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Biomedical subjects

M Swash

Publications and source records attributed to M Swash.

At least 19 recordsLinked to original sources
PubMed1992

Hippocampal and neocortical ubiquitin-immunoreactive inclusions in amyotrophic lateral sclerosis with dementia.

Amyotrophic lateral sclerosis (ALS) patients with dementia were found to have ubiquitin-immunoreactive (IR) inclusions in the dentate granule cells of the hippocampus. These inclusions were also present in some patients with minor cognitive changes but otherwise typical ALS. Ubiquitin-IR inclusions were also found in neurons of superficial layers of the frontal and temporal cortex and in the entorhinal cortex in patients with ALS and dementia. These ubiquitin-IR inclusions were non-argyrophilic, and were not labelled by antibodies which identify Alzheimer's neurofibrillary tangles and Pick bodies, nor were they typical of cortical Lewy bodies. Our findings indicate that ubiquitin-IR inclusions in small neurons of the hippocampus, entorhinal area and neocortex are a characteristic feature of degeneration of non-motor cortex in ALS, and are particularly associated with cognitive impairment and dementia of frontal lobe type.

Adult↗
PubMed1992

Fiber density in acute and chronic inflammatory demyelinating polyneuropathy.

The fiber density in the deltoid, extensor digitorum communis, and first dorsal interosseous muscles was measured using SFEMG in 11 patients with acute and chronic inflammatory demyelinating polyneuropathy. The fiber density was increased in 58% of the muscles studied. The deltoid muscle was the most abnormal of the 3 muscles studied. There was no correlation with the clinical syndrome, with conduction block or slowed motor conduction, or with the distribution of weakness. Changes were noted even in patients studied within 3 weeks of presentation, suggesting that reinnervation begins soon after the onset of the disease.

Adult↗
PubMed1992

Adverse effect of verapamil in myasthenia gravis.

Verapamil, a class IV anti-arrhythmic drug that blocks voltage-dependent calcium channels in cardiac and smooth muscle, also has effects on presynaptic and postsynaptic voltage-dependent calcium channels at the neuromuscular junction. In a postoperative patient with pre-existent myasthenia gravis, oral verapamil caused a marked exacerbation in myasthenic weakness.

Contraindications↗
PubMed1992

Cyclosporin A therapy in paraprotein-associated neuropathy.

A case of IgG paraprotein-associated demyelinating neuropathy complicated by respiratory failure, which was unresponsive to standard immunosuppressive drug therapy, is reported. Cyclosporin A therapy resulted in a marked clinical recovery with objective improvement in nerve conduction and vital capacity. The beneficial response suggests that cell-mediated immunity is an important pathogenetic mechanism, and that cyclosporin A may be useful in the treatment of other refractory cases of paraprotein-associated neuropathy.

Adult↗
PubMed1992

What do we really know about amyotrophic lateral sclerosis?

The cause of amyotrophic lateral sclerosis is unknown. In this review clinical and scientific data that are pertinent to understanding this disease are reviewed. There are currently several major controversies concerning the possible role of immunological factors, genetic factors, environmental toxins, and viral infection in pathogenesis. These concepts must be considered in relation to what is known about the disease in all its aspects, including epidemiological data, information on the classical and molecular pathology of the disease, and on associated involvement of other systems, e.g., the spinocerebellar pathways and frontal dementia. Only when all this information is assimilated can full understanding of the disease and, hopefully, a logical approach to treatment and prevention, be achieved.

Amyotrophic Lateral Sclerosis↗
PubMed1992

Criteria for diagnosis of familial amyotrophic lateral sclerosis. European FALS Collaborative Group.

Clinical criteria for the diagnosis of motor neuron disease, agreed at the inaugural meeting of the European Familial Amyotrophic Lateral Sclerosis Collaborative Group, are described. The criteria are derived from those developed for the study of sporadic amyotrophic lateral sclerosis, and allow the inclusion of certain recognized clinical sub-types of familial amyotrophic lateral sclerosis. They will require testing for consistency and sensitivity.

Amyotrophic Lateral Sclerosis↗
PubMed1992

Botulinum toxin in the treatment of chronic urinary retention in women.

Six women were identified as having difficulty in voiding or complete urinary retention due to abnormal myotonic-like electromyographic (EMG) activity in the striated muscle of the urethral sphincter. An attempt was made to improve voiding by injection of botulinum toxin into the striated sphincter muscle. Although 3 patients then developed transient stress incontinence, demonstrating that sufficient botulinum toxin had been given to cause sphincter weakness, no patient had significant symptomatic benefit.

Adult↗
PubMed1979

Pathogenesis of ano-rectal incontinence. A histometric study of the anal sphincter musculature.

Type 1 fibre predominance was found in the external anal sphincter, puborectalis and levator ani muscles of 17 control subjects, and of 16 patients with ano-rectal incontinence. In the external anal sphincter and puborectalis muscles of the control subjects the mean diameter of Type 2 fibres was slightly greater than that of Type 1 fibres, but in the levator ani muscles of control female subjects the mean diameter of Type 1 fibres was much greater than that of Type 2 fibres. In the patients with anorectal incontinence there was marked hypertrophy of fibres of both histochemical types. This was most marked in the puborectalis and external anal sphincter muscles. In 12 of the 16 incontinent patients there were histological and statistical features consistent with a neurogenic disorder. These histometric studies provide a quantitative basis for physiological and pathological studies of these muscles in incontinence and other anorectal disorders.

Adenosine Triphosphatases↗
PubMed1979

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↗
PubMed1979

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↗
PubMed1979

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↗