ECT in Catatonia Secondary to Autoimmune Encephalitis: State of Evidence
Direct Answer
ECT should be considered as an effective adjunctive treatment for catatonia in autoimmune encephalitis, particularly when benzodiazepines fail or when excited catatonia is present, with multiple case reports demonstrating complete resolution of catatonic symptoms when combined with immunotherapy. 1, 2, 3, 4
Evidence Quality and Limitations
The evidence base consists entirely of case reports and case series—no randomized controlled trials or systematic reviews exist specifically for this clinical scenario. 1, 2, 3, 4 Despite the low level of evidence, the consistency of positive outcomes across multiple published cases provides reasonable support for ECT use in this specific context.
Treatment Algorithm for Catatonia in Autoimmune Encephalitis
Primary Treatment: Immunotherapy Plus Benzodiazepines
First-line treatment must address the underlying autoimmune process with plasmapheresis, intravenous steroids, and/or intravenous immunoglobulin G (IgG), combined with lorazepam for catatonic symptoms. 1, 2, 4
Lorazepam should be initiated at 1-2 mg IV or IM, repeated every 1-2 hours as needed, with doses escalating up to 15 mg/day if necessary. 5, 3
Monitor vital signs, airway patency, and level of consciousness during benzodiazepine administration. 5, 6
When to Add ECT
ECT should be initiated when:
Benzodiazepines at adequate doses (up to 15 mg/day lorazepam) fail to improve catatonic symptoms after 5-6 treatment days. 5, 2, 3
Excited catatonia is present—characterized by agitation, disinhibition, violent behavior, and psychomotor excitement—which represents a medical emergency requiring immediate ECT rather than waiting for benzodiazepine response. 6, 2, 3
Life-threatening features develop, including severe malnutrition from food refusal, extreme suicidality, or autonomic instability (fever, tachycardia, blood pressure changes indicating malignant catatonia). 5, 6
ECT Protocol Specifics
Use bilateral electrode placement from the outset in autoimmune encephalitis with catatonia, as speed of response is critical and bilateral placement is more effective than unilateral. 5, 6
Administer ECT 2-3 times weekly, with most courses requiring 10-16 total treatments based on clinical response. 5, 2, 4
Use methohexital for anesthesia and succinylcholine for muscle relaxation. 5, 6
Monitor seizure duration, airway patency, vital signs, and adverse effects during each treatment. 5, 6
Observe patients for at least 24 hours post-ECT for potential complications such as tardive seizures. 5, 6
Clinical Evidence from Case Reports
Anti-NMDA Receptor Encephalitis Cases
A 27-year-old male with postherpetic anti-NMDA receptor encephalitis exhibited both akinetic and excited catatonia with violent behavior requiring 46 days of mechanical restraint; lorazepam up to 15 mg/day failed, but violent behavior resolved completely after the first ECT treatment, with full recovery after 16 total sessions. 3
Two cases (one adolescent, one young adult) with anti-NMDA receptor encephalitis presenting as excited catatonia showed limited improvement with immunotherapy and high-dose lorazepam but were effectively treated with ECT, demonstrating complete symptom resolution. 2
A 25-year-old female with anti-NMDA receptor encephalitis (titer 1:1280) failed to respond to intravenous steroids, IgG, plasma exchange, rituximab, haloperidol, and clonazepam, but improved remarkably following 12 rounds of ECT. 4
A 71-year-old female with anti-NMDA receptor encephalitis presenting with depression escalating to catatonia, delusions, and hallucinations had partial response to plasmapheresis and steroids but achieved complete resolution and return to premorbid state after multiple ECT sessions. 1
Critical Pitfalls to Avoid
Never delay ECT while attempting prolonged benzodiazepine trials in excited catatonia or malignant catatonia—these conditions demand immediate definitive treatment. 5, 6
Avoid typical antipsychotics in acute catatonia associated with autoimmune encephalitis, as they can worsen the syndrome and precipitate neuroleptic malignant syndrome. 5, 6
Do not use unilateral electrode placement in excited catatonia—bilateral placement is mandatory when speed of response is critical. 6
Do not consider ECT as monotherapy—it must be combined with immunotherapy addressing the underlying autoimmune process. 1, 2, 4
Proposed Mechanism of ECT Efficacy
While the exact mechanism remains unclear, ECT may work through multiple pathways: reducing neuroinflammation, modulating immune responses, restoring neurotransmitter balance disrupted by autoantibodies, and directly treating the catatonic syndrome independent of the underlying autoimmune etiology. 1
Special Considerations for Autoimmune Encephalitis
Catatonia in autoimmune encephalitis is typically resistant to standard benzodiazepine therapy alone, making ECT particularly valuable in this population. 1, 4
Excited catatonia can mimic delirium, psychosis, or mania, making diagnosis challenging—look for bizarre behavior, agitation, disinhibition, and psychotic symptoms in patients with no prior psychiatric history. 2
Continue immunotherapy (steroids, IgG, plasmapheresis, rituximab) concurrently with ECT, as both address different aspects of the disease process. 1, 2, 4