[1] Over time, seizures, decreased breathing, and blood pressure and heart rate variability typically occur.

[1][4][7] The underlying mechanism is autoimmune, with the primary target being the GluN1 subunit of the N-methyl-D-aspartate receptors (NMDAR) in the brain.

[19] During this acute phase, most patients require treatment in an intensive care unit to stabilize breathing, heart rate, and blood pressure.

[citation needed] One distinguishing characteristic of anti-NMDA receptor encephalitis is the concurrent presence of many of the above listed symptoms.

Whilst the exact pathophysiology of the disease is still debated, empirical evaluation of the origin of anti-NMDA receptor antibodies in serum and cerebrospinal fluid leads to the consideration of two possible mechanisms.

This implies that there are more NMDA receptor antibodies in the cerebrospinal fluid than would be predicted given the expected quantities of total IgG.

[citation needed] A more sophisticated analysis of the processes involved in antibody presence in the cerebrospinal fluid hints at a combination of these two mechanisms in tandem.

First and foremost is a high level of clinical suspicion, especially in young adults showing abnormal behavior as well as autonomic instability.

[citation needed] The initial investigation usually consists of clinical examination, MRI of the brain, an EEG, and a lumbar puncture for CSF analysis.

[30] CSF analysis often shows inflammatory changes with increased levels of white blood cells, total protein and the presence of oligoclonal bands.

In general, early diagnosis and aggressive treatment is believed to improve patient outcomes, but this remains impossible to know without data from randomized controlled trials.

[citation needed] The recovery process from anti-NMDAR encephalitis can take many months depending on its form and severity.

[11] In patients with herpesviral anti-NMDA encephalitis, the recovery process is typically met with poorer long-term outcomes due to extensive lesions caused by viral-indused necrosis in brain tissue [34].

[7] According to the California Encephalitis Project, the disease has a higher incidence than its individual viral counterparts in patients younger than 30.

[15] Anti-NMDA receptor encephalitis is suspected of being an underlying cause of historical accounts of demonic possession.

[36][37][38][39] New York Post reporter Susannah Cahalan wrote a book titled Brain on Fire: My Month of Madness about her experience with the disease.

[40] Dallas Cowboys defensive lineman Amobi Okoye spent 17 months battling anti-NMDA receptor encephalitis.

Knut, a polar bear at the Berlin Zoological Garden that died on 19 March 2011, was diagnosed with anti-NMDA receptor encephalitis in August 2015.