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Ient's illness, just like the above. PECULIAR CASE OF CEREBROVASCULAR ACCIDENT PRESENTING AS HEMIBALLISMUS Muhammad Sarfraz Nawaz1; Gaurav Goyal1; Toufik Mahfood Haddad1; Pranathi R. Sundaragiri1; Temple Brannan2, 1. 1Creighton University School of Medicine, Omaha, NE; 2Nebraska-Western Iowa Veterans Affairs Healthcare Center, Omaha, NE. (Tracking ID #2191582) Mastering OBJECTIVE #1: Recognize hemiballismus as initial presentation of acute cerebrovascular accident (CVA) Mastering OBJECTIVE #2: Highlight management of movement disorders in the setting of acute CVA CASE: A 72-year-old Caucasian male with past history of ischemic CVA, hypertension, diabetes mellitus, peripheral vascular illness and nicotine dependence presented with frequent involuntary jerking movements in the ideal upper and reduced extremities for 1 week duration. The symptoms initially started as twitching of right shoulder and progressively worsened. The symptoms have been absent throughout sleep but were prominent through the day and interfered with his activities of every day living. 	 The patient denied numbness, tingling, limb weakness, loss of consciousness, seizure-like activity, headaches or visual modifications. He had no family history of seizure or movement disorders. Physical examination revealed an elderly male, oriented and alert with elevated blood stress of 206/111 mm Hg with uncoordinated and unintentional movements of your proper upper and reduced extremities causing him to possess a limp throughout ambulation. Muscle strength was 4/5 in left biceps, triceps and hip flexors and 5/5 in other muscle groups, typical muscle tone and sensations, and absence of atrophy. Patellar reflexes and Babinski's sign were adverse bilaterally. Routine laboratory parameters were regular except for a hemoglobin A1C of 11.8  . Computed tomography (CT) scan of your head showed chronic right-sided thalamic lacunar infarct. Magnetic resonance imaging (MRI) from the brain confirmed chronic correct thalamic infarct and new smaller sub-acute infarcts in left lentiform nucleus. MR angiogram in the head was restricted by extreme motion artefacts but didn't demonstrate any clear vascular stenosis or cessation of flow. The patient was medically optimized on aspirin, simvastatin, haloperidol and lorazepam. The hemiballismus was attributed to the lentiform nuclear infarction. Patient's hyperkinetic movements dramatically decreased in intensity more than the subsequent 3 days and he was asymptomatic with no residual neurological challenges at 3 month follow-up. DISCUSSION: Hyperkinetic issues like chorea and hemiballismus are rare manifestations [http://www.ncbi.nlm.nih.gov/pubmed/1516647 1516647] of an acute CVA (0.5?  ).1 Having said that, CVAs are the most typical cause of acquired chorea and hemiballismus in adults. Other causes of non-genetic hemiballism contain non-ketotic hyperglycemia, encephalitis and vasculitis.2 Movement disorders secondary to cerebral ischemia most typically involve the contralateral lentiform nucleus, followed by the contralateral cortical, thalamic and subthalamic regions, although uncommon cases of ipsilateral subthalamic [http://05961.net/comment/html/?205126.html Joined Cases C-241/91 P And C-242/91 P] lesions with ipsilateral hemiballismus/hemichorea have already been reported as well.two,3 Diagnosis entails the use of CT scan and/or MRI, the diagnostic yield of which may be enhanced by using MR angiography.five Therapy of CVA-related hemiballismus follows standard stroke guidelines with added therapy for prevention of movement-disorder associated injury.2 Each neuroleptics and benzodiazepines have already been shown to be productive in managing symptoms of excessive involun.