1. Cans C. {{Pervasive developmental disorders in individuals with cerebral palsy}}. {Dev Med Child Neurol};2009 (Apr);51(4):254-255.
2. d’Orsi G, Demaio V, Minervini MG. {{Myoclonic status misdiagnosed as movement disorders in rett syndrome: a video-polygraphic study}}. {Epilepsy Behav};2009 (Mar 28)
Myoclonic jerks and myoclonic status (MS) were sometimes difficult to distinguish clinically from movement disorders such as hand stereotypies, tremor and dystonia in Rett syndrome. We described a rare and complete video-polygraphic study of a girl with Rett syndrome (MECP2 mutation) and MS misdiagnosed as movement disorders and disclosed after video-polygraphic recordings. Corresponding to closely recurring activity of diffuse spike and polispikes-wave-type paroxysms, rhythmic and, especially, arrhythmic myoclonias, usually asymmetrical and asynchronous, mainly involving right muscle deltoid and rarely followed by an inhibitory phenomenon, appeared. The MS improved and, most importantly, disappeared after the use of Levetiracetam, with an evident antimyoclonic efficacy and a marked improvement of daily life for the patient and her care-givers. The difficulty to differentiate some typical non-epileptic behavioural features and movement disorders of Rett patients from seizures can be overcome using prolonged video-polygraphic recordings.
3. Kilincaslan A, Mukaddes NM. {{Pervasive developmental disorders in individuals with cerebral palsy}}. {Dev Med Child Neurol};2009 (Apr);51(4):289-294.
The aim of the present study was to describe the prevalence and associated factors of pervasive developmental disorders (PDD), including autistic disorder and PDD not otherwise specified (NOS), in a clinical sample of 126 children and adolescents (75 males, 51 females; age range 4-18y, mean 8y 8mo, SD 3y 8mo) with tetraplegic, hemiplegic, diplegic, dyskinetic, or mixed types of cerebral palsy (CP); 28% could not crawl or walk even with support, 29% could move with support, and 43% walked independently. Participants were examined for PDD in two stages. In the first stage, probable participants were determined by direct observation, Autism Behavior Checklist score, and medical reports. In the second stage, those with ‘probable’ symptoms underwent psychiatric examination and their autistic symptoms were scored on the Childhood Autism Rating Scale. The final diagnosis of autistic disorder or PDD-NOS was given according to DSM-IV criteria. Fourteen (11%) and five (4%) of the participants met the criteria for autistic disorder and PDD-NOS respectively. Children with CP and PDD differed from those without PDD in terms of type of CP (p=0.02), presence of epilepsy (p<0.001), intellectual level (p<0.001), and level of speech (p<0.001). PDD was more common in children with tetraplegic, mixed, and hemiplegic CP, and in children with epilepsy, learning disability, and low level of speech. The findings corroborate the notion that CP is a complex disorder, often associated with additional impairments. PDD is not rare in CP and should be considered in patients with comorbid conditions such as epilepsy, learning disability, and language delay and in the presence of tetraplegic, mixed, and hemiplegic CP types.
4. Koyama T, Osada H, Tsujii H, Kurita H. {{Utility of the Kyoto Scale of Psychological Development in cognitive assessment of children with pervasive developmental disorders}}. {Psychiatry Clin Neurosci};2009 (Apr);63(2):241-243.
Based on the clinical records of 74 children with pervasive developmental disorders (PDD; mean age, 45.2 months; 62 boys), the utility of the Kyoto Scale of Psychological Development in cognitive assessment of young and/or mentally retarded PDD children was investigated. Because the overall developmental quotient (DQ) had the highest correlation with the IQ (Pearson’s r, 0.88) and the Cognitive-Adaptive DQ showed a non-significant difference in mean (65.8) from the IQ (66.4), they both seem useful as an equivalent to an IQ. The test would enable clinicians to carry out continual developmental assessments and to develop appropriate remedial programs for those children from infancy.
5. Li J, Vestergaard M, Obel C, Christensen J, Precht DH, Lu M, Olsen J. {{A nationwide study on the risk of autism after prenatal stress exposure to maternal bereavement}}. {Pediatrics};2009 (Apr);123(4):1102-1107.
OBJECTIVE: Prenatal stress has been linked to several adverse neurobehavioral outcomes, which may share a common pathophysiology with autism. We aimed to examine whether prenatal stress exposure after maternal bereavement is associated with an increased risk of autism later in life. METHODS: We conducted a nationwide population-based cohort study of all 1492709 singletons in Denmark born from 1978 to 2003. A total of 37275 children were born to women who lost a close relative during pregnancy or up to 1 year before pregnancy. These children were included in the exposed group, and the remaining children were in the unexposed group. All children were followed up from birth until their death, migration, onset of autism, or the end of 2006. Information on autism was obtained from the Danish Psychiatric Central Register. We used Cox regression models to estimate hazard ratios in the exposed group compared with those in the unexposed group. RESULTS: Maternal bereavement during the prenatal period was not associated with an increased risk of autism in the offspring. The hazard ratios did not differ by the nature of the exposure (maternal relationship to the deceased or cause of death). The hazard ratios were comparable between the 5 prenatal exposure periods under study (7-12 months before pregnancy, 0-6 months before pregnancy, first trimester, second trimester, and third trimester). CONCLUSIONS: This is the first population-based cohort study to examine the effect of prenatal stress on autism in childhood. Our data do not support any strong association between prenatal stress after maternal bereavement and the risk of autism.
6. Yamasue H, Kuwabara H, Kawakubo Y, Kasai K. {{Oxytocin, sexually dimorphic features of the social brain, and autism}}.{ Psychiatry Clin Neurosci};2009 (Apr);63(2):129-140.
The common features of autism spectrum disorder, a highly heritable representative pervasive developmental disorder with significant heterogeneity and multiple-genetic factors, are severe dysfunction in social reciprocity, abnormalities in social brain regions, and disproportionately low probability in the female gender. Concomitantly, certain domains of mental function, such as emotional memory and social reciprocity, show a significant sex difference. In addition, recent neuroimaging studies have shown significant sexual dimorphisms in neuroanatomical correlates of social cognition. Recently, some sexually dimorphic factors, including oxytocin, vasopressin, and genes linked with the x-chromosome, have received attention because of their possible contribution to mental development especially in the social cognitive domain. Taking this evidence together, it is hypothesized that a sexually dimorphic factor associated with social reciprocity could affect characteristics of autism spectrum disorder including dysfunction in social reciprocity, abnormalities in social brain regions, and disproportionately low probability in female gender. This review article overviews sexual dimorphisms in clinical features of autism spectrum disorder, in normal social cognition, and in social brain function and structure. The association of oxytocin with sexual dimorphisms, social reciprocity, neural correlates of social cognition, and the pathogenesis of autism spectrum disorder were further summarized. Recent studies have suggested that oxytocin plays a role in social attachment in experimental animals, in enhancing social interactive ability in human adults, and in the pathogenesis of autism spectrum disorder. Thus, the ongoing accumulated evidence suggests that oxytocin deserves to be examined as a candidate that causes the sexually dimorphic aspect of human social reciprocity, social brain development and the pathogenesis of autism spectrum disorder.
