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This is the commonest and gravest form of acute encephalitis About 2000 cases occur yearly in the United States, accounting for about 10 percent of all cases of encephalitis in this country Between 30 and 70 percent are fatal, and the majority of patients who survive are left with serious neurologic abnormalities HSV encephalitis occurs sporadically throughout the year and in patients of all ages and in all parts of the world It is due almost always to HSV-1, which is also the cause of the common herpetic lesions of the oral mucosa; rarely, however, are the oral and encephalitic lesions concurrent The type 2 virus may also cause acute generalized encephalitis, usually in the neonate and in relation to genital herpetic infection in the mother Type 2 infection in the adult may cause an aseptic meningitis and sometimes a polyradiculitis or myelitis, again in association with a recent genital herpes infection Exceptionally, the localized adult type of encephalitis is caused by the type 2 virus and the diffuse neonatal encephalitis by type 1
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ifestation of the illness, it may be mistaken for a stroke The CSF ndings have been mentioned and are typical of a meningoencephalitis Spinal uid that contains a large number of red cells may be attributed to a ruptured saccular aneurysm The electroencephalographic (EEG) changes, consisting of lateralized periodic highvoltage sharp waves in the temporal regions and slow-wave complexes at regular two- to three-per-second intervals, are highly suggestive in the appropriate clinical context, though they are not speci c for the disease CT scans show hypodensity of the affected areas in 50 to 60 percent of cases and MRI shows signal changes in almost all (increased signal in T2-weighted images; Fig 33-1) T1-weighted images demonstrate areas of low signal intensity with surrounding edema and sometimes with scattered areas of hemorrhage occupying the inferior parts of the frontal and temporal lobes Almost always the lesions enhance with contrast infusion or with gadolinium, indicating cortical and pial abnormalities of the blood-brain barrier It should be noted that these destructive lesions are almost unique among the viral encephalitides, being seen only occasionally in other viral infections of the brain, among them La Crosse encephalitis in children (McJunkin et al) A rising titer of neutralizing antibodies can be demonstrated from the acute to the convalescent stage, but this is not of diagnostic help in the acutely ill patient and may not be signi cant in patients with recurrent herpes infections of the oral mucosa More recently, tests for the detection of HSV antigen in the CSF by the application of PCR have been developed and are useful in diagnosis while the virus is replicating in the rst few days of the illness (Rowley et al) A re nement in this technique (a nested PCR assay), described by Aurelius and coworkers, reportedly has a sensitivity of 95 percent and gives virtually no false-positive tests in the rst 3 weeks of illness In the experience of Lakeman and colleagues, the test was 98 percent positive in cases proven by cultures of brain biopsy material and gave 6 percent false-positives Antiviral treatment did not appear to affect the test False-negative tests are most likely to
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occur in the rst 48 h of febrile infection The only alternative way to establish the diagnosis of acute HSV encephalitis is by uorescent antibody study and by viral culture of cerebral tissue obtained by brain biopsy; the approach to biopsy as a diagnostic test varies among centers but its use has declined with the availability of the PCR test We nd it necessary to perform biopsy in only a minority of cases, preferring to treat the patient with antiviral agents based on compatible clinical, radiologic, and CSF ndings while we await serologic and PCR test results Treatment Until the late 1970s, there was no speci c treatment for HSV encephalitis A collaborative study sponsored by the National Institutes of Health and also a Swedish study indicated that the antiviral agent acyclovir signi cantly reduces both mortality and morbidity from the disease (Whitley et al; Skoldenberg et al) For this reason, it is our practice to initiate treatment while con rmatory testing is being carried out Acyclovir is given intravenously in a dosage of 30 mg/kg per day and continued for 10 to 14 days in order to prevent relapse Acyclovir carries little risk and can be discontinued if further clinical or laboratory features point to another diagnosis The main problems that arise from the drug are local irritation of the veins used for infusion, mild elevation of hepatic enzymes, or transient impairment of renal function Nausea, vomiting, tremor, or an encephalopathy that is dif cult to distinguish from the encephalitis itself occur in a very few patients The matter of relapse after treatment with acyclovir has been recognized increasingly, particularly in children Several potential mechanisms have been suggested by Tiege and colleagues, includ` ing an immune-mediated in ammatory response, but treatment with too low a dose or for too brief a period is undoubtedly the main cause of the rare relapses that occur in adults In children, a second course of acyclovir is usually successful When a large volume of brain tissue is involved, the hemorrhagic necrosis and surrounding edema act as an enlarging mass that requires separate attention Coma and pupillary changes should
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Figure 33-1 Herpes simplex encephalitis Left: a T2-weighted coronal MRI in the axial plane, taken during the acute stage of the illness There is increased signal from practically all of the inferior and deep temporal lobe and the insular cortex Right: a T1-weighted image after gadolinium infusion showing enchancement of the left insular and temporal cortices and early involvement of the right temporal lobe
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