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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
Key points
- HSV-1 is the most common cause of sporadic viral encephalitis in the UK — predilection for temporal lobes
- Clinical triad: fever + altered consciousness + focal neurological signs (especially seizures, dysphasia, personality change)
- IV aciclovir 10 mg/kg TDS must be started IMMEDIATELY if encephalitis suspected — do NOT delay for investigations
- MRI shows high signal in temporal lobes on T2/FLAIR. CSF PCR for HSV confirms diagnosis
- Autoimmune encephalitis (e.g. anti-NMDA receptor) is an important differential — consider in young patients with psychiatric symptoms and seizures
Overview
Encephalitis is inflammation of the brain parenchyma, usually due to viral infection or autoimmune processes. Herpes simplex virus type 1 (HSV-1) is the most common cause of sporadic infectious encephalitis in the UK and has a mortality of ~70% if untreated, reduced to ~20% with prompt IV aciclovir. HSV-1 encephalitis has a predilection for the temporal and frontal lobes, causing characteristic features of temporal lobe dysfunction. Other viral causes include VZV, EBV, CMV (in immunocompromised), and enteroviruses. Autoimmune encephalitis (e.g. anti-NMDA receptor antibody encephalitis) is increasingly recognised, particularly in young women with ovarian teratoma.
Epidemiology
The incidence of encephalitis in the UK is approximately 5–8 per 100,000 per year. HSV-1 encephalitis has a bimodal age distribution affecting young adults and those over 50. Autoimmune encephalitis accounts for a significant and increasing proportion of cases. Immunocompromised patients (HIV, transplant recipients) are at risk from opportunistic pathogens including CMV, toxoplasma, JC virus (PML), and cryptococcus. Seasonal variation occurs with arboviral encephalitides (less relevant in the UK).
Clinical Features
Symptoms
Fever
Altered consciousness: confusion, drowsiness progressing to coma
Seizures — focal or generalised (common in HSV encephalitis)
Behavioural and personality change (temporal lobe involvement)
Headache
Dysphasia (dominant temporal lobe involvement)
Hallucinations — olfactory or gustatory in temporal lobe disease
Prodromal viral illness may precede neurological symptoms
Signs
Pyrexia
Reduced GCS — ranges from mild confusion to deep coma
Focal neurological signs: hemiparesis, cranial nerve palsies
Seizures — focal motor or generalised tonic-clonic
Signs of meningism may coexist (meningoencephalitis)
Movement disorders, involuntary movements (autoimmune encephalitis)
Investigations
First-line
Lumbar puncture and CSF analysisLymphocytic pleocytosis, mildly raised protein, normal glucose (viral pattern). CSF PCR for HSV-1/2, VZV, enterovirus. CSF may be normal early — does not exclude diagnosis
MRI brainInvestigation of choice. HSV encephalitis shows high signal in medial temporal lobes and inferior frontal lobes on T2/FLAIR, often asymmetric. May show haemorrhagic change
BloodsFBC, U&Es, LFTs, glucose, CRP, blood cultures, HIV test
Second-line
CT headIf MRI not immediately available or LP contraindicated — may show temporal lobe oedema or haemorrhage but less sensitive than MRI
EEGMay show periodic lateralised epileptiform discharges (PLEDs) in HSV encephalitis — supports diagnosis
Specialist
Autoimmune encephalitis antibodiesAnti-NMDA receptor, anti-LGI1, anti-CASPR2, anti-AMPA — especially in young patients with psychiatric features, seizures, or movement disorders
CT/MRI pelvisScreen for ovarian teratoma in young women with anti-NMDA receptor encephalitis
1
Empirical treatment — start IMMEDIATELY
- IV aciclovir 10 mg/kg TDS for 14–21 days (or until HSV excluded by CSF PCR)
- Do NOT delay aciclovir for LP, MRI, or any investigation
- Ensure adequate IV hydration — aciclovir is nephrotoxic (monitor renal function)
- If bacterial meningitis cannot be excluded: add IV ceftriaxone empirically
2
Supportive care
- Admit to neurocritical care or HDU
- Seizure management: IV lorazepam acutely, levetiracetam or phenytoin for ongoing seizures
- ICP management if cerebral oedema: elevate head, osmotherapy, neurosurgical input
- ABCDE monitoring, blood glucose control, VTE prophylaxis
3
Autoimmune encephalitis
- First-line immunotherapy: IV methylprednisolone 1 g/day for 3–5 days, IV immunoglobulin, or plasma exchange
- Second-line: rituximab or cyclophosphamide if poor response
- Remove teratoma if anti-NMDA receptor encephalitis with ovarian teratoma
Complications
- Persistent cognitive impairment: Memory deficits (temporal lobe damage), personality change, dysphasia — common even with treatment
- Epilepsy: Develops in up to 50% of survivors of HSV encephalitis
- Cerebral oedema and raised ICP: May require osmotherapy or decompressive surgery
- Death: ~20% mortality with treatment, ~70% without — early aciclovir is critical
- Relapse: HSV encephalitis can relapse weeks after treatment — may be viral or autoimmune-mediated
UKMLA Exam Tips
- 1HSV encephalitis: fever + seizures + temporal lobe signs (dysphasia, personality change) = IV aciclovir IMMEDIATELY
- 2MRI: high signal in temporal lobes on T2/FLAIR is classic for HSV encephalitis
- 3CSF PCR for HSV confirms diagnosis — but may be negative in first 24–48 hours (treat empirically)
- 4Aciclovir dose: 10 mg/kg TDS IV for 14–21 days — monitor renal function (nephrotoxic)
- 5Anti-NMDA receptor encephalitis: young woman with psychiatric symptoms + seizures + movement disorder ± ovarian teratoma
- 6Do NOT wait for investigations to start aciclovir — delay increases mortality dramatically
- 7Distinguish from meningitis: encephalitis has altered consciousness and focal neurology; meningitis has meningism but preserved consciousness (unless meningoencephalitis)
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