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Biomedical subjects

P A Nausieda

Publications and source records attributed to P A Nausieda.

At least 19 recordsLinked to original sources
PubMed1985

Sinemet "abusers".

It is generally assumed that parkinsonian patients perceive their need for antiparkinsonian drugs on the basis of emergent motor symptoms. We describe five patients in whom an apparent psychologic effect from levodopa prompted dosage escalation to the point of toxicity. Abstinence from dopaminergic drugs resulted in the appearance of drug-seeking behavior. Psychologic dependence on levodopa has not previously been reported, but appears to occur in a small subset of parkinsonian patients.

Antiparkinson Agents↗
PubMed1983

Chronic dopaminergic sensitivity after Sydenham's chorea.

We studied psychometric performance on the Minnesota Multiphasic Personality Inventory (MMPI) mini-mult and drug-induced choreic reactions in a group of patients with a history of Syndenham's chorea. Action tremor, motor signs, and residual chorea were common. One-half of the patients reported adverse choreic reactions to one or more agents. Patients with adverse reactions to central stimulants and anorectics had statistically significant elevations in the psychotic tetrad of the MMPI. Sydenham's chorea in childhood seems to confer persistent sensitivity to agents that augment central dopaminergic activity, which may be expressed as acute chorea. Central dopaminergic sensitivity may explain earlier reports of psychologic difficulties in survivors of rheumatic chorea.

Adult↗
PubMed1982

Modification of central serotonergic and dopaminergic behaviors in the course of chronic corticosteroid administration.

The effect of chronic cortisol administration (12.5 mg/kg per day p.o.) was studied in guinea pigs using two behavioral models; apomorphine-induced stereotypy (SB) and 1-5-HTP-induced myoclonus (MJB). Diurnal variations in behavioral sensitivity were evaluated by behavioral testing at five time points over a 24 h period at bi-weekly intervals. Cortisol succinate administration suppresses 1-5-HTP myoclonus in all animals and abolishes diurnal fluctuations in sensitivity during the first two weeks of therapy. At four weeks, a subgroup is observed which is behaviorally hypersensitive to 1-5-HTP. These changes occur in association with a reduction in the behavioral response to apomorphine but in the absence of major disruption in diurnal behavioral threshold variation to apomorphine. Chronic cortisol administration appears to induce major alterations in central serotonin-mediated behaviors. This observation may explain the therapeutic effect of corticosteroids in certain forms of myoclonus and the role of cortisol rhythm disturbances in the context of a variety of psychiatric disorders.

5-Hydroxytryptophan↗
PubMed1982

Sleep disruption in the course of chronic levodopa therapy: an early feature of the levodopa psychosis.

Sleep disruption is a common complaint in levodopa-treated parkinsonian patients. A survey of 100 parkinsonian patients revealed prominent sleep complaints in 74%. Sleep complaints were unrelated to patient age and the duration of disease but increased in prevalence with longer periods of levodopa therapy. Sleep abnormalities tended to increase in severity with continued treatment and insomnia tended to be followed by daytime somnolence, altered dream events, and episodic nocturnal vocalization and myoclonus. While dyskinetic side effects and on-off syndrome were encountered in patients with and without sleep complaints, 98% of patients experiencing psychiatric side effects also reported sleep disruption. It is suggested that sleep-related symptoms constitute an early stage of levodopa-induced dopaminergic psychiatric toxicity in the parkinsonian population. Clinical and experimental observations suggest that serotonergic mechanisms are important in this symptom complex.

Aged↗
PubMed1982

Drug-induced asterixis in Parkinson disease.

Asterixis was observed in five parkinsonian patients who were taking levodopa. A prospective study revealed that 4 of 55 consecutive patients had asterixis. Liver and metabolic functions were normal in all patients. Asterixis always occurred as part of a toxic confusional state superimposed on a parkinsonian state associated with some dementia. Insomnia, hallucinosis, and myoclonus were also prominent in the affected patients. Because of this association with other signs of chronic drug toxicity and its reversal with drug withdrawal, the asterixis seemed to be drug-related.

Aged↗
PubMed1982

Long-term suppression of central serotonergic activity by corticosteroids: a possible model of steroid-responsive myoclonic disorders.

Chronic administration of cortisol succinate (12.5 mg per kilogram per day) to guinea pigs suppressed jumping behavior induced by 1-5 hydroxytryptophan and abolished diurnal threshold variations of this behavior. Chronic corticosteroid administration did not alter threshold or diurnal variations of apomorphine-induced stereotypy. These observations suggest that the efficacy of corticosteroids in some human myoclonic movement disorders may be related to central serotonergic inhibition.

5-Hydroxytryptophan↗
PubMed1982

Tardive dyskinesia: pharmacology and clinical implications.

The basic pathogenesis of TD appears to relate to chronic pharmacologic denervation of specific dopaminergic receptor sites in the striatum. The pathophysiology of the disorder relates to the resultant denervation hypersensitivity. The mainstay of treatment includes withdrawal of neuroleptics when feasible and the use of dopamine-depleting agents. Enhancement of the striatal cholinergic input offers potential ancillary benefit to the alleviation of abnormal movements. The possibility of benefit from manipulating other neurotransmitters remains experimental. Treatment of TD with neuroleptics themselves is clearly treatment with the presumed offending agent and should be avoided. This shortsighted therapy may temporarily abate the pathophysiology of the condition, but it serves to aggravate its pathogenesis.

Animals↗