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)

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a chronic, proximal and distal, asymmetrical or symmetrical, motor and sensory demyelinating polyneuropathy with a progressive course for at least 2 months. The accurate diagnosis is crucial as CIDP is amenable to treatment. Recent advances have provided new strategies and options for management of this syndrome. In this article, we review the clinical and diagnostic features as well as discuss recent insights and treatment strategies along with our experience in the management of patients with CIDP.
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PMID:Management strategies in chronic inflammatory demyelinating polyradiculoneuropathy. 2064 61

Nerve enlargement has early been recognized in CIDP and plexus MRI hypertrophy has been reported in typical CIDP cases. Our aim is to determine plexus MRI value in the diagnosis of CIDP with an initial atypical presentation, which, up to now, has not been demonstrated. Retrospective study of 33 consecutive patients suspected of CIDP. Plexus MRI was performed on the most affected territory (brachial or lumbar). Were assessed: plexus trophicity, T2-STIR signal intensity and gadolinium enhancement. Final CIDP diagnosis was made after comprehensive workup. A histo-radiological correlation was performed. Final CIDP diagnosis was made in 25 (76%) including 21 with initial atypical clinical presentation. Eleven CIDP patients (52%) with initial atypical clinical presentation had abnormal plexus MRI including 9 suggestive of CIDP (43%) and none of the patients with an alternative diagnosis. Hypertrophy of the proximal plexus and/or extraforaminal roots was found in 8 cases and Gadolinium enhancement in 2 cases. Abnormalities were more frequent on brachial (86%) than lumbosacral MRIs (29%) and asymmetrical (72%) and most often associated with histological signs of demyelination. The nerve biopsy was suggestive of CIDP in 9/13 patients with normal MRI. Plexus MRI seems useful in the diagnostic strategy of patients with suspicion of CIDP with atypical presentation. Nerve biopsy remains important when other investigations are inconclusive.
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PMID:Contribution of plexus MRI in the diagnosis of atypical chronic inflammatory demyelinating polyneuropathies. 2672 95

SLE (systemic lupus erythematosus) is a multisystem autoimmune disorder of unknown aetiology which can present with myriad clinical presentation. The neurological manifestations of SLE consist of central nervous system (CNS) and peripheral nervous system manifestations (PNS). The CNS manifestations are aseptic meningitis, cerebrovascular accidents (stroke), demyelinating disorders, headache, involuntary movements like chorea, myelopathy, acute confusional states, cognitive dysfunction, mood disorder, seizures, psychosis and cranial nerve palsies.1 The PNS manifestations are Guillain Barre syndrome (GBS), autonomic disorder, mononeuropathy, polyneuropathy and plexopathy.1 Neuropathy in SLE can be clinically classified as mononeuritis multiplex and symmetrical and asymmetrical polyneuropathy. Symmetrical polyneuropathy being the most commonly seen clinical entity amongst the neuropathies in SLE. The neuropathy can be slowly progressive or acute in onset. Electrophysiologically, neuropathy is classified as axonal neuropathy, small fibre neuropathy, demyelinating neuropathy, mixed axonal-demyelinating sensorimotor polyneuropathy and plexopathy. Axonal neuropathy is further divided into sensory, sensorimotor and mononeuritis multiplex. Demyelinating neuropathy can be of two types: acute inflammatory demyelinating polyneuropathy (AIDP) and sensory demyelinating polyneuropathy. Anecdotal case reports also suggest that CIDP can occur as part of SLE neuropathy.2.
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PMID:SLE Neuropathy-Anything New? 2766 98

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is probably the best recognized progressive immune-mediated peripheral neuropathy. It is characterized by a symmetrical, motor-predominant peripheral neuropathy that produces both distal and proximal weakness. Large-fiber abnormalities (weakness and ataxia) predominate, whereas small-fiber abnormalities (autonomic and pain) are less common. The pathophysiology of CIDP is inflammatory demyelination that manifests as slowed conduction velocities, temporal dispersion, and conduction block on nerve conduction studies and as segmental demyelination, onion-bulb formation, and endoneurial inflammatory infiltrates on nerve biopsies. Although spinal fluid protein levels are generally elevated, this finding is not specific for the diagnosis of ClDP. Other neuropathies can resemble CIDP, and it is important to identify these to ensure correct treatment of these various conditions. Consequently, metastatic bone surveys (for osteosclerotic myeloma), serum electrophoresis with immunofixation (for monoclonal gammopathies), and human immunodeficiency virus testing should be considered for testing in patients with suspected CIDP. Chronic inflammatory demyelinating polyradiculoneuropathy can present as various subtypes, the most common being the classical symmetrical polyradiculoneuropathy and the next most common being a localized asymmetrical form, multifocal CIDP. There are 3 well-established, first-line treatments of CIDP-corticosteroids, plasma exchange, and intravenous immunoglobulin-with most experts using intravenous immunoglobulin as first-line therapy. Newer immune-modulating drugs can be used in refractory cases. Treatment response in CIDP should be judged by objective measures (improvement in the neurological or electrophysiological examination), and treatment needs to be individualized to each patient.
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PMID:History, Diagnosis, and Management of Chronic Inflammatory Demyelinating Polyradiculoneuropathy. 2986 82