A previously healthy 46-year-old right-handed man was admitted to the psychiatry ward after a one-week history of mild fever, behavioral changes, headaches, and reported facial twitches. His initial CT of the brain was negative. His neurological status continues to deteriorate, with reported episodes of lip smacking and facial twitches. Therefore, he was transferred to the medical ward. The neurology team was consulted, and a lumbar puncture (LP) was suggested. The cerebrospinal fluid (CSF) analysis showed elevated white count of 521 per microliter, 98% lymphocytes, elevated protein of 51/dL, and a normal glucose level. Polymerase chain reaction for the following viruses and bacteria were negative: herpes simplex virus I and II, varizella zoster virus, human herpes virus 6, cytomegalovirus, Epstein-Barr virus, enterovirus, mycoplasma pneumonia, and TB bacillus. There were no oligoclonal bands. The Gram stain was negative. A diagnosis of encephalitis was made, and he was started on acyclovir, ceftriaxone, and vancomycin. His initial EEG showed intermitted slowing of delta range over both frontocentral head regions with faster frequency superimposed representing extreme delta brush (Fig. 1). He was loaded with phenytoin, and a brain MRI was requested. The MRI of the brain with and without contrast was reported as normal. However, his neurological status has worsened, and he started to desaturate. He was transferred to the ICU where the neurology team was called to reevaluate him. Continuous EEG recording (CEEG) was advised, and it showed a rhythmical slowing over both frontocentral head regions with a clear evolution in voltage, frequency, and field consistent with nonconvulsive status epilepticus (NCSE) (Fig. 2). This evolution of the EEG pattern became more apparent when the EEG was compressed (Fig. 3). He was loaded with midazolam which was titrated up to burst suppression. Two days later, he continued to have facial twitches, and his CEEG was still showing electrical SE pattern. Levetiracetam was loaded and continued on a titrating dose of up to 2000 mg twice per day and on phenytoin with a titrating dose of 350 mg/day, with close drug level monitoring, followed in 2 days by a loading dose of valproic acid. Four days later, he continued to have episodes of facial twitches and lip smacking, and CEEG was still showing the previously reported pattern. The epilepsy team was consulted and they advised loading with propofol which was titrated up to 50 mg/h. However, every attempt to decrease the propofol would result in worsening facial twitches and, in a number of occasions, breakthrough tonic-clonic seizures. A diagnosis of ARNE was suspected based on clinical features and EEG pattern. A repeat MRI of the brain with and without contrast remained normal. Anti-NMDA receptor in the serum was requested, and an extensive search for a tumor was recommended but did not reveal any pathology. While waiting for the results of anti-NMDA receptor antibodies, IVIG was given over a 5-day course, along with a pulse of steroids. He was loaded with pentobarbital titrated up to burst suppression. However, breakthrough electrical SE was still apparent every time the level of suppression is reduced, and midazolam was restarted and titrated up to 12 mg/h. Over several weeks, his neurological status had not changed. His repeat LP showed white count of 24 per microliter and 90% lymphocytes. He continued on both propofol and midazolam while pentobarbital was discontinued. Topiramate was added and titrated over 2 days to a dose of 200 mg twice per day. Still, his CEEG was showing SE pattern, and he continued to have facial twitches. He also continued on a combination of high doses of levetiracetam 4 g/day, topiramate 400 mg/day, phenytoin 400 mg/day, valproic acid 3000 mg/day, clonazepam 5 mg/8 h, and phenobarbital 200 mg/day. A week later, his neurological status had not changed, and every attempt to reduce his anesthetics would result in recurrent clinical and electrical seizures. While in the ICU, his dose of phenobarbital was increased up to 150 mg twice per day, and he continued on propofol and midazolam. Intravenous magnesium sulfate was also tried but without success. He was also tried on IV ketamine, but his neurological status remained the same, and he continued to show the SE pattern when the level of sedation is reduced. The result of Anti-NMDA receptor antibodies came back positive and a repeat course of IVIG was recommended over a 4-day duration, 2 weeks after the first IVIG course was completed. However, his neurological status has not changed, and he remained in NCSE for 110 days, and a decision was made, after extensive discussions with the patient's family, to try VNS. A vagus nerve stimulator was implanted and interrogated to an output current of 2.5 mA over 4 days. His duty cycle was set at 30 s on and 5 min off. After 1 week of vagus nerve stimulator implantation, midazolam was weaned off successfully over 3 days and followed 4 days later by a weaning off propofol without any clinical or electrical seizure recurrences. His CEEG showed no evidence of electrical SE pattern. His neurological status continued to improve in the succeeding months with no reported clinical seizures. The dosages of antiepileptic drugs (AEDs) were gradually reduced one at a time. He was discharged from the hospital after 8 months of rehabilitation on no AEDs with mild-moderate cognitive impairment.