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Biomedical subjects

C D Marsden

Publications and source records attributed to C D Marsden.

At least 973 records · Page 54Linked to original sources
PubMed1976

Advances in the management of parkinson's disease.

The treatment of Parkinson's disease today is complex, time-consuming, but rewarding. The introduction of levodopa has not cured the disease, but has provided the most powerful therapy available yet. Its use is limited by side effects and careful titration to optimum dosage, often in combination with other drugs, is required. Despite best therapy, some patients never respond, and others begin to lose benefit after some years of therapy. New problems, such as the "on-off" effect have appeared with long-term treatment, and require careful adjustment of dosage. As with any replacement therapy, a balance between sub-optimal benefit and side effects has to be discovered and maintained by careful and frequent review. New approaches to treatment may offer further improvement in the near future.

Amantadine↗
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

Circling behaviour produced by unilateral lesions in the region of the locus coeruleus in rats.

Rats with unilateral lesions in the region of the locus coeruleus circled tightly to the opposite side when given apomorphine or amphetamine. This turning behaviour was transient and disappeared within some 30 days after surgery. It was seen most obviously in animals with severe unilateral destruction of the locus coeruleus, which caused on average a 55% reduction in the level of noradrenaline in the ipsilateral cerebral cortex. It was not marked in animals with partial unilateral lesions of the locus coeruleus, which caused only an average fall in cortical noradrenaline of 22%. It was not seen in sham operated animals or animals in which lesions were placed into adjacent structures such as the cerebellum above, superior cerebellar peduncle laterally, and brain stem ventrally. A clue to the mechanism of this phenomenon may lie in the observation that dopamine in the ipsilateral striatum was increased 5 days after operation, when circling occurred, but had returned to normal by 30 days when circling had ceased. It is suggested that the lesion causes a reduction in impulse traffic in the ipsilateral nigrostriatal pathway, and that circling is due to preferential stimulation of the ipsilateral striatal dopamine receptors by both drugs; apomorphine directly, amphetamine by release of endogenous dopamine.

Amphetamine↗
PubMed1975

Manipulation of brain serotonin in the treatment of myoclonus.

The response of myoclonus to oral and intravenous L-5-hydroxytryptophan (5-H.T.P.) in combination with a peripheral decarboxylase inhibitor (carbidopa) and to clonazepam has been examined in 9 patients. Moderate improvement or complete cessation of myoclonus followed treatment with one or both of these regimens in 5 patients, 1 of whom also responded to the concurrent administration of L-tryptophan and a monoamineoxidase inhibitor. The remaining 4 patients were at best only slightly improved by either 5-H.T.P. or clonazepam. The responsive group consisted of 3 patients with a history of anoxia, 1 patient with non-history of severe head injury, and 1 patient with non-progressive focal myoclonus and epilepsy. This group had low levels of 5-hydroxyindole acetic acid in the lumbar cerebrospinal fluid. It is suggested that 5-H.T.P. plus carbidopa, L-tryptophan plus a monoamine-oxidase inhibitor, and clonazepam may all act by elevating brain levels of serotonin (5-H.T.) and that some human myoclonic syndromes may be specifically related to a cerebral deficiency of 5-H.T.

5-Hydroxytryptophan↗