Many poststroke survivors develop spasticity. Spasticity is usually associated with other neurologic impairments, in particular paresis, which complicate the evaluation of its consequences and of treatment outcomes. The diagnosis and the assessment of spasticity are based on clinical examination, in particular resistance to passive movement and abnormal involuntary muscle contraction. Nonpharmacologic and pharmacologic treatments are commonly combined to manage spasticity, based on prespecified goals. There is evidence supporting the effectiveness and safety of most medications commonly used to treat spasticity; however, more evidence is needed regarding functional outcomes and the impact of combining treatment modalities.
Key points
- •
Spasticity from stroke is classified as cerebral-origin spasticity, characterized by hyperexcitability of monosynaptic pathways, a rapid rise in excitation, and stereotypical postures involving antigravity muscle groups.
- •
The prevalence of spasticity after stroke can be as high as 46% in the chronic phase (over 3 months).
- •
Spasticity is most often associated with other neurologic impairments, in particular paresis, which complicate its evaluation and management.
- •
Treating spasticity after a stroke entails combining nonpharmacological and pharmacologic interventions.
- •
There is emerging evidence suggesting that some treatments for spasticity improve upper and lower extremity functional performance.
Introduction
Spasticity is a movement disorder, defined as a velocity-dependent increase in stretch reflexes due to impaired supraspinal inhibitory signals. Recent observations suggest, however, that decreased homosynaptic depression (ie, impaired depletion of the release of excitatory neurotransmitters with repetitive afferent activation), rather than decreased presynaptic inhibition, is associated with poststroke spasticity. In addition, defective supraspinal control of various spinal inhibitory and facilitatory circuits is associated with abnormal muscle contraction during voluntary movement. Finally, changes in the rheologic and contractile properties of musculoskeletal soft tissue are frequently associated with chronic spasticity and in turn have been linked to increased spasticity.
Cerebral-origin spasticity after a stroke differs from spinal-origin spasticity as encountered in spinal cord injury and multiple sclerosis. Cerebral-origin spasticity is characterized by
- •
Hyperexcitability of monosynaptic pathways
- •
A rapid rise in excitation
- •
Stereotypical postures involving antigravity muscle groups. The hemiplegic posture commonly observed after a stroke consists of
- ○
In the upper extremity: shoulder adduction; forearm pronation; and elbow, wrist, and finger flexion
- ○
In the lower extremity: hip adduction, knee extension, ankle plantarflexion, and often pes varus
- ○
Spasticity is only one component of the upper motor neuron (UMN) syndrome. As a consequence, other features of the UMN syndrome most often accompany spasticity, such as weakness, loss of dexterity, and synkinetic movements. In one study, 100% of patients with spasticity exhibited limb weakness (vs 50% of patients without spasticity) when assessed over 3 months after a stroke. Because other neurologic impairments are commonly seen after a stroke (eg, visual, sensory, and cognitive), it may be difficult to isolate the specific impact of spasticity on functional limitations. It has been stated that the functional limitations experienced by stroke survivors are mostly related to neurologic deficits other than spasticity.
The prevalence of spasticity after stroke is difficult to ascertain in the absence of rigorous population-based studies. In a survey from the National Stroke Association, 57% of 504 stroke survivors reported tight or stiff muscles, suggesting the presence of spasticity. Clinician-based determination of the prevalence of spasticity is most often conducted in hospital stroke units, with sample sizes ranging from 50 to 200 individuals. Prevalence values are between 4% and 27% in the first month after stroke and between 17% and 46% past 3 months. Longitudinal studies generally report higher prevalence values at the chronic phase.
Introduction
Spasticity is a movement disorder, defined as a velocity-dependent increase in stretch reflexes due to impaired supraspinal inhibitory signals. Recent observations suggest, however, that decreased homosynaptic depression (ie, impaired depletion of the release of excitatory neurotransmitters with repetitive afferent activation), rather than decreased presynaptic inhibition, is associated with poststroke spasticity. In addition, defective supraspinal control of various spinal inhibitory and facilitatory circuits is associated with abnormal muscle contraction during voluntary movement. Finally, changes in the rheologic and contractile properties of musculoskeletal soft tissue are frequently associated with chronic spasticity and in turn have been linked to increased spasticity.
Cerebral-origin spasticity after a stroke differs from spinal-origin spasticity as encountered in spinal cord injury and multiple sclerosis. Cerebral-origin spasticity is characterized by
- •
Hyperexcitability of monosynaptic pathways
- •
A rapid rise in excitation
- •
Stereotypical postures involving antigravity muscle groups. The hemiplegic posture commonly observed after a stroke consists of
- ○
In the upper extremity: shoulder adduction; forearm pronation; and elbow, wrist, and finger flexion
- ○
In the lower extremity: hip adduction, knee extension, ankle plantarflexion, and often pes varus
- ○
Spasticity is only one component of the upper motor neuron (UMN) syndrome. As a consequence, other features of the UMN syndrome most often accompany spasticity, such as weakness, loss of dexterity, and synkinetic movements. In one study, 100% of patients with spasticity exhibited limb weakness (vs 50% of patients without spasticity) when assessed over 3 months after a stroke. Because other neurologic impairments are commonly seen after a stroke (eg, visual, sensory, and cognitive), it may be difficult to isolate the specific impact of spasticity on functional limitations. It has been stated that the functional limitations experienced by stroke survivors are mostly related to neurologic deficits other than spasticity.
The prevalence of spasticity after stroke is difficult to ascertain in the absence of rigorous population-based studies. In a survey from the National Stroke Association, 57% of 504 stroke survivors reported tight or stiff muscles, suggesting the presence of spasticity. Clinician-based determination of the prevalence of spasticity is most often conducted in hospital stroke units, with sample sizes ranging from 50 to 200 individuals. Prevalence values are between 4% and 27% in the first month after stroke and between 17% and 46% past 3 months. Longitudinal studies generally report higher prevalence values at the chronic phase.
Patient evaluation overview
Identifying Spasticity
The diagnosis of spasticity is based on clinical features, in the context of a central nervous system disorder. Spasticity is usually associated with some or all of the patient complaints presented in Table 1 . Even though these symptoms are suggestive of spasticity, they are not sufficient to establish the diagnosis. For example, difficulty moving a limb can be described as “stiffness” even when it is due to weakness. Pain can be related to spasticity (particularly if it is associated with spasms or occurs with passive movement), but central neuropathic pain (particularly after a thalamic stroke) or musculoskeletal pain may also be present.
| Complaints | Clinical Signs |
|---|---|
|
|
The diagnosis of spasticity is confirmed by clinical examination findings, summarized in Table 1 . Some of these signs are associated with passive stretch (resistance to passive movement, clonus); others are observed only with active movement, such as muscle co-contraction and spastic dystonia. Therefore, spasticity needs to be examined at rest and with voluntary movement (whenever possible) to better understand the functional consequences of spasticity. In addition, it is useful to assess spasticity in various positions (standing vs sitting vs supine) because position-dependent variations in spasticity have been reported and are commonly observed in practice.
Other signs of the UMN syndrome are almost always present, in particular paresis and loss of dexterity but also synergistic movement patterns. In addition, other neurologic impairments often increase the complexity of the clinical presentation but are important to document, because they have an impact on goal setting and treatment planning. Strength output is of particular importance, because increased weakness may occur as spasticity is treated. Finally, the presence of partial or total musculoskeletal contractures should be documented, because they have an impact on the treatment plan, whether or not they are directly related to spasticity.
Spasticity needs to be differentiated from other movement disorders associated with increased tone, in particular
- •
Dystonia, which causes abnormal sustained or intermittent muscle contractions with twisting movements and abnormal postures. Some of the features of dystonia, however, are observed with spasticity (spastic dystonia), as discussed previously.
- •
Extrapyramidal hypertonia, which is characterized by cogwheeling and rigidity
Velocity-dependent resistance to passive movement is a useful clinical feature to distinguish spasticity from these other movement disorders but may be difficult to assess in the presence of severe hypertonia and ROM limitations. In addition, various movement disorders may coexist, depending on the location of the stroke.
Measuring Spasticity
Once spasticity is identified, it is useful to rate its severity, particularly for monitoring treatment outcomes. Table 2 gives examples of some of the assessment tools available to clinicians and researchers.
| Name | Clinical Parameter Assessed | Scoring | Comments |
|---|---|---|---|
| Clinical examination scales | |||
| Ashworth Scale (AS) and Modified Ashworth Scale (MAS) | Resistance to passive movement | AS: 1 (no increase in muscle tone) to 5 (affected part[s] rigid in flexion or extension) MAS: 0 (no increase in muscle tone) to 4 (affected part[s] rigid in flexion or extension) Includes 1+ rating (catch followed by minimal resistance throughout the remainder of the range of motion) | Pros: easy to administer; frequently used in clinical trials Cons: lacks sensitivity to change; inter-rater reliability is an issue; resistance to passive movement is not equivalent to spasticity |
| Tardieu Scale (TS) and Modified Tardieu Scale (MTS) | Resistance to passive movement | TS: resistance to passive movement assessed at 3 speeds: V1 (as slow as possible), V2 (speed of the limb falling under gravity), V3 (as fast as possible) Two angles measured: R1 (first catch to a quick stretch) and R2 (total passive range of motion with slow stretch) R2–R1 = dynamic tone MTS: only 2 speeds (V1 and V3) | Pros: easy to administer; more detailed assessment than AS or MAS Cons: lacks sensitivity to change; inter-rater reliability is an issue |
| Triple Spasticity Scale | Change in resistance to passive movement between slow and fast speed, clonus, dynamic muscle length | Total score from 0 to 10 Three subscales: increased resistance between a slow stretch and a fast stretch (0–4), clonus (0–2), dynamic muscle length (0–4) | — |
| Self-report measures | |||
| Spasm Frequency Scale | Spasm frequency | 0 (No spasm) to 4 (more than 10 spontaneous spasms per hour) | Pros: easy to use; frequently used in clinical trials Cons: does not take into account fluctuations of spasm frequency; does not assess spasm severity or pain associated with spasms; lacks sensitivity to change |
| Spasm Frequency Score | Spasm frequency | 0 (No spasms) to 10 (10 or more spasms per day, or continuous contraction) | Pros and cons are similar to those cited for the Spasm Frequency Scale. Not as commonly used in clinical trials. |
| Spasticity numeric rating scale (NRS) | Global severity of spasticity | 0 (No spasticity) to 10 (worst possible spasticity) | Pros: easy to use, good test-retest reliability, correlates with other measures of spasticity Clinically important difference was calculated at 30% change in score (minimal clinically important difference: 18% change) Cons: validated only for multiple sclerosis–related spasticity |
| Instrumented measurements | |||
| Isokinetic dynamometry | Resistance to passive movement | Torque | Pros: high test-retest reliability; excellent control of stretch velocity and amplitude; quantification of resistance to passive movement Cons: equipment and time requirements; correlation with traditional clinical measures not always satisfactory |
| Pendulum test | Lower leg swing in patient sitting | Amplitude of leg swing around the knee (assessed with electrogoniometer), angle difference between start and finish positions | Pros: simple setup; correlates well with clinical measures of spasticity Cons: requires equipment; only assesses spasticity around the knee joint |
| EMG | EMG response to stretch, tendon tap (T reflex) and electrical stimulation of the peripheral nerve (H-reflex) | Threshold values H/M ratio (H = H-reflex threshold, M = M-reflex threshold) | Pros: measures reflex activity Cons: equipment and time requirements Poor or no correlation with clinical measures |
| Tonic stretch reflex threshold (TSRT) | Excitability of motoneurons without stretch (0°/s velocity) TSRT computed from angles where the EMG signal increases for a given velocity of stretch | The TSRT is defined as the intercept value of the linear regression line for dynamic stretch reflex thresholds (at various angular velocities) with the angle axis (dependent variable: angle; independent variable: velocity). | Pros: portable device; moderate inter- and intrarater reliability for moderate to high spasticity; tested in poststroke spasticity Cons: time consuming; did not correlate with MAS scores in preliminary validation study |
Most of the spasticity severity scales used in the clinic and in clinical trials measure resistance to passive movement (eg, Ashworth Scale and Tardieu Scale), despite the aforementioned limitations of this approach. In addition, patient-reported questionnaires have been used to quantify spasm frequency and, more recently, patients’ overall assessment of their spasticity (spasticity numeric rating scale). Instrumented tests measurements (electromyogram [EMG], dynamometry, and pendulum test) are not routinely used in the clinic, due to time and equipment requirements and because they do not always correlate with clinical findings.
Although functional tests and scales are increasingly used in clinical trials of treatments for spasticity, none of them was specifically developed and validated for this application, to the author’s knowledge. The appropriateness of a specific functional test depends on the limb(s) targeted for treatment, the treatment goals, the instrument’s psychometric properties, and feasibility. Among others, the Frenchay Arm Test, the Disability Assessment Scale have been used to assess upper limb function; timed walking tests to assess lower limb function; and the Barthel Index and Functional Independence Measure for overall functional status have been used in the evaluation of treatments of spasticity after stroke.
Other neurologic impairments need to be documented in the initial evaluation and taken into account for goal setting but may not need to be monitored in a quantitative manner, because they are expected to remain unchanged. The only notable exception is weakness, because it may also be impacted by treatment. The most common way to document strength in the clinic is the manual muscle testing (despite its limitations in the assessment of central paresis), whereas the Evaluation Database to Guide Effectiveness (EDGE) document published by the Neurology Section of the American Physical Therapy Association recommends the use of handheld dynamometry.
Treatment planning requires assessing the consequences of spasticity and defining realistic goals. Although it is a common process in medicine in general, and in the field of rehabilitation in particular, goal setting can be difficult because spasticity is most often not the only cause of the symptoms and functional limitations observed. Potential consequences of spasticity and related treatment goals are described in Table 3 .
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
