Overall, it is clear that substance use disorders in persons diagnosed with schizophrenia occur more frequently than in the general population; however, there is little evidence to suggest that persons with schizophrenia abuse substances for different reasons than the general population. Specifically, the literature demonstrates that patients with schizophrenia do not differentially choose to abuse specific drugs to ameliorate specific psychic states (e.g., anhedonia). Multiple studies also indicate that patients with schizophrenia do not preferentially abuse certain agents, nor does choice of agent correlate with extent of psychopathology; rather, these individuals use those substances most available and affordable (Cantor-Graae et al. 2001; Chambers et al. 2001; Lambert et al. 1997; Mueser et al. 1992). For the most part, research has also failed to find patterns of drug choice in persons with schizophrenia that differ from groups of patients with other major mental disorders. Thus, although the causes of dysphoria in schizophrenia may be linked to the illness (e.g., neuroleptic side effects, negative symptoms, demoralization), data simply do not support the notion that schizophrenic patients uniquely prefer certain drugs.
Evidence for the hypothesis that patients with schizophrenia do not abuse substances to alleviate certain mental states or medication side effects comes from research focusing on patients' reported reasons for substance use, which suggests that persons with schizophrenia abuse drugs for reasons that are similar to those for persons without schizophrenia (i.e., to get high, to feel better, to escape, and to be less depressed) (Dixon et al. 1991). The research on side effects and substance has generally produced mixed results when investigators examined tardive dyskinesia or other measures of extrapyramidal side effects; however, although Salyers and Mueser (2001) found no correlation between akathisia and extent of substance use, both akathisia and related dysphoria have been found in some studies to be associated with current alcohol use and increased risk of future alcohol use (Duke et al. 1994; Voruganti et al. 1997).
One of the better examples of research into reasons for substance use in schizophrenia is the study by Dervaux and colleagues of 100 patients diagnosed with schizophrenia, whose extent of substance use was assessed by diagnostic interview (Dervaux et al. 2001). Other assessment tools in this study included the Positive and Negative Symptom Scale (PANSS), self-report measures of impulsivity and sensation seeking, and a self-report measure of anhedonia. Forty-one percent of this cohort met lifetime criteria for substance abuse or dependence, but did not differ from the nonabusing patients with schizophrenia on the basis of ratings of anhedonia, or in symptom severity (as rated by PANSS). Interestingly, this study did not find differences between users and nonusers on the basis of age of first psychiatric contact or number of hospitalizations. Nonetheless, the substance abusers rated significantly higher on the measures of impulsivity and sensation seeking in a manner consistent with nonschizophrenic substance users; moreover, these measures were elevated even among the subgroup reporting only past abuse or dependence, leading the authors to suggest that impulsivity and drug-seeking behavior may not be induced by the use of substances, but rather is an inherent aspect of schizophrenia. It should be noted that some studies have found higher reported rates of depression among substance-using schizophrenics (Hambrecht and Hafner 2000), although others have not replicated this finding (Drake et al. 1989; Mueser et al. 1990).
Other observational data lend credence to the hypothesis that addictive behavior occurs independently as an inherent aspect of the neural abnormalities that contribute to schizophrenia, as opposed to being motivated or driven secondarily by symptoms of the disorder or negative psychic states induced by medication. A review of the literature on the biological basis for substance abuse in schizophrenia noted that some individuals do report symptomatic improvement during substance use, yet others note symptom exacerbation but persist in the use of substances (Chambers et al. 2001). Moreover, self-reports of improvement are often at variance with the clinical observation of symptomatic worsening. In addition, substances of abuse have widely divergent effects on neurotransmitters, weakening the assertion that the concurrent use of agents with opposing effects is intended to ameliorate a specific psychic state.
Another observation suggesting that schizophrenia and addictive behavior are independent manifestations of a common underlying dysregu-lation of neural circuitry is the finding that use of both drugs and alcohol commonly precedes psychosis, and that 77% of first-episode patients are smokers prior to neuroleptic treatment (Chambers et al. 2001). This relationship between substance use and symptom onset is thus an area of intense scrutiny for those who see the predilection toward psychosis and addictive behavior as independent but parallel processes engendered by common neuropsychiatric deficits.
In the literature review cited earlier, Cantor-Graae and colleagues noted two questions involving schizophrenia and substance use that are not clearly answerable with the current body of data. The first is "the extent to which substance use (especially psychoactive substance use) contributes to the development of schizophrenia, whether as an independent risk factor in itself or by precipitating illness onset in vulnerable individuals" (Cantor-Graae et al. 2001, p. 72).
Because substance use, particularly psychotomimetic agents (e.g., hallucinogens) and stimulants, may increase the likelihood of developing psychosis, investigators have examined this issue to determine the course of substance use in relation to onset of psychosis. To assess the temporal sequence of substance abuse and illness onset, Buhler and colleagues performed a structured interview on 232 first-episode patients with schizo phrenia, and then prospectively interviewed and followed another sample of 115 first-episode patients representing 86% of consecutive admissions for admissions in the local area (Buhler et al. 2002). The investigators found that 62% of those with drug abuse and 51% with alcohol abuse began their habit before any signs of the illness were manifest, including prodromal nonpsychotic symptoms. Significantly, there was no correlation found between onset of abuse and onset of psychotic symptoms, although it was noted that the onset of abuse and the psychotic disorder occurred in the same month in 18.2% who abused alcohol and 34.6% who used drugs, implying that there may be a subset of schizophrenia patients whose development of psychotic symptoms were speeded or precipitated by substance use, particularly cannabis use. These data from the combined pools of first-episode patients are similar to those reported for the original group of 232 first-episode patients analyzed separately (Hambrecht and Hafner 2000), in which 27.5% had a cannabis use problem more than 1 year (often more than 5 years) before onset of prodromal schizophrenia symptoms, 34.6% had the onset of symptoms and cannabis use in the same month, and in 37.9% symptoms of schizophrenia preceded substance use. As the genetics of the schizophrenia spectrum are elucidated, the role that substances play in the onset of schizophrenia among individuals with varying biological propensities will become clearer.
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