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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chicken sciatic nerves undergo demyelination following intraneural injection of diphtheria toxin and subsequent atrophy of some muscular cells. Paresis occurs after one week and lasts approximately three weeks; at the height of the lesion C14-leucine was injected into the ventral horn cells of the spinal cord. The axonal transport of fast flowing labelled proteins was followed down the sciatic nerve axons and flow rates at two different times were measured. Muscle cells were stained for succinic dehydrogenase and ATPase; fibre diameters, total protein, and total radioactivity associated with the nerves were also measured. The results showed that the fast flowing labelled proteins accumulated at the demyelination site while the muscle cells supplied by these nerves showed reduction of fibre diameter and evidence of degeneration. Further studies are in progress on slow moving proteins and muscle cells.
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PMID:Effect of diphtheritic demyelination on axonal transport in the sciatic nerve and subsequent muscle changes in the chicken. 8 Sep 47

A 3-year-old boy was referred for evaluation of psychomotor retardation. He had a waddling gait with proximal hypotonia and paresis. Computed tomography (CT scan) and magnetic resonance imaging (MRI) of the brain demonstrated symmetrical lesions in the basal ganglia suggesting bilateral necrosis. Lactate and pyruvate levels in blood and cerebrospinal fluid were persistently elevated. A biopsy of the quadriceps muscle showed normal light microscopic findings except for a slightly raised number of lipid droplets. Electron microscopy confirmed this and also showed a rather large number of subsarcolemmal mitochondria without crystalline inclusions. Biochemical studies showed a normal carnitine level and normal mitochondrial enzyme activities in muscle homogenate, including succinate-cytochrome c reductase. However, intact isolated mitochondria failed to oxidize succinate. An explanation for this paradoxical finding is a deficiency in that part of the coenzyme Q (CoQ) that is reduced by the succinate dehydrogenase complex. The differential diagnosis between Leigh's syndrome and infantile bilateral striatal necrosis (IBSN) is discussed. The role of neuroradiology in prompting complementary investigations is stressed.
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PMID:Defect in succinate oxidation by isolated muscle mitochondria in a patient with symmetrical lesions in the basal ganglia. 337 46

The vascular wall weakness caused by dysplastic alterations predisposes to the spontaneous dissection of cerebral arteries. The authors hypothesized for the first time that dysplasia might be the result of mitochondrial cytopathy. To test this hypothesis, the muscle biopsy was conducted in 3 male patients, aged 30-38 years, with the spontaneous dissection of the internal carotid (2) and posterior cerebral (1) arteries. Clinically dissections manifested by ischemic stroke (2) or the peripheral paresis of the hypoglossal nerve (1). The morphological study of fresh frozen sections of muscle by modified Gomori trichrome method revealed ragged-red fibers The histochemical study showed the severe decrease of the stain on succinate dehydrogenase and cytochrome-c-oxidase as well as the focal intensive staining of peripheral regions of muscle fibers. The complex of found changes is characteristic for a mitochondrial pathology. No patients had A3243G tRNA gene mutation, the most common mutation for MELAS. The serum lactate level was elevated only in one patient. We suggest that the mitochondrial disorder occurs not only in muscle, but also in cerebral artery wall--mitochondrial arteriopathy, which predisposes to spontaneous cerebral artery dissection.
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PMID:[Mitochondrial arteriopathy as a cause of spontaneous dissection of cerebral arteries]. 2073 20