Childs Nerv Syst (2006) 22:1493–1496
DOI 10.1007/s00381-006-0157-9

CASE REPORT

Posttraumatic infarction in the territory supplied
by the lateral lenticulostriate artery after minor head injury
Jung Yong Ahn & In Bo Han & Young Sun Chung &
Pyeong Ho Yoon & Sang Heum Kim

Received: 19 March 2005 / Published online: 30 August 2006
# Springer-Verlag 2006

Abstract
Background Occlusion of the intracranial arteries due to
blunt head traumas has been less frequently observed in
patients with minor head injuries.
Case report A 4-year-old boy presented with speech
disturbance 2 h after minor head injury. An initial computed
tomography (CT) scan showed a questionable finding of a
focal punctate high density in the left basal ganglia.
Hemiparesis developed on the right limbs 8 h post-injury,
and a subsequent CT scan revealed a discrete low-density
change around the focal high density. Diffusion-weighted
images revealed a clearly demarcated high-signal intensity
lesion in similar area on T2-weighted and fluid-attenuated
inversion recovery sequences images, compatible with
infarcted tissues on the territory supplied by the lateral
lenticulostriate artery. His hemiparesis improved gradually,
and by post-trauma day 10 he was able to walk briefly
without assistance. He was discharged on foot at posttrauma day 14.
Discussion and conclusion Children with minor head
trauma who have normal findings on initial CT scan may
rarely have basal ganglionic infarction resulting from
arterial spasm or thromboembolism of the perforating
J. Y. Ahn : I. B. Han : Y. S. Chung
Department of Neurosurgery,
Pochon CHA Medical University,
Sungnam, South Korea
P. H. Yoon : S. H. Kim
Department of Diagnostic Radiology,
Pochon CHA Medical University,
Sungnam, South Korea

arteries. Hospital admission and careful observation should
be considered for patients with minor head injury and
persistent neurologic deficits despite normal CT findings.
Magnetic resonance study is valuable for the evaluation of
posttraumatic infarction, differentiating from hemorrhagic
diffuse axonal injuries.
Keywords Minor head injury . Stroke . Basal ganglia .
Lenticulostriate artery

Introduction
Stroke after minor head trauma, especially in the basal
ganglia, is a rare event. They are usually hemorrhagic
lesions, either small or large, and are usually a consequence
of shearing forces in moderate to severe head injury [1].
Occlusion of the main intracranial arteries due to blunt head
traumas has also been less frequently observed in patients
with minor head injuries, often without loss of consciousness [2–7]. Spasms, emboli from the proximal major artery,
dissecting aneurysm, and thrombus formation have all been
suggested as causes [2, 7, 8]. But our knowledge about
posttraumatic cerebral infarction due to occlusion of the
perforating artery is very limited. We recently encountered
a pediatric patient presenting with unilateral basal ganglionic infarction confined to the territory of the lateral
lenticulostriate artery after a minor head injury. The clinical
and radiological features are delineated and the literature is
reviewed.

Case report
J. Y. Ahn (*)
Department of Neurosurgery, Pundang CHA Hospital,
351, Yatap-dong, Pundang-gu,
Sungnam 463-712, South Korea
e-mail: jyahn@cha.ac.kr

A 4-year-old boy fell to the ground while playing seesaw
and incurred bruising to the head. Although the boy’s
sensorium was clear immediately after the impact, speech

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disturbance was noted approximately 2 h later. On
admission, he could open his eyes, but his speech was
indistinct and he could not answer questions. There were no
focal neurological signs including that of motor power of
the extremities and cranial nerve functions.
Plain skull X-ray results showed no fracture line.
Computed tomography (CT) scans 2 h after injury revealed
a focal punctate high density in the left basal ganglia, a not
clearly delineated and questionable finding (Fig. 1a). The
patient was admitted to the hospital for close observation.
Hemiparesis developed on the right limbs (upper, grade II;
lower, grade IV), so repeat CT scans were performed 8 h
after injury. Compared with the previous CT scans, discrete
low-density change is noted around the focal high density
(Fig. 1b). Magnetic resonance (MR) studies were performed as a matter of differentiation tool of hemorrhagic or
ischemic lesion. Fluid-attenuated inversion recovery
(FLAIR) sequences images demonstrated a focal highsignal intensity area in the central portion of the left basal
ganglia and overlying centrum semiovale (Fig. 2a). T2weighted gradient echo (GRE) sequences images showed
no definite hypointense lesion corresponding with highsignal lesion on T2-weighted image (Fig. 2b). Diffusionweighted images (DWI) revealed a clearly demarcated
high-signal intensity lesion in similar area on T2-weighted
and FLAIR sequences images, compatible with infarcted
tissues on the territory supplied by the lateral lenticulostriate artery (Fig. 2c). MR angiography showed no gross
abnormalities including that of the left middle cerebral
artery and internal carotid artery (Fig. 3). To exclude the
possibility of a genetic predisposition to thrombosis,
platelet count with peripheral blood smear examination,
erythrocyte sedimentation rate, liver function test, lipid
profile, and plasma homocysteine levels were evaluated, all
of which were normal. To exclude the embolic cause of the
infarct, echocardiography and carotid Doppler examination
were also performed, all of which were normal.
The patient was treated conservatively with osmotic
diuretic agent and dextran. His hemiparesis improved

Fig. 1 a An initial CT scan 2 h after injury reveals a focal punctate
high density in the left basal ganglia, not clearly delineated and
questionable finding. b In repeat CT scan 8 h after injury, discrete lowdensity change is noted around the focal high density

Childs Nerv Syst (2006) 22:1493–1496

gradually, and by post-trauma day 10 he was able to walk
briefly without assistance and to grasp a colored pencil.
Follow-up CT scans showed low-density lesion with
minimal mass effect. He was discharged on foot by posttrauma day 14. A follow-up examination 2 months after
discharge documented complete resolution of the neurologic deficits. One year after discharge, his neurological status
remains stable.

Discussion
Posttraumatic cerebral infarction is a relatively rare complication of head trauma, but its frequency, cause, and
influence on mortality are not well defined [5]. Mirvis et al.
[5] reported that posttraumatic infarction was demonstrated
in 25 (1.9%) of 1,332 patients who required brain CT for
trauma and posterior cerebral artery and that the anterior
and middle cerebral arteries were the most frequently
involved vessels. But our knowledge about posttraumatic
infarction due to occlusion of the perforating arteries is very
limited. The lenticulostriate, thalamoperforating, or choroidal arteries have been found to be occluded against the
skull base, resulting in infarction on basal ganglia after
head traumas [5, 9–11]. Vascular lesions in the basal
ganglia may be disclosed in patients with shearing injury
due to angular acceleration forces as in our case. In most
major arteries occlusion, spasm, emboli from the proximal
major arteries, dissection, and thrombus formation have all
been accused for occurrence of infarction [2, 7, 8]. The
compression and distortion of the brain secondary to brain
herniation and increased intracranial pressure may also
induce focal areas of ischemic necrosis [10, 12]. However,
the injury mechanism of the perforating arteries has not
been demonstrated perfectly. The suggestive mechanisms
are spasm or thromboembolism. The lateral perforating
branches of the middle cerebral artery follow a recurrent
course to reach their points of penetration in the anterior
perforating space; their angle of origin is very acute.
Furthermore, the more lateral the origin the more acute
the angle. Dharker et al. [9] thought that stretching and
distorting the angle of perforating branches lead to damage
to the vessel, e.g., by ‘spasm’, with a consequent decrease
in local blood flow. In our case, we could identify the
punctate high-density lesion in initial CT scans, which is
suggestive of thrombus in the lenticulostriate artery. The
possible mechanism of the thrombus formation could be
postulated such that the differential motion between the
brain and the skull can lead to acute acceleration and
deceleration at the time of a head injury, which compresses
the arterial wall and sets in motion the thrombotic process.
Most of the patients may suffer minor head injuries,
often without loss of consciousness [9]. Although a

Childs Nerv Syst (2006) 22:1493–1496

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Fig. 2 a Fluid-attenuated inversion recovery sequences axial image
demonstrates a focal high-signal intensity area in the central portion of
the left basal ganglia and overlying centrum semiovale. b T2-weighted
gradient echo sequences image shows no definite hypointense
lesion corresponding with high-signal lesion on T2-weighted image.

c Diffusion-weighted images reveal a clearly demarcated high-signal
intensity lesion in similar area on T2-weighted and FLAIR sequences
images, compatible with infarcted tissues on the territory supplied by
the lateral lenticulostriate artery

relatively small area is affected, contralateral hemiparesis
with fasciobrachial predominance is unavoidable. The
distinctive features include the immediate weakness that
occurred more frequently in an upper limb than a lower
limb after minor injury as in the present case. The
associated findings of dysarthria, epilepsy, athetosis, and
cognate and behavioral abnormalities are reported [13].
Recovery is usually not rapid or complete, but neurological
recovery is observed within a week in most patients [9].
Subsequent recanalization in almost all perforators effectively limited the infarcted areas to pallidus, caudate
nucleus, anterior limb of the internal capsule, and centrum
semiovale. Most patients experienced complete recovery
within 4 months as our patient.
Exclusion of a treatable lesion such as hemorrhagic
lesions is important but is often difficult in practice. In our
case, neither unconsciousness nor definite neurological

signs were present immediately after the trauma, and
hypodense lesions in the cerebral parenchyma did not
appear in the initial CT images. Delayed CT images could
visualize low-attenuation regions. Differential diagnoses
included cerebral infarction, edema, contusion, or demyelination. Studies using MRI indicate that low-signal
intensity regions in T1-weighted images and high-signal
intensity lesions in T2-weighted images are often seen in
well-defined arterial distributions. For the differentiation
from hemorrhagic diffuse axonal injury (DAI) lesions in the
chronic stage, GRE sequences are conversely useful
because they can detect susceptibility effects of hemoglobin
degradation. In our patient, GRE sequences images showed
no definite hypointense lesion corresponding with highsignal lesion on a T2-weighted image. These findings mean
that it is an infarcted lesion as confirmed with DWI/MRI,
not a hemorrhagic DAI lesion. DWI is more sensitive than
T1- and T2-weighted images for the evaluation of acute
infarction [14, 15].

Conclusions

Fig. 3 MR angiography result shows no gross abnormalities
including that of the left middle cerebral artery and internal carotid
artery

We present a case of posttraumatic infarction in the territory
supplied by the lateral lenticulostriate artery after a minor
head injury in a child. Children with minor head trauma
who have normal findings on initial CT scan may rarely
have basal ganglionic infarction resulting from arterial
spasm or thromboembolism of the perforating arteries.
Hospital admission and careful observation should be
considered for patients with minor head injury and
persistent neurologic deficits (despite normal CT findings).

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MR study is valuable for the evaluation of posttraumatic
infarction, differentiating from hemorrhagic DAI lesions.

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