Schaeppi U, Krinke G
Agents Actions. 1982 Oct;12(4):575-82. doi: 10.1007/BF01965944.
Neurologic examination, electrophysiologic testing and microscopic post-mortem examination was used to study the neuropathy induced in the beagle dog by administration of excessive amounts of vitamin B6. Two female dogs received repeated daily oral doses of 3 g. The treatment was ceased when the dogs developed severe general morbidity, including uncoordinated gait and abnormal neurologic symptoms. The symptoms were most severe during and early after cessation of treatment, and in general they regressed during the subsequent 2 months of treatment-free observation. Sensory central and peripheral maximum nerve conduction velocity started to decrease after a considerable delay; the decrease progressed until late after termination of treatment and failed to fully regress. Morphologic lesions were confined to large, first order sensory neurons. The neurologic examination thus revealed the early changes, while electrodiagnostics and microscopic neuropathology were indicators of more advanced stages of toxic neuropathy and disclosed selective lesions in individuals whose gait appeared to be unremarkable.
通过神经系统检查、电生理测试和显微镜下尸检,研究了过量服用维生素B6诱导比格犬产生神经病变的情况。两只雌性犬每日重复口服3克维生素B6。当犬出现严重的全身不适,包括步态不协调和异常神经症状时,停止治疗。这些症状在治疗期间及停止治疗后早期最为严重,总体上在随后2个月的无治疗观察期内逐渐消退。感觉中枢和外周最大神经传导速度在相当长的延迟后开始下降;这种下降持续到治疗终止后很久,且未能完全消退。形态学病变局限于大型的一级感觉神经元。神经系统检查因此揭示了早期变化,而电诊断和微观神经病理学则是毒性神经病变更晚期阶段的指标,并揭示了步态看似正常的个体中的选择性病变。