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Biomedical subjects

C G Goetz

Publications and source records attributed to C G Goetz.

At least 235 records · Page 13Linked to original sources
PubMed1983

On the mechanism of sudden death in Moersch-Woltman syndrome.

A patient dying in the hospital with Moersch-Woltman Stiff-person syndrome (MWS) suffered from episodic, severe, uncompensated metabolic acidosis. Possible explanations for the acid-base abnormalities in this neurologic disorder are proposed.

Acidosis↗
PubMed1982

A pure parkinsonian syndrome following acute carbon monoxide intoxication.

A 50-year-old woman with carbon monoxide (CO)-induced parkinsonism was found to have bilateral lucencies of the globus pallidus on computed tomographic (CT) scan consistent with old necrotic lesions. She showed no clinical response to levodopa therapy, although she did improve with anticholinergic therapy. It is suggested that the parkinsonism in this patient is due to the pallidal lesions demonstrated on CT scan, and that such pallidal-related parkinsonism may not respond to dopaminergic therapy.

Acute Disease↗
PubMed1982

Pharmacology of hallucinations induced by long-term drug therapy.

The authors studied 20 patients with Parkinson's disease and prominent hallucinations related to dopaminergic or anticholinergic therapy. The character of the hallucinations appeared distinct from the classic description of either acute anticholinergic or acute aminergic hallucinatory states. Manipulation of either kind of drug could precipitate or relieve hallucinations in a given patient, which suggests that the dopaminergic/cholinergic systems are reciprocally active in the pathophysiology of long-term drug-induced hallucinatory states in this population.

Antiparkinson Agents↗
PubMed1982

Pergolide mesylate and idiopathic Parkinson disease.

We studied the effects of pergolide mesylate in an open trial of 23 patients with idiopathic Parkinson disease (PD). All had suffered from loss of efficacy or dose-limiting side effects on current antiparkinsonian regimens. On pergolide therapy, improvement, which was maintained for 6 months, was noted in some parkinsonian features in all 23 patients. All patients suffering from on-off phenomenon were helped by pergolide. Significant side effects were not encountered. Pergolide is useful in the treatment of PD.

Adolescent↗
PubMed1982

Cholinergic mechanisms in Tourette syndrome.

To examine the role of the cholinergic system in Tourette syndrome, we administered intramuscular physostigmine and scopolamine hydrobromide to 10 patients, evaluating both motor tics and involuntary vocalizations. Patients showed a consistent abatement of motor tics and exacerbation of vocal tics after scopolamine injection. The scopolamine effect was reversed by physostigmine. These data suggest that the cholinergic system plays a role in the pharmacologic pathophysiology of Tourette syndrome. The pharmacology of vocal and motor tics may differ, and cholinergic manipulation may benefit some patients.

Adolescent↗
PubMed1982

Primary writing tremor: a selective action tremor.

Progressive difficulty in handwriting due to jerking movements precipitated by the act of writing beginning between the ages of 8 to 54 is reported in six patients. There was no rest tremor, but three had mild postural tremor. Specific muscle activity (especially pronation of the wrist or abduction of the fingers) elicited the tremors that persisted as long as the evocative posture or muscle activity was maintained. None had a family history of tremors, but two had a history suggestive of hypoxia at birth. Unlike benign essential tremor, the movements did not respond to propranolol HCl, but most patients were benefited both acutely and chronically by centrally active anticholinergic agents.

Adolescent↗
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

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↗