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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
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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
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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
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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
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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
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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
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What is hypertonia?
increased mm tension and the ability to stretch
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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
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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
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Skeletal mm plasticity
- in spasticity there may be a secondary myopathy
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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
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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
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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
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WHat are the indications for treatment of spasticity?
- when spasticity produces disability or activity limitations (personal/ social)
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What are the tests and measures for mm performance?
- - static and dynamic mm tone: ashworth, tardieu, tendon jerks
- - mm strengthand selective motor control
- - function
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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)

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What are the common oral meds for spasticity?
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What are the advantages of oral medications?
- - non invasive, non permanent
- - effective management for some pts
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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
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Injected medications
- - 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
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Botulinum toxin aka botox what is the one for spasticity
- - type A serotype (BTX-A)
- - botox- A
- - dysport
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What is the selection criteria for botox?
- - focal spasticity- cant inject every mm
- - a specific functional gaol for treatment
- - intense therapy program
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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
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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
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BTX-A disadvantages
- - 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
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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
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Intrathecal baclofen
- - 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
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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
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Surgical management of spasticity
- Neurosurgery
- ortho surgery
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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
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rehab therapy
- - stretch
- - strengthen
- - fatigue
- - EMG biofeedback
- - weight bearing
- - hydrotherapy
- - PNF
- - bobath
- casting
- - orthosics
- - positioning
- - massage
- - edu
- - prevent nociceptive stim
- - ice/vib/ten.heat
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