Author(s): Rebecca Ann Speckman, MD, PhD, Ian J. Kim, MD, Michael J. Gallagher, MD
Originally published: August 3, 2020 Last updated: March 20, 2025
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Overview and Description

Introduction

Many pathologies can affect a person’s gait, or ability to walk. Gait abnormalities can contribute to increased fall risk, increased energy cost of walking, decreased safety during community ambulation, or otherwise negatively impact patients.1,2 A gait abnormality might also be the initial presentation of a disease or condition. It is important to identify abnormalities in gait so that the underlying pathology and/or the consequences of the gait abnormality itself can be addressed. Furthermore, the examiner must be able to differentiate primary gait dysfunction from compensatory strategies.3,4

Types of Underlying Pathologies

Pathological mechanisms of gait abnormalities are sometimes grouped into categories. An exhaustive consideration of specific pathological contributors to gait is beyond the scope of this article.

Normal gait. Briefly, the normal gait cycle is a sequence of events that occur from the initial contact of one foot with the ground to the subsequent contact of the same foot with the ground. Stance phase is the period of the gait cycle in which the foot is in contact with the ground. During stance phase, the lower limb accepts body weight and provides support while the body moves forward. Swing phase is the period in which the foot is off the ground and the limb is advancing forward. Further information regarding normal gait parameters is discussed in the “Biomechanics of Normal Gait” topic.

Structural or musculoskeletal deformities

Joint contractures. Joint contractures or other joint deformities can change the point(s) of contact of the foot with the ground during stance phase, altering origination of the ground reaction force (GRF). Contractures can also change the location of the GRF relative to the joint, all other things being equal. For example, knee flexion contractures would lead to the GRF being relatively more posterior to the knee in still standing or stance phase, creating a pathologically strong knee flexion moment. A person with a knee flexion contracture might dorsiflex their ankle more than normal during stance phase to allow their weight to get over their foot.

Painful joint. A classic antalgic (pain avoidance) gait pattern is characterized by decreased time spent in stance phase with the affected limb, which reduces the weightbearing through the limb.5,6 The patient may try to minimize motion at the affected joint.7  

Leg length discrepancy. Leg length discrepancy can be structural (for example, hemihypertrophy, knee extension contracture, knee extension brace) or functional (e.g., a prosthetic limb that is pistoning in swing phase).8 With the shorter limb, a “stepping in a hole” gait pattern might be observed, in which the person seems to step down when striking the ground on the shorter limb. The patient may have shorter stance time on the shorter leg.

During stance phase of the shorter limb, the patient may use compensatory mechanisms to effectively lengthen the shorter limb:

  • Vaulting – plantarflexing the foot earlier than normal push-off
  • Toe-walking – using the toe/forefoot for initial contact and as main point of contact throughout stance phase
  • Increasing knee extension in midstance.

These mechanisms help the patient clear the ground during pre-swing to swing phase with the contralateral (longer) limb.

During swing phase of the longer limb, the patient may compensate by a variety of mechanisms to help clear the longer limb:

  • Hiking the hip up – tilting the ipsilateral hip up
  • Circumduction – swinging the limb in a semicircle rather than straight through
  • Steppage gait – increased knee flexion and/or hip flexion during swing

Neurologic disorders

Bipedal locomotion is initiated and controlled by control centers in the brain and the spinal cord and effected by skeletal muscles. Maintaining balance utilizes multiple systems including proprioception, the visual system, and the vestibular system, with processing in the vestibular nucleus and cerebellum. Muscle tone (spasticity, rigidity, other) can affect gait, as can other musculoskeletal sequelae of neurologic disorders such as contractures or foot deformities.

Thus, a person with a central nervous system (CNS) disease process could have multiple contributors to gait abnormalities: muscle weakness, muscle spasticity, impaired muscle control, emergence of primitive locomotor patterns, and impaired balance.9 The relative contribution of these different elements can change over time, and it is particularly important for the clinician to remember that spasticity tends to be a later sequelae of CNS lesions.

Additionally, in neurologic conditions where no discrete lesion may exist such as various cognitive disorders and dementias, gait parameters also change. Studies have shown that a co-decline in gait speed and cognition is associated with increased risk of dementia.15 People with dementia have also been found to adopt longer stance phases and have greater variation between strides when asked to do an additional task besides walking.16

There are classic gait deviations that result from or may be associated with neurologic abnormalities (Table 1).17

Table 1. Classic neurologic gait deviations and common characteristics

Introduction to Abnormal Gait – Table 1

Problem-based Approach to Pathologic Gait

Many experts recommend using a problem-based approach, or sign-based approach, in the clinical setting rather than relying on classical disease- or condition-based abnormalities.10–12 For example, increased tone from spasticity or dystonia could have multiple different gait manifestations.13 In a problem-based approach, the clinician performs an observational gait analysis (visual gait analysis) with a goal to identify clinically significant gait problems, then works backward to identify possible causes. Here, we present a problem-based approach to selected gait abnormalities at the knee. Additional problem-based gait abnormalities are presented in Table 2.

Table 2. Gait abnormalities by anatomical area.

Introduction to Abnormal Gait – Table 2

Examples of Joint-Based Abnormalities: The Knee

For a given specific phase of gait, the clinician might observe less knee flexion than normal, more knee flexion than normal, alternating knee flexion and extension during a single phase (‘wobbling’), a hyperextended knee, extension thrust (forceful motion of the knee towards extension), varus or valgus angulation at the knee, forceful motion (thrust) towards varus or valgus, or other abnormalities.10

Limited knee flexion

Less-than-normal or complete lack of knee flexion during weight acceptance could decrease shock absorption and thus increase adverse forces at the knee, slow one’s progression forward through stance phase, or contribute to injury and stretching of the posterior capsule.3,10 Limited knee flexion during pre-swing to initial swing phase can cause the toe to drag, which impedes forward progression during swing phase and increases fall risk.

Primary pathologic contributors
  • Increased quadriceps tone (for example, knee extensor spasticity)
  • Knee extension contracture
  • Any abnormality or characteristics at the foot and ankle that moves the GRF relatively forward has the effect of decreasing the “normal” initial knee flexion moment, or even creating a knee extension moment.
    • A foot that goes flat faster than normal (e.g., “foot slap” from weak ankle dorsiflexors, or rapid foot flat from a single axis prosthetic foot with a soft posterior bumper).
    • Excess plantarflexion – plantarflexion contracture or injury (e.g., Achilles tendinopathy) may lead to a toe-walking pattern of gait with limited knee flexion.
As a compensatory mechanism
  • Knee flexor weakness. Knee flexor weakness would cause excess knee flexion during initial contact and perhaps even buckling (giving way) of the knee, were a person to enter stance phase with normal knee flexion. A patient could compensate by using their hip extensors or pelvis rotators to force the knee into extension during initial contact. In this case, the apparent abnormality on examination might be a lack of knee flexion or even the presence of knee extension in early stance, rather than excess knee flexion.
  • Knee pain.  Knee pain with flexion may present as an antalgic gait, where the patient limits time spent on the affected limb. Avoiding the painful range of knee flexion is one strategy that may be adopted here.
  • Impaired proprioception. Knee flexion introduces the potential for knee buckling in stance phase- (a flexed knee anterior to the GRF will experience an external knee flexion moment). A patient unable to sense where the lower limb is in space may adopted limited knee flexion as a compensation to reduce the risk of knee buckling/falling, as a relatively extended knee is more stable. 
  • The observer might be more likely to see complete lack of knee flexion or even an extension thrust in compensatory scenarios.14

Excess knee flexion

Excess knee flexion during weight acceptance increases risk of the knee buckling, causing instability and risk of falls.10 Increased effort from the knee extensors and hip extensors is needed to prevent the knee from buckling, and this can be very difficult or taxing. If a patient enters stance phase with excess knee flexion, they may be unable to use their heel for weight acceptance.

Primary pathologic contributors10
  • Knee flexion contracture
  • Increased tone of knee flexors
  • Uncompensated knee extensor weakness
  • Secondary to hip flexion contracture
  • Secondary to hip extensor weakness
  • Any structural, footwear, orthotic, or prosthetic factor that lengthens the time spent in first rocker can increase knee flexion during weight acceptance. A longer first rocker phase delays forward progression of the GRFV and/or predisposes the GRFV to be relatively more posterior to the knee.
    • Excess ankle dorsiflexion (for example, with congenital calcaneovalgus abnormality, cerebral palsy, or prosthetic foot).

Management Strategies

Gait impairments can be addressed by many different types of strategies. 

Therapeutic interventionscould include stretching, strengthening, gait training, balance programs, evaluation and training with assistive devices, or others.

Orthotic devices might be used to decrease or prevent contractures, for structural stabilization around a joint with excess laxity or that lacks muscular stabilization (e.g., a hinged AFO with metal side struts to control the ankle in the coronal plane), or to alter kinematics (e.g., a hinged AFO with a dorsiflexion assist spring could aid in clearance during swing phase).

Condition-specific management

Management of gait abnormalities could be a focused intervention to resolve or lessen the specific underlying disorder. For example, for gait impairments caused by spasticity, treatments to lessen spasticity might include a regular stretching program, splinting, pharmacologic intervention, or neurolysis. Likewise, a prosthetic limb that is too short can be lengthened. A plantarflexion contracture might be specifically addressed with a stretching program, splinting, or surgical release in extreme scenarios. If spasticity is a contributing etiology to contracture, then specific pharmacologic or interventional management could be included.

Preventive management

Whether a specific underlying disorder is identified, management can include strategies to decrease potential consequences of the gait abnormality, such as falls. Evaluation and training with a handheld assistive device or alternate means of mobility (for example, manual wheelchair) appropriate for the patient could help to reduce falls or other adverse events.

Cutting Edge/Unique Concepts/Emerging Issues

  • Gait analysis is a rapidly developing field, and technological innovation continues to advance our understanding of gait. Particularly, wearable technology and more sensitive methods of detection allow for both a greater diversity of gait observation without the need for a gait lab, as well as improving understandings of gait kinematics.
  • Patient-centered outcomes continue to be honed and may provide additional input into understanding the functional challenges of various gait deviations.
  • Gait-based parameters such as the 6-Minute Walk test and Timed-Up-and-Go test are becoming mainstays for fall risk screening in patients at-risk.

Gaps in Knowledge/Evidence Base

  • As in the “Cutting Edge” section, gait analysis remains a relatively new and developing field, and our understanding of kinematic parameters continues to evolve with improving measurement.
  • As technology improves, so too does our ability to modify gait – however, knowing when and which parameters to modify remains a key part of a physiatrist’s developing knowledge and skillset.

References

  1. Desforges JFMD, Sudarsky LMD. Current Concepts: Gait Disorders in the Elderly. N Engl J Med. 1990;322(20).
  2. Ambrose AF, Paul G, Hausdorff JM. Risk factors for falls among older adults: A review of the literature. Maturitas. 2013;75(1). doi:10.1016/j.maturitas.2013.02.009
  3. Perry J, Burnfield JM. Gait Analysis:  Normal and Pathological Function. 2nd ed. SLACK; 2010.
  4. Esquenazi A, Talaty M. Gait Analysis:  Technology and Clinical Applications. In: Cifu DX, ed. Braddom’s Physical Medicine and Rehabilitation. 5th ed. Elsevier; 2016.
  5. Lim MR, Huang RC, Wu A, Girardi FP, Cammisa FP. Evaluation of the elderly patient with an abnormal gait. In: Journal of the American Academy of Orthopaedic Surgeons. Vol 15. ; 2007. doi:10.5435/00124635-200702000-00005
  6. Whittle M, Levine D, Richards J. Pathological and other abnormal gaits. In: Whittle’s Gait Analysis. 6th ed. Elsevier; 2023.
  7. Pirker W, Katzenschlager R. Gait disorders in adults and the elderly: A clinical guide. Wien Klin Wochenschr. 2017;129(3-4). doi:10.1007/s00508-016-1096-4
  8. Gurney B. Leg length discrepancy. Gait Posture. 2002;15(2). doi:10.1016/S0966-6362(01)00148-5
  9. Perry J. Normal and Pathological Gait. In: Hsu JD, Michael JW, Risk JR, eds. AAOS Atlas of Orthoses and Assistive Devices. 4th ed. Mosby/Elsevier; 2008.
  10. Rancho Los Amigos National Rehabilitation Center. Observational Gait Analysis Handbook. Los Amigos Research and Education Institute, Inc.; 2001.
  11. Nonnekes J, Goselink RJM, Růzicka E, Fasano A, Nutt JG, Bloem BR. Neurological disorders of gait, balance and posture: A sign-based approach. Nat Rev Neurol. 2018;14(3). doi:10.1038/nrneurol.2017.178
  12. Alexander NB. Differential diagnosis of gait disorders in older adults. Clin Geriatr Med. 1996;12(4). doi:10.1016/s0749-0690(18)30196-4
  13. Sudarsky L. Neurologic disorders of gait. Curr Neurol Neurosci Rep. 2001;1(4). doi:10.1007/s11910-001-0089-4
  14. Cerny K. Pathomechanics of stance: Clinical concepts for analysis. Phys Ther. 1984;64(12). doi:10.1093/ptj/64.12.1851
  15. Collyer  TA, Murray  AM, Woods  RL,  et al.  Association of dual decline in cognition and gait speed with risk of dementia in older adults.   JAMA Netw Open. 2022;5(5):e2214647.
  16. Beauchet O, Allali G, Berrut G, Hommet C, Dubost V, Assal F. Gait analysis in demented subjects: Interests and perspectives. Neuropsychiatr Dis Treat. 2008;4(1):155-60. doi: 10.2147/ndt.s2070.
  17. Pirker, W, Katzenschlarger, R. Gait disorders in adults and the elderly: A clinical guide. Wien Klin Wochenschr. 2017;129:81-95. Doi: 10.1007/s00508-016-1096-4.

Original Version of the Topic

Heakyung Kim, MD, Hannah Aura Shoval, MD, Teerada Ploypetch, MD. Biomechanic of gait and treatment of abnormal gait patterns. 9/20/2014

Previous Revision(s) of the Topic

Julio Vazquez-Galliano, MD, Ibtehal Kimawi, MD, Lawrence Chang, DO, MPH. Biomechanic of Gait and Treatment of Abnormal Gait Patterns. 8/3/2020

 Author Disclosure

Rebecca Ann Speckman, MD, PhD
Nothing to Disclose

Ian J. Kim, MD
Nothing to Disclose

Michael J. Gallagher, MD
Nothing to Disclose