Neuritis acuta progressiva

Eichhorst, Hermann

doi:10.1007/bf02326118

Cited by 18 publications

(3 citation statements)

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“…Thus, central chromatolysis, which is now considered a secondary pathological finding of the anterior horn cells (because of the severe damage of the peripheral nervous axon cylinders), was only occasionally detected. This led to the incorrect assumption that the origin of GBS was the spinal cord, rather than the peripheral nerves …”

Section: Pathology Of Aidpmentioning

confidence: 99%

Pathology of Guillain–Barré syndrome

Nakano

Kanda

2016

Clinical & Exp Neuroim

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Guillain–Barré syndrome (GBS), a disease affecting the peripheral nervous system, is now well known. However, the disease concept has evolved over successive periods. For example, for approximately nine decades from the first report of GBS, it was considered to have a spinal cord origin. After the first clinical report, the accumulation of detailed clinicopathological data showed that GBS is composed of two distinct clinicopathological entities: acute inflammatory demyelinating polyneuropathy, and acute motor axonal neuropathy or acute motor and sensory axonal neuropathy. Acute inflammatory demyelinating polyneuropathy is characterized by the patchy distribution of demyelinative foci throughout the peripheral nervous system, whereas acute motor axonal neuropathy/acute motor and sensory axonal neuropathy shows primary axonal degeneration in the peripheral nervous system, which is particularly accentuated at the spinal nerve roots. The purpose of the present article was to provide an overview of the previous publications regarding the pathology of GBS and to thereby elucidate the pathological mechanisms of this still threatening disorder from a pathological viewpoint. The critical pathological feature of acute inflammatory demyelinating polyneuropathy is the complement–macrophage‐induced cytotoxic damage on the plasmalemma of the Schwann cells, whereas that of acute motor axonal neuropathy/acute motor and sensory axonal neuropathy is the antibody–complement‐mediated immune attack on the axolemma at the nodes of Ranvier.

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Section: Pathology Of Aidpmentioning

confidence: 99%

Pathology of Guillain–Barré syndrome

Nakano

Kanda

2016

Clinical & Exp Neuroim

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“…Octave Landry avait déjà rapporté en 1859 ce type d'atteinte dans sa « note sur la paralysie ascendante aiguë », mais n'avait pas démon-tré l'origine nerveuse périphérique de l'atteinte, malgré l'autopsie de deux patients décédés parmi les dix patients étudiés [2]. L'origine périphérique ou médullaire de ces paralysies était débattue, et c'est probablement Eischhorst, en 1877 qui, le premier, a rapporté les anomalies histologiques présentes dans un cas de ce qui sera plus tard appelé le syndrome de Guillain-Barré [3]. Rapidement de nombreuses descriptions anatomopathologiques de cas semblables ont été publiées, et dès 1904, Schmaus, s'appuyant sur 14 cas rapportés précédemment, décrivait la localisation inhabituelle, principalement proximale, des lésions [4].…”

Section: L'évolution Des Concepts Physiopathologiques Les Descriptionunclassified

Le syndrome de Guillain-Barré : nouveaux concepts et conséquences pratiques

Nicolas

2015

Pratique Neurologique - FMC

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“…Ross & Bury (13), Walton (14) and Schmaus (15) argued that the presence of clinical sensory involvement in the majority of patients effectively localized the site of involvement to the peripheral nerves. Postmortem pathological support, in the form of degenerative changes in the anterior and posterior roots, even in cases with only slight clinical sensory dysfunction was first described in 1876-1877 and reported frequently thereafter (6,16,17). More general involvement of peripheral nerves and their cell bodies was described by Mills (18) and degenerative changes at distal nerve ends was found by Rolly (19).…”

Section: Landry's Paralysis and The Recognition Of The Peripheral Nermentioning

confidence: 99%

The idiopathic polyradiculoneuropathies: a historical guide to an understanding of the clinical syndromes

Horowitz

1989

Acta Neurologica Scandinavica

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Recognition of the idiopathic polyradiculoneuropathies began with Graves, Landry and Dumenil who, respectively, suggested, implied and established the peripheral nervous system as a site of disease. Over the ensuing decades other neurologists separated the idiopathic disorders from neuropathies of known cause, poliomyelitis and myelopathies. Guillain, Barré and Strohl described the acute benign syndrome and its cerebrospinal fluid abnormalities. Haymaker & Kernohan solidified the features of the acute disorder as did Dyck et al and Prineas & McLeod for the relapsing and chronic conditions. Currently the idiopathic polyradiculoneuropathies are regarded as autoimmune in nature, clinically generalized with some cases having focal involvement, and of varying severity with only occasional fatalities. Neurologists are divided as to whether the acute and chronic disorders represent 2 different conditions or whether they are 2 forms in the spectrum of a single disorder. This author favors the concept of a single disorder with multifarious manifestations.

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Neuritis acuta progressiva

Cited by 18 publications

References 1 publication

Pathology of Guillain–Barré syndrome

Pathology of Guillain–Barré syndrome

Le syndrome de Guillain-Barré : nouveaux concepts et conséquences pratiques

The idiopathic polyradiculoneuropathies: a historical guide to an understanding of the clinical syndromes

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