Similarities between the Forssman carotid syndrome and experimental allergic encephalomyelitis.
The Forssman carotid syndrome was induced in guinea pigs to study the mechanism of demyelination-like lesions in this animal model and to compare it with experimental allergic encephalomyelitis days after intracarotid injection of rabbit anti-Forssman antibody and chronic lesions at 7-21 days post injection, using routine histological, immunofluorescent, and electron-microscopic techniques. The results were compared to those in a group of guinea pigs with acute or chronic lesions of EAE. The picture was remarkably similar in the two conditions, in regard to localization in the central nervous system (CNS), composition of cellular infiltrates, diameter of lesions produced, myelin loss and axonal degeneration, together with gamma globulin deposition in small vessels in affected areas. The differences were that in the Forssman carotid syndrome, in contrast to EAE, there were no mononuclear cell infiltrates in the acute phase, and no evidence of macrophages invading myelin sheaths was detected. Perivascular lesions consisted of demyelination within infiltrates of mono-nuclear cell in chronic relapsing EAE, but not in the Forssman carotid syndrome. It is suggested that investigation of the CNS may be of benefit in the pathogenetic study of demyelinating disease.
D000208:Acute Disease; D000818:Animals; D001921:Brain / Q000473:pathology / Q000648:ultrastructure; D001929:Brain Edema / Q000473:pathology* / Q000503:physiopathology; D002490:Central Nervous System / Q000098:blood supply*; D002908:Chronic Disease; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000473:pathology*; D005455:Fluorescent Antibody Technique; D006168:Guinea Pigs; D008297:Male; D008854:Microscopy, Electron; D012008:Recurrence; D013577:Syndrome; D014652:Vascular Diseases / Q000473:pathology* / Q000503:physiopathology