Abstract
Spasticity is commonly defined as a velocity-dependent increase in muscle tone with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex. Spasticity is one component of the upper motor neuron syndrome, which also includes hyperreflexia, clonus, muscle cocontraction, fatigability, and muscle weakness. Spasticity is not always a hindrance and each patient’s clinical situation should be carefully evaluated to look at the way spasticity is impeding his or her function, pain, physical condition, or caregiving. Furthermore, worsening of baseline spasticity should warrant a workup for noxious stimuli or infection as a cause. Options for treatment include oral medications such as baclofen and tizanidine as well as other interventional approaches such as chemodenervation coupled with rehabilitation, intrathecal baclofen, and/or surgical approaches.
Definition
Spasticity is commonly defined as a velocity-dependent increase in muscle tone with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex. This means that the faster the passive movement of the limb through its range, the greater the increase in muscle tone. Thus spasticity can be considered a component of an upper motor neuron (UMN) syndrome, which is also associated with hyperreflexia, clonus, muscle cocontraction, and muscle weakness.
Spasticity can be caused by a variety of conditions. It is often noted to be a major problem in spinal cord injury, multiple sclerosis, and traumatic brain injury. It is estimated to affect between 40% and 80% of patients with a spinal cord injury or multiple sclerosis, and the prevalence can be as high as 80% in patients with traumatic brain injury. Spasticity can also be present in other conditions like amyotrophic lateral sclerosis, brain and spinal cord tumors, and cerebral palsy.
Symptoms
Patients with spasticity may complain of increased tightness, worsening spasms, and pain. However, the main complaint can be worsening of functional activities. The ability to move affected limbs, actively or passively, is reduced. Spasticity significantly interferes with routine tasks and even hygiene (e.g., increased elbow flexor spasticity in a stroke survivor while walking; adductor spasticity in a paraplegic individual during bladder management) while at the same time causing pain and muscle cocontraction. These symptoms may reflect an increase in spasticity due to a secondary condition such as an infectious process, skin pressure injuries, and cord tethering. Therefore when a patient comes to clinic complaining of worsening spasticity, a thorough history and physical examination should be performed to identify the cause.
Physical Examination
Spasticity occurs in the presence of other signs and symptoms of UMN damage. The physical examination may show hyperreflexia, Babinski responses, and clonus. Other signs include muscle weakness, fatigue, reduced motor control, and loss of coordination. Increased muscle tone in the absence of these findings should lead to consideration of alternative causes such as dystonia, Parkinson disease, or pain-associated muscle spasm. Strength testing may not be valid, as the spasticity may affect joint range of motion due to contractures as cocontraction of antagonist muscles may interfere with the test.
Muscle contracture as well as other soft tissue changes can be a part of this UMN syndrome, and it may be difficult in some cases to determine how much contracture is present with the severe spasticity. A thorough physical examination can also show sensory disturbances (proprioception and spatial orientation), dysphagia, dysarthria, and skin problems. The skin should be inspected carefully, because abnormal positioning due to spasticity may directly cause skin injury (e.g., maceration of the palm due to a clenched fist) or contribute to the formation of pressure ulcers.
It is important to differentiate spasticity from rigidity, commonly seen in conditions like Parkinson disease. One must look at some physical examination findings that occur with spasticity, such as the clasp-knife phenomenon. There is also variability in evaluating antagonistic muscles. In spasticity, for example, some muscle groups are more affected than their antagonists. Rigidity is not velocity-dependent; it is constant throughout the whole range of motion.
Functional Limitations
Spasticity can cause significant functional limitations. In a spinal cord injury patient, for example, spasticity can have a serious impact on positioning. It can affect wheelchair positioning as well as transfers. Hygiene and bladder management may be affected by significant increases in hip adductor tone. It will affect dexterity and fine motor coordination in the upper extremities. The use of bracing or other modalities to assist with ambulation may be limited if the spasticity is significant. Studies have found that a significant number of patients with both spinal cord injury and traumatic brain injury have noted that spasticity affects quality of life. It is interesting that in some cases, spasticity may serve as a partial substitute for voluntary muscle contraction. A common example of substitution for voluntary muscle function is the hip and knee extensor spasticity seen after stroke, which may allow successful weight bearing through the hemiparetic leg and contribute to the restoration of walking ability.
Diagnostic Studies
Spasticity is a clinical diagnosis; there is no specific laboratory test for confirmation. Clinical measurement scales to quantify the severity of spasticity may be useful to monitor the efficacy of treatment. The most commonly used scales are the Ashworth Scale (and a modified version of this scale), which measures resistance of the muscle to passive stretch, and the Penn Spasm Frequency Scale, which characterizes the frequency of muscle spasms ( Tables 154.1 and 154.2 ).
Dystonia
Rigidity (e.g., Parkinson disease)
Paratonia
Pain-associated muscle spasm
Contracture
| 0 | No increase in muscle tone |
| 1 | Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end range of motion when the part is moved in flexion or extension/abduction or adduction |
| 1+ | Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the range of motion |
| 2 | More marked increase in muscle tone through most of the range of motion, but the affected part is easily moved |
| 3 | Considerable increase in muscle tone, passive movement is difficult |
| 4 | Affected part is rigid in flexion or extension (abduction or adduction) |
| How often are muscle spasms occurring? | |
| 0 | No spasms |
| 1 | Spasms induced only by stimulation |
| 2 | Spasms occurring less than once per hour |
| 3 | Spasms occurring between 1 and 10 times per hour |
| 4 | Spasms occurring more than 10 times per hour |
Treatment
Initial
The treatment of spasticity depends on the clinical and functional needs of the patient. As noted before, spasticity can be used to the patient’s advantage, such as ambulation in the presence of spastic hemiparesis. Treatment should be started when spasticity becomes an obstacle to functional goals, represents a safety risk (spasms while transferring, which could lead to a fall), impairs hygiene, or damages skin integrity. A change in previously well-controlled spasticity should always lead to the consideration of possible irritants or nociceptive stimuli that might be “triggering” the spasticity. Examples are urinary tract infections, skin pressure injuries, occult fractures, and an ingrown toenail in an insensate limb (e.g., in a paraplegic person).
Several oral medications ( Table 154.3 ) have been used to treat spasticity, depending on the underlying disease, with mixed results. Spasticity caused by injury to the spinal cord tends to respond better to baclofen and tizanidine than spasticity caused by a traumatic brain injury or stroke. However, centrally acting medications such as baclofen, tizanidine, and the benzodiazepines have significant side effects that may impair cognition and overall recovery after an acquired brain injury. Another commonly used drug is dantrolene, which works directly at the muscle level, preventing calcium flux at the sarcoplasmic reticulum and thereby reducing muscle force.
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