HSV Encephalitis
On this page
Direct answer
Herpes simplex encephalitis, mostly HSV-1, is the commonest sporadic fatal encephalitis: fever with headache, behavioural change, aphasia, hallucinations and seizures localising to the temporal and frontal lobes. The diagnosis rests on CSF polymerase chain reaction (sensitivity above 95 per cent), MRI showing temporal lobe signal change and EEG with periodic lateralising discharges — but intravenous aciclovir 10 mg per kg every eight hours is started empirically before any of it returns, because delay directly costs brain and life.
What you must remember
- Clinical localisation: personality change, bizarre behaviour, aphasia (dominant temporal lobe), olfactory or gustatory hallucinations, focal seizures and rapid deterioration — the "psychiatric" presentation is the trap.
- CSF: lymphocytic pleocytosis (often with red blood cells or xanthochromia reflecting haemorrhagic necrosis), moderately raised protein, normal or low glucose; PCR for HSV DNA is the diagnostic standard, though it can be falsely negative in the first day or two and after several days of aciclovir.
- MRI (FLAIR/T2) shows temporal lobe, insular and cingulate hyperintensity, often bilateral asymmetric; EEG shows temporal slowing and periodic lateralising epileptiform discharges; CT is insensitive early.
- Treatment: IV aciclovir 10 mg per kg every 8 hours (adults with normal renal function), adjusted for renal impairment, infused slowly with hydration to prevent crystal nephropathy, for 14–21 days; do not await PCR — treat empirically on suspicion.
- If clinical suspicion persists despite a negative PCR (early sampling, partial treatment), repeat the PCR and treat meanwhile; brain biopsy is a last resort of a previous era.
- Complications: status epilepticus, raised intracranial pressure, SIADH with hyponatraemia, and in children relapse — plus the memory and behavioural sequelae of temporal lobe destruction.
- The differential that changed modern practice: anti-NMDA-receptor encephalitis — prominent psychiatric features, dyskinesias (orofacial), autonomic instability, seizures, CSF antibodies, ovarian teratoma association in young women — treated with immunotherapy (steroids, IVIG, plasma exchange, rituximab) rather than antivirals alone.
- In the Indian context, Japanese encephalitis enters the differential with epidemic summer monsoon presentations, basal ganglia and thalamic MRI changes, and paediatric predominance.
- Outcomes are time-dependent: mortality falls from the untreated majority to well under a third with early aciclovir, and survivors can be left with Kluver-Bucy-type behaviour and amnesia.
The first 24 hours, in order
A 48-year-old is brought in after a week of "not being himself", then two generalized seizures; temperature is 38.6°C, he is aphasic and restless, neck is supple. Order of operations decides outcome. First: airway, glucose, control of seizures, and IV access — plus empirical coverage for bacterial meningitis until excluded, since the two overlap at the bedside. Second: aciclovir started within the hour on suspicion alone, 10 mg per kg over an hour every eight hours, hydration running to protect the kidneys; every hour of delay in herpetic encephalitis is temporal lobe that does not return. Third: the diagnostic battery — MRI (temporal/insular FLAIR change expected), EEG (periodic lateralising discharges over the left temporal region are the classic signature), CSF after imaging (lymphocytes, red cells, PCR sent, also testing for other viruses and, depending on the psychiatric prominence, NMDA-receptor antibodies in CSF rather than serum alone). Fourth: the management week — continuation of aciclovir for a minimum of 14 days, seizure control, sodium monitoring for SIADH, and vigilance for cerebral oedema. Fifth: the reflection step — if the CSF PCR returns negative but the syndrome fits, the modern instinct is not to stop but to repeat the PCR after 48–72 hours of treatment, because early false negatives and post-treatment false negatives are both well described.
Where students slip
The recurring failure is sequencing: waiting for PCR or MRI confirmation before starting aciclovir is the wrong answer in every format — empirical therapy on clinical suspicion is the tested reflex. Dose errors follow (10 mg per kg every eight hours, not the 5 mg per kg of mucosal HSV disease, and 14–21 days, not a week). The psychiatric-ward misdirection also trips candidates: the young patient with acute psychosis, orofacial dyskinesia and autonomic swings is anti-NMDA-receptor encephalitis until CSF antibody testing says otherwise, and the correct addition is immunotherapy. Finally, forgetting the kidney — aciclovir's crystalline nephropathy — costs easy viva marks that hydration and slow infusion would have earned.
Frequently asked questions
What dose and duration of aciclovir treat HSV encephalitis?
Intravenous aciclovir 10 mg per kg every eight hours, infused over an hour with adequate hydration, for 14–21 days, adjusted for renal function.
Which investigation is the diagnostic standard?
HSV DNA polymerase chain reaction on cerebrospinal fluid — sensitivity above 95 per cent — recognising early and post-treatment false negatives that warrant repeat testing.
What EEG pattern is classical in herpes simplex encephalitis?
Periodic lateralising epileptiform discharges over the affected temporal lobe, with background slowing.
When should anti-NMDA-receptor encephalitis be considered?
With prominent psychiatric onset, orofacial dyskinesias, autonomic instability, seizures and catatonia — send CSF antibodies, screen for ovarian teratoma in young women, and treat with immunotherapy.
Which epidemic encephalitis enters the Indian differential?
Japanese encephalitis — monsoon-season paediatric epidemics with thalamic and basal ganglia MRI changes — alongside scrub typhus and other regional infections in the febrile encephalopathy screen.