I recently started working part-time on an inpatient psychiatric unit at a large county medical center. The last time I worked in inpatient psychiatry was six years ago, and in the meantime I’ve worked in various office settings—community mental health, private practice, residential drug/alcohol treatment, and research. I’m glad I’m back, but it’s really making me rethink my ideas about mental illness.
An inpatient psychiatry unit is not just a locked version of an outpatient clinic. The key difference—which would be apparent to any observer—is the intensity of patients’ suffering. Of course, this should have been obvious to me, having treated patients like these before. But I’ll admit, I wasn’t prepared for the abrupt transition. Indeed, the experience has reminded me how severe mental illness can be, and has proven to be a “wake-up” call at this point in my career, before I get the conceited (yet naïve) belief that “I’ve seen it all.”
Patients are hospitalized when they simply cannot take care of themselves—or may be a danger to themselves or others—as a result of their psychiatric symptoms. These individuals are in severe emotional or psychological distress, have immense difficulty grasping reality, or are at imminent risk of self-harm, or worse. In contrast to the clinic, the illnesses I see on the inpatient unit are more incapacitating, more palpable, and—for lack of a better word—more “medical.”
Perhaps this is because they also seem to respond better to our interventions. Medications are never 100% effective, but they can have a profound impact on quelling the most distressing and debilitating symptoms of the psychiatric inpatient. In the outpatient setting, medications—and even psychotherapy—are confounded by so many other factors in the typical patient’s life. When I’m seeing a patient every month, for instance—or even every week—I often wonder whether my effort is doing any good. When a patient assures me it is, I think it’s because I try to be a nice, friendly guy. Not because I feel like I’m practicing any medicine. (By the way, that’s not humility, I see it as healthy skepticism.)
Does this mean that the patient who sees her psychiatrist every four weeks and who has never been hospitalized is not suffering? Or that we should just do away with psychiatric outpatient care because these patients don’t have “diseases”? Of course not. Discharged patients need outpatient follow-up, and sometimes outpatient care is vital to prevent hospitalization in the first place. Moreover, people do suffer and do benefit from coming to see doctors like me in the outpatient setting.
But I think it’s important to look at the differences between who gets hospitalized and who does not, as this may inform our thinking about the nature of mental illness and help us to deliver treatment accordingly. At the risk of oversimplifying things (and of offending many in my profession—and maybe even some patients), perhaps the more severe cases are the true psychiatric “diseases” with clear neurochemical or anatomic foundations, and which will respond robustly to the right pharmacological or neurosurgical cure (once we find it), while the outpatient cases are not “diseases” at all, but simply maladaptive strategies to cope with what is (unfortunately) a chaotic, unfair, and challenging world.
Some will argue that these two things are one and the same. Some will argue that one may lead to the other. In part, the distinction hinges upon what we call a “disease.” At any rate, it’s an interesting nosological dilemma. But in the meantime, we should be careful not to rush to the conclusion that the conditions we see in acutely incapacitated and severely disturbed hospital patients are the same as those we see in our office practices, just “more extreme versions.” In fact, they may be entirely different entities altogether, and may respond to entirely different interventions (i.e., not just higher doses of the same drug).
The trick is where to draw the distinction between the “true” disease and its “outpatient-only” counterpart. Perhaps this is where biomarkers like genotypes or blood tests might prove useful. In my opinion, this would be a fruitful area of research, as it would help us better understand the biology of disease, design more suitable treatments (pharmacological or otherwise), and dedicate treatment resources more fairly. It would also lead us to provide more humane and thoughtful care to people on both sides of the double-locked doors—something we seem to do less and less of these days.
Thought Broadcast 
As usual, a nice article. But I wouldn’t confuse setting of treatment with severity of illness. First off, there a lot of malingerers in need of money and housing who make it to an inpatient unit. Are they suffering? Yes. But do they hear voices constantly? No. They are sitting over at a table playing cards. And the voices disappear once the SSI check comes. And there is A LOT of Axis II pathology on inpatient units — girl gets dumped by boy,or boy gets dumped by girl, starts cutting and drinking, and lo and behold takes an impulsive overdose, etc.
I do think another psychiatrist/blogger (1boringoldman) has similar thoughts, especially with respect to depression and as I interpret his posts, feels that the DSM IV messed up by lumping all depressions together as MDD. Some depressions have definite “precipitants” (i.e. loss of loved one) while others appear more “organic”, more “biologic”, more “congenital”. And to think that a medication is going to bring back a loved one seems just silly to me…especially when medications (such as SSRIs) have complicated side effects and many people seem to have difficulty stopping them once they start (indicating addictiveness?). So my “beef” with the research is that we’ve been so consumed by the pharmocological approach that we’ve failed to do the research that might have lead us by now to a way to help those suffering from true “disease”. And we’ve gone nuts (IMHO) with the meds; couldn’t believe our family doc wanted to put my teen daughter on an SSRI for PMS. Really??
In the absence of biomarkers, or ANY objective marker for that matter, there is no way to differentiate normal from abnormal, let alone severe mental illness from not-so-severe mental illness.
Before we can make statements as to the differences between inpatients and outpatients, we need objective, measurable, robust, and reproducible diagnostic criteria. Now, we got zilch.
Yeah – Mental Illness is totally fake, just like Fibromyalgia and all those other “subjective” diseases with no biomarkers.
If you are defining disease by presently discovered bio-markers, that’s a pretty narrow view of illness and suffering.
Pathology can cause suffering. Sometimes it doesn’t. But the converse is also true. You can have suffering without pathology. Fibromyalgia is a terrific example. Irritable bowel syndrome is another. PANDAS is probably my favorite. Sure people suffer from the entities that we have given names to. But to call them ‘diseases’ is to commit a category error.
To reiterate, in the absence of objective, measurable, robust, and reproducible diagnostic criteria, there is no way to tell a healthy person from a sick person All we have to go on are inferences we draw from statements the sufferer makes (NB a schizophrenic often denies being ill).
It is anti-scientific to assert pathology when you’ve produced none, and foolish to treat it when you have no idea what you’re treating.
Thanks for the comments. I agree, Tom that “treatment setting” should not be the arbiter of which category the disorder falls into. Especially when, yes, you have malingerers in the hospital (see here, for example) and gravely disabled individuals wandering the streets. But it’s where the distinction has been most obvious to me.
Maybe we should pay more attention to the notions of “endogenous” vs. “exogenous,” or “functional” vs. “organic,” because I truly believe (along with 1boringoldman) that there are multiple forms of what we call depression, bipolar, schizophrenia, etc. (As a side note, this is what makes clinical trials essentially meaningless, and the DSM an irrelevant homogenizer. Although it does allow me to get paid.)
One point of concern, though: if we do happen to find a “biomarker,” or specific brain lesion, or “chemical imbalance” to justify a “real” diagnosis, what will we say to patients who don’t have those findings? Psychiatry is not prepared for that. We’ll probably create new biological theories to explain the others, and continue the cycle all over again.
“if we do happen to find a “biomarker,” or specific brain lesion, or “chemical imbalance” to justify a “real” diagnosis, what will we say to patients who don’t have those findings?”
If we will tell “biomarker-negative” people that they nevertheless have the illness they think they have, we might as well abandon the effort to find biomarkers.
“One point of concern, though: if we do happen to find a “biomarker,” or specific brain lesion, or “chemical imbalance” to justify a “real” diagnosis, what will we say to patients who don’t have those findings?”
For patients who “don’t have those findings”, I would tell them that so much is still unknown — as the medical/psychiatric connection in my next paragraph was until fairly recently — and that, for the time being, the goal is to alleviate symptoms. The “real” diagnosis may have to wait for the science to catch up, but in the meantime life has to be lived.
A young (early 20s) friend of ours had a spinal tap and other tests done recently to investigate his sudden, partial loss of vision. Brain lesions were found and attributed to his celiac disease (which had been diagnosed years ago and a strict gluten-free diet followed since then). WTF, I thought, celiac disease can do that? Then I learned that, yes it can, and can also lead to other psychiatric/brain problems .
Now I’m wondering if inpatient psychiatric patients are ever tested for immune disorders?
Jackie, my question about “what do we say to patients…” was a rhetorical one. The tendency, as you illustrate in your comment, is to say something along the lines of “there’s a biological basis but we just don’t know what it is yet.”
Maybe in some cases, there isn’t a biological basis. Maybe the basis of the disorder (and the cure) is psychological or behavioral or spiritual; maybe it’s a direct consequence of someone’s difficult environment (Does losing a job make someone depressed? You betcha!). And as much as I hate to say it because it seems to be anathema, maybe some people just aren’t doing enough (or are too lazy or careless?) to overcome their “depression” or “anxiety” or whatever.
It may sound like I’m passing judgment on people. That is not my intent. But we’re so fixated on finding an explanation for our problems (and a biological one at that), we sometimes fail to recognize that the problem is ourselves.
I agree with Steve. Steve, how would you respond to David Allen?
Thankk you so much for this post. I am a retired psychiatric social worker who worked in both a state hospital (called a mental health center) and a community mental health clinic, many of whose clients were “revolving door” patients at the state hospital.
I suspect that the state hospital was not quite like your inpatient unit since, while all the units were locked, there were some that housed people recovering from their need for acute treatment, some that housed the remaining few “chronic” patients in the area and one that housed people who’d gotten there via the criminal justice system.
I worked on the acute admissions unit which is probably not unlike where you are working now.
What seemed (and seems) apparent to me and to other people I worked with and to the patients (who later became clients) is not only that they had real, or more medical, illnesses, but that the variety was greater and the causes possibly more multiple than is currently talked about.
And while all our patients in the acute unit could for awhile be sufficiently calmed to move to another unit or back to the community –They tended to be discharged, by law, when they could no longer meet the admissions criteria which you describe though staff would try hard to protect those whom they knew couldn’t really make it — they were back, sometimes only days later. And in the intervening time, some committed crimes and others committed suicide and others got into drugs (again).
The structure of daily activities and group housing some of the clinics provided kept some of the folks out with reasonable success. But there were a lot of patients who lacked the ability to keep themselves together, and there didn’t seem to be any medication or therapy or group home that could really help them.
Since they needed diagnoses, they got personality disorder diagnoses, schizofreniform diagnoses, etc., but seeing them over a long period of time, you realized there were other issues as well: their brains just weren’t wired right, if you’ll excuse my non-medical terminology. Without drugging them into oblivion, there was no way, long term, to control the extreme panic,despair impulsiveness, rage and fear; or to deal with their inability to form reasonable judgments over time and to keep them away from danger. The currently available labels they received (and would today) just don’t fit.
The causes of these problems were probably multiple and might have included minimal brain damage (or maybe more than minimal), caused by any number of things; genetic problems, a physically and/or psychologically toxic environment, really bizarre or chaotic upbringing, and so forth.
Often these patients end up getting blamed for their problems because nobody is very good at fixing them. I suspect there is a lot more biology to them than we may have assumed. But as well as looking for biological causes of such illness, it would be I think very worthwhile to try to structure environments in which people with these problems could live more happily. I know that currently there is work being done to determine how people with schizophrenia might learn more effectively. But I think a different approach is needed: one in which external means are available in a home setting to turn down the volume for a person so that his mind isn’t pushed to the point of chaos. More creative use of medicine and a wider range of them would be in order but so would a greater understanding of each individual and in what conditions he functions well in and what pushes him too far and where he needs someone to act as his reasonable mind for him. Working with families and friends to learn about these people and how they function outside the hospital or the clinic would be very helpful. Then working with family and friends and, in addition, developing staff to assist and to sometimes provide tailored care in homes-away-from home would be very useful. I’m almost thinking of a hospice model, except for people with severe mental illness who deserve more out of life than many of them are currently getting.
This is obviously not something likely to happen soon, especially in the current economic climate. But a person can dream.
Rob,
You seem to be saying that syndromal evidence is completely worthless because we have not found the “cause” of certain mental conditions. That’s simplistic on several counts.
First, it’s a bit like saying that we did not know that head colds were a “real” illness until we discovered viruses. The human brain and its circuitry is impossibly complex, and our understanding is in its infancy.
Second, if two syndromes have a different specific presentation of several symptoms, time course, pervasiveness, specific predisposing factors, pattern of family histories, and response to medications,(like dysthymia has if you compare it to a melancholic depression); and they have both been described for centuries in a variety of different cultures, that is fairly good evidence that they are most likely both real and different. But it doesn’t tell us what the causes are, or whether genetic or environmental factors are more prominent in creating the syndrome.
The trouble with constructs like pediatric bipolar disorder, as opposed to true manic depressive illness, is that they are based entirely on vague similarities of symptoms and do not fulfill the criteria I mentioned above.
Your demand for absolute proof shows a misunderstanding of disease. Most diseases do not have a single “cause,” only risk factors. Even for pneumococcal pneumonia, the presence of the bacteria is just a risk factor, because of the body’s immune functions.
This is especially true in the brain: its’ 100X more complicated than any other organ because of the presence of very complicated gene/protein feedback loops, long-term potentiation of synapses and a variety of other mediators of gene-environmental interactions. And the presence of a disorder may depend on the cumulative effects of literally thousands of different genes.
All psychiatric syndromes are multidetermined. Whether or not they are “diseases” depends on your definition of disease, but doctors also treat pain. I assume you agree that emotional pain is real and deserves to be helped if possible.
URIs demonstrate objective, observable, robust, and reproducible pathology. Mental illness does not.
S. pneumoniae is not a risk factor for pneumococcal pneumonia. It is a sine qua non. The sines qua nons for mental illness, if there are any, are phenomenological, not pathological.
Wrong on both counts. On the first, you missed my point altogether. We have demonstrable pathology for URI’s NOW. Before microscopes and the germ theory, all we had to go on were runny noses and itchy eyes. And hay fever looks exactly the same. Somehow we recognized the difference, and knew they were “real.” You argument precludes FUTURE discoveries of objective and observable pathology with more advanced technology.
Second: Pnuemococcus is not the only bacteria that causes pneumonia, and the pathology of most bacterial pneumonias is pretty much the same. And you can have the pnuemococcis present and still not have pneumonia.
Nonsense. In what sense is coryza, cough, and inflamed mucous membranes absence of demonstrable pathology? Independent of the sufferer’s utterances!
And please let us not let the pneumococcal pneumonia argument descend into silliness. S. pneumoniae causes pneumococcal pneumonia. Klebsiella causes Klebsiella pneumonia, etc.
As for future discoveries of objective and observable pathology: By all means, bring on the future. Until the future arrives, we have no pathology, observable or otherwise.
So I guess all those people over the centuries have been just making up all that crap about hearing voices when no one’s around and completely and bizarrely misinterpreting sensory imput? They’re all liars?
You can fake a cough. Patients with panic attacks have tachycardia and sweat a lot. Pretty demonstrable.
Again, before microscopes and the germ theory, there was no way to tell that pneumonias had different pathogens.
And, I notice you still have not addressed my main points about syndromal evidence or the complexity of the brain.
Who says anybody made up their symptoms? My goodness David, are we going to argue about the plain meaning of the word “pathology”?
The argument was about our ability to recognize possible diseases before we have the technology to understand the nature of the disease. There was no way to know about certain types of pathology of certain apparent diseases before certain technological developments, and that’s the state were in about pathologies of neural networks in the brain. Of course we can’t be 100% sure given our current technology.
But we have a lot of syndromal evidence, as well as literally scores of biological risk factors for a number of different psychiatric syndromes.
You are the one who seems to be implying that because we don’t know the exact cause of psychiatric symptoms that we should never use meds to treat them. The psych medicines we have (whatever their drawbacks) clearly control certain symptoms (and not others); we just don’t know how they affect any underlying pathology. Just like we don’t know how aspirin works, but we know it treats headaches.
oops. hit reply to wrong comment; see below
I am so disappointed that this “discussion” seems to have taken on a hostile tone. I know Robert Whitaker, author of Anatomy of an Epidemic, is constantly imploring the community to just have a conversation about our paradigm of mental health care and to have some healthy skepticism about things we’re been accepting as “truth” when in fact they weren’t (chemical imbalances fixed by an SSRI, anyone?) but it is a shame when we can’t seem to have the conversation without taking potshots. No wonder Congress can’t get anything fixed.
That’s a misread of my argument. I argue that when we don’t know the pathology or pathophysiology of an entity, we treat it with drugs at our peril. Of course the drugs often control symptoms. But it is a logical error to infer pathology from this.
With respect, we do know the mechanism of action of aspirin.
http://en.wikipedia.org/wiki/Mechanism_of_action_of_aspirin
At last we agree! (although no one knew how aspirin worked until relatively recently, yet no one wanted to take it off the market).
Use of drugs can most assuredly have serious drawbacks – it’s always a case of risk versus benefit, monitoring patients for the emergence of serious side effects, etc. – and I absolutely agree that we can not infer pathology entirely from the effects of a drug on symptoms.
Thanks for an interesting exchange. gotta go.
I’m glad my post has spurred some interesting discussion. The sort of discussion that we need to encourage, not ignore.
The point of my post was not to say that the more severe manifestations of mental illness are “biological” while the others are not, but simply to point out that they are different. Profoundly different. And for me, at least, this difference was made most obvious to me when I returned to an inpatient setting.
I’m not making any arguments for or against the utility of psychiatric drugs, except to point out that they seem to work most reliably (although never 100%) in the more severe cases. Maybe there is a subset of patients whose symptoms are due to increased mesolimbic dopaminergic tone, or a forebrain serotonin deficiency, and who predictably respond to the medications we prescribe.
But it’s a fallacy to think that all forms of what we call “schizophrenia” or “bipolar disorder” or “depression” will respond the same way. I just hope that we can acknowledge this, and hopefully devote some resources to looking at the differences between the more severe and less severe cases of each, and adjust our treatment approaches accordingly.
“Maybe there is a subset of patients whose symptoms are due to increased mesolimbic dopaminergic tone”
We know with certainty that iatrogenic psychosis resulting from abrupt cessation of anti-psychotics causes increased mesolimbic dopaminergic activity. What percentage of new admissions recently discontinued their medications abruptly? It is worth considering that it is not the medication per se keeping them out of the hospital, but the absence of an abrupt discontinuation that keeps them out. If you, Steve, take Risperdal for several months, and then abruptly stop, you will become acutely psychotic due to increased mesolimbinc dopaminergic sensitivity combined with (relative) surge of dompaine.
Gary,
I’ve spent a day trying to locate (without success) an article in which the investigators determined that the majority of psych. admissions to their hospital could be attributed to drug discontinuation syndromes. Those “really, really sick” patients are “rebounding” – with amplification of their original symptoms plus some new ones, for good measure.
Good point. I have long believed that most (if not all) psychiatric admissions can be explained by one of the following: (a) discontinuation of medication (which may reflect either a “discontinuation syndrome” or simply the recurrence of intractable symptoms); (b) personality disorders; or (c) the effects of active substance abuse.
In other words, most patients aren’t admitted for worsening (or “progressive”) symptoms– as is the case with most medical conditions– but instead for the acute onset of symptoms that arise from factors independent of what we would otherwise consider a “natural disease process.”
What this says about psychiatry, I’m still trying to figure out.
Gary,
That is just flat out not true. I’ve taken bipolar patients who have been on long term anti-psychotic medication instead of lithium -some times after years on the medicine – and they do not become psychotic.
Presumably you do not take them off rapidly, as in “off a cliff”. It is no different than rebound TD. A return of normal levels of dopamine combined with hypersensitive dopamine receptors equals psychosis, TD, etc. Obviously there is a threshold here, as with anything. Not everyone that uses methamphetamine becomes psychotic. But, yes, writing “you will” as opposed to “you are vulnerable to” was overstated.
True or False? Sudden discontinuation of antipsychotics causes a return of normal levels of dopamine combined with hypersensitive domapine receptors?
“Evidence for a rapid onset psychosis (supersensitivity psychosis) following clozapine withdrawal was found and weaker evidence that this might occur with some other antipsychotic drugs. SOME CASES WERE REPORTED IN PEOPLE WITHOUT A PSYCHIATRIC HISTORY. It appears that the psychosis may be a feature of drug withdrawal rather than the re-emergence of an underlying illness, at least in some patients. Meta-analyses of withdrawal studies have suggested that antipsychotic discontinuation may also increase the risk of relapse over and above the risk because of the underlying disorder, but not all individual studies show this effect.”
Click to access actadrugwith.pdf
Again, absolute language like “will”, “always”, “never” is incorrect (there is no edit feature), but your contention that it is “Flat out” wrong is concerning. In regards to avoiding harm, just what do you think you’re doing to your patients’ dopaminergic systems, if not inducing an abnormal hypersensitivity?
I wish from the bottom of my heart that you all would think in terms of more than pharmaceutical treatment and in terms of environmental and social needs and adaptations as well as training.In the absence of better, more well-adapted medications, psychosocial adaptations and meeting social needs can be very, very helpful. With medications, they are also essential.
Well said.
Gary,
Of course all drugs active in the central nervous system should be tapered off to prevent withdrawal symptoms – which by the way, generally DO NOT INCLUDE delusions or hallucinations, which are the hallmarks of psychosis. In fact, the only drugs likely to cause psychotic symptoms during withdrawal are alcohol and barbiturates.
Unlike with drugs such as Paxil, dopaminergic drugs – the antipsychotics – can be tapered fairly quickly – like over the course of a week, depending on the dose.
You’re postulating something that would be called a tardive psychosis, similar to tardive dyskinesia, but frankly there is no good evidence that that happens.
How about tardive dyskinesia — see El-Mallakh et al (2011)? Or visit survivingantidepressants.org to see how withdrawal syndrome can “tardively” last months or years.
In the hospital, the problem is diagnosis. Quite often, the symptoms of a withdrawal reaction — which can be quite dramatic, understandably causing the patient to express vivid emotions — are misdiagnosed as an outbreak of severe mental illness, even psychosis. Bipolar disorder is a highly popular misdiagnosis. The patient goes into the hospital with, perhaps, situational depression and an adverse reaction and comes out on three or more psychiatric medications and a dire DSM label.
This is exactly how psychiatric treatment generates psychiatric disability.
42 case studies is hardly strong evidence. The article itself says: The existence of psychiatric disorders caused by withdrawal of psychiatric drugs is difficult to investigate. Technically, there is the problem of distinguishing the natural history of the underlying disorder from effects related to drug withdrawal.
Gary,
By the way, I’m not saying that antipsychotic drugs are harmless – far from it. But in many cases that’s all we have to stop people persecuted by delusions from living in cardboard boxes on skid row. I really wish they’d come up with better drugs!
I would like to add to StevebMD’s statement of what causes most psychiatric admissions – I went loony because of the meds I was prescribed, not illegal drug use, not drug withdrawal (although perhaps sometimes that was an issue also, since in the 90’s, docs didn’t have you taper off meds). Ever since going off meds a year and a half ago, I haven’t needed to be inpatient or go stay at a group home. Docs never see it, that the meds can be causing problems in some patients. They just started tagging me with a personality disorder label, with a straight face, as if you can suddenly develop a personality disorder in your mid 30’s.
I’m sure there are many people like me, where the meds are causing disinhibited behavior and agitation, and the docs are not figuring it out. I saw plenty of different psychiatrists, trying to figure out what to do, to save my life. No use. Psychiatrists cannot seem to manage diagnosing iatrogenic (did I spell that right?) problems.
Pat has an excellent point about iatrogenic “mental illness.” People suffering from adverse reactions to psychiatric medications and severe withdrawal syndrome also get hospitalized, misdiagnosed, escalated on medication, and made much, much worse by the attentions of specialists who should know better.
This happens ALL THE TIME. You’re not going to get accurate statistics because these adverse events are usually misdiagnosed as relapse or emergence of serious mental illness — some posters above express unclarity about this themselves.
You cannot treat the symptoms of an adverse reaction or withdrawal as if they were expression of a so-called mental illness along the lines of psychiatry’s “one drug per symptom” paradigm. The causes are entirely different, and the person’s nervous system has become destabilized. The brain is not made of rubber.
Back to Dr. Steve’s post: That psychiatrists even consider emotional problems of everyday people as on a continuum of disease with schizophrenia is very disturbing to me — but then, I find much about the thinking of psychiatrists to be very disturbing.
If I already didn’t know how extremely illogical and detached from reality psychiatry is, I would question the necessity to even discuss the distinction. I appreciate it that Dr. Steve so diplomatically presents it as food for thought for his colleagues.
Perhaps this is the underlying reason doctors have no compunction about making people worse with psychiatric medications and then rationalize the results: Any patient, already damaged goods, is on the road to psychosis anyway.
In academic terms, identifying true mental disease may be an “interesting nosological dilemma,” but in the real world, when more than 10% of the US population over the age of 6 is being medicated with psychiatric drugs (90% on antidepressants; 2/3 of them female), the pathologizing of the normal range of human expression is a very serious public health problem. (And will get more serious when people start quitting those useless medications in droves.)
Yes, mental illness does exist, but when psychiatry bandies about estimates of 25%-35% of the population suffering from it, one has to wonder whether garden-variety sadness or even what’s called mild to moderate depression truly belongs in the same category as schizophrenia.
Iatrogenia –
I agree with you about the overuse of psychiatric medications and the ridiculous percentage of the population rumored to have it. I rant, for instance, about the truly insane over-diagnosis of bipolar disorder on my blog and in my book -especially in kids.
However: tardive dyskinesia usually develops only after DECADES on antipsychotic medication. Very rarely does it appear after a short time, and usually in people with pre-existing brain problems.
You seem to imply that “tardive psychosis” develops in a much shorter period of time. If it exists at all, that still would not be the case.
You also speak as if we don’t have rather exquisite and extensive descriptions of schizophrenia and true bipolar disorder, and their course of illness, from way before antipsychotics were invented. Emil Kraepelin, who died in 1926 – about thirty years before thorazine – described it in ways that look almost exactly the same as what we see today. His work is still available and very detailed. You should read it before you start making suppositions.
Also, very few people on antidepressants get really severe withdrawal symptoms from them (except maybe with Paxil) and I’ve yet to see someone who is having it being misdiagnosed with something else. And I’ve been around a long time in a variety of clinical settings and supervising dozens of other psychiatrists.
You don’t have to make it sound like the situation is worse than it is, because it’s bad enough already!
My apologies, El-Mallakh et al (2011) wrote about tardive dysphoria, an iatrogenic condition they contend contributes to the Increase in “treatment-resistant depression” (a heinous term blaming the victim’s nervous system for inefficacy of antidepressant treatment).
Possibly related to the side effect of emotional blunting, tardive dysphoria is seen after medications are discontinued. As ever, whenever antidepressants are discontinued, it is unclear whether misdiagnosed withdrawal syndrome is being lumped in with tardive symptomology.
While the diagnoses of schizophrenia and bipolar disorder may be longstanding and fairly well-defined — aside from the skill with which they are applied — very, very few doctors grasp the diagnosis of antidepressant withdrawal syndrome, its severity, or potential duration of months or years.
Withdrawal syndrome can have intense and bizarre symptoms, including a particularly grueling insomnia, causing a great deal of distress to the patient. Symptoms often physically seem to be in the brain and patients truly wonder if they are losing their minds.
Naturally, some seek help at the hospital. When confronted with a doctor’s obtuseness, they may become passionate, angry, or argumentative. The doctor identifies the symptoms as agitation or delusion. Although patients in no way deserve a diagnosis of bipolar disorder or psychosis, they will get one anyway, because doctors don’t know what else to call it.
And that is how withdrawal syndrome generates spurious bipolar disorder and psychosis. It is very, very common. There are uncountable thousands of reports on the Web about this. There’s a very well-told one here: http://tinyurl.com/3zrxrm4
With all due respect, Dr. Allen, if you have not seen this, you may have been working in some extraordinary hospitals, and I would like to know which they were. Or, you may have mistakenly concurred in the misdiagnosis. After patients leave the hospital, you have no way of knowing whether it was correct. Psychiatry lacks feedback loops.
There is, actually, medical literature about how withdrawal from antidepressants “unmasks” bipolar disorder — another denial of adverse effects hidden in yet another heinous term.
Yes, unfortunately, the situation is worse than you know. It’s even worse than Robert Whitaker knows (http://tinyurl.com/3dcweda), as he’s only starting to delve into the long-term adverse effects of antidepressants.
As perhaps 100 million worldwide are taking these medications, most of them unnecessarily, we can expect the injured to number in the many millions, and every psychiatrist who has prescribed antidepressants will have patients in that population. Here’s Dr. Charles Raison expressing trepidation about that prospect http://tinyurl.com/3j2ynqr
Interesting. Thank you for the food for thought.
Being a patient who was at one time long ago on the other side of the locked doors I personally know the difference needed in interventions for me now verses 13 years ago.
Sometimes in my current regular doc sessions I wonder if I’m really sick, if I ever was or if I’m only one of the many worried well taking up the systems time.
Then I remember and connect briefly with the frightened scared woman raging, lost in overwhelming irrational thought and reacting with extremes from chair throwing to catatonia.
I’m not the same. Did the anti-psychotics or the SSRIs or the anti-convulsants or whatever other drug we desperately tried change the structure of my brain? Or was it the intensive therapy that helped me change my world view? Or the supportive and safe place I call home and loving family? Did all these change more than my behavior but actually alter me?
I dont know. No one tested my brain or took scans. I dont take the drugs anymore and the therapy is still around but not so hardcore. Am I really different on a biological scale (well other than being older?) I dont throw chairs or break plates now days. I have a job and friends and a life I love.
I’ve learned the answer to “WHY?” is irrelevant to my health. It matters not how I got sick or if I’m different – only that I remember one fundamental guiding concept:
My brain lies and I am not to trust it.
But that doesnt mean I’m not curious (-:
Iatrogenia,
Sorry, but antidepressant withdrawal lasting for years? That’s nonsense. Do you know for a fact that people who claim this were not taking other psychiatric medications at the same time, other medicines for physical conditions, or illegal drugs, or alcohol? That they are not taking other drugs even now?
Do you know for a fact that you are not seeing a sort of reverse placebo effect? Do you know for a fact what the person looked like before they took any drugs? Whenever I come across someone making unusual claims like that, and I form a relationship with them, there ALWAYS turns out to be a lot more to the story than you think.
You’re being sort of like the parents in denial about the effects they are having on their children. When in doubt, they blame some non-existant psychiatric condition. When in doubt, psychiatry critics always blame the drugs.
Somehow anti-depressants are ineffective against depression because the effects they have on neurotransmitters is not how they work, but withdrawing from them causes rebound depression because their effects on neurotransmitters IS how they work? Please.
I’m not saying they are not overprescribed, by the way. But the difference between chronic unhappiness, which the meds are useless for, and major depressive disorder- which usually does respond – is quite significant. And unfortunately ignored by an awful lot of psyciatrists.
No, Dr. Allen, prolonged antidepressant withdrawal syndrome is real. I’ve had prolonged Paxil withdrawal syndrome myself for 7 years, and I’m a very well-documented case. No drugs other than antidepressants.
Aside from many, many other bizarre, frightening, and recognized withdrawal symptoms, I initially had brain zaps for 6 months. Have you ever heard of brain zaps associated with any other condition?
There are many reports of tapering difficulties and prolonged withdrawal syndrome on SurvivingAntidepressants.org, which provides peer support for tapering and for prolonged antidepressant withdrawal syndrome. (We have a couple of cases of people having brain zaps for years, as well as other recognized withdrawal symptoms.)
Journal articles referring to 10 cases of prolonged antidepressant withdrawal syndrome are here: http://tinyurl.com/4ylsb3h
There was a collection of more than 100 prolonged withdrawal cases on paxilprogress,org, but the site changed direction and the management deleted them. However, they were captured by colleagues of Dr. Giovanni Fava, who are now collecting cases for journal articles, information here: http://tinyurl.com/3zuaxo9
This may well be the next shoe to drop, following the antidepressant-placebo controversy.
The underlying issue is probably that the nervous system does not recover from chronic serotonergic downregulation as readily as psychiatry likes to think. Withdrawal syndrome is not rebound — it’s dysautonomia.
I can well understand why doctors tend to deny the existence of prolonged antidepressant withdrawal syndrome. First, there’s the horror of having caused iatrogenic neurological damage. Then there’s the guilt of realizing one must have misdiagnosed and mistreated trusting patients.
And that is why, when their tapers go wrong, patients turn to the Web and to peer support rather than medicine for help — because very, very few doctors even recognize withdrawal syndrome, much less treat it.
Iatrogenia,
Iatrogenia
I can’t comment on your case because I don’t know anything about you, but I do know you can not be certain that all of your symptoms are due to Paxil withdrawal. Brain zaps can indeed go on for a while in some people, so that probably was. But I spend half my life getting patients off of inappropriate meds, and most of them get off even Paxil without any untoward effects at all.
And as to peer support groups? There are scores of people on the Child and Adolescent Bipolar Foundation Website who swear that their kids are bipolar and that they do next to nothing wrong as parents and that the meds are fixing things. Except other stuff they say contradicts all of that. I don’t think they’re lying; I think kidding themselves. And I don’t believe them either.
Dr. Allen, thank you for your attention to my posts.
You are not the first psychiatrist to suggest I am deluded. My opinion is that I am completely rational. Whose opinion takes precedence regarding my state of mind?
Psychiatry has a range of rationalizations about why prolonged antidepressant withdrawal (or other tardive symptomology from psychiatric drugs) cannot and does not exist. Yet there are thousands of people who, despite being told by their doctors, family, and society in general that they do not suffer from it, still insist they do, each coming to this conclusion independently. On which side is the mass delusion?
I can understand why any psychiatrist has difficulty coming to grips with the present situation in the field. All of your research is corrupt, there is no biological basis for prescription, every day reveals appalling (and previously concealed) adverse effects of the drugs you prescribe daily, and yet you must continue your profession or have no income.
I believe, as Dr. Steve hints in his article, that eventually psychiatry will be forced to focus on “true” mental illness, that very small minority of people who have no recourse but the trial-and-error of psychiatric medication. When the true risks of the drugs are acknowledged, the risk-benefit balance simply will not pan out in favor of the drugs for much of your customer base.
Iatrogenia,
Because Dr. Allen and others cannot “imagine” that a certain (small) percentage of antidepressant users may be vulnerable to permanent damage by the drugs, you and your fellow sufferers must simply be exhibiting delusions/hallucinations generated by your underlying psychiatric problem.
BTW, “permanent” antidepressant damage may not always manifest itself as CNS symptoms: eight months ago, my husband was asked to see a patient (a fellow physician!) who had been prescribed Doxepin by a psychiatrist and had (within 3 treatment days) essentially developed paralysis of the large bowel. To date, this unfortunate individual has had no return of bowel function.
Jane, I am accustomed to having the idea of prolonged withdrawal syndrome rejected in much harsher terms than Dr. Allen used.
The bowel issues are one symptom pattern of the syndrome, and not incompatible with the general issue of dysautonomia. Several people on survivingantidepressants.org suffer from post-medication gastroparesis.
Coincidentally, today Gianna Kali, a blogger well-known among psychiatric survivors, published an article about her very long recovery from psychiatric drug withdrawal (since 2007) and current struggle with the grueling insomnia that is a very common symptom https://bipolarblast.wordpress.com/2011/08/03/18227/
(A misdiagnosis of bipolar disorder is involved.)
She refers to a person named Alto Strata, who is my alter ego on survivingantidepressants.org, where I may be contacted if you wish to correspond.
Might I also suggest your husband’s colleague submit his case report to Dr. Carlotta Belaise to be included in the prolonged withdrawal syndrome study underway; instructions at http://tinyurl.com/3zuaxo9
JanePhD,
I never said Iatrogenia was delusional – that was her word. Some people do have severe idiosyncratic reactions to drugs – people have bled to death from one aspirin. But it was due to the effect of increased bleeding from aspirin, not from withdrawal.
Doxepin can cause severe constipation for sure, but if it persists after the doxepin is stopped then there is an extremely strong possibility that there was a pre-existing bowel or autonomic problem and the doxepin was the straw that broke the camel’s back. That effect, in other words, comes from the combined effect of doxepin plus probably several other complicating factors.
We were talking about drug withdrawal, which is not the same thing at all.
You see, there’s this logical fallacy called post hoc ergo propter hoc: if one event follows another, this does not represent proof that the first event caused the second. For instance, a lot of heroin addicts used pot first, but did the use of pot cause the heroin addiction? Even more heroin users drank coca-cola first. In this instance, the fallacy is known as post coke ergo propter coke.
Let it be known that Dr. Allen never suggested I was delusional, only mistaken.
Again, Dr. Allen, we have one world view against another. You have your anecdotal evidence based on your perception of your patients’ reactions, and I have another based on my perception of a different population.
Because few studies have been done on the longitudinal effects of withdrawal — and you can bet none will ever be funded by pharma — your argument that my conclusions are drawn from a possible erroneous inference is correct. But that is also true of your argument.
Because collection of psychiatric drug post-marketing data is so poor, adverse effects are always initially reported anecdotally and, historically, vigorously denied by the medical profession with the perfectly logical arguments Dr. Allen uses. It can take many reports and maybe a high-profile scandal (like the child bipolar death of Rebecca Riley) to get to the tipping point.
Now, we have a number of statistical meta-analyses (Kirsch, El-Mallakh, Andrews, Deshauer etc. see http://tinyurl.com/3dcweda) showing something untoward happens after discontinuation of antidepressants. In these studies, it is showing up as an increased rate of relapse over placebo and being interpreted as long-term lack of efficacy.
However, as I have contended for 5 years, the statistical base is confounded by withdrawal syndrome misdiagnosed as relapse. No study of antidepressant efficacy — ever — contains a protocol for distinguishing withdrawal syndrome from relapse, and none contains a single report of withdrawal syndrome, even STAR*D.
Marcia Angell just mentioned this in passing in the NY Review of Books http://tinyurl.com/3b8cvgk: “The problem with relapse studies, like that of John Geddes, which is cited by Friedman and Nierenberg, is that they don’t distinguish between a true relapse and withdrawal symptoms that result from the abrupt cessation of drugs.”
I have hopes this indicates the pervasive issue of withdrawal syndrome is about to break into medical consciousness. When Dr. Belaise’s study is published, perhaps some attention will be given to long-term adverse effects of antidepressants, and the general population will be relieved of the attentions of pharmapsychiatry.
Dr. Allen,
When an individual suffers a brain injury (a small stroke, for example), he may or may not experience a complete recovery. A neurologist may advise the patient’s family that a full recovery is anticipated but that scarring mechanisms could outpace repair mechanisms and the patient might be left with some deficits. It’s been my experience (with friends and relatives) that neurologists do not invoke an underlying disorder of suboptimal repair mechanisms to account for a less-than-full recovery – they invoke “bad luck”.
I think we can agree that the continuous administration of a psychoactive drug alters brain chemistry in a process that probably involves changes in microanatomy of the “target” neurons as well as compensatory changes in more remote neurons. Once the drug is removed, one would expect and hope that the system restores itself to its pre-drug wiring. Obviously, this does not happen for a significant minority of patients. More “bad luck”.
As for that SOL Doxepin patient – the individual has been exhaustively examined by a motility specialist. Final diagnosis: Doxepin toxicity. Really “bad luck”.
.
Jane,
Denying med side effects seems to exist quite a bit in medicine. There was a study recently which I am too lazy to look up that physicians commonly blew off legitimate complaints about statins.
It is only recently after an intense struggle that cancer patient complaints about “chemobrain” are now being taken seriously.
Unfortunately, it is alot worse as you know for patients with a “mental illness” label because that immediately diminishes their credibility in the eyes of psychiatry. How convenient as psychiatrists never have to be accountable for anything. Just blame everything on the patient.
Interestingly, when I lost my sense of taste after taking Listerine which fortunately came back upon discontinuation, my Dentist took my complaint seriously and didn’t blow me off as a nutcase. Sadly, if I had encountered a similar situation with someone like Dr. Allen, I wouldn’t been treated so nicely.
As one who was on Doxepin, I am blown away by what happened to that person who was seen by your husband.
That “wonderful” drug contributed to my lingering tinnitus that I still experience in spite of being off of meds for over a year. I also feel it contributed to the sleep difficulties I continue to experience.
AA,
You probably will not believe me, but I NEVER blow off one of my patient’s symptoms or complaints. I do, however, make sure I know them well enough not to attribute causes to the symptoms when there may be other factors involved.
Post hoc reasoning is unfortunately very common among us normal messed-up humans, including me. When in doubt, if a significant complaint even might be from a drug I’ve prescribed, and there’s no known countermeasure, I will stop the drug immediately and try something else, even if I don’t think it was the drug. Just to be on the safe side.
I also encourage patients to call me if they even THINK they are having a side effect that I have not already warned them about. I even return their calls! Then again, I usually see patients right at their appointment times, so I’m probably considered a freak of nature by some docs.
In Dr. Allen’s defense, I’ve interrogated him about his withdrawal practices and I believe he does monitor his patients closely, which is very rare and much appreciated.
Reinstatement of the medication is required at the very beginning of severe withdrawal symptoms to ensure an appropriately slow rate of taper. Dr. Allen appears to understand this.
Jane — “suboptimal repair mechanisms” — very good argument!
Addiction expert Stanton Peele recently wrote a brilliant blog piece at http://www.peele.net/blog/110616a.html paralleling the nervous system disruption of psychiatric drugs with those identified as addictive, and the obvious consequences of discontinuing either: withdrawal symptoms. Of course the underlying issues and dangers of physical dependence are the same!
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