Presentation on theme: "Abnormal Gait Department of Physical Therapy NEW YORK UNIVERSITY."— Presentation transcript:
Abnormal Gait Department of Physical Therapy NEW YORK UNIVERSITY
Historical Perspective zTendency to classify gait according to disease or injury state yHemiplegic gait yParkinsonian gait ySpastic gait yQuadra- or paraplegic gait yAmputee gait, etc.
Rationale zA specific disease or injury state manifested as a discrete and clinically describable problem with the mechanics of gait
Our Starting Point zWe’ll take a deficit-oriented vs. disease- oriented approach to abnormal gait analysis zExample: “How might a spastic hamstring on one side, secondary to hemiplegia caused by a CVA, affect gait mechanics?”
Answer zA spastic hamstring may limit step or stride excursion and/or pelvic transverse rotation
Preferred Rate of Ambulation zFree or comfortable walking speed zSelf-selected pace zRate at which the normal individual is most energy efficient zRange: ~ mph (cadence of ~ steps per minute) zWill vary from individual-to-individual
Walking Rates - Historical Perspective zHistorically walking rates classified as: ySlow: ~ steps per minute yMedium: ~ steps per minute yFast: ~ steps per minute
Energy Cost vs. Rate
Summary & Interpretation zOxygen expenditure is least while walking at a rate somewhere between ~85 to 110 steps per minute irrespective of stride (or step) length zIndividuals tend to gravitate toward a self-selected pace which is most energy efficient for that individual
Enter - The Idea of a ‘Preferred Rate’ zA preferred rate of ambulation is a self-selected walking pace that an individual assumes that is most energy efficient
Clinical Implication zSince there is apparently a rate- dependent issue that drives gait efficiency the PT should understand that going slower than and faster than the preferred rate will lead to inefficiency and potential stress on the cardiovascular and motor control systems
Why is Gait More Efficient at Preferred Rate? zWhat is the relationship between energy efficiency and a preferred rate of ambulation?
The Center of Gravity (COG) zCOG located at S 1 - S 2 zDuring preferred rate walking the COG approximates a sinusoidal curve from the: ySagittal perspective - no greater than a 2” peak-to-valley excursion yFrontal perspective - no greater than a 2” medial-to-lateral excursion
Path of the COG
Distortion of the Path of the COG zA distorted path of the COG will require mechanical and motor control compensations that will: yDisrupt normal timing of events yOver-ride normal gait control xChange from ‘automatic’ to ‘manua’l control strategies yLead to over-correction of gait mechanics
The Result Increased energy expenditure
A Simple Example zWalking with a stiff-knee (“stiff-knee gait”) with a cylinder cast zDuring stance the HAT will vault over the fixed foot (especially during mid-stance) zCOG will be deflected higher than the usual 2” upward vertical displacement with increased energy cost
Who Walks with a Stiff Knee? zTransient knee injury patient (e.g., surgical repair of a ligament zHemiplegic with loss of knee control zThe AK amputee with a locked-knee prosthesis zThe BK amputee with poor knee control zShould we consider each case the SAME?
The Control of Gait zMotor control options: y‘Manual’ control theory - thinking about having to take a step each time you want to advance the foot forward y‘Automatic control theory - an automatic control system that accounts for gait mechanics without having to think about foot placement and other metrical details
Which one is it? Think about this...
An Everyday Occurrence zYou’re walking along 23rd Street, heading west toward your bus stop zYou’re thinking about what was discussed in Kinesiology class today zYou’re also thinking that there is a lot a traffic and it’s going to take you forever to get home tonight...
Questions zAre you thinking about foot placement? zAre you thinking about how long each step should be? zAre you thinking about trunk and pelvic rotation in the transverse plane and maintaining reciprocal arm-swing? zAre you thinking about...
Answer zProbably NOT! zWhy? zYour gait control is on ‘automatic pilot’ zWhen do you have to think about gait control? zWhen there’s a perturbation
Central Pattern Generator (CPG) zCPG - a group of synaptic connections probably at the spinal cord level which are triggered by an event or condition zWhen a threshold is met via a triggering mechanism the CPG appears to be activated and takes over automatic control of gait metrics - i.e., you don’t have to think about it
Evidence zSpinalized (cord transected) cats suspended over a treadmill will walk with an alternating, striding quadripedal gait zHuman quadriplegics have also “walked” this way
CPG and Supraspinal Influence zGait perturbations yExample: Someone walks across your path from the side that you didn’t see yThere’s a need to take immediate corrective action to avoid a collision zSupraspinal centers appear to over-ride the CPG and switch to a ‘manual control’ strategy
What Triggers a CPG? zThere seems to be a close relationship between activating a CPG for gait control and preferred rate of ambulation zIn other words, there is a rate- dependent relationship between normal gait mechanics and its control mechanism
So... It appears we maintain the path of the COG within very tight limits and therefore expend the least amount of energy by assuming a preferred rate which in turn leads to an activation of a CPG
Think About This... What’s one of the most common things heard during gait training in a PT clinic?
“Mr. Jones, while you’re walking, I want to go…”
What are some possible implications of this? zMr. Jones will be safe - probably won’t fall and break his hip (good news). zMr. Jones won’t sue you (good news). zThe path of the COG may be distorted (bad news). zEnergy cost may increase (bad news) ySuppose Mr. Jones has a cardiac condition?
What are some possible implications of this? zMr. Jones may never reach his pre- injury/disease preferred rate of ambulation and therefore never trigger a CPG that automates gait (bad news). zMr. Jones’ gait may never look ‘normal’ (bad news).
Is it possible that... …going very slow might actually cause Mr. Jones to lose his balance and fall? Why?
Factors That Lead to the Initiation of Gait zAssume right LE will advance first: zWeight shift to left LE (unloads right hip) zLeft hip moves into (hyper-) extension and precedes right hip flexion zRight side of pelvis rotates medially preceding right hip flexion zCOG moves over right foot after it’s advanced
Factors That Lead to the Initiation of Gait zSuccessful completion of these events probably leads to a triggering of a CPG as preferred rate is attained
Gait Training Scenario Mrs. Flanagan is standing in the parallel bars with her physical therapist, Dudley Doright, getting ready to take a left step to start walking. We hear the PT say, “Now, Mrs. Flanagan, I want you to put your left foot forward and take a step…”
What wrong with this picture? zWhere is the patient’s COG relative to her base-of-support? zWhat is probably the size of the left step (step length) relative to the right? zWhat impact will this likely have on her forward velocity? zWhat are the chances of attaining her pre-injury/disease preferred rate?
Deficit-Oriented Gait Analysis zQuestions: Do diseases/injuries specifically manifest as a stereotypical gait pattern? or Does the disease/injury lead to a deterioration of control parameters which cause gait deficits?
Response zIf you believe the latter…it shouldn’t matter what the patient’s problem is zIf you understand the consequence of the disease or injury (loss of motor control, weakness, damaged supportive structures, loss of a part of or an entire limb, etc.)...
…you should be able to anticipate or predict what impact a deficit has on gait irrespective of their state of injury or disease.
Hip Extensors - Stance
Analysis of Deficits Hip Extensors - Stance zEarly stance HS) yPrevent hip flexion (jack-knifing) zEarly stance (HS - FF) yGuide hip into flexion eccentrically z Early stance HS) weakness/absence yHip/trunk collapses into flexion z Early stance (HS - FF) yTrunk falls forward
Hip Abductors - Stance
Hip Abductors zPrevent contra-lateral hip from dipping greater than zStance-side abductors active zLoss of abductors: yStatic analysis - + Trendelenburg sign yDynamic analysis - weakness o f abductors manifests as ‘lurching gait’ (toward stance- side)
Analysis of Deficits Abductors - Stance zEarly stance yCOG shifts away from stance side LE yIncreases moment arm of COG relative to stance side hip yStance side abductors generate counter- rotational torque to prevent contra-lateral from dropping > z Early stance weakness/absence yContra-lateral hip drops > yCompensation is to lean (‘lurch’) over stance-side LE
Quadriceps - Stance
Analysis of Deficits Quadriceps - Stance zEarly stance (HS - FF) yGuides knee into 20 0 of flexion eccentrically (controls unlocking of the knee) zLate stance (HR - TO) yControls for knee flexion (~40 0 at TO) z Early stance weakness/absence yInability to absorb energy yBuckling z Late stance weakness/absence yKnee collapse into flexion -premature flexion into early swing - ‘rubber knee’
Pre-Tibial Group - Stance
Analysis of Deficits Pre-tibial Group - Stance zEarly stance (HS - FF) yLowers forefoot to floor eccentrically yAfter forefoot contacts floor- pull tibia forward over foot z Early stance weakness/absence yForefoot slaps to the floor - ‘drop-foot’ gait yLoss of forward pull of tibia
Plantar Flexors - Stance
Analysis of Deficits Plantar Flexors - Stance zLate mid-stance yConcentrically pulls tibia forward zLate stance (HR - TO) yProvides propulsive thrust during push off z Early stance weakness/absence yLoss of forward pull of tibia yLoss of forward thrust - poor transition to early swing
Ankle Stability - Late Stance zAnkle less stable and subject to injury (e.g., sprains) in plantar flexion vs.dorsiflexion yPosterior trochlea in mortise yCollateral ligaments swing out of collateral position zPosition of ankle during push-off (late stance) = plantar flexed
Analysis of Deficits Peroneals - Stance zLate stance (HR - TO) yDynamically provide collateral stability to ankle when plantar flexed ySecondary plantar flexor for forward thrust z Late stance weakness/absence yAnkle instability causing medial-lateral movement yPotential for ankle injury - sprains yPoor transition from late stance to early swing
Analysis of Deficits Plantar Intrinsics - Stance zLate stance (HR - TO) yProvide medial - lateral stability to MTP joints (especially nos. 1 & 2) - cancels second degree of freedom yImproves forward propulsion and transition to early swing z Late stance weakness/absence yExcessive medial - lateral ‘shimmy’ of hindfoot during HR yInefficient forward thrust
Analysis of Deficits Paraspinals - Stance zEarly stance (HS - FF) & late stance (HR - TO) yPrevent forward flexion of trunk acting on pelvis z Early & late stance weakness/absence yTrunk falls forward yLoss of head and neck control
Analysis of Deficits Hip Flexors - Swing zLate stance - early swing (acceleration) yForward flexion of femur working with plantar flexors to accelerate LE in early swing yFunctionally shortens LE (with eccentric action of quadriceps and dorsiflexors) to prevent ‘toe-drag’ z Late stance - early swing weakness/absence of forward acceleration after TO z Toe may not clear the floor during swing through yCompensate with circumduction at hip
Dorsiflexors - Swing
Analysis of Deficits Dorsiflexors - Swing zMid-to-late swing (deceleration) yAffects ‘toe-up’ concentrically yFunctionally shortens LE during swing through z Mid-to-late swing weakness/absence yLoss of ‘toe-up’ yCompensation xIncreased hip flexion - ‘steppage gait’ xCircumduction at hip
Hamstrings - Swing
Analysis of Deficits Hamstrings - Swing zLate swing (deceleration) yDecelerates tibial shank yProvides for smooth transition between late stance and early swing z Late swing weakness/absence y‘Impact on terminal extension’ - knee slapped into extension or hyperextension
Gait in the Elderly Men - Murray, Kory & Clarkson z Gait did not appear vigorous or labored z Gait pattern did not resemble that of patients with CNS damage z Gait was guarded and restrained - attempt to maximal stability and security
Gait in the Elderly Men - Murray, Kory & Clarkson z Gait resembled someone walking on a slippery surface ydecreased step & stride legnth ywider dynamic BOS yincreased lateral head movement ydecreased rotation of pelvis
Gait in the Elderly Men - Murray, Kory & Clarkson ytoe/floor clearance distance slightly decreased ylower stance-to-swing ratio ydecreased reciprocal arm swing more from elbow than shoulder
Spasticity and its Impact on Gait zSpasticity - resistance to passive stretch yResults from CNS (UMN) injury/disease yIncreased source of uncontrolled/poorly controlled tension yProbably due to loss of inhibiting action of the CNS yWhile tension production may be significant the time-rate-of-tension development may be delayed
Spasticity & Gait zSpastic response may be caused by: yUnexpected quick stretch of muscles yFoot contact with floor ySupraspinal overlay zEffects: yRestrict joint excursion yDelay transition from one gait phase to the next
Spasticity & Gait zDubo et al. showed that EMG activity of spastic muscles increased during mid- stance i.e., there was a loss of phasic control of muscles
Spasticity & Gait Examples zQuadcriceps yMay prevent knee from unlocking during interim between HS and FF xKnee maintained in extension leading to a ‘vaulting’ over stance limb or circumduction of hip xDisrupts (timing) transition to mid- and late stance xMay prevent LE bending during swing phase
Spasticity & Gait Examples zPlantar flexors yIncrease in spastic tone may limit forward rotation of tibia between MS and PO xMay locate ground reaction force well behind knee causing significant flexion moment during late MS and knee buckling tendency yAnkle may be locked up during PO decreasing propulsive thrust forward - inefficient transition from TO to early swing
Spasticity & Gait Examples zHamstrings yMay limit forward swing of LE - decreasing step length yMay prevent knee from reaching a terminally extended position just prior to HS
Gait Training - Questions zIf gait is controlled by a rate-dependent chain of synaptic connections at the spinal cord level (i.e., a CPG), is it possible for a PT to effect (physiological) changes in the gait control system?
Gait Training - Questions zIf gait is initiated (and sustained) as described previously (e.g., unloading of hip, pelvis rotates medially, COG loads over stance foot, etc.), how do we train patients to start walking?
Gait Training - Questions zWhat impact will ‘assistive devices’ have on gait performance? yParallel bars yWalkers yBilateral & unilateral crutches and canes yPTs using contact guarding from the side or behind
Gait Training - Questions zIf the rhythmic, symmetrical alternating characteristics of gait are triggered when a patient assumes their preferred rate, will gait symmetry and a ‘normal’ appearing gait be possible if the patient walks substantially slower than her preferred rate?
Gait Training - Questions zAre all patients’ objectives concerning walking the same? zAre your objectives for Ms. Walksalot, a 39 year old healthy female who broke her ankle two weeks ago in an intensive tennis match, the same as for Mr. Livesinathirdstorywalkup, a frail 87 year old male, with emphysema and a fractured, pinned hip?
Gait Training - Questions zWhat’s the best thing a PT can say to their patient while gait training?...