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Biomedical subjects

B M Patten

Publications and source records attributed to B M Patten.

At least 73 records · Page 4Linked to original sources
PubMed1975

A syndrome of acute zinc loss. Cerebellar dysfunction, mental changes, anorexia, and taste and smell dysfunction.

Oral administration of the amino acid histidine to six patients with progressive systemic sclerosis produced anorexia, taste ans smell dysfunction, changes in mentation, and cerebellar dysfunction in each patient; these changes were associated with significant decreases in serum zinc concentration and significant increases in urinary zinc excretion. Administration of zinc ion, even with continued histidine administration, returned each of the signs and symptoms to or toward normal within 8 to 24 hours in each patient at the same time that correction of the serum zinc concentration occurred. The signs and symptoms noted constitute a syndrome related to acute zinc loss.

Adult↗
PubMed1975

A hypothesis to account for the Mary Walker phenomenon.

Certain myasthenic patients show that their skeletal muscles produce a substance during ischemic exercise which, when released into the circulation, increases muscle weakness. This phenomenon has been named after Mary Walker, the physician who popularized its demonstration. It is suggested that ischemic exercise produces lactic acid that binds calcium, reducing ionized and total serum calcium. The decreased calcium has an adverse effect on skeletal muscle function especially in patients with myasthenia gravis, where neuromuscular function is often so precarious it may be interrupted by weak inhibitors.

Acetylcholine↗
PubMed1975

Neuromuscular disease in secondary hyperparathyroidism.

Neuromuscular function was evaluated in six patients with osteomalacia or secondary hyperparathyroidism, or both, as demonstrated by bone biopsy showing osteomalacia or increased immunoreactive parathyroid hormone, or both. Each patient had weakness, atrophy, and fatigability of proximal muscles, especially of the lower extremities. Most also showed involuntary fine movements of the tongue, hyperactive tendon reflexes with abnormal spread, and decreased vibration sensation, abnormalities similar to those observed in primary hyperparathyroidism. Every patient studies had evidence of neuropathic muscle disease, either on electromyography or muscle biopsy studies histochemically or both. Muscle biopsies showed no definite myopathic features. Treatment of the osteomalacia improved muscle strength. Patients with osteomalacia therefore have a treatable neuromuscular disease that is neuropathic in nature and resembles closely that found in primary hyperparathyroidism.

Adolescent↗
PubMed1972

Multiple sclerosis associated with defects in neuromuscular transmission.

Three patients with multiple sclerosis characterized by exacerbations and remissions of nervous system signs and symptoms disseminated in time and space also had the kind of easy fatiguability seen in myasthenia gravis. In each case abnormal decrements to repetitive stimulation were electromyographically demonstrated and treatment with ephedrine or anticholinesterase drugs increased the patient's functional capacity while improving the electromyographic abnormality. The suggestion is that these patients represent an overlap syndrome, analogous to the overlap syndrome existing between systemic lupus erythematosus and rheumatoid arthritis where clinical and laboratory features of two diseases coexist in the same patient at the same time. Presumably some patients with multiple sclerosis have deficient production of acetylcholine, just like patients with myasthenia, and treatment with agents useful in myasthenia is able partially to correct the symptoms caused by the deficiency. The cases illustrate how in neurology greater attention to the more immediate cause of clinical symptoms, in the absence of a known aetiology, may result in benefit to the patients.

Adult↗