Spasticity is a motor disorder characterized by velocity-dependent increase in tonic stretch reflexes resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles. Clinically, this results in increased muscle tone, exaggerated tendon reflexes, clonus and re-emergence of primitive reflexes.1
Disorders of the central nervous system, such as strokes, traumatic brain injuries, neoplasms, cerebral palsy, multiple sclerosis and spinal cord injuries result in neural reorganization causing abnormal neural and muscle control. Spasticity develops as a result of an imbalance between excitatory and inhibitory input to α motor neurons resulting in disinhibition of the stretch reflex and increased muscle excitability.2 The pattern of spasticity depends on the location of the injury in the CNS. Alterations in neural pathways lead to changes in mechanical properties of muscles and joints that account for some features of spasticity.
The epidemiology of spasticity is specific to the type and severity of CNS injury. For example, it is estimated that spasticity affects 65-78% of chronic spinal cord injury (SCI) patients3, 25% of stroke patients,4 80% of patients with MS at some point during their clinical course,5,6 and more than 90% in CP.7
The mechanism behind spasticity is not completely understood and likely varies depending on the site of the CNS injury. This process begins with damage to upper motor neuron followed by any number of maladaptive neural changes, including8,9,10,11
- Loss of inhibitory control by descending pyramidal and reticulospinal tracts
- Maladaptive branching of residual corticospinal and reticulospinal tracts
- Hyperexcitability of reticulospinal, vestibulospinal and rubrospinal projections12
- Increased sensitivity of stretch-activated muscle spindles.
The above alterations result in changes to the classic sensory-motor reflex arc, such that a stretched muscle results in abnormal activation causing the pathological velocity-dependent resistance, defined as spasticity.
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
New onset/acute (CNS injury)
- During the acute period following CNS injury, affected trunk and limb muscles are typically flaccid. After traumatic SCI, spinal shock occurs, which is a temporary conduction block of electrical transmission through the spinal cord, characterized by hypotension, bradycardia, and loss of sympathetic stimulation. In contrast, stroke patients present with flaccidity without associated autonomic symptoms.4
- Reflexes can become brisk and increasingly more exaggerated followed by observable increases in muscle tone and spasticity of the affected muscle groups. The progression of spasticity is variable between disorders and individuals, and the emergence of symptoms is progressive.
- Chronic untreated spasticity may cause bony deformity (e.g., tibial torsion or hip dysplasia seen in children with cerebral palsy), remodeling of soft tissue, and muscle and soft tissue contractures that limit range of motion (ROM).10 Eventually, this remodeling may result in postural and functional abnormalities.4
Specific secondary or associated conditions and complications
Spasticity can be associated with the following features of the upper motor neuron syndrome13
|• Increased tendon reflexes with radiation|
• Babinski reflex
• Extensor spasms
• Flexor Spasms
• Mass Reflex
• Dyssynergistic patterns of co-contraction during movement
• Associated reactions and other dyssynergistic and stereotypical spastic dystonias
|• Muscle weakness|
• Loss of dexterity
• Easy fatigability – notable decline in peak force, power, speed or accuracy during continuous performance of a prolonged task
Essentials of Assessment
A thorough history regarding the onset and mechanism of injury or pathological process should be obtained. Additional history regarding functional deficits, mobility and quality of life should be assessed. 4 Qualitative questions about spasticity include information about:
- Interference with function, hygiene, and safety
- Temporal changes of symptoms
- Patterns of overflow (stereotypical synergistic movement patterns, e.g. Upper extremity flexion patterns associated with stroke)
- Possible benefits (e.g., assisting with transfers)
- Previous treatments
- Recent and current medical problems
It is also important to note changes in function, social history and caregiver burden. Other medical conditions, such as urinary and bowel dysfunction or skin breakdown known to exacerbate spasticity should also be explored. Last, a full medication list should be obtained.8,11
Spasticity is the velocity dependent sensation of resistance felt when a joint is ranged. In other words, greater resistance is felt when a joint is ranged with greater velocity. Affected joints should be examined for degrees of range of motion and intensity of spasticity based on a reproducible scale. A spastic muscle will have the tendency to remain in a shortened position, with simultaneous co-contraction of antagonistic muscles. For example, an individual affected by spasticity will have co-contraction of the triceps when trying to flex their elbow, resulting in less efficient movement, weakness, and loss of dexterity.
Joint ROM needs to be monitored over time because spasticity may result in contractures unless appropriately treated.
The Modified Ashworth Scale (MAS) is a commonly used and easily applicable scale used to score passive individual muscle movement as the limb is moved through its entire arc of joint motion over a one-second time period.14 The amount of non-volitional resistance the examiner encounters is quantified to indicate the intensity of spasticity:
- 0 – no increase in muscle tone
- 1 – slight increase in muscle tone (usually a catch and release feeling)
- 1+ – slight increase in muscle tone, manifested by a catch, with minimal resistance throughout remainder (less than half) of motion
- 2 – marked increase in muscle tone through most of the ROM but easily moved
- 3 – increased muscle tone with difficult passive movement
- 4 – rigid without movement
The tardieu scale measures the quality and angle of muscle reaction. The patient is seated when testing upper extremities and supine when testing lower extremities. A standard goniometer is used to measure the joint angles.
There are three speed definitions:
- V1 – As slow as possible
- V2 – Speed of a limb falling under gravity
- V3 – Moving as fast as possible
Quality of Muscle Reaction:
- 0 – No resistance throughout passive movement
- 1 – Slight resistance throughout, with no clear catch at a precise angle
- 2 – Clear catch at a precise angle followed by release
- 3 – Fatiguable Clonus (< 10 secs) occurring at a precise angle
- 4 – Unfatiguable Clonus (> 10 secs) occurring at a precise angle
- 5 – Joint immobile
R1 – Angle of catch seen at V2 or V3
R2 – Full range of motion achieved when muscle is at rest and tested at V1 velocity
The stretching velocity of V1 and V3 are applied to measure R2 and R1, respectively. The quality of muscle reaction is graded at the velocity of V3. The difference between R2 and R1 is the measure of the dynamic component of spasticity.
The patient can be observed performing activities that may exacerbate spasticity in order to fully understand how spasticity influences their function. Ideally, this assessment would occur at multiple times over several days because spasticity is variable and can be affected by time of day, training effect, emotional state of patient, and concurrent illness.14
Outcome measures can be grouped according to parameters that they measure:
- Physiological measures eg shortening of individual muscle cells, Hmax/Mmax ratio (has been shown to correlate with clinically observed increased in muscle stretch reflex activity)
- Measures of passive activity: Goniometric Measurement, resistance to movement (e.g.Ashworth and Modified Ashworth scales, Tardieu scale)
- Measures of voluntary activity (e.g.,9-hole peg test, Timed walking test)
Functional goals may be classified as relieving symptoms (e.g., pain, spasms), facilitating passive function (e.g., ease of caregiver assisted positioning, transfers, personal care) and active function (e.g., self-transfers, gait quality and velocity). Assessment tools should be tailored to measure the identified goal (e.g., pain scales, spasm frequency scales, walking speeds, overall comfort rating).
It is important to note that there can be benefits to having spasticity. For example, extensor spasticity in the lower extremity can help facilitate transfers by maintaining the hip and knee in extension while standing. It may also maintain muscle bulk in an otherwise weakened limb or body section.
There are no laboratory studies that identify spasticity, however LFTs should be monitored when certain pharmacological treatments, such as dantrolene or tizanidine, are used. Baclofen should be used cautiously in the presence or renal disease. Additionally, acute conditions such as infections or electrolyte disturbances may suddenly worsen spasticity and thus changes in spasticity severity should be investigated. 15
Imaging may help in the assessment for noxious stimuli that can exacerbate spasticity, such as fractures, heterotopic bone formation, or deep venous thrombosis.
Supplemental assessment tools
The intensity of spasticity is often quantified according to two common scales: the Modified Ashworth Scale (see above) or Tardieu Scale, used most commonly in Europe. Although the MAS has been standardized and thoroughly tested, it has limited inter-rater reliability. Furthermore, it fails to convey functional or prognostic information. The advantage of the Tardeiu scale is it uses a fast and slow speed of movement, measures range of movement and includes a subjective rating scale. However, few studies reflect the validity and reliability of this test. Electromyography (EMG) and nerve conduction measures (NCS) have been used in the assessment of spasticity. Needle and surface EMG can be used to identify overactive muscles. A ratio of the H-reflex to M-wave has been used as an index of spasticity but it lacks correlation with prognosis, function, or response to various treatments.14,16
Early predictions of outcomes
Understanding the natural history of the underlying neurological injury will drive predictions about the course of spasticity. There are no validated prognostic models of spasticity available.
Spasticity will affect the way the individual interacts with the environment by influencing independence with transfers, ambulation, and performance of activities of daily living. Environmental modifications, wheelchairs, transfer techniques, and positioning with cushions and supports can affect the intensity of spasticity and its functional impact.
Involvement of the patient, caregivers, and interdisciplinary team, including therapists, social workers, and nursing staff are essential in setting realistic goals and for optimal management of spasticity and function.
Rehabilitation Management and Treatments
Available or current treatment guidelines
The goal of spasticity management is to reduce maladaptive, abnormal tone while improving function. 4,13,14 No universal, evidence-based guidelines exist in spasticity management. The initial management should focus on reducing exacerbating causes before specific treatment is considered. Most clinicians employ a stepped approach to spasticity management utilizing simple and non-invasive strategies before resorting to treatments that carry a greater burden of risks and side effects. Treatment strategies are employed based on several principles, including desired goals and whether spasticity is generalized, focal (affecting a localized part of the limb) or multifocal (affecting multiple parts of a limb or multiple limbs).
Desired outcomes are often patient- and caregiver-specific. They range from complex goals such as improved mobility to more basic aims such as improved hygiene and decreased pain. Effectiveness of spasticity interventions can be assessed by technical factors, functional changes, patient satisfaction, and cost effeciency.14
An appropriate treatment regimen may employ numerous modes of treatment as outlined below.
Basic ROM activities remain the cornerstone for managing spasticity and preventing complications. Interdisciplinary treatment, with patient and caregiver involvement is critical for maintaining a dedicated daily regimen. 15,17
Application of cold modalities has been used to assist stretching by decreasing muscle spindle reactivity. Hydrotherapy (i.e., pool therapy) assists some patients with decreasing oral medications and improving function. Heat, especially via ultrasound, can enhance stretching of collagen fibers but can also trigger increased spasticity.3, 18 Early research indicates that functional electrical stimulation may assist in decreasing spasticity when paired with functional activities.19
Seating and positioning
Proper patient positioning can positively impact tone, spasticity, and preservation of ROM. Cushioning and body supports incorporated into beds, wheelchairs, and standing frames can be used to optimize positioning.
Orthoses, splinting, and casting
Orthoses resist a patient’s spasticity, provide sustained muscle stretch and prevent joint contractures. They may be used functionally during rest as with a nocturnal hand splint or functionally such as a walking ankle foot orthosis.
If a joint is significantly contractured that adversely impacts function, serial casting may be employed to lengthen shortened muscles by sarcomere addition,19 thereby increasing functional range of motion. Caution and close follow up are needed when using casts and orthoses on insensate limbs.
Medications, as presented below, can decrease overall muscle tone but may result in side effects such as somnolence, lethargy, and weakness.21
|Medication||Mechanism||Daily PO Dosage||Side Effect|
|Benzodiazepines||GABA A agonist||Varies||somnolence|
|Baclofen||GABA B agonist||15 – 80mg||Drowsiness, weakness, withdrawal syndrome possible|
|Dantrolene||Hydantoin Deriative that inhibits calcium release (works directly on skeletal muscle)||25 – 300mg||Drowsiness, dizziness, hepatotoxicity|
|Tizanidine||Alpha 2 presynaptic receptor Agonist||8 – 36mg||Orthostatic hypotension, constipation, dry mouth, hepatotoxicity|
|Clonidine||Alpha 2 presynaptic agonist||0.1 – 2.4mg||dry mouth, hypotension / syncope|
|Gabapentin||Selective inhibitor of voltage-gated calcium channels||100 – 2400mg||dizziness, somnolence|
|Lamotrigine||Inhibits sodium channels||25 – 500mg||dizziness, rash|
|Cyproheptadine||Alters serotonin, histamine, acetylcholine||4 – 32mg||Sedation|
|Tetrahydrocannabinol||CB1 and CB2 receptors||Varies||Potential cognitive impairment, Anxiety|
Alcohol or phenol neurolytic injections of motor nerves or small motor branches can be effective for focal spasticity. These injectates denature proteins in neural tissue thus preventing transmission. Administration of neurolytic medications requires significant technical skill. Systemic absorption can result in hypotension, tremor or convulsions. Possible side effects include swelling and injection in proximity to sensory nerves may result in dysthesias.15
Focal spasticity, especially in the upper limb, hand, or foot muscles, may be effectively treated with botulinum toxin which inhibits pre-synaptic release of acetylcholine in the neuromuscular junction. The effects of botulinum toxin injections typically last three to four months.14 A limitation of this method is the expense and duration of effect. EMG, electrical stimulation and ultrasound guidance, used in isolation or combination can help with anatomic localization of muscles to inject. The FDA issued a black box warning on botulinum toxin in 2009 regarding the potential for toxin spread when used for spasticity with risks for life-threatening swallowing and breathing difficulties with the potential for death.22
An intrathecal baclofen (ITB) pump delivers medication directly into the intrathecal space and its effectiveness is well validated. ITB administration limits systemic side effects such as somnolence seen with oral administration. This results from more direct access to GABA-B receptors in the spinal cord which also enhances spasticity relief.4,22 A number of adverse events, such as constipation, urinary retention, pump and catheter malfunction, and the need for battery replacement, should be considered. Physicians familiar with ITB systems should manage medication dosing and pump issues.16 Recipients of ITB pumps need to be carefully screened to ensure they have the resources and ability to follow up for regularly scheduled pump refills and maintenance in order to avoid potentially life-threatening baclofen withdrawal.
Surgical management may be required to treat the contractures and other joint deformities caused by spasticity. Surgical interventions may include peripheral neurotomies, tendon releases, tendon lengthening and rhizotomies which are utilized sparingly due to the inherent risks.24
Coordination of care
A coordinated rehabilitation team consisting of the patient, their family / caregivers with physiatrist, physical therapist (PT), occupational therapist (OT), and speech and language pathologist (SLP) when appropriate, can assist in the management of spasticity. These caregivers can help the patient identify functional goals, provide education and treatment, and assist with initial assessment and response to therapy.23
Patient & family education
Patients and family should be educated early about the sequelae of the upper motor neuron syndrome. When spasticity treatments are offered, education about potential side effects is necessary, including the potential for reduced muscle strength or function (e.g., transfers). Certain therapies require significant patient and caregiver commitment and treatment adherence, such as ITB.
Intrathecal baclofen can cause life-threatening problems if a patient is overdosed or if they are withdrawn from treatment abruptly. Strict adherence to refill schedules and watchfulness for any changes in spasticity pattern can help patients and families avoid complications. As changes in spasticity can also herald a new disease process, patients and families should communicate changes to their care team. Similarly, botulinum toxins, when used for spasticity, carry a black box warning for potential toxin spread that may result in respiratory failure and death22, particularly if injected in close proximity to facial and neck structures.
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
Sudden increases in spasticity can be caused by worsening of a disease process or by irritants. Common irritants include heterotopic ossification, urinary tract infections, urolithiasis, stool impaction, pressure ulcers, fractures or dislocations, ingrown toenails, growth spurts, and emotional stress.15,17, 29
Cutting Edge/Emerging and Unique Concepts and Practice
Cutting edge concepts and practice
Human recombinant hyaluronidase is under investigation to address muscle stiffness resulting from prolonged joint immobility that arises from spasticity. Excessive accumulation of hyaluronan in muscles immobilized by CNS injury and spasticity is theorized to contribute to muscle stiffness by developing cross linkage of molecules and increased viscoelasticity of the extracellular matrix, inhibiting muscle movement. Local injection of hyaluronidase hydrolyzes hyaluronan, with the potential to reduce stiffness. Further research is needed to study the optimal dosing, duration, number/locations of injections and the possibility of placebo effect. 26
Gaps in the Evidence-Based Knowledge
There is a lack of understanding of the exact pathophysiology underlying spasticity. The difficulty in measuring spasticity intensity in response to treatments impedes efforts in determining therapy effects. Most clinical scales that assess spasticity and quantify response to treatment are ordinal and poorly quantify the response to treatment. Additionally, severity of spasticity can vary throughout the day thus further clouding clinical assessment. Global scales measuring functional limitation such as the Functional Independence Measure and the Barthel Index are not sensitive enough to record change after therapeutic interventions. Furthermore, none of these techniques incorporate the subjective experience of spasticity, nor how it affects the quality of people’s lives. Reliable and reproducible quantitative measures are needed for evaluation of spasticity.27
- Lance, JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurology 1980;30:1303-13.
- Young RR. Spasticity: a review. Neurology 1994;44(suppl9):S12-20.
- Holtz KA, Lipson R, Noonan VK, Kwon BK, Mills PB. Prevalence and Effect of Problematic Spasticity After Traumatic Spinal Cord Injury. Arch Phys Med Rehabil. Jun 2017;98(6):1132-1138. doi:10.1016/j.apmr.2016.09.124
- Zeng H, Chen J, Guo Y, Tan S. Prevalence and Risk Factors for Spasticity After Stroke: A Systematic Review and Meta-Analysis. Systematic Review. Frontiers in Neurology. 2021-January-20 2021;11(1884)
- Bethoux F, Marrie RA. A cross-sectional study of the impact of spasticity on daily activities in multiple sclerosis. Patient. 2016;9(6):537–546.
- L. Hemmett, J. Holmes, M. Barnes, N. Russell, What drives quality of life in multiple sclerosis?, QJM: An International Journal of Medicine, Volume 97, Issue 10, October 2004, Pages 671–676
- Yeargin-Allsopp M, Van Naarden Braun K, Doernberg NS, Benedict RE, Kirby RS, Durkin MS. Prevalance of cerebral palsy in 8-year old children in three areas of the United States in 2002: a multisite collaboration. Pediatrics 2008;121:547-54.
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- Bareyre FM, Kerschensteiner M, Raineteu O, Mettenleiter TC, Weinmann O, Schwab ME. The injured spinal cord spontaneously forms a new intraspinal circuit in adult rats. Nature Neuroscience. 2004;7(3):269-277.
- Mayer NH. Clinicophysiologic concepts of spasticity and motor dysfunction in adults with an upper motoneuron lesion. Muscle & Nerve. 1997;6(S):S1-S13.
- Trompetto C, Marinelli L, Mori L, et al. Pathophysiology of spasticity: implications for neurorehabilitation. Biomed Res Int. 2014;2014:354906. doi:10.1155/2014/354906
- Barnes MP. An Overview of the Clinical Management of Spasticity, in Upper Motor Neuron Syndrome and Spasticity: Clinical Management and Physiology, eds. Barnes MP and Johnson GR. Cambridge University Press, New York, 2001.
- Pierson SH. Outcome measures in spasticity management. Muscle & Nerve. 1997;6(S):S37-S60.
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- Yablon SA, Stokic DS. Neurophysiologic evaluation of spastic hypertonia. Am. J. Phys. Med. Rehabil. 2004;10(S):S10-S18.
- Smania N, Picelli A, Munari D, et al. Rehabilitation procedures in the management of spasticity. European Journal of Rehabilitation Medicine. 2010;46:423-438.
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- O’Dell MW, Lin CCD, Harrison V. Stroke rehabilitation: Strategies to enhance motor recovery. Annual Review of Medicine. 2009;60:55-68.
- Boakes JL, Foran J, etal. Muscle adaptation by serial sarcomere addition 1 year after femoral lengthening. Clin Orthop Relat Res. 2007 Mar;456:250-3.
- Zafonte R, Lombard L, Elovic E. Antispasticity medications: Uses and limitations of enteral therapy. Am. J. Phys. Med. Rehabil. 2004;10(S):S50-S58.
- Kuehn BM. FDA requires black box warning on labeling for botulinum toxin products. JAMA. 2009;301(22):2316.
- Francisco GE. The role of intrathecal baclofen therapy in the upper motor neuron syndrome. Eur. Med. Phys. 2004;40:131-143.
- Chambers HG. The surgical treatment of spasticity. Muscle & Nerve. 1997;6(S):S121-S128.
- Taub, E; Uswatte, G; Pidikiti, R (1999). “Constraint-Induced Movement Therapy: A new family of techniques with broad application to physical rehabilitation–a clinical review”. Journal of rehabilitation research and development. 36 (3): 237–51.
- Mori F The use of repetitive transcranial magnetic stimulation (rTMS) for the treatment of spasticity. Prog Brain Res. 2009;175:429-39.
- Raghavan P, Lu Y, Mirchandani M, Stecco A. Human Recombinant Hyaluronidase Injections For Upper Limb Muscle Stiffness in Individuals With Cerebral Injury: A Case Series. EBioMedicine. 2016;9:306-313. doi:10.1016/j.ebiom.2016.05.014
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- Haugh AB, Pandyan AD, Johnson GR. A systematic review of the Tardieu Scale for the measurement of spasticity. Disabil Rehabil. Aug 15 2006;28(15):899-907.
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Original Version of the Topic
Craig C. DiTommaso, MD, Kathleen R. Bell, MD. Spasticity. 6/7/2013.
Previous Revision(s) of the Topic
Marika Hess, MD, Damon Gray, MD. Spasticity. 3/29/2017.
Krupali Chokshi, MD
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Steven Flanagan, MD
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