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Fraser Trevor Fraser Trevor Author
Title: Evidence of Dopamine Deficiency in Cocaine Addicts
Author: Fraser Trevor
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Illustration of the Parkinson disease by Sir William Richard Gowers from A Manual of Diseases of the Nervous System in 1886 showing the...
Illustration of the Parkinson disease by Sir W...
Illustration of the Parkinson disease by Sir William Richard Gowers from A Manual of Diseases of the Nervous System in 1886 showing the characteristic posture of PD patients (Photo credit: Wikipedia)
Dackis and Gold (1985) have postulated that chronic use of cocaine
appears to lead to dysregulation of brain dopaminergic systems. This
hypothesis is clinically supported by preliminary findings showing a
lasting decrease in dopamine (DA) in the brains of cocaine addicts
(Wilson et al. 1992) and reported hyperprolactinemia (Dackis and
Gold 1985; Mendelson et al. 1988). More recent studies showed
multiphasic changes in prolactin release that are temporally correlated
with different phases of cocaine abstinence: High plasma prolactin
levels were observed during the immediate abstinence (crash) phase,
reduced levels during early withdrawal, and modestly increased levels
during the later phases of withdrawal (Gawin et al. 1993). Deficiency
of dopaminergic functions in cocaine abusers is suggested by
observed reduced uptake of dopa to presynaptic dopamine neurons in
the striatum (Baxter et al. 1988), and by decrease of dopamine type 2
(D2) receptor density in the cerebral cortex measured by PET
(Volkow et al. 1993). Moreover, the incessant hypodopaminergia
accompanied by possible lesions in basal ganglia are implicated in
chronic cocaine abusers by persistent extra-pyramidal symptoms
including dystonic and choreoathetoid movements, tics, and increased
resting hand tremor, resembling those manifestations seen in
Parkinson's disease (Bartzokis et al., this volume; Bauer 1993, this
volume; Daras, this volume).
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