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There are no pathognomonic clinical findings associated with HSE. Focal neurologic deficits, CSF pleocytosis, and abnormalities on CT scanning may be absent initially. Therefore, a high index of suspicion is required to make the diagnosis, particularly in immunocompromised patients with febrile encephalopathy. Expeditious evaluation is indicated after the diagnosis of HSE is considered.
HSE occurs as 2 distinct entities:
In children older than 3 months and in adults, HSE is usually localized to the temporal and frontal lobes and is caused by HSV-1
In neonates, however, brain involvement is generalized, and the usual cause is HSV-2, which is acquired at the time of delivery
Meningeal signs may be present, but meningismus is uncommon. Unusual presentations also occur. Both HSV-1 and HSV-2 may produce a more subacute encephalitis, apparent psychiatric syndromes, and benign recurrent meningitis. Less commonly, HSV-1 may produce a brainstem encephalitis, and HSV-2 may produce a myelitis.