Prognosis

Due to the varied etiology, survivors of the critical phases of the illness are a heterogeneous group. Mortality and morbidity vary depending on the underlying etiology, the immune status of the host, the extent and location of anatomic lesions, the development of complications, and the time to initiate treatment. Mortality as an outcome occurs in 6% to 9% in the US, and in 12% in England in infectious encephalitis.[3][6][7][124]​​ Age >65 years old, immunocompromised (HIV or immunosuppressive medication-induced), mechanical ventilation, coma, acute thrombocytopenia, elevated cerebrospinal fluid polymorphonuclear count, cerebral edema, and status epilepticus are associated with poor outcomes.[124][125]

The development of the late sequelae depends on age, etiology of the encephalitis, and severity of the clinical episode.[75] Severe disability occurs in more than half of survivors. In children, long-term morbidity occurs in up to two-thirds of patients. This includes fatigue, cognitive impairment, attention and deficit disorders, dysphasia, motor impairment, ataxia, epilepsy, and personality changes.[126][127][128][129] Children with isolated cerebellar involvement or respiratory syncytial virus encephalitis tend to have a good prognosis.

Postencephalitic epilepsy occurs in 10% by 5 years and 20% by 20 years.[130] The presence of seizures during hospitalization and an abnormal brain magnetic resonance imaging are the strongest predictors of development of postencephalitic epilepsy. The etiology of encephalitis, presence of focal neurologic deficits, and interictal electroencephalographic abnormalities do not influence development of postencephalitic epilepsy.[131]

For herpes simplex virus encephalitis, older age, decreased level of consciousness, and delay or lack of treatment with acyclovir are associated with high mortality rates. Diffuse cerebral edema and intractable seizures are additional poor prognostic indicators. Survivors frequently have disabling neurologic sequelae such as (short-term) memory impairment, personality and behavioral changes, psychiatric issues, and anosmia.[132] Some have observed associations of anti-NMDAR encephalitis after HSV encephalitis.[133]​ Severe behavioral and personality changes including Kluver-Bucy syndrome, seen before acyclovir became widely available, are no longer common.

Mortality rates in autoimmune encephalitis are generally lower than in infectious cases; however, prolonged recovery and potential for relapse make longer-term management challenging.[1] Mortality rates for anti-N-methyl-D-aspartate (NMDA) receptor encephalitis are up to 6%, and relapse occurs in 12% to 25% of patients.[31][134][135]​ Earlier immune treatment has been associated with better outcomes but cognitive and behavioral changes may persist.[31][135]​​[136]​ Mortality rates may be lower for anti-leucine-rich glioma-inactivated 1 encephalitis than anti-NMDA encephalitis, but longer-term relapse rates might be higher.[1][137][138]

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