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Acute ischemic stroke in a 19 month old following minor head trauma: case report and review of the literature.

Minor head trauma is a very rare cause of ischemic stroke in the pediatric population. We describe a nineteen month old patient who developed left hemiparesis and subsequently left facial palsy after a fall. MR! of the brain showed hypo densities in the basal ganglia, internal capsule and caudate nucleus consistent with stroke. Echocardiogram and MRA were normal. Hypercoaguable work up showed that the patient was a carrier for a single MTHFR gene. The patient was heated conservatively. On follow up two weeks later his facial palsy had resolved and strength in the extremities improved. Although a rare condition awareness about this is necessary as there can he considerable delay in its recognition.


Childhood stroke has an annual incidence of from 2-3 to 13/100,000. (1) It is an important cause of pediatric mortality and morbidity. Recent studies have shown a mortality rate of two to eleven percent and persistent neurological deficits were observed in sixty eight to seventy three percent of patients. (2) Although this disorder is being increasingly recognized owing to the advances in neuroimaging, there is still a considerable delay in its recognition due to lack of awareness and the vast number of stroke mimics which can occur in childhood. (1) Minor head trauma is a rare cause of childhood ischemic stroke and accounts for less than two percent of all the cases. (3)

We present the case of a 19 month old male child who developed an ischemic stroke secondary to minor head trauma.

Case description

A nineteen month old male child with no significant past medical history was brought to our emergency room with increased sleepiness and decreased use of his left upper and lower extremities. About a day prior to the admission the child fell down from a chair of about three feet in height. He cried immediately after the fall and had no reported loss of consciousness The next day the child developed a left hemiparesis and was brought to the emergency department. On neurological exam pupils and cranial nerves were intact; a left hemiparesis affecting the upper and lower extremities was noted. Reflexes were normal. CT scan of the head showed a hypodense area in the posterior limb of the right internal capsule. The child was admitted to the pediatric intensive care unit for serial neurologic exams. By the next day the child developed drooping of the left side of his face. The patient did not have any inability to close his eyes or raise his eyebrows. The diagnosis of right sided upper motor neuron facial palsy was made. A brain MRI with contrast was done which demonstrated an infarction of the right internal capsule, caudate nucleus and basal ganglia (figure 1) CT angiogram of the head was performed and showed no aneurysms or dissections. An echocardiogram was done which ruled out the heart as source of an embolus. A hypercoaguability work up revealed normal levels of factor V leiden, protein C, proteins S, antithrombin III, and homocystine. Genetic analysis revealed that the child was a carrier for a single MTHFR gene mutation. The child was treated conservatively and was discharged home with physical therapy three days after admission. On follow up two weeks later the facial paresis had resolved; there was an increase in gross motor movement in the left lower extremity but minimal improvement in left upper extremity.


Pediatric stroke consists of both ischemic stroke and hemorrhagic stroke. Ischemic stroke can be further classified into arterial ischemic stroke and sinus venous thrombosis. Alternatively they are also classified as perinatal or neonatal stroke (occurring between twenty eight weeks of gestation and twenty eight weeks after birth) and childhood stroke. The classification is important as the etiologies and management of each subtype is different. (4)

Childhood arterial ischemic stroke is defined as arterial ischemic stroke occurring between ages one month and eighteen years. (4) Risk factors of adult ischemic stroke such as hypertension and atherosclerosis are rare in children. Instead, childhood arterial ischemic stroke is associated with congenital heart disease, vascular anomalies, prothrombotic conditions, genetic or metabolic disease and head trauma. (2)

Striatocapsular infarction in children following minor head trauma is a rare occurrence, consisting of less than two percent of all childhood ischemic strokes. (3) A variety of factors are thought to be responsible. The anatomy of a child's brain is different from thaf of an adult. The lenticulostriate arteries are end branches of the middle cerebral arteries which supply the caudate, putamen and the internal capsule. In children these arteries arise at a more acute angle as compared to adults and follow a recurrent course before going into the anterior perforated substance. This creates a mobile segment between the two fixed segments (extraparenchymal and intraparenchymal) of the lenticulostriate arteries which is vulnerable to stretching and injury during head trauma. Moreover, the sphenoid bone is not completely developed in children, which allows for more movement of the brain during head trauma and may contribute to damage of the lenticulostriate arteries. (3,5) Stretching of these arteries can result in vasospasm and also in endothelial injury which may subsequently lead to thrombus formation. Maki et al described four patients with basal ganglia lesions following minor head trauma. The authors noted that if the stretching force was severe it resulted in rupture of the vessel wall but milder forces only gave rise to endothelial rupture. (6)

Varicella zoster can cause arteriopathy of the large proximal cerebral arteries. Shaffer et al suggested that infection with varicella zoster may sensitize the smaller arteries to vasospasm in children and may contribute in the development of stroke following minor head trauma. A rare condition characterized by massive cerebral edema and stroke due to mutation of a calcium channel gene CACNA1A has been reported. (3) Although it is likely that other genetic factors exist which increase the risk of developing a stroke following minor head trauma, our understanding of them has so far been limited. (5)

The diagnosis of a stroke in children is often delayed due to the rarity of the disorder as well as a number of stroke mimics occurring in childhood. Migraines, tumors, encephalitis, and seizures can all present with stroke like symptoms. (4) Gabis et al showed that the average time from symptom onset to seeking clinical attention was 28 5 hours and 35.7 hours before the diagnosis was made. (7)


The most common clinical manifestation of childhood arterial ischemic stroke is hemiparesis. Younger patients may present with decreased level of consciousness. MRI is the preferred modality of neuroimaging for diagnosing ischemic stroke. Further evaluation would include a MRA or angiography to rule out arteriopathy or dissections, echocardiogram to rule out cardiac anomalies and a hypercoaguability work up. The prognosis of childhood ischemic stroke due to minor head trauma is favorable. Landi et al have reported 9 cases al! of which showed clinical improvement at 13 months. (3)


Childhood arterial ischemic stroke is an important cause of pediatric mortality and morbidity. Patients suspected to have this condition should have emergent brain imaging done and a thorough search for the risk factors of stroke. Increased awareness of this condition is essential as studies have shown a considerable delay in diagnosis.


(1.) Braun KP, Kappelle LJ. Kirkham FJ, Deveber G. Diagnostic pitfalls in paediatricischaemic stroke.Dev Med Child Neurol. 2006; 48(12):985-90.

(2.) Bernard TJ, Goldenberg NA, ArmstrongWells J. Amlie-Lefond C, Fullerton HJ. Treatment of childhood arterial ischemic stroke. Ann Neurol. 2008; 63(6):679-96.

(3.) Landi A. Marotta N. Mancarella C, Marruzzo D, Salvati M, Delfini R. Basalganglia stroke due to mild head trauma in pediatric age clinical and therapeutic management; a case report and 10 year literature review. Hal J Pediatr 20116; 37:2.

(4.) Amlie-Lefond C, Sebire G, Fullerton HJ. Recent developments in childhood arterial ischaemic stroke Lancet Neurol. 2008; 7(5):425-35.

(5.) Shaffer L, Rich PM, Pohl KR, Ganesan V Can mild head injury cause ischaemic stroke? Arch DIs Child. 2003; 88(3):2S7-9.

(6.) Maki Y, Akimoto H, Enmoto T. Injuries of basal ganglia following head trauma in children. Childs Brain 1980; 113-23

(7.) Gabis LV. Yangala R, Lenn NJ Time lag to diagnosis of stroke in children. Pediatrics. 2002; 110(5):924-8.

Vishnu Garla, MD Department oi Pediatrics, Marshal! University Joan C. Edwards School of Medicine

Eduardo Pino, MD Department of Pediatrics, Marshall University Joan C Edwards School of Medicine

Richard Coulon, MD Department of Neurology, Marshall University Joan C Edwards School of Medicine

Rebecca Wolfer, MD Department of Surgery, Marshall University Joan C. Edwards School of Medicine.

Corresponding Author: Vishnu Garla, MD, Marshall University, JCESOM, 1600 Medical Center Drive, Huntington, WV 25701;
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Author:Garla, Vishnu; Pino, Eduardo; Coulon, Richard; Wolfer, Rebecca
Publication:West Virginia Medical Journal
Article Type:Report
Geographic Code:1USA
Date:May 1, 2014
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