The term spasticity was defined by Lance in the 1980s [5] as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflex (muscle tone) with exaggerated tendon jerks, resulting hyper-excitability of the stretch reflex as one component of the upper motor neuron syndrome (UMNS).” Muscles affected by UMNS frequently exhibit weakness, loss of reciprocal inhibition, decreased movement control, and spasticity.

The stroke lesion generally affects the cortex and/or subcortical regions. It is considered to be an “upper motor neuron syndrome” if it affects the areas controlling motor strength and muscle tone. For example, the corticospinal tract (CST) is the dominant descending motor pathway connecting the motor cortex to the limbs through the spinal cord to control limb strength and voluntary movement. There are other nondominant subcortical tracts as well. For example, the vestibulospinal tract receives excitatory input from vestibular organs and deep cerebellar nuclei, subsequently synapses on ipsilateral interneurons that excite alpha motor neurons to the limb and trunk muscles, and excites the extensors to regulate posture and balance. The reticulospinal tract is another subcortical tract receiving input from both cortices and ascending sensory input from spinoreticular tract neurons. It innervates interneurons that excite motor neurons to limbs muscles, and mainly excites flexors, thereby facilitating the regulation of voluntary movements. Although we do not know the exact anatomic correlation of PSLS, the injury from stroke affecting the corticospinal tract or other subcortical tracts likely contributes to hemiparesis as well as spasticity [6, 7] (Fig. 19.2 shows this highlighted patient suffered a left pontine infarct and injured the left corticospinal tract; the patient exhibits moderate-to-severe spasticity with both upper and lower extremities after stroke).

Limb spasticity is a common complication after stroke and is frequently associated with pain, contractures, fatigue, functional limitations, diminished self-image, poor gait, increased falls, pressure sores, skin breakdown, etc. Spasticity should be comprehensively assessed at the level of impairment and its corresponding impact on function. The spasticity and impairment level can be assessed using the Ashworth Spasticity Scale (or the modified Ashworth) and Tardieu Scale. The Ashworth spasticity scale [8] measures the resistance to stretching when a limb is passively moved. It is a 6-point scale that provides information on the severity of spasticity and can be used to indicate responses to treatment. The Tardieu scale [9] measures spasticity that takes into account resistance to passive movement at both slow and fast speeds. Impact on function can be assessed using the modified Rankin Scale, Barthel index, and Functional Independence Measurement and Disability Assessment Scale (DAS). The DAS [10] is a scale specially designed to assess disability linked to upper extremity spasticity, while the other three scales assess overall disability from spasticity. Pain usually accompanies spasticity. Therefore, pain scale, such as the numeric pain rating scale (NPRS), which is an 11-point scale (0 is no pain and 10 is worst pain imaginable), is also used for assessment.

Spasticity can occur in either a single muscle or a group of muscles in both arms and legs. Typical manifestations of spasticity in stroke patients are shown below (Table 19.1).

Management of spasticity requires a multidisciplinary effort, including the patient and/or caregiver, stroke neurologist or physiatrist, occupational therapists, physical therapist, and psychologist. The focus of treatment is usually tailored to the specific needs or goals of the patient and/or caregiver. Spasticity management should be aimed at reducing the effects of disability on daily activities, including limb position, hygiene, dressing, walking, and a healthy self-image. The treatment is also crucial for the caregiver because stroke survivors require various degrees of assistance from the caregiver for dressing, hygiene, walking, and other ADLs. Generally speaking, spasticity reduction, functional improvement, pain relief, self-image enhancement, and reduction of caregiver burden are common goals for both patients and caregivers.

The key element of treatment is spasticity reduction. There are several treatment options for PSLS, including pharmacological agents [11], such as baclofen (oral or intrathecal), tizanidine, or benzodiazepine; rehabilitation therapy (muscle stretching or muscle strength training), electric stimulation [12], and chemodenervation approaches [13], including botulinum toxin regional muscle injection, phenol injection, and alcohol injection. Most of the pharmacological agents carry significant central nervous system related side effects, which can be intolerable to some stroke patients. For example, tizanidine is an effective antispasmodic agent, but it easily causes somnolence, sleepiness, hypotension, and bradycardia. As a result, Botulinum toxin has emerged as the first-line treatment for focal PSLS due to the fact that it has no cognitive side effect.