Gait Disorders by Sruthi Meenaxshi

1. Gait disorders
-S.R.Sruthi Meenaxshi
MODERATOR:DR.DHIRAJ KISHORE

2. Gait
• Defined as Bipedal, biphasic , forward
propulsion of centre of gravity of the human
body, in which there are alternate sinuous
movements of different segments of body
with least expenditure of energy.
• In humans two thirds of total body weight is
centered in the upper body which makes for
inherent instabilty.

3. • The limits of stability have
been defined as an inverted
cone with the apex at the
feet and base defining
perimeter at the head .
• Sway outside of this
perimeter results in
instabilty. The dimensions
of the base of the cone are
roughly 12.5 degrees in
anteroposterior diameter
and 16 degrees laterally

4. Requirement for normal gait
 Antigravity support of the body
 Stepping
 Maintenance of equilibrium
 Propulsion

5. GAIT CYCLE
• A gait cycle consists of two
steps or one stride ‘the
activities that occur from
the point of initial contact
of one lower extremity to
the point at which the
same extremity contacts
the ground again ‘
• During one gait cycle, each
extremity passes through
two phases, a single
stance phase and a single
swing phase

6. Components of stance phase
• Stance phase comprises 60% of the gait cycle
• Heel strike – moment when the heel first strikes
the ground
• Foot flat – from heel strike to when the full foot is
in contact with the ground
• Midstance – body weight is directly over the
stance leg
• Heel off – moment the heel of the stance leg
leaves the ground
• Toe off – when only the toe of the stance leg is in
contact with the ground

8. Components of the Swing Phase
• Swing phase comprises 40% of the gait cycle
• Acceleration – the toe of the stance leg leaves the
ground and begins to swing forward
• Midswing – the swinging leg is directly beneath
the body
• Deceleration – the swinging leg continues
forward towards knee extension but is slowing
down as it travels, stopping just prior to full knee
extension and heel contact with the ground

9. SWING PHASE

12. Things to look for while observing gait
• Feet separation
• Stride length
• Foot drop
• Pelvic tilt
• Arm swing

13. ABNORMAL GAITS

14. Gait disturbances can arise from disorders of
• Frontal lobe lesions
• Sensory pathways (sensory ataxia )
• Cerebellum
• Posterior column, dorsal root ganglia, peripheral
nerves
• Extrapyramidal system
• Vestibular system

15. SENSORY ATAXIA
• Disturbances in the sensory input to the
cerebellum
• The nervous system is deprived of sensory
information primarily proprioception and joint
position sense
• Romberg sign
• Loss of tendon reflexes
• Features of peripheral neuropathy
• WIDE BASED HIGH STEPPAGE GAIT

16. • 26 year old female , presented with C/0
progressive tingling/ numbness, weakness,
Ataxia with high steppage gait. On
examination there was spastic parapersis with
extensor plantar. Sensory examination
revealed diminished touch, pressure, vibration
and proprioception.Rombergs test was
positive.

17. • 8 year old male present ed with C/o
Progressive ataxia , with weakness of limbs
and frequent falls, visual impairment with
incoordination.On examination patient had
scoliosis , spasticity , plantar was extensor ,
knee and ankle reflexes were absent with
foot deformity . Sensory examination revealed
decreased proprioception and vibration.

18. • FRIEDREICH ATAXIA
• - Autosomal Recessive
• -unstable expansion of GAA repeats Frataxin
protein iron accumulation in mitochondria 
mitochondrial injury neuronal injury
• Dorsal root ganglion : absent reflexes
• Dorsal column degeneration : dec post col senses
• Spinocerebellar tract : gait ataxia , dysrthria
• Corticospinal tract – Babinski positive
• Associated cardiomyopathy (90%) Diabetes ( 10
%) , optic atrophy , spine and foot deformity

19. • CAUSES OF SENSORY ATAXIA:
Causes-subacute combined degeneration of the
cord (vit B12 deficiency), diabetes sensory
neuropathy
tabes dorsalis, Friedreich ataxia, cervical
spondylosis , meningioma

22. Cerebellar Ataxia
• Wide based gait, clumpsy, staggering, unsteady,
lurching titubating
• The patient is unable to walk in a straight line , tandem
walking is impaired
• With hemispheric lesion the patient will stagger and
deviates towards the involved side
• With lesion of cerebellar vermis,the patient will exhibit
a lurching, staggering gait, but without laterality
• Cerebellar ataxia is present with both eyes open and
closed( romberg negative)

24. Approach to patient with cerebellar
ataxia

25. PROGRESSION
• Progessive
• Static
• Intermittent symptoms
• Reversible Ataxia

26. • STATIC ATAXIAS : Vascular causes
• REVERSIBLE ATAXIA :
• infectious causes – post viral
• thyroid
• drugs / toxins
- INTERMITTENT ATAXIA
- Episodic Ataxia ( inherited Etiology)

27. FOCAL/SYMMETRIC ATAXIA
• Cerebellar symptoms on same side of lesionor
bilateral symptoms
• FOCAL ATAXIAS: vascular causes , multiple
sclerosis, cerebellar abscess, cerebellar
glioma, PML , HIV, congenital causes
• SYMMETRICAL ATAXIA :
-intoxication , nutritional, Post
infectious,Hypothyroid, Autoimmune causes

29. ACQUIRED ATAXIA
• First rule out structural causes ( MRI/ CT
HEAD )
• CV J anomalies
• Posterior fossa tumours
• Demyelinating diseases
• Hypoxic encephalopathies
• Vascular causes – infarct, hemorhage

30. TOXINS
• Cancer chemotherapeutics -5 FU, Cytarabine
• Metals : bismuth , Mercury (Ataxia,
paresthesia, restricted visual defects, LEAD (
anemia , ataxia, foot drop, wrist drop,
basophilic stippling )
• Solvents : paint thinner , toluene cognitive
defects plus pyramidal tract signs )
• Anticonvulsants –phenytoin (purkinje cell loss
)avoid in epileptics with ataxia

31. Infections
• VZV
• HSV
• EBV
• Bickerstaffs encephalitis (brain stem : post
infectious / external ophthalmoplegia/lower limb
areflexia , extensor plantar, ataxia , drowsiness
• HIV ( lymphoma , PML, Toxoplasmosis )
• CJD ( 17 % classic CJD , Ataxic variant of CJD)
• Syphilis
• Whipple disease

32. • 54 year old male recently diagnosed diabetic and hypertensive came with
complaints of acute onset dhe noticed progressively He gradually developed
progressive truncal ataxia with ataxic dysarthria and intentional tremor, rapidly
worsening over a period of 2 weeks.on examination . Prominent ataxic dysarthria,
dysmetria of upper limbs more than lower limb, dysdiadochokinesia and
intentional tremors were observed. No cranial neuropathy . Upper and lower limb
power was 5/5, with brisk tendon reflexes, hypotonia in the upper limbs and mild
spasticity in the lower limbs.No chronic medication intake.
• On MRI inital3 weeks of illness was normal. All hematological and biochemical
parameters were within normal limits. ANA, Anti DSDNA, APLA, Canca, Panca, CSF
analysis were within normal. CSF electrophoresis was negative for oligoclonal
bands and malignant cells. CSF Cr Ag, PCR-TB, HSV I and II and arbovirus were
negative. A 4cm lympnode was palpable over the axilla. Lymphnode biopsy
revealed hogkins lymphoma . Anti TR anti body was performed was found to be
positive. Mri was repeated showed hyperintensites in bilateral cerebellar
hemisphere.
• Patient was treated with 6 cycles of chemotherapy. Treatment options are limited
and are largely dependent on treating the underlying malignancy to lower
antibody titers. Other therapeutic interventions such as intravenous
immunoglobulins, plasmapheresis and immunosuppressive therapy

33. Case of acute paraneoplastic
pancerebellitis

34. AUTOIMMUNE CAUSES
• Paraneoplastic Syndromes
- Anti HU abs – small cell cancer lung (
extrapyramidal signs)
- Anti YO Abs – ovarian cancer
- Anti Ri abs – breast cancer
- Anti Tr Antibody – hodgkins lymphoma

35. • 60 year old man presented with
incoordination of movements with tremor ,
with wide based staggering gait , nystagmus
and scanning speech. He gives a history than
his 32 year old son has similar complaints. On
examination power is normal, Tone is
spastic,knee and ankle reflex was absent
plantar was extensor. Dymmetria,
dysdiadakinesis , pendular knee jerk was
present. MRI showed diffuse cerebellar
atrophy

36. Spinocerebellar Ataxia
• Autosomal dominant
• SCA 1-36 types , SCA1,2,3,7,17 due to CAG
triplet repeat expansion codes for glutamine
Protiens termed as ATAXINS- more than -40
glutamines potentially toxic for the neurons –
leads to neuronal loss and gliosis SCA 8- CTG
repeat,SCA 10 forms pentanucleotide repeats
• Anticipation ( earlier age on onset and
aggressive course in successive generation )

37. • SCA 1 middle life progressive cerebellar ataxia
,scanning sppech, nystagmus , dysarthria mild
spascity , parkinsonian tremor , knee and
ankle reflexes are lost. Extensor plantar
response. Urinary and Fecal incontinence.
Variable loss of purkinje cells. Gross atrophy of
cerebellum
• SCA2- onset 2-65 years , ataxia , dysarthria,
parkinsonian rigidity, optic atrophy and retinal
degeneration
• Most common in India

38. • MachadoJoseph disease (SCA3)
• Type 1 (amyotrophic lateral sclerosis-parkinsonism-
dystonic type)
- Weakness , spasticity, broad based lurching gait, ankle and
patellar clonus. Extensor plantar.ophthalmoparesis and
ocular prominence is early manifestion.
- There is no truncal titubation
- Prominence of horizontal and vertical nystagmus
- Loss of fast saccadic movements of eye
- Facial fasciculation,facial myokymia, lingual fasciculation
without atrophy

39. - Type 2 MC ( ataxia type)
- 2 nd and 3 rd decade with corticospinal and
extrapyramidal symptoms
- Dysarthria,cerebellar defects,opthalomoparesis, facial
myokymia, facial fasciculation ,spasticty is present
- Type 3 MJD ( Ataxia- Amyotrophic type )
- Mean age on onset 25 years
- Pancerbellar (dysarthria/ gait distubance)
- Distal sensory loss with features of peripheral neuropathy
(loss of deep tendon reflexes )
- No extrapyramidal or corticospinal involvement

40. • SCA 6:
• Late onset AD ataxia
• Loss of vibration and proprioception
• Familial hemiplegic migraine
• Cerebellar atrophy
• SCA7:
• Presence of retinal pigment degeneration

41. • 55 year old male hypertensive and Diabetic
came with C/O weakness of right upperlimb
and lowerlimb. On examination BP was
240/110 mm hg there was hypertonia ,
spasticity , plantar on right was extensor and
left was flexor. CT head was revealed
hemorrhage involving the internal capsule.
• GAIT ? Circumduction / Spastic gait

42. Spastic gait
• Spastic gait/ hemiparetic gait
is caused by lesion
interrupting the corticospinal
pathway.
• Usually arms are
flexed,adducted and internally
rotated and legs extended.
• Patient drags the foot and
scrapes the toes.

44. Spastic-ataxic gait
• Features of both spasticity and ataxia,it usually results in a
spastic-ataxic gait.
• ‘jiggling’ or ‘bobing’ with tremulous,bouncing up and
down body movements.
• Causes-vit-B12 deficiency, multiple sclerosis,
HTLV/TSP, HIV associated vacuolar myelopathy,
Copper deficiency

45. Parkinsonian gait
• The gait is slow,stiff and
shuffling.as if patient is
trying to catch his own
centre of gravity
• Usually patient is
stooped,with head and
neck forward and knee
flexed;the upper extrimities
are flexed at the shoulders
elbow and wrist.
• Cog wheel rigidity
• Arm swing is decreased

46. • 60 year old male presented with gait disturbance in
the short shuffling festinant gait , bradykinesia ,
pillrolling tremors with rigidity. Patient was diagnosed
with parkinsons was started on levodopa with no
benefit .six months later he c/o about gait disturbance
with a feeling of right leg dragging with postural
imbalance, and difficulties in swallowing and
articulation.Toxic screen , gene testing for SCA was
negative. Patient cognitive function gradually
detetoriated.MRI revealed atrophy of cerebellum,
pons and middle cerebellar peduncle .(Positron
emission tomography (PET) was performed using 18F-
fluorodeoxyglucose (FDG), and showed decreased
cerebral glucose metabolism on the bilateral basal
ganglia, cerebellum, both parietal lobes, and left
posterior cingulate gyrus .

47. Multisystem atropy

48. Multisystem atrophy
• Sporadic neurodegenerative disorder
• Pathology : cell loss , gliosis, glial cytoplasmic
inclusions( alpha synnuclein) in several CNS
structures
• Mutation of COQ2 gene
• Affects both men and women
• Main features : autonomic failure
,parkinsonism(80 % MSA P), cerebellar ataxia
(MSA c type)

49. Consensus statement for clinical
diagnosis of MSA
• Autonomic and urinary dysfuntion
1)Orthostatic hypotension (reduction in atleast 30
mmhg systolic bp or atleast 15 mm hg of
reduction of diastolic pressure after 3min of
standing )
2) Urinary incontinence (persistant, involuntary
partial or total bladder emptying , accompanied
by erectile dysfunction or both )

50. • MSA P associated Parkinsonism :
• Progressive akinesia and rigidity
• Jerky postural tremor and resting tremor
• Orofacial or craniocervical dystonia associated
with high pitched dysarthria
• Postural instability early in disease with
frequent falls

51. • MSA – C:
• Gait ataxia
• Limb kinetic ataxia
• Scanning dysarthria
• Cerbellar and oculomotor disturbances

52. Disease progression
• Parkinsonism poorly responds to levodopa
• Cerebellar ataxia
• Early instablity and falls occur within 3 years
of disease onset
• Rapid progression of the disease ( wheelchair
bound despite dopaminergic treatment within
5 years of disease onset )

53. • 60 year old male presented with H/o
asymmetrical onset involuntary jerky
movements, bradykinesia , forgetfulness,
difficulty in swallowing, articulation.On
examination muscle bulk was normal with no
fasciculation .Tone of all limbs were increased
(R>L) with marked axial rigidity.Reflexes were
brisk with Right sided plantar flexor and left
equivocal.sensory examination was normal.
Patient had a stooped posture with short
shuffling gait. Patient was started on levodopa
but with no benefit . Patient developed repetitive
contraction of muscle with feeling of arm and
legs disconnected body.MRI was done revealed
atrophy of fronto temporal region.

55. Case of corticobasal degeneration

56. Frontal gait disorder
• Also called gait apraxia where
there is loss of ability to use
legs properly in walking w/o
demonstrable sensory
impairment, weakness, or
incoordination.
• Usually occurs in frontal lobe
lesion ,NPH, Binswanger
disease, Pick’s disease.
• It is characterized by slightly
flexed posture, short,
shuffling steps and an
inability to integrate and
coordinate lower extremity
movement to accomplish
normal ambulation.

57. Normal pressure Hydrocephalus

58. • 76 year old female came with C/O
forgetfullness , difficulty in remembering
names , decreased fluency had trouble in
performing learned motor skills with difficulty
in initiating gait (GAIT APRAXIA) On
examination there was decline in memory and
orientation with no sensory or motor
weakness.MRI and CT scan showing
predominant cortical and hippocampal
atrophy.

59. ALZHEIMER DISEASE
• RISK Factors : Old age / female sex / low level
of education / diabetes
• Mutations in gene encoding presinilin1 and
presinilin 2
• Characterised by memory impairment –
difficulty in naming , Aphasia is early and
prominent feature .
• Normal results on lab
• MRI shows predominant hippocampal atrophy

60. Steppage gait
Weakness of dorsiflexor- Tibialis anterior ,
The steps are regular and even, but the advancing foot
hangs with the toes pointing toward the ground.
high steppage gait in order to help the foot clear the
floor and avoid tripping.
Double tap
Causes: u/l foot drop - peroneal nerve palsy,
L5 radiculopathy.
polio, Multiple Sclerosis , GBS, Spinal disc
herniation
peroneal muscle atrophy, Peroneal nerve injury
polyneuropathy

61. Waddling /Trendelenburg gait
• During stance phase of gait cycle centre of
gravity is tranferred to the stance leg .
• Hip abducters stabilizes the pelvis.
• Abducter weakness of the stance leg causes
downward tilt of opposite pelvis to reduce
the load by deceasing the lever arm
• The patient walks with a broad base,with an
exaggerated rotation of pelvis that results in
a waddling gait.
. Causes-proximal muscle weakness, cushings
,polymyositis dermatomyosiitis
,LGMD,CDH, MND