Antipsychotics Are For Psychosis, Not Insomnia

For quite some time, psychiatrists have known that in many cases of severe chronic schizophrenia, over the long term there was dramatic evidence of marked shrinking of brain tissue and enlarged cerebral ventricles (fluid-filled hollow parts at the center of the brain) - cerebral atrophy.  I had been taught that this phenomenon was first discovered in patients who had never been treated with antipsychotic medication. 

When I mentioned that in an argument on an anti-psychiatry blog, however, I was immediately challenged on whether the subjects studied had really not been treated. 

When I did a literature search, I was surprised to find out that what I had been taught was wrong, and that the other folks were right.  As far as I could find on the search, the subjects whose brains were scanned had almost all taken antipsychotic medication at some point during their lives.   (Hey guys, I can admit when I was wrong!  Can you?)

The black areas on the scan are empty of brain cells

Of course, that still begs the question, what caused the atrophy?  Was it the disease, the drugs used to treat it, or a combination of both?  Of course, even if it was entirely due to the drugs, one would still have to weigh the risks of cerebral atrophy versus the risk of being chronically tortured by accusatory hallucinations and living out on the street, as was well-portrayed in the movie The Soloist. 

Go check out Skid Row in L.A. in person if you don't believe it.  That part of town is actually marked with a sign that says, "Skid Row."  See the folks on street corners loudly preaching incoherent gibberish about the Gospels for hours to an audience one at all.

Unfortunately, due to pharmaceutical marketing techniques and to psychiatrists who cannot tell sedation from other therapeutic effects, atypical antipsychotics are being used for a lot of other things besides psychosis.  Seroquel is being used commonly as a sleeping medication!  Because of TV commercials, most people think Abilify is an antidepressant. 

Now, we've known for decades that in some patients with real and severe melancholic clinical depression antipsychotics can indeed augment an antidepressant in treatment-resistant cases.  But so does lithium, which is both way more effective and a hell of a lot safer than antipsychotics. 

Now, in this month's Archives of General Psychiatry comes a study that adds more information to address the initial question about cerebral atrophy ("Long-term Antipsychotic Treatment and Brain Volumes: A Longitudinal Study of First-Episode Schizophrenia," Beng-Choon Ho, MRCPsych; Nancy C. Andreasen, MD, PhD; Steven Ziebell, BS; Ronald Pierson, MS; Vincent Magnotta, PhD, Arch Gen Psychiatry 2011;68(2):a128-137). The authors followed first-break patients with schizophrenia for many years who were all treated with antipsychotics and took serial MRI tests to continuously measure brain volume. 

On average, each patient had 3 scans (≥2 and as many as5) over 7.2 years (up to 14 years). Unfortunately, there was no control group of patients with schizophrenia who were not treated with antipsychotics, because it is considered unethical to withhold treatment.

They instead controlled mathematically for severity of the underlying disorder under the theory that more severe cases were likely to have been given more antipsychotic medication, thereby clouding the picture of whether it was the disease or the treatment causing the atrophy.

The results: more antipsychotic treatment was associated with smaller gray matter (one type of brain tissue) volumes when disease severity was adjusted for.  Progressive decrement in white matter (the othert type of brain tissue) volume was also most evident among patients who received more antipsychotic treatment. Illness severity had relatively modest correlations with tissue volume reduction, and alcohol/illicit drug misuse had no significant associations when effects of the other variables were adjusted.

The conclusion: it appears that both the disease itself and the medication appeared to both contribute to cerebral atrophy.  Of course, without the control group, this can not be a definitive conclusion.  Also, we do not know if the drugs would do anything like this on patients who do not have schizophrenia but some other psychiatric disorder, or no disorder at all.

Nonetheless, these results should certainly give pause to any doctor treating a non-psychotic patient with anti-psychotic medication - especially since much safer alternative drugs are available.  This potential risk is on top of the serious risks that these medications may cause diabetes, high cholesterol, and a chronic untreatable neurological condition called tardive dyskinesia.  As all these risks are cumulative, long term treatment of non-psychotic individuals with anti-psychotics before all other measures are tried is particularly reprehensible.


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