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Biology 202
2001 Second Web Report
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BINSWANGER'S DISEASE

S.L.

Even though I knew my grandmother for 17 years before she died my mother told me that I had never met her. According to her my grandmother had not been "herself" for years because the affects of her advanced age had basically destroyed the person she once was and turner her into a living zombie. Although humans live an average of 85 years, things such as memory loss and lack of motor control can completely change a person and in a way kill her years before she dies. Vascular Dementia has the same general symptoms as "old age" only it typically occurs in younger people. Binswanger's Disease is a specific type of vascular dementia, probably the most common form, which affects people at approximately age 60. Most people diagnosed with this disease do not live past five years of its onset(1). Currently, not much is known about Binswanger's Disease; in many ways it resembles various other neurological disorders making it difficult to diagnose. The trademark of this disease is damage to the blood vessels in the deep white matter of the brain(1),(4),(5). The pons, basal ganglia, and thalamus are typical sites for these lesions(5),(7). A Magnetic Resonance Imaging scan is one of the most reliable ways to see this damage(5),(6). However, with outward symptoms such as depression, strokes, and disease of heart valves(1),(2),(3),(5) an MRI is not typically one of the first diagnostic tool used and the disease proceeds unchecked.

My original thought surrounding Binswanger's Disease related to my mother's opinion of my grandmother; the people with the disease became different people due to the changes in their brains. In other words, one of the physical changes that takes place in the brain must somehow affect the victim's I-function effectually transforming him or her into a different individual. From the point of view that brain equals behavior and there is nothing else this analysis made logical sense. However, it seemed like a very simplistic summary of the disease's effects, and after deeper investigation into the course of the disease I realized that the answer would not be so easy. One of the facts I uncovered is that occasionally victims will partially recover and stabilize for a period of time, thus reverting to their pre-Binswanger's Disease selves(1),(5). So the I-function cannot, most probably, be destroyed in these instances since the victims return to their original behavior, even though their brains have undergone alterations. Therefore something more complicated must take place in the brain of a victim with this disease.

First, I would like to explain some of the physical changes that occur in the brain of a person with vascular dementia of the Binswanger's type and the various symptoms that stem from these changes. This will give evidence to the statement that the changes to the brain do in fact result in changes in the behavior to the extent of changing the person. The smooth muscle cells of small arteries within the brain degenerate as extracellular matrix builds up on the walls, creating structural rigidity and restricting blood flow(7). There is a diffuse and patchy loss of the myelin in the white matter and an increase in fibrinogen levels(5),(7). One of the current theories for why these changes occur is a change in the vascular permeability within the brain. The most common symptom recognized I patients is memory loss, similar to Alzheimer's Disease(5). However, other common symptoms are difficulties with decision making and cognition, mood changes, especially depression, loss of coordination, hemiparalysis, and Parkinsonian-like tremors(1),(2),(3),(5). Since there is presently no cure for Binswanger's Disease treatment is symptomatic, the most effective treatments being antihypertensive medication and aspirin prophylaxis(3),(4),(5). The reasons for the effects of the aspirin treatment are not currently know, but it seems to at least slow the progression of the illness. If understood as a list of causes and effect all of the preceding facts show that by changing the brain of a Binswanger victim the behavior of that person is changed, and by stopping the alterations to the brain, as with aspirin, the behavior remains as it was.

The onset of this disease is often sudden and the progression is swift, yet since temporary recover of behavior is possible it seems as if the I-function is suppressed or overridden rather than destroyed, at least in the instances of patients who demonstrate this form of partial recovery. When a patient chooses to try a form of treatment, I theorize that the patient, i.e.-the patient's I-function or the conscious, decisions making part of that patient, is choosing to fight the disease. This is probably no only in an attempt to live longer, since death within five years is practically guaranteed, but also to prevent a loss of I-function capabilities. So in a way it is a battle between two parts of the brain; the I-function and the deep white matter.

In one case study of Binswanger's Disease that I came across a 57 year old man who had been social, a competent and diligent worker, and involved in many different activities completely transformed. His wife described his behavior as being essentially opposite of what it had been. The man's employer said that he: "had undergone an abrupt personality change. His personality had changed from jovial with a good sense of humor to docile, introverted and unwilling to confront typical work situations. His work performance deteriorated. He slept during important meetings and was frequently found wandering among buildings(5)." While the man in this case study seems to have changed into a different individual I argue that his I-function was still intact, and in fact he was using part of it. If the smooth muscle cells in the small arteries of his brain could be restored and the deposits of extracellular matrix removed then his aimless wandering would probably stop and he would return to telling jokes and socializing.

While few in depth analysis of Binswanger's Disease have been performed the data that exists seems to show that it prevents the I-function from carrying out its typical duties. Current research on living patients focuses on the benefits of aspirin treatment which have recently been discovered, but unfortunately some of the most illuminating data has been collected from autopsies by which point it is most likely too late to help the patient. Regrettably, one of the greatest risk factors for this disease after advanced age is low income. Without the proper money to supply an adequate diet and medical care it is near impossible to help a patient. If money were not a factor then performing MRI's on people with symptoms of vascular dementia could help to determine if the patient actually has vascular dementia rather than another similar neurological disorder and what form of dementia the patient has so that a treatment plan can be established. If progression of Binswanger's Disease can be halted or slowed with treatments such as aspirin prophylaxis then there is that much more time that the patient can properly function and retain his or her personality. Until more studies can be done however all this is speculation and Binswanger's Disease is still a sentence of life-imprisonment to the I-function and eventual death to the body.

WWW Sources

1) Binswanger's Disease information page , on the National Institute of Neurological Disorders and Stroke web site

2) Binswanger's Disease information page, on the National Organization for Rare Disorders, Inc web site

3) Binswanger's Disease information page, on the Jewish Hospital HealthCare Services web site

4) posting about Binswanger's Disease by a neurologist, Massachusetts General Hospital web site through Harvard University

5) "Senile Dementia of the Binswanger's Type" , American Academy of Family Physicians web site

6) "New Insight Into Binswanger's Disease" , American Medical Association article

7) "Vascular Dementia: the role of changes in the vessels" , journal article from the National Cardiovascular Center, Osaka, Japan




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