Gait Abnormalities – Assessment and Causes

geekymedics.com/gait-abnormalities/

Sunil Aggarwal July 1,

2018

Normal Gait Cycle

The normal gait cycle is divided into two phases (swing and stance phase). Each limb will
alternate between these two phases.

Stance phase
Limb with the foot on the ground
Starts with “heel strike” (heel comes into contact with the floor); ends with toe-off
Hip abductors of the limb in stance phase contract to stabilise the pelvic girdle and
prevent the pelvis dropping on the contralateral side (failure to do so causes a
waddling gait)

Swing phase
Limb with the foot not touching the ground
Starts with toe-off, when foot plantar flexes to push the foot off the ground
Knee and hip flex to draw the limb forward
Foot dorsiflexes immediately after toe-off so the foot clears the floor and does not
drag (failure to do so leads to a foot drop and a high stepping gait)

Hemiplegic Gait

Gait
Asymmetrical gait; one limb is normal while the affected limb is stiff (spastic)

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 Affected limb held in extension (knee extension and foot plantar flexion) with feet
inverted
Toes on the affected side may drag on the floor due to fixed ankle plantar flexion
and knee extension lengthening the leg
Affected leg swings around (i.e. circumducts) during the swing phase to prevent the
feet from dragging

Associated clinical features

Other signs of upper motor neuron pyramidal weakness are typically

found on the affected side (upper and lower limb):
Increased tone with clasp-knife spasticity
Hyperreflexia with or without clonus
Upgoing plantars (i.e. positive Babinski)
Reduced power
The upper limb may have flexor posturing of elbows and wrist with shoulders and
fingers in adduction

NB: If upper motor neuron signs are present in the upper limb, the site of the lesion
must be at or above the level of the cervical spine.

Other features
Sensory deficit – the pattern of sensory loss is important to give clues to the cause
(see differential diagnosis)
Surgical scars on the spine or head

Differential diagnosis
Caused by a unilateral upper motor neuron lesion.

Unilateral brain lesion on the contralateral side of the affected limb (most
likely cause)
Ischaemic/haemorrhagic stroke
Brain tumour
Trauma
Demyelination (e.g. multiple sclerosis)
Space-occupying lesion

Hemisection of the spinal cord (Brown-Sequard syndrome) on the

ipsilateral side of the affected limb (rarer):
Prolapsed intervertebral disc
Spinal spondylosis
Spinal tumour
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 Demyelination
Spinal infarct

Key points
Hemisection of the spinal cord causes ipsilateral loss of proprioception and
vibration sensation and contralateral loss of pain and temperature sensation
Complete transection of the spinal cord would normally cause a diplegic gait
Spinal cord lesions usually cause impairment in sensation, whereas brain lesions
may leave sensation intact

Diplegic Gait (a.k.a. Scissoring Gait)

Gait
Findings are similar to hemiplegic gait but bilateral in nature
Limbs are stiff and held in extension with feet inverted and internally rotated
Hips are drawn together due to excessive adductor tone
Legs are forced together due to spasticity which results in leg overlap when
walking
Circumduction of both legs during the swing phase
Symmetrical movement of the lower limb

Associated clinical features

Other signs of an upper motor neuron pyramidal deficit on the affected

side (upper and lower limb):
Increased tone with clasp-knife spasticity
Reduced power
Hyperreflexia with or without clonus
Upgoing plantars (positive Babinski)
The upper limb may have flexor posturing of elbows and wrist with shoulders and
fingers in adduction

NB: If upper motor neuron signs are present in the upper limb, the site of the lesion
must be at or above the level of the cervical spine

Other clinical features:

Sensory deficit – if a diplegic gait is caused by spinal cord pathology, the ‘sensory
level’ (ie. the lowest dermatome level with normal sensation) correlates with the
level of spinal cord pathology
A urinary catheter may be in situ if nerves supplying lumbosacral plexus are
involved
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 Surgical scars on back or head
If lower motor neuron signs are present (e.g. wasting or fasciculations) consider
motor neuron disease

Differential diagnosis
Similar causes as hemiplegic gait but with complete transection of the spinal cord and/or
bilateral brain involvement.

Spinal cord lesion (sensation usually affected)

Prolapsed intervertebral disc
Spinal spondylosis
Spinal tumour
Transverse myelitis
Spinal infarct
Syringomyelia
Hereditary spastic paraparesis

Bilateral brain lesion

Cerebral palsy
Multiple sclerosis
Bilateral brain infarcts
Midline tumour (e.g. paraspinal meningioma)

Motor neuron disease

Associated with lower motor neuron findings

NB: Quadriplegia – a term used to describe upper motor neuron weakness found in all
four limbs.

Parkinsonian Gait (a.k.a. Festinant Gait)

Gait
‘Festinant gait’ – short-stepping, shuffling
Minimal arm swing (an early feature of a Parkinsonian gait)
Difficulty/hesitancy when asked to start, turn around and stop walking
Difficulty initiating new movements
Stooped posture
Hypomimia (expressionless face)
Hypokinetic gait

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NB: hypomimia and reduced arm swing may be early features of Parkinson’s before the
development of the characteristic short-shuffling gait.

Associated clinical features

Idiopathic Parkinson’s disease classically presents with a triad of:

Tremor
Rigidity
Bradykinesia

There may be other associated features including:

Cogwheel rigidity
Asymmetrical tremor (typically pin-rolling)
Bradykinesia
Difficulty getting up from a seated position

Differential diagnosis
Features of the Parkinsonian gait are observed in both idiopathic Parkinson’s
disease and other Parkinsonian disorders.
Idiopathic Parkinson’s disease usually has most features of the gait described
above and the classic triad of tremor, rigidity and bradykinesia.
Other Parkinsonian disorders may only have a few of the gait features, may not
have all features of the triad, and may be associated with other findings.

Examples of disorders with Parkinsonian features include:

Vascular Parkinson’s disease
Dementia with Lewy bodies
Parkinson’s plus syndromes
Multisystem atrophy – associated with autonomic and cerebellar signs
Progressive supranuclear palsy – associated with vertical gaze palsies
Drug-induced (dopamine antagonists)
Antipsychotics
Antiemetics
Dementia pugilistica

Ataxic Gait

Gait
Broad-based

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 Unsteady
Foot stamping
May require support with a walking frame
If unilateral cerebellar lesion present, the patient may veer towards the side of the
lesion
Heel-toe walking may help elicit ataxia if gait initially appears normal

Associated clinical features

Ataxic gait implies either cerebellar, vestibular or sensory impairment.
If cerebellar disease is the cause, other signs of cerebellar disease may be present.
If the cerebellar lesion is unilateral then the signs are present on the same side of
the lesion.

Cerebellar ataxia
Nystagmus (on the affected side of the lesion if unilateral cerebellar lesion)
Ataxic dysarthria
Dysmetria (i.e. past-pointing or under-shooting)
Intentional tremor (on the affected side of the lesion if unilateral cerebellar lesion)
Dysdiadokokinesia (on the affected side of the lesion if unilateral cerebellar lesion)

Sensory ataxia
Sensory neuropathy gives the appearance of an ataxic gait due to impaired limb
sensation
Signs include:
Positive Romberg’s sign
Impaired proprioception (joint position sense)
Impaired vibration sense
The absence of other cerebellar signs (e.g. dysmetria, nystagmus, dysarthria etc)

Vestibular ataxia
Vestibular disturbance can give a gait similar to an ataxic gait
Associated with vertigo, nausea and vomiting

Differential diagnosis

Unilateral cerebellar disease (unilateral cerebellar findings):

Ischaemic (posterior circulation infarct) or haemorrhagic stroke – vascular events
produce hyperacute symptoms
Space-occupying lesion

Bilateral cerebellar disease (giving bilateral cerebellar findings):

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 Multiple sclerosis
Alcoholism
B12 deficiency
Drugs:
Phenytoin
Carbamazepine
Barbiturates
Lithium
Genetic:
Frederich’s Ataxia
Spinocerebellar ataxia
Ataxic telangiectasia
Paraneoplastic disease
Multi-systems atrophy – associated with Parkinsonian and autonomic features

Neuropathic Gait (a.k.a. High Steppage Gait)

Caused by a motor weakness of the nerves supplying the ankle dorsiflexor muscle
(tibialis anterior).

Gait
Foot drop- there is a weakness of dorsiflexion, so the foot drops and toes drag
during the swing phase
To prevent the toes from dragging on the floor, the knee and hip flexes excessively,
thereby creating a “high stepping” gait
Feet stamp on the floor

Associated clinical features

Ankle-foot orthoses:
Aid to keep ankle fixed in dorsiflexion

Unilateral foot drop with sensory impairment:

Common peroneal nerve disease- usually with a sensory loss on the dorsum of the
foot and lateral calf
L5 nerve route disease- usually with sensory loss in the distribution of the L5
dermatome

Bilateral distal muscle weakness with foot drop:

Seen in peripheral neuropathies or motor neurone disease

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 The appearance of pes cavus and “inverted champagne bottle calf” are features of
hereditary motor and sensory neuropathies

Reflexes:
Reduced or absent in peripheral neuropathies
Brisk with upgoing plantars and fasciculations (a mixture of upper and lower motor
neurone signs) in motor neurone disease

Differential diagnosis
Foot drop implies weakness of the muscles of ankle dorsiflexion (tibialis anterior)
supplied by the common peroneal nerve (L4, L5 and S1 nerve root).

This is due to either:

Isolated common peroneal nerve palsy

L5 radiculopathy (weakened foot inversion)

OR

Part of generalized polyneuropathy involving multiple nerves

NB: Unilateral foot drop with no other muscles or nerves involved suggests an isolated
neuropathy- common peroneal palsy or L5 radiculopathy, and not a polyneuropathy.
Common peroneal nerve palsy or L5 radiculopathy is usually unilateral, but can be
bilateral.

Common peroneal nerve palsy (preserved foot inversion):

Trauma or compression – especially as the nerve passes around the head of the
fibula (e.g. head of fibular fracture or plaster cast)

Bilateral foot drop

A bilateral foot drop with other neurological features (muscle wasting, reduced reflexes,
impaired sensation in a distribution outside common peroneal nerve/L5 dermatome,
and weakness in muscles other than ankle dorsiflexors) is seen in more diffuse disease:

Polyneuropathies:
Diabetic neuropathy
Hereditary motor and sensory neuropathies (Charcot-Marie Tooth disease is
a type of hereditary motor and sensory neuropathy)
Vasculitis
Guillain-Barré syndrome

Motor neurone disease:

Associated with upper and lower motor neurone findings
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Sensory Gait (a.k.a. stomping gait)
Caused by sensory impairment.

Gait
Caused by peripheral sensory nerve impairment
The patient cannot sense where the foot is (i.e. impaired proprioception), nor when
the foot hits the ground. To compensate the patient slams their foot on the ground
in order to sense when the foot has hit the ground.
Gait may also appear ataxic with sensory impairment (sensory ataxia)

Associated clinical features

Romberg’s test positive:
Balance is maintained by vestibular input, visual input and proprioception
(joint position sense). We need two out of three to be intact in order to
maintain balance. In a healthy person when visual input stops (closed eyes),
we rely on vestibular and proprioception (two inputs) to maintain balance.
In a patient with peripheral sensory impairment (proprioception impaired),
when the eyes are closed (visual input removed), they only have their
vestibular input to maintain balance. One input is not enough and so the
patient becomes unsteady.

Stomping is exacerbated in the dark

Impaired sensation to the feet must be present in order to confirm the diagnosis
Usually due to diseases affecting the spinal dorsal columns (dorsal column disease
causes impaired proprioception and vibration sense)

Other features of peripheral neuropathy may be present:

Diminished ankle reflexes
Peripheral motor weakness (causing a neuropathic gait with foot drop)

Features of subacute degeneration of the cord may be seen in B12

deficiency:
Diminished proprioception and vibration sense with absent ankle reflexes
Exaggerated knee reflex
Upgoing (positive) Babinski reflex

Differential diagnosis

Dorsal column disease:

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 B12 deficiency
Tabes dorsalis (syphilis)

Peripheral nerve disease:

Diabetes
Vasculitis
B12 deficiency
Hereditary motor and sensory neuropathies (e.g. Charcot-Marie Tooth Disease)
Guillain-Barré syndrome
Post-infection

Myopathic Gait (a.k.a. Waddling Gait or Trendelenburg Gait)

Gait
Hip abductors are weak so they are unable to contract and stabilize the pelvis during the
stance phase. Therefore, the pelvis tilts down (instead of staying horizontal) towards the
leg in swing phase.

The body compensates to prevent the swinging foot from dragging by:

Laterally flexing the torso away from the leg in swing phase- this draws the pelvis
and leg up off the floor, and gives the characteristic ‘waddling’ appearance
Circumducting the leg

Associated clinical features

Trendelenburg’s sign positive:

When the patient stands on one leg, the pelvis drops towards the contralateral
side

Signs of proximal myopathy:

Difficulty standing from a seated position without using arms
Difficulty standing from a squat or sitting up from a lying position

Differential diagnosis

Systemic disease
Hyperthyroidism
Hypothyroidism
Cushing’s syndrome
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 Acromegaly
Polymyalgia rheumatica
Polymyositis
Dermatomyositis

Muscular dystrophies
Duchenne’s muscular dystrophy
Becker’s muscular dystrophy
Myotonic dystrophy

Choreiform Gait (a.k.a. Hyperkinetic Gait)

Gait
Normal gait with involuntary choreic movements present throughout the body such as:

Oro-facial dyskinesia (grimacing or lip-smacking)

Choreic movements of the upper and lower limbs (writhing, dance like semi-
purposeful movements)

Involuntary movements are usually present at rest. However, walking can accentuate
these movements.

Differential diagnosis

Basal ganglia disease:

Huntington’s disease
Sydenham’s chorea
Cerebral palsy (choreiform type)
Wilson’s disease
Dopaminergic medications (e.g. Parkinson’s medications)

Antalgic Gait (a.k.a. Painful Gait)

Gait
Gait may appear painful.
Shortened length of time in the stance phase on the affected leg.

Differential diagnosis

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Any cause of pain in the lower limb such as:
Osteoarthritis
Inflammatory joint disease
Lower limb fracture
Nerve entrapment (e.g. sciatica)

Editor

Andrew Gowland

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