Abstracts

Rationale: Relapse of Herpes Simplex Virus (HSV) encephalitis following successful antiviral therapy is uncommon but well described. It is more frequent in children and usually occurs within 3 months of initial infection. Later relapse is rare. A case of reactivation of HSV encephalitis triggered by epilepsy surgery 16 years after initial infection is reported, and similarities to a single previous case report are reviewed. Methods: A case of recurrent HSV encephalitis following right frontal topectomy for intractable epilepsy is presented, with comparison to a prior report (Bourgeois M et al, Reactivation of herpes virus after surgery for epilepsy in a pediatric patient with mesial temporal sclerosis. Neurosurgery, 1999; 44(3):632-635.) Results: A 19 year old woman with prior HSV encephalitis at age 3 years developed refractory frontal lobe epilepsy (10-20 seizures/day). After 7 days of invasive monitoring with subdural electrodes, right inferior frontal gyrus topectomy and MST of surrounding area was performed. She was seizure-free until postoperative day (POD) 10 when she presented with fever, headache and CSF WBC=125(68% PMN). MRI showed acute right frontoparietal infarction and small areas of restricted diffusion in left hemisphere. Mental status worsened with persistent fever despite IV vancomycin, ceftriaxone and open irrigation of surgical site. On POD 19 fever had resolved but MRI showed new areas of bilateral infarction, CSF WBC=10 (83% Lymph) and CSF PCR positive for HSV. Despite initiation of acyclovir there was extension of intracranial edema and patient expired on POD 25. Postmortem confirmed HSV encephalitis with positive virus immunostaining. Comparison is made to a single previous case report of HSV encephalitis at age 16 months with reactivation following amygdalohippocampectomy at age 8 years. That case presented similarly on POD 6 with fever, deterioration in neurological status and diffuse cerebral involvement, maximal at surgical site. Patient survived with severe disability. Notable differences were the shorter interval between original infection and recurrence (7 years vs. 16 years), lack of invasive subdural monitoring, and status epilepticus at presentation. Conclusions: Epilepsy surgery may induce reactivation of HSV encephalitis in previously affected patients. The use of subdural electrodes, corticosteroids and surgical manipulation may have acted as triggers for reactivation in the current case. Diagnosis was complicated by the preceding invasive monitoring, which increased suspicion for bacterial infection, and by neuroimaging which suggested infarction rather than encephalitis. Length of time between original encephalitis and surgery does not appear to mitigate the risk for reactivation, as our case represents the longest reported interval between initial infection and reactivation. The poor outcome of these patients underscores the need for a high index of suspicion for herpes reactivation and early use of acyclovir in at risk postoperative patients. Prophylactic acyclovir should be considered in patients with a history of encephalitis undergoing invasive monitoring.