Synopsis
Recognise subacute immune-mediated encephalopathy among psychiatric, epileptic and infectious mimics, obtain paired diagnostic samples and coordinate early neurological, tumour and critical-care treatment.
- Autoimmune encephalitis typically evolves over days to fewer than three months with impaired memory, altered mental state or psychiatric change plus seizures, focal findings, CSF inflammation, EEG abnormalities or compatible MRI features.
- A first psychotic presentation with catatonia, seizures, dyskinesia, fluctuating consciousness or autonomic disturbance needs an organic assessment; age alone must not divert the patient exclusively into a psychiatric pathway.
- Anti-NMDA-receptor encephalitis often progresses from psychiatric and cognitive symptoms to seizures, oro-facial dyskinesia, autonomic instability and hypoventilation, especially in younger people.
Key red flags
A younger patient develops anxiety, insomnia, psychosis or cognitive change, then seizures, catatonia, oro-lingual or limb dyskinesia, autonomic swings and central hypoventilation. An ovarian teratoma is an important association.
Investigation priorities
Identify limbic or extra-limbic inflammation and exclude stroke, tumour, abscess, demyelination and other structural causes.
Management branches
Encephalopathy is accompanied by seizure, autonomic instability, hypoventilation or falling consciousness.
- Use ABCDE, check bedside glucose, protect the airway, treat status epilepticus through the emergency protocol and obtain critical-care input for hypoventilation, dysrhythmia or severe autonomic fluctuation.
- After blood cultures and prompt lumbar puncture when safe, start intravenous aciclovir at the locally adjusted encephalitis dose while HSV remains plausible; add antibacterial therapy if meningitis cannot be excluded.