AIM: The etiology of cerebrovascular disease in the paediatric population, remains unknown in up to 40% of the cases ("idiopathic"), but recent advances could improve this percentage. We devised a comprehensive study protocol for such investigation aimed at the identification of potentially modifiable risk factors for paediatric stroke. PATIENTS AND METHODS: From the 141 patients initially registered in our data base for stroke population (from January 1984 until December 1995), we invited all the patients with idiopathic cerebrovascular disease to complete the study protocol. New cases appeared from January 1996 until July 1999 were also included. RESULTS: A total of 68 cases were identified. We found an etiology in 38% and in 76% of the cases we found at least one risk factor for stroke. Mild hyperhomocysteinemia was the most frequent risk factor identified (36% of patients versus 5% of controls), one of them an infant with fatal haemorrhagic infarct with classic homocystinuria. 31% of the patients had thrombotic risk factors (protein S, protein C, antithrombine III deficiency, factor V Leiden, etc). 17.6% had unspecific febrile illness at the time of the cerebral infarction and 11.6% had minor head injuries before the stroke. CONCLUSIONS: The use of the protocol improves the identification of potentially modifiable risk factors for stroke in childhood and may serve as a practical guideline for clinicians. The stroke protocol is as important as management strategies for acute stroke or for recurrence prevention, currently under consideration in the adult population.
AIM: The etiology of cerebrovascular disease in the paediatric population, remains unknown in up to 40% of the cases ("idiopathic"), but recent advances could improve this percentage. We devised a comprehensive study protocol for such investigation aimed at the identification of potentially modifiable risk factors for paediatric stroke. PATIENTS AND METHODS: From the 141 patients initially registered in our data base for stroke population (from January 1984 until December 1995), we invited all the patients with idiopathic cerebrovascular disease to complete the study protocol. New cases appeared from January 1996 until July 1999 were also included. RESULTS: A total of 68 cases were identified. We found an etiology in 38% and in 76% of the cases we found at least one risk factor for stroke. Mild hyperhomocysteinemia was the most frequent risk factor identified (36% of patients versus 5% of controls), one of them an infant with fatal haemorrhagic infarct with classic homocystinuria. 31% of the patients had thrombotic risk factors (protein S, protein C, antithrombine III deficiency, factor V Leiden, etc). 17.6% had unspecific febrile illness at the time of the cerebral infarction and 11.6% had minor head injuries before the stroke. CONCLUSIONS: The use of the protocol improves the identification of potentially modifiable risk factors for stroke in childhood and may serve as a practical guideline for clinicians. The stroke protocol is as important as management strategies for acute stroke or for recurrence prevention, currently under consideration in the adult population.