Updated: Jun 28, 2019
  • Author: Krupa Pandey, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
  • Print

Practice Essentials

Spasticity is increased, involuntary, velocity-dependent muscle tone that causes resistance to movement. The condition is typically a result of insult to the central nervous system or motor neurons. It may occur as a primary condition such as in degenerative conditions or as a result of secondary causes such as spinal cord injury, trauma to the brain, or inflammatory conditions such as multiple sclerosis.

Signs and symptoms

Typically, the most common sign on exam is resistance to a passive change in a joint angle. It is most commonly noted in the flexor muscles of the upper extremities, the proximal extensor muscles of the lower extremities, and the distal flexor muscles of the lower extremities. As such, depending on the insult, specific patterns may arise that can aide in treatment.

Cerebral palsy

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 present in patients with cerebral palsy, stroke, or traumatic brain injury (TBI): [1]

  • 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 can occur in patients with cerebral palsy, MS, or TBI or who have suffered a stroke: [1]

  • Hip adduction and flexion

  • Knee flexion

  • Ankle plantar flexion or equinovarus positioning

The following extensor patterns may be 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, including family history, and physical examination are crucial. Additional tests such as electromyography for evaluation of motor neuron disease, determination of nerve conduction velocities, or imaging studies of the head, neck, and spine may be useful in eliminating treatable causes of increased tone. [2]

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, [3] 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 may 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:

  • Preventative measures

  • Therapeutic interventions (physical therapy, occupational therapy, hippotherapy, aquatics) and physical modalities (ultrasonography, electrical stimulation, biofeedback) [4, 5]

  • Positioning/orthotics (including taping, dynamic and static splints, wheelchairs, and standers)

  • Oral medications (such as baclofen and dantrolene) [6]

  • Injectable neurolytic medications (botulinum toxins and phenol)

  • Intrathecal baclofen

  • Surgical intervention (including selective dorsal rhizotomy and orthopedic procedures)

See Treatment and Medication for more detail.



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):

  • Clonus

  • Clasp-knife phenomenon

  • Hyperreflexia

  • Babinski sign

  • Flexor reflexes

  • Flexor spasms

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. [7]

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 [8] and F-wave amplitudes. [9] 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

  • Hydrocephalus

  • 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)

  • Bladder distention

  • Bowel impaction

  • Cold weather

  • Fatigue

  • Seizure activity

  • Stress

  • Malpositioning



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.

Multiple sclerosis

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 [10] :

  • 15.7% had no spasticity

  • 50.3% had minimal to mild spasticity

  • 17.2% had moderate spasticity

  • 16.8% had severe spasticity


In several studies examining patients at 12 months post-stroke, spasticity has been estimated to occur in up to 46% of patients 12 months after stroke. [11, 12, 13] Spasticity is associated with a negative impact on the health-related quality of life (HRQoL) of stroke survivors with statistically and clinically meaningful differences existing between stroke survivors with and without spasticity. These results suggest an opportunity to improve HRQoL among stroke survivors with spasticity. [1]

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

  • Sleep disturbance

  • 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


Patient Education

Resources and advocacy groups

Christopher & Dana Reeve Foundation

636 Morris Turnpike

Suite 3A

Short Hills, NJ 07078, USA

TEL: (800) 225-0292 or

(973) 379-2690 (outside the United States)

American Stroke Association, a division of the American Heart Association

7272 Greenville Avenue

Dallas, TX 75231, USA

TEL: (888) 478-7653

Brain Injury Association of America

1608 Spring Hill Road

Suite 110

Vienna, VA 22182, USA

TEL: (703) 761-0750


Multiple Sclerosis Association of America

706 Haddonfield Road

Cherry Hill, NJ 08002, USA

TEL: (800) 532-7667 or (856) 488-4500

FAX: (856) 661-9797

Email: (general information) or (MS questions)

Multiple Sclerosis Foundation

6520 N Andrews Avenue

Ft Lauderdale, FL 33309-2130, USA

TEL: (888) 673-6287 or (954) 776-6805

FAX: (954) 351-0630


National Multiple Sclerosis Society

733 3rd Avenue, 6th Floor

New York, NY 10017-3288, USA

TEL: (800) FIGHT MS (344-4867) or (212) 986-3240

FAX: (212) 986-7981


National Spinal Cord Injury Association

A program of the United Spinal Association

75-20 Astoria Blvd

Jackson Heights, NY 11370, USA

TEL: (718) 803-3782

National Stroke Association

9707 East Easter Lane

Suite B

Centennial, CO 80112, USA

TEL: (800) 787-6537

FAX: (303) 649-1328

Stroke Clubs International

Contact: Ellis Williamson

805 12th Street

Galveston, TX 77550, USA

TEL: (409) 762-1022


United Cerebral Palsy

1825 K Street NW

Suite 600

Washington, DC 20006, USA

TEL: (800) 872-5827 or (202) 776-0406