This document provides an overview of gait disorders, including normal gait cycle components and subdivisions, physiological and anatomical aspects of gait, common causes and types of abnormal gait, clinical symptoms and examination of gait. Key points covered include definitions of stance and swing phases, centers of pressure and gravity, neurological structures involved in locomotion, epidemiology of gait disorders in older adults, gait abnormalities due to weakness, spasticity, sensory deficits and imbalance. Classification of gait patterns such as myopathic, neurogenic, sensory ataxia, vestibular imbalance and spastic hemiparetic gaits are described.

1. CLINICAL APROACH TO
GAIT DISORDERS
DR. SUMIT KAMBLE
DM SENIOR RESIDENT
DEPT. OF NEUROLOGY
GMC, KOTA
MODERATOR
DR. DILIP MAHESHWARI
ASSOCIATE PROFF. NEUROLOGY

2. NORMALGAIT CYCLE
• Single gait cycle or stride is defined:
• Period when 1 foot contacts the ground to when that same foot contacts
the ground again
• Each stride has 2 phases:
• Stance Phase
• Foot in contact with ground
• Swing Phase
• Foot not in contact with ground

3. SUB-DIVISIONS OFSWING PHASE

4. SUB COMPONENT OFSTANCE PHASE

5. PHYSIOLOGICAL AND BIOMECHANICAL
ASPECTS OFGAIT
• Posture- based on mechanical musculoskeletal linkages and
neurological control detecting and correcting body sway.
• Postural response
1. Automatic righting reflexes keeping head upright on trunk
2. Supporting reactions controlling antigravity muscle tone
3. Anticipatory (feed-forward) postural reflexes occurring
before limb movement
4. Reactive (feedback) postural adjustments counteracting body
perturbations during movement.

6. • Initiation of gait - heralded by a series of shifts in the center of
pressure beneath the feet—first posteriorly, then laterally toward
the stepping foot, and finally toward the stance foot to allow the
stepping foot to swing forward.
• Center of Gravity (CG)
• Midway between the hips
• Few cm in front of S2

7. ANATOMICAL ASPECTS OFGAIT
• Neuroanatomical structures responsible for equilibrium and
locomotion -
1. Brainstem (subthalamic, midbrain)
2. Cerebellar locomotor regions
project through descending reticulospinal pathways from the
pontomedullary reticular formation into ventromedial spinal cord.

8. • Prefrontal cortex - modulates midbrain and cerebellar locomotor
regions
• Parietal cortex - integrates sensory inputs indicating position
and orientation in space, the relationship to gravitational forces,
the speed and direction of movement.
• Cerebellum - modulates the rate, rhythm, amplitude, and force
of stepping.

9. EPIDEMIOLOGYAND IMPACT
• Gait disorders affect up to 15% of people > 60 years of age
• >80% who are >85 years.
• Patients hospitalized with neurologic disorders, 60% have gait
disturbance.
1. Sensory deficits, 18%
2. Myelopathy, 17%
3. Multiple infarcts, 15%
4. Unknown cause, 14%
5. Parkinsonism, 12%
6. Cerebellar degeneration, 7%
7. Hydrocephalus, 7%
8. Miscellaneous, 5%
9. Psychogenic, 3 %
10.Toxic/metabolic, 2.5%

10. ABNORMALGAIT
1. Pain
2. Impaired Joint Mobility (arthritis, contractures)
3. Muscle weakness (Myopathy, neuropathy)
4. Spasticity (stroke, cord lesion)
5. Sensory/balance deficit (neuropathy, stroke)
6. Impaired central processing (dementia, stroke, delirium,
drugs)

11. HISTORY: COMMON SYMPTOMSAND
ASSOCIATIONS
WEAKNESS
• Hemiplegia or foot drop caused by weakness of ankle
dorsiflexion - Catching or scraping a toe on the ground and a
tendency to trip
• Weakness of knee extension - sensation that the legs will give
way while standing or walking down stairs.

12. • Weakness of ankle plantar flexion - interferes with ability to
stride forward, resulting in a shallow stepped gait.
• Proximal muscle weakness- Difficulty in climbing stairs or
rising from a seated position.
• Axial muscle weakness - interfere with truncal mobility

13. SLOWNESS
• Slowness of walking
1. Normal reaction to unstable or slippery surfaces
2. Elderly
3. Those who feel their balance is less secure because of any
musculoskeletal or neurological disorder
4. Parkinson disease (PD) and other basal ganglia diseases

14. STIFFNESS
• Presenting symptoms of a spastic paraparesis or hemiparesis.
• Drag their legs, catch the toes of their shoes on any surface
irregularity and their legs suddenly give way, causing stumbling
and falls.
• Leg muscle tone in some upper motor neuron syndromes and
dystonia may be normal when the patient is examined in the
supine position but is increased during walking.

15. • In childhood, an action dystonia of the foot is a common initial
symptom of primary dystonia with stiffness, inversion, and
plantar flexion of the foot and walking on the toes only
becoming evident after walking or running.
• Patients with dopa-responsive dystonia typically develop
symptoms in the afternoon (“diurnal fluctuation”).

16. IMBALANCE
1. Cerebellar ataxia
2. Sensory ataxia
3. Vestibulopathy
4. Vascular lesions of thalamus, and basal ganglia.
5. Wide-based unsteady gait is also feature of frontal lobe
diseases
6. Imbalance in subcortical cerebrovascular disease and basal
ganglia disorders manifests when turning while walking,
stepping backwards, bending over to pick up something, or
performing several tasks simultaneously,

17. FALLS
1. Collapsing falls(Tone is lost )- syncope or seizures.
2. Toppling falls (Muscle tone is retained) - impaired static and
dynamic postural responses that control body equilibrium
during standing and walking.

18. Toppling falls (Muscle tone is retained)
• Tripping - foot drop or shallow steps, may also be a
consequence of carelessness secondary to inattention, dementia,
or poor vision.
• Proximal muscle weakness- legs giving way and falls.
• Unsteadiness and poor balance
• Impairment of postural responses.
• Spontaneous falls, especially backward, are an important clue to
diagnoses such as multiple system atrophy and progressive
supranuclear palsy

19. SENSORY SYMPTOMS AND PAIN
• Distribution of any accompanying sensory complaints provides
clue to the site of the lesion producing walking difficulties.
• Radicular pain or paresthesias,
• Sensations of tight bands around the trunk
• Distal symmetrical paresthesias of the limbs
• Neurogenic claudication of the cauda equina
• Vascular intermittent claudication
• Skeletal pain due to degenerative joint disease

20. URINARY INCONTINENCE
• Spinal cord lesion
• Parasagittal cerebral lesions such as frontal lobe tumors
(parasagittal meningioma), frontal lobe infarction caused by
anterior cerebral artery occlusion, and hydrocephalus.
• Urinary urgency and urge incontinence are also common in
parkinsonism and subcortical white-matter ischemia.

21. COGNITIVE CHANGES
• Slowing of gait may be a marker of impending cognitive
impairment and dementia.
• Executive dysfunction including inattention, impaired
multitasking, and set switching may predict later development
of falls in older adults without dementia or impaired mobility
• Dementia with disinhibition and impulsivity are associated with
reckless gait problems and falls.

22. EXAMINATION OFPOSTUREAND WALKING
ARISING TO STAND FROM SEATED POSITION
1. Proximal muscle strength
2. Organization of truncal and limb movements
3. Stability
4. Stance base
STANDING
1. Posture
2. Stance base
3. Body sway
4. Romberg test
5. Postural reflexes (pull test)

23. WALKING
1. Initiation of stepping
2. Speed
3. Stance base
4. Step length
5. Cadence
6. Step trajectory (shallow, shuffling, or high stepping)
7. Associated trunk and arm movements
8. Trunk posture
TURNING WHILE WALKING
1. Number of steps to turn
2. Stabilizing steps
3. En bloc (truncal and limb movement)
4. Freezing
OTHER MANEUVERS
1. Tandem walking
2. Walking backwards
3. Running Walking on toes, heels

24. CLASSIFICATION OFGAIT PATTERNS
A. MYOPATHIC GAIT (waddling gait)
• Weakness of proximal leg and hip-girdle muscles interferes with
stabilizing the pelvis and legs on the trunk.
• Exaggerated rotation of the pelvis with each step and a
waddling gait.
• Hips are slightly flexed as a result of weakness of hip extension,
and an exaggerated lumbar lordosis occurs.
• Gower’s sign.

26. NEUROGENIC WEAKNESS (STEPPAGE GAIT)
• Seen in patients with foot drop (weakness of foot dorsiflexion),
• Lift the leg high enough during walking so that the foot does
not drag on the floor.
• Unilateral- Peroneal and Sciatic nerve palsy and L5
radiculopathy.
• Bilateral - amyotrophic lateral sclerosis, Charcot-Marie-Tooth
disease and other peripheral neuropathies and scapuloperoneal
syndromes.

27. • Weakness of ankle plantar flexion produces a shallow stepped
gait.
• Femoral neuropathy produces weakness of knee extension and
buckling of the knee when walking or standing. This may first
be evident when walking down stairs.

29. SENSORY ATAXIA (SLAPPING/STAPMING GAIT)
• Adopt a wide base and advance cautiously, taking slow steps
under visual guidance.
• Feet are thrust forward with variable direction and height.
• Sole of the foot strikes floor forcibly with a slapping sound
(slapping gait).
• Walking on uneven surfaces and dark is particularly difficult.
• Romberg test.
• Large-diameter peripheral neuropathies, posterior root or dorsal
root ganglionopathies, and dorsal column lesions.

30. VESTIBULAR IMBALANCE AND GAIT
• Acute peripheral vestibular disorders result in leaning and
unsteady veering to the side of the lesion
• Unsteadiness and veering while running may be less evident
than when walking in acute vestibulopathy.
• In chronic vestibular failure, gait may be normal, though
unsteadiness can be unmasked during eye closure and rotation
of the head from side to side while walking.

31. SPASTIC HEMIPARETIC GAIT
• Arm is adducted, internally rotated at the shoulder, and flexed at
the elbow, with pronation of the forearm and flexion of the wrist
and fingers.
• Leg is slightly flexed at the hip and extended at the knee, with
plantar flexion and inversion of the foot.
• Swing phase of each step is accomplished by slight lateral
flexion of the trunk toward the unaffected side and
hyperextension of the hip on that side to allow slow
circumduction of the extended paretic leg as it swings forward
from the hip, dragging the foot or catching the toe on the ground
beneath.

33. SCISSORS GAIT
• Bilateral spastic paresis of legs
• Legs move slowly and stiffly and the thighs are strongly
adducted such that the legs may cross as the patient walks

35. CEREBELLAR ATAXIA
• Midline cerebellar structures, vermis, and anterior lobe - loss of
truncal balance, increased body sway, dysequilibrium, and gait
ataxia.
• Stance- Wide-based
• Lurching and staggering quality that is more pronounced when
walking on a narrow base or during heel-to-toe walking,
resembling acute alcohol intoxication.
• Anterior lobe atrophy develop a 3-Hz anteroposterior sway of
the trunk and a rhythmic truncal and head tremor (titubation)
that is superimposed on the gait ataxia.

36. • Flocculonodular lobe - exhibit multidirectional body sway,
dysequilibrium, and severe impairment of body and truncal
motion. Standing and even sitting can be impossible, although
when lying down, the heel-shin test may appear normal, and
upper limb function may be relatively preserved.
• Limb ataxia due to involvement of the cerebellar hemispheres is
characterized by a decomposition of normal leg movement.
Steps are irregular and variable in timing (dyssynergia), length,
and direction (dysmetria).

38. HYPOKINETIC (PARKINSONIAN) GAIT
• Posture - stooped, with flexion of the shoulders, neck, trunk,
and knees.
• Asymmetrical reduction of arm swing and slowing in gait,
particularly when turning
• Start hesitation before breaking into a more normal stepping
pattern with small, shallow steps on a narrow base.
• Freezing
• Festination.
• Retropulsion and propulsion

40. FRONTAL LOBE GAIT DISORDERS
• Cautious gait, a consequence of compensatory adjustments in
response to real or perceived disequilibrium
• Isolated gait ignition failure, characterized by difficulty
initiating or maintaining locomotion, and caused by lesions in
the frontal lobe, white matter connections, or basal ganglia
• Frontal gait disorder(Magnetic gait) characterized by variable
base (narrow to wide), decreased foot clearance, short shuffling
steps, disequilibrium, and start and turn hesitation, and caused
by lesion in the frontal lobe and white matter

42. CHOREIC GAIT
• Random movements of chorea are often most noticeable during
walking.
• Superimposition of chorea on the trunk and leg movements of
the walking cycle gives the gait a dancing quality owing to the
exaggerated motion of the legs and arm swing.
• Chorea can also interrupt the walking pattern, leading to a
hesitant gait.

44. DYSTONIC GAIT
• Childhood-onset primary torsion dystonia - sustained abnormal
posturing of the foot (typically plantar flexion and inversion) on
attempting to run.
• Walking forward or backward or even running backward may
be normal at an early stage.
• Early stages - tonic extension of the great toe (striatal toe) when
walking.
• Birdlike (peacock) gait - excessive flexion of the hip and knee
and plantar flexion of the foot in a during the swing phase.

46. PSYCHOGENIC GAIT DISORDERS (ATASIA-ABASIA)
• 1. transient fluctuations in posture while walking,
• 2. knee buckling without falls,
• 3. excessive slowness and hesitancy,
• 4. crouched, stooped or other abnormal posture of the trunk,
• 5. complex postural adjustments with each step,
• 6. exaggerated body sway or excessive body motion especially
brought out by tandem walking, and
• 7. trembling, weak legs.

48. NON-NEUROLOGIC CAUSES
1. Visual loss
2. Orthopedic disorders
3. Rheumatologic disorders
4. Pain
5. Cardiorespiratory problems

49. THANKYOU

50. REFERENCES
• Bradleys Neurology in Clinical Practice 7th edition
• DeJongs The Neurological Examination 7th edition
• Uptodate. Com
• Jacquelin perry, GAIT ANALYSIS normal and pathological
function
• Gait Disorders Evaluation and Management Jeffrey M.
Hausdorff