Spasticity is a motor disorder marked by a velocity-dependent increase in muscle tone or tonic stretch reflexes associated with hypertonia.

Spasticity can present variably in a clinical setting, Spasticity can lead to many complications eg interference with daily function, hygiene, comfort, and nursing care as well as contractures (increasing the risk of pressure ulcers and subsequent infections). Also, spasticity poses an increased risk of subluxation and/or dislocation as well as heterotopic ossification. 

Spasticity can prove to be beneficial for some patients, allowing them to ambulate or simply stand/bear weight, decreasing their risk of developing osteoporosis and helping improve circulation and overall mental health[1].


Spasticity is a consequence of neuromuscular disorders, which affects quality of life in those who experience this phenomenon. Spasticity results from an upper motor neuron lesion that disinhibits the tendon stretch reflex; spasticity results in a velocity dependent tightness of muscle.[2]

The most well-known and referenced description of spasticity is the physiological definition proposed by Lance in 1980. [3]

  • 'Spasticity is a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neurone syndrome

More recently, a definition from Pandyan et al (2005) [4] states that spasticity is:

  • 'Disordered sensorimotor control, resulting, resulting from an upper motor neuron lesion (UMN), presenting as an intermittent or sustained involuntary activations of muscles [5]


Many clinical scenarios can lead to spasticity, such as stroke, cerebral palsy (CP), anoxia, traumatic brain injury (TBI), spinal cord injury (SCI), multiple sclerosis (MS), and other central nervous system (CNS) neurodegenerative diseases eg MND

Spasticity affects approximately

  • 35% of those with stroke,
  • more than 90% with CP
  • about 50% of TBI patients
  • 40% of SCI patients
  • between 37% and 78% of MS patients.[1]

Anatomy and Etiology

Spasticity is considered to be a positive sign of the upper motor neuron syndrome (UMNS), which refers to motor behaviors resulting from lesions proximal to the alpha motor neuron, therefore within the spinal cord or brain. Other positive features of UMNS include exaggerated muscle stretch reflexes and up-going plantar reflex. Negative features include motor weakness, slowed movement, loss of dexterity, or selective motor control. A UMN injury leads to loss of inhibition downstream and hypersensitivity of the reflex arc within the spinal cord.[1]

Primary impairments from an upper motor neuron lesion (UMNL) are usually due to the disruption of supraspinal control of descending pathways that control excitatory and inhibitory influences on proprioceptive, cutaneous and nociceptive spinal reflexes.

The Inhibitory System

Corticorecticular Fibres form the Corticoreticular Spinal Tract. These tracts travel with, but are separate from, the Corticospinal Tract, and is responsible for the facilitation of the inhibitory area within the medulla called the ventromedial reticular formation. Here, the Dorsal Reticulospinal Tract originates, which is responsible for an inhibitory action on both the stretch and flexor reflexes.

The Excitatory System

The bulbopontine tegmentum gives rise to the Medial Reticulospinal Tract and, acting weakly with the Vestibulospinal Tract, is excitatory to both stretch and extensor reflexes and like the Dorsal Reticulospinal Tract, is also inhibitory to the flexor reflexes.


Different Lesions and Their Presentations

The signs and symptoms between Cortical UMN Lesions and Spinal Cord UMN Lesions vary due to the location of where the disruption has taken place. [7]


Both the inhibitory system (Corticospinal Tract and Dorsoreticulospinal Tract) and excitatory systems (Medial Reticulospinal and Vestibulospinal Tract) are in dynamic balance and therefore the inhibition to the spinal cord is easily adjusted according to demand.

Corticospinal Tract Lesion

Although the Corticospinal Tract has an inhibitory influence on stretch and flexor reflex, the main inhibitory system produced by the Dorsal Reticulospinal Tract remains intact and therefore the balance of excitatory and inhibitory influences are maintained.

Internal Capsule Lesion

Leads to interruption of both the Corticospinal Tract and Corticoreticular Tract pathways that are responsible for the inhibitory response and some loss of inhibition to stretch and flexor stretches. The excitatory systems from both the Medial Reticulospinal and Vestibulospinal Tract are more dominant which leads to the facilitation of extensor and stretch reflexes but inhibition of flexors.

Incomplete Spinal Cord Lesion

Signs and symptoms will vary dependant on site and extent. If the inhibitory system is affected then there will be an unopposed excitatory drive to stretch and extensor reflexes with partial inhibition of flexor reflexes.

Complete Spinal Cord Lesion

Spinal reflexes are unopposed due to the complete loss of supraspinal control. Both flexor and extensor reflexes are disinhibited and therefore people may experience both flexor and extensor spasms.

Clinical Presentation

On physical exam, hallmark findings include

  • high muscle tone in muscle groups such as the shoulder adductors; elbow, wrist, and finger flexors; and forearm pronators. In the lower extremities, the increased tone is especially prominent in the hip adductors, knee flexors and extensors, and plantar flexors and invertors of the ankle.
  • Patients may report difficulty with footwear if their spasticity involves constant, high tone of the extensor hallucis longus or long toe flexors.
  • Spasticity varies with speed of movement; meaning the faster the muscle is moved or stretched, the greater the resistance to stretch or passive elongation is felt.
  • Clonus, spastic co-contractions, and spastic dystonia may be evident. ie Clonus is defined as an alternating muscle contraction and relaxation of the agonist and antagonist muscles. Spastic co-contractions are abnormal antagonist contractions that present during voluntary agonist effort. Spastic dystonia is a muscle contraction that is present at rest, leading to a constant clinical posture that is highly sensitive to stretch.[1] 

Spasticity is usually accompanied by one of more components of an upper motor neurone lesion seen in the table below, and is seldom exists in isolation. The impact of spasticity varies from person to person, ranging from being a clinical sign with no impact on function or a large increase in tone that affects transfers, mobility and personal care. It can also lead to contracture due to the shortening of muscles and tendons. [9][10]

Positive Component Negative Component
Exaggerated Tendon Reflexes Spastic Co-Contractions
Released Reflexes Motor Weakness
Babinski Sign Slowed Movements
Increased Tone Loss of Dexterity
Clonus Loss of Selective Motor Control
Spastic Dystonia

Permanent loss of joint range has been known to occur 3-6 weeks after both stroke and brain injury and therefore it is important that spasticity is identified early on in the assessment in order for it to be monitored and managed as required. In a person with hemiplegia the lower limb pattern is plantar flexion and inversion of the ankle with hamstring tightness limiting knee range of motion as well as adductor spasticity. Upper limb presentation is usually shoulder adduction, internal rotation, elbow flexion, forearm pronation with wrist and elbow flexion. [9][10]
UL Tone.jpg
UL + LL Tone.png


Spasticity has a number of characteristics that differentiates it from rigidity:

  1. Velocity dependence
  2. Clasp Knife Phenomenon: Limb initially resists movement and then suddenly gives way
  3. Distribution: Antigravity muscles being more affected
  4. Stroking Effect: Stroking the surface of the antagonist muscle may reduce tone in spasticity.

Diagnostic Procedures

Modified Ashworth Scale

Modified Ashworth Scale' scores exhibited better reliability when measuring upper extremities than lower[11]. The scale is as below:

0 No increase in muscle tone

1 Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion when the affected part(s) is moved in flexion or extension

1+ Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM

2 More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved

3 Considerable increase in muscle tone, passive movement difficult

4 Affected part(s) rigid in flexion or extension

Ashworth Scale

The Ashworth scale is the most widely used assessment tool to measure resistance to limb movement in a clinic setting, although it is unable to distinguish between the neural and non-neural components of increased tone.[12]

The scale is as follows:

0 No increase in muscle tone

1 Slight increase in tone giving a catch when the limb is moved

2 More marked increase in tone but limb easily moved

3 Considerable increase in tone - passive movement difficult

4 Limb is rigid in flexion or extension

Tardieu Scale

This scale quantifies muscle spasticity by assessing the response of the muscle to stretch applied at specified velocities. Grading is always performed at the same time of day, in a constant position of the body for a given limb. For each muscle group, reaction to stretch is rated at a specified stretch velocity. [13]

Velocity to Stretch

V1 As slow as possible

V2 Speed of the limb segment falling  

V3 As fast as possible (> Natural Drop)  

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

Joint Immobile 

Spasticity Angle

R1 Angle of catch seen at Velocity V2 or V3

R2 Full range of motion achieved when muscle is at rest and tested at V1 velocity


A large difference between R1 & R2 values in the outer to middle range of normal m. length indicates a large dynamic component. [14]

A small difference in the R1 & R2 measurement in the middle to inner range indicates predominantly fixed contracture. [14]

Outcome Measures

Since the severity of Spasticity may vary from one neurological condition to another and even from one patient to other with the same condition, disease specific spasticity measurement scales are developed. For example, in the Multiple Sclerosis (MS) population (The Multiple Sclerosis Society Spasticity Scale, MSSS-88). This is an 88-item, patient-based, interval level scale that not only looks at spasticity symptoms but also incorporates the person’s experience of spasticity and how spasticity affects their daily life. [15] However, in general the outcome measures include: [16]

  1. Goniometric Measurement
  2. Range of Passive Hip Abduction
  3. Ashworth Scale
  4. Adductor Tone Rating - Five-point Ordinal Rating of Tone, but is confined to the Adductors. [17]
  5. Spasm Frequency Scale - Ordinal Rank Scale (0 - 4) based on self-reporting of lower-limb spasm frequency in people with spinal cord related spasticity. It is scored depending on how many spasms are experienced in an average hour. [18]
  6. Clonus and Spasm Score (Self-Report). This is a further Ordinal Scale (0 - 3), based on self-reporting of the frequency and provocation of both spasms and clonus. [19]
  7. Numeric Rating Scale for Leg Stiffness.
  8. Walking and Falls Score - An estimate of fall frequency scored in an ordinal fashion (0 - 4), with 0 being no falls and 4 equating to more than 1 per day. If appropriate, a timed 10-metre walk is also recorded. [20]
  9. Overall Comfort Rating.




Spasticity is one of the components of the UMN syndrome but should not be considered in isolation when it comes to management strategies. It is essential that management targets function and is always patient focused rather than aimed at reducing the degree of spasticity[22]

Neurorehabilitation comprises four main categories of spasticity management targets.

  • Client care: Preventing or treating contractures; preventing or treating pressure areas; proper positioning of the body on the bed/wheelchair; easy orthotics fitting.
  • Movement improvement:The unmasking of voluntary movements previously covered by significant spasticity in cases of incomplete lesions; accelerating the “spontaneous” recovery process; modifying the “immature” motor pattern; using new recovery techniques to promote guided neuroplasticity, e.g. robotic rehabilitation; new functional pattern in moving and walking.
  • ADL's: transfers, getting around, putting on clothes, personal hygiene, driving, etc.
  • Quality of life: Independent living; social and professional reintegration[23]
The informative video below outlines some basic treatment strategies ( MS specifically, but can be extrapolated).

The Evidence for Interventions

  • Progressive Resistance Strength Training - No evidence shows that strength training increases spasticity in patients with stroke. Musculoskeletal impairment are significantly reduced after resistance strength training. [25]
  • Biofeedback combined with functional electrical stimulation and occupational therapy does not increase the degree of spasticity after treatment. It also showed a greater reduction in spasticity compared to patients who performed functional electrical stimulation and occupational therapy alone. [26]
  • Nabiximols (a specific Cannabis extract ) effectiveness in MS-related spasticity combined with a PT program may improve overall response to the reduction in spasticity.[27].
  • Shock wave therapy on flexor hypertonic muscles of the forearm and interosseus muscles of the hand in patients with stroke showed significant reduction of muscle tone (>3months). [28]
  • Amelio reported significant reduction of muscle tone (>12 weeks) of plantar flexors in children with cerebral palsy. [29]
  • Significant reduction of ankle plantar flexor spasticity in patients with stroke after fifteen 10-minute sessions of continuous ultrasound therapy over a 5-week period (frequency 1MHz and intensity 1,5 W/cm2). [30][31]
  • Cryotherapy, using cold packs (12°C) for 20-minutes, can lower the muscle temperature to reduce the spasticity. [32]
  • Electric Stimulation using agonist stimulation showed a significant improvement in Ashworth Scores, while antagonist stimulation showed an increase of stretch reflex-initiating angle. [33]
  • A scoping review (March 2020) summarises management strategies: medication, physical therapy, and other physical rehabilitative strategies, with surgical management techniques used for treating and preventing spasticity after traumatic brain injury in children[34].

Patients should be educated on maintaining a daily stretching and range of motion program. In addition to the patient, the family and caregivers should be educated about proper positioning, daily skin inspection, an adequate and regular bowel/bladder regimen, avoiding noxious stimuli, and identifying signs of infection and pain.[1]


If the spasticity is widespread then systemic medication is used. This includes:

  • Dantrolene (Dantrium)
  • Baclofen (Lioresal and others)
  • Tizanidine (Zanaflex)
  • Diazepam (Vallium)

If the spasticity is locallised then local medication is used. This includes:

  • Boutulinum Toxin (Botox)
  • Baclofen (Inrathecally - High concentration more locally).
  • Phenol / Nerve Block
  1. Baclofen: The most common systemic agent. Baclofen acts on the receptors of excitatory nerve terminals, in particular the 'GABA B G-Protein receptor. Once the baclofen has attached to this G-Protein on the pre-synaptic terminal, potassium channels open while calcium channels close, hyperpolarising the cell. The inability for calcium to enter the cell means the release of glutamate, an excitatory neurotransmitter, is prohibited.
  2. Tizanidine: Follows the same mechanism as Baclofen, however attaches to the a2 adrenoreceptor on the pre-synaptic cell membrane.
  3. Botulinum Toxin (Botox): Injected locally into muscle. Prevents the excytotic release of acetylcholine at the level of the neuromuscular junction which further prevents release of calcium from the sarcoplasmic reticulum which leads to excitation-contraction coupling.
  4. Diazepam (Vallium): Less common. Increases the effect of GABA, an inhibitory neurotransmitter, that is released from inhibitory interneurons which decreases the excitability within the post-synaptic nerve terminal.
  5. Dantrolene: Provided orally. Blocks the release of calcium from the sarcoplasmic reticulum within the muscle which prevents excitation-contraction coupling.

Other Considerations

It is important to identify and address potential triggers and aggravating factors that can cause an exaccerbation in spasticity [9]. These may include:

  • Pressure Ulcers
  • Ingrown Toenails
  • Skin Infections
  • Injuries
  • Constipation
  • UTI
  • DVT
  • Improper Seating
  • Ill Fitting Orthotics

Clinical Guidelines

The Royal College of Physicians (RCP) latest clinical guidelines in 2016 recommend the following for the management of spasticity: [35]

  1. People with motor weakness after stroke should be assessed for spasticity as a cause of pain, as a factor limiting activities or care, and as a risk factor for the development of contractures.
  2. People with stroke should be supported to set and monitor specific goals for interventions for spasticity using appropriate clinical measures for ease of care, pain and/or range of movement.
  3. People with spasticity after stroke should be monitored to determine the extent of the problem and the effect of simple measures to reduce spasticity e.g. positioning, passive movement, active movement (with monitoring of the range of movement and alteration in function) and/or pain control.
  4. People with persistent or progressive focal spasticity after stroke affecting one or two areas for whom a therapeutic goal can be identified (e.g. ease of care, pain) should be offered intramuscular botulinum toxin. This should be within a specialist multidisciplinary team and be accompanied by rehabilitation therapy and/or splinting or casting for up to 12 weeks after the injections. Goal attainment should be assessed 3-4 months after the injections and further treatment planned according to response.
  5. People with generalised or diffuse spasticity after stroke should be offered treatment with skeletal muscle relaxants (e.g. baclofen, tizanidine) and monitored for adverse effects, in particular sedation and increased weakness. Combinations of antispasticity drugs should only be initiated by healthcare professionals with specific expertise in managing spasticity.
  6. People with stroke should only receive intrathecal baclofen, intraneural phenol or similar interventions in the context of a specialist multidisciplinary spasticity service.
  7. People with stroke with increased tone that is reducing passive or active movement around a joint should have the range of passive joint movement assessed. They should only be offered splinting or casting following individualised assessment and with monitoring by appropriately skilled staff.
  8. People with stroke should not be routinely offered splinting for the arm and hand.



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