Let's Kill the Schizoaffective Diagnosis

Following is a chopped (or should I say slashed?) version of a new article on mcmanweb (with the rather less provocative title of "Schizoaffective Disorder"), which in turn is based on copy-and-paste of extracts from several mcmanweb articles on psychosis and various diagnostic headaches in bipolar ...

Think of schizoaffective as occupying that middle ground where bipolar overlaps with schizophrenia. But what are we dealing with? Schizophrenia lite, BP heavy, a separate illness, two co-occurring illnesses, or something occupying the psychosis spectrum?

The DSM-5, which is scheduled to replace the current DSM-IV in 2013, spells it out: "The current DSM-IV-TR diagnosis schizoaffective disorder is unreliable," but then makes no changes to make the diagnosis reliable.

What We’re Up Against

A number of years back, the International Society for Bipolar Disorders came up with their own recommendations for improving the diagnostic criteria for bipolar. According to their report, genetic studies lend credence to an overlap between bipolar and schizophrenia, with a clustering of both in family groups, and shared suspect genes in both illnesses.

Schizoaffective is thought to occur in less than one percent of the general population (women predominate), but the patient population is much higher owing to clinicians making the diagnosis when they are uncertain.

In schizoaffective, "there must be a mood episode that is concurrent with active-phase symptoms of schizophrenia." This is different than a "mood disorder with psychotic features" or "mood symptoms in schizophrenia." Not that it's easy to tell. Confounding matters is the discomforting reality that schizoaffective is a moving target - the relative proportion of mood to psychotic symptoms may change over the course of the disturbance, not to mention over the long term. Not surprisingly, most patients who receive an initial diagnosis of schizoaffective are later diagnosed with something else.

With all this in mind, the ISBD panel considering the matter recommended eliminating the designation, schizoaffective, in its entirety and substituting it with additional specifiers to schizophrenia, bipolar I, bipolar II, and major depression.

Another Perspective ...

In a research article, psychiatric geneticists Craddock and Owen contend that the current definition of schizoaffective disorder is too narrow to be clinically useful. Instead, it is treated as a glorified "NOS" diagnosis. Compared with the much broader definitions of schizophrenia and mood disorders, "it is inevitable" that the schizoaffective category will seem less reliable to clinicians. This is especially true if clinicians pay little attention to the different ways psychosis presents itself over time.

Despite the lack of respect for schizoaffective, the authors note that "genetic epidemiology supports a strong genetic component to schizoaffective illness." Based on their findings, the authors suggest the concept of "schizoaffective spectrum phenotype" incorporating various shades of mood and psychosis.

What Are We Looking At?

At a 2007 "Deconstructing Psychosis" planning session sponsored by the American Psychiatric Association, the NIMH, and WHO, Carol Tamminga MD of the University of Texas Southwestern Medical Center noted that although mood stabilizers alone can treat psychotic symptoms in acute mania, they are not effective in treating psychosis in schizophrenia. Dr Tamminga offered three possible explanations:

Psychosis has a distinct pathophysiology, common to both schizophrenia and bipolar disorder, and antipsychotics target that molecular mechanism; 2) psychosis is mediated by neural systems which are different in schizophrenia and bipolar disorder, which can be stimulated and treated from multiple points and by many different pharmacologic strategies; and 3) psychosis is a response analogous to "fever" and should not be a primary target for treatment.

Trying to Make Sense of All This

The operative phrase to the DSM-IV schizoaffective diagnosis is:

There is either a Major Depressive Episode, a Manic Episode, or a Mixed Episode concurrent with symptoms that meet Criterion A for Schizophrenia.

Criterion A lists other symptoms besides psychosis, and calls for a minimum time of one month. (There is a Criterion C for schizophrenia, which mandates a six-month minimum for "continuous signs of the disturbance," but there is no reference to this in the schizoaffective diagnosis.)

Schizoaffective, then, is basically short-form schizophrenia punctuated by relatively brief overlays of depression or mania (the DSM minimum for mania, for instance, is one week). The assumption is that it is highly likely that there will be long periods when the schizophrenia symptoms manifest with no mood symptoms, and indeed this is a DSM requirement.

Thus, schizophrenia symptoms can appear without mood symptoms, but mood symptoms can't appear without schizophrenia symptoms.

Does this sound like schizophrenia to you? Short form or not? Say, schizophrenia with mood symptoms? Is schizoaffective, then, a euphemism diagnosis for clinicians too chicken to tell their patients the truth? It appears that way.

Let's kill the schizoaffective diagnosis, then, and go with the ISBD specifiers approach. Their recommendations:

In schizophrenia, these specifiers::

1. With symptoms meeting criteria for mania or mixed features.
2. With symptoms meeting criteria for major depressive disorder.

In bipolar I and II and major depression, these specifiers:

1. With psychotic symptoms meeting Criterion A for schizophrenia (ie hallucinations or delusions over one month) and for at least two weeks without prominent mood features.
2. With psychotic symptoms meeting Criterion A for schizophrenia with consistent concurrent mood features.

Meanwhile, Back in the Real World ...

A few questions you need to be asking:

Is your psychiatrist using the diagnosis to bring your clinical condition into sharper relief? In other words, has a competent clinician who really knows you figured out that your bipolar comes with serious complications? And if so, is he or she ready to work with you - including spending extra time with you - in helping you manage?

Or has your psychiatrist basically given up on you? In other words, is your diagnosis a result of the frustration of a lazy clinician who barely knows you and has already written you off as untreatable?

Or is your psychiatrist over-reacting? In other words, is your diagnosis the result of a lazy clinician who barely knows you and assumes that anything that even remotely resembles psychosis must be connected to schizophrenia or schizoaffective? In other words, are you about to be over-treated and over-medicated?

What's in a name? Sometimes nothing. Sometimes everything.

Gold Standard Clinical Trials - Science or Marketing?: Part III

The story so far ...

At the 12th International Congress on Schizophrenia Research in April 2009, J&J debuted a “randomized, double blind, placebo-controlled” study which found its antipsychotic Invega produced a better result on a population of schizoaffective patients than did the placebo.

Researchers point to studies of this type as representing the gold standard of clinical research, but there is a major fallacy in their reasoning, and this study in particular represents a splendid example: Although the methodology of the study was flawless - even dazzling - the result showed us nothing. We already knew antipsychotics, including Invega, worked (with obvious limitations) for conditions involving psychosis. Psychiatrists already prescribe antipsychotics to patients with schizoaffective.

The result was meaningful to one party, and one party only: J&J (which owns Janssen, which manufactures Invega). Thanks to the success of this trial (and to the decidedly less convincing success of an earlier one), J&J had a bullet-proof brief to take to the FDA. In July, the company announced in a press release:

“The U.S. Food and Drug Administration (FDA) today approved the first and only [my emphasis] antipsychotic for the acute treatment of schizoaffective disorder.”

J&J had received clearance to market its Invega as a treatment for schizoaffective - which, since it was the only player in the field, translated to a golden opportunity to market an illness rather than simply a product. Thus, in its press release:

Among people who frequently use mental health services, schizoaffective disorder may account for approximately 24 percent of cases.

And again:

“Schizoaffective disorder can be challenging to diagnose because of the broad range of symptoms patients experience," said Nina Schooler PhD, SUNY Downstate Medical Center.

And again:

"Schizoaffective disorder is a chronic, disabling condition," said Husseini Manji MD, FRCPC, Global Therapeutic Area Head, Neuroscience, Johnson & Johnson Pharmaceutical Research & Development. "This new indication for Invega further demonstrates Janssen's commitment to helping people with serious mental illnesses."

In the article of the second study, published in the Oct, 2010 Journal of Clinical Psychiatry, we are told that schizoaffective was first identified in 1933, and the first study article in the April JCP we are informed that:

Although schizoaffective disorder occurs less commonly than schizophrenia, it may account for up to one-quarter of admissions to inpatient mental health facilities.

Back in the glory days of Pharma, J&J would have sponsored at least two dinner (or luncheon or breakfast) symposia at the American Psychiatric Association’s annual meeting. Anywhere from five hundred to a thousand psychiatrists would have crowded into a hotel ballroom to hear a panel of experts expound on “Schizoaffective Disorder, the Forgotten Illness” or “Treatment Modalities for Schizoaffective Disorder” or something similar. The psychiatrists (and other clinicians) would have received CME credits for their attendance.

From 2002 to 2009, I must have attended more than 60 symposia of this nature at APAs. Some of them were blatant advertorials, but most were highly educational and a large number of them were outstanding. I actually recall congratulating some Wyeth people for sponsoring a luncheon symposium the year before that had nothing to do with depression or Effexor. They looked at me funny, as if to say, “How did we screw that up?”

But in the eight consecutive APAs I attended, never once did I see in the program an industry-sponsored symposium devoted to schizoaffective disorder. If I had, I’m sure I would have penciled it in.

The APA has done away with industry-sponsored symposia at its annual meetings, but J&J would have had ample opportunity to get out the word in the exhibit hall. I did not attend last year’s APA, but I guarantee any clinician approaching their exhibit could have watched a multimedia display on schizoaffective, helped themselves to the literature, put their names on a contact list, and had their questions answered by a phalanx of J&J eager beavers. If the clinician expressed an interest in knowing more, one of the eager beavers would have escorted him or her to a back area to talk one-on-one with a J&J big cheese. 

Meanwhile, J&J would have been getting out the word in the poster area of the annual meeting. Perhaps attendees there would have viewed the same poster I did at the Schizophrenia Congress. In all likelihood they would have been exposed to many many more, of little significance, something like “Paliperidone ER Taken with Bottled Water vs Tap Water in a Nursing Home Mongolian Population with Schizoaffective Disorder.”

The multiple poster effect would have been wall-to-wall, marketing dressed up as research, with illness and product occupying an attendee’s entire field of vision. Working the posters would be an academic superstar with his or her minions, eager (okay, perhaps not eager) to answer questions.

In the meantime, away from the APA, J&J would be staging its own events with expert speakers, as well as launching its drug reps on special missions of search and sell. Moreover, they would be placing articles in publications. In a recent piece on his Carlat Psychiatry Blog, Daniel Carlat, author of “Unhinged,” had this to say about a feature in Current Psychiatry, which goes out free to psychiatrists:

Another promotional CME Supplement was published in October 2010, and is entitled  "Differential Diagnosis and Therapeutic Management of Schizoaffective Disorder." It is supported by Janssen, the maker of Invega, which was recently the first medication FDA approved for - you guessed it - schizoaffective disorder. I haven't read it yet, but this is a de facto advertisement simply by virtue of the choice of topic. Janssen makes the only approved product for schizoaffective disorder, and in order to advertise it, they paid off Current Psychiatry to write a huge article about the disorder. It doesn't need to be "biased;" it just needs to be focused on a topic that is of inherent commercial benefit to the supporter.

The article doesn’t tell us what we don’t already know about about schizoaffective, but it does hit on all the talking points in the J&J press release and related literature, including the fact that:

Only 2 randomized, double-blind, placebo-controlled studies of an atypical antipsychotic (paliperidone extended-release, now FDA-approved for the treatment of SAD), have been conducted in a well-defined SAD patient population.

Even a squeaky-clean expert in a forum uncorrupted by Pharma would be obliged to mention something to this effect. There is no way of avoiding it, and that is the beauty of J&J’s strategy.

But when all it said and done, psychiatrists will not be changing the way they treat patients with psychotic features, whether you call it schizoaffective or something else. They will still use an antipsychotic, just as they have been doing for the last fifty years. It’s just that a few more of them will be doing it with Invega.

Gold Standard Clinical Trials - Science or Marketing?

This is the second in a new series on analyzing information. Credit Robert Whitaker’s “Anatomy of an Epidemic” for getting the ball rolling, as there is no way of critiquing his book without evaluating the evidence he relied upon. Only then can we ask ourselves if his conclusions are justifiable.

This is a different proposition entirely than whether Whitaker is right or wrong. You can decide that for yourself.

In my previous piece, I commented on some findings at the very bottom of the evidence food chain (a series of wholly unscientific reader polls I had conducted here), but that actually told us something. In this piece, I will flip it. I will talk about a study at the very top of the food chain, but that tells us nothing. Let’s get started ...

Two years ago, in my capacity as a journalist, I was at the 12th International Congress on Schizophrenia Research in San Diego, just down the hill from where I live. The top brain scientists in the world were presenting and in attendance, including 2000 Nobel Laureate Arvid Carlsson. I recall going to a table with my morning coffee and greeting the researchers there with, “Hi, I’m the only C student at this table.”

Part of the Congress involved poster sessions, where scientists stand in front of blow-ups of their latest findings. This affords an invaluable opportunity for the researchers at the conference to engage their fellow researchers in one-on-one discussion. It also affords a golden opportunity for people like me to walk up to some future Nobel Laureate and ask, “What’s a neuron?”

The first three or four days of posters involved cutting edge brain research. I was like a kid in a candy store ... a wrestler in a chair factory, a hippie in a drum circle. (Did you see that Super Bowl commercial?) The last day of the conference featured posters on treatment. Instantly, I felt I had been sucked back in time a half century.

Some very enthusiastic Johnson&Johnson people informed me of a new study of theirs that shed some very important new light on schizoaffective disorder.

Really? I thought. Schizoaffective is probably the most confusing diagnostic classification in the entire DSM. Everyone agrees that it has something to do with that undelineated middle ground where bipolar and schizophrenia bleed into one another, but what is it exactly? Schizophrenia lite? Bipolar heavy? Some kind of schizophrenia-bipolar mix? Or a stand-alone illness in its own right?

Naturally, I was interested. I looked at the poster. "A Randomized, Double Blind, Placebo-Controlled Study of Flexible Dose Paliperidone ER in the Treatment of Patients with Schizoaffective Disorder," I read.

I smiled politely, engaged in very short chit-chat, then made my way to other posters. In one glance, I knew, the study told me nothing. Here’s the deal:

Randomized, double blind, placebo-controlled studies are the gold standard of treatment research. Perhaps the most celebrated example of a clinical trial is James Lind’s 1747 experiment involving 12 scurvy-infected sailors. He divided his patients into six pairs. Five of the pairs showed no improvement. Of the pair receiving oranges and lemons, one had fully recovered after five days, the other had almost recovered. (Then they ran out of fruit.)

A more refined study would have pitted a much larger group of orange-and-lemon people against a proportionally large group taking a look-alike, taste-alike placebo (say a citrus pill vs a sugar pill). To keep the study honest, one would have made sure the clinicians handing out the pills had no way of knowing which pill was which (the double-blind).

I knew at a glance the J&J people had all their “i”s dotted and “t”s crossed. Studies of this nature are immensely expensive - my best guess is the $20 million-range - designed by some of the smartest people in the world overseeing an immense and highly complex undertaking where an infinity of things can go wrong (and often do).

The catch? Even though the study was conducted scientifically, to rigorous standards, it was not a scientific study. It was a marketing exercise.

Paliperidone is the generic name for J&J’s recently-approved Invega, which is Son of Risperdal. Risperdal represents the first of the new-generation atypical antipsychotics (discounting Clozaril) introduced in the early 1990s and hyped as superior to old-generation antipsychotics.

We already know that as problematic as antipsychotics may be, they are very effective in knocking out psychosis. The first studies involving Thorazine proved that six decades ago. Since then, antipsychotics have been the treatment of choice for schizophrenia and any condition involving psychosis, including bipolar and schizoaffective, accounting for some $20 billion annually in sales.

So what’s new? Nothing much, really, except that no drug company had ever undertaken a trial on a schizoaffective population. What was the point?

Keep in mind that when James Lind was investigating scurvy, the British Royal Navy was not issuing citrus fruit to its sailors. His findings would give them cause to change their practice, though it would take them another fifty years to get around to it.

Contrast this with the Invega study. Is a clinician, reading this study, really going to change his or her practice by putting all his schizoaffective patients on an antipsychotic? He already has them on an antipsychotic.

But could the study possibly be persuasive in getting a clinician to change her practice from prescribing say Geodon or Zyprexa to Invega? Ah, a marketing question.

More to come ...  

The People’s DSM: My Alternative Bipolar (Cycling) Diagnosis - Part III

Thus far (in Part I and Part II), I have kept what I refer to as “cycling illness” simple. As long as we appreciate that down and up are connected as different phases in the same cycle, there is little room for confusion. But there is a major complication called psychosis. If the psychosis is severe enough and prevalent enough, suddenly clinicians are faced with some very tricky diagnostic calls.

The current DSM recognizes psychosis as an illness in its own right and acknowledges its occurrence in other illnesses, including depression, bipolar, and schizophrenia, not to mention the hybrid diagnosis of schizoaffective. In theory, clinicians have a rough guide to work with. In practice, uncertainty prevails, namely:

How, precisely, does psychosis tie in to mood? And, while we’re at it, is there actually one person in the whole wide world who can explain schizoaffective, much less the reason for its existence?

Brain science and genetics promise to yield far more definitive answers than we presently have, which may explain why the draft DSM-5 changed virtually nothing. My view is we need to do our best based on the knowledge we have now, even if future scientific discovery proves us wrong. Let’s get to work:

The current DSM treats “with psychotic features” as a specifier to bipolar rather than to depression or mania. Let’s keep the specifier approach, but find more precise applications, thus:

Euphoric Mania with Psychosis

Various euphoric mania characteristics (such as enhanced positive abilities) may manifest as delusional thinking or hallucinations, in which the subject may see him or herself or his or her situation in a grossly exaggerated light (such as a superman on a special humanitarian mission).

Dysphoric Mania (Mixed) with Psychosis

Various dysphoric mania characteristics (such as enhanced negative abilities) may manifest as delusional thinking or hallucinations, in which the subject may see him or herself or his or her situation in a grossly exaggerated light (such as the only one in the world aware of a vast conspiracy).

And a copy and paste from the Alternative Depression Diagnosis Part II:

Vegetative (or Mixed) Depression with Psychosis

Various vegetative domain characteristics (such as excessive guilt) may manifest as delusional thinking or hallucinations, in which the subject may see him or herself as deserving of punishment (such as being tracked by agents for an imaginary crime).

Agitated (or Mixed) Depression with Psychosis

Various agitated domain characteristics (such as a sense of exaggerated bad luck) may manifest as delusional thinking or hallucinations, in which the subject may see him or herself as the object of unwarranted harassment (such as being tracked by agents as a result of a frame-up).

***

Thus, in these situations, psychosis is strongly linked to different phases of the cycle in terms of both timing and congruency. When the mania recedes, for instance, so does the psychosis. This suggests mood stabilizers as a first option rather than an antipsychotic.

If, on the other hand, the psychosis appears have a life independent of the cycle, then the clinician needs to spell it out, such as: “Cycling l, with Co-Occurring Psychotic Disorder.” (The current DSM lists “Delusional Disorder” and “Brief Psychotic Disorder”.)

This suggests different treatment options, such as an antipsychotic for the psychosis plus a mood stabilizer for the cycle (with perhaps the antipsychotic serving double duty in lieu of a mood stabilizer).

It is important to emphasize that psychosis with a life of its own is not synonymous with schizophrenia. Generally, more is going on with schizophrenia than just psychosis. Nevertheless, a very compelling case can be made for an overlap between bipolar and schizophrenia. Unfortunately, the DSM’s ‘tweener diagnosis of schizoaffective is more of a problem than a solution. Thus:

Kill the Schizoaffective Diagnosis

The operative phrase to the schizoaffective diagnosis is: “There is either a Major Depressive Episode, a Manic Episode, or a Mixed Episode concurrent with symptoms that meet Criterion A for Schizophrenia.”

Criterion A lists other symptoms besides psychosis, and calls for a minimum time of one month. (There is a Criterion C for schizophrenia, which mandates a six-month minimum for “continuous signs of the disturbance,” but there is no reference to this in the schizoaffective diagnosis.)

Schizoaffective, then, is basically short-form schizophrenia punctuated by relatively brief overlays of depression or mania (the DSM minimum for mania, for instance, is one week). The assumption is that it is highly likely that there will be long periods when the schizophrenia symptoms manifest with no mood symptoms, and indeed this is a DSM requirement.

Thus, schizophrenia symptoms can appear without mood symptoms, but mood symptoms can’t appear without schizophrenia symptoms.

Does this sound like schizophrenia to you? Short form or not? Say, schizophrenia with mood symptoms? Is schizoaffective, then, a euphemism diagnosis for clinicians too chicken to tell their patients the truth? It appears that way.

Let’s kill the schizoaffective diagnosis, then. And while we’re at it, let’s rethink schizophrenia, complete with a name that accurately describes the illness. But that’s for later, along with a full review of psychosis. In the meantime, to sum up:

1. When the psychosis can be linked to a phase of the cycle: Specify the phase within the cycling diagnosis.
2. When the psychosis appears independent of the cycle but does not meet criteria for schizophrenia: Stick to cycling diagnosis, with a co-occurring psychotic disorder.
3. When the psychosis appears related to schizophrenia: Go with a schizophrenia diagnosis, with a mood symptoms specifier.

Please note that I do not regard this draft as anything approaching the final word. If you have your own approach to breaking down psychosis, or can think of a hybrid bipolar-schizophrenia diagnosis that makes sense - or for that matter can make a good case for not fixing what ain’t broken - then, please, let’s hear from you.

My DSM-5 Report Card: Grading Bipolar - Part IV

Part I, Part II, and Part III to Grading Bipolar placed heavy emphasis on that largely unmapped middle ground where bipolar bleeds over into clinical depression. Why this is critically important is that clinical ignorance leads to misdiagnosis and wrong treatments, which translates into years and even decades of unnecessary suffering.

The current DSM abets numerous opportunities for bad psychiatric practice, which the DSM-5 was supposed to redress. Unfortunately, the Task Force and its various workgroups suffered an extreme outbreak of dereliction of duty.

So, can the DSM-5 do better where bipolar bleeds over in the other direction into schizophrenia? First a little background ...

Back in the early twentieth century, the pioneering diagnostician Emil Kraepelin separated out “manic depression” (bipolar and recurrent depression) from “dementia praecox” (schizophrenia). This distinction provided psychiatry with its first real navigational aid, which continues to guide diagnostic practice to this very day.

But Kraepelin also recognized the limits to making a clear categorical split, and recent genetic findings are backing his reservations. Virtually all the leading candidate genes for bipolar happen to be leading candidate genes for schizophrenia, as well.

The current DSM recognizes some of the crucial fine shadings. Thus we have “with psychotic features” as specifiers to both major depressive disorder and bipolar disorder. In addition, there exists the separate diagnosis of “schizoaffective disorder” that is widely interpreted as a hybrid between bipolar and schizophrenia.

The issue: Should those charged with the DSM-5 attempt to fix what doesn’t appear to be broken? Or is there considerable room for improvement?

On with the grading ...

Psychosis, a Clear Definition

The current DSM makes various references to psychotic features, but what precisely is “psychotic”? To find out, one needs to flip the pages to the rather obscure diagnosis of “brief psychotic disorder,” which mandates one or more of the following symptoms:

Delusions; hallucinations; disorganized speech; psychomotor symptoms, including catatonic behavior.

The DSM-5 would leave this unchanged.

Fine, that provides a breakdown of the component parts to psychosis, but what is psychosis? The glossary to the DSM-IV concedes that none of the historic definitions “has achieved universal acceptance.” Narrowly viewed, psychosis refers to hallucinations and delusions to which the patient lacks insight. A wider view would incorporate patient insight. Still wider are the symptoms listed for the positive symptoms of schizophrenia (same as for a brief psychotic episode) and wider still would incorporate “loss of ego boundaries or gross impairment in reality testing.”

The current DSM punted in coming up with an authoritative definition and set of distinctions. It appears the DSM-5 is similarly opting out.

Grade: F.

With Psychotic Features

Psychosis looms large in mania and less so in depression. The DSM-IV operative term is “with psychotic features,” which the DSM-5 would leave unchanged. Presumably, a “feature” is less intense than a “symptom,” but it would be helpful to see this spelled out. Is this asking too much? Apparently yes.

Grade: F.

Mood Congruent/Incongruent

When adding a “with psychotic features” specifier to depression or mania, the DSM-5 would mandate clinicians to differentiate “mood congruent” from “mood incongruent.” In a depression context, mood congruent psychosis might translate to, say, irrational feelings of deserved punishment. A manic context might involve delusions of a special relationship to a deity.

Mood incongruent, by contrast, involves no apparent linkage between mood and disordered thinking.

The current DSM buries this distinction way back in Appendix C. Moving this up front and center is a major step forward. But will clinicians have to flip to the back pages to find the definitions?

Grade: B.

How Psychotic is Psychotic?

We know we can have a mood disorder “with psychotic features.” What is unclear is whether we can have a mood disorder with full-blown psychosis. Or is that something else? Say schizophrenia or schizoaffective disorder?

Misinterpreting psychosis leaves no room for error, as a diagnosis of schizophrenia sends (very wrongly) a clear message to abandon all hope.

Grade: F.

Schizoaffective Disorder

The DSM-5 spells it out: “The current DSM-IV-TR diagnosis schizoaffective disorder is unreliable.”

To start, the current DSM classifies schizoaffective under “Schizophrenia and Other Psychotic Disorders,” but is this the right place to put it?

Too often, schizoaffective is employed as a glorified NOS diagnosis by clinicians who can’t decide whether their patient has bipolar or schizophrenia. As Goodwin and Jamison and others point out, the current DSM leaves wide room for mutually exclusive interpretations, such as:

A form of bipolar with psychosis, a form of schizophrenia with mood swings, co-occurring schizophrenia and bipolar, a separate illness, or a different phenomenon entirely occupying the psychosis spectrum.

Just to make things more confusing, a patient may appear to have schizophrenia during one phase of his or her life and bipolar in another.

So how would the DSM-5 fix a diagnosis it regards as “unreliable”?

“We recommend the following, minor change in the text ..."

A MINOR textual change? Is that it? Yes, apparently.

Grade: F-minus.

More to come ...