Week 10 Spasticity Management Flashcards
This is not accepted in the medical community anymore/
People might start out flaccid and then start to develop spasticity and muscle synergies at the 2-3 week mark, then spasticity gets more severe, then the spasticity might go away and at stage 6 they’ll be back to normal – Bruunstrom stages
Spasticity is not a one off continuum and it can fluctuate. Some people develop spasticity that goes away, majority of the time once developed it does not go away.
We all have muscle tone. Muscles are resting in a state of tension that is normal. Spasticity can be more global but generally in specific muscle groups.
When describing muscle tone don’t say “that person has tone”.
Say they have spasticity in their left elbow flexors and right wrist extensors.
People can be rigid (Parkinson’s),
Spasticity – have to move joint fast - velocity (independent/dependent)
Rigidity – velocity (independent/dependent)
Treat spasticity and rigidity differently.
Hypotonic – muscle tones are lower than normal resting tone and they are more floppy. People can be flaccid, atrophying, and no contraction might be present .
When you go to describe muscle tone, really know the descriptors and be precise with your language.
dependent; independent;
How does the CNS select particular solutions from the innumerable options afforded by the many effectors (muscles, joints, and limbs) that typically take part in natural movements?
Abnormal synergies are a result of increased recruitment of brainstem pathways
The body knows what muscles to turn on to have an efficient movement when grabbing for a water bottle.
Don’t need spasticity to have a muscle synergy.
When people have spasticity the corticospinal tract likely gets insulted. This tract has influences to the lateral reticulospinal tract and has an inhibitory effect. Big X through the corticospinal tract and you lose the positive component to the LMN and the inhibitory component (lateral reticulospinal) to the LMN. Other tracts in green are positive which creates that positive effect and leads to spasticity.
Measure synergies through the fugl myers – don’t need to know how to grade any of these.
Could use these
Stiffness – muscle undergoes fibrotic changes
At the muscle belly things are happening
Central impact – spasticity is a biproduct of the CNS being impacted.
A different version of what we went over with the boxes earlier.
WON’T BE TESTED ON SENSITIVITY/SPASTICITY
If comes back negative – pretty confident there is no spasticity.
Limitations of the MAS (Modified Ashworth Scale)
In spasticity it is dependent on the person being relaxed. But is the spasticity you feel really a product of the central nervous system or the impact from the muscle belly itself and the muscle being tight?
“The rationale behind the SNOUT rule is that if a test has a high sensitivity, one can be confident that it will detect the clinical event and so if the test result is negative, one can be nearly certain that the clinical condition is not present.”
Spasticity does not impact function
AR is thought to result from irradiation or overflow of neural excitation across the cortex or spinal cord during voluntary movement (Honaga et al 2007)
Associative Reactions – when someone has spasticity, when they exert themselves walking, transfers, getting their HR up, their spasticity will temporarily get worse. Classic example – biceps spasticity , holding arm in flexed pattern, as they walk the biceps will incrementally be in a more flexed position due to the increased metabolic demand.
Pain – if muscles are constantly turned on 24/7, it can lead to pain.
Abnormal movement patterns – CC gait lecture
Skin breakdown – elbow constantly bent, think of skin folds and they are touching, or spasticity on gastroc and toe walking on one side - plantar surface of the foot has to absorb a lot more
Increased caregiver burden – spasticity in hips can be so severe that you can’t put on and take off pants.
Contractures – muscle gets tighter and tighter and tighter and once it reaches a contracture – game over
Painful stimuli – could be WB, touching the muscle, etc. anything that is noxious to the body that causes the spasticity to be triggered.
If muscle gets hyper stretched it might trigger it.
Not uncommon when going to the bathroom and the spasticity gets worse temporarily.
Positioning is a long term prevent contracture solution
Think of different positioning devices to make sure the joint doesn’t develop a contracture
Left arm and left leg – open packed position
Good - How can I get the joint in its most open pact position
Left hand side individual – not good – fully flexed position of the elbows, knees, and hips – consequence – skin breakdown of the popliteal area because there is no air to breathe. Can get pressure injuries on the back of the knee (probably right knee).
Individual on the right – not good. Back of their neck and occiput, sacrum, skin breakdown, respiratory function, qol will be impacted due to needing more assistance, person is not transferring walking because they probably lack the ROM.
Even if someone hasn’t developed severe spasticity, still have to position them in good positions.
Have to educate people on decent positioning.
Even if someone hasn’t developed severe spasticity, still have to position them in good positions.
Have to educate people on decent positioning.
Will also use modalities for pain
Vibration:
- high = facilitation
- low = inhibition
Take home message – our techniques that we do that aren’t pharmacological based are temporary no matter how hard you try.
The big theme with all of these examples – these are all being applied to the muscle and they provide an inhibitory affect to reestablish the homeostasis. We are taking a bottom approach to the CNS to override the positive affect and to reduce the muscle tone. Anything you can do to impact the muscle will have an afferent input to reestablish homeostasis.
These examples work for as long as you are using the device. If you stretch for 15 min – will reduce the spasticity for 15 min. tens for four hours lasts 4 hours. So, the more realistic scenario with these examples that helps with spasticity management would be TENS/NMES – slap some tens on them and they can do functional exercises with it on.
https://www.youtube.com/watch?v=1yccRAlm9_M
Serial casting – dying art in therapy.
Serial casting is indicated for this
Serial casting – temporary cast if you were to break a bone to ^^^^
These casts are on for like a week to address one or more of these issues
Want Grade A evidence!!!!
Wont be tested no why serial casting works !!!!!
Impaired sensation – make sure they are doing skin hygiene, clearing off dead skin
Impaired cognition – need caregiver to help assist.
Edema – might not be casting appropriate where the fluid has nowhere to go
Open wounds – don’t stick a cast on them
Heterotopic ossification – bone growth where it is not meant to be
Myositis ossificans – bone growth in a muscle – have to go in and cut it out
Active – could create a wound or limit ability to take antibiotics
Contracted ankles might benefit from serial casting which can positively impact their GAIT kinematics because of the increase in ROM
Get casted every week for 6-8 weeks = 6-8
Can walk on these, but won’t be the prettiest walk in the world.
Need two be stretched into maximal ROM and then be casted. This is how it helps develop that ROM because the muscle is stuck in that max range for that week
Cast – is it dirty, smell funny, etc
Capillary refills in the toes and the finger there?
Skin integrity – check above and below and then after the cast is taken off that week, is the skin tolerating this cast ?
Discussed bivalve casting
Knee flexion contracture – achieved full terminal knee extension when walking
Lower muscle tone – don’t over stretch
Positioning – open pack
Is this more static like down syndrome, or spinal shock
WON’T BE TESTED ON THIS
Neuroplasticity matters in the context of spasticity because work on the task the person can’t do to get enough reps to manage the spasticity. Brain rewires itself so muscle doesn’t start to get tight. Have to learn how to recruit it.
Will only temporarily reduce spasticity with modality we choose.
Why else might you address spasticity? – have to manage it in some capacity to prevent contractures by stretching (teach pts to stretch), skin integrity – if someone gets a pressure injury, it could potentially kill them.
Most optimal way to stretch for most people for a minimum of at least 30 seconds to truly stretch the muscle. If stretching for 10 seconds it won’t cut it.
More optimal ways/positions to stretch?
Cueing him – learned how to flex his leg when he took a step
Might need more punch - use pharmacological interventions
First line of defense when spasticity is at play – oral meds
The thinking is that baclofen reduces the release of excitatory neurotransmitters in the pre-synaptic neurons and stimulates inhibitory neuronal signals in the post-synaptic neurons with resultant relief of spasticity
Tizanidine (Zanaflex) inhibitsthe release of excitatory amino acids like glutamate and aspartate from spinal interneurons. Consequently, tizanidine enhances the presynaptic inhibition of motor neurons.
Valium - increases GABA in CNS… Thisshift in charge leads to ahyperpolarization of the neuronal membrane and reduced excitability of theneuron
Depress the CNS excitability is what these medications do – reason for the side effects
Side effects don’t outweigh the therapeutic impact.
https://www.youtube.com/watch?v=b0oQ3b-xjAQ
Second line of defense is injections
Blocks acetylcholine release – paralyzes the muscle – why there is no wrinkles as well lol.
Dysport can be used if pt has Medicaid, less copay
Takes 7-14 days to really pack a punch
If person gets botox on august 1st, want pt scheduled for therapy after two weeks
If you paralyze a muscle the muscle might get weak. A lot of these individuals can use their spasticity to their advantage.
Not all spasticity is bad. If spasticity is getting in the way of a functional activity, that is when you can choose to intervene
Repeat injections – wears off the effectiveness. Don’t want the immune system to develop a resistance.
Botox
Cost is major issue
Used with (smaller/larger) muscle groups
Need insurance approval prior to start of treatment
Repeat injections are more difficult to get covered
Botulinum toxin type A in the treatment of lower limb spasticity in children with cerebral palsy (Blumetti et. al 2019)
“BoNT-A is not more effective than ankle serial casting to treat ankle contractures for any of the assessed outcomes, but is more effective than orthotics at improving range of motion and spasticity.”
$13 a unit
smaller
People that tend to get botox and something else tend to do better than just one modality alone. Casting + botox > just better than one modality
Neurolytic – dissolving of the nerve, kills the nerve
Phenol – an option for pts if cost is a barrier, a quicker acting medication
Greater side effects for phenol
Shorter acting for phenol
Botox is longer lasting and fewer side effects but more effective
Botox is better with spasticity and AROM in the cerebral palsy pop.
Insurance is the biggest player in what someone gets.
New research indicating we should consider use of ITB earlier with severe spasticity to reduce long term contractures, improve comfort in severe TBI/SCI related spasticity.
Pts with bad spasticity, they’ll get this and this is a pump where it is dispensed into the spinal cord and it continuously gives lower levels of baclofen 24/7.
Nice option for a lot of spasticity management
Can give someone months or years of use following an injury
7% of pumps need replacement
Most commonly caused by kinks in the catheter
Evaluated by X ray
Battery failure, infection, occlusion are other common causes of failure
Putting something in the spinal cord so there could be back up CSF as wellas the others listed
Overdose – settings are too much and too much baclofen pumping through the system
LAST RESORT if nothing worked.
Get tendon lengthened in order to increase ROM. It is the flavour of the month.
They go in to the spastic muscle, lengthen it at the tendon, casted for 3 months to allow to heal and then begin therapy.
Likely NWB for three months so some people physically can’t do it.
Seen in the CP pop.
Full contracture – botox doesn’t work
LAST RESORT if nothing worked.
Get tendon lengthened in order to increase ROM. It is the flavour of the month.
They go in to the spastic muscle, lengthen it at the tendon, casted for 3 months to allow to heal and then begin therapy.
Likely NWB for three months so some people physically can’t do it.
Seen in the CP pop.
Full contracture – botox doesn’t work
Mild spasticity – 1 or 1+ on MAS
Best option – task specific training/functional training to power through or “compensate?”
More severe – try to reduce the spasticity in some way. Ice, tens, anything . Need arm in position to do the task specific training.
If spasticity isn’t bothering someone do the functional training. If very severe, need to address it first before task specific training.
PLOF – Prior Level of Function
ASIA LEVEL: C3 ASIA A (Noon sign)
Neurological level: C3
Go to motor level that has a 3 as long as everything above it as a 5. Make sure sensory is 2/2 on both sides.
C3 ASIA A
Bed mobility: dependent
Transfers: dependent
Ambulation: Probably not
Elevations: probably not on the functional aspect but could independent with caregiver instructions
Floor transfers: dependent
Wheelchair mobility: modified independent at a power wheelchair level.
Wheelchair mobility – can a person propel the wheelchair physically? Can they also manage the components of the chair? Can they lock their brakes, elevate their leg rests. Anything that involves the wheelchair.
Zone of partial preservation – some sensory or motor below the neurological level.
Modified independent – pt is doing the task
Interventions:
Bed mobility – rolling – has arm movement on the left hand side. Can participate in some capacity. Working on rolling for weight shifts in bed vs a caregiver or nurse. Rolling is good for hygiene (helps the therapist).
Caregiver instructions with Transfers – have to teach the caregiver to put the harness on properly, joint positioning. the pt can learn how to teach the caregiver. Have to test or quiz the pt on how to put on the harness or anything of those things they need to be able to do.
C3 ASIA A on ventilator – if there is innervations, strengthen the hell out of it. Can potentially get them off of the ventilator if they can regulate their breathing on their own. Think zone of partial preservation from C3-C5 (still some innervation for the diaphragm). Strengthen strengthen.
Ambulation – get them upright (tilt table). At a huge loss for Bone mineral loss, fxs, etc. stimulation might have good value for them. Add some juice with stim for this pt.
If the person has to do a weight shift – tilt back weight shift. Cant’ do the other weight shifts due to no trunk control and cant do push up because of obvious muscle reasons.
