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Peter J Dyck - One of the best experts on this subject based on the ideXlab platform.

  • natural history of Brachial Plexus Neuropathy
    2017
    Co-Authors: Peter Tsairis, Peter J Dyck, Donald W Mulder
    Abstract:

    A clinical analysis of 99 patients with Brachial Plexus Neuropathy (BPN) and the outcome of 84 of these patients are presented. The disease may involve the upper, the lower, or the entire Plexus; the involvement may be complete or incomplete, and it may often be bilateral. Although the etiologic factor or factors remain unknown, our studies support the contention that this form of Neuropathy is a clinical entity with, in most cases, a fairly typical pattern of symptoms and signs. The overall prognosis is excellent despite the severity and extent of the lesion. There is no apparent difference in the clinical aspects and recovery rates between patients who had antecedent immunizations and those who did not. While improvement may begin in one to two months, complete functional recovery may not be achieved for up to three years or longer in some cases. (27:109-117, 1972)

  • sept9 mutations and a conserved 17q25 sequence in sporadic and hereditary Brachial Plexus Neuropathy
    JAMA Neurology, 2009
    Co-Authors: Christopher J Klein, Julie M Cunningham, Anthony J Windebank, James P B Dyck, Scott M Friedenberg, Diane M Klein, Peter J Dyck
    Abstract:

    Background The clinical characteristics of sporadic Brachial Plexus Neuropathy (S-BPN) and hereditary Brachial Plexus Neuropathy (H-BPN) are similar. During attacks, inflammation of the Brachial Plexus nerves has been identified in both conditions. SEPT9 mutations (Arg88Trp, Ser93Phe, 5′UTR c.-131G>C) occur in some families with H-BPN. These mutations were not found in North American kindreds with H-BPN with a conserved 500-kilobase sequence of DNA at the 17q25 chromosomal region (where SEPT9 localizes) where a founder mutation has been suggested. Objective To study the 17q25 sequence and SEPT9 in S-BPN (56 individuals) and H-BPN (13 kindreds). Methods Allele analysis at 17q25, SEPT9 DNA sequencing, and messenger RNA analysis from lymphoblast cultures were performed. Results A conserved 17q25 sequence was found in 5 of 13 kindreds with H-BPN and 1 individual with S-BPN. This conserved sequence was not found in the family with a SEPT9 mutation (Arg88Trp) or in 182 control subjects. SEPT9 messenger RNA expression levels did not differ between forms of H-BPN and control subjects. No known mutations of SEPT9 were found in S-BPN. Conclusions Rarely, individuals with S-BPN may have the same conserved 17q25 sequence found in many North American kindreds with H-BPN. Individuals with BPN with this conserved sequence do not seem to have SEPT9 mutations or alterations of messenger RNA expression levels in lymphoblast cultures and are predicted to have the most common genetic cause in North America by a founder-effect mutation.

  • inflammation and neuropathic attacks in hereditary Brachial Plexus Neuropathy
    Journal of Neurology Neurosurgery and Psychiatry, 2002
    Co-Authors: Christopher J Klein, Peter J Dyck, Anthony J Windebank, S M Friedenberg, T M Burns, Peter James Dyck
    Abstract:

    Objective: To study the role of mechanical, infectious, and inflammatory factors inducing neuropathic attacks in hereditary Brachial Plexus Neuropathy (HBPN), an autosomal dominant disorder characterised by attacks of pain and weakness, atrophy, and sensory alterations of the shoulder girdle and upper limb muscles. Methods: Four patients from separate kindreds with HBPN were evaluated. Upper extremity nerve biopsies were obtained during attacks from a person of each kindred. In situ hybridisation for common viruses in nerve tissue and genetic testing for a hereditary tendency to pressure palsies (HNPP; tomaculous Neuropathy) were undertaken. Two patients treated with intravenous methyl prednisolone had serial clinical and electrophysiological examinations. One patient was followed prospectively through pregnancy and during the development of a stereotypic attack after elective caesarean delivery. Results: Upper extremity nerve biopsies in two patients showed prominent perivascular inflammatory infiltrates with vessel wall disruption. Nerve in situ hybridisation for viruses was negative. There were no tomaculous nerve changes. In two patients intravenous methyl prednisolone ameliorated symptoms (largely pain), but with tapering of steroid dose, signs and symptoms worsened. Elective caesarean delivery did not prevent a typical postpartum attack. Conclusions: Inflammation, probably immune, appears pathogenic for some if not all attacks of HBPN. Immune modulation may be useful in preventing or reducing the neuropathic attacks, although controlled trials are needed to establish efficacy, as correction of the mutant gene is still not possible. The genes involved in immune regulation may be candidates for causing HBPN disorders.

  • immune Brachial Plexus Neuropathy suggestive evidence for an inflammatory immune pathogenesis
    Neurology, 1996
    Co-Authors: Guillermo A Suarez, Caterina Giannini, E P Bosch, R J Barohn, J Wodak, Peter R Ebeling, R Anderson, Paul E Mckeever, Mark B Bromberg, Peter J Dyck
    Abstract:

    We report Brachial Plexus biopsy findings from two Australian and two American patients with Brachial Plexus Neuropathy. There were florid multifocal mononuclear inflammatory cell infiltrates. Present evidence suggests that these Brachial neuropathies have an immune basis.

Jean M. Panneton - One of the best experts on this subject based on the ideXlab platform.

  • Arteritis and Brachial Plexus Neuropathy as Delayed Complications of Radiation Therapy
    Mayo Clinic Proceedings, 2001
    Co-Authors: Devon I Rubin, Paula J. Schomberg, Roger F.j. Shepherd, Jean M. Panneton
    Abstract:

    Radiation-induced arteritis of large vessels and Brachial Plexus Neuropathy are uncommon delayed complications of local radiation therapy. We describe a 66-year-old woman with right arm discomfort, weakness, and acrocyanosis that developed 21 years after local radiation for breast adenocarcinoma. Arteriography revealed arteritis, with ulcerated plaque formation at the subclavian-axillary artery junction, consistent with radiation-induced disease, and diffuse irregularity of the axillary artery. Electromyography showed a chronic Brachial plexopathy. The patient's acrocyanosis, thought to be due to digital embolization from her vascular disease, improved with antiplatelet therapy. The concurrent combination of radiation-induced arteritis and Brachial plexopathy is uncommon but should be considered in patients presenting with upper extremity pain or weakness after radiation therapy.

Kristin Ørstavik - One of the best experts on this subject based on the ideXlab platform.

Huanxin Lin - One of the best experts on this subject based on the ideXlab platform.

H H Lucraft - One of the best experts on this subject based on the ideXlab platform.

  • Brachial Plexus Neuropathy following mantle radiotherapy
    Clinical Oncology, 1998
    Co-Authors: N J Wadd, H H Lucraft
    Abstract:

    We report two cases of presumed radiation-induced Brachial Plexus Neuropathy in patients with lymphoma who were treated with standard mantle radiotherapy to a dose of 40 Gy in 20 fractions. Radiation-induced Brachial plexopathy has not previously been reported following mantle irradiation at this dose. Both patients received chemotherapy in relapse. We postulate three possible causes: enhanced radiation sensitivity; an interaction between the chemotherapy and the radiotherapy; or an increased dose in axilla owing to a smaller separation at that point.