ILLUSTRATIVE CASE

A Case of Lenticulostriate Stroke Due to Minor Closed
Head Injury in a 2-Year-Old Child
Role of Mineralizing Angiopathy
Emin Fidan, MD,* Dana D. Cummings, MD, PhD,† and Mioara D. Manole, MD‡

Objective: Cerebral infarction due to minor head injury is rare. Mineralizing angiopathy is considered a predisposing factor for lenticulostriate
stroke after minor closed head injury. This entity is characterized by infarction of the basal ganglia and most often occurs in young children, from infancy to 2 years of age. Symptoms usually occur immediately after the injury.
Methods and Results: We present the case of a previously healthy
2-year-old female child presenting with right facial hemiparesis and aphasia, along with right arm and leg weakness that occurred immediately after
a fall from the couch onto a carpeted floor. A brain computed tomography
scan revealed small and linear calcifications of the basal ganglia and
subcortical frontoparietal area, in the absence of signs of intracranial
hemorrhage. Brain magnetic resonance imaging with stroke protocol revealed restriction of water diffusion in the left basal ganglia on
diffusion-weighted imaging sequences as well as apparent diffusion coefficient sequences, suggesting an acute infarct of the left basal ganglia
within the distribution of the lenticulostriate vessels. The patient was
treated with aspirin and conservative management and had gradual improvement over the next few days, with full recovery of the aphasia, facial
nerve function, and arm and leg mobility, within 2 months.
Conclusions: Some infants can present with the onset of stroke-like
symptoms after minor head injuries. Presence of linear calcifications of
the basal ganglia noticed on brain computed tomography in many of these
patients suggests that mineralizing angiopathy may be a predisposing
factor for lenticulostriate stroke after minor closed head injury in infants. Brain magnetic resonance imaging to further delineate possible
cerebral infarction is indicated.
Key Words: concussion, mineralizing angiopathy, stroke
(Pediatr Emer Care 2017;00: 00–00)

E

ach year, almost half a million children experience traumatic
brain injury in the United States, with 80% having mild closed
head injury (CHI).1,2 Most of the patients with mild CHI have an
uneventful course.3 A rare complication of mild pediatric CHI occurring in some infants is infarction of the basal ganglia.4–6 Mineralizing angiopathy of lenticulostriate arteries is postulated to
be a risk factor for infarction of the basal ganglia after mild
CHI.6 We present a case of a 2-year-old female child who developed hemiparesis just minutes after a mild CHI. We describe the
clinical and radiological features of this case and review the predisposing factors, pathophysiology, and clinical evaluation of
lenticulostriate strokes occurring after CHI.
From the Divisions of *Pediatric Critical Care Medicine, †Child Neurology,
and ‡Pediatric Emergency Medicine, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, Pittsburgh, PA.
Disclosure: The authors declare no conflict of interest.
Reprints: Mioara D. Manole, MD, Division of Pediatric Emergency Medicine,
Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center,
4401 Penn Ave, Pittsburgh, PA 15224 (e‐mail: manomd@upmc.edu).
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ISSN: 0749-5161

Pediatric Emergency Care • Volume 00, Number 00, Month 2017

CASE
A previously healthy 2-year-old female child presented to
our emergency department for evaluation of acute facial droop, inability to speak, and gait abnormality, which developed within 3 to
5 minutes after a fall. Parents reported that the patient fell off a
couch onto a carpeted floor, hitting her occipital area. She had
no loss of consciousness and no emesis; she cried immediately.
Shortly after the fall, the parents noticed that the patient had a
facial droop and was less active than usual; she had a language
disturbance consistent with aphasia; she communicated by crying
and grunting. She continued to ambulate and was active. She was
initially evaluated at an urgent care center, where she was assessed
as being a neurologically intact 2-year-old child; however, she was
transferred to our tertiary care center at mother's request. Initial
physical examination at our hospital 90 minutes after the event
showed an awake and alert patient. She was able to follow commands, but she was not communicating verbally. Neurological
examination was positive for right-sided facial weakness limited
to the lower half of the face, associated with slight drooling. Cranial nerve function was otherwise intact. Right hemiparesis was
noted. Strength was 3/5, tone was decreased, but muscle mass
was normal. Deep tendon reflexes were absent in the right upper
and lower extremity, but they were normal in the left upper and
lower extremity. Plantar reflexes were absent on the right side
and downgoing on the left side. Sensation was grossly intact.
Her gait was wide based, hemiparetic, but without ataxia.
A computed tomography (CT) scan of the brain obtained
in the emergency department revealed small bilateral calcifications of the basal ganglia (Fig. 1A), as well as small calcium
deposition over the left frontoparietal area, without signs of intracranial hemorrhage or any obvious hypoattenuation suggesting
ischemic infarct. Brain magnetic resonance imaging (MRI) with
stroke protocol revealed restriction of diffusion in the left basal
ganglia with apparent diffusion coefficient correlate, suggesting
an acute infarct in the area of the basal ganglia within the
distribution of the lenticulostriate vessels (Fig. 1B). Magnetic
resonance spectroscopy demonstrated elevated lactate in the
left basal ganglia, without definite evidence of elevation of
lactate in the contralateral basal ganglia. Laboratory evaluation
obtained to exclude hematological, metabolic, or infectious causes
was normal, including the following: complete blood count, comprehensive metabolic panel, inflammatory markers (erythrocyte
sedimentation rate, C-reactive protein, antinuclear antibody, rheumatoid factor, anti-neutrophil cytoplasmic antibody), lactate, pyruvate, iron studies, thyroid studies, Lyme screen, serum amino
acids, creatine phosphokinase, urine organic acids, hypercoagulable
profile, and lipoprotein A panels. Echocardiography was normal.
The patient was diagnosed with lenticulostriate stroke precipitated by mild CHI and was admitted to the intensive care unit
for monitoring. Aspirin was started in the emergency department
at a dose of 5 mg/kg per day. The right-sided hemiparesis improved during the following 48 hours. All symptoms gradually
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Pediatric Emergency Care • Volume 00, Number 00, Month 2017

Fidan et al

FIGURE 1. Brain CT and MRI images of a 2-year-old patient with signs and symptoms of stroke after a minor CHI. A, The brain CT image shows
calcifications of the basal ganglia suggesting mineralizing angiopathy (solid arrows). B, The brain MRI image shows an infarct in the
distribution of the lenticulostriate artery (open arrow).

improved over the next weeks, and the patient had full recovery of
aphasia, facial nerve function, and upper and lower extremity
function within 2 months.

DISCUSSION
A very small subset of children with mild CHI can present
with signs and symptoms of cerebral infarction. A thorough neurological examination will identify the infants and children with
abnormal neurological examination who need further evaluation
and imaging. Mineralizing angiopathy is believed to be a predisposing factor for lenticulostriate stroke occurring after CHI in infants and toddlers.
Lenticulostriate stroke has been previously reported in infants and constitutes less than 2% of all childhood ischemic
strokes.4 Despite rarity of lenticulostriate stroke, there have been
few case reports and 2 case series suggesting an association of
mild CHI with lenticulostriate stroke, especially in infants younger than 2 years.4–13 Recently, Yang et al5 described a series of
16 infants who developed cerebral infarction after mild CHI. Similar to our patient, 10 of the 16 patients had basal ganglia calcifications detected on brain CT. In addition, lenticulostriate artery
mineralization was observed in a series of 23 infants with basal
ganglia ischemic stroke after mild CHI. The authors describe the
following characteristics of lenticulostriate stroke after CHI:
(i) age 6 to 24 months, previously healthy patient; (ii) neurological
deficits of rapid onset, minutes to hours after a mild CHI; (iii)
hemiparesis on the affected side; (iv) bilateral linear mineralization along lenticulostriate arteries on brain CT; and (v) good
short-term and long-term outcome, with the exception of patients
with recurrent stroke.6
Several mechanisms are postulated for lenticulostriate stroke
occurring after mild CHI. Vasospasm or thromboembolism of the
lenticulostriate artery due to rapid brain displacement during the
traumatic impact is one proposed mechanism.14 The lenticulostriate
arteries, responsible for the flow to the basal ganglia, are end arteries originating from the initial segment of middle cerebral artery.15
These vessels originate at an acute angle from the middle cerebral artery, and in infants and children, the angle is more acute.
Stretching and distorting of the arteries during trauma may lead
to vasospasm, with consequent decrease in regional blood flow.14,16,17
Another anatomical age variation is at the level of the sphenoid
bone, which is not fully developed in children, possibly predisposing

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this age group to a higher risk of stretch injury secondary to increased brain mobility.18 Supporting this hypothesis, in one large
case series, patients with stroke were 36 more times likely to have
had head trauma in the week before the stroke.19 In addition, mineralizing angiopathy represents another predisposing factor for
lenticulostriate stroke after a mild CHI in the pediatric population.
Mineralizing angiopathy can be idiopathic or secondary to infection such as cytomegalovirus, echovirus, Epstein-Barr virus, and
mycoplasma.5 Mineralizing angiopathy might result in more rigid
vessels and increased sensitivity to stretch injury, with vascular
maturation occurring as the child ages, mineralizing angiopathy
might regress so that the risk of stroke by this mechanism would
decline in older children.20
Pediatric patients with lenticulostriate stroke generally have
onset of symptoms within an hour after the injury.4–6,9–14 A thorough neurological examination in the emergency department will
identify these abnormalities. Brain imaging is indicated for the
acute evaluation of children with focal neurological deficits after
mild CHI.21 Recent studies highlight the higher diagnostic ability
of thin-section spiral CTwith multiplanar reconstructions as an alternative choice to standard CT5,6; however, in young children,
there is a concern of increased radiation administered using the
thin-section spiral CT. Magnetic resonance imaging can further
delineate the ischemic injury; however, if head CT is not obtained,
the pathological entity of mineralizing angiopathy might not be
recognized. Exclusion of other possible etiologies of stroke in
children should be performed using hematological, metabolic,
cardiac, and infection investigations.
In conclusion, although most infants presenting with CHI
will present with headache, nausea, vomiting, or altered consciousness, a few infants will present with focal hemiparesis or
other acute stroke deficits. Basal ganglia infarction after minor
CHI in infants with mineralizing angiopathy requires a high index
of suspicion and thorough neurological examination. Imaging including brain CT to detect calcified vessels and MRI to detect
acute cytotoxic edema can confirm the suspected diagnosis.
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Pediatric Emergency Care • Volume 00, Number 00, Month 2017

Stroke after Minor Closed Head Injury

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