Tone Management Flashcards
what is ms tone and why is it adaptive
resting tension in ms
resistance to elongation/stretch when relaxed
state of partial ms contraction at rest that supports posture and provides baseline tension for volitional contractions
what are anatomical structures that contribute to the complex control of a ms fiber (5)
cortex
brainstem
cerebellum
spinal stretch reflexes
ms spindles
clinical reasoning: do you always want to dec ms tone if person has hypertonicity?
not necessarily
clinical reasoning: do you always want to inc ms tone if person has hypotonicity?
yes
what are 4 pathologies can result in hypotonicity and how
LMNL:
- impacts ant horn of SC, ventral nerve root, spinal nerves, or peripheral nerves
UMNL:
- damage to corticospinal tract -> have hypotonicity in acute/shock phases & even long term s/p stroke
chromosomal abnormalities (ie downs)
cerebellar lesions
what is hypotonicity and how does it present
dec resistance to passive elongation
limbs/trunk feel heavy/floppy
- ms are soft/squishy to palpation
what is hypotonicity associated with (2)
dec stretch reflex
dec DTRs
why do you commonly see secondary weakness in hypotonicity
those w normal strength w low tone require more energy for more tension to be generated in extrafusal ms fibers to make up for that low baseline tension
- takes more energy to move and endurance may be a problem
what are secondary complications that result from hypotonicity (2)
atrophy, weakness
joint misalignment, subluxation
what is a common manifestation that you can observe in people who have low tone
poor postural alignment
- forward flexed trunk
- forward head
- post pelvic tilt
- W-sitting in children
what is the goal when treating hypotonicity
improve motor response and mvmt patterns for inc safety and independence w functional activities
what are 5 strategies to inc ms response w sensory input
approximation
ms tapping, quick swipe
light, graded resistance
wt bearing positions
moveable/pliable surfaces
how does approximation inc ms response
inc proprioceptive input from joint receptors
-> help facilitate co-contraction in wt bearing position -> help w extensor response primarily (some flexor, but mostly extensor)
how does ms tapping inc ms response
activate ms spindle
-> if activate briskly can inc motor response
how does light, graded resistance inc ms response
tracking resistance -> facilitatory to encourage smoother mvmt
how does wt bearing inc ms response
stability, postures, co-contraction, proprioceptive input
- get approximation -> facilitate co-contraction and inc extensor response
how does moveable/pliable surfaces inc ms response
if hypotonicity -> activates reticular system and facilitates a ms response
what is the focus of treating someone w hypotonicity
focus on strengthening ms and proper postural alignment
what is a consideration of when to implement strategies to inc ms response in hypotonic pts
preparatory techniques that are not a treatment in and of itself
-> prepping to optimize motor system and prepare for work
if preparatory techniques don’t work, what is the next approach to use and examples of that
compensatory approach
- ex: external support via bracing, orthotics, splints for stability, improved function and joint protection
what is hypertonicity
inc resistance to passive stretch
-> difficult to move limb and elongate ms
what are 2 conditions that you see hypertonicity in
UMNLs
basal ganglia disorders
- ie Parkinsons
what is hypertonicity associated with
inc stretch reflex and hyper-reflexia DTRs
how does hypertonicity impact ms
preserves ms bulk (dont see much atrophy)
-> still can have underlying weakness
what are examples of hypertonicity (3)
rigidity
spasticity
clonus
when do you want to minimize hypertonicity
if it interferes w function, causes pain, positioning problems, hygiene issues (maladaptive)
when do you NOT want to minimize hypertonicity
if supports posture and improves balance, mobility (adaptive)
-> may rely on passive tension to help w posture and transfers
what is spasticity
velocity dependent inc resistance of ms or ms groups to passive stretch d/t loss of suppression of spinal stretch reflex
what is the cause of spasticity
overactive spinal stretch reflex
what are 2 functional classifications of spasticity
weak and spastic
strong and spastic
how is spasticity measured (3)
clinical exam
MAS
tardieu
what is a common sx to be associated w hypertonicity and why
pain
- esp w adaptive shortening of ms
what are 3 activities to assess as part of a comprehensive clinical exam
balance
functional mobility
ADLs
what are 5 modalities that can treat hypertonicity and what does the literature say ab their use
US
cryotherapy
vibration
estim (TENS, FES)
neutral warmth
literature doesn’t strongly support any of them
- some anecdotal success through trial and error
how could estim be helpful in treating hypertonicity
could apply to spastic ms to fatigue and tire out
could apply to antagonists to get a stronger contraction and overcome the tone in spastic ms to allow for mobility/motion
what are 3 manual techniques to temporarily modify hypertonicity and what as sheri baby found to be the most successful
deep pressure **
prolonged stretch (slow speed)
RRo
how does deep pressure temporarily modify hypertonicity
deep (but not painful) pressure on ms spindle or tendon (GTO) to induce reflexive relaxation
- after few seconds ms relaxes, can then start to open limb up slowly
why is it important that deep pressure to temp modify hypertonicity not be painful? what is a strategy to avoid this?
if painful stim will trigger guarding and inc ms contraction
use widely distributed pressure
what are examples of using a prolonged stretch to temporarily modify hypertonicity
splints & air sleeves for longer term management
serial casting
how does RRo help to modify hypertonicity
rotating along long axis of limb
- can do for trunk in hooklying or SL
- rotation can be inhibitor to nervous system and relax ms
what are 2 examples of noninvasive neuromodulation (NINM) for spasticity management, what are outcomes, & when/where is this seen
repetitive transcranial magnetic stim (rTMS)
transcranial direct current stim (tDCS)
more effective when combined w other interventions, safe and low risk
more on a research level, not seen in practice yet
- not FDA approved, not widely clinically available
what does the evidence say about serial casting
no/little evidence on permanently altering ms tone or improving function
- evidence to improve PROM
who is most appropriate for serial casting
if complex spasticity and want to aggressively manage tone and prevent contractures
what is the process of serial casting
prolonged stretch over 3-5 days
-> then remove and apply new cast in further elongated position and continue until desired effect achieved
what are 3 types of medical management options for hypertonicity
meds
- oral
- intrathecal (baclofen)
injections
surgical interventions
*rTMS and tDCS still in trials
what is PT’s role in the team’s selection of a medical management option
we have insight on how tone is affecting pt function and how the intervention is or isn’t working
- we can advise on what may be the best option for the pt
what are 5 types of oral meds for managing hypertonicity
tizanidine (zanaflex)
dantrolene
gabapentin
diazepam
baclofen
what are advantages and disadvantages of oral meds
advantages:
- easy to admin & make changes quickly
- non-invasive
- acts globally to target multiple ms groups
disadvantages:
- large doses may be needed
- systemic side effects
- compliance
- acts globally (if focal spasticity, may cause relaxation of ms throughout body and can lead to weakness and fatigue)
tizanidine (zanaflex): purpose, MOA, dosage, adverse effects
reduce spasms
acts on alpha-2 adrenergic system at spinal and supraspinal levels to dec spinal stretch reflex
starting dose 1-4mg at bedtime
- avoid side effects
max dosage = 36mg
common adverse effects:
- fatigue, dizziness, drowsiness
- weakness, anxiety, nausea, HAs
dantrolene: purpose, MOA, adverse effects
spasticity, dec ms contraction
affects release of calcium from sarcoplasmic reticulum of skeletal ms
- acts peripherally at level of ms fiber
adverse effects:
- drowsiness, dizziness, fatigue
- ms weakness, **abdominal pain
gabapentin (neurontin): MOA, adverse effects
binds to calcium channel receptors on neurons interfering w transmission
- works at nerve level
- interferes w nerve signal transmission
usually well tolerated**
side effects of fatigue, reduced concentration
diazepam (valium): MOA, adverse effects
inc affinity of neurotransmitter GABA to its receptor in brainstem and SC (works centrally)
- results in inc in presynaptic inhibition and dec of monosynaptic and polysynaptic reflexes
side effects:
- drowsiness, dizziness, fatigue
- weakness, nausea
- memory impairment, constipation
oral baclofen: purpose, MOA, adverse effects, dosage, and important pt ed and why
treat spasticity
interacts w GABA neurotransmitter and works w/i CNS pre and post-synaptically to inhibit spinal reflexes
- enters CSF and crosses BBB causing side effects
Side Effects:
- fatigue, weakness
- hypotonia, somnolence, n/v
- HA, dizziness, paresthesias, withdrawal
starting dose 5-10mg 2-3x/day
-> inc slowly to 80mg/day
education of importance of compliance and dosing schedule
- can cause serious side effects if quickly withdraw
what pts are appropriate for a intrathecal baclofen pump trial (6)
person w global spasticity, spasms, and/or clonus
progressive/chronic dz
primarily LE involvement
varying functional needs
potentially failed focal management
on high dose of oral baclofen
- ie need >80mg of baclofen
what is intrathecal baclofen
surgically implanted pump to deliver baclofen into spinal thecal subarachnoid space
advantages and disadvantages of an intrathecal baclofen pump
advantages
- lower med doses bc delivered directly into CSF -> dec SE
- ability to tailor delivery times to needs
- systemic effect
- ability to do trial before implantation
disadvantages
- surgical implant (invasive)
- compliance is important (regular f/u, interrogate it, make sure working properly)
- doesn’t effect UE as well as trunk and LE
what happens on trial day for a ITB pump
battery of tests
admin med which peaks 3-4hrs post
- we will retest at 1.5hr increments after injection
what are some tests and assessments we may perform during a trial of ITB pump (7)
ROM
spasticity - MAS
strength
functional assessment
- mobility & transfers
- postural control & alignment
PSFS
pain
caregiver burden
what are indications of a successful ITB pump trial (5)
reduction of spasticity per MAS, PSFS
no adverse reactions
inc ROM, function, positioning
dec in pain, spasms
dec caregiver burden & inc (I)
botox injection: indication, MOA, duration of effectiveness and why, SE, and outcomes
focal spasticity
inhibits acetylcholine release at NMJ
-> causes weakness of ms injected & temporary paralysis
wears off in 3mo secondary to nerve sprouting and re-innervation
- can’t do multiple injections in same spot bc of this effect
no systemic side effects
dec spasticity by 1-2pts on MAS
- improves ROM
- improves mobility
phenol injection: indication, MOA, duration, and effects
focal lesions
injected directly into nerves -> damages both motor and sensory nerves via chemical neurolysis
lasts 9-12mo
effects: ms paralysis, immediate response to injection
phenol vs botox
phenol works directly at nerve
- causes more paralysis
- prevents any contraction at all
- no delay
botox works at NMJ
- may still have some underlying contraction
- may have slight delay
what are surgical interventions
selective dorsal rhizotomy
msk surgeries
- tenotomy
- myotomy
- tendon lengthening or transfer
what is a selective dorsal rhizotomy and what does this do? SE?
surgical procedure to cut a portion of dorsal nerve roots in lumbosacral spinal cord
-> dec sensory input or afferent arc of stretch reflex at segmental spinal level and dec excitability
SE: sensory loss, weakness
what population is there good evidence for dec in spasticity after a selective dorsal rhizotomy
children w CP
- spastic diplegia
what is the purpose of a tenotomy or myotomy as a surgical intervention
prevent contraction to dec hypertonicity
what populations do you tend to see MSK surgeries in
more adults than peds
why would they do a tendon or ms transfer after a tenotomy or myotomy
try to preserve function that may be lost in surgery
when do we intervene for hypotonicity
almost always
- almost always marked as mal-adaptive
