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Gait Cycle Terminology; graphical representation of stride and step lengths

Walking is a coordinated action that requires the integration of sensory and motor functions. A gait disturbance is a gait pattern that deviates from a "normal" gait. Synchrony, fluency, smoothness, and symmetry may be affected. Gait disturbance may be an important clue in looking for other relevant findings on examination, and can be caused by problems at any level of the neuraxis, and they can be classified on an anatomical basis. This type of classification scheme categorises gait disturbances into low-level, middle-level, and high-level gait disorders. Particularly in the elderly, multiple factors may be in play causing a gait disturbance. The most common patterns of abnormal gait are: hemiplegic, parkinsonian, marche à petits pas, ataxic and unsteady gaits. Romberg’s test is performed after examining the gait. This is a simple test primarily of joint position sense. [1][2]

Gait Cycle

The walk and run gait cycle.

Gait is a cyclic process take place between the time a foot touches the ground and when the same foot returns to the ground once again (heel-strike to heel-strike). It consists of:

  • Stance phase. The stance phase of a limb is when some part of the foot is touching the ground. It makes up 60% of the gait cycle and incorporates heel strike, foot flat, mid-stance, and push-off (heels-off and toes-off).
  • Swing phase. The swing phase is when it is off the ground. This phase has an acceleration, mid-swing, and deceleration components.

The stride is the distance between consecutive initial contacts of the same foot with the ground.

The step is the distance between initial contacts of the alternating feet.

Stance Phase

Initial contact (heel strike): This occurs when the foot contacts the ground. The hip extensors contract to stabilize the hip. The quadriceps and tibialis anterior contract eccentrically.

Loading response (initial double limb support): This marks the beginning of the initial double limb stance. It occurs after initial contact until elevation of the contralateral limb. The bodyweight is transferred on to the supporting limb. The ankle dorsiflexors (tibialis anterior) contract eccentrically to control plantar flexion moment. The quadriceps contract to stabilise knee and counteract the flexion moment (about the knee).

Mid-stance (single limb support): This is the initial period of single leg support. It is from elevation of opposite limb until both ankles are aligned in coronal plane. The hip extensors and quadriceps undergo concentric contraction.

Terminal stance (single limb support): This begins when the supporting heel rises from the ground and continues until the opposite heel touches the ground. The toe flexors contract and are the most active during this phase

Pre-swing (second double limb support): This is the start of the second double limb stance in the gait cycle. It is from initial contact of opposite limb to just prior to elevation of ipsilateral limb. The hip flexors contract to propel advancing limb

Swing Phase

Initial swing (toe off): This is the start of single limb support for the contralateral limb. It is from elevation of limb to point of maximal knee flexion. The hip flexors concentrically contract to advance the swinging leg

Mid-swing (foot clearance). This follows knee flexion to point where tibia is vertical. The ankle dorsiflexors contract to ensure foot clearance

Terminal swing (tibia vertical): This is from point where tibia is vertical to just prior to initial contact. The hamstring muscles decelerate forward motion of thigh.

Variables Affected During Gait Cycle

Pelvic rotation: The pelvis rotates 4 degrees medially (anteriorly) on swing side. It lengthens the limb as it prepares to accept weight.

Pelvic tilt: The pelvis drops 4 degrees on swing side, lowering the centre of gravity at midstance.

Knee flexion in stance: early knee flexion (15 degrees) at heel strike. This lowers the centre of gravity, decreasing energy expenditure. It also absorbs shock of heel strike.

Foot mechanisms: ankle plantar flexion at heel strike and first part of stance.

Knee mechanisms: at midstance, the knee extends as the ankle plantarflexes and foot supinates. This restores leg to original length. It reduces fall of pelvis at opposite heel strike.

Lateral displacement of pelvis: The pelvis shifts over stance limb. The centre of gravity must lie over base of support (stance limb) .

Centre of gravity: In standing position the centre of gravity (COG) is 5cm anterior to S2 vertebral body. There is vertical displacement during gait cycle in a rhythmic pattern. The highest point is during midstance phase, and the lowest point occurs at the time of double limb support. There is also horizontal displacement of the COG, where it displaces horizontally during adult male step

Gait Disorder Classifications

Higher, Middle, and Lower Level Gait Disorder Anatomical Correlations. [1]
Levels Anatomical Level Balance and Gait Pattern
Higher Psychological / psychiatric Variable: slow, buckling knees
Higher Cortical and subcortical Different patterns: cautious, parkinsonian, ataxic, spastic, magnetic, gait ignition failure, disequilibrium
Middle Basal ganglia Parkinsonian / dystonic / choreic
Middle Thalamus Astasia / ataxia
Middle Cerebellum Cerebellar ataxia
Middle Brain stem Ataxia / spasticity
Middle Spinal cord Spastic gait / tabetic gait
Lower Peripheral nerve
Proprioception, vestibular visual
Sensory ataxia / vestibular disequilibrium / visual disequilibrium
Lower Neuromuscular junction Waddling
Lower Muscle Waddling, steppage, Trendelenburg
Lower Skeleton Antalgic / compensatory for deformities

See below for a demonstration of neurological gait conditions (Hemiplegic, Parkinsonian, Cerebellar, Stomping, Scissoring, Trendelenburg, Foot-drop, Choreiform)

Lower Level Gait Disorders

Lower level gait disorders are caused by pathology of the muscles, skeleton, peripheral nerves, peripheral vestibular system, and anterior visual pathway.[1]

Antalgic Gait

The occurs when there is a protective adaptation to minimise pain during weightbearing. The patient removes weight from the painful side as quickly as possible. The stance phase of the affected side, and the swing phase of the unaffected side are lessened. Stride length and velocity are decreased.

Trendelenburg and Waddling Gaits

The distance from the midline to the femoral head is almost twice that between the abductors and femoral head. The abductors generate very large forces across the hip weight bearing area, about 3 times that of upper body weight.[3] Trendelenburg gait manifests as ipsilateral lurching of the torso with a contralateral hip drop during the stance phase of the affected side. It is caused by unilateral hip abductor weakness.[1] There is an exaggerated up and down motion of the pelvic.

A waddling gait pattern is seen with weakness of the bilateral hip abductors as well as in bilateral hip joint osteoarthritis or other bilateral hip joint diseases such as bilateral congenital hip dislocation. The gait is wide based, and has short steps. There is increased alternating lateral body sway, and excessive drop of the hips. By swaying laterally the patient places their weight down the centre of gravity through each hip to reduce pain. There may be increased arm abduction and an exaggerated lumbar lordosis. [1]

The abductor lurch is seen with further abductor mechanism weakness, where the trunk muscles come into play. The entire body and shoulder tilts to the diseased side in the stance phase of the ipsilateral limb. The abductor lurch can also occur in the setting of a painful hip. By tilting the body to the affected side the centre of gravity is shifted towards the centre of the femoral head, thereby reducing the reaction force and resultant pain. In this situation there is no drop of the hemipelvis as seen with a Trendelenburg gait.

Short Limb Gait

To compensate for length, the pelvis on the affected short side tilts down (hip hiking). This allows the longer limb to more easily clear the ground. The foot may supinate or there may be toe walking. The longer limb may compensate by flexing at the hip or knee.[3]

Steppage Gait

This is seen with weakness of foot dorsiflexion, which may be due to peroneal nerve injury, radiculopathy, and demyelinating neuropathy. It may be unilateral or bilateral. The patient exaggerates knee and hip flexion to avoid tripping. The step is high and short, and at the end of each swing phase the foot may slap the floor.[1]

Gluteus Maximus or Extensor Lurch

Normally the gluteus maximus prevents the torso toppling forward in the stance phase, because the centre of gravity is anterior to the hip. With gluteus maximus weakness, the torso lurches backwards at heel strike on the affected side. This is a compensatory mechanism to interrupt forward motion of the trunk due to a weakness of hip extension. The pelvis is thrusted forward, and the torso backwards, in order to shift the centre of gravity more posteriorly.[3]

Flexion Contracture of Hip or Knee

This results in increased lumbar lordosis, stopping, and a short stride length. Evaluate this laterally.[3]

Knee Considerations

See also: Knee Examination

Evaluate varus and valgus thrusting by squatting or sitting to inspect the patient from the level of their knees. Varus thrust is the most common. In the stance phase the knee collapses into varus with the lateral border laterally thrusting. This can be seen in advanced osteoarthritis, varus from malunited tibial plateau fracture, and tibia varum. A ligamentous laxity will usually add a recurvatum thrust visualised laterally. Valgus thrust is less common, and patients may circumduct their limb to avoid knocking their knees.[3]

A stiff knee gait with the knee extended may be seen with patients avoiding patellofemoral pain. This can also be seen when compensating for quadriceps weakness with locking in the stance phase. On the other hand, a stiff knee gait with the knee flexed - even 5 degrees can cause a gait disturbance - can result in a short stride, a heel strike replaced by an almost flat foot to start phase, and a jerky up-down motion from apparent shortening.[3]

Ankle and Foot Considerations

See also: Ankle Examination

An equinus contracture can be seen as a high stepping gait during the swing phase of the affected side. There is an abnormally early heel raise, with hyperextension of the ipsilateral knee to compensate for the contracture.[3]

Patients with a stiff 1st MTP joint walk mainly on the lateral border of their foot. This may be more easily visualised by observing for lateral wear on their shoes. There is a hurried push-off, which occurs directly from the heel.[3]

In pes planus the heel raise is avoided, and so the heel and ball of the foot rise together. The toes are usually splayed outwards.[3]

Sensory Ataxia

The sensory ataxic gait is wide based with a variable step length and marked stride-to-stride variability. There is usually unsteadiness. Romberg sign is often positive. This gait pattern is not specific to any anatomical location, and may be seen in pathology of proprioception (sensory ataxia), cerebellum (cerebellar ataxia), pons, and thalamus.[1] Common causes are peripheral neuropathy and posterior column loss.

Visual Disequilibrium

Acute visual distortion such as using new prescription glasses may cause a sense of loss of balance. There may be cautiousness in gait, with tentative steps and an increased base of support.[1]

Vestibular Disequilibrium

Acutely there may be vertigo, nystagmus, and a tendency to fall onto the affected side. Chronically, the symptoms may be less marked, but the gait is often still wide based and cautious. There is difficulty with Romberg test and tandem walking, but assistance is not required to walk.[1]

Sensory Disequilibrium

There is conflict among inputs from the visual, proprioceptive, and vestibular pathways. Loss of two of these pathways, or loss of one without CNS adaptation, may lead to this becoming chronic. The gait is slow and cautious, and there is increased bipedal support.[1]

Middle Level Gait Disorders

In middle level gait disorders are caused by lesions in the ascending or descending sensorimotor tract, cerebellar dysfunction, bradykinesia, and hyperkinetic movement disorders.[1]

Spastic Gait and Scissoring

Corticospinal tract lesions cause spastic gaits that can be hemi or paraparetic depending on whether the lesion is unilateral or bialteral. There is often an associated weakness. [1] Common causes of spastic paraparesis are cerebral palsy, multiple sclerosis, and cord compression.

Spastic hemiparetic gaits show lower limb hyperextension with difficulty in hip and knee flexion and excessive plantarflexion and inversion of the foot. The arm may have a flexor posture or may dangle. The support base is narrowed, and there is a semicircular movement at the hip during the swing phase which is needed to clear the ground due to the hyperextension of the leg. With more mild spasticity and good proximal muscle strength the patient may clear the floor during the swing phase with increased hip flexion.[1]

Spastic paraparetic gaits is more common in spinal cord injury and there is some shared features with hemiparetic gaits. Arm swing and the posture of the upper limb may be relatively normal depending on the lesion level.[1]

Spastic diplegic gait is a bilatearl hemiparetic gait with particular features. The knees and hips are significantly flexed. The hips are adducted during the gait cycle causing a scissoring pattern from leg crossing. Compared to bilateral hemiparesis, in spastic diplegia the upper limbs and bulbar muscles are much less affected than the lower limbs.[1]

Cerebellar Ataxia

The patient veers towards side of lesion. The common causes are drugs (e.g. phenytoin), alcohol, multiple sclerosis, and cerebrovascular disease.

Parkinsonian Gait

A parkinsonian gait indicates basal ganglion dysfunction. There are small paces and reduce arm swing. The reduced arm swing is usually unilateral, and is one of the earliest signs of parkinsonism. There may be be difficulty in starting and stopping. Festination may be worse on one side. The tremor may increase with walking. The common causes are Parkinson's disease and major tranquillisers.

Marche à Petit Pas

This indicates bilateral diffuse cortical dysfunction. The common cause is diffuse cerebrovascular disease ‘lacunar state.’

Apraxic Gait

This indicates that cortical integration of the movement is abnormal and there is usually frontal lobe pathology. Common causes are normal pressure hydrocephalus and cerebrovascular disease.

Hemiplegic Gait

There is seen in unilateral upper motor neurone lesion. Common causes are stroke and multiple sclerosis.

Choreic Gait

Choreic gait is a type of abnormal walking pattern observed in individuals with chorea, a neurological disorder characterized by involuntary, rapid, and irregular movements. In patients with choreic gait, the involuntary movements interfere with the coordination required for smooth walking, resulting in jerky and unpredictable steps, as well as imbalance and difficulty in maintaining a steady pace.

Dystonic Gait

Dystonic gait is associated with dystonia, a neurological movement disorder marked by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements or postures. In individuals with dystonic gait, the muscle contractions can affect walking by causing twisting, turning, or dragging movements of the legs or feet, leading to an unsteady, bizarre, and awkward walking pattern. The severity of dystonic gait can vary and may be exacerbated by specific triggers, such as stress or voluntary movements.

Higher Level Gait Disorders

These gait disorders are caused by impairment of the cortico-basal ganglia-thalamocortical pathways. Gait disorders in this category include cautious gait, fear of falling, freezing of gait, and frontal and subcortial disequilibrium.

Psychiatric disorders may also affect the gait cycle. Functional gaits are variable, may be worse with observation, and are inconsistent with the rest of the examination. It may be mistaken for choreic gait especially in Huntington's disease.[2]


Gait Assessment

There should be a general, neurological, and musculoskeletal examination in order to localise the lesion. The gait should be assessed by observing the gait parameters, posture, range of motion, and tandem walking. [2]

  • Symmetrical gait
    • Size of the paces are they small or normal
      • If small paces, look at the posture and arm-swing
        • If they are stooped with reduced arm-swing this is a parkinsonian gait
        • Upright with marked arm-swing: marche à petits pas
      • If normal paces, look at the lateral distance between the feet
        • Widely separated is broad-based
        • Legs uncoordinated is cerebellar
        • Crossing over with toes dragging is scissoring
    • Normal paces
      • Look at the knees
        • Knees lifting high is high-stepping
      • Look at the pelvis and shoulders
        • Marked rotation of pelvis and shoulders is waddling
      • Look at the whole movement
        • Disjointed movements as if the patient has forgotten how to walk, and is frequently rooted to the spot is apraxic
        • Bizarre, elaborate, and inconsistent is functional.
  • asymmetrical gait
    • Is there pain?
      • Painful or antalgic gait
      • Bony deformity is an orthopaedic gait
      • Leg swinging out to the side is a hemiplegic gait
      • One leg lifting higher than the other is foot drop

Romberg's Test

The Romberg test is done after gait assessment and is a test of joint position sense. Ask the patient to stand with his feet together. Allow them to stand like this for a few seconds. Reassure them that you will catch them if they fall. If they falls with their eyes open do not proceed. Romberg’s test is not positive in cerebellar disease.[2]

  • Negative Romberg's test: stands with eyes open, stands with eyes closed
  • Positive Romberg's test: stands with eyes open, falls with eyes closed
    • This indicates loss of joint position sense.
    • It can occur with:
      • A posterior column lesion in the spinal cord with cord compression (cervical spondylosis, tumour). Rare causes include tabes dorsalis, vitamin B12 deficiency, and degenerative spinal cord disease.
      • Peripheral neuropathy
  • Severe unsteadiness: unable to stand with eyes open and feet together
    • Common causes are cerebellar syndromes, central and peripheral vestibular syndromes.
  • Cerebellar syndrome: Stands with eyes open, rocks backwards and forwards with eyes closed.


Test tandem gait by asking them to walk as if on a tight-rope. The gait is unsteady if the fall consistently. Elderly patients are often slightly unsteady. Ask the patient to walk on their heels, and if unable to do so this is foot drop. Ask them to walk on their toes, and if unable to do so this is weakness of gastrocnemius. The neurological examination should focus on pyramidal signs, tremor, sensory changes, and dysmetria. The general examination may include a brief cardiorespiratory and ophthalmologic examination. A general screening and focused musculoskeletal examination should be performed. A vestibular examination may be also indicated.[2]



  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 Biller, José. Practical neurology. Philadelphia: Wolters Kluwer, 2017.
  2. 2.0 2.1 2.2 2.3 2.4 Fuller, Geraint. Neurological examination made easy. Edinburgh: Churchill Livingstone/Elsevier, 2013.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8