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Biomedical subjects

J M S Pearce

Publications and source records attributed to J M S Pearce.

At least 73 records · Page 4Linked to original sources

Heubner's artery.

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Anterior Cerebral Artery↗

A note on aphasia in bilingual patients: Pitres' and Ribot's laws.

Johann Gesner in 1770 probably provided the first description of dissociation in reading ability in different languages in a bilingual patient, who after brain damage was able to read Latin but not German. Clinical studies have since shown that bilingual 'aphasics' do not necessarily manifest the same language disorders with the same degree of severity in both languages. Superficially, different case findings indicate instances of shared and divergent representation of components of language in the bilingual brain. This paper considers a selection of many empirical studies, which have failed to reconcile the parallel recovery of language in many reported bilingual aphasiacs and the differential recovery in others. It reviews Pitres' rule (recovery of the most used acquired language) and Ribot's law (recovery of the native language) that are important concepts during recovery and rehabilitation of bilingual aphasiacs.

Aphasia↗

Théodore Herpin: neglected contributions in the understanding of epilepsy.

In contrast to earlier notions of epilepsy, Théodore Herpin considered that when symptoms started in the periphery or the viscera their origin was in the brain, a view later lauded by Hughlings Jackson. His respected book Des accès incomplets did not attempt to deal with disordered physiology but was designed to help physicians to recognise and treat epilepsy early in its course. He described juvenile myoclonic epilepsy and vividly and accurately portrayed many other clinical phenomena of epilepsy.

Anticonvulsants↗

Rhinorrhoea/otorrhoea.

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Cerebrospinal Fluid Otorrhea↗

Richard Morton: origins of anorexia nervosa.

Sir William Gull coined the name 'anorexia nervosa'. Examples of self-starvation appeared in the Hellenistic era. Holy anorexics abused their bodies, rejected marriage and sought religious asylum where many perished and became saints. The condition then paled into obscurity until the 19th century. Louis-Victor Marce (1828-1864) described such a patient in 1859, but Richard Morton is generally credited with the first medical description of anorexia nervosa in 1689. Two neurologists in 1873 separately described anorexia nervosa. Ernest Charles Lasegue, a student friend of Claude Bernard, and a favourite pupil of Trousseau wrote of a refusal of food that may be indefinitely prolonged. Historical precedence is explored and citations included.

Anorexia Nervosa↗

Some neurological aspects of laughter.

This brief survey of laughter attempts an analysis of its neurological mechanisms, evolution, role in social behaviour and its clinicopathological importance. The mechanisms of laughter, its physiological consequences and its demonstration by sound spectrography are considered. Something resembling laughter occurs in certain primates, and possibly rodents, though there are important differences. The evolution of laughter in a social context is appraised. Pathological laughter arises rarely, usually caused by diseases of the frontal or temporal lobes, and in hypothalamic hamartomata in children.

Animals↗

A note on gelastic epilepsy.

Laughter epilepsy or gelastic seizures have been described in various epilepsies arising from the temporal or frontal lobes, but most commonly from hypothalamic hamartomata. Gelastic seizures also arise from temporal and frontal lobe tumours and atrophic lesions. The essential clinical features are: stereotyped recurrence; absence of external precipitants; concomitance of other manifestations generally accepted as epileptic; presence of interictal or interictal EEG epileptiform discharges, and absence of conditions in which pathological laughter might occur. The history and clinical significance are discussed.

Epilepsies, Partial↗

Myofascial pain, fibromyalgia or fibrositis?

The terms myofascial pain, fibromyalgia and fibrositis are critically examined. They constitute diagnostic labels for non-specific musculoskeletal aches and pains. Analysis of the evidence shows that none of these labels is substantiated by hard physical signs or by laboratory evidence of consistent pathological or biochemical abnormality. What is the objective evidence for disorder(s) of muscle, fascia or fibrous tissues, so clearly indicated by these diagnostic names? Alternative terms such as 'regional pain syndrome' or 'chronic pain syndrome' merely redefine the clinical problem without providing a mechanism or basis for diagnosis. Despite different diagnostic criteria, these conditions, along with chronic fatigue syndrome, have many demographic and clinical similarities, most notably tender trigger points. Indeed, the terms are often used interchangeably. There are few differences in the symptoms, physical findings, laboratory tests, functional status, psychosocial features and psychiatric disorders. This paper seeks not to deny the existence of aches and pains, but to critically examine the utility of these terms. The only claimed physical sign is the presence of tender trigger points over muscles or muscle attachments. Research suggests that tender points are a measure of general distress related to pain complaints but separately associated with fatigue and depression. They are present in some normal subjects and are variable in occurrence in time in the same individual. They reflect no demonstrable pathology. It is therefore argued that none of these commonly used diagnoses represent distinct disease entities. A possible but unproven alternative hypothesis is that such symptoms relate to neural pain with both peripheral and central components, and in some instances psychological or wilful embellishment.

Facial Pain↗