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

Practice 8 questions · Untimed · Unlimited attempts

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Q1 OR8.1 1 pt

A 28-year-old man presents with a history of acute febrile illness at age 3, followed by progressive weakness of the right lower limb. Examination reveals flaccid paralysis of the right quadriceps with absent knee jerk, wasting of the thigh, and a valgus knee deformity. Power in the hamstrings and hip extensors is 4/5. The MOST accurate description of the neurological lesion underlying his condition is:

A Demyelination of corticospinal tracts causing spastic paralysis
B Destruction of anterior horn cells causing flaccid lower motor neuron paralysis
C Peripheral nerve demyelination causing sensory and motor deficits
D Neuromuscular junction blockade causing fatigable weakness

Correct. Poliovirus selectively destroys anterior horn cells (LMN cell bodies), producing the classic flaccid, areflexic, wasting pattern of PPRP without sensory loss.

Post-polio residual paralysis results from destruction of anterior horn cells (lower motor neurons) by poliovirus. This produces an LMN pattern: flaccid paralysis, areflexia, wasting, and no spasticity.

Polio causes LMN lesions via anterior horn cell destruction — not UMN (corticospinal), peripheral nerve, or NMJ pathology.

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Q2 OR8.1 1 pt

A surgeon plans a tibialis posterior tendon transfer to restore active dorsiflexion in a 22-year-old woman with post-polio foot drop. Pre-operatively the tibialis posterior muscle is assessed. What is the MINIMUM MRC power grade required in the donor muscle for a tendon transfer to be considered effective?

A Grade 2 (active movement with gravity eliminated)
B Grade 3 (active movement against gravity only)
C Grade 4 (active movement against gravity and some resistance)
D Grade 5 (normal power)

Correct. Donor muscle must be grade 4 or above. Transfer typically costs one grade, leaving at least grade 3 for functional power after re-routing.

The cardinal rule for tendon transfer: donor muscle must be at least grade 4 (active movement against gravity AND resistance). After transfer, one grade is typically lost, so grade 4 gives grade 3 — enough for functional use.

The minimum is grade 4. Grades 2 and 3 are insufficient — after transfer the muscle loses approximately one grade, so grade 3 would become grade 2, which is non-functional for weight-bearing dorsiflexion.

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Q3 OR8.1 1 pt

A 19-year-old patient with post-polio residual paralysis of the right lower limb has a severe equinovarus deformity of the foot. Serial casting and physiotherapy have failed. The patient is skeletally mature (growth plates closed). The orthopaedic surgeon recommends a triple arthrodesis. Which joints are fused in a triple arthrodesis?

A Tibiotalar, subtalar, and calcaneocuboid joints
B Subtalar, talonavicular, and calcaneocuboid joints
C Tibiotalar, talonavicular, and subtalar joints
D Calcaneocuboid, naviculocuneiform, and tarsometatarsal joints

Correct. Triple arthrodesis fuses subtalar (talocalcaneal), talonavicular, and calcaneocuboid joints — the three joints that control hindfoot inversion/eversion and midfoot rotation.

Triple arthrodesis fuses three hindfoot joints: subtalar (talocalcaneal), talonavicular, and calcaneocuboid. It is indicated in skeletally mature patients with fixed hindfoot deformities to provide a stable, plantigrade foot.

Triple arthrodesis spares the tibiotalar (ankle) joint. It fuses: subtalar + talonavicular + calcaneocuboid.

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Q4 OR9.1 1 pt

A 7-year-old boy with spastic diplegic cerebral palsy is assessed in clinic. He walks independently with a crouched gait but cannot run. He can climb stairs with a railing. Using the Gross Motor Function Classification System (GMFCS), which level best describes him?

A GMFCS Level I — walks without limitations
B GMFCS Level II — walks with limitations on some surfaces
C GMFCS Level III — walks using handheld mobility device
D GMFCS Level IV — self-mobility with limitations; uses powered mobility

Correct. GMFCS Level II describes a child who walks independently on most surfaces but cannot run and has difficulty on stairs without railing — matching this boy's profile.

GMFCS Level II: walks independently on most surfaces but has limitations in uneven terrain and stairs, cannot run. GMFCS Level I: walks without restrictions. Level III: uses handheld mobility devices. Levels IV-V: limited or no independent ambulation.

This child walks independently (excluding Level III/IV). He cannot run and needs a railing for stairs, distinguishing him from Level I (no functional limitations).

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Q5 OR9.1 1 pt

A 6-year-old girl with spastic hemiplegia has equinus deformity of the left ankle on weight-bearing but the foot can be passively dorsiflexed to neutral with the knee extended. Which of the following BEST characterises her deformity and guides management?

A Fixed equinus contracture — requires tendo Achilles lengthening
B Dynamic equinus deformity — managed with physiotherapy, AFO and/or botulinum toxin A
C Spastic drop foot due to peroneal nerve palsy — requires AFO only
D Structural bony equinus — requires calcaneal osteotomy

Correct. Passively correctable equinus = dynamic deformity (muscle overactivity, not structural contracture). First-line: physiotherapy, AFO, and botulinum toxin A to the gastrocnemius-soleus; surgery reserved for fixed contractures.

Dynamic (functional) deformity in CP: the deformity is present on standing/walking but the joint can be passively corrected. This is managed non-surgically (physiotherapy, AFO, botulinum toxin A). Fixed deformity (contracture) cannot be passively corrected and requires surgical intervention.

The ability to passively dorsiflex to neutral is the key finding that distinguishes dynamic from fixed deformity and directs non-surgical management first.

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Q6 OR9.1 1 pt

A child with CP is being considered for botulinum toxin A injection into a spastic muscle. At which step in neuromuscular transmission does botulinum toxin A exert its effect?

A Blocks nicotinic acetylcholine receptors on the motor end plate (postsynaptic blockade)
B Cleaves SNAP-25, inhibiting presynaptic acetylcholine vesicle release
C Inhibits acetylcholinesterase, prolonging acetylcholine action in the synaptic cleft
D Depolarises the motor end plate causing sustained muscle contraction

Correct. Botulinum toxin A cleaves SNAP-25, a SNARE protein required for vesicle docking. Without SNAP-25, ACh vesicles cannot fuse with the presynaptic membrane — neuromuscular transmission is blocked.

Botulinum toxin A cleaves SNAP-25 protein, preventing docking and fusion of acetylcholine vesicles at the presynaptic terminal — blocking ACh release at the NMJ and causing temporary chemical denervation of the muscle.

Botulinum toxin acts PRESYNAPTICALLY by cleaving SNARE proteins (SNAP-25), not by blocking postsynaptic receptors or inhibiting acetylcholinesterase.

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Q7 OR8.1 1 pt

A 10-year-old boy with post-polio residual paralysis has a paralysed gluteus medius and tensor fascia lata resulting in a Trendelenburg gait. To restore lateral stability at the hip, the surgeon plans a muscle transfer. Which of the following is the MOST appropriate donor for hip abductor reconstruction in PPRP?

A Tibialis anterior tendon transfer
B Iliopsoas tendon transfer (Mustard procedure) to the greater trochanter
C Hamstring tendon transfer to the lateral condyle
D Peroneus longus transfer to the gluteus maximus

Correct. The Mustard procedure transfers the iliopsoas around the iliac wing to the greater trochanter to substitute for paralysed hip abductors — a well-described technique for PPRP Trendelenburg gait.

For hip abductor weakness in PPRP, the tensor fascia lata or iliopsoas can be transferred to reconstruct abductor function. Donor must be grade 4+. The external oblique or iliopsoas transfer (Mustard procedure) is a recognised option.

The Mustard procedure (iliopsoas to greater trochanter) is the standard transfer for hip abductor paralysis in PPRP. Tibialis anterior and hamstrings are distal leg transfers unrelated to hip stabilisation.

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Q8 OR9.1 1 pt

A 16-year-old girl with spastic diplegic CP has persistent scissoring gait despite physiotherapy and two prior botulinum toxin A injections. Clinical examination reveals fixed adductor spasticity with a hip abduction of only 20 degrees bilaterally. Gait analysis confirms continuous adductor overactivity. What is the MOST appropriate next step?

A Repeat botulinum toxin A injection at higher dose
B Bilateral hip adductor release (adductor myotomy ± anterior obturator neurectomy)
C Bilateral femoral osteotomy for derotation
D Triple arthrodesis of the foot bilaterally

Correct. Fixed adductor contracture with failed conservative and botulinum toxin therapy is an indication for surgical adductor release. Anterior obturator neurectomy may be added to reduce recurrence.

Once deformity is fixed (not correctable with passive stretch) and conservative/botulinum toxin management has failed, surgical intervention is indicated. For hip adductor spasticity, adductor release (adductor myotomy/tenotomy ± anterior obturator neurectomy) is the appropriate surgical option.

Once deformity is fixed and botulinum toxin A has failed (2 injections), surgical adductor release is indicated. Femoral osteotomy addresses rotational deformity; triple arthrodesis addresses hindfoot deformity.

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