The efficacy of Equine Assisted Therapy intervention in gross motor function, performance, and spasticity in children with Cerebral Palsy

PurposeTo evaluate the efficacy of Equine Assisted Therapy in children with Cerebral Palsy, in terms of gross motor function, performance, and spasticity as well as whether this improvement can be maintained for 2 months after the end of the intervention.MethodsChildren with Cerebral Palsy participated in this prospective cohort study. The study lasted for 28 weeks, of which the equine assisted therapy lasted 12 weeks taking place once a week for 30 min. Repeated measures within the subject design were used for the evaluation of each child’s physical performance and mental capacity consisting of six measurements: Gross Motor Function Measure-88 (GMFM-88), Gross Motor Performance Measure (GMPM), Gross Motor Function Classification System (GMFCS), Modified Ashworth Scale (MAS) and Wechsler Intelligence Scale for Children (WISC III).ResultsStatistically significant improvements were achieved for 31 children in Gross Motor Function Measure and all its subcategories (p < 0.005), also in total Gross Motor Performance Measure and all subcategories (p < 0.005). These Gross Motor Function Measure results remained consistent for 2 months after the last session of the intervention. Regarding spasticity, although an improving trend was seen, this was not found to be statistically significant.Conclusion and implicationsEquine Assisted Therapy improves motor ability (qualitatively and quantitatively) in children with Cerebral Palsy, with clinical significance in gross motor function

Isolated abducens nerve palsy after closed head injury in a child

The authors present the rare case of a 5-year-old child with an isolated right abducens nerve palsy following a minor closed head injury. Occlusion of the left eye for 4 h daily was prescribed, and the child remained under close ophthalmological follow-up. Significant improvement was noticed in the following 6 months

Refining the locus of branchio-otic syndrome 2 (BOS2) to a 5.25 Mb locus on chromosome 1q31.3q32.1

In 1991, a large family was described with an autosomal dominant inheritance of otological and branchial manifestations which was termed branchio-otic syndrome type 2 (BOS2). This trait was mapped by linkage analysis in this family to a region of 23-31 Mb on chromosome 1q25.1q32.1. In the present report we describe the clinical features of two patients with a deletion in this region: one patient has a deletion but no otological or branchial manifestations, the other patient manifests mild conductive hearing loss resulting from bilaterally malformed middle ear ossicles, as well as a preauricular pit. Mapping of the deletion breakpoints allowed to delineate the region involved in BOS2 to a 5.25 Mb region containing 27 protein-coding genes. A detailed medical history of both patients is provided and they are compared with the literature on other detected interstitial deletions of 1q25q32. These findings will aid in the identification of the genetic cause underlying BOS2.status: publishe

Refining the locus of branchio-otic syndrome 2 (BOS2) to a 5.25 Mb locus on chromosome 1q31.3q32.1

In 1991, a large family was described with an autosomal dominant inheritance of otological and branchial manifestations which was termed branchio-otic syndrome type 2 (BOS2). This trait was mapped by linkage analysis in this family to a region of 23-31 Mb on chromosome 1q25.1q32.1. In the present report we describe the clinical features of two patients with a deletion in this region: one patient has a deletion but no otological or branchial manifestations, the other patient manifests mild conductive hearing loss resulting from bilaterally malformed middle ear ossicles, as well as a preauricular pit. Mapping of the deletion breakpoints allowed to delineate the region involved in BOS2 to a 5.25 Mb region containing 27 protein-coding genes. A detailed medical history of both patients is provided and they are compared with the literature on other detected interstitial deletions of 1q25q32. These findings will aid in the identification of the genetic cause underlying BOS2. (C) 2009 Published by Elsevier Masson SAS