1. Department of Physical Therapy NEW YORK UNIVERSITY
Abnormal Gait
Department of Physical Therapy
NEW YORK UNIVERSITY

2. 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.

3. Rationale
A specific disease or injury state manifested as a discrete and clinically describable problem with the mechanics of gait

4. 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?”

5. Answer
A spastic hamstring may limit step or stride excursion and/or pelvic transverse rotation

6. Preferred Rate of Ambulation
Free or comfortable walking speed
Self-selected pace
Rate at which the normal individual is most energy efficient
Range: ~ mph (cadence of ~ steps per minute)
Will vary from individual-to-individual

7. Walking Rates - Historical Perspective
Historically walking rates classified as:
Slow: ~ steps per minute
Medium: ~ steps per minute
Fast: ~ steps per minute

8. Energy Cost vs. Rate

9. 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

10. 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

11. 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

12. Why is Gait More Efficient at Preferred Rate?
What is the relationship between energy efficiency and a preferred rate of ambulation?

13. 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

14. Path of the COG

15. 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

16. The Result
Increased energy expenditure

17. 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

18. 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?

19. 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

20. Which one is it?
Think about this...

21. 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...

22. 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...

23. 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

24. 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

25. Evidence
Spinalized (cord transected) cats suspended over a treadmill will walk with an alternating, striding quadripedal gait
Human quadriplegics have also “walked” this way

26. 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

27. 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

28. 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

29. Think About This...
What’s one of the most common things heard during gait training in a PT clinic?

30. “Mr. Jones, while you’re walking, I want to go…”

31. “...very slow!”

32. 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?

33. 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).

34. Is it possible that...
…going very slow might actually cause Mr. Jones to lose his balance and fall?
Why?

35. 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

36. 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

37. 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…”

38. 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?

39. 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?

40. 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.)...

41. …you should be able to anticipate or predict what impact a deficit has on gait irrespective of their state of injury or disease.

42. Hip Extensors - Stance

43. Analysis of Deficits Hip Extensors - Stance
Early stance HS)
Prevent hip flexion (jack-knifing)
Early stance (HS - FF)
Guide hip into flexion eccentrically
Early stance HS) weakness/absence
Hip/trunk collapses into flexion
Early stance (HS - FF)
Trunk falls forward

44. Hip Abductors - Stance

45. Hip Abductors
Prevent contra-lateral hip from dipping greater than
Stance-side abductors active
Loss of abductors:
Static analysis - + Trendelenburg sign
Dynamic analysis - weakness o f abductors manifests as ‘lurching gait’ (toward stance- side)

46. Analysis of Deficits Abductors - Stance
Early stance
COG shifts away from stance side LE
Increases moment arm of COG relative to stance side hip
Stance side abductors generate counter-rotational torque to prevent contra-lateral from dropping > 5-80
Early stance weakness/absence
Contra-lateral hip drops > 5-80
Compensation is to lean (‘lurch’) over stance-side LE

47. Quadriceps - Stance

48. Analysis of Deficits Quadriceps - Stance
Early stance (HS - FF)
Guides knee into 200 of flexion eccentrically (controls unlocking of the knee)
Late stance (HR - TO)
Controls for knee flexion (~400 at TO)
Early stance weakness/absence
Inability to absorb energy
Buckling
Late stance weakness/absence
Knee collapse into flexion -premature flexion into early swing - ‘rubber knee’

49. Pre-Tibial Group - Stance

50. Analysis of Deficits Pre-tibial Group - Stance
Early stance (HS - FF)
Lowers forefoot to floor eccentrically
After forefoot contacts floor- pull tibia forward over foot
Early stance weakness/absence
Forefoot slaps to the floor - ‘drop-foot’ gait
Loss of forward pull of tibia

51. Plantar Flexors - Stance

52. Analysis of Deficits Plantar Flexors - Stance
Late mid-stance
Concentrically pulls tibia forward
Late stance (HR - TO)
Provides propulsive thrust during push off
Early stance weakness/absence
Loss of forward pull of tibia
Loss of forward thrust - poor transition to early swing

53. 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

54. Analysis of Deficits Peroneals - Stance
Late stance (HR - TO)
Dynamically provide collateral stability to ankle when plantar flexed
Secondary plantar flexor for forward thrust
Late stance weakness/absence
Ankle instability causing medial-lateral movement
Potential for ankle injury - sprains
Poor transition from late stance to early swing

55. Analysis of Deficits Plantar Intrinsics - Stance
Late stance (HR - TO)
Provide medial - lateral stability to MTP joints (especially nos. 1 & 2) - cancels second degree of freedom
Improves forward propulsion and transition to early swing
Late stance weakness/absence
Excessive medial - lateral ‘shimmy’ of hindfoot during HR
Inefficient forward thrust

56. Paraspinals -Stance

57. Analysis of Deficits Paraspinals - Stance
Early stance (HS - FF) & late stance (HR - TO)
Prevent forward flexion of trunk acting on pelvis
Early & late stance weakness/absence
Trunk falls forward
Loss of head and neck control

58. Analysis of Deficits Hip Flexors - Swing
Late stance - early swing (acceleration)
Forward flexion of femur working with plantar flexors to accelerate LE in early swing
Functionally shortens LE (with eccentric action of quadriceps and dorsiflexors) to prevent ‘toe-drag’
Late stance - early swing weakness/absence of forward acceleration after TO
Toe may not clear the floor during swing through
Compensate with circumduction at hip

59. Dorsiflexors - Swing

60. Analysis of Deficits Dorsiflexors - Swing
Mid-to-late swing (deceleration)
Affects ‘toe-up’ concentrically
Functionally shortens LE during swing through
Mid-to-late swing weakness/absence
Loss of ‘toe-up’
Compensation
Increased hip flexion - ‘steppage gait’
Circumduction at hip

61. Hamstrings - Swing

62. Analysis of Deficits Hamstrings - Swing
Late swing (deceleration)
Decelerates tibial shank
Provides for smooth transition between late stance and early swing
Late swing weakness/absence
‘Impact on terminal extension’ - knee slapped into extension or hyperextension

63. 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

64. 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

65. 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

66. 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

67. Spasticity & Gait Spastic response may be caused by: Effects:
Unexpected quick stretch of muscles
Foot contact with floor
Supraspinal overlay
Effects:
Restrict joint excursion
Delay transition from one gait phase to the next

68. 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

69. 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

70. 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

71. 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

72. 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?

73. 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?

74. 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

75. 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?

76. 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?

77. Gait Training - Questions
What’s the best thing a PT can say to their patient while gait training?...

78. ...Probably very little!