Overview and Description
Normal gait is a series of rhythmical, alternating movements of the trunk and limbs which results in the forward progression of the center of gravity. It is generally established by 4-8 years of age.1 Toddler’s gait has increased trunk movement, wide base of support, arms in high guard position, high foot lift during swing, flat-footed contact, and short, quick, rigid steps with the toes pointing outward.2 Mature gait has reciprocal arm-swing and heel strike with increased velocity, cadence, step length, single-limb stance time, and ratio of pelvis span to ankle spread when both feet are on the ground, due to increased stability and limb length.3
The center of gravity (COG) of the human body is a hypothetical point around which the force of gravity appears to act. It is point at which the combined mass of the body appears to be concentrated25. COG is 5cm anterior to second sacral vertebra with 5 cm horizontal and vertical displacement during average adult male step.4 Maintaining COG over the base of support, including legs and assistive device, prevents falls. Minimized center of gravity (COG) movement vertically and horizontally creates gait efficiency. 4 Six determinants of gait minimize the excursion of COG and energy expenditure.5 The first five minimize vertical motion, horizontal planar pelvic rotation, frontal planar pelvic tilt, knee flexion, ankle and knee mechanisms. The sixth minimizes horizontal motion by lateral pelvic displacement.5
Ground reaction force (GRF) applies Newton’s Law of equal and opposite force so that during standing, GRF passes through the center of the foot anterior to the ankle (counterforce plantar flexors), slightly anterior to the knee (counterforce posterior ligamentous capsule), and slightly posterior to the hip (counterforce iliofemoral ligaments).6 In the frontal plane, the gluteus medius exerts abduction counterforce when standing on one leg.
Important measures of gait include walking speed, cadence (number of steps per minute), walking base width (measured from midpoint to midpoint of both heels), step length (measured from the point of foot contact to the point of contralateral foot contact) and stride length (linear distance covered by one gait cycle). The gait cycle is divided into stance and swing phases. Stance is weight bearing on a single leg; swing is advancing the limb while off the floor. During walking, 60% of time is stance and 40% is swing, with 20% of time in double support, and 40% in single limb support.6 Stance phase is subdivided into initial contact (from 0% to 2% of the gait cycle), loading response (from 2% to 12% [opposite toe off] of the gait cycle), mid stance (from 12% to 31% [heel rise] of the gait cycle), terminal stance (from 31% to 50% [initial contact from opposite foot] of the gait cycle) and pre-swing (from 50% to 62% [toe off] of the gait cycle). Swing phase is subdivided into initial swing (from 62% to 75% [foot of the swing limb is next to the foot of the stance limb] of the gait cycle), mid swing (from 75% to 87% [tibia of the swing limb is vertical] of the gait cycle) and terminal swing (from 87% to 100% [immediately before the next initial contact] of the gait cycle) 27.
The preferred walking speed in healthy adults up to the age of 59 years is approximately 1.4 m/s. Average stride lengths in healthy adults range between 150 and 170 cm. The average cadence in young adults was reported to range between 115 and 120 steps/min. 26
Relevance to Clinical Practice
Ageing is associated with a decline in gait speed, shorter step length and slower cadence. These changes provide greater stability because both feet are on the ground simultaneously for a greater percentage of the cycle. Elderly subjects prefer a 40 % wider step width than young persons (average step width in elderly women approximately 8 cm and in elderly men 10 cm).26,30
Pathologic gait results from impaired strength range of motion, proprioception, pain, or balance combined with mechanical compensations, and can have musculoskeletal and neuromuscular etiologies.
A. Musculoskeletal etiologies
1) Pain: “Antalgic gait”
Causes: Pain with weight bearing
Pathomechanism: Characterized by a shorter step length and stance time on the side of the painful lower extremity. It may be accompanied by ipsilateral trunk lean with hip pain or a contralateral trunk lean with knee and foot pain.
Treatment: treat underlying cause, analgesia, assistive device (AD) in contralateral hand.
2) Leg length discrepancy (LLD)9
Causes: True or apparent leg length discrepancy
Pathomechanism: Shortened side: pelvic drop, decreased hip and knee flexion, ankle plantar flexion (vaulting, toe walking). Lengthened side: hip hiking, circumduction, excessive hip and knee flexion (steppage gait), foot hyperpronation.
Treatment10: For <2cm: no treatment. For >2cm: shoe lift or consider surgery. Lift <2cm inside shoe, >2cm outside shoe. Surgical options: shortening surgery (epiphysiodesis or femoral shortening), lengthening surgery (femur/tibia), correction muscle or joint contracture.
B. Neuromuscular Etiologies
B-1. Lower Motor Neuron Lesion (LMNL) (or other causes of muscular weakness)
1) Hip abductor weakness (Trendelenburg gait): Excessive downward drop of the contralateral pelvis during stance. Referred to as positive Trendelenburg sign if present during single-limb standing.
Pathomechanism: Compensated gait causes the trunk to lean laterally toward the stance lower extremity of the weak side. If bilateral, it is referred to as a waddling gait.
Treatment: AD in contralateral hand, gluteus medius strengthening.
2) Hip extensor weakness (Posterior lurch gait): Backward trunk lean with hyperextended hip during stance phase of affected limb. This action moves the line of gravity of the trunk behind the hip and reduces the need for hip extension torque.
Pathomechanism: Use of iliofemoral ligament to lock hip in extension to prevent trunk falling forward.
Treatment: Strengthen gluteus maximus. Keep compensatory mechanism, do not fix lumbar hyperlordosis
3) Knee extensor weakness: Knee buckling (uncompensated), genu recurvatum (compensated).
Pathomechanism: Knee remains fully extended throughout the stance. An associated anterior trunk lean in the early part of stance moves the line of gravity of the trunk slightly anterior to the axis of rotation of the knee. This keeps the knee extended without action of the knee extensors. This gait deviation may lead to an excessive stretching of the posterior capsule of the knee.
Treatment: Ankle Foot Orthosis (AFO):11(p342) Solid AFO set at a few degrees of plantar flexion or a hinged AFO with a neutral dorsiflexion stop. Quadriceps strengthening.
4) Ankle dorsiflexion weakness (Steppage gait and foot slap)
Pathomechanism: When there is severe weakness, the initial contact with the ground is made by the forefoot followed by the heel region. Mild weakness, the initial contact is made with the heel followed by a rapid ankle plantar flexion, causing a “foot slap” During the swing phase, toes may drag/catch. Compensatory is “steppage gait” with excessive hip and knee flexion or body shift to clear foot.
Treatment: Posterior leaf spring AFO or hinged AFO with dorsiflexion assist or plantar flexion stop for mediolateral instability. Role of electrical stimulation (ES) to prevent atrophy of anterior tibialis and/or functional ES (FES) to activate ankle dorsiflexor.
5) Ankle Plantar Flexor Weakness (Calcaneal gait):
Pathomechanism: Heel remains in contact with the ground late in terminal stance. Lack of eccentric contraction of ankle plantar flexor causes GRF to pass behind knee, creating knee flexion moment with excess tibial motion over ankle during mid to late stance. Increased quadriceps contraction needed to prevent knee buckling. Contralateral leg step length (swing duration) reduced by unstable stance of affected limb. Heel off delayed and push off phase decreased.
Treatment: Hinged AFO with dorsiflexion stop or solid AFO set at a few degrees plantar flexion to pass GRF anterior to knee to prevent buckling.
6) Myopathic gait (Waddling gait):
Pathomechanism: Proximal muscle weakness (hip girdle muscles) resulting in combination of posterior lurch and bilateral Trendelenburg, “waddling gait”. Toe-walking with disease progression. Compensatory mechanism moves GRF anterior to knee joints to prevent knee buckling from extensor weakness.12
Treatment: submaximal aerobic and low-resistant strength training, prevent fixed contractures by stretching and night-time braces. Lengthening surgery may be considered to prolong ambulation in patients with good muscle strength limited by contractures.13
7.) Neurogenic Claudication:Pain and neurological deficits with ambulation
Pathomechanism: Usually secondary to lumbar spinal stenosis. Will have hyperlordosis with stenosis and vertebral shift if walking/standing.21 Pain and neurologic deficits better with spinal flexion – better walking uphill or cycling.21 Symptoms worse on hyperextension.
Treatment: Lumbar brace and physical therapy to correct lordotic posture. May need surgical decompression of spine if symptoms not better with conservative measures.21
B-2. Upper Motor Neuron Lesion (UMNL) (or other causes involving the central nervous system)
Spastic hemiplegia, spastic diplegia/quadriplegia, from cerebral palsy and stroke. 14 Weakness in UMNL can be treated with bracing as above, including FES.15For details: http://www.aacpdm.org/UserFiles/file/IC19_v1.pdf
1) True Equinus Gait
Pathomechanism: ankle in plantar flexion throughout stance and hips/knees extended related to spasticity/contracture of ankle plantar flexors or weakness of ankle dorsiflexors.. May present with compensatory genu recurvatum.14
Treatment: Hinged AFO with dorsiflexion assist and/or plantar flexion stop; chemoneurolysis of gastroc-soleus muscle; surgical treatment is Tendo-Achilles Lengthening (TAL).
2) Jump Gait
Pathomechanism: the ankle is in equinus, the knee and hip are in flexion, there is an anterior pelvic tilt and an increased lumbar lordosis. May be related to hamstring/hip flexor spasticity/contractures. May present with “stiff knee gait” from hamstring quadriceps co-contraction.14
Treatment: Hinged or solid AFO, according to the integrity of the plantar-flexion, knee-extension couple. Single event multi-level chemoneurolysis or single event multi-level surgery of hamstring, iliopsoas, gastroc-soleus +/- rectus femoris. Selective dorsal rhizotomy. It is important to distinguish jump knee with true equinus from apparent equinus.
3) Apparent Equinus
Pathomechanism: Not true equinus but walk in equinus position to compensate for severe hip and knee flexion throughout the stance phase; the ankle has a normal range of dorsiflexion. May be related to spasticity/contractures of hip/knee flexors.14
Treatment: Single-event multi-level chemoneurolysis or surgical lengthening of iliopsoas/hamstrings +/- gastrocsoleus. Do not solely relax gastroc-soleus muscle, as that causes more hip and knee flexion and iatrogenic crouched gait.
4) Crouch Gait
Pathomechanism: excessive dorsiflexion or calcaneus at the ankle in combination with excessive flexion at the knee/hip. Common with severe diplegia and spastic quadriplegia, especially in older or overweight children. Most common cause in spastic diplegia16,17: isolated lengthening of heel cord in younger children without control of spasticity/contracture of hamstrings/iliopsoas, leading to rapid increase in hip/knee flexion.18Result is energy-inefficient gait, with anterior knee pain, patellar pathology in adolescence. Also caused by botulinum injections to gastroc-soleus without addressing hamstrings/iliopsoas or providing adequate orthotic support.
Treatment: Single-event multi-level chemoneurolysis in younger and less involved children. Lengthening of hamstrings and iliopsoas, adequate correction of bony problems (medial femoral torsion, lateral tibial torsion), foot stabilization in older children with contractures. Solid ground reaction AFO (GRAFO) or articulated GRAFO with dorsiflexion stop only with fully knee extension (after chemoneurolysis or surgery), otherwise solid AFO.
5) Parkinsonian Gait
Pathomechanism: rigidity (pelvis/thorax rotating en bloc, reduced arm swing), postural instability (trunk flexion, protracted shoulders, flexed hips/knees), bradykinesia (slow motion, inability to change direction) with possible festination.
Treatment: external tactile, auditory, or visual cues timed with step initiation or step maintenance. Rolling walker improves efficiency, independence, safety.
6.) Cautious Gait (also known as “Senile Gait”)
Pathomechanism: Associated with older age-related brain disease or dysfunction and fear of falling.21 Slow, wide based gait, with stooped posture and reduced arm swing.21
Treatment: Gait and balance training. Contact guard to mid assist and reassurance may be of help to prevent fear of falling.
7.) Spastic Gait
Pathomechanism: Usually secondary to brain injury
A.) Hemiparetic: Paretic side with flexor muscle synergy noted. Typical features are as follows for the affected side: Upper arm is adducted and internally rotated with flexion at the shoulder, elbow, and wrist. Hip and knee flexed. Foot inverted and plantarflexed. Lower leg circumducts during swing phase, also known as “Wernicke-Mann gait.”21
B.) Paraparetic: similar to hemiparetic gait but involves bilateral lower legs. Gait is spastic, spastic and ataxic and/or scissoring.21
Treatment: Physical therapy for gait and balance training. Anti-spastic medications and botulinum injections to reduce muscle tone and spasticity. Pain control. Need to emphasize importance of hygiene to prevent infections and pressure injuries.
8.) Cerebellar Ataxic Gait
Pathomechanism: Usually secondary to cerebellar injury. Balance worse than leg placement. Differentiate from sensory ataxia which is proprioceptive deficits from dorsal column injury and worse with Romberg testing. Cerebellar gait initiation is normal. However, leg coordination is inconsistent and “broad-based, insecure, and wobbly.”21 Unilateral cerebellar lesions have ipsilateral ataxia, whereas vermis causes truncal ataxic gait.
Treatment: Usually gait and balance training. Assistive devices may help with gait instability.
9.) Frontal Gait Ataxia
Pathomechanism: Usually secondary to injury to frontal lobe and connecting networks. May be secondary to vascular disease or hydrocephalus. May involve other lobes of brain and associated with Alzheimer’s disease. Difficult to classify condition. Not Parkinsons disease or any neurologic tremor. Patients have lost the ability to walk, change positions from sit to stand, and have a broad base gait with short stride length and are unable to initiate gait on own.21 Will also have en bloc gait, freezing episodes, and retropulsion. Treatment: Gait and balance training. Anti-Parkinsons medications or therapeutic modalities has not clinically been shown to work for this condition.
Cutting Edge/Unique Concepts/Emerging Issues
Pathologic gait is slower, requiring more energy and is disability objectively measured by oxygen consumption or heart rate changes. In normal subjects hinged knee orthosis increases oxygen consumption with slower speeds as degree of knee flexion contracture is increased. 19,20Displacement of center of gravity or other biomechanical factors give an objective indication of energy efficiency before and after an intervention. 7 Technological advancement in recording physiology, biomechanics, and kinesiology of gait are improving assessment for intervention and improvements after intervention. New technological advances for improving gait are wearable sensors and non-wearable cameras, platforms, and walkways which allow for identification of gait dysfunctions and inform us on how to adapt to them,23 while robotics, weight supported treadmills, harnesses, belts, exoskeletons, platforms, and EMGs/FES systems are all being used for functional gait training.24
Future treatments may involve regenerative medicine for reforming tendon/muscle/bone in pathological gait in combination with surgical correction.
Gaps in Knowledge/Evidence Base
Technological advances will allow more sophisticated assessment gait and help elucidate appropriate interventions. Additionally, electrical stimulation, neurolysis, and surgical correction should be explored for the optimal treatment regimens.
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- Graham HK, Selber P, Rodda J, et al. “The knee in cerebral palsy: Current management from lessons learnt through three dimensional gait analysis.”American Academy for Cerebral Palsy and Development Web site. http://www.aacpdm.org/UserFiles/file/IC19_v1.pdf. Accessed August 19, 2014.
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- Shanahan CJ, Boonstra FMC, Cofré Lizama LE, et al. Technologies for Advanced Gait and Balance Assessments in People with Multiple Sclerosis. Front Neurol. 2018;8:708.
- Mikolajczyk T, Ciobanu I, Badea DI, Iliescu A, Pizzamiglio A, Schauer T, Seel T, Seiciu PL, Turner DL, Berteanu M. Advanced technology for gait rehabilitation: An overview. Sage. Advances in Mechanical Engineering. 2018;10(7):1-19.
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Original Version of the Topic
Heakyung Kim, MD, Hannah Aura Shoval, MD, Teerada Ploypetch, MD. Biomechanic of gait and treatment of abnormal gait patterns. 09/20/2014
Julio Vazquez-Galliano, MD
Nothing to Disclose
Ibtehal Kimawi, MD
Nothing to Disclose
Lawrence Chang, DO, MPH
Nothing to Disclose