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Jamal Ahmad - One of the best experts on this subject based on the ideXlab platform.
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cross sectional study to evaluate the effect of duration of type 2 diabetes mellitus on the nerve conduction velocity in diabetic peripheral Neuropathy
Diabetes and Metabolic Syndrome: Clinical Research and Reviews, 2014Co-Authors: Gauhar Hussain, Aijaz Abbas S Rizvi, Sangeeta Singhal, Mohammad Zubair, Jamal AhmadAbstract:Abstract Objective To study the nerve conduction velocity in clinically undetectable and detectable peripheral Neuropathy in type 2 diabetes mellitus with variable duration. Material and methods This cross sectional study was conducted in diagnosed type 2 diabetes mellitus patients. They were divided in groups: Group I ( n = 37) with clinically detectable diabetic peripheral Neuropathy of shorter duration and Group II ( n = 27) with clinically detectable diabetic peripheral Neuropathy of longer duration. They were compared with T2DM patients ( n = 22) without clinical Neuropathy. Clinical diagnosis was based on Neuropathy symptom score (NSS) and Neuropathy disability score (NDS) for signs. Nerve conduction velocity was measured in both upper and lower limbs. Median, ulnar, common peroneal and posterior tibial nerves were selected for motor nerve conduction study and median and sural nerves were selected for sensory nerve conduction study. Results The comparisons were done between nerve conduction velocities of motor and sensory nerves in patients of clinically detectable Neuropathy and patients without Neuropathy in type 2 diabetes mellitus population. This study showed significant electrophysiological changes with duration of disease. Nerve conduction velocities in lower limbs were significantly reduced even in patients of shorter duration with normal upper limb nerve conduction velocities. Conclusion Diabetic Neuropathy symptom score (NSS) and Neuropathy disability score (NDS) can help in evaluation of diabetic sensorimotor polyNeuropathy though nerve conduction study is more powerful test and can help in diagnosing cases of Neuropathy.
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serum levels of tnf α in peripheral Neuropathy patients and its correlation with nerve conduction velocity in type 2 diabetes mellitus
Diabetes and Metabolic Syndrome: Clinical Research and Reviews, 2013Co-Authors: Gauhar Hussain, Aijaz Abbas S Rizvi, Sangeeta Singhal, Mohammad Zubair, Jamal AhmadAbstract:Abstract Objective To compare serum levels of TNF-α in patients of peripheral Neuropathy and patients without Neuropathy in type 2 diabetes mellitus. Material and methods This cross sectional study was conducted in diagnosed type 2 diabetes mellitus patients. They were divided in groups, Group I ( n = 37) with clinically detectable diabetic peripheral Neuropathy of shorter duration and Group II ( n = 27) with clinically detectable diabetic peripheral Neuropathy of longer duration. They were compared with patients without clinical Neuropathy ( n = 22), clinical diagnosis was based on Neuropathy symptom score (NSS) and Neuropathy disability score (NDS) for signs. Blood samples were collected for baseline investigations and estimation of serum TNF-α. Nerve conduction velocity was measured in both upper and lower limbs. Median, Ulnar, Common Peroneal and Posterior Tibial nerves were selected for motor nerve conduction study and Median and Sural nerves were selected for sensory nerve conduction study. Results The comparisons were done between various clinical and biochemical parameters in clinically detectable and undetectable peripheral Neuropathy groups of type 2 diabetes mellitus. The study showed raised serum levels of TNF-α in peripheral Neuropathy patients and significant correlation with nerve conduction velocity. Conclusion High level of TNF-α in serum of T2DM patients with Neuropathy shows possible contribution in development of Neuropathy. Due to its independent association this cytokine might be used as biomarker for diabetic peripheral Neuropathy.
Roy Freeman - One of the best experts on this subject based on the ideXlab platform.
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treatment induced Neuropathy of diabetes an acute iatrogenic complication of diabetes
Brain, 2015Co-Authors: Christopher H Gibbons, Roy FreemanAbstract:Treatment-induced Neuropathy in diabetes (also referred to as insulin neuritis) is considered a rare iatrogenic small fibre Neuropathy caused by an abrupt improvement in glycaemic control in the setting of chronic hyperglycaemia. The prevalence and risk factors of this disorder are not known. In a retrospective review of all individuals referred to a tertiary care diabetic Neuropathy clinic over 5 years, we define the proportion of individuals that present with and the risk factors for development of treatment-induced Neuropathy in diabetes. Nine hundred and fifty-four individuals were evaluated for a possible diabetic Neuropathy. Treatment-induced Neuropathy in diabetes was defined as the acute onset of neuropathic pain and/or autonomic dysfunction within 8 weeks of a large improvement in glycaemic control—specified as a decrease in glycosylated haemoglobin A1C (HbA1c) of ≥2% points over 3 months. Detailed structured neurologic examinations, glucose control logs, pain scores, autonomic symptoms and other microvascular complications were measured every 3–6 months for the duration of follow-up. Of 954 patients evaluated for diabetic Neuropathy, 104/954 subjects (10.9%) met criteria for treatment-induced Neuropathy in diabetes with an acute increase in neuropathic or autonomic symptoms or signs coinciding with a substantial decrease in HbA1c. Individuals with a decrease in HbA1c had a much greater risk of developing a painful or autonomic Neuropathy than those individuals with no change in HbA1c (P 4% points over 3 months the absolute risk of developing treatment-induced Neuropathy in diabetes exceeded 80%. Treatment-induced Neuropathy of diabetes is an underestimated iatrogenic disorder associated with diffuse microvascular complications. Rapid glycaemic change in patients with uncontrolled diabetes increases the risk of this complication.
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diabetic autonomic Neuropathy
Handbook of Clinical Neurology, 2014Co-Authors: Roy FreemanAbstract:Diabetes mellitus is the commonest cause of an autonomic Neuropathy in the developed world. Diabetic autonomic Neuropathy causes a constellation of symptoms and signs affecting cardiovascular, urogenital, gastrointestinal, pupillomotor, thermoregulatory, and sudomotor systems. Several discrete syndromes associated with diabetes cause autonomic dysfunction. The most prevalent of these are: generalized diabetic autonomic Neuropathy, autonomic Neuropathy associated with the prediabetic state, treatment-induced painful and autonomic Neuropathy, and transient hypoglycemia-associated autonomic Neuropathy. These autonomic manifestations of diabetes are responsible for the most troublesome and disabling features of diabetic peripheral Neuropathy and result in a significant proportion of the mortality and morbidity associated with the disease.
Richard J Barohn - One of the best experts on this subject based on the ideXlab platform.
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multifocal acquired demyelinating sensory and motor Neuropathy the lewis sumner syndrome
Muscle & Nerve, 1999Co-Authors: David Saperstein, A Amato, Gil I Wolfe, Jonathan S Katz, Sharon P Nations, Carlayne E Jackson, Wilson W Bryan, Dennis K Burns, Richard J BarohnAbstract:We report 11 patients with multifocal acquired demyelinating sensory and motor (MADSAM) Neuropathy, defined clinically by a multifocal pattern of motor and sensory loss, with nerve conduction studies showing conduction block and other features of demyelination. The clinical, laboratory, and histological features of these patients were contrasted with those of 16 patients with multifocal motor Neuropathy (MMN). Eighty-two percent of MADSAM Neuropathy patients had elevated protein concentrations in the cerebrospinal fluid, compared with 9% of the MMN patients (P < 0.001). No MADSAM Neuropathy patient had elevated anti-GM1 antibody titers, compared with 56% of MMN patients (P < 0.01). In contrast to the subtle abnormalities described for MMN, MADSAM Neuropathy patients had prominent demyelination on sensory nerve biopsies. Response to intravenous immunoglobulin treatment was similar in both groups (P = 1.0). Multifocal motor Neuropathy patients typically do not respond to prednisone, but 3 of 6 MADSAM Neuropathy patients improved with prednisone. MADSAM Neuropathy more closely resembles chronic inflammatory demyelinating polyNeuropathy and probably represents an asymmetrical variant. Given their different clinical patterns and responses to treatment, it is important to distinguish between MADSAM Neuropathy and MMN. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 560–566, 1999
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multifocal acquired demyelinating sensory and motor Neuropathy the lewis sumner syndrome
Muscle & Nerve, 1999Co-Authors: David Saperstein, A Amato, Gil I Wolfe, Jonathan S Katz, Sharon P Nations, Carlayne E Jackson, Wilson W Bryan, Dennis K Burns, Richard J BarohnAbstract:We report 11 patients with multifocal acquired demyelinating sensory and motor (MADSAM) Neuropathy, defined clinically by a multifocal pattern of motor and sensory loss, with nerve conduction studies showing conduction block and other features of demyelination. The clinical, laboratory, and histological features of these patients were contrasted with those of 16 patients with multifocal motor Neuropathy (MMN). Eighty-two percent of MADSAM Neuropathy patients had elevated protein concentrations in the cerebrospinal fluid, compared with 9% of the MMN patients (P < 0.001). No MADSAM Neuropathy patient had elevated anti-GM1 antibody titers, compared with 56% of MMN patients (P < 0.01). In contrast to the subtle abnormalities described for MMN, MADSAM Neuropathy patients had prominent demyelination on sensory nerve biopsies. Response to intravenous immunoglobulin treatment was similar in both groups (P = 1.0). Multifocal motor Neuropathy patients typically do not respond to prednisone, but 3 of 6 MADSAM Neuropathy patients improved with prednisone. MADSAM Neuropathy more closely resembles chronic inflammatory demyelinating polyNeuropathy and probably represents an asymmetrical variant. Given their different clinical patterns and responses to treatment, it is important to distinguish between MADSAM Neuropathy and MMN.
Gauhar Hussain - One of the best experts on this subject based on the ideXlab platform.
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cross sectional study to evaluate the effect of duration of type 2 diabetes mellitus on the nerve conduction velocity in diabetic peripheral Neuropathy
Diabetes and Metabolic Syndrome: Clinical Research and Reviews, 2014Co-Authors: Gauhar Hussain, Aijaz Abbas S Rizvi, Sangeeta Singhal, Mohammad Zubair, Jamal AhmadAbstract:Abstract Objective To study the nerve conduction velocity in clinically undetectable and detectable peripheral Neuropathy in type 2 diabetes mellitus with variable duration. Material and methods This cross sectional study was conducted in diagnosed type 2 diabetes mellitus patients. They were divided in groups: Group I ( n = 37) with clinically detectable diabetic peripheral Neuropathy of shorter duration and Group II ( n = 27) with clinically detectable diabetic peripheral Neuropathy of longer duration. They were compared with T2DM patients ( n = 22) without clinical Neuropathy. Clinical diagnosis was based on Neuropathy symptom score (NSS) and Neuropathy disability score (NDS) for signs. Nerve conduction velocity was measured in both upper and lower limbs. Median, ulnar, common peroneal and posterior tibial nerves were selected for motor nerve conduction study and median and sural nerves were selected for sensory nerve conduction study. Results The comparisons were done between nerve conduction velocities of motor and sensory nerves in patients of clinically detectable Neuropathy and patients without Neuropathy in type 2 diabetes mellitus population. This study showed significant electrophysiological changes with duration of disease. Nerve conduction velocities in lower limbs were significantly reduced even in patients of shorter duration with normal upper limb nerve conduction velocities. Conclusion Diabetic Neuropathy symptom score (NSS) and Neuropathy disability score (NDS) can help in evaluation of diabetic sensorimotor polyNeuropathy though nerve conduction study is more powerful test and can help in diagnosing cases of Neuropathy.
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serum levels of tnf α in peripheral Neuropathy patients and its correlation with nerve conduction velocity in type 2 diabetes mellitus
Diabetes and Metabolic Syndrome: Clinical Research and Reviews, 2013Co-Authors: Gauhar Hussain, Aijaz Abbas S Rizvi, Sangeeta Singhal, Mohammad Zubair, Jamal AhmadAbstract:Abstract Objective To compare serum levels of TNF-α in patients of peripheral Neuropathy and patients without Neuropathy in type 2 diabetes mellitus. Material and methods This cross sectional study was conducted in diagnosed type 2 diabetes mellitus patients. They were divided in groups, Group I ( n = 37) with clinically detectable diabetic peripheral Neuropathy of shorter duration and Group II ( n = 27) with clinically detectable diabetic peripheral Neuropathy of longer duration. They were compared with patients without clinical Neuropathy ( n = 22), clinical diagnosis was based on Neuropathy symptom score (NSS) and Neuropathy disability score (NDS) for signs. Blood samples were collected for baseline investigations and estimation of serum TNF-α. Nerve conduction velocity was measured in both upper and lower limbs. Median, Ulnar, Common Peroneal and Posterior Tibial nerves were selected for motor nerve conduction study and Median and Sural nerves were selected for sensory nerve conduction study. Results The comparisons were done between various clinical and biochemical parameters in clinically detectable and undetectable peripheral Neuropathy groups of type 2 diabetes mellitus. The study showed raised serum levels of TNF-α in peripheral Neuropathy patients and significant correlation with nerve conduction velocity. Conclusion High level of TNF-α in serum of T2DM patients with Neuropathy shows possible contribution in development of Neuropathy. Due to its independent association this cytokine might be used as biomarker for diabetic peripheral Neuropathy.
David Saperstein - One of the best experts on this subject based on the ideXlab platform.
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multifocal acquired demyelinating sensory and motor Neuropathy the lewis sumner syndrome
Muscle & Nerve, 1999Co-Authors: David Saperstein, A Amato, Gil I Wolfe, Jonathan S Katz, Sharon P Nations, Carlayne E Jackson, Wilson W Bryan, Dennis K Burns, Richard J BarohnAbstract:We report 11 patients with multifocal acquired demyelinating sensory and motor (MADSAM) Neuropathy, defined clinically by a multifocal pattern of motor and sensory loss, with nerve conduction studies showing conduction block and other features of demyelination. The clinical, laboratory, and histological features of these patients were contrasted with those of 16 patients with multifocal motor Neuropathy (MMN). Eighty-two percent of MADSAM Neuropathy patients had elevated protein concentrations in the cerebrospinal fluid, compared with 9% of the MMN patients (P < 0.001). No MADSAM Neuropathy patient had elevated anti-GM1 antibody titers, compared with 56% of MMN patients (P < 0.01). In contrast to the subtle abnormalities described for MMN, MADSAM Neuropathy patients had prominent demyelination on sensory nerve biopsies. Response to intravenous immunoglobulin treatment was similar in both groups (P = 1.0). Multifocal motor Neuropathy patients typically do not respond to prednisone, but 3 of 6 MADSAM Neuropathy patients improved with prednisone. MADSAM Neuropathy more closely resembles chronic inflammatory demyelinating polyNeuropathy and probably represents an asymmetrical variant. Given their different clinical patterns and responses to treatment, it is important to distinguish between MADSAM Neuropathy and MMN. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 560–566, 1999
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multifocal acquired demyelinating sensory and motor Neuropathy the lewis sumner syndrome
Muscle & Nerve, 1999Co-Authors: David Saperstein, A Amato, Gil I Wolfe, Jonathan S Katz, Sharon P Nations, Carlayne E Jackson, Wilson W Bryan, Dennis K Burns, Richard J BarohnAbstract:We report 11 patients with multifocal acquired demyelinating sensory and motor (MADSAM) Neuropathy, defined clinically by a multifocal pattern of motor and sensory loss, with nerve conduction studies showing conduction block and other features of demyelination. The clinical, laboratory, and histological features of these patients were contrasted with those of 16 patients with multifocal motor Neuropathy (MMN). Eighty-two percent of MADSAM Neuropathy patients had elevated protein concentrations in the cerebrospinal fluid, compared with 9% of the MMN patients (P < 0.001). No MADSAM Neuropathy patient had elevated anti-GM1 antibody titers, compared with 56% of MMN patients (P < 0.01). In contrast to the subtle abnormalities described for MMN, MADSAM Neuropathy patients had prominent demyelination on sensory nerve biopsies. Response to intravenous immunoglobulin treatment was similar in both groups (P = 1.0). Multifocal motor Neuropathy patients typically do not respond to prednisone, but 3 of 6 MADSAM Neuropathy patients improved with prednisone. MADSAM Neuropathy more closely resembles chronic inflammatory demyelinating polyNeuropathy and probably represents an asymmetrical variant. Given their different clinical patterns and responses to treatment, it is important to distinguish between MADSAM Neuropathy and MMN.
