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1/76. The treatment of chronic inflammatory demyelinating polyradiculoneuropathy with acupuncture: a clinical case study.

    Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), also referred to as chronic relapsing guillain-barre syndrome, is a rare neurological disease characterized by progressive symmetrical motor and sensory loss. Current biomedical treatments for this disease are often only short term in nature and have limitations with respect to side-effects and cost. The authors review CIDP from the perspectives of Western biomedicine and traditional Chinese medicine. A case report of a 17-year-old female diagnosed with CIDP and treated successfully with acupuncture is reviewed. ( info)

2/76. The spectrum of chronic inflammatory demyelinating polyneuropathy.

    research criteria for the diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) were proposed by an Ad Hoc Subcommittee of the American Academy of neurology (AAN) in 1991, and since then these criteria have been widely used in clinical studies. We have been impressed by the frequent finding of electrophysiological changes of a demyelinating neuropathy in patients whose clinical presentation does not conform to the usually accepted clinical phenotype of CIDP. To determine the clinical spectrum of CIDP, we conducted a retrospective review of patients of the peripheral electrophysiology laboratory of the University of Miami-Jackson Memorial Medical Center. Diagnostic criteria for acquired demyelination of an individual nerve were adapted from the AAN research criteria for the diagnosis of CIDP (1991). patients were accepted for inclusion when such evidence was demonstrated in at least one motor nerve or at least two sensory nerves. We then reviewed the clinical phenotype and the underlying etiology of the neuropathy in these cases. Eighty-seven patients, 63 male and 24 female, age of onset 4-84 (mean 49.3) years, met these inclusion criteria. Forty-seven patients (54%) had distinct features outside the usual clinical presentation of CIDP. Of these, 15 (17%) had predominantly distal features, 13 (15%) had exclusively sensory polyneuropathy; seven (8%) had markedly asymmetric disease, seven (8%) had associated CNS demyelination, four (5%) had predominant cranial nerve involvement, and one (1%) had only the restless legs syndrome. An associated medical condition that may have been responsible for the acquired demyelinating neuropathy was present in 60% of the patients. We conclude that spectrum of CIDP is broader than would be indicated by the strict application of the AAN research criteria, and that many of the cases meeting more liberal criteria frequently respond to immunosuppressive therapy. ( info)

3/76. Chronic inflammatory demyelinating polyneuropathy after treatment with interferon-alpha.

    Treatment with interferon-alpha (IFN-alpha) has been associated with the occurrence of a number of autoimmune disorders. We report a case of chronic inflammatory demyelinating polyneuropathy (CIDP) occurring in a patient with a chronic viral hepatitis c infection who received a novel, long-acting form of IFN-alpha. After withdrawal of the interferon treatment, this patient responded to a single extended course of plasma exchange that resulted in a complete clinical remission of symptoms without relapse. ( info)

4/76. Ataxic form of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).

    We reported a 64-year-old male with an eight-month history of gait disturbance and sensory impairment. The patient initially noticed unsteadiness of gait and numbness in his feet, and these symptoms progressed until he was unable to walk without assistance five months later. Vibratory sensation and position sense were markedly diminished, and deep tendon reflexes were absent in all extremities. Motor conduction velocities were slow with prolonged distal latencies, and sensory nerve action potentials (SNAP) were not elicited. sural nerve biopsy revealed a mild loss of myelinated fibres and segmental demyelination. cerebrospinal fluid showed normal cell count with protein 526 mg/dL. Anti-GM1, anti-GM2 and anti-GA1 antibodies in serum were positive. We diagnosed chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) presenting ataxia. Steroid therapy provided immediate improvement of symptoms and signs. This case suggests that CIDP should be considered as one of the potential causes of ataxic neuropathy. ( info)

5/76. Chronic inflammatory demyelinating polyradiculoneuropathy and severe peripheral oedema: a renal explanation.

    Inflammatory demyelinating neuropathies have been associated with membranous and focal sclerosing glomerulonephritis. Here we describe a 58 year old man with a clinical history, physical examination and laboratory investigations consistent with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), who also had severe lower limb and sacral oedema resistant to medical therapy. Mild proteinuria was present and a renal biopsy showed features consistent with focal sclerosing glomerulonephritis (FSGN). The patient's weakness and oedema did not respond to i.v. immunoglobulin or plasmapheresis but responded to high dose oral prednisone. The oedema was not explained by immobility, hypoproteinaemia or local factors. The occurrence of the oedema in a person with CIDP and FSGN and its improvement with prednisone, together with improvement in CIDP and FSGN, suggests that it was immune mediated, possibly due to increased capillary permeability. The presence of renal disease in patients with inflammatory demyelinating neuropathies may be more common than currently realised. ( info)

6/76. Chronic inflammatory demyelinating polyneuropathy associated with membranous glomerulonephritis: case report.

    A case of Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) with Membranous glomerulonephritis (MGN) is reported. This is the second case recorded in the literature and the article compares this case with the other reported case, including immunological implications. ( info)

7/76. Chronic relapsing multifocal sensory-motor neuropathy with conduction block.

    A 47 years old man had 13 episodes of relapsing and remitting sensory-motor neuropathy involving the upper limbs over the last 20 years. All but the last episode resolved spontaneously within 2 months. neurophysiology revealed multifocal motor and sensory conduction block in the upper limbs with normal terminal latencies. CSF analysis was normal and anti-GM1 antibodies were not detected. There was a dramatic clinical improvement after intravenous immunoglobulin treatment. This case represents an unusual multifocal variant of chronic inflammatory demyelinating neuropathy. ( info)

8/76. Sonographic detection of diffuse peripheral nerve hypertrophy in chronic inflammatory demyelinating polyradiculoneuropathy.

    Chronic inflammatory demyelinating polyradiculoneuropathy is an autoimmune disease characterized by recurrent demyelination and remyelination with resultant thickening of the peripheral nerves. We report a case in which sonography was instrumental in demonstrating diffuse peripheral nerve hypertrophy. On sonography, both brachial plexuses were found to be diffusely hypertrophic and hypoechoic. Similar findings were noted for the median, sciatic, and femoral nerves. The brachial plexus findings were confirmed by MRI. ( info)

9/76. Inflammatory demyelinating polyneuropathy: a complication of immunotherapy in malignant melanoma.

    paraneoplastic syndromes (PNS) involving the central nervous system are a rare manifestation of malignant disease. As they commonly precede the diagnosis of malignancy their acute manifestations do not often present themselves to oncologists in the first instance. It is currently believed that most, if not all, neurological PNS are autoimmune in nature. proteins expressed ectopically on the surface of tumour cells generate an immune response which cross-reacts with the same, or similar, proteins in the nervous system resulting in damage. This can involve a single cell type of the nervous system whilst in other cases the impairment is more widespread. The following report is of a case of chronic inflammatory demyelinating polyneuropathy (CIDP) occurring in metastatic malignant melanoma, following treatment with interferon-alpha. We review the current literature on this rare association and speculate on its pathogenesis, and the implications for future therapeutic strategies in melanoma targeting tumour antigens. ( info)

10/76. Severe exacerbation of hepatitis after short-term corticosteroid therapy in a patients with "latent" chronic hepatitis B.

    We present a case of severe exacerbation of hepatitis after short-term corticosteroid therapy for chronic inflammatory demyelinating polyneuropathy (CIPD) with "latent" chronic hepatitis B showing no HBV-related antigens and antibodies. After corticosteroid pulse therapy for CIPD, the patient had severe exacerbation of hepatitis twice. Although she did not show any hepatitis b virus (HBV)-related antigens or antibodies, sequences of HBV were detected in serum and liver by a nested polymerase chain reaction. A sequence analysis of HBV at the second exacerbation showed that the G-to-A point mutation at nucleotide 1896 that converted codon 28 from tryptophan (TGG) to a stop codon (TAG) in the precore region resulted in amino acid change, which has been frequently observed in fulminant hepatitis and severe hepatitis in japan. ( info)
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