The pharmacological management of spasticity
Spasticity is formally defined as a velocity-dependent increase in resistance to passive range of motion. It is a hallmark of neurological diseases that affect the central nervous system, including conditions that are congenital (e.g., cerebral palsy), acquired (traumatic brain injury), static (stroke), and progressive (multiple sclerosis). Spasticity results in involuntary contractions of synergistic muscles in the extremities, which are clinically manifested as flexor or extensor spasms (Mayer & Esquenazi, 2003; Meythaler, 2001).
Spasticity can be both beneficial and deleterious. Therefore, clinicians who care for such patients must consider all aspects of a patient's spasticity before embarking on a treatment plan. Spasticity beneficially contributes to assistance with mobility, maintenance of posture, vascular circulation, preservation of muscle mass and bone mineral density, prevention of venous thrombosis, and reflexive bowel and bladder function. Conversely, spasticity can interfere with positioning, mobility, comfort, and hygiene. Impaired dexterity can be observed in individuals with both spasticity and some voluntary muscle movement. Ambulatory patients can benefit from formal gait analysis to precisely assess the impact of hypertonicity on locomotion. Spasticity has also been linked to increased metabolic demands in patients who are not adequately nourished (Saulino, Kancherla, & Phillips, 2004). Spontaneous spasms can interfere with sleep or duration of wheelchair use. Spasms can also lead to skin breakdown because of shearing effects or to impaired healing of surgical wounds due to tension along suture lines (Satkunam, 2003).
The relationship of spasticity to pain is complex. Spasticity can limit the range of motion around a joint and result in musculoskeletal pain. Reduction of spasticity may reduce the pain associated with biomechanical problems. However, central nervous system disease can also produce neuropathic pain. Modulation of spasticity may not be effective in reducing neuropathic pain (Ward & Kadies, 2002).
Because the effects of spasticity can be complex, the goal of treatment may not be its complete elimination but rather titration to maximize the risk-benefit ratio. Traditionally, this syndrome is managed in a sequential fashion. However, most practitioners currently apply a more synergistic approach to reducing spasticity. Regardless of the approach, any anti-spasticity regimen must be tailored to the patient.
The two mainstays of nonpharmacological spasticity management are the removal of noxious stimuli that can drive hypertonicity and the application of physical modalities. Comorbidities of neurological disease can act as noxious stimuli that trigger increased spasticity. Examples include urinary tract infections, bladder distention, urolithiasis, bowel impaction, decubitus ulcers, and osteomyelitis. Such problems should be treated before beginning pharmacological treatment for spasticity. As patients become more aware of their reactions to such triggers, they can help the healthcare professional with the ongoing management of their spasticity.
Physical measures can also modulate spasticity. Stretching of the involved muscles is often helpful. Continuous or static stretching is preferred to short-duration or ballistic stretching (Gracies, 2001a). Long-duration stretching techniques can be applied manually or by means of adaptive equipment such as casts or splints. Application of heat and cold has been reported to reduce spasticity. Cryotherapy has the more extensive history; methods for...
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