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by inflammatory cells and perivascular lymphocytic of patients. Neuroimaging may be normal in the early
cuffing [Figure 4] with occasional multinucleated giant stages. DNA detection may be negative. [17]
cells, consistent with the well-known pathology of HSE.
The patient was discharged on the 10th postoperative Untreated HSE is progressive and often fatal in
day in a recovering condition. 7-14 days. A landmark study by Whitley et al. [18] in
1977 revealed a 70% mortality in untreated patients
Over the next few months, the patient made a remarkable and severe neurologic deficits in most of the survivors.
neurological recovery. He regained full consciousness Mortality in patients treated with acyclovir was 19% in
and normal cognition. He did not have further episodes the trials that established its superiority to vidarabine.
of seizures. He has no residual neurological deficits. Subsequent trials reported lower mortalities (6-11%),
Two months after the craniectomy, the bone flap was perhaps because they included patients who were
replaced. diagnosed by PCR rather than brain biopsy and who

DISCUSSION
Table 2: Histopathology of the right temporal lesion
Parameters Results
In HSE, delay in treatment leads to severe neurological Microscopy Sections show pieces of cerebral cortex and
sequelae. Therefore, early diagnosis is of great subcortical white matter in which there is edema,
importance. Diagnostic criteria include clinical focal hemorrhage and infarction with infiltration by
symptoms, MRI, EEG, and CSF studies [Table 3]. The inflammatory cells
Perivascular lymphocytic cuffing and occasional
sensitivity is increased with the combination of these multinucleated giant cells noted
neurodiagnostic tests. [12] When HSE is suspected, No viral inclusions/granuloma seen
MRI brain should be done as early as possible as signs of Diagnosis There is no evidence of malignancy
Brain biopsy: consistent with herpes simplex
HSE could be detected by MRI earlier than CT scan. [13] encephalitis
Because MRI is a more sensitive and specific diagnostic
tool, it is used instead of CT scans in the majority of Table 3: Diagnostic criteria for HSE. HSE is diagnosed in
patients. [13-15] The characteristic MRI finding of HSE a febrile patient with an altered level of consciousness
is hyperintense areas (T2-weighted sequences) in the *in the presence of any 3 of the following diagnostic tests
inferior part of temporal lobes, medial part, and insula. Criteria
This may also be observed in the frontal and parietal EEG showing background slowing and frequent PLEDs over the
lobes. Bilateral temporal lobe involvement has been temporal lobe [8]
reported to be pathognomonic of HSE. [16] Diffusion MRI‑Brain showing gyral edema in T1‑weighted sequences and
high signal intensities over the medial temporal lobe and the
limitation observed in T2-FLAIR sequences are also cingulate gyrus in T2, FLAIR and diffusion‑weighted sequences,
thought to be typical. [16] often with foci of hemorrhage [9]
CSF showing lymphocytic pleocytosis, elevated protein and
elevated CSF opening pressure [10]
Herpes simplex encephalitis is a medical emergency Detection of herpes simplex virus DNA in the CSF by polymerase
that requires prompt diagnosis and therapy. However, chain reaction: gold standard for diagnosis [11]
both are often delayed for several reasons. For instance, *With or without focal neurological deficits. EEG: electroencephalography;
the clinical presentation itself is non-specific and may PLEDs: periodic lateralized epileptiform discharges; MRI‑Brain: magnetic resonance
imaging of brain; CSF: cerebrospinal fluid; HSE: herpes simplex encephalitis; FLAIR: fluid‑
be mistaken for stroke, epilepsy, delirium or a primary attenuated inversion recovery; DNA: deoxyribonucleic acid
psychiatric disorder. CSF cell count is normal in 5-10%

Figure 4: Histopathology of the right temporal lesion showing infiltration by
Figure 3: Electroencephalography showing diffuse right hemispherical slowing inflammatory cells and perivascular lymphocytic cuffing, which is consistent
in theta to delta range with herpes simplex encephalitis

184 Neuroimmunol Neuroinflammation | Volume 2 | Issue 3 | July 15, 2015 Neuroimmunol Neuroinflammation | Volume 2 | Issue 3 | July 15, 2015 185