(Stroke. 1995;26:326-328.)
© 1995 American Heart Association, Inc.
Articles |
Unilateral Upper Limb Asterixis Related to Primary Motor Cortex Infarction
From the Service d'Urgences Neurovasculaires et Centre de Recherches sur l'Ataxie (N.N., P.T.), the Laboratoire d'Electromyographie, Service du Pr Bady B (C.V.), and the Service de Neuroradiologie et d'Imagerie en Résonance Magnétique (J.C.F.), Lyon, France.
Correspondence to Dr N. Nighoghossian, Service de Neurologie du Pr Trouillas P, Hôpital Neurologique, 59 Blvd Pinel, Lyon, 69003 France.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsCase ReportDiscussionReferences |
|---|
Background Unilateral upper limb asterixis related to cortical infarct is an unusual clinical picture. We found this association in two patients. Magnetic resonance imaging (MRI), somatosensory evoked potentials (SEPs), and electromyographic recording were performed.
Case Descriptions Two patients developed an acute upper limb ataxia with asterixis. This consisted of frequent arrhythmic loss of extensor muscle tone on instruction to maintain the wrist and fingers extended. Voluntary electromyographic activity in the left extensor digitorum communis muscle showed abrupt periods of interruption ranging from 90 to 260 milliseconds in duration in the first case and from 60 to 220 milliseconds in the second case. SEPs were normal. MRI disclosed a right cortical infarct within the primary motor cortex in both cases.
Conclusions These findings indicate that asterixis was not related to a failure in the processing of proprioceptive input controlling the regulation of postural tone of the distal upper limbs because SEPs were normal. The involvement of primary motor cortex might suggest that asterixis results from an impairment of a centrally generated motor-command signal controlling the postural tone of the distal upper limb.
Key Words: cerebral cortex • cerebral infarction • motor activity
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsCase ReportDiscussionReferences |
|---|
Unilateral asterixis has been associated with a variety of focal brain lesions.1 2 3 4 5 6 Asterixis can be related to a failure in the processing of proprioceptive input that controls the postural tone of the distal upper limb.1 7 8 9 Conversely, unilateral asterixis has been described in patients without proprioceptive loss.2 We report here two cases of unilateral asterixis related to an involvement of primary motor cortex without somatosensory deafferentation, which was demonstrated by the recording of somatosensory evoked potentials (SEPs).
|
Methods |
|---|
|
TopAbstractIntroductionMethodsCase ReportDiscussionReferences |
|---|
Neuroimaging studies included brain computed tomographic (CT) scan and magnetic resonance imaging (MRI) using multiecho axial T2 (2500/90 milliseconds) and coronal T1-weighted and sagittal T1-weighted (520/22 milliseconds) pulse sequences that provided 1.2-mm-thick slices. The site of the ischemic lesion was assessed using the coplanar stereotaxic atlas of the human brain from Talairach and Tournoux.10
SEP recording was performed as described by Mauguière and
Desmedt.11 12 13 Electromyographic recording was performed
with a Nicolet Vicking II four-channel system. The system bandpass was
20 Hz to 5 kHz. The gain was 100 µv/div, and the sweep speed was 500
ms/div. Recordings (Fig 1
) were made with bipolar needle
electrodes placed from the extensor digitorum communis (channel A) and
flexor digitorum sublimis (channel B). The patients were asked to
voluntarily extend their arms and wrists straight in front of them.
|
|
Case Report |
|---|
|
TopAbstractIntroductionMethodsCase ReportDiscussionReferences |
|---|
An 83-year-old patient with chronic nonvalvular atrial fibrillation developed an acute left hand weakness on May 30, 1993. One day later, while the weakness improved, neurological examination disclosed a mild ataxia of the left upper limb with hypotonia, delayed initiation of movement, hypermetria, dyssynergia, and tremor during finger-to-nose test; eye closure had no effect on ataxia. Deep tendon reflexes were more brisk in the left arm. Touch, joint, vibration, and temperature sensation, as well as stereognosis, were preserved on the left side. Asterixis was confined to the left wrist and fingers. It consisted of frequent arrhythmic loss of extensor muscle tone on instruction to maintain the wrist and fingers extended, producing intermittent brief lapses in the assumed posture. CT scan (Fig 1
) and
MRI (Fig 2) showed an infarction located within the
primary motor cortex. SEP responses were normal. At this time the
voluntary electromyographic activity in the left extensor digitorum
communis muscle showed abrupt interruptions during 60 to 220
milliseconds (mean, 134 milliseconds) (Fig 1, A2) without
concomitant activity in the left flexor digitorum sublimis muscle (Fig 1, B2). Metabolic screening, including liver enzyme values
and electroencephalogram, was normal.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsCase ReportDiscussionReferences |
|---|
Asterixis, described originally by Adams and Foley,14 denotes a dysfunction of the mechanism underlying sustained muscular contraction.15 It is characterized by arrhythmic, brief total lapses in or relaxation of tonically contracting muscles, as noted in our patients. MRI disclosed in both cases an infarct within the primary motor cortex, a site where a lesion might impair some of the neural mechanisms responsible for maintaining posture.
Our patients had mild cerebellar ataxia. A contribution of the cerebellum in the maintenance of tonic postures opposing gravity has been advocated by Gordon Holmes.16 Considering the location of the lesion, the interruption of neocerebellar pathways that originate in the pericentral cortex of Brodmann's areas 6, 4, 3, 2, 1, and 517 might account for both the asterixis and the upper limb ataxia. Asterixis has previously been described with cerebellar symptoms4 8 9 18 and was thought to be due to a reduction of afferent information caused by the loss of the dentato-thalamo-cortical input. However, the occurrence of asterixis in patients with ataxic hemiparesis is so exceptional that it cannot be considered without reservation as a mere consequence of dysfunction in the cortico-cerebello-cortical loop. In this study, SEPs were normal in both cases; therefore, a failure in the processing of proprioceptive inputs cannot explain the asterixis.
Jennings et al19 demonstrated in monkeys that some units in Brodmann's somatosensory areas 3A and 2 that failed to respond to passive manipulation were nevertheless activated during maintained steady posture. It was therefore suggested that the activity of these neurons results from central rather than peripheral input.20 This input to neurons of the primary somatesthetic area might originate in the central motor structures, such as the primary motor cortex. Consistent with this possibility is the finding that the activity of primary motor cortex neurons is related to the amount of muscle activity associated with the maintenance of a given force at a given position.21 22 23 In addition, evidence has been presented that perception of exerted force derives from a centrally generated motor-command signal rather than from peripheral receptors.24 25 Our patients' SEPs were normal, and the mechanism of the asterixis might be consistent with an abnormality of this corollary discharge because the lesions were confined to the primary motor cortex.
Young and Shahani26 later suggested that the underlying mechanism of asterixis might be hyperactivity of the inhibitory mechanism in the central nervous system. The term "negative myoclonus" is used in the literature to describe an inhibitory phasic phenomenon characterized by simultaneous silent periods of agonist and antagonist muscles during posture maintenance.
We did not study asterixis with the method described by Ugawa et al,27 which allows analysis of electroencephalographic events associated with sudden pauses in ongoing electromyographic activity (silent-period locked averaging method). Asterixis in the present study was not associated with myoclonic jerking. Therefore, it must be differentiated from both the positive myoclonus and asterixis occurring in the elderly28 and the epileptic negative myoclonus that caused a form of "postural" epilepsia partialis continua characterized by phasic motor inhibition instead of activation.29
|
Received August 26, 1994; revision received October 10, 1994; accepted October 28, 1994.
|
References |
|---|
|
TopAbstractIntroductionMethodsCase ReportDiscussionReferences |
|---|
1. Leavitt S, Tyler HR. Studies in asterixis. Arch Neurol. 1964;10:360-368.
2. Young RR, Shahani BT, Kjelberg RJ. Unilateral asterixis produced by a discrete CNS lesion. Trans Am Neurol Assoc. 1976;101:306-307. [Medline] [Order article via Infotrieve]
3.
Degos JD, Verroust J, Bouchareine A, Serdaru M, Barbiset J.
Asterixis in focal brain lesions. Arch Neurol. 1979;36:705-707.
4.
Donat JR. Unilateral asterixis due to thalamic hemorrhage.
Neurology. 1980;30:83-84.
5. Peterson DI, Peterson GW. Unilateral asterixis due to ipsilateral lesions in the pons and medulla. Ann Neurol. 1987;22:661-663. [Medline] [Order article via Infotrieve]
6.
Tarsy D, Lieberman B, Chirico-Post J, Benson DF. Unilateral
asterixis associated with a mesencephalic syndrome. Arch
Neurol. 1977;34:446-447.
7. Feldmeyer JJ, Bogousslavsky J, Regli F. Asterixis uni-ou bilatéral en cas de lésion thalamique ou parietale: un trouble moteur afférentiel? Schweiz Med Wochenschr. 1984;114:167-171. [Medline] [Order article via Infotrieve]
8. Trouillas P, Nighoghossian N, Mauguière F. Syndrome cérébelleux et asterixis unilatéral par hématome thalamique: mécanismes présumés. Rev Neurol. 1990;146:484-489. [Medline] [Order article via Infotrieve]
9. Nighoghossian N, Trouillas P, Vial C, Mauguière F. Monoparésie ataxique du membre supérieur et suspension du tonus d'attitude par lésion pariétale. Rev Neurol. 1993;149:262-266. [Medline] [Order article via Infotrieve]
10. Talairach J, Tournoux P. Co-planar Stereotaxic Atlas of the Human Brain. Three-Dimensional Proportional System: An Approach to Cerebral Imaging. Stuttgart/New York, NY: Georg Thieme Verlag Publishers; 1988.
11.
Mauguière F, Desmedt JE. Thalamic pain syndrome of
Dejerine Roussy: differentiation of four subtypes assisted by
somatosensory evoked potential data. Arch Neurol. 1988;45:1312-1320.
12. Desmedt JE, Brunko E, Debecker J. The system bandpass required to avoid distortion of early components when averaging SEPs. Electroencephalogr Clin Neurophysiol. 1974;30:407-410.
13. Mauguière F, Gonnaud PM, Ibanez V, Schott B. Potentiels évoqués somesthésiques précoces et déficits sensitifs dans les lésions thalamiques et juxta-thalamiques. Rev Neurol. 1987;143:643-656. [Medline] [Order article via Infotrieve]
14. Adams RD, Foley JM. The disorder of movement in the more common varieties of liver disease. Electroencephalogr Clin Neurophysiol. 1953;3:51.
15. Shahani BT, Young RR. Asterixis: a disorder of the neural mechanisms underlying sustained muscle contraction. In: Shahani BT, ed. The Motor System: Neurophysiology and Muscle Mechanisms. Amsterdam, Netherlands: Elsevier Scientific Publishing; 1976:301-306.
16.
Holmes G. The cerebellum of man. Brain. 1939;62:1-30.
17. Brodal P. Principles of organization of the monkey corticopontine projections. Brain Res. 1978;148:214-218. [Medline] [Order article via Infotrieve]
18. Pullicino P, Xuereb M, Farrugia B. Hémorragie cérébelleuse et asterixis unilatéral. Rev Neurol. 1990;11:697-698.
19.
Jennings VA, Lamour Y, Solis H, Fromm C. Somatosensory cortex
activity related to position and force. J Neurophysiol. 1983;49:1216-1229.
20.
Mountcastle VB, Lynch JC, Georgopoulos A, Sakata H, Acuna C.
Posterior parietal association cortex of the monkey: command functions
for operations within extrapersonal space. J Neurophysiol. 1975;38:871-907.
21.
Cheney PD, Fetz EE. Functional classes of primate
corticomotoneural cells and their relation to active force. J
Neurophysiol. 1980;44:773-791.
22.
Evarts EV. Activity of pyramidal tract neurons during postural
fixation. J Neurophysiol. 1969;32:375-385.
23.
Evarts EV, Fromm C, Kröller J, Jennings VA. Motor cortex
control of finely graded forces. J Neurophysiol. 1983;49:1199-1215.
24.
McCloskey DI. Kinesthetic sensibility. Physiol Rev. 1978;58:763-820.
25. McCloskey DI, Ebeling P, Goodwin GM. Estimation of weights and tensions and apparent involvement of `a sense of effort.' Exp Neurol. 1974;42:220-232. [Medline] [Order article via Infotrieve]
26. Young RR, Shahani BT. Asterixis: one type of negative myoclonus. In: Fahn S, Marsden CD, Woert MHV, eds. Advances in Neurology: Myoclonus. New York, NY: Raven Press Publishers; 1986;43:137-156.
27.
Ugawa Y, Genba K, Shimpo T, Mannen T. Onset and offset of
electromyographic (EMG) silence in asterixis. J Neurol Neurosurg
Psychiatry. 1990;53:260-262.
28. Hashimoto S, Kawamura J, Yamamoto T, Kinoshita A, Segawa Y, Harada Y, Suenaga T. Transient myoclonic state with asterixis in elderly patients: a new syndrome? J Neurol Sci. 1992;109:132-139. [Medline] [Order article via Infotrieve]
29. Cirignotta F, Lugaresi E. Partial motor epilepsy with negative myoclonus. Epilepsia. 1991;32:54-58.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  K. Noda, H. Miwa, N. Miyashita, S. Tanaka, and Y. Mizuno Monoataxia of upper extremity in motor cortical infarction Neurology, May 22, 2001; 56(10): 1418 - 1419. [Full Text] [PDF]
|
|
|
|
|
|
J. S. Kim Asterixis after unilateral stroke: Lesion location of 30 patients Neurology, February 27, 2001; 56(4): 533 - 536. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. S. Kim Involuntary Movements After Anterior Cerebral Artery Territory Infarction Stroke, January 1, 2001; 32(1): 258 - 261. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||