Although little can be done to counter the muscle weakness that occurs in MS, several forms of treatment can be applied to help limit the adverse effects of spasticity. However, treatment plans must be designed to meet individual patient needs and must take into consideration both the benefits and the risks of specific interventions. For some ambulatory patients, for example, treatment of spasticity is less desirable if increased stiffness of the legs facilitates walking by offsetting muscle weakness. Management of spasticity often involves a combination of therapeutic approaches, including control of secondary factors that stimulate spasticity, proper positioning, physiotherapy, and medications. Surgical procedures, such as tendon release, are sometimes used when other interventions are not effective.

Spasticity can be triggered or worsened by a variety of painful or unpleasant stimuli, such as urinary tract infections, fecal impaction, contractures, tight clothing, or ill-fitting footwear. A treatment plan should ensure that these sources of secondary stimulation are eliminated or controlled. Careful attention to balanced and symmetrical positioning when patients are standing, sitting, or lying down is important for preventing fixation in distorted postures induced by spasticity. Proper positioning can help stimulate muscles that are antagonists to those subject to spasticity. Physical therapy helps in maintaining balanced muscle tone, in preventing or treating contractures, and in training muscles in coordinated movement.

Baclofen and tizanidine are the two medications used most often to treat spasticity, with cloazepam and gabapentin usually reserved as secondary medications (Table 3.3). Baclofen, an agonist of γ-aminobutyric acid-B (GABA B) receptors, reduces presynaptic release of excitatory neurotransmitters and, at higher concentrations, acts postsynaptically to antagonize their actions. Generally given orally, baclofen can also be administered intrathecally through subcutaneous pump to treat more severe spasticity in long-standing MS.¹²⁷ Tizanidine stimulates a₂-andrenergic receptors in the spinal cord, which inhibits presynaptic