Autonomic functions in 1 patient12 had demonstrated impaired cardiovagal and cardiovascular adrenergic function along with reduced quantitative sudomotor axon reflex test response in the foot. double incontinence (3), spastic speech (2), YF-2 dysphagia (2), behavioral disturbances (2), seizures (1), and cold intolerance (1). Neurologic examination revealed myokymia (12), hyperactive tendon reflexes (10), and tremor (6). EMG revealed neuromyotonia (12) and increased spontaneous activity (7). Autonomic function tests conducted in 8 patients revealed definite autonomic dysfunction (4), orthostatic hypotension (2), early dysfunction (1), and postural orthostatic tachycardia syndrome (1). Polysomnography findings in 6 patients revealed insomnia (3), absence of deep sleep (1), high-frequency beta activity (1), REM behavior disorder (1), and periodic leg movements (1). Neuropsychological evaluation showed subtle involvement of the left frontal and temporal lobe. Malignancy workup was negative. All patients were treated with steroids. There was complete neurologic resolution in follow-up with persistent neuropathic pain in 5 patients. Conclusions This study has contributed to the growing knowledge on CASPR2-related YF-2 Morvan syndrome. It is important for an increased awareness and early recognition as it is potentially treatable by immunotherapy. Augustine Marie Morvan described a rare disorder termed la choree fibrillaire (Morvan syndrome) associated with autonomic dysfunction and severe insomnia in 1890.1 It is characterized by central, autonomic, and peripheral hyperexcitability due to contactin-associated protein 2 (CASPR2) antibodies.2,3 CASPR2 is an axonal transmembrane protein of the neurexin superfamily expressed in the central and peripheral nervous system that binds to contactin-2. Its cytoplasmic domain is involved in the clustering of Kv1 potassium channels in the juxtaparanodal region, resulting in promotion of axon myelination.4 Mutations and polymorphisms of the CNTNAP2 gene that encodes CASPR2 are found to result in schizophrenia, epilepsy, and peripheral nerve hyperexcitability.5 The clinical spectrum of CASPR2 antibodyCassociated neurologic disorder is diverse, found in association with Morvan syndrome, epilepsy, pain, anterior horn cell disorder, and limbic encephalitis.6 Morvan syndrome is diagnosed when the following triad of clinical features is observed: (1) CNS: confusion, cognitive dysfunction, hallucinations, insomnia, and myoclonus; (2) autonomic symptoms: hyperhidrosis and fluctuations in blood pressure; and (3) peripheral nerve hyperexcitability: clinical or electrophysiologic evidence of spontaneous muscle overactivity in the form of painful cramps, fasciculations, myokymia, and neuromyotonia.2,3 In the past 2 decades, various solitary case reports and short case series of Morvan syndrome have been described. Initial reports of Morvan syndrome were found in association with voltage-gated potassium channel (VGKC) antibodies mainly CASPR2 and leucine-rich glioma-inactivated 1 (LGI-1) antibodies. But eventually Morvan syndrome YF-2 is more commonly associated with only CASPR2 antibody involvement.7,8 Few cases of Morvan syndrome have occurred following exposure YF-2 to indigenous drug use9 and heavy metal exposure.1 Malignancy of the thymus, lung, and prostate is reported in nearly 40% of Morvan syndrome.1,C3 The present study has been conducted to further characterize Morvan syndrome with an emphasis on its clinical spectrum, imaging, autonomic, electrophysiologic profile, polysomnography (PSG), and neuropsychological findings. Methods The retrospective chart review was conducted at a tertiary neuropsychiatric hospital between 2016 and 2019. Patients with positive serum CASPR2 antibodies presenting with various neurologic manifestations were assessed. They were found to have Morvan syndrome (24), autoimmune encephalitis (4), anterior horn cell disorder (3), and other disorders (5). The patients with CASPR2-positive Morvan syndrome form the study population. Patients’ data regarding the demographic profile (table 1), clinical features, and investigations (table 2) were retrieved from the case records. Written informed consent was obtained from all the patients where personal details were available (photographs, videos, and PSG). Table 1 Clinical Profile of CASPR2-Related Morvan Syndrome Open in a separate window Table 2 MPH1 Investigation Findings of YF-2 Patients With CASPR2-Related Morvan Syndrome Open in a separate window Standard Process Approvals, Registrations, and Individual Consents The scholarly research is a retrospective graph.