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

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 muscarinic receptor antagonist tropicamide suppresses tremulous jaw movements in a rodent model of parkinsonian tremor: possible role of M4 receptors

“…Degeneration of nigrostriatal dopamine (DA) neurons is a major neuropathological feature of idiopathic Parkinson's disease (Bergman and Deuschl 2002;Marsden et al 1975). Moreover, parkinsonian symptoms also can be induced or exacerbated by various drugs, including DA antagonists and DA-depleting agents that are used as antipsychotic drugs McEvoy 1983;Tarsy et al 1975Tarsy et al , 2002. Although idiopathic parkinsonism typically is treated by drugs that stimulate DA tone (Lang and Lees 2002a, b;Mailman et al 2001;Pogarell et al 2002), current models of basal ganglia function indicate that parkinsonian symptoms are produced by neurochemical interactions involving several transmitters in various parts of basal ganglia circuitry (Delong 1990;Hauber 1998;Obeso et al 2000;Young and Penney 1993;Finn et al 1997b;Wichmann et al 2001;Trevitt et al 2002;Carlson et al 2003;Correa et al 2003Correa et al , 2004Wisniecki et al 2003;Simola et al 2004).…”

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].…”