Abstract
Tardive dyskinesia (TD) is thought to result from nigrostriatal dopaminergic supersensitivity secondary to prolonged neuroleptic exposure. Preclinical studies have demonstrated that the opiate antagonist naloxone can acutely reverse a haloperidol-induced hyperdopaminergic state. In a trial of high-dose naloxone, 20 patients with TD received i.v. naloxone (20 mg, 40 mg, and placebo) under double-blind conditions. At baseline and at regular postdrug intervals, patients were evaluated using a battery of motor, clinical, and neuropsychological measures to study effects on neurological, behavioral, and cognitive functions. There was a significant improvement in involuntary movements at 30 min postnaloxone, together with improvement in clinical ratings at that time point, as well as some cognitive changes. The implications of these findings for the putative functional relationship between dopaminergic and enkephalinergic systems in the nigrostriatal area are discussed.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 19-28 |
| Number of pages | 10 |
| Journal | Psychiatry Research |
| Volume | 26 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1988 |
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Keywords
- involuntary movements
- naloxone
- psychiatric symptoms
- Tardive dyskinesia
ASJC Scopus subject areas
- Psychiatry and Mental health
- Biological Psychiatry
- Psychology(all)
Cite this
High-dose naloxone in tardive dyskinesia. / Lindenmayer, Jean Pierre; Gardner, Eliot; Goldberg, Elkhonon; Opler, Lewis A.; Kay, Stanley R.; van Praag, Herman M.; Weiner, Michelle; Zukin, R. Suzanne.
In: Psychiatry Research, Vol. 26, No. 1, 1988, p. 19-28.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - High-dose naloxone in tardive dyskinesia
AU - Lindenmayer, Jean Pierre
AU - Gardner, Eliot
AU - Goldberg, Elkhonon
AU - Opler, Lewis A.
AU - Kay, Stanley R.
AU - van Praag, Herman M.
AU - Weiner, Michelle
AU - Zukin, R. Suzanne
PY - 1988
Y1 - 1988
N2 - Tardive dyskinesia (TD) is thought to result from nigrostriatal dopaminergic supersensitivity secondary to prolonged neuroleptic exposure. Preclinical studies have demonstrated that the opiate antagonist naloxone can acutely reverse a haloperidol-induced hyperdopaminergic state. In a trial of high-dose naloxone, 20 patients with TD received i.v. naloxone (20 mg, 40 mg, and placebo) under double-blind conditions. At baseline and at regular postdrug intervals, patients were evaluated using a battery of motor, clinical, and neuropsychological measures to study effects on neurological, behavioral, and cognitive functions. There was a significant improvement in involuntary movements at 30 min postnaloxone, together with improvement in clinical ratings at that time point, as well as some cognitive changes. The implications of these findings for the putative functional relationship between dopaminergic and enkephalinergic systems in the nigrostriatal area are discussed.
AB - Tardive dyskinesia (TD) is thought to result from nigrostriatal dopaminergic supersensitivity secondary to prolonged neuroleptic exposure. Preclinical studies have demonstrated that the opiate antagonist naloxone can acutely reverse a haloperidol-induced hyperdopaminergic state. In a trial of high-dose naloxone, 20 patients with TD received i.v. naloxone (20 mg, 40 mg, and placebo) under double-blind conditions. At baseline and at regular postdrug intervals, patients were evaluated using a battery of motor, clinical, and neuropsychological measures to study effects on neurological, behavioral, and cognitive functions. There was a significant improvement in involuntary movements at 30 min postnaloxone, together with improvement in clinical ratings at that time point, as well as some cognitive changes. The implications of these findings for the putative functional relationship between dopaminergic and enkephalinergic systems in the nigrostriatal area are discussed.
KW - involuntary movements
KW - naloxone
KW - psychiatric symptoms
KW - Tardive dyskinesia
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U2 - 10.1016/0165-1781(88)90083-2
DO - 10.1016/0165-1781(88)90083-2
M3 - Article
VL - 26
SP - 19
EP - 28
JO - Psychiatry Research
JF - Psychiatry Research
SN - 0165-1781
IS - 1
ER -