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Biomedical subjects

S Fahn

Publications and source records attributed to S Fahn.

At least 361 records · Page 20Linked to original sources
PubMed1978

Dystonia: a disorder often misdiagnosed as a conversion reaction.

The authors studied the records of 84 patients who had idiopathic torsion dystonia. Thirty-seven cases had originally been misdiagnosed as primarily psychiatric illness. Only 1 patient presented with dystonic movements that were clearly part of a more general psychiatric disorder. The authors believe her to be the first reported patient whose dystonia is undeniably of psychogenic origin.

Adolescent↗
PubMed1978

Strokes and ulcerative colitis.

One adolescent and two young adults had ulcerative colitis and cerebral thrombosis. All survived with neurologic deficit. These patients had no other predisposing factor for cerebrovascular disease. Systemic arterial and venous thromboembolic complications occur often in ulcerative colitis, but stroke is uncommon. Abnormalities in the early stages of clotting may be responsible, and the risk of thromboembolic phenomena in young patients seems to increase with exacerbations of this form of chronic inflammatory bowel disease, and possibly with regional enteritis as well.

Adolescent↗
PubMed1977

New approaches in the management of hyperkinetic movement disorders.

This review covers recent advances in a variety of dyskinesias. Introduction of new drugs for the treatment of myoclonus and sensory biofeedback therapy for focal dystonia are expanding our concepts of these types of movement disorders. Progress in the treatment of action myoclonus is especially noteworthy and has led to the implication of serotonin deficit in the pathophysiology of this syndrome. Knowledge of the biochemical pathology of Huntington's chorea has outpaced therapy for this disorder, but new forms of therapy have been proposed based on the chemical findings. Basic pharmacologic studies suggest pathophysiologic mechanisms for the syndrome known as tardive dyskinesia, but treatment is still far from ideal for this disorder. Other movement disorders with recent therapeutic advances include essential tremor and hemiballism. This review will cover only those dyskinesias in which new therapies have been advanced in the last few years. Aside from parkinsonism, which will not be discussed here, progress in the treatment of movement disorders has been slow, but steady. New drugs are being tested constantly, and the purpose of this review is to call attention to the ongoing evaluation in this field. Descriptions and etiologies for these dyskinesias are covered elsewhere (Fahn, 1976a) and therefore are not repeated here.

5-Hydroxytryptophan↗
PubMed1977

Is dopamine a neurohormone of the adrenal medulla? Studies with morphine stimulation.

Dopamine (da) concentrations in rat adrenals, plasma and brain were variably elevated 1 h after a large parenteral dose of morphine. In adrenals, unlabelled DA increased 2-fold and labelled DA, synthesized from 3H-tyrosine, increased more than 4-fold. The increases could be prevented by inhibition of DA-synthesizing enzymes and spinal cord transection, respectively. Labelled DA in plasma increased 2.7-fold after morphine in intact rats but did not increase in those with spinal cord transection. It is concluded that: (1) morphine stimulates the adrenal by increasing nerve impulse flow, (2) increased nerve impulse flow increases DA synthesis and levels, and (3) the increased DA levels result in increased release of DA into the bloodstream.

Adrenal Medulla↗
PubMed1977

Treatment of vascular hemiballism and hemichorea.

Hemichorea and hemiballism have been considered debilitating and irreversible disorders. Eight patients with vascular hemichorea were treated with perphenazine. All were elderly and hypertensive. Three had primarily choreic movements while five had, in addition, proximal flailing movements of hemiballism. In seven, dramatic response to perphenazine therapy was seen, with virtual cessation of movements. In one case, only partial response was obtained with a high dose of perphenazine, and this dose had to be reduced because of drowsiness and hepatotoxicity. In four patients, movement did not recur after the drug was stopped. This study indicates that perphenazine can be a highly effective agent for the treatment of hemichorea and hemiballism and that improvement can be maintained in some patients even after therapy is discontinued.

Cerebrovascular Disorders↗
PubMed1977

Interaction between bromocriptine and levodopa. Biochemical basis for an improved treatment for parkinsonism.

The present investigation examined the biochemical interaction of bromocriptine and levodopa with respect to monoamine and gamma-aminobutyric acid metabolism in the brain. Rats were treated with levodopa, 250 mg per kilogram of body weight intraperitoneally, with or without carbidopa, 25 mg per kilogram, 1 or 2 hours before sacrifice. Some were also given bromocriptine, 5.0 mg per kilogram, 4 hours before sacrifice. Rats were killed 1 and 2 hours after levodopa and brain levels of gamma-aminobutyric acid and monoamines, and their metabolites were measured. Dopamine levels and metabolism were not markedly altered when bromocriptine was added to levodopa treatment. The level of serotonin, which was reduced 25 to 40 percent by levodopa alone, was close to normal with the combination treatment. Serotonin metabolism was also enhanced by the addition of bromocriptine as shown by increased levels of 5-hydroxyindoleacetic acid. The results suggest that bromocriptine not only may improve the motor disorder of parkinsonism but also may reduce some side effects of levodopa therapy, such as depression, which could be due to serotonin depletion.

Animals↗
PubMed1976

Correlation of behavioural inhibition or excitation produced by bromocriptine with changes in brain catecholamine turnover.

The dopamine agonist, bromocriptine, produced either inhibition or stimulation of motor behaviour in rats depending upon the dose and time after administration. Stimulation of motor activity occurred only with high doses after a 1-2 h delay. Both inhibition and stimulation were associated with decreased turnover of dopamine in the brain. Release of noradrenaline in brain and noradrenaline plus adrenaline in adrenal varied with motor activity. It is suggested that low doses of bromocriptine inhibit behaviour by activating an inhibitory presynaptic receptor, resulting in reduced synthesis and release of dopamine, whilst high doses cause behavioural excitation by activating the post-synaptic dopamine receptor.

Animals↗
PubMed1976

Primary sensory symptoms in parkinsonism.

Forty-three of 101 outpatients with parkinsonism reported that they regularly experienced primary sensory symptoms, i.e., spontaneous abnormal sensations not caused by somatic disease. This is in contrast to similar symptoms reported by only 8 percent of a control population. The most striking and severe symptom was burning of the trunk and proximal extremities, occurring in 11 patients. Twenty-nine patients reported spontaneous pain; a variety of other paresthesialike sensations, e.g., tingling, numbness, and formication, occurred in 32 patients. These subjective sensory phenomena were not associated with sensory loss or autonomic or motor signs. In 20 percent of affected individuals (9 percent of the total), sensory symptoms preceded the onset of the movement disorder, causing difficulty in diagnosis. It is concluded that at least some sensory symptoms originate within the nervous system as a manifestation of the disease process and are not secondary effects of the motor disorder.

Aged↗