Neurosurgical Experiences with Herpes Simplex Encephalitis*
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Neurosurgical Experiences with Herpes Simplex Encephalitis* LARRY K. PAGE, M.D., H. RICHARD TYLER, M.D., AND JOHN SIIILLITO, JR., M.D. Departments of Neurosurgery and Neurology, Peter Bent Brigham Hospital, and the Harvard Medical School, Boston, Massachusetts ~ EUROSURGEONS nlust differentiate tures of cercbrospinal fluid, however, are herpes simplex cnccphalitis from rarely if ever positive. 9,12 Diagnosis is usually N other rapidly-expanding middle fossa established in retrospect by the demonstra- lesions by early diagnostic procedures in- tion of a greater than fourfold rise in serum eluding brain biopsy. Successful therapy antibody titer to herpes simplex virus, s,22 may depend upon prompt surgical decom- Early diagnosis is made from brain biopsy pression of the massive cerebral edema that material by demonstrating the characteristic is often found. The purpose of this paper is inflammatory changes of acute encephalitis to record our experiences with various in association with Cowdry type-A intra- methods of reducing increased intraeranial nuclear inclusion bodies, 1,12,'5 or by direct pressure in three consecutive eases of proven isolation of herpes simplex virus from brain herpes simplex encephalitis during a ~-year tissue.21,a0 period. Herpes simplex encephalitis may vary in In 1941, Smith, et al., 29 demonstrated both severity,2~ but spontaneous recovery is herpes simplex virus and Cowdry type-A extremely rare in any patient who has intranuclear inclusion bodies in the brain of become comatose. 25 It commonly is asso- a child with encephalitis. Since then, herpes ciated with severe neurological residua or simplex has been suggested as the etiologic death, 9,24 which often may be secondary to agent in cases variously labeled as acute cerebral edema, intracranial hypertension, inclusion body encephalitisp '9'15 acute nec- and transtentorial herniations rather than rotizing encephalitis, ~'n acute necrotizing to irreversible neuronal damage by the virus hemorrhagic encephalitis, 4 and even acute itself, n,a2 It would seem reasonable that hemorrhagic leukoencephalitis.22 when increased intraeranial pressure is The patient with acute encephalitis due present, its relief prior to the stage of per- to herpes simplex virus often presents a manent brain-stem damage might increase characteristic appearance 9 which begins with the chances for useful survival?,7,14,22 the abrupt onset of fever, headache, drowsi- Case Reports ness, occasional stiff neck, and convulsions. More specific symptoms such as dysphasia, Case 1. The patient, a ~5-year-old white psychomotor phenomena, and olfactory man, developed malaise, nausea, photo- hallucinations point toward the maximally phobia, and temperature elevations to 106~ affected temporal and orbital regions. Early The next day he became lethargic, confused, involvement may be predominantly unilat- and disoriented. eral. Electroencephalograms, radioisotope Examination. The patient was admitted to scans, and x-ray contrast studies may all lo- the hospital 4 days after the onset of symp- calize to one temporal lobe. Abscess or other toms with a temperature of 1OS~~ and a rapidly expanding lesions of the temporal pulse rate of 80 per minute. Somnolence area must then be ruled out. 1'4'19'22'26 and dysphasia were present, yet he could Cerebrospinal fluid pressure may be perform simple calculations. Mild right facial elevated, and pleocytosis is usual. Viral cul- weakness and right-sided hyperreflexia were found. The peripheral blood white-cell Received for publication Feburary 1, 1967. count was 18,500 with 85% polymorphonu- * Supported in part by National Institutes of Health clear cells. Cerebrospinal fluid cell count was Grant NB 5519. Presented at the meeting of the Con- gress of Neurological Surgeons, San Juan, Puerto Rico, 160 with 95% lymphocytes, 40 nlg% pro- October 8, 1966. tein, 64 rag% glucose, and an opening pres- 346 Herpes Simplex Encephalitis 347 sure of 300 mm of water. There was focal electroencephalographic slowing in the left frontotemporal area. On the day of admission bilateral carotid arteriograms showed a slow circulation time but no further abnormality. Operation. A left temporal burr hole was made and a needle biopsy taken, which showed extensive necrosis with perivascular cuffing, focal polymorphonuclear and plasma cell infiltration, vascular congestion, and hemorrhage. Intranuelear inclusion bodies were not found. On the sixth postoperative day, bilateral sixth nerve palsies and myoclonic movements were noted. The patient received penicillin, chloromycetin, streptomycin, isoniacid, am- FIG. 1. Cystic necrosis of temporal lobes ~89months photericin B, and dexamethasone. However, after the onset of illness. Case 1. he became increasingly lethargic, and cere- brospinal fluid pressures rose to 550 mm of to the Peter Bent Brigham Hospital with a water over the next 10 days. Constant temperature of 104~ a pulse of 11~ per ventricular drainage was established. A minute, a stiff neck, and bilateral Kernig's ventriculogram showed dilatation of both signs. She was disoriented, had difficulty lateral ventricles without shift or filling naming common objects or parts of her body, defect. Cardiac arrest occurred on two occa- and exhibited a right facial weakness and sions during anesthesia induction for the right homonymous visual inattention. The placement of a ventriculo-peritoneal shunt. peripheral blood white-cell count was 8,000 The shunt was finally established after 35 with 57% lymphocytes. Electroencephalog- days of external ventricular drainage. Seven raphy showed slowing over the left hemi- days later, the shunt required revision, and sphere, echoencephalography showed devia- biopsy again revealed necrotizing encephali- tion of the midline toward the right, and tis, this time with extensive gliosis. In spite Hg 2~ scanning showed increased radioac- of a functioning shunt, the patient remained tivity over the left temporal area (Fig. ~). comatose until his death 16 days later. Antibiotics were started. On the second Postmortem examination. There was ex- hospital day a left carotid arteriogram tensive cystic necrosis of both temporal showed marked elevation of the middle lobes and mild dilatation of the ventricular cerebral artery with minimal left-to-right system (Fig. 1). Virus was not recovered shift of midline vessels (Fig. 3). On the third from cerebral tissue in this case, but a rise in serum antibody titer to herpes simplex virus from less than 1 : 4 to greater than 1 : ~56 was demonstrated. Case 2. A 30-year-old white woman was vacationing in Austria when she suffered two generalized convulsions which were fol- lowed by several days of headache and lethargy. She returned to this country and was admitted to a local hospital with mild temperature elevation and a tendency to "talk in a stream." Lumbar puncture re- vealed an opening pressure of 160 mm of water, 50 mgV-/v protein, 30 lymphocytes, and negative bacterial cultures. FIG. ~. Anterior coronal Hg2~ scan. Note the increased Examination. The patient was transferred left temporal uptake. Case 2. .