Injection of polidocanol foam (PF) in varicose veins as a trigger for attacks of migraine with visual aura.
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Adult↗
Biomedical subjects
H Ratinahirana
Publications and source records attributed to H Ratinahirana.
Time course of degeneration and regeneration of myelinated nerve fibres following chronic loose ligatures of the rat sciatic nerve: can nerve lesions be linked to the abnormal pain-related behaviours?
This study of a mononeuropathy of 1-15 weeks (W) duration was induced in rats by setting 4 loose ligatures around the common sciatic nerve. This chronic lesion, in which the continuity of the nerve was maintained, has been introduced as a model for experimental pain. Quantitative analyses of teased nerve fibres and a morphometric analysis of semi-thin transverse sections, were performed and completed by electron microscopic examination. Morphological changes were observed mainly distal, but also proximal, to the ligatures, indicating significant axonopathy with simultaneous degeneration and regeneration. The lesions were analysed in parallel with the time course of the pain-related behaviours. Both were at their maximum 2 weeks after ligature with progressive recovery beginning between W3 and W4. However, the largest fibres had not totally recovered by W15, contrasting with the disappearance of abnormal nociceptive reactions between W8 and W10. Although the damage to unmyelinated fibres is of importance, the abnormal pain-related behaviours seen in these rats appeared to be closely linked to the presence of both degenerative and regenerative changes in the A delta-range fibres, which did not necessarily correspond to initial A delta fibres.
Animals↗
Ganglioside GD1b is the target antigen for a biclonal IgM in a case of sensory-motor axonal polyneuropathy: involvement of N-acetylneuraminic acid in the epitope.
We report on a 54-year-old man with a sensory-motor polyneuropathy associated with a biclonal IgM-kappa gammopathy, which reacted with the ganglioside GD1b. Examination of nerve biopsy specimens showed some reduction in the density of myelinated fibers and axonal degeneration with a loss of large fibers and a relative increase in the density of small fibers. Immunodetection on thin-layer chromatography of the glycolipid antigens showed strong reactivity of the patient's serum IgM-kappa with GD1b ganglioside and weak binding to GD1a. biclonal IgM antibodies did not react with GM1, asialo-GM1, GT1b, GD2, or GD3. Indirect immunofluorescence staining showed binding of IgM-kappa mainly in a crescent-like pattern on the internal side of myelin sheaths, which could correspond either to an enlarged periaxonal (adaxonal) space or to the internal mesaxon or to both. The immunostaining was abolished after absorption of the serum with GD1b.
Antigens↗
[Characterization of inflammatory cell infiltrates of peripheral neuropathies in human immunodeficiency virus infection].
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HIV Infections↗
Alterations in myelinated fibres in the sciatic nerve of rats after constriction: possible relationships between the presence of abnormal small myelinated fibres and pain-related behaviour.
Morphology or peripheral myelinated fibres was analyzed in rats exhibiting hyperalgesia and allodynia with mechanical and thermal stimuli, consecutive to a mononeuropathy induced by 4 loose ligatures around a sciatic nerve. This preliminary study was based on weeks 2-3 after surgery, the time of the maximum alterations of the pain-related behaviour. At this time, contrasting with a marked decrease of the large afferent fibres a consistent number of much less than 5 micron fibres was pointed out. In addition to their extremely short internodal length, the majority of these fibres had an abnormal g-ratio, thus an abnormal myelin sheath. It is suggested that this group of abnormal fibres might be related to the A delta fibres described in neuromas and involved in pain-related behaviours seen in the mononeuropathic rats.
Animals↗
The spectrum of changes on 20 nerve biopsies in patients with HIV infection.
Nerve and muscle biopsies were performed on 20 patients with HIV infection and peripheral neuropathy. Nine patients had distal symmetrical peripheral neuropathy (DSPN) (six ARC and three AIDS), six had inflammatory demyelinating polyneuropathy (IDP) (three ARC, one AIDS, and two otherwise asymptomatic patients), one had mononeuropathy multiplex (MM) (AIDS), 1 had mononeuropathy (ARC), one had meningoradiculitis (AIDS), and two had areflexia-associated lymphocytic meningitides (ARC), DSPN exhibited axonal degeneration in four of nine cases and was associated with segmental demyelination in five of nine cases. IDP exhibited segmental demyelination associated with axonal degeneration in four of six cases. Demyelination was more frequent in asymptomatic patients (2 of 2 cases) and in ARC (7 of 12 cases), whereas axonal degeneration was predominant in AIDS (6 of 6 cases). Mononuclear cell infiltration was seen in 1 of 2 asymptomatic patients and in 11 of 12 ARC patients but was exceptionally found in AIDS (1 of 6 cases). Involvement of the walls of small vessels, mostly venules ("subacute microvasculitis"), was found in 1 of 2 asymptomatic patients, in 8 of 12 ARC patients, and never in AIDS. The polyclonal mononuclear cell population was composed mainly of Leu 2 (T8) positive cells in seven cases of ARC. No virions were seen in electron microscopy. HIV was isolated in two cases from the CSF or the nerve biopsy.
Acquired Immunodeficiency Syndrome↗
Peripheral neuropathies during treatment with almitrine: report of 46 cases.
Almitrine bismesylate is thought to cause sensory peripheral neuropathy. Forty-six patients are reported who received almitrine bismesylate alone for chronic respiratory failure or in combination with raubasine for various cerebrovascular diseases. Polyneuropathy appeared between 9 and 25 months after the onset of treatment. Sensory signs and symptoms were confined to the distal parts of the lower limbs and involved large and small fibres. Histological and electrophysiological findings indicated axonal degeneration. Respiratory failure could have caused the polyneuropathy in some cases but many had no chest disease. Patients began to improve between 3 and 6 months after withdrawal of the drug. Recovery was usually complete after 12 months.
Aged↗
[A simple system for semi-automatic image analysis].
A device using a Macintosh microcomputer and a light microscope equipped with a drawing tube is described. The mirror of the drawing tube is turned to the screen of the microcomputer. An example of its use in morphometry of peripheral nerves is given. At a 1000X magnification, the resolution of the system is 10 pixels per 2.6-microns. The coefficient of variation between 20 measurements of diameter of thin (3 microns in diameter) and large (12 microns in diameter) myelinated fibers was 8% and 2% respectively. This precise and inexpensive system could be easily run in laboratories of morphology.
Humans↗
[Study of antiglycolipid antibodies in IgM monoclonal dysglobulinemias associated with peripheral neuropathy].
An immunological mechanism may be responsible for the peripheral neuropathies related to IgM monoclonal gammopathies. Myelin-associated glycoprotein (MAG) has been found to be one the main target antigens for these paraproteinemias. Glycosphingolipids of peripheral nerve have been also found to be targets for these antibodies, especially a sulfated glycosphingolipid containing glucuronic acid (GLSG) specific for peripheral nerve. Crossed reactivity has been found between MAG and GLSG. Anti-glycolipid antibodies were determined in 14 patients with IgM gammopathy and polyneuropathy. Glycosphingolipids from human peripheral nerve were purified and chromatographed by thin-layer chromatography for immunodetection of the antibodies. The 12 patients who had GLSG antibody activity had a clinical status identical to the reported cases of dysglobulinemic neuropathies with anti-MAG antibodies.
Adult↗