Spasticity

Introduction

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Lesions to the central nervous system (brain or spinal cord) can lead to both positive and/ or negative upper motor neurone syndrome (UMNS) features:

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

Spasticity is seen to be a positive feature of upper motor neuron syndrome. This is because it is due to a loss of inhibition of the lower motor neuron pathways, rather than a loss of connection to the lower motor neuron (or other pathways). This results from disordered sensorimotor control of movement due to a lesion of the upper motor neuron which regulate muscle control. Therefore, there is an imbalance of the signals between the central nervous system (CNS) and muscles, presenting as intermittent or sustained involuntary activation of muscles.

All muscles have some tone to maintain function, for example, activation of antigravity muscles to maintain sitting or standing postures. In an individual with spasticity, there is a velocity-dependent increase in muscle tone to passive movement. This creates an inability to stretch muscles or coordinate movements effectively.

This inhibition can result from central nervous system pathology, such as:

• Cerebral Palsy
• Multiple Sclerosis
• Motor neurone disease
• Stroke
• Hypoxic Brain Injury
• Traumatic Brain Injury
• Parkinson’s Disease
• Spinal cord injury
• Spinal cord compression
• Metastesis / tumour

Spasticity can have an impact on an individual’s function, affecting upper and lower limbs, as well as trunk. If this is not managed effectively, it can lead to fixed deformity contractures (changes to soft tissue), which affect skin care, comfort and hygiene, as well as complications for daily tasks.

The management of spasticity needs to be carefully considered as some patients rely on aspects of spasticity to allow them to maintain enough tone for functions such as standing or walking. Physiotherapy management may include facilitating individuals to utilise this to maintain weight bearing and ambulation to decrease their risk of developing osteoporosis, strengthen muscles, help improve circulation and promote overall mental health.

Definition

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

‘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)  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 .

Classification of Spasticity into various components of spasticity into sub-definitions:

1. Intrinsic Tonic Spasticity: Exaggeration of the tonic component of the stretch reflex (manifesting as increased tone),
2. Intrinsic Phasic Spasticity: Exaggeration of the phasic component of the stretch reflex (manifesting as tendon hyper-reflexia and clonus), and
3. Extrinsic Spasticity: Exaggeration of extrinsic flexion or extension spinal reflexes.

Epidemiology

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.

Anatomy and Etiology

A UMN injury leads to loss of inhibition downstream and hypersensitivity of the reflex arc within the spinal cord. 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

Corticoreticular Spinal Tract: These tracts travel with, but are separate from, the Corticospinal Tract, and are 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. 

Normal

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.

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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. Antigravity muscles are predominantly affected.
• 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 (velocity dependent); 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. i.e., 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. 
• Clasp knife phenomenon: Limb initially resists movement and then suddenly gives way 
• Stroking Effect: Stroking the surface of the antagonist muscle may reduce tone in spasticity. 

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. 

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Outcome measures

Useful objective measures to monitor changes in spasticity can include:

Subjective:

• Pain:
  • Numeric Pain Scale (e.g. for pain, comfort, stiffness)
  • Observing grimacing / pulling away
• Arm A and Arm B
• LegA

Objective:

• Resting Position: photographs, description, measuring bony landmarks
• Passive range of movement
  • Adductor Tone Rating
• Active range of movement
• Muscle strength: Oxford Scale
• Spasms:
  • Modified Penn Spasm Frequency Scale
  • Clonus and Spasm Score
• Function
  • Walking: 10m times walk
  • Transfers: Times up and go
  • Upper Limb Function: 9 hole peg test
  • Speech: Speech comprehension score 
  • Walking and Falls Score
• Muscle tone: Ashworth Scale / Modified Ashworth Scale, Tardieu (outlined below)

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.

The scale is as follows:

Ashworth Scale
Grade	Description
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

Modified Ashworth Scale

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

Modified Ashworth Scale
Grade	Description
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

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. 

Tardieu
Velocity to Stretch
V1	As slow as possible
V2	Speed of the limb segment falling (with gravitational pull)
V3	At a fast rate (>gravitational pull)
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 angleFatiguable 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 Velocity V2 or V3
R2	Full range of motion achieved when muscle is at rest and tested at V1 velocity

Management

It important to consider the triggers of spasticity when planning interventions. There are a number of stimuli which can exacerbate spasticity, some may need multidisciplinary input alongside implementing physiotherapy management. These include:

• Skin: pressure ulcers, ingrown toe nails
• Bladder or bowel: constipation, full bladder
• Pain / discomfort: restrictive clothing, wheelchair straps, catheter straps
• Seating / positioning
• Fatigue
• Infections: UTI, pneumonia, skin
• Stress
• Disease progression
• Menstruation
• Other medical condistions (e.g. kidney stones)
• Ill fitting orthotics

Physiotherapy

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 identified impairments to function and is always patient focused rather than aimed at reducing the degree of spasticity Planned interventions should consider a balance between movement and positioning. This includes:

• Standing
  • Standing frame
  • Treadmill training (body-weight supported if needed)
  • Tilt table
• Active exercises
• Passive movements
• Functional electrical stimulation
• 24 hour positioning management
• Splinting and the use of orthotics
• Stretches

Considerations for managing spasticity :

• Client care:
  • Preventing or treating contractures
  • Monitoring skin to preventing pressure areas
  • Positioning of trunk, head and limbs in supine and in chair/ wheel chair
    • If possible, standing promotes anti-gravity muscle activity in the trunk and lower limbs. It also maintains or improves soft tissue and joint flexibility and modulation of the neural component of spasticity.
  • Orthotics to maintain / improve available range
• 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 and transfers
  • Getting around
  • Putting on clothes
  • Personal hygiene
  • Driving, etc.
  • Occupation
• Quality of life
  • Independent living
  • social and professional reintegration
  • Task specific activities can have a positive psychological effect

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.

Pharmacological

Some individuals may benefit from medications to manage spasticity. These can be generalised, focal or intrathecal interventions.

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

• Dantrolene (Dantrium)
• Baclofen (Lioresal and others)
• Tizanidine (Zanaflex)
• Diazepam (Vallium)
• Benzodiazepines
• Gabapentin
• Pregabalin
• Canabinoids

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

• Boutulinum Toxin (Botox)
• Regional Nerve Block

Intrathecal medications can also be used. These include:

• Baclofen
• Phenol

Medication
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.
Tizanidine	Follows the same mechanism as Baclofen, however attaches to the a2 adrenoreceptor on the pre-synaptic cell membrane.
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.
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.
Dantrolene	Provided orally. Blocks the release of calcium from the sarcoplasmic reticulum within the muscle which prevents excitation-contraction coupling.

Considerations of medication:

• Optimise timings of sessions alongside medications
• Exposing weakness in limbs of trunk
• Monitor effects and when dose may need adjusting
• Side effects, such as fatigue

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