Fifty dangerous years

Another 50-something year-old passes away; another "unknown" cause of death; and another awaited autopsy.

Also, another opportunity to delve further into neurology.


E. (Everette) Lynn Harris was a prolific author, who introduced the uninitiated to the "down low," starting with his book, Invisible Life. Prior to hitting the scene as one of the most influential black (and later) openly gay author, he worked at IBM, Hewlett-Packard and AT&T.

At the University of Arkansas he became the first black editor of the school newspaper and the first black male Razorbacks cheerleader. Just as he gave courage to his readers to not keep everything on the "down low," he gained courage from them and came out of the closet. He gave many black (and other races) gay men who were living their public lives as married heterosexuals while having sex with other men, the courage to be more open about their sexuality.


So, how does this all tie into neurology?

He was only 54 years-old and died fairly suddenly. His publicist, Laura Gilmore, has been quoted as saying that he fell ill on a train to Los Angeles a few days ago and blacked out for a few minutes, but seemed fine after that.

In neurology (as in much of medicine, hopefully), we start with an extensive history. Unfortunately here, all we know is that we have (we presume) a previously healthy 54 year-old man who develops a sub-acute illness with a brief loss of consciousness. We know that this occurred on a train ride and this may or may not be an important detail (or it may be a red herring).

Unfortunately, we do not know his past medical history (besides diabetes) or family history. His social history may be significant for him being a homosexual, but he was a strong and vocal anti-HIV/AIDS advocate (we cannot exclude this as a possibility, though).

We would then move on to a physical examination, which obviously cannot be performed with this “patient” (after all, isn’t an examination done with the patient and not on or to the patient?).

We have no laboratory or imaging studies to review, which means we have to rely on the history of the present illness alone.

How apt for a writer.


“Feeling ill” is a very nonspecific phrase and could be interpreted as an antecedent symptom to the ‘blacking out” or it could be a further description of the “blacking out” – note the word “and.” Does “and” mean that there are two separate symptoms or does it the illness simply an alternate description of the blacking out? Furthermore, if they are two separate symptoms, then which one occurred first: feeling ill or blacking out? Could we use the backing out as the physical exam of a patient who has a symptom of feeling ill?

Some may argue that there was no one there to examine Mr. Harris, so how could we refer to an examination. We do know that in many lifetime diagnoses (remember, not chronic diseases – language may be stigmatizing), the patient’s exam may be more reliable than the physician’s exam (what is more important, the reflex hammer or the description of further weakness – actually, both are important).

Returning to the “case” at hand (last time I checked, cases were left to bellhops or lawyers), let’s first address the “blacking out.”

Where does a loss of consciousness localize to?

1. Neurologic
2. Non-neurologic


a. Syncope (fainting) may be neurologic or it may cardiologic. A transient decrease in blood flow to the brain, may lead to a brief loss of consciousness. Usually this should last for less than “a few minutes,” but observers are notoriously bad at estimating the length of an event, such as loss of consciousness or seizures, for example. Vasovagal syncope is the most common form in adults, but he seems not to have had any accompanying autonomic features. He may have had a cardiac arrhythmia (abnormal heart rhythm) leading to his brief loss of consciousness and later to death.

b. Seizure. As far as we are aware, he had no history of epilepsy, in which case this is the first seizure. 6% of the U.S. population will have a nonfebrile seizure sometime during their life. There is a cumulative risk in developing epilepsy (more than one seizure): By 20 years of age, 1% of the population has epilepsy and by 75 years of age, 3% of the population has been diagnosed with epilepsy, and 10% will have experienced some type of seizure. Seizures are more common in blacks than in whites. Seizures themselves have a differential diagnosis, including different types of seizures, drug intoxication and psychogenic nonepileptic pseudoseizures. He “seemed fine” after the event, so there was presumably no postictal state. Most seizures last well below two minutes, but as we noted above observers (even medically trained ones) often overestimate the amount of time a person is “out.” People with seizures may also cause SUDEP (Sudden Unexplained Death in Epilepsy), which is the sudden, unexpected death of someone with epilepsy, but who was otherwise healthy, and for whom no other cause of death can be found. SUDEP accounts for 10% of all epilepsy-related deaths; 85% of these fatalities occur between the ages of 20-50 years. The incidence of SUDEP is approximately 1 in 1000 people with epilepsy per year which is at least 10 times of the sudden death rate found in the general population. How should neurologists discuss the risk for SUDEP with their epilepsy patients? Should it be discussed with everyone or those you are trying to scare into be more compliant with the treatment regimen or should it be “don’t ask, don’t tell?”

c. Central nervous system (CNS) infection (meningitis or encephalitis) - - he “seemed fine” after the event (and presumably before), which makes an infectious cause less likely, but it may explain his fairly rapid death.

d. Hypoglycemia (low blood sugar) could cause a loss of consciousness, but without receiving any sugar after it happened, it would seem less likely that he would seem “fine after that” (he did, however, have diabetes mellitus). The same would be true for dehydration.

e. Narcolepsy (from the Greek for “seized by somnolence”) could cause him to suddenly fall into REM (rapid eye movement) sleep. It has an incidence of 0.02% to 0.18% (similar to multiple sclerosis and like MS, it may take 10 years from first symptom to finally being diagnosed). Also like MS, narcolepsy seems to involve the T cells and is associated with HLA-DQB1*0602.

f. Intoxication would seem less likely because he “seemed fine after that.”

g. Stroke (especially vertebrobasilar insufficiency -- temporary lack of blood flow in the arteries in the back of the head) would not allow him to “seem fine” after the event. He was, however, on a train ride, which can lead to dehydration and blood clots. A deep venous thrombosis (blood clot in the vein) could be dislodged from the leg and return via the venous system to the heart. 20% of the population have a patent foramen ovale (opening between the right and left side of the heart, which usually closes around the time of birth), and then this clot could shoot up into the carotid or vertebral arteries and obstruct blood flow to the brain or the clot could travel to the blood vessels in the brain itself). A venous blood clot could also form in the superior sagittal sinus (a big vein that drains blood from the arteries feeding the brain, and then returns the blood to the right side of the heart). This cerebral sinus thrombosis could lead to venous strokes, which have a tendency to bleed.



So, what did E. Lynn Harris die from?




We’ll have to wait and see.



- Dr. Daniel Kantor, MD BSE
Medical Director
Neurologique


info@neurologique.org
www.neurologique.org