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  • Title: [Brain lesions of perinatal and late prenatal origin in a neuropediatric context].
    Author: Garaizar C, Prats-Viñas JM.
    Journal: Rev Neurol; 1998 Jun; 26(154):934-50. PubMed ID: 9658464.
    Abstract:
    INTRODUCTION: The obstetric and neonatal technological advances have changed the frequency and syndromic classification of perinatal brain lesions. OBJECTIVE: To study all prevalent patients during 1996, with perinatal or late intrauterine brain lesions, in the outpatient neuropediatric clinic at our hospital. METHODS: Selection of patients according to neuroimaging findings, and/or neurological sequela with documented perinatal antecedent. EXCLUSION CRITERIA: a normal MRI, brain lesions of doubtful origin, or uncertain sequela with normal CT or echography studies. Descriptive study, and also analytical, using logistic regression to study the relationship between antecedents and sequela. RESULTS: A total of 111 patients with: brain lesions due to hypoxic-ischemic encephalopathy (22 cases), lesions due to prematurity (29), late intrauterine infection or neonatal meningitis as the only cause of fixed neurological impairment (12), unexpected vascular brain lesions during the neonatal period (11), late intrauterine brain lesions (37). The neurological sequela observed were: cerebral palsy (68%), epilepsy (47%), mental retardation (45%), learning disorders in (34%) of those of school age and free from mental retardation, strabism (26%), microcephaly (19%), visual impairment (14%), hyperkinesis (10%). The neuroimaging findings were: focal lesions (45%), hydrocephaly (28%), intraventricular haemorrhage (22%), white matter lesions (24%), venous thrombosis (2%). The multivariable analysis showed, as the most noticeable finding, the relationship between the antecedent of mechanical ventilation and late development of hyperkinesis (OR: 10), in this sample of patients with severe sequela. Three patients should be noted: a case of late-onset dystonia secondary to a late intrauterine brain lesion, a child with exclusively cerebellar symptoms due to a destructive cerebellar lesion of prenatal onset, and a patient with an acquired perinatal biopercular lesion and pseudobulbar palsy as the only long-term sequelae.
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