The September issue of the Journal of Neuropathology and Experimental Neurology reports the first pathological evidence that repetitive brain trauma in contact sports may be associated with motor neuron disease (MND) or ALS — popularly called Lou Gehrig's disease.

The suspicion that traumatic head and neck injury might trigger ALS began more than 100 years ago. One recent study showed the incidence of ALS among 7325 professional Italian soccer players was 6.5 times higher than expected. In addition, the risk for ALS for veterans of the 1991 Gulf War was 2-fold 10 years after the conflict. Repetitive concussions are associated with chronic traumatic encephalopathy (CTE), a degenerative brain disease that impairs memory, destabilizes emotions, and may progress to dementia.

CTE is the focus of the Center for the Study of Traumatic Encephalopathy. In the study, researchers analyzed the donated brains and spinal cords of 12 former football players, boxers, and professional hockey players. All 12 evidenced the build-up of abnormal tau protein found in CTE. However, the spinal cords of the 3 athletes thought to have ALS also contained the abnormal protein, a finding not characteristic of sporadic ALS.

The study authors concur that more research is needed. They recommend looking at how repetitive head injury may use other biological mechanisms such as inflammation to trigger neurodegenerative diseases, the role played by genetics, and the potential for therapeutic intervention. The long period of latency between traumatic brain injury and the onset of CTE and MND could become a window for treatment that would either dampen or block the "neurodegenerative cascade" that follows such brain trauma.

Increased awareness of the cumulative effects of concussion has resulted in improved football helmet design as well as how coaches manage players.

When trying to sleep, have you ever experienced strange feelings in legs that compel you to move them? If so, you may have experienced Restless legs syndrome (RLS). It most commonly affects the legs, but can also affect the arms or torso. Moving the affected body part provides relief for a brief period, but then the sensation returns.

RLS may start at any age, including early childhood. For some people it is a progressive disease. For others, it happens only under certain conditions, such as extreme fatigue, and then disappears. The sensations are unusual and unlike other common sensations. People who suffer from RLS have a hard time describing them but use words such as: uncomfortable, “antsy”, electrical, creeping and many others. While it may be impossible to describe the sensation to someone without RLS, other RLS sufferers can easily relate to the peculiar sensation. Some people have little or no sensation, yet still have a strong urge to move.

A National Institutes of Health (NIH) consensus panel established the following criteria for the diagnosis: 1) an urge to move the limbs with or without sensations, 2) improvement with activity, 2) worsening at rest, 3) worsening in the evening or night.

The diagnosis of RLS is made on a good medical history and physical examination. Other than preventing an underlying cause, such as anemia, no method of preventing restless legs has been established or studied. Treatment of restless legs syndrome involves identifying the cause of symptoms when possible. Stretching the muscles in the legs can bring instant and permanent relief, lasting several days or longer. This does not work for everyone: sometimes relief is temporary, and discomfort can return within seconds.

Benign paroxysmal positional vertigo (BPPV) is a common clinical disorder characterized by brief recurrent spells of vertigo (dizziness) often brought about by certain head position changes, such as looking up, turning over in bed, or straightening up after bending over. BPPV is an important cause of vertigo with a prevalence of 11 to 64 per 100,000. In one study, 9% of elderly patients that underwent a comprehensive evaluation for nonbalance-related problems were found to have previously unrecognized BPPV. Delays in the proper diagnosis and treatment of this condition are still common, and can lead to unnecessary costs and limitations of function. The importance of recognizing this condition is underscored by the ease and effectiveness of treatment techniques that eliminate symptoms and the need for expensive testing.

BPPV is caused when small calcium carbonate particles that form in part of the middle ear move into one of the semicircular canals. When the calcium carbonate crystals move within the semicircular canal they cause vertigo. When this happens the eyes develop jerky movements (called nystagmus). The presence of nystagmus during the exam help make the diagnosis.

The reason for these calcium crystals are formed is not well understood. The calcium debris may break off following trauma or viral infections, but in many instances it seems to occur without identifiable illness or trauma. It may have to do with age-related changes in the protein. Patients with BPPV have recently been found to have more osteopenia and osteoporosis than matched controls, and those with recurrent BPPV tended to have the lowest bone density scores.

Treatment is to move a patient’s head in the correct direction to move the calcium crystals into a region of the middle ear where they will be normally adsorbed. Once gone, the symptoms resolve. If properly done, the repositioning maneuver eliminates BPPV immediately in greater than 85% of patients..

At present, the generally accepted recurrence rate of BPPV after successful treatment is 40 to 50% at 5 years of average follow up. There does appear to be a subset of individuals prone to multiple recurrences.

I want to point out a very well written comment to a blog I posted last week. Mark, from Memphis, wrote:

The treatment of epilepsy will always be a complex issue, with complex and varying results, and rate of success, which degree of success can also vary over time. Further, you know how close the connection is between brain neuronal function, mood, and behavior.

I feel any increase in suicidal behaviors, whether attempted (as in some personality disorders) or the unfortunately successful suicide, is due to similarly complex pathology and disorder. Neuronal dysfunction leads to though or mood disorders, depression, and is further aggrevated by the social isolation, difficulty in finding employment, and lowered self-esteem many patients with epilepsy face. Medications can also complicate patients' function, especially in patients who have refractory, difficult-to- control epilepsy.

Having known your work in the past, I am proud to have worked with you, and have seen many patients who underwent successful surgery for their epilepsy, and reported significantly improved mood and cognition in their postoperative course.

Regardless of the degree of connection between medication and suicide, we see it is vital (in the truest sense of the word) to get patients the best control of their seizures by any means possible.

Patients with primary headache disorders, such as migraine, may use a variety of drugs chronically. Some examples are ergotamine, analgesics, opioids, and triptans. These may be taken alone or in combination. However, chronic use of such drugs can end up causing headache, a condition called medication overuse headache (MOH).

The prevalence of this condition is increasing worldwide and in the general population is 1–1.4% with a peak prevalence in women in their 50s. It’s therefore considered a major health problem. The reason medication overuse headaches occur is not known, and is still a matter of debate.

The treatment of MOH generally includes discontinuation of the overused medication. But stopping medications can lead to "withdrawal headache.” Various therapeutic protocols for removing chronic medications without causing severe side effects are not proven, which makes the treatment of a difficult problem even more complex. Probably the best way to prevent MOH from happening is to use medications as sparingly as possible.

For years it has been known that people taking antiepileptic drugs (AED) have a higher risk for suicide. The question has been, what is responsible for this; the disease for which a patient is being treated or the drugs used to treat it? Examples of common illnesses treated with AEDs are chronic pain, depression, and bipolar disorder.

In January 2008, the FDA issued a safety alert on the risk for suicidality in people taking AED medications. The alert stemmed from analysis of 199 placebo-controlled AED trials of 11 AEDs. It found a 2-fold increased risk for suicidal thoughts or actions among AED-treated patients compared with placebo-treated patients and suggested that the risk was increased regardless of AED type and indication for use. However, the assessment of suicidality in analysis was "subject to several limitations such as the lack of systematic or standardized language to define suicidal ideation and behavior across clinical trials." To investigate further, data from The Health Improvement Network database looked at the association between AEDs and "harder" endpoints (attempted and completed suicides) in patients with epilepsy, depression, or bipolar disorder.

A new study in the August 5 issue of The New England Journal of Medicine suggests that it might not be antiepileptic drugs (AEDs) themselves that raise the suicide risk in patients, but the underlying disease for which these drugs are prescribed. This new study analyzed more than 5 million patients, so the validity of the data is quite compelling.

A new report from the Framingham published in the August 2 edition of Circulation shows that decreased cardiac function is correlated with increased risk of dementia.

"Generally speaking, it seems that heart and brain health are related, so proper management of cardiovascular risk factors may have important implications on brain health," says Angela Jefferson, PhD, from the Boston University School of Medicine in Massachusetts.

Using Framingham data, the researchers looked at 1504 participants free of clinical stroke, transient ischemic attack, or dementia. They reviewed brain and cardiac magnetic resonance images and neuropsychological and laboratory data. They found that cardiac index (a measure of heart health) was positively related to total brain volume and information processing speed but was inversely related to lateral ventricular volume. Data revealed that participants with the lowest and middle cardiac indices had significantly lower brain volumes than participants with the best cardiac indices.

In an accompanying editorial, Clinton Wright, MD, and Ralph Sacco, MD, from the University of Miami in Florida, suggest the finding that even intermediate reductions in cardiac index were associated with declines in brain volume is striking.

The mechanism for associations between cardiac index and evidence of brain aging is unknown. However, the study authors suggest reduced systemic blood flow may contribute to subclinical brain injury because of its impact on cerebral blood flow homeostasis. In other words, poor heart function may injure the brain long-term.
"It will take years to know the fate of all 1504 Framingham participants," the editorialists add. "Whether lower cardiac index leads to reduced brain volumes and accelerates neurodegeneration on an eventual path to dementia is not yet clear. What is known is that various vascular risk factors, including decrements in cardiac function, are determinants of dementia — both Alzheimer disease and variants of vascular dementia. This provides opportunities to find interventions that modify the course of these diseases predicted to be of major impact on our aging population."

Bottom line: use that gym membership.