Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-three styrene exposed workers from three different industrial sites were examined with electroencephalography and motor and sensory neurography. The three groups had respective styrene exposures of clearly above the threshold limit value (50 ppm), at about this level, and clearly below it. The neurophysiological results were compared with those of a group of normal controls and a group of 17 patients judged to suffer from sequelae after long-term heavy exposure to organic solvents (mainly painters). Ten subjects in the styrene group presented signs of a mild sensory neuropathy with polyphasic sensory responses of a low amplitude. The same pattern was commonly found among the reference group heavily exposed to solvents. The ten subjects in the styrene group with mild polyneuropathy had a significantly higher age and significantly heavier styrene exposure than the rest of the group. Age difference could not explain the difference in the neurophysiological parameters, and therefore the contributing role of styrene exposure has to be considered. The electroencephalographic analysis showed no changes of the dominant alpha frequency. An increased amount of diffuse slow activity was seen in many of the heavily exposed mixed-solvent cases and was seen in some of the styrene-exposed cases without a clear relation to degree of exposure. An increased occurrence of fast activity in central and precentral areas of the brain was found in the styrene group, as well as in the mixed-solvent group. This pilot study indicates that the same type of neurophysiological changes from the strictly normal are seen among workers exposed to styrene as those found among a group of patients judged to suffer from sequelae after chronic exposure to various organic solvents. The neurophysiological "profile" is (a) sensory nerve responses with low amplitude and long duration, (b) somewhat low sensory conduction velocities, (c) close to normal motor neurographic findings, and (d) an increased amount of fast activity in central and precentral regions in the electroencephalogram in combination with normal occipital alpha activity.
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PMID:Neurophysiological observations after chronic styrene exposure. 73 4

Disturbances of the central and peripheral nervous system in Crohn's disease can be directly or indirectly caused by the disease itself or by the treatment. The first mentioned disturbances are very seldom. Cerebral arterial and venous thromboses can be attributed to hypercoagulation. Malabsorption of vitamin B 12 or folic acid can lead to a subacute combined degeneration of the spinal cord, sometimes in combination with a polyneuropathy and an encephalopathy. Spinal abscesses very seldom occur. An opticusneuropathy can be caused either by vasculitis or by a lack of vitamin A and/or vitamin B. Polyneuropathies in Crohn's disease which are not induced by drugs are manifested as mononeuritis multiplex or as symmetrical sensory neuropathy. An autoimmune process is being discussed as the probable cause of there diseases. In some cases large doses and prolonged administration of metronidazole can lead to cerebral dysfunctions with state of confusion, alterations of consciousness, cerebral convulsions and cerebellar syndrome. Most of these symptoms disappear rapidly after this drug is not longer administered. In long-term administration of metronidazole 10-50% of the patients develop a sensory polyneuropathy with a total dosis of at least 22.5 g, but mostly above 60 g. After the use of metronidazole is stopped, it takes a substantial period of time until there is a full recovery from the symptoms.
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PMID:[Neurologic concomitant diseases in Crohn disease]. 128 45

The clinical electrophysiological and histological features of 10 cases of "chronic sensory demyelinating neuropathy" (CSDN) are reported. This entity is characterised by: 1) subacute or chronic progression; 2) pure sensory neuropathy; 3) high spinal fluid protein in the majority of cases; 4) electrophysiological evidence of demyelination affecting motor as well as sensory nerve fibres; 5) demyelination on sural nerve biopsy and 6) good response to immunotherapy in progressive phase. It is believed that this entity represents chronic inflammatory demyelinating polyneuropathy (CIDP) presenting as pure sensory neuropathy.
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PMID:"Chronic sensory demyelinating neuropathy": chronic inflammatory demyelinating polyneuropathy presenting as a pure sensory neuropathy. 132 1

A Japanese kindred with dominantly inherited amyloid polyneuropathy, commonly called familial amyloid polyneuropathy (FAP), has been identified. Amyloid protein was transthyretin (TTR) related and the patients were heterozygous for the mutant gene encoding TTR with a single amino acid substitution of cysteine for tyrosine at position 114. This family originated in Nagasaki Prefecture, Japan, and 12 of the 36 known members of six generations have been affected. The initial symptoms occurred in their thirties with the cardinal features of polyneuropathy, vitreous opacities and cardiac disease. Sensory neuropathy was severe in the lower limbs. Autonomic disturbances, especially postural hypotension, were the most debilitating to the patients. Amyloid deposits were detected widely in most organs except for the central nervous system. The duration from the onset of the disease to death was within 10 yrs. Heart failure caused by heavy amyloid deposits was the most common cause of sudden death.
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PMID:Familial amyloid polyneuropathy associated with the transthyretin Cys114 gene in a Japanese kindred. 133 Feb 2

Rational treatment of diabetic polyneuropathy depends upon establishing its cause, which is at present unknown. A number of animal models of diabetes have been examined and although abnormalities are detectable in the peripheral nervous system they do not duplicate the degenerative neuropathy encountered in the human. The relevance of these abnormalities is therefore uncertain, although they may reflect the earlier changes in man. For human neuropathy, it is likely that vascular lesions or an abnormal susceptibility to mechanical injury are responsible for focal neuropathies. The evidence that ischaemia and hypoxia are responsible for the diffuse sensory neuropathy and autonomic polyneuropathy is still equivocal and it is often difficult to establish whether the vascular changes are primary or secondary. Metabolic explanations, such as sorbitol accumulation in nerve, have not so far been adequately validated by responses to treatment. The manifestations of diabetic neuropathy are complex and a single explanation should not be sought.
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PMID:Diabetic neuropathy: models, mechanisms and mayhem. 156 4

The spontaneously diabetic BB/W-rat has emerged as an important model system for somatic and autonomic diabetic polyneuropathy. In this study we examined visual evoked potentials and the presence of morphometric and structural changes in the optic nerve and the retinal ganglion cells and their afferent axons contained in the retinal nerve fibre layer. A six-month duration of diabetes mellitus was associated with significant increases in the latencies of the visual evoked potentials. The latency of the first positive potential showed a 44% increase, and that of the first negative potential was prolonged by 41%. No significant changes were demonstrated at any of the amplitudes. In the optic nerve mean myelinated fibre size was significantly reduced to 82% of control values, which was accounted for by a significant reduction in axonal size. Axo-glial dysjunction, a prominent structural defect of diabetic somato-sensory neuropathy in both man and diabetic rodents, was non-significantly increased in the optic nerve. In diabetic animals retinal ganglion cells displayed dystrophic changes. No such changes were observed in age- and sex-matched control animals. Proximal axons of the retinal nerve fibre layer showed an increase in dystrophic axons in diabetic BB/W-rats. Morphometric analysis of optic nerve capillaries revealed no abnormalities except for basement membrane thickening. The present data suggest that the diabetic BB/W-rat develops a central sensory neuropathy, characterized functionally by prolonged latencies of the visual evoked potentials and structurally by an axonopathy of optic nerve fibres.
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PMID:Impaired visual evoked potential and primary axonopathy of the optic nerve in the diabetic BB/W-rat. 164 37

We report a patient with a progressive, predominantly sensory neuropathy and a IgM kappa M-protein that binds to Schmidt-Lantermann incisures. A sural nerve biopsy showed primary axonal damage and IgM deposits at Schmidt-Lantermann incisures were seen by direct immunoperoxidase. Serum from the patient injected into rat sciatic nerve reacts with the incisures as with those in the patient's nerve. The IgM kappa M-protein reacts with chondroitin sulfate C and binds to a broad nerve protein band with a mobility of between 170 and 118 kDa. Peripheral neuropathy may be related to the M-protein, which had immunocytochemical reactivity not previously described for patients with polyneuropathy and IgM monoclonal gammopathy.
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PMID:Axonal neuropathy in a patient with monoclonal IgM kappa reactive with Schmidt-Lantermann incisures. 164 11

Sensory ataxia as the chief manifestation of acute neuropathy is rather rare. Of the 224 cases of acute polyneuropathy seen over 6 years (1984-1990) only 10 patients (M:F 3:7) had disabling ataxia as the presenting feature. Their ages ranged from 14-61 years. Antecedent febrile illness was present in 6 patients and the peak deficit evolved over 2-25 days. Severe ataxia, paresthesia, distal areflexia and predominant joint sense loss were common to all, motor weakness was either absent or insignificant. CSF was acellular and revealed elevated protein in 3 subjects. All patients had electrophysiological evidence of severe sensory neuropathy with mild or no motor neuropathy. Sural nerve biopsy in one patient showed loss of large, as well as small, diameter myelinated fibres, secondary demyelination, but no evidence of inflammation. At follow up marginal to moderate improvement in ataxia was noted in only 5 patients. Absence of ophthalmoplegia and motor weakness, poor prognosis and characteristic electrophysiological and histopathological observations suggest that acute ataxic neuropathy may be a distinct entity.
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PMID:Acute ataxic neuropathy: a clinical, electrophysiological and morphological study. 166 83

We report a case of severe subacute autonomic and sensory neuropathy in a 52 year-old man. Cerebrospinal fluid protein was 275 mg/dl. Electrophysiological data were consistent with an axonal sensory neuropathy. Nerve biopsy showed a severe decrease in myelinated fibers, and a less severe loss of unmyelinated fibers. No cause was found and recovery was almost complete over 4 years, with minimal persistent dysautonomia. This case and 4 similar reported cases are compared with pure dysautonomia and with sensorimotor dysautonomic neuropathy. The site of damage is discussed and it is suggested that these cases are axonal forms of inflammatory polyneuropathy.
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PMID:[Sensory neuropathy and subacute dysautonomia. Clinical and pathological study]. 176 56

Three patients with hypereosinophilia showed different forms of peripheral neuropathy: severe polyneuropathy of prevalently sensory type (case 1), mild sensory neuropathy (case 2), acute mononeuropathy of the median nerve with subclinical polyneuropathy (case 3). Hypereosinophilia was probably idiopathic, however the presence of atypical findings suggested transition to vasculitides or collagen disease. Sural nerve biopsy in cases 1 and 2 showed features of axonopathy in both, although of different severity, reflecting the variability of clinical involvement and, probably, heterogeneous pathogenic mechanisms. Peripheral nerve involvement associated with hypereosinophilia may be related to neurotoxicity of eosinophils, or to vascular damage.
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PMID:Peripheral neuropathy associated with hypereosinophilia. 185 60


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