PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6684236

Hypertrophic neuropathy and multiple sclerosis.

N L Rosenberg·D Bourdette
View original source ↗Export metadata ↓

Abstract

In a 62-year-old man with multiple sclerosis, postmortem examination disclosed clinically unsuspected findings of hypertrophic neuropathy. The brain and spinal cord contained many typical plaques of multiple sclerosis. Most spinal roots were thickened, and microscopic examination showed onion-bulb changes characteristic of hypertrophic neuropathy. This is the eleventh reported case of a sporadic hypertrophic neuropathy in a patient with multiple sclerosis.

Explore related subjects

Central Nervous System DiseasesHumansHypertrophyMaleMiddle AgedMultiple SclerosisCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

N L Rosenberg, D Bourdette. 1983. Hypertrophic neuropathy and multiple sclerosis.. https://doi.org/10.1212/wnl.33.10.1361

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

A rare symptomatic presentation of ecchordosis physaliphora: neuroradiological and surgical management.

We report a case of ecchordosis physaliphora, an uncommon benign lesion originating from embryonic notochordal remnants, intradurally located in the prepontine cistern, that unusually presented associated with symptoms. MRI detected and precisely located the small mass. At surgery, a cystic gelatinous nodule was found ventral to the pons, contiguous with the dorsal wall of the clivus via a small pedicle. Histological examination diagnosed the lesion as an ecchordosis physaliphora. Here we focus on the analysis of the neuroradiological aspects that play a crucial role from both a diagnostic and a therapeutic standpoint.

Central Nervous System Diseases↗
PubMed2006

Motion-onset VEPs: characteristics, methods, and diagnostic use.

This review article summarises the research on the motion-onset visual evoked potentials (VEPs) and important motion stimulus parameters which have been clarified. For activation of the visual motion processing system and evocation of the motion-onset specific N2 peak (with latency of 160-200ms) from the extra-striate temporo-occipital and/or parietal cortex, the following stimulus parameters can be recently recommended: low luminance (<ca. 20cd/m(2)) and low contrast (<ca. 10%-sinusoidally modulated) of a moving structure with low velocity and temporal frequency (<ca. 6Hz). A short (up to 200ms) duration of motion and a long (at least 1s) inter-stimulus interval reduce adaptation to motion and predominance of a pattern-related P1 peak. Radial motion (with increasing velocity and decreasing spatial frequency towards the periphery) produces larger reactions as compared to a unidirectional translation. In view of the slow maturation (up to the age of 18 years) and early ageing of the visual motion processing system, the use of age-dependent latency norms may be necessary. Since early or selective involvement of the motion processing system is suspected in some CNS disorders, we suggest an evaluation of the utility of motion-onset VEPs as part of the electrophysiological CNS examination since this method may recognise motion processing involvement better than other methods. Motion-onset VEPs might increase the sensitivity of this examination for diagnosing CNS diseases including Multiple Sclerosis, Neuroborreliosis, Glaucoma, Dyslexia and Encephalopathies.

Central Nervous System Diseases↗