Spasticity/ spastic paraplegia Flashcards
What is spasticity
Disordered sensorimotor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles
Name some positive and negative aspects of motor activity
Negative- weakness, reduced dexterity, reduced postural responses
Positive- spasms, spasticity, clonus, brisk tendon reflexes, positive support reaction.
What is a stretch reflex?
And how do they work?
What would you see?
A stretch reflex is a response to a muscle stretch.
Sensory axons, arising from muscle spindles embedded within connective tissues in the muscles are activated.
The sensor axons relay information to the brain and spinal cord from the spindles about the length changes of the muscles (amplitude and speed of stretch)
Ventral horns off the spinal cord form excitatory connections with the motor neuron supplying same middl muscle = contraction of the muscle
Features- tendon reflex, knee or ankle jerk (phasic stretch reflex)
Modulation of monosynaptic stretch reflex
3 inhibitory pathways
1: reciprocal inhibition
- inhibitory connections to the motor neurons of antagonist muscles
- therefore, there is a rapid contraction of stretched muscle and simultaneous relaxation of antagonist muscle
3: Recurrent inhibition
What effect does spasticity have on the stretch reflex?
There is a reduced threshold for activation of the stretch reflex
Increase of the grain of response ( ratio between size of stretch reflex and velocity of the stretch)
Stretch reflex lasts longer = tonic stretch reflexes
Clasp knife phenomenon ( sudden education in tone when moving limb with spasticity = decline in velocity when resistance increases)
^ (tonic stretch also length dependent so sensitivity to stretch reflexes reduces)
What are key patholophysiological features of spasticity
It develops over time
Requires:
Upper motor neuron pathway lesions
Reduced inhibition within spinal cord circuits
Adaptive changes in properties of:
- motor neuron
- spinal inter neurons
Explain 3 lesion areas of the UMN pathways
- Cortex (pre-motor, supplementary motor) (lessons here can affect spasticity)
- ventromedial reticular formation
- bulbopontine tegmentum
- vestibular nucleus - Spinal interneuronal network ‘
Describe the mechanism underlying the onset of spasticity
Unm lesion
Lack of descending modulation of sc inhibitory circuits
- leads to a lack of inhibition to turn off plateau/ sustain firing
MOTOR NEURON
- leads to prolonged EPSPs and plateau potential in response to afferent inputs
= enhanced response to stretch
OR
Damage to noradrenergic/ serotonergic pathways
- this leads to intrinsic motor neuron changes occur over time
MOTOR NEURON
- leads to prolonged EPSPs and plateau potential in response to afferent inputs
= enhanced response to stretch
Explain tissue changes and abnormal Co-contraction
- connective tissues changes can contribute to stiffness
Neural stiffness = medication
Non-neural stiffness = stretching and splinting
-Example-
- abnormal co-contractions can appear after strike (requiring stretching as it is non-neuronal stiffness
Co-contraction and excessive muscle activity during movements are independent from stretch related muscle activation (spasticity)
What sensory inputs may increase spasticity and spasms
- skin
- bladder
- bowels
- seating and positioning
- pain, skin
What is clonus ?
When might you see it?
- rhythmic pattern of contraction at a rate of several times per second
- demonstrated by a sudden stretch of muscle
- commonly observed in the leg muscles with rhythmic contractions in response to ankle dorsiflexion
What are spasms?
When might you see them?
Types?
- sudden involuntary movements (often painful)
- can be precipitated by muscle stretch, loading abs unloading joint movement
- can be triggered by peripheral, oculus and visceral afferents (pressure sores, infection, urinary retention)
- Flexor
- Extensor
- Adductor
- Combined
What are the associated reactions of spasticity?
Babe some positive (+) reactions
- pp with UMN syndrome, when activating 1 pasta is the body, experience involuntary activity in scores part of body
- weight bearing in paretic leg, plantar flex ion and inversion of foot (with it without knee extension) (disinfected primitive reflex)
^ can interfere with standing and walking rehabilitation
Name some impacts of spasticity
- discomfort
- stiffness
- spasms
- pain
- effect on function (walking)
- emotional impact
GOOD
- in cases of weakness, can be beneficial to standing and walking
What are the types of assessments and other factors to consider
Multidisciplinary team
- medical history/ comorbidities e.g Stroke
- past and present medications
- triggers e.g bladder
- physical management (splints)
Type of assessments
- Ashworth Scale 0-4 ( muscle tone)
- Modified Penn Spasm Frequency Scale
Spasm frequency (0-4)
Spasm Severity (1-3)
Management plan of spasticity
Spasticity diagnosis
Is it useful for function
(Yes - physio, plan for management) *
(No - does it need treatment ( affecting range, care, function or causing pain)
^ yes*
- assess spasticity and record measures
- assess for triggers abs aggravating factors
Devise physiotherapy and treatments plan
(Splinting etc)
Is it still problematic
(Yes ( focal or generalised) *
(No ( continue plan and monitoring)
- focal spasticity (botulinum + physio)
Spasticity continues ( drug treatment, intrathecal interventions, therapy and interventions)
Name some treatments
Aims of treatment
- botulinum
- peripheral chemical neurolysis)
- oral treatments (baclofen)
- intrathecal baclofen
- intrathecal phenol
- surgery
aims:
- pain reduction
- dressing
- hand movement and limb positio
- perineal hygiene
What is botulinum and how and should it be used?
- injected directly into targeted muscle
- Within 12 hours, it is taken into nerve endings
- effect begins immediately and lasts between 10-14 days after injection
- clinical affect peak 3-6 weeks after admin
- requires continuous treatment
Should be given in conjunction with physio to gain maximum benefit
1. Initial phase = 28days see axonal sprouting
2. 91days = renewed vesicles, returning dominance is functional loss of spores abs terminals)
Useful for focal spasticity
Explain the treatment, peripheral chemical neurolysis
Used in combination with physical management
Can be used alone or in combination with botulinum toxin
^ alternative option for focal spasticity
- local injection of ethanol or more commonly phenol
- permanent effect
-partial nerve regeneration abs sprouting may occur - clinical effects wave after weeks or months, injections can be repeated
Name and explain oral treatments for spasticity
Baclofen - most commonly used. (Inhibition of monosynaptic and polysynaptic reflexes at the spinal level - suppress release of excitatory neurotransmitter)
Gabapentin - modulates cell function through alterations in calcium ion influx reduces release of monoamine transmitters
Benzodiazepines - modulation of GABAergic transmission. Reduction in mono- and poly synaptic spinal reflexes.
Oral spray
Nabiximols - oralmucosal spray
2.7mg tretrahydrocannabinol and 2.5g cannabidiol in each spray.
Approved in uk as an add on ardent
Painful spasms and sleep disturbances
Typical side effects:
- drowsiness and weakness
Weakness could be due to unmasking of due to reduction in spasticity
What is an advanced treatment of oral medications and botulinum injections are not effective
Intrathecal baclofen requires a pump implanted in the abdomen, with a catheter conveying the baclofen to the intrathecal space.
Concentration in the lumbar spinal cord allows for small doses to be effective without causing systemic side effects (lower dose than oral <1% off oral dose)
Candidates:
- risk of lumbar puncture bolus dose
- patient commitment, regular refills and replacements
Risks:
- infection 3-26%
- catheter/ pump dysfunction 4-24% of patients
- withdrawal or overdose (overdose is rare but often due to pump malfunction or prescribing error)
Withdrawal note commo n due to catheter malfunction
Name and explain an injectable treatment of other treatments are ineffective
Intrathecal phenol
- used of medication are ineffective and spasticity preventing eating hoisting
- reserved for people with no functional movement, lost bladder control and impaired sensation in the legs as it damages motor and sensory nerves
- requires expert administration
- neither long term maintenance it cost issues
- single injection often lasts months and can be repeated if effects wane.
What are the surgery options for those with spasticity
Orthopaedic surgery - tendon lengthening, correction of contractures, tendon Ranger, joint fusion
Dorsal root entry zone lesion/ dorsal rhizotomy/ peripheral neurotomies
Selective dorsal rhizotomies - involve sectioning some of the others of each targeted dorsal root to reduce the afferent input while preserving sensory and sphincter function
Used mainly in children with cerebral palsy; requires intensive rehabilitation
Rarely used in adults
