Ketamine Infusion Associated with Improved Neurology in a Patient with NMDA Receptor Encephalitis

A young lady was ventilated on intensive care for a prolonged period with NMDA receptor encephalitis. She had undergone steroid, immunoglobulin, and plasmapheresis with no evidence of recovery. Her main management issue was the control of severe orofacial and limb dyskinesia. Large doses of sedating agents had been used to control the dystonia but were ineffective, unless she was fully anaesthetised. The introduction of a ketamine infusion was associated with a dramatic improvement in her symptoms such that it was possible to remove her tracheostomy two days after commencement. She was discharged shortly after that and is making a good recovery. The successful use of ketamine has not previously been described in this context, and we hope this case report will provide some insight into the management of this rare but serious condition. 1. Introduction We would like to report a strong temporal relationship between the commencement of ketamine sedation and a dramatic improvement in the clinical features of NMDA receptor encephalitis. 2. Case Presentation A previously fit and healthy 21-year-old female presented to the psychiatric services with uncharacteristic behaviour. She was noted to be extremely anxious, with repetitive phrases and evidence of disordered thought. She was admitted to a psychiatric hospital and treated for acute psychosis. However, her care was transferred to the acute medical services following the development of acute dystonia of the face, tongue, and symmetrical jerking movements of the limbs. This progressed over the next 48 hours to what appeared to be atypical generalised seizures while still maintaining some degree of volitional control, with a documented Glasgow Coma Scale between 3 and 11. Autonomic dysfunction was also evident with hyperpyrexia and varying tachycardia. She was intubated and ventilated for airway protection. CT imaging was unremarkable, and an EEG, although was encephalopathic, did not show status epilepticus. CSF was not pleocytic with normal biochemistry. Initially, she was treated for atypical status epilepticus with propofol, phenytoin, and midazolam; however, ongoing seizure-like activity and orofacial dyskinesia were noted with no EEG correlate. A provisional diagnosis of NMDA receptor encephalitis was made by the neurology team, and although a serum anti-NMDA receptor antibody assay was negative, treatment with methylprednisolone was commenced. The main clinical problem for the ICU team was managing her profound dyskinesia and agitation without acquiring iatrogenic complications such as