Lecture 12: Gait Deviations Flashcards
Gait Deviations quiz: Will be lots of video questions
* No degrees on quiz
* Will get RLA terminology and old terminology (so you’ll have both)
Pathology: Toes or Forefoot Contact on inital contact (remember, the heel should hit first)
* Name some potential causes
Possible causes:
* Leg length discrepancy
* PF contracture (causing contraction of the gastroc)
* Spasticity - so if PF are spastistic they DF might not be waek but they just can’t overcome this excess tone. Or if they’re going to pull they foot up into DF they could trigger that spasticity in PF’s because spasticity is velocity dependent
* Profound DF weakness (doesnt eccentrically contract enough to pull toes up)
* Painful heel - want to avoid landing on it
* Excessive knee or hip flexion with impairment that limits neutral ankle (try it, makes sense)
* Ankle ROM impaired into DF
Analysis / Examine:
* Range of motion ankle / hip / knee flexion
* Leg length
* Ankle PF contractures
* Muscle tone and timing of activity in PF’s
* Heel pain
* Pre tibial strength
NOTE: Contractures form quickly in people w/ abnoraml pathways and much slower w/ those people w/ normal pathways.
Foot Flat on initial contact
* Name some possible causes
Description: Entire foot simultaneously touches the ground
Possible causes
* PF contracture
* Weak DF’s
* Knee flexion contracture that prevents optimal tibial alignment prior to intial contact - do this yourself, you’ll see that that knee needs to be bent for the foot slap to occur baring other pathologies (I think excessive hip flexion could also cause a similar effect)
Analysis/Examine:
* ROM at ankle and knee
* Strength of anterior tibialis
Foot slap on initial contact
* Most common possible cause
This is very similar to foot flat
Description: Forefoot Slaps ground following heel first initial contact
* So audible slap
Typically caused by weak dorsiflexors (eccentric)
Analysis/Examine:
* Strength of ankle DF’s
* Muscle activation timing of pretibial muscles - look at muscle timing and figure out why its happening
This is now 2 step so you need to know that a week anterior tib causes that foot slap and that the deep fib innervates that anterior tib
3 step. need to know what LMN vs UMN is. Need to know what correlates to that decreased sensation
Excess PF in mid stance and/or terminal stance
Description: Ankle fails to achieve 5 degrees of DF in mid stance and/or 10 degrees of DF in terminal stance (do it and see)
* decreased tibial translation - so think your tibia going over your foot when you’re walking. If you’re not going into that full DF you wouldnt get as much of that tibial translation (try it)
* Causes
* Why might it be intential
Possible causes
* PF contracture - litteraly can’t get into that DF position
* Overactivity or spasticity of the PF’s thats stopping
* Intentional to avoid ankle and knee collapse if PF’s and vastii are weak
Analysis / Examine:
* ROM-PF contracture
* PF tone (spasticity)
* Strength of calf msucles and vastii
* Intentional due to dual areas of weakness - if you have to too much ankle DF it causes the knee to flex which could lead to collapse (because the gastroc is being stretched and it covers both the ankle and knee joint) - so its so the knee doesnt collapse
If you have lots of DF what happens to the knee?
It flexes because the gastroc wants to shorten and it covers both the ankle and knee joint
What is vaulting?
Going up on toe to get contralatearl foot forward (and not have that toe drag)
* so its done so we don’t drag toes
* often done due to lack of hip/knee ROM (because that leg would drag if we werent going up onto toes w/ otehr leg)
* Weak DF’s of ipsilatearl leg causing toe drag could be a reason we vault w/ the contraltaeral leg
Spasticity making you go into PF of the leg on the ground cause cause the tip toe apperance making you go into vaulting (even if theres not a problem w/ the swing leg)
NOTE: Vault is often inconsistent because its ineffeicent. They might circumduct, vault, and do other things because they get tried of doing just one position because this is an inefficient position
* It hurts to walk w/ gait deviations
Excess DF: Ankle collapses into more than 5 degrees of DF at mid stance and/or more than 10 DF at terminal stance
* so think almost collapsing down
* Possible causes?
Causes:
* Inability of PF’s to control tibial advance
* Knee flexion contractures
* Hip flexion contractures
Analysis/Examine:
* ROM ankle
* PF strength
* Hip and knee flexion contractures
Early Heel Rise in Mid stance
* Discription: Heel comes off the ground in mid stance
* causes?
Causes:
* Spasticity
* Contracture of PF’s
Analysis/Examination
* ROM - can just be lack of ROM at heel
* Tone for PF spasticity
* However some people just walk like this - these are our bouncy walkers
No Heel off:
* Discription: heel fails to elevate from ground appropriately during terminal stance
* causes?
They really need that heel off to gain adequate propulsion. If they lift their entire foot instead of pushing –> decreased stride length / pace. Messes up entire gait
Possible causes:
* Weak PF’s
* weak invertors that fail to lock midfoot in terminal stance
* Inadequate toe extension ROM - if they can’t have this then they cannot come over that toe and up into that heel off. Things like turf toe / plantafascitis
* Painful forefoot or toes
Analysis/Examination:
* Strength of PF’s and tibialis posterior
* Toe extension ROM and strength
* Forefoot pain
Toe Clawing: - toes flex and grab the floor
* What often causses this?
* Spasticity of waht can cause this?
Sensory stuff. Think stimulation to bottom of feet
* think walking barefoot on somewhere like the beach
Spasticity of toe flexors
Excessive activation of toe flexors to compensate for weakness of the gastrocnemius and soleus
Plantar grasp reflex that is only partially integrated
Positive supporting reflex
Analysis / examin:
* Tone of toe flexors
* Strenght of PF’s
* Presence of primitive reflexes
Excessive inversion / Eversion at the ankles - in stance or swing phase
* Description: Subtalar joint excessively inverted or everted (expected position)
* Possible causes?
Excessive inversion possible causes:
* Overactivity or contracture of invertors
* Reduced activity of evertors (so think weakened)
* Primitive Extensor pattern
Excessive eversion:
* Overactivity or contracture of evertors
* Reduced activity or strength of invertors
* primitive Flexor pattern
Analysis/Examin:
* Strength and timing of LE movements and tone
* ROM/contractures - so maybe they don’t have much movement at that subtaylor joint
basically w/ this its tight on one side or weak on one side
Toe Drag:
- happens in swing phase
- some portion of reference foot contacts ground during swing
- possible causes?
Causes?
* Pretibial muscle weakness (think anterior tib)
* Plantarflexor spasticity or contractures (locking them in that toe down position)
* Inadequate knee or hip flexion
Analysis/Examine:
* ROM of ankle, knee and hip - decreased ROM into flexion could be causing it to drag
* Strength of muscles critical for limb clearance (think pretibial / hamstring / hip flexors)
Another cause of this can be decreased balance. They don’t pick that foot up because they’re scared to, so they drag it.
Excessive knee flexion - in any phase
Possible causes:
possible causes:
* knee flexor spasticity or contracture that exceeds position required for given phase
* Painful or effused knee
* Proprioceptive loss at knee - what happens is when you lose proprioception at any joint you hold it rigid - so if they don’t know where their joint is, than they just don’t move it, then they don’t have to worry about knowing where it is.
* Shorter LE on contralateral side (would mean you need more knee flexion to decrease toe drag and avoid falling)
* Weak calf or hip flexion contracture if during single lim support
Analysis / Examine:
* Tone
* Spasticity
* ROM
* Contractures
* Pain
* Effusion
* Proprioceptive loss at knee
* Leg length discrepancy
Limited knee flexion - loading phase (remember, you should have slight knee flexion in loading phase)
* Description: Knee achieves less than expected 20 degrees of flexion
* Causes?
Causes
* Intentional to decrease demand on weak quad muscles (so they basically fling it out into extension using momentum, then don;t slightly flex it to land on it so they don’t have to eccentrically lengthen quads, and they don’t have to achieve that extension w/ the quads as much because they just flung it out there)
* Plantarflexor or quadriceps tone, spasticity, or contracture
* Proprioceptive impairment at knee - again if they don’t have that good propriocetion they arent going to want to move the joint at all, so it can get locked into that extra extension
Analysis/Examine: Plantarflexors and quads
* Strength
* Tone
* Spasticity
* Plantarflexion and knee exntesion ROM
* Knee proprioception
Limited Knee flexion: - during pre swing and initial swing
* Description: Knee achieves less than expected flexion for a given phase
* causes?
Causes:
* Plantarflexor tone, spasticity, or contracture - i think this is just because if you’re in PF you’re dragging and unable to bend knee
* Quadriceps tone, spasticity
* Proprioceptive impairment at the knee - don’t want to bend it because they’re unable to locate it in space
* Knee pain or effusion - don’t want to move it
* Calf weakness or hip flexion contracture that limits ability to achieve trailing limb terminal stance - meaning you will drag foot more
* Knee flexor weakness
Analysis/Examine
* Tone and spasticity of plantarflexors, vastii, and rectus femoris
* ROM
* Knee propropcetion
* Pain
* Effusion
* Plantarflexor strength and for hip flexion contracture
* Knee flexor strength
Knee hyperextension - stance phase
* Description: Extension of knee beyond anatomical neutral
* Causes?
Causes:
* Structural abnoramlity
* Flaccid/weak quadriceps or hamstrings
* Quads spasticity - nails them into extension
* Accommodation to a fixed plantarflexion deformity - PF goes w/ knee extension
* Impaired proprioception
Analysis/Examine:
* Strength
* Tone
* Spasticity of plantarflexors and quadriceps
* ROM
* Knee proprioception
She suggested if the pt has a tone of knee hyperextension, maybe shell use an ace wrap to put them in DF (because adding DF theoretically pulls the knee into flexion [gastroc biomechanics]). If they’re still walking w/ knee hypertension than im thinking its NOT coming from the foot and vice versa
* If you did the beighton scale and everythings hypermobile and they’re walking w/ tons of hyperextension, than you might not be able to fix it. Because thats really joint laxity more than anything. might need something more external
increased PF goes with what knee movement?
Knee extension
Increased DF goes w/ what knee movement?
Knee flexion
* makes sense, gastroc is being stretched and knee wants to bend
Wobble - Stance phase
* just a little wobble when taking a stap.
* Description: Alternating flexion and extension at the knee joint (wobble)
* Causes?
Causes:
* Proprioceptive Impairments - dont know where knee is so they make those little adjustments that seem like wobbles
* Alternating spasticity of knee flexors and extensors
Analysis/Examine:
* Proprioception
* Tone/spasticity
Limited Hip Flexion - any phase
* Description: Hip positioned in less flexion (thigh relative to vertical) than expected for given phase
* Causes
Causes:
* Intentional to limit demand on waek hip extensors during loading response - if they have weakness of hip extensors they might actaully decrease their hip flexion so they don’t have as big of a range to go through - you need more m control as the range gets bigger
* Weak hip flexors
* Hamstring spasticity or contracture - makes sense - pulling into flexion
Analysis/Examine
* Strength of hip flexors and extensors
* ROM of hip
* Tone/spasticity of hip exnsors and hamstrings
Circumduction - swing phase
* Description: Lateral circular movement of limb consisting initially of abduction, external rotation, followed by adduction and internal rotation in latter portion of swing - think leg out and around - note this can coexist w/ vaulting and go back and forth
* causes
Causes:
* Weak hip flexors/decreased Df / decreased knee flexion
* Inability to shorten leg for limb clearance - swing limb (leg length descrepancy, tone etc..)
Analysis/examine:
* Strength of hip flexors, knee flexors, and ankle dorsiflexors
* ROM in hip and knee flexion, and ankle DF
* Abnormal tone/extension pattern
Increased Hip Internal rotation
* all phases
* Description: internal rotation of femur
* causes?
Causes:
* Spasticity or contractures of internal rotators
* Weakness of external rotators (so internal take over)
* Excessive forward rotation of contralateral pelvis
Analysis/Examine:
* Tone
* Internal rotation ROM
* Strength of external rotators
Increased hip external rotation
* all phases
* External rotation of femur
* Causes?
Causes:
* Spasticity or contractures of external rotators
* Weakness of internal rotators
analysis/examine:
* Tone (might be increased for external rotation pulling them into it)
* External rotation ROM (might be increased)
* Strength of internal rotators (might be weak)
Is someone w/ Ataxias gait pattern consistent or inconsistent?
Very inconsistent
* they might have loads of hip flexion w/ one step and next to none the following step
* consistently inconsistent
Does someone w/ ataxia have over shooting or under shooting?
Both! remember, that gait is very inconsistent and all over the place
Does someone w/ ataxia have a narrow or wide BOS?
Increased due to their unsteadiness
Does someone w/ ataxia have increased or decreased single leg stance time?
Decreased
Ataxia can be bigger or smaller. No one set ataxia. Some more severe some not
What is cissoring?
* what most likely causes it?
Crossing the midline w/ steps
Spastic adductors
* could also result from weak abductors
Path deviation = when you’re walking forward and take a step in the lateral direction
NOTE: Ataxia is not the same as spasticity. Infact w/ ataxia they often have hypotonia at the trunk which impacts all 4 limbs
Crouched posture
* this is what it sounds like, everything is kind of in flexion
Causes:
* Hip flexion contractures or tightness
* Knee flexion contractures or tightness
* Excessive plantar flexor muscle weakness - leads to increased DF - also weak because they’re in DF all the time and a lengthened muscle is typically a waekened muscles (not in the optimal contractile state)
* Impairments in motor control
* Some combination of the above
shorter stride because they dont get the push off because they’re in so much DF
Increased flexion seen at all joints in the sagittal plane
KNOW: Crouch posture = staright plane (saggital plane)
Spastic diplegic = has some rotational part to it as well
What is hemiplegia?
* Why do they have an improved chance of independent ambulation?
One side of the body impacted (think R arm/R leg)
They have an improved chance of independent ambulation because they still have one “good” side
however, typically the good side isnt really that good. You’ll see deviations on the good side to compensate for the bad side - so even the good side isnt great
What is spastic Diplegic?
* Which way is the pelvis tilted
* Which way is their upper trunk positioned
* What happens at the scapula
* What happens at the neck
* What happens at the hips?
* What gait deviation is common?
* What happens at the knee
Bilatearl LE impacted (if it was quad it’d be all 4 extremeities)
* Pelvis in posterior tilt
* Forward flexion of the upper trunk (do these to and see how they make eachother do this)
* Protacted scapula
* Excessive neck extension
* Excessive hip flexion
* They do scissoring when walking (adduction and internal roation stance)
* Either excessive knee flexion or hyperextension - this is if they have a lot of tone
Late stance-Plantarflexor weakness may allow ankle to collapse into excess DF and knee excess flexion
Ankle excess DF in late stance to ctronol knee flexion contracture or hamstring tightness/spasticity
What kind of gait pattern is this - Crutch/Cane moves at same time as opposite LE
Two point
Modified two point would be if you only have 1 device and you’re still walking with the two steps
What kind of gait pattern is this - Assistive device-inolved side, uninvolved side
Three point
Device, step, step
* can have a three point w/ a bilatearl device like crutches, you just move them together
For this you could use a walker, bilatearl crutches, bilatearl cane, loftstrand crutches, key is that each UE has something and they move together
What kind of gait pattern is this - device then opposite LE then device and opposite LE
Four point
Explain a swing to gait pattern
Device thand then bilatearl LE together
Explain a swing through
Device and then bilatearl LE pass device
legs stay together
Prognosis for INdependent Gait
* Depends on severity of brain lesion
* Good prognosis if they can sit independently by _
* If they dont have independent ambulation by _ they most likely won’t walk
Good if they can sit by age 2 (for ambulation)
If they don’t have ambulation by 8 the most likely wont walk
* NOTE: if they arent walking by puberty it gets much harder because they increase their body mass
These 3 have a decent chance of being able to walk:
* Spastic hemiplegia - one side can take over
* Mild to moderate spastic diplegia - their tone kind of helps them - they don’t have coordinated gait, its not pretty
* Mild ataxia - if its mild they can often ambulate independently
How do you fit an anterior/posterior walker?
Wrist crease (styloid process)
How do you decide wether to use a posterior or anterior walker for a pt?
Posture
w/ the posterior walker they’re more upright. W/ anterior they’re leaning forward more
Posterior walker = more stable
Occupation - can get up in personal w/ shleves and counters and shit.
NOTE: Posterior walkers are heavier
* So strength is a factor - do they have enough arm strength and trunk strength to move it
*
How do you measure loft strand crutches?
* measure straight up and down or in tripod
Measure straight up and down (not in tripod)
Cuft 1-2 inches below elbow
Hand held portion ~wrist crease/styloid process
Very hard to get these 2 exactly right on most people
Mobility stability curve
Energy requirement
KNOW: increasing the pattern slows down the pt
* for instance if they’re going too fast you can take them from a 2 point pattern –> 4 point pattern
What has more stability the posterior walker or anterior walker
Case 1:
* 3 year old unable to walk independently
* Can stand w/o UE for 1 minute
* Can take a few steps with hand held assist
* Generalized hypotonicity
* Intact cognitive
Posterior walker - provides lots of stability (they have hypotonicity)
* obvisouly they could use an anterior walker as well - they’re cheaper and more readily avialable and lighter.
3 year old not really able to use crutches - not great cognitively
* can change per pt
* she likes liftstands because they’re easier to progress. Can for from 2 –> 1 to make it harder
Case 2:
* 5 year old with spastic quadriplegic CP (spasticity in all 4 extremeitities)
* Unable to sit or stand independently
* Decreased cognitive function
Wheel chair
They won’t ever be able to walk so progression doesnt matter
Case 3:
* 7 year old with spastic diplegic CP (spasticity of bilatearal LE)
* Has been using posterior walker “for years”
* pt reports unsafe and moves to quickly w/ no LE dissociation
* Intact cognitive
4 point loft stand crutches
* this is specifically targeted at slowing them down
We also don’t want to go to a wheelchair which would kind of be the only other option
Case 4:
* 7 year old with spasticity of bilatearl LE’s
* Has been using bilatearl loftstrand crutches and 2 point pattern “for years”
* Frequent falls and loss of balance
* Intact cognitive
4 point loft strand to promote stability
