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NEUROSCIENCE OF PSYCHOACTIVE SUBSTANCE USE AND DEPENDENCE

al., 1987), this may reflect diminished need to self-medicate negative
symptoms with cigarette smoking after the more efficacious treatment of
these symptoms with atypical antipsychotics. This may also be related to the
fact that atypical antipsychotics do not stay on the dopamine D2 receptor as
long as do the traditional neuroleptics, thereby allowing more physiological
dopamine transmission (Kapur & Seeman, 2001). Thus atypical antipsychotics
do not have as many side-effects, and the need for nicotine to reduce these
side-effects is decreased. Taken together, the above results suggest that
nicotine has a beneficial effect on negative symptoms in patients with
schizophrenia, and this effect may be one of the reasons why these patients
smoke excessively. The most likely neurobiological mechanism for this effect
is the increase in dopaminergic and cholinergic function in the brain. Further
research on this subject is necessary to determine the exact mechanisms that
will provide insight into the etiology and treatment of both schizophrenia
and nicotine dependence.
Although the available clinical data do not offer support for one versus
the other two interpretations for reduced smoking with atypical antipsychotic
medications, such findings have led to promising speculations that these
medications “may play a unique role in the treatment of substance-using
patients with schizophrenia” for reasons that are poorly understood (Wilkins,
1997; Krystal et al., 1999; McEvoy, Freudenreich & Wilson, 1999). In addition,
as indicated above, patients with schizophrenia may smoke for improvement
in all three domains, that is negative symptoms, cognitive deficits, and
extrapyramidal side-effects induced by neuroleptic medications. Finally, it
must be emphasized that the degree of comorbidity between smoking and
schizophrenia will also depend on the levels of smoking in the general
population of a given country. Comparative international studies are needed
to clarify the relative role of neurobiology and environment on comorbidity
between smoking and schizophrenia.

Psychostimulant (cocaine and amphetamine) dependence and
schizophrenia
There is a high degree of comorbidity between schizophrenia and
psychostimulant use in countries with high high rates of cocaine and
amphetamine use. Psychostimulant use is 2–5 times higher among patients
with schizophrenia compared with the general population, and more
prevalent than in other psychiatric populations (LeDuc & Mittleman, 1995).
It was estimated that 19–50% of patients with schizophrenia use
psychostimulant drugs (Cuffel, 1992; Ziedonis et al., 1992; LeDuc &
Mittleman, 1995; Patkar et al., 1999). Interestingly, however, patients with
schizophrenia appear to prefer psychostimulants to psychoactive
substances with sedative properties, such as opiates, barbiturates and
alcohol (Schneier & Siris, 1987; Dixon et al., 1990; Mueser et al., 1990).
Certain symptoms of psychostimulant withdrawal also resemble the

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