Spasticity

Author(s): Marika Hess, MD and Damon Gray, MD

Originally published:11/27/2012

Last updated:03/29/2017

1. DISEASE/DISORDER:

Definition

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, enhanced tendon reflexes, clonus and re-emergence of primitive reflexes.1

Etiology

Disorders of the central nervous system, such as strokes, brain injuries, 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.

Epidemiology

The epidemiology of spasticity is specific to the type and severity of CNS injury. For example, it is estimated that spasticity affects 65 -78%3 of chronic spinal cord injury (SCI) patients, 17 – 39% of stroke patients,4 between 37 – 78% of patients with MS,5,6 and more than 90% in CP.7

Patho-anatomy/physiology

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 an upper motor neuron followed by any number of maladaptive neural changes, including:8,9,10,11

  1. Loss of inhibitory control by descending pyramidal and reticulospinal tractsMaladaptive branching of residual corticospinal and reticulospinal tracts

Increased effect of rudimentary brainstem- mediated descending tracts denervation supersensitivity causing  increased excitability of α-motoneuronslocal sprouting from neighboring spinal interneuronsIncreased sensitivity of stretch-activated muscle spindlesThe above alterations result in changes to the classic sensory-motor reflex arc, whereby when a limb is moved either passively or actively, the stretched muscle is activated abnormally, thereby causing the pathological velocity-dependent resistance, defined as spasciticy.

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 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

Subacute

  • Reflexes can become brisk and even more exaggerated followed by observable increases in muscle tone and spasticity for the affected muscle groups. The progression of spasticity is variable between disorders and individuals, and the emergence of symptoms is progressive.

Chronic

  • 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 syndrome12:

            Positive             Negative
  • Increased tendon reflexes with radiation
  • Clonus
  • Positive Babinsky
  • 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
  • Fatigueability

2. ESSENTIALS OF ASSESSMENT

History

A thorough history regarding the mechanism of injury or pathological process should be taken. Additional history regarding functional impact and quality of life shoule be assessed. 4 Qualitative questions about spasticity include information about:

  • Severity
  • Localization
  • Triggers
  • Interference with function, safety, and pain
  • Patterns of overflow (stereotypical synergistic movement patterns, eg. Upper extremity flexion patterns associated with stroke)
  • Possible benefits (e.g., assisting with transfers)
  • Temporal changes of symptoms

Changes in function and caregiver burden are important to note. Other medical conditions, such as urinary and bowel dysfunction or skin breakdown, that could exacerbate spasticity should be explored and a full medication list obtained.8,11

Physical examination

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 ROM, intensity of spasticity based on a reproducable 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.

The ROM of joints needs to be monitored over time because spasticity will result in contractures over time 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.13 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 with minimal resistance throughout remainder of motion
  • 2 – marked increase in muscle tone but easily moved
  • 3 – increased muscle tone with difficult passive movement
  • 4 – rigid without movement.

Functional assessment

The patient can be observed performing activities that may exacerbate spasticity in order to fully understand how spasticity influences 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.13

Outcome measures can be grouped according to parameters that they measure:

  1. Physiological measures eg shortening of individual muscle cells, H reflex
  2. Measures of passive activity: Goniometric Measurement, resistance to movement ( eg Ashworth and Modified Ashworth scales, Tardieu scale)
  3. Measures of voluntary activity (eg. 9 hole peg test, walking speed)

Functional goals may be classified as relieving symptoms (eg. pain, spasms), facilitating passive function (eg. ease of caregiver assisted positioning, transfers, personal care) and active function (eg. self-transfers, gait quality and velocity ). Assessment tools should be tailored to measure the identified goal (. eg pain scales, spasm frequency scales , walking speeds, overall comfort rating).

It is important to note that spasticity is not always a negative phenomenon that should be treated at all cost. Spasticity can be beneficial when patients use it to gain function with transfers, standing, and when primitive synergistic movements can be used functionally. It may be helpful in maintaining muscle bulk in an otherwise weakened limb or body section.

Laboratory studies

There are no laboratory studies that identify spasticity, however LFTs should be monitored when pharmacological treatment is employed to treat spasticity. When spasticity intensity worsens, an underlyng cause must be investigated, and exacerbating conditions such as infections and electrolyte disturbances should be considered.14

Imaging

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. 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.13,15

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.

Environmental

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 in turn affect the intensity of spasticity and its functional impact.

Professional Issues

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.

3. 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 benign strategies before resorting to treatments that carry a greater burden of risks and side effects. Since spasticity may be generalized, focal (affecting a localized part of the limb) or multifocal (affecting multiple parts of a limb or multiple limbs), treatment strategies are employed accordingly.

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. Spasticity improvements can be assessed by technical factors, functional changes, patient satisfaction, and cost effectiveness.13

An appropriate treatment regimen may employ numerous modes of treatment as outlined below.

Physiotherapy

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. 14,16

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 ultrasound, can enhance stretching of collagen fibers but can also trigger increased spasticity.3, 17 Early research indicates that functional electrical stimulation may assist in decreasing spasticity when paired with functional activities.18

Seating and positioning

Proper patient positioning, can positively impact tone, spasticity, and preservation of ROM. Cushioning and body supports with beds, wheelchairs, and standing frames can be used to optimize positioning.Orthoses, splinting, and casting

Orthoses resist a patient’s spasticity 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 found to be affected by a significant contracture that is adversely impacting function, serial casting may be employed to cause lengthening of the muscle by serial sarcomere addition19 to allow increased functional range of motion.

Pharmacological management

Medications, as presented below, can decrease overall muscle tone but may result in side effects such as somnolence, lethargy, and weakness.20

Medication Mechanism PO Dosage Side Effect
Benzodiazepines GABA A hyperpolarization Varies somnolence
Baclofen GABA B hyperpolarization 15 – 80mg somnolence
Dantrolene Inhibits calcium release 25 – 300mg somnolence, hepatic dysfunction
Tizanidine Alpha 2 antagonist 8 – 36mg constipation, dry mouth
Clonidine Alpha 2 antagonist 0.1 – 2.4mg dry mouth, hypotension / syncope
Gabapentin Unknown 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 Anxiety

 

Neurolysis

Alcohol or phenol neurolytic injections of motor nerves or small motor branches can be effective for local spasticity. Administration of neurolytic medications requires significant technical skillsand dysthesia is a possible adverse effect.14

Botulinum toxin

Localized spasticity problems, especially in the upper limb, hand, or foot muscles, may be effectively treated with  botulinum toxin which affects the release of acetylcholine from the presynaptic terminal. The relaxation effect of botulinum toxin injections will usually last three to four months in most patients.14 A limitation of this method is the expense and duration of effect. The FDA issued a black box warning on botulinum toxin in 2009 warning about the potential for toxin spread when used for spasticity with risks for life-threatening swallowing and breathing difficulties with the potential for death.21

Intrathecal baclofen

An intrathecal baclofen (ITB) pump delivers medication directly into the intrathecal space and is well validated. ITB administration limits systemic side effects seen with oral administration, such as somnolence, and improves medication effectiveness.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.15Surgical interventions

Methods of spasticity control involving surgery, such as tendon releases and rhizotomy, are utilized sparingly due to the inherent risks.23

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.22

Patient & family education

Patients and family should be educated early about the sequelae of the UMN 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.

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 death.21

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.14,16

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

NA

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

There is a lack of understanding of the exact pathophysiology underlying spasticity.  The difficulty in measuring spasticity intensity and change in spasticty 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. 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.26

REFERENCES

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  2. Young RR. Spasticity: a review. Neurology 1994;44(suppl9):S12-20.
  3. Adams MM, Hicks AL. Spasticity after spinal cord injury. Spinal Cord. 2005;43:577–586.
  4. Brainin M, Norrving B, Sunnerhager KS, et al. Poststroke chronic disease management: towards improved identification and interventions for post-spasticty-related complications. International Journal of Stroke. 2001;6:42-46.
  5. Barnes MP, Kent RM, Semlyen JK, McMullen KM. Spasticity in multiple sclerosis. Neurorehabil Neural Repair 2003;17:66-70.
  6. Goodin DS. Survey of multiple sclerosis in northern California. Northern California MS Study Group. Mult Scler 1999;5:78-88.
  7. 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.
  8. Gracies JM. Pathophysiology of spastic paresis. I: Paresis and soft tissue changes. Muscle & Nerve. 2005;31:535-551.
  9. Gracies JM. Pathophysiology of spastic paresis. II: Emergence of muscle overactivity. Muscle & Nerve. 2005;31: 552-571.
  10. 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.
  11. Mayer NH. Clinicophysiologic concepts of spasticity and motor dysfunction in adults with an upper motoneuron lesion. Muscle & Nerve. 1997;6(S):S1-S13.
  12. 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.
  13. Pierson SH. Outcome measures in spasticity management. Muscle & Nerve. 1997;6(S):S37-S60.
  14. Gracies JM, Elovic E, McGuire J, Simpson D. Traditional pharmacological treatments for spasticity: part I-Local treatments. Muscle & Nerve. 1997;6(S):S61-S91.
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  17. Wantanabe T. The role of therapy in spastic management. Am. J. Phys. Med. Rehabil. 2004;10(S):S45-S49.
  18. O’Dell MW, Lin CCD, Harrison V. Stroke rehabilitation: Strategies to enhance motor recovery. Annual Review of Medicine. 2009;60:55-68.
  19. 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.
  20. Zafonte R, Lombard L, Elovic E. Antispasticity medications: Uses and limitations of enteral therapy. Am. J. Phys. Med. Rehabil. 2004;10(S):S50-S58.
  21. Kuehn BM. FDA requires black box warning on labeling for botulinum toxin products. JAMA. 2009;301(22):2316.
  22. Francisco GE. The role of intrathecal baclofen therapy in the upper motor neuron syndrome. Eur. Med. Phys. 2004;40:131-143.
  23. Chambers HG. The surgical treatment of spasticity. Muscle & Nerve. 1997;6(S):S121-S128.
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Bibliography:

Gormley ME, O’Brien CF, Yablon SA. A clinical overview of treatment decisions in the management of spasticity. Muscle & Nerve. 1997;6(S):S14-S20.

Ivanhoe CB, Reistetter TA. Spasticity: The misunderstood part of the upper motor neuron syndrome. Am. J. Phys. Med. Rehabil. 2004;83(10):S3-S9.

Original Version of the Topic

Craig C. DiTommaso, MD, Kathleen R. Bell, MD. Spasticity. 06/07/2013.

Author Disclosure

Marika Hess, MD
Nothing to Disclose

Damon Gray, MD
Nothing to Disclose

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