Locomotion-Assessment and Intervention In Persons w/Brain Injury Flashcards
what are the typical structures impaired in pw stroke?
SMA, pre-motor cortex
M1 motor cortex (+/-BS)
sensory cortex
frontal lobe
when the pre-motor cortex is impaired in pw stroke, what is the impairment?
they can’t figure out how to set their posture to take a step
what structure is responsible for the motor plan of gait?
SMA and pre-motor cortex
what structure is responsible for the motor output for gait?
the M1 motor cortex
what system functions are typically impaired in pw stroke?
motor fxn
sensory fxn
postural alignment
gait patterns impairment
what motor fxn impairments are typical in pw stroke?
dec active, fractionated (isolated) motor control
abnormal tone, typically hypertonicity and clinical hypertonicity
chronic learned non-use and secondary MSK impairments, weakness
what sensory fxn impairments are typical in pw stroke?
hemisensory deficits
proprioception and kinesthesia in a % if the primary somatosensory cortex is affected
what postural alignment impairment is typical in pw stroke?
asymmetrical WB in standing
what gait patterns impairments are typical in pw stroke?
typical “classic” stroke gait deviations
increased clinical hypertonicity
t/f: bc the MCA is the most commonly affected artery in stroke, gait tends to look very similar in pw stroke in the acute phase
true
t/f: walking is mediated by complex neural systems both automatic and voluntary
true
t/f: damage to all BS descending pathways and corticospinal tracts decrease fractionated mov’t
true
what is the postural alignment of the limbs in pw stroke?
assymetrical WB bw limbs
involved limb in relative ER and adduction w outtoeing
what is often the cause of relative ER and adduction w outtoeing in the acute phase in pw stroke?
often from retraction
what is often the cause of relative ER and adduction w outtoeing in chronic phase in pw stroke?
often from ROM deficits
what is the postural alignment of the trunk on the involved side in pw stroke?
trunk shortening
scap depression and Retraction
pelvic retraction
what is often the only active muscle control in pw stroke?
adductors
t/f: pw stroke will often use the adductors to advance the limb forward in gait
true
in the acute phase, what are postural alignment impairments likely due to?
lack of activation
in the chronic phase, what are postural alignment impairments likely due to?
likely due to sitting a lot and getting stuck like that
what muscles are often the strongest in pw stroke?
extensor synergy muscles
t/f: in pw stroke, the trunk leans towards the involved side w/scap and pelvic retraction
true
what is the problem with unilateral ADs in pw stroke?
it promotes even more lean to the uninvolved side
what is the locomotor central pattern generator (CPG)?
a complex network of spinal interneurons to generate rhythmic, alternating activities of flexion and extension at the hips and knees
what are the 2 inputs to the CPG?
afferent input from stretch receptors
jt loading at IC
the afferent input stretch receptors facilitates what?
flexion
t/f: stretch of the hip flexors in gait facilitates hip flexion
true
jt loading at IC drives what?
extension
step length on the ____ side is key in facilitating hip flexion
uninvolved
what are 3 steps in activating the CPGs in pw stroke?
alignment of the foot facing forward
taking a big step with the uninvolved leg to get a good stretch of the hip flexors
make sure to get good heel strike and repeat
what can we work on in pregait to get a good swing phase on the involved side?
work on getting a good big step w/the uninvolved leg
why do we care about the CPG?
bc we set up our pts to use automatic gait patterns generators to our advantage to make interventions easier
what are the 2 most important phases in gait for facilitating gait recovery in stroke?
heel strike/initial contact
terminal hip ext/terminal stance phase on the trailing limb
what is the importance of effective heel strike/IC?
maximizing IC at the ankle maximizes sensory input and facilitates LE extension to stance
what is the importance of terminal hip ext/terminal stance phase?
the trailing limb in good hip extension maximizes sensory input through stretch of the hip flexors to facilitate hip flexion for swing
why are CPGs so important in interventions?
lots of our interventions will be focused on terminal limb ext
we can try to regain ROM in chronic pw stroke
if we want to intervene on gait with less degrees of freedom (DOF), what can we do?
have the pt in kneeling on the involved limb and lunging into it to get the stretch of the hip flexors
when we see clinical hypertonicity come into play, what might this tell us?
what we are doing doesn’t have enough stability or is too difficult for the pt
t/f: there is a typical set of gait deviations and resultant biomechanical adaptations that we can expect in pw stroke
true
what are the typical kinematic deviations at initial contact (heel/foot contact and loading)?
limited ankle DF
lack of knee flexion (knee hyperextension)
in the acute phase, what is the cause of limited ankle DF at IC?
decreased activation of ant tib muscles
contractile block of advancement (hypertonicity of calf muscles)
in the chronic phase, what is the cause of limited ankle DF at IC?
consider jt immobility/PROM, contracture, contractile block
what are the causes of lack of knee flexion (knee hyperextension) at IC?
contracture of soleus paired w/limited control of quads at 0-15 deg
contracture a/or hypertonicity of calf muscles w/premature activation
what are the typical kinematic deviations at midstance?
knee hyperextension
lack of knee extension (knee remains flexed 10-15 deg w/excessive ankle DF)
excessive lateral pelvic shift
what are the mechanical causes of knee hyperextension at midstance?
failure to progress body mass forward over the foot due to limited tibial advancement (DF) and terminal hip extension
in the acute phase, what are the mechanical causes of knee hyperextension at midstance?
decreased activation of ant tib muscles
contractile block of advancement-contracture and/or hypertonicity of calf muscles
mechanical block of advancement created by an orthosis
in the chronic phase, what are the mechanical causes of knee hyperextension at midstance?
contractures, jt immobility, and PROM
what is the behavioral cause of knee hyperextension in midstance?
fear of limb collapse due to weakness of muscles controlling the knee as an adaptation
t/f: normally the tibia advances over the foot going forward w/a little knee flexion
true
what are the causes of lack of knee ext in midstance?
synergistic activation of the LE musculature (flexor synergy or co-contraction)
what are the causes of excessive lateral pelvic shift in midstance?
decreased ability to activate stance hip abductors and control hip and knee extensors
what are the typical kinematic deviations in late stance (pre-swing)?
excessive pelvic retraction and lack of terminal hip ext
lack of knee flexion and ankle PF
what are the causes of excessive pelvic retraction and lack of terminal hip extension in late stance?
no stretch of the hip flexors
no “driver” for the LE flexor arm of SPG/CPG to initiate swing phase
what are the causes of lack of knee flexion and ankle DF in late stance?
weakness of calf muscles (GS)
inadequate PROPULSION
even though we have tone of the calf muscles, there is a lack of activation
t/f: even though we have tone of the calf muscles, there is a lack of activation of the muscles in late stance that limit knee flexion and ankle PF
true
in early and mid swing phase, the dominant muscle activity in the LE is…
extensor tone
when the extensor tone is dominant in the LE in early and mid swing phase, what muscles are weak?
hip flexor activity is weak
what are the typical kinematic deviations in early and mid swing phase?
limited hip flexion
limited knee flexion
when hip flexion is limited during early and mid swing, what do we often see pts doing?
hip hiking or circumducting
OR
advancing the limb with hip adductors (limb ER and outward toe angle)
when the adductors are used to advance the limb in early and mid swing, what is the position of the limb?
ER and outward toe angle
what are the causes of limited hip flexion in early and mid swing phase?
decreased activation of flexor muscles, often with hypertonicity of extensor muscles/extensor synergy dominance
what causes limited knee flexion in early and mid swing?
decreased activation of HS often with hypertonicity of rectus fem
reciprocal inhibition of the HS w/lots of quad activation
the ____ needs to be facilitated out of synergy early on
HS
what can we do to decrease reciprocal inhibition to the HS?
calm the rectus fem and facilitate active HS
get into hooklying for low stress HS activation
what are the typical kinematic deviations in late swing?
limited knee extension and ankle DF for IC
decreased loading response
what are the causes of limited knee ext and ankle DF for IC at late swing?
contracted/hypertonic calf muscles
decreased DF activity
what are the causes of decreased loading response at late swing?
inadequate heel strike and no jt loading “driver” to activate the LE extensor arm of the SPG/CPG
what is the secondary impairment of spatiotemporal adaptations?
decreased ROM
what are the composite impairments of spatiotemporal adaptations?
increased “learned non-use”
clinical hypertonicity
what are the spatiotemporal gait adaptations?
decreased walking speed
short and/or uneven step and stride length
increased stride width
increased double limb support phase
dependence on support through the hands
how do we measure gait velocity?
the a forward 10m WT (2m ramp up, 6m walk, 2m deceleration)
why do we do the 10mWT with max speed too?
bc we want to see what happens when pts change speed for things like going to the bathroom, getting the phone, or getting the door
what is the range for normal walking speeds?
1.2-1/4 m/s
what is an important gait velocity threshold for community ambulation and independence in ADLs?
0.8 m/s
what is the MCID for gait velocity?
0.1 m/s
t/f: a change in gait velocity of 0.1 m/s is significant for mortality
true
people who fell had significantly slower ____ times
3mBWT
3mBWT times slower than ____ indicated a pt is very likely to fall
4.5s
3mBWT times faster than ____ indicated a pt is unlikely to fall
3s
what is the procedure for the 3mBWT?
align heels w/start tape
walk backwards as quickly and safely as possible without looking back
instructed to stop (timing stops) when they reach the 3m tape mark (no ramp up or deceleration)
documentation of gait should always include what things?
level of assistance, gait velocity, and distance
gait fxnal classifications based upon the velocity
description of gait patterns limitations (OGA)
distances of >____ft will jeopardize qualification (insurance coverage) for PT
100
to avoid distances over 100 ft, what should we do?
keep distances low to increase velocity, control and decrease level of assistance
improve safety and independence w/in reduced distances when you’re setting goals
what is the cutoff gait velocity for household walker?
0.4 m/s