A Undetectable Gemstone Of SB431542

11 Our case had refractory SE and initial EEG revealed bitemporal epileptiform discharges with generalisation and background slowing whereas an MRI revealed signal changes in hippocampus, left temporal, insular and medial frontal lobes. A case of NORSE needs extensive workup to rule out infectious aetiology like encephalitis, immunological disorders like collagen vascular disorders, neoplastic, paraneoplastic, metabolic-induced and toxin-induced disorders.6 In our case CSF for HSV PCR was positive which has a high-sensitivity and specificity,5 thus SB431542 confirming the diagnosis of HSE. Despite receiving multiple AEDs, she responded clinically with complete seizure control only after receiving acyclovir. The clinical features of HSE are often non-specific and misleading, which include focal encephalitis with fever, altered sensorium and focal neurological signs. Frontotemporal involvement leads to aphasia, personality change and focal seizures. Seizures can be the presenting feature in about 50% cases because of the involvement of a highly epileptogenic frontotemporal cortex. Alteration in excitability of the hippocampal A3 neuronal network and HSV1-induced neuronal loss results in mossy fibre reorganisation which may play an important role in epileptogenesis.12 Seizures can be acute symptomatic or remote symptomatic. Seizures include focal seizures (complex partial), focal onset generalised or generalised seizures. SE can complicate the illness, although its occurrence as a presenting feature is uncommon. According to a study by Misra13 UK, 39.8% cases with SE (most common type was convulsive status epilepticus) had CNS infections of which 8% had herpes simplex infection. Gunduz14 reported a case of non-convulsive SE due to HSV infection. Our case had a convulsive SE along with behavioural changes and hallucinations (auditory and visual). A cranial MRI is essential for an early diagnosis as well as for defining the distribution of cerebral injury in HSE. The MRI scan in HSE typically shows early changes of focal oedema in the medial aspects of the temporal lobes, orbital surfaces of the frontal lobes, insular cortex and cingulate gyrus.15 An EEG is abnormal in almost all cases and may reveal focal abnormalities like slowing, spikes, lateralised or multifocal epileptiform discharges involving the frontotemporal leads; however, none of these findings are specific for HSE. The imaging features and EEG changes can resemble those occurring in NORSE as observed in our case. Exact guidelines for the management of NORSE have not been defined; however, the treatment strategy includes intravenous infusion of propofol, midazolam and pentobarbitol alone or in combination. If seizures are still refractory, intravenous ketamine and inhalational anaesthetics can be used.16 Newer agents like topiramate and leviteracetam have been tried and found to be useful.