Reply to Letter on “Stroke After Minor Head Trauma in Infants and Young Children With Basal Ganglia Calcification: A Lenticulostriate Vasculopathy?”

We thank the authors Chang and Chiu for their interest in our article. ¹ Basal ganglia stroke after minor head trauma in infants and young children has been known for long and is considered to be related to the anatomical peculiarities of the origin and the course of lenticulostriate arteries and the greater mobility of the brain at the skull base during infancy. Both these factors render lenticulostriate arteries vulnerable to injury and vasospasm/thrombosis following head injury. ² With the recent findings of basal ganglia calcification / calcified lenticulostriate arteries on computed tomographic (CT) imaging in infants with basal ganglia stroke after minor head trauma, the emphasis has now rightly shifted from the anatomical peculiarities to the lenticulostriate vasculopathy as the pathologic substrate for stroke. The mineralized arteries become rigid and, therefore, are easily injured following minor head trauma. ³

Lenticulostriate vasculopathy, as an ultrasonographically defined entity, has gained recent emphasis in neonatal and radiologic literature. Initially described in association with congenital infections and trisomy 13, lenticulostriate vasculopathy is now considered to be a nonspecific marker of perinatal and/or post-natal brain injury, as it is associated with a wide variety of etiologies including intra- and extrauterine infections, metabolic abnormalities such as hypoglycemia, hypoxic-ischemic encephalopathy, chromosomal aberrations, inborn errors of metabolism, maternal alcohol or drug abuse, and prematurity. ^4,5 Neurodevelopmental outcome of these neonatal disorders is determined by underlying pathology rather than the presence of lenticulostriate vasculopathy. To our knowledge, lenticulostriate vasculopathy associated with these conditions has never been reported to predispose infants to basal ganglia stroke after minor head trauma. An idiopathic or isolated form of lenticulostriate vasculopathy, in the absence of neonatal conditions mentioned above, has also been described and is associated with normal neurodevelopmental outcome. ⁶ Because the infants who sustain basal ganglia stroke after minor head trauma have no history of prenatal or perinatal adverse events, and are developmentally and neurologically normal at the time of stroke, ^3,7,8 idiopathic lenticulostriate vasculopathy can be presumed. With the current state of knowledge, it is, however, difficult to surmise that lenticulostriate calcification represents a more severe pathologic condition. Not only basal ganglia stroke following minor head trauma has been described in infants in the absence of basal ganglia calcification on CT, ⁹ incidental basal ganglia calcification has been identified in 1% of the head CTs done for unrelated indications. ³ At best, mineralization represents an end-stage pathology of lenticulostriate vasculopathy. ⁷

We agree with the Chang and Chui about the role of cranial ultrasonography in emergency care in the evaluation of basal ganglia stroke after minor head trauma in infants with anterior fontanel window. Cranial ultrasound clearly offers advantages over CT but few cranial ultrasonographic studies are available in the setting of basal ganglia stroke after minor head trauma to make such recommendations. CT is still needed in cases beyond 18 months of age when the anterior fontanel has closed. Also, CT imaging is necessary to follow the course of basal ganglia calcification. Brain magnetic resonance imaging (MRI), anyway, is indispensable in stroke evaluation. As of now, there is probably a role for each of these modalities in the evaluation of basal ganglia stroke in infants after minor head trauma. In future, novel MRI and magnetic resonance angiographic techniques might obviate the need for cranial ultrasonography and CT imaging.

Infections may play a role in the causation of basal ganglia stroke after minor head trauma but in the absence of robust clinical and laboratory evidence, such an association would remain conjectural. As far as cytomegalovirus infection is concerned, only 1 study has identified cytomegalovirus infection as a risk factor for stroke on the basis of presence of cytomegalovirus DNA in plasma or urine. From the study, it is difficult to know the timing (pre- or postnatal) and nature (chronic persistent but inactive or a chronically active) of infection. ¹⁰ Further studies are needed to clarify the role of cytomegalovirus in the causation of basal ganglia stroke in infants after minor head trauma.

To summarize, although basal ganglia stroke after minor head trauma is well recognized, its association with lenticulostriate vasculopathy has only recently been described. Risk factors for the isolated or idiopathic lenticulostriate vasculopathy underlying stroke predisposition after minor head trauma are still not known and need to be the focus of future research.