DSM-5 and Psychosis: Hopes and Limitations

There has been a lot of recent press regarding the National Institute of Mental Health (NIMH) and its research vision. Dr. Thomas Insel, the director of NIMH has recently come out explaining that the NIMH will no longer utilize the Diagnostic and Statistical Manual of Mental Disorders (DSM) when conducting further research. He clarified those remarks in a subsequent joint statement with the president-elect of the American Psychiatric Association (APA), Jeffrey Lieberman.

While that long term process is developing, we are left with the imperfect descriptive system that is the DSM. What follows is my brief take on the historical roots of the DSM as a diagnostic framework in the area of psychosis, and key changes that have been made for this version, the DSM-5, which is due out on May 18, in areas of importance to NAMI members.

The DSM system is designed to produce reliable diagnoses that hold up on different days and across different practitioners. This path to organize symptoms, which impact research, payment and services, isn’t driven by a corresponding neurobiology, however; the field simply does not have the capacity to do that yet. Perhaps Dr. Insel’s researchers can help us get there in the not too distant future. For now though, collecting symptoms into syndromes, a diagnosis can offer some insight into some of the elements of a recovery plan. Pragmatists know that DSM is the only game in town right now to inform clinical practice and research as the underlying work to develop biological roots to diagnosis is years or even decades away.  

A Brief History on Diagnosis

I find it helpful to think about the roots of descriptive psychiatry in the area of psychosis. The work of Emil Kraeplin a German psychiatrist in the 1890s forms the base of our modern day symptom driven framework. His work focused on the course of people who came to a hospital with psychosis. He first organized his framework by interviewing any hospitalized patients who presented symptoms of psychosis. After years of observation, he organized these presentations of psychosis into what we now call schizophrenia and bipolar disorder (his pioneering terms were dementia praecox and manic depressive insanity, respectively).

Kraeplin, like his colleague Alois Alzheimer, focused on cognitive problems at different stages of life. Dementia praecox translates to precocious dementia and was the way Kraeplin first thought of what we now call schizophrenia. Kraeplin’s young patients weren’t demented per se—they could often recall facts and know the date, time and place—but they did have issues with memory and other thinking functions. Interestingly, a recent intervention called cognitive enhancement therapy (CET) has shown potential to improve cognition in people with schizophrenia, thus validating Kraeplin’s original interpretation of the condition. He was a keen observer, and Kraeplin believed we would someday unlock the underlying neuroscience that he was observing in people.

Changes Coming to the DSM

One key change in the area of schizophrenia is that DSM-5 has deleted all the subtypes of schizophrenia. This is a logical choice to me as I did not feel that the symptoms were distinct enough to make these more precise diagnoses. I didn’t find the subtypes to be helpful in informing care and they didn’t add to the person’s understanding of their experience. The DSM-5 replaces these widely ignored subtypes in schizophrenia with a dimensional system that looks at different important areas (such as positive symptoms, negative symptoms and cognition). While I haven’t used these dimensions yet, I am hopeful that a more detailed description of what people are actually experiencing will result in more helpful treatment for an individual over time. The description of symptoms is of course imperfect but better descriptions in this dimensional concept are likely to make incremental progress in getting people better care.

Gene studies have shown us that these conditions may be more biologically related that we have previously thought. Schizoaffective disorder for example, is an under-researched diagnosis that encompasses symptom elements both of schizophrenia and of bipolar disorder. It represents a clinically observed but biologically elusive overlap in the original Kraeplin system of diagnosis. There was talk initially of eliminating the diagnosis from the DSM-5, which alarmed me given its prevalence. In the end, the DSM-5 includes a more longitudinal view of symptoms in the diagnosis of schizoaffective disorder as opposed to a more point in time symptom description for the condition. Given that schizophrenia and bipolar disorder are also best understood over years this change makes good sense to me as a clinician. Recovery is a long term process so it makes sense that this diagnosis is similarly understood over time.

There is a growing interest in the field on earlier intervention in psychosis in order to get people help sooner. The APA studied whether it was possible to identify people earlier in their course, who may go on to develop schizophrenia. The proposed diagnostic concept was first called risk syndrome and later, attenuated psychosis. This is a controversial area of inquiry as overlooking people with this issue presents risks and so does over-identifying people. This remains an important question as we do know from the research and our own survey of people with schizophrenia that it can take nine years on average to get a diagnosis from the onset of symptoms in our current world. This delay adds suffering and missed opportunities to accelerate recovery for people who develop schizophrenia. Proponents of an attenuated psychosis diagnosis cite non-medication (and side effect free) strategies that have been shown to be helpful, and made comparisons to the earlier and helpful diagnosis of hypertension in medicine. On the other hand, psychiatric diagnosis unfortunately can come with a price in society and it is also important not to label something that won’t develop into a bona fide illness process.

The field trial team of the DSM tried to see if they could make this work—if attenuated psychosis could identify young people who were first hearing voices or who had paranoid thoughts to inform who would go on to have a later psychosis diagnosis like schizophrenia. The field trials showed that the proposed diagnosis of Attenuated Psychosis did not accomplish both key tasks of identifying people at risk and not identifying people who were not. The idea of attenuated psychosis as a diagnosis is therefore in the “needs further study” area of the DSM-5 and is not a reimbursable diagnosis. Formal diagnosis or not, I encourage people who are having early symptoms of psychosis to get assessment and help—many of the psychotherapy strategies have shown good results with no downside. There is a national movement to provide services to young adults and teens that are having early psychosis symptoms and information on these ideas and programs is available at www.nami.org/psychosis. I work at such a program in Boston called PREP and I love my time there.

This is a humbling line of work and the DSM-5 reflects that. It doesn’t surprise me that understanding the human brain is going to offer many more challenges than say, blood pressure. We don’t know precisely how our treatments work at the neurobiological level but it is quite helpful to know that they often do work. How exactly does cognitive enhancement therapy or lithium work? We simply cannot say after offering some reasonable hypotheses. I take comfort that this was the state of the field of infectious disease for decades after the advent of antibiotics. The field of medicine knew they worked but we didn’t know why. Thousands if not millions of lives were saved along the way without any detailed knowledge of the underlying process of action. In psychiatry, we need to do both—look for true biological underpinnings for diagnosis and for the linked treatment that will follow, and work to improve knowledge and care now to serve people better today.