Minor head injury as cause and co-factor in the aetiology of stroke in childhood: a report of eight cases
- 1Department of Paediatrics, Paediatric Neurology, Johann Wolfgang Goethe University, Frankfurt/Main, Germany
- 2Department of Paediatrics, Paediatric Haematology and Oncology (Coagulation Disorders), Johann Wolfgang Goethe University
- 3Department of Paediatrics, Paediatric Neurology, St Hedwig Hospital for Sick Children, University Regensburg, Germany
- Correspondence to: Dr Matthias Kieslich, Department of Paediatrics, Paediatric Neurology, Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, 60590 Frankfurt/Main, Germany; matthias.kieslich{at}kgu.de
- Received 31 October 2001
- Accepted 12 March 2002
- Revised 11 March 2002
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.
