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DIAGNOSIS AND THERAPY OF HERPES SIMPLEX VIRUS (HSV) ENCEPHALITIS

Diagnosis
Routine diagnostic tests are of limited utility in HSV type 1 encephalitis. Examination of cerebrospinal fluid (CSF) often shows a mononuclear cell pleocytosis (10 to 1000 cells/mm3), an elevated protein concentration, and a normal or slightly low glucose level. The most helpful CSF finding, if present, is red blood cells in the absence of a traumatic lumbar puncture. This suggests necrotizing HSV type 1 encephalitis in the appropriate clinical setting. MRI with enhancement demonstrates lesions earlier than computed tomographic scan and is superior in localizing lesions to the orbital-frontal and temporal lobes. The EEG pattern in HSV type 1 encephalitis is distinctive and consists of periodic sharp-and-slow wave complexes emanating from the temporal lobe that occur at regular intervals of 2 to 3 seconds. These discharges can be unilateral or bilateral and are seen in two thirds of pathologically proven cases of HSV encephalitis. Although clinical and imaging studies can suggest HSV type 1 encephalitis, the diagnosis is correct only approximately 50% of the time when based on these criteria. Therefore, laboratory confirmation of the diagnosis is required. Polymerase chain reaction (PCR) on CSF for HSV type 1 is the procedure of choice, and results can be obtained in 1 hour. In one series, PCR was shown to be 98% sensitive and 100% specific. Serum antibodies are unhelpful, and CSF viral culture has low sensitivity. Cerebral biopsy with virus isolation has been the gold standard for diagnosis. It is rarely indicated unless CSF abnormalities are atypical, a CSF PCR study is negative, MRI and EEG are nonspecific, or clinical course is progressive despite acyclovir therapy. If CSF PCR is not available, early stereotactic brain biopsy is favored over empiric antiviral treatment, since the clinical diagnosis is only 50% accurate and alternative treatable diagnoses are found in as many as 15% of cases when biopsy is performed.
Therapy
Acyclovir is the treatment of choice for herpes encephalitis and should be instituted upon suspicion of the disease. The effects of the illness can be significantly reduced if acyclovir is begun before there is a major alteration in the patient’s level of consciousness. Therapy has reduced the mortality rate to 19% (versus 70% in untreated control subjects), with 38% of patients returning to normal function. The recommended dose is 10 mg/kg intravenously every 8 hours for 10 to 14 days. The dose should be adjusted in patients with renal failure. Patients with a Glasgow Coma Score below 6 at the beginning of therapy, age older than 30 years, or the presence of encephalitis for more than 4 days before the initiation of treatment have a very poor outcome.
Patients who survive herpes encephalitis may have severe, debilitating sequelae, including motor and sensory deficits, aphasia, and problems with cognitive function. Relapse of encephalitis is occasionally seen 1 week to 3 months after completion of acyclovir therapy and initial improvement. Retreatment with acyclovir or acyclovir and vidarabine is indicated in these cases.
*22/348/5*

DIAGNOSIS AND THERAPY OF HERPES SIMPLEX VIRUS (HSV) ENCEPHALITISDiagnosis Routine diagnostic tests are of limited utility in HSV type 1 encephalitis. Examination of cerebrospinal fluid (CSF) often shows a mononuclear cell pleocytosis (10 to 1000 cells/mm3), an elevated protein concentration, and a normal or slightly low glucose level. The most helpful CSF finding, if present, is red blood cells in the absence of a traumatic lumbar puncture. This suggests necrotizing HSV type 1 encephalitis in the appropriate clinical setting. MRI with enhancement demonstrates lesions earlier than computed tomographic scan and is superior in localizing lesions to the orbital-frontal and temporal lobes. The EEG pattern in HSV type 1 encephalitis is distinctive and consists of periodic sharp-and-slow wave complexes emanating from the temporal lobe that occur at regular intervals of 2 to 3 seconds. These discharges can be unilateral or bilateral and are seen in two thirds of pathologically proven cases of HSV encephalitis. Although clinical and imaging studies can suggest HSV type 1 encephalitis, the diagnosis is correct only approximately 50% of the time when based on these criteria. Therefore, laboratory confirmation of the diagnosis is required. Polymerase chain reaction (PCR) on CSF for HSV type 1 is the procedure of choice, and results can be obtained in 1 hour. In one series, PCR was shown to be 98% sensitive and 100% specific. Serum antibodies are unhelpful, and CSF viral culture has low sensitivity. Cerebral biopsy with virus isolation has been the gold standard for diagnosis. It is rarely indicated unless CSF abnormalities are atypical, a CSF PCR study is negative, MRI and EEG are nonspecific, or clinical course is progressive despite acyclovir therapy. If CSF PCR is not available, early stereotactic brain biopsy is favored over empiric antiviral treatment, since the clinical diagnosis is only 50% accurate and alternative treatable diagnoses are found in as many as 15% of cases when biopsy is performed.
TherapyAcyclovir is the treatment of choice for herpes encephalitis and should be instituted upon suspicion of the disease. The effects of the illness can be significantly reduced if acyclovir is begun before there is a major alteration in the patient’s level of consciousness. Therapy has reduced the mortality rate to 19% (versus 70% in untreated control subjects), with 38% of patients returning to normal function. The recommended dose is 10 mg/kg intravenously every 8 hours for 10 to 14 days. The dose should be adjusted in patients with renal failure. Patients with a Glasgow Coma Score below 6 at the beginning of therapy, age older than 30 years, or the presence of encephalitis for more than 4 days before the initiation of treatment have a very poor outcome.Patients who survive herpes encephalitis may have severe, debilitating sequelae, including motor and sensory deficits, aphasia, and problems with cognitive function. Relapse of encephalitis is occasionally seen 1 week to 3 months after completion of acyclovir therapy and initial improvement. Retreatment with acyclovir or acyclovir and vidarabine is indicated in these cases.*22/348/5*

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