Neurosurgical experiences with herpes simplex encephalitis.

Abstract

N ~ EUROSURGEONS n l u s t differentiate herpes simplex cnccphalitis from other rapidly-expanding middle fossa lesions by early diagnostic procedures ineluding brain biopsy. Successful therapy may depend upon prompt surgical decompression of the massive cerebral edema that is often found. The purpose of this paper is to record our experiences with various methods of reducing increased intraeranial pressure in three consecutive eases of proven herpes simplex encephalitis during a ~-year period. In 1941, Smith, et al., 29 demonstrated both herpes simplex virus and Cowdry type-A intranuclear inclusion bodies in the brain of a child with encephalitis. Since then, herpes simplex has been suggested as the etiologic agent in cases variously labeled as acute inclusion body encephalitisp '9'15 acute necrotizing encephalitis, ~'n acute necrotizing hemorrhagic encephalitis, 4 and even acute hemorrhagic leukoencephalitis. 22 The patient with acute encephalitis due to herpes simplex virus often presents a characteristic appearance 9 which begins with the abrupt onset of fever, headache, drowsiness, occasional stiff neck, and convulsions. More specific symptoms such as dysphasia, psychomotor phenomena, and olfactory hallucinations point toward the maximally affected temporal and orbital regions. Early involvement may be predominantly unilateral. Electroencephalograms, radioisotope scans, and x-ray contrast studies may all localize to one temporal lobe. Abscess or other rapidly expanding lesions of the temporal area must then be ruled out. 1'4'19'22'26 Cerebrospinal fluid pressure may be elevated, and pleocytosis is usual. Viral cul-