Float like a butterfly……Head injury and dementias

So, the film “Ali” is on TV and it has me thinking about the (Parkinson syndrome) dementia he would later develop as a result of his boxing career (and likely mixed with dementia pugilistica – boxer’s dementia).

And I started thinking about that line that someone says if they look like they got a beating, “yeah, but you should see the other guy!” And I started to wonder, what did happen with Ali’s opponents?

I had to look it up, because I don’t know that much about boxing. I like these little research projects. Sure, I missed half of the movie, but I think I learned a lot more!

So here’s what I found about Ali’s opponents in under an hour:

Jerry Quarry did go on to develop dementia pugilistica and has passed away.

Floyd Patterson developed dementia pugilistica and has passed away.

Tunney Hunsaker had a long battle with Alzheimer’s disease and has passed away.

Leon Spinks developed dementia pugilistica at a young age.

Jimmy Ellis developed dementia pugilistica and has passed away.

Jimmy Young was showing symptoms of dementia pugilistica and has passed away.

Joe Frazier is rumored to have symptoms.

I think he really did and does live like a champion. And he has always had the attitude to go with 😉 When I was working at an Adult Day Center through the Alzheimer’s Association in Dallas, Texas (2004), one of the volunteers had been a repeated contact point for Muhammad Ali when he came to town for medical appointments. She said he was just the sweetest man!

You have heard in the news lately, that there is talk of concussions and head trauma leading to dementia. You have heard the outcomes of sport’s greats, such as:

So, now you wonder how and why. Hopefully, some research and these articles will help you understand. You can also read my other post on sports and dementia here.

Dementia Pugilistica:  About “Punch-Drunk” Syndrome

From Protect The Brain

Dementia pugilistica, is commonly referred to as punch-drunk syndrome, due to the fact that it was originally discovered in boxers in the 1920s. In fact, the term itself derives from the Latin word pugil, which translates as “boxer” or “fighter.” It occurs in people who have suffered multiple concussions, and it commonly manifests itself as dementia – or declining mental ability – along with problems with memory, and Parkinsonism, which is characterized by a lack of coordination.

A study published in 1928 in the Journal of the American Medical Association was the first to describe dementia pugilistica. The report noted that boxers who suffer from this condition will commonly experience tremors, slowed movement, speech problems and confusion. Dementia pugilistica frequently goes undiagnosed, due to the fact that it will commonly not begin to cause symptoms for many years or even decades. Further, its symptoms are often mistakenly ascribed to the effects of old age or conditions such as Alzheimer’s disease.

Dementia Pugilistica and Chronic Traumatic Encephalopathy

Dementia pugilistica is actually a variant of chronic traumatic encephalopathy (CTE), which is itself a serious type of brain damage resulting from repeated concussions and is found in many professional athletes and military personnel who have been subjected to multiple impacts to the head. Severe concussions and mild traumatic brain injury are both capable of causing CTE, and the likelihood of developing this condition is increased with the number of impacts. Whereas CTE was formerly believed to be a disease which affected primarily only professional and amateur boxers, it is now understood to be an affliction suffered by many more people. The doctors at the Brain Injury Research Institute have made considerable contributions to raising public awareness of CTE and are working to find effective solutions for prevention and treatment.

Well, what is traumatic brain injury, exactly?

(information from the Alzheimer’s Association)

Traumatic brain injury results from an impact to the head that disrupts normal brain function. Traumatic brain injury may affect a person’s cognitive abilities, including learning and thinking skills

Falls are the leading cause of traumatic brain injury for all ages. Those aged 75 and older have the highest rates of traumatic brain injury-related hospitalization and death due to falls.

Doctors classify traumatic brain injury as mild, moderate or severe, depending on whether the injury causes unconsciousness, how long unconsciousness lasts and the severity of symptoms. Although most traumatic brain injuries are classified as mild because they’re not life-threatening, even a mild traumatic brain injury can have serious and long-lasting effects.

Traumatic brain injury is a threat to cognitive health in two ways:

  1. A traumatic brain injury’s direct effects, which may be long-lasting or even permanent, can include unconsciousness, inability to recall the traumatic event, confusion, difficulty learning and remembering new information, trouble speaking coherently, unsteadiness, lack of coordination and problems with vision or hearing.
  2. Certain types of traumatic brain injury may increase the risk of developing Alzheimer’s or another form of dementia years after the injury takes place. Learn more.

If a Head Injury Occurs

If you or someone you’re with experiences an impact to the head and develops any symptoms of traumatic brain injury, seek medical advice even if symptoms seem mild. Call emergency services for anyone who is unconscious for more than a minute or two or who experiences seizures, repeated vomiting or symptoms that seem to worsen as time passes. Also seek emergency care for anyone whose head was injured during ejection from a vehicle, who was struck by a vehicle while on foot, or who fell from a height of more than 3 feet. Even if you don’t lose consciousness and your symptoms clear up quickly, a brain injury still may have occurred.


Symptoms of a brain injury include:

  • Unconsciousness
  • Inability to remember the cause of the injury or events that occurred Immediately before or up to 24 hours after
  • Confusion and disorientation
  • Difficulty remembering new information
  • Headache
  • Dizziness
  • Blurry vision
  • Nausea and vomiting
  • Ringing in the ears
  • Trouble speaking coherently
  • Changes in emotions or sleep patterns

The severity of symptoms depends on whether the injury is mild, moderate or severe.

  • Mild traumatic brain injury, also known as a concussion, either doesn’t knock you out or knocks you out for 30 minutes or less. Symptoms often appear at the time of the injury or soon after, but sometimes may not develop for days or weeks. Mild traumatic brain injury symptoms are usually temporary and clear up within hours, days or weeks, but they can last months or longer.
  • Moderate traumatic brain injury causes unconsciousness lasting more than 30 minutes. Symptoms of moderate traumatic brain injury are similar to those of mild traumatic brain injury but more serious and longer-lasting.
  • Severe traumatic brain injury knocks you out for more than 24 hours. Symptoms of severe traumatic brain injury are also similar to those of mild traumatic brain injury but more serious and longer-lasting.


Evaluations by health care professionals typically include:

  • Questions about the circumstances of the injury
  • Assessment of the person’s level of consciousness and confusion
  • Neurological examination to assess memory and thinking, vision, hearing, touch, balance, reflexes and other indicators of brain function

Depending on the nature of the traumatic brain injury and the severity of symptoms, brain imaging with computed tomography (CT) may be needed to determine if there’s bleeding or swelling in the brain.

Causes and risks

Falls are the most common cause of traumatic brain injury, and falling poses an especially serious risk for older adults. When a senior sustains a traumatic brain injury in a fall, direct effects of the injury may result in long-term cognitive changes, reduced ability to function and changes in emotional health.

Vehicle crashes are another common cause of traumatic brain injury. You can reduce your risk by keeping your vehicle in good repair, following the rules of the road, and buckling your seat belt.

Sports injuries are also a cause of traumatic brain injury. You can protect your head by wearing a helmet and other protective equipment when biking, inline skating or playing contact sports.

Other causes include

  • Indirect forces that jolt the brain violently within the skull, such as shock waves from battlefield explosion
  • Bullet wounds or other injuries that penetrate the skull and brain

Dementia and traumatic brain injury Over the past 30 years, research has linked moderate and severe traumatic brain injury to a greater risk of developing Alzheimer’s disease or another type of dementia years after the original head injury.

  • One of the key studies showing an increased risk found that older adults with a history of moderate traumatic brain injury had a 2.3 times greater risk of developing Alzheimer’s than seniors with no history of head injury, and those with a history of severe traumatic brain injury had a 4.5 times greater risk.

Does every hit to the head lead to dementia?

Not everyone who experiences a head injury develops dementia. There’s no evidence that a single mild traumatic brain injury increases dementia risk. More research is needed to confirm the possible link between brain injury and dementia and to understand why moderate, severe and repeated mild traumatic brain injuries may increase risk.

Other studies — but not all — have found a link between moderate and severe traumatic brain injury and elevated risk.

Emerging evidence suggests that repeated mild traumatic brain injuries, such as those that can occur in sports like American football, hockey and soccer, may be linked to a greater risk of a type of dementia called chronic traumatic encephalopathy. Research has shown that boxers have an increased risk of chronic traumatic encephalopathy.

Current research on how traumatic brain injury changes brain chemistry indicates a relationship between traumatic brain injury and hallmark protein abnormalities (beta-amyloid and tau) linked to Alzheimer’s.

Some research suggests that traumatic brain injury may be more likely to cause dementia in individuals who have a variation of the gene for apolipoprotein E (APOE) called APOE-e4. More research is needed to understand the link between APOE-e4 and dementia risk in those who’ve had a brain injury.

Treatment and outcomes

The most serious traumatic brain injuries require specialized hospital care and can require months of inpatient rehabilitation. Most traumatic brain injuries are mild and can be managed with either a short hospital stay for observation or at-home monitoring followed by outpatient rehab, if needed.

Treatment of dementia in a person with a history of traumatic brain injuries varies depending on the type of dementia diagnosed. Strategies for treating Alzheimer’s or another specific type of dementia are the same for individuals with and without a history of traumatic brain injury.

Alzheimer’s disease and other dementias that may occur as a long-term result of traumatic brain injury are progressive disorders that worsen over time. As with all dementias, they affect quality of life, shorten lifespan and complicate the effort to manage other health conditions effectively.

Dementia Help and Support are Available

The Alzheimer’s Association can help you learn more about Alzheimer’s and other dementias, and help you find local support services. Call our 24/7 Helpline at 800.272.3900.
Brain Injury Association of America  (HDSA) is an education, advocacy and research organization that offers support to people with brain injuries and their families. Call their information center at 800.444.6443.
Centers for Disease Control (CDC) has a traumatic brain injury section that offers information about research studies and prevention and education programs.

‘Brain Games’:  preventing, diagnosing sub-concussive brain trauma

This article comes form Telehealth and Telecare Aware’s website, May 16, 2014.

Tuesday 13 May, presented at NYC MedTech-the NYC Medical Technology Forum, at Troutman Sanders LLP, Chrysler Building, New York City

In a packed (agenda and attendees) two hour evening meeting, three presenters detailed the latest research on the clinical signs of chronic traumatic encephalopathy (CTE), along with new technologies for detecting it as it happens and diagnosing it plus monitoring recovery: Robert Stern, PhD, professor of neurology and neurosurgery at the Boston University School of Medicine and a leading clinical researcher on CTE (as our long-time readers know) ; Isaiah Kacyvenski, head of the sports segment of electronics designer MC10 which developed the Checklight head impact indicator for Reebok; and Uzma Samadani, MD, PhD, co-founder of Oculogica which presented at ELabNYC a few weeks ago.

Dr. Stern’s presentation reviewed his clinical work with primarily NFL players in how CTE manifests in both behavior patterns and the brain. His focus remains on sub-concussive trauma, the ‘bottom of the iceberg’ in his analogy, and its cumulative, long-term effects.  Repetitive brain trauma–neuronal shearing which is produced by linear, lateral and rotational forces to the head–produce a cascade of brain changes leading to destruction of brain tissues that show as dark patches on post-mortem samples and scans. These differ from Alzheimer’s disease in the abundance of tau protein distributed fairly early in life around the brain’s blood vessels and in the depths of the cortical sulci, where Alzheimer’s signature beta amyloid does not locate. Dr. Stern’s research also incorporates the behavioral changes that precede diagnosis: the emotional ‘short fuse’, the difficulty in memory, accidents, suicide, drastic changes in behavior and impulse control. There are many examples of degeneration and early death among players [TTA 6 Dec 12 which also refers to Dr. Stern’s research published in Brain; also see TTA 5 June 2013 on his German Center presentation which has additional background on his and his team’s research.]

In addition to the work he has done relating to (American) football (he is on the NFL Players Association brain injury committee and his research was instrumental in the PA’s lawsuit against the NFL), he studies other contact sports such as hockey (brain injury clusters among the ‘enforcers’), soccer (football everywhere ex US), baseball (pitchers ‘beaning’ batters) and rugby (rough and unprotected all over, making this sport a favorite of orthopedic surgeons). Routinely, football players experience 20-30G blows up to 1,000 times per year of play which are not prevented by those impressive helmets designed to protect against skull fracture.) These repetitive blows start in junior football in boys as young as 8 or 9. In no-helmet soccer, the danger is in heading the ball; the force can be 15Gs. It seems that all you need is adequate (not high) G force to create neuronal changes, but detection is difficult because these events have no immediate physical symptoms.

The research around CTE has produced changes in the practice of contact sports and protection against head blows. Texas is synonymous with high school football, but even they have restricted the amount of full-contact practices both during and pre-season (Forbes); California and Arizona also adopted similar rules (NPR) with Illinois the latest in April (Breitbart).

Dr. Stern’s newest research is not yet published, but he shared two preliminary findings and overall status with this audience of clinicians, academics, attorneys, investors:

  • Football players who started in the game before the age of 12 had three times the likelihood of self-reported executive function problems: changes in mood, behavior, cognition.
  • CTE has been found in a developmentally disabled person who is a repetitive head banger.
  • Among soldiers, blast trauma in combat may be leading to CTE.
  • The next step is to find biomarkers (the Dr. Inga Koerte research)–the DETECT study using lumbar puncture– and brain imagery (early PET scan, Siemens) to locate abnormal tau levels so that CTE can be diagnosed earlier and more definitively.

Dr. Stern concluded that his work has only reached the ‘infant stage’ of development. Questions which badly need answers: Is CTE common? Why do some contact sports athletes get it and others never do? What are the risk factors? Genetics? Exposure? Far larger sample sizes–and funding–are needed, and unfortunately NIH funding has grown scarce.

[A note to the Howard Hughes Medical Institute: Mr. Hughes was the poster child for head trauma due to at least 14 airplane and car crashes. Could this have led to his bizarre behavior over years, culminating in debilitating mental illness? ]

Beyond the research

MC10 develops electronics which are stretchable and wearable for sports and fitness, consumer health and medical products. If this sounds familiar, the company’s co-founder and ‘father of conformal electronics technology’ is John Rogers, professor at the University of Illinois, Champaign-Urbana. [More here on his stretchy sensor patches powered by tiny biodegradable batteries.] Isaiah Kacyvenski presented an overview of their new product to detect head concussion, the Reebok Checklight, which premiered at International CES [TTA 15 Nov 13] and retailing for about $150. Where the breakthrough in adoption could be is reduction in insurance liability, but further and wider research will have to be done to accumulate the data. Mr. Kacyvensky is a former NFL player (with six concussions), graduating from Harvard with a pre-med degree and post-NFL, a Harvard Business School MBA.

This Editor profiled Oculogica at the ELab Pitch Day [TTA 17 Apr] and on 2 May in our overview of concussion diagnostics. Dr. Uzma Samadani primarily discussed the neurodiagnostics science behind the development of EyeBox CNS. The idea came from tracking eyes watching TV. What it does is quantify the physiologic tracking of eyes moving together (convergence). In about 120 seconds, a normal person’s eyes will track a box pattern about five times. Not only in head trauma but also in brain tumors and diabetes, this tracking can be disrupted. EyeBox also can track recovery time–the time it takes for the eyes to revert back to a box pattern. Early subject studies are finding a wide variation, much greater than expected, in recovery.

Credit for this exemplary meeting goes to John Lieberman, CPA of Perelson Weiner LLP, founder of NYC MedTech, for his excellent organization and host Heather Ettinger of Troutman Sanders LLP for their hospitality. 

You can read a bit more on boxers with dementia pugilistica here

A clinical summary of it here 

More about dementia pugilistica here

More on Parkinsonism-Pugilistica here

And more about the different types of dementia here 


6 thoughts on “Float like a butterfly……Head injury and dementias

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