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      Polymicrogyria and Congenital Parvovirus B19 Infection

      case-report
      , M.D., Ph.D. 1 , , M.D. 1 , 2 , , M.D. 1 , 2
      AJP Reports
      Thieme Medical Publishers
      Parvovirus, polymicrogyria, teratogen, congenital infection

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          Abstract

          Fetal parvovirus B19 infection causes anemia, hydrops, and pregnancy loss but is generally not considered teratogenic. Nevertheless, disturbances of neuronal migration have been described with congenital parvovirus infection. We evaluated a term infant with congenital parvovirus disease and polymicrogyria. We compared this case with four other reports of central nervous system disease after birth to parvovirus-infected mothers. After an extensive diagnostic evaluation, this infant was found to have congenital parvovirus disease with severe anemia and nonimmune hydrops as well as extensive polymicrogyria. Although rare, this report and literature review suggest that parvovirus B19 has the potential to disrupt normal neurodevelopment. We suggest that infants with severe congenital parvovirus infection have close developmental surveillance and if symptomatic undergo neuroimaging to assess for disorders of neuromigration.

          Most cited references13

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          Parvovirus B19.

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            Neuronal migration disorders.

            Lissencephaly-pachygyria-severe band heterotopia are diffuse neuronal migration disorders (NMDs) causing severe, global neurological impairment. Abnormalities of the LIS1, DCX, ARX, TUBA1A and RELN genes have been associated with these malformations. NMDs only affecting subsets of neurons, such as mild subcortical band heterotopia and periventricular heterotopia, cause neurological and cognitive impairment that vary from severe to mild deficits. They have been associated with abnormalities of the DCX, FLN1A, and ARFGEF2 genes. Polymicrogyria results from abnormal late cortical organization and is inconstantly associated with abnormal neuronal migration. Localized polymicrogyria has been associated with anatomo-specific deficits, including disorders of language and higher cognition. Polymicrogyria is genetically heterogeneous and only in a small minority of patients a definite genetic cause has been identified. Mutations of the GPR56 and SRPX2 genes have been related to isolated polymicrogyria. Focal migration abnormalities associated with abnormal cell types, such as focal cortical dysplasia, are highly epileptogenic and variably influence the functioning of the affected cortex. The functional consequences of abnormal neuronal migration are still poorly understood. Conservation of function in the malformed cortex, its atypical representation, and relocation outside the malformed area are all possible. Localization of function based on anatomic landmarks may not be reliable. Copyright 2009 Elsevier Inc. All rights reserved.
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              Clinical and imaging heterogeneity of polymicrogyria: a study of 328 patients.

              Polymicrogyria is one of the most common malformations of cortical development and is associated with a variety of clinical sequelae including epilepsy, intellectual disability, motor dysfunction and speech disturbance. It has heterogeneous clinical manifestations and imaging patterns, yet large cohort data defining the clinical and imaging spectrum and the relative frequencies of each subtype are lacking. The aims of this study were to determine the types and relative frequencies of different polymicrogyria patterns, define the spectrum of their clinical and imaging features and assess for clinical/imaging correlations. We studied the imaging features of 328 patients referred from six centres, with detailed clinical data available for 183 patients. The ascertainment base was wide, including referral from paediatricians, geneticists and neurologists. The main patterns of polymicrogyria were perisylvian (61%), generalized (13%), frontal (5%) and parasagittal parieto-occipital (3%), and in 11% there was associated periventricular grey matter heterotopia. Each of the above patterns was further divided into subtypes based on distinguishing imaging characteristics. The remaining 7% were comprised of a number of rare patterns, many not described previously. The most common clinical sequelae were epileptic seizures (78%), global developmental delay (70%), spasticity (51%) and microcephaly (50%). Many patients presented with neurological or developmental abnormalities prior to the onset of epilepsy. Patients with more extensive patterns of polymicrogyria presented at an earlier age and with more severe sequelae than those with restricted or unilateral forms. The median age at presentation for the entire cohort was 4 months with 38% presenting in either the antenatal or neonatal periods. There were no significant differences between the prevalence of epilepsy for each polymicrogyria pattern, however patients with generalized and bilateral forms had a lower age at seizure onset. There was significant skewing towards males with a ratio of 3:2. This study expands our understanding of the spectrum of clinical and imaging features of polymicrogyria. Progression from describing imaging patterns to defining anatomoclinical syndromes will improve the accuracy of prognostic counselling and will aid identification of the aetiologies of polymicrogyria, including genetic causes.
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                Author and article information

                Journal
                AJP Rep
                AJP Rep
                AJP Reports
                Thieme Medical Publishers (333 Seventh Avenue, New York, NY 10001, USA. )
                2157-6998
                2157-7005
                02 August 2011
                December 2011
                : 1
                : 2
                : 105-110
                Affiliations
                [1 ]Department of Pediatrics, Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
                [2 ]Division of Neonatology, Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
                Author notes
                Address for correspondence and reprint requests Jörn-Hendrik Weitkamp, M.D. 2215 B Garland Ave, 1125 MRB IV/Light Hall Nashville, TN 37232-0656 hendrik.weitkamp@ 123456vanderbilt.edu
                Article
                01105
                10.1055/s-0031-1285984
                3653533
                23705097
                8bea73a9-1008-4d09-9958-f4e638d295ef
                © Thieme Medical Publishers
                History
                : 21 April 2011
                : 20 June 2011
                Categories
                Article

                parvovirus,polymicrogyria,teratogen,congenital infection

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