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Biomedical subjects

C D Marsden

Publications and source records attributed to C D Marsden.

At least 829 records · Page 46Linked to original sources
PubMed1981

Lisuride in parkinsonism.

Lisuride is a soluble ergolene derivative with endocrine effects similar to but more potent than those of bromocriptine. In nine subjects with idiopathic, postencephalitic, or drug-induced parkinsonism, lisuride at a dosage of 0.05 to 0.15 mg intravenously caused an immediate improvement in tremor, rigidity, akinesia, and postural deformity, but also caused chorea and orofacial dyskinesia. Improvement lasted 2 to 3 hours. Lisuride had little or no effect in a single patient with progressively supranuclear palsy. Oral lisuride therapy, 0.8 to 4.8 mg daily, had similar effects but occasionally caused reduced awareness and hallucinations.

Administration, Oral↗
PubMed1981

Kainic acid lesions of striatum and decortication reduce specific [3H]sulpiride binding in rats, so D-2 receptors exist post-synaptically on corticostriate afferents and striatal neurons.

Unilateral kainic acid lesions of rat striatum reduced specific striatal [3H]spiperone and [3H]sulpiride binding sites (Bmax) by 52 and 67% respectively compared with the intact side. The dissociation constant (KD) for [3H]spiperone binding was unchanged but that for [3H]sulpiride binding was reduced. Specific striatal [3H]spiperone and [3H]sulpiride binding was reduced by 22 and 37% respectively in unilateral decorticate animals, but there was no change in KD. Unilateral 6-hydroxydopamine lesions of the medial forebrain bundle caused no change in striatal [3H]spiperone binding sites or KD value, but produced a 27% increase in [3H]sulpiride binding sites with no change in KD. These data support the hypothesis of D-2 receptors located on cortico-striate glutamate fibres, but also indicate the presence of both D-1 and D-2 receptors on the cell bodies of striatal neurons.

Animals↗
PubMed1981

Reliability and efficacy of the long-latency stretch reflex in the human thumb.

1. The amount of positional compensation afforded by the long-latency reflex in the flexor pollicis longus has been investigated in ten normal human subjects. 2. The interphalangeal joint of the thumb was extended by between 2 and 40 degrees at up to 900 deg/s by suddenly increasing the standing force applied to the lever against which the subject was pressing with the pad of the thumb. 3. Electromyographic (e.m.g.) responses at spinal-latency were very small or absent for stretches of this magnitude. The long-latency stretch reflex produced an average positional correction of about 50% for disturbances in the range of 5-25 degrees. The response began to saturate for disturbances of greater than 25 degrees. 4. The e.m.g. response was pulsatile, lasting only some 50 ms, even during continuously increasing disturbances; frequently it terminated despite a remaining positional error. 5. There was a large variation from subject to subject in the average amount of positional correction provided by the stretch reflex. Examination of single responses to the same stretch in individual subjects showed an even greater variation from trial to trial. 6. Variation in the compensation produced by the long-latency stretch reflex from trial to trial could not be explained by the slight variation in size or maximum velocity of the individual stretches.

Adult↗
PubMed1981

Simple tics in Gilles de la Tourette's syndrome are not prefaced by a normal premovement EEG potential.

EEG events prior to simple tics have been examined in six patients with Gilles de la Tourette's syndrome, and compared to EEG changes occurring when the same subjects voluntarily mimicked their own tics. Voluntary jerks were prefaced by a premovement negative potential commencing about 500 ms prior to the muscle EMG discharge and reaching an amplitude of about 7 muV. No such premovement potential was evident in the EEG prior to spontaneous tics in five of the six patients; a very small event was seen in the sixth patient but it was only about one-tenth of the size of the premovement potential seen prefacing voluntary jerks in the same subject. These data indicate that simple tics in Gilles de la Tourette's syndrome are physiologically distinct from normal self-paced willed movements.

Action Potentials↗
PubMed1981

Neuroleptic-induced acute dystonic reactions may be due to enhanced dopamine release on to supersensitive postsynaptic receptors.

Oral administration of butaperazine (40 mg per kilogram) to rats increased dopamine turnover, as measured by elevation of striatal and mesolimbic concentrations of homovanillic acid and 3,4-dihydroxyphenylacetic acid, for 24 to 48 hours. Initially, this dose of butaperazine inhibited stereotyped behavior in response to subcutaneous administration of apomorphine, but this effect was reversed at 12 hours. Later, animals had normal or exaggerated responses to apomorphine. The data suggest that the critical 20- to 28-hour period after butaperazine administration, when most human acute dystonic reactions occur, normal or supersensitive cerebral dopamine receptors are exposed to an excessive synaptic release of dopamine. This may be responsible for the drug-induced dystonia.

3,4-Dihydroxyphenylacetic Acid↗