The Prevention of Sensory Neuron Degeneration in the Pig, With Special Reference to the Rôle of Various Liver Fractions 1

Wintrobe, M. M.; Mushatt, Cecil; Kolb, Lawrence C.; Stein, Harold J.; Lisco, Hermann

doi:10.1172/jci101281

Cited by 12 publications

(3 citation statements)

References 7 publications

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“…Of interest is the study of vitamin B 6 deficiency that lasted the longest time, as long as 20 weeks, in pigs. 17 That study observed abnormalities in gait and "early degen- In the current study, the walking-track abnormalities began to be apparent at 4 months. Demonstration that the vitamin B 6 -deficient diet in fact produced a nutritional deficiency state was provided by quantitation of pyridoxol, pyridoxal, pyridoxal phosphate, and pyridoxic acid in the rat serum.…”

Section: Annals Of Plastic Surgerysupporting

confidence: 49%

“…Pyridoxine deficiency causes arteriosclerosis, fatty liver, and convulsions in monkeys 8 ; weakness, growth retardation, and convulsions in chickens 9 ; and neutropenia, 10 xanthuria, convulsions, 11,12 and seborrheic dermatitis 13,14 in humans, but has not been observed to have any effect on reproduction 15 or taste sensitivity 16 in the rat. The only neurological observations have been abnormal gait in pigs 17 and "sensory neuritis" in 3 of 50 people 14 in a short-term study of B 6 dietary deficiency.…”

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confidence: 99%

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Experimental Model of Pyridoxine (B6) Deficiency-Induced Neuropathy

Dellon¹,

Dellon²,

Tassler³

et al. 2001

Annals of Plastic Surgery

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A pyridoxine (B6) dietary deficiency was studied in female adult Sprague-Dawley rats by hind-limb walking-track analysis. Serum levels of pyridoxine and three metabolites were quantified by high-pressure liquid chromatography with fluorescence measurement. Morphometric analysis of the sciatic and posterior tibial nerves (from within the tarsal tunnel) was performed after 1 year on a diet deficient in vitamin B6. The B6-deficient rats developed abnormal walking-track patterns by 8 months, and these track parameters were different from age- and sex-matched normal diet control rats at the p < 0.05 level. Adding B6 at 10 parts per million to the diet then partially corrected these parameters, whereas the addition of 30 parts per million B6 corrected the abnormal pattern completely. Serum pyridoxal concentration correlated with the functional parameters, dropping from a mean of 115 mg per liter to 39.5 mg per liter (p < 0.05), and correcting with the B6 additive. Morphometric analysis demonstrated that the B6-deficient nerve from the tarsal tunnel had a decreased nerve fiber density (p < 0.001), with a normal total myelinated nerve fiber number, and an increased axon-to-myelin ratio (p < 0.003). It is concluded that a diet totally deficient in vitamin B6 results in a peripheral neuropathy.

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Section: Annals Of Plastic Surgerysupporting

confidence: 49%

mentioning

confidence: 99%

Experimental Model of Pyridoxine (B6) Deficiency-Induced Neuropathy

Dellon¹,

Dellon²,

Tassler³

et al. 2001

Annals of Plastic Surgery

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“…Convulsions and ataxia appear in pigs deficient in vitamin B, (Wintrobe, Mushatt, Miller, Kolb, Stein & Lisco, 1942; Follis & Wintrobe, 1945). There is demyelination of the sciatic and brachial nerves which is later found also in dorsal root fibres and the dorsal columns of the spinal cord.…”

Section: The Role Of Vitamins In Metabolic Processesmentioning

confidence: 99%

Nutritional Aspects of Pyrldoxal as a Coenzyme

Sinclair

1953

Proc. Nutr. Soc.

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Subacute Necrotizing Encephalomyelopathy

Namiki¹

1965

Arch Neurol

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In 1951, Leigh1 published a case report of a peculiar neuropathological disorder in an infant. The disease, which he called subacute necrotizing encephalomyelopathy, was characterized by (1) multiple, frequently symmetrical foci of necrosis with predilection for the periaqueductal and periventricular structures and the tegmentum of the brain stem, (2) breakdown of the interstitial tissue of the nerve parenchyma with relative preservation of the cell bodies of the neurons, and (3) the prominence of small blood vessels. Although Leigh suggested that the disorder might represent Wernicke's disease in infants, there has been no convincing proof as to the etiology of this disorder. Subsequently, Feigin and Wolf (1954),2 Richter (1957),3 and Reye (1960)4 added several cases of a similar neuropathological disease.The case reported here is the first recorded instance of the disease in Japan. The importance of the associated pathology of the peripheral nerves, spinal roots, and dorsal white columns of the spinal cord is also stressed. Report of CaseThis patient, a 15-year-old Japanese girl, was the first child of parents who were first cousins. It was alleged that the mother's nutritional status during the pregnancy was very poor; the delivery occurred at term and was not complicated. The details of the feeding and development of the patient in early infancy were not available. At four months of age, the patient suffered from bilateral otitis media and for about the following year, she had a relapsing fever, often to 40 C (104 F). She started to laugh late and could not hold her head upright for long periods. She sat up at the end of the first year, was able to stand by herself at the age of 22 months, and began to walk at 30 months. Around the age of two, lordosis appeared. At that time, she could understand her parents but was scarcely able to speak or laugh. Walking required her mother's help, and by the time of her school admission her walking difficulty had gradually worsened. She swayed to the left, wore her left shoe with difficulty, and her left leg trembled while standing. Her school record indicated gradual de¬ terioration.When she was 13 years old, she was seen at the eye clinic of the Nagasaki University Hospitals. At that time she weighed 29.5 kg (65 lb) and measured 132 cm (4 ft 4 inches) in height (normal values at this age for Japanese girls are 42.2 kg (93 lb) and 149.0 cm (4 ft 11 inches). Both the tuberculin skin test and a Wassermann test were negative. She was said to have had abnormal gaze (strabismus) since the age of three or four. The visual acuity of both eyes was within normal limits. Her right eye was dominant, and when she focused on an object with her left eye, horizontal nystag¬ mus was provoked. A diagnosis of strabismus concomitans divergens sinistra was made. About four months prior to death she was seen at a Nagasaki hospital because of general fatigue. She died at home, and the details of her terminal illness are not known.She was the eldest of four siblings. One of her younger siblings...

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The Prevention of Sensory Neuron Degeneration in the Pig, With Special Reference to the Rôle of Various Liver Fractions 1

Cited by 12 publications

References 7 publications

Experimental Model of Pyridoxine (B6) Deficiency-Induced Neuropathy

Experimental Model of Pyridoxine (B6) Deficiency-Induced Neuropathy

Nutritional Aspects of Pyrldoxal as a Coenzyme

Subacute Necrotizing Encephalomyelopathy

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