Abnormal Gait

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Gait and balance abnormalities occur in 8-19% of older people living in the community.[1]

As the body moves forward, one limb typically provides support while the other limb is advanced in preparation for its role as the support limb. The gait cycle (GC) is composed of stance and swing phases. The stance phase is further subdivided into 3 segments including:

  • Initial double stance.
  • Single limb stance.
  • Terminal double limb stance.

Duration of each aspect of stance decreases as walking velocity increases. The transition from walking to running is marked by elimination of double support.
A stride is the equivalent of a gait cycle. The duration of a stride is the interval between sequential initial floor contacts by the same limb.

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Walking posture changes only slightly with age:

  • Unless the elderly have diseases such as osteoporosis with kyphosis, they walk upright with no forward lean.
  • Elderly people also walk with about a 5° greater 'toe out', possibly due to a loss of hip internal rotation or in a subconscious strategy to increase stability.
  • Ground clearance as the foot swings is the same in elderly as in younger people.
  • Gait velocity remains stable until about the age of 70, then falls about 15% per decade for normal gait. It has been shown that slow walking speed in the elderly is strongly associated with an increased risk of cardiovascular mortality.[3]
    • Velocity is lower because older people take shorter steps.
    • One explanation for this is that calf muscles are weaker and cannot produce sufficient plantar flexion.
    • Another is that the elderly are reluctant to generate plantar flexion power because of poor balance and poor control of the centre of mass whilst standing on one foot momentarily.
  • Cadence (rhythm) does not change with age.
    • Everyone has a preferred cadence, which relates to leg length and usually represents the most energy-efficient rhythm for individual body structure.
    • Tall people take longer steps at a slower cadence.
    • Short people take shorter steps at a faster cadence.
  • Double stance (the time when both feet are on the ground) increases with age - from 18% of a total gait cycle in young adults to approximately 26% in healthy elderly people.
    • During double stance, the centre of mass is between the feet, which is a stable position.
    • Increased time in the double stance position reduces momentum and therefore reduces time for the swing leg to advance, contributing to short step length.
    • Increased double stance may be needed on uneven ground or when balance is impaired, so that step length is compromised for stability. Elderly people with a fear of falling increase their double stance time.
  • Joint motion changes with age.
    • Ankle plantar flexion is reduced during the late stage of stance, just before the back foot lifts off.
    • Maximal ankle dorsiflexion is not reduced.

The presence of neurological gait abnormalities in the elderly (without dementia) at baseline assessment, is a significant predictor of the risk of development of dementia - especially non-Alzheimer's dementia.[4]

Pathology Gait seen if predominantly symmetrical problem Gait seen if predominantly asymmetrical problem
Upper motor neurone disorder Diplegia
Brain stem problem Ataxic  
Lower motor neurone disorder Spina bifida Femoral nerve palsy
Sensory problem Neuropathic  
Basal ganglia disorder Athetoid  
Cortical problem Apraxia - loss of the ability to carry out familiar, purposeful movements in the absence of paralysis or other motor or sensory impairment  
Orthopaedic problem Femoral anteversion
Tibial torsion
Congenital dislocation of the hip
Amputee   Trans-tibial amputation gait
Trans-femoral amputation gait

In this the patient avoids certain movements to avoid acute pain. It can be seen as a feature of:

Ataxia is a neurological sign characterised by the inco-ordination of voluntary movements.

Ataxia is the most prominent manifestation of cerebellar disease. The cardinal features of cerebellar dysfunction involve disturbances of stance and gait. Eye movements, muscle tone, skilled movements and speech are also affected by cerebellar disease.


This may include trauma, toxic and metabolic causes, neoplasms, immune mechanisms and genetic diseases.[5] It may also arise from multiple sclerosis. It may also arise developmentally as congenital ataxia. In children this is a nonprogressive disorder in which co-ordination will usually improve with age. Children aged between 2 and 10 years may also present with subacute reversible ataxia stemming from a viral infection.


  • Broad-based gait
  • Lurching quality
  • Difficulty with turning
  • Difficulty walking in a straight line
  • Broad-based posture

Assessment should include asking the patient to walk heel to toe. The duration of the problem should be established and knowledge of previous and early motor abilities may be helpful.
Diurnal variation with morning unsteadiness which decreases later in the day may suggest raised intracranial pressure. It is also possible that patients may present with cerebellar ataxia of extremely acute onset and this may be accompanied by headache, vertigo, vomiting, altered consciousness and neck stiffness. In this case, urgent referral for diagnosis is needed.

The bradykinesia and slowness of postural adjustments, together with a forward-flexed posture produces the 'festinant gait' typical of Parkinson's disease.

After a cerebrovascular event:

  • The strong gluteal and quadriceps muscle groups are generally spastic.
  • The hip flexors, hamstrings and dorsiflexors of the foot are generally weak.
  • The hip and knee will thus be stiff and slightly flexed.
  • The foot will be plantar-flexed and tending to drag along the floor.

This indicates pyramidal pathway damage - and the residual power left is dependent on non-pyramidal pathways and there being enough residual cortical function.


These disorders can arise from:

  • Diabetes
  • Alcoholism
  • HIV
  • Toxin exposure
  • Metabolic abnormalities
  • Vitamin deficiency
  • Adverse effects of certain drugs

However 32-70% of all peripheral neuropathies are idiopathic.[6]


Unsteady gait, often high-stepping. This is virtually diagnostic of neuropathies when present.

Patients may fall over if asked to close their eyes.

Damage to the descending corticospinal tract, eg by a tumour, may present initially with a generalised stiffening of the legs. The patient may find it impossible to walk quickly or run because of a stiff-legged gait.

Ankle clonus may be a feature, and eventually develops into a spastic, foot dragging 'shoe-scuffing' gait.


Usually seen in spastic cerebral palsy, usually diplegic and paraplegic varieties.

Characteristic features

  • Legs flexed slightly at the hips and knees, giving the appearance of crouching, with the knees and thighs hitting or crossing in a scissors-like movement.
  • Often mixed with, or accompanied by, spastic gait - a stiff, foot-dragging walk caused by one-sided, long-term muscle contraction.
  • The individual is forced to walk on tiptoe unless the dorsiflexor muscles are released by an orthopaedic surgical procedure.
  • Muscle contractures of the adductors result in thighs and knees rubbing together and crossing in a manner analogous to scissors.
  • There may also be complicated assisting movements of the upper limbs when walking.

These features are typical and are usually present to some degree regardless of the mildness or severity of the cerebral palsy.

Patients with unilateral vestibular disorders:

  • Will veer to the affected side (as opposed to a generalised instability with bilateral vestibular or cerebellar disorders).
  • There is a wide-based gait and their difficulties are exaggerated by asking them to walk heel-to-toe.

Many patients respond well to a simple home programme of vestibular rehabilitation head movement exercises. This results in reduced symptoms of imbalance during stance and gait.[7]

This is a videotape-based analysis of 16 facets of human gait.[8] The gait abnormality rating scale (GARS) comprises three categories:

  • Five general categories.
  • Four lower limb categories.
  • Seven trunk, head and upper limb categories.

Each item has a score range from 0 (good function) to 3 (poor function). The total GARS score is the sum of the 16 individual items. The total score represents a rank ordering of risk for falling, based on the number of gait abnormalities recognised and the severity of any abnormality identified.

Abnormal gait patterns can also be identified by neuro-orthopaedic specialists using dynamic electromyography (EMG) or three-dimensional kinematic and kinetic studies.[9] This can, for example, reveal paralysis of the peroneal evertors or continuing EMG activity and even clonic contractions in the tibialis muscles during the swing phase of walking, allowing effective treatment.

Further reading & references

  • Bogey R; Gait analysis, eMedicine, Oct 2009
  • Thomann KH, Dul MW; Abnormal gait in neurologic disease. Optom Clin. 1996;5(3-4):181-92.
  • University of Utah; Neurologic Exam - demonstration videos of gait abnormalities; Some have spoken commentary, which may falter on lower specification computers or those with a slow internet connection. A good resource - requires QuickTime. A link is provided for download if required
  1. Martin MP, O'Neill D; Vascular higher-level gait disorders--a step in the right direction? Lancet. 2004 Jan 3;363(9402):8.
  2. Gait Disorders: Chapter 21, Merck Manual of Geriatrics
  3. Dumurgier J, Elbaz A, Ducimetiere P, et al; Slow walking speed and cardiovascular death in well functioning older adults: BMJ. 2009 Nov 10;339:b4460. doi: 10.1136/bmj.b4460.
  4. Verghese J, Lipton RB, Hall CB, et al; Abnormality of gait as a predictor of non-Alzheimer's dementia. N Engl J Med. 2002 Nov 28;347(22):1761-8.
  5. Morrison DR, Chapes SK, Guikema JA, et al; Experiments with suspended cells on the Space Shuttle. Physiologist. 1992 Feb;35(1 Suppl):S31-4.
  6. Dyck PJ, Oviatt KF, Lambert EH; Intensive evaluation of referred unclassified neuropathies yields improved diagnosis. Ann Neurol. 1981 Sep;10(3):222-6.
  7. Cohen HS, Kimball KT; Decreased ataxia and improved balance after vestibular rehabilitation. Otolaryngol Head Neck Surg. 2004 Apr;130(4):418-25.
  8. Wolfson L, Whipple R, Amerman P, et al; Gait assessment in the elderly: a gait abnormality rating scale and its relation to falls. J Gerontol. 1990 Jan;45(1):M12-9.
  9. Patrick JH, Keenan MA; Gait analysis to assist walking after stroke. Lancet. 2007 Jan 27;369(9558):256-7.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Hayley Willacy
Current Version:
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Document ID:
1740 (v21)