Saturday, December 4, 2010

Many of us routinely use aspirin to decrease the risk of stroke from blood clots that form either on our heart valves or our carotid arteries. Some people also believe that aspirin also slows the progression of Alzheimer’s Disease (AD). However, a recent review in the journal Stroke suggests that the drug does not slow progression of the disease and may increase the risk for intracerebral hemorrhage (ICH).

"What we know is that there's no indication to prescribe aspirin in order to slow down cognitive decline, and there's a potential increased risk of hemorrhage, so if there's no clear cardiovascular indication, I think doctors should refrain from prescribing aspirin to Alzheimer's disease patients," said one of the study's authors, Edo Richard, MD, PhD.
For this analysis, researchers searched PubMed and the Cochrane Library for randomized trials up that investigated the effect of aspirin for AD and registered complications of aspirin therapy, including ICH. They found only 2 relevant trials, neither of which had shown an effect of aspirin on progression of cognitive decline. But doctors are sometimes tempted to prescribe aspirin to AD patients if there is any indication of vascular damage, he added. "That, I think, is not a good idea."

Approached for a comment on the study, Ronald C. Petersen, MD, PhD, director of the Mayo Alzheimer's Disease Research Center, Rochester, Minnesota, called the results "important," "well founded," and "timely," especially with the growing concern about microbleeds and microhemorrhages in AD patients. "The study raises awareness of this complicated issue of blood vessels, hemorrhages, and Alzheimer's disease," said Dr. Petersen.
He pointed out that it is possible aspirin may aggravate small bleeds in the brain. "If the micro bleeds are occurring because of a loss of integrity of the blood vessel wall, be it amyloid being deposited (a substance associated with causing AD) in the wall or whatever, the aspirin, being a blood thinner, would just increase the likelihood of a leak and a bleed," he added.
The results should help convince physicians not to "throw aspirin out there as a panacea, like water, with the idea that it's just aspirin so don't worry about it," said Dr. Petersen. "No, aspirin could be a concern in the right situation. On the other hand, if the person has cardiovascular risk factor where aspirin may very well be important as a prophylaxis, don't be dissuaded from giving it."

Wednesday, November 10, 2010

A study in the November issue of the British Journal of Psychiatry reports that participating in regular leisure-time physical activities of any intensity can lead to a decrease in depression. In a study of more than 40,000 Norwegian residents, investigators found that those who were not active during their time away from work were almost twice as likely to have symptoms of depression that those who were regularly active.

The investigators note that social benefits associated with exercise, such as increased number of friends and social support, may be more important contributors to this association than biological changes. However, there was no association found between workplace exertion (such as walking or heavy lifting) and decreased symptoms of depression.

Although many past studies have found lower rates of depression for people who are more active, "almost all of the published research on this topic has focused exclusively on intense leisure-time activity such as organized sports, jogging, and fitness classes," write the study authors. They note that results have been mixed when studies have considered other types of activities.

These participants (50.9% female; mean age, 45.9 years) were asked how often they engaged in light or intense physical activity during their leisure time and how active they were in their workplace. Light activity was defined as any activity not leading to being sweaty or out of breath.

They also underwent a physical examination and completed the Hospital Anxiety and Depression Scale questionnaire regarding symptoms of depression and anxiety. Social factors were also collected, including age, sex, marital status, education, social class, cigarette or alcohol use, any mental illnesses in immediate relatives, any somatic diseases, and level of social support.

Results showed that 10.1% had case-level symptoms of depression, 15.2% had symptoms of anxiety, and 5.6% had comorbid depression and anxiety. Those who participated in both light and intense leisure-time activities had decreasing rates of both depression and comorbid depression and anxiety symptoms based on amount of time spent on the activities.

In other words, "there was an inverse relationship between the amount of leisure-time physical activity and case-level symptoms of depression," investigators write. Although those who participated in light leisure activity had a slightly lower prevalence of anxiety, there was no association found with intense leisure-time activity. There were also no associations found between workplace activity and decreasing symptoms of any of the disorders studied.

However, the take-home message is that "we know from different sets of data that, at least for depression, some level of physical activity is helpful as opposed to not having activity." There is a large proportion of people who think exercise is too hard or that they do not have time for it. "For that population clinicians should be thinking about recommending that they should at least be engaging in the amount of physical activity that they think they're capable of. So again, little is better than nothing — which is actually a very good message.

Sunday, November 7, 2010

A recent article in New York Times pointed out that one of the first signs of impending dementia is an inability to understand money and credit, contracts and agreements.

The Financial Industry Regulatory Authority, the largest nongovernmental regulator for securities firms doing business in the United States, recently met with individual financial services companies and the Alzheimer’s Association to formulate guidelines on how to deal with clients who have trouble remembering and reasoning, a problem that is not new but is increasing as the population ages.

The issue promises to become more complicated as doctors diagnose Alzheimer’s earlier and earlier. If tests indicate that a person is developing dementia, does that mean the patient should be watched, or that should limits be placed on his or her abilities to make financial or legal decisions?

Financial firms are in “a dicey situation” if they have to decide whether a client can make major decisions about finances or future plans, said John M. Gannon, senior vice president for investor education with the financial regulatory agency. And yet, according to research by Daniel C. Marson, a neuropsychologist at the University of Alabama, Birmingham, confusion over money and finances is perhaps the most important and most predictable early functional change as people descend into dementia.

This makes sense because managing finances requires long range planning, risk evaluation, a varying degrees of arithmetic skill, all of which are brain functions lost with the varying forms of dementia.

Thursday, October 28, 2010

Alzheimer’s Disease is only one cause of dementia. Until recently the diagnosis was based on the clinical symptoms along brain images the brain showing atrophy. The diagnosis was confirmed with a brain biopsy. Now there is an assay of proteins in the cerebrospinal fluid (CSF) can help specify the diagnosis.

Despite more than 5 million Americans with Alzheimer's disease, and millions more at risk, these CSF tests have yet to be widely adopted by neurologists. In part because the ability to make an improved early diagnosis raised the question: does this matter? The argument in favor of earlier diagnosis is being able to treat the disease and thus slow the progression. However, not only is there no "magic bullet" for the prevention of Alzheimer's disease, there is no bullet at all. The current treatments offer modest, temporary, and symptomatic improvement at best.
A more persuasive argument in support of the CSF test is this provides more accurate diagnosis when testing new, possibly effective, treatments. The success of clinical trials requires not only that the treatment be effective, but that all subjects be correctly diagnosed. Subjects who have other diseases contaminate the sample and confound results.

At present, CSF and other biomarker Alzheimer's testing should be reserved for patients who present a diagnostic dilemma and patients entering clinical trials.

Friday, October 15, 2010

Walking at least 6 miles per week appears to maintain brain volume and preserve memory in old age, according to new research. Kirk I. Erickson, PhD, with the University of Pittsburgh, Pennsylvania, and colleagues reported the findings in the October 13 online issue of Neurology.
"These findings are really quite astonishing," Dr. Erickson said. "Other studies have previously shown that exercise is related to brain function, but the fact that we found that walking as little as 1 mile a day is related to brain volume 9 years later, and dementia 13 years later, is truly novel and really quite impressive," he said.

According to the researchers, the volume of gray matter shrinks in late adulthood and often precedes cognitive impairment. Participation in physical activity and exercise has been "hypothesized to protect against the deterioration of brain tissue, but this hypothesis has not been tested in longitudinal studies."

In the current study, 299 dementia-free people from the Cardiovascular Health Cognition Study were assessed for physical activity, as measured by the number of blocks they walked in 1 week. Nine years after the physical activity assessment, magnetic resonance imaging (MRI) scans were used to measure brain size. Four years later, the participants were tested for cognitive impairment and dementia.

Participants who walked at least 72 blocks — approximately 6 to 9 miles — per week had more gray matter than people who walked less; however, walking more than 72 blocks did not appear to increase gray matter volume any further.

In the 4-year follow-up, 116 of the participants, or 40%, had developed cognitive impairment or dementia. Greater gray matter volume with physical activity was associated with a 2-fold reduced risk for cognitive impairment.
"Based on our results, we can conclude that there is a relation between the amount of walking earlier in life and brain volume in later adulthood and that greater volume of tissue related to walking is associated with a reduced risk of cognitive impairment," the study authors suggest.
Dr. Erickson added that much more work is needed from randomized trials that assign people to an exercise treatment for long periods. "Only under these conditions will we be able to determine the extent to which exercise augments brain function in late life," he said.

Friday, October 8, 2010

Here’s an interesting finding: the relation between the ability to lose weight and lack of sleep. According to the October 5 issue of the Annals of Internal Medicine, lack of sleep appears to compromise the efficacy of dieting to lose weight.

The study of 10 people conducted in a sleep laboratory showed that there are multiple hormonal changes associated with sleep and these may affect the ability of dieters to lose weight. Not getting enough sleep increased the subjects’ hunger, and affected their leptin and ghrelin serum concentrations (ghrelin is a hormone that reduces metabolism and promotes retention of fat). The study found that the reduced sleep decreased the proportion of weight lost as fat by 55%. Subjects who slept 8.5 hours per night lost a mean of 1.4 kg, and those who slept 5.5 hours per night lost a mean of 0.6 kg.

The major limitation to the study is that the number of subjects was quite small, so the results may not be generalized to the majority of dieters. However, I use any excuse I can to get my 8 hours of sleep.

Friday, September 24, 2010

A new study of high-dose B vitamins suggest the rate of brain shrinkage may be slowed by treatment in elderly people with mild cognitive impairment (MCI). Overall, B vitamins given at a dose high enough to reduce homocysteine (an amino acid) by 31.7% in this trial had a "pretty dramatic effect" on the rate of brain atrophy also of about 30% compared with placebo.

The effect was greater among those subjects with the highest homocysteine levels. "The treatment actually reduced the rate of shrinkage by 53%, which is a huge effect," said Dr. Smith, the study leader. "We were absolutely delighted with this strong result."

Neuroimaging studies have established that even in the healthy elderly, the brain shrinks at a rate of about 0.5% per year. In those with Alzheimer's disease, the rate is accelerated to about 2.5% per year, and those with MCI fall somewhere in between, with an intermediate rate of about 1%.
Homocysteine has been confirmed a risk factor for brain atrophy, as well as cognitive impairment and dementia. "Since homocysteine levels can be regulated by B vitamins, because they are the main cofactors in the enzymes involved in metabolizing homocysteine, the question is, 'If you lower homocysteine by giving B vitamins, will you reduce the rate of shrinkage of the brain?'"

Of course, the big question is whether this reduction in the rate of brain atrophy translates into maintaining cognition. The trial was not big enough to answer that question statistiaclly. However, another study, NORVIT also looked at cognitive outcomes, and showed no effect of B vitamins in improving cognitive performance over 2 years in otherwise healthy elderly subjects (N Engl J Med. 2006;354:2764-2772, 2817-2819).

For now, I’m going to continue taking vitamins.

Thursday, September 16, 2010

At a recent meeting, neurologists described resting-state connectivity of brain regions associated with introspection. This network is chronically hyperactivated and hyperconnected in patients with schizophrenia. When healthy people are at rest, parts of the frontal lobes are not correlated, but in patients with schizophrenia and bipolar disorder, they are linked. This may help explain cognitive dysfunction in both disorders.

Michael Greicius, MD also addressed the default-mode network of the brain during his talk on Alzheimer's disease. The posterior regions of the default-mode network tend to overlap considerably with brain regions that show reduced metabolism in the earliest stages of Alzheimer's disease. “Using these functional connectivity approaches, our group and others have demonstrated reduced functional connectivity in the default-mode network in Alzheimer's disease, mild cognitive impairment, healthy older controls with prominent amyloid plaque burden, and healthy older carriers of the ApoE4 allele,” he said. In addition to functional changes, this brain network also appears to undergo structural changes and overlap with maps of amyloid plaque distribution (amyloid causes brain cell death in Alzheimer’s Disease).

Classically, neurologists study and describe brain anatomy whereas psychiatrists are concerned with human behavior. As new brain imaging techniques become more robust, the distinction between these fields of medicine blur.

Wednesday, September 15, 2010

There’s not been a lot of new information to discuss. But there was a recent review of the various factor believed to contribute to the delay or prevention of cognitive decline. To be included, studies had to have adult participants who were 50 years or older, drawn from general populations, and followed for at least 1 year. 127 observational studies and 22 randomized control trials (RCT), and 16 systematic reviews were reviewed. There was limited evidence to supported the benefits of selected nutritional factors or cognitive and physical activities. Factors associate with an increased risk were current tobacco use, a gene associated with Alzheimer’s Disease, and certain medical conditions. One RCT found a small, sustained benefit from cognitive training and another RCT reported that physical exercise helps to maintain cognitive function. Although the review concluded that there were few potentially beneficial factors in preventing cognitive decline, the overall quality of the evidence is low.

Friday, September 10, 2010

Cell phone use has increased dramatically since being introduced in the early 1980s. But its use has raised questions as to whether repeated low-level exposure to radiofrequency (RF) energy can damage human tissue to the point of causing malignancy. Because most users hold the cell phone against their ear, there is concern usage may cause tumors to either the ear (acoustic neuromas), salivary glands, adjacent brain (gliomas), or the tissue lining of the skull (meningiomas).

To address this question, an international study, INTERPHONE, was conducted. The study included users with at least 10 years of exposure. In addition it contained users with the greatest cumulative hours of use of any prior study, making it the largest study to date addressing this controversy. The data analysis was quite extensive, but overall the results indicate that cell phone users did not appear to have an increase in risk of either glioma or meningioma. However, there was a suggestion of an increased risk of glioma for those users who had the highest exposure levels of RF energy. This higher exposure could be from either in an increased number of calls or prolonged calls.

Wednesday, September 1, 2010

The August 19 issue of the New England Journal of Medicine reported that Tai chi may be a helpful intervention for patients with fibromyalgia. "Previous research has suggested that tai chi offers a therapeutic benefit in patients with fibromyalgia," wrote Chenchen Wang, MDl. "...[Tai chi] combines meditation with slow, gentle, graceful movements, as well as deep breathing and relaxation, to move vital energy (or qi) throughout the body. It is considered a complex, multicomponent intervention that integrates physical, psychosocial, emotional, spiritual, and behavioral elements."

66 participants were randomly assigned to receive classic Yang-style tai chi or a control intervention consisting of wellness education and stretching. In both groups, participants received 60-minute sessions twice weekly for 12 weeks. Fibromyalgia Impact Questionnaire score at the end of 12 weeks was the main study outcome, with higher scores indicating more severe symptoms. There were additional test to measure other aspects of outcome. To assess durability of the response, these tests were performed again at 24 weeks.

Improvements in the FIQ total score and quality of life in the tai chi group were clinically important. The tai chi group also fared better than the wellness intervention group in physical component scores of the Short-Form Health Survey and mental component scores. These improvements were still present at 24 weeks with no reported adverse events. Limitations of this study include lack of double blinding, lack of generalizability because treatment was delivered by a single tai chi master at a single center, and follow-up limited to 24 weeks.

Monday, August 23, 2010

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.

Friday, August 20, 2010

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.

Monday, August 16, 2010

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.

Sunday, August 15, 2010

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.

Wednesday, August 11, 2010

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.

Sunday, August 8, 2010

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.

Friday, August 6, 2010

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.

Thursday, July 29, 2010

An article in the July 29 issue of the New England Journal of Medicine reviewed evidence for the use of acupuncture for chronic low back pain.
"Acupuncture is a therapeutic intervention characterized by the insertion of fine, solid metallic needles into or through the skin at specific sites," write Brian M. Berman, MD, from the University of Maryland School of Medicine in Baltimore. "The technique is believed to have originated in China, where it has remained a fundamental component of a system of [medicine that] espouses an ancient physiological system (not based on Western scientific empiricism) in which health is seen as the result of harmony among bodily functions and between body and nature. Internal disharmony is believed to cause blockage of the body's vital energy, known as qi, which flows along 12 primary and 8 secondary meridians."

Tenderness on palpation is thought to be evidence of blockage of qi, and inserting acupuncture needles at specific points along the meridians is believed to restore the proper flow of qi. The analgesic effects of acupuncture appear to be based on neural innervation, because they are completely blocked by local anesthesia at needle-insertion sites. Furthermore, acupuncture stimulates the release of endogenous opioids in brainstem, subcortical, and limbic structures, as well as producing mechanical stimulation of connective tissue and other effects on local tissues. Despite these effects, the mechanisms underlying chronic pain relief by acupuncture are not completely understood.

Acupuncture is seldom regarded as the first choice of treatment, in part because randomized controlled clinical trials and large meta-analyses have not proven it to be more effective than sham acupuncture in relieving low back pain. However, it may be useful as part of a multidisciplinary approach to the management of chronic low back pain, along with physical therapy, pain medication, and/or exercise.
"Acupuncture is a regulated discipline, and patients should be referred only to practitioners who are licensed by the state in which they practice," the review authors write. "A diploma from the National Certification Commission for Acupuncture and Oriental Medicine is a requirement for licensure in most states. Physicians may practice acupuncture in the United States after completing one of several medical acupuncture programs."

Contraindications to acupuncture include coagulation and bleeding disorders, use of anticoagulants, severe psychiatric disease, and local skin infections or trauma. Electroacupuncture should not be used at the site of pacemakers or other implanted electrical devices. Pregnant women may undergo acupuncture, but not at specific acupuncture points known to be especially sensitive to needle insertion or at acupuncture points in the abdominal regions.

One treatment is considered to be insufficient, and recent trials of acupuncture for low back pain used at least 12 acupuncture sessions, often starting with 2 sessions a week and tapering off after 4 weeks to once weekly, with booster treatments sometimes used monthly or every other month. Acupuncture should be discontinued if there are no apparent effects after 10 to 12 sessions.
"There is continuing debate in the medical community regarding the role of the placebo effect in acupuncture," the review authors write. "The most recent well-powered clinical trials of acupuncture for chronic low back pain showed that sham acupuncture was as effective as real acupuncture. The simplest explanation of such findings is that the specific therapeutic effects of acupuncture, if present, are small, whereas its clinically relevant benefits are mostly attributable to contextual and psychosocial factors, such as patients' beliefs and expectations, attention from the acupuncturist, and highly focused, spatially directed attention on the part of the patient."

Joint clinical practice guidelines from the American College of Physicians and the American Pain Society recommend that clinicians consider acupuncture as one possible treatment option for patients with chronic low back pain refractory to self-care (level of supporting evidence, fair). According to the North American Spine Society, acupuncture offers better short-term pain relief and functional improvement than no treatment, and adding acupuncture to other treatments is more effective than other treatments alone, but high-quality, randomized controlled trials are still needed comparing acupuncture with no treatment and with sham acupuncture.

Sunday, July 25, 2010

A report in the Archives of Neurology suggests that Vitamin E may play a modest role in altering the course of dementia. Compared with participants with the lowest intake, investigators found that those patients with higher vitamin E intake were 25% less likely to develop dementia.

"When beta-amyloid — a hallmark of pathologic Alzheimer disease — accumulates in the brain, an inflammatory response is likely evoked that produces nitric oxide radicals and downstream neurodegenerative effects," report investigators led by Elizabeth Devore, ScD, from the Erasmus Medical Center in Rotterdam, the Netherlands. "Vitamin E is a powerful fat-soluble antioxidant that may help to inhibit the pathogenesis of dementia."

Vitamin E is found in whole-grain foods, eggs, milk, nuts, seeds, avocado, spinach, and unheated vegetable oils. The Rotterdam Study previously found that higher dietary intakes of vitamins E and C were associated with a lower risk for dementia and Alzheimer's disease.

In this new long-term follow-up of the Rotterdam Study, investigators followed participants for 9.6 years. The population-based prospective cohort study included 5395 people free of disease at baseline.
A total of 465 people developed dementia. Of these, 365 were diagnosed with Alzheimer's disease. The investigators found that higher dietary intake of vitamin E, but not vitamin C, beta carotene, or flavonoids, was associated with lower long-term risk for dementia.

These results conflict with previous findings, which suggested a link between vitamin C intake and dementia risk. Probably the bottom line is to eat a healthy diet.

Tuesday, July 20, 2010

The most common sleep complaint in adults is insomnia and is a significant health concern. The criteria for a diagnosis of primary insomnia include difficulty with falling asleep, difficulty remaining asleep, waking up too early, or failing to achieve restorative sleep for a period of 1 month or more while experiencing significant distress and/or impairment in daily functions. One poll found that 64% of participants reported a sleep problem at least a few nights each week, with 41% reporting problems almost every night. Insomnia is 41% more common in women than in men.

Although there are several different degrees of insomnia, three types of insomnia have been clearly identified: transient, acute, and chronic. Transient insomnia lasts for less than a week. It can be caused by another disorder, by changes in the sleep environment, by the timing of sleep, severe depression, or by stress. Its consequences - sleepiness and impaired psychomotor performance - are similar to those of sleep deprivation. Acute insomnia is the inability to consistently sleep well for a period of less than a month. Chronic insomnia lasts for longer than a month. It can be caused by another disorder, or it can be a primary disorder. Its effects can vary according to its causes. They might include being unable to sleep, muscular fatigue, hallucinations, and/or mental fatigue; but people with chronic insomnia often show increased alertness.

Patterns of insomnia are:
Onset insomnia - difficulty falling asleep at the beginning of the night, often associated with anxiety disorders.
Middle-of-the-Night Insomnia - Insomnia characterized by difficulty returning to sleep after awakening in the middle of the night or waking too early in the morning
Terminal (or late) insomnia - early morning waking. Often a characteristic of clinical depression.

Poor sleep quality can occur as a result of sleep apnea or major depression. Poor sleep quality is caused by the individual not reaching stage 3 or delta sleep which has restorative properties.

A common misperception is that the amount of sleep required decreases as a person ages. The ability to sleep for long periods, rather than the need for sleep, appears to be lost as people get older. Some elderly insomniacs toss and turn in bed and occasionally fall off the bed at night, diminishing the amount of sleep they receive.

Treatment for insomnia varies depending on the cause. This is why a good workup by a sleep specialist is the best way to make a proper diagnosis and lay out a treatment plan.

Saturday, July 17, 2010

The July issue of the Archives of Neurology reported a longitudinal study of more than 3,000 subjects in which a link between vitamin D and Parkinson’s disease was found. In the 29-year follow-up period, there were 50 incident cases of Parkinson's disease. The study was carried out in Finland where there is restricted sunlight exposure. It is a population that typically has low vitamin D levels. The mean serum level was about 50% of the suggested optimal level of 75 to 80 nmol/L.
The investigators found that individuals with a serum vitamin D concentration of at least 50 nmol/L had a 65% lower risk for Parkinson's than those with values less than 25 nmol/L after adjustment for several potential confounders. The relative risk between the highest and lowest vitamin D levels was 0.35.

Vitamin D is no longer considered a vitamin, but rather a hormone that has autocrine and paracrine functions well beyond those of regulating calcium absorption and bone health.

The exact mechanisms by which vitamin D may protect against Parkinson's disease are not fully understood. Vitamin D has, however, been shown to exhibit neuroprotective effects through antioxidative mechanisms, neuronal calcium regulation, immunomodulation, enhanced nerve conduction, and detoxification mechanisms.

The association with and possible causal role of insufficient vitamin D in many chronic diseases, such as Multiple Sclerosis, is becoming more widely appreciated yet what constitutes an optimal blood concentration of vitamin D for humans, and specifically for the human nervous system, remains unknown.

Friday, July 16, 2010

Making the news this last week was a gene for Alzheimer’s Disease (AD). This prompted a friend to ask me, “Why would you want to know if you were going to develop the disease?” Good question. One reason is for genetic planning. Another reason is that early diagnosis may lead to earlier treatment, and thus better prognosis. After all, this approach has been successful in preventing diseases such as cervical cancer and heart attacks.

But early treatment requires early diagnosis and not all people with dementia have AD. To this end solid criteria must be developed to identify a “preclinical state.” Put another way, we need to be able to identify AD far in advance of symptoms. Genetic testing will be helpful but in itself is not sufficient.

Okay, so what test might yield such information? Probably it will come from imaging studies (MRI or PET scans) that measure the metabolism and accumulation of amyloid, an insoluble protein. Amyloid accumulates in neurons of AD patients, causing cell death. Microscopically AD patients’ brains show “tombstones,” which are small deposits of amyloid that remain after neurons die. So amyloid accumulation is likely to become one metric for defining preclinical AD, allowing people with positive family histories of the disease to be successfully diagnosed and treated.

Tuesday, July 13, 2010

The Framingham study is a large prospective study of over 5,000 men and women living in Framingham, Massachusetts who have been followed every 2 years since 1948. Data from it is used to estimate risk of heart and other diseases. The dementia part of the study began in 1975 using several neuropsychological tests. Recent data from the study reports that people who participate in moderate to heavy physical activity have a 45% lower risk for dementia over time.

"A reduced risk of dementia may be one of the additional health benefits that can actually be derived from maintaining at least moderate physical activity," lead author Zaldy Tan, MD, MPH, from the Brigham and Women's Hospital, VA Boston, and Harvard Medical School, in Massachusetts, concluded. Dr. Tan presented the results at the Alzheimer's Association International Conference on Alzheimer's Disease 2010.

Previous findings from the Framingham have already shown moderate or high physical activity to be associated with a number of positive outcomes, including a reduced risk for stroke and cardiovascular disease, higher high-density lipoprotein cholesterol levels, a reduced risk for colon cancer, and lower overall rates of mortality.

Physical activity is a potential preventive factor that would likely take years to manifest its effect, "so the fact that we've followed them for over 20 years, this is something that suggests that long-term physical activity actually works," Dr. Tan noted. The mechanism is not clear, he added, but reduction of cardiovascular risk factors such as hypertension, or the release of neurotrophic factors, are possible effects.

The Framingham study is not the only one to demonstrate this relationship. A recent review showed that 20 of 24 population-based studies showed a link between physical activity and reduced risk for dementia or cognitive decline. The flip side of this is that four of those studies did not support the correlation. However, the Framingham study is one of the best because it has such well designed, long-term follow-up.

Saturday, July 10, 2010

As a back pain sufferer, I was interested to read in the July 7th issue of the Journal of the American Medical Association (JAMA) that glucosamine is not significantly different from placebo for reducing pain-related disability or improving health-related quality of life in patients with chronic low back pain. Years ago I’d tried the dietary supplement without success even though a lot of people swear by it.

Because glucosamine is a precursor molecule involved in building tendons, ligaments, and cartilage it’s widely believed that it helps restore cartilage as well as having anti-inflammatory properties. Despite conflicting data on its efficacy it has been widely used as a treatment for osteoarthritis. Some estimates suggest that more than more than 25% of patients with chronic LBP have tried glucosamine in various forms.

The research was a well-designed clinical study conducted at the Oslo University Hospital Outpatient Clinic using 250 patients with nonspecific chronic pain in the lower back. Patients were randomized to receive either a daily dose of 1500 mg of glucosamine sulfate or identical placebo administered as 3500-mg capsules. (The study design was double-blind cross over). The outcome was measured by a pain scale as well as one to assess quality of life.

Unfortunately low back pain is a significant cause of disability and medical cost in the United States. Too bad it doesn’t seem to have a significant therapeutic effect for relieving the symptoms.

Friday, July 9, 2010

A recently reported study of more than 3,000 people identified 9 modifiable risk factors for reducing more than 90% of all strokes. None of these will come as any big surprise. It’s been known for years that high blood pressure is associated with a higher incidence of brain hemorrhage (intracerebral hematoma) that results in either death of long-term injury. This relationship has been reaffirmed. This finding was based on the definition of hypertension as a systolic blood pressure greater than 150 mm Hg instead of the newer parameter of > 120 mm Hg.

A second, not surprising factor contributing to stroke, is smoking. For years it has been known that smoking increases the risk of both cardiac and stroke disease, mainly because it is associated with increased vascular problems. Diabetes is another factor that leads to vascular problem and stroke.

Two additional factors are obesity (as measured by abdominal girth) and regular exercise. These two have an obvious relationship with each other in that exercise helps maintain weight reduction in most people. Regardless of their interrelationship, they independently factored into the risk of stroke. Excessive alcohol consumption was also identified as a contributing factor.

So, your mother was right when she warned you to eat right, exercise, don’t smoke, and don’t drink excessively. The difference is that we probably didn’t believe our mothers. Now evidence based medicine shows she was correct.

Sunday, July 4, 2010

I went to the dentist the other week for a chipped tooth. He used a local anesthetic to numb the nerves to my maxilla, or upper jaw. So I thought I’d write a few words about local anesthetics. When injected near a nerve, these drugs cause reversible loss of function of that nerve. So, if the nerve carries fibers for sensation, blocking it results in anesthesia (lack of sensation).

Nerves transmit information by conducting action potentials, or brief impulses. They do this by allowing sodium and potassium to rapidly flow in and out of the fiber, a process called depolarization and repolarization. If you can chemically block this process, you can block the transmission of action potentials, thus rendering the nerve incapable of sending information. And this is exactly how local anesthetics, such as Novocain work.

All nerve fibers are sensitive to local anesthetics, but generally smaller diameter fiber are more sensitive than larger fibers. Local anesthetics block conduction in the following order: small myelinated axons (e.g. those carrying pain impulses), non-myelinated axons, then large myelinated axons. Because pain fibers are the smallest diameter fibers, a differential block can be achieved (i.e. block pain sensation more readily than other senses, such as light touch).

Permanent nerve damage can occur after a peripheral nerve block but is rare. Symptoms are very likely to resolve within a few weeks. The vast majority of those affected recover within four to six weeks. 99% of these people have recovered within a year. Very few nerve blocks result in some degree of permanent persistent nerve damage.

Nerve fibers are not the only tissues that use potassium and sodium conduction as the basis for their action. So do muscle fibers. For this reason, the amount of anesthetic injected must be carefully monitored. This is also the reason that some local anesthetics are effective in treating some severe types of cardiac arrhythmias.

True allergies to local anesthetics is very rare.

Monday, June 28, 2010

I bought a Kindle the other day. One of the reasons was I found I wasn’t reading as many books as I used to. I thought about why? Well, one reason is eye strain. Without realizing it, I was tiring more when reading printed pages. As a result, I found reasons not to sit down and spend a couple hours reading. But the other week I bought a Kindle and am amazed at the improvement I now have in reading stamina. I had heard Kindles were easier on the eyes than printed books, but really thought it was just marketing hype. Well, for me it isn’t.

So what is eye strain? Several muscles control the eyes, moving them in back and forth and converging to focus at various distances. In addition to the actual muscles that move the eyes are the facial muscles that control the lids. Like any muscle they can fatigue. Our eyes were really designed to see far away and at different focal lengths. But if we look at one focal length for sustained periods of time (as I do during TV football season), we essentially produce a repetitive strain injury to the muscles. This results in aching eye muscles and/or even dry-feeling eyes. A trick I’ve adopted to relieve this problem is to stop every ten minutes or so and look away, at a corner of the room, or at something out the window. The problem, of course, is remembering to do this. In any event, I love my new Kindle. If you’ve ever thought of owning one, seriously consider it. They’re seriously fun.

Friday, June 18, 2010

A strange pain disorder called Causalgia can occur when the nerves that run from the spinal cord to the limbs are partially damaged, especially when the damage involves the bundles of nerves to the arms called the brachial plexus. Partial damage can come from accidents (that stretch the shoulder away from the neck, literally pulling some nerve fibers apart), from hand surgery, or from war injuries. A more recent name for the disorder is Complex Regional Pain Syndrome.
The pain is burning, constant, and usually involves the hand or foot. Sensory stimulation, such as rubbing the area, can worsen the pain. The pain usually is adjacent to any neurological deficit if there is one. Meaning that the pain may not be located in a region of numbness, but adjacent to it.

What makes this pain syndrome so different from other forms of chronic pain is that changes can occur in the skin and bones of the affected limb. The skin can become swollen and red because of loss of the normal tone of the blood vessels. In fact, comparing the temperature of the affected limb compared to the other normal limb is one aid to making the diagnosis (thermography). Abnormal sweating can also be seen. Interestingly, in some case patchy osteoporosis can be shown on X-rays of the limb in as little as three weeks from onset.

The cause is not really understood, but because of the vascular and skin changes, it has been suggested that the sympathetic nervous system is involved. In severe cases nerve blocks to the sympathetic ganglia in the base of neck can provide enough pain relief so that aggressive physical therapy can be started. Cigarette smokes are at much higher risk for developing the painful disorder than non-smokers.

Monday, June 14, 2010

I worked for a couple of medical device companies. One of the was Northstar Neuroscience. It was based a very cool concept. We developed a small battery powered electrode that could be implanted on the motor area of stroke victim’s brain. The system could be turned on to provide a tiny electrical current to the brain while the patient was participating in physical therapy. Guess what? It worked. Patients who were partially paralyzed on one side of their body regained a remarkable amount of movement. But timing is everything and before we could commercialize the device and obtain FDA approval, the stock market ran into a brick wall and there was no way the company could continue without another stock offering, so it went under. Actually, Saint Jude bought the technology but never really did anything with it.

The thing I loved about working at Northstar was all the bright energetic minds. I’m happy to say that many of the engineers and thinkers migrated from Northstar to another start-up company, NeuroVista. What they’re working on is a really cool sensor that is able to predict when a person with epilepsy is going to have a seizure.

There is a genetic line of dogs that have seizures and the company has successfully tried the device on the seizure-prone dogs with good success. Enough so that the company is starting their first clinical trial on humans in Australia. Check them out at

If you’re interested, check out a recent interview that was broadcast on Australian TV:

Sunday, June 6, 2010

Here’s one from the Whatever-Happened-To department: Cryonics. The idea was that a life could be suspended if lowered to subzero temperatures (typically at -196 degrees F ) for an indefinite period of time. The rationale being that people who are considered dead by current legal or medical definitions may not necessarily be dead according to more stringent definitions of death. So, cryopreserved them until they can someday be recovered by using highly advanced technology that is presently not available. Because most chemical reactions slow with decreasing temperature, it stands to reason that lowering a tissue’s temperature will place it in a state of suspended life. Presently cryopreservation is can be done for sperm (for future in vitro fertilization) and other biological tissues such as blood and stem cells.

According to their website, Alcor, ( is a foundation established in 1972 in California. Their mission is to enhance the cryonics movement. In 1987 Alcor “cryopreserved” its first human.

Interesting subject. It contains all the stuff I love to mull over when thinking up plots. On the other hand, the scientist in me always asks, “Whoa, what are some of the risks, the basic problems in biology?” There are several, making the physiology complicated. When tissues are cooled slowly, water migrates out of cells and ice forms in the extracellular space. Too much extracellular ice can cause crush injury to the cell membrane. Also, moving water out of the cell can cause dehydration damage. Although some tissues can tolerate some extracellular ice, most can’t tolerate ice inside the cell. To mitigate some of these problems, tissue can be flash frozen. In 1963 Peter Mazur, at Oak Ridge National Laboratory in the USA, showed that lethal intracellular freezing could be avoided if cooling was slow enough to permit sufficient water to leave the cell during progressive freezing of the extracellular fluid. That rate differs between cells of differing size and water permeability: a typical cooling rate around 1°C/minute is appropriate for many mammalian cells after treatment with cryoprotectants such as glycerol or dimethyl sulphoxide, but the rate is not a universal optimum. Even so, problems arise when trying to thaw frozen tissue.

The issues go on and on, and to me the bottom line is the process is not ready for prime time.

Saturday, May 29, 2010

New research shows that a gene which is the major genetic risk factor for Alzheimer's disease (AD) may also influence the actual expression of the disease and account for some of the variations in the types of cognitive problems seen in patients with AD.

"This work provides proof of concept that genetics may not only impact the risk for dementia but also the nature of a dementia syndrome," said author David A. Wolk, MD, the author of a paper published online May 17 in an early edition of the Proceedings of the National Academy of Sciences United States of America.

Drs. Wolk and Bradford C. Dickerson, MD, investigated cognitive and neuroanatomical phenotypic variability in gene carriers and noncarriers with mild AD. Only patients proven to have AD on the basis of a cerebrospinal fluid molecular profile were studied. They found that APOE ε4 allele carriers displayed significantly greater impairment on measures of memory retention, whereas noncarriers displayed greater impairment on tests of working memory, executive control, and word retrieval. In addition, carriers exhibited greater medial temporal lobe atrophy, whereas noncarriers had greater frontoparietal atrophy.

"What was particularly remarkable about this study was the high correspondence between the differential effect of APOE status on cognitive symptoms and on evidence of brain atrophy," Dr. Wolk said.

Friday, May 28, 2010

It happens to all of us at one time or another. We’re in a conversation when and suddenly can’t remember the name of someone very familiar to us. We might even be able to visualize their face or remember the first letter of their name. It doesn’t even have to be a person’s name – it can be an object. There’s a name for this: The Tip of The Tongue Phenomenon, or TOT. I kid you not. The French term this Presque vu, for “almost seen.”

Reference to TOT appeared in non-academic literature as early as 1885 when Chekhov mentioned it in a short story. Harvard psychologists Roger Brown and David McNeill reported the first empirical investigation of the tip-of-the-tongue state in 1998. They recounted, "[t]he signs of it were unmistakable" and "he [a research participant] would appear to be in mild torment, something like on the brink of a sneeze, and if he found the word his relief was considerable." They reported that TOT is a fairly universal phenomenon occurring about once a week but will increase in frequency with age. While experiencing TOT we are often able to access the first letter of the intended word as well as remember related words.

Okay, but what causes it to happen?

Although it is safe to say no one knows for certain, the literature includes hypotheses that include both the psycholinguistic and memory oriented. Psycholinguists can get wrapped around the axel debating non-testable hypotheses, so I’ll not go into those. Suffice it to say from what I’ve been able to read about TOT, it appears to be like a temporary mild form of aphasia. We know the word but can’t pull it from memory. It’s frustrating and, often, the more we try, the more elusive the word is. And it’s usually after we stop trying the word pops back to the surface like a submerged balloon.

What we do know for sure is TOT happens at all age groups and becomes more frequent with age. This again suggests a memory problem because studies suggests that older adults remember less information about the intended word and thus have more difficulty resolving the TOT experience when it happens. It is a harbinger of dementia? Probably not. But like everything else, the symptom must be taken within the context of the broader neuropsychological examination.

Sunday, May 23, 2010

It’s been a while since I’ve contributed to this blog, but I’ve been swamped with work. Looks like CHOP SHOP will be released May 1, 2012. That’s a long way away, but it’s surprising just how fast deadlines creep up. For those of you who don’t know about it, it deals with the huge lucrative market for cadavers and assorted body parts. In doing my research for the story I was amazed to learn that selling bodies is illegal in most states. Yet every few years you read in the news about someone in a funeral home or coroner’s office who is busted for dealing. It’s rumored that a fresh body in good condition can fetch up to $300,000 dollars.

Some medical schools still use cadavers to teach anatomy, although this is becoming more the exception. It’s not that a supply of bodies is lacking, it’s that this gross anatomy is no longer considered essential curriculum in some schools. So how are bodies obtained by med schools? Because people will their bodies to “science,” usually to a local medical school. But this isn’t the need that drives the black market. Demand comes from a variety of parts that can be “salvaged” from a fresh body. Skin for grafting on burn patients, corneas to replace cloudy ones, bone for use in spinal fusions, This doesn’t count the need for the soft tissue organs used for transplants – kidneys, liver, hearts. I could go on and on, but I think you get the idea. For remain functional, organs such as kidneys, are usually harvested from living patients and immediately transplanted in the recipient. This because anoxia (being without oxygen) can severely damage them.

If you want to learn more about this intriguing but grizzly subject, keep an eye out for CHOP SHOP. I will, or course, push it on my website and send out the usual spam to anyone unlucky enough to be on my mailing list. The other books after SHOP will be STEM SELL and CUCKOO’S NEST. Stay tuned.

Thursday, May 13, 2010

Sorry if you came here looking for a new post. I've been snowed under with a ton of work. This week I signed a three book deal with Medallion Press for CHOP SHOP, STEM SELL, and CUCKOO'S NEST. These are all stand alones and SHOP will be comming out May 1, 2012. My agent Robert Astle wants me to adapt all three stories to screenplays. Shortly after DEAD HEAD was released, a Hollywood production company showed interest in optioning it. At the moment I'm also very involved in the International Thriller Writers association. I'll get back to posting new material here as soon as I can come up for breath. Keep checking, I'll be posting again soon.

Friday, May 7, 2010

I’m a supporter of legalizing marijuana. For a variety of reasons. But first, some history. I doubt that most readers realize that the drug was legal in the United States until 1906 when the first pprohibitions of cannabis were instated. By the mid-1930s, cannabis was regulated in every state by laws instituted through The Uniform State Narcotic Act. In the 1970s, some states started to decriminalize cannabis. Most places that have decriminalized cannabis have one or more of civil fines, drug education, drug treatment in place of incarceration, criminal charges for possession of small amounts of cannabis, or have made various cannabis offenses the lowest priority for law enforcement. In the 1990s many states began to legalize medical cannabis. This conflicts with federal laws because cannabis is a Schedule I drug according to the Controlled Substances Act of 1970. (The DEA classifies drugs into several tiers based on numerous criteria. To prescribe medications, physicians must have a license and prescribe only within the levels for which they’re licensed.) Washington, where I live, approved the use in 1998 for any medical condition in which the “potential benefits of the medical use of cannabis would likely outweigh the health risks.” Patients diagnosed with cachexia; cancer; HIV or AIDS; epilepsy; glaucoma; and multiple sclerosis are given legal protection under this act. Other medical conditions are subject to approval by the Washington Board of Health.

In Washington State patients may legally possess or grow no more than a 60-day supply of cannabis. The American Medical Association and the California Medical Association have both, separately, called for more research on Marijuana. “...CMA considers the criminalization of marijuana to be a failed public health policy; and be it further resolved that CMA encourage and participate in debate and education regarding the health aspects of changing current policy regarding cannabis use.”

My personal and professional opinion is that marijuana is no more physically harmful or carry more potential for abuse than does alcohol. Certainly, the most addictive legalized drug presently available to citizens is tobacco. With increasing medical costs and decreasing ability to fund these costs, a reasonable tax on legalized marijuana would be another revenue source.

Tuesday, May 4, 2010

Got a couple comments on my April 21 blog about memory. Both referred to a segment on the TV show 60 Minutes in which the use of Adderall in college campuses to facilitate studying was discussed. I didn’t see the show, but apparently students are using the drug to help cram for exams.

Adderall is the brand-name for a psychostimulant (a stimulant or “upper”) medication that is used commonly to treat people with ADHD because such patients often have a paradoxical reaction to it. Instead of becoming stimulated, they are calmed down. Adderall is also used to treat Narcolepsy (see the April 30 blog). It requires a prescription drug and may or may not be addictive depending upon the addictive potential of the individual using it. The drug is thought to work by increasing the amount of two neurotransmitters (see earlier blog), dopamine (which is deficient in Parkinson’s disease) and norepinephrine. Its main effect is to increase alertness, libido, concentration, and overall cognitive performance while decreasing user fatigue. So it’s easy to see why students might use it. It is available in two formulations – an instant release and extended release. It is a cousin to methamphetamine and dextroamphetamine and there is some dextroamphetamine in both formulations.

Use of uppers by students is not new and started when amphetamines were first introduced in the 60s as “diet pills.” In fact, when Shire, the pharmaceutical firm that introduced Adderall in 1996, did so as an obesity treatment. Since then pediatricians have tumbled to the fact that it is effective for treating some children with ADHD.

As is the case with all drugs, there is the potential for “off label” use – using the drug for indications not approved to be on the dispensing label. Off label use is not illegal. Physicians commonly prescribe drugs for indications not officially approved by the FDA. As an example, Tegretol, a widely used anticonvulsant was initially introduced for treatment of trigeminal neuralgia. Neurologist quickly adopted the medication to treat seizure disorders. It wasn’t until a decade later, after clinical trials demonstrated it’s anticonvulsant effect, that the FDA approved it for that use.

This issues raised by the two blog readers is a good one. Is the use of a psychoactive drug for the purposes of studying bad? Probably not. In actuality, it’s not much different than brewing a pot of strong coffee for a night of cramming. The difference, of course, is that caffeine does not require a prescription. Both caffeine and Adderall can be addictive, so the difference here is how to obtain the drug. Most doctors will not prescribe it as a study aid, so it is commonly obtained illegally.

I thank the two readers who raised this question. As I've written before, please ask questions about the brain and brain function.

Friday, April 30, 2010

We spend about one third of our lives asleep. This, if you think about it, is a pretty astounding percentage. Historically, this very important part of our brain’s health has been ignored until the last century. Partly, this because we had no method to really study the phenomenon. The EEG gave us the ability to observe the brain’s electrical activity during sleep, and beginning in the 1950s sleep research became a reality. Now, most major hospitals have sleep laboratories for diagnosing sleep disorders. In addition, neuroscientists have studied the mechanisms by which the brain produces sleep.

There is no single sleep center in the brain. Rather, there are nuclei along the brain stem into the base of the brain (hypothalamus) that are actively involved in producing and maintaining sleep. These centers are also associated with the activating systems that produce wakefulness. An old anatomic name for this arrangement of neurons was the reticular activating system. One of the neurotransmitters in these nuclei is serotonin, synthesized from the amino acid tryptophan. This is perhaps one reason it is common to become sleepy after eating a meal loaded with tryptophan – turkey, pumpkin seeds, cheddar and other cheeses.

Because we are not conscious during sleep we tend to think of the state as equivalent to putting a transmission in neutral, with the foot off the gas. It really is an active process. As we fall asleep the brain waves begin to slow and transition into a state termed Slow Wave Sleep. Subjects may dream during SWS, but the images are ill formed and difficult to recall if the subject is awakened. After about ninety minutes the EEG speeds up and our limb muscles become relative paralyzed, while our eyes begin moving in rapid jerks. This is termed rapid eye movement sleep. If you’ve ever watched a pet dog sleep you may see the eyes moving behind the lids. It is during this period we have our most vivid and easily recalled dreams. REM episodes last approximately 20 minutes before quieting down to SWS. As time passes, the REM periods begin to occur more frequently but last the same duration.

Why do muscles become paralyzed during REM sleep? Scientists don’t know for sure but suspect it may be an evolutionary advantage. It wouldn’t be good news to start moving around while asleep in a tree.

There are problems that can occur if the sleep centers become active during wakefulness. One of the most commonly known is narcolepsy, a sleep disorder characterized by excessive sleepiness. Two major forms happen depending upon the presence or absence of the muscle paralysis that accompanies REM sleep. If an attack of REM occurs during wakefulness, the patient can become extremely weak and even fall. This is known as cataplexy. Without the REM component, patients may just fall asleep at their desk or on an assembly line, which obviously can result in severe workplace accidents. For years this has been treated with stimulants like amphetamine. A newer drug, Nuvigil, has also been introduced.

Another cause of excessive sleepiness is inadequate regular sleep due to airway obstruction. For patients who have anatomical causes – such as overgrown tonsils – surgery may be helpful. Extreme obesity can also cause obstruction. Dickens wrote about an extremely fat person who constantly fell asleep. This is now recognized as Pickwickian syndrome.

The take-home message is that sleep disorders are now easily diagnosed and treated. But they need to be worked up at a comprehensive sleep center.

Tuesday, April 27, 2010

One of my wife’s favorite movies is The English Patient, primarily because she loves Ralph Fiennes, the male lead. I like it because the depiction of amnesia is very realistic. The word comes from Greek and refers to a memory disturbance, and the experience is more global than a person being able to recall who he or she is.

Memory is a complex process that includes recognizing an event, person, or object and then storing it in the brain. But memories are of no value unless they can also be retrieved. Typically, amnesia results from disrupting either the laying down or the retrieval of memory. The causes have traditionally been divided into “organic” or “functional.” Organic causes include damage to the brain through physical injury (like the plane crash in The English Patient), neurological disease such as Alzheimer’s disease, or the use of certain (generally sedative) drugs (my favorite is alcohol). Functional causes are psychological factors such as mental disorder, post-traumatic stress or, in psychoanalytic terms, defense mechanisms.

As we experience things the circuits in our brain are activated and monitored by the process we call consciousness. This is purely an electrical phenomenon served by multiple networks of neurons. The moment our attention turns to something else, so does the firing of the involved neurons. But for several seconds a trace of activity remains, just like the spot that lingers after staring into a bright light and closing your eyes. This is the first hint of memory, because the trace is now of something in the past. If this is not worth saving the signal is overtaken by other experiences. If, however, it’s something we want to remember a chemical reaction begins that takes several hours. Scientists are not exactly sure how memories are stored chemically, but hints suggest it involves a protein. Sleep, particularly slow-wave sleep, probably has a significant role in consolidating memories.

Also poorly understood is how memories are retrieved and brought back to consciousness. Specific brain areas, such as the temporal lobe, are rich in memories, but removal of a temporal lobe does not necessarily result in significant memory loss. However, the destruction of both hippocampi results in the inability to lay down or retrieve memory.

As newer more sophistocated methods are developed that can unravel the physiology of the brain, more of these questions will be answered. This is an exciting time in brain research.

Wednesday, April 21, 2010

The April 20 edition of the online publication of NATURE published a study showing that in more than 11,000 healthy adults between 18 and 50 years of age brain training exercises were of no benefit. The group did the exercises three times a week for 6 weeks. At the end of the study the ones trained actually showed less improvement in cognitive function than control patients.

"A couple of years ago, I reviewed the literature on brain training and was surprised to find that, despite the fact that many millions of people are now involved in these types of activities, there is very little solid peer-reviewed scientific evidence out there to show that it actually works," lead author Adrian M. Owen, MD, from the Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, United Kingdom, told reporters at a telephone press briefing. "This is a multi-million-pound industry, and given that so many people are involved, it is interesting that the scientific evidence was lacking."

Dr. Owen and his colleagues conducted an online study to investigate whether regular brain training leads to any improvement in cognitive function. Participants were randomly assigned to 1 of 3 groups. The first group trained in tasks that emphasized reasoning, planning, and problem-solving. The second group trained in a broader range of cognitive functions, which included tests of short-term memory, attention, visuospatial processing, and mathematics. To continuously challenge the participants' cognitive performance and maximize any benefits of training, the difficulty of the training increased as the participants improved.

The control group surfed the Internet to find answers to general knowledge questions.

At the end of 6 weeks, the participants were reassessed to see whether their cognitive functioning had improved. The researchers found that none of the brain training tasks transferred to other mental or cognitive abilities beyond what had been specifically practiced by each group. The control group also improved in their ability to answer obscure knowledge questions, although the effect size was small.
The study found that the training groups did get much better on the test that they actually practiced. In addition, participants got better the more they trained. However, even people who trained much more than average showed no generalization of training to untrained tasks — even those that were cognitively closely related.

Surf on!

Tuesday, April 20, 2010

The peripheral nervous system is the nerves from the spinal cord to muscles and organs. Nerves to muscles are ones we use to play tennis, type on the computer, or move our eyes to read these words. There is also the autonomic nervous system for controlling organ function such as heart rate, gut motility, and bladder. The Vagus Nerve is one and originates in the brainstem just above the neck. It travels far down into the abdominal cavity, making connections to the heart, lungs, and stomach. Not only does it send impulses to organs, it also relays information back to the brain, making it both afferent and efferent.

In the late 70s it was discovered that pulsing the Vagus Nerve with small electric currents could help reduce seizures in some forms of epilepsy. So, Cyberonics began selling a small device similar to a cardiac pacemaker that could be implanted into patients’ chests – Vagus Nerve Stimulators, or VNS. Many people with seizure disorders do not have seizures adequately controlled with medication, so must rely on alternative treatments.

It was noted that some patients with depression in addition to epilepsy showed an improvement in depression regardless of any improvement in seizure control. Soon, VNS devices were being implanted in patients suffering only from depression.

There is no question this treatment is effective for a small number of patients. The question that still is not understood is why this should be.

Thursday, April 15, 2010

I recently overheard a person authoritatively state, “You know, we only use about ten percent of our brain.” I laughed. This wasn’t the first time I’ve heard this outrageous statement and have always wondered where it started. Like a lot of folklore, it’s not true.

Early Greeks realized that a severe depressed skull fracture, say on the left side, could result in paralysis on the right side of the body. But how or where this cross-connectivity between brain and body occurred wasn’t known. For centuries it wasn’t clear that the brain had anything to do with consciousness or thought. The microscope demonstrated neurons and supportive glial tissue, but how they communicated with each other and the rest of the body remained a mystery until a neuroanatomist, Santiago Ramon Cajal, invented a special dye that could demonstrate individual neurons and fiber tracts.

Prior to the last century brain function was localized by carefully correlating obvious brain damage (usually from strokes) with findings from the pre-death neurologic examination. But this only gave anatomists clues to obvious behavior, like movement or speech. Until the mid 20th century there were no methods to measure “silent” brain activities such as memory or solving math problems. The largest lobe of the human brain is the frontal lobe. For centuries anatomists suspected it was important in personality and behavior but there was no methodology to test these hypotheses. Now, with newer imaging techniques, such as Positron Emission Tomography (PET scans) there are elegant ways to visualize brain activity during many subtle functions.

Although we may not be able to ascribe functional labels to every square millimeter of brain, there really are no “unused” areas.

Monday, April 12, 2010

HM is one of the most famous patients in the history of neurosurgery because of what he taught us about memory.

A great many cases of epilepsy are associated with scarring on the brain surface from a variety of causes – stroke, infection, trauma, etc. One brain area commonly responsible for seizures is the temporal lobe, located on each side directly behind the eye and bone of the temple. In the late 1930s surgery was being developed to remove brain scars as one method of seizure control in an era when there were no effective medications. In cases where seizure-causing scars could be easily approached surgically, the results were quite good.
Patient HM developed seizures as a result of a bike accident at age 9. A New England neurosurgeon diagnosed HM’s seizures as originating from both his right and left temporal lobes. In September, 1953, both of HM’s temporal lobes were removed, rendering him seizure free. However, although he could remember how to do previously learned tasks, he was no longer able to commit new events to long-term memory (termed anterograde amnesia). He also suffered moderate retrograde amnesia, and could not remember most events in the 1-2 year period before surgery, and some events up to 11 years before, meaning that his amnesia was temporally graded. However, his ability to form long-term procedural memories was still intact; thus he could, as an example, learn new motor skills, despite not being able to remember learning them.
Until his death, HM was the subject of numerous psychological studies aimed at learning more about the process of memory. Up until his surgery, it was unclear what parts of the brain are crucial for the various processes involved in laying down, storing, and retrieving memories. Even after his death, HM’s brain continues to teach us about the complex physiology of memory.

Friday, April 9, 2010

A critical component of traumatic brain injury (TBI) is brain swelling. Contents inside of the skull include the brain matter itself, spinal fluid (around the brain and inside ventricles), and the blood in vessels. Because the skull is a rigid container, a change in volume of any one of these three components can dramatically alter intracranial pressure.

Under normal conditions the brain’s blood vessels are partially constricted. Immediately following a blow to the head, the normal control of these vessels is lost. As a result, the vessels dilate, causing an increase in intracranial pressure. The CO2 content of blood affects vessels; high CO2 dilates them whereas low CO2 constricts them. To lower intracranial pressure neurosurgeons hyperventilate the patient; over-breathing quickly lowers the blood’s CO2 content, which constricts the vessels.

Brain tissue has a great deal of water in it. So sucking water out of brain can also lower pressure. This is accomplished by injecting a non-metabolized sugar into the blood stream. The sugar molecules (such as mannitol) are too large to pass from blood into brain tissue, but their presence pulls water from the brain into the blood by osmosis. The water then excreted by the kidneys. For obvious reasons, these sugars are termed osmotic diuretics.

Finally, intracranial pressure can be lowered by carefully draining small amounts of fluid from the chambers in the brain. Severely head injured patients however may have already collapsed these spaces, making this option impossible.

Why is controlling intracranial pressure so important? Because the higher the pressure the harder it is to push blood through the brain. When the pressure inside the skull exceeds arterial pressure blood flow to the brain stops. If this happens, massive brain damage results. To help manage a patient, pressure sensors are commonly placed directly inside the skull.

Wednesday, April 7, 2010

My last post discussed subdural hematomas, so it’s a good time to talk about epidural hematomas. As previously mentioned, the Dura is a fibrous membrane attached to the inner surface of the skull. Like all tissue, it needs a blood supply. The artery feeding it (the Middle Meningeal artery) runs just in front of the ear where the skull is quite thin and easily fractured. When fractured, the bone edge can be quit sharp and cut this artery. Unlike veins that transmit blood at low pressure, arteries carry blood at high pressure. So when the meningeal artery is cut a blood clot forms between the skull and dura; hence the name of epidural hematoma. Because the bleeding is under arterial pressure, the clot can grow large quickly.

As the clot enlarges it pushes brain aside. But since the skull can’t expand the compressed brain becomes squeezed. And just like a tube of toothpaste, the squeezed brain seeks the path of least resistance, which is out the base of the skull – a phenomenon termed herniation. This is considered a surgical emergency.

Epidural hematomas seldom occur in isolation and are usually accompanied by additional forms of traumatic brain injury. For this reason, even with prompt removal, a patient may remain in coma depending upon any other injuries.

Monday, April 5, 2010

Lining the inside of the skull is a tough fibrous tissue called Dura. Between the Dura and brain is a space filled with Cerebrospinal Fluid (CSF). Young people have a very thin subdural space, but as we age and the brain shrinks because of loss of neurons and, as a result, this space grows larger. Blood is supplied to the brain by two carotid and two vertebral arteries that travel up the neck and cross this space. Veins bridge this space along the midline of the head and at the temples, to drain eventually into the Jugular Veins on either side of the neck.

When the head is struck by an object (either deceleration or acceleration) the brain moves within the skull and tugs on these bridging veins. A strong enough tug will tear a vein, causing bleeding into the subdural space. This results in a clot which is called a subdural hematoma. Because older people have smaller, atrophic brains, there is more space for the brain to move on impact, even with relatively minor trauma, such as falls. For this reason, subdural hematomas are more common in seniors.

The pressure a subdural hematoma exerts on the brain may cause weakness on the opposite side of the body. However, the mass may not cause enough symptoms for the patient to seek medical evaluation. Over time, the center of the clot liquefies while the outer layers form a tough fibrous capsule of scar tissue and the clot changes from an acute, to sub-acute, to a chronic subdural hematoma.

CT or MRI scans easily show the mass.

The treatment is surgical removal. But this can become problematic in chronic cases where the membranes are well formed and rich in small blood vessels, thus potentially causing more problems than leaving them undisturbed.

Sunday, April 4, 2010


Because my previous blog dealt with concussion I thought I’d continue talking about traumatic brain injury (TBI). A brain stem contusion is just one more step in the continuum of TBI. As with a concussion, the kinetic forces of impact are channeled down and out the base of the skull and thus travel through the brain stem. But unlike concussions, which temporarily disrupts neurons from functioning without causing damage to the tissue itself, these forces are strong enough to rupture the small blood vessels that nourish the brain stem, and this results in small (called petechial) hemorrhages. The location of each hemorrhage determines the symptoms it produces. Because the brain stem contains so many pathways for the control of the eyes, movement and coordination, consciousness, and other senses, the damage can cause numerous combinations of neurologic problems involving coma, double vision, paralysis, loss of hearing, and others.

In addition to producing hemorrhages, the shock wave causes a massive release of brainstem synapses, flooding the area with neurotransmitters which can compound the cause of unconsciousness.

Usually these hemorrhages are too small to be seen on a routine MRI or CT scan, so the diagnosis is based on the clinical exam. Treatment is supportive, giving the brain time to recover. Often, however, some symptoms, such as double vision or lethargy may linger for years.

Saturday, April 3, 2010


I was channel surfing the other day when I came across a boxing match. I watched for a few moments out of amazement rather than interest. Boxing appears to be a sport with one purpose only – to inflict brain damage on one’s opponent. There may be a lot of body blows in a round, but what boxers are really trying to do is get a good shot at their opponent’s head for a knock down, or better yet, a knock out. How sick is that?

The past decade has seen a redefinition of what constitutes a concussion. Used to be it was a head injury characterized by a brief loss of consciousness. The requirement for loss of consciousness has been removed, leaving only the symptoms of temporary confusion and amnesia after a blow to the head.

When a force impacts the skull a shock wave of energy is transmitted to the brain. Like electricity, the shock wave travels the route of least resistance, which is out the base of the skull into the spinal canal. This route includes the brainstem, an area crucial to consciousness. If the force is great enough, the neurons supporting consciousness are temporarily disrupted, possibly resulting in a period of unconsciousness. But this period may be extremely short or never even occur. Nevertheless, brainstem circuits are temporarily disrupted, leaving symptoms of confusion, amnesia, headache, dizziness, ringing in the ears, nausea or vomiting, slurred speech, and fatigue. These symptoms may not appear until hours after the injury.

A common misperception is that concussions are trivial, leaving no residual. Actually repetitive concussions have a cumulative effect on brain function. A good example is the “punch drunk” retired boxer who may show slowed movement, Parkinson like tremors, and elements of dementia. For this reason professional neurosurgical organizations have spent a great deal of effort to encourage the use of protective helmets for sports that place the athlete at risk for head injury.

Thursday, April 1, 2010


What’s the difference between encephalitis and meningitis? As most of you know, attaching -itis to a word indicates inflammation. The word encepha – refers to the brain itself. So encephalitis is a condition in which brain tissue is inflamed. The causes of inflammation may be numerous and include bacterial or viral infections. The meninges are three separate layers of tissue that surround the brain and spinal cord (the dura, the arachnoid, the pia). So the term meningitis refers to inflammation of the meninges, also without indicating the cause, which can include bacterial or viral infections.

Many cases of meningitis are transmitted from the environment (from another individual) into the person through the air. The nerves for smell (olfactory nerve), located in the roof of the nose, provides a common direct route for bacteria to reach the brain and meninges. Often, the cause of the infection is unknown.

Meningitis and encephalitis are potentially life threatening diseases that require prompt diagnosis and treatment. Signs of meningitis include sleepiness, nausea, vomiting, headache, fever, and a stiff neck. Because the brain is bathed in spinal fluid (CSF), obtaining a sample of fluid through a “spinal tap” is the most accurate method of diagnosis. Normally CSF has no cells in it and contains protein and sugar. If the meninges are infected the CSF shows white cells, bacteria, and abnormal amounts of protein and glucose. Cases of encephalitis may show only an increase in cells. MRI and/or CT scans are usually also required as part of the evaluation.

Monday, March 29, 2010


The causes of strokes can be broken down into three main categories: 1) hemorrhage, 2) embolic, 3) thrombotic. Intracerebral hemorrhage occurs when a blood vessel breaks, releasing blood directly into the brain tissue. This can happen from a weakness in the vessel wall, when the blood pressure is too high, or when a person’s blood is not able to clot, for example, when they are placed on “blood thinners.” The resulting blood clot forms a mass and can squeeze surrounding brain, rapidly leading to death or severe brain damage. Often, by the time the patient reaches medical care, it is too late to reverse the damage and many neurosurgeons believe surgery is not worthwhile.

Embolic strokes occur when a blood clot or piece of cholesterol plaque breaks off a heart valve or inside of a blood vessel and flows upstream to becomes lodged in a smaller vessel. This prevents blood from nourishing to the tissue supplied by the vessel. The size of the stroke depends upon where along the vessel it is blocked. Disease that damages the heart valves or the lining of the heart chambers are common causes for emboli.

Thrombotic strokes occur commonly in the carotid and vertebral arteries that supply the brain. Vessel disease, like arteriolosclerosis can narrow the inside of the vessel, slowing blood like a kink in a hose and eventually resulting in a clot that stops flow entirely. There is a narrow window of time that, if this the cause of the stroke is diagnosed and the proper facilities are available, drugs called “clot busters” may help dissolve the blockage and restore flow.

More hospitals are establishing stroke teams, a group of specialized doctors and nurses who can provide the expertise to diagnose and treat stroke as rapidly as possible.

Saturday, March 27, 2010


In my last blog I mentioned preprogrammed motor activity, so I thought this might be a good time to expand on that concept. There is a vast literature on motor control – the physiology of how we execute movements - and the brain pathways involved in even simple tasks are complex.

Think back to when you learned how to ride a bike. Initially there were several things you needed to learn; how to balance, how to peddle, how to turn, how to stop, and how to shift gears. To help balance, you may initially have used trainer wheels. But as you progressed, the trainer wheels came off and you became more confident. Part of this learning process was that repetitive movements like peddling were becoming programmed into your nervous system so that you didn’t have to think about them and you could focus on more important tasks, such as where to turn.

Another example is shooting baskets. The first time you threw a basketball at a hoop you probably didn’t come close to hitting it, much less sinking the shot. The weight of the ball was new and you had no concept of the forces needed to send it in the right trajectory. As you practiced, your nervous system learned to make numerous calculations extremely rapidly and your accuracy improved. Some of these calculations went from the conscious to the unconscious level. In addition your nervous system transitioned from linear processing to parallel processing. In parallel processing a process is broken down into several component tasks which are solved simultaneously and then made whole again.

Friday, March 26, 2010


A comment to the 3/22/ post asked. “… An "expert" said that when you are driving and receiving information through the phone, your brain goes into something he called sensory overload. Your peripheral vision is severely reduced and you basically are looking straight ahead. I can understand this when actually holding a cell phone to your ear. They did not make a distinction between hands free devices and holding a phone however. So my question is this.....would it be different if you were hands free and talking on the phone or would you still be overloaded. And if this is the case, how does this relate to talking to a passenger? Is that the same dynamic or different? Explain sensory overload.”

Sensory overload is a condition where the senses are strained and to the point it becomes difficult to focus on the task at hand. We commonly experience this situation if, say, we’re talking on the phone and our spouse asks us a question. It’s impossible to carry on the phone conversation and answer, so we pause the conversation long enough to take care of our spouse. Okay, you say, but that’s not the same as driving and talking. Well, yes it is. Can you type a letter while carrying on a conversation? No you can’t. And it doesn’t make any difference if you’re holding the phone or not – concentrating on the conversation at hand detracts from paying attention to driving.

The deceiving thing about driving is that much of the brain’s motor activity is automatic in that the visual information coming into our brain elicits a preprogrammed response, like turning through a curve in the road. This lulls us into believing we can do other things while driving. (I’ve seen drivers putting on makeup while driving 60 mph on the freeway). But the truth is the brain really can only really concentrate on one task at a time. The more you try to multitask, the poorer your performance in any of the tasks.

Driving requires constant vigilance. The more that vigilance that is distracted, the longer the reaction time to an unplanned event and the less we are aware of what’s going on around us. This holds true regardless of whether the conversation is on the phone or with the passenger next to us.

Thursday, March 25, 2010


Having just mentioned the Blood Brain Barrier, it’s a good time to discuss Multiple Sclerosis. MS is an autoimmune disease. Auto immune diseases are strange in that the same immune system that guards our body against infections for some reason turns against certain our own body and attacks them in the same manner.
When this occurs in the brain to cause MS, lymph cells attack the blood brain barrier to break it down, allowing other immune system components into the brain where they attack the myelin, the insulation on neurons. When this happens, the myelin becomes damaged to the point the nerves no longer can transmit information. The name multiple sclerosis refers to the multiple scars (known as plaques) that form as a result of the immune attack. Although myelin also coats peripheral nerves, they are seldom involved in the disease.

Neuroscientists know a great deal about MS, but they do not know what causes or triggers this autoimmunity. Some believe it results from a prior infection as if an immune response against the infection gets confused and attacks the BBB and myelin instead. Genetics does not play a strong role in this disease. The frustrating aspect about this disease is it is intermittent, meaning a person may have one or two attacks and no others. Another person may have attacks one after another in a very progressive course. Once the diagnosis is made, there is no way to predict what will happen. The good news is that there are at least five-modifying treatments that are approved for treatment and have various degrees of efficacy.