Senior registrar presentation by Dr Umar Mohammed in NOHIL.

1. Discuss Gait
and its
Abnormalities
Dr Umar Mohammed
Moderated By Dr Izuagba
17th Feb., 2022

2. Outline
• Introduction
– Definition
– Orthopaedic Importance
– Historical Background
– Gait Cycle
• Stand Phase
• Swing Phase
• Development of Mature Gait
– Evaluation of Gait
– Abnormalities of Gait
– Conclusion
– References

3. Introduction
• Human gait is a bipedal locomotion
• Pattern can vary in a normal or physiological manner
depending on age or speed as well as pathological
conditions
• In order to appreciate the Abnormal gait associated
with pathology, it is essential to have a basic
understanding of normal human gait
• Prevalence increase with ageing population and
increasing morbidity index
• Loss of personal freedom and Reduced quality of life
• Tendency to fall

4. Definition
• A Persons manner of walking
• Gait is a series of bipedal rhythmic and
alternating movements of trunk and limbs which
result in forward progression of centre of gravity
and the body with minimal energy expenditure
• A sequence of foot movements by which a
person moves forward
• Gait Disorder
– An altered gait pattern, in Rhythm and Cycle

5. Orthopaedic Importance
• Diagnosis and Treatment plans arrived from
knowledge and correct gait analysis helps to
improve treatment outcome in orthopaedics.

6. Historical Background
• Aristotle (384 – 322 BCE) can be attributed to the earliest recorded
comment regarding the manner in which humans walk
• It was not until renaissance that another progress was made
through experiment and theorizing of Giovanni Borelli (1608 –
1679)
• Ernst Heinrich (1795 – 1878), Wilhelm Edward (1804 -1892),
Edward Fedrich Weber (1806 – 1871)1871 working in Liegzig made
the next major contribution based on very simple measurements
• AdvancesinmeasurementbiotechnologiesbyJulesEtienneMarey&Mu
ybridge
• Force plates and Kinematics Otto Fischer & Wilhelm Braune
• Clinical application by David Sutherland & Jacquelyn Perry(1923-
2006)
• Advent of modern computers

7. Gait Requirements
Functional Elements
• Normal functioning of musculoskeletal system
of lower limbs and spine
• Good sensory feedback from proprioceptive
sensation from feet and the joints
• Visual, labyrinthine sensory inputs &
coordination
• ADDS SMOOTHNESS, rhythm & elegance to
the human gait

8. Gait Cycle
• The gait cycle is a
repetitive pattern
involving steps and
strides
• Step; Starts with the
initial contact of one foot
and ends with the initial
contact of the other foot
• Stride; Starts with the
initial contact of one foot
and ends with the next
initial contact of that
same foot
• Classification of gait cycle
involves two main phases:
1. Stance phase: 60%
2. Swing phase: 40%
• Gait involves a
combination of open and
close chain activities
• Cadence; is the number
of steps per minutes
(100 to 115/min)

9. • Old terminologies
1. Heel strike
2. Foot Flat
3. Mid-stance
4. Heel-off
5. Toe-off
6. Acceleration
7. Mid-swing
8. Deceleration
• New terminologies
1. Initial contact
2. Loading response
3. Mid-stance
4. Terminal-stance
5. Pre-Swing
6. Initial-swing
7. Mid-swing
8. Terminal-swing

11. Development of mature gait
• The child start walking by 12-14
months age
• The toddler has
– Broad base gait which looks to be
high stepped & flat footed with
arms outstretched for balance
– Legs are externally rotated
– Mild bowing
• Heel strike develops at around
15-18months with reciprocal arm
swing
• Running and change of direction
occur after the age of 2 years
• Adult pattern by age of 4 to 8
years
• Stride length & speed are lower

12. Gait in Elderly- Senile Gait
• Age related changes in gait takes
place in decade 6 to 7
• Decreased stride length,
increased cycle time (decreased
cadence)
• Relative increase in duration of
stance phase of gait cycle
• Speed almost always reduced
• Reduction in total range of hip
flexion and extension
• Reduction in swing phase and
knee flexion
• Difficulty in balance
• Forward of upper portion of trunk
with flexion arms and knees

13. Running
• Propulsive forward
movement without the
period of double support
• Speed = Stride length x
Stride frequency
• Inadequate
extension=inadequate
power generation
• Swing phase takes 62% of
the gait cycle

14. Evaluation of gait
• Clinical analysis Gait Analysis
– Careful history taking & Examination focused on:
• Gait pattern
• Physical examination
– Neurological assesment
– Orthopaedic Evaluation
• Observational
– Can use videos,photos, mobile apps, or the clinicians eye
• Video Assisted Observational Gait Analysis (VAOGA)
• Computerized Gait Analyses
– VGA Laboratory: Videographic Gait Laboratory
Analysis
• Multichannel Functional Electrical Stimulation
(MFES)
• Detect underlying cause

15. Abnormality of Gait
• Abnormalities of Gait are often complex
• Include deviations at multiple joints and in
multiple planes of motion
• May involves multiple joints

16. Abnormalities of Gait
• In general gait deviations fall under the
following headings
1. Deformities
2. Pain: Inflammatory or infective
3. Joint muscle range of motion limitation
4. Muscular paralysis / Loss of motor control
5. Neurological involvement (UMN, LMN)
6. Limb lenght discrepancies

17. Causes of Gait Disorder
Physiological Pathological
• Paediatric gait < 4years
• Elderly gait > 60 years
• Musculoskeletal causes
– Antalgic gait
– Inflammatory joint disease
– Bone and joint infection
– Tendinopathy
– Trauma
– Congenital/ developmental
– LLD
– Contracture
• Neuro Vascular Disorders
– Sensory Ataxia
– Cerebral Ataxia
– LMN: polio, neuropathies
– UMN: cerebral palsy, CVA
– Dystonia
– Myopathies
– Dysvascular

18. Pathological Causes of Gait disorder
Cont’d
Limping & Lurching
• Limping
– Antalgic gait
• Lurching
– Waddling gait
– Trendelenburg gait
– Spastic gait
• Lurching Paralytic
– High stepping gait
– Quadriceps gait
– Gluteal medius gait
– Gluteal maximus gait
• Lurching Structural
Abnormalities
– Short limb gait
– In toeing gait
– Out toeing gait
– Knock knee gait
– Genu recurvatum gait
– Stiff hip gait
– Festinate gait

19. Pathological Causes of Gait disorder
• Limping
– Weight bearing avoided
on affected side as far as
possible
– Diminished stance phase
– It denotes a painful
condition on the
affected side

20. Pathological Causes of Gait disorder
Cont'd
• Lurching
– Prolongs stance phase to
improve the stability
– It denotes variable failure
of abduction mechanism
• Causes:
– Muscular weakness
– Structural deformity of
joints and bones
– Neurological disorders
– Miscellaneous

21. Antalgic Gait
• Stance phase on affected side
is shortened due to pain in the
weight bearing limb
• There is a corresponding
increase in stance phase on
unaffected side
• Young children may only
refuse to walk or bear weight
• Common causes are OA, LCPD,
SCFE, Fractures, Tendinitis
• An index of suspicion is
required in children

22. Trendelenburg Gait & Waddling Gait
• Weakness of hip abductors
• During weight-bearing on the ipsilateral side, the
pelvis drop on the contralateral side, rather than
rising as is normal
• With bilateral hip weakness, this result in a
waddling ‘’rolling sailor’’ gait with hips, knees,
and feet externally rotated
• LCPD, SCFE, DDH, JIA, inherited myopathies,
neurologic conditions (spina bifida, CP, & spinal
cord injury)

23. Trendelenberg & Waddling Gaits

24. Backward Lurch - Gluteus maximus
Gait
• Weakness in gluteus
maximum muscle
• While the body propels
forward during
midstance, the trunk is
Lurched posterior to
effect posterior pelvic and
shifting the centre of
gravity towards stance hip
• Causes: Poliomyelitis, AKA
with prosthesis

25. Spastic Gait Patterns – Cerebral palsy
• Circumduction Gait
• Scissoring Gait
• Ataxic
• Ethetoid
• Drunkers Gait
• Chorioform
• Hemiplegic Gait
• Diplegic Gait

26. Spastic Gait Pattern Cont'd
• Different gait patterns
observed in CP depends
on the involvement of
spasticity or contracture
of different muscles
• Variation depends on the
topographical type of CP
• Best seen in contrast
between unilateral spastic
CP and bilateral spastic CP

27. Hemiplegic Gait – Circumduction Gait
• The shoulder is adducted
and the elbow & wrist are
flexed
• To avoid the foot from
scrapping the ground, the
hip and the lower limb
rotates outward
• The patient swings the
paraplegic limb outwards
& ahead in a
Circumduction to avoid
foot scrapping the ground
• It is seen in CVD

28. Spastic Hemiplegic Gait
• In spastic Hemiplegia, there is more
involvement distally and therefore true
equinus is the basis of common patterns
• Winter et al. Described four gait patterns in
hemiplegics based on saggital kinematics
– Type1 – Drop foot type
– Type2 – True equinus +/- recurvatum knee
– Type3 – Stiff knee gait
– Type4 – Jump / Scissors

29. Spastic - Diplagia
• Involvement on both sides
• Spasticity in lower extremities worse than upper
extremities
• Walks with abnormally narrow base, dragging
both legs and scrapping the toes
• Cause: CP – Bilateral periventricular lesions
• Characteristic extreme tightness of hip adductors
which can cause legs to cross the midline referred
to as Scissors gait
• The hip adductor release is to minimize scissoring

30. Spastic Diplegia Cont'd
• There are four common patterns of gait in
spastic diplegia as described by Rodda et al.
– Type1 – True equinus
– Type2 – Jump gait
– Type3 – Apparent equinus
– Type4 – Crouch gait

32. Scissoring – Scissors Gait
• One leg cross directly over the
other with each step due to
adductor tightness
• The gait is characteristic of a
child with marked bilateral
adductor spasm at hip &
equinus in the ankle
• Leg goes into marked
adduction in swing phase so
that the foot with equinus
goes across to the opposite
side
• Such repeated crossing of leg
while walking gives scissoring
appearance called scissor gait

33. Cerebellar Ataxic Gait – Drunkers
(Reeling Gait)
• Clumsy, staggering movements with a
wide-based gait
• While standing the patients body
may swagger back & forth and from
side to side, known as titubation
• Patient tend to walk irregularly on
wide base, not able to walk from heel
to toe or in straight line, swinging
sideways without stability and
balance
• The gait of acute alcohol intoxication
• With unilateral lesion of cerebellum,
balance is lost towards the side of the
lesion
• Causes: Cerebellar lesion & lesion
connecting pathway to/& from the
cerebellum – midline cerebellar
disease at vermis

34. Chorioform – Hyperkinetic Gait
• The patient has chorea
(irregular, jerky, involuntary
movements) more in upper
limbs and has unstable gait
• Walking may accentuate their
baseline movement disorder
• Seen in patients with
extrapyramidal symptoms
• Cause: Basal ganglia disorders
including Sydenham’s chorea,
Huntington's Disease and
other forms of chorea,
Athetosis or Dystonia

35. Steppage / High Stepping gait
• On attempt of heel strike, the
toe drops to the ground first
• To avoid this, the patient flexes
the hip and knee extensively
to raise the foot, and slaps it
on the floor forcibly
• Cause:
– Foot drop
– Paralysis of Tibialis anterior &
other extensors of ankle and
toes
– LMN lesion
– Multiple neuritis
– Anterior motor horn cells
– Cauda equina

36. Stamping / Stomping Gait
Sensory Ataxia Gait
• Occurs in sensory ataxia in
which there is loss of
sensation in lower extremity
• Due to absence of deep
position sense, the patient
constantly observes placing of
his feet
• Hip is hyperflexed & externally
rotated and forefoot is
dorsiflexed to strike ground
with a stamp
• Causes: Peripheral neuritis,
Brain stem lesion in children,
Tabes dorsalis in adult

37. Quadriceps Gait
• Normally the knee is
locked by quadriceps
contraction while
transmitting weight to the
lower limb during
midstance
• Hence patient with weak
quadriceps stabilizes his
knee by leaning forward
on the affected side and
pressing over lower thigh
by his ipsilateral hand or
fingers

38. Weakness – Hip Flexors
• The patient will have
difficulty in initiating swing
through
• To compensate for ths
specific muscular weakness,
patient externally rotates
leg & uses hip adductors for
swing through
• This Circumduction of hip
exaggerates energy
expenditure & produces
extreme trunk & pelvis
motion

39. Festinant Gait
• The steps are short so
that feet barely clear
floor
• Steps are successively
more rapid as if trying
to catch up with centre
of gravity
• Cause: Parkinson’s
disease

40. Short Limb Gait
• Shortening < 1.5cm
compensate by pelvic tilt
– Low shoulder
– Low iliac crest
– Low ASIS
• Shortening upto 5cm
compensate by equinus
– Put foot & ankle into equinus
– Hip & knee of normal limb in
flexion
• Shortening > 5cm, the
patient dips his body on
that side

41. Other types of Gait
• Calcaneal Gait
• Knock knee Gait
• Genu Recurvatum Gait
• Stiff Hip Gait
• Hip knee Contracture
Gait
• Gait with Walking aid
– Swing-to gait
– Swing-through gait
– Two point gait
– Three point gait
– Four point gait

42. Alderman’s Gait
• Patient walks with head and chest thrown
backward with protuberant abdomen and legs
thrown wide apart
• Cause: TB spine (thoracolumbar junction)

43. Psychogenic Gait Disorders
• Atypical gait that cannot be explained by neurological or
other disease
• Non genuine findings on examination
• Psychiatric disease, conversion reaction or malingering
• Gait Pattern:
– Lurching erratically, holding onto walls, and staggering from
side to side (‘’astasia-abasia’’), and inconsistent
– “Walking on ice“ (small, cautious steps with fixed Flexed LL
joints)
– Quasimodo gait (dragging one leg), without falling
• Hysterical Gait: Bizarre +/- falls

44. Fear of Falling
• Elderly individuals who have fallen in the past
• Cautious and slow gait, holding on to furniture
and walls
• Fear of falling can be a significant contributor
to gait instability
• They need physical therapy and rehabilitation.

45. Conclusion
• Knowledge of the normal pattern and
mechanics of gait is important in identifying
the pathological gait
• Every pathology must be understood for
proper diagnosis and treatment
• Need for record keeping that involves data,
pictures and videos

46. Thank you

47. References
• Orthopaedic Management of Cerebral palsy. Eugene E
Bleck. 1979. WB Saunders
• Orthopaedic Management of Cerebral palsy. Helen W
Horstmann & Eugene Bleck. 2007
• Cerebral Palsy. Freeman Miller. 2005. Springer
• Multiple literatures from Google.com
• Videos prepared and sheared in Youtube channels
– Dr Sadam Mazar Baloch
– Dr Shahzaib Baloch
– Dr Nida Hameed @ Dr Ziuaddin University, Karachi