Wednesday, November 3, 2010
Supersensitivity Psychosis: Is There Such a Thing, and If There Is Then Why the Hell Haven't We Heard About It Before?
In his book, "Anatomy of an Epidemic," Robert Whitaker easily debunked the chemical imbalance myth (see earlier blog piece), which rested on nothing more than some observations in search of an explanation.
The observation: "Certain drugs reduce psychiatric symptoms."
The explanation: "It must be because they correct a chemical imbalance."
The reality: "The brain is not chemical soup."
Whitaker then went on to cite with approval a different set of observations in search of an explanation called "supersensitivity psychosis." Supersensitivity psychosis is central to the whole point of Whitaker's book, which posits that our meds may actually worsen rather than improve the natural course of our illness.
This goes much further than stating that well-known side effects tend to make us feel worse rather than better. Suppose, instead, Whitaker asks, our meds actually amplify the very symptoms they are supposed to remedy? We know, for instance, that indiscriminate use of antidepressants can turn depressives into bipolars and classic bipolars into rapid-cycling bipolars.
What about antipsychotics? Are they really as "anti" as psychiatry makes them out to be, or is there a bit of "pro" to their effect? After all, if these meds truly worked the way Pharma would have us believe, there would be a lot less incidence of mental illness, with a lot less severity, rather than a lot more. Consider this the observation. The explanation may have something to do with many of us being hypersensitive to our meds. But does reality bear this out?
The story begins with the investigations of Guy Chouinard and Barry Jones of McGill University back in the late seventies. We know that antipsychotics knock out psychosis by blocking post-synaptic dopamine D2 receptors. But the brain compensates by, amongst other things, increasing the receptor binding sites on these very same neurons. This has been shown in postmortem brain samples of rats, and more recently in brain scans of humans.
If the antipsychotic (or neuroleptic) is suddenly withdrawn, the brain takes time to readjust, during which all manner of bad things may happen. Down in the nigrostriatal dopamine pathway, neurons are firing too rapidly to maintain full motor control, resulting in facial tics, agitation, and other disturbances. Or, should the patient stay on the med, the morphed neurons may reach a point of no-return. These disturbances may in time manifest as tardive dyskinesia, which is permanent.
So far, so good. But what if, Chouinard and Jones asked, something similar went on in the very dopamine pathway - the mesolimbic pathway - that antipsychotics are supposed to restore to normal? If you suddenly withdrew the antipsychotic, could "rebound" psychosis occur? And could a permanently altered brain turn good prognosis patients into chronic bad prognosis ones? As the authors explained in a 1980 article:
According to this hypothesis, the cessation of maintenance neuroleptic medication induces a relative increase in the mesolimbic dopamine function, leading to psychotic relapse or deterioration in the same manner as tardive dyskinesia can emerge or worsen when medication is stopped or decreased.
In a 1990 paper, Chouinard estimated the likelihood of 43 percent of patients on neuroleptics being affected in this manner. In one of his case studies, he cited "Mrs B," who had five relapses of acute psychosis over the first 22 years of her illness vs six in the last 10, and was no longer responding to increased doses.
"What was psychiatry supposed to do with this information?" asks Whitaker in his book. "It clearly imperiled the field's very foundation." Whitaker then relates how the dean of receptorology, Solomon Snyder of Johns Hopkins, came to psychiatry's rescue by assuring readers in a 1986 book that talk of supersensitivity psychosis was premature. Soon after, the hypothesis was consigned to the "interesting" file and the field breathed a sigh of relief.
Today, Whitaker observes, "the notion that antipsychotics increase the likelihood that a person diagnosed with schizophrenia will become chronically ill seems, on the face of it, absurd." Ask anyone - the top experts, the man on the street - and they "will attest that antipsychotics are essential for treating schizophrenia."
So is psychiatry to be damned for turning its back on us, or is Whitaker reaching too far in his quest for an explanation? Or are there simply a lot more nuances to the issue than he suggests?
Next: We look at the nuances ...
Previous blog pieces:
Tuning Out the Distractions
Thanks to Stupid Advocacy, Your Life is Worth Just One Penny
The Study Psychiatry Wishes Would Just Go Away - Part II
The Study Psychiatry Wishes Would Just Go Away
Is the Cure Worse Than The Illness?
The Whitaker Controversy: An Irony in Search of Nuance
If Meds Work as Well as Our Psychiatrists Tell Us, Why Do We Have MORE Mental Illness Today Rather Than Less?
RIP: Chemical Imbalance in the Brain