Multiple sclerosis, or M.S., is a devastating, chronic, debilitating illness, that has defied until recently most treatment approaches. It hits the young adult in the prime of life typically, more young women than men. It is like ALS though much slower, and not quite as destructive neurologically as ALS but well bad enough. Only in the last two decades or so, have treatments started to be even minimally effective. I have followed M.S. patients in my decades of psychiatric practice since I started in the neurosciences, brain science as a collegian, then aspired to go into neurosurgery before I decided on psychiatry as a medical student. I have long enjoyed practicing medical centers and general hospitals on the “psychiatry consult liaison services,” almost specializing in seeing neurology patients and M.S. patients most of all.
M.S. is like many other chronic illnesses. For decades we had only paltry symptomatic treatments. That is to say, our treatment only treated symptoms, or brought episodes to a close and did not treat the etiological, causative basis of M.S. When one had a flare of M.S. with “shorting out,” loss of a sense, use of a limb, sight, balance, etc., then one was given intravenous treatments with whatever immunosuppressant was in vogue at the time. These over the last 40 years or more have included ACTH, prednisone, methotrexate, bee venom (which like many other briefly popular treatments, did NOT work) and other agents de jure.
Then the advent of more scientifically based, more specific anti-immune system based medications came out in the 1990’s, the family of the interferons. These were much better for many M.S. patients at stopping an episode in its tracks than the previous agents. But they had like so many modern medicines in all branches of medical practice, enormous side and adverse effects. Betaseron based medicines tended to be given by injection shallowly into the subcutaneous tissues every other day and would cause in the vast majority of persons, a day of in-the-bed-flu like syndrome. “Flu without the flu” as many called it. And on an every other day schedule, you got the shot, had the flu and then the next day when the flu like aches and low grade fever and fatigue passed, you got your next shot and braced yourself for starting to feel bad physically that evening…it was awful and many many patients tolerated this for years and then en masse stopped the interferon based therapies. A newer, slightly different family of agents came out nearly a decade ago but were no better.
One medicine was the first to show signs of reversing the loss of insulation, the myelin sheath protein covering of the nerve wires, the axons, that were like the insulation of all electrical wires. This is itself the basic damage that is done by M.S. in patients that causes the losses in M.S., i.e., “shorting out.” However, this medicine had the horrific emergence of an adverse side effect that became clearer after its release, of causing a “Jacob-Creutzfeldt” like dementia that was rapid and fatal. The drug was pulled for a few years from the market so frightening was this by product of its use. The cure in effect was worse than the disease for which it was used to treat. It was later returned to market after the fairly low incidence rate of the dementing process was delineated. But its use was highly restricted with extremely close monitoring of all patients on it. Needless to say, it was so daunting a risk, that it was remained largely not utilized except by the truly desperate. My wife and I for instance, never considered its use for her.
Schizophrenia can be compared, loosely, to M.S. It is a chronic and often debilitating illness that has cumulative, worsening effects on the person as they age with it. Its causes are still not well understood. Our treatments still are pathetically incompletely effective on the illness itself, often not effecting its course all that much in a substantial percentage of patients. It carries with it, like M.S., a growing adverse burden on the individual but also on society. Most persons with M.S. become unable to work and support themselves. Consequently many of them end up dependent on their families and society, the government for their income/support. Schizophrenia is present in a known, largely constant, predictable portion of the population that is not insignificant, up to 1% or so of every society’s total population, a huge number, greater than M.S. even.
Our medicines starting with the first anti-psychotic, Thorazine, or chlorpromazine, through the several ‘zines, or phenothiazines, were entirely and only good for treating or suppressing or lessening, a portion of the symptoms of schizophrenia. The anti psychotics did not treat the basis of schizophrenia itself in perhaps anyone. The illness continued under the surface even in the best and most responsive of patients. Up to a third or half, this is not yet clear, of patients with schizophrenia, had progression other symptoms and would develop deficits in personal elements of their personalities, such as emotional responsiveness and expressivity, truncation of verbal abilities, increasing loss of initiative, passivity and severe self imposed isolation socially to a hermit like reclusive approach to life. Indeed many of the famous “hermits” of modern times, were likely chronic schizophrenics, so called recluses.
Now we are in the era of the “second generation,” or “atypical” anti psychotics. When the first two came out in the early 1990’s, Clozaril (clozapine) and Zyprexa (olanzepine), they were hailed and widely regarded as genuine breakthroughs. And they were, but only in part. They were known to seemingly be more effective than the previous phenothiazines. They worked in some previously unresponsive patients with schizophrenia. Indeed clozapine was regarded as the drug for the large percentage (?30 to 50%?) of schizophrenic patients who did not respond to anything, the truly “treatment resistant.” They seemed not to cause the dreaded movement disorder of “tardive dyskinesia.” And in keeping with the price gouging ethos of the modern pharmaceutical industry, they were incredibly highly priced, many times the price ranges of their predecessors.
But as time wore on, and our experience with these medications enlarged, we came to realize, the bloom was off the anti-psychotic rose. These medications had a different set of tough and health destructive side effects, largely in the endocrine realm. Most if not all of them, more or less, cause increase in glucose levels, weight gain and appetite. This leads in many persons taking them, obesity and consequently, medically facilitated diabetes, as if we did not have enough of that public health epidemic already. They were not sedating or motorically slowing and because the absence of such well known side effects in their predessors, came to be more widely utlized and came to be the standard of care nonetheless.
And they may help with the “negative” symptoms of schizophrenia, the above mentioned, apathy, passivity, decline in initiative, social withdrawal issues. So there is some progress but it is very incremental as illustrated by my introductory discussion of M.S.
More of the now recognized many possible causes of schizophrenia are starting to emerge in M.S. and schizophrenia. M.S. may as it turns out be simpler than schizophrenia. Its causes seem to be more inter-related than schizophrenia which may have hundreds of causes in its dozens of forms. They range from intra-uterine insults to the fetus, advanced age of the father, the mother having flu during gestation, to environmental toxins never on Earth before, to inborn random genetic mutations or genetic heritage in families with inter-generational incidence of schizophrenia in the family tree.
In summary, if this clinician were to hazard a guess, our grasp and ability to treat M.S. is likely to be more advanced in the coming lifetimes of those younger today, than the similar fronts concerning the psychiatric brain illness of the schizophrenias.