Summary
Thiamine is important for oxidative metabolism, and B1 deficiency is thought to give rise to polyneuropathies. A group of male Wistar rats (n = 15) received a vitamin B1 deficient diet (group-a), and the pair fed control group (n= 20, group-b) received a normal diet with no vitamin deficiency.
A second control group (group-c) was fed unrestrictedly with a standard diet (n = 19). All animals were examined for 25 weeks. The sensory nerve conduction velocity, the compound radicular, spinal and brain stem responses and the SEP were derived for tail and hind paw stimulation. The examination was repeated at 6-week intervals.
There was no difference in nerve conduction between group-a and -b, but for both groups the conduction velocity was significantly slower than in group-c. The SEP latencies were significantly increased in group-a compared with group-b and also with group-c. The spinal and cerebral latencies were delayed in group-a. The diameters of myelinated nerve fibres were decreased in group-a compared with group-b, and in group-b compared with group-c.
The results indicate that a specific polyneuropathy exits as a result of B1 deficiency, and that the sequelae of the lack of thiamine are pronounced in the CNS.
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Claus, D., Eggers, R., Warecka, K. et al. Thiamine deficiency and nervous system function disturbances. Eur Arch Psychiatr Neurol Sci 234, 390–394 (1985). https://doi.org/10.1007/BF00386056
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DOI: https://doi.org/10.1007/BF00386056