Minor head injury as cause and co-factor in the aetiology of stroke in childhood: a report of eight cases

Abstract

Background: Traumatic stroke usually occurs after dissection of large extracranial or intracranial vessels, leading to disseminated cerebral embolism. Stretching and distorting forces in cerebral intraparenchymal end arteries can cause intimal lesions followed by an occluding thrombus. Objective: To investigate the importance of traumatic endothelial lesions in intraparenchymal end arteries after minor head injuries. Methods: The cases of eight children are reported. They were aged between two and seven years (mean 6.2 years), and they developed significant neurological deficits at 15 minutes to 72 hours (mean 16.3 hours) after minor head injuries. Results: The the patients all had hemiparesis combined with other signs, including central facial paralysis, dysphasia, dysphagia, and extrapyramidal signs. Computed tomography or magnetic resonance imaging showed cerebral infarctions affecting branches of the middle cerebral artery (n = 3), anterior cerebral artery (n = 1), posterior cerebral artery (n = 1), and basilar artery (n = 3). These lesions affected the basal ganglia, the internal capsule, and the brain stem. Neither heart disease nor dissections of large vessels were present. Two children had prothrombotic risk factors (an increase in lipoprotein (a) and a factor V Leiden mutation). The follow up period was between three months and 13 years (mean 3.9 years). Outcome was classified according to the Glasgow outcome scale as moderate disability (n = 4), severe disability (n = 2), non-disabling sequelae (n = 1), and total recovery (n = 1). Conclusions: Minor head injuries can be cause and co-factor in the aetiology of stroke. The frequency of this may be underestimated, and detailed medical history of the days before stroke manifestation may identify more traumatic events, especially in the group of so called "idiopathic" strokes.

Management of Stroke in Infants and Children

“…Even among patients with a given disorder, it is often the severity of the bleeding tendency rather than the specific defect that determines the risk of ICH. In the absence of trauma, the risk of ICH from thrombocytopenia is low as long as the platelet count remains above 20 000 mm 3 . Similarly, more severe coagulation deficiencies are more likely to cause ICH than milder deficiencies independently of the specific deficiency.…”

“…Heart disease and chronic anemia (including SCD and ␤-thalassemia) also are risk factors for CVST, but the list of associated conditions ranges from head and neck infections to systemic conditions such as inflammatory bowel disease and autoimmune disorders. 2 Head trauma appears to be a trigger for arterial stroke 1,3 and dehydration for venous stroke, 4 -6 whereas infections, including varicella, meningitis, tonsillitis, and otitis media, 1 and anemia, leukocytosis, and prothrombotic disorders are probably risk factors for both. 1,[5][6][7] It is increasingly evident that many children have multiple risk factors that together determine the risk of stroke or stroke recurrence.…”

“…119,120 The significance of ischemic events in children usually proves more difficult to diagnose because of the patient's age and limited communication skills, leading to delayed recognition of the underlying moyamoya condition. 3 Associated Conditions. Although the cause and pathogenesis of moyamoya disease are poorly understood, genetic factors play a major role.…”

“…Basal ganglia infarction after relatively trivial trauma may be secondary to stretching of the deep arterial perforators. 3 Hanging or strangulation may result in injury to cervical arteries or veins. The carotid artery can be stretched over the transverse process of C2 or compressed by direct pressure over the transverse process of C6.…”

Posttraumatic Cerebral infarction: A Rare Complication in a pediatric patient after mild head injury

“…The relative delay of symptoms in most of the cases can be explained on the basis of thrombus generation and immediate onset of symtoms can be explained mechanical disruption of blood or spasm. [3] Early diagnosis and treatment are not possible because the post-traumatic ischemic stroke in a child is relatively rare; many of the patients do not lose consciousness and disease symptoms may begin late. In our case, neurological symptoms began 6 hours later and the first neuroimaging study was performed at that time.…”