Carotid artery stenosis is a leading cause of ischemic stroke. While management of symptomatic carotid stenosis is well established, the optimal approach in asymptomatic carotid artery stenosis (aCAS) remains controversial. The rapid evolution of medical therapies within the time frame of existing landmark aCAS surgical revascularization trials has rendered their findings outdated. In this review, we sought to summarize the controversies in the management of aCAS by providing the most up-to-date medical and surgical evidence. Subsequently, we compile the evidence surrounding high-risk clinical and imaging features that might identify higher-risk lesions. With this, we aim to provide a practical framework for a precision medicine approach to the management of aCAS.

Anti-NMDA receptor encephalitis can coexist with an overlapping demyelinating syndrome. c An atypical presentation of a single autoimmune disorder should prompt investigation for coexistent autoimmune disorders. c Discovery of overlap syndromes is important because the management and prognosis may be different. Oysters c In autoimmune encephalitis, shorter time from symptom onset to treatment initiation has been associated with better outcome. 1 c Treatment should not be delayed until the result of autoantibody testing is available. Case report A 31-year-old man developed a subacute onset of headache, left-sided numbness, and anterograde amnesia. In the following 2 weeks, he experienced personality changes, anxiety, paranoid thoughts, 7 kg weight loss, and worsening cognitive changes. He said that he felt as though he was trapped in a time loop, meaning that events seemed to be constantly recurring to him. He denied fever, night sweats, viral prodromal symptoms, or recent vaccinations. He was diagnosed with acute disseminated encephalomyelitis (ADEM) in 2007 from which he made a full recovery. On neurologic examination, he was inattentive and agitated. His word registration and short-term recall at 5 minutes were 0 of 5. He had verbal and motor perseveration with echolalia. He had decreased sensation to pinprick on his entire left side. He also had left pronator drift and bilateral athetosis of the upper limbs. The remainder of his examination was normal. His overall clinical examination finding was consistent with a multifocal process involving subcortical and cortical regions. On day 1, routine blood testing including complete blood cell count with differential, metabolic panel, liver function test, RPR, ESR, ANA, thyroid function tests, thiamine, B12, urinalysis, urine toxicology screen, heavy metal screening, and HIV were normal or negative. Brain MRI revealed multiple T2 hyperintensities within the right internal capsule, periventricular white matter, and bilateral mesial temporal lobes. There were contrast-enhancing lesions involving the right dorsal pons and right internal capsule and thalamus (figure, A-F). CSF analysis demonstrated 9 nucleated cells/μL with lymphocytic predominance. On day 2, CT of the chest, abdomen, and pelvis and testicular ultrasound were negative for malignancy. Cervical and thoracic spine MRI was performed to look for any past or active demyelinating lesions, especially in the setting of previous history of ADEM, and the result was normal. Video EEG did not demonstrate abnormal ictal or interictal epileptiform discharges. By this time, CSF Gram stain, cultures, and viral PCRs returned negative, and 8 CSF-specific oligoclonal bands were present. Serum and CSF NMDA-R IgG and serum MOG-IgG1 antibodies were sent to the laboratory. On hospital day 3, IV methylprednisolone

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