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)

Neurofibromatosis 2 (NF2) is an autosomal dominant disease characterised by development of tumours in the central and peripheral nervous system. Some NF2 patients develop acro-distal sensory motor polyneuropathy that can hardly be explained by the tumour burden alone. In the present study eight sural nerve biopsy specimens from seven NF2 patients suffering from polyneuropathy were investigated, data including clinical course of the disease, electrophysiological findings, teased fibre preparations, histopathological, morphometric, immunohistochemical, electron microscopic and molecular genetic findings. All patients suffered from distal symmetric reflex loss, symmetrical stocking-like hypalgesia and hypesthesia and loss of vibration sense later followed by a slowly progressive distal muscle atrophy and paresis. Sural nerve biopsy specimens revealed a pathological reduction of nerve fibre density correlating with age. In addition, diffuse proliferation of Schwann cells was observed in five of eight biopsies, and small endoneurial tumourlets of schwannomas and perineuriomas were found in two of eight and one of eight samples, respectively. Ki-67 labelling revealed a slight endoneurial proliferative activity in three cases. Schwann cell onion bulbs with or without central myelinated axon were seen in two cases. The findings suggest an axonopathy of multifactorial origin resulting not only from gross tumour growth but, in addition, from small endoneurial tumourlets, diffuse proliferation of Schwann cells and proliferation of perineurial cells.
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PMID:Polyneuropathy in neurofibromatosis 2: clinical findings, molecular genetics and neuropathological alterations in sural nerve biopsy specimens. 1211 61

Palatopharyngeal paresis has never been reported to be contralateral in the lateral medullary infarction (LMI). A 65-year-old lady with acute dorsolateral infarction in the left medulla presented mild hoarseness, mild dysphagia, mild gait ataxia along with marked hypalgesia and thermal anesthesia on the right limbs. To our surprise, palatal weakness was on the right side, instead of being on the left side as expected in typical Wallenberg syndrome. The palatal paresis was noted during voluntary phonation but turned into normal movement while gag reflex was induced. An involvement of corticobulbar fibers before synapsing into the ipsilateral caudal medulla or a selective involvement of the peri-ambigual reticular formation and/or its post-synaptic connection fiber destined to the contralateral swallowing center presumably underlies such a rare contralateral palatal paresis.
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PMID:Lateral medullary infarction presenting contralateral palatal paresis. 1928 Aug 67


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