Blowing The Whistle On Sports Concussions

Chris Borland, a star rookie linebacker for the 49ers, announced in March of 2015 that he would retire early from football. He had 2 concussions and walked away from a multimillion-dollar contract and possible superstardom. He said, “I don’t think it’s worth the risk.” The NFL estimates that 30% of former players will develop dementia.

The term chronic traumatic encephalopathy is new, but the disorder was recognized as far back as 1928 when a Dr Harrison Martland described a condition in boxers who were recognized to be “punch-drunk” that was similar to Parkinson’s. The condition seemed irreversible and worsened steadily, even after retirement from boxing. Severity correlated with the number of professional bouts. Muhammad Ali was the poster child. A similar syndrome has been reported in non-athletes who had repetitive brain injuries, such as abuse victims, veterans, autistic patients with head-banging behavior, and in fact a circus clown. The sports most likely to cause chronic traumatic encephalopathy (CTE) are professional football, hockey, rugby, professional wrestling, and soccer. There is evidence that repetitive “subconcussive” head trauma, meaning that the trauma affects the brain but does not cause symptoms, may contribute to CTE. Thus, athletes who were never recognized to have a concussion may still be at increased risk.

There are many unanswered questions. Is there a threshold number of concussive or subconcussive injuries that will increase risk? The National Institutes of Health recently funded 2 large research projects, utilizing funds contributed by the NFL.

The symptoms of CTE are usually mood disorders, headaches, cognitive difficulties, suicidal ideation, difficulties with speech, and aggressive behavior. These athletes tend to have poor impulse control and are short-tempered.

Understanding why some athletes develop CTE and others do not is a major public health challenge.

See Neurology, October 27, 2015, page 1442 and 1504.

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Patient-Driven Research In Parkinson’s

Finding effective treatments for Parkinson’s has been difficult. Part of the problem is recruiting patients in clinical trials. Allowing patients to participate in the design of the trial can go far in solving this problem.

The disease drastically affects quality of life, and a network that shares knowledge would be a boon for professionals and patients alike. There are several models of this type of collaboration. One is termed ParkinsonNet, founded in the Netherlands in 2004, and more recently the Parkinson’s Excellence Network in the UK. A third is Parkinson’s Movement, which is part of the Cure Parkinson’s Trust, which is a patient-based think tank in the US and UK. Recently, a partnership was formed between ParkinsonNet and the Van Andel Research Institute based in Grand Rapids, Michigan. Kaiser Permanente is testing the feasibility of ParkinsonNet in a setting in California. This is based on the Dutch model.

Key focus areas are better treatment, improved services, and getting patients more control of their disorder. The goal is a new era of patient-driven research in healthcare.

See Lancet Neurology, November 2015, page 1077-1078.

Age is the most important risk factor in developing Alzheimer’s

By 2050, the number of elderly individuals older than 80 years is projected to triple globally. This has been termed the “coming epidemic.” Ten years ago, research demonstrated that aged liver tissue exposed to young blood has greater regenerative capacity, and studies showed similar benefit in muscle tissue. These studies have been replicated several times but only in mice.

The hippocampus is a key brain structure in memory, and atrophy of that area of the brain is almost always seen in Alzheimer’s patients. The brain is protected by “the blood-brain barrier,” but an area in the hippocampus is closely associated with blood vessels and thus is exposed to systemic factors. Even though the effects of transfusing young blood into aged mice are strong, the aged brain so exposed shows much less regeneration than young rodents’ brain. Transfusing young blood leads to enhanced neurogenesis, meaning new nerve cells and synaptic plasticity, meaning more connections between nerve cells. Memory and other higher order cognitive functions can be measured and are improved.

There are many issues. Although blood plasma products are widely used in humans and considered relatively safe, the potential for cancer has not been studied.

Two studies have been started to examine improvement in symptoms in patients with mild to moderate Alzheimer’s disease following the removal or addition of blood factors that impair or improve brain function. One study is named AMBAR (Alzheimer’s Management By Albumin Replacement) and the other PLASMA (PLasma for Alzheimer SymptoM Amelioration). All clinical trials are registered at the web site These 2 trials are numbered NCT01561053 and NCT02256306.

These research approaches sound too good to be true, but how lovely to contemplate the possibility that they may succeed.

See JAMA Neurology, October 2015, Castellano, PhD, et al.

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CoQ10 For Parkinson’s Is Back

Coenzyme Q10 is the electron acceptor for complexes I and II in the organelle in the cells termed mitochondria. A toxin can cause parkinsonism through inhibition of complex I. These scientific findings led to trials of CoQ10 in Parkinson’s. The first study using 200 mg a day seemed to improve symptoms in early Parkinson’s, but a larger study failed to confirm these results.

Now a new study, published in Parkinsonism & Related Disorders by lead author Asako Yoritaka, August 2015, was a placebo-controlled pilot trial of the reduced form of CoQ10 termed ubiquinol-10. There were only 14 patients in the treated group and 12 in the placebo group, but there seemed to be benefit in improving “off” time. Results do not lead to the conclusion that the medication may help early Parkinson’s. Furthermore, the very small numbers of patients tested limits significance of the results.

Nevertheless, ubiquinol is a widely available supplement. A dose of 300 mg a day has been found to be safe in healthy volunteers and was also safe in patients in the study. Those patients were given 2 of the 50 mg capsules 3 times a day for a total dose of 300 mg a day. The brand by Kaneka was used. This is easy to purchase online. This dose would probably cost $30 to $40 a month.

Can You Improve Your Cognitive Function With Supplements And Exercise?

Most research studies with long-term Mediterranean and heart-healthy diets have shown improved cognitive function. Some studies of regular exercising have also resulted in improved function. Results of 2 new randomized trials showed surprising results.

In the first, 3741 older adults with mean age of 73 received either 3 supplements thought to help cognitive function or placebo. In 5 years, both groups were the same.

In the second study, 635 sedentary older adults with no cognitive impairment attended home exercise programs of walking and strength training and increased their weekly exercise by over 2 hours. This was compared with a health education-only group. At 2 years, cognitive scores were not different.

Nutritional supplements are not food, and findings do not contradict those of healthy diets. The same caveat applies to some extent for physical activity. The specific components of exercise that enhance cognitive function have not been well defined.

Supplements used were mainly types of omega-3 fatty acids.

See JAMA, August 25, 2015.

Can Noninvasive Device Help Cluster Headaches?

The pain of cluster headaches is so severe that they are often termed “suicide headaches.” They last from 15 minutes to several hours and can occur up to 8 times a day. Injectable sumatriptan is usually rapidly effective, but the cost becomes prohibitive when needed several times daily for weeks to months at a time. Further, the medication cannot be used in people with coronary artery disease or risk factors for this, as it may trigger a myocardial infarction in that group.

Vagal nerve stimulation, targeting a nerve on the side of the neck and requiring surgery, is used to treat intractable epilepsy. There is now a noninvasive vagal nerve stimulation device, which looks like a large ultrasound probe and is applied to the side of the neck. It led to a doubling of the percentage of sustained responders compared to a placebo group. This was defined as an improvement in headache at both 15 minutes and 1 hour after treatment. It seemed to work better for patients with “episodic” cluster, meaning that the period of headaches lasts for several months and then clears, as opposed to those with chronic headache, which means that patients have daily headaches for 1 year or more. More studies are planned.

Results were presented at the American Headache Society’s 2015 Annual Scientific Meeting (abstract LBP07).