Tag Archive | vascular dementia

The Little Things – Mother’s Day 2017

Mama and DaddyIt’s the little things that I think and dream about now that Mama is gone. Some of them are real and some, those in my dreamworld, are reconfigured to how I wished or hoped they had turned out.

As time passes between my parents’ deaths, I find more and more Daddy and Mama are together, the two of them and sometimes with my sisters and and sometimes just with me, but we all seem to be younger, when our lives were more together than they are now and we shared the little things that glued us together.
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Transcatheter Aortic Valve Replacement (TAVR) Linked to Increased Risk of Neurological Microbleeds and Vascular Dementia

healthy vs failing aortic valveAortic valve failure is a cardiac condition in which the aortic valve fails to open and close properly, negatively affecting healthy blood flow both to the brain and to the body. 

There are two surgical methods currently that can restore normal aortic valve functioning. Continue reading

Super Bowl 50, Football, and the Everpresent Looming Specter of Dementia

Football carries a huge risk of neurological damage and the development of dementiaToday, February 7, 2016, the 50th Super Bowl game in NFL (National Football League) history will be played by the Carolina Panthers and the Denver Broncos. Therefore, it is appropriate to discuss the other dark and dangerous side of this football game – and all the ones played before and all the ones that will be played after – before it is played.

Super Bowl games have become extravagant and lavish productions in the last ten years or so, intended to bring into the audience people who normally either don’t have interest in the game or don’t normally watch football. Super Bowl games also represent an obscenely huge financial windfall for the NFL and for advertisers with enough money to pay for the coveted and outrageously expensive advertising spots during the game. Continue reading

Profiles in Dementia: Woodrow Wilson (1856 – 1924)

President Wilson had suffered from arteriosclerosis since 1906 and was showing signs of vascular dementia by 1917.I have been, over the last couple of months, reading a lot of books about the history of World War I – before, during, and after – and the last book I’ve read in this series so far gave intimate and detailed portraits of the four world leaders who were ultimately responsible for the Treaty of Versailles, which may have been the most-poorly and ignorantly (in some cases, deliberately) constructed end-of-war agreement ever made. Continue reading

The Layperson’s Guide to Neural Disorders That Often Lead to Neurodegeneration and Dementia

Normal brain cellMost dementias – Lewy Body dementia, vascular dementia, early-onset dementias, alcohol-related dementia, and Alzheimer’s Disease among them – appear seemingly suddenly as primary and distinct neurodegenerative processes without definitive causes (except in the case of genetic inheritance, which primarily occurs in rare dementias like Corticobasal Degeneration, Progressive Supranuclear Palsy, and Fatal Familial Insomnia and some of the early-onset dementias).

However, there are a group of neural disorders, which are caused by the same genetic mutation that affects lipid storage in the body, that often have dementia as a secondary symptom as the diseases progress.  

Structure of cell membraneThese neural disorders (all these have sphingolipid metabolism dysfunction in common) – which include Niemann-Pick disease, Tay Sachs disease, and Gaucher disease – are characterized by by increased levels of a particular type of sphingolipid.

There is no cure for these neural disorders and they are all fatal (in many cases, during childhood).

Anatomy of a sphingolipidSpingolipids are the biological product of a chemical process that creates a protective layer on nerve cell membranes and ensures proper – and protective – cell signaling and are critical to optimal brain function.

The genesis of sphingolipids are long-chain – also known as sphingoid – bases that normally have a length of 18 carbons, although they can also have lengths of 16 or 20 carbons. The length of long-chain bases is determined by serine palmitoyltransferase (STP), a multiprotein enzyme.

Chemistry of sphingolipidIn neural disorders like Niemann-Pick disease, Tay Sachs disease, and Gaucher disease, a mutation (known as Stellar) in one of the proteins that makes up STP creates an abnormally high number of 20 carbon long-chain bases, which dramatically interferes with sphingolipid metabolism.

This causes neurodegeneration to occur. In all these neural disorders, much of the neurodegeneration begins soon after birth.

In Tay Sachs disease, neurodegeneration of the brain and spinal cord begins at about six months of age. The average lifespan is four years.

Gaucher disease has three subtypes.

In Type 1 Gaucher disease, symptoms, which include anemia, bone deterioration, and liver and spleen impairment, are non-neurological and do not materialize until middle age. The average life expectancy for Type 1 is 68 years.

Type 2 and Type 3 Gaucher disease are both neuropathic forms of the disease.  Neurodegenerative symptoms include abnormal eye movements, seizures, and systemic brain damage.

In Type 2 Gaucher disease, the onset of symptoms is within three to six months of age. Deterioration is rapid; the average life expectancy is about two years of age.

 Type 3 Gaucher disease is a slower onset and involving version of Type 2. The average onset of neurological involvement is late childhood into adolescence. Life expectancy ranges from the mid-twenties to, in extremely rare cases, the early forties.

Niemann-Pick disease has four types: Type A, Type B, Type C1 and Type C2.

Niemann-Pick disease Type A occurs in infants. Symptoms include enlargement of the liver and spleen (around three months of age) and a failure to thrive during the first year of life. At one year, widespread damage to the lungs occurs, and there is a progressive loss of neurological and motor function.

A cherry red spot on the macula is a common denominator in Tay Sachs Disease and Niemann Pick disease Type 1Along with Tay Sachs disease, Niemann-Pick disease Type A also has a common eye deformity consistent with neurometabolic disease, known as a cherry spot, that occurs within the macula and is often what initially identifies the two neural disorders.

While most children born with Niemann-Pick disease Type A die in infancy, a few may live as long as four years.

Niemann-Pick disease Type B includes most of the same symptoms as Type A (motor skills are not usually affected), but the onset of symptoms is during adolescence. Most people with Niemann-Pick disease Type B survive into adulthood, but mortality rates climb dramatically between twenty and thirty years of age.

Niemann-Pick disease Type C (C1 and C2 are caused by different gene mutations, but the symptoms are the same) is characterized by severe liver disease, severe pulmonary infections, progressive neurodegeneration, and increasing difficulty with speech and swallowing that deteriorates completely over time.

The onset of Niemann-Pick disease Type C can be at any age, but it is most commonly seen by the age of five. The life expectancy with this type is under twenty years of age when symptoms appear in childhood. When symptoms appear later, the life expectancy is ten to twenty years after symptoms begin.

 

 

Profiles In Dementia: Winston Churchill (1874-1965)

Winston Churchill Vascular DementiaWinston Churchill had a health profile most of his adult life that pointed to the inevitability of cognitive impairment in his later years.

Churchill was an alcoholic (during War War I and II, when the British needed strategic decisions to be made in the middle of the night, an inebriated Churchill was in the thick of things because even drunk he apparently was a better strategist than most of his sober peers).

Churchill also had chronic and worsening hypertension, in part from stress and in part from an unrestrained diet of much rich and artery-clogging food.

As early as 1947, Churchill’s physician, who was complicit in the lies about Churchill’s health all the years he held public office and who propped him up with amphetamines and calmed him down with depressants, noted in his diary that “[Churchill] is no longer fertile in ideas…his once-teeming mind has run dry.”

Beginning in 1948, Churchill began to regularly experience TIA’s in different parts of his brain. Accompanying the mini-strokes, at times, was temporary numbness on one or the other sides of his body, which resolved in a few hours or a few days.

Churchill would also experience the temporary dysphasia in the 30 minutes to an hour afterward that is characteristic of TIA’s, but the language center of his brain was spared permanent damage until his last major stroke in 1953.

With amphetamines and carefully scripted speeches, therefore, Churchill was able, at least from a verbal aspect, to hide the neurological damage and the cognitive decline that those closest to him were aware was progressing rapidly.

But the signs were everywhere in retrospect. Churchill’s speeches and governing were rooted in the first and second world wars. He was glaringly oblivious to post World-War-II politics, issues, and legislation.

He was literally in the-all-too-common vascular dementia time warp of the past and increasingly unaware of the present and had no concept of the future.

With his doctors and his staff carefully concealing his progressing dementia from the public, Churchill managed to limp along in office through continuous TIA’s and three major strokes, until 1955, when he finally resigned because his cognitive impairment and the physical effects of the strokes and dementia were impossible to conceal anymore.

Churchill lived for 10 more years, but vascular dementia was his constant companion and as it progressed, he retreated and regressed until he remembered no one and nothing and it was impossible to see the man he’d been at the zenith of his life.

 

 

Profiles in Dementia: Bill Guthridge (1937 – 2015)

Bill Guthridge UNC-Chapel Hill Basketball Coach 1997-2000On May 13, 2015, former University of North Carolina – Chapel Hill basketball coach Bill Guthridge died from heart failure. However, it was Coach Guthridge’s incurable heart condition that led to his development of vascular dementia, and with its progression, his placement for the last several years in a Chapel Hill assisted living facility. 

If Bill Guthridge doesn’t look familiar to you as a UNC-Chapel Hill head basketball coach, there’s a very good reason for that. He was and has been overshadowed and a bit lost in the shuffle of UNC basketball coaches by his lifelong friend, former UNC head coach Dean Smith (1961 to 1997), and current UNC head coach Roy Williams, who was an assistant coach along with Guthridge at UNC from 1978 to 1988.

However, Coach Guthridge served as the perfect replacement as head basketball coach when Coach Smith unexpectantly announced his retirement from the University of North Carolina at Chapel Hill in 1997.

UNC Coach Dean Smith and UNC Coach Bill Guthridge 1970'sCoach Guthridge had been Coach Smith’s assistant coach at UNC for 30 years, so he knew Coach Smith’s style, plays, and strategies inside and out. Coach Guthridge was the right choice to lead the transition to another, younger leader of the famed basketball program at the University of North Carolina.

Unfortunately, it took UNC two tries to find that leader.

The university made a huge misstep when it hired former UNC player, Matt Doherty, a young, untested coach in the league of the Atlantic Coast Conference (ACC) and a 180-degree change from the coaching styles of Coach Smith and Coach Guthridge, as its head basketball coach in 2000, when Coach Guthridge retired.

University of North Carolina Chapel Hill Head Coach Roy WilliamsAfter a three-year disastrous tenure under Doherty, the University of North Carolina hired Roy Williams from Kansas and got the leadership and gravitas that had characterized the UNC basketball program under Coach Smith and Coach Guthridge.

After Coach Guthridge’s retirement in 2003, he and Coach Smith stayed in close contact, visiting each other frequently. Ironically, both coaches developed dementia along the way (Coach Smith died in January 2015 of complications from dementia).

Coach Smith began showing signs of cognitive impairment before Coach Guthridge did. It was profoundly hard for Coach Guthridge to watch his lifetime friend become forgetful and lose the memories they shared together, not just as the architects of a fantastic and highly-ethical college basketball program, but as friends who regarded each other and their respective families as their own.

Coach Guthridge Early Years as UNC Assistant CoachWhen Coach Smith died, Coach Guthridge knew that his friend was gone, but he quickly moved back to their time together when they were younger and dementia had not knocked on their doors yet.

My guess is that Coach Guthridge probably never came back from that place after Coach Smith’s death and I would speculate that Coach Smith’s death may have been the final straw of an increasingly-unfamiliar and disconnected life for Coach Guthridge. Perhaps, at last, somewhere in his mind, Coach Guthridge finally made the decision to retire from this physical life.

Perhaps, at last, somewhere in his mind, Coach Guthridge finally made the decision it was time for him to retire from this physical life.

Coach Guthridge made his retirement official on May 13, 2015.