Spasticity

Disease/Disorder

Definition

Spasticity is a motor disorder classically defined by velocity-dependent increase in tonic stretch reflexes resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles. This results in increased muscle tone, exaggerated tendon reflexes, clonus and re-emergence of primitive reflexes.¹ Spasticity is also described by its clinical presentation, etiology, localization, and associated CNS manifestiations.² 

An updated definition of spasticity has been proposed describing it as involuntary muscle overactivity in the setting of central paresis, elicited by slow or rapid passive joint movement or sensory stimulation. ³ It relates post-stroke spasticity to motor recovery to better account for its pathophysiology and the complex nuances arising from different definitions of motor recovery. More specifically, it defines spasticity in resting muscles as a velocity- and muscle length–dependent increase in resistance to externally imposed muscle stretch, resulting from hyperexcitable descending excitatory brainstem pathways and the resultant exaggerated stretch reflex responses. The definition proposes that abnormal synergies, inappropriate muscle activation, and anomalous muscle coactivation coexist with spasticity and share similar pathophysiological origins. It also elaborates on how spasticity interference with recovery of pre-injury motor function.⁴ 

Etiology

Disorders of the central nervous system, such as strokes, traumatic brain injuries (TBI), neoplasms, cerebral palsy (CP), multiple sclerosis (MS) and spinal cord injuries (SCI) result in neural reorganization causing abnormal neural and muscle control. Spasticity develops because of an imbalance between excitatory and inhibitory input to α motor neurons resulting in disinhibition of the stretch reflex and increased muscle excitability.⁵ 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 40% of people with SCI⁶ 35% of those with stroke,³ 50% of those with TBI, between 37%, -78% of people with MS at some point during their clinical course,^7,8 and more than 90% people with CP.⁹

Patho-anatomy/physiology

The mechanism behind spasticity is incompletely understood and likely varies depending on the site of the CNS injury. This process begins with damage to upper motor neurons followed by maladaptive neural changes, including^10,11,12,13

• Loss of inhibitory control by descending pyramidal and reticulospinal tracts
• Maladaptive branching of residual corticospinal and reticulospinal tracts
• Hyperexcitability of reticulospinal, vestibulospinal and rubrospinal projections¹⁴
• Increased sensitivity of stretch-activated muscle spindles.

These alterations result in changes to the classic sensory-motor reflex arc, such that a muscle stretch results in abnormal activation causing the pathological velocity-dependent resistance, classically 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, loss of sympathetic stimulation, and loss of motor reflexes.  Loss of motor reflexes with associated muscle flaccidity may also occur acutely post-stroke but without the associated autonomic symptoms occurring acutely after SCI.³

Subacute

Reflexes may 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

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 restrict range of motion (ROM).¹² Eventually, this remodeling may result in postural and functional abnormalities. ³

Specific secondary or associated conditions and complications

Spasticity is often associated with the following features of the upper motor neuron syndrome¹⁵

Essentials of Assessment

History

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.³ Qualitative questions about spasticity include information about

• Severity
• Localization
• Pain
• Spasms
• Triggers
• 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.

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 to measure their range of motion (ROM) 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 managed.

Modified Ashworth Scale

The Modified Ashworth Scale (MAS) is a commonly used and easily applicable ordinal scale used to grade resistance encountered during passive individual muscle movement as the limb is moved through its entire arc of joint motion over a one-second time period.^{1, 6} 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) towards end-of-ROM
• 1+ – slight increase in muscle tone, manifested by a catch, with minimal resistance throughout remainder (less than half) of the ROM
• 2 – marked increase in muscle tone through the majority of the ROM but still easily moved
• 3 – increased muscle tone with difficult passive movement throughout the majority of the ROM
• 4 – rigid (in flexion or extension) without movement

Modified Tardieu Scale

The Modified Tardieu Scale (MTS) measures the quality and angle of muscle reaction in response to different applied velocities (V1 – V3, slow to fast). The patient is seated when testing upper extremities and supine when testing lower extremities. A standard goniometer is used to measure the joint angles. Muscle Reaction is graded 0 through 5, and Spasticity Angle is graded as R1 or R2, all of which are defined below.

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

Spasticity Angle

• 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.

Penn Spasm Frequency Scale (PSFS)

The PSFS is a patient self-reporting tool used to provide subjective information on severity and frequency of spasticity-related spasms, commonly applied in studies assessing spasticity in the SCI population. ^17,18

• 0 – no spasms experienced
• 1 – spasms experienced are only elicited by vigorous sensory and motor stimulation
• 2 – spasms are easily induced and occasionally spontaneous, and occur less than once per hour
• 3 – spasms occur between 1 and 10 times per hour
• 4 – patient experiences more than 10 spasms per hour

Functional assessment

The patient can be observed performing functional activities in order to better understand how spasticity influences their daily activities. Ideally, this assessment should occur at multiple times over several days because spasticity is variable and can be affected by time of day, training effect, emotional state of the patient, and concurrent illness.¹⁶

Outcome measures can be grouped according to parameters they measure

• Physiological measures e.g., shortening of individual muscle cells, Hmax/Mmax ratio, also known as the “EMG ratio,” which describes or quantifies the maximal reflex excitability (activation) of the motor pool for a given muscle, which 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., MAS, MTS)
• 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 spasticity may offer potential functional benefits. 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.

Laboratory studies

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 of renal disease. Additionally, acute conditions such as infections, injuries or electrolyte disturbances may suddenly worsen spasticity, prompting an investigation to determine its etiology.¹⁹

Imaging

Imaging may help determine the etiology underlying unexpected changes spasticity, such as fractures, heterotopic bone formation, spinal cord syrinx or deep venous thrombosis.

Supplemental assessment tools

The intensity of spasticity is often quantified according to two common scales: the MAS (see above) or the MTS (see above), the latter of which is 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. MTS offers the advantage of assessing spasticity using both fast and slow movements, measuring range of movement and including a subjective rating scale. However, few studies reflect its validity and reliability, noting good inter-rater and test-retest reliability was reported, particularly among patients with SCI.²⁰ Electromyography (EMG) and nerve conduction measures (NCS) have also been used in the assessment of spasticity. Needle and surface EMG can be used to identify overactive muscles. The H-reflex to M-wave ratio (Hmax/Mmax) has been used as an index of spasticity but it lacks correlation with prognosis, function, or response to various treatments.^16,21

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 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.

Rehabilitation Management and Treatments

Available or current treatment guidelines

The goals of spasticity management are to reduce maladaptive, abnormal tone while improving function.^3,15,16 The American Academy of Physical Medicine & Rehabilitation (AAPMR) published evidence-based, best practice consensus guidance for the assessment and management of spasticity.²² Initial management focuses on reducing exacerbating causes before specific treatment is considered. Most clinicians employ a step-wise approach to management, utilizing non-invasive strategies before resorting to treatments that carry higher risks of undesirable 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.¹⁶

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

Physical/occupational therapy

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.^19,23

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.^6,24 Early research indicates that functional electrical stimulation may assist in decreasing spasticity when paired with functional activities.²⁵ Other nonpharmacological modalities used may include vibration, biofeedback, and direct tendon pressure.

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. Conversely, poor seating can trigger or exacerbate spasticity.

Orthoses, splinting, and casting

Orthoses resist spasticity by providing sustained muscle stretch and preventing joint contractures. They may be used during rest as with a nocturnal hand splint, or functionally, such as an ankle foot orthosis for ambulation. Orthoses can be plastic, carbon fiber or metal. Metal uprights may be preferred with fluctuating edema and sensory impairments because they do not come directly into contact with the patient’s skin, thereby decreasing the risk of pressure injuries in vulnerable populations.²⁶ An ill-fitting orthosis can trigger or contribute to exacerbation of spasticity.

If a joint is significantly contracted and adversely impacts function, serial casting may be employed to lengthen shortened muscles through sarcomere addition,²⁵ thereby increasing functional range of motion. Caution and close follow up are needed when using casts and orthoses on insensate limbs in order to avoid skin breakdown.

Pharmacological management

Medications, as presented below, can decrease overall muscle tone but may result in side effects such as somnolence, lethargy, and weakness.²⁷

Diagnostic nerve blocks

Injecting a local anesthetic (usually lidocaine or bupivacaine) perineurally under electrostimulation guidance will block motor conduction for several hours. This will provide clinicians an opportunity to assess potential benefits and plan more accurately for specific anti-spasticity interventions, such as chemoneurolysis or botulinum toxin.

Neurolysis

Ethyl alcohol (45% to 100%) or phenol (typically 5%) injections of motor nerves or small motor branches can be effective in managing 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 dysesthesias if injected in close proximity to sensory nerves, which in some reports affected 10-30% of patients, lasting weeks to months.  This more often occurs with phenol because it is more toxic. Spasticity reduction following neurolysis typically lasts greater than 6 months.¹⁹

Botulinum toxin

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.¹⁶ 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.Patients with an underlying neuromuscular disease, such as amyotrophic lateral sclerosis (ALS), myasthenia gravis, Lambert-Eaton syndrome, or peripheral motor neuropathic disease, are at increased risk of severe reactions including respiratory depression or dysphagia.²⁹ Most commonly used, and FDA-approved formulations include onabotulinumtoxin A, incobotulinumtoxin A, abobotulinumtoxin A, and rimabotulinumtoxin B.

Intrathecal baclofen

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.^3,29 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.²¹ 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 interventions

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.³⁰

Coordination of care

A coordinated rehabilitation team led by a physiatrist and consisting of the patient, their family / caregivers, physical therapist (PT), occupational therapist (OT), orthotist, neurosurgeon, orthopedic surgeons, and speech and language pathologist (SLP), when appropriate, can assist in managing spasticity.  These caregivers can help the patient identify functional goals, provide education and treatment, and assist with initial assessment and response to therapy.³¹

Patient & family education

Patients and family / caregivers 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 treatment is abruptly withdrawn. 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,²⁹ particularly if injected in close proximity to facial or 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.^19,23,32 Abrupt changes in spasticity while undergoing ITB treatment warrants immediate assessment for pump failure or errors occurring during pump refill or programming.

Cutting Edge/Emerging and Unique Concepts and Practice

Human recombinant hyaluronidase is under investigation to address muscle stiffness resulting from prolonged joint immobility arising 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.^33,34

Gaps in the Evidence-Based Knowledge

The exact pathophysiology underlying spasticity has not been fully elucidated.  The difficulty in measuring spasticity intensity in response to treatments impedes efforts in determining therapeutic effects. Most clinical scales that assess spasticity and treatment responses are ordinal and poorly quantify therapeutic efficacy. 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 insufficiently sensitive enough to record changes after therapeutic interventions. Furthermore, none of these measures 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.³⁵

References

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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, Steven Flanagan, MD. Spasticity. 10/13/2021

Author Disclosure

Steven Flanagan, MD
Nothing to Disclose

Jessica Rivetz, MD
Nothing to Disclose