BACKGROUND AND PURPOSE: Recent studies have been made of the novel treatment of lower limb spasticity after stroke with botulinum toxin A, and the results were based mostly on the clinical assessment made before and after treatment. This study investigated the effects of toxin on ankle muscle activity during gait in patients with severe extensor spasticity. The questions posed were whether the toxin particularly diminishes the so-called premature muscle activity as a major cause of equinovarus deformity and whether different types of altered motor control allow a prediction of the outcome of the treatment. METHODS: In 12 chronic hemiparetic outpatients with pronounced lower limb spasticity, we injected 400 U botulinum toxin A into the soleus and tibialis posterior muscles and both heads of the gastrocnemius muscles. Ankle spasticity and complex gait analysis including kinematic electromyography (EMG) of the soleus and tibialis muscles were assessed before treatment and 4 weeks after the injection. RESULTS: Nine patients profited with a reduction of spasticity, improved gait ability, and a more normal temporal pattern of muscle activity with a prominent reduction of the premature activity of the plantar flexors. Eight patients exhibited a qualitative pattern (type I) corresponding to an increased stretch-reflex excitability. Three patients did not profit; their muscle tone, gait ability, and muscle activation remained stable or even deteriorated. CONCLUSIONS: This study further supports the beneficial effects of botulinum toxin in the treatment of lower limb extensor spasticity. A correlation was observed between the clinical reduction of muscle tone, functional gait parameters, and a more normal EMG pattern with a predominant reduction of the premature activity of the plantar flexors. The qualitative type of EMG pattern corresponding to an increased stretch-reflex excitability (type I) was a positive predictor for the outcome.
BACKGROUND AND PURPOSE: Recent studies have been made of the novel treatment of lower limb spasticity after stroke with botulinum toxin A, and the results were based mostly on the clinical assessment made before and after treatment. This study investigated the effects of toxin on ankle muscle activity during gait in patients with severe extensor spasticity. The questions posed were whether the toxin particularly diminishes the so-called premature muscle activity as a major cause of equinovarus deformity and whether different types of altered motor control allow a prediction of the outcome of the treatment. METHODS: In 12 chronic hemiparetic outpatients with pronounced lower limb spasticity, we injected 400 U botulinum toxin A into the soleus and tibialis posterior muscles and both heads of the gastrocnemius muscles. Ankle spasticity and complex gait analysis including kinematic electromyography (EMG) of the soleus and tibialis muscles were assessed before treatment and 4 weeks after the injection. RESULTS: Nine patients profited with a reduction of spasticity, improved gait ability, and a more normal temporal pattern of muscle activity with a prominent reduction of the premature activity of the plantar flexors. Eight patients exhibited a qualitative pattern (type I) corresponding to an increased stretch-reflex excitability. Three patients did not profit; their muscle tone, gait ability, and muscle activation remained stable or even deteriorated. CONCLUSIONS: This study further supports the beneficial effects of botulinum toxin in the treatment of lower limb extensor spasticity. A correlation was observed between the clinical reduction of muscle tone, functional gait parameters, and a more normal EMG pattern with a predominant reduction of the premature activity of the plantar flexors. The qualitative type of EMG pattern corresponding to an increased stretch-reflex excitability (type I) was a positive predictor for the outcome.
Authors: D Richardson; G Sheean; D Werring; M Desai; S Edwards; R Greenwood; A Thompson Journal: J Neurol Neurosurg Psychiatry Date: 2000-10 Impact factor: 10.154
Authors: A Berardelli; G Abbruzzese; L Bertolasi; G Cantarella; F Carella; A Currà; D De Grandis; G DeFazio; G Galardi; P Girlanda; P Livrea; N Modugno; A Priori; G Ruoppolo; L Vacca; M Manfredi Journal: Ital J Neurol Sci Date: 1997-10