Dystonia, Spasticity and Botulinum Toxin Therapy: Rationale, Evidences and Clinical Context
نویسنده
چکیده
Perhaps among the central nervous system (CNS) conditions with muscle hyperactivity, dystonia and spasticity figure as those that are disabling and requiring therapeutic intervention. Dystonia is a neurological syndrome characterized by sustained muscle contractions usually producing twisting and repetitive movements or abnormal postures. The sustained movements of dystonia may have overlying spasms similar to tremor but have a directional preponderance. Three other important clinical features of dystonia are occurrences of pain, sensory trick phenomenon (i.e. touching “hot spots” in body surface that abolishes the dystonia), and changes in severity depending on activity and posture . Spasticity is typified by a velocity-dependent occurrence of a “catch” following passive limb movement. Recently, the scope of spasticity has been broadened in its definition as a disordered sensori-motor control resulting from an upper motor neuron (UMN) lesion presenting as intermittent or sustained involuntary activation of muscles(1-2) . Although their etiopathogenesis differ, both conditions overlap as regard the following: [a] occurrence of muscle co-contractions; [b] Overactivity involves not only extrafusal but also intrafusal muscles(3-4) [c] Intrinsic muscle changes in size and visceco-elastic properties (5-6); [d] contractures if left unattended (7);[e] muscular spread in synergy, “overflow” and compensatory muscles; [f ] loss of dexterity; [g] occurrence of pain to varying degrees; [h] secondary bone and joint abnormalities; [i] may lead to “compensatory circuitry changes” at segmental and suprasegmental levels (4) ; [j] May lead to posturing and cosmesis issues, and [k] hygiene, quality of life and social impact . Another common thread between dystonia and spasticity is the reduction in muscle tone following botulinum neurotoxin therapy (BoNT), and effectively addressing the disordered sensori-motor control in both conditions. Intuitively, BoNT will be most efficacious in cases with a combination of spasticity and dystonia (i.e. spastic dystonia), such as in childhood spasticity(8). This chapter summarizes the clinical efficacy of BoNT in both dystonia and spasticity.
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The Effect of Foot Serial Casting Along with Botulinum Toxin Type-A Injection on Spasticity in Children with Cerebral Palsy
Background & Aims: The goal of this study was to determine the effect of foot serial casting along with botulinum toxin type-A injection on spasticity in children with cerebral palsy. Methods: This study was a randomized clinical trial performed as a pre-post, double blind study. It was performed on 25 children with hemiplegia and diplegia (2-8 years) in Tehran city, who were referred to valias...
متن کاملBotulinum toxin and spasticity
The clinical eVects of botulinum toxin have been recognised since the end of the 19th century. It is the most potent neurotoxin known and it is produced by the gram negative anaerobic bacterium Clostridium botulinum. The paralytic eVect of the toxin is due to blockade of neuromuscular transmission. Injection into a muscle causes chemodenervation and local paralysis and this eVect has led to the...
متن کاملBotulinum toxin and spasticity
The clinical eVects of botulinum toxin have been recognised since the end of the 19th century. It is the most potent neurotoxin known and it is produced by the gram negative anaerobic bacterium Clostridium botulinum. The paralytic eVect of the toxin is due to blockade of neuromuscular transmission. Injection into a muscle causes chemodenervation and local paralysis and this eVect has led to the...
متن کاملBotulinum toxin and spasticity
The clinical eVects of botulinum toxin have been recognised since the end of the 19th century. It is the most potent neurotoxin known and it is produced by the gram negative anaerobic bacterium Clostridium botulinum. The paralytic eVect of the toxin is due to blockade of neuromuscular transmission. Injection into a muscle causes chemodenervation and local paralysis and this eVect has led to the...
متن کاملBotulinum toxin and spasticity
The clinical eVects of botulinum toxin have been recognised since the end of the 19th century. It is the most potent neurotoxin known and it is produced by the gram negative anaerobic bacterium Clostridium botulinum. The paralytic eVect of the toxin is due to blockade of neuromuscular transmission. Injection into a muscle causes chemodenervation and local paralysis and this eVect has led to the...
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