Indian Journal of Dermatology
: 2011  |  Volume : 56  |  Issue : 6  |  Page : 749--751

Poor neurological sequelae of herpes simplex virus encephalitis in an infant despite adequate antiviral and adjunct corticosteroid therapy

Ratna B Basak1, Varsha Malpani1, Khalid Kakish1, Susan Vargese1, Nageshwar Chauhan2, Andreas Boeck1,  
1 Department of Pediatrics, Alain Hospital-affiliate to Medical University of Vienna, Alain, United Arab Emirates
2 Department of General Medicine Hospital, Jagadhri, Yamunanagar, Haryana, India

Correspondence Address:
Ratna B Basak
Brookdale University Hospital and Medical Center, 1 Brookdale Plaza, Brooklyn, NY
United Arab Emirates


A 2-month-old infant presented to our emergency department with fever, altered consciousness, and focal seizures of acute onset. He had vesicular skin lesions over the right preauricular region. CT brain showed a large hypodense lesion involving the left temporo-parietal region, left basal ganglia and left thalamus. MRI brain revealed bilateral multifocal corticomedullary lesions suggestive of encephalitis. CSF-PCR was positive for herpes simplex virus (HSV) type I. He was treated with standard dose intravenous acyclovir for 15 days along with a trial of pulse methylprednisolone, but was readmitted within a week with features of an early relapse. The infant survived but developed significant neurological sequelae. Although treatment of HSV is available, the neurological outcome is guarded even with adequate antiviral therapy. Adjunct corticosteroid therapy did not appear to attenuate the neurological sequelae.

How to cite this article:
Basak RB, Malpani V, Kakish K, Vargese S, Chauhan N, Boeck A. Poor neurological sequelae of herpes simplex virus encephalitis in an infant despite adequate antiviral and adjunct corticosteroid therapy.Indian J Dermatol 2011;56:749-751

How to cite this URL:
Basak RB, Malpani V, Kakish K, Vargese S, Chauhan N, Boeck A. Poor neurological sequelae of herpes simplex virus encephalitis in an infant despite adequate antiviral and adjunct corticosteroid therapy. Indian J Dermatol [serial online] 2011 [cited 2022 Sep 26 ];56:749-751
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Full Text


Herpes simplex encephalitis (HSE) in children has high rates of morbidity and mortality. Early diagnosis and antiviral therapy HSE has significantly reduced the case fatality rate, but relapses occur even after adequate therapy. [1] We present a case of HSE treated with acyclovir and methylprednisolone, who developed significant neurodeficits after a relapse.

 Case Report

A 2-month-old male infant presented with high-grade fever, intermittent right sided tonic clonic seizures since day one of admission. He was irritable 2 days prior to arrival. He was born full term normal delivery to consanguineous parents. On examination, he was febrile (39.5°C), poorly responsive, with a glasgow coma scale (GCS) of 8. The pupils were constricted but reactive to light. There was generalized hypertonia with brisk deep tendon reflexes. Grouped vesicular skin lesions were noted in the right preauricular region over a 2 × 3 cm area [Figure 1]. After initial fluid resuscitation and seizure control with IV diazepam and phenytoin, CT brain revealed a large hypodense lesion in the left temporoparietal region suggestive of encephalitis or infarction [Figure 2]. Investigations showed normal blood count and CRP of 12 mg/L. Renal functions were normal and serum albumin 2.6 g/dL. CSF showed WBC 2 cells/cumm, RBC <1 cell/cu mm, protein 139 mg/dL, glucose 51 mg/dL and chloride 679 mg/dL. Gram stain and latex agglutination for bacterial antigens were negative. Blood, CSF and urine cultures showed no growth. Serum immunoglobulin profile was normal. MRI brain showed left cortical and subcortical temporoparietal irregular high signal with gyral enhancement. The multifocal bilateral corticomedullary lesions were suggestive of encephalitis. EEG was consistent with diffuse encephalopathy showing greater involvement of right hemisphere. Tzanck smear showed multinucleated giant cells suggestive of viral infection. CSF qualitative PCR was positive for herpes simplex virus (HSV) type1.The infant was diagnosed with HSE and started on IV acyclovir at 45 mg/kg/day. IV ceftriaxone and vancomycin started on admission were discontinued after 72 hours following negative blood and CSF cultures. Although the fever settled after 3 days and seizures reasonably well controlled, the GCS remained at 8. A trial of pulse methylprednisolone therapy was given from day 5 to day 7. [2] The infant became alert, responsive, and began accepting oral feeds. IV acyclovir was continued for 15 days and the child discharged on day 18 on phenytoin, with recommendations for close follow up. Five days following discharge, he was readmitted with low grade fever and seizures lasting less than 30 seconds, occurring more than 10 times/day. CT scan showed a new infarct in right temporoparietal region and right basal ganglia and an area of fresh hemorrhage in the right cerebellum and occipital lobe. CSF showed protein 287 mg/dL, glucose 57 mg/dL, numerous RBC, WBC 170/cumm, 92% lymphocytes, 8% neutrophils. Blood and CSF cultures again revealed no growth. Repeat CSF-PCR for HSV was negative. MRI done during this readmission showed marked cystic changes representing liquefying encephalomalacia involving bilateral temporoparietal regions, more pronounced on the right [Figure 3]. HSV IgM was positive in the infant while it was negative in the mother. The presentation was consistent with an early relapse, and he was treated with IV acyclovir at 60 mg/kg/d for further 21 days. The child was, however, left with poor visual fixation, decerebrate posturing, hypertonia and poor suck-swallow coordination. He was discharged on nasogastric feeds, carbamazepine, baclofen and daily physiotherapy.{Figure 1}{Figure 2}{Figure 3}


Children and adolescents account for nearly one-thirds of all cases of HSE. [3] After the neonatal period, HSE is routinely caused by HSV type 1 although HSV type 2 may rarely be involved. [1] Two biological properties of HSV that directly influence human disease are neurovirulence and latency. [4] Transneuronal transmission of HSV type 1 causes HSE in both children and adults while hematogeneous spread of HSV type 2 or HSV type 1 causes CNS infections in neonates. [5] HSE exhibits a striking predilection for temporal lobe involvement suggesting that the olfactory tract might be the main pathway of access to the CNS. About 5-10% patients may have a normal CSF on initial evaluation, particularly in children. [3],[6] Diffusion weighted MRI is the most sensitive modality for early detection of CNS disease. [1] EEG may show focal or diffuse slowing, focal sharp waves or spikes or periodic lateralized epileptiform discharges, but no pattern is pathognomonic for HSE. [1],[3] HSV-PCR has replaced brain biopsy as diagnostic method of choice. [7] However, PCR has lower sensitivity in children compared to adults, particularly during the initial days of the disease. [6] Early administration of intravenous acyclovir 10 mg/kg every 8 hrs (30 mg/kg/d) for 14-21 days is the standard treatment for HSE in children and adults and is recommended by the International Herpes Management Forum. [8] While this has drastically reduced the mortality of HSE from 70 to 10%, [9] neurological morbidity is still unacceptably high. Twenty-six percent children with HSE tend to relapse, and thus a minimum of 15 days of acyclovir at 45 mg/kg/d is recommended to prevent early relapse in children. [10],[11] Neurologic relapses of HSE could either involve the extrapyramidal system or manifest as fever and severe neurological symptoms with lack of extrapyramidal movements. In this latter form, resumption of cerebral viral replication is highly suspect because cerebral imaging shows new necrotichemorrhagic lesions. [10] This may have been the basis of the early relapse in the case presented. HSV-DNA may or may not be demonstrable in the CSF during relapse [10],[12] The role of corticosteroids in HSE is not well defined. Neurological damage in HSE results not only from viral invasion, but also from intense inflammatory changes and cerebral edema secondary to the immune response to the virus. [2],[13] Corticosteroids in the acute stage of HSE may improve brain edema, regulate host immune response and may be beneficial in the management of HSV encephalitis. [2],[14],[15]

Until further data is available, adjunct steroid therapy is currently recommended as a therapeutic option. [16]


Tzanck positive grouped vesicles with seizures point to a diagnosis of HSE. Neurological morbidity in survivors of HSE in children remains high despite timely initiation of IV acyclovir. Adjunct corticosteroid therapy did not appear to attenuate the neurological sequelae.


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