Efficacy of therapeutic ultrasound and transcutaneous electrical nerve stimulation compared with botulinum toxin type a in the treatment of spastic equinus in adults with chronic stroke: a pilot randomized controlled trial.

BACKGROUND: Therapeutic ultrasound and transcutaneous electrical nerve stimulation (TENS) have been described as being effective in the treatment of spasticity. No previous study compared these physical modalities with a first-line treatment for spasticity, such as botulinum toxin type A. OBJECTIVE: To compare the effects of therapeutic ultrasound and TENS with botulinum toxin type A on spasticity after stroke. METHODS: Thirty patients with chronic stroke and spastic equinus were randomly assigned to 3 groups: 1 group received therapeutic ultrasound to the affected leg calf muscles, 1 group underwent TENS to the tibial nerve of the affected leg, and 1 group was injected with onabotulinum toxin A in the spastic gastrocnemius. All patients were evaluated immediately before treatment and 15, 30, and 90 days after the first clinical evaluation. The following outcome measures were considered: ankle passive dorsiflexion range of motion and the modified Ashworth scale. RESULTS: Patients injected with botulinum toxin type A had significantly better ankle passive range of motion than those treated with physical modalities at all posttreatment evaluations. At second and third posttreatment evaluations, the modified Ashworth scale indicated significantly greater improvement in patients injected with botulinum toxin type A than in those treated with physical modalities. No difference was found between groups treated with physical modalities. CONCLUSIONS: Our findings support the hypothesis that botulinum toxin type A is more effective than therapeutic ultrasound and TENS for treating focal spasticity in patients with chronic stroke

Novel mutations in ACVR1 result in atypical features in two fibrodysplasia ossificans progressiva patients

Fibrodysplasia Ossificans Progressiva (FOP) is a rare, heritable condition typified by progression of extensive ossification within skeletal muscle, ligament and tendon together with defects in skeletal development. The condition is easily diagnosed by the presence of shortened great toes and there is severe advancement of disability with age. FOP has been shown to result from a point mutation (c.617G>A) in the ACVR1 gene in almost all patients reported. Very recently two other mutations have been described in three FOP patients. We present here evidence for two further unique mutations (c.605G>T and c.983G>A) in this gene in two FOP patients with some atypical digit abnormalities and other clinical features. The observation of disparate missense mutations mapped to the GS and kinase domains of the protein supports the disease model of mild kinase activation and provides a potential rationale for phenotypic variation