Experimental allergic encephalomyelitis. I. Optic nerve and central nervous system manifestations.

Experimental allergic encephalomyelitis (EAE) was produced in six adult rhesus monkeys. The animals were evaluated serially by ocular, ophthalmoscopic, fluorescein fundus angiographic, pupillary, visual evoked potential, neurologic, cerebrospinal fluid (CSF), and hematologic examinations and by postmortem detailed histopathologic examination. All the animals developed acute EAE. Four of the monkeys, surviving longer than 1 month, developed chronic relapsing EAE and were sacrificed 3 to 14 months after sensitization. All 12 eyes developed acute optic neuritis (with variable degrees of optic disc edema and visual loss). Later on, all the eyes of animals with chronic EAE developed optic atrophy with total or almost total blindness. Histopathologic examination of the optic nerve and central nervous system revealed inflammatory infiltrates, extensive demyelination, and axonal degeneration, without inflammation in the retina or optic nerve head (i.e., nonmyelinated neural tissue). Relapsing EAE was reflected in episodic increases of CSF proteins and pleocytosis. The various findings are correlated.

Electroencephalographic absence status with minimal behavior change.

Difficulty in correlating EEG abnormalities with clinical seizures is emphasized in this case report of an epileptic patient with electrical status epilepticus and normal behavior. In addition, the usefulness of dichotic listening tests in the identification of subtle perceptive and expressive impairments is illustrated in this same patient at a time of noncompliance with anticonvulsant therapy.