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Normal Gait
Normal gait is generally established by 4-8 years of age.1(p100)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.2Mature 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

Minimized center of gravity (COG) movement vertically and horizontally creates gait efficiency. COG is 5cm anterior to second sacral vertebra with 5 cm horizontal and vertical displacement during average adult male step.4Maintaining COG over the base of support, including legs and assistive device, prevents falls.4Six determinants of gait minimize the excursion of COG and energy expenditure.5The 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).6In the frontal plane, the gluteus medius exerts abduction counterforce when standing on one leg.

A step is the distance covered by one foot. Cadence is the frequency of steps. A stride is heel strike to heel strike on the same foot7including 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 10% of time in double support, and 40% in single limb support.6Stance phase is subdivided into initial contact, loading response, midstance, terminal stance and pre-swing. Swing phase is subdivided into initial swing, midswing and terminal swing

Stance PhaseDescriptionGRF DiagramJoint6,8Concentric ContractionEccentric Contraction (for Control)6,8
Initial ContactRight foot contacts ground (Heel strike)Hip: Flexion 30°Gluteus Maximus/ Hamstring

Gluteus Medius (pelvic stabilization)

Knee: ~full extensionHamstring/ Quadriceps stabilize
Ankle: NeutralPretibial (tibialis anterior, extensor digitorum longus and extensor hallucislongus)
Loading ResponseWeight acceptance, shock absorptionHip: Flexion 30°

High flexion torque

Gluteus Maximus, Hamstrings (shock absorption/limit hip flexion)

Adductor Magnus (shock absorption)

Gluteus Medius (pelvic stabilization)

Knee: flexion 15-18°Quadriceps (advances femur over tibia)
AnklePretibial (Pulls tibia over Calcaneus)
MidstanceLeft toe comes off ground; right leg supports weightHip (Initial Flex 30° Final: Flex 10°)Gluteus Medius/Glut Max- Hip Abduction

Gluteus Maximus- Initially: Hip extension

Knee (Initial Flex 15° Final: Netural position)Quadriceps (early midstance only)Lateral collateral ligament (Counters varus force)
Ankle (Initial: PF 10° Final: DF 7°)Calf (Soleus/Gastrocnemius) (advances tibia over foot and provides stability)
Terminal StanceRight heel comes off groundPelvis (5° rotation which increases step length)
Hip (Extension 10°)IliopsoasGluteus Medius

Tensor Fasciae Lata (counters posterior hip vector)

KneePassive Joint Stability and forward action
Ankle (DF to 10°)Calf (“Forefoot Rocker”)
Pre-SwingLeft foot floor contact. Right pre-swing stage begins with right knee quickly bending and preparing to swing forwardHip (flexes to neutral)Iliopsoas

Rectus femoris Sartorius

Adductor Longus (decelerates abduction)

Knee (moves to 35° of flexion)Passive knee flexionQuadriceps
Ankle (moves from DF 10° to PF 20°)Calf
Swing PhaseDescriptionGRFJointConcentricEccentric
Initial SwingRight toe comes off ground accelerating forwardHip (flexion 20°)Iliopsoas, gracilis, sartorius
Knee (Flexion to 60-65°)gracilis, sartorius, biceps femorisQuadriceps
Ankle (PF 20° to PF 5-10°)Pretibial muscles reduce plantar flexion (foot clearance)
MidswingRight foot swings past left and right foot deceleratesPelvic Neutral
Hip (flexion 30°)Iliopsoas, Pretibial muscles (clears leg)
Knee (extends from PF 60° to PF 30°)Passively extending kneeHamstrings (midway deceleration)
Ankle (PF ~1cm clearance)Pretibial muscles (clears foot)
Terminal SwingRight tibia vertical to floor and right knee continues extension, swinging right foot forward. Right foot decelerates in preparation for landing.Pelvis Rotation
Hip (deceleration to stop flexion at 30°)Gluteus Max


KneeHamstrings (stabilizes knee)
AnklePretibial muscles (foot clearance, then placement)



Pathologic Gait

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: Weight bearing avoided on painful limb. Decreased step length of uninvolved side.
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): Drop of pelvis on the unaffected side.
Pathomechanism: Compensated gait causes the trunk to leans toward the affected side.
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.
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: Posterior capsule locks affected knee joint, hyperextending knee by forward trunk leaning.
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: Unable to heel strike, leading to initial contact with toes. Incomplete lesion still has heel strike but unable to control transition to foot flat causing “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: 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 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

B-2. Upper Motor Neuron Lesion (UMNL)

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 from spasticity/contracture of ankle plantar flexor or ankle dorsiflexion weakness. 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: hamstring and hip flexor spasticity/contractures in addition to true equinus. 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 spasticity/contractures.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: similar to jump knee with hip/knee flexion spasticity/contractures but walks in ankle dorsiflexion from weak ankle plantar flexor. 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.


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, 20 Displacement 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.

Future treatments may involve regenerative medicine for reforming tendon/muscle/bone in pathological gait in combination with surgical correction.


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.


1. Esquenazi A, and Mukul Talaty M.Gait Analysis: Technology and Clinical Applications. In: Braddom RL. Physical Medicine and Rehabilitation. St. Louis, MO: Elsevier Health Sciences; 2010.

2. Ivanenko YP, Dominici N, Lacquaniti F. Development of independent walking in toddlers.Exerc Sport Sci Rev. 2007;35(2):67-73.

3. Sutherland DH, Olshen R, Cooper L, Woo SL. The development of mature gait.J Bone Joint Surg Am. 1980;62(3):336-353.

4. Cuccurullo S, ed.Physical Medicine and Rehabilitation Board Review. 2nd ed. New York, NY: Demos Medical Publishing; 2010:459

5. Saunders JB, Inman VT, Eberhart HD. The major determinants in normal and pathological gait.J Bone Joint Surg Am. 1953;35-A(3):543-558.

6. Gonzalez EG, Meyers SJ, Edelstein JE, et al. eds.Downey & Darling’s physiological basis of rehabilitation medicine, 3rd ed. Boston: Butterworth-Heinemann; 2001.

7. Frontera WR.DeLisa’s Physical Medicine and Rehabilitation: Principles and Practice, Two Volume Set Prof. Lippincott Williams & Wilkins; 2010.

8. Ayyappa E. Normal human locomotion, Part 2: motion, ground reaction force and muscle activity. Journal of Prosthetics and Orthotics. 1997.

9. DeLisa JA. Gait Analysis in the Science of Rehabilitation. Darby, PA: DIANE Publishing; 1998.

10. Weinstein, SL, Flynn JM, eds.Lovell and Winter’s Pediatric Orthopaedics. Baltimore, MD: Lippincott Williams & Wilkins; 2005:1632.

11. Hennessey WJ. Lower limb orthotic devices. In: Braddom RL.Physical Medicine and Rehabilitation. St. Louis, MO: Elsevier Health Sciences; 2010.

12. Alexander M, Matthews D, eds.Pediatric Rehabilitation: Principles and Practice,. 4th ed. New York, NY: Demos Medical Publishing; 2009:281-282.

13. Bushby K, Finkel R, Birnkrant DJ, et al. Diagnosis and management of Duchenne muscular dystrophy, part 2: implementation of multidisciplinary care.Lancet Neurol. 2010;9(2):177-189.

14. Rodda J, Graham HK. Classification of gait patterns in spastic hemiplegia and spastic diplegia: a basis for a management algorithm.European Journal of Neurology. 2001;8(Supp 5):98-108.

15. 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.

16. Sutherland DH, Cooper L. The pathomechanics of progressive crouch gait in spastic diplegia.Orthop Clin N Am. 1978;9:143-154.

17. Borton DC, Walker K, Pirpiris M, Nattrass GR, Graham HK. Isolated calf lengthening in cerebral palsy: outcomeanalysis of risk factors.J Bone Joint Surg (Br). 2001;83:364-370.

18. Miller F, Dabney K, Rang M. Complications in cerebral palsy treatment. In: Epps CH, Bowen JR, eds.,Complications in Pediatric Orthopaedic Surgery. Philadelphia: JB Lippincott, 1995;498-500.

19. Waters RL, Lunsford BR. Energy expenditure of normal and pathological gait: application to orthotic prescription. In:Atlas of Orthotics. St. Louis, MO: Mosby, 1985.

20. Waters RL, Mulroy S. The energy expenditure of normal and pathologic gait.Gait Posture. 1999;9(3):207-231.

Author Disclosure

Heakyung Kim, MD
Allergan: Honorarium, Consulting; Allergan: PI, Research Grants, Other roles

Hannah Aura Shoval, MD
Nothing to Disclose

Teerada Ploypetch, MD
Nothing to Disclose