Normal gait cycle

The gait cycle has six phases:

Heel-strike: initial contact of the heel with the floor.
Foot flat: weight is transferred onto this leg.
Mid-stance: the weight is aligned and balanced on this leg.
Heel-off: the heel lifts off the floor as the foot rises but the toes remain in contact with the
floor.
Toe-off: as the foot continues to rise the toes lift off the floor.
Swing: the foot swings forward and comes back into contact with the floor with a heel
strike(and the gait cycle repeats).

Assess gait:

Patients with neurological disease are often at an increased risk of falls so make sure
to remain close to the patient during the assessment so that you are able to intervene if
required.

Ask the patient to walk to the end of the examination room and
then turn and walk back whilst you observe their gait paying attention to:

 Stance: a broad-based ataxic gait is typically associated with midline cerebellar

pathology (e.g. a lesion in multiple sclerosis or degeneration of the cerebellar
vermis secondary to chronic alcohol excess).
 Stability: a staggering, slow and unsteady gait is typical of cerebellar
pathology. In unilateral cerebellar disease, patients will veer towards the side
of the lesion.
 Arm swing: often absent or reduced in Parkinson’s disease (typically unilateral
initially).
 Steps: small, shuffling steps are characteristic of Parkinson’s disease. High-
stepping may indicate the presence of foot drop.
 Turning: patients with cerebellar disease will find the turning manoeuvre
particularly difficult.
Tandem (‘heel-to-toe’) gait

Ask the patient to walk to the end of the examination room and back with
their heels to their toes (known as ‘tandem gait’). Heel-to-toe walking exacerbates
underlying unsteadiness making it easier to identify more subtle ataxia.

Tandem gait is particularly sensitive at identifying dysfunction of

the cerebellar vermis (e.g. alcohol-induced cerebellar degeneration). Difficulties with
heel-to-toe walking may also suggest weakness of the flexors muscles of the leg or
sensory ataxia.

Gait abnormalities

 Ataxic gait: broad-based, unsteady and associated with either cerebellar pathology or
sensory ataxia (e.g. vestibular or proprioceptive dysfunction). In the context of
proprioceptive sensory ataxia, patients typically watch their feet intently to compensate
for the proprioceptive loss. If a cerebellar lesion is present the patient may veer to the
side of the lesion.
 Parkinsonian gait: small, shuffling steps, stooped posture and reduced arm swing
(initially unilateral). The patient will require several small steps to turn around. The
gait appears rushed (festinating) and may get stuck (freeze). Hand tremor may also be
noticeable.
 High-stepping gait: can be unilateral or bilateral and is typically caused by foot drop
(weakness of ankle dorsiflexion). The patient also won’t be able to walk on their
heel(s).
 Waddling gait: shoulders sway from side to side, legs lifted off ground with the aid of
tilting the trunk. Waddling gait is commonly caused by proximal lower limb weakness
(e.g. myopathy).
 Hemiparetic gait: one leg held stiffly and swings round in an arc with each stride
(circumduction). This type of gait is commonly associated with individuals who have
had a stroke.
 Spastic paraparesis: similar to hemiparetic gait but bilateral, with both legs stiff and
circumducting. The patient’s feet may be inverted and “scissor”. This type of gait is
typically associated with hereditary spastic paraplegia.

Hemiplegic gait
- A hemiplegic gait is typically caused by a lesion in the central nervous system (e.g. stroke)
which results in unilateral weakness and spasticity. [they’re weak on one side of body]
- Patients with hemiplegia exhibit spastic flexion of the upper limb and extension of the
lower limb. [arm fixed bent and stiff]
- Due to the extension of the lower limb (fixed ankle plantar flexion and knee extension), the
leg is elongated meaning patients have to circumduction their leg to prevent their foot from
dragging on the ground. [leg is straight – looks longer and has to swing it around]
- Clinical features which may be associated with a hemiplegic gait include: [upper motor
neuron signs]
o Increased tone with clasp-knife spasticity
o Hyperreflexia with or without clonus
o Upgoing plantars (i.e. positive Babinski)
o Reduced power
o Sensory deficit: the pattern of sensory loss depends on the site of the lesion in the nervous
system

Causes

Unilateral cerebral lesion: Hemi section of the spinal cord:

Stroke Trauma
Space-occupying lesion
Trauma
Multiple sclerosis
 Diplegic gait => SPASTIC GAIT
As for hemi but both sides
- A diplegic gait (a.k.a scissoring gait) may be caused by a lesion in the central nervous system
(e.g. stroke, or complete transection of the spinal cord).
Clinical findings are similar to those in hemiplegic gait but are bilateral in nature.
- Spasticity is typically worse in the lower limbs compared to the upper
limbs.
 Stiff and resist movement make walking difficult
- The hips and knees are flexed and adducted whilst the ankles are
extended and internally rotated.
- The knees are forced together due to spasticity in the adductor muscles
resulting in leg overlap when walking (a.k.a. scissoring).
- In an attempt to overcome this adduction, the patient circumducts both
legs during the swing phase.
- The upper limb may have flexor posturing of the elbows and wrist with shoulders and
fingers in adduction (known as ‘low guard’ or ‘mid-guard’ position). They also typically lack
the swinging movements present in a normal gait.

Clinical features which may be associated with a diplegic gait include:

o Increased tone with clasp-knife spasticity
o Hyperreflexia with or without clonus
o Upgoing plantars (i.e. positive Babinski)
o Reduced power
o Sensory deficit – if a diplegic gait is caused by spinal cord pathology, the ‘sensory level’
(I.e. The lowest dermatome level with normal sensation) correlates with the level of
spinal cord pathology
o Wasting and fasciculations (consider motor neuron disease)

Bilateral brain lesion:
Cerebral palsy
Multiple sclerosis
Bilateral brain infarcts
Midline tumour (e.g. paraspinal
meningioma)
Spinal cord lesion (sensation usually Motor neuron disease:
affected):
Prolapsed intervertebral disc associated with lower motor
Spinal tumour neuron findings
Transverse myelitis
Spinal infarct
Syringomyelia
Hereditary spastic paraparesis
Parkinsonian gait
- A Parkinsonian gait (a.k.a. festinant gait) is caused by rigidity and bradykinesia as a result
of the lossof dopaminergic neurons in the basal ganglia.
Features of a Parkinsonian gait include:
- Initiation: typically slow to start walking due to failure of gait ignition and hesitancy.
- Step length: reduced stride length with short steps is common (shuffling gait). Each step may
getprogressively smaller as the patient attempts to retain balance (known as festinant gait).
- Arm swing: reduced arm swing on one or both sides (often an early feature of Parkinson’s
disease).
- Posture: flexed trunk and neck causing a stooped appearance.
- Tremor: resting tremor can be observed when the patient is distracted by walking.
- Turning: impaired balance on turning or hesitancy is common due to postural instability.

Clinical features which may be associated with a Parkinsonian gait include:

o Tremor
o Rigidity
o Bradykinesia
o Hypomimia

Causes
Features of the Parkinsonian gait are observed in both idiopathic Parkinson’s disease and
otherParkinsonian disorders.
Idiopathic Parkinson’s disease usually has most features of the gait described above and the
classictriad of tremor, rigidity and bradykinesia.
Other Parkinsonian disorders may only have a few of the gait features, may not have all features
of thetriad, 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 (e.g. multisystem atrophy and progressive supranuclear palsy)
Drug-induced Parkinsonism (e.g. antipsychotics, antiemetics)
Dementia pugilistica
 Ataxic gait = unsteady, clumsy
An ataxic gait is typically broad-based and associated with [damage to the things that help us
keep co-ordination]
1. midline cerebellar disease (e.g. alcoholic cerebellar degeneration) [cerebellum at base of
brain co ords balance, so damage here disrupts co ord]
2. vestibular disease (e.g. labyrinthitis) [vestibular system, maintains balance and spatial
orientation – in the inner ear]
3. loss of proprioception (known as sensory ataxia). [proprioception is the body's ability to
sense its position and movement in space. Lost due to peripheral neuropathy or damage to
dorsal column in spinal cord. Poor sensory feedback means they have difficulty co ord
movements]
Features of an ataxic gait include:
1. Stance: a broad-based ataxic gait is typically associated with midline cerebellar
pathology (e.g., a lesion in multiple sclerosis or degeneration of the cerebellar vermis
secondary to chronic alcohol excess).
2. Stability: a staggering, slow and unsteady gait is typical of cerebellar pathology. In
unilateral cerebellar disease, patients will veer towards the side of the lesion.
3. Turning: patients with cerebellar disease will find the turning manoeuvre particularly
difficult.

CAUSES
CEREBELLAR SENSORY VESTIBULAR
o Cerebellar stroke (ischaemic or Peripheral neuropathy (e.g. diabetes o Labyrinthitis
haemorrhagic) mellitus) o Meniere’s disease
o Space-occupying lesion o Acoustic neuroma
o Multiple sclerosis
o Alcoholism
o B12 deficiency
o Drugs (e.g. phenytoin, carbamazepine,
barbiturates, lithium)
o Genetic disease (e.g. Frederich’s
ataxia, spinocerebellar ataxia)
o Paraneoplastic disease

Clinical features

Nystagmus Positive Romberg’s sign Vertigo

Ataxic dysarthria Impaired proprioception Nausea
Dysmetria Impaired vibration sensation Vomiting
Intention tremor Absence of other cerebellar signs
Dysdiadokokinesia (e.g. dysmetria, nystagmus,
dysarthria)
Neuropathic gait
 Neuropathic gait (a.k.a. high-steppage gait) is caused by weakness of the muscles in the
distal limb (typically the dorsiflexors of the foot) as a result of damage to the peripheral
nerves providing motor innervation.
- Weakness of the dorsiflexors of the foot results in foot drop and dragging of the toes during
the swing phase of the gait cycle.
- To prevent the toes from dragging on the floor, the knee and hip flex excessively, thereby
creating a “high stepping” gait.

Clinical features which may be associated with a neuropathic gait include:

Peripheral vascular disease
Peripheral sensory impairment
Distal muscle weakness
Reduced or absent reflexes

Causes
Foot drop is caused by weakness of the muscles of ankle dorsiflexion (tibialis anterior)
supplied by the common peroneal nerve (L4, L5 and S1 nerve root).
Foot drop may therefore be caused by:
o Isolated common peroneal nerve palsy (e.g., secondary to trauma or compression)
o L5 radiculopathy (e.g., disc prolapse)
o Generalized polyneuropathy involving multiple nerves (e.g., diabetic neuropathy, motor
neurone disease, Charcot-Marie Tooth disease)
Myopathic gait
A myopathic gait (a.k.a. waddling gait or Trendelenburg gait) occurs due to weakness of the hip
abductors resulting in a waddling appearance.
Hip abductor weakness results in an inability to stabilize the pelvis during the stance phase. As a
result, the pelvis tilts downwards towards the unsupported side during the swing phase of the
gait cycle.6/7
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 (causing the characteristic ‘waddling’ appearance)
Circumduction the leg

Associated clinical features

Clinical features which may be associated with a myopathic gait include:
Difficulty standing from a seated position without the use of the arms
Difficulty standing from a squat or sitting up from a lying position
Positive Trendelenburg’s sign; when the patient stands on one leg, the pelvis drops towards the
contralateral side

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

Muscular dystrophies:
Duchenne’s muscular dystrophy
Becker’s muscular dystrophy
Myotonic dystrophy
Choreiform gait
A choreiform gait (a.k.a. hyperkinetic gait) presents with involuntary movements such as:
Oro-facial dyskinesia (grimacing or lip-smacking)
Choreic movements of the upper and lower limbs (writhing, dance like semi-purposeful
movements)

The involuntary movements are usually present at rest; however, walking can accentuate the
movements.
Causes
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
An antalgic gait is an abnormal gait pattern which develops as a result of pain. Typically the
stance phase is reduced on the affected leg resulting in a limping appearance.
Causes
Any cause of lower limb pain such as:
Osteoarthritis
Inflammatory joint disease
Lower limb fracture
Nerve entrapment (e.g. sciatica)

Sensory Gait
As our feet touch the ground, we receive propioreceptive information to tell us their
location. The sensory ataxic gait occurs when there is loss of this propioreceptive input. In
an effort to know when the feet land and their location, the patient will slam the foot hard
onto the ground in order to sense it. A key to this gait involves its exacerbation when
patients cannot see their feet (i.e. in the dark). This gait is also sometimes referred to as a
stomping gait since patients may lift their legs very high to hit the ground hard. This gait
can be seen in disorders of the dorsal columns (B12 deficiency or tabes dorsalis) or in
diseases affecting the peripheral nerves (uncontrolled diabetes). In its severe form, this
gait can cause an ataxia that resembles the cerebellar ataxic gait.