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Biomedical subjects

D Tarsy

Publications and source records attributed to D Tarsy.

At least 55 records · Page 3Linked to original sources
PubMed1978

Withdrawal syndromes associated with antipsychotic drugs.

Withdrawal symptoms frequently follow abrupt discontinuation of antipsychotic compounds. In addition to other somatic symptoms, withdrawal-emergent dyskinesias may be observed. "Covert dyskinesia" refers to a masked form of tardive dyskinesia that becomes clinically detectable only after antipsychotic drugs are withdrawn or their dosage is reduced. Withdrawal dyskinesia appears under similar circumstances but disappears spontaneously in 6 to 12 weeks. Cholinergic overactivity and changes in dopamine-acetylcholine balance in the basal ganglia may underlie these withdrawal syndromes. The principal value of the concept of covert dyskinesia is in the secondary and tertiary prevention of tardive dyskinesia through early discovery and treatment.

Acetylcholine↗
PubMed1977

Unilateral asterixis associated with a mesencephalic syndrome.

Unilateral asterixis due to a focal brain lesion is a rare occurrence. Acute asterixis restricted to the left upper extremity appeared in a patient in association with signs of acute midbrain dysfunction, without changes in mental status or in the EEG, and in the absence of metabolic or toxic disturbance. Electromyography disclosed features typical of asterixis due to metabolic causes.

Brain Diseases↗
PubMed1977

Deanol acetamidobenzoate treatment in choreiform movement disorders.

Deanol acetamidobenzoate was administered in double-blind, crossover fashion with placebo to five patients with tardive dyskinesia, three patients with Huntington's chorea, and one patient with posthemiplegic chorea. No significant effect on dyskinesia was observed. Preliminary administration of physostigmine salicylate to patients with tardive dyskinesia had a variable effect, while benztropine mesylate produced no change. Since the status of deanol as an effective precursor of acetylcholine is uncertain, further trials with putative cholinergic agents remain warranted in choreiform syndromes.

Benztropine↗
PubMed1977

Plasma DOPA levels and growth hormone response to levodopa in parkinsomism.

It has been suggested that the therapeutic response to levodopa in patients with Parkinson's disease may be related to changes in plasma growth hormone concentration. In order to examine this problem, we have determined plasma DOPA and growth hormone levels after a standard oral levodopa load in 32 patients with Parkinson's disease. Levodopa caused an increase in plasma growth hormone concentration in 30 subjects. The magnitude and timing of this growth hormone response was not related to the clinical response, the presence or absence of response swings, or the occurrence of dyskinesias. The growth hormone response to levodopa is normal in patients with Parkinson's disease and not altered by long-term levodopa treatment.

Adult↗
PubMed1977

Tardive dyskinesia in young adults.

The authors describe two cases of tardive dyskinesia in which severe axial dystonia and intense facial grimacing produced marked discomfort as well as social and physical disability. Both patients experienced the onset of psychiatric symptoms as young adults, showed a prompt response to antipsychotic drug therapy, and were subsequently left on maintenance treatment for indefinite periods. The severity of this frequently irreversible and disabling condition warrants careful consideration in the use of long-term antipsychotic drug treatment in the young psychiatric outpatient population.

Adult↗
PubMed1977

The pathophysiologic basis of tardive dyskinesia.

The prolonged course of tardive dyskinesia (TD) associated with antipsychotic drugs suggests that permanent structural alterations of the brain occur, though neurohistopathological studies have provided little to support this view. An alternative view is that functional adaptive changes may account for the manifestations of TD. A currently popular hypothesis is that there may be a functional excess in the activity of dopamine (DA) as a synaptic neurotransmitter in the basal ganglia. A cholinergic mechanism has also been implicated in TD, but the clinical effects of acetylcholine agonists and antagonists in TD are variable. In animals, nigrostriatal neurons respond to the blockade of DA synapses by treatment with antipsychotic agents in several ways, including acute and transient increases in the turnover of DA, and more slowly evolving "disuse" supersensitivity, possibly of postsynaptic receptors. The latter effects have been studied extensively in animal models of presumably DA-mediated behavior, by chemical studies of DA-sensitive adenylate cyclase in caudate nucleus in vitro, and by studies of labeled dopamine receptors. The phenomenon of DA-supersensitivity might help to explain some of the acute "withdrawal dyskinesias" that follow the abrupt discontinuation of high doses of antipsychotic agents, and might contribute to other reversible forms of the syndrome, but may be too short-lived to explain the persistent forms of TD. It must be concluded that an explanation of the latter syndrome of persistent drug-related TD remains uncertain.

Animals↗
PubMed1975

Inhibition of circling behavior by neuroleptic drugs in mice with unilateral 6-hydroxydopamine lesions of the striatum.

The development of circling behavior to apomorphine, amphetamine and L-Dopa in mice with unilateral 6-hydroxydopamine lesions of the dopaminergic nerve terminals in the striatum has been studied, and the effect of a range of neuroleptic and sedative drugs on this circling behaviour has been investigated. Circling induced by all the stimulant drugs was inhibited in a dose-dependent manner by haloperidol, pimozide, chlorpromazine, metoclopramide and clozapine (in descending rank order of potency), but not by phenoxybenzamine, diazepam, promethazine and pentobarbitone sodium. This relatively simple animal model appears useful for screening neuroleptic drugs which may block striatal dopamine receptors, thereby predicting their potency to cause unwanted extrapyramidal effects but not their antipsychotic efficacy.

Animals↗
PubMed1975

Clonidine in Parkinson disease.

Several theoretical considerations suggest that potentiation of central norepinephrine mechanisms may improve motor performance in patients with Parkinson disease receiving concurrent treatment with levodopa. Clonidine hydrochloride, an antihypertensive drug believed to directly stimulate brain norepinephrine receptors, was administered to a group of patients with relatively mild Parkinson disease and coexisting essential hypertension and to three patients with Parkinson disease manifesting the "on-off" response to levodopa. Although a significant antihypertensive effect was achieved, a change in parkinsonian disability could not be demonstrated.

Aged↗
PubMed1975

Pharmacological evidence for cerebral dopamine receptor blockade by metoclopramide in rodents.

Metoclopramide antagonises apomorphine-induced stereotypy in rats (ED50 1.5 mg/kg), apomorphine reversal of reserpine-induced locomotor suppression in mice (50% inhibition produced by 17 mg/kg), and apomorphine- or amphetamine-induced turning behaviour in mice with unilateral lesions of the striatal dopaminergic nerve terminals (ED505.0 and 4.0 mg/kg respectively). Metoclopramide resembles pimozide in all these respects and appears to be a relatively potent antagonist of striatal dopamine receptors. Yet metoclopramide, in anti-emetic doses, has no effect on disability in Parkinson's disease or on the therapeutic benefit of L-Dopa and L-Dopa dyskinesias.

Animals↗