Table 1.

Comparison of antibody‐associated encephalitides.

Encephalitis	Demographical features	Affected CNS area	Clinical course	Neuronal loss	Possible cytotoxic mechanisms
Rasmussen encephalitis	Peak of onset 6 years, occasionally in about 10% adolescent or adult onset	One hemisphere, starts usually in peri‐insular area	Progression over approximately 1 year, then neurological stabilization with fluctuating seizure frequency	Yes	T‐cell cytotoxicity
Antibody‐associated encephalitis
Intracellular antigens
Anti‐Hu	Usually older adults, almost all have paraneoplastic disease	Mediotemporal (brain stem, cerebellum)	Either progression to death or chronic deterioration	Yes	T‐cell cytotoxicity
Anti‐Ma2	Young men with testicular cancer or older people with other types of neoplasms. Almost all have paraneoplastic disease	Mediotemporal (brain stem)	Often better than in anti‐Hu	Yes	T‐cell cytotoxicity
Anti‐GAD65	Mainly young female adults	Mediotemporal	Chronic, treatment resistant temporal lobe epilepsy	Yes	T‐cell cytotoxicity
Surface antigens
Anti‐NMDAR	Mainly young females (peak early twenties). ¼ to ½ of the patients have ovarian teratomas.	Functionally: whole brain	Mostly complete or good remission after weeks to years, speeded up by tumor removal and immunotherapy	Little	Antibody‐mediated decrease of NR1 receptors
Anti‐VGKC complex	Usually older people, men two times more frequently than females	Mediotemporal	Complete or good remission within months to 2 years, speeded up by immunotherapy	Yes	Antibody‐mediated, complement activation, lysis