Quantitative morphology of the caudate and putamen in patients with cocaine dependence.

OBJECTIVE Deficits in dopaminergic function may contribute to hypertrophy of striatal structures associated with typical neuroleptic treatment. In light of a body of research that has associated chronic cocaine use with extrapyramidal symptoms and striatal dopaminergic depletion, the authors looked for evidence of striatal dysmorphology in patients with chronic cocaine dependence. METHOD Caudate, putamen, and total brain volumes were quantified by means of magnetic resonance imaging in 25 cocaine-dependent and 20 healthy subjects. RESULTS Normalized caudate and putamen volumes were 3.40% and 9.18% larger, respectively, in the cocaine-dependent subjects. CONCLUSIONS These observations suggest that deficits in dopaminergic function associated with cocaine dependence may contribute to striatal hypertrophy.

[1]  M. Kreek,et al.  Chronic administration of a cocaine "binge" alters basal extracellular levels in male rats: an in vivo microdialysis study. , 1995, The Journal of pharmacology and experimental therapeutics.

[2]  L. Bauer.  Resting hand tremor in abstinent cocaine-dependent, alcohol-dependent, and polydrug-dependent patients. , 1996, Alcoholism, clinical and experimental research.

[3]  M. Gold,et al.  Neurotransmitter and neuroendocrine abnormalities associated with cocaine use. , 1985, Psychiatric medicine.

[4]  N. Volkow,et al.  Cerebral Blood Flow in Chronic Cocaine Users: A Study with Positron Emission Tomography , 1988, British Journal of Psychiatry.

[5]  G. E. Alexander,et al.  Parallel organization of functionally segregated circuits linking basal ganglia and cortex. , 1986, Annual review of neuroscience.

[6]  G. Paxinos,et al.  Distribution of catecholamine uptake sites in human brain as determined by quantitative [3H] mazindol autoradiography , 1991, The Journal of comparative neurology.

[7]  G. Bartzokis,et al.  Choreoathetoid movements in cocaine dependence , 1999, Biological Psychiatry.

[8]  J. Fleiss.  The design and analysis of clinical experiments , 1987 .

[9]  Gorelick Da.  Alcohol and cocaine. Clinical and pharmacological interactions. , 1992 .

[10]  W. Brady,et al.  Cocaine-associated dystonic reaction. , 1997, The American journal of emergency medicine.

[11]  S. J. Gatley,et al.  Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects , 1997, Nature.

[12]  A. Levey,et al.  Striatal dopamine, dopamine transporter, and vesicular monoamine transporter in chronic cocaine users , 1996, Annals of neurology.

[13]  Faith M. Gunning-Dixon,et al.  Differential aging of the human striatum: a prospective MR imaging study. , 1998, AJNR. American journal of neuroradiology.

[14]  R. Fisher,et al.  Alterations in the Spontaneous Release of Dopamine and the Density of the DA D2 Receptor mRNA After Chronic Postnatal Exposure to Cocaine , 1997, Brain Research Bulletin.

[15]  E. Attig,et al.  Cocaine induced chronic tics. , 1994, Journal of neurology, neurosurgery, and psychiatry.

[16]  Jagath C. Rajapakse,et al.  Quantitative Magnetic Resonance Imaging of Human Brain Development: Ages 4–18 , 1996 .

[17]  N C Andreasen,et al.  Change in basal ganglia volume over 2 years in patients with schizophrenia: typical versus atypical neuroleptics. , 1999, The American journal of psychiatry.