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Biomedical subjects

C D Marsden

Publications and source records attributed to C D Marsden.

At least 613 records · Page 34Linked to original sources
PubMed1986

The physiology of orthostatic tremor.

This article describes the physiological findings in a patient with orthostatic tremor. The tremor primarily affected the legs, was alternating between antagonist muscle groups, and had a remarkably rapid frequency of 16 Hz. It was present only during certain postures and appeared to be of central origin. A tremor of the same frequency was also recorded in the arms during particular movements, but was cocontracting. We suggest that orthostatic tremor may be generated by spontaneous oscillation in those central structures responsible for organizing the motor programs for standing.

Electromyography↗
PubMed1986

Ipsilateral blepharospasm and contralateral hemidystonia and parkinsonism in a patient with a unilateral rostral brainstem-thalamic lesion: structural and functional abnormalities studied with CT, MRI, and PET scanning.

A patient developed progressive right hemidystonia in childhood. Subsequently, left-sided blepharospasm, slurred and stuttering speech, and right-sided rigidity and bradykinesia, responsive to dopamine agonists, appeared. Investigation with computed tomography and magnetic resonance imaging (MRI) at age 43 years revealed a left-sided calcified rostral brainstem-thalamic lesion of uncertain aetiology. Although no structural lesion was seen in the striatal regions, L-[18F]-fluorodopa uptake was severely diminished in the left striatum but normal on the right. Dopamine receptor binding identified by [11C]-methylspiperone was in the normal range on both sides.

Adult↗
PubMed1986

Brain energy metabolism and dopaminergic function in Huntington's disease measured in vivo using positron emission tomography.

A 48-year-old man with typical Huntington's disease was investigated with computed tomography (CT) and positron emission tomography. Regional cerebral blood flow, oxygen extraction, oxygen and glucose utilisation, L-Dopa uptake, and dopamine (D2) receptor binding were measured using several positron-labelled tracers. CT showed slight atrophy of the head of caudate but no cortical atrophy, although distinct frontal lobe dysfunction was present on psychometric testing. Oxygen and glucose metabolism and cerebral blood flow were decreased in the striata and to a lesser extent in frontal cortex. Cerebral blood flow was in the low normal range throughout the remainder of the brain. A normal metabolic ratio was found in all regions, since the changes in glucose utilisation paralleled those in oxygen consumption. The capacity of the striatum to store dopamine as assessed by L-[18F]-fluorodopa uptake was normal, but dopamine (D2) receptor binding was decreased when compared to normal subjects.

Carbon Radioisotopes↗
PubMed1986

Electrophysiology of the corticomotoneurone pathways in patients with movement disorders.

The corticomotoneurone pathways were examined in 21 patients with movement disorders, using the technique of percutaneous electrical stimulation of the motor cortex. Conduction in these pathways was assessed by measuring the latency to onset of electromyographic activity in the muscles of the upper limb after cortical stimulation. In all patients [five with primary (idiopathic) torsion dystonia and two with secondary (symptomatic) hemidystonia, seven with Huntington's disease, four with essential tremor, and three with Parkinson's disease] central motor conduction was normal. This and other evidence suggests that the origin of the disorder of movement in these conditions lies in the delivery of abnormal motor commands to a normal corticomotoneuronal system.

Adult↗
PubMed1986

Administration of MPTP to the common marmoset does not alter cortical cholinergic function.

The administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets induced persistent motor deficits and decreased concentrations of dopamine, homovanillic acid, and 3,4-dihydroxy-phenylacetic acid (DOPAC) and [3H]dopamine uptake in the caudate-putamen. There was an 80% reduction in tyrosine hydroxylase immunoreactive cells in substantia nigra. At 10 days following the start of MPTP administration, the activity of choline acetyltransferase in the thalamus and frontal cortex was unchanged compared with control animals. Similarly, specific [3H]QNB binding was unaltered. At 4-6 weeks following the start of MPTP treatment, choline acetyltransferase activity and [3H]QNB binding in the frontal cortex and thalamus remained unaffected. There was no evidence for cell loss in the nucleus basalis of Meynert or alteration in the intensity of staining for acetylcholinesterase. MPTP treatment of the common marmoset produces a nigrostriatal lesion. In contrast, MPTP did not alter cortical cholinergic function and was not neurotoxic to the cholinergic cells in the nucleus basalis of Meynert.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Ramsay Hunt syndrome and coeliac disease: a new association?

Two patients with the syndrome of Ramsay Hunt (dyssynergia cerebellaris myoclonica, DCM), associated with malabsorption due to adult coeliac disease, are reported. Both presented with progressive cerebellar ataxia, action myoclonus, and epilepsy. One had gastrointestinal symptoms (recurrent diarrhea and weight loss which responded satisfactorily to a gluten-free diet), but the other did not. In both patients, jejunal biopsy revealed subtotal villous atrophy; serum folate and vitamin E level were also reduced. Neither a gluten-free diet nor vitamin supplements improved the neurological picture. However, some symptomatic relief was afforded by treatment with clonazepam, sodium valproate, carbamazepine, and piracetam. It could be argued that the association between these two disorders is coincidental. However, since we have found this combination in 2 of 14 consecutive cases with DCM, a causal relationship seems likely, although the underlying mechanism remains unknown. Patients with the Ramsay Hunt syndrome should be investigated for malabsorption, and also undergo small intestinal biopsy.

Adult↗
PubMed1986

Do enkephalins in basal ganglia mediate a physiological motor rest mechanism?

Thermal injury (30-s immersion in water at 62 degrees C) of one hind limb of rats caused a gradual withdrawal of the limb from use, such that after 1 week 50% of the animals walked on three legs. At 24 h following thermal lesion and at a time when the lesioned paw was still used for walking there was a reduction in met- and leu-enkephalin content in the periaqueductal grey (PAG) and bilateral reduction in leu-enkephalin content of the globus pallidus, but no change in enkephalin levels in caudate-putamen. One week following the lesion, animals exhibiting complete withdrawal of the injured limb, showed bilateral reduction of met- and leu-enkephalin content of PAG. Both met- and leu-enkephalin content in caudate-putamen. In each case the change was more marked in basal ganglia areas contralateral to the lesion. In animals lesioned 1 week previously and which did not use the injured limb, there was no change in the monoamine (or metabolite) content of caudate-putamen or in the spontaneous or potassium-evoked release of 3H-dopamine from strial slices. Thermal injury did not cause any general change in pain sensitivity and the time of change in pain threshold in the injured limb did not parallel the withdrawal of the affected limb from walking. The results suggest that after a thermal limb lesion, delayed changes in basal ganglia enkephalin content may be important in withdrawing the injured limb from the normal pattern of locomotion. Basal ganglia enkephalins may be involved in a physiological rest mechanism, which allows healing of the affected part.

Animals↗
PubMed1986

Simple and complex movements in a patient with infarction of the right supplementary motor area.

The role played by the supplementary motor area (SMA) in the higher-level organization of motor behaviour (motor programming) has been highlighted by the study of cerebral blood flow during voluntary movements in normal humans. We present a detailed physiological investigation from a patient with a right SMA lesion and show that the right SMA plays a role in programming simultaneous and sequential movements in both arms, though the contralateral arm was the more severely impaired. In addition, we obtained evidence to suggest that the precentral motor cortex may be more responsive to peripheral perturbations when the modulating influence of the SMA is absent. In view of the similarity of the physiological findings in this subject to those in patients with Parkinson's disease, we suggest that the defect of motor programming in Parkinson's disease is likely to reflect functional deafferentation of the SMA.

Aged↗
PubMed1986

Acute dystonia induced by neuroleptic drugs.

About 2.5% of patients treated with neuroleptic drugs develop acute dystonia within 48 h of commencing therapy. The symptoms remit on drug withdrawal or following anticholinergic therapy. Acute dystonia can also be reliably induced in many primate species by neuroleptic treatment with comparable time course, symptomatology and pharmacological characteristics to those observed in man. In general, New World monkeys appear more susceptible to acute dystonia than Old World primates. It is at present not clear whether all primates, including man, would exhibit dystonia if a sufficiently high dose of neuroleptic was administered. Alternatively, some unknown, possibly species-specific or even genetic, factors may determine an individual's susceptibility to develop dystonia. Use of a rodent model of dystonia might enable more detailed analysis of biochemical correlates of dystonic behaviour. Whilst rodents do not exhibit overt dystonic behaviour after neuroleptic treatment, they may develop oral dyskinesias which bear a close pharmacological similarity to dystonia in man and primates. However, it is not known whether chewing induced by neuroleptic drugs in rats resembles acute dystonia in primates or whether this is another movement disorder possibly unique to rodent species. The pathophysiology of acute dystonia remains unknown, but may involve striatal dopaminergic and cholinergic function. In view of the close similarity between dystonia in man and other primates, studies on the mechanisms whereby neuroleptic drugs cause acute dystonic reactions in monkeys may give some clues to the pathogenesis of spontaneous dystonia in man.

Acute Disease↗
PubMed1986

Habituation and conditioning of the human long latency stretch reflex.

The effects of stretch repetition rate, prior warning stimuli and self administered stretch were examined on the size of the short and long latency components of the stretch reflex electromyographic EMG response in flexor pollicis longus and the flexor muscles of the wrist and fingers. Stretches of constant velocity and extent were given every 10 s, 5 s, 2 s, or 1 s to either the wrist or thumb during a small background contraction of the flexor muscles. The size of the long latency component of the stretch reflex (measured as the area under the averaged rectified EMG responses) declined dramatically at faster repetition rates, especially in the wrist and finger flexors. The size of the short latency component was relatively unaffected. The size of the electrically elicited H-reflex in forearm muscles also failed to habituate under the same conditions. If each individual trial of a series was examined, the long latency component of the stretch reflex EMG could be seen to decrease in size over the first three to six stretches if stretches were given every 1 s, but not if stretches were given every 10 s. When stretches were given every 5 s to either wrist or thumb, an electrical stimulus applied to the digital nerves of the opposite hand 1 s before stretch reduced the size of the long latency component of the reflex EMG response. The short latency component was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effects of somatostatin on dopamine sensitive adenylate cyclase activity in the caudate-putamen of the rat.

The effect of somatostatin-14 (SRIF) on dopamine-sensitive adenylate cyclase in caudate-putamen pellets was studied in naive female rats, and in rats with chemical lesions of the nigrostriatal dopaminergic tract produced by injection of 6-hydroxydopamine, or of the caudate-putamen itself produced by injection of kainic acid 3 week earlier. In unlesioned rats somatostatin at a concentration of 10(-7) moles/l inhibited adenylate cyclase activation by submaximal concentrations of dopamine, increasing the apparent Km but not altering Emax. In 6-hydroxydopamine lesioned rats somatostatin no longer influenced adenylate cyclase activity, whereas in kainic acid lesioned rats somatostatin still increased the apparent Km for dopamine activation. The effect of somatostatin in untreated and lesioned rats is compatible with a partial competitive antagonism to dopamine. Although the data from the lesioned rats present preliminary results, the dose response characteristics and the effects in lesioned animals suggest a more complex interaction, possibly by binding of somatostatin to an inhibitory subunit of regulatory adenylate cyclase components.

Adenylyl Cyclases↗
PubMed1986

Motor strategies involved in the performance of sequential movements.

The present study analyses the strategies adopted by normal subjects when they are asked to make two separate movements as rapidly as possible one after the other. Five subjects performed the following sequential movements in their own time. 1) Squeeze an isometric force transducer between fingers and thumb to a force of 30 N and then flex the elbow of the same arm through 15 degrees. 2) Squeeze the transducer with one hand and then flex the elbow of the other arm. 3) Perform an isotonic opposition of finger and thumb and then flex the elbow of the same arm. 4) First flex the elbow through 15, 30 or 45 degrees and then squeeze the transducer. 5) Flex and then extend the elbow as rapidly as possible. In tasks 1-4 there was no correlation between the times taken to complete the two separate components of the sequence. Because of this we suggest that the two movements remained under the control of two separate motor programmes. In contrast, in task 5, the times taken for the two components were correlated and hence we suggest that in this case a single programme was used to perform the sequence. In tasks 1-3, in which the mean duration of the first movement was some 135-162 ms, there was a mean pause of about 85 ms before the start of the second movement. Subjects tended to chose a minimum inter-onset latency between the start of the first and the start of the second movement of a sequence of some 230 ms. The reason for this appeared to be that if subjects were encouraged to decrease their inter-onset latencies to less than 200 ms, the speed of the second movement decreased sharply. However, if the duration of the first movement was prolonged as in task 4, the second movement could be delayed, although there now was little or no pause between the two movements. We conclude that when a single motor programme is run, it is followed by a "relative refractory period". If a second programme is run within this period, it cannot be executed without loss of speed. Switching from one motor programme to another is achieved with an optimal minimum delay of 200 ms. Sequential movements which are controlled by a single programme do not share this limitation.

Adult↗
PubMed1986

The effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on striatal and limbic catecholamine neurones in white and black mice. Antagonism by monoamine oxidase inhibitors.

Albino mice and pigmented mice were treated for 6 days with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at the maximum tolerated doses (2 days at 30 mg/kg i.p., 2 days at 40 mg/kg i.p. and 2 days at 50 mg/kg i.p. in white mice, 6 days at 30 mg/kg i.p. in pigmented mice) and the effects of simultaneous treatment with the monoamine oxidase inhibitors, deprenyl (1 mg/kg, i.p.), MDL 72145 (0.5 mg/kg, i.p.) and clorgyline (5 mg/kg, i.p.), determined behaviourally (daily for 6 days and for 4 days after withdrawal) and biochemically (92 hr after withdrawal of drug). In albino mice MPTP caused depletions of dopamine (90%), dihydroxyphenylacetic acid (DOPAC; 82%) and homovanillic acid (HVA; 65%) in the striatum and in dopamine (54%), DOPAC (51%) and HVA (53%) in the nigra. However, MPTP was not selective in its action since the levels of dopamine and its metabolites were also reduced in limbic tissue. Further, MPTP affected the function of noradrenaline, with reduced levels in tissues of the striatum (74%) and nigra (46%). Pigmented mice were as susceptible as albino mice to the actions of MPTP to reduce the levels of dopamine and metabolites in the striatum. However, the limbic areas and substantia nigra of the pigmented mouse were more resistant to the actions of MPTP. Treatment with deprenyl and MDL 72145 (but not clorgyline) could be shown to reduce the biochemical and behavioural consequences of the action of MPTP (although behavioural changes, development of severe motor incapacitation and prostrate appearance, appeared to be non-specific).(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

MPP+ can disrupt the nigrostriatal dopamine system by acting in the terminal area.

Acute intracerebral injections of MPP+ in the mouse can cause behavioural and biochemical correlates of nigrostriatal dopamine dysfunction, but these are most marked and consistent when injections are directed at the dopamine nerve terminal area (CP) rather than the cell body area (SN). This adds further support to the hypotheses that a locus of neurotoxic action of MPTP/MPP+ may reside in the dopamine cell terminal regions.

3,4-Dihydroxyphenylacetic Acid↗