Lecture and practical 1 - Spasticity

Question 1

What are the outdated and currently accepted definitions of spasticity?

Answer 1

Outdated = Velocity-dependent increase/overactivity of tonic stretch reflexes

Currently accepted = Disordered sensory-motor control due to upper-motor neuron lesion leading to intermittent or sustained involuntary activation of muscles

Question 2

Describe the stretch reflex including the roles of the different types of motor neurons

Answer 2

Sensory 1a afferent neurones are activated due to stretch detected by golgi tendon organs and spindles

Synapse in ventral horn with alpha motor neurons which contract the extrafusal muscle fibres to contract the muscle

Gamma motor neurons control sensitivity of stretch reflex by controlling myofibrils to set normal muscle tone and length for the alpha neurons

Question 3

What is reciprocal inhibition?

Answer 3

The 1a afferent neuron bifurcates in the ventral horn.

Synapses with alpha motor neurons to contract the muscle fibres of the agonist

Synapses with inhibitory interneurons which innervate the alpha motor neurons for the antagonist inhibiting this

Question 4

What is normal tone

Answer 4

Sufficient tension to maintain stability and to enable movement

Question 5

Give 5 standard things that impact tone

Answer 5

Posture
Temperature
Emotions i.e. stress
Visual/auditory stimuli
Medical factors i.e. skin ulcers, UTIs etc

Question 6

Identify and categorise the neural components of upper motor neuron lesions

Answer 6

Positive:
- Spasticity
- Spasms
- Clonus
- Associated Reactions

Negative:
- Weakness
- Impaired motor control
- Decreased range of movement

Question 7

What are the non-neural impacts of an upper motor neuron lesion

Answer 7

Secondary adaptive changes:
- Contractures
- Muscle stiffness

Question 8

What are associated reactions?

Answer 8

An increase in spasticity/tone due to voluntary activation of unaffected muscles or involuntary movements such as coughing and sneezing

Question 9

What are contractures?

Answer 9

Shortening of muscles, tendons, skin and nearby soft tissues impacting range of movement at a joint

Question 10

Give 2 clinical scales for assessing tone, identify the more accepted one and explain why

Answer 10

Tardieu Scale - measures at 3 different velocities
Modified Ashworth Scale

The Tardieu scale is more accepted because the MAS overdiagnoses spasticity in cases of contracture

Question 11

What is the common pattern of spasticity in the upper limb

Answer 11

Flexor synergy:
Elbow = flexed
Forearm = supinated
Wrist = flexed
Fingers and thumb = flexed and adducted

Question 12

What is the common pattern of spasticity in the lower limb

Answer 12

Extensor synergy:
Hip = flexed, adducted and internally rotated
Knee = extended
Foot = plantar flexed and inverted

Question 13

What is neuroplasticity and how does it relate to spasticity rehabilitiation

Answer 13

Neuroplasticity is the ability of the brain to form synaptic connections after injury (or in response to learning)

Repetition required to build synaptic connections, movements must be performed and repeated even if imperfectly, the MDT must be on board to ensure a 24 hour approach to rehabilitation to enable repetition/frequency required for effective neuroplasticity use

Question 14

Describe the method of administration and mechanism of botulinum toxin

Answer 14

Administration = focal, directly into the muscles affected (guided by ultrasound)

Mechanism = binds to receptors on the pre-synaptic neuron, the toxin-receptor complex is taken into the neuron by endocytosis, the toxin is then released and binds to SNARE proteins and prevents the vesicles containing acetylcholine (an excitatory neurotransmitter) from binding to the membrane and releasing the contents into the synapse

Question 15

Describe the method of administration and mechanism of baclofen

Answer 15

Administration = systemically and intrathecally

Mechanism = Binds to gaba receptors to increase inhibitory effects reducing muscle spindle sensitivity to acetylcholine from alpha motor neurons

Question 16

Describe the method of administration and mechanism of tinzanadine

Answer 16

Administration = systemically

Mechanism = Pre-synaptic inhibition increases and prevents release of excitatory neurotransmitters

Question 17

What were considerations inspired by the practical session regarding medication for managing spasticity

Answer 17

Medication for managing spasticity can have side effects that heighten some other already disabling effects of the patient’s neurological impairments. For example the stroke patient we met at the session was greatly impacted by neurofatigue and medication for his spasticity worsened this. They can also increase cognitive issues.

Question 18

How can positioning be used across lying, sitting and standing for spasticity management?

Answer 18

Lying = modified supine and side-lying positions and use of supportive aids

Sitting = alignment focused to improve stability of pelvis and hips

Standing = gravity can facilitate extensor activity - this is enabled by therapists and equipment such as standing frames

Question 19

Why is splinting debated within spasticity management?

Answer 19

Greater than 6 hours of stretching a day can be required to see meaningful change

2023 Stroke guidelines indicate focus needs to be on treatment of activity and functional movement and not passive features

Question 20

In what situations is splinting required regarding spasticity management

Answer 20

Risks to skin-integrity i.e. fingernails digging into palm of hand and creating cuts

Personal hygiene risks i.e. fists clenched meaning unable to wash hands

Question 21

What is the main aim of therapy/exercise treatment for spasticity management and give 3 sub aims this can entail

Answer 21

To maximise function and activity:
- Prevent secondary complications
- Strengthen muscles
- Promote normal movement patterns

Question 22

Give two types of surgical intervention for spasticity

Answer 22

Tendon lengthening/replacement

Selective dorsal rhizotomy - Cutting of afferent sensory neurons at certain spinal cord levels

Question 23

What is learnt disuse and how does it apply to spasticity rehab

Answer 23

Patients need to be massively encouraged to carry out movement (even if imperfect) in affected limb and not just adapt to using a single limb (learnt disuse).

Question 24

What is the Ashford Goal Classification?

Answer 24

A goal classification based on patients receiving botox for spasticity.

Helps give more structure to the goal-setting process.

Divides goals into 2 categories, symptoms/impairments and activities/functions with 3 subcategories in each

Question 25

What is goal attainment scaling

Answer 25

Goal attainment scaling is a way of statistically/more objectively measuring progress across varied patient-decided goals

Question 26

What are the 3 domains of the ICF problem list

Answer 26

Body functions
Activities
Participation

Question 27

Why do contractures occur?

Answer 27

Sarcomeres (muscular units) partake in the sliding filament theory (myosin binds to actin and slides, dettaches then reattaches further down)

Continuous shortening of muscles causes a reduction in the number of sarcomeres

This impacts the length of the muscle impacting ability to generate force and achieve range of movement

Question 28

What does electrical stimulation do and not do for shortened muscles

Answer 28

It doesn’t prevent loss of sarcomeres in muscle tissue but it does prevent connective tissue change

Question 29

What spinal tracts are involved in spasticity and how?

Answer 29

Lesions to corticospinal tracts lead to weakness

Lesions in non-pyramidal tracts such as the rubrospinal tract lead to mixed effects and imbalance between inhibitory and excitatory influence on alpha motor neurones leading to uncontrolled overactivity of certain muscle groups