Safe handover : safe patients

This document:• provides guidance to doctors on best practice in handover• provides examples of good models of handover that doctors and hospital managerscan learn from• aims to drive further developments in standardising handover arrangementsin UK hospitals

Botulinum toxin treatment of spasticity in diplegic cerebral palsy : a randomised, double-blind, placebo-controlled, dose-ranging study

This study evaluated the efficacy and safety of three doses of botulinum toxin A (BTX-A; Dysport®) in 125 patients (meanage 5.2 years, SD 2; 54% male)with dynamic equinusspasticity during walking. Participants were randomized toreceive Dysport (10, 20, or 30 units/kg) or placebo to thegastrocnemius muscle of both legs. Muscle length wascalculated from electrogoniometric measurements and thechange in the dynamic component of gastrocnemiusshortening at four weeks was prospectively identified as theprimary outcome measure. All treatment groups showedstatistically significant decreases in dynamic componentcompared with placebo at 4 weeks. Mean improvement indynamic component was most pronounced in the 20 units/kggroup, being equivalent to an increase in dorsiflexion with the knee extended at 19°, and was still present at 16 weeks. The safety profile of the toxin appears satisfactory

Clinical, electrophysiological, and molecular genetic studies in a new family with paramyotonia congenita

OBJECTIVES—To characterise the clinical and electrophysiological features and to determine the molecular genetic basis of pure paramyotonia congenita in a previously unreported large Irish kindred.
METHODS—Clinical and neurophysiological examination was performed on three of the five affected family members. Five unaffected and three affected members of the family were available for genetic testing. Direct sequence analysis of the SCN4A gene on chromosome 17q, was performed on the proband's DNA. Restriction fragment length polymorphism (RFLP) analysis was used to screen other family members and control chromosomes for the SCN4A mutation identified.
RESULTS—Each affected member had clinical and examination features consistent with pure paramyotonia congenita. Electrophysiological studies disclosed a 78% drop in compound muscle action potential (CMAP) amplitude on cooling to 20°C. DNA sequence analysis identified a heterozygous point mutation G4367A in exon 24 of the SCN4A gene which segregated with paramyotonia and was absent in 200 control chromosomes. The mutation is predicted to result in a radical amino acid substitution at a highly conserved position within the voltage sensing fourth transmembrane segment of the fourth repeated domain of the sodium channel.
CONCLUSIONS—The G4367A mutation is likely to be pathogenic and it associates with a pure paramyotonia phenotype. In keeping with other paramyotonia mutations in this region of the skeletal muscle sodium channel, it is predicted that this mutation will impair voltage sensing or sodium channel fast inactivation in a temperature dependent fashion. This study provides further evidence that exon 24 in SCN4A is a hot spot for paramyotonia mutations and this has implications for a DNA based diagnostic service.