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Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
 19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vitro studies seem to indicate that a serum factor may be involved in the pathogenesis of motor neuron disease. If so, plasmaphoresis might influence the course of amyotrophic lateral sclerosis (ALS) favorably. In the present study, therefore, ALS patients were subjected to weekly 21 plasma exchanges, using a Haemonetics blood separator. Seven other ALS patients, matched as closely as possible with the treatment group regarding age, sex, duration of symptoms as well as degree of involvement, served as control group. The progression of the disease was followed by an arbitrary grading system, assessment of muscular power by Zadig's dynamometer, and by tests for motor speed, coordination and for pulmonary function. Duration of treatment was from 6 to 15 months. Monthly evaluations indicated that the rate of deterioration was approximately the same in treatment and control groups. Plasmaphoresis carried out in this way does thus not alter the downhill course of ALS.
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PMID:Plasma exchange in motor neuron disease. A controlled study. 9 37

The neurologic status of 2,000 veterans who had had surgery for peptic ulcer between 1952 and 1957 was evaluated. In 1970, a total of 156 of these men were examined, 97 of whom had procedures that disrupted the normal continuity of the upper gastrointestinal tract. Twenty-one had neurologic disorders, including 17 patients with peripheral neuropathies. Procedures bypassing the ampulla of Vater were performed in 15 of these. The only detected factor associated with neurologic manifestations was weight loss since surgery. A mortality study of the total population revealed 865 patients had died by the end of 1973. There were seven deaths attributed to neurologic causes, one in a patient with amyotrophic lateral sclerosis and one in another with spinal paralysis. All seven were among the 70% of the deceased who had had surgery that disrupted the continuity of the upper gastrointestinal tract. Thus, we conclude that the type of surgery influenced the likelihood of neurologic complications, but at least for motor neuron disease, the increased risk was not appreciable.
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PMID:Neurologic disorders following surgery for peptic ulcer disease. 16 68

In certain genetically susceptible populations of wild mice a progressive motor neuron disease with a long latent period is caused by indigenous type C leukemia virus. Neuronal damage appears to be due primarily to a direct neurotropic effect of the virus and not to an immunogenic mechanism. The disease can be prevented by antiviral genetic means. Search for a similar virus in humans with ALS has been negative.
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PMID:Lower motor neuron disease in wild mice caused by indigenous type C virus and search for a similar etiology in human amyotrophic lateral sclerosis. 19 66

Clinical evaluation and pulmonary function tests were performed in 218 patients with motor neuron disease, mainly amyotrophic lateral sclerosis (ALS). Serial studies were obtained in 103 patients, in 31 until death from ALS. Most patients, regardless of the pattern of motor neuron involvement, had characteristic abnormalities in pulmonary function, including reduced forced vital capacity (FVC) and maximum voluntary ventilation (MVV). Reductions in the FVC and MVV to as low as 50% were commonly missed by clinical evaluators. Spirometry is therefore of value in detecting early involvement of respiratory neurons. Progressively greater reductions in the FVC and MVV in all the fatal cases indicate that serial spirometry has prognostic value in ALS.
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PMID:Spirometry in amyotrophic lateral sclerosis. 42 Jun 26

Hereditary canine spinal muscular atrophy is a newly recognized motor neuron disease occurring in Brittany Spaniels. The clinical manifestations, pattern of inheritance, electrodiagnostic findings, and muscle biopsies have features in common with human spinal muscular atrophy. Neuropathological examination discloses some loss of motor neurons in the spinal cord and brainstem. Many of the surviving motor neurons have neurofibrillary swellings in proximal axons, an abnormality similar to that which occurs early in the course of human amyotrophic lateral sclerosis. These axonal swellings are filled with maloriented skeins of neurofilaments. Since the proteins comprising neurofilaments are carried by slow axonal transport, their accumulation within axons suggest that the swellings may result from impaired slow transport, a hypothesis that can be tested in affected Brittany Spaniels. Hereditary canine spinal muscular atrophy is a new genetic, clinical, and pathological entity, and, at present, it appears to be the best currently available animal model of motor neuron disease.
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PMID:Hereditary canine spinal muscular atrophy. 43 62

Creatine phosphokinase (CPK) is usually elevated in inflammatory and degenerative muscle disease but is usually reported as normal in neuropathic diseases. A review of the literature indicates, however, that it is elevated in 50 to 75% of patients who have motor neuron diseases, and that these elevations are usually 5 to 6 times normal. The effect of bedrest and moderate exercise on serial CPK values in a patient with motor neuron disease is assessed. Bedrest for 24 hours decreased his CPK to 0.58 of the baseline value; 5 hours following moderate exercise it increased to 1.71 of the basal value. This phenomenon appears to be a response to exercise stimuli rather than to the disease process itself. CPK values up O 1000 IU/L are compatible with the diagnosis of amyotrophic lateral sclerosis (ALS). In patients whose CPK values seem atypical, it is best to have them rest 48 hours before repeating the test.
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PMID:Exercise effect on creatine phosphokinase elevation in motor neuron disease. 49 5

Calcium metabolism was studied prospectively in 12 patients with amyotrophic lateral sclerosis. Two patients showed mild hypocalcemia, malabsorption of calcium, and elevated plasma parathyroid hormone concentrations. Serum 25-hydroxyvitamin D was decreased in one and low-normal in the second. These two patients and a third showed aminoaciduria on thin layer chromatography. Calcium metabolism was apparently restored to normal by dihydrotachysterol, a vitamin D analog, but no improvement in neurologic function resulted. Bone radiographs taken in search of metabolic bone disease showed a significant increase in the incidence of congenital vertebral anomalies in the ALS patients (50% versus 8%). The relationship of the abnormalities in calcium metabolism and in vertebral structure to the etiology of motor neuron disease is not known.
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PMID:Calcium metabolism in amyotrophic lateral sclerosis. 86 4

To identify antecedent events contributing to the development of amyotrophic lateral sclerosis, we studied 25 amyotrophic lateral sclerosis patients in whom we tabulated the incidence of factors previously associated with motor neuron disease and compared the incidences with those found in 25 hospitalized patients and 25 normal people. More amyotrophic lateral sclerosis patients reported exposure to lead and mercury, participation in athletics, and consumption of large quantities of milk. Exposure to lead and mercury, athletic participation, and milk ingestion are possible risk factors that may predispose to the development of amyotrophic lateral sclerosis.
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PMID:Antecedent events in amyotrophic lateral sclerosis. 94 26

Intercostal muscle end-plates were measured in patients with amyotrophic lateral sclerosis (ALS) and more benign motor neuron disease (MND). The length of the intact end-plates in ALS and MND was not different from the controls. Segmented end-plates were increased in both ALS and benign MND, and the end-plate length was greatest in ALS. In individual ALS cases, no correlation was found between the end-plate abnormalities and relevant clinical variables.
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PMID:End-plate morphology in amyotrophic lateral sclerosis. 118 Jul 38

In a retrospective study of the charts of 39 patients who had motor neuron disease we found that over 50 percent of patients had radiographic abnormalities of bone and over 20 percent had serum calcium concentrations out of the range observed in normal controls. Statistical analysis indicated that, in respect to serum calcium levels, patients who have motor neuron disease are a separate population. These findings, which might reflect a disturbance in bone or calcium metabolism in patients with motor neuron disease, are of interest in view of the known ability of divalent ions other than calcium, such as lead and mercury, to simulate motor neuron disease, and the discovery that patients with proven primary and secondary hyperparathyroidism may have features of amyotrophic lateral sclerosis.
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PMID:Motor neuron disease: retrospective study of associated abnormalities. 127 82


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