about 2.3 million people were affected globally with rates varying widely in different regions and among different populations.[12][13] That year about 20,000 people died from MS, up from 12,000 in 1990.[14] The disease usually begins between the ages of 20 and 50 and is twice as common in women as in men.[15] MS was first described in 1868 by Jean-Martin Charcot.[16] The name multiple sclerosis refers to the numerous scars (sclerae—better known as plaques or lesions) that develop on the white matter of the brain and spinal cord.[16] A number of new treatments and diagnostic methods are under development.[17]

Signs and symptoms

Main symptoms of multiple sclerosis

A person with MS can have almost any neurological symptom or sign, with autonomic, visual, motor, and sensory problems being the most common.[2] The specific symptoms are determined by the locations of the lesions within the nervous system, and may include loss of sensitivity or changes in sensation such as tingling, pins and needles or numbness, muscle weakness, very pronounced reflexes, muscle spasms, or difficulty in moving; difficulties with coordination and balance (ataxia);problems with speech or swallowing, visual problems (nystagmus, optic neuritis or double vision), feeling tired, acute or chronic pain, and bladder and bowel difficulties, among others.[2] Difficulties thinking and emotional problems such as depression or unstable mood are also common.[2]Uhthoff’s phenomenon, a worsening of symptoms due to exposure to higher than usual temperatures, and Lhermitte’s sign, an electrical sensation that runs down the back when bending the neck, are particularly characteristic of MS.[2] The main measure of disability and severity is the expanded disability status scale (EDSS), with other measures such as the multiple sclerosis functional composite being increasingly used in research.[18][19][20]

The condition begins in 85% of cases as a clinically isolated syndrome (CIS) over a number of days with 45% having motor or sensory problems, 20% having optic neuritis, and 10% having symptoms related to brainstem dysfunction, while the remaining 25% have more than one of the previous difficulties.[8] The course of symptoms occurs in two main patterns initially: either as episodes of sudden worsening that last a few days to months (called relapses, exacerbations, bouts, attacks, or flare-ups) followed by improvement (85% of cases) or as a gradual worsening over time without periods of recovery (10-15% of cases).[15] A combination of these two patterns may also occur[5] or people may start in a relapsing and remitting course that then becomes progressive later on.[15] Relapses are usually not predictable, occurring without warning.[2] Exacerbations rarely occur more frequently than twice per year.[2] Some relapses, however, are preceded by common triggers and they occur more frequently during spring and summer.[21] Similarly, viral infections such as the common cold, influenza, or gastroenteritis increase their risk.[2]Stress may also trigger an attack.[22] Women with MS who become pregnant experience fewer relapses; however, during the first months after delivery the risk increases.[2] Overall, pregnancy does not seem to influence long-term disability.[2] Many events have been found not to affect relapse rates including vaccination, breast feeding,[2] physical trauma,[23] and Uhthoff’s phenomenon.[21]

Causes

The cause of MS is unknown; however, it is believed to occur as a result of some combination of genetic and environmental factors such as infectious agents.[2]Theories try to combine the data into likely explanations, but none has proved definitive. While there are a number of environmental risk factors and although some are partly modifiable, further research is needed to determine whether their elimination can prevent MS.[24]

Geography

MS is more common in people who live farther from the equator, although exceptions exist.[2][25] These exceptions include ethnic groups that are at low risk far from the equator such as the Samis, Amerindians, Canadian Hutterites, New Zealand Māori,[26] and Canada’s Inuit,[15] as well as groups that have a relatively high risk close to the equator such as Sardinians,[15] inland Sicilians,[27]Palestinians and Parsis.[26] The cause of this geographical pattern is not clear.[15] While the north-south gradient of incidence is decreasing,[25] as of 2010 it is still present.[15]

MS is more common in regions with northern European populations[2] and the geographic variation may simply reflect the global distribution of these high-risk populations.[15] Decreased sunlight exposure resulting in decreased vitamin D production has also been put forward as an explanation.[28][29][30] A relationship between season of birth and MS lends support to this idea, with fewer people born in the northern hemisphere in November as compared to May being affected later in life.[31] Environmental factors may play a role during childhood, with several studies finding that people who move to a different region of the world before the age of 15 acquire the new region’s risk to MS. If migration takes place after age 15, however, the person retains the risk of his home country.[2][24] There is some evidence that the effect of moving may still apply to people older than 15.[2]

Genetics

HLA region of Chromosome 6. Changes in this area increase the probability of getting MS.

MS is not considered a hereditary disease; however, a number of genetic variations have been shown to increase the risk.[32] Some of these genes appear to have higher levels of expression in microglial cells than expected by chance.[33] The probability of developing the disease is higher in relatives of an affected person, with a greater risk among those more closely related.[3] In identical twins both are affected about 30% of the time, while around 5% for non-identical twins and 2.5% of siblings are affected with a lower percentage of half-siblings.[2][3][34] If both parents are affected the risk in their children is 10 times that of the general population.[15] MS is also more common in some ethnic groups than others.[35]

Specific genes that have been linked with MS include differences in the human leukocyte antigen (HLA) system—a group of genes on chromosome6 that serves as the major histocompatibility complex (MHC).[2] That changes in the HLA region are related to susceptibility has been known since the 1980s,[36] and additionally this same region has been implicated in the development of other autoimmune diseases such as diabetes type I and systemic lupus erythematosus.[36] The most consistent finding is the association between multiple sclerosis and alleles of the MHC defined as DR15 and DQ6.[2] Other loci have shown a protective effect, such as HLA-C554 and HLA-DRB1*11.[2] Overall, it has been estimated that HLA changes account for between 20 and 60% of the genetic predisposition.[36] Modern genetic methods (genome-wide association studies) have discovered at least twelve other genes outside the HLA locus that modestly increase the probability of MS.[36]

Infectious agents

Many microbes have been proposed as triggers of MS, but none have been confirmed.[3] Moving at an early age from one location in the world to another alters a person’s subsequent risk of MS.[7] An explanation for this could be that some kind of infection, produced by a widespread microbe rather than a rare one, is related to the disease.[7]Proposed mechanisms include the hygiene hypothesis and the prevalence hypothesis. The hygiene hypothesis proposes that exposure to certain infectious agents early in life is protective, the disease being a response to a late encounter with such agents.[2] The prevalence hypothesis proposes that the disease is due to an infectious agent more common in regions where MS is common and where in most individuals it causes an ongoing infection without symptoms. Only in a few cases and after many years does it cause demyelination.[7][37] The hygiene hypothesis has received more support than the prevalence hypothesis.[7]

Evidence for a virus as a cause include: the presence of oligoclonal bands in the brain and cerebrospinal fluid of most people with MS, the association of several viruses with human demyelination encephalomyelitis, and the occurrence of demyelination in animals caused by some viral infection.[38]Human herpes viruses are a candidate group of viruses. Individuals having never been infected by the Epstein–Barr virus are at a reduced risk of getting MS, whereas those infected as young adults are at a greater risk than those having had it at a younger age.[2][7] Although some consider that this goes against the hygiene hypothesis, since the non-infected have probably experienced a more hygienic upbringing,[7] others believe that there is no contradiction, since it is a first encounter with the causative virus relatively late in life that is the trigger for the disease.[2] Other diseases that may be related include measles, mumps and rubella.[2]

Other

Smoking has been shown to be an independent risk factor for MS.[28]Stress may be a risk factor although the evidence to support this is weak.[24] Association with occupational exposures and toxins—mainly solvents—has been evaluated, but no clear conclusions have been reached.[24]Vaccinations were studied as causal factors; however, most studies show no association.[24] Several other possible risk factors, such as diet andhormone intake, have been looked at; however, evidence on their relation with the disease is “sparse and unpersuasive”.[28]Gout occurs less than would be expected and lower levels of uric acid have been found in people with MS. This has led to the theory that uric acid is protective, although its exact importance remains unknown.[39]

Pathophysiology

Multiple sclerosis

The three main characteristics of MS are the formation of lesions in the central nervous system (also called plaques), inflammation, and the destruction of myelin sheaths of neurons. These features interact in a complex and not yet fully understood manner to produce the breakdown of nerve tissue and in turn the signs and symptoms of the disease.[2] Additionally, MS is believed to be an immune-mediated disorder that develops from an interaction of the individual’s genetics and as yet unidentified environmental causes.[3] Damage is believed to be caused, at least in part, by attack on the nervous system by a person’s own immune system.[2]

Lesions

Demyelination in MS. On Klüver-Barrera myelin staining, decoloration in the area of the lesion can be appreciated (Original scale 1:100)

The name multiple sclerosis refers to the scars (sclerae – better known as plaques or lesions) that form in the nervous system. These lesions most commonly affect the white matter in the optic nerve, brain stem, basal ganglia, and spinal cord, or white matter tracts close to the lateral ventricles.[2] The function of white matter cells is to carry signals between grey matter areas, where the processing is done, and the rest of the body. The peripheral nervous system is rarely involved.[3]

To be specific, MS involves the loss of oligodendrocytes, the cells responsible for creating and maintaining a fatty layer—known as the myelin sheath—which helps the neurons carry electrical signals (action potentials).[2] This results in a thinning or complete loss of myelin and, as the disease advances, the breakdown of the axons of neurons. When the myelin is lost, a neuron can no longer effectively conduct electrical signals.[3] A repair process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes are unable to completely rebuild the cell’s myelin sheath.[40] Repeated attacks lead to successively less effective remyelinations, until a scar-like plaque is built up around the damaged axons.[40] These scars are the origin of the symptoms and during an attack magnetic resonance imaging (MRI) often shows more than ten new plaques.[2] This could indicate that there are a number of lesions below which the brain is capable of repairing itself without producing noticeable consequences.[2] Another process involved in the creation of lesions is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons.[2] A number of lesion patterns have been described.[41]

Inflammation

Apart from demyelination, the other sign of the disease is inflammation. Fitting with an immunological explanation, the inflammatory process is caused by T cells, a kind oflymphocyte that plays an important role in the body’s defenses.[3] T cells gain entry into the brain via disruptions in the blood–brain barrier. The T cells recognize myelin as foreign and attack it, explaining why these cells are also called “autoreactive lymphocytes”.[2]

The attack of myelin starts inflammatory processes, which triggers other immune cells and the release of soluble factors like cytokines and antibodies. Further breakdown of the blood–brain barrier in turn causes a number of other damaging effects such as swelling, activation of macrophages, and more activation of cytokines and other destructive proteins.[3] Inflammation can potentially reduce transmission of information between neurons in at least three ways.[2] The soluble factors released might stop neurotransmission by intact neurons. These factors could lead to or enhance the loss of myelin, or they may cause the axon to break down completely.[2]

Blood–brain barrier

The blood–brain barrier is a part of the capillary system that prevents the entry of T cells into the central nervous system. It may become permeable to these types of cells secondary to an infection by a virus or bacteria. After it repairs itself, typically once the infection has cleared, T cells may remain trapped inside the brain.[3]Gadolinium cannot cross a normal BBB and, therefore, Gadolinium-enhanced MRI is used to show BBB breakdowns.[42]

Diagnosis

Animation showing dissemination of brain lesions in time and space as demonstrated by monthly MRI studies along a year

Multiple sclerosis as seen on MRI

Multiple sclerosis is typically diagnosed based on the presenting signs and symptoms, in combination with supporting medical imaging and laboratory testing.[8] It can be difficult to confirm, especially early on, since the signs and symptoms may be similar to those of other medical problems.[2][43] The McDonald criteria, which focus on clinical, laboratory, and radiologic evidence of lesions at different times and in different areas, is the most commonly used method of diagnosis[13] with the Schumacher and Poser criteria being of mostly historical significance.[44] While the above criteria allow for a non-invasive diagnosis, some state that the only definitive proof is an autopsy or biopsy where lesions typical of MS are detected.[2][45][46]

Clinical data alone may be sufficient for a diagnosis of MS if an individual has had separate episodes of neurological symptoms characteristic of the disease.[45] In those who seek medical attention after only one attack, other testing is needed for the diagnosis. The most commonly used diagnostic tools are neuroimaging, analysis of cerebrospinal fluid and evoked potentials. Magnetic resonance imaging of the brain and spine may show areas of demyelination (lesions or plaques). Gadolinium can be administeredintravenously as a contrast agent to highlight active plaques and, by elimination, demonstrate the existence of historical lesions not associated with symptoms at the moment of the evaluation.[45][47] Testing of cerebrospinal fluid obtained from a lumbar puncture can provide evidence of chronic inflammation in the central nervous system. The cerebrospinal fluid is tested for oligoclonal bands of IgG on electrophoresis, which are inflammation markers found in 75–85% of people with MS.[45][48] The nervous system in MS may respond less actively to stimulation of the optic nerve and sensory nerves due to demyelination of such pathways. These brain responses can be examined usingvisual– and sensory-evoked potentials.[49]

Clinical course

Progression of MS subtypes

Several phenotypes (commonly named types), or patterns of progression, have been described. Phenotypes use the past course of the disease in an attempt to predict the future course. They are important not only for prognosis but also for treatment decisions. In 1996, the United States National Multiple Sclerosis Society described four clinical courses.[5] This set of courses was later reviewed by an international panel in 2013, adding clinically isolated syndrome (CIS) and radiologically isolated syndrome (RIS) as phenotypes, but leaving the main structure untouched.[50]

  1. relapsing-remitting (RRMS)
  2. secondary progressive (SPMS)
  3. primary progressive (PPMS)
  4. progressive relapsing (PRMS). This entity was removed in the 2013 review.[50]

The relapsing-remitting subtype is characterized by unpredictable relapses followed by periods of months to years of relative quiet (remission) with no new signs of disease activity. Deficits that occur during attacks may either resolve or leave problems, the latter in about 40% of attacks and being more common the longer a person has had the disease.[2][8] This describes the initial course of 80% of individuals with MS.[2] When deficits always resolve between attacks, this is sometimes referred to as benign MS,[51]although people will still build up some degree of disability in the long term.[2] On the other hand, the term malignant multiple sclerosis is used to describe people with MS having reached significant level of disability in a short period.[52] The relapsing-remitting subtype usually begins with a clinically isolated syndrome (CIS). In CIS, a person has an attack suggestive of demyelination, but does not fulfill the criteria for multiple sclerosis.[2][53] 30 to 70% of persons experiencing CIS later develop MS.[53]

Nerve axon with myelin sheath

Secondary progressive MS occurs in around 65% of those with initial relapsing-remitting MS, who eventually have progressive neurologic decline between acute attacks without any definite periods of remission.[2][5] Occasional relapses and minor remissions may appear.[5] The most common length of time between disease onset and conversion from relapsing-remitting to secondary progressive MS is 19 years.[54]

The primary progressive subtype occurs in approximately 10–20% of individuals, with no remission after the initial symptoms.[8][55] It is characterized by progression of disability from onset, with no, or only occasional and minor, remissions and improvements.[5] The usual age of onset for the primary progressive subtype is later than of the relapsing-remitting subtype. It is similar to the age that secondary progressive usually begins in relapsing-remitting MS, around 40 years of age.[2]

Progressive relapsing MS describes those individuals who, from onset, have a steady neurologic decline but also have clear superimposed attacks. This is the least common of all subtypes.[5]

Unusual types of MS have been described; these include Devic’s disease, Balo concentric sclerosis, Schilder’s diffuse sclerosis, and Marburg multiple sclerosis. There is debate on whether they are MS variants or different diseases.[56] Multiple sclerosis behaves differently in children, taking more time to reach the progressive stage.[2] Nevertheless, they still reach it at a lower average age than adults usually do.[2]

Management

Although there is no known cure for multiple sclerosis, several therapies have proven helpful. The primary aims of therapy are returning function after an attack, preventing new attacks, and preventing disability. As with any medical treatment, medications used in the management of MS have several adverse effects. Alternative treatments are pursued by some people, despite the shortage of supporting evidence.

Acute attacks

During symptomatic attacks, administration of high doses of intravenouscorticosteroids, such as methylprednisolone, is the usual therapy,[2] with oral corticosteroids seeming to have a similar efficacy and safety profile.[57] Although, in general, effective in the short term for relieving symptoms, corticosteroid treatments do not appear to have a significant impact on long-term recovery.[58] The consequences of severe attacks that do not respond to corticosteroids might be treatable by plasmapheresis.[2]

Disease-modifying treatments

Relapsing remitting multiple sclerosis

As of 2016, nine disease-modifying treatments have been approved by regulatory agencies for relapsing-remitting multiple sclerosis (RRMS) including: interferon beta-1a, interferon beta-1b, glatiramer acetate,mitoxantrone, natalizumab, fingolimod,[59]teriflunomide,[60]dimethyl fumarate[61] and alemtuzumab.[62] Their cost effectiveness as of 2012 is unclear.[63] In May 2016 the FDA approved daclizumab for the treatment of relapsing multiple sclerosis in adults, with requirements for postmarketing studies and submission of a formal risk evaluation and mitigation strategy.[64][65]

In RRMS they are modestly effective at decreasing the number of attacks.[59] The interferons and glatiramer acetate are first-line treatments[8] and are roughly equivalent, reducing relapses by approximately 30%.[66]Early-initiated long-term therapy is safe and improves outcomes.[67][68] Natalizumab reduces the relapse rate more than first-line agents; however, due to issues of adverse effects is a second-line agent reserved for those who do not respond to other treatments[8] or with severe disease.[66] Mitoxantrone, whose use is limited by severe adverse effects, is a third-line option for those who do not respond to other medications.[8]Treatment of clinically isolated syndrome (CIS) with interferons decreases the chance of progressing to clinical MS.[2][69] Efficacy of interferons and glatiramer acetate in children has been estimated to be roughly equivalent to that of adults.[70] The role of some newer agents such as fingolimod, teriflunomide, and dimethyl fumarate, as of 2011, is not yet entirely clear.[71]

Progressive multiple sclerosis

No treatment has been shown to change the course of primary progressive MS[8] and as of 2011 only one medication, mitoxantrone, has been approved for secondary progressive MS.[72] In this population tentative evidence supports mitoxantrone moderately slowing the progression of the disease and decreasing rates of relapses over two years.[73][74]

Adverse effects

Irritation zone after injection of glatiramer acetate.

The disease-modifying treatments have several adverse effects. One of the most common is irritation at the injection site for glatiramer acetate and the interferons (up to 90% with subcutaneous injections and 33% with intramuscular injections).[75] Over time, a visible dent at the injection site, due to the local destruction of fat tissue, known aslipoatrophy, may develop.[75] Interferons may produce flu-like symptoms;[76] some people taking glatiramer experience a post-injection reaction with flushing, chest tightness, heart palpitations, and anxiety, which usually lasts less than thirty minutes.[77] More dangerous but much less common are liver damage from interferons,[78]systolic dysfunction(12%), infertility, and acute myeloid leukemia (0.8%) from mitoxantrone,[73][79] and progressive multifocal leukoencephalopathy occurring with natalizumab (occurring in 1 in 600 people treated).[8][80]

Fingolimod may give rise to hypertension and slowed heart rate, macular edema, elevated liver enzymes or a reduction in lymphocyte levels.[71] Tentative evidence supports the short-term safety of teriflunomide, with common side effects including: headaches, fatigue, nausea, hair loss, and limb pain.[59] There have also been reports of liver failure and PML with its use and it is dangerous for fetal development.[71] Most common side effects of dimethyl fumarate are flushing and gastrointestinal problems.[61][71] While dimethyl fumarate may lead to a reduction in the white blood cell count there were no reported cases of opportunistic infections during trials.[81][82]

Associated symptoms

Both medications and neurorehabilitation have been shown to improve some symptoms, though neither changes the course of the disease.[83] Some symptoms have a good response to medication, such as an unstable bladder and spasticity, while others are little changed.[2] For neurologic problems, a multidisciplinary approach is important for improving quality of life; however, it is difficult to specify a ‘core team’ as many health services may be needed at different points in time.[2] Multidisciplinary rehabilitation programs increase activity and participation of people with MS but do not influence impairment level.[84] There is limited evidence for the overall efficacy of individual therapeutic disciplines,[85][86] though there is good evidence that specific approaches, such as exercise,[87][88] and psychology therapies, in particular cognitive behavioral approaches are effective.[89]

Alternative treatments

Over 50% of people with MS may use complementary and alternative medicine, although percentages vary depending on how alternative medicine is defined.[9] The evidence for the effectiveness for such treatments in most cases is weak or absent.[9][90] Treatments of unproven benefit used by people with MS include dietary supplementation and regimens,[9][91][92] vitamin D,[93]relaxation techniques such as yoga,[9]herbal medicine (including medical cannabis),[9][94]hyperbaric oxygen therapy,[95]self-infection with hookworms, reflexology, and acupuncture.[9][96] Regarding the characteristics of users, they are more frequently women, have had MS for a longer time, tend to be more disabled and have lower levels of satisfaction with conventional healthcare.[9]

Prognosis

Disability-adjusted life year for multiple sclerosis per 100,000 inhabitants in 2004

  no data
  <13
  13–16
  16–19
  19–22
  22–25
  25–28
  28–31
  31–34
  34–37
  37–40
  40–43
  >43

The expected future course of the disease depends on the subtype of the disease; the individual’s sex, age, and initial symptoms; and the degree of disability the person has.[10] Female sex, relapsing-remitting subtype, optic neuritis or sensory symptoms at onset, few attacks in the initial years and especially early age at onset, are associated with a better course.[10][97]

The average life expectancy is 30 years from the start of the disease, which is 5 to 10 years less than that of unaffected people.[2] Almost 40% of people with MS reach the seventh decade of life.[97] Nevertheless, two-thirds of the deaths are directly related to the consequences of the disease.[2]Suicide is more common, while infections and other complications are especially dangerous for the more disabled.[2] Although most people lose the ability to walk before death, 90% are capable of independent walking at 10 years from onset, and 75% at 15 years.[98][needs update?]

Epidemiology

Deaths from multiple sclerosis per million persons in 2012

  0-0
  1-1
  2-2
  3-5
  6-12
  13-25

MS is the most common autoimmune disorder of the central nervous system.[11] As of 2010, the number of people with MS was 2–2.5 million (approximately 30 per 100,000) globally, with rates varying widely in different regions.[13][15] It is estimated to have resulted in 18,000 deaths that year.[99] In Africa rates are less than 0.5 per 100,000, while they are 2.8 per 100,000 in South East Asia, 8.3 per 100,000 in the Americas, and 80 per 100,000 in Europe.[13] Rates surpass 200 per 100,000 in certain populations of Northern European descent.[15] The number of new cases that develop per year is about 2.5 per 100,000.[13]

Rates of MS appear to be increasing; this, however, may be explained simply by better diagnosis.[15] Studies on populational and geographical patterns have been common[37] and have led to a number of theories about the cause.[7][24][28]

MS usually appears in adults in their late twenties or early thirties but it can rarely start in childhood and after 50 years of age.[13][15] The primary progressive subtype is more common in people in their fifties.[55] Similar to many autoimmune disorders, the disease is more common in women, and the trend may be increasing.[2][25] As of 2008, globally it is about two times more common in women than in men.[13] In children, it is even more common in females than males,[2] while in people over fifty, it affects males and females almost equally.[55]

History

Medical discovery

Detail of Carswell’s drawing of MS lesions in the brain stem and spinal cord (1838)

Robert Carswell (1793–1857), a British professor of pathology, and Jean Cruveilhier (1791–1873), a French professor of pathologic anatomy, described and illustrated many of the disease’s clinical details, but did not identify it as a separate disease.[100] Specifically, Carswell described the injuries he found as “a remarkable lesion of the spinal cord accompanied with atrophy”.[2] Under the microscope, Swiss pathologist Georg Eduard Rindfleisch (1836–1908) noted in 1863 that the inflammation-associated lesions were distributed around blood vessels.[101][102]

The French neurologistJean-Martin Charcot (1825–1893) was the first person to recognize multiple sclerosis as a distinct disease in 1868.[100] Summarizing previous reports and adding his own clinical and pathological observations, Charcot called the disease sclerose en plaques.

Diagnosis

The first attempt to establish a set of diagnostic criteria was also due to Charcot in 1868. He published what now is known as the “Charcot Triad”, consisting in nystagmus,intention tremor, and telegraphic speech (scanning speech)[103] Charcot also observed cognition changes, describing his patients as having a “marked enfeeblement of the memory” and “conceptions that formed slowly”.[16]

Diagnosis was based in Charcot triad and clinical observation until Schumacher made the first attempt to standardize criteria in 1965 by introducing some fundamental requirements: Dissemination of the lesions in time (DIT) and space (DIS), and that “signs and symptoms cannot be explained better by another disease process”.[103] Both requirements were later inherited by Poser criteria and McDonald criteria, whose 2010 version is currently in use.

During the 20th century theories about the cause and pathogenesis were developed and effective treatments began to appear in the 1990s.[2]

Historical cases

Photographic study of locomotion of a MS female patient with walking difficulties created in 1887 byMuybridge

There are several historical accounts of people who probably had MS and lived before or shortly after the disease was described by Charcot.

A young woman called Halldora who lived in Iceland around 1200 suddenly lost her vision and mobility but, after praying to the saints, recovered them seven days after. Saint Lidwina of Schiedam (1380–1433), a Dutchnun, may be one of the first clearly identifiable people with MS. From the age of 16 until her death at 53, she had intermittent pain, weakness of the legs, and vision loss—symptoms typical of MS.[104] Both cases have led to the proposal of a “Viking gene” hypothesis for the dissemination of the disease.[105]

Augustus Frederick d’Este (1794–1848), son of Prince Augustus Frederick, Duke of Sussex and Lady Augusta Murray and the grandson of George III of the United Kingdom, almost certainly had MS. D’Este left a detailed diary describing his 22 years living with the disease. His diary began in 1822 and ended in 1846, although it remained unknown until 1948. His symptoms began at age 28 with a sudden transient visual loss (amaurosis fugax) after the funeral of a friend. During his disease, he developed weakness of the legs, clumsiness of the hands, numbness, dizziness, bladder disturbances, and erectile dysfunction. In 1844, he began to use a wheelchair. Despite his illness, he kept an optimistic view of life.[106][107] Another early account of MS was kept by the British diarist W. N. P. Barbellion, nom-de-plume of Bruce Frederick Cummings (1889–1919), who maintained a detailed log of his diagnosis and struggle.[107] His diary was published in 1919 as The Journal of a Disappointed Man.[108]

Research

For the journal formerly known as Multiple Sclerosis, see Multiple Sclerosis Journal.

Medications

Chemical structure of alemtuzumab

There is ongoing research looking for more effective, convenient, and tolerable treatments for relapsing-remitting MS; creation of therapies for the progressive subtypes;neuroprotection strategies; and effective symptomatic treatments.[17]

During the 2000s and 2010s, there has been approval of several oral drugs that are expected to gain in popularity and frequency of use.[109] Several more oral drugs are under investigation, including ozanimod and laquinimod. Laquinimod was announced in August 2012 and is in a third phase III trial after mixed results in the previous ones.[110]Similarly, studies aimed to improve the efficacy and ease of use of already existing therapies are occurring. This includes the use of new preparations such as the PEGylatedversion of interferon-β-1a, which it is hoped may be given at less frequent doses with similar effects.[111][112] Request for approval of peginterferon beta-1a is expected during 2013.[112]

Monoclonal antibodies have also raised high levels of interest. Alemtuzumab, daclizumab, and CD20 monoclonal antibodies such as rituximab, ocrelizumab and ofatumumabhave all shown some benefit and are under study as potential treatments.[82] Their use has also been accompanied by the appearance of potentially dangerous adverse effects, the most important of which being opportunistic infections.[109] Related to these investigations is the development of a test for JC virus antibodies, which might help to determine who is at greater risk of developing progressive multifocal leukoencephalopathy when taking natalizumab.[109] While monoclonal antibodies will probably have some role in the treatment of the disease in the future, it is believed that it will be small due to the risks associated with them.[109]

Another research strategy is to evaluate the combined effectiveness of two or more drugs.[113] The main rationale for using a number of medications in MS is that the involved treatments target different mechanisms and, therefore, their use is not necessarily exclusive.[113]Synergies, in which one drug improves the effect of another are also possible, but there can also be drawbacks such as the blocking of the action of the other or worsened side-effects.[113] There have been several trials of combined therapy, yet none have shown positive enough results to be considered as a useful treatment for MS.[113]

Research on neuroprotection and regenerative treatments, such as stem cell therapy, while of high importance, are in the early stages.[114] Likewise, there are not any effective treatments for the progressive variants of the disease. Many of the newest drugs as well as those under development are probably going to be evaluated as therapies for PPMS or SPMS.[109]

Disease biomarkers

MRI brain scan produced using aGradient-echo phase sequenceshowing an iron deposit in a white matter lesion (inside green box in the middle of the image; enhanced and marked by red arrow top-left corner)[115]

While diagnostic criteria are not expected to change in the near future, work to develop biomarkers that help with diagnosis and prediction of disease progression is ongoing.[109] New diagnostic methods that are being investigated include work with anti-myelin antibodies, and studies with serum and cerebrospinal fluid, but none of them has yielded reliably positive results.[116]

At the current time, there are no laboratory investigations that can predict prognosis. Several promising approaches have been proposed including: interleukin-6, nitric oxideand nitric oxide synthase, osteopontin, and fetuin-A.[116] Since disease progression is the result of degeneration of neurons, the roles of proteins showing loss of nerve tissue such as neurofilaments, tau, and N-acetylaspartate are under investigation.[116] Other effects include looking for biomarkers that distinguish between those who will and will not respond to medications.[116]

Improvement in neuroimaging techniques such as positron emission tomography (PET) or magnetic resonance imaging (MRI) carry a promise for better diagnosis and prognosis predictions, although the effect of such improvements in daily medical practice may take several decades.[109] Regarding MRI, there are several techniques that have already shown some usefulness in research settings and could be introduced into clinical practice, such as double-inversion recovery sequences, magnetization transfer, diffusion tensor, and functional magnetic resonance imaging.[117] These techniques are more specific for the disease than existing ones, but still lack some standardization of acquisition protocols and the creation of normative values.[117] There are other techniques under development that include contrast agents capable of measuring levels of peripheralmacrophages, inflammation, or neuronal dysfunction,[117] and techniques that measure iron deposition that could serve to determine the role of this feature in MS, or that of cerebral perfusion.[117] Similarly, new PET radiotracers might serve as markers of altered processes such as brain inflammation, cortical pathology, apoptosis, or remylienation.[118] Antibiodies against the Kir4.1 potassium channel may be related to MS.[119]

Chronic cerebrospinal venous insufficiency

In 2008, vascular surgeon Paolo Zamboni suggested that MS involves narrowing of the veins draining the brain, which he referred to as chronic cerebrospinal venous insufficiency (CCSVI). He found CCSVI in all patients with MS in his study, performed a surgical procedure, later called in the media the “liberation procedure” to correct it, and claimed that 73% of participants improved.[120] This theory received significant attention in the media and among those with MS, especially in Canada.[121] Concerns have been raised with Zamboni’s research as it was neither blinded nor controlled, and its assumptions about the underlying cause of the disease are not backed by known data.[122] Also, further studies have either not found a similar relationship or found one that is much less strong,[123] raising serious objections to the hypothesis.[124] The “liberation procedure” has been criticized for resulting in serious complications and deaths with unproven benefits.[122] It is, thus, as of 2013 not recommended for the treatment of MS.[125] Additional research investigating the CCSVI hypothesis are under way.[126]

See also

https://en.wikipedia.org/wiki/Multiple_sclerosis

Amyotrophic lateral sclerosis

From Wikipedia, the free encyclopedia
  (Redirected from Lou Gehrig Disease)
“ALS” redirects here. For other uses, see ALS (disambiguation).
“Motor neurone disease” redirects here. For the broader group of diseases, see Motor neuron disease.
Amyotrophic lateral sclerosis
Lou Gehrig’s disease, Charcot disease
ALS Coronal.jpg

An MRI with increased signal in the posterior part of the internal capsule which can be tracked to themotor cortex consistent with the diagnosis of ALS.
Classification and external resources
Specialty Neurology
ICD10 G12.2
ICD9-CM 335.20
OMIM 105400
DiseasesDB 29148
MedlinePlus 000688
eMedicine neuro/14emerg/24pmr/10
Patient UK Amyotrophic lateral sclerosis
MeSH D000690
GeneReviews
Orphanet 803

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease and motor neurone disease (MND), is a specific disorder that involves the death of neurons that control voluntary muscles.[1][2][3][4] Some also use motor neuron disease for a group of five conditions of which ALS is the most common.[5] ALS is characterized by stiff muscles, muscle twitching, and gradually worsening weakness due to muscles decreasing in size.[6] This results in difficulty in speaking,swallowing, and eventually breathing.[3][6]

The cause is not known in 90% to 95% of cases.[1] About 5–10% of cases are inherited from a person’s parents.[7] About half of these genetic cases are due to one of two specific genes. The diagnosis is based on a person’s signs and symptoms with testing done to rule out other potential causes.[1]

No cure for ALS is known.[1] A medication called riluzole may extend life by about two to three months.[8]Non-invasive ventilation may result in both improved quality and length of life.[9] The disease usually starts around the age of 60 and in inherited cases around the age of 50.[7] The average survival from onset to death is three to four years.[10] About 10% survive longer than 10 years.[1] Most die from respiratory failure. In much of the world, rates of ALS are unknown.[7] In Europe and the United States the disease affects about two people per 100,000 per year.[7][11]

Descriptions of the disease date back to at least 1824 by Charles Bell.[12] In 1869, the connection between the symptoms and the underlying neurological problems was first described by Jean-Martin Charcot, who in 1874 began using the term amyotrophic lateral sclerosis.[12] It became well known in the United States in the 20th century when in 1939 it affected the baseball player Lou Gehrig,[2] and later worldwide when physicist Stephen Hawking, diagnosed in 1963 and expected to die within two years, became famous.[13] In 2014 videos of the ice bucket challenge went viral on the Internet and increased public awareness.[14]

Signs and symptoms

The disorder causes muscle weakness and atrophy throughout the body due to the degeneration of the upper and lower motor neurons. Individuals affected by the disorder may ultimately lose the ability to initiate and control all voluntary movement, although bladder and bowel function and the muscles responsible for eye movement are usually spared until the final stages of the disorder.[15]

Cognitive function is generally spared for most people, although some (about 5%) also develop frontotemporal dementia.[16] A higher proportion of people (30–50%) also have more subtle cognitive changes which may go unnoticed, but are revealed by detailed neuropsychological testing. Sometimes, ALS coexists in individuals who also experience dementia, degenerative muscle disorder, and degenerative bone disorder as part of a syndrome called multisystem proteinopathy.[17]Sensory nerves and the autonomic nervous system are generally unaffected, meaning the majority of people with ALS maintain hearing, sight, touch, smell, andtaste.[18]

Initial symptoms

The start of ALS may be so subtle that the symptoms are overlooked.[19] The earliest symptoms of ALS are muscle weakness and/or muscle atrophy. Other presenting symptoms include trouble swallowing or breathing, cramping, or stiffness of affected muscles; muscle weakness affecting an arm or a leg; and/or slurred and nasal speech. The parts of the body affected by early symptoms of ALS depend on which motor neurons in the body are damaged first.[citation needed]

About 75% of people contracting the disorder first experience weakness or atrophy in an arm or leg and this is known as “limb-onset” ALS. Awkwardness when walking or running or even tripping over or stumbling may be experienced and often this is marked by walking with a “dropped foot” which drags gently on the ground. Or if arm-onset, difficulty with tasks requiring manual dexterity such as buttoning a shirt, writing, or turning a key in a lock may be experienced. Occasionally, the symptoms remain confined to one limb for a long period of time or for the duration of the illness; this is known as monomelic amyotrophy.[citation needed]

About 25% of cases begin as progressive bulbar palsy termed “bulbar-onset” ALS. Initial symptoms will mainly be of difficulty speaking clearly or swallowing. Speech may become slurred, nasal in character, or quieter. There may be difficulty in swallowing and loss of tongue mobility. A smaller proportion of people experience “respiratory-onset” ALS, where the intercostal muscles that support breathing are affected first. A small proportion of people may also present with what appears to be frontotemporal dementia, but later progresses to include more typical ALS symptoms.[citation needed]

Over time, people experience increasing difficulty moving, swallowing (dysphagia), and speaking or forming words (dysarthria). Symptoms of upper motor neuron involvement include tight and stiff muscles (spasticity) and exaggerated reflexes (hyperreflexia) including an overactive gag reflex. An abnormal reflex commonly called Babinski’s sign also indicates upper motor neuron damage. Symptoms of lower motor neuron degeneration include muscle weakness and atrophy, muscle cramps, and fleeting twitches of muscles that can be seen under the skin (fasciculations) although twitching is not a diagnostic symptom and more of a side effect so twitching would either occur after or accompany weakness and atrophy. Around 15–45% of people experience pseudobulbar affect, a neurological disorder also known as “emotional lability”, which consists of uncontrollable laughter, crying, or smiling, attributable to degeneration of bulbar upper motor neurons, resulting in exaggeration of motor expressions of emotion.[citation needed] For ALS to be diagnosed, symptoms of both upper and lower motor neuron damage that cannot be attributed to other causes must be present.[citation needed]

Progression

Although the order and rate of symptoms varies from person to person, most people eventually are not able to walk or use their hands and arms. They also lose the ability to speak and swallow food, while most end up on a portable ventilator, called bilevel positive airway pressure. The rate of progression can be measured using an outcome measure called the “ALS Functional Rating Scale Revised (ALSFRS-R)”, a 12-item instrument administered as a clinical interview or patient-reported questionnaire that produces a score between 48 (normal function) and 0 (severe disability). Though the degree of variability is high and a small percentage of people have a much slower disorder, on average, patients lose about 0.9 FRS points per month. A survey-based study amongst clinicians showed that they rated a 20% change in the slope of the ALSFRS-R as being clinically meaningful.[20] Regardless of the part of the body first affected by the disorder, muscle weakness and atrophy spread to other parts of the body as the disorder progresses. In limb-onset ALS, symptoms usually spread from the affected limb to the opposite limb before affecting a new body region, whereas in bulbar-onset ALS, symptoms typically spread to the arms before the legs.[citation needed]

Disorder progression tends to be slower in patients who are younger than 40 at onset,[21][22] are mildly obese,[23] have disorder restricted primarily to one limb, and those with primarily upper motor neuron symptoms.[24] Conversely, progression is faster and prognosis poorer in people with bulbar-onset disorder, respiratory-onset disorder, and frontotemporal dementia.[24]

The CX3CR1allelic variants have also been shown to have an effect on the disorder’s progression and life expectancy.[25]

Late stages

Although respiratory support can ease problems with breathing and prolong survival, it does not affect the progression of ALS. Most people with ALS die within three to five years from the onset of symptoms. In one study, the median survival time from onset to death was around 39 months, and only 4% survived longer than 10 years.[26] Newer data point to around 10% of people surviving beyond 10 years.[1] Guitarist Jason Becker has lived since 1989 with the disorder, while physicist Stephen Hawking has survived for more than 50 years, but they are considered unusual cases.[27]

Difficulty in chewing and swallowing makes eating very difficult and increases the risk of choking or of aspirating food into the lungs. In later stages of the disorder, aspiration pneumonia can develop, and maintaining a healthy weight can become a significant problem that may require the insertion of a feeding tube. As the diaphragm and intercostal muscles of the rib cage that support breathing weaken, measures of lung functionsuch as vital capacity and inspiratory pressure diminish. In respiratory-onset ALS, this may occur before significant limb weakness is apparent. Most people with ALS die of respiratory failure or pneumonia.[7]

In late stages, the oculomotor nerve that controls the movements of the eye can be affected as can the extraocular muscles (EOMs). The eye movements remain unaffected largely until the later stages due to differences in the extraocular muscles compared to the skeletal muscles that are initially and readily affected. In the disease’s final stages, a person’s condition may resemble locked-in syndrome.[28]

Causes

Genetics

About 5–10% of cases are directly inherited from a person’s parents.[7] Overall, first-degree relatives of an individual with ALS have a 1% risk of developing ALS.[29][30]

A defect on chromosome 21, which codes for superoxide dismutase, is associated with about 20% of familial cases of ALS, or about 2% of ALS cases overall.[31][32][33] This mutation is believed to be transmitted in anautosomal dominant manner, and has over a hundred different forms of mutation. The most common ALS-causing mutation is a mutant SOD1 gene, seen in North America; this is characterized by an exceptionally rapid progression from onset to death. The most common mutation found in Scandinavian countries, D90A-SOD1, is more slowly progressive than typical ALS, and people with this form of the disorder survive for an average of 11 years.[34]

In 2011, a genetic abnormality known as a hexanucleotide repeat was found in a region called C9orf72, which is associated with ALS combined with frontotemporal dementia ALS-FTD,[35] and accounts for some 6% of cases of ALS among white Europeans.[36]

The UBQLN2 gene encodes production of the protein ubiquilin 2 in the cell, which is a member of the ubiquilin family and controls the degradation of ubiquitinated proteins. Mutations in UBQLN2 interfere with protein degradation, leading to neurodegeneration and causing dominantly inherited, chromosome X-linked ALS and ALS/dementia.[37]

To date, a number of genetic mutations have been associated with various types of ALS. The currently known associations are:

Type OMIM Gene Locus Inheritance Remarks
ALS1 105400 SOD1 21q22.1 autosomal dominant (?),autosomal recessive (?) The most common form of familial ALS
ALS2 205100 ALS2 2q33.1 autosomal recessive (?) Juvenile-onset
ALS3 606640 (?) 18q21 (?)
ALS4 602433 SETX 9q34.13 autosomal dominant (?)
ALS5 602099 SPG11 15q21.1 autosomal recessive (?) Juvenile onset
ALS6 608030 FUS 16p11.2 (?)
ALS7 608031 (?) 20p13 (?)
ALS8 608627 VAPB 20q13.3 autosomal dominant (?)
ALS9 611895 ANG 14q11.2 (?)
ALS10 612069 TARDBP 1p36.2 autosomal dominant (?) ALS with or without frontotemporal dementia
ALS11 612577 FIG4 6q21 (?)
ALS12 613435 OPTN 10p13 (?)
ALS13 183090 ATXN2 12q24.12 autosomal dominant (?) Spinocerebellar ataxia 2
ALS14 613954 VCP 9p13.3 (?) Recent new study shows strong link in ALS mechanism[38][39]
ALS15 300857 UBQLN2 Xp11.21 X-linked dominant (?) Described in one family[37]
ALS16 614373 SIGMAR1 9p13.3 autosomal recessive (?) Juvenile onset, very rare, described only in one family[40]
ALS17 614696 CHMP2B 3p11.2 autosomal dominant (?) Very rare, reported only in a handful of people
ALS18 614808 PFN1 17p13.2 (?) Very rare, described only in a handful of Chinese families[41]
ALS19 615515 ERBB4 2q34 autosomal dominant (?) Very rare, as of late 2013 described only in four people[42]
ALS20 615426 HNRNPA1 12q13.13 (?) Very rare, as of late 2013 described only in two people[43]
ALS21 606070 MATR3 5q31.2 autosomal dominant (?) Very rare. Formerly known as “distal myopathy type 2” (MPD2) and “vocal cord and pharyngeal dysfunction with distal myopathy” (VCPDM)
ALS22 616208 TUBA4A 2q35 autosomal dominant (?) “Amyotrophic lateral sclerosis 22 with or without frontotemporal dementia”
FTDALS1 105550 C9orf72 9p21.2 autosomal dominant (?) “Frontotemporal dementia and/or amyotrophic lateral sclerosis type 1”. Accounts for around 6% of ALS cases among white Europeans[citation needed]
FTDALS2 615911 CHCHD10 22q11.23 autosomal dominant (?) “Frontotemporal dementia and/or amyotrophic lateral sclerosis type 2”
FTDALS3 616437 SQSTM1 5q35.3 autosomal dominant (?) “Frontotemporal dementia and/or amyotrophic lateral sclerosis type 3”
FTDALS4 616439 TBK1 12q14.2 autosomal dominant (?) “Frontotemporal dementia and/or amyotrophic lateral sclerosis type 4”

SOD1

In 1993, scientists discovered that mutations in the gene (SOD1) that produces the CuZnsuperoxide dismutase (SOD1) enzyme were associated with around 20% of familial ALS. This enzyme is a powerfulantioxidant that protects the body from damage caused by superoxide, a toxic free radical generated in the mitochondria. Free radicals are highly reactive molecules produced by cells during normal metabolism. Free radicals can accumulate and cause damage to DNA and proteins within cells. To date, over 110 different mutations in SOD1 have been linked with the disorder, some of which (such as H46R) have a very long clinical course, while others, such as A4V, are exceptionally aggressive. When the defenses against oxidative stress fail, programmed cell death (apoptosis) is upregulated.

A defect in SOD1 could be a loss or gain of function. A loss of SOD1 function could lead to an accumulation of free radicals. A gain of SOD1 function could be toxic in other ways.[44][45]

Aggregate accumulation of mutant SOD1 is suspected to play a role in disrupting cellular functions by damaging mitochondria, proteasomes, protein folding chaperones, or other proteins.[46] Any such disruption, if proven, would lend significant credibility to the theory that aggregates are involved in mutant SOD1 toxicity. Critics have noted that in humans, SOD1 mutations cause only 2% or so of overall cases and the etiological mechanisms may be distinct from those responsible for the sporadic form of the disease. To date, the ALS-SOD1 mice remain the best model of the disease for preclinical studies, but it is hoped that more useful models will be developed.

Head injury

While moderate to severe traumatic brain injury is a risk for ALS, it is unclear if mild traumatic brain injury increases rates.[47][48]

In 1994 the National Institute for Occupational Safety and Health (NIOSH) reported a nonsignificant increase in nervous system disorders due to four cases of ALS among NFL football players. It was unclear if this was due to chance or not.[49] Another study from 2012 also found a possible increase in ALS in NFL football players.[50] An older study did not find an increased risk among high school football players.[47] A 2007 review found an increased risk among soccer players.[48] ALS may also occur more often among the US military veterans however the reason is unknown.[51] This may be due to head injury.[52]

Other factors

Where no family history of the disease is present – i.e., in around 90% of cases – no cause is known for ALS. Possible associations for which evidence is inconclusive include military service, frequent drug use, and participation in contact sports.[medical citation needed]

Studies also have focused on the role of glutamate in motor neuron degeneration. Glutamate is one of the neurotransmitters in the brain. Scientists have found, compared with healthy people, people with ALS have higher levels of glutamate in their serum and spinal fluid.[32]Riluzole is currently the only FDA-approved drug for ALS and targets glutamate transporters. It only has a modest effect on survival, however, suggesting that excess glutamate is not the sole cause of the disease.

Certain studies suggested a link between sporadic ALS, specifically in athletes, and a diet enriched with branched-chain amino acids, a common dietary supplement among athletes, which cause cell hyperexcitability resembling that usually observed in people with ALS. The proposed underlying mechanism is that cell hyperexcitability results in increased calcium absorption by the cell, and thus brings about cell death of neuronal cells, which have particularly low calcium buffering capabilities.[53]

Some evidence supports superoxide dismutase 1 (SOD1) protein misfolding propagates between molecules in a similar fashion to prions.[54] Similarly, it has been proposed that incorporation of the cyanobacterial toxin β-methylamino-l-alanine (BMAA) leads to another prion-like protein misfolding propagation.[55][56]

Another very common factor associated with ALS is a lesion to the motor system in areas such as the frontotemporal lobes.[57] Lesions in these areas often show signs of early deficit, which can be used to predict the loss of motor function, and result in the spread of ALS.[57] The mechanisms of ALS are present long before any signs or symptoms become apparent.[58] Before any muscular atrophy becomes apparent during ALS, roughly one-third of the motor neurons must be destroyed.[58]

Other potential risk factors including chemical exposure, electromagnetic field exposure, occupation, physical trauma, and electric shock, have been investigated, but are without consistent findings.[59][60] There is a tentative association with exposure to a number of pesticides including the organochlorine insecticidesaldrin, dieldrin, DDT, and toxaphene.[61][62][63]

Pathophysiology

The defining feature of ALS is the death of both upper and lower motor neurons in the motor cortex of the brain, the brain stem, and the spinal cord. Prior to their destruction, motor neurons develop protein-richinclusions in their cell bodies and axons. This may be partly due to defects in protein degradation.[37] These inclusions often contain ubiquitin, and generally incorporate one of the ALS-associated proteins: SOD1,TAR DNA binding protein (TDP-43, or TARDBP), and/or FUS.[64]

Diagnosis

MRI (axial FLAIR) demonstrates increased T2 signal within the posterior part of the internal capsule, consistent with the diagnosis of ALS.

No test can provide a definite diagnosis of ALS, although the presence of upper and lower motor neuron signs in a single limb is strongly suggestive.[1] Instead, the diagnosis of ALS is primarily based on the symptoms and signs the physician observes in the person and a series of tests to rule out other diseases.[1] Physicians obtain the person’s fullmedical history and usually conduct a neurologic examination at regular intervals to assess whether symptoms such as muscle weakness, atrophy of muscles, hyperreflexia, and spasticity are worsening.[1]

Differential diagnosis

Because symptoms of ALS can be similar to those of a wide variety of other, more treatable diseases or disorders, appropriate tests must be conducted to exclude the possibility of other conditions.[1] One of these tests is electromyography (EMG), a special recording technique that detects electrical activity in muscles.[1] Certain EMG findings can support the diagnosis of ALS.[1] Another common test measures nerve conduction velocity (NCV).[1] Specific abnormalities in the NCV results may suggest, for example, that the patient has a form of peripheral neuropathy (damage to peripheral nerves) or myopathy (muscle disease) rather than ALS. While a magnetic resonance imaging (MRI) is often normal in people with early stage ALS, they can reveal evidence of other problems that may be causing the symptoms, such as a spinal cord tumor, multiple sclerosis, aherniated disk in the neck, syringomyelia, or cervical spondylosis.[1]

Based on the person’s symptoms and findings from the examination and from these tests, the physician may order tests on blood and urine samples to eliminate the possibility of other diseases, as well as routine laboratory tests.[1] In some cases, for example, if a physician suspects the person may have a myopathy rather than ALS, a muscle biopsy may be performed.[1]

Viralinfectious diseases such as human immunodeficiency virus (HIV), human T-cell leukaemia virus (HTLV), Lyme disease,[65]syphilis[66] and tick-borne encephalitis[67] can in some cases cause ALS-like symptoms.[1]Neurological disorders such as multiple sclerosis, post-polio syndrome, multifocal motor neuropathy, CIDP, spinal muscular atrophy, and spinal and bulbar muscular atrophy can also mimic certain aspects of the disease and should be considered.[1]

ALS must be differentiated from the “ALS mimic syndromes” which are unrelated disorders that may have a similar presentation and clinical features to ALS or its variants.[68] Because of the prognosis carried by this diagnosis and the variety of diseases or disorders that can resemble ALS in the early stages of the disease, people should always obtain a specialist neurological opinion, so alternative diagnoses are clinically ruled out. Benign fasciculation syndrome is another condition that mimics many of the symptoms of ALS, but is accompanied by normal EMG readings and no major disablement.[citation needed]

However, most cases of ALS are readily diagnosed and the error rate of diagnosis in large ALS clinics is less than 10%.[69][70] In one study, 190 patients who met the MND/ALS diagnostic criteria, complemented with laboratory research in compliance with both research protocols and regular monitoring. Thirty of these patients (16%) had their diagnosis completely changed during the clinical observation development period.[71] In the same study, three patients had a false negative diagnosis, myasthenia gravis (MG), an autoimmune disease. MG can mimic ALS and other neurological disorders leading to a delay in diagnosis and treatment. MG is eminently treatable; ALS is not.[72] Myasthenic syndrome, also known as Lambert-Eaton syndrome, can mimic ALS and its initial presentation can be similar to that of MG.[73][74]

Management

Management of ALS attempts to relieve symptoms and extend life expectancy. This supportive care is best provided by multidisciplinary teams of health care professionals working with the person and their caregivers to keep them as mobile and comfortable as possible.[citation needed]

Medications

Riluzole (Rilutek) has been found to modestly improve survival.[75] It lengthens survival by several months, and may have a greater survival benefit for those with a bulbar onset. It also extends the time before a person needs ventilation support. People taking it must be monitored for liver damage (occurring in about 10% of people taking the drug).[76] It is approved by Food and Drug Administration (US) and recommended by the National Institute for Clinical Excellence (UK). Riluzole does not reverse damage already done to motor neurons.[77]

Other medications may be used to help reduce fatigue, ease muscle cramps, control spasticity, and reduce excess saliva and phlegm. Drugs also are available to help patients with pain, depression, sleep disturbances, dysphagia, and constipation. Baclofen and diazepam are often prescribed to control the spasticity caused by ALS, and trihexyphenidyl or amitriptyline may be prescribed when people with ALS begin having trouble swallowing their saliva.[15]

Breathing support

When the muscles that assist in breathing weaken, use of ventilatory assistance (intermittent positive pressure ventilation, bilevel positive airway pressure (BiPAP), or biphasic cuirass ventilation (BCV) may be used to aid breathing. Such devices artificially inflate the person’s lungs from various external sources that are applied directly to the face or body. When muscles are no longer able to maintain oxygen and carbon dioxide levels, these devices may be used full-time. BCV has the added advantage of being able to assist in clearing secretions by using high-frequency oscillations followed by several positive expiratory breaths.[78] People may eventually consider forms of mechanical ventilation (respirators) in which a machine inflates and deflates the lungs. To be effective, this may require a tube that passes from the nose or mouth to the windpipe (trachea) and for long-term use, an operation such as a tracheotomy, in which a plastic breathing tube is inserted directly in the person’s windpipe through an opening in the neck.[citation needed]

Persons and their families should consider several factors when deciding whether and when to use one of these options. Ventilation devices differ in their effect on the person’s quality of life and in cost. Although ventilation support can ease problems with breathing and prolong survival, it does not affect the progression of ALS. Patients need to be fully informed about these considerations and the long-term effects of life without movement before they make decisions about ventilation support and have deep discussions on quality of life. Some persons under long-term tracheotomy intermittent positive pressure ventilation with deflated cuffs or cuffless tracheotomy tubes (leak ventilation) are able to speak, provided their bulbar muscles are strong enough, though in all cases speech will be lost as the disease progresses. This technique preserves speech in some persons with long-term mechanical ventilation. Other persons may be able to use a speaking valve such as a Passey-Muir speaking valve with the assistance and guidance of a speech-language pathologist.[citation needed]

External ventilation machines that use the ventilation mode of BiPAP are frequently used to support breathing, initially at night, and later during the daytime, as well. The use of BPAP (more often referred to as noninvasive ventilation, NIV) is only a temporary remedy, however, and long before BPAP stops being effective, persons should decide whether to have a tracheotomy and long-term mechanical ventilation. At this point, some persons choose palliative hospice care.[citation needed]

Therapy

A man with ALS communicates with his wife by pointing to letters and words with a head mounted laser pointer.

Using low tech to communicate. A man with ALS communicates by pointing to letters and words using an head mounted laser pointer.

Physical therapy plays a large role in rehabilitation for individuals with ALS. Specifically, physical and occupational therapists can set goals and promote benefits for individuals with ALS by delaying loss of strength, maintaining endurance, limiting pain, preventing complications, and promoting functional independence.[79]

Occupational therapy and special equipment such as assistive technology can also enhance patients’ independence and safety throughout the course of ALS. Gentle, low-impact aerobic exercise such as performing activities of daily living, walking, swimming, and stationary bicycling can strengthen unaffected muscles, improve cardiovascular health, and help patients fight fatigue and depression. Range of motion and stretching exercises can help prevent painful spasticity and shortening (contracture) of muscles. Physical and occupational therapists can recommend exercises that provide these benefits without overworking muscles. They can suggest devices such as ramps, braces, walkers, bathroom equipment (shower chairs, toilet risers, etc.), and wheelchairs that help patients remain mobile. Occupational therapists can provide or recommend equipment and adaptations to enable people to retain as much safety and independence in activities of daily living as possible.[citation needed]

People with ALS who have difficulty speaking may benefit from working with a speech-language pathologist. These health professionals can teach patients adaptive strategies such as techniques to help them speak louder and more clearly. As ALS progresses, speech-language pathologists can recommend the use of augmentative and alternative communication such as voice amplifiers, speech-generating devices (or voice output communication devices) and/or low tech communication techniques such as head mounted laser pointers, alphabet boards or yes/no signals.[citation needed]

Nutrition

Patients and caregivers can learn from dieticians how to plan and prepare numerous small meals throughout the day that provide enough calories, fiber and fluid, and how to avoid foods that are difficult to swallow. Patients may begin using suction devices to remove excess fluids or saliva and prevent choking. Occupational therapists can assist with recommendations for adaptive equipment to ease the physical task of self-feeding. Speech-language pathologists make food choice recommendations that are more conducive to their unique deficits and abilities. When patients can no longer get enough nourishment from eating, doctors may advise inserting a feeding tube into the stomach. The use of a feeding tube also reduces the risk of choking and pneumonia that can result from inhaling liquids into the lungs. The tube is not painful and does not prevent patients from eating food orally if they wish.[citation needed]

Researchers have stated, “ALS patients have a chronically deficient intake of energy and recommended augmentation of energy intake”[80] and have a severe loss of appetite.[81] Both animal[82] and human research[80][unreliable medical source?][83][unreliable medical source?] suggest that ALS patients should be encouraged to consume as many calories as possible and not to restrict their caloric intake. As of 2012, “a lack of robust evidence for interventions” remained for the management of weight loss.[84]

End of life care

Social workers and home care and hospice nurses help people with ALS, their families, and caregivers with the medical, emotional, and financial challenges of coping, particularly during the final stages of the disease. Social workers provide support such as assistance in obtaining financial aid, arranging durable power of attorney, preparing a living will, and finding support groups for patients and caregivers. Home nurses are available not only to provide medical care, but also to teach caregivers about tasks such as maintaining respirators, giving feedings, and moving patients to avoid painful skin problems and contractures. Home hospice nurses work in consultation with physicians to ensure proper medication, pain control, and other care affecting the quality of life of patients who wish to remain at home. The home hospice team can also counsel patients and caregivers about end-of-life issues.[citation needed]

Epidemiology

In much of the world, rates of ALS are unknown.[7] In Europe, the disease affects about 2.2 people per 100,000 per year.[7] In the United States, more than 5,600 are diagnosed every year, and up to 30,000 Americans are currently affected. ALS is responsible for two deaths per 100,000 people per year.[85]

ALS is classified as a rare disease, designated by the FDA as an “orphan” disease (affecting fewer than 200,000 people in the United States), but is the most common motor neuron disease. People of all races and ethnic backgrounds are affected. One or two of 100,000 people develop ALS each year.[86] Amyotrophic lateral sclerosis affects around 30,000 Americans.[87] ALS cases are estimated at 1.2–4.0 per 100,000 individuals in Caucasian populations with a lower rate in other ethnic populations.[88]Filipinos are second to Caucasians in terms of ALS prevalence with 1.1-2.8 per 100,000 individuals.[87]

Reports have been made of several “clusters” including three American football players from the San Francisco 49ers, more than 50 association football players in Italy,[89] three association football-playing friends in the south of England,[90] and conjugal (husband and wife) cases in the south of France.[91][92][93][94][95] Although many authors consider ALS to be caused by a combination of genetic and environmental risk factors, so far the latter have not been firmly identified, other than a higher risk with increasing age.

History

Descriptions of the disease date back to at least 1824 by Charles Bell.[12]

English scientist Augustus Waller described the appearance of shriveled nerve fibers in 1850. In 1869, the connection between the symptoms and the underlying neurological problems were first described by Jean-Martin Charcot, who introduced the term amyotrophic lateral sclerosis in his 1874 paper.[12] In 1881, the article was translated into English and published in a three-volume edition of Lectures on the Diseases of the Nervous System.

ALS became a cause célèbre in the United States in 1939 when baseball legend Lou Gehrig‘s career, and two years later, his life, were ended by the disease.[96]

In the 1950s, an epidemic occurred among the Chamorro people on Guam which bore similarities to many conditions, including ALS.[97]

By 1991, researchers had linked chromosome 21 to familial ALS (FALS). In 1993, the SOD1 gene on chromosome 21 was found to play a role in some cases of FALS. In 1996, riluzole became the first FDA-approved drug for ALS.[citation needed]

In 1998, the El Escorial criteria were developed as the standard for classifying ALS patient in clinical research. The next year, the revised ALS Functional Rating Scale was published and soon becomes a gold standard for rating the declines in ALS patient in clinical research. Noncoding repeat expansions in C9ORF72 were found to be a major cause of ALS and frontotemporal dementia in 2011.[citation needed]

Name

Amyotrophic comes from the Greek word amyotrophia: a- means “no”, myo refers to “muscle”, and trophia means “nourishment”; amyotrophia therefore means “no muscle nourishment,” which describes the characteristic atrophy of the sufferer’s disused muscle tissue. Lateral identifies the areas in a person’s spinal cord where affected portions of the nerve cells are located. Degeneration in this area leads to scarring or hardening (“sclerosis“).

In the United Kingdom, India,[98] Australia[99] and some other Commonwealth countries the term motor neurone disease (MND) is commonly used.[4]

Society and culture

In August 2014, a challenge went viral online which was commonly known as the “ALS Ice Bucket Challenge“.[100] Contestants fill a bucket full of ice and water, then state who nominated them to do the challenge, and nominate three other individuals of their choice to take part in it. The contestants then dump the buckets of ice and water onto themselves. However, it can be done in a different order. The contestants then donate at least US $10 (or a similar amount in their local currency) to ALS research at the ALS Association, or Motor Neurone Disease Association in the UK. Any contestants who refuse to have the ice and water dumped on them are expected to donate at least US$100 to ALS research. As of July 2015, the Ice Bucket Challenge had raised $115 million for the ALS Association.[101] Many celebrities have taken part in the challenge.[102] The Ice Bucket Challenge was credited with helping to raise funds that contributed to the discovery that the gene NEK1 may potentially contribute to the development for ALS.[103][104]

ALS is the central topic of the 2014 movie You’re Not You, directed by George C. Wolfe, with Hilary Swank, Emmy Rossum and Josh Duhamel playing the main characters.[105]

American football

After this 2012 report was released, some NFL players involved in the legal settlement with the NFL complained that the NFL, which initially agreed to pay $765 million, was not doing enough to help players. The judge in the case concurred, and the NFL then agreed to pay an unlimited amount of damages for players found to have ALS, Parkinson’s disease, Alzheimer’s disease and dementia.[106]

Research

A number of clinical trials are underway globally for ALS; a comprehensive listing of trials in the US can be found at ClinicalTrials.gov. A large genetic study, called project MinE, initiated by two people with ALS is going on currently. It is a crowdfunded research project with many countries involved to discover more genes.[107] A division of the US Centers for Disease Control and Prevention maintains a registry of Americans with ALS.[108]

https://en.wikipedia.org/wiki/Amyotrophic_lateral_sclerosis

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The Pronk Pops Show Podcasts

Pronk Pops Show 747: August 31, 2016 

Pronk Pops Show 746: August 30, 2016 

Pronk Pops Show 745: August 29, 2016 

Pronk Pops Show 744: August 26, 2016 

Pronk Pops Show 743: August 25, 2016

Pronk Pops Show 742: August 24, 2016 

Pronk Pops Show 741: August 23, 2016 

Pronk Pops Show 740: August 22, 2016

Pronk Pops Show 739: August 18, 2016

Pronk Pops Show 738: August 17, 2016

Pronk Pops Show 737: August 16, 2016

Pronk Pops Show 736: August 15, 2016

Pronk Pops Show 735: August 12, 2016

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Pronk Pops Show 732: August 8, 2016

Pronk Pops Show 731: August 4, 2016

Pronk Pops Show 730: August 3, 2016

Pronk Pops Show 729: August 1, 2016

Pronk Pops Show 728: July 29, 2016

Pronk Pops Show 727: July 28, 2016

Pronk Pops Show 726: July 27, 2016

Pronk Pops Show 725: July 26, 2016

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Pronk Pops Show 713: July 6, 2016

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Pronk Pops Show 710: June 30, 2016

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Pronk Pops Show 707: June 27, 2016

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Pronk Pops Show 704: June 22, 2016

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Pronk Pops Show 702: June 20, 2016

Pronk Pops Show 701: June 17, 2016

Pronk Pops Show 700: June 16, 2016

Pronk Pops Show 699: June 15, 2016

Pronk Pops Show 698: June 14, 2016

Pronk Pops Show 697: June 13, 2016

Pronk Pops Show 696: June 10, 2016

Pronk Pops Show 695: June 9, 2016

Pronk Pops Show 694: June 8, 2016

Pronk Pops Show 693: June 6, 2016

Pronk Pops Show 692: June 3, 2016

Pronk Pops Show 691: June 2, 2016

Pronk Pops Show 690: June 1, 2016

Pronk Pops Show 689: May 31, 2016

Pronk Pops Show 688: May 27, 2016

Pronk Pops Show 687: May 26, 2016

Pronk Pops Show 686: May 25, 2016

Pronk Pops Show 685: May 24, 2016

Pronk Pops Show 684: May 23, 2016

Pronk Pops Show 683: May 20, 2016

Pronk Pops Show 682: May 19, 2016

Pronk Pops Show 681: May 17, 2016

Pronk Pops Show 680: May 16, 2016

Pronk Pops Show 679: May 13, 2016

Pronk Pops Show 678: May 12, 2016

Pronk Pops Show 677: May 11, 2016

Pronk Pops Show 676: May 10, 2016

Pronk Pops Show 675: May 9, 2016

Pronk Pops Show 674: May 6, 2016

Pronk Pops Show 673: May 5, 2016

Pronk Pops Show 672: May 4, 2016

Pronk Pops Show 671: May 3, 2016

Pronk Pops Show 670: May 2, 2016

Story 1: Make America Great Again and Remember The Alamo — Future President Donald J. Trump Meets Current Mexican President Pena — I Shall Return When The Wall Is Built and Paid For by Mexican Illegal Aliens In United States — Made In America — Videos

The-AlamoAlamoCongress Anti-Trump

DES MOINES, IA - AUGUST 15: Republican presidential candidate Donald Trump greets fairgoers while campaigning at the Iowa State Fair on August 15, 2015 in Des Moines, Iowa. Presidential candidates are addressing attendees at the Iowa State Fair on the Des Moines Register Presidential Soapbox stage and touring the fairgrounds. The State Fair runs through August 23. (Photo by Win McNamee/Getty Images)

funny-cartoon-cops1 illegal alien lock thme up mexico will pay for the wall presidentrumpProTrumpRecruitmentTool-NeverTrump-Mexican-AFBranco-ComicallyIncorrect-052616the great trump wallmexico-border-wall trump-and-immigration-cartoon-darkowtrump deportation plan trump-camps

RemembertheAlamoSanAntonioTexasalamo

Trump FULL Speech From Mexico

THE ALAMO: THE REAL STORY (WILD WEST HISTORY DOCUMENTARY)

Remember the alamo – Johnny Cash

Johnny Cash – Remember The Alamo

The Alamo – Davy Crockett Playing Violin

Full: Donald Trump and Mexican President Nieto Hold Press Conference 8/31/16

Donald Trump arrives in Mexico

What to expect from Trump’s meeting with Mexican prez

Weighing Issues Raised By Trump’s Mexican Visit

Vincente Fox “Donald Trump Is Not Welcome In Mexico” CNN Full Interview 8/31/16

BATTLE OF THE ALAMO 1836

The Alamo (1960) – Final Battle

Trump reveals how he would force Mexico to pay for border wall

Trump captures the nation’s attention on the campaign trail

April 5

Donald Trump says he would force Mexico to pay for a border wall as president by threatening to cut off the flow of billions of dollars in payments that immigrants send home to the country, an idea that could decimate the Mexican economy and set up an unprecedented showdown between the United States and a key regional ally.

In a two-page memo to The Washington Post, Trump outlined for the first time how he would seek to force Mexico to pay for his 1,000-mile border fence, which Trump has made a cornerstone of his presidential campaign and which has been repeatedly scoffed at by current and former Mexican leaders.

The proposal would jeopardize a stream of cash that many economists say is vital for Mexico’s struggling economy. But the feasibility of Trump’s plan is unclear both legally and politically, and it would test the bounds of a president’s executive powers in seeking to pressure another country.

In the memo, Trump said he would threaten to change a rule under the USA Patriot Act antiterrorism law to cut off a portion of the funds sent to Mexico through money transfers, commonly known as remittances. The threat would be withdrawn if Mexico made “a one-time payment of $5-10 billion” to pay for the border wall, he wrote.

“It’s an easy decision for Mexico,” Trump said in the memo, on campaign stationery emblazoned with “TRUMP Make America Great Again!”

After the wall was funded, Trump wrote, transfer payments could continue “to flow into their country year after year.” He gave the memo to The Post in response to a written question provided to him before an interview last week.

Nearly $25 billion was sent home by Mexicans living abroad in 2015, mostly in the form of money transfers, according to the Mexican central bank. In his memo, Trump said that “the majority of that amount comes from illegal aliens.”

But that figure includes cash from around the world, not just the United States. In addition, aGovernment Accountability Office report in January said it is difficult to track how much money Mexican immigrants working illegally in the United States are sending vs. money sent by those working legally.

Another complication in Trump’s remittance proposal is that he also wants to deport all 11 million immigrants living il­legally in the United States, many of whom come from Mexico.

President Obama sharply criticized Trump’s remittances proposal Tuesday and told reporters at the White House that foreign leaders are peppering him with questions “about some of the wackier suggestions” coming from Trump and his main Republican rival, Sen. Ted Cruz (Tex.).

“This is just one more example of something that is not thought through and is primarily put forward for political consumption,” Obama said. “The notion that we’re going to track every Western Union bit of money that’s being sent to Mexico, good luck with that.”

Cristóbal Alex, president of the Latino Victory Fund, blasted the idea as “a very dangerous and unrealistic proposal.”

“This is nothing but another attack against immigrants that would have devastating consequences for Latinos and Americans overall, endangering our economy, our democracy, our foreign policy and security,” Alex said.

Throughout the campaign, Trump has claimed that he could build his proposed U.S.-Mexico barrier for about $8 billion — a figure that numerous experts have described as dubious because of the costs and other obstacles to building a lengthy, impenetrable concrete barrier through numerous jurisdictions.

Trump’s proposal to pay for such a wall is also fraught with challenges. Although there is a shortcut in the Administrative Procedure Act that allows for ­“interim” regulations that take effect immediately without going through the regular public notice and comment process, there are limitations on that authority.

Based on the process for changes laid out in the Federal Register, Trump as president could potentially invoke a change by making the argument that illegal immigration is an emergency that must be addressed immediately or is a threat to public health or safety.

But such a rule would presumably apply to limiting wire transfers, canceling visas or raising visa fees — not about directly limiting immigration. That could make it harder for Trump to argue that any of those criteria meet the exceptions, according to some experts.

After reviewing Trump’s proposal, one expert on immigration law said he is skeptical.

“Trump is giving an extremely broad definition of this section of the Patriot Act and what it allows, and it’d surely be litigated,” said Stuart Anderson, executive director of the National Foundation for American Policy, a nonpartisan think tank in Virginia. “It would be a large expansion beyond what the text reads.”

Anderson said Trump’s memo also leaves unaddressed how normal financial transactions across borders would be affected and whether there would be an overly aggressive federal intrusion into the growing number of financial transactions that take place over the Internet.

With the subject line “Compelling Mexico to Pay for the Wall,” the memo is the latest attempt by the Republican presidential front-runner to offer more specifics about his proposal at a time when he faces tough head winds, including a loss to Cruz on Tuesday night in Wisconsin’s Republican primary.

The memo includes rationales for a number of potential intim­idation tactics, including increased trade tariffs, the cancellation of visas and higher fees for border-crossing cards.

But at the core of Trump’s approach is a focus on the remittances of illegal immigrants, which he argues are crucial to Mexican economic stability and are a way of pressuring the country to disburse billions of dollars to the United States to fund construction of his wall.

Trump’s official immigration plan, released last year, featured a pledge to “impound all remittance payments from illegal wages” and to hike fees on temporary visas, among other actions, but it did not go into further detail.

The playbook outlined in Trump’s memo echoes suggestions that have long been made by Sen. Jeff Sessions (R-Ala.), a Trump confidant and a hard-line voice on immigration policy within the Republican Party. Stephen Miller, a former top aide to Sessions, is Trump’s policy adviser.

Starting on “day 1,” Trump writes, he would issue a warning to Mexico that unless it pays his desired amount, he will promulgate a new federal provision that would lead to a sweeping confiscation of funds sent by Mexicans in the United States who lack documentation of their “lawful presence.”

On “day 2,” Trump continued, “Mexico will immediately protest.” But he would declare that Mexico must choose between the enforcement of his provision or acquiescing.

To explain how he would have the standing to pursue his aggressive strategy, Trump begins by citing a provision in the Code of Federal Regulations that sets the standards for financial institutions in identifying their customers.

That provision, Trump says, makes it possible for the executive branch to “issue detailed regulations on the subject.” He predicted that Mexico would react by initially balking, then doing what he wants.

Trump writes that “if the Mexican government will contribute $_ billion to the United States to pay for the wall, the Trump Administration will not promulgate the final rule, and the regulation will not go into effect.”

Many academics and economists have said that Trump’s notion of impounding remittances could have devastating consequences, harming poor communities and families that rely on funds from abroad to provide food and shelter.

Trump leaves open the option of using other methods to coerce Mexico, including “trade tariffs, or enforcement of existing trade rules,” “cancelling visas” and “visa fees.”

“Our approvals of hundreds of thousands of visas every year is one of our greatest leverage points,” Trump writes. “We also have leverage through business and tourist visas for important people in the Mexican economy.”

Trump ends with a scathing critique of Mexico, claiming that it has “taken advantage” of the United States for years through “gangs, drug traffickers and cartels” responsible for “the extraordinary daily cost of this criminal activity.”

“We have the moral high ground here,” Trump concludes, “and all the leverage.”

https://www.washingtonpost.com/politics/trump-would-seek-to-block-money-transfers-to-force-mexico-to-fund-border-wall/2016/04/05/c0196314-fa7c-11e5-80e4-c381214de1a3_story.html

 

 

Live: Donald Trump Calls Mexican President ‘a Friend’

Trump lands in Mexico for last-minute meeting with President Peña Nieto

August 31, 2016

U.S. presidential candidate Donald Trump landed here in his private jet Wednesday for a hastily arranged meeting with Mexican President Enrique Peña Nieto, according to local media reports, marking Trump’s first formal international trip as the Republican nominee to a country where he is broadly despised for his vilification of illegal immigrants.

Trump and Peña Nieto plan to meet Wednesday afternoon, ahead of a major immigration speech Trump is scheduled to deliver in the evening in Phoenix. His campaign manager, Kellyanne Conway, said Trump intends to talk to Peña Nieto about “shared concerns” including trade, illegal immigration and drugs.

“It’s very important to show that you’re willing to work with a neighboring country before you’re president,” Conway said on Fox News Channel.

She said the two will take questions from American and Mexican reporters and that it will be “up to them” to decide whether they want to make a joint statement. But American reporters who cover Trump regularly expressed concerns on social media about Trump’s decision not to bring his regular press corps with him.

El Universal, a major newspaper, reported the arrival, quoting airport sources, and said Trump would travel by helicopter from the airport’s presidential hangar to the presidential palace in Mexico City.

Republican presidential candidate Donald Trump, shown here in Sacramento in June, has landed in Mexico for a hastily arranged meeting with President Enrique Peña Nieto. (Josh Edelson/AFP/Getty Images)
Peña Nieto has sharply condemned Trump for repeatedly declaring that Mexico is sending predatory killers and rapists into America, but he is now the target of condemnation at home for extending an invitation to Trump last Friday. Democratic nominee Hillary Clinton also received an invitation but has not arranged a meeting yet.

Speaking at the American Legion convention in Cincinnati, Clinton went after Trump, saying coalition building and leadership will take more than a “photo-op.”

“It certainly takes more than trying to make up for a year of insults and insinuations by dropping in on our neighbors for a few hours and then flying home again. That is not how it works,” she said without naming her rival.
Former president Vicente Fox, an outspoken Trump critic, said on Mexican television that the visit would be an opportunity for Trump to mock Peña Nieto on his home turf. Fox told Milenio TV that Trump is not welcome and that “he has offended us, he has deceived us, he has discriminated against us.”

[Mexicans are angry at their own president for meeting with Trump]

Trump responded to Fox’s criticism by renewing his regular feuding with Fox, engaging directly with him in a bitter war of words on Twitter.

“Former President Vicente Fox, who is railing against my visit to Mexico today, also invited me when he apologized for using the ‘f bomb,” Trump tweeted Wednesday morning.

Mexican President Enrique Peña Nieto is meeting with U.S. presidential candidate Donald Trump Wednesday in Mexico City. (Pat Sullivan/AP)
Fox responded: “@realDonaldTrump, I invited you to come and apologize to all Mexicans. Stop lying! Mexico is not yours to play with, show some respect.”

Discussions of the meeting appear to have been closely held. Several Mexican officials and diplomats contacted Tuesday had no notion that Trump had even been invited, let alone planned to visit the next day.

When The Washington Post first reported on consideration of the trip Tuesday night, Mexico’s foreign minister, Claudia Ruiz Massieu, was in Milwaukee for the opening of a new Mexican consulate. Members of her staff said they were unaware of a possible Trump visit.

Trump’s trip to Mexico will give U.S. voters their first glimpse of how he carries himself in a high-level meeting with a foreign leader. Trump visited Scotland earlier this year before he was the GOP nominee in a trip characterized as personal, though he did praise Britain’s vote to exit the European Union in remarks to reporters.

Trump spent Wednesday morning in California at a home he owns in Beverly Hills and is scheduled to deliver his immigration speech in the evening at the Phoenix Convention Center.

The speech will come after Trump has wavered for weeks on whether he will continue to hold his hard-line positions on the central and incendiary issue of his campaign, in particular his call to deport an estimated 11 million immigrants who are living in the United States illegally.
In addition to vows of mass deportations, Trump has repeatedly promised to build a wall along the U.S.-Mexico border and force Mexico to pay for it. Peña Nieto and other Mexican leaders have dismissed the idea as preposterous.

“There is no way that Mexico can pay [for] a wall like that,” Peña Nieto said in a July interview on CNN, adding that he did not agree with Trump’s frequent characterization of illegal immigrants from Mexico as rapists and killers.

[The Fix: Trump’s high-risk, low-reward trip to Mexico is sort of baffling]

Questions about what would become of the estimated 11 million undocumented immigrants if Trump is elected have gone largely unanswered by the candidate and his team in recent days. The campaign has suggested that Wednesday’s speech will address those questions and concerns.

“I expect the speech to be a refinement of the goals he’s always stated,” said Rep. Kevin Cramer (R-N.D.), a Trump supporter. Cramer said that he would like to see Trump lay out a “chronology” of actions that he would try to achieve. The congressman said he is open to a plan that would afford illegal immigrants who have not committed crimes some form of legal status.

Trump has offered glimpses of his policy priorities even as he has skirted questions about their implementation. He remains publicly committed to building the border wall, has extolled the need to crack down on those who overstay their visas and has proposed expanding the E-Verify program, used by employers to determine whether an immigrant is legally able to work in the country.

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The campaign has also said Trump would prioritize the deportation of criminals, a policy that the Obama administration has pursued.

Mark Krikorian, a hard-line opponent of illegal immigration, said in an interview that he has been troubled by Trump’s recent language because it has echoed viewpoints championed by reform advocates such as former Florida governor Jeb Bush and Sen. Marco Rubio (R-Fla.).

“Anything that seems to suggest the kind of guarantee of an amnesty would, I think, as a policy matter be a bad idea — and as a political matter it would be a bad idea,” Krikorian said.
According to a study by the Migration Policy Institute, an estimated 690,000 undocumented immigrants have significant criminal histories — felony convictions or serious misdemeanors — that make them top priorities for deportation under current administration policy. The number of people prioritized for deportation would grow to about 5.5 million if visa overstays were included, according to some data, although those estimates are not considered very reliable.

https://www.washingtonpost.com/politics/trump-lands-in-mexico-for-last-minute-meeting-with-president-pena-nieto/2016/08/31/6e1a9f8c-6f8f-11e6-8533-6b0b0ded0253_story.html

 

Story 2: Trump Speech On Immigration Will Be Watched By 10 Million Plus Americans — Will Trump Flip Flop on Deportation of 30-50 Million  Illegal Aliens in United States? No, but Big Lie Media Will Say He Did! — Videos

Donald Trump Immigration Plan – O’Reilly

Hannity, Ingraham Team Up Again for 2nd Straight Day of Bashing ‘Arrogant’ #NeverTrump ers Mediait

Katrina Pierson previews Trump’s immigration speech

Kellyanne Conway: Donald Trump Will Lay Out Immigration Policy During Speech | TODAY

Is Donald Trump changing his immigration vision?

The Pronk Pops Show Podcasts Portfolio

IMMIGRATION REFORM THAT WILL MAKE AMERICA GREAT AGAIN

The three core principles of Donald J. Trump’s immigration plan

When politicians talk about “immigration reform” they mean: amnesty, cheap labor and open borders. The Schumer-Rubio immigration bill was nothing more than a giveaway to the corporate patrons who run both parties.

Real immigration reform puts the needs of working people first – not wealthy globetrotting donors. We are the only country in the world whose immigration system puts the needs of other nations ahead of our own. That must change. Here are the three core principles of real immigration reform:

1. A nation without borders is not a nation. There must be a wall across the southern border.

2. A nation without laws is not a nation. Laws passed in accordance with our Constitutional system of government must be enforced.

3. A nation that does not serve its own citizens is not a nation. Any immigration plan must improve jobs, wages and security for all Americans.

Make Mexico Pay For The Wall

For many years, Mexico’s leaders have been taking advantage of the United States by using illegal immigration to export the crime and poverty in their own country (as well as in other Latin American countries). They have even published pamphletson how to illegally immigrate to the United States. The costs for the United States have been extraordinary: U.S. taxpayers have been asked to pick up hundreds of billions in healthcare costs, housing costs, education costs, welfare costs, etc. Indeed, the annual cost of free tax credits alone paid to illegal immigrants quadrupled to $4.2 billion in 2011. The effects on jobseekers have also been disastrous, and black Americans have been particularly harmed.

The impact in terms of crime has been tragic. In recent weeks, the headlines have been covered with cases of criminals who crossed our border illegally only to go on to commit horrific crimes against Americans. Most recently, an illegal immigrant from Mexico, with a long arrest record, is charged with breaking into a 64 year-old woman’s home, crushing her skull and eye sockets with a hammer, raping her, and murdering her. The Police Chief in Santa Maria says the “blood trail” leads straight to Washington.

In 2011, the Government Accountability Office found that there were a shocking 3 million arrests attached to the incarcerated alien population, including tens of thousands of violent beatings, rapes and murders.

Meanwhile, Mexico continues to make billions on not only our bad trade deals but also relies heavily on the billions of dollars in remittances sent from illegal immigrants in the United States back to Mexico ($22 billion in 2013 alone).

In short, the Mexican government has taken the United States to the cleaners. They are responsible for this problem, and they must help pay to clean it up.

The cost of building a permanent border wall pales mightily in comparison to what American taxpayers spend every single year on dealing with the fallout of illegal immigration on their communities, schools and unemployment offices.

Mexico must pay for the wall and, until they do, the United States will, among other things: impound all remittance payments derived from illegal wages; increase fees on all temporary visas issued to Mexican CEOs and diplomats (and if necessary cancel them); increase fees on all border crossing cards – of which we issue about 1 million to Mexican nationals each year (a major source of visa overstays); increase fees on all NAFTA worker visas from Mexico (another major source of overstays); and increase fees at ports of entry to the United States from Mexico [Tariffs and foreign aid cuts are also options].  We will not be taken advantage of anymore.

Defend The Laws And Constitution Of The United States

America will only be great as long as America remains a nation of laws that lives according to the Constitution. No one is above the law. The following steps will return to the American people the safety of their laws, which politicians have stolen from them:

Triple the number of ICE officers. As the President of the ICE Officers’ Council explained in Congressional testimony: “Only approximately 5,000 officers and agents within ICE perform the lion’s share of ICE’s immigration mission…Compare that to the Los Angeles Police Department at approximately 10,000 officers. Approximately 5,000 officers in ICE cover 50 states, Puerto Rico and Guam, and are attempting to enforce immigration law against 11 million illegal aliens already in the interior of the United States. Since 9-11, the U.S. Border Patrol has tripled in size, while ICE’s immigration enforcement arm, Enforcement and Removal Operations (ERO), has remained at relatively the same size.” This will be funded by accepting the recommendation of the Inspector General for Tax Administration and eliminating tax credit payments to illegal immigrants.

Nationwide e-verify. This simple measure will protect jobs for unemployed Americans.

Mandatory return of all criminal aliens. The Obama Administration has released 76,000 aliens from its custody with criminal convictions since 2013 alone. All criminal aliens must be returned to their home countries, a process which can be aided by canceling any visas to foreign countries which will not accept their own criminals, and making it a separate and additional crime to commit an offense while here illegally.

Detention—not catch-and-release. Illegal aliens apprehended crossing the border must be detained until they are sent home, no more catch-and-release.

Defund sanctuary cities. Cut-off federal grants to any city which refuses to cooperate with federal law enforcement.

Enhanced penalties for overstaying a visa. Millions of people come to the United States on temporary visas but refuse to leave, without consequence. This is a threat to national security. Individuals who refuse to leave at the time their visa expires should be subject to criminal penalties; this will also help give local jurisdictions the power to hold visa overstays until federal authorities arrive. Completion of a visa tracking system – required by law but blocked by lobbyists – will be necessary as well.

Cooperate with local gang task forces. ICE officers should accompany local police departments conducting raids of violent street gangs like MS-13 and the 18th street gang, which have terrorized the country. All illegal aliens in gangs should be apprehended and deported. Again, quoting Chris Crane: “ICE Officers and Agents are forced to apply the Deferred Action for Childhood Arrivals (DACA) Directive, not to children in schools, but to adult inmates in jails. If an illegal-alien inmate simply claims eligibility, ICE is forced to release the alien back into the community. This includes serious criminals who have committed felonies, who have assaulted officers, and who prey on children…ICE officers should be required to place detainers on every illegal alien they encounter in jails and prisons, since these aliens not only violated immigration laws, but then went on to engage in activities that led to their arrest by police; ICE officers should be required to issue Notices to Appear to all illegal aliens with criminal convictions, DUI convictions, or a gang affiliation; ICE should be working with any state or local drug or gang task force that asks for such assistance.”

End birthright citizenship. This remains the biggest magnet for illegal immigration. By a 2:1 margin, voters say it’s the wrong policy, including Harry Reid who said “no sane country” would give automatic citizenship to the children of illegal immigrants.

Put American Workers First

Decades of disastrous trade deals and immigration policies have destroyed our middle class. Today, nearly 40% of black teenagers are unemployed. Nearly 30% of Hispanic teenagers are unemployed. For black Americans without high school diplomas, the bottom has fallen out: more than 70% were employed in 1960, compared to less than 40% in 2000. Across the economy, the percentage of adults in the labor force has collapsed to a level not experienced in generations. As CBS news wrote in a piece entitled “America’s incredible shrinking middle class”: “If the middle-class is the economic backbone of America, then the country is developing osteoporosis.”

The influx of foreign workers holds down salaries, keeps unemployment high, and makes it difficult for poor and working class Americans – including immigrants themselves and their children – to earn a middle class wage. Nearly half of all immigrants and their US-born children currently live in or near poverty, including more than 60 percent of Hispanic immigrants. Every year, we voluntarily admit another 2 million new immigrants, guest workers, refugees, and dependents, growing our existing all-time historic record population of 42 million immigrants. We need to control the admission of new low-earning workers in order to: help wages grow, get teenagers back to work, aid minorities’ rise into the middle class, help schools and communities falling behind, and to ensure our immigrant members of the national family become part of the American dream.

Additionally, we need to stop giving legal immigrant visas to people bent on causing us harm. From the 9/11 hijackers, to the Boston Bombers, and many others, our immigration system is being used to attack us. The President of the immigration caseworkers union declared in a statement on ISIS: “We’ve become the visa clearinghouse for the world.”

Here are some additional specific policy proposals for long-term reform:

Increase prevailing wage for H-1Bs. We graduate two times more Americans with STEM degrees each year than find STEM jobs, yet as much as two-thirds of entry-level hiring for IT jobs is accomplished through the H-1B program. More than half of H-1B visas are issued for the program’s lowest allowable wage level, and more than eighty percent for its bottom two. Raising the prevailing wage paid to H-1Bs will force companies to give these coveted entry-level jobs to the existing domestic pool of unemployed native and immigrant workers in the U.S., instead of flying in cheaper workers from overseas. This will improve the number of black, Hispanic and female workers in Silicon Valley who have been passed over in favor of the H-1B program. Mark Zuckerberg’s personal Senator, Marco Rubio, has a bill to triple H-1Bs that would decimate women and minorities.

Requirement to hire American workers first. Too many visas, like the H-1B, have no such requirement. In the year 2015, with 92 million Americans outside the workforce and incomes collapsing, we need companies to hire from the domestic pool of unemployed. Petitions for workers should be mailed to the unemployment office, not USCIS.

End welfare abuse. Applicants for entry to the United States should be required to certify that they can pay for their own housing, healthcare and other needs before coming to the U.S.

Jobs program for inner city youth. The J-1 visa jobs program for foreign youth will be terminated and replaced with a resume bank for inner city youth provided to all corporate subscribers to the J-1 visa program.

Refugee program for American children. Increase standards for the admission of refugees and asylum-seekers to crack down on abuses. Use the monies saved on expensive refugee programs to help place American children without parents in safer homes and communities, and to improve community safety in high crime neighborhoods in the United States.

Immigration moderation. Before any new green cards are issued to foreign workers abroad, there will be a pause where employers will have to hire from the domestic pool of unemployed immigrant and native workers. This will help reverse women’s plummeting workplace participation rate, grow wages, and allow record immigration levels to subside to more moderate historical averages.

https://www.donaldjtrump.com/positions/immigration-reform

 

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The Pronk Pops Show 726, July 27, 2016, Story 1: Sanders Sellsout Socialist Supporters — Videos — Story 2: Smooth Operator Bill Clinton Reveals Real Hillary: My Ding-A-Ling — I did not have sex with that wonderful woman; What difference does it make? Vince did. The Sweetest Taboo — Videos — Story 3: The Trump Strikes Back — They are coming to take Hillary and Huma away HA HA — The Future of Freedom –Videos

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