Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerous studies have been devoted to the various histopathologic changes of the surface of the tongue. The muscles of the tongue and their changes in the process of ageing as well as in neurogenic atrophies, however, have not been systematically examined so far. Enlarging upon previous studies, an autopsy material of 170 tongues from all age groups was histologically examined in order to identify the steps in the development of age-related atrophy. These are characterized by a histometrically documented atrophy of the musculature with progressive lipomatosis. Fatty infiltration starts in the 2nd/3rd decade at three sites of predilection: body, root and tip of the tongue in the region of the anterior lingual gland (NUHN). The age-dependent atrophy and the known clinical behaviour of neurogenic atrophies of the tongue are correlated with the histopathology of three typical forms: a neurogenic myasthenic atrophy of the tongue with high-grade symmetrical fatty replacement as an expression of a progressive myasthenic denervation; a lipomatous atrophy of the tongue as a late stage of poliomyelitis and long-term treatment in the "Iron Lung", and a lipomatous hemiatrophy due to posttraumatic extracranial hypoglossus paresis. The paretic part of this tongue consists of 85-90% fatty tissue. The different degrees of muscular atrophy of the tongue are largely compensated by metaplasia of fatty tissue in the perimysium following muscular degeneration (in the sense of a fatty replacement). With the exception of general and severe myasthenic atrophy, size, form and function of the tongue fail to show any significant changes in age-related atrophy and hemiatrophy.
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PMID:Histopathology of different types of atrophy of the human tongue. 358 8

Lumbar spinal tumoral calcinosis and spinal epidural lipomatosis are rare conditions. We present a 70-year-old female patient with serology negative spondyloarthropathy who developed paresis due to tumoral calcinosis in the left facet joint between L5 and S1 levels and spinal epidural lipomatosis at L5 and S1 levels. Surgery was performed to excise the lesions en bloc. Neural decompression was provided. Neurological symptoms improved after surgery. Here, we report the first serology negative spondyloarthropathy case that had concomitant development of tumoral calcinosis and spinal epidural lipomatosis.
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PMID:Tumoral calcinosis and epidural lipomatosis of the lumbar spine. 2129 3