Case Presentation: A 69-year-old Brazilian female who moved to the US in the 1990s with history of COPD, hypertension, and depression (treated 5 years ago with Seroquel) presented to the ER with 2 weeks of cough, diarrhea, and post-tussive emesis. The patient was febrile to 103 F, BP 96/58, tachycardic to 110, and hypoxic to 92% on room air. Admission physical exam was pertinent for decreased breath sounds over the left lower lobe but was otherwise normal with no focal neurologic deficits. Labs were notable for a leukocytosis of 12.6 with neutrophilic predominance. Other labs were within normal limits. Chest x-ray was notable for left lower lobe infiltrate concerning for pneumonia. The patient was admitted and started on Ceftriaxone and Azithromycin. She remained febrile throughout the first 48 hours of admission. Infectious workup including blood, urine, and stool cultures, legionella antigen, respiratory viral panel, Flu swab, HIV antibody, RPR, and stool C Difficile were negative. Sepsis labs including lactate were negative. Her fevers were associated with delirium and rigors. Fevers resolved on day 3 of admission. Further into the hospital course, the patient was noted to have persistent altered mental status and automatism lip smacking and tongue protrusion movements. Head CT was notable for calcified foci indicative of prior neurocysticercosis. Neurology was then consulted with recommendation for MRI and video EEG. Patient’s MRI was notable for calcified foci and video EEG was remarkable for abnormal discharges due to diffuse background slowing indicating global or multifocal cerebral dysfunction without epileptiform discharges.
Discussion: In this case, the patient’s febrile illness was ultimately attributed to pneumonia. The more complex and puzzling finding in this patient’s admission was the development of abnormal movements including tremors, convulsions, and automatisms. The initial rigors seen were believed to be associated with the patient’s fever. However, after these movements resolved she began to develop automatism movements including lip smacking and tongue protrusion. It was first theorized that these movements could be related to tardive dyskinesia given her prior use of Seroquel. While it would be unusual to develop tardive dyskinesia for the first time 5 years after the last use of this medication, it is possible that these symptoms could develop at any point after treatment. In addition to these automatisms the patient began developing shoulder jerking and repetitive hand movements while sleeping. These movements were witnessed by the primary and neurology teams on exam. At that time video EEG was obtained with evidence of global abnormal discharge, more consistent with a seizure like process. The abnormal movements, along with calcifications present on head imaging, were likely due to focal seizures in the setting of lower seizure threshold from her febrile illness.
Conclusions: Tardive dyskinesia most commonly involves the mouth and tongue but the arms, legs, trunk, and respiratory muscles can also be affected which is why this diagnosis was initially considered. Since it is uncommon (although reported in the literature) for tardive dyskinesia to present 5 years after antipsychotic use, it was important to rule out other etiology causing her abnormal movements. It is important to remember that structural brain abnormalities can be a foci for seizures. The patient’s prior neurocysticercosis infection was a foci for seizures in the setting of lowered seizure threshold from a febrile illness.