control on the internal segment of the globus pallidus is fol-lowed by disinhibition of the thalamus,16 leading tochorea/ballismus.

Recently, Kim and colleagues17 found altered CBF in boththe contralateral thalamus and basal ganglia, reflecting loss ofinhibitory input from the pallidum to the thalamus in vascularhemichorea. The primary insult to the striatum thus led to adysfunction of GABAergic neurons projecting through the GPeto the subthalamic nucleus.

In our case, the giant aneurysm impinged mainly on theputamen, globus pallidus, thalamus, midbrain, and mostlikely the subthalamic nucleus, all critical areas of the basalganglion circuitry involved in triggering chorea.1–3,7,18 –20 Inaddition to chorea, our patient exhibited myoclonic jerks inthe hand probably due to posterior thalamic involvement.20

Successful aneurysm treatment resulted in progressive im-provement of the involuntary movements over severalmonths, probably due to decreased aneurysm volume andshape as well as the disappearance of surrounding edema.Our case highlights the need to carry out imaging studies incases of focal chorea, to avoid overlooking potentially treat-able life-threatening conditions.

Legend to the Video

Abnormal involuntary movements consistent with choreaare evident on the right arm, both when attempting to writeand on outstretched hands. Occasional arm and hand jerkingis also shown.

References

1. Kase CS, Maulsby GO, deJuan E, Mohr JP. Hemichorea-hemibal-lism and lacunar infarction in the basal ganglia. Neurology 1981;31:452–455.

2. Shan DE, Ho DM, Chang C, Pang HC, Teng MM. Hemichorea-hemiballism: an explanation for MR signal changes. Am J Neuro-radiol 1998;19:863–870.

3. Redondo L, Chacon J, Valencia J, Vinuelas F, Perez Alonso JL,Garcıa Flores C. Symptomatic chronic hemichorea of a vascularlesion in the contralateral putamen. Rev Neurol 1996;24:303–305.

4. Krauss JK, Kiriyanthan GD, Borremans JJ. Cerebral arteriovenousmalformations and movement disorders. Clin Neurol Neurosurg1999;101:92–99.

5. Piccolo I, Causarano R, Sterzi R, et al. Chorea in patients withAIDS. Acta Neurol Scand 1999;100:332–336.

6. Kujawa KA, Niemi VR, Tomasi MA, Mayer NW, Cochran E,Goetz CG. Ballistic-choreic movements as the presenting featureof renal cancer. Arch Neurol 2001;58:1133–1135.

7. Krauss JK, Nobbe F, Wakhloo AK, Mohadjer M, Vach W, Mund-inger F. Movement disorders in astrocytomas of the basal gangliaand the thalamus. J Neurol Neurosurg Psychiatry 1992;55:1162–1167.

8. Chu K, Kang DW, Kim DE, Park SH, Roh JK. Diffusion-weighted and gradient echo magnetic resonance findings ofhemichorea-hemiballismus associated with diabetic hyperglyce-mia: a hyperviscosity syndrome? Arch Neurol 2002;59:448 –452.

9. Waubant E, Simonetta-Moreau M, Clanet M, Berry I, Bonafe A.Left arm monoballism as a relapse in multiple sclerosis. MovDisord 1997;12:1091–1092.

10. Sugama S, Kusano K. A case of dyskinetic cerebral palsy resem-bling post-anoxic action myoclonus. Brain Dev 1995;17:210–212.

11. Jankovic J, Ashizawa T. Huntington’s disease. In: Appel SH,editor. Current neurology, Vol 15. Chicago: Mosby Year Book;1995. p 29–60.

12. Ueno S, Maruki Y, Nakamura M, et al. The gene encoding a newlydiscovered protein, chorein, is mutated in chorea-acanthocytosis.Nat Genet 2001;28:121–122.

13. Danek A, Rubio JP, Rampoldi L, et al. McLeod neuroacanthocy-tosis: genotype and phenotype. Ann Neurol 2001;50:755–764.

14. Sakai K, Kyoshima K, Ohigashi Y, Kobayashi S, Meguro M.[Generalized choreic movement associated with subarachnoidhemorrhage]. Japanese. No To Shinkei 1991;43:875–880.

15. Read D, Eisiri MM. Fusiform basilar aneurysm in a child. Neu-rology 1979;29:1045–1049.

16. DeLong MR. Primates models of movement disorders of basalganglia origin. Trends Neurosci 1990;40:281–285.

17. Kim JS, Lee KS, Lee KH, Kim YI, Kim BS, Chung YA, ChungSK. Evidence of thalamic disinhibition in patients with hemicho-rea: semiquantitative analysis using SPECT. J Neurol NeurosurgPsychiatry 2002;72:329–333.

18. Shan DE, Ho DM, Chang C, Pan HC, Teng MM. Hemichorea-hemiballism: an explanation for MR signal changes. Am J Neuro-radiol 1998;19:863–870.

19. Lee MS, Marsden CD. Movement disorders following lesions of thethalamus or subthalamic region. Mov Disord 1994;9:493–507.

20. Ghika J, Bogousslavsky J, Henderson J, Maeder P, Regli F. Thejerky dystonic unsteady hand: a delayed syndrome in posteriorthalamic infarctions. J Neurol 1994;241:537–542.

Transient Ischemic Attacks Presentingas Hemiballism

Jae Woo Kim, MD, PhD,* Seoung-Ho Choi, MD,Wook-Joo Kim, MD, and Sang-Myung Chun, MD

Department of Neurology, Dong-A University Hospital,Busan, Korea

Abstract: Hemiballism is continuous, nonpatterned involun-tary movement characterized by irregular, coarse, flingingmovement involving the limbs on one side. Hemiballism ismost commonly caused by stroke. However, very rarely atransient ischemic attack (TIA) presents as hemiballism. Wedescribe 2 such patients with hemiballism presenting as TIA.© 2003 Movement Disorder Society

Key words: hemiballism; stroke; transient ischemic attack

Ballism is a form of forceful, flinging, large amplitude, coarsechorea. Ballism and chorea are often interrelated and may occur

A videotape accompanies this article.*Correspondence to: Dr. Jae Woo Kim, Parkinson’s Disease and

Movement Disorders Clinic, Department of Neurology, Dong-A Uni-versity Hospital, 1, 3 Ga, Dongdaisin-Dong, Seo-Gu, Busan 602-715,Korea. E-mail: jwkim@mail.donga.ac.kr

Received 28 December 2002; Revised 6 May 2003; Accepted 21May 2003

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in the same patient. The involuntary movement usually affectsonly one side of the body; therefore, the term hemiballism isused to describe unilateral ballism. Although various structurallesions have been associated with ballism, damage to the sub-thalamic nucleus and the pallidosubthalamic pathways appearsto play a critical role in the expression of this hyperkineticmovement disorder.1 Stroke is the most common cause ofhemiballism, but transient ischemic attack (TIA) presenting ashemiballism, to our knowledge, has been reported rarely.2,3

Case Reports

Case 1

A 62-year-old man was admitted because of recurrent jerkymovement involving his left limbs. One day before admission,he suddenly developed rapid, irregular involuntary movementsinvolving both proximal and distal limbs while he was driving.They lasted approximately 10 minutes then disappeared spon-taneously. The movement reappeared and lasted in the samemanner five more times until the next morning, when he visitedthe emergency room of our hospital. He has not been known tobe hypertensive, but his blood pressure was 190/110. On neu-rological examination, his mental status examination was nor-mal. There were no motor and sensory abnormalities betweenthe attacks. The involuntary movements were forceful, jerky,irregular, flinging, and large amplitude movements involvinghis left arm and leg, proximal as well as distal. He sometimesshowed dyskinesia in his left face and tongue protrusion. Rou-tine laboratory examinations and thyroid function test werenormal. Electrocardiogram and echocardiogram revealed noabnormalities. Serum antiphospholipid antibody and serologictests for syphilis were negative. T2-weighted brain magneticresonance imaging (MRI) showed several high signal intensitylesions in the periventricular areas corresponding to lacunarinfarction, but no lesion adjacent to subthalamic nucleus. How-ever, a diffusion brain MRI study demonstrated no recentlesions. Magnetic resonance angiography (MRA) revealed atight stenosis in the M1 and distal portion of right middlecerebral artery and some irregularities in the left internal ca-rotid artery (Fig. 1). Brain perfusion SPECT using 99mTc

HMPAO showed a mild perfusion defect in the left temporalarea. The involuntary movement has not reappeared for morethan 3 years since administration of an antiplatelet agent.

Case 2

A 61-year-old man suddenly developed involuntary move-ment involving his left limbs. One day before he visited ourclinic, he experienced, while bicycling, sudden dyskinesia inhis left limbs, which was jerky, forceful, irregular, and flinging.The involuntary movement lasted for 2 minutes and disap-peared spontaneously. He had had a previous episode of tran-sient right hemiparesis lasting 2 to 3 minutes 2 weeks before hisvisit. Five years earlier, he had developed visual disturbance inhis left visual field. He had been diagnosed with and treated forhypertension and hyperthyroidism for 15 years before his visit.His blood pressure was 160/110. On neurological examination,he had left homonymous hemianopia and bilateral foot drop.Pain and temperature sensations were decreased in the leftlateral lower leg. Otherwise, no abnormal neurological deficitswere found. Routine laboratory examinations and thyroid func-tion test were normal. Electrocardiogram and echocardiogramrevealed no abnormalities. Serum antiphospholipid antibodyand serologic tests for syphilis were negative. Electromyogra-phy revealed bilateral lumbosacral radiculopathy. T2-weightedbrain MRI showed right posterior cerebral infarction but nolesion in or adjacent to the right subthalamic nucleus. A diffu-sion brain MRI study demonstrated no recent lesions. MRAdemonstrated a stenosis in the M2 portion of right middlecerebral artery (Fig. 2). Since administration of an antiplateletagent, no involuntary movement has occurred during follow-upfor almost 3 years.

Discussion

Hemiballism is usually caused by cerebrovascular disorders.It is mostly seen in middle-aged or elderly patients and has

FIG. 1. Magnetic resonance angiography reveals a tight stenosis in theM1 and distal portion of right middle cerebral artery and some irreg-ularities in the left internal carotid artery.

FIG. 2. Magnetic resonance angiography demonstrates stenosis in theM2 portion of right middle cerebral artery.

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sudden onset. When due to other causes such as tumors, infec-tions, multiple sclerosis, trauma, or metabolic abnormalities,younger patients may be affected and the onset may be pro-longed over days or weeks.4,5 The ages of our patients were 61and 62, typical and close to the age seen in one of the majorseries reported.5,6 Additionally, both patients had hypertensionand an arterial stenosis contralateral to the limbs with involun-tary movement. It was conceivable that, although MRI can misssmall infarcts, hemiballism in our patients was due to TIA,because the duration of the dyskinesia ranged from several to10 minutes and no abnormal signal intensities responsible forthe hemiballism were found in the diffusion-weighted MRI.Diffusion-weighted imaging can miss small infarcts. However,it was not likely that the patient had an infarct, because hepresented brief, recurrent abnormal movements rather thancontinuous ones. It is known that a lesion causing hemiballismmay be located in either the subthalamic nucleus or the struc-tures with which the subthalamic nucleus has afferent or effer-ent connections.7 These sites include the striatum, globus pal-lidus, thalamus, and rarely, distant sites such as the coronaradiata and precentral or postcentral gyrus.8–10 Paroxysmaldyskinesias have been rarely reported in patients with hyper-thyroidism.11 However, our patients were euthyroid when theydeveloped their involuntary movements. No other possiblecauses for sudden and transient hemiballism were found inthese patients. Considering that Case 1 had recurrent hemibal-lism in the same limbs and both patients had severe stenoses inthe middle cerebral arteries and no potential embolic sources, itis assumed that thrombosis rather than embolism contributedthe involuntary movements. The reason why Case 1 also hadinvoluntary movements involving face and tongue as well aslimbs remains to be determined. It is conceivable that a largerischemic area has more opportunity to cause involuntary move-ment involving larger part of body than a smaller area. Our twocases demonstrate that TIAs can present as hemiballism, a raremovement disorder.

Acknowledgment: This study was supported by the Dong-A Uni-versity Research Fund, in 2002.

Legend to the Video

The patient (Case 1) shows irregular, jerky, flinging move-ment involving his left limbs and choreic movement involvinghis left face, which suddenly develop and last about 10 minutes.

References

1. Buruma OJS, Lakke JP. In: Vinken PJ, Bruyn GW, Klawans HL,editors. Handbook of clinical neurology. Vol. 5. Extrapyramidal dis-orders. New York: Elsevier Science Publishers; 1986. p 369–380.

2. Bedwell SF. Some observations on hemiballismus. Neurology1960;10:619–622.

3. Margolin DI, Marsden CD. Episodic dyskinesias and transientcerebral ischemia. Neurology 1982;32:1379–1380.

4. Riley D, Lang AE. Hemiballism in multiple sclerosis. Mov Disord1988;46:88–94.

5. Dewey RB, Jankovic J. Hemiballism-hemichorea. Clinical andpharmacologic findings in 21 patients. Arch Neurol 1989;46:862–867.

6. Klawans HL, Moses H, Nausieda PA. Treatment and prognosis ofhemiballismus. N Eng J Med 1976;295:1348–1350

7. Shannon KM. Hemiballismus. Clin Neuropharmacol 1990;13:413–425.

8. Lang AE. Persistent hemiballismus with lesions outside the sub-thalamic nucleus. Can J Neurol Sci 1985;12:125–128.

9. Carpenter MB. Ballism associated with partial destruction of thesubthalamic nucleus of Luys. Neurology 1955;5:479–489.

10. Schwarz GA, Barrows LJ. Hemiballism without involvement ofLuys body. Arch Neurol 1960;2:420–434.

11. Baba M, Terada A, Hishida R, Matsunaga M, Kawabe Y, TakebeK. Persistent hemichorea associated with thyrotoxicosis. InternMed 1992;31:1144–1146.

Subthalamic Lesion andParoxysmal Tonic Spasms

Pedro J. Garcia-Ruiz, MD,1* Vicente Villanueva, MD,1

Eva Gutierrez-Delicado, MD,1 Amaia Echeverrıa, MD,1

Antonio Perez-Higueras, MD,2 and Jose M. Serratosa, MD1

1Department of Neurology, Fundacion JimenezDıaz, Madrid, Spain

2Department of Neuroradiology, Fundacion JimenezDıaz, Madrid, Spain

Abstract: Paroxysmal dyskinesia due to a subthalamic lesion isa rare finding. We describe a patient with paroxysmal tonicspasms due to a well-defined lesion in the subthalamic area. Inthis case, we confirm the nonepileptic nature of the episode andcollect with detail the clinical features by means of a video-electroencephalographic recording. We also report an excellentresponse to carbamazepine in subthalamic paroxysmal dyski-nesias. © 2003 Movement Disorder Society

Key words: subthalamic lesion; paroxysmal dyskinesias;paroxysmal tonic spasms

Paroxysmal dyskinesias (PDs) are a heterogeneous group ofdisorders characterized by the presence of sudden and transientabnormal movements.1,2 PD can be classified as idiopathic,familial, and secondary.1,2 Occasionally focal lesions, includ-ing vascular and demyelinating, can result in secondary PD1–7;the location of such focal lesions includes mainly the thalamus,there being very rarely subthalamic localization. Although sec-ondary PDs are well-known movement disorders, the fre-quently transient nature of these dyskinesias and the absence ofvideotape documentation in most patients to ensure diagnosisof a nonepileptic event, leads to common misdiagnosis. Inaddition, pathological or neuroradiological findings have beendescribed rarely. We report a case of PD confirmed by video–

A videotape accompanies this article.Drs. Garcia-Ruiz and Villanueva contributed equally to this work.*Correspondence to: Dr. Pedro J. Garcia-Ruiz, Department of Neu-

rology, Fundacion Jimenez Dıaz, Av. Reyes Catolicos 2, 28040 Ma-drid, Spain. E-mail: pgarcia@fjd.es

Received 20 December 2002; Revised 2 April 2003; Accepted 29April 2003

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