Idiopathic Toe Walking • Persistent toe walking after 2 years of age • No identified underlying diagnosis • May or may not have equinus contractures • Knee not affected – full knee extension at initial contact

Toe Walking: How to Know Wh to Who t Worry W About Ab t Part 2 Sylvia Õunpuu, MSc Kristan Pierz, MD AACPDM 2013

Eastwood et al., JPOB, 1997.; Hicks et al., JPO, 1988.; Williams et al., J Child Neurol, 2013

Idiopathic Toe Walking

Idiopathic Toe Walking - Kinematics Hip Flexion-Extension

60

• Ability to isolate voluntary control at foot and ankle • No evidence of spasticity

• Video of chair exam

• Increased ankle plantar flexion through out stance and swing • Full knee extension at initial contact • Full knee flexion in swing • Compensatory increased hip flexion

Flx

Ext -20

80

Knee Flexion-Extension

Flx

Ext -20

Plantar-Dorsiflexion

40 Dor deg Pla -40

25%

50%

75%

Gait Cycle

Idiopathic Toe Walking - Kinetics 40

• Typical peak power generation in terminal stance • Consistent with typical yp ankle plantar flexor strength

EMG – Idiopathic Toe Walking • Premature onset gastrocnemius activity in terminal swing • Early termination tibialis activity in terminal swing and activity in mid stance • Very V similar i il findings fi di for f same muscles l in i CP toe walking • No EMG response to passive stretch

Plantar-Dorsiflexion

Dor

deg

Pla

-40

2.0

Ankle Moment

Ext

Nm/kg

Flx

-1.0

3.0

Right Side EMG

Ankle Power

5

Right Gastrocnemius

5

Right Gastrocnemius*

5

Right Gastrocnemius**

Gen

W/kg

V

V

V

-5

-5

-5

Abs

5 -2.0

-5

IC #33 Toe Walking – Case Examples

% Gait Cycle

Right Anterior Tibialis

V

5

% Gait Cycle

Right Anterior Tibialis*

V % Gait Cycle

-5

5

% Gait Cycle

Right Anterior Tibialis**

V % Gait Cycle

-5

% Gait Cycle

Part 2 - 1

Idiopathic Toe Walking • May be able to normalize some kinematic and kinetic variables on demand • “Doctor walk” may look better but still have subtle differences

• Treatment depends on severity – Reassurance – Stretching/PT – Casting – Bracing/night splinting – Surgery (level depends on Silfverskiöld test) – No role for BOTOX due to lack of spasticity

S

Alvarez et al., Gait Posture, 2007.; Engstrom et al., JBJS, 2013.; Stricker & Angulo, JPO, 1998

Pendharkar et al., Gait Posture, 2012

Pre – Post Sx for Toe Walking • Kinematic changes in stance and swing • Heel initial contact and pplantar grade g foot • Power generation at push off maintained

40

Unilateral Idiopathic Toe Walking

Plantar-Dorsif lexion

• Red flag • If diagnosis of hemiplegia is negative • Examine for other possibilities

Dor deg Pla

-40

Ankle Moment

2.0

– Spinal – Tumor – Etc.

Ext Nm/kg Flx

-1.0

Ankle Pow er

3.0

Pre – dashed line Post – solid line

Idiopathic Toe Walking Treatment

W/kg

-2.0

25%

50%

75%

Gait Cy c le

Cerebral Palsy • Lack of selective inhibition can result in unrestricted muscle firing/spasticity +/plantar flexor contracture • Gastrocnemius more involved than soleus • Knee may or may not be involved • Can’t voluntarily correct

Cerebral Palsy • Equinus alone • Equinus plus limited knee extension • Limited knee extension without equinus

80

Knee Flexion-Extension

Flx

Ext

E

-20

40

Plantar-Dorsiflexion

Dor deg Pla -40

E 25%

50%

75%

Rose et al, JPO, 1999

IC #33 Toe Walking – Case Examples

Part 2 - 2

Cerebral Palsy • Equinus alone • Equinus plus limited knee extension (dashed) • Limited knee extension without equinus (solid)

80

EMG – Cerebral Palsy

Knee Flexion-Extension

Flx

Ext

E

-20

40

Plantar-Dorsiflexion

• Continuous activity for 100% gait cycle for gastrocnemius common • Increased of anterior tibialis activity at toe off with minimal lower level activity through remainder of gait cycle • EMG response to passive stretch

Dor

Right Side EMG

deg

5

Pla -40

E 50%

75%

-5

5

% Gait Cycle

Right Anterior Tibialis*

% Gait Cycle

-5

V -5

% Gait Cycle

• Kinematic differences • Vaulting side:

– Vaulting

• Hemiplegia p g • Clinical exam differences

– Dorsiflexion in swing – Typical yp dorsiflexion at initial contact – Typical knee modulation

video

% Gait Cycle

80

Knee Flexion-Extension

Flx

A49595 Ext -20

40

– Passive ROM – Ability to isolate voluntary contraction – Typical strength

% Gait Cycle

Right Anterior Tibialis**

5

V

Vault vs. Involved Side

Cerebral Palsy – Vault vs. Involved Side

Plantar-Dorsiflexion

Dor deg Pla

Hemiplegic side = dashed line Vault side = solid line

Vault vs. Involved Side 40

– Dorsiflexor moment loading response (not shown) – Reduced power generation terminal stance

% Gait Cycle

Right Anterior Tibialis

Right Gastrocnemius**

5 V

-5

-5

• Kinetic differences • Vault

Right Gastrocnemius*

-5

V

• Compensatory toe walking

5 V

5

25%

Right Gastrocnemius

V

Plantar-Dorsiflexion

40

Dor

Dor

deg

deg

Pla

Pla

-40

2.0

2.0

Ext

Ext

Nm/kg

Nm/kg

Flx

Flx

-1.0

-1.0

3.0

Ankle Power

3.0

Gen

Gen

W/kg

W/kg

Abs

Abs

-2.0

25%

50%

75%

Gait Cycle

Cerebral Palsy Treatment

Plantar-Dorsiflexion

-40

Ankle Moment

-40

Ankle Moment

Ankle Power

• • • • •

Stretching/PT Casting Bracing/night splinting Surgery (level depends on Silfverskiöld test) Botox can decrease spasticity but will not address contracture

-2.0

(vault)

(involved)

IC #33 Toe Walking – Case Examples

Part 2 - 3

Pre vs. Post Involved Side • Ankle Kinematics

80

Flx

– Improved dorsiflexion in stance and swing (gastrocnemius lengthening) – Possible due to positive confusion test

-20 20

Plantar-Dorsiflexion

40

Dor

– Changes a result of multi-level surgery (hamstrings and rectus procedures included)

deg

Pla

-40

A49595 Ankle Moment

2.0

Ext

Nm/kg

Flx

-1.0

Ankle Power

3.0

Gen

W/kg

-40

25%

50%

75%

Abs

Gait Cy cle

80

Ext

40

A49595 Plantar-Dorsiflexion

Dor

deg

-2.0

25%

50%

75%

Gait Cy c le

Pre vs. Post Non-involved Side Plantar-Dorsiflexion

40

• Ankle Kinetics

Flx

-20

(Pre = dashed, Post = solid)

Knee Flexion-Extension

– Improved dorsiflexion in stance and swing – Increased peak knee flexion in swing to clear limb (not needed prior to treatment due to contralateral toe walking)

Dor

Pla

Pre vs. Post Non-involved Side

• Knee Kinematics

– Improved peak plantar flexor moment and power generation terminal stance – Improved ankle moment and power modulation (shape of curve)

deg

(Pre = dashed, Post = solid)

• Ankle Kinematics

Plantar-Dorsiflexion

40

• Ankle Kinetics

A49595

Ext

• Knee Kinematics

Pre vs. Post Involved Side

Knee Flexion-Extension

– Heel initial contact unchanged – Improved peak power generation i terminal i l stance – Ankle functioning more optimally with elimination of the vault

Dor

deg

Pla

-40

2.0

Ext

Ankle Moment

A49595

Nm/kg

Flx

-1.0

Ankle Power

3.0

Gen

Pla W/kg

-40

25%

50%

Abs

75%

Gait Cyc le

(Pre = dashed, Post = solid)

-2.0

25%

(Pre = dashed, Post = solid)

Charcot-Marie-Tooth Disease • Hereditary Motor and Sensory Neuropathies – > 40 genes associated with different forms of disease (CMT 1A, CMT 1B, CMT 2, CMT 3, CMT 4,, CMT X,, etc,, etc)) – Abnormalities in myelin sheath or axon – Peripheral nerves affected – motor and/or sensory

IC #33 Toe Walking – Case Examples

50%

75%

Gait Cy c le

CMT is characterized by: distal muscle weakness and imbalance associated foot and ankle deformities resulting compromised gait function

Gait function is a very important quality of life indicator for persons with CMT.

Part 2 - 4

CMT – toe walking

Ankle Function

Plantar-Dorsiflexion

40

Dor

Deg

• Least common presentation

• Equinus through out the gait cycle • Toe contact pattern • Plantar flexor contracture (add values) • Reduced power generation in terminal stance • Strength profile variable plantar flexor weakness

Õunpuu et al., Gait and Posture, 2013.

Knee Function

-40

2.0

*

Pfl

Nm/kg

Dfl

-1.0

*

Ankle Moment

*

3.0

Ankle Power

Gen

W /kg

*

Abs

-2.0

Hip Dysplasia • Toddler w/ unilateral toe walking (if unilateral hip dislocation) • Limited hipp abduction • Supple ankle/knee • May be associated with h/o other “packaging problems” (torticollis, metatarsus adductus)

• Typical extension at initial contact • Typical peak and timing to peak flexion in swing

Hip Dysplasia • Toe walking is a compensation for the leg length difference due to dislocated hip • Apparent leg length difference since hip is high riding • Treat the hip not the limp

*

Pla

40

Leg Length Difference

Plantar-Dorsiflexion

Dor deg

• A60628 Pla -40

25%

50%

75%

Gait Cycle

hip dislocation = dashed line

IC #33 Toe Walking – Case Examples

• Similar to DDH, but there is an actual LLD rather than just “apparent” • Scoliosis may also give “apparent” LLD if associated w/ pelvic obliquity • Too many reasons to cover here (list included for reference) • Careful history (congenital vs acquired)

Part 2 - 5

Congenital • Hypoplasia syndrome • Proximal femoral focal deficiency • Tibial deficiencies • Fibular Fib l deficiencies d fi i i • Hemiatrophy • Hemihypertrophy • Idiopathic • Klippel-Trenaunay-Weber syndrome

Aquired

• Beckwith-Wiederman syndrome • Proteus syndrome • Skeletal dysplasia • Ollier Olli di disease • Fibrous displasia • Neurofibromatosis • Multiple hereditary exostosis

• • • • • • • • • • • • •

Leg Length Difference • Which is the abnormal limb? (shortening vs overgrowth) • Toe walking g is one compensation • Patients may also compensate w/ asymmetric knee/hip/pelvis ROM

40

Plantar-Dorsiflexion

deg

•PlaB41910 25%

50%

Hemophilia Pigmented villonodular synovitis Neurologic Acute brain injury Spinal cord injury Peripheral nerve injury Cerebral palsy Myelomeningocele Poliomyelitis Tumors Tumor treatment Enchondromatosis Hemangiomas

Tumor

Dor

-40

• • • • • • • • • • • • •

Trauma Acute bone loss Physeal Injury Fracture healing Burns Irradiation Iatrogenic Infection Osteomyelitis Septic arthritis Pupura fulminans Inflammation Juvenile rheumatoid arthritis

75%

Gait Cycle

short leg = dashed line

• Tumor can put pressure on calf muscle itself or a nerve • Vascular malformation may result in gastrocnemius spasm/contracture • Unilateral; may be associated w/ tenderness

Song et al., JBJS, 1997 Domb et al., CORR, 2004. Skabelund & Andrews, J Orthop Sports PT, 2013

Hereditary Spastic Paraparesis (Familial Spastic Paraplegia) • Progressive lower extremity weakness and increased tone/spasticity • Selective voluntaryy control including ankle • MRI brain/spine usually normal • Positive family history • > 50 types Fink JK, Acta Neuropathol, 2013; Wolf et al. Gait Posture, 2011

IC #33 Toe Walking – Case Examples

Disease Progression • Bilateral crouch maintained • Bilateral increasingg toe walking due to increasing equinus • Bilateral increasing plantar flexor contracture: 5◦ to -20 ◦ (R) and -10 ◦ (L)

80

Knee Flexion-Extension 80

Flx

Knee Flexion-Extension

Flx

C41858 Ext

Ext

-20

40

-20

Plantar-Dorsiflexion

40

Dor deg

deg

Pla -40

Plantar-Dorsiflexion

Dor

E

25%

50% Gait Cycle

2007

75%

Pla -40

25%

50%

75%

Gait Cycle

2010

right (solid) / left (dashed) knee and ankle sagittal plane kinematics

Part 2 - 6

Other Etiologies - Syrinx • MRI documented Syrinx from T1 – T4 • Age 4+11 years • Plantar flexor contracture right side only: -5 ◦ with knee flexed and -15 ◦ with knee extended • Difficulties isolating right ankle motion

Syrinx – con’t • Right excessive plantar flexion knee extension couple with equinus and knee extension in stance (right = solid line) • Left typical function (left = dashed line)

B48382 video 840-4

80

Knee Flexion-Extension

Flx

B48382 Ext -20

40

Plantar-Dorsiflexion

Dor deg Pla -40

25%

50%

75%

Gait Cycle

Syrinx – con’t • Right excessive plantar flexion knee extension couple with equinus and knee extension in stance (right = solid line) • Compensatory toe walking left side (left = dashed line) • Primary vs. compensatory toe walking

80

Other Etiologies - Myopathies

Knee Flexion-Extension

Flx

Ext -20

Plantar-Dorsiflexion

40 Dor deg Pla -40

25%

50%

• Add video for D30009 • 1143-3 – 2012 • 1086 – 3 - 2010

75%

Gait Cycle

Ullrich Congenital Myopathy • Progressive increase in toe walking over time • Progressive increase in ankle pplantar flexor contracture over time

• Diseases of skeletal muscle that can be progressive • Inherited, inflammatory, y or caused by endocrine or metabolic problems • Result in skeletal muscles weakness and atrophy

40 Dor deg Pla -40

25% 50% D30009

75%

Gait Cycle

2010 – right (solid) / left (dashed) 40

Plantar-Dorsiflexion

Dor deg Pla -40

Other Etiologies - Tumors

Plantar-Dorsiflexion

25%

50%

75%

Gait Cycle

2012 – right (solid) / left (dashed)

IC #33 Toe Walking – Case Examples

• Concern: unilateral toe walking • increasing tightness in his left ankle • pain/discomfort with left rapid passive dorsiflexion and palpation around the musculo-tendon junction of the left gastrocnemius

Part 2 - 7

Toe Walking Diagnostic Matrix

Tumors con’t 40

• Equinus of left ankle in stance and swing – - 15 deg (knee 0 & 90)

• Toe initial contact with absence of dorsiflexor moment at loading response • Reduce ankle power generation – Unable to test plantar flexor strength due to limited ROM

Plantar-Dorsiflexion

Dor

deg

Pla

TOE WALKING

-40

2.0

Ankle Moment

Ext

Nm/kg

Flx

CEREBRAL PALSY TRAMATIC BRAIN INJURY CVA

-1.0

3.0

Ankle Power

Gen

OTHER

W/kg

Abs

-2.0

Diagnostic Matrix

Diagnostic Matrix OTHER

CEREBRAL PALSY TRAMATIC BRAIN INJURY CVA

DETERMINING A DIAGNOSIS PATIENT HISTORY OF TOE WALKING FAMILY HISTORY OF TOE WALKING UNILATERAL VS BILATERAL CLINICAL EXAMINATOIN STRENGTH PASSIVE ROM

REAL OR VISUAL (equinus and/or knee flexion)

DOCUMENTATION OF MOVEMENT PATHOLOGY REAL vs. COMPENSATION

PRIMARY or SECONDARY

TREATMENT DECISION MAKING and EVALUATION

Assessment of Toe Walking • What you need to know to make treatment decisions: – – – – – – – – –

Medical and birth history Family history of similar problems Ankle passive ROM Ability to isolate function at the ankle Assessment of spasticity Ankle function during gait (kinematics and kinetics) Knee function during gait (kinematics) EMG during gait and in response to passive stretch Imaging when appropriate

IC #33 Toe Walking – Case Examples

References •

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Alvarez C, De Vera M, Beaucham R, Ward V, Black A: Classification of idiopathic toe walking based on gait analysis: development and application of the ITW severity classification. Gait Posture. 2007 Sept;26(3):428-35. Armand S, Watelain E, Mercier M, Lensel G, Lepoutre FX: Identification and classification of toe-walkers based on ankle kniematics, using a data-mining method. Gait Posture. 2006 Feb;23(2):240-8. Bonnefoy-Mazure A, Turcot K, Kaelin A, De Coulon G, Armand S: Full body gait analysis may improve diagnostic discrimination between hereditary spastic paraplegia and spastic diplegia: a preliminary study. Res Dev Disabil. 2013 Jan;34(1):495-504 ( ) ((Epub p 2012 Oct 17). ) Davids JR, Foti T, Dabelstein J, Bagley A: Voluntary (normal) versus obligatory (cerebral palsy) toewalking in children: a kinematic, kinetic, and electromyographic analysis. J Pediatr Orthop.. 1999 JulAug;19(4):461-9. Domb BG, Khanna AJ, Mitchell SE: Frassica FJ: Toe-walking attributable to venous malformation of the calf muscle. Clin Orthop Rel Res. 2004 Mar;(420):225-9. Eastwood DM, Dennett X, Shield LK, Dickens DR: Muscle abnormalities in idiopathic toe-walkers. J Pediatri Orthop B. 1997 Jul;6(3):215-8.

Part 2 - 8

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Engstrom P, Bartonek A, Tedroff K, Orefelt C, Haglund-Akerlind Y, Gutierrez-Farewik EM: Botulinum toxin A does not improve the results of cast treatment for idiopathic toe-walking: a randomized controlled trial. J Bone Joint Surg Am. 2013 Mar 6;95(5):400-7. Engstrom P, Van’t Hooft I, Tedroff K: Neuropsychiatric symptoms and problems among children with idiopathic toe-walking. J Pediatr Orthop. 2012 Dec;32(8):848-52. Ferrarin M, Bovi G, Rabuffetti M, Mazzoleni P, Montesano A, Moroni I, Pagliano E, Marchi A, Marchesi C, Beghi E, Pareyson D: Reliability of instrumented movement analysis as outcome measure in CharcotMarie-Tooth disease: results from a multitask locomotor protocol. Gait Posture. 2011 May;34(1):36-43. Fink JK: Hereditary spastic paraplegia: clinico-pathologic features and emerging molecular mechanisms. Acta Neuropathol. 2013 Sep;126(3):307-28. Hicks R, Durinick N, Gage JR: Differentiation of idiopathic toe-walking and cerebral palsy. J Pediatr Orthop. p 1988 Mar-Apr;8(2):160-3. p; ( ) Hirsch G, Wagner: The natural history of idiopathic toe-walking: a long-term follow-up of fourteen conservatively treated children. Acta Paediatr. 2004 Feb;93(2):196-9. Kelly IP, Jenkinson A, Stephens M, O’Brien T: The kinematic patterns of toe-walkers. J Pediatr Orthop. 1997 Jul-Aug;17(4):478-80. Klebe S, Stolze H, Kopper F, Lorenz D, Wenzelburger R, Volkmann J, Porschke H, Deuschl G: Gait analysis of sporadic and hereditary spastic paraplegia. J Neurol. 2004 May;251(5):571-8.

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Kogan M, Smith J: Simplified approach to idiopathic toe-walking. J Pediatr Orthop. 2001 NovDec;221(6):790-1. Oetgen ME, Peden S: Idiopathic toe walking. J Am Acad Orthop Surg. 2012 May;20(5):292-300. Õunpuu S, Garibay E, Solomito M, Bell K, Pierz K, Thomson J, Acsadi G, Deluca P: A comprehensive evaluation of the variation in ankle function during gait in children and youth with Charcot-Marie-Tooth disease. Gait Posture. 2013 May 20 (Epub ahead of print). Pendharkar G, Percival P, Morgan D, Lai D. Automated method to distinguish toe walking strides from normal strides in gait of idiopathic toe walking children from heel accelerometrydata. Gait Posture. 2012 Mar;35(3):478-82. Piccinini L, Cimolin V, D’Angelo MG, Turconi AC, Crivellini M, Galli M: 3D gait analysis in patients with hereditary spastic paraparesis and spastic diplegia: a kinematic, kinetic and EMG comparison. Eur J Paediatr Neurol. 2011 Mar;15(2):138-45 (Epub 2012 Sep 15). Rose J, Martin JG, Torbum L, Rinsky LA, Gamble JG: Electromyographic differentiation of diplegic cerebral palsy from idiopathic toe walking: involuntary coactivation of the quadriceps and gastrocnemius. J Pediatr Orthop. 1999 Sep-Oct;19(5):677-82. Song KM, Halliday SE, Little DG: The effect of lim-length discrepancy on gait. J Bone Joint Surg Am. 1997 Nov;79(11):1690-8. Skabelund J, Andrews RS: Venolymphatic malformation of the proximal gastrocnemius muscle in a girl. J Orthop Sports Physical Therapy. 43(5):349, 2013. Stricker SJ, Angulo JC: ;Idiopathic toe walking: a comparison of treatment methods. J Pediatr Orthop. 1998 May0Jun;18(3):289-93.

Westberry DE, Davids JR, Davis RB, de Morais Filho MC: Idiopathic toe walking: a kinematic and kinetic profile. J Pediatr Orthop. 2008 Apr-May;28(3):352-8. Williams CM, Tinley P, Curtin: Idiopathic toe walking and sensory processing dysfunction. J Foot Ankle Res. 2010 Aug 16;3:16. Williams CM, Tinley P, Curtin M, Wakefield S, Nielsen S: Is idiopathic toe walking really idiopathic? The motor skills and sensory processing abilities associated with idiopathic toe walking gait. J Child Neurol. 2013 Jan 24 (Epub ahead of print). Wolf SI, Braatz F, Metaxiotis D, Armbrust P, Dreher T, Doderlein L, Mikut R: Gait analysis may help distinguish hereditary spastic paraplegia from cerebral palsy. Gait Posture. 2011 Apr;33(4):556-61 (Epub 2011 Feb 16).

IC #33 Toe Walking – Case Examples

Part 2 - 9