The most interesting aspect of this disease is that it can easily be diagnosed, yet many patients in the past were left to die in psychiatric institutions without access to treatment. Spoiler alert: this is similar to what Cahalan experienced and reflects the core of her message, which is to raise awareness of this disorder so that less individuals are misdiagnosed. Once admitted to these institutions, patients will have progressed to the late stage of symptoms, such as catatonia, and will be closer to death. In addition, since Anti-NMDAR Encephalitis is a widely unknown and underdiagnosed disorder, psychiatrists will misdiagnose encephalitic patients with schizophrenia and will refer them to psychiatric institutions. This explains the cognitive restoration of patients after being given treatment, but the exact mechanism for this reversibility is still unknown.īecause the early symptoms pertain to changes in behavior and one’s mental state, patients will often seek help from psychiatrists. Dalmau noticed that NMDAR clusters were increasing back to baseline. After stopping this infusion for several days, Dr. Rat neurons were infused with patient’s antibodies, which caused clusters of NMDAR’s to decrease. The hippocampus is a region of the brain responsible for memory consolidation, and is especially rich in NMDAR’s. Dalmau published a paper in 2008, in which he observed the antibodies’ reversible effect in the hippocampus of rats. In fact, the many theories that explain the causes of schizophrenia revolve around NMDA hypofunction and explain why encephalitic patients commonly experience hallucinations and delusions. NMDA hypofunction (a decrease in NMDA activity) can prove to be very harmful to one’s cognition and behavior. What causes the severity of these symptoms? NMDAR’s are crucial for learning and memory they play a key role in synaptic plasticity which is a process that determines how neurons communicate according to learning and experiences. The sooner patients are treated, the more their cognition will be restored. Fortunately, patients may recover from this disease, but the percent of cognitive restoration depends on how swiftly the treatment is given. Anti-NMDAR Encephalitis can be fatal if treatment, such as immunosuppressive therapy or tumor removal, is not administered in time. If left untreated, patients will later suffer from seizures and catatonia. Patients may also experience behavioral shifts, including being more anxious or aggressive. Patients may often experience psychosis and schizophrenia-like symptoms, such as delusions and hallucinations. These antibodies will eventually spread to the brain, where individuals will progressively suffer from worsening symptoms. Ovarian teratomas express NMDAR’s, which the body treats as foreign bodies and subsequently, creates antibodies of type IgG to attack them. Dalmau noticed that the majority of encephalitic patients were female and diagnosed with a tumor, particularly, an ovarian teratoma. What triggers this autoimmune response is still uncertain, as this disease was only discovered in 2007 by Dr. Anti-NMDA Receptor Encephalitis is an autoimmune disease caused by the body synthesizing antibodies which attack N-methyl-D-aspartate receptors (NMDAR’s) in the brain. Her story of battling this disorder is truly remarkable and inspiring. Both the novel and film tell Cahalan’s story of suffering from the strange disorder: Anti-NMDA Receptor Encephalitis. You may have seen the movie “Brain on Fire” on Netflix or read the novel “Brain on Fire: My Month of Madness” written by Susanah Cahalan.
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