- Author: Zeba F Vanek, MD, MBBS, DCN; Chief Editor: Stephen A Berman, MD, PhD, MBA more...
Spasticity is increased, involuntary, velocity-dependent muscle tone that causes resistance to movement. The condition may occur secondary to a disorder or trauma, such as a tumor, a stroke, multiple sclerosis (MS), cerebral palsy, or a spinal cord, brain, or peripheral nerve injury.
Signs and symptoms
Children with cerebral palsy tend to exhibit one of the following spasticity patterns:
Diplegic pattern: Scissoring, crouching, and toe walking
Quadriplegic pattern: Diplegic patterning in addition to flexion of the elbow, flexion of the wrist and fingers, adduction of the thumb, and internal rotation, pronation, or adduction of the arms
Hemiplegic pattern: Plantar flexion of the ankle, flexion of the knee, adduction of the hip, flexion of the wrist and finger, adduction of the thumb, and flexion, internal rotation, pronation, or adduction of the arms
Equinovarus positioning of the foot is a common posture in the lower extremity, and it can be a major limitation to functional transfers or gait as a child grows older.
Spasticity of the upper extremities
The following patterns often are seen in patients with cerebral palsy, stroke, or traumatic brain injury (TBI):
Adduction and internal rotation of the shoulder
Flexion of the elbow and wrist
Pronation of the forearm
Flexion of the fingers and adduction of the thumb
The following flexor patterns often are seen in patients with cerebral palsy, MS, or TBI or who have suffered a stroke:
Hip adduction and flexion
Ankle plantar flexion or equinovarus positioning
The following extensor patterns often are seen in patients following TBI:
Knee extension or flexion
Equinus and/or valgus ankle
Great toe dorsiflexion or excessive toe flexion
See Clinical Presentation for more detail.
In patients with new-onset spasticity, a thorough history and physical examination, as well as examination using electromyography, a determination of nerve conduction velocities, or imaging studies of the head, neck, and spine may be useful in eliminating treatable causes of increased tone.
In patients with a previous neurologic insult, a thorough history and physical examination is necessary to rule out any factors that can exacerbate spasticity (eg, medication changes, noxious stimuli, increased intracranial pressure).
Laboratory studies (eg, complete blood count [CBC] and culturing of urine, blood, cerebrospinal fluid) may help to rule out infection.
Spasticity is difficult to quantify, but clinically useful scales include the following:
Ashworth Scale/Modified Ashworth: From 0-4 (normal to rigid tone)
Physician's Rating Scale: Gait pattern and range of motion assessed
Spasm Scale: From 0-4 (no spasms to >10/h)
See Workup for more detail.
Interventions for spasticity vary from conservative (therapy and splinting) to more aggressive (surgery); most often, a variety of treatments are used at the same time or are employed interchangeably. Treatment options do not need to be used in a stepladder approach and indeed should not be. Current spasticity management options include the following:
Therapeutic interventions (physical therapy, occupational therapy, hippotherapy, aquatics) and physical modalities (ultrasonography, electrical stimulation, biofeedback) [3, 4]
Positioning/orthotics (including taping, dynamic and static splints, wheelchairs, and standers)
Oral medications (such as baclofen and dantrolene) 
Injectable neurolytic medications (botulinum toxins and phenol)
Surgical intervention (including selective dorsal rhizotomy and orthopedic procedures)
Spasticity is increased, involuntary, velocity-dependent muscle tone that causes resistance to movement. The condition may occur secondary to a disorder or trauma, such as a tumor, a stroke, multiple sclerosis (MS), cerebral palsy, or a spinal cord, brain, or peripheral nerve injury. (See Pathophysiology and Etiology.)
Spasticity usually is accompanied by paresis and other signs, such as increased stretch reflexes, which collectively are called upper motor neuron syndrome. Paresis particularly affects distal muscles, with loss of the ability to perform fractionated movements of the digits. (See Clinical Presentation.)
Upper motor neuron syndrome results from damage to descending motor pathways at the cortical, brainstem, or spinal cord levels. When the injury that leads to spasticity is acute, muscle tone is flaccid with hyporeflexia before the appearance of spasticity. The interval between injury and the appearance of spasticity varies from days to months according to the level of the lesion. In addition to weakness and increased muscle tone, the signs in spasticity include the following (see Clinical Presentation):
Spasticity can be severely debilitating, but with appropriate neurologic, surgical, rehabilitative, and psychosocial interventions, its manifestations can be treated, thus greatly improving the quality of life of affected individuals. (See Prognosis, Treatment, and Medication.)
While the incidence of spasticity is not known with certainty, the condition likely affects over half a million people in the United States and over 12 million people worldwide.
The pathophysiologic basis of spasticity is incompletely understood. Polysynaptic responses may be involved in spinal cord–mediated spasticity, while enhanced excitability of monosynaptic pathways is involved in cortically mediated spasticity.
Spasticity-related changes in muscle tone probably result from alterations in the balance of inputs from reticulospinal and other descending pathways to the motor and interneuronal circuits of the spinal cord, along with the absence of an intact corticospinal system. Loss of descending tonic or phasic excitatory and inhibitory inputs to the spinal motor apparatus, alterations in the segmental balance of excitatory and inhibitory control, denervation supersensitivity, and neuronal sprouting may be observed.
Once spasticity is established, the chronically shortened muscle may develop physical changes, such as shortening and contracture, that further contribute to muscle stiffness.
Cortical and spinal cord damage
Selective damage to area 4 in the cerebral cortex of primates produces paresis that improves with time, but increases in muscle tone are not a prominent feature. Lesions involving area 6 cause impairment of postural control in the contralateral limbs. Combined lesions of areas 4 and 6 cause both paresis and spasticity to develop.
Physiologic evidence suggests that interruption of reticulospinal projections is important in the genesis of spasticity. In spinal cord lesions, bilateral damage to the pyramidal and reticulospinal pathways can produce severe spasticity and flexor spasms, reflecting increased tone in flexor muscle groups and weakness of extensor muscles.
Mechanisms of spasticity
The pathophysiologic mechanisms causing the increase in stretch reflexes in spasticity also are not well understood. Unlike healthy subjects, in whom rapid muscle stretch does not elicit reflex muscle activity beyond the normal short-latency tendon reflex, patients with spasticity experience prolonged muscle contraction when spastic muscles are stretched. After an acute injury, the ease with which muscle activity is evoked by stretch increases in the first month of spasticity; then, the threshold remains stable until declining after a year.
During the development of spasticity, the spinal cord undergoes neurophysiologic changes in the excitability of motor neurons, interneuronal connections, and local reflex pathways. The excitability of alpha motor neurons is increased, as is suggested by enhanced H-M ratios and F-wave amplitudes. Judged by recordings from Ia spindle afferents, muscle spindle sensitivity is not increased in human spasticity.
Local anesthetic injections into spastic muscles in man can diminish spasticity through an effect on gamma motor neurons. Renshaw cells receive inputs from descending motor pathways, and recurrent collateral axons from motor neurons activate Renshaw cells, which inhibit gamma motor neurons. Renshaw cell activity is not reduced significantly in spasticity.
Reciprocal inhibition between antagonist muscles is mediated by the Ia inhibitory interneuron, which also receives input from descending pathways. Altered activity in Ia pathways has been shown in spasticity. Inhibitory interneurons acting on primary afferent terminals of the alpha motor neuron also influence the local circuitry.
Finally, plasticity and the formation of new aberrant connections in the central nervous system (CNS) is another theoretical explanation for some of the events in spasticity.
Treatable factors that may cause sudden onset of spasticity include the following:
Tethered spinal cord
Nerve impingement peripherally or centrally
Intracranial, epidural, or subdural bleeding
Factors that can exacerbate preexisting spasticity from spinal injury, brain tumor/injury, cerebral palsy, or MS include the following:
Infection (eg, otitis, urinary tract infection, pneumonia)
Noxious stimulus (eg, ingrown toenail, ill-fitting orthotics, occult fracture)
Spasticity can have a devastating effect on function, comfort, and care delivery, and it also may lead to musculoskeletal complications. Spasticity does not always require treatment, but when it does, a wide range of effective therapies—used alone or in combination—are available.
Rizzo et al, in an analysis of a cross-sectional database of 17,501 patients with MS (NARCOMS registry), reported the following with regard to the prevalence of spasticity :
15.7% had no spasticity
50.3% had minimal to mild spasticity
17.2% had moderate spasticity
16.8% had severe spasticity
A review of spasticity after stroke showed that it affects less than one quarter of stroke victims. Ninety-five patients were studied immediately after and 3 months after a first-time stroke. Seventy-seven (81%) were initially hemiparetic, of whom 20 had spasticity. Modified Ashworth score was grade 1 in 10 patients, grade 1+ in 7 patients, and grade 2 in 3 patients. At 3 months, 64 patients (67%) were hemiparetic and 18 were spastic, reflecting 5 whose tone normalized and 3 who became spastic in the interim.
Disadvantages of spasticity
The negative impacts of spasticity on health and quality of life include the following:
Orthopedic deformity, such as hip dislocation, contractures, or scoliosis
Impairment of activities of daily living (eg, dressing, bathing, toileting)
Impairment of mobility (eg, inability to walk, roll, sit)
Skin breakdown secondary to positioning difficulties and shearing pressure
Pain or abnormal sensory feedback
Poor weight gain secondary to high caloric expenditure
Depression secondary to lack of functional independence
Advantages of spasticity
Spasticity can confer certain benefits to the patient, including the following:
Substitutes for strength, allowing standing, walking, gripping
May improve circulation and prevent deep venous thrombosis and edema
May reduce the risk of osteoporosis
Resources and advocacy groups
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