Acute disseminated encephalomyelitis historical perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sujaya Chattopadhyay, M.D.[2]

Encephalomyelitis was primarily an experimental finding discovered after injection of rabbits with rabbit spinal cord infused with solutions of sodium chloride and lecithinase, adjuvants, like [[bayol F],] and killed tubercle bacilli, and human spinal cord treated with formaldehyde solution. Clinical signs were spasticity, ataxia, weakness and even death. The perivascular inflammatory lesions had a predilection for the white matter and demyelination was seen in all ages. Older lesions had glial scars.

In the year 1933, Rivers, Sprunt and Berry observed encephalomyelitis and demyelination in monkeys after serial injections of extracts and saline suspensions of normal rabbit brain.This finding was further confirmed in 1940 by Ferraro and Jervis. In their experiments, the monkeys exhibited forced head position, nystagmus, tremor, spastic paresis. The lesions were distributed throughout the central nervous system with a predilection for white matter. They were perivascular and contained multinucleated giant cells.

Schwentker and Rivers demonstrated that the antigenicity of nervous tissue increased with age and was more characteristic of the white matter. It hinted towards a possible antigenic property of lipid-rich myelin sheath.

Morgan reproduced extensive encephalomyelitis in monkeys by using heat-killed turbercle bacilli. The reaction time for producing changes was reduced by Kabat, Wolf and Bezer who employed heterologous antigen.

Alpha –lecithinase of Clostridium welchii has also been shown to damage the myelin sheath in vitro.

More recent studies showed development of encephalomyelitis regardless of the potency or nature of the injected antigen. A pervivascular hematogenous insterstitial infiltrate gradually evolved to demyelination, fatty degeneration and astrocytic scar formation. It is possible that some of the antibodies originated in the Virchow-Robin spaces which then migrated across at least the blood–cerebrospinal fluid barrier, suggested by Greenfield in his report of post-vaccination encephalomyelitis.