Traditional pharmacological treatments for spasticity part II: General and regional treatments

Spasticity after spinal cord injury

“…22 The resultant increase in muscle tone is thought to be due to a combination of increased denervation hypersensitivity 2,3,5,9,33 and changed muscle properties. 11,13,22,34,35 Denervation leads to an initial downregulation of neuronal membrane receptors, followed by an upregulation, with enhanced sensitivity to neurotransmitters. 2 Gradual changes in muscle proper-ties also occur following SCI, such as fibrosis, atrophy of muscle fibers, decrease in the elastic properties, decrease in the number of sarcomeres, accumulation of connective tissue, and alteration of contractile properties toward tonic muscle characteristics, which likely contribute to the increased passive tension.…”

“…2 Gradual changes in muscle proper-ties also occur following SCI, such as fibrosis, atrophy of muscle fibers, decrease in the elastic properties, decrease in the number of sarcomeres, accumulation of connective tissue, and alteration of contractile properties toward tonic muscle characteristics, which likely contribute to the increased passive tension. 11,13,22,[34][35][36] Intrinsic phasic spasticity Intrinsic phasic spasticity encapsulates symptoms such as tendon hyper-reflexia and clonus, and is due to exaggeration of the phasic component of the stretch reflex. 2 Tendon hyper-reflexia is identified as an exaggerated muscle response to an externally applied tap of deep tendons.…”

“…35,39 Management of spasticity following SCI In contrast to the general lack of agreement within the literature about the definition and evaluation of spasticity, there appears to be widespread agreement that decisions regarding the management of spasticity must be based on the goal of achieving balance between the useful and detrimental effects of spasticity on an individual's QOL. 2,10,16,34 The management of spasticity may be desired for the reduction of 'passive problems', such as preventing contracture, reducing pain, facilitating splint wearing, easing positioning and hygiene, and preventing contractures, or of 'functional problems', including the individual's reduced ability to perform useful work with the motor system. 9 In general, no one treatment option will successfully manage spasticity in all individuals; the most conservative tactics are utilized first, with a progression from physical rehabilitation modalities, pharmacologic interventions, injection techniques, intrathecal baclofen, and lastly, surgery.…”

“…42 In the case of SCI, the distribution of spasticity tends to be more diffuse, making regional or systemic treatment preferable. 34 The decision whether or not to treat spasticity and, if so, in what manner, is summarized nicely in a flow chart by Parziale et al (Figure 1 16 ).…”

“…34 Most antispasticity medications can be grouped roughly into three functional categories: (1) 'GABAergic' -drugs that act at interneurons that use the neurotransmitter gamma-aminobutyric acid (GABA) in the CNS (eg, baclofen and diazepam), (2) alpha-2-adrenergicthose that act at alpha-2 receptors in the CNS (eg, tizanidine and clonidine), and (3) peripheral actingthose that act at the neuromuscular level (eg, dantrolene). 48 Numerous factors are taken into consideration when the physician and patient are deciding upon the role of pharmacologic management, including time since injury, onset of spasticity, severity, prognosis, available support system, cognitive status, concurrent medical problems, geographic location, symptom location, and financial issues.…”