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References
1. Gowers WR. Hysterie. In: Handbuch der Neurologie. Band III.
Bonn: Vlg. Friedrich Cohen; 1892. p 351–397.
2. Fahn S. Psychogenic movement disorders. In: Marsden CD, Fahn
S, editors. Movement disorders 3. Oxford, London: ButterworthHeinemann; 1994. p 359 –372.
3. Glosser DS, Stern MB. Psychogenic movement disorders: theoretical and clinical considerations. In: Adler CH, Ahlskog JE, editors.
Parkinson’s disease and movement disorders: diagnosis and treatment guidelines for the practicing physician. Totowa, NJ: Humana
Press; 2000. p 435– 451.
4. Koller W, Lang A, Vetere-Overﬁeld B, Findley L, Cleeves L,
Factor S, Singer C, Weiner W. Psychogenic tremors. Neurology
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5. Deuschl G, Köster B, Lücking CH, Scheidt C. Diagnostic and
pathophysiological aspects of psychogenic tremors. Mov Disord
1998;13:294 –302.
6. Monday K, Jankovic J. Psychogenic myoclonus. Neurology 1993;
43:349 –352.
7. Nowak M. Psychogenic paralysis in childhood and adolescence. Z
Kinder Jugendpsychiatr Psychother 2002;30:199 –210.
8. Spierings C, Poels PJ, Sijben N, Gabreels FJ, Renier WO. Conversion disorders in childhood: a retrospective follow-up study of
84 inpatients. Dev Med Child Neurol 1990;32:865– 871.
9. Pakalnis A, Paolicchi J, Gilles E. Psychogenic status epilepticus in
children: Psychiatric and other risk factors. Neurology 2000;54:
969 –970.
10. Thomas NH. Somatic presentation of psychogenic disease in child
neurologic practice. Neurology 2002;58(Suppl. 3):A28.
11. Manyam BV. Uncommon forms of tremor. In: Watts RL, Koller
WC, editors. Movement disorders; neurologic principles and practice. New York, St. Louis: McGraw-Hill; 1997. p 387– 403.
12. Fahn S, Williams DT. Psychogenic dystonia. Adv Neurol 1988;
50:431– 455.
13. Ranawaya R, Riley D, Lang A. Psychogenic dyskinesias in patients with organic movement disorders. Mov Disord 1990;5:127–
133.
14. Lang AE, Koller WC, Fahn S. Psychogenic parkinsonism. Arch
Neurol 1995;52:802– 810.
15. Hayes MW, Graham S, Heldorf P, de Moore G, Morris JGL. A
video review of the diagnosis of psychogenic gait: appendix and
commentary. Mov Disord 1999;14:914 –921.
16. Keane JR. Hysterical gait disorders: 60 cases. Neurology 1989;39:
586 –589.
17. Deuschl G, Bain P, Brin M. Tremor: basic mechanisms and clinical
aspects. Abstracts and consensus-statement of the Scientiﬁc Committee of the Tremor Symposium, July 11/12, 1997. Kiel: Scientiﬁc Committee of the Tremor Symposium; 1997; p 1– 45.
18. Srinath S, Bharat S, Girimaji S, Seshadri S. Characteristics of a
child inpatient population with hysteria in India. J Am Acad Child
Adolesc Psychiatry 1993;32:822– 825.
19. Factor SA, Podskalny GD, Molho ES. Psychogenic movement
disorders: frequency, clinical proﬁle, and characteristics. J Neurol
Neurosurg Psychiarty 1995;59:406 – 412.
20. Kramer U, Carmant L, Riviello JJ, Stauffer A, Helmers SL, Mikati
MA, Holmes GL. Psychogenic seizures: video telemetry observations in 27 patients. Pediatr Neurol 1995;12:39 – 41.
21. Fine J, Stergiopoulos V, Nieves A, Feinstein A, Lang AE. Longterm follow-up psychogenic movement disorders. Neurology
2000;54(Suppl. 3):A50 –A51.
22. Grattan-Smith P, Fairley M, Procopis P. Clinical features of conversion disorders. Arch Dis Child 1988;63:408 – 414.
23. Walters AS, Hening WA. Noise-induced psychogenic tremor associated with post-traumatic stress disorder. Mov Disord 1992;7:
333–338.
24. Kim YJ, Pakiam AS, Lang AE. Historical and clinical features of
psychogenic tremor: a review of 70 cases. Can J Neurol Sci
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25. Alper K, Devinsky O, Perrine K, Vasquez B, Luciano D. Nonepileptic seizures and childhood sexual and physical abuse. Neurology 1993;43:1950 –1953.
26. Lempert T, Brandt T, Dieterich M, Huppert D. How to identify
psychogenic disorders of stance and gait. A video study in 37
patients. J Neurol 1991;238:140 –146.
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28. Quane T, Chambers CV, Synderman D. Conversion disorder presenting as gait disturbance in an adolescent. Arch Fam Med 1995;
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Patterns of referral in patients with medically unexplained motor
symptoms. J Psychosom Res 2000;49:217–219.

Arm Chorea Secondary to an Unruptured
Giant Aneurysm
Luis M. Barreiro de Madariaga, MD,1 José E. Sian, MD,1
Ignacio Casas Parera, MD,2 and Federico Micheli, MD3*
1

Hospital Central de Formosa, Formosa, Argentina
2
Instituto de Oncologı́a Ángel H. Roffo,
Servicio de Neurologı́a, Buenos Aires, Argentina
3
Parkinson’s Disease and Movement Disorders Program,
Institute of Neurosciences, José de San Martı́n Hospital de
Clı́nicas, Buenos Aires, Argentina

Abstract: We describe the case of a 20-year-old male who
developed right-arm choreic movements secondary to a giant
unruptured aneurysm impinging upon the left thalamus, putamen, globus pallidus, cerebral peduncle, midbrain, and subthalamic nucleus. The aneurysm was treated successfully with
coils and a supraclinoid balloon. Abnormal movements initially
failed to ameliorate, but within a few months, it was possible to
discontinue symptomatic haloperidol therapy, with only mild
residual abnormal movements. © 2003 Movement Disorder
Society
Key words: chorea, aneurysm, vascular
Commonly affecting elderly patients with a cerebrovascular
accident, hemichorea is on occasion accompanied by proximal ballistic movements, attributable to disorders involving
the contralateral caudate nucleus, putamen, and globus pallidus.1,2 We report on a young patient with a giant unrup-

A videotape accompanies this article.
*Correspondence to: Dr. Federico Micheli, Juncal 1695-P 5 Dpto J
(1062), Buenos Aires, Argentina. E-mail: Fmicheli@ﬁbertel.com.ar
Received 15 August 2002; Revised 2 May 2003; Accepted 8 May
2003

Movement Disorders, Vol. 18, No. 11, 2003

1398

CLINICAL/SCIENTIFIC NOTES

tured aneurysm who slowly developed choreic movements
in his right arm.

Case Report
A 20-year-old, previously healthy man developed abnormal
involuntary choreic movements in his right hand that over 2
weeks progressed slowly to involve the whole arm and shoulder girdle. Movements worsened with stress and disappeared
during sleep.
Neurological examination showed an alert and cooperative patient oriented in time and space. Fundus oculi were
normal and visual ﬁelds full. Cranial nerve testing was
normal. The right upper limb was slightly hypotonic with
pendular deep tendon reﬂexes. Arrhythmic, irregular, abnormal involuntary movements of the right upper limb associated with hand jerks, consistent with negative myoclonus,
were observed and these interfered markedly with voluntary
movements but were also present at rest and when sustaining
a posture. The remainder of the neurological examination
was normal.
Magnetic resonance imaging (MRI) of the brain showed a
rounded T1-weighted image with void signal, surrounded by a
hypointense signal displacing the left lenticular nucleus and the
internal capsule, compatible with a giant aneurysm surrounded
by edema. The mass impinged upon the left thalamus and on
the left cerebral peduncle and midbrain (Fig. 1).
Athough MRI T1- and T2-weighted images showed hyperintensity consistent with turbulent ﬂow, an MRA (3-D
TOF–3-D PC) disclosed intraluminal ﬂow with typical aneurysmatic features, conﬁrmed by four-vessel angiography
showing a left M1 giant aneurysm. Laboratory workup including VDRL, FAN, LE, ASTO, and ESR, were all normal
or negative, as was a chest X-ray, an electrocardiogram
(EKG), and an echocardiogram.
The aneurysm was treated uneventfully with coils and a
balloon in the supraclinoid pre-aneurysmatic segment. A control MRI 2 months later showed a decrease in peri-aneurysmatic edema. Unfortunately, choreic movements failed to improve initially. Treatment with ﬂunarizine 10 mg/day was
ineffective, but haloperidol 2.5 mg q.i.d. markedly diminished
involuntary movements. After a few months, medication was
discontinued successfully with only mild residual involuntary
arm movements.

Discussion
Secondary chorea may result from focal basal ganglion lesions including stroke,3 arteriovenous malformations,4 infections,5 brain tumors either as paraneoplastic syndromes6 or
causing a mass effect,7 diabetes,8 multiple sclerosis,9 and cerebral palsy.10 Chorea is also a feature of many neurodegenerative diseases including Huntington’s disease,11 chorea-acanthocytosis,12 and McLeod neuroacanthocytosis.13
While several arteriovenous vascular malformations are
known to induce movement disorders,4 several mechanisms
have been identiﬁed for such symptoms including mass effect,
diaschisis, local alterations in blood ﬂow, and hemorrhage or
ischemic structural lesions.
Conversely, aneurysms have rarely been reported in association with movement disorders and, to the best of our knowledge, only three such cases of chorea secondary to aneurysms

Movement Disorders, Vol. 18, No. 11, 2003

FIG. 1. Magnetic resonance of the brain showing a rounded T1-weighted
image with void signal, surrounded by a hypointense signal displacing the
left ventricular nucleus and the internal capsule. This is compatible with a
giant aneurysm surrounded by edema. The mass impinged upon the left
thalamus (top) and the left cerebral peduncle and midbrain (bottom).

have been documented.3,14,15 Two were due to ischemic lesions
in the basal ganglia interpreted as secondary to emboli from the
aneurysm in one3 and to vasospasm in the other,14 and the third
to brainstem compression by a giant fusiform aneurysm of the
basilar artery.15
Development of involuntary movements associated with
myoclonic jerks in our patient was relentless in his right hand
and arm. Although a slowly progressive focal movement disorder strongly suggests an enlarging mass-occupying lesion,
our case illustrates that progressive focal chorea may be caused
by a giant unruptured aneurysm. Loss of subthalamic nucleus

CLINICAL/SCIENTIFIC NOTES
control on the internal segment of the globus pallidus is followed by disinhibition of the thalamus,16 leading to
chorea/ballismus.
Recently, Kim and colleagues17 found altered CBF in both
the contralateral thalamus and basal ganglia, reﬂecting loss of
inhibitory input from the pallidum to the thalamus in vascular
hemichorea. The primary insult to the striatum thus led to a
dysfunction of GABAergic neurons projecting through the GPe
to the subthalamic nucleus.
In our case, the giant aneurysm impinged mainly on the
putamen, globus pallidus, thalamus, midbrain, and most
likely the subthalamic nucleus, all critical areas of the basal
ganglion circuitry involved in triggering chorea.1–3,7,18 –20 In
addition to chorea, our patient exhibited myoclonic jerks in
the hand probably due to posterior thalamic involvement.20
Successful aneurysm treatment resulted in progressive improvement of the involuntary movements over several
months, probably due to decreased aneurysm volume and
shape as well as the disappearance of surrounding edema.
Our case highlights the need to carry out imaging studies in
cases of focal chorea, to avoid overlooking potentially treatable life-threatening conditions.

Legend to the Video
Abnormal involuntary movements consistent with chorea
are evident on the right arm, both when attempting to write
and on outstretched hands. Occasional arm and hand jerking
is also shown.

References
1. Kase CS, Maulsby GO, deJuan E, Mohr JP. Hemichorea-hemiballism and lacunar infarction in the basal ganglia. Neurology 1981;
31:452– 455.
2. Shan DE, Ho DM, Chang C, Pang HC, Teng MM. Hemichoreahemiballism: an explanation for MR signal changes. Am J Neuroradiol 1998;19:863– 870.
3. Redondo L, Chacón J, Valencia J, Viñuelas F, Pérez Alonso JL,
Garcı́a Flores C. Symptomatic chronic hemichorea of a vascular
lesion in the contralateral putamen. Rev Neurol 1996;24:303–
305.
4. Krauss JK, Kiriyanthan GD, Borremans JJ. Cerebral arteriovenous
malformations and movement disorders. Clin Neurol Neurosurg
1999;101:92–99.
5. Piccolo I, Causarano R, Sterzi R, et al. Chorea in patients with
AIDS. 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 feature
of renal cancer. Arch Neurol 2001;58:1133–1135.
7. Krauss JK, Nobbe F, Wakhloo AK, Mohadjer M, Vach W, Mundinger F. Movement disorders in astrocytomas of the basal ganglia
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8. Chu K, Kang DW, Kim DE, Park SH, Roh JK. Diffusionweighted and gradient echo magnetic resonance ﬁndings of
hemichorea-hemiballismus associated with diabetic hyperglycemia: 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. Mov
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10. Sugama S, Kusano K. A case of dyskinetic cerebral palsy resembling post-anoxic action myoclonus. Brain Dev 1995;17:210 –212.

1399

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 newly
discovered protein, chorein, is mutated in chorea-acanthocytosis.
Nat Genet 2001;28:121–122.
13. Danek A, Rubio JP, Rampoldi L, et al. McLeod neuroacanthocytosis: 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 subarachnoid
hemorrhage]. Japanese. No To Shinkei 1991;43:875– 880.
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16. DeLong MR. Primates models of movement disorders of basal
ganglia origin. Trends Neurosci 1990;40:281–285.
17. Kim JS, Lee KS, Lee KH, Kim YI, Kim BS, Chung YA, Chung
SK. Evidence of thalamic disinhibition in patients with hemichorea: semiquantitative analysis using SPECT. J Neurol Neurosurg
Psychiatry 2002;72:329 –333.
18. Shan DE, Ho DM, Chang C, Pan HC, Teng MM. Hemichoreahemiballism: an explanation for MR signal changes. Am J Neuroradiol 1998;19:863– 870.
19. Lee MS, Marsden CD. Movement disorders following lesions of the
thalamus or subthalamic region. Mov Disord 1994;9:493–507.
20. Ghika J, Bogousslavsky J, Henderson J, Maeder P, Regli F. The
jerky dystonic unsteady hand: a delayed syndrome in posterior
thalamic infarctions. J Neurol 1994;241:537–542.

Transient Ischemic Attacks Presenting
as 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 involuntary movement characterized by irregular, coarse, ﬂinging
movement involving the limbs on one side. Hemiballism is
most commonly caused by stroke. However, very rarely a
transient ischemic attack (TIA) presents as hemiballism. We
describe 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, coarse
chorea. 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 University 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 21
May 2003

Movement Disorders, Vol. 18, No. 11, 2003