Abstract
The present study quantifies the effect of the two botulinum toxin type A products, Xeomin and Dysport, with approval from the National Agency for Medicines and Medical Devices of Romania (ANMDMR), for the treatment of the spastic upper limb following a stroke. The results obtained in the present study show a good efficiency of using both products in the spasticity of the upper limb, and a maintenance of the results obtained for both products for a minimum period of 3 months. Also, at higher doses, the results of the study show better improvement of spasticity and upper limb function on the evaluation scales, but the local effect is not maintained for a longer period. Keywords: toxinum botulinum type A, Xeomin, Dysport, spasticity
Highlights
The present study quantifies the effect of the two botulinum toxin type A products, Xeomin and Dysport, with approval from the National Agency for Medicines and Medical Devices of Romania (ANMDMR), for the treatment of the spastic upper limb following a stroke
It is clinically easy to identify and the most frequent definition given by the American Academy of Neurology is the one described by Lance in 1980: Spasticity is a motor disorder characterized by a speed dependent increase in stretch reflexes, with exaggerated tendon reflexes resulting from a hyperexcitability of the stretch reflexes as a component of the central motor neuron syndrome [2]
What is the optimal starting dose? In the present study we want to compare the effect on spasticity and upper limb function of two products containing botulinum toxin: Xeomin and Dysport
Summary
The present study quantifies the effect of the two botulinum toxin type A products, Xeomin and Dysport, with approval from the National Agency for Medicines and Medical Devices of Romania (ANMDMR), for the treatment of the spastic upper limb following a stroke. At higher doses, the results of the study show better improvement of spasticity and upper limb function on the evaluation scales, but the local effect is not maintained for a longer period. It is clinically easy to identify and the most frequent definition given by the American Academy of Neurology is the one described by Lance in 1980: Spasticity is a motor disorder characterized by a speed dependent increase in stretch reflexes (muscle tone), with exaggerated tendon reflexes resulting from a hyperexcitability of the stretch reflexes as a component of the central motor neuron syndrome [2]. Detailed clinical evaluation is vital to identify patientcentered spasticity issues and other factors that contribute to its impact, such as muscle retraction, weakness, and dexterity loss. Rehabilitation goals for spastic upper limb management include restoring active function, if there is any return of motor function, or, if not possible, improving passive function to facilitate limb care [7,8]
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