TY - JOUR
T1 - Alterations in sleep polygraphy after neuroleptic withdrawal
T2 - A putative supersensitive dopaminergic mechanism
AU - Thaker, Gunvant K.
AU - Wagman, Althea M.
AU - Kirkpatrick, Brian
AU - Tamminga, Carol A.
N1 - Funding Information:
From the Maryland Psychiatric Research Center, Department of Psychiatry. School of Medicine, University of Maryland at Baltimore, Baltimore, MD. Supported in part by NIMH Grants R03 MH40641-01, R01 MH37073-OlA1 and MH35996. Address reprint requests to Dr. G. K. Tbaker. Maryland Psychiatric Research Center. P.O. Box 21247. Baltimore. MD 21228. Received December 8, 1986: revised February 29, 1988.
PY - 1989/1/1
Y1 - 1989/1/1
N2 - Although a number of studies have reported sleep disturbances following neuroleptic withdrawal, a full description of such changes in sleep architecture is not available. Polysomnographic, plasma prolactin, and clinical measurements were carried out in a small number of patients on chronic neuroleptic treatment and after drug withdrawal. Preliminary findings show that in these chronically treated schizophrenic patients with and without tardive dyskinesia (TD), abrupt neuroleptic withdrawal induces reductions in total sleep, rapid eye movement (REM) sleep, and plasma prolactin. Furthermore, an increase in delta sleep was observed only in patients without TD. The REM suppression occurred significantly earlier in TD patients compared to the non-TD schizophrenic patients. These changes were transient, and both sleep measures and plasma prolactin stabilized during the 2-4 weeks after withdrawal to levels somewhere between the values observed during chronic treatment and withdrawal (week 1) periods. As the withdrawalinduced exaggerated changes mimicked the dopamine agonist effect on these sleep and hormonal measures, one can hypothesize that the observed changes are due to unmasking of supersensitive dopamine receptors following drug cessation. Normalization of these receptors and/or adaptational changes in other nondopaminergic system(s) can hypothetically explain the eventual stabilization of these measures during the following weeks.
AB - Although a number of studies have reported sleep disturbances following neuroleptic withdrawal, a full description of such changes in sleep architecture is not available. Polysomnographic, plasma prolactin, and clinical measurements were carried out in a small number of patients on chronic neuroleptic treatment and after drug withdrawal. Preliminary findings show that in these chronically treated schizophrenic patients with and without tardive dyskinesia (TD), abrupt neuroleptic withdrawal induces reductions in total sleep, rapid eye movement (REM) sleep, and plasma prolactin. Furthermore, an increase in delta sleep was observed only in patients without TD. The REM suppression occurred significantly earlier in TD patients compared to the non-TD schizophrenic patients. These changes were transient, and both sleep measures and plasma prolactin stabilized during the 2-4 weeks after withdrawal to levels somewhere between the values observed during chronic treatment and withdrawal (week 1) periods. As the withdrawalinduced exaggerated changes mimicked the dopamine agonist effect on these sleep and hormonal measures, one can hypothesize that the observed changes are due to unmasking of supersensitive dopamine receptors following drug cessation. Normalization of these receptors and/or adaptational changes in other nondopaminergic system(s) can hypothetically explain the eventual stabilization of these measures during the following weeks.
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U2 - 10.1016/0006-3223(89)90149-2
DO - 10.1016/0006-3223(89)90149-2
M3 - Article
C2 - 2563233
AN - SCOPUS:0024534396
SN - 0006-3223
VL - 25
SP - 75
EP - 86
JO - Biological Psychiatry
JF - Biological Psychiatry
IS - 1
ER -