実験的ビタミン欠乏症における末梢神経病変

A Histopathological Study on Peripheral Nerve Tissue of Experimental Vitamin Deficiency

はじめに

　ビタミン欠乏症，とくにB群欠乏時の末梢神経病変はいわゆる実質性変性として末梢神経病理の重要な分野をなしている。しかし，B₂をはじめ多くのビタミンがつぎつぎにB₁から分離されたにもかかわらず，それぞれのビタミン欠乏時の神経組織，とくに末梢神経の変化は，まだ十分に明らかにされていない。

　そこで著者は，実験的に白米病，B₁，B₂，B₆，ニコチン酸，パントテン酸，B₁₂および葉酸のB群の欠乏症における末梢神経の病変について検索した結果を中心に述べ，あわせて近年ようやく論議されるようになつたEおよびA欠乏のさいの末梢神経の変化についても簡単にふれておくことにする。

A histopathological study has been preformedon the peripheral nervous tissue of rats andpigeons, in experimental deficiencies of variousvitamins, such as thiamine, riboflavin, pyridox-ine, pantothenic acid, niacin, vitamin B12, folicacid, vitamin A and α-tocopherol.

In case of thiamine deficiency, lesion was ini-tiated by appearance of myelin droplets atSchmidt-Lantermann's incissures and dissociationof myelin sheath from axolemma. The chaneeswere followed by disintegration of myelin sheath,later causing bubbling and destruction of axons,more marked in distal portion of nerve fibers.Axonal reaction were found in both motor cellsof spinal cord and sensory spinal ganglion cells.These changes were identical to those of expe-rimental pyruvic acid administration. However,lcwering of Ch E activity and disruption ofend-plates of motor neurons were observed inthiamine dificienciy, whereas the changes werenot found in pyruvic acidapplication.

Riboflavin dificiency was characterized byshrinkage and clumping of neurofibrils, andacute swelling or liquefaction of nerve cells inspinal cord, spinal ganglia and Auerbach's andMeissner's plexus. In spite of severe damagesin neuron somas, alterations of distal nerve fiberswere surprisingly slight, possibly due to rapidcourse to death of animals.

Experiment of pyridoxine deficiency demon-strated the same type of alteration to those ofriboflavin deficiency, though the pathologicalchanges were slighter in degree. But degenerativechanges of nerve fibers were more marked thanthe former, because pyridoxine dificient animalsmay live longer.

In pantothenic acid deficiency, both nerve cellsand fibers were damaged at the same time. De-generative changes were demonstrable in motor,sensory and vegetative neurons. Lowering ofChE activity and destruction of end-plates werealso demonstrated.

Almost the same degenerative changes werefound in case of niacin deficiency in both nervecells and fibers. End-plates are less affected.

In vitamin B₁₂ deficiency, stainability of nervecell nuclei was reduced, being accompanied bydecrease of Nissl substance and disappearanceof neurofibrils. These were demonstrated innerve cells of spinal cord, spinal ganglia andAuerbach's and Meissner's plexus. Slight dege-nerative changees of nery fibers were demonstratedin the periterminal region.

Decrease of Nissl substance in neuron somas wasobserved as the first change in case of folic aciddeficiency. The change was followed by vacuolardegeneration and clumping of neurofibrils. Al-terations of periterminal areas were also demon-strated in this deficiency.

In vitamin A deficiency, marked degenerativechange of nerve fibers were specifically demon-strated in cornea. Slight vacuolar degenerationand decrease of Nissl substance were demon-strated in neuron somas of trigeminus ganglion,spinal ganglia and spinal cord. Degenerativechanges of motor neurons were not extended tothe end-plates, whereas moderate destruction ofsensory ending was observed.

In α-tocopherol deficiency, severe degenerativechanges were found in nerve cells of brain, spinalcord, spinal ganglia, Auerbach's and Meissner'splexus. Changes in peripheral nerve and endappartus were affected secondarily.