In this case report, acute mania with psychotic features deteriorating to catatonic state revealed anti-NMDA-receptor encephalitis. This encephalitis is a multistage illness that progresses from psychosis, memory deficits, seizures, and language disintegration to a state of unresponsiveness with catatonic features . Psychiatric symptoms, including delusions, anxiety, insomnia, and mania, can occur initially, and they usually present less than 2 weeks after prodromal symptoms (headache, fever, nausea, diarrhea or upper respiratory tract symptoms) . The patients are often initially seen by psychiatrists. Anti-NMDA-Receptor encephalitis predominantly affects children and young adults [4, 13] and may or may not be associated with a tumor. Approximately 80% of patients are women. The presence of a tumor is more frequent in women who are older than 18 years and who are black . Because of the initial psychiatric presentation, high dosages of antipsychotics were administrated to the patient. Even if the role of antipsychotics is not clear and that catatonic features occur in anti-NMDA-Receptor encephalitis, they may aggravate the catatonic symptoms.
Therapeutic approaches to catatonia are mainly symptomatic. It is recommended to use high dosages of benzodiazepines and to perform electroconvulsive therapy in case of resistance or a life threatening condition . Treatment of the causal organic condition is also warranted. In this case, the patient did not respond to high doses of lorazepam. ECT was discussed but postponed due to signs of acute encephalitis.
A recent literature review showed that organic causes of catatonia in young people make up 20% of all cases , and this rate was confirmed in a prospective study . Among the organic causes, encephalitis, caused by infection or immune mechanisms requires specific treatments. In particular, neuropsychiatric systemic lupus erythematosus (SLE) can be revealed by a catatonic syndrome. It is crucial to diagnose and begin an appropriate treatment quickly to improve the patient's prognosis. Plasma exchange appears to be an efficient treatment option in SLE and catatonia, and it avoids the use of ECT [17, 18].
In the present case, given the increased antinuclear antibodies, the MRI results (non-specific white matter hyperintensities) and the PET hypometabolism, clinicians first hypothesized the presence of SLE. The presence of antinuclear and/or thyroid peroxidase antibodies, in addition to NMDAR antibodies, has been previously described, most typically in children and can suggest a predisposition to this type of auto immunity [4, 13]. Associated plasma exchanges and immunosuppressive therapy were used as treatment. After improvement of the malignant catatonia, neurological markers led to a diagnosis of anti-NMAD-receptor encephalitis, which indicated the need for continuation of immunomodulatory therapy with immunoglobulins. This treatment led to a major improvement in catatonic, psychiatric and neurological symptoms. Management of anti-NMDAR encephalitis is focused on immunotherapy and the detection and removal of a teratoma . Based on an extensive review (400 patients over a 3-year period), Dalmau and colleagues proposed an algorithmic strategy to guide treatment . The first line of immunotherapy consists of corticosteroids, intravenous immunoglobulins, and plasma exchange (alone or in combination). The second line of immunotherapy (rituximab or cyclophosphamide or both) is usually needed in the case of a delayed diagnosis or in the absence of a tumor .
Regarding the patient's cognitive impairment, NMDA receptors are known to play a crucial role in synaptic plasticity, which is involved in memory, learning and cognition . Disruption of these receptors can result in seizures and changes in memory, learning and behavior . It is possible to explain the patient's sequelae by a diagnosis of diffuse encephalopathy that is mainly due to frontal and limbic dysfunction. Similarly, an early manifestation with acute severe psychiatric signs and catatonia may be related to dysfunction of the NMDA-R circuitry, as the NMDA-R has been implicated in psychotic symptomatology [20, 21].
Interestingly, another case of adolescent catatonia associated with encephalitis has been reported . In that case, encephalitis was paraneoplastic and improved after an ovarian tumor ablation. In retrospect, it is possible that that case also presented was anti-NMDA-receptor encephalitis, given its frequent association with ovarian teratoma [12, 13]. Another recent case report showed an excellent recovery after immunotherapy (plasma exchange and corticosteroids) in a case of anti-NMDAR encephalitis in a 12-year-old girl .
Recognition of encephalitis by psychiatrists is important because patients may initially present with psychiatric symptoms and catatonic features. Here, symptoms and paraclinical data are in accordance with cases of anti NMDAR encephalitis already reported: severe psychiatric symptoms, seizures, orofacial dyskinesia. In the case of severe and possible life-threatening anti-NMDA-receptor encephalitis, it is essential that a quick and adapted treatment is implemented. Indeed, the prognosis of anti NMDA-R encephalitis varies: 75% of cases recover with immunotherapy and tumor ablation (when present), while 25% of cases lead to severe sequelae and even death . Relapse occurs in 15% of all cases .
This case report emphasizes the importance to search for a medical condition in catatonic syndrome of young people to treat and avoid severe neurological sequelae or death. The proposal of the DSM-V workgroup to make catatonia a "specifier" added as a fifth digit to other diagnoses seems likely to reduce rather than enhance clinician awareness of importance of recognizing this syndrome and researching for medical condition, particularly during psychiatric training. By contrast, a large group of experts advocated a unique and broadly-defined code for catatonia as a syndrome, which can be diagnosed acutely in addition to any suspected or established associated disorders . In this case, the initial psychiatric clinical presentation was complicated by a malignant catatonic state, which is now well-described in anti-NMDA-Receptor encephalitis. Child psychiatrists need to know that anti-NMDA-Receptor encephalitis occurs frequently in children and adolescents. Plasma exchanges and immunosuppressive therapy treatments can dramatically improve catatonic syndrome associated with autoimmune dysfunction such as SLE [17, 18], PANDAS  and NMDA-receptor encephalitis.