Nutritional Neuropathies

Kumar, Neeraj

doi:10.1016/j.ncl.2006.11.001

Cited by 90 publications

(67 citation statements)

References 238 publications

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“…A deficiency of vitamins, particularly groups B (thiamine, cobalamin, pyridoxine, and niacin) and E, generally produces an axonal type of polyneuropathy. 22,41 However, riboflavin (vitamin B2) deficiency is characterized by demyelination with hypertrophy of Schwann cells, marked lipid accumulation, paranodal tomacula, and fibroblastic onion bulbs. [6][7][8]19,20 There is, at least initially, sparing of axons, and spinal cord and brain are apparently unaffected.…”

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confidence: 99%

Selective Vulnerability of Peripheral Nerves in Avian Riboflavin Deficiency Demyelinating Polyneuropathy

et al. 2009

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Abstract. Riboflavin (vitamin B2) deficiency in young chickens produces a demyelinating peripheral neuropathy. In this study, day-old broiler meat chickens were fed a riboflavin-deficient diet (1.8 mg/kg) and killed on posthatch days 6, 11, 16, 21, and 31, while control chickens were given a conventional diet containing 5.0 mg/kg riboflavin. Pathologic changes were found in sciatic, cervical, and lumbar spinal nerves of riboflavin-deficient chickens from day 11 onwards, characterized by endoneurial oedema, hypertrophic Schwann cells, tomacula (redundant myelin swellings), demyelination/remyelination, lipid deposition, and fibroblastic onion bulb formation. Similar changes were also found in large and medium intramuscular nerves, although they were less severe in the latter. However, by contrast, ventral and dorsal spinal nerve roots, distal intramuscular nerves, and subcutaneous nerves were normal at all time points examined. These findings demonstrate, for the first time, that riboflavin deficiency in young, rapidly growing chickens produces selective injury to peripheral nerve trunks, with relative sparing of spinal nerve roots and distal nerve branches to muscle and skin. These novel findings suggest that the response of Schwann cells in peripheral nerves with riboflavin deficiency differs because either there are subsets of these cells in, or there is variability in access of nutrients to, different sites within the nerves.Key words: Avian species; demyelination; neuropathy; peripheral nerves; riboflavin deficiency.The normal functioning of the nervous system depends on a constant supply of nutrients. A deficiency of vitamins, particularly groups B (thiamine, cobalamin, pyridoxine, and niacin) and E, generally produces an axonal type of polyneuropathy.22,41 However, riboflavin (vitamin B2) deficiency is characterized by demyelination with hypertrophy of Schwann cells, marked lipid accumulation, paranodal tomacula, and fibroblastic onion bulbs. [6][7][8]19,20 There is, at least initially, sparing of axons, and spinal cord and brain are apparently unaffected. 7 Riboflavin (7,8-dimethyl-10-ribityl-isoalloxazine) is a water-soluble vitamin and a dietary requirement in both chickens and humans. It is a precursor of flavin mononucleotide and flavin adenine dinucleotide, and decreased levels of these coenzymes impair oxidative phosphorylation. 36 Riboflavin deficiency leads to decreased beta-oxidation of fatty acids with relative preservation of the tricarboxylic acid cycle. 37 The lipid deposition in Schwann cells and the formation of paranodal redundant loops of normal myelin (paranodal tomacula) suggest a disturbance of lipid metabolism and control of myelin membrane formation in the myelinating Schwann cell.The novel findings in this study that Schwann cells in spinal nerve roots and subcutaneous and distal intramuscular nerves do not show these pathologic changes suggest that Schwann cells in different parts of the peripheral nerve system respond differently to riboflavin deficiency. Materials and MethodsOur a...

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Selective Vulnerability of Peripheral Nerves in Avian Riboflavin Deficiency Demyelinating Polyneuropathy

et al. 2009

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“…These biochemical events result in reduced cerebral glucose use, impaired cellular energy metabolism, membranes that are unable to maintain osmotic gradients, and a reduction in astrocyte function [17••, 18, 19]. Glutamate-mediated excitotoxicity, mitochondrial dysfunction, decreased synaptic transmission, and increased intracellular oxidative stress are also hypothesized to play a role in the neurologic complications of vitamin B 1 deficiency [18,19].…”

Section: Selected Specific Micronutrient Deficiencies Associated Withmentioning

confidence: 99%

“…Reduced intake, reduced absorption, increased metabolic requirement, increased losses, and/or defective transport often combine to result in thiamine deficiency [18]. Aside from the obvious decreased smallintestinal exposure resulting from bariatric surgeries, intractable vomiting and small-intestinal bacterial overgrowth also contribute to the thiamine deficiency seen [20].…”

Section: Selected Specific Micronutrient Deficiencies Associated Withmentioning

confidence: 99%

Micronutrient-Related Neurologic Complications Following Bariatric Surgery

Kazemi

Frazier

Cave

2010

Curr Gastroenterol Rep

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Nearly two thirds of American adults are either overweight or obese. Accordingly, bariatric surgery experienced explosive growth during the past decade. Current estimates place the worldwide volume of bariatric procedures at greater than 300,000 cases annually. Micronutrient deficiencies are well-described following bariatric surgery, and they may present with devastating and sometimes irreversible neurologic manifestations. Clinical symptoms range from peripheral neuropathy to encephalopathy, and are most commonly caused by thiamine, copper, and B(12) deficiencies.

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“…The course and severity of DPN found to be further affected by a wide range of comorbid conditions. Most importantly accumulation of homocystine (Hcy), an intermediary metabolite of amino acid methionine and methylmalonicacid (MMA) 6,7 in the blood. Homocysteinemia have been implicated in the pathogenesis of peripheral sensory-motor and autonomic neuropathy.…”

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confidence: 99%

Plasma total homocysteine is not associated with peripheral neuropathy in a groups Bangladeshi type 2 diabetic subjects

Rahman

Hassan

Biswas

et al. 2012

Bangladesh J Med Sci

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Aims: The present study was undertaken to explore the relationship of plasma homocysteine in the pathogenesis of neuropathy in diabetic patients. Subjects and Methods: Forty two type 2 diabetic patients [22 with neuropathy (DN group) and 20 without neuropathy (DNN group)], age range between 35-70 years had relatively controlled glycemia and duration of diabetes 7-15 years, were studied. Motor and sensory nerve conduction velocities and action potential amplitudes of peripheral nerves were determined by following standard protocol. HbA1c was estimated by modified HPLC (BIO-RAD Variant, USA). Serum C-peptide was measured by enzyme linked immunosorbentassay (ELISA), plasma total homocysteine by Fluorescent Polarization Immunoassay (FPIA). Results: Age, BMI and blood pressure of the study subjects were. Duration of diabetes between DN and DNN groups was comparable. DN group had significantly higher fasting glucose levels (9.8±3.8, mmol/l) compared to the DNN group (6.9±1.8, p=0.004). This trend was also reflected in the HbA1c level: 8.7± 2.1 vs 7.2±1.6 in DN group and DNN group respectively (p=0.009). The two diabetic groups had relatively higher absolute C-peptide level compared to the controls (p=ns). DN and DNN groups had significantly higher plasma homocysteine level compared to the Controls. But between the two diabetic groups no significant difference was observed. Ulnar and peroneal motor nerve conduction velocities and compound muscle action potentials in the diabetic neuropathy group significantly lower compared to diabetic counterpart and the controls. Ulnar and sural sensory nerve conduction velocities and action potentials were significantly lower in the diabetic neuropathy group compared to the diabetic counterpart and the controls. Plasma homocysteine did not show any correlation with nerve conduction velocities and action potential amplitudes. Conclusions: The data concluded that (i) Diabetic neuropathy may not be related to hyperhomocysteinemia in type 2 diabetic patients of Bangladeshi origin; (ii) Hyperglycemia, even at milder level, is related to neuronal dysfunction in these subjects; and (ii) Hyperinsulinemia don't seem to be prerequisite for neuropathy in these subjects.

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Nutritional Neuropathies

Cited by 90 publications

References 238 publications

Selective Vulnerability of Peripheral Nerves in Avian Riboflavin Deficiency Demyelinating Polyneuropathy

Selective Vulnerability of Peripheral Nerves in Avian Riboflavin Deficiency Demyelinating Polyneuropathy

Micronutrient-Related Neurologic Complications Following Bariatric Surgery

Plasma total homocysteine is not associated with peripheral neuropathy in a groups Bangladeshi type 2 diabetic subjects

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