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Biomedical subjects

M Swash

Publications and source records attributed to M Swash.

At least 271 records · Page 15Linked to original sources

Diagnosis and management of tuberculous paraplegia with special reference to tuberculous radiculomyelitis.

Paraplegia occurred in eight of 17 patients with central nervous system tuberculosis. In six of these paraplegia was the presenting feature. Paraplegia may complicate tuberculous meningitis, or vertebral tuberculosis, but it may also occur, as in three of our cases, as a primary localised spinal tuberculous radiculomyelitis. These cases are presented in relation to the concept that paraplegia complicating these forms of tuberculosis is caused by radiculomyelitis.

Adolescent↗

Infection of the brainstem by Listeria monocytogenes.

A case of brainstem infection by Listeria monocytogenes is described. The patient was a 63 year old man previously in good health and his illness did not follow the usual bi-phasic pattern. There was no prodromal phase, and the progressive brainstem signs with a lymphocytosis and a normal sugar level in the CSF led to a tentative diagnosis of viral brainstem encephalitis. Ampicillin was begun only when signs of pulmonary infection developed. Clinical diagnosis is difficult but ampicillin should probably be used in any doubtful case in which a "viral" brainstem encephalitis is being considered.

Brain Abscess↗

Significance of immunoglobulin deposition in peripheral nerve in neuropathies associated with paraproteinaemia.

Direct and indirect immunofluorescent studies of sural nerves were carried out in two patients with paraproteinaemia and neuropathy, in four other patients with axonal or demyelinating neuropathies, and in one normal sural nerve. IgM was demonstrated directly in the two cases of paraproteinaemia and neuropathy, and indirectly, using the serum of one of these cases, in a case of axonal neuropathy and in one case of chronic Guillain-Barré syndrome. In the latter case, IgM deposition also occurred after exposure to normal serum. These results suggest that the paraprotein itself did not directly cause neuropathy, but that immunoglobulin deposition is probably a secondary process, caused by diffusion into damaged nerves.

Aged↗

Benign postinfection polymyositis.

Six patients developed persistent muscular cramps, aching pain, and fatigability after an influenza-like illness. Electromyography showed myopathic changes, although results of routine laboratory investigations were normal in all but one patient, whose serum creatine kinase concentration was slightly increased. All but one of the patients improved: three were asymptomatic within one to two years. The syndrome was probably a benign form of polymyositis.

Adult↗

Possible biochemical basis of memory disorder in Alzheimer disease.

Damage to the hippocampal formation, whether focal or diffuse, leads to severe impairment of short-term memory. The most common presenting symptom of Alzheimer disease is loss of short-term memory, and histologically the hippocampus is characteristically affected. Choline acetyltransferase, which is involved in the synthesis of acetylcholine, is depleted in the hippocampus in the disorder. Anticholinergic drugs administered to normal subjects can simulate some aspects of the memory defect seen in Alzheimer disease. It is postulated that damage to a cholinergic neuronal pathway running to or from the hippocampus underlies the memory disorder. This suggestion implies that it may be possible to improve memory in patients with Alzheimer disease by pharmacological means.

Acetylcholine↗

The significance of ragged-red fibres in neuromuscular disease.

The pathological significance of ragged-red fibres is uncertain. We have studied ragged-red fibres in the muscle biopsies of 3 adults; one with polymyositis and two with progressive external ophthalmoplegia. All the ragged-red fibres were Type 1 fibres. In two patients the mean diameter of the ragged-red fibres was significantly smaller than the unaffected Type 1 fibres. Some of these fibres showed features of regeneration, and others of degeneration. In the patient with polymyositis the mitochondria were proliferated and contained osmiophilic dense bodies; in the other two patients paracrystalline mitochondrial inclusions were prominent. These findings suggest that ragged-red fibres do not represent a single pathological process.

Adult↗

Myopathy in Whipple's disease.

We report a patient with Whipple's disease who developed a myopathy that improved during antibiotic therapy. The muscle biopsy showed mild type 2 fibre atrophy, type 1 fibre preponderance, variability in fibre size, and changes in the myofibrillar pattern of affected fibres. Interfascicular macrophages contained PAS-positive material. With the electron microscope these macrophages contained membranous inclusions and bacillary bodies, similar to those seen in the jejunal biopsy.

Biopsy↗

Sphincter denervation in anorectal incontinence and rectal prolapse.

Biopsies of the external anal sphincter, puborectalis, and levator ani muscles have been examined in 24 women and one man with long-standing anorectal incontinence, 18 of whom also had rectal prolapse, and in two men with rectal prolapse alone. In 16 of the women anorectal incontinence was of unknown cause, but in eight there was a history of difficult labour. Similar biopsies were examined in six control subjects. In all the incontinent patients there was histological evidence of denervation, which was most prominent in the external anal sphincter muscle biopsies, and least prominent in the levator ani muscles. Myopathic features, which were thought to be secondary, were present in the more abnormal biopsies. There were severe histological abnormalities in small nerves supplying the external anal sphincter muscle in the three cases in which material was available for study. We suggest that idiopathic anorectal incontinence may be the result of denervation of the muscles of the anorectal sling, and of the anal sphincter mechanism. This could result from entrapment or stretch injury of the pudendal or perineal nerves occurring as a consequence of rectal descent induced during repeated defaecation straining, or from injuries to these nerves associated with childbirth.

Adult↗

Implications of longitudinal muscle fibre splitting in neurogenic and myopathic disorders.

Histological and electromyographic studies indicate that longitudinal muscle fibre splitting is a common finding in neuromuscular disorders. Separated fragments derived by splitting may undergo degeneration or enlarge to become separate, innervated fibres, thus leading to an increased number of fibres within motor units. Splitting may, therefore, lead to the formation of clusters of fibres of uniform histochemical type, but of variable diameter and length, both in neurogenic and in myopathic disorders. Fibre splitting is thus a factor leading to functional compensation in these disorders.

Action Potentials↗

Effects of oral amines on the EEG.

Oral tyramine activated pre-existing episodic EEG abnormalities--namely, sharp waves, spike and wave, and localised theta activity--in epileptic patients. Little change was found in the EEGs of migrainous subjects after chocolate or beta-phenylethylamine. The implications of the findings with tyramine are discussed.

Administration, Oral↗

Neostigmine-induced end-plate proliferation in the rat. A study using supra-vital methylene blue.

The supra-vital methylene blue technique was used to study motor end-plate morphology in 21 BD-1X rats, treated for 7 to 16 weeks with oral neostigmine bromide, and in five control animals. Motor endings of treated animals showed preterminal, terminal, and ultraterminal sprouting and an increase in mean end-plate length (p less than 0.001). These changes were most prominent after 14 weeks of treatment. After 16 weeks of therapy, mean end-plate length decreased and the proliferative abnormality became less evident. The adverse effect of neostigmine on motor end-plates may have clinical relevance in the management of myasthenia gravis and may be partly responsible for the end-plate abnormalities previously reported in this disease.

Administration, Oral↗