Attempted use of haloperidol in the treatment of L-dopa induced dyskinesias

Abstract

SYNOPSIS Haloperidol was used in 12 patients in an attempt to improve L-dopa induced dyskinesias. In eight patients any improvement in dyskinesias was associated with increased Parkinsonism. In four patients the dyskinesias initially improved without clinical deterioration. Within several weeks, however, the disability due to Parkinsonism increased in these four patients as well. These observations suggest that long term haloperidol does not effectively decrease L-dopa induced dyskinesias without worsening Parkinsonism.

Metoclopramide and pimozide in Parkinson's disease and levodopa-induced dyskinesias.

“…Drugs which block dopamine receptors, such as phenothiazines or butyrophenones, reverse the anti-Parkinsonism effect of levodopa and abolish levodopa-induced involuntary movements (Klawans and Weiner, 1974). In this study pimozide was quite potent in its ability to increase Parkinsonism and abolish levodopainduced involuntary movements, an effect similar to that of haloperidol (Klawans and Weiner, 1974).…”

“…The choreiform and dystonic involuntary movements commonly produced by levodopa are probably due to a central dopaminergic effect and are readily abolished by drugs known to block dopamine receptors (Klawans and Weiner, 1974). The effect of metoclopramide on levodopainduced involuntary movements should therefore serve as an additional index of central antidopaminergic effect.…”

The pharmacological therapeutic management of levodopa-induced dyskinesias in patients with Parkinson’s disease

“…D2 antagonists, such as neuroleptics, can fully suppress dyskinesias, but this results in a concomitant and unacceptable suppression of antiparkinsonian response to levodopa [42,80]. Thus these drugs are unsuitable for the treatment of dyskinesia in parkinsonian patients.…”

The synaptic significance of metoclopramide induced dyskinetic-dystonic head and neck movements in pregnancy

“…In chronic administration it produces acute dyskinesias but does not produce parkinsonism [7,8]; 2. the extrapyramidal side-effects appear in usual doses and not in high doses as demanded by the phenothiazines [57]; 3. MP fails to worsen parkinsonism [53] as is the case with antipsychotics [31]; 4. failure to reverse levodopa induced involuntary movements [54] as opposed to antipsychotics [31]; 5. amino-oxyacetic acid (AOAA) which increases the gammaamino-butyric acid (GABA) concentration [58] antagonises the effects of neuroleptics on the striatal DA metabolism [2] but does not alter the MP induced increases in striatal HVA concentration; 6. MP has no antipsychotic activity, a property apparently associated with the DRB effect in the mesolimbic area [57] as do neuroleptics [3].…”