Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reported is a case of multiple mononeuropathy which appeared during the administration of recombinant interferon-alpha 2a (rIFN-alpha 2a) for treatment of chronic hepatitis C. A 38-year-old man received an intramuscular injection of rIFN-alpha 2a, 6 x 10(6) IU, every one or two days for a nine week period. Seven weeks after the initiation of rIFN-alpha 2a therapy he developed numbness of the tongue and extremities and weakness of the upper extremities. Neurological examination revealed an asymmetrical disturbance of touch and pain sensation in the tongue, trunk, left shoulder and extremities accompanied by painful dysesthesia. Moderate weakness and muscular atrophy were noted in the right hand and left shoulder. Electrophysiological studies showed the amplitude of the compound muscle action potentials and sensory nerve action potentials were significantly decreased, when the right median and ulnar nerves were stimulated. Additionally, the conduction velocities were normal and needle electromyography showed fibrillation potentials suggesting an axonal form of multiple mononeuropathy. Biopsies of the muscle and nerve failed to show pathological changes, however. The clinical and electrophysiological abnormalities reduced gradually with methyl-prednisolone pulse therapy and administration of prednisolone and mizoribine. Therefore, in this case, administration of rIFN-alpha 2a may have induced multiple mononeuropathy of the axonal form.
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PMID:[Multiple mononeuropathy during recombinant interferon-alpha 2a therapy for chronic hepatitis C]. 130 Feb 64

Ischemia plays an important role in the development of neuropathies associated with various disorders, such as peripheral vascular occlusive diseases, necrotizing vasculitides, diabetes mellitus and nerve compression or trauma. Although a multiple mononeuropathy or an asymmetrical polyneuropathy is the usual clinical presentation of ischemic neuropathy, some patients present with a neuropathy that is mainly distal and symmetrical. Pathologically, nerve ischemia results in focal or multifocal central fascicular or sector fiber degeneration. These ischemic lesions tend to begin at mid-upper arm or midthigh level, which is the watershed zone of poor perfusion, and become more diffuse distally. Nerve ischemia at the level of distal small fascicles often induces sub-perineurial crescent lesion rather than central fascicular fiber degeneration. Physiologically, reduced nerve blood flow with endoneurial hypoxia has been demonstrated in experimental diabetic and galactose neuropathies. Endoneurial ischemia/hypoxia in galactose neuropathy appears to be due to increased intercapillary distances and constriction of trans-perineurial vessels resulting from endoneurial edema. Although acute ischemic neuropathy has been well investigated, little is known about functional or structural responses of peripheral nerve to chronic ischemia.
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PMID:[Ischemic neuropathy]. 209 82

Recently a subset of chronic demyelinating inflammatory polyneuropathies with asymmetrical involvement limited to upper limbs, at least at the onset, resembling a multifocal mononeuropathy has been described. Electrodiagnostic testing disclosed multifocal CB outside the common entrapment sites has been described. We report a 55 years old man with a 4 years history of paresis, numbness, fasciculations, myokymia, cramps and mild amyotrophy. Electrophysiological evaluation showed proximal multifocal conduction block and abundant spontaneous activity as fasciculations, myokymia and scarce denervation activity. The importance of taking into account this entity in the differential diagnosis of patients with suspected mononeuritis multiplex or motoneuron disease is emphasized. The nosologic place of this entity is also discussed.
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PMID:[Multifocal polyneuropathy with persistent conduction blockage. A new subset of chronic inflammatory polyneuropathies]. 255 98

A 33 year-old male homosexual infected with human immunodeficiency virus type I developed an asymmetrical and painful neuropathy in the lower limbs. Neuro-muscular biopsy showed a necrotizing vasculitis. There were no clinical features indicative of systemic vasculitis. Prednisone therapy dramatically improved the neuropathy, without adverse effects. Although rare, necrotizing arteritis must be considered in HIV-1 patients with neuropathy, especially in case of mononeuropathy multiplex and when immunodepression is mild or absent, since a successful corticosteroid therapy can be prescribed.
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PMID:[Neuropathy caused by necrotizing vasculitis in HIV-1 infection]. 827 36

A 35-year-old woman presented with a 4 year history of stepwise sensory loss which progressed in an asymmetrical fashion (mononeuropathy multiplex) and developed into a relatively symmetric polyneuropathy which was purely sensory by clinical and electrodiagnostic criteria. Sural nerve biopsy revealed demyelination with axonal sparing. Extensive laboratory evaluation failed to reveal a definite cause. This case is unique among well-documented cases of chronic inflammatory demyelinating polyneuropathy (CIDP) in that it is purely sensory by both clinical and electrodiagnostic criteria, and may represent a distinct entity rather than an extension of the spectrum of CIDP.
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PMID:Clinically and electrodiagnostically pure sensory demyelinating polyneuropathy. 873 35

We report a 23-year-old woman, who had a relapsing-remitting multiple mononeuropathy with multifocal nerve enlargement. The patient was characterized by asymmetrical, marked enlargement of multiple nerves in the arms (median and ulnar nerves) and neck (accessory nerve) bilaterally. Sequential nerve conduction studies revealed persistent demyelinative abnormalities, especially across the segment of nerve thickening. The MRI of the proximal arm confirmed the markedly enlarged median and ulnar nerves which showed high signal intensity on T2-weighted images and partial enhancement after administration of gadolinium. We consider that the patient had the clinical features of "multifocal pseudohypertrophic neuropathy" described by Adams et al, and that chronic demyelination and inflammation associated with impairment of the blood-nerve barrier might be underlying mechanisms.
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PMID:[A case of relapsing demyelinating multiple mononeuropathy with multifocal nerve enlargement]. 890 85

We reported a case of mononeuropathy multiplex associated with anti-GM1 and -SGLPG antibodies in a patient with ongoing Hashimoto disease. A 56-year-old woman was admitted with asymmetrical patchy sensory and motor disturbance in the extremities. Muscle atrophy and weakness in the left palm and bilateral tibialis anterior muscles were also noted. Deep tendon reflexes were normal in all the extremities. Superficial and deep sensations were reduced in the hands and feet bilaterally, and the distribution of sensory loss was irregular. Her serum was positive for antinuclear antibody, rheumatoid factor, anti-RNP antibody, and anti-SS-A antibody. Serial electrophysiological studies suggested that the predominant process was axonal degeneration of the sensorimotor nerves. On sural nerve biopsy, there were no findings of vasculitis but severe axonal degeneration was observed. Thin-layer chromatography with immunostaining revealed anti-GM1 and -SGLPG antibodies. Treatment with corticosteroids was successful. In this case, the anti-GM1 antibody may have played a role in the pathogenesis of mononeuropathy multiplex associated with autoimmune disease.
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PMID:[A case of mononeuropathy multiplex associated with anti-GM1 and -SGLPG antibodies in a patient with ongoing Hashimoto disease]. 1020 76

The association between the use of statins and neuromuscular disease is currently being intensely discussed. We relate a 63 years old man with possible case of statin-induced neuropathy in a patient with dislipidemia in use of simvastatina at high doses. The electrophysiologic studies disclosed findings compatible with mononeuropathy multiplex, suggested by clinical prescutation of asymmetrical numbness and weakness. More common causes of mononeuropathy multiplex were excluded and the patient improved after the discontinuation of the drug.
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PMID:Simvastatin-induced mononeuropathy multiplex: case report. 1527 60

A 75-year-old man, previously diagnosed as having chronic hepatitis C virus (HCV) infection, suddenly developed left foot drop, followed by progressive motor weakness and sensory disturbance in all of the extremities. Because of an elevated level of the rheumatoid factor (RF), he had been treated with antirheumatic drugs three years before the onset of his neurological symptoms. Within two months, he became unable to walk any more, and was transferred to our hospital. Neurologic examination showed asymmetrical severe muscular weakness and atrophy of all the limbs, and a sensory deficit under the level of the wrists and knees. Livedo reticularis was also noted in bilateral legs. Nerve conduction study revealed severe sensorimotor axonal neuropathy, and muscle biopsy specimens showed necrotizing vasculitis of small arteries in the perimysium. Serological tests indicated type II cryoglobulinemia (monoclonal IgAkappa + polyclonal IgG). A diagnosis of vasculitic neuropathy associated with HCV-related mixed cryoglobulinemia was made. A high-dose intravenous immunoglobulin therapy (IVIg) and a high-dose steroid therapy were not effective, and he died of alveolar hemorrhage probably due to pulmonary vasculitis. Postmortem pathological examination revealed severe vasculitis, accompanied by fibrinoid degeneration and the infiltration of predominant mononuclear cells into the small and medium-sized vascular walls of multiple organs such as the liver, kidney, pancreas and intestine as well as the peripheral nerves and skeletal muscles. A severe loss of myelinated fibers were also observed in the multiple peripheral nerves examined. We emphasize that patients with HCV infection and mixed cryoglobulinemia may develop severe systemic vasculitis resembling polyarteritis nodosa leading to often life-threatening polyvisceral failure, particularly in patients showing progressive mononeuropathy multiplex.
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PMID:[An autopsy case of systemic vasculitis associated with hepatitis C virus-related mixed cryoglobulinemia presenting severe peripheral neuropathy]. 1556 85

The hereditary neuropathy with liability to pressure palsies (HNPP) is an autossomal dominant disorder manifesting recurrent mononeuropathies. Objective Evaluate its clinical and nerve conduction studies (NCS) characteristics, searching for diagnostic particularities. Method We reviewed the neurological manifestations of 39 and the NCS of 33 patients. Results Family history was absent in 16/39 (41%). The onset complaints were weakness in 24, pain in 6, sensory deficit in 5 and paresthesias in 4. Pain was seen in 3 other patients. The following neuropathy patterns were found: multiple mononeuropathy (26), mononeuropathy (7), chronic sensorimotor polyneuropathy (4), chronic sensory polyneuropathy (1) and unilateral brachial plexopathy (1). NCS showed a sensorimotor neuropathy with focal conduction slowing in 31, two had mononeuropathy and another brachial plexopathy. Conclusion HNPP presentation is variable and may include pain. The most frequent pattern is of an asymmetrical sensory and motor neuropathy with focal slowing at specific topographies on NCS.
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PMID:Clinical and neurophysiological features of the hereditary neuropathy with liability to pressure palsy due to the 17p11.2 deletion. 2698 83


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