| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2001;32:258.)
© 2001 American Heart Association, Inc.
Case Report |
Involuntary Movements After Anterior Cerebral Artery Territory Infarction
From the Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, South Korea.
Correspondence to Jong S. Kim, MD, Department of Neurology, Asan Medical Center, Song-pa PO Box 145, Seoul 138-600, South Korea. E-mail jongskim{at}www.amc.seoul.kr
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Background and Purpose—Patients with anterior cerebral artery territory infarction presenting with involuntary movements have rarely been described in the literature.
Case Descriptions—The author reports 9 such patients: 3 with asterixis, 5 with hemiparkinsonism (tremor, rigidity, hypokinesia), and 1 with both. Asterixis developed in the acute stage in patients with minimal arm weakness, whereas parkinsonism was usually observed after the motor dysfunction improved in patients with initially severe limb weakness. Asterixis correlated with small lesions preferentially involving the prefrontal area; parkinsonism is related to relatively large lesions involving the supplementary motor area.
Conclusions—Anterior cerebral artery territory infarction should be included in the differential diagnosis of asterixis and hemiparkinsonism.
Key Words: cerebral arteries • cerebrovascular disorders • dyskinesias • movements • Parkinson disease • tremor
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Involuntary movements (IMs), such as chorea, dystonia, asterixis, and tremor, may occur as a consequence of stroke,1 most often due to involvement of the basal ganglia or thalamus/subthalamus. However, IMs caused by anterior cerebral artery (ACA) territory infarction have rarely been reported.2 The author describes 9 patients who developed IMs after ACA infarction.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Between May 1995 and December 1999, the author prospectively identified 9 patients with ACA infarction who presented with IMs at the Asan Medical Center. All the patients were examined and followed up by the author. The observed IMs were either asterixis or hemiparkinsonism. To assess the presence of asterixis, the patients were asked to stretch their arms with the wrists dorsiflexed. Legs were also extended with feet dorsiflexed at the ankle. Selected patients (n=4) were videotaped and repeatedly assessed.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
There were 4 men and 5 women, ranging in age from 47 to 79 years. No patients received medications, such as antiepileptics or antipsychotics, that might have caused IMs. History taking showed that there were no such IMs before the onset of stroke in these patients. Family history of IMs was also denied. Laboratory results, including serum ammonia, calcium, and electrolytes, were all within normal limits. The clinical findings are briefly summarized in Table 1
, and 3 cases are described below. All patients had
hemiparesis worse in the leg, and 4 had speech disturbances.
None showed significant sensory loss or limb ataxia. Two patients
showed alien hand signs; when asked to perform a task using both arms,
the action of the right hand was not under conscious control, so that
the patients often used the left hand to restrain the right
one.3
|
Involuntary Movements
In all patients, IMs occurred in the arms, most
markedly in the fingers, but never occurred in the legs. Four patients
had asterixis; 1 (patient 6) had bilateral asterixis, more severe on
the side contralateral to the lesion. Asterixis started
immediately after the onset of stroke and disappeared within 2 to 7
days. Electromyography, performed in 1 patient (patient 8), confirmed
episodes of electrical silence. Six patients had hemiparkinsonism:
tremor, cogwheel rigidity, and hypokinesia. The tremors, of 4 to 5 Hz,
started to appear gradually as the motor weakness improved at 2 to 4
weeks in the patients with initially severe arm weakness. Tremor
occurred mainly during rest in 3 patients; in another 3, it was more
prominent on arm stretching. The patients’ gait was slow and
hemiparetic, and arm swing was greatly reduced. The dearth of movement
was obvious in the involved arm. Patient 9 initially had asterixis that
disappeared as her limb weakness progressed. One month later, as her
motor dysfunction improved, she developed hemiparkinsonism.
L-dopa was tried in 4
patients (patients 1,3,5, and 9); only 1 (patient 3) showed partial
improvement of tremor. During the follow up of 2 to 33 (mean 19)
months, the tremor and cogwheel rigidity gradually diminished in
severity
(Table 1
).
Imaging Findings and Vascular Study
The lesions, analyzed by brain MRI in 7
patients and CT in 2 patients, are schematically presented in
Figure 1. The patients with hemiparkinsonism (patients 1
through 5) usually had relatively large, rostral-dorsal lesions,
probably involving the supplementary motor area (SMA), whereas those
with asterixis (patients 6 through 8) had small lesions mainly
involving the prefrontal area. Cerebral angiography was performed in 7
patients (transfemoral in 3, MR in 4). Atherosclerotic
stenosis/occlusion at the proximal ACA was found in 6 patients.
Patient 1, with a normal angiogram, had valvular heart disease.
To assess the perfusion of the basal ganglia,
[99mTc]-L,
L-ethylcysteinate dimer
(ECD) SPECT was performed in 2 patients (patients 5 and 9) and showed
perfusion defect in the ACA territory but not in the basal
ganglia.
|
Patient 1
A 79-year-old hypertensive woman with valvular
heart disease suddenly developed left hemiparesis (II/V, on the 0-V
Medical Research Council scale, in the arm and II/V in the leg),
and urinary incontinence. She was apathetic and nearly mute. The muscle
strength gradually improved, and 1 month later she experienced only
minimal hand weakness, although leg weakness (II/V) remained. Sensation
was normally perceived. There was no ataxia on the finger-to-nose test.
She started to show a resting tremor of 4 to 5 Hz in her left fingers.
The tremor was rhythmic and of variable amplitude. Also observed
were cogwheel rigidity, hypokinesia in the left limbs, and a loss of
arm swing during walking. There was no tremor or cogwheeling in the
foot. Brain MRI showed an acute infarct in the frontal lobe of the
right ACA territory. MR angiography showed normal results, although a
distal part of the ACA was not evaluated.
L-dopa (200 mg)/benserzide
(50 mg) 3 times a day did not improve her symptoms and was
discontinued. Nevertheless, the tremor gradually decreased in
intensity; 3 years later, mild cogwheel rigidity remained in the left
arm but without tremor.
Patient 6
A 55-year-old hypertensive man suddenly developed right
hemiparesis III/V in the leg, and only slightly in the arm. He was
alert but apathetic. Although there was no obvious speech problems he
had difficulties in initiating the speech. Position sensation was
mildly decreased in the right toes. He showed an alien hand sign in the
right arm. A finger-to-nose test did not reveal ataxia. On stretching
of the arms, there was asterixis in both hands, which was worse in the
right. MRI showed an acute infarct in the left ACA territory.
Transfemoral angiography showed an occlusion of the A2 portion of the
left ACA. The asterixis gradually decreased in intensity, and was no
longer observed 1 week later.
Patient 9
A 59-year-old hypertensive woman suddenly developed
involuntary, shaking movements of the right forearm after 3 episodes of
transient, right-sided weakness. Neurological examination showed that
there was a slight weakness in the right leg. The gross arm shaking
rapidly diminished in intensity and was observed as a pattern of
asterixis only when her hands were stretched. Over the next 3 days, her
limb weakness progressed to III/V, when the asterixis disappeared. She
also developed transcortical mixed aphasia and alien hand sign. The arm
weakness gradually improved; 1 month later, only slight clumsiness of
the hand was observed while the leg was still severely weak (III/V).
She started to show a resting tremor of 4 to 5 Hz in the right fingers.
There was cogwheel rigidity and slight spasticity in the right arm and
a loss of arm swing on gait. The tremor and rigidity gradually
improved, and 2 years later there only remained a very mild,
intermittent hand tremor.
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
I found that there are 2 distinct types of IMs caused by ACA infarction: asterixis and hemiparkinsonism.
Hemiparkinisonism
The parkinsonism usually occurred after the patients’
limb weakness improved in the setting of initially severe hemiparesis.
Their resting and monotonous tremor was similar to that of idiopathic
Parkinson’s disease (IPD), but the tremor occurred more distinctly in
half of the patients when their arms were stretched. However, whether
this postural tremor differentiates it from a tremor of IPD remains
unclear, because the patients with IPD occasionally show prominent
postural tremor.4 The
patients’ hemihypokinesia may be attributed at least in part to the
pyramidal dysfunction. However, the dearth of arm movement
and the loss of arm swing during gait were clearly more prominent than
would be expected from the mild pyramidal dysfunction.
Moreover, the cogwheel rigidity cannot be explained by hemiparesis or
hemispasticity. Rather, the delayed onset of symptoms in patients with
severe limb weakness and the observation that parkinsonian symptoms
occurred in the arm but not in the leg suggest that the
extrapyramidal symptoms are manifested only after the
recovery of the initially severe pyramidal
dysfunction.
Previously, frontal lobe tumors have been repeatedly
described as a cause of
hemiparkinsonism.5 6 7 8
However, parkinsonism due to ACA infarction has received surprisingly
little
attention.2 9 Our
imaging studies showed that hemiparkinsonism is usually related to SMA
or cingulate gyrus involvement
(Figure 1, panels 1 through 5). Leenders et
al6 hypothesized that local
tissue pressure on the basal ganglia produced hemiparkinsonism in their
patient with frontal meningioma. However, this mechanism seems unlikely
in our patients, considering that there was no compressive effect on
the basal ganglia on MR imaging, including coronal cuts (data not
shown), and that the symptoms occurred in the subacute-chronic but
not the acute stage. Thus, a more plausible explanation for the
hemiparkinsonism would be a functional disconnection of the
striatum-SMA circuitry.8
There has been ample evidence of anatomic connections between the
striatum and the
SMA,10 11 12
and the disconnection of the basal ganglia output to the SMA by an ACA
infarction could produce parkinsonism. Previously, Playford et
al13 demonstrated an
impaired basal ganglia facilitation of medial frontal activation in
patients with IPD. Dick et
al9 even suggested that IPD
symptoms actually reflect functional deafferentation of the SMA from
the basal ganglia. The disconnection does not appear to be related to
an alteration of the basal ganglionic blood flow, because SPECT studies
showed normal perfusion in the basal ganglia in our patients. In a
study using PET scan, Miyagi et al8 found
decreased glucose metabolism and normal dopamine
metabolism in the basal ganglia of a patient with
meningioma at the SMA area that produced hemiparkinsonism. They
speculated that the tumor might have caused synaptic dysfunction of the
striatum as a whole, but without an impairment of the presynaptic
dopaminergic nerve terminals. Consistent with this observation,
L-dopa was not effective in
most of our patients. Nevertheless, the hemiparkinsonism spontaneously
improved in all the patients.
Asterixis
Unlike hemiparkinsonism, the asterixis correlated with
initially mild limb weakness associated with small, anteriorly located
lesions
(Figure 1, panels 6 through 8). Asterixis, one type of
negative myoclonus,14
results from a sudden cessation of electrical activity in the extensor
muscles, due possibly to an intermittent inhibition of the spinal
neuronal system that mediates voluntary tonic extension of the limb.
Asterixis may occur after focal cerebral lesions involving the
midbrain, thalamus, parietal lobe, or the frontal
cortex.14 15 16
However, ACA infarction as a cause of asterixis has received little
attention. Young and
Shahani14 suggest that
sustained muscle contraction is related to the neural subsystem
involving the medial frontal cortex, parietal lobe, and the
ventrolateral thalamus. This system may have been disrupted in our
patients with lesions mainly involving the prefrontal cortex. It is
noteworthy that asterixis was bilateral in patient 6. Although
concomitant involvement of the contralateral frontal cortex may be
possible, previous studies have also reported bilateral asterixis due
to unilateral brain
lesions,15 17
which suggests that the focal unilateral ACA infarction itself produced
bilateral asterixis.
Received May 22, 2000; revision received August 7, 2000; accepted August 28, 2000.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Ghika J, Bogousslavsky J. Abnormal movements. In: Bogousslavsky J, Caplan L, eds. Stroke Syndrome. New York, NY: Cambridge University Press; 1995:91–101.
2. Nagaratnam N, Davies D, Chen E. Clinical effects of anterior cerebral artery infarction. J Stroke Cerebrovasc Dis. 1998;7:391–397.[Medline] [Order article via Infotrieve]
3.
Goldberg G, Mayer
NH, Toglia JU. Medial frontal cortex infarction and the alien hand
sign. Arch Neurol. 1981;38:683–686.
4. Deuschl G, Krack P, Tremors. Differential diagnosis, neurophysiology, and pharmacology, In: Jankovic J, Tolosa E, eds. Parkinson’s Disease and Movement Disorders. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 1998:419–452.>
5. Nicholson AN, Turner EA. Parkinsonism produced by parasagittal meningioma. J Neurosurg. 1964;21:104–113.[Medline] [Order article via Infotrieve]
6.
Leenders KL,
Findley LJ, Cleeves L. PET before and after surgery for tumor-induced
parkinsonism. Neurology. 1986;36:1074–1078.
7.
Straube A, Sigel K.
Parkinsonian syndrome caused by a tumour of the left supplementary
motor area. J Neurol Neurosurg
Psychiatry. 1988;51:730–731.
Letter.
8. Miyagi Y, Norioka T, Otsuka M, Fukui M. Striatal glucose metabolism and [18F] fluorodopa uptake in a patient with tumor-induced hemiparkinsonism. Neurosurgery. 1993;32:838–841.[Medline] [Order article via Infotrieve]
9. Dick JP, Benecke R, Rothwell JC, Day BL, Marsden CD. Simple and complex movements in a patient with infarction of the right supplementary motor area. Mov Disord. 1986;1:255–266.[Medline] [Order article via Infotrieve]
10.
Kemp JM, Powell
TRS. The cortico-striate projections in the monkey.
Brain. 1970;93:525–546.
11. Yeterian EH, van Hoesen GW. Cortico-striate projections in the rhesus monkey: the organization of certain cortico-caudate connections. Brain Res. 1978;139:43–63.[Medline] [Order article via Infotrieve]
12. Jürgens U. The efferent and afferent connections of the supplementary motor area. Brain Res. 1984;300:63–81.[Medline] [Order article via Infotrieve]
13. Playford ED, Passingham RE, Nutt J, Frackowiak RSJ, Brooks DJ. Impaired activation of medial frontal areas during movement in Parkinson’s disease: a PET study. J Cereb Blood Flow Metab. 1991;11[suppl 2]:S1. Abstract.>
14. Young RR, Shahani BT. Asterixis, one type of negative myoclonus. In: Fahn S, ed. Advances in Neurology, Volume 43: Myoclonus. New York, NY: Raven Press; 1986;43:137–156.
15. Rio J, Montalbán J, Pujadas F, Alvarez-Sabin J, Rovira A, Codina A. Asterixis associated with anatomic cerebral lesions: a study of 45 cases. Acta Neurol Scand. 1995;91:377–381.[Medline] [Order article via Infotrieve]
16.
Nighoghossian
N, Trouillas P, Vial C, Froment JC. Unilateral upper limb asterixis
related to primary motor cortex infarction.
Stroke. 1995;26:326–328.
17. Kim HK, Kim JS, Lee MC. Astasia and asterixis due to unilateral thalamic infarction. J Korean Neurol Assoc. 1995;13:104–108.
This article has been cited by other articles:
 |
|
 |
|
  A. Handley, P. Medcalf, K. Hellier, and D. Dutta Movement disorders after stroke Age Ageing, May 1, 2009; 38(3): 260 - 266. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Y. Kang and J. S. Kim Anterior cerebral artery infarction: Stroke mechanism and clinical-imaging study in 100 patients Neurology, June 10, 2008; 70(24_Part_2): 2386 - 2393. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F Alarcon, J C M Zijlmans, G Duenas, and N Cevallos Post-stroke movement disorders: report of 56 patients J. Neurol. Neurosurg. Psychiatry, November 1, 2004; 75(11): 1568 - 1574. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||