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Table 4: Diagnosis of HSE in the present case
Diagnostic tests Characteristic findings Present case
EEG [8] Background slowing and frequent PLEDs over the temporal lobe Showed diffuse right hemispherical
Usually, present from day 2 to day 14 after disease onset slowing in theta to delta range
Neuroimaging [9] MRI is more sensitive and specific than CT T2‑weighted sequence showed swollen
Early findings include gyral edema in T1‑weighted sequences and edematous right temporal lobe.
and high signal intensities over the medial temporal lobe and the Restricted diffusion and abnormal
cingulate gyrus in T2, FLAIR and diffusion‑weighted sequences, leptomeningeal enhancement were also
often with foci of hemorrhage noted
Bilateral assymetrical temporal lobe and cingulate gyrus involvement
is nearly pathognomonic of HSE but is a late development
CSF study [10] Elevated CSF opening pressure CSF protein: 60 mg/dL
Lymphocytic CSF pleocytosis CSF sugar: 87 mg/dL
3
Elevated proteins CSF cells: 200 cells/mm with
Normal glucose predominantly lymphocytes (P28, L64)
Virological Gold standard for diagnosis CSF meningoencephalitis profile: positive
diagnosis [11] Detection of herpes simplex virus DNA in the CSF by PCR for herpes simplex‑1
Brain biopsy [27,28] Microscopically, necrosis is associated with diffuse inflammation and Inflammatory cell infiltration and
perivascular lymphocytic infiltration. Viral intranuclear inclusions are perivascular lymphocytic cuffing consistent
inconstant, and viral antigens are detectable only at early stages with HSE. No herpes inclusions were seen
HSE: herpes simplex encephalitis; EEG: electroencephalography; PLEDs: periodic lateralized epileptiform discharges; MRI: magnetic resonance imaging; CT: computed
tomography; CSF: cerebrospinal fluid; PCR: polymerase chain reaction; FLAIR: fluid‑attenuated inversion recovery; DNA: deoxyribonucleic acid

thus may have been identified earlier with milder the initial neurologic deficit does not affect the
cases of HSE. [19] long-term clinical outcome if decompression is done
in the early stages. [26]
Sequelae among survivors are significant and depend
on the patient’s age and neurologic status at the time In conclusion, we were able to diagnose HSE with
of diagnosis. Patients who are comatose at diagnosis the help of clinical findings, MRI-brain, analysis of
have a poor prognosis regardless of their age. In CSF profile showing lymphocytic pleocytosis and
non-comatose patients, the prognosis is age related, detection of HSV DNA, in our patient [Table 4]. EEG
with better outcomes occurring in patients younger showed diffuse right hemispherical slowing in theta to
than 30 years. Anterograde memory often is impaired delta range and brain biopsy was consistent with HSE.
even with successful treatment of HSE. Retrograde Initially, the patient was initiated on empirical acyclovir
memory, executive function, and language ability may therapy and anti-cerebral edema medications but later
also be impaired. A study by Utley et al. [20] showed that on decompressive craniectomy was necessary to treat
patients who had a shorter delay (< 5 days) between refractory intracranial hypertension. Following surgery
presentation and treatment had better cognitive the patient showed remarkable neurological recovery.
outcomes. Furthermore, Marschitz et al. [21] reported a Hence, we conclude that, for patients with HSE, it is
case of chorea after HSE. important for the clinician to detect deterioration of
consciousness because of the mass effect caused by
Despite adequate medical treatment, some HSE patients the disease-associated inflammatory process as early as
worsen because of refractory intracranial hypertension. possible. Timely recognition of refractory intracranial
A decompressive craniectomy (in which the skull hypertension and surgical decompression in HSE can
flap is not immediately replaced, allowing the brain be life-saving. Increased intracranial pressure during
to swell, thus reducing intracranial pressure), with HSE may be so grave that it may cause a shift of
or without anterior temporal lobe resection, can be intra-cerebral structures, thus increasing the morbidity
effective in controlling intractable, elevated intracranial and mortality. Decompressive surgery for HSE with
pressure in HSE. [22,23] refractory hypertension can positively affect patient
survival, with good outcomes in terms of neurological
Taferner et al. [24] reported the long-term sequelae recovery.
(1.5-8 years after craniectomy) of four cases with HSE
and confirmed its appropriateness, as it led to full REFERENCES
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