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Results for “POLYNEURITIS”

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At least 19 recordsLinked to original sources
PubMed1978

HLA antigens in the Landry-Guillain-Barré syndrome and chronic relapsing polyneuritis.

Forty-four patients with inflammatory demyelinating polyneuritis (22 with Landry-Guillain-Barré syndrome, 6 with subacute polyneuritis, and 16 with chronic relapsing polyneuritis) were typed for genetic markers in and around the HLA region of chromosome 6. Patients with chronic relapsing polyneuritis showed a definite association with HLA-AW30 and AW31 and probable associations with HLA-B8, HLA-DW3, and glyoxalase I. No significant associations were demonstrated with the Landry-Guillain-Barré syndrome although an increase in glyoxalase I was significant if combined with the results of typing in chronic relapsing polyneuritis. The total patient group showed significant increases in HLA-AW30, HLA-AW31, and HLA-DW3. The results support the view that HLA-linked genetic factors influence susceptibility to chronic relapsing polyneuritis and may contribute to the differences in clinical patterns observed in inflammatory demyelination of the peripheral nervous system.

Chromosome Mapping↗
PubMed1989

[Etiological aspects of polyneuritis in Senegal].

This study of 115 cases documented by the Neurology Unit between 1970 and 1984, stresses the relative frequency of deficiency etiology. The study was conducted clinically, biologically and electrophysiologically. Distribution between the sexes is almost equal, and the main age group concerned, those between 20 and 40 years. The various ethnic groups are all similarly affected. "Tropical Neuropathies" (most frequently of deficiency origin) are very important and account for half the cases. They are followed, in decreasing order of frequency, by toxic polyneuritis (ethanol and INH), degenerative polyneuritis with Charcot Marie-Tooth's sickness leading, and finally metabolic polyneuritis-diabetic (but diabetes creates no more polyneuritis than multineuritis) and uremic. The frequency of polyneuritis is the same as in European statistics. "Tropical Neuropathy" is a vast, ill defined subject which has been made to include many polyneurites which, in the end after a number of years, turned out to be degenerative polyneuritis. The result of this study will probably be to erode the classification "Tropical Neuropathy", which already displays inexactitudes in long term studies because of the discovery of a significant number of degenerative etiologies wrongly included in the past.

Adolescent↗
PubMed1976

Chronic relapsing polyneuritis.

Clinical, electrophysiological and pathological findings in 23 patients with subacute and relapsing idiopathic demyelinating polyneuropathies are described. In 17 patients with relapsing polyneuropathy, the neurological illness was unaccompanied by any systemic disturbances. The term preferred for the neuropathy in this group of patients is chronic relapsing polyneuritis. The findings in this group suggest that the common form of this syndrome is due to a single disease entity. Chronic relapsing polyneuritis differs from acute idiopathic polyneuritis chiefly in regard to the rate of evolution and the severity of the initial episode of polyneuropathy. If these two polyneuropathies have the same pathogenesis, the factor which determines whether the disease is acute and self-limiting or chronically relapsing is often present at the time of onset of the disease. The relationship of chronic relapsing polyneuritis to relapsing hypertrophic polyneuropathy and progressive hypertrophic polyneuropathy is also discussed and it is concluded that these diseases may constitute a spectrum of pathogenetically related disorders. In chronic relapsing polyneuritis, as in other demyelinating polyneuropathies, a marked segmental reduction in axon diameter accompanies demyelination. This corresponds to a more than 50% reduction in the volume of the affected region of the axon and it is associated with increased packing of axoplasmic organelles and wrinkling of the axolemma. It is suggested that in the normal myelinated nerve fibre, the Schwann cell and myelin sheath maintain fluid locally within the axon.

Acute Disease↗
PubMed1983

Acute cranial polyneuritis with vertigo after stapedectomy.

Acute vertigo occurring 48 hours after stapedectomy is assumed to be related to inner ear trauma. Similarly, acute vertigo occurring weeks after stapedectomy could be related to a fistula of the oval window. No one has tested the hypothesis that some of these cases could represent concomitant cranial polyneuritis. We report the development after stapedectomy of five cases of acute cranial polyneuritis with vertigo diagnosed by physical examination of the cranial nerves. In another case we determined that vertigo occurring after stapedectomy was not related to concomitant cranial polyneuritis. Although all the patients were treated with corticosteroids, the vertigo resolved within 12 to 24 hours only in those whose vertigo we had ascribed to polyneuritis.

Adult↗
PubMed1983

[Polyneuritis in periarteritis nodosa].

The authors observed 16 patients suffering from nodular periarteritis with the polyneuritis syndrome. The development and clinical characteristics of polyneuritis due to nodular periarteritis were studied, its course and outcome were also recorded. Some data helpful for recognizing the etiology of polyneuritis are presented. It is demonstrated that when multiple modality treatment (with corticosteroids as a component) is initiated at the early stages of disease, some patients exhibit prolonged remission of nodular periarteritis, including notable regression of polyneuritis manifestations.

Adolescent↗
PubMed1982

Chronic relapsing polyneuritis. A light- and electron-microscopic study.

The clinico-pathologic findings in two patients with chronic relapsing polyneuritis are reported. The patients had several attacks of diffuse polyneuritis followed by partial recovery. The tendency to persisting disability increased following relapses and in the late stages there was a progressive motor deterioration suggesting a continuing activity of nerve damage. The biopsies of peripheral nerves, obtained in the advanced stages of the disease, showed severe loss of myelinated fibers and aspects of repeated demyelination and remyelination, with formation of onion bulb complexes. Completely demyelinated axons together with remyelinating fibers as well as remyelinated fibers invested by macrophages were seen at the same time. The clinical and pathological evidences suggest that in chronic relapsing polyneuritis, at least in the late stages of the disease, besides clinical relapses, there is a continuing activity of nerve damage. Thus, due to this ongoing activity of demyelination and remyelination, the elimination of the supernumerary Schwann cells does not take place satisfactorily and hypertrophic changes of the nerve fascicles are produced.

Aged↗
PubMed2000

Predominant arm weakness in acute idiopathic polyneuritis: a distinct regional variant.

Acute idiopathic polyneuritis is a heterogeneous disorder with a number of clearly established variants. We describe four patients who present with an acute neuropathy predominantly affecting the arms which we believe should be considered as a distinct variant of acute polyneuritis. In two cases a primary demyelinating process affecting both motor and sensory nerves is suggested whereas in the other two the features were of a pure motor axonal degeneration. The relationship between these neuropathies, other variants of acute idiopathic polyneuritis and multifocal motor neuropathy is considered.

Acute Disease↗