gait and disorders

1. Gait disorders

2. Introduction
 The maintenance of an upright posture and the act
of walking are among the first, and ultimately most
complex, motor skills humans acquire.
 individual’s pattern of walking may be so distinctive
they can be recognized by the characteristics of
their gait or even the sound of their steps.
 Many diseases of the nervous system are identified
by the disturbances of gait and posture.

3. Anatomical aspects of gait
 2 basic systems responsible for equilibrium and
locomotion
1. Brainstem locomotor centers
 pedunculopontine &
 adjacent nuclei of midbrain
2. Spinal locomotor centers
 Additional level of supraspinal control is needed to
maintain bipedal stance and gait
1. Frontal cortex
2. Parietal cortex
3. cerebellum

4. Brainstem locomotor centers:
 Projects from the pontomedullary reticular formation, through
reticulospinal pathways into ventromedial spinal cord.
 Stimulation results in increase in axial and limb muscle tone
to assume an upright posture before stepping begins
Spinal locomotor centers:
 Assemblies of spinal interneurons
 Activate motor neurons of limb and trunk muscles in a
patterned and repetitive manner to drive stepping
movements
 propriospinal networks that link the trunk and limbs to
facilitate synergic coordinated limb and trunk movements of

5. Frontal cortex
prefrontal cortex
◦ via corticobulbar and corticostriatal tracts
◦ modulates midbrain and cerebellar locomotor
regions.
Frontal motor projections
 to the pontomedullary reticular formation
◦ innervate axial muscles modulate postural
responses associated with stepping
 to the spinal motor neurons,
◦ enables precision of foot movements.

6. Parietal cortex
 It integrates sensory inputs
 indicates position and orientation in space, the
relationship to gravitational forces,
Cerebellum
 Modulates the rate,rhythm,amplitude and force of
stepping
 contributes to medial brainstem efferent system
through projections from flocculonodular and
anterior lobes
◦ Controlls the equilibrium and truncal posture

7. PHYSIOLOGICAL ASPECTS OF GAIT
 Stability when standing is based on
◦ musculoskeletal linkages between the trunk and
legs
◦ neurological control detecting and correcting
body sway i.e, postural responses.
 Synergitic action axial and proximal limb muscle
and postural responses maintain static postural
control.

8. Postural reflexes:
2 types
◦ anticipatory postural reflexes:
 feed-forward
 occurring before limb movement.
◦ Reactive postural reflexes:
 feedback
 postural adjustments counteracting body
perturbations during movement.
◦ modified by voluntary control.
◦ generated by the integration of visual,
vestibular, and proprioceptive inputs in the
context of voluntary intent.

9.  Once the trunk is upright and stable, locomotion can
begin.
 The initiation of gait is heralded by a series of shifts in
the center of pressure beneath the feet.
◦ first posteriorly,
◦ then laterally toward the stepping foot
◦ finally toward the stance foot to allow the stepping
foot to swing forward
 This sequence is then followed by the stereotyped
stance, swing, and step phases of the gait cycle.

10. GAIT CYCLE
Period between two successive points at which the
heel of the same foot strikes the ground
Cadence:“the rhythm and number of steps per minute”

11. Gait
cycle
2 phases
8 events
Phases
stance
swing
Events
4 stance phase
events
4 swing phase
events

12. Stance phase Swing phase
Accounts for 60% gait
cycle.
Consists of 4 phases
 initial contact
 loading
 mid-stance
 terminal stance.
Accounts for 40% gait
cycle.
Consists of 4 phases
 Preswing
 Initial swing
 Mid swing
 Terminal swing

13. Events during stance phase
1. Heel strike:
 initiates gait cycle
 body’s center of gravity is at its lowest position
2. Foot flat :
 plantar surface of the foot touches the ground
3. Mid stance
 Swinging contra lateral foot passes the stance foot
 Center of gravity at its highest position
4. Heel off
 Heel looses contact with ground.
5. Toe off
 terminates the stance phase as foot leaves the ground

14. Events during swing phase
1. Acceleration:
 begins as soon as foot leaves the ground
 activation of hip flexors to accelerate leg forward
2. Mid swing:
 foot passes directly beneath the body
 coincident with mid stance of other foot
3. Deceleration:
 describes the action of muscles as they slow
 the leg and stabilize the foot in preparation for next
heel strike

16. Distance measures:
Stride length
◦ distance between heels from one heel strike to the next heel strike on
same side
◦ distance travelled by a person during a gait cycle
Step length
◦ length between heel strike of one foot to other
◦ Rt + Lt step length = stride length
Step width
◦ medio lateral distance between feet

17.  A typical adult walking parameters comfortably on a
level surface includes:
◦ velocity of about 80 m per minute,
◦ about 113 steps per minute,
◦ stride length of 1.41 m.
◦ About 60% of the gait cycle is spent in stance phase
◦ 40% in swing phase
◦ 10% in double limb support.
 The body's center of mass is located just anterior to
the S2 vertebral body.

18. Evaluation of gait

19. HISTORY
 A detailed history provides the first clues to diagnosis.
 note the circumstances in which walking difficulty
occurs.
 Ask for any associated symptoms, especially falls.
 Walking over uneven ground exacerbates most
walking difficulties.
 Often an individual is unaware of their gait
abnormality, and family or friends note altered
cadence, shuffling or slowness.

20. Weakness:
 weakness of certain muscle groups produces
characteristic difficulties during particular movements
of the gait cycle.
◦ weakness of ankle dorsiflexion - foot drop
◦ Weakness of knee extension - buckling attacks
◦ Weakness of ankle plantar flexion - shallow stepped
gait.
◦
◦ proximal muscle weakness
- Difficulty in climbing stairs or rising from a
seated position
 Catching or scraping a toe on the ground and a

21. Slowness and Stiffness:
 Slowness of gait is normal reaction when walking
on slippery surfaces.
 Similarly, when the balance was threatened any
musculoskeletal or neurological disorder patient
will have slowness of gait.
 In Parkinson disease (PD) and other basal ganglia
diseases, slowness of walking is due to shuffling
with short, shallow steps.
 Difficulty rising from a chair or turning in bed may
be clues to loss of truncal mobility in diffuse
cerebro vascular disease, hydrocephalus, and
basal ganglia diseases.

22.  Complaints of stiffness, heaviness in the limbs are
the symptoms of a spasticity.
 It is important to remember that 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.
 In childhood, an action dystonia of the foot is a
common initial symptom, walking on the toes only
becoming evident after walking or running.

23. Imbalance:
 poor balance and unsteadiness are cardinal features
of cerebellar ataxia and sensory ataxia.
 cerebellar gait ataxia complains of
◦ Unsteadiness and inability to walk in a straight line
and near falls.
◦ Turning and suddenly changing direction results in
veering to one side.
◦ Symptoms are exacerbated by an uneven support
surface.

24. Sensory ataxia:
◦ presents with unsteadiness when walking in the
dark.
◦ Patients complain of being uncertain of the exact
position of their feet when walking.
◦ impression of walking on a spongy surface or cotton
wool.
Acute vestibulopathy:
◦ Is associated with vertigo and severe imbalance.
Chronic vestibular dysfunction
◦ often causes veering and problems in an
environment with many moving objects.

25.  A wide-based unsteady gait also is a feature of frontal
lobe diseases
◦ normal pressure hydrocephalus,
◦ diffuse small vessel ischemia of frontal sub cortical
white matter.
 Imbalance in sub cortical cerebro vascular disease
commonly manifests when
◦ turning while walking,
◦ stepping backwards,
◦ bending over to pick up something.

26. Falls:
 Toppling Falls
◦ muscle tone is retained
◦ falling like a tree trunk
◦ due to impaired static and dynamic postural
responses that control body equilibrium
 collapsing falls
◦ muscle tone is lost
◦ imply a loss of consciousness characteristic of
syncope or seizures
 Tripping falls:
◦ many people attribute falls to tripping when in
fact tripping did not occur.
◦ Tripping may be due to foot drop or shallow
steps
◦ also be a consequence of secondary to
inattention, dementia, or poor vision.

27.  Proximal muscle weakness may result in the legs
giving way and falls.
 Unsteadiness and poor balance in an ataxic
syndrome may lead to falls.
 falls associated with postural adjustments, or falls
occurring when performing multiple tasks suggest
an impairment of postural responses.
 Backward falls in early stages
◦ Feature of an akinetic-rigid syndromes
◦ Favors a diagnosis of MSA or PSP rather than
PD
◦ Falls do occur in PD but are late feature.
• In PD falls are usually forward and may also occur
while turning and changing the posture.
 Collapsing falls related to orthostatic hypotension, a

28. Sensory Symptoms and Pain:
 distribution of sensory complaints provides a clue
to the site of the lesion.
◦ Ex: Distal symmetrical paresthesias of limbs
S/O peripheral neuropathy.
 Skeletal pain due to degenerative joint disease is
aggravated by movement of the affected joints.
 The normal pattern of walking is frequently
modified by joint disease.
 strategies to minimize pain by avoiding full weight
bearing on the affected limb will produce limping.

29. Urinary Incontinence:
 Urinary urgency and urge incontinence seen in
◦ spinal cord lesion
◦ parkinsonism
◦ subcortical white-matter ischemia.
 frontal lobe tumors, frontal lobe infarction, and
hydrocephalus also produce urinary
incontinence.
Cognitive Changes:
 Slowing of gait may be a marker of impending
cognitive impairment and dementia.
 executive dysfunction including inattention may
produce falls.
 disinhibition and impulsivity are associated with
reckless gait problems and falls.

30. EXAMINATION OF POSTURE AND GAIT
 First observe the overall pattern of limb and body
movement during walking.
 Normal walking progresses in a smooth and
effortless manner.
 The truncal posture is upright, and the legs swing in a
fluid motion with a regular stride length.
 Synergistic head, trunk, and upper-limb movement
flow with each step.
 After the overall walking pattern is observed, the
specific aspects of posture and gait should be
examined.

31. specific aspects of posture and gait includes:
1. Arising to stand from seated position
2. Stance and posture
3. Walking
4. Turning while walking
5. Other maneuvers
◦ Tandem walking
◦ Walking backwards
◦ Running
◦ Walking on toes, heels

32. Arising from Sitting:
 informs about
◦ pelvic girdle strength,
◦ control of truncal movement,
◦ coordination, and balance.
 proximal muscle weakness:
Inability to rise when the feet are appropriately
placed under the body.
 incoordination or imbalance:
An abnormally wide stance base when
standing.
 Frontal lobe diseases:
Feet are not positioned directly under the
body

33. Stance:
 Stance base = the distance between the feet
 gives an indication of balance.
 Wide stance base indicates poor balance.
 Wide-based gaits are
◦ typical of cerebellar or sensory ataxia
◦ diffuse cerebro vascular disease
◦ frontal lobe lesions.
 Eversion of the feet to increase stability seen in
diffuse cerebrovascular disease.
 In mild ataxia, a widened base may only be evident
with turning.
 Tandem (heel to toe) walking is a good objective
measure of walking stability.

34. Trunk Posture:
 Flexion of the trunk and a stooped posture - PD.
 Upright posture with neck and trunk extension- PSP.
 Slight flexion at the hips to lower the trunk
- feature of cautious gait.
 Neck flexion – MND
Myasthenia gravis
MSA
Parkinsonism
 Tilt of the trunk to one side - dystonia.
 exaggerated lumbar lordosis
◦ stiff person syndrome[d/t Paraspinal muscle spasm]
◦ Proximal myopaties.

36. Truncal tilt away from the side of the lesion
◦ acute vascular lesions of the thalamus( postero
lateral) and basal ganglia.
Truncal tilt away from the side of the lesion
◦ Acute vestibular imbalance in the lateral medullary
syndrome
Truncal flexion (camptocormia)
◦ paraspinal myopathies that produce weakness of
trunk extension.
 restricted range of spinal movement and persistence
of the abnormal spinal posture when supine or
during sleep are useful pointers toward a bony spinal
deformity.

37. Postural Responses:
1.Reactive postural responses
2. anticipatory postural responses.
3.protective postural responses.
.

38. pull test
Reactive postural responses
are examined by “the pull
test”.
 Examiner sharply pulls the
upper trunk backward or
forward while the patient is
standing.
 The pull should be sufficient
to require the patient to
step to regain their balance.
 The examiner must be
prepared to prevent the
patient from falling.
 A few short, shuffling steps
backward or an impending
fall backward or forward
suggests impairment of
righting reactions

39.  Falls after postural changes such as arising from a
chair or turning while walking suggest impaired
anticipatory postural responses.
 Falls without rescue arm movements or stepping
movements to break the fall indicate loss of
protective postural responses.
 Injuries sustained during falls provide a clue to the
loss of postural responses
 A tendency to fall backward spontaneously is a
sign of impaired postural reflexes in PSP and gait
disorders associated with frontal lobes

40. Romberg test
 Patients with proprioceptive loss depends on visual
cues.
 the removal of vision greatly exaggerates the ataxia.
 This is the basis of the Romberg test.
 In which eye closure leads to a dramatic increase in
unsteadiness and even falls in the patient with sensory
ataxia.
 When performing the Romberg test, it is important the
patient is standing comfortably before eye closure and
to remember that a modest increase in body sway is a
normal response to eye closure.

41. Walking:
Initiation of Gait:
start hesitation – difficulty in gait initiation.
slipping clutch phenomenon
◦ few short, shuffling steps on the spot without
forward progress.
magnetic foot phenomenon.
◦ complete immobility with the feet seemingly glued
to the floor
 Patients may make exaggerated upper-body
movements or alter the step pattern.

42.  Start hesitation seen in
◦ frontal lobe disease,
◦ diffuse cerebrovascular disease,
◦ hydrocephalus.
◦ gait ignition failure.
◦ PD
 Isolated start hesitation is seen in the syndrome of
gait ignition failure.

43. Stepping:
 length and trajectory of each step and the rhythm of
stepping should be noted.
 Short, regular, shallow steps or shuffling and a slow gait
-
akinetic-rigid
syndromes.
 Freezing typically occurs when turning, when walking
has been interrupted by an obstacle.
 Festination (increasingly rapid, small steps) is common
in PD but rare in other akinetic-rigid syndromes.

44.  Unilateral loss of synergistic arm swing while walking
1. valuable sign of early PD
2. Unilateral UMN lesion
3. acute cerebellar syndrome
Turning:
 Requires more balance more than walking in a straight
line.
 Slowing on turns may be the first abnormality in walking in
PD
 Multiple steps on turning
◦ PD

45. More Challenging Tests of Walking:
Tandem walking:
 Subtle degrees of cerebellar ataxia unmasked by
tandem walking.
Walking on toes and heels:
 may bring out abnormal movements as well as
deficits in the strength of dorsiflexion and plantar
flexion of the ankle.
Walking backward:
 will sometimes reduce or abolish the dystonic foot
posturing observed walking forward in action dystonia
of the foot.
Running:
 examine the patient running to identify an action
dystonia of the legs in early stages.

46. Associated and Synergistic Limb Movements While
Walking:
Dystonic posturing of an arm or leg
◦ dystonia,
◦ parkinsonism,
◦ old hemiparesis.
Choreiform movements are more prominent during
walking than at rest in
◦ most chorea syndromes,
◦ levodopa-induced dyskinesia,
◦ tardive dyskinesia.
Parkinsonian tremor of the dependent upper limb is
often observed while walking.

47. MOTOR AND SENSORY EXAMINATION:
 motor and sensory function in the limbs is examined
with the patient sitting or supine.
 The size and length of the limbs should be measured
in any child presenting with a limp.
 The spinal column should be inspected for scoliosis,
and the lumbar region for skin defects or hairy
patches indicative of spinal dysraphism.

48. DISCREPANCIES ON EXAMINATION OF GAIT:
 minimal abnormal signs on physical examination of
the recumbent patient, in contrast to the observed
difficulty when walking.
Cerebellar gait ataxia caused by a vermis lesion:
◦ perform the heel-to-shin test normally when
supine but is ataxic when walking.
Action dystonia:
◦ Abnormal posturing of the feet only when
walking.
◦ A dystonic gait may be evident only when
running or walking forward but not when walking
backward.

49. Frontal lobe lesion, hydrocephalus,or diffuse
cerebrovascular disease :
◦ Patient totally unable to walk when standing.
◦ Gegenhalten (paratonia), with or without brisk
tendon reflexes, may be the only abnormal sign in
the recumbent patient
◦ Such patients perform the heel-shin test and make
bicycling movements of their legs normally when
lying on a bed.
Leg tremor of orthostatic tremor
◦ only appears during weight bearing, especially
when standing still.

50. GAIT DISORDERS

51. CLASSIFICATION OF GAIT PATTERNS:
 A scheme based on Hughlings Jackson’s three orders
of neurological function.
 Lower Level Gait Disorders (simplest)
 Middle Level Gait Disorders
 Higher Level Gait Disorders
(complex, integrative )
 Each level contributes sensory and motor function,
but that of higher centers is more complex and
dispersed within the nervous system.

52. Lower Level Gait Disorders
 manifest physical signs such as weakness or
sensory loss.
 are due to diseases of the muscle and peripheral
nerves that produce muscle weakness.
 Lower level sensory gait disorders follow loss of
one of the three basic senses important for gait and
balance:
◦ proprioception
◦ vision
◦ vestibular sensation.

53. Low level (sensory and motor) gait disorders:
1. Waddling gait - proximal weakness (myopathy)
2. high stepping gait - distal weakness (neuropathy)
3. Sensory ataxia – proprioception loss.
4. Vestibular ataxic gait -acute peripheral vestibulopathy
5. Gait difficulty due to acute visual impairment

54. Myopathic Weakness and Gait:
 Weakness of proximal leg and hip-girdle muscles
 interferes with stabilizing the pelvis and legs on the trunk.
 produces exaggerated rotation of the pelvis with each step
and a
waddling gait.
 The hips are slightly flexed (d/t hip extensor weakness).
 exaggerated lumbar lordosis.
 Gower’s sign positive
 myopathy is the most common cause of proximal muscle
weakness,
 neurogenic weakness of proximal muscles can also

56. Neurogenic Weakness and Gait:
 Muscle weakness of peripheral nerve origin.
 typically affects distal leg muscles
 results in a steppage gait.
 The patient lifts the leg and foot high above
the ground with each step because of
weakness of ankle dorsiflexion and foot drop.
 unilateral foot drop:
◦ common peroneal or sciatic nerve palsy or
an L5 radiculopathy
 Less common is foot drop caused by
myopathic weakness, as in the
scapuloperoneal syndromes.
 Weakness of ankle plantar flexion - shallow
stepped gait.

58.  A femoral neuropathy as in diabetes mellitus:
◦ produces weakness of knee extension and
buckling of the knee when walking or standing.
 This may first be evident when walking down stairs.
 similar weakness:
◦ Progressive muscular atrophy in MND
◦ quadriceps myopathy
◦ inclusion body myositis

59. Sensory Ataxia:
 wide stance base
 advance cautiously
 taking slow steps under visual guidance.
 the feet are thrust forward with variable direction and
height.
 The sole of the foot strikes the floor forcibly with a
slapping sound - slapping gait.
 Romberg test positive.
 Walking on uneven surfaces is particularly difficult.
 Results from
◦ peripheral neuropathies,
◦ posterior root or dorsal root ganglionopathies,
◦ dorsal column lesions.

60. Vestibular Imbalance, Vertigo, and Gait:
 Acute peripheral vestibulopathy
◦ produce veering to the side of the lesion.
◦ Veering less prominent while running than walking.
◦ Patients prefer to lie stand still.
 In chronic vestibular failure,
◦ gait may be normal,
◦ unsteadiness can be unmasked during eye closure
and rotation of the head from side to side while
walking.

61. Middle-Level Gait Disorders
 Related to impaired modulation of force generated by
the lower level motor system
include:
(1) spastic gait from corticospinal tract lesions
(2) ataxic gait arising from disturbances of the
cerebellum and its connections.
(3) hypokinetic gaits associated with parkinsonism.
(4) hyperkinetic gaits associated with chorea,dystonia,
and

62. Spastic Gait:
Spasticity of the arm and leg on one side:
 The leg is slightly flexed at the hip and
extended at the knee, with plantar flexion
and inversion of the foot.
 During the swing phase
◦ lateral flexion of the trunk toward the
unaffected side.
◦ circumduction of the extended paretic
leg.
◦ dragging the foot or catching the toe on
the ground.
◦ Minimal associated arm swing occurs on
the affected side.
 Muscle tone was increased on effected
side along with brisk DTR and extensor
plantar response.

63. Spasticity of both legs:
 legs are stiffly extended at the knees,
plantar flexed at the ankles, and
slightly flexed at the hips.
 Both legs circumduct, and the toes of
the plantar flexed feet catch on the
floor with each step.
 There is a tendency to adduct the
legs, particularly when the disorder
begins in childhood. [scissoring gait]
 Occasionally, bilateral leg dystonia
(dystonic paraparesis) mimics a
spastic paraparesis.

64.  This typically occurs in doparesponsive dystonia in
childhood.
 may be misdiagnosed as HSP or cerebral diplegia.
 Clinical differentiation between these conditions can
be difficult.
 Brisk tendon reflexes occur in both, and spontaneous
extension of a great toe in patients with striatal
disorders may be interpreted as a Babinski response.
 Fanning of the toes and knee flexion suggest spastic
paraplegia.
 Other distinguishing features include changes in
muscle tone, such as spasticity in HSP and rigidity in
dystonic paraparesis.

65. Cerebellar Ataxic gait:
 Lesions of spino cerebellum produces gait
ataxia.
 wide-based stance.
 Steps are taken slowly and carefully.
 tendency to lurch and stagger.
 Accentuated by tandem walking
 Gait with lurching and staggering quality
- midline cerebellar
pathology.
 Swaying to one side

67. A pure truncal ataxia
- midline (vermis) cerebellar syndrome.
- normal examination in supine position
Patients with anterior lobe atrophy:
◦ develop a 3-Hz antero posterior sway of the
trunk and a rhythmic truncal and head tremor
(titubation) that is superimposed on the gait
ataxia.
Lesions of vestibulo cerebellum:
 exhibit multidirectional body sway, & dysequilibrium.

68. Lesions of neo cerebellum:
 produce limb ataxia
 characterized by a decomposition of normal leg
movement.
 Steps are irregular and variable in timing
(dyssynergia), length, and direction (dysmetria).
 With lesions confined to one cerebellar hemisphere,
ataxia is limited to the ipsilateral limbs
 there is little postural instability or truncal imbalance
if the vermis is not involved.
 Cerebellar gait ataxia is exacerbated by the rapid
postural adjustments like turning.

69. Spastic Ataxic gait:
 A combination of spasticity and ataxia produces a
distinctive “bouncing” gait.
 Gait is wide based
 clonus is precipitated by standing or walking,
creating a bouncing motion.
 Compensatory movements, made in an effort to
regain balance, set up a vicious cycle of ataxic
movements, clonus, and increasing unsteadiness,
rendering the patient unable to stand or walk.
 Bouncing gaits must be distinguished from action
myoclonus of the legs and cerebellar truncal tremors.

70. Hypokinetic (Parkinsonian) Gait:
Early PD:
◦ Asymmetrical reduction of arm swing and
◦ Mild slowing in gait, particularly when turning.
Advanced PD:
◦ stooped posture with flexion of the shoulders,
neck, trunk.
◦ little associated limb movements while walking.
◦ the arms are held immobile at the sides or
slightly forward.
◦ Rest tremor of the upper limbs is often apparent
when walking but leg tremor is rare during
walking.
◦ Begins with start hesitation with a few rapid,
short, shuffling steps.
◦ Followed by shuffling gait with small, shallow
steps on a narrow base with freezing episodes
◦ In the long term, levodopa therapy may induce

71.  The posture of generalized flexion of the patient with
PD exaggerates the normal tendency to lean forward
when walking.
 To maintain balance when walking and avoid falling
forward, the patient may advance with a series of
rapid, small steps (festination).
 The shuffling gait of PD that is responsive to
levodopa characterizes the mid-level gait pattern.
 As the disease progresses, dysequilibrium and falls
emerge as features of a higher level gait disorder.

74. Choreic Gait:
 random movements of chorea - increased during
walking.
 The superimposition of chorea on the trunk and leg
movements gives the gait a dancing quality.
 Chorea can also interrupt the walking pattern,
leading to a hesitant gait.
 Huntington disease
◦ causes a stumbling and stuttering gait with
steps forward, backward, or to one side.
◦ Variable stance but generally wide-based
◦ Excessive swaying of trunk.
◦ Balance and equilibrium are maintained until the
terminal stages

76. Dystonic Gait:
 Produce bizzare gait pattetns.
 classic presentation of childhood-onset primary
torsion dystonia:
◦ action dystonia of a leg, with sustained abnormal
posturing of the foot (typically plantar flexion and
inversion) on attempting to run.
 In contrast, walking backward or even running
backward may be normal at an early stage.
Striatal toe:
 tonic extension of the great toe.
 Important early sign.

78.  A characteristic feature common to dystonic gaits is
excessive flexion of the hip when walking.
 Patients may hop or walk sideways in a crab-like
fashion.
 Hyperflexion of the hips and knee produce an
attitude of general body flexion in a simian
posture.
 excessive flexion of the hip and knee and plantar
flexion of the foot produce a birdlike (peacock)
gait during the swing phase of each step.
 Many patients have been thought to be hysterical

79. Dopa-responsive dystonia
◦ characteristically presents in childhood with
walking difficulties
◦ child walks normally in the early morning
◦ dystonic posturing of the legs increases as the
day progresses or after exercise.
◦ Symptoms may be relieved by a nap (“sleep
benefit”).
◦ Examination reveals dystonic plantar flexion and
inversion of the foot, with brisk tendon reflexes.
◦ Some of these patients respond dramatically to
levodopa.
◦ Indeed, all children presenting with a dystonic
foot or leg should have a therapeutic trial of
levodopa before other therapies such as
anticholinergic drugs are commenced.

80. Paroxysmal kinesogenic choreoathetosis:
◦ present with difficulty walking as the result of
dystonic postures and involuntary movements of
the legs.
◦ often appearing after standing from a seated
position.
◦ These attacks are typically brief, lasting a matter of
seconds.

81. Mixed Movement Disorders and Gait:
Athetoid cerebral palsy:
 Produce motor signs reflecting abnormalities at
many levels of the nervous system.
 These include spasticity of the legs, truncal and gait
ataxia, dystonia, and dystonic trunk and limb
spasms.
 DD - primary torsion dystonia.
 patient with cerebral palsy usually has a
◦ history of perinatal injury or birth asphyxia.
◦ history of hypotonia.
◦ delayed developmental motor milestones.
◦ presence of spasticity and ataxia.

82. Tremor of the trunk and Legs:
 Leg tremor in benign essential tremor occasionally
symptomatic.
 Trunk and leg tremor may contribute to unsteadiness in
cerebellar disease.
 Orthostatic tremor:
◦ has a unique frequency (16 Hz) and distribution.
◦ rapid tremor produces an intense sensation of
unsteadiness often with little obvious shaking of the
legs.
◦ relieved by walking or sitting down.
◦ Patients avoid standing still (e.g., in a queue) and
may shuffle on the spot in an effort to relieve the
unsteadiness.
◦ Examination reveals a rippling of the quadriceps
muscles during standing.

83. Action Myoclonus:
 Postanoxic action myoclonus of the legs is often
accompanied by negative myoclonus (asterixis)
that disrupts standing and walking.
 Repetitive action myoclonus produces jerky
movements of the legs.
 Lapses of muscle activity between the jerks
(negative myoclonus) cause the patient to sag
toward the ground.
 sequence of events gives rise to an exaggerated
bouncing appearance, which is sustainable for only
a few seconds before falling.

84.  Difficulty walking is one of the major residual
disabilities of post-anoxic myoclonus.
 Stimulus sensitive cortical reflex myoclonus
◦ similar disorder of stance and gait,
◦ reflex myoclonus of the quadriceps, resulting in a
bouncing posture.
 acute onset negative myoclonus can occur with
vascular lesions , particularly of the thalamus and
frontal lobes.

85. Higher Level Gait Disorders
 characterized by varying combinations of
◦ dysequilibrium,
◦ Falls due to impaired postural responses
◦ short shuffling steps, and freezing.
 formal neurological examination fails to reveal signs
that adequately explain the gait disturbance.
 Slowness of sequential leg movement and poor
truncal control are often present.

86.  Stepping patterns are influenced by environmental
cues that induce freezing of gait.
 Freezing or falling while performing multiple
simultaneous tasks is common.
 a variety of terms for higher level gait disorders such
as
◦ apraxia of gait,
◦ magnetic gait,
◦ lower half parkinsonism,
◦ frontal gait,

87. Hypokinetic Higher Level and Freezing Gait Patterns:
 With progression of PD,
◦ freezing of gait,
◦ disequilibrium,
◦ loss of postural responses and falls become
increasingly troublesome.
 This will poorly respond to levodopa therapy.
 DBS of ( STN / Gpi ) may improve or worsen gait with
increased falls.
 DBS in the region of the pedunculopontine nucleus is
under investigation for dysequilibrium and freezing of
gait.

88. Akinetic rigid syndromes:
 most common are MSA,PSP,CBD.
 Gait patern was similar to PD except festination is less
common.
 Another distinguishing feature is early appearance of
falls due to loss of postural and righting responses.
 Falls occur in 80% of patients with progressive
supranuclear palsy and can be dramatic, leading to
injury.
 Dramatic response to levodopa that is typical of PD
does not occur in these other akinetic rigid syndromes.

89. Gait in frontal lobe lesions:
 Varies from an ataxic gait to an akinetic-rigid gait
 Often had combination of these features.
 early stages - wide stance base with turning difficulty.
 There may be episodes of freezing.
 Arm swing is normal or even exaggerated, giving the
appearance of a “military two-step” gait.
 The normal fluidity of trunk and limb motion is lost.
 voluntary upper limb and hand movements are normal
and there is a lively facial expression.

90.  There difficulty in gait initiation [slipping clutch or
magnetic feet].
 Once walking is underway, steps may be better.
 freezing re-emerge while attempting to turn.
 Upper motor neuron signs including pseudobulbar palsy
paratonic rigidity (gegenhalten) , Frontal releasing signs
commonly occurs.
 Postural and righting reactions are impaired and
eventually lost.
 Urinary incontinence and dementia frequently occur.

91. Called as “lower half parkinsonism”
or
marche à petits pas of Dejerine
or
Critchley’s atherosclerotic
parkinsonism.
 Commonly seen in diffuse small vessel
cerebrovascular disease.
 upper motor neuron signs including pseudobulbar
palsy, and the absence of a resting tremor
distinguish this syndrome from PD.

93. syndrome of gait ignition or gait initiation failure:
◦ Also called as “pure akinesia” or “primary progressive
freezing of gait.”
◦ exhibit profound start hesitation and freezing.
◦ but step size and rhythm are normal once walking is
underway.
◦ These findings are similar to those seen with walking in
PD.
◦ but speech and upper limb function are normal
◦ there is no response to levodopa.

94.  some elderly patients experience severe walking
difficulties that resemble those described in frontal lobe
disease.
 The history is usually of gradual onset, without stroke-
like episodes.
 No identifiable lesions of the frontal lobes or in white
matter on imaging.
 The criteria for normal pressure hydrocephalus are not
fulfilled.
 there are no signs of parkinsonism and levodopa is
ineffective.
 There is no evidence of more generalized cerebral
dysfunction.
The cause of these syndromes is unknown although it is
increasingly recognized that subcortical white-matter

95. ELDERLY GAIT PATTERNS
CAUTIOUS GAITS:
 Healthy, neurologically normal
elderly people
◦ Walk at slower speeds
◦ Shorter and shallower steps
◦ Stance width slightly wider than
normal
◦ Synergistic associated arm
movements are less vigorous.
◦ The rhythmicity of stepping is
preserved.

96.  These changes give the normal elderly gait a
cautious or guarded appearance.
 Factors contributing to a general decline in mobility
of the elderly include
◦ degenerative joint disease,
◦ reducing range of limb movement,
◦ decreased cardiovascular fitness,
◦ limiting exercise capacity.

97.  A cautious gait is a normal response to the
perception of impaired or threatened balance.
 They may be unable to walk without support.
 The gait improves dramatically when support is
provided.
 Accordingly, a cautious gait should be interpreted
as compensatory and not specific for any level of
the gait classification.
 A formal program of gait retraining may help
restore confidence and improve the ability to walk.

98. RECKLESS GAIT PATTERNS:
 seen in patients with impaired postural responses and
poor truncal control.
 Patients do not recognize their instability and take risks
that result in falls and injuries.
 Such patients make inappropriate movements of the
feet and trunk when sitting or standing.
 The most striking examples occur in frontal dementia.
 impulsivity and a failure to adapt to the precarious
balance are part of the cognitive decline.

99. HYSTERICAL GAIT DISORDERS
The typical gait patterns encountered include:
1. transient fluctuations in posture while walking
2. knee buckling without falls
3. excessive slowness and hesitancy
4. 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.

100.  common features of psychogenic gait (and
movement) disorders are:
◦ Suggestibility
◦ Variability
◦ Improvement with distraction,
◦ History of sudden onset
◦ Rapid, dramatic, and complete recovery.
 Other signs like give away weakness or non
physiological sensory loss will be present.
 Hoover sign:
◦ As the patient lifts the normal leg, the examiner
places a hand under the “paralyzed” leg and
feels the presence (and strength) of synergistic
hip extension.

101. ASTASIA – ABASIA:
 Unable to either stand or walk,
 More or less normal use of their legs while in bed
 Normal neurologic examination
 When such patients are placed on their feet, they may take a
few steps and then become unable to advance their legs.
 they lurch in all directions and crumple to the floor if not
assisted
BEFORE LABELLING A HYSTERICAL GAIT, RULE OUT
1. Lesions of anterosuperior cerebellar vermis
2. NPH
3. Frontal lobe disease
4. Intoxications such as with phenytoin