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Biomedical subjects

I Shoulson

Publications and source records attributed to I Shoulson.

At least 91 records · Page 5Linked to original sources
PubMed1979

Bromocriptine inhibits norepinephrine release.

Bromocriptine is a dopamine agonist that induces postural hypotension and can be used as an antihypertensive. The drug inhibits release of norepinephrine (NE) from an isolated artery by stimulating presynaptic receptors. In normotensive subjects it lowers both plasma and cerebrospinal fluid (CSF) levels of NE by 50% and lowers blood pressure moderately in standing subjects and slightly in recumbent subjects. Through central and peripheral mechanisms, bromocriptine inhibits sympathetic nervous discharge of NE.

Adult↗
PubMed1978

Huntington's disease: treatment with muscimol, a GABA-mimetic drug.

Muscimol, a gamma-aminobutyric acid (GABA) analogue that exerts potent and specific agonist effects on GABA receptors, was administered orally to 10 patients with Huntington's disease. In this double-blind study, muscimol treatment did not result in improvement in these patients' motor or cognitive functions. However, muscimol administration did ameliorate chorea in the most severely hyperkinetic patient, and it was associated with the appearance of dystonic features, electroencephalographic changes, and behavioral alterations in some patients. These latter observations support a functional relationship between GABA-ergic activity and the genesis of both systonia and EEG abnormalities in humans. The therapeutic failure of muscimol indicates that the GABA disturbances in Huntington's disease does not alone account for the clinical features of this disorder.

Activities of Daily Living↗
PubMed1976

Serotonergic functions in man.

Abundant preclinical evidence suggests that serotonin-containing neural systems may participate in the regulation of both extrapyramidal and neuroendocrine function. In an attempt to examine these possibilities in man, patients with various neurologic disorders received drugs believed to facilitate or inhibit serotonergic function. Extrapyramidal signs in patients with parkinsonism or Huntington's disease showed no consistent change with L-tryptophan or parachlorophenylalanine. Unexpectedly, L-5-hydroxytryptophan, given in combination with a peripheral decarboxylase inhibitor, caused a worsening of parkinsonian akinesia and rigidity. Fenfluramine, at doses which appeared to diminish central serotonin but not dopamine turnover, had no consistent effect on the severity of involuntary movements in patients with Huntington's chorea, but did produce a significant rise in plasma prolactin.

Animals↗
PubMed1976

Huntington's disease: treatment with dipropylacetic acid and gamma-aminobutyric acid.

Dipropylacetic acid (DPA), and anticonvulsant known to raise brain gamma-aminobutyric acid (GABA), was administered orally to eight patients with Huntington's disease. Both alone and in combination with high oral doses of GAGA, DPA failed to ameliorate and motor signs of this disorder. At maximum dose levels, combined DPA and GABA treatment led to an apparent increase in the central turnover of both dopamine and serotonin, as estimated by the oral probenecid-loading test. These latter observations may indicate a close functional interrelation between monoaminergic and GABAnergic neural pathways in the central nervous system of man.

Adult↗
PubMed1976

Studies with bromocriptine. Part 2. Double-blind comparison with levodopa in idiopathic parkinsonism.

A double-blind crossover study was performed in 12 patients with idiopathic parkinsonism to compare their response to bromocriptine with their response to previous optimal drug treatment, including levodopa. There was a 26 percent overall improvement with bromocriptine; rigidity, tremor, and facial expression showed the greatest response. Seven of eight patients who were taking levodopa at the beginning of the study was taken off the drug completely. Adverse reactions were transient and dose-dependent. Bromocriptine promises to be an effective new therapeutic agent in the treatment of idiopathic parkinsonism.

Aged↗
PubMed1976

Studies with bromocriptine: III. Concomitant administration of caffeine to patients with idiopathic parkinsonism.

Caffeine was administered to six patients with idiopathic parkinsonism in an attempt to potentiate the therapeutic response of bromocriptine, a dopamine (DA) receptor agonist, by inhibition of phosphodiesterase. In a double-blind study at doses of 1,000 mg daily, caffeine failed to enhance the antiparkinsonian action of bromocriptine (40 mg daily) given concomitantly. Although effective in potentiating the action of levodopa and other agonists in animal models of parkinsonism, caffeine is inactive in parkinsonism in man.

Bromocriptine↗
PubMed1976

Reversal of systemic manifestations of cryoglobulinemia. Treatment with melphalan and prednisone.

In a patient with essential cryoglobulinemia with systemic, cutaneous, and neurologic manifestations and a mixed IgG-IgM cryoprotein, elimination of systemic and cutaneous disease manifestations, as well as notable reversal of neurologic impairment, followed therapy with melphalan. Levels of circulating cryoprotein decreased, but protein structure was unchanged by chemotherapy. Experience to date with alkylating agents suggests that this mode of treatment is the most effective currently available.

Cryoglobulins↗