Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated neuropathy with heterogeneous features. Appropriate treatment will produce a favorable outcome, but a poor treatment response and severe disability have also been reported. The roles of the clinical phenotypes and electrophysiological features of CIDP as well as of autoantibodies against nodal and paranodal proteins have been highlighted previously due to their association with the treatment response and long-term prognosis. This review addresses the diverse factors associated with the prognosis of CIDP.
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Tendon-Sparing Extraocular Muscle Enlargement Associated With Chronic Inflammatory Demyelinating Polyradiculoneuropathy Antonios D. Dimopoulos, Anne Barmettler Ophthalmic Plastic & Reconstructive Surgery.2024; 40(2): e38. CrossRef
It was sometimes difficult to differentiate between acute-onset chronic inflammatory demyelinating polyneuropathy (A-CIDP) and subacute inflammatory demyelinating polyneuropathy (SIDP). The CNS involvement of these polyneuropathies has rarely reported in the literature. We present the case of a 42-year-old man who developed rapidly developing inflammatory demyelinating polyneuropathy followed by right optic neuritis. This case showed progressive motor weakness and sensory dysfunction with time to nadir at 8 weeks, demyelination in nerve conduction study, no other etiology of neuropathy, no relapse during follow-up of 18 months, good response to steroid and complete recovery which favor SIDP more than A-CIDP. We experienced the case of SIDP associated with optic neuritis.
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated polyneuropathy. Corticosteroids,intravenous immunoglobulin (IVIG) and plasmapheresis have been reported to be effective treatment. Rarely, CIDP can occurin the patients with HIV infection. The clinical features and electrophysiological findings of CIDP are known to be similarin patients with and without HIV infection. We report a 30-year-old male with HIV infection associated CIDP who improvedafter the administration of intravenous immunoglobulin and long term oral prednisone.
Background Peripheral neuropathy is the most frequent neurological complication in human immunodeficiency virus (HIV)infection, related with diverse etiologies including inflammation, opportunistic infection and side effects of medications. Thepurpose of the present study was to evaluate characteristics of HIV associated neuropathy according to the stage of HIVinfection. Methods: In reviewing the medical records of HIV patients who underwent electrodiagnostic studies between 1997and 2011, total 11 patients (all males; median age, 47 years; range, 28-71 years) with comorbid neuropathy were enrolled. Stageof HIV infection was categorized according to the Centers for Disease Control and Prevention (CDC) criteria. Classificationof peripheral neuropathy was based on clinical and electrophysiological features. Results: Distal symmetric polyneuropathywas observed in 8 patients (72.7%), inflammatory demyelinating polyneuropathy in 2 patients (18.1%), and polyradiculopathyin 1 patient (9.1%). Median CD4+ T cell count was 123/mm3 (range, 8-540/mm3) and 7 patients (60%) had the mostadvanced HIV disease stage (CDC-C3). There was no neuropathy caused by CMV infection. Conclusions: Distal symmetricpolyneuropathy was the most common type of neuropathy in HIV infection, but various forms of neuropathy such asinflammatory demyelinating polyneuropathy and polyradiculopathy were also present. HIV associated neuropathy is morefrequently associated with advancing immunosuppression, although it can occur in all stages of HIV infection.