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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 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 foot not touching the ground
  • Starts with toe-off, when foot plantar flexes to push 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)
  • 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 plantarflexion 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 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
  • Demyelination
  • Spinal infarct

 

Key points:

  • Hemisection of 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 give 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 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
  • Urinary catheter may be in situ if nerves supplying lumbosacral plexus are involved
  • 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

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
  • 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):

  • 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 weakness of dorsiflexion, so the foot drops and toes drag during 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
  • 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)

 

 

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

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 a peripheral neuropathy may be present:

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

 

Features of sub-acute 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:
    • 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

 

  • Evidence of systemic disease or a muscular dystrophy causing proximal myopathy

 

Differential diagnosis

Any cause of a proximal myopathy (there are many), including:

  • 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.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

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