Erfan Bashar
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Autoimmune Encephalitis — Clinical Patterns

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Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.

Autoimmune encephalitis presents subacutely, over days to weeks. That tempo sits between stroke (minutes to hours) and neurodegenerative dementia (months to years). Progression under 3 months of memory, mental-status, or psychiatric change is itself an entry criterion for the diagnosis, and it is one of the most useful early clues.

Infectious encephalitis looks similar at first. Autoimmune and infectious causes are pursued together from the start, with cerebrospinal fluid viral testing as the key early branch point.

Limbic encephalitis

Limbic encephalitis is the best-known pattern. Progressive memory loss, confusion, seizures, and behavioural change develop over weeks. The inflammation centres on the medial temporal lobes, usually on both sides.

Anti-NMDA receptor encephalitis

Anti-NMDA receptor encephalitis is the prototype syndrome. About 80% of patients are young and female, with a median age near 20. The illness often unfolds in stages. A viral-like prodrome gives way to behavioural change, memory loss, or psychosis within about 2 weeks. Speech disturbance, seizures, and movement disorders follow, progressing to global encephalopathy with autonomic instability and hypoventilation.

Roughly one third of patients has a tumour. Ovarian teratoma in young women is the classic association, though the disease occurs more widely.

LGI1 disease and faciobrachial dystonic seizures

LGI1 disease looks different. Short-term memory loss dominates, with other seizures, psychiatric symptoms, sleep disturbance, and low blood sodium each affecting a substantial share of patients. Low sodium occurs in about half and supports the pattern without confirming it.

Faciobrachial dystonic seizures are brief, stereotyped jerks of the face and one arm lasting seconds. They are closely associated with LGI1 antibodies and often precede the limbic encephalitis phase. Recognising them allows treatment before the full syndrome develops.

Tumours such as lung cancer or thymoma occur in fewer than 1 in 5 patients. The typical patient is around 60.

Brainstem and rarer patterns

Brainstem encephalitis brings cranial nerve signs, eye movement disturbance, instability, and jaw dystonia. It is reported with ANNA-2 (anti-Ri) antibodies, including in association with breast adenocarcinoma.

Less common patterns include opsoclonus-myoclonus, stiff-person physiology with axial rigidity, and presentations dominated by seizures or by a fluctuating dementia-like course with headache and spontaneous remissions.

Demographic clues such as young age with teratoma or brief dystonic jerks are suggestive, not pathognomonic. Any of them may be absent.

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