Abnormal Gait
Department of Physical
Therapy
NEW YORK UNIVERSITY
Historical Perspective
Tendency to classify gait according to
disease or injury state
Hemiplegic gait
Parkinsonian gait
Spastic gait
Quadra- or paraplegic gait
Amputee gait, etc.
Rationale
A specific disease or injury state
manifested as a discrete and clinically
describable problem with the mechanics
of gait
Our Starting Point
We’ll take a deficit-oriented vs. disease-
oriented approach to abnormal gait
analysis
Example: “How might a spastic hamstring
on one side, secondary to hemiplegia
caused by a CVA, affect gait mechanics?”
Answer
A spastic hamstring may limit step or
stride excursion and/or pelvic transverse
rotation
Preferred Rate of
Ambulation
Free or comfortable walking speed
Self-selected pace
Rate at which the normal individual is
most energy efficient
Range: ~2.5 - 4.0 mph (cadence of ~75
- 120 steps per minute)
Will vary from individual-to-individual
Walking Rates - Historical
Perspective
Historically walking rates classified as:
Slow: ~75 - 90 steps per minute
Medium: ~90 - 105 steps per minute
Fast: ~105 - 120 steps per minute
Energy Cost vs. Rate
Summary & Interpretation
Oxygen expenditure is least while walking
at a rate somewhere between ~85 to 110
steps per minute irrespective of stride (or
step) length
Individuals tend to gravitate toward a self-
selected pace which is most energy
efficient for that individual
Enter - The Idea of a
‘Preferred Rate’
A preferred rate of ambulation is a
self-selected walking pace that an
individual assumes that is most energy
efficient
Clinical Implication
Since 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?
What is the relationship between energy
efficiency and a preferred rate of
ambulation?
The Center of Gravity
(COG)
COG located at S1 - S2
During preferred rate walking the COG
approximates a sinusoidal curve from the:
Sagittal perspective - no greater than a 2”
peak-to-valley excursion
Frontal perspective - no greater than a 2”
medial-to-lateral excursion
Path of the COG
Distortion of the Path of
the COG
A distorted path of the COG will require
mechanical and motor control
compensations that will:
Disrupt normal timing of events
Over-ride normal gait control
Change from ‘automatic’ to ‘manua’l control
strategies
Lead to over-correction of gait mechanics
The Result
Increased energy expenditure
A Simple Example
Walking with a stiff-knee (“stiff-knee
gait”) with a cylinder cast
During stance the HAT will vault over the
fixed foot (especially during mid-stance)
COG will be deflected higher than the
usual 2” upward vertical displacement
with increased energy cost
Who Walks with a Stiff
Knee?
Transient knee injury patient (e.g., surgical
repair of a ligament
Hemiplegic with loss of knee control
The AK amputee with a locked-knee
prosthesis
The BK amputee with poor knee control
Should we consider each case the SAME?
The Control of Gait
Motor control options:
‘Manual’ control theory - thinking about
having to take a step each time you want to
advance the foot forward
‘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
You’re walking along 23rd Street, heading
west toward your bus stop
You’re thinking about what was discussed
in Kinesiology class today
You’re also thinking that there is a lot a
traffic and it’s going to take you forever to
get home tonight...
Questions
Are you thinking about foot placement?
Are you thinking about how long each
step should be?
Are you thinking about trunk and pelvic
rotation in the transverse plane and
maintaining reciprocal arm-swing?
Are you thinking about...
Answer
Probably NOT!
Why?
Your gait control is on ‘automatic pilot’
When do you have to think about gait
control?
When there’s a perturbation
Central Pattern Generator
(CPG)
CPG - a group of synaptic connections
probably at the spinal cord level which are
triggered by an event or condition
When 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
Spinalized (cord transected) cats
suspended over a treadmill will walk with
an alternating, striding quadripedal gait
Human quadriplegics have also “walked”
this way
CPG and Supraspinal
Influence
Gait perturbations
Example: Someone walks across your path
from the side that you didn’t see
There’s a need to take immediate corrective
action to avoid a collision
Supraspinal centers appear to over-ride
the CPG and switch to a ‘manual control’
strategy
What Triggers a CPG?
There seems to be a close relationship
between activating a CPG for gait control
and preferred rate of ambulation
In 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…”
“...very slow!”
What are some possible
implications of this?
Mr. Jones will be safe - probably won’t fall
and break his hip (good news).
Mr. Jones won’t sue you (good news).
The path of the COG may be distorted
(bad news).
Energy cost may increase (bad news)
Suppose Mr. Jones has a cardiac condition?
What are some possible
implications of this?
Mr. Jones may never reach his pre-
injury/disease preferred rate of
ambulation and therefore never trigger a
CPG that automates gait (bad news).
Mr. 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
Assume right LE will advance first:
Weight shift to left LE (unloads right hip)
Left hip moves into (hyper-) extension and
precedes right hip flexion
Right side of pelvis rotates medially preceding
right hip flexion
COG moves over right foot after it’s advanced
Factors That Lead to the
Initiation of Gait
Successful 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?
Where is the patient’s COG relative to her
base-of-support?
What is probably the size of the left step
(step length) relative to the right?
What impact will this likely have on her
forward velocity?
What are the chances of attaining her pre-
injury/disease preferred rate?
Deficit-Oriented Gait
Analysis
Questions:
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
If you believe the latter…it shouldn’t
matter what the patient’s problem is
If 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
Early stance (@ HS) Early stance (@ HS)
Prevent hip flexion weakness/absence
(jack-knifing) Hip/trunk collapses
Early stance (HS - FF) into flexion
Guide hip into flexion Early stance (HS - FF)
eccentrically Trunk falls forward
Hip Abductors - Stance
Hip Abductors
Prevent contra-lateral hip from dipping
greater than 5 - 80
Stance-side abductors active
Loss of abductors:
Static analysis - + Trendelenburg sign
Dynamic analysis - weakness o f abductors
manifests as ‘lurching gait’ (toward stance- side)
Analysis of Deficits
Abductors - Stance
Early stance Early stance
COG shifts away from weakness/absence
stance side LE Contra-lateral hip
Increases moment arm drops > 5-80
of COG relative to Compensation is to
stance side hip lean (‘lurch’) over
Stance side abductors stance-side LE
generate counter-
rotational torque to
prevent contra-lateral
from dropping > 5-80
Quadriceps - Stance
Analysis of Deficits
Quadriceps - Stance
Early stance (HS - FF) Early stance
Guides knee into 200 weakness/absence
of flexion eccentrically Inability to absorb energy
(controls unlocking of Buckling
the knee)
Late stance (HR - TO) Late stance
Controls for knee weakness/absence
Knee collapse into flexion
flexion (~400 at TO)
-premature flexion into
early swing - ‘rubber knee’
Pre-Tibial Group - Stance
Analysis of Deficits
Pre-tibial Group - Stance
Early stance (HS - FF) Early stance
Lowers forefoot to weakness/absence
floor eccentrically Forefoot slaps to the
After forefoot contacts floor - ‘drop-foot’ gait
floor- pull tibia Loss of forward pull of
forward over foot tibia
Plantar Flexors - Stance
Analysis of Deficits
Plantar Flexors - Stance
Late mid-stance Early stance
Concentrically pulls weakness/absence
tibia forward Loss of forward pull of
Late stance (HR - TO) tibia
Provides propulsive Loss of forward thrust
thrust during push off - poor transition to
early swing
Ankle Stability - Late
Stance
Ankle less stable and subject to injury (e.g.,
sprains) in plantar flexion vs.dorsiflexion
Posterior trochlea in mortise
Collateral ligaments swing out of collateral
position
Position of ankle during push-off (late
stance) = plantar flexed
Analysis of Deficits
Peroneals - Stance
Late stance (HR - TO) Late stance
Dynamically provide weakness/absence
collateral stability to Ankle instability
ankle when plantar causing medial-lateral
flexed movement
Secondary plantar Potential for ankle
flexor for forward injury - sprains
thrust Poor transition from
late stance to early
swing
Analysis of Deficits
Plantar Intrinsics - Stance
Late stance (HR - TO) Late stance
Provide medial - weakness/absence
lateral stability to MTP Excessive medial -
joints (especially nos. lateral ‘shimmy’ of
1 & 2) - cancels hindfoot during HR
second degree of Inefficient forward
freedom thrust
Improves forward
propulsion and
transition to early
swing
Paraspinals -Stance
Analysis of Deficits
Paraspinals - Stance
Early stance (HS - FF) Early & late stance
& late stance (HR - weakness/absence
TO) Trunk falls forward
Prevent forward Loss of head and neck
flexion of trunk acting control
on pelvis
Analysis of Deficits
Hip Flexors - Swing
Late stance - early Late stance - early
swing (acceleration) swing
Forward flexion of femur weakness/absence of
working with plantar forward acceleration
flexors to accelerate LE after TO
in early swing
Toe may not clear the
Functionally shortens LE
(with eccentric action of floor during swing
quadriceps and through
dorsiflexors) to prevent Compensate with
‘toe-drag’ circumduction at hip
Dorsiflexors - Swing
Analysis of Deficits
Dorsiflexors - Swing
Mid-to-late swing Mid-to-late swing
(deceleration) weakness/absence
Affects ‘toe-up’ Loss of ‘toe-up’
concentrically Compensation
Functionally shortens Increased hip flexion -
LE during swing ‘steppage gait’
through Circumduction at hip
Hamstrings - Swing
Analysis of Deficits
Hamstrings - Swing
Late swing Late swing
(deceleration) weakness/absence
Decelerates tibial ‘Impact on terminal
shank extension’ - knee
Provides for smooth slapped into extension
transition between or hyperextension
late stance and early
swing
Gait in the Elderly Men -
Murray, Kory & Clarkson
Gait did not appear
vigorous or labored
Gait pattern did not
resemble that of
patients with CNS
damage
Gait was guarded and
restrained - attempt to
maximal stability and
security
Gait in the Elderly Men -
Murray, Kory & Clarkson
Gait resembled
someone walking on a
slippery surface
decreased step & stride
legnth
wider dynamic BOS
increased lateral head
movement
decreased rotation of
pelvis
Gait in the Elderly Men -
Murray, Kory & Clarkson
toe/floor clearance
distance slightly
decreased
lower stance-to-swing
ratio
decreased reciprocal
arm swing more from
elbow than shoulder
Spasticity and its Impact
on Gait
Spasticity - resistance to passive stretch
Results from CNS (UMN) injury/disease
Increased source of uncontrolled/poorly
controlled tension
Probably due to loss of inhibiting action of the
CNS
While tension production may be significant the
time-rate-of-tension development may be
delayed
Spasticity & Gait
Spastic response may be caused by:
Unexpected quick stretch of muscles
Foot contact with floor
Supraspinal overlay
Effects:
Restrict joint excursion
Delay transition from one gait phase to the
next
Spasticity & Gait
Dubo 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
Quadcriceps
May prevent knee from unlocking during
interim between HS and FF
Knee maintained in extension leading to a
‘vaulting’ over stance limb or circumduction of hip
Disrupts (timing) transition to mid- and late stance
May prevent LE bending during swing phase
Spasticity & Gait
Examples
Plantar flexors
Increase in spastic tone may limit forward
rotation of tibia between MS and PO
May locate ground reaction force well behind knee
causing significant flexion moment during late MS
and knee buckling tendency
Ankle may be locked up during PO decreasing
propulsive thrust forward - inefficient
transition from TO to early swing
Spasticity & Gait
Examples
Hamstrings
May limit forward swing of LE - decreasing
step length
May prevent knee from reaching a terminally
extended position just prior to HS
Gait Training - Questions
If 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
If 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
What impact will ‘assistive devices’ have
on gait performance?
Parallel bars
Walkers
Bilateral & unilateral crutches and canes
PTs using contact guarding from the side or
behind
Gait Training - Questions
If 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
Are all patients’ objectives concerning walking
the same?
Are 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
What’s the best thing a PT can say to
their patient while gait training?...
...Probably very
little!