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Biomedical subjects

C D Marsden

Publications and source records attributed to C D Marsden.

At least 541 records · Page 30Linked to original sources
PubMed1988

Dopa-responsive dystonia.

DRD is a distinctive clinical entity and an unexpectedly common subgroup of torsion dystonia. Diurnal fluctuation is often but not always present and does not reliably distinguish the disorder from ITD. DRD must be considered in the differential diagnosis of the child or adolescent presenting with a dystonic gait disorder, diplegic cerebral palsy, sporadic spastic paraplegia, ataxic syndromes, and juvenile parkinsonism. The response to L-DOPA is so dramatic and occurs so quickly that a diagnostic therapeutic trial should be undertaken in all patients presenting with these syndromes.

Adolescent↗
PubMed1988

Writer's cramp.

Explore the source record for details and available documents.

Adult↗
PubMed1987

Pilocarpine-induced purposeless chewing behaviour in rats is dependent on intact central stores of 5-HT.

Pilocarpine-induced purposeless chewing behaviour in rats was partially antagonised by pretreatment with reserpine, tetrabenazine or p-chlorophenylalanine (PCPA). In contrast, pretreatment with alpha-methyl-p-tyrosine (AMPT) had no effect on pilocarpine-induced chewing. These data suggest that enhancement of purposeless chewing by pilocarpine is dependent, in part, on intact central stores of 5-HT.

Animals↗
PubMed1987

Localization of neurotensin receptors in the forebrain of the common marmoset and the effects of treatment with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

The distribution of neurotensin binding sites was mapped in the brain of the common marmoset using [3H]neurotensin as the ligand. Autoradiographic techniques show that the density of receptors is particularly high in the substantia nigra, ventral tegmental area, olfactory tubercle and cerebral cortex and that the distribution of neurotensin receptors in the cerebral cortex and striatum is heterogenous. In the cerebral cortex neurotensin receptors are concentrated in layers I, II, III and V, whilst receptor density is generally less in all layers of middle temporal cortex. Striatal neurotensin receptors conformed to a striosomal distribution as defined by acetylcholinesterase staining with the highest density of binding sites in the matrix. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine selectively destroyed over 80% of the dopaminergic neurons of the marmoset substantia nigra and almost 60% of those in the adjacent ventral tegmental area. The subsequent loss of a large proportion of neurotensin receptors from marmoset substantia nigra and striatum suggests their presence on the dopaminergic nigrostriatal pathway.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine as monoamine oxidase substrates: a second ring is not necessary.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is oxidised to a neurotoxic metabolite by monoamine oxidase B (MAO B). Using two colorimetric assays, we have examined a range of its structural analogues as possible further substrates of this enzyme in order to identify the types of environmental or endogenous compounds that might also be neurotoxic. Compounds with fully saturated or unsaturated pyridine rings were not substrates; nor were a range of tetrahydro-beta-carbolines or isoquinolines. Four substrates for MAO were found, 1-methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine (2'-Me-MPTP), 4-phenyl-1,2,3,6-tetrahydropyridine (PTP), 4-(p-chlorophenyl)-1,2,3,6-tetrahydropyridine (Cl-PTP) and ethyl-1-methyl-1,2,3,6-tetrahydro-4-pyridine-carboxylate (ethyl-MTP-carboxylate). Ethyl-MTP-carboxylate is of particular interest as it shows that a tetrahydropyridine without a phenyl ring can also be a substrate. Cl-PTP, PTP and ethyl-MTP-carboxylate appeared to be partially metabolised by MAO A. The inhibitor sensitivity of 2'-Me-MPTP oxidation was more complex.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Chronic trifluoperazine treatment does not induce lipid peroxidation in the rat cortex.

Rats received continuous chronic trifluoperazine hydrochloride (4.4-4.9 mg/kg/day) treatment for 15 months via their drinking water. Drug treatment did not alter the content of polyunsaturated fatty acids in the cerebral cortex when compared to age-matched control animals. Similarly, there was no change in basal levels of malondialdehyde (MDA) when measured by a fluorimetric or spectrophotometric technique. Incubation of cortical homogenates in air, or with FeSO4 plus ascorbic acid or H2O2 plus FeSO4, stimulated MDA production to the same extent in tissue from drug-treated and control animals. The chronic administration of trifluoperazine to rats does not appear to promote lipid peroxidation as has been suggested for haloperidol.

Animals↗
PubMed1987

Modulation of the long-latency reflex to stretch by the supplementary motor area in humans.

Surface-recorded, electromyographic responses to 200-ms ramp stretches were studied in the wrist flexor muscles from both arms of a patient with clinical and radiographic evidence of infarction in the right supplementary motor area (SMA). They were compared with those from 8 age-matched control subjects. The latencies of the spinal component of the stretch reflex were slightly longer than normal in both arms of the patient (normal subjects: 28.5 +/- 2.6 ms; patient: 35 ms, right arm and 32 ms left arm). However, the amplitude and duration of the short-latency response were identical in both arms. The onset of the long-latency response to stretch was symmetrical in both the patient's arms and was slightly later than normal (normal subjects 55.5 +/- 4.0 ms, patient: 72 ms right arm and 70 ms left arm); however, its duration was considerably prolonged in the arm contralateral to the SMA lesion (normal subjects: 44.8 +/- 6.0 ms; patient: 48 ms right arm. 105 ms left arm). These results are consistent with the hypothesis that the long-latency stretch reflex is mediated via a transcortical loop.

Adult↗
PubMed1987

Different sites of action of electrical and magnetic stimulation of the human brain.

The latency of the surface recorded electromyographic response to either an electrical or magnetic stimulus applied to the scalp has been measured in the first dorsal interosseous and abductor pollicis brevis muscles of 3 subjects. In the contracting muscle the response latency to the magnetic stimulus was longer by 1.4-2.7 ms compared to the electrical stimulus. Poststimulus time histograms of the firing of single motor units of first dorsal interosseous muscle were studied in 4 subjects. The first period of increased probability of firing of the single motor units showed a similar latency difference (mean 2.8 ms) to the two modes of stimulation. It is concluded that the extra delay to magnetic stimulation is consumed in central motor pathways. This implies that the two modes of stimulation activate the brain at different sites. It is suggested that the magnetic stimulus excites the corticospinal neurones transynaptically, whereas the electrical stimulus excites these neurones directly.

Brain↗