Congenital cytomegalovirus (CMV) infection is the most common transplacentary transmitted viral infection, affecting 1% live born neonates but clinically symptomatic in only 10%. Both symptomatic and asymptomatic infected neonates may develop a wide range of neurodevelopmental disorders, the most severe being sensorineuronal hearing loss, cerebral palsy (CP), mental retardation (MR) and epilepsy. We present 6 children suffering cerebral palsy and their magnetic resonance/computer tomography findings in the examined group of 39 children in total with proven congenital CMV infection.Out of these 39 children, 14 were symptomatic at neonatal age. The remaining 25 asymptomatic infants were referred after neonatal age (1,5-18 months), for deviant neurological signs, accompanied by microcephaly and/or gastrointestinal problems.Two children were sent due to deafness. In all children examined CMV infection was proven by specific serology, PCR for CMV DNA and /or isolation of virus in the urine. All 39 children had prospective neurodevelopmental follow up for 2-11 years, undergoing repeated neurological, hearing tests, ophthalmologic, developmental assessment including speech and behaviour. Classification of CP was done according to the Surveillance of Cerebral Palsy in Europe (SCPE) proposal, including functional grading: the gross motor function classification system (GMFCS) and bimanual fine motor function (BFMF) criteria. Out of 14 symptomatic children, 5 were multihandicapped . All of them were microcephalic. One out of 25 asymptomatic children with CP was multihandicapped and microcephalic. Out of 6 children with cerebral palsy 4 have dyskinetic CP, two of them GMFCS and BFMF grade V, and two GMFCS IV and BFMF IV. Two children have bilateral spastic CP, GMFCS III and BFMF III. Cranial MRI/CT was performed in all 6 children with CP. In two multicandicaped children MRI demonstrated complex brain malformations: polymicrogyria, hypoplastic cerebellum, callosal hypoplasia. The other two multihandicapped children have multifocal leukoencephalopathy with temporal cysts. One multihandicapped child underwent cranial CT showing pacygyria, paraventricular cyst and calcification. In one asymptomatic multihandicapped child repeated MRI demonstrated brain atrophy, hypomyelination and calosal hypoplasia. Conclusion: 6/39 children examined with congenital CMV infection have CP accompanied by additional severe neurodevelopmental disorders. 5/39 children with CP had symptomatic CMV infection. Cranial MRI and CT demonstrated various brain abnormalities: two children have complex brain malformations (severe cortical dysgenesis, cerebellar hypoplasia, callosal hypoplasia), two widespread leukoencephalopathy with temporal cysts, and one diffuse brain atrophy. The spectrum of brain abnormalities in children with CP is related to the onset of congenital infection .
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