When seizures are not what they seem: A case of Anti-NMDA receptor encephalitis with psychogenic nonepileptic seizures

Dear Editor, A 31-year-old female was hospitalized due to the sudden onset of disorganized behavior. Her symptoms, included repeatedly switching the lights on and off without reason, shouting the name of their tenant, engaging in irrelevant conversations, pacing around the house, muttering to herself, staring spells, performing repetitive dancing movements, crying at the feet of a goddess statue, pleading for a cure, without any explanation for her actions. Along with the reduced sleep, appetite, and impaired self-care for 5 days, with a significant worsening and difficulty managing at home for 1 day. She had a history of fever 10 days before the onset of these symptoms, for that she received symptomatic treatment and recovered completely. Her past medical history included pulmonary tuberculosis, which she completed treatment for 2 years ago. On examination, she was short-statured, conscious, oriented to time and person, and able to obey simple commands. However, she was non-cooperative for further examination. She was admitted with a suspicion of viral encephalitis. Laboratory tests revealed a raised total leukocyte count, elevated prothrombin time (PT), and international normalized ratio, (INR), and reduced. Activated partial thromboplastin time, (aPTT), while other routine blood investigations were normal. cerebrospinal fluid (CSF) analysis indicated raised proteins and total leucocyte count (TLC) with no growth on culture. The patient was started on Inj. Acyclovir 250 mg I.V. Three times a day (TDS) and Inj. Levetiracetam 500 mg. Despite treatment, she continued to experience seizure-like activity, prompting the initiation of Inj. Lacosamide 50 mg BD. Her Electroencephalogram (EEG) was abnormal, suggestive of right frontal epileptic activity with secondary generalization [Figure 1]. The viral panel was negative. Magnetic resonance imaging (MRI) brain scan (plain and contrast) showed no obvious abnormality or contrast enhancement. However, she continued to have tonic-clonic movements throughout her body and was suspected to have Psychogenic nonepileptic seizures (PNES). No active intervention was advised by psychiatry due to the EEG findings suggestive of seizure. This was followed by a seizure, during which she bit her tongue and had active bleeding, frothing at the mouth, and a postictal state, leading to a low Glasgow coma scale score (GCS). She was subsequently transferred to intensive care and put on mechanical ventilation. After tongue suturing, she was sedated and paralyzed. Inj. Brivaracetam 50 mg I.V. BD and Inj. Lacosamide I.V. 100 mg BD was initiated. A repeat Complete blood count (CBC) showed reduced hemoglobin, decreased platelets, and an increased TLC, with a rising trend. CSF analysis revealed normal proteins and lymphocytes. Autoimmune encephalitis was suspected. A CSF panel confirmed N-methyl-D-aspartate (NMDA)receptor antibody positivity. The patient underwent plasma exchange, but after three cycles, she developed cardiogenic shock and subsequently passed away in intensive care.Figure 1: EEG shows 60Hz artefact. Sharp and slow wave discharges in the right hemisphere, with secondary generalization in a few places, and occasional runs of delta activity in the right frontal region. Abnormal EEG suggestive of right frontal epileptic activity with secondary generalizationAnti-NMDA receptor (NMDAr) encephalitis is an autoimmune disorder marked by diverse neuropsychiatric symptoms, frequently seen in young females, and often linked to ovarian teratomas. The disorder predominates in females (80%), although in patients younger than 12 years, the frequency of males is higher (40%).[1] PNES can occur in this condition, complicating the clinical presentation as they may be misdiagnosed as epileptic seizures. PNES is known to be more prevalent amongst women, with a consistent female preponderance in most studies.[2] Symptoms of NMDAr encephalitis include psychiatric manifestations like psychosis and agitation, alongside neurological signs, such as seizures and movement disorders.[1,3] Diagnosis is confirmed by detecting antibodies against the NMDAr.[2] The pathophysiology involves the production of autoantibodies that leads to receptor dysfunction and altered neuronal activity.[4,5] Treatment includes immunotherapy. Early diagnosis and intervention are vital for a favorable prognosis, though PNES can complicate treatment responses, necessitating a multidisciplinary approach.[1] Awareness of the overlap between psychiatric and neurological symptoms is crucial for accurate diagnosis and effective management. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed. Authors’ contributions Concept and design of paper: AJ, SC. Drafting the article and revising it critically: AJ, SC. Final editing and approval of the version to be published: AJ, SC, SR, SB. All authors have read and approved the manuscript. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.