Effects of Thiamine Deficiency on the Central Nervous System

Dreyfus, P; Victor, Maurice

doi:10.1093/ajcn/9.4.414

Cited by 131 publications

(37 citation statements)

References 17 publications

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“…This rise is then followed in these structures by a rapid decline in LeaU, followed by the appearance of clinical illness, and finally histological abnormalities (Hakim and Pappius, 1983). The two models result in histological lesions that are similar in nature and distribution (Dreyfus and Victor, 1961;Troncoso et ai., 1981). We have therefore used the two models here in a complementary sequence; metabolic data are obtained from the DD animals only prior to the development of clinical illness and from DD + PT animals only after the appearance of clinical se quelae.…”

Section: Figmentioning

confidence: 99%

Metabolic and Histological Reversibility of Thiamine Deficiency

Hakim

Carpenter

Pappius

1983

J Cereb Blood Flow Metab

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Summary:The rapid improvement in the clinical mani festations of thiamine deficiency with thiamine supple mentation is well known. To study this process in more detail, we rendered rats thiamine deficient either by di etary deprivation alone (DD) or, in addition, by daily pyr it hi amine administration (DD + PT). We observed the cerebral metabolic and histological responses of these rats after 1 or 7 days of thiamine supplementation both prior to and at the onset of clinical sequelae. The cerebral metabolic response to thiamine deficiency and replenish ment was determined with the [14C]deoxygJucose tech-

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Section: Figmentioning

confidence: 99%

Metabolic and Histological Reversibility of Thiamine Deficiency

Hakim

Carpenter

Pappius

1983

J Cereb Blood Flow Metab

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“…5 Ataxia with white matter degeneration is reported in lions, 28,32 cheetahs, 33 cats, 20,26 English Foxhounds, 41 Landrace-cross pigs, 31 rats, 11 and nonhuman primates 11,36,47 where deficiencies in vitamins A, B 12 (cobalamin), 41 B 3 (nicotinamide), 31 B 6 (pyridoxine), 47 and B 1 (thiamine) 11,20,26,36 have been implicated. In affected cats 26 and rats, 11 the thiamine content of the diet was between 0.1 and 0.3 and 0.1 and 0.5 mg/kg, 11 respectively, whereas no thiamine was present in the diet fed to nonhuman primates. 36 Ionizing gamma-radiation has been used safely for over 40 years to prolong the shelf life, to improve the microbiologic safety, and to reduce the use of chemical fumigants and additives in human and animal feedstuffs.…”

Section: Introductionmentioning

confidence: 99%

The Experimental Induction of Leukoencephalomyelopathy in Cats

et al. 2009

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Abstract. Leukoencephalomyelopathy of undetermined etiology has been described in specific pathogen-free cats. A study was established to assess if the long-term feeding of a gamma-irradiated diet could induce this disease. Cats fed exclusively on diet irradiated at 25.7-38.1 kGy (''typical'' dose) and 38.1-53.6 kGy (high-end dose), respectively, developed typical lesions with attendant, progressively severe ataxia between study days 140 and 174. The onset of ataxia at day 140 and the number of animals affected at this time were similar in animals fed each ration. A maximum ataxia ''score'' was first reached by an animal on the high-end dose diet on day 167 and by 2 cats fed the ''typical-end'' dose diet 21 days later. Ataxic cats and 1 animal euthanized on day 93 prior to the onset of ataxia exhibited varying degrees of Wallerian degeneration in the spinal cord and brain, similar to the spontaneous disease. The elevated total antioxidant status of spinal cord segments and hepatic superoxide dismutase concentration of cats fed typical and high-end treated diets suggested free-radical involvement in the pathogenesis. The significantly elevated peroxide concentrations of the irradiated diets (1,040% and 6,440% of untreated values) may have resulted in increased oxidative insult, a factor possibly exacerbated by the treated diets' reduced vitamin A content. This study has reproduced leukoencephalomyelopathy in cats similar to spontaneous outbreaks by feeding a gamma-irradiated dry diet with elevated peroxide and reduced vitamin A concentrations.

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“…In various animal species as well as in man, cerebral and spinal cord transketolase, like other enzymes of the pentose phosphate pathway, have been found predominantly in myelin-rich areas of the nervous system (e.g., subcortical white matter, brain stem, spinal cord) whereas two other thiamine-dependent enzymes, pyruvate decarboxylase and alpha ketoglutarate decarboxylase, were shown to have higher activity in the neurosomal masses of the nervous tissue (15)(16)(17)(18)(19)(20)(21)40). …”

Section: Resultsmentioning

confidence: 99%

“…McCandless, Schenker, and Cook observed that diminished transketolase activity may not be the sole factor responsible for the first signs of encephalopathy in acutely thiamine-deficient rats (21). Such an early symptomatology however, is rarely associated with conspicuous axon degeneration, demyelination, and glia proliferation in affected areas of the peripheral and central nervous tissue as seen with prolonged depletion of vitamin B, (40,42,43).…”

Section: Resultsmentioning

confidence: 99%

Relationship of nervous tissue transketolase to the neuropathy in chronic uremia

Sterzel¹,

Semar²,

Lonergan³

et al. 1971

J. Clin. Invest.

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A B S T R A C T Patients with chronic uremia develop neurologic defects which are similar to the demyelinating lesions seen in thiamine deficiency. The Hemodialysis markedly reduced the inhibitory effects of the patients' plasma and the data indicate that uremic patients who received effective long-term dialysis treatment show a parallel decline of transketolase inhibition and uremic neuropathy.

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Effects of Thiamine Deficiency on the Central Nervous System

Cited by 131 publications

References 17 publications

Metabolic and Histological Reversibility of Thiamine Deficiency

Metabolic and Histological Reversibility of Thiamine Deficiency

The Experimental Induction of Leukoencephalomyelopathy in Cats

Relationship of nervous tissue transketolase to the neuropathy in chronic uremia

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