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What is spasiticty?
- a motor disorder that is characterised by a velocity dependent increase in tonic stretch reflexes (mm tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome
What are the positive signs of UMNS (upper motor neuron syndrome)?
- - spasticity: co contraction or dystonia (neuro disorder with mm contractures causing rot and not proper mm contraction)
- - rigidity
- - hyperreflexia
- - primitive reflexes
- - clonus
What are the negative signs of UMNS (upper motor neuron syndrome)?
- - lack of strength
- - lack of motor control
- - lack of coordination
- - these signs are more of a problem than the +ve signs
What are the other definitions of spasiticty?
- - tone- compliance of tissue, spasticity can contribute
- - hypertonia- low tone- not used much, flaccid
- - clonus- fast stretch and hold on stress, contraction/ relax to maintain stretch
- - rigidity: cogwheel - when resistance gives way, leadpipe- constant resistance to stretch throughout movt
- - claspknife phenomenon- like shutting pocket knife
- - contracture- shortening of saccromeres
How does rigidty differs from spasticity?
- The resistance to passive stretch is:
- - bidrirectional- spasticity- resistance both flex and ext
- - relatively independent to the speed of the movement
- - does not result from hyperactive stretch reflexes
Difference between contracture and spasticity?
- - no relationship between spasiticty and contracture development
- - hypertonia associated wiht contracture but not hyperreflexia
- - the stiffness associated with contracture can contribute to hypertonia and can be confused with spasticity
- - no correlation between contracture and spasiticty
What is hypertonia?
increased mm tension and the ability to stretch
Acitivty limitations and spasticity
- - spasticity (if you get rid of this you cant increase the pt function) and activity are not correlated
- - spasiticty doesnt make an independent contribution to activity limitations after stroke
- - dereasing spasiticity doent improve acitivty
What are the three proposed theires of spasticity?
- - imbalance between excitatory and inhibitory impulses to the alpha motor neurons- due to lack of descending inhibitory input to the alpha motor neuron- cause hyper excitable reflexes from a lesion
- - descening pathways also influences renshaw cells (neurons located in ventral horn) which suppress repeated firing of alpha motor neurons- lesion decreases activity of renshaw cells alpha neurons = reduce their inhibitory activity- this results in rapid, repeated firing of alpha motor neurons from repetitve stretch reflexes triggered by vountary or passive stretch of mm
- - descending pathways also inhibit golgitendon organ (GTO)- proprioceptors at junction of mm tendon, mm belly- protect mm from source- lesion results in lack of inhibition of GTO = excitation of stretch reflex
Skeletal mm plasticity
- in spasticity there may be a secondary myopathy
Normal vs spastic mm
- - random things happen in spasticity
- - fibre size- loss of variability
- - the mm is shorter but the sacromeres are longer
- - the contrature tissue around the cell makes it 10 x stiffer than non spastic cells
- - fibre type distribution
- - more connective tissue around fibres make less compliance
What are some adverse effects of spasticity?
- - interferes with functional recovery: may affect mobility, functional independence
- - impaired hygiene (axilla, palm) and sexual function
- - may cause pain jts forced in wrong position
- - impaired sleep- rol over and have a spastic response
- - icreased carer burden
- - all goals for treatment
What are the benefits of spasticity?
- - esp for spinal cord injuries
- - an aid to standing and walking via extensor spasms
- - increased strength in isometric and eccentric volntary contractions, facilitated by hyperactive stretch reflexes
- - maintenance of mm mass- not so much instroke but significant in spinal cord injusires
- - can also prevent pressure area sores
- - maintained bone mineralisation/ density
- - improved venous return
- - reduced DVT risk
- - reduced dependent oedema in paralysed limbs
WHat are the indications for treatment of spasticity?
- when spasticity produces disability or activity limitations (personal/ social)
What are the tests and measures for mm performance?
- - static and dynamic mm tone: ashworth, tardieu, tendon jerks
- - mm strengthand selective motor control
- - function
What are goals for spasticity management?
- - prevention of spasticity- takes a while to develop- positioning, seating, PROM- AROM and stretching? handling techniques?
- - find nociceptive stimulus- spasticity triggered by pain eg bowel, bladder, skin
- - relieve pain and symptoms
- - improve function (ADLS, seating, mobility)
What are the common oral meds for spasticity?
What are the advantages of oral medications?
- - non invasive, non permanent
- - effective management for some pts
What are the disadvantages of oral medications?
- -difficult to achieve a steady state
- - following a schedule may be diffcult
- - sid effects: drowsiness, hypotonia, and weakness my limit effectiveness
- - peripheral nerve block- into nerve -can cause perm damage
- - motor point blocks- pt mm where it is responsive- botox
- - numerous agents used
- - duration of effects varies
- - numerous complications
Botulinum toxin aka botox what is the one for spasticity
- - type A serotype (BTX-A)
- - botox- A
- - dysport
What is the selection criteria for botox?
- - focal spasticity- cant inject every mm
- - a specific functional gaol for treatment
- - intense therapy program
What does BTX-A do?
- - blocks neuromuscular transmission by inhibiting release of arch trom the presynaptic terminals, resulting in a reversible denervation atrophy
- - chemicals denervation develops over a few days and last 3-4 months
- - collateral sprouting from the adjacent axons limits the duration of clinical effects
BTX- A advantages
- - diffuses easily through mm membranes therefore doesnt require precise location of motor points
- - simple injection technique
- - no CNS side effects
- - no sensory disturbance
- - weakness resolves
- - safe
- - well tolerated
- - lasts 3/12 months
- - injection pain
- - limited maximum dose
- - cost
- - EMG gudieance- locate hard mm. Other is a clearing affect after a pt doesnt matter how much u give
What are some adverse effects of BTX-A?
- - excessive weakness decrease function
- - adjacent mm weakness
- - transient fatigue, nausea and H/A
- - local pain and haematoma
- - flu like illness
- - clinical resistance
- - contraindications- neuro mm junction problems, antibiotcis, pregas, temp, breast feeding
- - baclofen is delivered directly to the spinal cord resulting in effectively a chemical rhizotomy
- - benefit is less cognitive SEs
- - indications are for: serve spasticity, ineffectiveness of oral agents, positive response to test dose via LP
- the one where the machine is in the body
adverse effects of IT-B?
- - cost 30 grand
- - respiratory depression ( drug overdose)
- - drowsiness/ increased weakness
- - seizures
- - nausea and vomiting
- - infection
- - skin nevrosis
- - pump/ battery/ catheter problmes
Surgical management of spasticity
- ortho surgery
What are the advantages and disadvantages of surgery
- ad- perm- one time procedure, evidence for efficacy in reducing spasticity and improving function in children with spastic diplegia
- dis- perm- may need spasticity, potential adverse effects
- - stretch
- - strengthen
- - fatigue
- - EMG biofeedback
- - weight bearing
- - hydrotherapy
- - PNF
- - bobath
- - orthosics
- - positioning
- - massage
- - edu
- - prevent nociceptive stim
- - ice/vib/ten.heat