Search

Your search keyword '"Dyck, P. James B."' showing total 787 results
Start Over Author "Dyck, P. James B."
787 results on '"Dyck, P. James B."'

207. Editorial by concerned physicians: Unintended effect of the orphan drug act on the potential cost of 3,4-diaminopyridine.

Author

Burns, Ted M., Smith, Gordon A., Allen, Jeffrey A., Amato, Anthony A., Arnold, W. David, Barohn, Richard, Benatar, Michael, Bird, Shawn J., Bromberg, Mark, Chahin, Nizar, Ciafaloni, Emma, Cohen, Jeffrey A., Corse, Andrea, Crum, Brian A., David, William S., Dimberg, Elliot, Sousa, Eduardo A. De, Donofrio, Peter D., Dyck, P. James B., and Engel, Andrew G.

Published
2016
Full Text
View/download PDF

208. “Unequivocally Abnormal” vs “Usual” Signs and Symptoms for Proficient Diagnosis of Diabetic Polyneuropathy

Author

Dyck, Peter J., primary, Overland, Carol J., additional, Low, Phillip A., additional, Litchy, William J., additional, Davies, Jenny L., additional, Dyck, P. James B., additional, Carter, Rickey E., additional, Melton, L. Joseph, additional, Andersen, Henning, additional, Albers, James W., additional, Bolton, Charles F., additional, England, John D., additional, Klein, Christopher J., additional, Llewelyn, Gareth, additional, Mauermann, Michelle L., additional, Russell, James W., additional, Selvarajah, Dinesh, additional, Singer, Wolfgang, additional, Smith, A. Gordon, additional, Tesfaye, Solomon, additional, and Vella, Adrian, additional

Published
2012
Full Text
View/download PDF

210. Epidermal Nerve Fiber Quantification in Patients With Erythromelalgia

Author

Mantyh, William G., Dyck, P. James B., Dyck, Peter J., Engelstad, Janean K., Litchy, William J., Sandroni, Paola, and Davis, Mark D. P.

Abstract

IMPORTANCE: Erythromelalgia is a clinical diagnosis based on intermittent warmth, erythema, and pain in the distal extremities. One problem facing physicians is how to objectively test for this disease. Given that other painful conditions of the distal extremities (ie, neuropathy related to human immunodeficiency virus, diabetes, or Fabry disease) can be evaluated with a skin biopsy to visualize pathologically decreased densities of the small nerve fibers that innervate the epidermis, one hypothesis is that erythromelalgia could similarly be associated with a loss of epidermal nerve fiber density (ENFD). OBJECTIVES: To examine whether erythromelalgia is associated with a structural loss of small fibers using the ENFD technique and to compare this with functional studies of small nerve fibers. DESIGN, SETTING, AND PARTICIPANTS: In a retrospective study of 52 consecutive patients with erythromelalgia who were seen between September 1, 2010, and September 22, 2015, patients were interviewed and examined and their conditions clinically diagnosed by a board-certified dermatologist at a large tertiary referral center, where ENFD testing became a routine part of evaluating erythromelalgia in 2010. Thus, all 52 consecutive patients were included solely based on their clinical diagnosis of erythromelalgia. For quantification of ENFD, observers were masked to all patient information except for name and clinic number. MAIN OUTCOMES AND MEASURES: The hypothesis that patients with erythromelalgia would have decreased ENFD was formulated before data collection. Epidermal nerve fiber density, the primary outcome, is a measurement of the density of small nerve fibers within the epidermis. Secondary measures included functional small fiber evaluation, such as autonomic (heart rate, blood pressure, and sweat testing) and subjective testing of pain. RESULTS: In this cohort study, 52 consecutively seen patients were identified (female, 42 [80%]; median age, 44 years; age range, 13-82 years). Whereas only 5 of 52 patients (10%) had ENFD at or below the fifth percentile of healthy control individuals, most patients had functional abnormalities of these small fibers; 29 patients (60%) had abnormal sweat test results, 21 (42%) had abnormal pain thresholds, and 20 (38%) had abnormal blood pressure or heart rate control. CONCLUSIONS AND RELEVANCE: Unlike other diseases of the small nerve fibers that cause acral pain syndromes, erythromelalgia is not characterized by loss of ENFD. However, most patients have impaired function of these small fibers. Physicians would benefit from performing functional rather than structural small fiber studies when evaluating erythromelalgia.

Published
2017
Full Text
View/download PDF

211. Can Intraneural Perineuriomas Occur Intradurally? An Anatomic Perspective

Author

Prasad, Nikhil K., Tubbs, R. Shane, Amrami, Kimberly K., Dyck, P. James B., Mauermann, Michelle L., Giannini, Caterina, de Divitiis, Oreste, and Spinner, Robert J.

Abstract

BACKGROUND:Intraneural perineuriomas are rare, benign lesions produced by the neoplastic proliferation of perineurial cells. They typically present in adolescents and affect nerves of the limbs. In our experience, we have not encountered a single case of classic intraneural perineurioma at an intradural location.OBJECTIVE:To determine whether intraneural perineuriomas could occur intradurally, given the prevalence of intradural nerve sheath tumors, and explain our findings with an anatomic perspective.METHODS:We retrospectively reviewed the high-resolution magnetic resonance images of 56 patients from an institutional registry of patients with intraneural perineurioma. All cases were analyzed for signs of proximal extension toward spinal nerves, roots, and spinal cord. A literature review was performed. The clinical, radiological, and histopathological features of potential intradural lesions were critically appraised against strict criteria for a diagnosis of classic intraneural perineurioma.RESULTS:Fifteen of 56 (27%) patients with intraneural perineurioma had a proximal localization in the lumbosacral or brachial plexus. Not a single case occurred proximal to the dorsal root ganglia (DRG). One case of trigeminal intraneural perineurioma occurred distal to the gasserian ganglion. A literature review did not reveal any convincing cases of classic intraneural perineuriomas occurring in an intraspinal intradural location and revealed only 1 possible case in an intracranial intradural location.CONCLUSION:Based on our study, the occurrence of classic intraneural perineuriomas intradurally is exceedingly rare, if at all present. This may be related to the paucity of perineurial cells at the nerve root level and reciprocal interactions between neuroglial cells at the central-to-peripheral transition zones.

Published
2017
Full Text
View/download PDF

212. Clinical, physiological and pathological characterisation of the sensory predominant peripheral neuropathy in copper deficiency

Author

Taylor, Sean W, Laughlin, Ruple S, Kumar, Neeraj, Goodman, Brent, Klein, Christopher J, Dyck, Peter J, and Dyck, P James B

Abstract

IntroductionMyelopathy is considered the most common neurological complication of copper deficiency. Concurrent peripheral neuropathy has been recognised in association with copper deficiency but has not been well characterised.ObjectivesTo characterise the clinical, physiological and pathological features of copper-deficient peripheral neuropathy.MethodsPatients with simultaneous copper deficiency (<0.78 μg/mL) and peripheral neuropathy seen at the Mayo Clinic from 1985 to 2005 were identified.Results34 patients were identified (median age 55 years, range 36–78) including 24 women and 10 men. Myelopathy was found in 21 patients. Median serum copper level was 0.11 μg/mL (range 0–0.58). The most frequent clinical and electrophysiological pattern of neuropathy was a sensory predominant length-dependent peripheral neuropathy (71%). Somatosensory evoked potentials demonstrated central slowing supporting myelopathy (96%). Quantitative sensory testing demonstrated both small and large fibre involvement (100%). Autonomic reflex screens (77%) and thermoregulatory sweat test (67%) confirmed sudomotor dysfunction. 14 cutaneous nerve biopsies revealed loss of myelinated nerve fibres (86%), increased regenerative clusters (50%), increased rates of axonal degeneration (91%) and increased numbers of empty nerve strands (73%). 71% of biopsies demonstrated epineurial perivascular inflammation.ConclusionsAn axonal, length-dependent sensory predominant peripheral neuropathy causing sensory ataxia is characteristic of copper deficiency usually co-occurring with myelopathy. Neurophysiological testing confirms involvement of large, greater than small fibres. The pathological findings suggest axonal degeneration and repair. Inflammatory infiltrates are common but are small and of doubtful pathological significance.

Published
2017
Full Text
View/download PDF

219. Peripheral Nerve Society Guideline* on the classification, diagnosis, investigation, and immunosuppressive therapy of non-systemic vasculitic neuropathy: executive summary

Author

Collins, Michael P., primary, Dyck, P. James B., additional, Gronseth, Gary S., additional, Guillevin, Loïc, additional, Hadden, Robert D. M., additional, Heuss, Dieter, additional, Léger, Jean-Marc, additional, Notermans, N.C., additional, Pollard, John D., additional, Said, Gérard, additional, Sobue, Gen, additional, Vrancken, A.F.J.E., additional, and Kissel, John T., additional

Published
2010
Full Text
View/download PDF

222. Epidemiologic Investigation of Immune-Mediated Polyradiculoneuropathy among Abattoir Workers Exposed to Porcine Brain

Author

Holzbauer, Stacy M., primary, DeVries, Aaron S., additional, Sejvar, James J., additional, Lees, Christine H., additional, Adjemian, Jennifer, additional, McQuiston, Jennifer H., additional, Medus, Carlota, additional, Lexau, Catherine A., additional, Harris, Julie R., additional, Recuenco, Sergio E., additional, Belay, Ermias D., additional, Howell, James F., additional, Buss, Bryan F., additional, Hornig, Mady, additional, Gibbins, John D., additional, Brueck, Scott E., additional, Smith, Kirk E., additional, Danila, Richard N., additional, Lipkin, W. Ian, additional, Lachance, Daniel H., additional, Dyck, P. James. B., additional, and Lynfield, Ruth, additional

Published
2010
Full Text
View/download PDF

225. An outbreak of neurological autoimmunity with polyradiculoneuropathy in workers exposed to aerosolised porcine neural tissue: a descriptive study

Author

Lachance, Daniel H, primary, Lennon, Vanda A, additional, Pittock, Sean J, additional, Tracy, Jennifer A, additional, Krecke, Karl N, additional, Amrami, Kimberly K, additional, Poeschla, Eric M, additional, Orenstein, Robert, additional, Scheithauer, Bernd W, additional, Sejvar, James J, additional, Holzbauer, Stacy, additional, DeVries, Aaron S, additional, and Dyck, P James B, additional

Published
2010
Full Text
View/download PDF

236. Chronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype.

Author

Mathey, Emily K., Park, Susanna B., Hughes, Richard A. C., Pollard, John D., Armati, Patricia J., Barnett, Michael H., Taylor, Bruce V., Dyck, P. James B., Kiernan, Matthew C., and Lin, Cindy S. -Y.

Subjects
CHRONIC diseases, DEMYELINATION, SENSORIMOTOR cortex, AUTOANTIBODIES, NEUROLOGICAL disorders, T cells
Abstract

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an inflammatory neuropathy, classically characterised by a slowly progressive onset and symmetrical, sensorimotor involvement. However, there are many phenotypic variants, suggesting that CIDP may not be a discrete disease entity but rather a spectrum of related conditions. While the abiding theory of CIDP pathogenesis is that cell-mediated and humoral mechanisms act together in an aberrant immune response to cause damage to peripheral nerves, the relative contributions of T cell and autoantibody responses remain largely undefined. In animal models of spontaneous inflammatory neuropathy, T cell responses to defined myelin antigens are responsible. In other human inflammatory neuropathies, there is evidence of antibody responses to Schwann cell, compact myelin or nodal antigens. In this review, the roles of the cellular and humoral immune systems in the pathogenesis of CIDP will be discussed. In time, it is anticipated that delineation of clinical phenotypes and the underlying disease mechanisms might help guide diagnostic and individualised treatment strategies for CIDP. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

237. Toxic Neuropathies.

Author

Karam, Chafic and Dyck, P. James B.

Subjects
*POLYNEUROPATHIES, *ETIOLOGY of diseases, *DRUG toxicity, *HEAVY metal toxicology, *SYSTEMATIC reviews
Abstract

Toxic neuropathies are a rare, but important cause of acquired polyneuropathy. In this review article, the authors discuss the general principles of toxic neuropathies and provide a systematic review of neuropathies related to drugs, heavy metals, environmental and industrial agents, and alcoholic neuropathies. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

239. Application of whole exome sequencing in undiagnosed inherited polyneuropathies.

Author

Klein, Christopher J., Middha, Sumit, Xiaohui Duan, Yanhong Wu, Litchy, William J., Weihong Gu, Dyck, P. James B., Gavrilova, Ralitza H., Smith, David I., Kocher, Jean-Pierre, and Dyck, Peter J.

Subjects
POLYNEUROPATHIES, NUCLEOTIDE sequencing, METABOLIC disorders, FAMILIAL spastic paraplegia, SENSORY neurons, MOTOR neurons, GENE expression
Abstract

Background: Inherited polyneuropathies often go undiagnosed. We investigated whole exome sequencing (WES) in utility to identify the genetic causes of diverse forms of inherited polyneuropathies without genetic diagnosis. Methods: WES was applied to 24 cases from 15 kindreds. These kindreds had earlier unsuccessful candidate gene testing and five probands were initially thought to have acquired neuropathy. We assessed the efficacy of WES in screening 74 known neuropathy genes and 5195 reported pathogenic mutations for hereditary motor and sensory neuropathy, distal hereditary motor neuropathy, hereditary sensory and autonomic neuropathy, complicated hereditary spastic paraplegia, and select hereditary metabolic neuropathies. Results: Pathogenic mutations were identified in five kindreds: (1) ATL1-p.Val253Ile; (2) LITAF-p.Gly112Ser; (3) MFN2-p.Arg94Gln; (4) GARS-p.Ile334Phe; and (5) BSCL2-p.Ser 90Leu. Complexities in establishing inheritance, difficulties in selecting candidate genes and high cost of gene testing all hindered earlier gene discoveries. WES expanded the phenotypic spectrum of the identified known mutations. Possible causal mutations in known genes (SPTLC1, DCTN1, REEP1) were identified in three kindreds. In the remaining seven kindreds, multiple rare or novel variants were identified in novel genes not previously linked with neuropathy. Our results demonstrate an average sequencing depth of 140×, >98% coverage and >10× sequencing depth for 93% (range 89%-96%) of the diverse neuropathy genes and their known mutations. Conclusions: Diverse inherited neuropathy patients without genetic discovery by candidate gene testing have a favourable probability of receiving a genetic diagnosis by WES. Frequently, atypical phenotypes account for earlier failed candidate approaches, and WES is demonstrated to expand the clinical spectrum of known pathogenic mutations. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

250. Reply

Author

Dyck, Peter James, primary, O'Brien, Peter C., additional, Litchy, William J., additional, Harper, C. Michel, additional, Daube, Jasper R., additional, and Dyck, P. James B., additional

Published
2001
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results