Long-term chlorpromazine in rhesus monkeys: Production of dyskinesias and changes in social behavior

McKinney, William T.; Moran, Elaine C.; Kraemer, Gary W.; Prange, Arthur J.

doi:10.1007/bf00433805

Cited by 26 publications

(8 citation statements)

References 12 publications

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“…Although not well established on the basis of existing data, there is a potentially more fundamental relationship between neuroleptic drug action and negative symptoms. Psychological and behavioral changes similar to negative symptoms (e.g., apathy, lack of spontaneity, and impaired affective arousal) have been induced in infrahuman primates (McKinney et al 1980; Carlson 1981; McKinney and Moran 1981) and nonpsychotic humans (Baldessarini 1980) by neuroleptic drugs. Furthermore, preclinical evidence suggests that the negative symptom-like effects of neuroleptic drugs cannot be simply ascribed to a generalized motor depression resulting from sedation.…”

Section: Treatment Of Secondary Negative Symptomsmentioning

confidence: 99%

Treatment of Negative Symptoms

Carpenter¹,

Heinrichs²,

Alphs³

1985

Schizophrenia Bulletin

493

172

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The rational treatment of the negative symptoms of schizophrenia requires a careful differentiation of those secondary to a range of other factors and those that constitute enduring primary or deficit symptoms. Secondary negative symptoms are usually responsive to treatment of the underlying cause. In contrast, there is no intervention currently available with established efficacy in treating deficit symptoms. These distinctions serve to reduce the heterogeneity of negative symptoms. A discussion of the diagnosis and treatment of the various forms of secondary negative symptoms is followed by suggestions for future research in the treatment of deficit symptoms.

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Section: Treatment Of Secondary Negative Symptomsmentioning

confidence: 99%

Treatment of Negative Symptoms

Carpenter¹,

Heinrichs²,

Alphs³

1985

Schizophrenia Bulletin

493

172

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“…Among other species of primates treated with haloperidol, TD has appeared in two of 21 rhesus (Bedard et al 1977;Paulson 1972Paulson , 1973, but not among 31 squirrel, eight green, or two iris monkeys (Casey et al 1980;Gunne and B~ir~iny 1976;Liebman and Neale 1980;Weiss and Santelli 1978). Chlorpromazine has been administered chronically to a total of 35 rhesus monkeys (Deneau and Crane 1969;Paulson 1972Paulson , 1973McKinney et al 1980), but only four (11%) displayed TD (McKinney et al 1980). The contention that TD was produced in the chlorpromazine-treated rhesus monkeys of Paulson (1972Paulson ( , 1973 is not tenable, because in those particular animals dyskinesias worsened after each injection and were not exacerbated by drug withdrawal.…”

Section: Discussionmentioning

confidence: 99%

Fluphenazine-induced acute and tardive dyskinesias in monkeys

Kovacic

Domino

1984

Psychopharmacology

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Five Cebus apella monkeys were treated with biweekly injections of fluphenazine enanthate (0.1-3.2 mg/kg IM). Three of these completed 1 full year of treatment, one injured its leg after 6 months of treatment and was killed, and another died of unknown causes after 9 months of treatment. All monkeys displayed abnormal movements corresponding to the early appearing extrapyramidal symptoms of neuroleptic-treated patients. These consisted initially of slowing or absence of volitional movement, trembling of the hands, trembling of the entire body, and general drowsy behavior. As treatment progressed, a variety of abnormal postures and movements appeared after each injection that were not exacerbated by drug withdrawal and, as tested at the end of the year, could be abolished or prevented with benztropine mesylate (0.2-0.5 mg/kg IM). The three monkeys that completed 1 year of treatment with fluphenazine were then withdrawn from the drug. After withdrawal, all three developed movements similar in appearance to those of patients with tardive dyskinesia (TD). Reinstitution of fluphenazine treatment, as tested in one monkey, abolished all movements resembling TD.

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“…Yet, because it is not convenient to administer neuroleptics to monkeys in the same way as given to humans (several times daily for many months), this is rarely the practiced drug regimen. Domino and Kovacic (1983), in fact, concluded that of 121 monkeys that have been given neuroleptics in several published studies, most developed only the acute dystonic or parkinsonism syndrome, and only 10 developed TD (some of those of Gunne and Barany, 1976;Bedard et al, 1977;McKinney et al, 1980). Kovacic and Domino (1984), Johansson (1989), and Gunne et al (1984) subsequently increased this sample, but the number of documented cases is clearly very low.…”

Section: Primate Studiesmentioning

confidence: 99%