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At least 55 records · Page 3Linked to original sources
PubMed1996

Wallerian degeneration in peripheral nerve disease.

Wallerian-like degeneration can be regarded as the final shared pathway of the most prevalent diseases of the peripheral nervous system, including many degenerative, metabolic, heritable, toxic, inflammatory and ischaemic disorders. The cellular responses that take place during Wallerian degeneration, including the elaboration of neurotrophins, are increasingly recognized to set the stage for the success or failure of subsequent regeneration, and manipulations of Wallerian degeneration are being investigated as a potential means of altering the outcome of nerve regeneration.

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PubMedDate not supplied

[Globoid cell leucodystrophy (Krabbe's disease). Peripheral nerve lesion (author's transl)].

Morphological study of peripheral nerves in two patients with globoid cell leucodystrophy (Krabbe's disease) demonstrates: 1degree segmentary demyelination; 2degrees marked loss of large (8-10 micra) myelinated fibres; 3degrees significant increase of the mean transverse fascicular area by proliferating collagen fibres; 4degrees electron-microscopic signs of remyelination with small onion-bulb formations. These findings can explain clinical features such as the disappearance of the deep tendon reflexes, the gradual transition of hypertonia into combined hypertonia-hypotonia and the concomitant slowing of nerve conduction velocity. The ultrastructural study reveals the presence of large and small inclusions which are either located within lysosomes or free in the cytoplasm of Schwann cells and fibroblasts. The inclusions are probably consequences of the disturbed metabolism of cerebrosides. Their appearance is sufficiently specific in order to allow a diagnosis of Krabbe's disease.

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PubMedDate not supplied

Humoral factors in peripheral nerve disease.

Humoral factors including soluble substances transported by the blood stream and factors released at a target tissue may play a role in diseases of the peripheral nervous system. Various criteria have to be met in order to accept humoral factors as potential pathogens. In this review these general criteria are discussed, including the evidence provided by plasma exchange therapy, demonstration of circulating or deposited autoantibodies and immune complexes, identification of antigenic molecules, animal model diseases, passive transfer experiments, and the demonstration of circulating factors not directed against specific targets. In acute, chronic, and chronic relapsing inflammatory polyneuropathies, and in the polyneuropathy associated with monoclonal gammopathy, humoral factors have been identified, but their exact pathogenic role is not fully understood. In the Lambert-Eaton myasthenic syndrome, a disorder of the motor nerve terminal, pathogenic IgG-antibodies have been demonstrated by passive transfer experiments. In the experimental animal model disorders, the acute and chronic variants of experimental allergic neuritis, humoral factors including antibodies to myelin basic proteins and galactocerebroside and nonspecific humoral factors may all contribute to the ultimate peripheral nerve damage, but their relative importance in relation to cell-mediated immune reactions is not yet clear.

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PubMed1984

Glial bundles in spinal nerve roots. An immunocytochemical study stressing their nonspecificity in various spinal cord and peripheral nerve diseases.

Glial bundles (GBs) in spinal nerve roots in 86 autopsy cases with various spinal lesions were examined using the peroxidase-antiperoxidase technique for glial fibrillary acidic protein (GFAP). In 19 of 22 cases of Werding-Hoffmann disease (WHD), GBs were present in the anterior roots (ARs) but absent in the youngest age group (age less than 1.5 months at death). GBs were numerous in classical cases (age 3-24 months), accompanying severe damage of the anterior horns and roots, but were less prominent in most cases of protracted course (age 2-8.5 years). Thus, development of GBs in the ARs of motor neuron disease at a young age seems to depend on the clinical type (age at onset and disease duration) and degree of damage to motor neurons and ARs. Varying numbers of GBs were found also in the posterior roots (PRs) of 12 cases of WHD. In 13 patients with amyotrophic lateral sclerosis (ALS), few GBs were observed in the ARs of two and PRs of five cases without apparent relation to other clinicopathologic data. GBs in the PRs of both WHD and ALS might indicate spreading of the degenerative process to sensory neurons despite the absence of pathology detectable by routine histological stains. Numerous GBs were found also in adults affected with polymyelitis in childhood. Varying numbers of GBs were present, however, in many different diseases, such as Friedreich ataxia, Guillain-Barré syndrome, various polyneuropathies, cervical spondylosis, ataxia telangiectasia, metachromatic leukodystrophy, and Leigh syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

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