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Lewis rats develop experimental allergic neuritis (EAN) when injected with bovine dorsal root (BDR) emulsified in complete Freund's adjuvant (CFA). In this study the susceptibility to EAN and subsequent relapse was studied in animals ranging from 4 to 25 weeks of age. Older animals exhibited a severe acute illness which was monophasic over the period of observation, whereas younger animals developed a less severe and frequently relapsing illness. Very young animals often relapsed more than once and sometimes to a more severe degree than shown in their first attack. Older animals which were in the late recovery stage of EAN (44 days after injection with BDR/CFA) were completely resistant to a second challenge with antigen. Young adult animals also developed resistance but not as strongly as the older animals. Animals first injected at weaning developed resistance as in the adults, but the analysis is complicated by the occurrence of spontaneous relapses. Because of differences in disease pattern between EAN and acute inflammatory polyneuropathy (Guillain-Barré syndrome) in man, caution should be exercised in drawing too close a parallel between the animal model and the human disease. The affinities may be closer to chronic relapsing inflammatory polyradiculopathy in man.

Severe hypothermia and an ascending impairment of shivering are previously undescribed clinical signs in hyperacute experimental allergic encephalomyelitis (EAE) in the Lewis rat. These occurred in hyperacute EAE induced by inoculation with guinea pig spinal cord homogenate and heat-killed Bordetella pertussis. Hypothermia was first detected on day 6-7 post-inoculation, within 12-24 h of the onset of neurological signs, and became more severe as the disease progressed. Rectal temperatures less than or equal to 30 degrees C were common at ambient temperatures of 19-22 degrees C. Shivering was assessed by palpation and by cold tremor electromyography. Shivering was absent in the tail by day 6-7 post-inoculation. The impairment then progressed to affect the hindlimbs, thorax and occasionally the forelimbs. Shivering was absent in hindlimbs with only mild or moderate weakness. Histological studies revealed perivascular inflammation with polymorphonuclear and mononuclear cells, oedema, fibrin deposition, haemorrhage, primary demyelination and axonal degeneration in the spinal cord, dorsal root ganglia and spinal roots. The brainstem was also involved but the cerebral hemispheres, including the hypothalamus, were spared. The close relationship between the severity of hypothermia and the extent of shivering impairment indicates that reduced shivering is an important cause of hypothermia in hyperacute EAE. It is concluded that this impairment of shivering is due not to hypothalamic damage but to lesions elsewhere in the central and peripheral nervous systems.