Drugs Used to Treat Spasticity

Abstract

Spasticity is a common and disabling symptom for many patients with upper motor neuron dysfunction. It results from interruption of inhibitory descending spinal motor pathways, and although the pathophysiology of spasticity is poorly understood, the final common pathway is overactivity of the alpha motor neuron. Therapy for spasticity is symptomatic with the aim of increasing functional capacity and relieving discomfort. Any approach to treatment should be multidisciplinary, including physical therapy, and possibly surgery, as well as pharmacotherapy. It is important that treatment be tailored to the individual patient, and that both patient and care giver have realistic expectations. Pharmacotherapy is generally initiated at low dosages and then gradually increased in an attempt to avoid adverse effects. Optimal therapy is the lowest effective dosage. Baclofen, diazepam, tizanidine and dantrolene are currently approved for use in patients with spasticity. In addition, clonidine (usually as combination therapy), gabapentin and botulinum toxin have shown efficacy, however, more studies are required to confirm their place in therapy. Intrathecal baclofen, via a surgically implanted pump and reservoir, may provide relief in patients with refractory severe spasticity.

Spasticity after spinal cord injury

“…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.…”

“…10,17,36 The goal of physical therapy is to diminish spasticity in order to allow expression of voluntary mobility and movements and/or to improve the comfort and independence in tasks related to QOL, such as transfers, dressing, and using the washroom. 43 The literature on the conservative/physical treatment of spasticity is sparse, and some have questioned the effectiveness of these management strategies.…”

“…15,34 Rather, it binds postsynaptically near GABA A receptors, facilitates GABA-mediated chloride conductance and, therefore, hyperpolarizes the membrane. 9,10,15,48 The result of diazepam administration is an increase in presynaptic inhibition of afferent neuronal terminals and, thus, a reduction of monosynaptic and polysynaptic reflexes. 9,13,34 Diazepam is often mentioned as being most effective in the treatment of hyperactive reflexes and painful spasms in individuals with SCI (compared to individuals with stroke or multiple sclerosis).…”

“…There remains, however, discrepancy in the literature about the definition of spasticity; whereas some authors include symptoms such as clonus, hyperactive tendon reflexes, and spasms within the umbrella term 'spasticity', 1,[5][6][7] others discuss these same symptoms as related to but separate from spasticity, which is defined by these authors as increased muscle tone. 3,[8][9][10][11] Decq 2 recently has suggested the use of a modified definition, whereby spasticity, in general, is defined as a symptom of the upper motor neuron syndrome characterized by an exaggeration of the stretch reflex secondary to hyperexcitability of spinal reflexes. He follows by separating the various components of spasticity into sub-definitions: (1) intrinsic tonic spasticity: exaggeration of the tonic component of the stretch reflex (manifesting as increased tone), (2) intrinsic phasic spasticity: exaggeration of the phasic component of the stretch reflex (manifesting as tendon hyper-reflexia and clonus), and (3) extrinsic spasticity: exaggeration of extrinsic flexion or extension spinal reflexes.…”

“…Furthermore, it must be noted that, although spasticity can have a negative impact on QOL, it has been suggested that symptoms of spasticity may increase stability in sitting and standing, facilitate the performance of some ADL and transfers, increase muscle bulk and strength of spastic muscles (thereby helping prevent osteopenia), and increase venous return (possibly diminishing the incidence of deep vein thrombosis). 10,[14][15][16] This potential for a beneficial effect of spasticity on QOL has a large impact upon decisions regarding its management. 7,16 The use of varied definitions of spasticity complicate its valid and reliable assessment.…”