The Experts below are selected from a list of 282 Experts worldwide ranked by ideXlab platform
Bryan R Mcrae - One of the best experts on this subject based on the ideXlab platform.
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a new treatment option for laryngeal Sensory Neuropathy
Laryngoscope, 2009Co-Authors: Stacey L. Halum, David L Sycamore, Bryan R McraeAbstract:OBJECTIVES/HYPOTHESIS: Laryngeal Sensory Neuropathy (LSN) may produce a variety of symptoms, including chronic cough, globus sensation, odynophonia, and/or odynophagia. Etiologies are often iatrogenic, viral, or idiopathic, although the diagnosis is generally one of exclusion. The aim of this study is to introduce pregabalin (Lyrica, Pfizer Inc., New York, NY) as a potential new therapy for LSN. STUDY DESIGN: Retrospective clinical investigation. METHODS: : Charts were reviewed from 12 consecutive patients who were prescribed pregabalin for symptoms of LSN. Outcomes were reviewed by analyzing pre and post-treatment questionnaires asking patients to rate symptoms on a scale from 0 to 5. Adverse effects and evidence of drug tolerance were also recorded. RESULTS: Two patients did not tolerate pregabalin due to somnolence. Of those that tolerated the medication, mean pretreatment chief complaint symptom severity rating was 3.9, whereas mean post-treatment symptom rating was 1.2 after 1 month of pregabalin therapy. None of the patients developed drug tolerance effects over time. CONCLUSIONS: Pregabalin therapy appears to be an effective treatment option for laryngeal Sensory Neuropathy. Future prospective studies are needed to compare outcomes between pregabalin and other medications as treatments for LSN.
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a new treatment option for laryngeal Sensory Neuropathy
Laryngoscope, 2009Co-Authors: Stacey L. Halum, David L Sycamore, Bryan R McraeAbstract:Objectives/Hypothesis: Laryngeal Sensory Neuropathy (LSN) may produce a variety of symptoms, including chronic cough, globus sensation, odynophonia, and/or odynophagia. Etiologies are often iatrogenic, viral, or idiopathic, although the diagnosis is generally one of exclusion. The aim of this study is to introduce pregabalin (Lyrica, Pfizer Inc., New York, NY) as a potential new therapy for LSN. Study Design: Retrospective clinical investigation. Methods: Charts were reviewed from 12 consecutive patients who were prescribed pregabalin for symptoms of LSN. Outcomes were reviewed by analyzing pre and post-treatment questionnaires asking patients to rate symptoms on a scale from 0 to 5. Adverse effects and evidence of drug tolerance were also recorded. Results: Two patients did not tolerate pregabalin due to somnolence. Of those that tolerated the medication, mean pretreatment chief complaint symptom severity rating was 3.9, whereas mean post-treatment symptom rating was 1.2 after 1 month of pregabalin therapy. None of the patients developed drug tolerance effects over time. Conclusions: Pregabalin therapy appears to be an effective treatment option for laryngeal Sensory Neuropathy. Future prospective studies are needed to compare outcomes between pregabalin and other medications as treatments for LSN. Laryngoscope, 2009
Robert H. Brown - One of the best experts on this subject based on the ideXlab platform.
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SPTLC1 is mutated in hereditary Sensory Neuropathy, type 1
Nature genetics, 2001Co-Authors: Khemissa Bejaoui, Margaret D. Scheffler, Geoffry Haan, Peter Ashby, Peter De Jong, Robert H. BrownAbstract:Hereditary Sensory Neuropathy type 1 (HSN1, MIM 162400; ref. 1) genetically maps to human chromosome 9q22 (refs. 2-4). We report here that the gene encoding a subunit of serine palmitoyltransferase is located within the HSN1 locus, expressed in dorsal root ganglia (DRG) and mutated in HSN1.
Stacey L. Halum - One of the best experts on this subject based on the ideXlab platform.
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a new treatment option for laryngeal Sensory Neuropathy
Laryngoscope, 2009Co-Authors: Stacey L. Halum, David L Sycamore, Bryan R McraeAbstract:OBJECTIVES/HYPOTHESIS: Laryngeal Sensory Neuropathy (LSN) may produce a variety of symptoms, including chronic cough, globus sensation, odynophonia, and/or odynophagia. Etiologies are often iatrogenic, viral, or idiopathic, although the diagnosis is generally one of exclusion. The aim of this study is to introduce pregabalin (Lyrica, Pfizer Inc., New York, NY) as a potential new therapy for LSN. STUDY DESIGN: Retrospective clinical investigation. METHODS: : Charts were reviewed from 12 consecutive patients who were prescribed pregabalin for symptoms of LSN. Outcomes were reviewed by analyzing pre and post-treatment questionnaires asking patients to rate symptoms on a scale from 0 to 5. Adverse effects and evidence of drug tolerance were also recorded. RESULTS: Two patients did not tolerate pregabalin due to somnolence. Of those that tolerated the medication, mean pretreatment chief complaint symptom severity rating was 3.9, whereas mean post-treatment symptom rating was 1.2 after 1 month of pregabalin therapy. None of the patients developed drug tolerance effects over time. CONCLUSIONS: Pregabalin therapy appears to be an effective treatment option for laryngeal Sensory Neuropathy. Future prospective studies are needed to compare outcomes between pregabalin and other medications as treatments for LSN.
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a new treatment option for laryngeal Sensory Neuropathy
Laryngoscope, 2009Co-Authors: Stacey L. Halum, David L Sycamore, Bryan R McraeAbstract:Objectives/Hypothesis: Laryngeal Sensory Neuropathy (LSN) may produce a variety of symptoms, including chronic cough, globus sensation, odynophonia, and/or odynophagia. Etiologies are often iatrogenic, viral, or idiopathic, although the diagnosis is generally one of exclusion. The aim of this study is to introduce pregabalin (Lyrica, Pfizer Inc., New York, NY) as a potential new therapy for LSN. Study Design: Retrospective clinical investigation. Methods: Charts were reviewed from 12 consecutive patients who were prescribed pregabalin for symptoms of LSN. Outcomes were reviewed by analyzing pre and post-treatment questionnaires asking patients to rate symptoms on a scale from 0 to 5. Adverse effects and evidence of drug tolerance were also recorded. Results: Two patients did not tolerate pregabalin due to somnolence. Of those that tolerated the medication, mean pretreatment chief complaint symptom severity rating was 3.9, whereas mean post-treatment symptom rating was 1.2 after 1 month of pregabalin therapy. None of the patients developed drug tolerance effects over time. Conclusions: Pregabalin therapy appears to be an effective treatment option for laryngeal Sensory Neuropathy. Future prospective studies are needed to compare outcomes between pregabalin and other medications as treatments for LSN. Laryngoscope, 2009
P. K. Thomas - One of the best experts on this subject based on the ideXlab platform.
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An epidemic of optic Neuropathy and painful Sensory Neuropathy in Cuba: Clinical aspects
Journal of Neurology, 1995Co-Authors: P. K. Thomas, G. T. Plant, P. Baxter, C. Bates, R. Santiago LuisAbstract:An epidemic of bilateral optic Neuropathy and painful Sensory Neuropathy occurred in Cuba in 1991–1993. Over 45 000 individuals were stated to have been affected. We report a clinical study on 25 patients seen in Cuba in 1993–1994. Affected patients showed either bilateral optic Neuropathy with caecocentral scotomata or a distal predominantly Sensory Neuropathy sometimes associated with deafness, or a combination of both optic and peripheral Sensory Neuropathy. The nature of the epidemic is discussed. The clinical features in patients with confirmed neurological deficits were consistent with a diagnosis of Strachan's syndrome, probably related to nutritional deficiency. Other patients with similar symptoms showed no evidence either of optic or peripheral Neuropathy and were considered to represent disease mimicry on a psychoneurotic basis.
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Autosomal recessive hereditary Sensory Neuropathy with spastic paraplegia
Brain, 1994Co-Authors: P. K. Thomas, V. P. Misra, Rosalind H.m. King, J. R. Muddle, S. Wroe, Kailash P. Bhatia, Milne Anderson, Ana Cabello, Juan J. Vílchez, N. H. WadiaAbstract:Five patients are described with a progressive Sensory Neuropathy in association with a spastic paraplegia and a mutilating lower limb acropathy. Disease onset was in childhood. Two pairs of siblings were both the offspring of normal consanguinous parents, suggesting autosomal recessive inheritance. The fifth case was sporadic; her parents were normal and non-consanguinous. Nerve biopsy in three patients showed an axonopathy with a loss of myelinated nerve fibres of all diameters and also of unmyelinated axons. In combination with the previous report by Cavanagh et al. (Brain 1979; 102: 79-94), the present patients establish the existence of an autosomal recessive form of hereditary Sensory Neuropathy with spastic paraplegia. There have been previous descriptions of a dominantly inherited form.
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Hereditary neuralgic amyotrophy associated with a relapsing multifocal Sensory Neuropathy.
Journal of Neurology Neurosurgery & Psychiatry, 1993Co-Authors: P. K. Thomas, I. E. C. OrmerodAbstract:A family with neuralgic amyotrophy (idiopathic brachial plexus Neuropathy) associated with a multifocal Sensory Neuropathy is described. Four members over two generations were affected by neuralgic amyotrophy, inherited as an apparent autosomal dominant trait; two also had a multifocal relapsing Sensory Neuropathy with the clinical features of Wartenberg's migrant Neuropathy.
N. H. Wadia - One of the best experts on this subject based on the ideXlab platform.
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Autosomal recessive hereditary Sensory Neuropathy with spastic paraplegia
Brain, 1994Co-Authors: P. K. Thomas, V. P. Misra, Rosalind H.m. King, J. R. Muddle, S. Wroe, Kailash P. Bhatia, Milne Anderson, Ana Cabello, Juan J. Vílchez, N. H. WadiaAbstract:Five patients are described with a progressive Sensory Neuropathy in association with a spastic paraplegia and a mutilating lower limb acropathy. Disease onset was in childhood. Two pairs of siblings were both the offspring of normal consanguinous parents, suggesting autosomal recessive inheritance. The fifth case was sporadic; her parents were normal and non-consanguinous. Nerve biopsy in three patients showed an axonopathy with a loss of myelinated nerve fibres of all diameters and also of unmyelinated axons. In combination with the previous report by Cavanagh et al. (Brain 1979; 102: 79-94), the present patients establish the existence of an autosomal recessive form of hereditary Sensory Neuropathy with spastic paraplegia. There have been previous descriptions of a dominantly inherited form.
