Demyelination and Remyelination in Lead Neuropathy Electron Microscopic Studies

Lampert, Peter W.; Schochet, Sydney S.

doi:10.1097/00005072-196810000-00001

Cited by 123 publications

(59 citation statements)

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“…In our study, this blebbing was identified as segmental demyelination, which was characterized by wide distention of the myelin sheath due to interlamellar splitting, accompanied by reduction of axon diameter. This separation of myelin has been seen in immune-mediated diseases such as experimental allergic encephalomyelitis [ 18, 271, experimental allergic neuritis [28,291, and Landry-Guillain-Barrk syndrome in man [25], as well as in toxic neuropathies of lead [21], alkyl-tin [l], and tellurium [20]. Especially in experimental allergic neuritis [28], it was shown that this demyelination resulted in a reduction of axon diameter.…”

Section: Discussionmentioning

confidence: 97%

An Ultrastructural Study of Spinal Nerve Roots and Dorsal Root Ganglia in Aging Rats with Spontaneous Radiculoneuropathy

Mitsumori¹,

Maita²,

Shirasu³

1981

Vet Pathol

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Abstract. The spinal nerve roots and dorsal ganglia of 104-to 135-week-old rats with spontaneous radiculoneuropathy were examined by light and electron microscopy.Demyelination was common in myelinated fibers of various diameters of both ventral and dorsal roots. The most striking alteration was wide distention of myelin sheaths, which extended throughout the entire internode. The spaces formed between separated lamellae frequently were invaded by macrophages. Subsequent vesicular degeneration of myelin seemed to be mediated by invading macrophages. These processes caused complete myelin destruction, but most axons showed no degenerative changes except for obvious reduction in diameter. Occasionally, there were clumping and partial degradation of neurofilaments and ruptured axolemma in the severely demyelinated axons. A few fibers also were undergoing walleriantype degeneration, perhaps secondary to the severe demyelinative changes. Remyelinating fibers in various phases of repair were coexistent with markedly demyelinated ones. Demyelinative changes described above also developed within some of these remyelinated internodes.There were no remarkable changes in neurons of the dorsal root ganglia, though accumulation of lipofuscin was common.Our findings suggest that the changes in the nerve roots are essentially a primary segmental demyelination in aging rats with radiculoneuropathy.It is well known that posterior paralysis occurs spontaneously in senile rats more than 2 years old. Degenerative changes of the peripheral nervous system are common in these rats [3, 6, 7, 14, 361. These changes have been reported as "radiculoneuropathy" in Sprague-Dawley rats [3, 41, and have been found in SPF Wistar strain [36], Charles River CD@ strain [8, 141 and BN/Bi, WAG/Rij and (WAG/BN)FI rats [6, 71. It has been shown that the lesions are prominent in the spinal nerve roots, especially from the lumbar roots to the cauda equina, but are not found in the nerve cells of the dorsal root ganglia and ventral horn of the spinal cord, the origin of these nerve fibers [3, 361. There is still no consensus on the primary site of the lesion, however, because nerve lesions in the peripheral nervous system usually include segmental demyelination with or without wallerian degeneration. Some investigators suggested that the segmental demyelination might be a primary change [3, 141. In contrast, another investigator stated that the lesion combines wallerian degeneration and demyelination, with the former possibly being primary [36].

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Section: Discussionmentioning

confidence: 97%

An Ultrastructural Study of Spinal Nerve Roots and Dorsal Root Ganglia in Aging Rats with Spontaneous Radiculoneuropathy

Mitsumori¹,

Maita²,

Shirasu³

1981

Vet Pathol

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“…Electronmicrographs suggest that vacuolation is the result of separation of the outer lamellae of the myelin sheath which may be secondary to focal accumulation of fluid between the myelin layers. Oedematous changes in myelin have been demonstrated to play a major role in a number of neurotoxic injuries (Powell et al, 1980), including those associated with exposure to lead (Lampert & Schochet, 1968), isoniazid (Blakemore et al, 1972) and hexachlorophene (Lampert et al, 1973;Towfight et al, 1974).…”

Section: Discussionmentioning

confidence: 99%

Effects of vigabatrin on evoked potentials in dogs.

Arezzo

Litwak

et al. 1989

Brit J Clinical Pharma

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1 The purpose of this study was to evaluate possible changes in brain morphology and evoked potentials associated with daily administration of 300 mg kg-l vigabatrin in dogs. 2 Somatosensory evoked potentials (SEP) and auditory evoked potentials (AEP) were recorded at baseline and weekly for 12 weeks of treatment and every 2 weeks for 17 weeks of recovery. Morphology was assessed immediately after treatment for two treated dogs and after recovery for the remaining five treated and two control dogs. 3 Vigabatrin produced a significant slowing of the central transmission measure of the SEP with no alteration in the AEP. Vigabatrin was associated with microvacuolation in select regions of the brain including the fornix, septum, optic tract, hypothalamus, thalamus and cortex. In addition, some microglial proliferation was noted. 4 Changes in SEP and the microvacuolation fully recovered after 17 weeks of treatment. 5 The study confirms vigabatrin-induced microvacuolation in the dog and suggests these changes are associated with functional slowing of conduction in the somatosensory pathways.

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“…Subsequent studies have shown variability in this change in myelin during chronic lead exposure. This variability has been attributed in part to age and species differences in animals and to differences in duration ofexposure and doses of lead employed in such studies (2)(3)(4)(5)(6). Although there is no conclusive evidence as to whether lead primarily affects neuronal elements, non-neuronal elements, or both, studies dealing with this question (3)(4)(5) have suggested that lead produces a primary lesion in Schwann cells and that the neuronal lesions are due, in part, to pathological changes that occur in these supporting cells.…”

Section: Introductionmentioning

confidence: 99%

Porphyrin-heme biosynthesis in organotypic cultures of mouse dorsal root ganglia. Effects of heme and lead on porphyrin synthesis and peripheral myelin.

Whetsell¹,

Sassa²,

Kappas³

1984

J. Clin. Invest.

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A s bstract. Well-myelinated cultures of mouse dorsal root ganglia incubated for 48 h with 6-aminolevulinic acid (ALA) showed intense porphyrin fluorescence localized in myelin sheaths but not in axons or neuronal somata. When the cultures were continuously incubated with a high concentration of lead, focal swelling and segmental degeneration of myelin began to develop within 2 wk. Incubation of cultures with ALA after 3 wk of lead treatment revealed markedly decreased porphyrin fluorescence in myelin sheaths compared with untreated controls. After 6 wk of lead treatment, myelin showed severe segmental degeneration. Porphyrin fluorescence from ALA at this time was barely detectable in these cultures. No fluorescence was visible in the demyelinated axons; however, silver-impregnation staining after fixation demonstrated continuity of the axon despite the severe loss of myelin. When cultures were continuously incubated with lead and heme together for 6 wk, the segmental demyelination seen in cultures treated with lead alone did not occur. These findings suggest that the lead-induced segmental demyelination in cultured mouse dorsal root ganglia may be due to toxic effects of the metal on the heme biosynthetic pathway in myelinating cells and that exogenous heme may counteract this toxic effect of lead.

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Demyelination and Remyelination in Lead Neuropathy Electron Microscopic Studies

Cited by 123 publications

References 0 publications

An Ultrastructural Study of Spinal Nerve Roots and Dorsal Root Ganglia in Aging Rats with Spontaneous Radiculoneuropathy

An Ultrastructural Study of Spinal Nerve Roots and Dorsal Root Ganglia in Aging Rats with Spontaneous Radiculoneuropathy

Effects of vigabatrin on evoked potentials in dogs.

Porphyrin-heme biosynthesis in organotypic cultures of mouse dorsal root ganglia. Effects of heme and lead on porphyrin synthesis and peripheral myelin.

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