Sandra Steingard, MD, is a practicing psychiatrist who from time to time posts articles on Robert Whitaker’s Mad in America website.
Dr. Steingard apparently prescribes psychotropic drugs in her practice, but she is by no means a pill-for-every-problem practitioner, and her articles are always interesting and thought-provoking.
Dr. Steingard posted A Paradox Revealed – Again on Mad in America on July 7, 2013. In this article she mentions the recent study by Lex Wunderink et al, which found that people being treated for first episode psychosis were doing a great deal better functionally after seven years if their neuroleptic drugs had been discontinued or reduced relatively early in the process, as compared to individuals who were retained on the drugs for two years.
Dr. Steingard also mentioned a 1980’s study by Timothy Crow, MD, a British psychiatrist. In that study, those individuals who were randomly assigned to a placebo for follow-up were doing better functionally after two years than those assigned to maintenance neuroleptics.
Dr. Steingard mentions a third study. This was conducted in Australia by J.F. Gleeson et al, from 2003-2007. The object of this study was to assess the effectiveness of relapse prevention therapy [RPT] in improving adherence to neuroleptic drug treatment in first episode psychosis. Dr. Gleeson and his colleagues found that the RPT was effective in encouraging people to keep taking the pills. But at 30-month follow-up, they found that employment outcomes for this group were worse. In other words, all the encouragement to keep taking the pills was pushing people in a negative direction!
All of these results, in my view, pose serious challenges to conventional psychiatric practice, and it is my general perception that most psychiatrists deal with these kinds of results by ignoring them. The Timothy Crow study was published in the British Journal of Psychiatry in August 1990: 23 years ago!
Dr. Steingard, however, is obviously taking this material seriously, and is trying to reconcile the findings with her day-to-day work as a psychiatrist. She writes:
“First of all, there is a wide variability in outcome and response. I continue to believe that there are those who benefit from these drugs in both the short and long term. I am not able to accept the notion that neuroleptics are no different from other tranquilizers since they seem to yield a specificity of response – a decrease in voices, an increase in coherence – in someone who is appearing fully alert. But this is only for some and there are others for whom the response is not so great and there are those who recover without taking them. Unfortunately, we have no way of knowing who these people are.”
This paragraph raises enormous issues, and is, I believe, the heart of Dr. Steingard’s article. For these reasons, I thought it might warrant some comment.
“… a wide variability in outcome and response.”
I don’t think anyone would argue with that.
“I continue to believe that there are those who benefit from these drugs in both the short and long term.”
This is more complex. We know that neuroleptic drugs are neurotoxic and have devastating side effects, including reduced life expectancy and irreparable brain damage. It also seems likely that the damage begins with the first dose and continues as long as the drugs are ingested. These drugs were initially marketed as major tranquilizers, and the name changes (to “neuroleptics” and then to “anti-psychotics”) were more a matter of marketing than anything substantive. So any perceived benefit of these products is in the area of tranquilization. The PDR and psychiatrists often talk about weighing risks and benefits of these and other psychotropic products. But while this sounds good, it strikes me as an empty formula. How can one weigh the risk of tardive dyskinesia of unknown severity five years from now with some temporary tranquilizing now?
“I am not able to accept the notion that neuroleptics are no different from other tranquilizers since they seem to yield a specificity of response – a decrease in voices, an increase in coherence – in someone who is appearing fully alert.”
This statement is the fundamental justification for neuroleptic treatment, and is also the justification for changing the name to “anti-psychotic.” It is also, in my view, false. There have been at least two experiments in which professional mental health workers took these products and recorded their experiences. The first was by Belmaker and Wald, Haloperiodol in normals, British Journal of Psychiatry, 1977, 131:222-223. The authors each took a single 5mg dose of Haldol. They described the results as follows:
“‘The effect was marked and very similar in both of us: within ten minutes a marked slowing of thinking and movement developed, along with a profound inner restlessness. Neither subject could continue work, and each left work for over 36 hours. Each subject complained of paralysis of volition, a lack of physical and psychic energy. The subjects were unable to read, telephone or perform household tasks of their own will, but could perform these tasks if demanded to do so.'” (quoted from Richard Bentall, Madness Explained, p 500.)
The second study, which was conducted by Juan Artaloytia et al in 2006, was a double blind randomized trial of a single dose of placebo, haloperidol, and risperidone administered to 32 healthy volunteers in random order. Doses of haloperidol were 5mg, and of risperidone 2.5mg. Drowsiness was assessed by means of a self-reporting analog scale. The mean drowsiness for the three conditions were: placebo 4.01; haloperidol 9.02; risperidone 13.05.
The haloperidol vs. placebo difference was statistically significant at the 0.001 level; the risperidone vs. placebo at less than the 0.001 level. It is clear that there is a marked sedative effect with both neuroleptics. And this was with a single does. (There was a minimum washout period of 48 hours between administrations.)
In addition to which I should add that every client I’ve ever worked with who was under the influence of these products seemed sedated except those individuals who had been taking the drugs for an extended period. In these clients, the movement disorders tended to be the dominant presenting feature.
Nor has it been my experience that these drugs entirely suppressed the psychotic speech. It usually seemed to me that this was still present, but in a more subdued and less intrusive form, which is consistent with a generally tranquilizing effect.
I’m certain that Dr. Steingard has seen a great many more people under the influence of neuroleptic drugs than I have, and perhaps we’ll just have to agree to differ. But I find the notion that these drugs specifically target auditory hallucinations and incoherence a bit of a stretch.
I know that there has been some neurological research as to whether neuroleptics, after ingestion, are concentrated in certain areas of the brain. I have very little knowledge of neurophysiology, but the impression I get is that the question is still open. But even if there were local concentrations, that doesn’t really address the issue. The question is: do neuroleptics reduce the incidence/intensity of auditory hallucinations and incoherence but otherwise leave people fully alert? It would not be all that difficult to design and carry out a study to address this question, but to my knowledge, this has not been done.
In the passage quoted above, Dr. Steingard identifies auditory hallucinations and cognitive incoherence as two items that would attract psychiatric treatment. On the face of it this seems true – perhaps even obvious. But in my view it’s not quite the full picture.
What I mean is this. I can sit on my front porch experiencing auditory hallucinations of the most bizarre and florid variety, but I will never come to the attention of the mental health system unless someone becomes disturbed or worried about my behavior. Similarly with incoherence. In the privacy of my home, my speech can be disjointed and incomprehensible, but I will attract no psychiatric attention unless I start disturbing other people.
In my experience, the factor that attracts psychiatric attention is not “craziness” in itself, but rather agitation. Sitting in my rocking chair, benignly sharing bizarre and incoherent fantasies with my neighbors, will get me labeled as an eccentric old geezer. But if these verbalizations are accompanied by agitation, especially if it is severe, they will land me in a mental health office. And this is true even though the things I am saying in the latter scenario are essentially the same as in the former.
Obviously I have no knowledge of the clients who come to Dr. Steingard’s office, but in the clients I have seen and heard of over the years, who were being or had been treated with neuroleptics, the primary presenting feature was agitation, especially if the agitation had a pressured or aggressive or threatening quality.
Here’s what I think happens in practice. If a person is disturbing the peace, the police are called to the scene. The police implement a fairly simple algorithm:
agitated and “crazy”: mental health center
agitated but not “crazy”: jail
agitated and drunk: secure detox center
agitated and drugged (street drugs): secure detox center
Obviously in practice it’s more complex and more individualized than this, but I believe that the general outline here is accurate. What’s particularly noteworthy is that individuals who are “crazy” but are not agitated and not causing any kind of disturbance are absent from the picture. I realize that these people can attract psychiatric attention. They might, for instance, be brought to the mental health center or to a psychiatrist’s office by a concerned spouse. But for the most part, and certainly in the publicly-funded system, the presence of agitation and disturbance is usually the critical factor.
A great deal of police time is spent responding to and resolving disputes: domestic disputes, arguments in bars and other locations, conflicts between neighbors, etc… In my experience police officers generally are highly skilled in this kind of conflict resolution. They routinely separate the parties and try to engage them individually in dialogue, with a view to establishing why the parties are upset. If they find that a crime has already been committed, they often take formal action, and one of the contenders is taken to jail. But very often they manage to calm people down, identify the cause of the conflict, and elicit agreement to a ceasefire, with promises of more involved follow-up the next day.
When one of the parties is psychotic, however, they usually don’t even attempt reconciliation. The psychotic individual is put in a safe place (usually the back of the squad car) and taken to the mental health center.
Here again, there are endless variations on this theme, but the central point I’m making is that if an agitated person is behaving in a manner that is considered crazy, little or no attempt is made to find out why he’s agitated. This is because it is assumed that agitation is an intrinsic component of “craziness” and is not amenable to the kind of empathic, interactive resolution that is generally effective with “ordinary” people.
In my view this prejudice is a direct consequence of the standard psychiatric assumption: that psychotic behavior is an illness that resides in the individual. So, when “ordinary” people become agitated, it is assumed that something in their environment “set them off.” When a psychotic person becomes agitated – well that’s just the way they are – one of the “symptoms of the mental illness.”
Nor is this prejudice confined to the police. When the agitated individual gets to the mental health center, the intake worker’s primary task is to assign a “diagnosis” and initiate involuntary commitment proceedings. Here again, the agitation, which by this time is usually a good deal worse, is seen as a symptom. A neuroleptic injection is often administered, and the person is taken to the state hospital in secure transport.
At the hospital, little or no attempt is made to find out why he was agitated. The object of the exercise is to find out what “meds” work best for him and in what dosages. In other words, how much of what chemicals will keep him from getting agitated. When the hospital psychiatrist believes he’s got this about right, the person will be discharged to a community psychiatrist who continues the process. But, again in my experience, it’s rare that anyone looks back with a client and tries to figure out what happened and what might be learned from the incident. The agitation was a symptom of an illness and the illness is now – thanks to the “meds” – in remission.
During my career (I’m now retired), I worked with a good many people who had been through this kind of procedure. I always made a point of asking them about the precipitating incidents, and I tried to gain an understanding of why they had been agitated. Most people were usually able to give a coherent account of their agitation, and these accounts tended to be generally similar to the reasons “ordinary” people become agitated: feeling particularly tired; feeling under-appreciated or put upon; family tensions; etc… Intoxication was frequently mentioned, and sometimes heavy use of psychoactive substances for extended periods.
Agitation is a difficult term to define, but I think most people would see it as anger or incipient anger.
However – and this is the central point of this post – if an “ordinary” person attracts official attention because of anger, frustration, agitation, etc., he will likely be assigned to an anger management, social skills, or conflict resolution training program. But a psychotic person in the same situation is given neuroleptics, sometimes forcibly. The drugs do have a dampening effect on the outbursts, but little or no attempt is made to train the person in skills that might alleviate the sense of frustration, or help him to not become agitated in the future
When we read in the paper of an “ordinary” person becoming angry and getting into a scrape, we wonder what happened – what triggered the incident? But when we read of a mental health client in similar circumstances, there is a tendency to see the anger as an integral part of his “mental illness.” This differential perspective, which I suggest is widespread, is a direct consequence of psychiatry’s spurious medicalization of all behavioral/emotional problems, and is the dynamic underlying the increased stigma associated with “mental illness.”
I realize that this post has been largely an expression of my opinion, my perceptions. Maybe I’m mistaken. Maybe agitation isn’t the critical issue. It could be argued that I should wait until more research has been done before challenging the orthodoxy in this way.
On the other hand, neuroleptics, which used to be administered to a relatively circumscribed group of people, are fast becoming commonplace for the control of behavioral problems in children, elderly people in nursing homes, and people with developmental disabilities in group homes. They are also being prescribed widely to soldiers on return from active duty.
I’m not sure that we can afford the luxury of waiting until all the facts are known. We know that the drugs are damaging, and we know that there has been a marked increase in their use in the past two decades (from 6.2 million treatment visits in 1995 to 14.3 million treatment visits in 2008, and still climbing!) And we know that there are better ways to help people deal with feelings of agitation, anger, and frustration.
Dr. Steingard acknowledges that neuroleptics don’t help everybody. In others, she tells us, the response is “…not so great, and there are those who recover without taking them.” She then laments the fact that there is no way to distinguish these groups in advance. Dr. Steingard resolves this dilemma by maintaining an attitude of “…active shared decision making with the individual and her support system,” and by keeping to low doses. The problem with this approach, however, is that the drugs are still doing damage, and it seems unlikely, at least to me, that a client who was new to the system would have any idea as to how devastating the side effects of these products can be. In my experience, it is still widely believed by the general public that tardive dyskinesia and akathisia are symptoms of mental illness, rather than side effects of the drugs used to “treat” these “illnesses.” And even within professional circles, psychiatrists maintained for years that the brain shrinkage was caused by the schizophrenia!
Discussing risks with a client may create the impression that responsibility has been shared. But the sharing is inevitably unequal – the lion’s share must sit on the psychiatrist’s shoulders.
There’s also another problem. For the past five decades, pharma-psychiatry has been promoting the notion that virtually every behavioral/emotional problem is an illness, and that the primary “treatment” for these “illnesses” is drugs. This philosophy has been widely accepted by the medical and legal communities, by the media, by the government, and by the general public. A psychiatrist who decides not to prescribe neuroleptics to someone who has been assigned a “diagnosis” of “schizophrenia” is opening him/herself to liability in the same way that a medical doctor will be liable if he doesn’t administer an antibiotic to someone with pneumonia. The neuroleptics have become the “standard of care,” and although the whole concept is spurious, it is still the norm, and it is the standard by which a psychiatrist will be judged in a law suit.
Don’t misunderstand me. I’m not arguing for psychiatry. It was psychiatrists who created these spurious diagnoses and these destructive standards of care in the first place and, apart from very few exceptions, such as Dr. Steingard, are showing no signs of letting up, or even questioning these standards. Indeed, with DSM-5, the process is accelerated.
My point is that we need to keep drawing attention, vigorously and widely, to the fact that psychiatry is flawed and destructive, and that “antipsychotics” are neurotoxic drugs with devastating side effects.