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Paroxysmal Hemiballism/Hemichorea Resulting from Transient Ischemic Attacks

2015; Wiley; Volume: 3; Issue: 3 Linguagem: Inglês

10.1002/mdc3.12268

2330-1619

Carmen Gasca‐Salas, Anthony E. Lang,

Genetic Neurodegenerative Diseases

Movement Disorders Clinical PracticeVolume 3, Issue 3 p. 303-305 Case ReportFree Access Paroxysmal Hemiballism/Hemichorea Resulting from Transient Ischemic Attacks Carmen Gasca-Salas MD, Carmen Gasca-Salas MD Toronto Western Hospital, Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, Toronto, Ontario, CanadaSearch for more papers by this authorAnthony E. Lang MD, FRCPC, Corresponding Author Anthony E. Lang MD, FRCPC Toronto Western Hospital, Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, Toronto, Ontario, CanadaCorrespondence to: Dr. Anthony E. Lang, Toronto Western Hospital, Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, McLaughlin Pavilion, 399 Bathurst Street, 7th Floor, Toronto, Ontario, Canada M5T 2S8; E-mail: lang@uhnresearch.caSearch for more papers by this author Carmen Gasca-Salas MD, Carmen Gasca-Salas MD Toronto Western Hospital, Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, Toronto, Ontario, CanadaSearch for more papers by this authorAnthony E. Lang MD, FRCPC, Corresponding Author Anthony E. Lang MD, FRCPC Toronto Western Hospital, Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, Toronto, Ontario, CanadaCorrespondence to: Dr. Anthony E. Lang, Toronto Western Hospital, Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, McLaughlin Pavilion, 399 Bathurst Street, 7th Floor, Toronto, Ontario, Canada M5T 2S8; E-mail: lang@uhnresearch.caSearch for more papers by this author First published: 09 December 2015 https://doi.org/10.1002/mdc3.12268Citations: 4 Relevant disclosures and conflicts of interest are listed at the end of this article. AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Hemiballism is a rare movement disorder that presents with involuntary irregular, poorly patterned, flinging movements of one side of the body with an acute or subacute onset.1 In approximately 50% of cases, there is also facial involvement. Large-amplitude movements are characteristic, but lower-amplitude hemichorea commonly coexists in the same patient and the pathophisiology of hemiballism and hemichorea is the same. Although the classical localization of lesions causing hemiballism is the subthalamic nucleus (STN), lesions affecting various areas, such as striatum, thalamus, globus pallidus, and cortex, are also possible, with lesions of the contralateral striatum being the commonest cause.2 We present an unusual patient with recurrent episodes of hemiballism/hemichorea resulting from presumed transient ischemic attacks (TIAs) secondary to middle cerebral artery (MCA) stenosis. Case Report This 51-year-old man, with a past medical history of arthritis and depression, presented with paroxysmal left hemibody involuntary movements. The first episode occurred in April 2013 while he was driving. He had sudden and violent left-limb movements for around 10 minutes with no alteration of consciousness. Over the subsequent month, he continued to have similar episodes with a frequency ranging from once a week to 20 a day. Typically, they were shorter than the first episode, lasting 2 to 3 minutes. He was unaware of any triggers, such as sudden movements, startle, hyperventilation, or exercise. He underwent three conventional and one sleep-deprived EEGs that were normal. He was treated with levetiracetam, and in June 2013, the episodes resolved completely. A brain MRI in May 2013 showed ischemic changes in the right caudate and right pallidum that showed restriction on diffusion-weighted imaging (DWI) sequence, as well as scattered ischemic lesions through subcortical white matter and right parietal cortex. One month later, a new MRI showed an increase of these lesions, in the right basal ganglia (Fig. 1A,B). There was a suspicion of demyelinating disease and a lumbar punture was performed in September 2013, showing normal cerebrospinal fluid findings. The episodes returned after the lumbar puncture. A few days later, the patient presented with an acute episode of left-sided facial droop and left hemiparesis that lasted 15 to 20 minutes. This episode recurred once on the same day and again 2 days later. He was admitted to our hospital. During this admission, he experienced two further episodes of left-side involuntary movements for 2 minutes each. These episodes were described as identical to the previous ones. Another brain MRI showed a chronic stroke with a subacute area of infarction in the right parietal region and acute smaller foci in the right frontal lobe, and right periventricular white matter were observed. An MR angiogram showed a moderate narrowing of a short segment in the right middle cerebral artery (MCA) trunk, likely atherosclerotic (Fig. 1C). During his hospitalization, the patient provided us a home video of his typical episodic abnormal movements (see Video 1). The involuntary movements involving his left arm and leg were consistent with hemiballism/hemichorea. They were both large (flinging) and lower-amplitude, continuous irregular movements with additional athetoid movements involving the left hand and foot. He was treated with dual antiplatelet (clopidogrel for 21 days and acetylsalicylic acid), and levetiracetam was discontinued. He had a good recovery from stroke, and, to date, involuntary movements have not recurred. Figure 1Open in figure viewerPowerPoint (A) May 2013. Ischemic changes in the right caudate (T2), subcortical white matter, and right parietal cortex (FLAIR). DWI images showed restriction in the right caudate. (B) June 2013. Increase of the right basal ganglia lesions (also involving putamen and globus pallidus) (T2). (C) September 2013. MRI showed a chronic stroke with a subacute area of infarction in the right parietal region and acute smaller foci in the right frontal lobe and right periventricular white matter (FLAIR and DWI). Moderate narrowing of the proximal MCA-M1 (MR angiogram). FLAIR, fluid-attenuated inversion recovery. Discussion We report a case with video documentation of TIA presenting as hemiballism in a patient with MCA stenosis. Stroke remains the most common cause of hemiballism,2 whereas TIA presenting as hemiballism is extremely uncommon. It can be a consequence of MCA3 or carotid stenosis.4 It has also been reported to be associated with TIAs in Moya-Moya disease,5-7 but commonly induced by hyperventilation. Limb shaking is a well-known hyperkinetic movement associated with transient cerebral ischemia resulting from internal carotid artery stenosis or occlusion. This consists of irregular brief jerking8 and it may be a form of asterixis.9 The phenomenology of limb-shaking TIAs is clearly different from the poorly patterned, flinging movements observed in hemiballism. Contrary to traditional teaching, lesions causing hemiballism may be located outside of the STN, specifically in those structures with which the STN has afferent or efferent connections, such as the striatum, globus pallidus, thalamus, and frontal and parietal cortex. Therefore, an interruption of these connections may lead to ballistic movements.2 In the present case, strokes involving the basal ganglia were present and there was an increase in these over time. The parietal cortex was also damaged, and this might further explain the involuntary movements.10, 11 Some of the episodes of hemiballism may have been related to ischemic strokes, and the response to leviteracetam could have been coincidental to a resolution of symptoms resulting from a permanent stroke, given that the episodes later returned despite this treatment. Although fluctuant symptoms can occur with completed strokes with surrounding ischemic penumbra, the recurrent episodes lacking clear triggers (e.g., changes in posture or blood pressure, hyperventilation, and so on) and resolving after the introduction of antiplatelet agents favor transient ischemia as the underlying causative mechanism. This paroxysmal occurrence of hemiballism/hemichorea secondary to TIA should be recognized encouraging further appropriate investigations such as cerebrovascular imaging in order to prevent a delay in diagnosis with resultant increased risk of stroke leading to greater long-term disability. Author Roles (1) Research Project: A. Conception, B. Organization, C. Execution; (2) Statistical Analysis: A. Design, B. Execution, C. Review and Critique; (3) Manuscript Preparation: A. Writing of the First Draft, B. Review and Critique. C.G.: 1A, 1B, 3A, 3B A.E.L.: 1A, 1B, 3A, 3B Disclosures Funding Sources and Conflicts of Interest: The authors report no sources of funding and no conflicts of interest. Financial Disclosures for previous 12 months: The authors declare that there are no disclosures to report. Supporting Information A video accompanying this article is available in the supporting information here. Filename Description mdc312268-sup-0001-VideoS1.movvideo/mov, 78.4 MB Video 1. The patient is lying down watching TV and involuntary left extremities movements suddenly arise. The movements are irregular, continuous, flinging, and often large amplitude with intermittent flexion-extension and rotation of the elbow and knee. Distal athetoid movements can also be observed. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. References 1Shefner J. Ballism. In: AB Joseph, RB Young, eds. Movement Disorders in Neurology and Neuropsychiatry. Malden, MA: Blackwell Science; 1999: 475– 480. 2Postuma RB, Lang AE. Hemiballism: revisiting a classic disorder. Lancet Neurol 2003; 2: 661– 668. 3Kim JW, Choi SH, Kim WJ, Chun SM. Transient ischemic attacks presenting as hemiballism. Mov Disord 2003; 18: 1399– 1401. 4Margolin DI, Marsden CD. Episodic dyskinesias and transient cerebral ischemia. Neurology 1982; 32: 1379– 1380. 5Han SH, Kim YG, Cha SH, Chung SY. Moyamoya disease presenting with singing induced chorea. J Neurol Neurosurg Psychiatry 2000; 69: 833– 834. 6Spengos K, Tsivgoulis G, Toulas P, Vemmos K, Vassilopoulos D, Spengos M. Hyperventilation-enhanced chorea as a transient ischaemic phenomenon in a patient with moyamoya disease. Eur Neurol 2004; 51: 172– 175. 7Im SH, Oh CW, Kwon OK, Cho BK, Chung YS, Han DH. Involuntary movement induced by cerebral ischemia: pathogenesis and surgical outcome. J Neurosurg 2004; 100: 877– 882. 8Baquis GD, Pessin MS, Scott RM. Limb shaking—a carotid TIA. Stroke 1985; 16: 444– 448. 9Yoon Y, Kim JS. Limb-shaking TIA: an asterixis. Neurology 2013; 81: 931– 932. 10Mizushima N, Park-Matsumoto YC, Amakawa T, Hayashi H. A case of hemichorea-hemiballism associated with parietal lobe infarction. Eur Neurol 1997; 37: 65– 66. 11Hwang KJ, Hong IK, Ahn TB, Yi SH, Lee D, Kim DY. Cortical hemichorea-hemiballism. J Neurol 2013; 260: 2986– 2992. Citing Literature Volume3, Issue3May/June 2016Pages 303-305 FiguresReferencesRelatedInformation