In considering the potential nosological impact of emerging findings about substance-induced psychotic disorder or difficulties in distinguishing “substance-induced” from “independent” psychoses, it is important to recall that clinical challenges in diagnosis or new etiological findings have no straightforward relationship to amending the diagnostic system, itself. The difficulties in distinguishing substance-induced from independent psychotic symptoms are hardly new and were well known to framers of DSM-III
, and DSM-IV
criteria. The current guidelines embody the thinking of previous workgroups on the optimal way of handling these issues. Likewise, the impact of drug use on etiology of schizophrenia is one of many factors contributing to the disorder, and the general policy of the DSM
(International Classification of Diseases
) systems is to base diagnostic groupings on phenomenology of disorders and not on causes, given the lack of definitive knowledge about causes of any of the major mental disorders.16
If changes are to be made in DSM-IV related to comorbid psychotic disorders and SUDs, these can take place at several different levels including (a) rearrangement of groups of disorders (eg, subsuming SUDs, eating disorders, and impulse control disorders under a general category of “Addictions” or “Impulse Control Disorders”), (b) adding or deleting a diagnostic category, (c) changing diagnostic criteria, or (d) changing textual guidelines for determining the presence or absence of criteria. Response to the problems of differentiating substance-induced vs independent disorders would most likely be in the text or in the criteria for specific substance-induced syndromes. Changes made on the basis of emerging findings about enduring psychoses caused by drug abuse could be at the syndrome level (eg, adding a “cannabis-induced enduring psychosis” diagnosis) or in the text describing characteristics of disorders.
To inform the diagnostic decision between substance-induced and independent psychotic symptoms, 2 kinds of information would be useful: (a
) identification of early markers that clearly differentiate the 2 conditions and (b
) more precise information about the duration of substance-induced psychotic symptoms. At present, the most definitive method for making this distinction is longitudinal assessment after a period of sustained abstinence from psychoactive substances. This is time consuming and often impractical given the relapsing nature of substance abuse and limited access to inpatient care. First, more rapid diagnosis could be facilitated by the identification of “markers” or distinctive clinical features that would identify patients with psychotic symptoms as having transient, substance-induced syndromes or enduring independent disorders. Such markers might take the form of biological indices (eg, a genetic profile suggesting schizophrenia), symptom profiles, or features of the psychiatric history. Recent works by Caton and colleagues17
and C. L. M. Caton, D. S. Hasin, P. E. Shrout, R. E. Drake, B. Bominguez, S. Samet, B. Shanzer (unpublished data) illustrate this approach. In a sample of 319 treatment-entering patients with psychosis and SUDs, reevaluation at 1-year follow-up revealed that 25% of psychotic diagnoses that had originally been designated as substance-induced were reclassified as independent. At initial evaluation, the reclassified patients differed from those with transient psychoses by being more likely to report parental mental illness, having poorer premorbid adjustment, and having less insight into their psychosis. Second, more definitive information could be gathered on the duration of substance-induced psychotic symptoms and syndromes. Numerous studies have evaluated characteristics and course of stimulant-induced psychosis,13,18–21
but less is known about the time course of transient psychotic syndromes resulting from use of other classes of drugs or from polysubstance abuse. At present, for purposes of differential diagnosis, “sustained” remission is considered to be around 4 weeks of abstinence. Conceivably, this duration of abstinence may be too short for psychoses induced by some substances (eg, cannabis or hallucinogens) or too long for those induced by others (eg, benzodiazepines).
Recent evidence suggesting that cannabis use may contribute as a cause of “schizophrenia” diagnosis14
could have an important impact on the understanding of psychotic illnesses and on the system for classifying these illnesses. From a practical, clinical standpoint, intervening with teenage marijuana use could prevent the development of a full psychotic syndrome in susceptible individuals. Such a preventive substance abuse intervention could be coupled with early antipsychotic pharmacotherapy to intervene in the “prodromal” period of schizophrenia or other psychotic conditions.22
For understanding etiology, research on mechanisms of cannabis effects may point to neurobiological pathways underlying vulnerability to schizophrenia. Nosological changes that might be made on the basis of these findings would require considerably more evidence than is currently available. For example, enduring psychotic syndromes associated with prior cannabis use may constitute disorders that are distinctly different from what is now called “schizophrenia” and that would warrant classification as separate disorders. Delineation of such a syndrome (or syndromes) would require a considerable body of work documenting diagnostic distinctiveness, course, symptom features, and other types of evidence articulated by Robins and Guze5
for defining psychiatric disorders. Alternatively, the concept of schizophrenia that is “caused” by cannabis use suggests the possibility of designating subtypes of psychotic disorders on the basis of differing etiological factors, which could include genetic, developmental, or other causes.