OR8.1,OR9.1 | Neuromuscular Orthopaedics — Graded Quiz

Correct. Paralysed plantar flexors (gastrocnemius-soleus grade 1/5) plus functioning dorsiflexors (grade 4/5) = unopposed dorsiflexion force → calcaneus foot.

Calcaneus deformity in PPRP results from paralysis of the plantar flexors (triceps surae) with preserved or overactive dorsiflexors. The unopposed dorsiflexion force causes a calcaneus stance — the converse of equinus (paralysed dorsiflexors, intact plantar flexors).

Calcaneus = plantar flexors paralysed + dorsiflexors intact. Equinus is the reverse. Spasticity is a UMN (CP) feature, not PPRP.

Correct. Crouched gait reflects bilateral spastic hip/knee flexor overactivity (iliopsoas, rectus femoris, hamstrings) preventing full extension in stance. This is the defining pattern of spastic diplegia.

Crouched gait in spastic diplegia results from spastic hip flexors and knee flexors combined with weak hip extensors. Tight hamstrings acting across both hip and knee maintain the flexed posture. The crouch pattern is distinct from equinus gait seen in hemiplegia.

Crouched gait in diplegia is driven by spastic flexors (hip flexors + hamstrings) across multiple joints, not by plantar flexor spasticity (which causes jump/equinus gait) or isolated foot drop.

Correct. Transferring the complete tibialis posterior to the dorsum removes the only significant invertor, allowing unopposed eversion forces to drive the foot into planovalgus. A split or partial transfer preserves invertor function.

Transferring the entire tibialis posterior (a plantar flexor and invertor) to the dorsum without leaving a portion as an invertor creates an invertor-free foot that may drift into planovalgus. The split transfer technique (half to extensor hallucis longus, half to extensor digitorum) balances this risk. A full transfer without balancing inversion leads to overcorrection into valgus.

Planovalgus post-transfer = loss of invertor balance. Grade 3 donor would have failed due to insufficient power (not overcorrection). Skeletal maturity and routing are relevant but not the primary cause of this specific valgus complication.

Correct. Dynamic equinus (passively correctable) in a 5-year-old is managed conservatively: physiotherapy + AFO + botulinum toxin A. Surgery is premature and carries risks of overcorrection in a growing child.

In young children with CP and correctable (dynamic) equinus, the priority is non-surgical management: intensive physiotherapy, ankle-foot orthosis (AFO), and botulinum toxin A injection into the gastrocnemius-soleus to reduce spasticity and allow normal gait development. Surgery is reserved for fixed deformity or failure of conservative treatment.

Dynamic deformity + young age = conservative treatment first. Surgery (TAL, osteotomy, arthrodesis) is deferred unless deformity becomes fixed or conservative treatment fails.

Correct. Triple arthrodesis eliminates the motion of the subtalar and midtarsal joints, which normally absorb and dissipate ground impact. The knee subsequently receives increased mechanical load, accelerating degenerative changes.

Triple arthrodesis eliminates hindfoot shock absorption (subtalar and midtarsal joints). The resulting increased stress is transmitted proximally to the ankle and knee. Long-term complications include ipsilateral knee osteoarthritis due to loss of hindfoot cushioning during gait.

Loss of hindfoot motion after triple arthrodesis transfers stress proximally. Increased knee loading causes premature degenerative arthritis — the key long-term complication counselled before surgery.

Correct. Dyskinetic CP is extrapyramidal (basal ganglia), not pyramidal. Involuntary movements increase with intentional action. Orthopaedic interventions targeting spasticity are less helpful; DBS is a newer option.

Dyskinetic CP results from basal ganglia/extrapyramidal damage (typically from kernicterus or hypoxic-ischaemic injury). Unlike spastic CP (pyramidal tract, UMN signs), dyskinetic CP features involuntary movements that worsen with intentional movement. Botulinum toxin A and orthopaedic surgery are less effective in dyskinetic CP; deep brain stimulation may be considered.

Dyskinetic CP is basal ganglia/extrapyramidal (NOT cerebellar or posterior column). Its management differs from spastic CP — botulinum toxin and surgery are less effective here.

Correct. Quadriceps function (grade ≥3) is the single most important determinant for independent weight-bearing gait. Bilateral grade 2 quads cannot prevent knee buckling — callipers or knee-locking orthoses are necessary.

Quadriceps power is the most critical determinant of community ambulation in PPRP. Grade ≥3 quadriceps (against gravity) allows functional walking without knee-locking orthosis. Bilateral quadriceps grade 2 (cannot overcome gravity) means the patient cannot lock the knee in stance — independent ambulation without callipers is not feasible.

Quadriceps, not hip flexors or tibialis anterior, is the critical muscle for independent knee stability during stance phase. Bilateral grade 2 quads = cannot walk without orthotic knee support.

Correct. The ideal SDR candidate: spastic diplegia, GMFCS II-III, aged 3-8 years, good selective motor control, no fixed contractures — this profile optimises the benefit-risk ratio.

Ideal candidates for SDR: spastic diplegia (not dyskinetic or ataxic), GMFCS Level II-III, age 3-8 years, adequate selective motor control, adequate muscle strength and hip/knee extension against gravity, no fixed contractures, and motivated family. SDR is less effective in dyskinetic CP or children with significant weakness.

SDR is best for spastic diplegia GMFCS II-III in the 3-8 year window. Dyskinetic CP, ataxic CP, very high GMFCS levels, older age, and fixed contractures are relative or absolute contraindications.

Correct. Paralysis of both quadriceps and hamstrings leaves the knee without active dynamic support. The patient hyperextends the knee to use the posterior capsule as a passive lock — progressively stretching it into genu recurvatum.

With paralysed quadriceps (grade 1) and paralysed hamstrings, the knee has no active stabilisation. Intact hip flexors and body weight on a flexible knee leads to genu recurvatum (hyperextension deformity) — the patient uses passive posterior capsule tightness to lock the knee in extension for weight bearing. This is the most common knee deformity in PPRP with quadriceps paralysis.

With paralysed quads AND hamstrings, the knee has no active muscle control. The patient locks it in hyperextension → genu recurvatum. Spasticity does not occur in PPRP (LMN disease).

Correct. Excessive TAL weakens the gastrocnemius-soleus complex beyond neutral, allowing the dorsiflexors to dominate — producing calcaneus foot (heel walking, inability to push off). This is why intraoperative TAL is performed judiciously under tension.

Overcorrection of equinus by excessive tendo Achilles lengthening results in calcaneus deformity — the plantar flexors are excessively weakened, the foot drops into persistent dorsiflexion. This is the most feared complication of TAL in CP, as calcaneus foot causes a crouch gait pattern that is functionally more disabling than the original equinus.

New calcaneus foot post-TAL = overcorrection (over-lengthened Achilles). DVT, infection, and nerve injury do not explain this specific new deformity pattern.