Middle Cerebral Artery Occlusion Compromising the Sensory and Motor Cortices CASE REPORT

K. H. Lin, W. C. Shyu
Middle Cerebral Artery Occlusion Compromising the Sensory and
Motor Cortices
Kuan-Hung Lin , Woei-Cherng Shyu
Department of Neurology , Buddhist Tzu Chi General Hospital, Hualien, Taiwan; Department of Neurology , Chung Gung
Memorial Hospital, Taoyuan, Taiwan
We report a patient with mild motor and sensory dysfunction of the face and hand, which was caused by a middle cerebral artery
occlusion with infarction in the sensory and motor cortices of the dominant hemisphere. She showed striking recovery in three days.
We discuss some of the possible circulatory variants that might underlie this pattern of infarction. (Tzu Chi Med J 2006; 18:382384)
Key words: MCA occlusion, infarction, central sulcus, collateral circulation
Infarctions in the middle cerebral artery (MCA) area
may present with different clinical features depending
on which divisions or branches are occluded and on the
extent of the infarct [1]. If the anterior (superior) division is involved, the most common consequences are
contralateral hemiparesis and hemisensory loss. In
addition, aphasia usually accompanies lesions in the left
hemisphere, whereas sensory neglect phenomena and
anosognosia accompany right hemispheric lesions. Here
we provide a clinical description of one case of complete left MCA occlusion at the distal part of M1 segment of the dominant hemisphere that only affected the
precentral and postcentral gyrui.
An 88 year old right-handed woman without a his-
tory of hypertension and previous stroke suffered an
acute episode of dizziness and collapse at home when
she got up in the early morning. In the emergency room
she had mildly slurred speech without aphasia, a shallow right nasolabian fold without dysphagia, numbness
over right lower face, right distal hand and moderate
weakness of the right arm, but no weakness of the right
leg (NIHSS=7). A head CT scan showed only brain diffused atrophy correlated to her old age and a brain MRI
scan according to the Diffusion Weighted Image revealed
multiple small lacunar infarcts as well as a new left MCA
infarct that only involved the precentral and postcentral
gyrui. A brain MRA scan showed patent anterior cerebral arteries (ACA), and an attenuated flow-related signal for the left MCA at the distal part of M1 segment;
the superior division of this artery was not visualizable.
A neck MRA scan and carotid ultrasound were
unremarkable. Her neurological deficits improved strikingly and she asked to be discharge after three days
Received: March 7, 2006, Revised: April 25, 2006, Accepted: June 7, 2006
Address reprint requests and correspondence to: Dr. Kuan-Hung Lin, Department of Neurology, Buddhist Tzu Chi General
Hospital, 707, Section 3, Chung Yang Road, Hualien, Taiwan
Tzu Chi Med J 2006 18 No. 5
MCA infarct involving only sensory and motor cortices
Fig. 1. (A) Brain MRA showing an occlusion of the left MCA
distal M1 branch; the superior division of the left
MCA is not visualizable. (B) Brain MRI-DWI revealing an acute infarct in the left lateral precentral
gyrus. (C,D,E) Brain MRI-T2, FLAIR, ADC mapping images showed a ischemic lesion in the left lateral precentral gyrus.
The middle cerebral artery is the largest branch of
the internal carotid artery. The artery supplies a portion
of the frontal lobe and the lateral surface of the temporal and parietal lobes, including the primary motor and
sensory areas of the face, throat, hand and arm and in
the dominant hemisphere, the areas for speech. The clinical abrupt sensory-motor symptoms over right face and
right upper limb of the patient show a possible anatomic
Tzu Chi Med J 2006 18 No. 5
K. H. Lin, W. C. Shyu
localization of the vascular lesion to the lateral part of
the left precentral and postcentral gryus [2,3]. The lateral precentral gyrus contains the motor representation
for the contralateral face and arm and the lateral postcentral gyrus contains the sensory functions. Both of
them are normally supplied by a distal branch of the
middle cerebral artery, the lateral Rolandic artery [4].
This area is normally included in all infarctions involving the superior division of the MCA.
In order to explain the sparing of other branch of
the MCA observed in this case of MCA occlusion, at
least four different mechanisms may be suspected. In
the first, a shower of small emboli resulting from the
break up of a large proximal embolus would block distal branches of the MCA. Only precentral and postcentral gryus underwent ischemic infarction and the other
areas of the cortices were spared because of spontaneous emboli lysis except for the lateral Rolandic artery.
However, in previously reported embolic cases of this
type, the hemiparesis was dense initially and improved
subsequently, namely a "spectacular shrinking deficit"
[5,6]. However, in this case, the motor deficit was minimal at presentation, which therefore does not support
this model for the mechanism.
A second possibility is spontaneous local recanalization of the occluded vessels, with or without additional
good leptomeningeal collateralization, which could lead
to selective restoration of flow except for the lateral Rolandic branch of the MCA. This would be able to explain the rapid recovery after the initial focal weakness
and numbness. Recanalization occurring within the first
few days after an acute event is known to improve the
outcome after MCA infarction. However, further MRA
follow-up would be required after the initial stroke to
show that recanalization has occurred.
A third possibility is the presence of pre-existing
collateral circulation established because of chronic poor
MCA perfusion [7-9], except for the lateral Rolandic
branch. This would provide a reasonable explanation for
isolated Rolandic infarct effect of the MCA occlusion
in this patient. Unfortunately, we were unable to demonstrate such selective collateral circulation, because our
patient did not receive conventional angiography due to
her age. Without this information, other potential changes
including the possibility of an embolus break up with
distal migration, as described in situation 1 above, cannot be entirely ruled out.
The final possible explanation for pathogenesis of
the cortical infarction resulting from MCA occlusion is
that it is the result of a combination of multiple stroke
mechanisms, such as both local branch occlusion and
embolism [10,11]. To confirm this hypothesis, there
would be a need for serial DWI/MRA imaging and
microembolic signal monitoring by transcranial Doppler in order to provide supportive evidence.
In conclusion, we suggest that further prospective
studies of similar patients using catheter angiography
or follow-up MRA are necessary because they might
reveal how such a stroke mechanism might be exploited
to improve the treatment.
1. Ringelstein EB, Biniek R, Weiller C, Ammeling B, Nolte
PN, Thron A: Type and extent of hemispheric brain
infarctions and clinical outcome in early and delayed
middle cerebral artery recanalization. Neurology 1992;
2. Seitz RJ, Hoflich P, Binkofski F, Tellmann L, Herzog H,
Freund HJ: Role of the premotor cortex in recovery from
middle cerebral artery infarction. Arch Neurol 1998; 55:
3. Portera-Cailliau C, Doherty CP, Buonanno FS, Feske
SK: Middle cerebral artery territory infarction sparing the
precentral gyrus: Report of three cases. J Neurol
Neurosurg Psychiatry 2003; 74:510-512.
4. Racy A, Jannotta FS, Lehner LH: Aphasia resulting from
occlusion of the left anterior cerebral artery. Report of a
case with an old infarct in the left Rolandic region. Arch
Neurol 1979; 36:221-224.
5. Minematsu K, Yamaguchi T, Omae T: 'Spectacular
shrinking deficit': Rapid recovery from a major hemispheric syndrome by migration of an embolus. Neurology 1992; 42:157-162.
6. Kraemer N, Thomalla G, Soennichsen J, et al: Magnetic resonance imaging and clinical patterns of patients
with 'spectacular shrinking deficit' after acute middle
cerebral artery stroke. Cerebrovasc Dis 2005; 20:285290.
7. Wei L, Erinjeri JP, Rovainen CM, Woolsey TA: Collateral growth and angiogenesis around cortical stroke.
Stroke 2001; 32:2179-2184.
8. Mull M, Schwarz M, Thron A: Cerebral hemispheric lowflow infarcts in arterial occlusive disease. Lesion patterns and angiomorphological conditions. Stroke 1997;
9. Coyle P: Spatial relations of dorsal anastomoses and
lesion border after middle cerebral artery occlusion.
Stroke 1987; 18:1133-1140.
10. Caplan LR, Hennerici M: Impaired clearance of emboli
(washout) is an important link between hypoperfusion,
embolism, and ischemic stroke. Arch Neurol 1998; 55:
11. Lee DK, Kim JS, Kwon SU, Yoo SH, Kang DW: Lesion
patterns and stroke mechanism in atherosclerotic middle
cerebral artery disease: Early diffusion-weighted imaging study. Stroke 2005; 36:2583-2588.
Tzu Chi Med J 2006 18 No. 5