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Local revision copy · not clinical advice

Neuromuscular

Topic 21 · slides 584–598 · 15 slides · 75 questions
15 slides
▸ Slide 584 · NeuromuscularNeuromuscular · 2 questions expand
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slide 584
Question list
Q1-Q22 questions — tap to reveal all answerslist
  1. Which topic does this slide introduce?
  2. Which conditions are discussed in this neuromuscular section?
Answers · Q & A
Q1.Which topic does this slide introduce?
  • Neuromuscular disorders in paediatric orthopaedics
  • Not covered in the speaker notes - section divider slide
Q2.Which conditions are discussed in this neuromuscular section?
  • Not covered in the speaker notes
  • The slide is an image-only section divider
▸ Slide 585 · ArthrogryposisNeuromuscular · 10 questions expand
slide 585
Question list
Q1-Q1010 questions — tap to reveal all answerslist
  1. How does arthrogryposis present and what does the neurological examination indicate?
  2. What are the other manifestations of arthrogryposis?
  3. How is arthrogryposis assessed and what is the natural history?
  4. What is the aetiology and what are the forms of arthrogryposis?
  5. What is amyoplasia?
  6. What are the Drummond principles of operative management?
  7. What are the limb positions and associated deformities in arthrogryposis?
  8. What are the upper limb operative options in arthrogryposis?
  9. How is hip involvement in arthrogryposis treated?
  10. What is the role of physiotherapy in arthrogryposis?
Answers · Q & A
Q1.How does arthrogryposis present and what does the neurological examination indicate?
  • Non-progressive congenital disease with limited movement involving 2 or more joints
  • Limbs: tubular, fusiform, featureless, without skin creases
  • Positions: pronated forearm, extended elbow, hand in palm; FABER, foot deformity
  • UL: shoulder abducted, IR, elbow extended, wrist UD + flexed, fingers flexed at MCPJ and IPJ, thumb adducted (in palm)
  • Normal neuro exam: amyoplasia, distal arthrogryposis, generalised connective tissue disorder or fetal crowding
  • Abnormal neuro exam: diminished in-utero movement due to abnormal CNS, PNS, motor endplate or muscle
Q2.What are the other manifestations of arthrogryposis?
  • Upper extremity deformity
  • Teratologic hip subluxation and dislocation
  • Knee contractures
  • Foot: clubfoot, vertical talus
  • Possible: DDH, dislocated knee, clubfoot
  • Neuromuscular C-shaped scoliosis 33%; fractures 25%
  • Extraskeletal: haemangioma on forehead, abdominal wall anomalies (inguinal hernia, gastroschisis)
Q3.How is arthrogryposis assessed and what is the natural history?
  • Diagnosis: EMG, muscle biopsy, enzyme study, genetic study
  • X-ray spine and pelvis
  • MDT: paediatrician, ortho, geneticist, physio, P&O, psychologist
  • Normal face, IQ and normal life expectancy
  • Aim: increase joint mobility and muscle strength to develop adaptive use patterns that allow for walking and independence with ADLs
  • 25% non ambulatory
Q4.What is the aetiology and what are the forms of arthrogryposis?
  • 1 in 3000 births; the direct factor causing akinesis is unknown
  • Intrinsic causes: myopathic, neuropathic, fibropathic (neurogenic 90%, myopathy)
  • Extrinsic: decreased IU movement, IU infection, oligohydramnios, multiple pregnancy, amniotic bands
  • Maternal disease: diabetes, myasthenia gravis
  • Sporadic Arthrogryphosis multiplex congenita (4 limbs); distal arthrogryphosis
  • Larsen (4 limbs, knee dislocation, clubfoot)
  • Freeman Shelton (hand, foot, scoliosis + face (microstomia))
  • Pteryrium syndrome (flexor web)
Q5.What is amyoplasia?
  • Classic form of AMC: sporadic multiple contracture syndrome
  • Symmetrical involvement of multiple UL and LL joints; CNS normal
  • Muscle tissue replaced by fibrofatty tissue; most commonly seen form
  • 1 in 10,000 births, 30% of all congenital contractures
  • Types: I localised; II full expression (thin limbs, elbows extended, wrists flexed and ulnarly deviated, intrinsic plus hands, adducted thumbs); III adds polydactyly
Q6.What are the Drummond principles of operative management?
  • Deformity recurrence is common - dense inelastic soft tissue does not elongate with growth
  • Regain muscle balance if muscle is functional
  • Delay osteotomy until maturity
  • Maximal correction by surgery (tenotomies + capsulectomies) as conservative treatment is ineffective
  • Shortening procedure if recurrence (e.g. talectomy)
Q7.What are the limb positions and associated deformities in arthrogryposis?
  • Upper limb: shoulder abducted and internally rotated, elbow extended, wrist ulnar deviated + flexed, fingers flexed at MCPJ and IPJ, thumb adducted (in palm)
  • Lower limb: hip flexed, externally rotated, abducted (FABER), knee flexed (contracture), equinus
  • Also check the spine for scoliosis; possible DDH, dislocated knee, clubfoot; normal face and IQ
Q8.What are the upper limb operative options in arthrogryposis?
  • IR contracture of shoulder: external humeral rotational osteotomy
  • Elbow extension contracture preventing hand to mouth: posterior capsulotomy and triceps lengthening
  • Wrist: dorsal carpal wedge osteotomy +/- FCU transfer to preserve arc of motion
  • Correction of the thumb-in-palm deformity
Q9.How is hip involvement in arthrogryposis treated?
  • Unilateral: operative reduction (OR)
  • Bilateral: controversial - used to be conservative, now a trend towards sequential reduction
Q10.What is the role of physiotherapy in arthrogryposis?
  • Passive range will improve
  • Active range and muscle power will not improve
▸ Slide 586 · CMT/ hereditary motor sensory neuropathyNeuromuscular · 6 questions expand
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slide 586
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Q1-Q66 questions — tap to reveal all answerslist
  1. What is CMT/hereditary motor sensory neuropathy and how is it inherited?
  2. Compare CMT type 1 and type 2.
  3. What is the differential diagnosis of pes cavus?
  4. What muscle imbalances cause cavus, varus, claw toe and big toe plantarflexion?
  5. What is the management goal and conservative management of CMT?
  6. What are the operative options in CMT?
Answers · Q & A
Q1.What is CMT/hereditary motor sensory neuropathy and how is it inherited?
  • Most common inherited neurological disease
  • Inheritance: most AD, some AR/XR
  • Chromosome 17 in CMT1A
Q2.Compare CMT type 1 and type 2.
  • Type 1: AD, demyelinating, onset 10-20 y.o., cavus foot
  • Type 2: most AD, some AR, direct axonal death, onset >20 y.o., flaccid foot
Q3.What is the differential diagnosis of pes cavus?
  • Unilateral: polio, post-ischaemia contracture, Charcot
  • Bilateral: CP, syringomyelia, Friedrich ataxia, spinal bifida, CMT
Q4.What muscle imbalances cause cavus, varus, claw toe and big toe plantarflexion?
  • Cavus: PL > tib ant
  • Varus: tib post > PB
  • Claw toe: extrinsic > intrinsic
  • Big toe plantarflexion: weak TA with recruitment of ELH
Q5.What is the management goal and conservative management of CMT?
  • Investigation: EMG, DNA test
  • Goal: stable, plantigrade, shoeable, painless foot best with mobility
  • Prefer bony procedures as the disease is progressive
  • Conservative: lateral wedge insole to correct hindfoot varus; AFO if footdrop
Q6.What are the operative options in CMT?
  • Varus: PL to PB transfer, lateral sliding osteotomy
  • Cavus: Steindler procedure, Jone’s procedure, dorsal closing wedge osteotomy
  • Planter flexed big toe: Jone’s procedure
  • Claw toes: EDL lengthening, EDB tenotomy, PP excisional arthroplasty, TA lengthening
▸ Slide 587 · Peroneal muscle atrophyNeuromuscular · 6 questions expand
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slide 587
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Q1-Q66 questions — tap to reveal all answerslist
  1. What is the epidemiology and genetics of hereditary motor sensory neuropathy?
  2. What are the three main types of hereditary motor sensory neuropathy?
  3. How does peroneal muscle atrophy present?
  4. What are the examination findings in peroneal muscle atrophy?
  5. What other orthopaedic manifestations are associated with peroneal muscle atrophy?
  6. How is peroneal muscle atrophy diagnosed?
Answers · Q & A
Q1.What is the epidemiology and genetics of hereditary motor sensory neuropathy?
  • 1:2500, most common, affects motor more than sensory
  • Usually autosomal dominant (can be AR, X-linked)
  • Peripheral myelin protein 22 (PMP22)
  • Duplication of chromosome 17
Q2.What are the three main types of hereditary motor sensory neuropathy?
  • Demyelinating: 10-20s, AD, cavus foot
  • Axonopathy: 20s+, AD, flaccid foot, less disabling
  • Both demyelinating and axonal degeneration
Q3.How does peroneal muscle atrophy present?
  • Motor deficits: weakness, instability, clumsiness, frequent ankle sprains, difficulty with stairs
  • Lateral foot pain
  • Sensory deficit
Q4.What are the examination findings in peroneal muscle atrophy?
  • Cavovarus +/- rigid hindfoot
  • Weakened tibialis anterior and peroneal muscles (foot drop during swing phase)
  • Hyporeflexia or areflexia
Q5.What other orthopaedic manifestations are associated with peroneal muscle atrophy?
  • Hip dysplasia
  • Scoliosis
  • Hand muscle atrophy and weakness
Q6.How is peroneal muscle atrophy diagnosed?
  • NCV / EMG
  • DNA - look for PMP22 gene mutation
  • Chromosome analysis - duplication of chromosome 17
▸ Slide 588 · Friedreich's AtaxiaNeuromuscular · 5 questions expand
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slide 588
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Q1-Q55 questions — tap to reveal all answerslist
  1. What is the inheritance, genetics and neuroanatomical involvement of Friedreich's ataxia?
  2. What is the classic triad and gait finding of Friedreich's ataxia?
  3. What conditions are associated with Friedreich's ataxia?
  4. How is Friedreich's ataxia diagnosed?
  5. At what age does loss of ambulation (LOC) occur and what is the life expectancy in Friedreich's ataxia?
Answers · Q & A
Q1.What is the inheritance, genetics and neuroanatomical involvement of Friedreich's ataxia?
  • Commonest spinocerebellar degenerative disease
  • Autosomal recessive (frataxin mutation affecting mitochondria production)
  • Affects the cerebellar system, dorsal root ganglia, corticospinal tract and sensory peripheral nerve
Q2.What is the classic triad and gait finding of Friedreich's ataxia?
  • Ataxia
  • Areflexia
  • Upgoing plantar response
  • Staggering wide based gait
Q3.What conditions are associated with Friedreich's ataxia?
  • Cardiomyopathy (if plan OT)
  • Cavovarus foot
  • Scoliosis
Q4.How is Friedreich's ataxia diagnosed?
  • Clinical + family history + genetic testing
Q5.At what age does loss of ambulation (LOC) occur and what is the life expectancy in Friedreich's ataxia?
  • Wheelchair bound by 30 y (loss of ambulation)
  • Death by 50 y
▸ Slide 589 · XR of this skeletally immature patient showing broken shenton and dislocated lefNeuromuscular · 14 questions 1 check expand
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slide 589
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Q1-Q1414 questions — tap to reveal all answerslist
  1. What are the radiographic findings in this skeletally immature patient with a dislocated left hip?
  2. What history should be taken in a child with a neuromuscular hip dislocation?
  3. How is function classified and prognosis assessed in cerebral palsy?
  4. What is cerebral palsy and how is it classified?
  5. What are the principles of managing cerebral palsy?
  6. How is hip dysplasia in cerebral palsy prevented and treated?
  7. What does the physical examination include in neuromuscular disease?
  8. How is spasticity defined and treated globally vs focally?
  9. What is a contracture and how is it treated?
  10. What are the four types of lever arm dysfunction?
  11. What are the hemiplegic gait patterns and their management?
  12. What are the diplegic gait patterns?
  13. What are the timing and components of surgery in cerebral palsy?
  14. What soft tissue releases are used for early hip subluxation in CP?
Answers · Q & A
Q1.What are the radiographic findings in this skeletally immature patient with a dislocated left hip?
  • Broken Shenton's line and dislocated left hip
  • Increased acetabular index and increased neck-shaft angle, perhaps with more anteversion
  • Relatively well formed tear drop and femoral head suggest neuromuscular dislocation rather than DDH
  • Pelvis looks like an inlet view due to pelvic anteversion from tight rectus; look for VP drain
  • Triradiate cartilage fuses at 11-13 years old
Q2.What history should be taken in a child with a neuromuscular hip dislocation?
  • Perinatal and birth history
  • Developmental milestones (age of sitting and walking)
  • Problems faced by patient him/herself; Problems faced by cares (perineal hygiene, pain, transfer, sitting)
  • Determine GMFCS level
  • Other medical problems and social support
  • Prognostication if very young - good: head control by 9 months, sit by 2 years, hemiplegic; bad prognosis: bleck, lack of head control by 20 months, non ambulatory by 7 yr
Q3.How is function classified and prognosis assessed in cerebral palsy?
  • GMFCS I no restriction, II stairs with rails, III wheelchair, IV powered wheelchair, V self mobility limited
  • If non-ambulatory and >1 year old, test primitive reflexes; 2 or more = poor prognosis for walking (Bleck)
  • Gait analysis lab for quantitative measurements
Q4.What is cerebral palsy and how is it classified?
  • Non-progressive insult to the immature brain; primary insult non-progressive but musculoskeletal features evolve with growth
  • Topographically: diplegic, hemiplegic, quadriplegic
  • Neurologically: spastic, hypotonic, mixed, athetoid, ataxic
  • Functionally: GMFCS
  • Deviations: primary (loss of selective motor control), secondary (growth related), tertiary (compensatory)
  • Secondary deviation examples: Anatomic shortening of muscle tendon unit (e.g. myostatic contractures); Persistent bone deformities due to HV principle (e.g. femoral anteversion); Joint subluxations/ dislocations
Q5.What are the principles of managing cerebral palsy?
  • Multi-disciplinary approach (MDT); orthopaedics has a role only in spastic type and cannot reverse the primary insult
  • Overall aim: maximize patient’s function consistent with the current disease status and prevent deterioration
  • Walker aims (Gage) and prevention of early OA; sitter aims: spinopelvic balance, perineal hygiene, mobile knees, plantigrade feet
  • Medical spasticity: physio, analgesia, oral or intrathecal baclofen, botox (3-6 months)
  • Surgery: delay until >6 years but before tertiary issues; SEMLS vs OSSCS (release/lengthen biarticular muscles, preserve monoarticular antigravity muscles)
Q6.How is hip dysplasia in cerebral palsy prevented and treated?
  • Spastic biarticular adductors overpower monoarticular abductors, so the hip displaces; hip dysplasia is preventable
  • Surveillance per NICE guidelines and the Swedish CPUP study: X-ray before 3 years; repeat one in 6 y.o; monitor Reimer migration index, hip abduction; refer if abduction <30 degrees or RMI >33%
  • Early subluxation RMI 33-50%: botox/soft tissue release (adductor tenotomy, iliopsoas +/- hamstring lengthening) and night abduction splint
  • Moderate subluxation RMI >50%: VDRO/pelvic osteotomy; dislocation: <1yr reconstruct, >1 year observe if painless, salvage if painful (Girdlestone, capsule interpositional arthroplasty, McHale)
  • Evidence suggests less than 50% of asymptomatic dislocated hips will develop pain in the long run, so observation can be supported
  • Psoas spastic, hip flexed, reduced torque on proximal femur, femur cannot derotate, so anteversion; Valgus as non weight bearing
Q7.What does the physical examination include in neuromuscular disease?
  • General: IQ, sitting balance, gait (stance and swing phase), orthosis
  • Hip: tone, ROM, Thomas or Staheli test for FFC, Phelps test for abduction tightness, Duncan Ely for rectus, Ober for ITB
  • Knee: tone, ROM, popliteal angle (hamstring shift more accurate to see if psoas contracture contributes)
  • Ankle: tone, ROM, Silverskiold test, bony impingement or impending ulcers
  • Spine for scoliosis, pelvic obliquity, LLD
Q8.How is spasticity defined and treated globally vs focally?
  • Velocity dependent increase in tone due to loss of supraspinal inhibition
  • Global: selective dorsal rhizotomy - decrease afferent input from muscle spindle
  • Global: baclofen - GABA agonist, increase K channel opening --> easy hyperpolarization
  • Global: gabapentin - VGCC deactivator, decrease nerve excitation and decrease neurotransmitter release
  • Focal: botox
Q9.What is a contracture and how is it treated?
  • Shortening of the musculotendinous unit due to slowing of growth from lack of tensile loading
  • Muscle: release or transfer; joint: release; bone: osteotomy
Q10.What are the four types of lever arm dysfunction?
  • Unstable fulcrum (hip dislocation)
  • Floppy lever (pes planus)
  • Short lever (coxa valga)
  • Malrotation (tibial ER)
Q11.What are the hemiplegic gait patterns and their management?
  • Foot drop -> hinged AFO / solid AFO
  • True equinus (gastroc soleus contracture) -> hinged AFO -> heel cord lengthening
  • Jump knee (spastic hamstring + triceps surae) -> hinged AFO -> no OT
  • Apparent equinus (iliopsoas contracture + gastroc weakness) -> solid AFO -> psoas lengthening
Q12.What are the diplegic gait patterns?
  • True equinus
  • Jump knee
  • Apparent equinus
  • Crouch knee
  • Recurvatum knee
  • Stiff knee (swing phase problem)
Q13.What are the timing and components of surgery in cerebral palsy?
  • Timing: delay OT as long as possible (>6 years) but before tertiary issues - contain the hip before dislocation, modify gait before deviation
  • SEMLS vs OSSCS (orthopaedic selective spasticity control surgery)
  • OSSCS: correct lever arm dysfunction by releasing or lengthening biarticular muscles and preserving monoarticular antigravity muscles
  • Components: balance spasticity, prevent contractures, correct lever arm dysfunction
Q14.What soft tissue releases are used for early hip subluxation in CP?
  • Adductor longus transect - protect the anterior branch of the obturator nerve
  • Gracilis myotomy and adductor brevis lengthening
  • Iliopsoas lengthening +/- hamstring lengthening
  • Nighttime abduction splint
Fact check

Triradiate cartilage fuses at 11-13 years old — imprecise age range — Triradiate cartilage closes at about 12 years bone age in girls and 14 in boys (radiographic closure roughly 13-14 years in females and 15-16 in males); overall quoted range is about 12-16 years. — medium confidence — source

▸ Slide 590Neuromuscular · 2 questions expand
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slide 590
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Q1-Q22 questions — tap to reveal all answerslist
  1. What is the topic of this slide?
  2. What clinical content is shown on this slide?
Answers · Q & A
Q1.What is the topic of this slide?
  • Neuromuscular
  • Not covered in the speaker notes - slide image only
Q2.What clinical content is shown on this slide?
  • Not covered in the speaker notes
▸ Slide 591 · GMFCS (Gross Motor Function classification score)Neuromuscular · 4 questions expand
slide 591
Question list
Q1-Q44 questions — tap to reveal all answerslist
  1. What are the GMFCS levels?
  2. What is the most predictive factor for becoming an independent walker?
  3. What are the goals for a non-ambulator with cerebral palsy?
  4. What are the Gage principles for an ambulator?
Answers · Q & A
Q1.What are the GMFCS levels?
  • Level 1: no restriction in walking, limited in advanced motor skills
  • Level 2: no aids, some limitation outdoors or in the community
  • Level 3: needs assistive aids, limitation outdoors or in the community
  • Level 4: self mobility with limitation, needs transport or powered mobility outdoors
  • Level 5: self mobility severely limited even with assistive technology
Q2.What is the most predictive factor for becoming an independent walker?
  • independent sitting at 2 y.o
Q3.What are the goals for a non-ambulator with cerebral palsy?
  • Good sitting balance, forward gaze, use UL for feeding
  • Spine straight, shoulder and pelvis level
  • Hip located, stable, pain free with good ROM
  • Knee mobile, flexed for sitting, extends in brace for transfer
  • Foot plantigrade for standing
Q4.What are the Gage principles for an ambulator?
  • Stability in stance
  • Good clearance in swing
  • Preposition of the foot at end of swing
  • Adequate step length
  • Energy conservation
▸ Slide 592 · Crouch gaitNeuromuscular · 5 questions expand
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slide 592
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Q1-Q55 questions — tap to reveal all answerslist
  1. What are the midstance features of crouch gait?
  2. What are the causes of crouch gait?
  3. Briefly explain the mechanism of crouch gait.
  4. How is crouch gait managed?
  5. What are the sequelae of hamstring lengthening and why is the semiT transferred?
Answers · Q & A
Q1.What are the midstance features of crouch gait?
  • Excess ankle dorsiflexion
  • Knee flexion
  • Hip flexion
  • Overall short stride length and muscle atrophy
Q2.What are the causes of crouch gait?
  • Weakness (triceps surae, quads)
  • Spasticity (hamstrings, iliopsoas)
  • Joint contracture (knee flexion contracture)
  • Lever arm dysfunction (increased femoral anteversion, increased tibial torsion, collapse tripod)
Q3.Briefly explain the mechanism of crouch gait.
  • Weak gastrocsoleus / excessive ankle dorsiflexion means the knee extension / ankle plantarflexion couple cannot work
  • GRF falls posterior to the knee, producing a knee flexion moment
Q4.How is crouch gait managed?
  • Weakness: avoid iatrogenic excessive gastrocsoleus release/recession; GRAFO for gastroc; hamstring transfer for quads
  • Spasticity: hamstring lengthening (semiM + gracilis fractional +/- biceps femoris) and semiT to adductor tubercle transfer
  • Psoas spasticity: release at the pelvic brim or LT
  • Joint contracture: extension osteotomy
  • Lever arm dysfunction: reconstruct hip, tibia or foot
Q5.What are the sequelae of hamstring lengthening and why is the semiT transferred?
  • Sequelae: weak hip extension + anterior pelvic tilt
  • SemiT to adductor tubercle transfer converts a biarticular to monoarticular muscle
  • Aim: prevent hip extension and decrease anterior pelvic tilt
▸ Slide 593 · Recurvatum gaitNeuromuscular · 3 questions expand
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slide 593
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Q1-Q33 questions — tap to reveal all answerslist
  1. What compensatory mechanisms maintain balance in recurvatum gait?
  2. What is the cause of recurvatum gait and how does age guide treatment?
  3. What operations are used for fixed triceps surae contracture in recurvatum gait?
Answers · Q & A
Q1.What compensatory mechanisms maintain balance in recurvatum gait?
  • Knee recurvatum with the ankle in plantarflexion at midstance
  • Hip flexion moves the CG anterior to balance the GRF
  • Contralateral crouch occurs due to pelvic obliquity
Q2.What is the cause of recurvatum gait and how does age guide treatment?
  • Contracture of triceps surae
  • <6 years / spasticity: botox, stretching, solid AFO
  • Contracture + >6 years: assess with Silverskiold
Q3.What operations are used for fixed triceps surae contracture in recurvatum gait?
  • Gastroc only: gastroc recession
  • Gastroc + soleus: ETA
  • Applied when there is contracture and the patient is >6 years old
▸ Slide 594 · Jump knee gaitNeuromuscular · 4 questions expand
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slide 594
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Q1-Q44 questions — tap to reveal all answerslist
  1. What are the features of jump knee gait?
  2. What causes jump knee gait and how is it managed?
  3. What is gait analysis?
  4. What is the set-up for gait analysis?
Answers · Q & A
Q1.What are the features of jump knee gait?
  • Ankle equines in late stance
  • Knee flexion in early stance and terminal swing
  • Hip flexion in early stance
  • Pelvis normal or anteriorly tilted
Q2.What causes jump knee gait and how is it managed?
  • Problem is spastic hamstring and triceps surae
  • No OT
  • Serial cast, botox, stretching, hinged AFO
Q3.What is gait analysis?
  • Systematic description, assessment and measurement of the quantities that characterise human locomotion
  • Components: kinematic, kinetic, EMG, energy consumption
Q4.What is the set-up for gait analysis?
  • 2D video analysis
  • 3D computer analysis using specialised markers on specific bony landmarks
  • Force plates to measure GRF
  • EMG to look at muscle firing patterns
▸ Slide 595 · Stiff knee gaitNeuromuscular · 3 questions expand
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slide 595
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Q1-Q33 questions — tap to reveal all answerslist
  1. What causes stiff knee gait and when is knee flexion reduced?
  2. How is stiff knee gait managed in a child under 6 years?
  3. What are the indications for rectus to pes transfer?
Answers · Q & A
Q1.What causes stiff knee gait and when is knee flexion reduced?
  • Spastic rectus femoris or rectus firing out of phase
  • Decreased knee flexion in terminal stance and throughout the swing phase
Q2.How is stiff knee gait managed in a child under 6 years?
  • Botox and stretching
Q3.What are the indications for rectus to pes transfer?
  • Peak knee flexion <50 degrees
  • Peak knee flexion later than 30% of swing
  • Active rectus in the mid 3/5 of swing
  • Toe dragging
▸ Slide 596 · Winters classificationNeuromuscular · 4 questions expand
slide 596
Question list
Q1-Q44 questions — tap to reveal all answerslist
  1. What is Winters type 1 gait?
  2. What is Winters type 2 gait?
  3. What is Winters type 3 gait?
  4. What is Winters type 4 gait?
Answers · Q & A
Q1.What is Winters type 1 gait?
  • Type 1 = 'drop foot' = equinus in swing phase only
Q2.What is Winters type 2 gait?
  • Type 2a = 'true equinus' = equinus in the whole gait cycle
  • Type 2B = true equinus + recurvatum knee
Q3.What is Winters type 3 gait?
  • 'Jump knee' = equinus + tight hamstrings
Q4.What is Winters type 4 gait?
  • Equinus + tight hamstrings + tight flexors and adductors
  • Results in adduction and internal rotation deformity
▸ Slide 597 · Sutherland classificationNeuromuscular · 4 questions expand
slide 597
Question list
Q1-Q44 questions — tap to reveal all answerslist
  1. What is true equinus and how is it managed?
  2. What is apparent equinus and how is it managed?
  3. What is crouch gait (equinoplanovalgus) and how is it managed?
  4. What is jump gait in the Sutherland classification and how is it managed?
Answers · Q & A
Q1.What is true equinus and how is it managed?
  • Tight gastrocsoleus complex
  • Mx: hinged AFO (allows dorsiflexion while blocking plantarflexion)
Q2.What is apparent equinus and how is it managed?
  • Ankle goes into dorsiflexion due to persistent loading with lengthening of the Achilles tendon
  • Ankle ROM is still normal
  • Mx: solid AFO
Q3.What is crouch gait (equinoplanovalgus) and how is it managed?
  • Excessive dorsiflexion due to an overlengthened Achilles
  • Can be caused iatrogenically by releasing the Achilles while ignoring hamstring tightness
  • Mx: GRAFO
Q4.What is jump gait in the Sutherland classification and how is it managed?
  • Tight hamstrings flex the knee and the hip flexes to push the CG in front, with progressively worse equinus
  • Mx: hinge AFO
▸ Slide 598 · Strayer --> gastroc release from soleus proximal to conjoint tendon --> 1cmNeuromuscular · 3 questions expand
slide 598
Question list
Q1-Q33 questions — tap to reveal all answerslist
  1. Describe the Strayer, Vulpius and Baker techniques.
  2. Describe the White and Hoke PETA techniques.
  3. Which zone is preferred in cerebral palsy and why?
Answers · Q & A
Q1.Describe the Strayer, Vulpius and Baker techniques.
  • Strayer: gastroc release from soleus proximal to the conjoint tendon -> 1 cm
  • Vulpius: chevron at the MST junction -> 1.5 cm
  • Baker: central fascial tongue
Q2.Describe the White and Hoke PETA techniques.
  • White PETA: 1 medial + 1 lateral incision -> 2-4 cm
  • Hoke PETA: 2 medial + 1 lateral incision -> 4 cm
Q3.Which zone is preferred in cerebral palsy and why?
  • Zone 1 is more preferred in CP
  • It allows a more selective release