2. Prevalence, Morbidity and
Mortality
Gait disorders has been described in 15% individuals
older than age 65 yrs
By the age 80 yrs 1 in 4 person will require mechanical
aid to assist ambulation.
30 % of those with age >65yr fall every year
8% of those with age >75 yrs suffer serious fall related
injury
One in five elderly limit activity voluntarily because of
fear of falling.
3. Physiology of gait
Station is the way patient stands and gait is the way
patient walks.
In human, bipedal gait and erect position over narrow
base require more efficient maintenance and control
of equilibrium and have more complex mechanism
than quadruped animals.
Standing may be considered a postural reflex
mechanism mediated through brainstem.
4. Various CNS centres and their role
“Central pattern generators’’ in spinal cord and
brainstem found in lower animals.
These are group of interneurons that co-ordinate with
motor neurons to produce patterned movements like
walking.
Their existence is unproven in human but locomotion
likely depends on their activity.
Their activity is modulated by higher centres in
subthalamus and mid-brain especially pedunculopontine nucleus through reticular fibres.
5. Command and control centres in brainstem,
cerebellum and forebrain modify action of spinal
pattern generators to promote stepping.
Step generation is dependant on locomotor centres in
pontine tegmentum, midbrain and sub thalamic
regions.
Locomotor synergies are established through reticular
formation and descending pathways in ventromedial
spinal cord.
6. Cerebral control
Goal and purpose of walking.
Avoidance of obstacles.
Adaption of locomotor programme to context and
terrain.
7. Postural control
Maintenance of centre of mass over base of support
through the gate cycle.
Unconscious postural adjustments
Vestibular nuclei and midline cerebellum contribute to
balance control.
8. Sensory information for postural
control primarily generated by
Visual system
2. Vestibular system
3. Proprioceptive receptors in muscle spindles and
joints
1.
9. Gait
Gait cycle refers to the events that transpire between
the time that one heel strikes the ground and the time
the same heel strikes the ground again.
For a single limb it comprises of 4 events
Initial contact>>>Stance phase>>Pre-swing phase
>>Swing phase
Periods of single limb support alternates with periods
of double limb support.
10.
11. Various parameters to measure gait are gait velocity,
stride time, stride length and step length.
A typical adult walking on a level surface has velocity
80 m/min, 113 steps /min, stride length – 1.41 m.
60% stance phase+ 40% swing phase+ 10%double limb
support.
Centre of mass of human body is located just anterior
to the s2 vertebral body.
An effective gait has minimal displacement of centre of
mass.
12. Examination of station
Patient asked to stand with feet closely together.
Stand with eyes open and eyes closed.
One foot at a time
On toes and heels
Tandem with one heel in front of other.
Light push.
13. Cerebellar disease there is broad base and swaying.
Lesion in the vermis – swaying on backward, forward
and either side.
Hemispheric lesion / unilateral vestibular diseasepatient sways or falls towards affected side OR
There may be tilting of the head towards the involved
side with chin rotated towards sound side.
Patient will lose balance more easily when pushed
towards involved side.
14. Movement disorder may become apparent.
Skeletal abnormality- kyphosis, scoliosis. Lordosis.
Developmental anamolies
Hemiparesis- flexed and pronated upper extremities
and extended lower extremity.
Parkinson’s disease- flexed posture, stooped over, with
head and shoulder bent forward and arms and knees
flexed.
15. Depressed – stooped and dejected
Manic states- erect, aggressive posture
Schizophrenia- may assume bizarre posture and
maintain it for long time.
16. Examination of Gait
Width of the base- normally medial malleoli should
pass within about 2 inches of each other during stride
phase.
Asymmetry of toe lift- foot drop.
Stride length- shortened stride length may be early
evidence of bifrontal or extra pyramidal disease.
Decreased arm swing on one side may be early
indicator of Hemiparesis or hemi parkinsonism.
Tandem walking
17. Movements of hip – excessive in proximal muscle
weakness.
Brisk walk with abrupt stop and turn
Walking on heel and toes
To hop on either foot
21. Cautious gait (senile gait)
Older patients
Non-specific
Abbreviated stride, lowered centre of mass, slow
velocity, short steps, wide base.
No difficulty in foot-floor clearance, no shuffle, no
difficulty with initiation of gait, no freezing.
“walking on icy/ slippery surface”
An adaptation to perceived postural threat
Age related degeneration of sensory apparatus
Physical therapy
22. Spastic gait (stiff legged gait)
A hemiparetic posture with arms flexed, adducted and
internally rotated.
Plantar flexion of the foot on the affected side
(equinus deformity).
Holds arm tightly by side, rigid and flexed while
walking. No arm swing.
circumduction and hip hike, dragging and shuffling
of the feet
Upper motor neuron signs in physical examination.
23. compromise of corticospinal command and
overactivity of spinal reflexes.
SPINAL CORD CAUSES
Myelopathy from cervical spondylosis
Demyelinating disease and trauma
hereditary spastic paraplegia
structural lesion -tumor or spinal vascular
malformation.
24. With cerebral spasticity, asymmetry is common,
involvement of the upper extremities is usually
observed, and dysarthria is often an associated feature.
Common causes include vascular disease (stroke),
multiple sclerosis, and perinatal injury to the nervous
system (cerebral palsy).
25. Parkinsonian Gait
Akinetic-rigid.
Rigidity, bradykinesia and loss of associated movements.
Stooped with head and neck forward, knees flexed.
Upper extremities usually flexed at shoulder, elbow and
wrist. Fingers usually extended.
Slow, stiff and shuffling. Patient walks with small, mincing
steps.
Involuntary acceleration (festination), decreased arm
swing, en bloc turning, start hesitation, freezing when
encountered an obstacle.
26. Freezing of gait is even more common in some of the
Parkinson's-related neurodegenerative disorders.
Progressive supranuclear palsy
multiple-system atrophy
corticobasal degeneration.
These patients frequently present with axial
stiffness, postural instability, and a shuffling gait while
lacking the characteristic pill-rolling tremor of
Parkinson's disease. Falls within the first year suggest
the possibility of progressive supranuclear palsy.
27. Hyperkinetic movement disorders
Chorea, Huntington’s disease – abnormal movement
become more marked when walking.
Huntington’s disease- gait may be grotesque, dancing
or prancing with abundant erroneous movements.
28. Frontal gait disorder
"gait apraxia“
a shuffling, freezing gait with imbalance and other signs of
higher cerebral dysfunction.
A wide base of support, short stride, shuffling along the
floor, and difficulty with starts and turns.
difficulty with gait initiation --"slipping clutch" syndrome.
lower body parkinsonism- Strength is preserved, patients
are able to make stepping movements when not standing
and maintaining balance at the same time.
a higher level motor control disorder.
29. most common cause of frontal gait disorder is vascular
disease, particularly subcortical small-vessel disease.
Lesions are frequently found in the deep frontal white
matter and centrum ovale.
Binswanger’s disease
Communicating hydrocephalus.
30. Cerebellar Ataxias
a wide base of support, lateral instability of the trunk,
erratic foot placement, and decompensation of
balance when attempting to walk tandem.
Difficulty maintaining balance when turning and
sudden stopping.
unable to walk tandem heel to toe.
Truncal sway in narrow-based or tandem stance.
31. Two types of lesion
1) Lesion in cerebellar vermis – a lurching, staggering
gait without laterality.
2) Hemispheric lesion – persistent swaying and
deviation towards affected side.
“compass deviation” or “star shaped gait” .
33. Sensory ataxia
balance depends on high-quality afferent information
from the visual and the vestibular systems and
proprioception.
When this information is lost or degraded, balance
during locomotion is impaired and instability results.
Joint position and vibration sense are diminished in
the lower limbs. The stance in such patients is
destabilized by eye closure; they often look down at
their feet when walking and do poorly in the dark
Tabes dorsalis, SACD of spinal cord, sensory
peripheral neuropathy.
34. Cerebellar ataxia
Sensory ataxia
Base of support
Wide-based
Narrow base, looks Wide-based
down
Velocity
Variable
Slow
Very slow
Stride
Irregular, lurching
Regular with path
deviation
Short, shuffling
Romberg
+/–
Unsteady, falls
+/–
Heel shin
Abnormal
+/–
Normal
Initiation
Normal
Normal
Hesitant
Turns
Unsteady
+/–
Hesitant, multistep
+++
++++
Postural instability +
Frontal gait
Poor postural
synergies getting up
from a chair
Falls
Late event
Frequent
Frequent
35. Steppage (equine) gait
Patient lifts one or both legs high during respective
stride phases
FOOT DROP : Weakness of dorsiflexors of foot and
toe.
To prevent tripping patient compensates by lifting the
foot as high as possible, hiking the hip and flexing the
hip and knee.
Double tap sound may be heard.
SENSORY ATAXIA : patient lifts up feet then slaps
them on the floor to improve proprioceptive feedback.
37. Myopathic (waddling) gait
Weakness of hip girdle muscle.
Myopathy and muscular dystrophy.
Pronounced lordosis in case of weak hip flexors.
Trendelenberg’s sign - an abnormal drop of pelvis on
the side of swing leg due to hip abductor weakness.
Bilateral weakness cause an exaggerated pelvic swing
resulting inn waddling gait.
38. Toxic and metabolic disorders
Alcohol intoxication
chronic renal disease
hepatic failure
Sedative drugs, especially neuroleptics and long-acting
benzodiazepines
39. Psychogenic Gait Disorder
Some patients with extreme anxiety or phobia walk
with exaggerated caution with abduction of the arms,
as if walking on ice.
Hysterical gait disordersOdd gyrations of posture
wastage of muscular energy (astasia-abasia),
extreme slow motion,
dramatic fluctuations over time may be observed in
patients with somatoform disorders and conversion
reaction.
