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Today I would like to share with you the stories of two men who are beating the opinions of the medical profession and are living productive lives.

A few months back my son-in-law conned me into going to a local taping of one of the Worldwide Entertainment (WWE, formerly World Wrestling Federation) shows. I met someone there whose life has a few lessons for everyone with a brain-related disability. In the interest of confidentiality I’ll call him Mike.

Mike and his older brother had seats next to ours. Mike, being the more outgoing, introduced himself as well as his brother when they took their seats. Mike is a big time fan of wrestling to the point that he can tell you what happened at every pro wrestling event as far back as 10 years ago. Since we had about 30 minutes before the show started, the four of us chatted the time away.

Mike related how he only worked part time at the local office of Catholic Charities, where he sorted donations of food, clothing, or whatever happened to come through the door. When he wasn’t working he spent his time helping his mother with “house stuff” such as laundry, cleaning, mowing the lawn, shopping for groceries, “whatever needs doing,” as he called it.

His brother told us how Mike had to overcome a number of health problems in his 24 years of life.

First came open heart surgery to repair a valve in his heart. Then came another surgery to fix a tight spot in his esophagus. The doctors eventually told his parents that he was probably autistic and that he would wind up in an institution some day. Fortunately, for Mike, his parents told his doctors that they would prove them wrong.

Mike received home schooling in addition to his regular special education schoolwork. It soon became apparent that he was functioning better than kids with classic autism and, thanks to an alert school counselor, he was re-evaluated by a team of neuropsychologists who diagnosed Mike as having “high functional” autism or, more formerly, Asperger’s Syndrome. Mike lives at home, and he never saw the inside of an institution.

To put it mildly, Mike had one Hell of a good time that night. The show may have been scripted and choreographed in advance, but it was just what Mike wanted.

Lawrence’s story is pretty much the same as Mike’s, but a recent event in his life involves something that shouldn’t happen in America or any other country.

Lawrence is also a “high function” autistic. He works in the produce department of a Belen, NM Wal-Mart Superstore and has been there for 10 years. His employee evaluations have been excellent, he has been named “Employee of the Month” several times and, on top of that, he loves his job. Until a new department manager arrived, that is.

This new manager, in Lawrence’s presence, demanded of the store manager that Lawrence be fired because “he’s retarded,” “he sets a bad example” and the he “can’t read and write.” She further demanded that Lawrence take his yearly vacation time immediately and be terminated the day that he returned to work.

Needless to say, that pissed this writer off.

Since your humble correspondent spent a year of his misguided youth in law school, I reverted to a state best described as that of “lawyer prick.”

I recommended that Lawrence and his parents to immediately send a letter to the store manager in which they should “suggest” that he and the meat and produce department managers should devote a few hours to familiarize themselves with the provisions of the Americans with Disabilities Act (ADA). Specifically, they should “suggest” that the Wal-Mart managers read the sections regarding “harassments” and “threats.” They also should “suggest” that, since the department managers have initiated demands that Lawrence be fired, if Lawrence should be dismissed for anything other than willful employee misconduct that Wal-Mart, the store manger, and the meat and produce managers individually, will be sued for violating Lawrence’s civil rights under the Civil Rights Act of 1991 and for illegal harassment and terminations as described in the ADA.

I’ve said it before and will say it again and again: as long as jerks like the above-mentioned Wal-Mart managers are allowed to get away with such reprehensible behavior, Dr. King’s immortal words in his “Letter from the Birmingham Jail” will give a concise summary of the world that those of us with physical or mental handicaps are facing:

“Injustice anywhere is a threat to justice everywhere.”

I’m Wayne McDonald and I’m a brain injury survivor. And I hate bigots.

It is well known that obesity is a risk factor in cardiovascular disease and diabetes, but recent research indicates that obesity may be initiated by the brain.

At a recent symposium sponsored by the London-based Journal of Physiology and Blackwell Publications devoted to basic research in the relationship between metabolic disturbances and the brain, the presenting scientists provided a “state of the art” review of current research on this topic.

Barry Levin, MD of the New Jersey Medical School, and a long time researcher in how the brain senses and regulates metabolism, presented laboratory evidence suggesting that the brain may be a central factor in the well-known tendency to gain weight after dieting.  He noted that when the body has gone through a process of negative energy balance (as when dieting, where food intake is reduced and body fat is used as a supplemental energy source) the brain may signal the body to begin restoring fat when dieting ceases.

In a similar vein, Mary Dallman, PhD, of the University of California at San Francisco, presented a laboratory study based on rats that demonstrated that when rats were subjected to physiologic stress (such as cold or sleep deprivation) that they would gain weight once the stress was removed.  These results become part of a growing body of evidence linking stress to obesity by altering the process of dopamine metabolism in the brain.

Gregory Morton, PhD of the University of Washington presented evidence that the brain in the regulation of glucose and other nutrients in the bloodstream.  He noted that there is clear evidence that the brain senses a decrease in circulating glucose (with oxygen, the brain’s energy source) it responds by signaling the body to begin the conversion of fat to glucose as well as increasing the appetite.  Any disturbance in the brain-glucose-hormonal axis, he noted, could be a causative factor in the development of Metabolic Syndrome.

Metabolic Syndrome is a condition that is associated with 1) obesity, 2) abnormal lipid/cholesterol levels in the bloodstream, 3) cardiovascular disease, and 4) Type 2 diabetes (high blood “sugar” and abnormal results on a glucose tolerance test). 1, 2

The papers presented at the symposium are published in the September issue of the Journal of Physiology.

In a recent publication of note Knopman et al reported their results that strongly suggest that women diagnosed with age-related dementia (also known as senile dementia) demonstrated a consistent pattern of weight loss, beginning 10-11 years before diagnosis, when compared to an age and sex-matched cohort of those without dementia. 3

Surprisingly, the study found that this pattern of weight loss did not occur in men diagnosed with dementia.

Comment

The symposium presentations mentioned above are certainly remarkable in that they add even more credibility to the probable role of the brain in obesity.  Particularly, the laboratory models suggesting that a reduction of stress in the lifestyle may be beneficial in planned weight loss through dieting.

The study linking a pattern of unintended weight loss in women that were eventually diagnosed with dementia is also noteworthy.  As the authors suggested in their paper, further research is indicated to determine the possible utility of weight loss as a “marker” for the subsequent development of dementia in older (> 60 years of age) women.

It must be noted that dementia and Alzheimer’s Disease are not the same disease process in that there are many causes of dementia (such as vascular or metabolic causes) while Alzheimer’s is associated with the presence of amyloid plaque buildup in the brain itself.

Notes

1. For more information about Metabolic Syndrome and its associated medical risks, see my earlier essay published at Associated Content.com.

2. Perez-Tilve, Diego; Stern, Javier, and Tschop, Matthias (2006): The Brain and the Metabolic Syndrome: Not a Wireless Connection, Endocrinology 147(3): 1136-1139.

3. Knopman, DS; S. D. Edland, SD; Cha, Petersen, RH, and W. A. Rocca, WA (2007): Incident dementia in women is preceded by weight loss by at least a decade, Neurology 69:739-746.

The Glasgow Coma Scale (GCS) is widely used in the clinical evaluation of disorders of consciousness that are the result of traumatic brain injury (TBI). 1 The GCS is usually first assessed “in the field” by emergency medical personnel to establish a “baseline” against which further changes in the level of consciousness may be evaluated.

The GCS consists of three parameters:

·         EYES – Graded on a scale of 1 (eyes closed) to 4 (eyes open, or opens eyes on command.

·         VERBAL – Graded on a scale of 1 (silent) to 5 (responds normally and appropriately).

·         MOTOR – Graded on a scale of 1 (absence of movement) to 6 (normal, purposeful movement).

The scores in each of the 3 categories are then added.  The total score is usually interpreted as follows:

·         3 – 8 = severe (most critical and requiring intensive medical management)

·         9 – 12 = moderate (will require hospitalization until improvement)

·         13 + = minor (minimal care or brief admission for observation)

The US Centers for Disease Control and Prevention (CDC) has recommended adoption of the GCS as the preferred method of evaluating head injury in mass casualty situations.

Other Scales that Include the GCS

There are several other scales that include the GCS as one of their components.  These scales are primarily used in the Intensive Care Unit (ICU) to evaluate the victim’s overall recovery  Among the more widely used are the APACHE II (Acute Physiology and Chronic Health Evaluation II) 2 and the SAPS II (Simplified Acute Physiology Score). 3

These scales, as well as others, are not limited the status of consciousness but are more general in nature and are designed to evaluate combined physiologic derangements.

GCS and Prognosis for Recovery

There have been many clinical studies published that document the relationship between the GCS score and its predictive value regarding both short- and long-term survival.  While a review of these studies is beyond the intent of this posting, their results are easily summarized.

The poorest outcomes, meaning either death or substantial permanent disability, are a function of two parameters. First, the lowest scores on admission correlate closely with death during the first week of hospitalization  Secondly, the length of time over which clinical improvement occurs is a strong indicator of the level of permanent disability.  These two findings are, of course, only generalizations and it is well-documented in the medical literature that considerable individual variations may occur.

Recent advances in imaging of the brain have demonstrated the possibility that there may be some residual sensory awareness in those who have suffered significant brain injury.  While these findings are indeed exciting, it must be remembered that their incorporation into the clinical decision-making process remains many years in the future. 4

Notes

1. Teasdale, G and Jennett, B (1974) Assessment of coma and impaired consciousness; a practical scale, Lancet 13:2(7872):81-84.

2. Knaus, W; Draper, E; Wagner D, and Zimmerman J (1985) “APACHE II: a severity of disease classification system”. Critical Care Medicine 13: 818-29.

3. Le Gall, J-R; Stanley Lemeshow, S;, and Saulnier, F (1993). A New Simplified Acute Physiology Score (SAPS II) Based on a European/North American Multicenter Study. JAMA 270:2957-2963.

4. Pickard, J; Coleman, M; Aigbirhio, F; Carpenter, T, and Owen, A (2006) Head Injury: From the Glasgow Coma Scale to Quo Vadis, Clinical Neurosurgery, 53: 53-57.

 

I’m sorry about the inactivity here over the past week but, as anyone with brain injury will tell you, we have good days and bad days. Hopefully, I’ve gotten the bad days out of the way for now and I can get this blog up to date.

While I was out of action for the past week I had plenty of time for some serious thinking regarding a project that has been bouncing around inside my head for over a year. What follows is an explanation regarding that project and why I’m bringing it to your attention.

Over the past several years there have been several reports in the medical literatures indicating that there is evidence that there is some degree of preserved sensory processing present in those that are in the vegetative and minimally conscious states, (VS and MCS, respectively) [1], [2], [3] particularly the sense of hearing. Furthermore, the reports by Owen et al [4] and Schiff et al[5] indicate that not only is sensory processing preserved but that consciousness can be restored, even after a period of years. These reports raise two important issues that, to the best of my knowledge, have yet to be addressed.

The first of these questions is quite straightforward: “What happens to the victim’s consciousness when they are in the vegetative or minimally conscious states?” It would seem, based on the published data, that consciousness is “suppressed” rather than “lost” during these conditions. In other words, what an observer may perceive as a patient in the VS or the MCS may actually be a patient that is indeed “living in their own world” and whose degree of consciousness suppression has not lifted to the point that they can communicate with their surroundings. Are these patients in a condition that may be analogous to a deep sleep?

The second question is predicate on a “yes” answer to the question above. If cerebral function is present although consciousness is suppressed, what ethical issues must be considered? Should resources be directed at determining which patients are “more conscious” than others? Or, more ominously, should such results be used to decide who will receive more intensive therapy?

At the risk of destroying my credibility as an essayist, I will now disclose my reason for introducing the above questions.

During my own recovery I had several experiences that proved, at least to me, that the brain does indeed continue processing sensory inputs (such as hearing) even though consciousness is suppressed. And, since I’m convinced that I have no reason to believe that I am unique in that I am the only person to experience this phenomenon, I would like to hear from other brain injury survivors that may have had similar experiences. Even if you have no memory of such events I would like to hear from you.

If you, or a family member or friend, would care to share what you might have (or didn’t have, for that matter); drop by my web site at www.freewebs.com/waynemcdonald and then follow the first link.

On my word as a gentleman, I promise that any and all responses will be held in the strictest confidence.

Thanks for stopping by my blog.

I’m Wayne McDonald and I’m a brain injury survivor.

 


 

[1] For a description of the general definitions of the vegetative and minimally unconscious states, see my post “What Are Disorders of Consciousness?

[2] Laureys, Steven (2004) Functional neuroimaging in the vegetative state, NeuroRehabilitation 19: 335-341.

[3] Di, HB; Yu, SM; Weng, SC; and Laureys, Steven et al (2007) Cerebral response to patient’s own name in the vegetative and minimally conscious states. Neurology 68: 895-899.

[4] Owen, AM; Coleman, MR; Boly, M; and Davis, MH (2006) Detecting awareness in the minimally conscious state. Science 313 (5792): 1402

[5] Schiff, ND; Giacino, JT; Kalmer, K; Victor, JD; and Baker, K et al (2007) Behavioural improvements with thalamic stimulation after severe traumatic brain injury. Nature 448 (7153): 600-603.

In my personal opinion, the saying that “Old habits are hard to break” is probably one of the most accurate statements ever made regarding human behavior.

Before my retirement, I spent almost 30 years as a medical para-professional as first a Physician’s Assistant and then as an ultrasonographer with special qualifications in adult and pediatric cardiology as well as in vascular testing. And, even though I’m retired, I still make the trips down to the medical library in order to read the latest medical journals. A report in the journal Neurology caught my attention a few months back and, as a brain injury survivor, I would like to share the gist of that report with you.

In “The Portrayal of Coma in Contemporary Motion Pictures,” which appeared in the “Reports and Reviews” section of the May 9, 2006 issue of Neurology1 Eelco Wijdicks, MD of the Mayo Clinic in Rochester, Minnesota, reports on a study in which he and his son, Coen, identified 30 movies released between 1970 and 2004 in which actors depicted characters that had been in prolonged coma with the goal of evaluating the accuracy of those depictions, which they defined as “by appearance, the complexity of care, accurate cause of coma and probability of awakening, and appropriate compassionate discussion between the physician and family members.” From these 30 movies, 22 clips were shown to a panel of neurologists and intensive care nurses and then to 72 non-medical viewers.

The medical viewers identified numerous inaccuracies in these clips, including 1) sudden awakening “with cognition intact, even after prolonged time in a coma,” 2) portrayal of comatose patients as “Sleeping Beauty” (with eyes closed, beautifully groomed and perfect complexion, and the absence feeding tubes or other common supportive measures), and 3) showing “patients’ that emerged from coma that immediately began walking around, and in some cases “fighting” with the “bad guys,” without even a hint of residual disability.

The 72 viewers without a medical background were then shown the same clips. None of these viewers were able to identify the misrepresentations pointed out by the medical-background viewers. Furthermore, when asked if they strongly agreed with the statement “If my family member would be in the same situation, it is possible that I would remember what happened in the scene and allow it to influence any decisions that I would make, ” 39 percent said that they would allow the scenes to influence their decisions.

It is well known that, at least to those who have experienced the stressful environment surrounding the care of a family member in a coma, movies present inaccurate depictions of coma patients as well as their prospects for recovery. What is indeed surprising (at least to this writer) is the number of viewers that, knowing what they had seen was purely fictional, would still let these fictional portrayals influence their own decisions.

Admittedly, what a person would do in an actual situation is probably much different than their response should they find themselves forced to make what could amount to a life or death decision involving a loved one. My point is simply to point out that, with the exception of those that have been in a “real-life” situation, the general public has been misled by the entertainment industry into unfounded beliefs regarding coma.

The movie industry is not solely to blame for such misunderstandings, as the media “hype” regarding the case of Terry Wallis demonstrates.

Terry Wallis: “The Man who slept for 19 Years”

The case of Terry Wallis has become perhaps the most widely-cited example of a patient who “suddenly awoke” from a “coma”. Mr. Wallis received a severe brain injury at the age of 19 as a result of an automobile accident. Initially comatose following this accident, he progressively improved over the course of several weeks before stabilizing in a minimally conscious state. He remained in this state until June of 2003 when he, for reasons that remain medically unexplainable, began to communicate with family members.

Mr. Wallis’ dramatic recovery instantly became national news with everyone from CNN to the New York Times, and even the New Scientist, covering his “sudden recovery from a coma.” Unfortunately, their reporting gave the impression that Mr. Wallis had made a “Hollywood recovery.”

Mr. Wallis is indeed speaking, but his speech is almost unintelligible. He remains confined to his bed, with occasional periods in a bedside chair or wheelchair, due to the severe muscle wasting and joint immobility that invariably develops among the long term bedridden. He is still unable to feed or care for himself and will, in all probability, never be able to do so. His actual condition is certainly a far cry from that depicted in the media.

I do not intend this essay to in any way minimize the fact that Mr. Wallis did make an unexpected recovery of skills that were long thought to have been lost as a consequence of his accident. I am simply pointing out that the media is quite often more concerned with the viewer impact content of its news coverage rather than its accuracy.2, 3

I’m Wayne McDonald and I’m a brain injury survivor.

Notes

1. Wijdicks, Eelco and Wijdicks, Coen (2007) The Portrayal of Coma in Contemporary Motion Pictures, Neurology 66:1300-1303.

2. Mr. Wallis’ is the focus of the documentary “The Man who Slept for 19 Years.” This documentary is scheduled for broadcast on August 26, 2007 at 5:00PM EDT on the Discovery Health Channel. Please check the local listings for your area regarding broadcast time.

3. For perhaps the most nauseating example of how the Internet “promotes discussion” regarding news about Mr. Wallis and his struggle to recover, see Patient Revives After 19 Years By Rewiring Brain posted at Slashdot.

A clinical study published in the medical journal Neurology1 has demonstrated that donepezil (Aricept®, Eisai) preserves or improves the brain’s ability to perform cognitive functions such as basic mathematics and facial recognition as well as more global functions such as motor skills and self-awareness in patients diagnosed with severe Alzheimer’s disease

The report, authored by an international team represented by clinicians from Canada, the United Kingdom, and the United States, compared results of several commonly used diagnostic tests of cognitive function in Alzheimer’s disease before and after several weeks of therapy with donepezil.  The study found that a once daily dosage of 10mg donepezil was associated with either an improvement, or delayed progression of impairment, in cognitive function as documented by several widely used tests of neuropsychological function (63% of treated subjects vs. 39% in the placebo group).

Donepezil is a member of the class of chemical agents known as acetyl-cholinesterase inhibitors, which means that it blocks the chemical which normally causes the breakdown of the neurotransmitter acetyl-choline in the area that separates neurons (nerve cells) from one another within the brain. While it has long been known that acetyl-choline is associated with the processes of memory storage and recall, the study is the first to demonstrate the beneficial effects of an acetyl-cholinesterase inhibitor in the more severe stages of Alzheimer’s disease.

Side effects associated with donepezil in the current study (such as low blood pressure, fainting, and gastro-intestinal distress) were no more frequent than in reports from previous studies involving patients with less severe manifestations of Alzheimer’s disease.

The study was funded by Eisai, Inc which produces the proprietary brand of donepezil, Aricept ® and by Pfizer, Inc.

Comment

Donepezil has been approved for use in mild to moderate cases of dementia in Alzheimer’s disease since 1996. The importance of the report in Neurology is that it is the first study to clearly demonstrate that the drug causes significant improvements in patient’s with the more severe manifestations of the constellation of signs and symptoms associated with Alzheimer’s disease.

For More Information

Information about Aricept®, including links for families and caregivers, can be found at the Aricept® information page.

As always, for more information about Alzheimer’s, see the National Institute of Neurological Diseases and Stroke information pages devoted to Alzheimer’s disease.

Information on clinical trials relative to AD can be found at Clinical Trials.gov website.

Reference

S. E. Black, MD, R. Doody, MD, H. Li, PhD, T. McRae, MD, K. M. Jambor, MA, Y. Xu, PhD, Y. Sun, PhD, C. A. Perdomo, MS and S. Richardson, PhD (2007):  Donepezil preserves cognition and global function in patients with severe Alzheimer disease, Neurology 2007;69:459-469

According to participants in a symposium convened as part of this year’s meeting of the American Psychological Association (APA), literally hundreds of “therapies” purporting to “treat;” “cure;” or “reverse” Autism Spectrum Disorder are flooding the Internet.

According to symposium moderator James Mulick, professor of psychology and pediatrics at Ohio State University, many of these treatment programs have never been evaluated for both their effectiveness and safety.

In a press release accompanying the symposium, Dr. Mulick noted that “Developmental disabilities like autism are a magnet for all kinds of unsupported or disproved therapies…

“There’s no cure for autism, and many parents are willing to believe anything if they come to think it could help their child.”

Dr. Mulick, who is also a contributing editor of Controversial Therapies for Developmental Disabilities: Fad, Fashion, and Science in Professional Practice, noted that when he began treating autistic children in the early 1970s about 3 children in 10,000 were diagnosed as having autism but now, due to a “relaxing” of diagnostic criteria related to the condition, the incidence is estimated to be near 1 in 150 children.

Another speaker at the symposium, Ohio State University doctoral candidate Tracy Kettering, remarked that when she conducted Google™ search for the phrase “autism treatment” the search returned more than 2 million matches.

“You get hundreds of different types of therapies that come up, and many have quotes from parents that claim a particular therapy ‘cured’ their child …” Kettering said.

Anne Snow, an Ohio State psychology graduate student, noted that while many of these treatments have never been adequately studied, that doesn’t mean they aren’t extensively promoted online.

“One of the characteristics of fad treatments is that they are discussed in the media and on the Internet, where many parents can be exposed to them.”

The symposium panelist agreed that the lifelong, “highs and lows,” manifestations of autism behavior may have led some parents to adopt a strategy of “try anything until something works.”

So far, according to Dr. Mulick, the only therapy that has been shown to have a long-term positive affect on autism is called Early Intensive Behavioral Intervention (EIBI)

EIBI is a highly structured approach to learning, in which children with autism are taught first to imitate their teachers. Unfortunately, this treatment is expensive, time-consuming and labor intensive. It involves one-on-one behavioral treatment with the child for up to 40 hours a week for several years.

“It’s expensive and difficult for many parents to use, that’s got to be one reason other (less well-documented and studied) treatments look attractive to them.”

The symposium, “Outrageous Developmental Disabilities Treatments,” was presented as part of the APA’s annual meeting, held this year in San Francisco, CA.

Comment

Autism isn’t the only neurological disease that has attracted the attentions of the “hucksters of hope and hypertext” marketing strategy.  Families of victims of conditions such as Alzheimer’s and Parkinson’s diseases, Multiple Sclerosis, and traumatic brain injury will certainly attest to the number of “treatment programs” that have arisen over the years.  Such programs do have one well-documented, proven effect: they are quite effective at separating people from their money.

If you want to try one after another of these “treatments,” don’t let me stop you.  Just remember that, as I have said in other posts, “miracle” cures simply don’t exist!  This is even more so when dealing with Internet-based operations.

As Washington Post columnist William Raspberry once noted “Saying that you saw it on the Internet is like saying that you heard it at the barbershop.”

According to a study to be published in an upcoming issue of the Annals of Neurology, a clinical trial has demonstrated that a new DNA-specific vaccine blocks the body’s immune system’s response to a specific protein is both safe and effective in reducing the size and number of brain lesions associated with Multiple Sclerosis (MS).

The vaccine, known as BHT-3009 after the specific protein that it targets, is the first vaccine to produce magnetic resonance imaging (MRI)-documented improvements in the brain lesions known to be associated with MS.  During the study, which was conducted at 4 US centers and 1 in Canada, 30 patients were given periodic injections of the vaccine.  Adverse effects of the treatment, which included abdominal discomfort, fatigue, and weakness, were the same in both the vaccination and placebo groups.

Multiple Sclerosis affects an estimated 400,000 Americans and is felt to be a class of autoimmune disease.  This means that, for reasons that are not well understood, the body’s immune system attacks the coatings of nerve cells within the central nervous system (the brain and spinal cord).  The clinical course of MS is notoriously difficult to predict with some patients experiencing only mild weakness and muscle changes while others will eventually progress to complete paralysis.

In an accompanying interview with online medical news service Medscape which accompanied publication of the study, Hideki Garren, MD, who led the clinical trial, noted that “these vaccines have not worked out exactly as expected and have failed in the sense that they have not met an approvable end point. However, they have shown that they can achieve some immune response in humans.”

While the reported results involved only 30 patients, the researches concluded that BHT-3009 and similar vaccines may represent a potential new treatment for those with MS.

The paper by Dr. Garren and associates was published in the August 13 online, early access edition of the Annals of Neurology. 

It should be noted that Dr. Garren is a founder of, and has a financial interest in, Bayhill Therapeutics of Palo Alto, CA.  Bayhill Therapeutics manufactures the BHT-3009 vaccine and funded the clinical trial mentioned previously in this posting.

Notes

More information on Multiple Sclerosis can be found at the Montel Williams MS Foundation and the National Multiple Sclerosis Society web pages.

The Bayhill Therapeutics web site can be found at this link.

 

Two new studies have shown that women who have a history of migraine headaches that are preceded by visual disturbances can be at a 10 time higher risk for stroke when compared to women without migraine.

In a paper that appears in the August 9 online, early access edition of the American Heart Association’s journal Stroke a team headed by Dr Leah MacClellan reviewed data collected in the Stroke Prevention in Young Women Study and found that women under the age of 55 that had a history of migraine headaches with aura were at 7-fold increased risk for stroke. 

An “aura” is a set of symptoms, usually involving disturbances in vision, which precedes the onset of a migraine headache.

When migraine with aura occurred in women with additional risk factors related to stroke such as smoking, hypertension (high blood pressure), or use of oral contraceptives, the risk of stroke was found to be 10 times higher than among women without migraine or at least 1 risk factor.   Migraine headache without aura, however, was not demonstrated to be a risk factor among the same study group.

The elevated risk in women with the combination of migraine with aura was confirmed in a separate paper that was also published online.

Dr. Tobias Kurth, who has published several studies concerning the possible relationship between headaches and stroke, concentrated his research within the same area and found that migraine with aura alone was the most common risk factor for stroke in women under the age of 55.

Neither of the studies evaluated the possible protective effect of medical therapy directed at preventing migraine headaches or relieving their associated symptoms.

Comment

Migraine headaches, with and without aura, are thought to be caused by a temporary decrease in the electrical activity of some parts of the brain.  The mechanisms behind such disturbances are poorly understood and are the subject of considerable clinical and laboratory research.

In 2004 clinicians from University Hospital in Bern, Switzerland reported on their results regarding migraine headaches and the surgical closure of a specific heart defect known as a patent foramen ovale (PFO).  They found that there was a doubling in the incidence of migraine headache in those with a documented PFO when compared to the general population. At one year following closure of the PFO, they found that the number of patients reporting a reduction in the number of headaches and/or the severity of symptoms was nearly 60%.  Several clinical studies to test the possible interrelationship between PFO, migraine headache, and stroke are underway at this time.

In light of the above studies it should appear obvious that women with a history of migraine with aura, particularly younger women should promptly seek medical attention if they develop any of the recognized signs of stroke such as numbness or paralysis affecting one side of the body, difficulty speaking or swallowing, loss of vision or other visual disturbance affecting only one eye.

Notes

Tobias Kurth (2007):  Migraine with Aura and Ischemic Stroke: Which Additional Factors Matter?  Stroke, Published online August 9, 2007, 10.1161/ STROKEAHA.107.494179.

Tobias Kurth et al (2004): Headache, migraine, and the risk of stroke in women. Poster S24.001, presented at the American Academy of Neurology Annual Meeting, San Francisco, April 27, 2004.

Leah R. MacClellan, Wayne Giles, John Cole, Marcella Wozniak, Barney Stern, Braxton D. Mitchell, and Steven J. Kittner (2007):  Probable Migraine with Visual Aura and Risk of Ischemic Stroke: The Stroke Prevention in Young Women Study, Stroke, Published online August 9, 2007, 10.1161/STROKEAHA.107.488395.

When the general public is asked to describe the consequences of brain injury, the most frequent responses will involve some concept of the victim’s loss of consciousness. This is unfortunate since, as those of us that deal with the long-term consequences are all too aware, the real “battle” doesn’t begin until after consciousness returns. For the purpose of this general overview, we may define any change from a state of full self-awareness to a state of decreased (or absent) self-awareness as a disorder of consciousness.

In the medical literature, recovery from a disorder of consciousness is defined as occurring along a continuum; which is to say that such recovery progresses in a direct, linear, and predictable fashion. The rapidity and completeness of recovery, of course, varies between individuals and with the underlying disease process that is the cause of such disorders. None the less, it will be helpful to review the general stages that may or may not be encountered.

The first, and by far the most serious, stage in the disorders of consciousness is that of coma; a state of profound (deep) unconsciousness in which the victim is unable to move, open his/her eyes, or respond appropriately in any way to external stimulation. Those in a coma are unable to breathe on their own and depend on mechanical support of respiratory activity, as well as intensive medical and nursing care, in order to survive.

Coma as a distinct clinical condition is very rarely a persistent condition, meaning that those surviving the initial event which induced coma will either progress to a less severe level of neurological compromise or will die. Despite the occasional “sensational” or “anecdotal” reports in the news media, there has never been a documented case of spontaneous recovery from coma directly to “consciousness. Such “miracle” recoveries have always been from a less severe level of impaired consciousness and have further been complicated by marked loss of motor skills such as speaking, use of table utensils, or the ability to perform simple self-care functions.

The next stage in the continuum is the vegetative state (VS), which is defined as a state in which the patient may be able to breathe without assistance yet remains dependent on skilled medical and nursing care in order to survive. Those in the vegetative state may open their eyes and may even make occasional non-purposeful sounds such as grunting or laughter but they are incapable of making intentional responses to external events. In the vegetative state, the patient has an established sleep/wake cycle, which can give the illusion of conscious activity.

The vegetative state, unlike coma, may persist for years upon years without obvious improvement in the victim’s clinical condition

The final stage, and the stage that is currently the focus of intense clinical research (Owen, 2006; Schiff, 2007), is the minimally conscious state (MCS). In this state the victim demonstrates

“…limited and intermittent capacity for conscious behavior. These patients occasionally demonstrate clear-cut signs of self- or environmental awareness… the diagnosis of MCS is based on the presence of specific behavioral manifestations of conscious awareness. These behaviors occur inconsistently, must be differentiated reliably from reflexive, random, and spontaneous behavior, and include functions such as simple command following, production of yes/no responses, intelligible verbalization, and contingent behavioral responses… (Hirsch, 2005).”

As with the vegetative state, the minimally conscious state may also persist for years. But, in contrast to the vegetative state, the victim may continue to demonstrate a slow overall improvement. Once again, changes are impossible to predict.

Notes

Hirsch, Joy (2005): Raising Consciousness, Journal of Clinical Investigation, 115:1102.

Owen, Adrian et al (2006): Detecting awareness in the vegetative state, Science 313 (5792), 1402.

Schiff, Nicholas et al (2007): Behavioural improvements with thalamic stimulation after severe traumatic brain injury, Nature 448, 600-603 (2 August 2007).

 

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