A case of limbic syndrome characteristic of anti-NMDAr encephalitis associated with ovarian teratoma is retrospectively observed in a patient treated in our clinic in 2003. Patient K., a 20-year-old female, had 3 days of experience of an influenza-like state, including fever up to 37.8 C, headaches, sore throat, general malaise, and sleep disturbance (prodromal stage). One week later, she had sharply developed a schizophreniform state with agitation, motor stimulation, and hallucinations (stage of mental disorders). Following hospitalization in the psychiatric ward and the initiation of sedative therapy with diazepam, she suffered from fluctuating consciousness during the day from stunning to stupor, an impaired verbal contact, apart from pronouncing individual sounds, and loss of control over sphincters. The status epilepticus presentation included passive supine position, mostly with the eyes open, stiff neck muscles, floating eyeballs, divergent strabismus, dissociation of responses to external stimuli, a non-localized delayed reaction to pain, and resistance to opening eyes, resembling the action of dissociative anesthetics-NMDA antagonists, such as phencyclidine or ketamine. There were also opercular hyperkinesis, choreoathetosis of the extremities more to the right, torticollis to the right, and impaired swallowing (stage of motor and vegetative disorders). Breathing was intact. In the CSF, there was a slight increase in the protein content (0.78 g/L) and predominantly lymphocytic pleocytosis (up to 187 x 106/L cells, 179 x 10/L were lymphocytes), no oligoclonal antibodies, and no antibodies to NMDAr were performed at that time. No brain lesions were recorded on the MRI of the brain, and EEG demonstrated the predominance of the SW and D-BEA, characteristic of the anti-NMDAr type of LE, without epileptiform discharges. The TPWs were observed in the leads F4-A2, C4-A2, and BDP in C3-A1 (Figure 1).
A teratoma of the right ovary was found, regarded at that time as an unrelated finding. A differential diagnostic search was carried out, aimed at ruling in tuberculosis, rabies, and the use of psychotropic and narcotic drugs; none of the above was confirmed. As a result, the disease was defined as viral lethargic encephalitis. Within 3 weeks, the patient received posidrome, antibiotics, and immunotherapy (human Ig). GCs were not used, as there were no data on the presence of actual autoimmune pathology. There were some positive dynamics on days 12 to 14:an increase in activity, recognition of relatives, improvement of speech (pronounced separate syllables and simple words), and the patient began to perform simple commands. The patient had suffered from lethal thromboembolism to the pulmonary artery after 3.5 weeks of treatment.