BK is a Caucasian male with no previous psychiatric problems, aged 18 years at presentation. His only medical problem was alopecia areata treated since age 12 years. Despite moderate-range intellectual disability (ID) based on school testing prior to development of catatonia, he demonstrated higher-than-expected adaptive functioning, including playing the piano, reading and working part-time. He pitched Special Olympics Softball and excelled in team soccer. Family history was positive for adult-onset hypothyroidism, Raynaud's and anxiety. There were no identifiable initiating stressors. Symptoms emerged at age 18 years, 4 months, with progressive psychomotor slowing, episodic immobility, freezing, reduced speech and eye-blink rate, loss of hedonic capacity, grimacing and holding his tongue out, repeated shrugging and turning of the shoulders, slow eating, and stereotyped movements of the fingers. He became negativistic. There were no sleep problems and minimal snoring. Neurological examination revealed overall motor slowing with general but mild body stiffness, anisocoria that was considered within normal range by neuro-ophthalmology and a change from right to left-handedness for eating. Neurologic studies were unremarkable, including brain MRI and routine and 24 hr EEGs. Extensive neurologic and medical evaluations, as described in Methods, to identify conditions that may cause or mimic catatonia failed to provide an alternative diagnosis. The pretreatment BFCRS Screening score was 8 and the Severity score 25. Based on these findings, his response to a diagnostic trial of lorazepam and lack of evidence to suggest another underlying medical or neuropsychiatric disorder, BK was diagnosed with unspecified catatonia. Lorazepam was titrated to a maximum dose of 20 mg/day over an 11-month period. Parental report, based on their subjective symptom levels endorsed a 75% return to baseline function. Other medications were tried including minocycline, which was discontinued within a week due to dizziness, and memantine, used for a short period, appeared to exacerbate catatonia symptoms. Due to failure to achieve baseline functions, bifrontal ECT treatments were initiated after 15 months resulting in an immediate and robust response, with more spontaneous speech and fluidity of movement. He maintained this response on no other catatonia specific treatments for approximately 2 years. Gradual reemergence of symptoms including loss of spontaneous speech, motor slowing and freezing, and decreased interest in activities led to reinstitution of medical treatment. Low dose lorazepam appeared to stabilize symptoms; he has returned to playing the piano, working part time and exercising. Parents did not see a benefit of NAC or dextromethorphan/quinidine and decided against repeat ECT, though he is not completely back to baseline. He is on 3.5 mg of lorazepam per day, which parents increase to 4.5 mg if symptoms increase. Current BFCRS Screening scale is 1 and Severity scale 2.5.