Paeds Vivas · neurology-neurodisability-and-neuromuscular
Duchenne and Becker muscular dystrophy: Viva
Branching clinical structured oral on Duchenne and Becker muscular dystrophy covering the creatine kinase and the genetic confirmation by multiplex ligation-dependent probe amplification, the reading-frame hypothesis and the dystrophin-associated glycoprotein complex, the glucocorticoid backbone with prednisolone or deflazacort started at the motor plateau, the cardiac and respiratory surveillance, and the appraisal of the FOR-DMD and EMBARK trials and the precision therapies.
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Study tools
Target exams
Branch 1: Confirming the diagnosis
The candidate should recognise the classic picture of Duchenne muscular dystrophy, with the delayed walking, the frequent falls, the calf pseudohypertrophy, the Gowers sign, the reduced reflexes, and a creatine kinase of 24,000 units per litre that is off the scale. A strong candidate states that the creatine kinase is typically above 10,000 and between 10,000 and 100,000 in Duchenne, that it is raised from birth before any weakness, and that a value of this magnitude in a weak boy points to a dystrophic process until the genetics prove otherwise. The candidate should add that the mildly raised transaminases are muscle-derived, because the same enzymes leak from the damaged fibre, and that a high transaminase in a weak boy is muscle, not liver. [3]
If the examiner presses on the confirmation, the candidate should state that the genetic test has now replaced the muscle biopsy as the first investigation, with multiplex ligation-dependent probe amplification as the first-line method for the exon deletions and duplications, and whole-gene sequencing for the point and splice mutations when the multiplex is normal. A muscle biopsy with dystrophin immunostaining is reserved for the inconclusive case. The candidate should offer the carrier testing of the mother and the female relatives, because the disease is X-linked recessive, with about two thirds inherited and one third new mutations. [4]
References6ShowHide
- [1]Hoffman EP, Brown RH Jr, Kunkel LM Dystrophin: the protein product of the Duchenne muscular dystrophy locus. Cell, 1987.PMID 3319190
- [2]Koenig M, Beggs AH, Moyer M The molecular basis for Duchenne versus Becker muscular dystrophy: correlation of severity with type of deletion. Am J Hum Genet, 1989.PMID 2491009
- [3]Bushby K, Finkel R, Birnkrant DJ Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and pharmacological and psychosocial management. Lancet Neurol, 2010.PMID 19945913
- [4]Birnkrant DJ, Bushby K, Bann CM Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and neuromuscular, rehabilitation, endocrine, and gastrointestinal and nutritional management. Lancet Neurol, 2018.PMID 29395989
- [7]Griggs RC, Miller JP, Greenberg CR Efficacy and safety of deflazacort vs prednisone and placebo for Duchenne muscular dystrophy. Neurology, 2016.PMID 27566742
- [10]Mendell JR, Muntoni F, McDonald CM AAV gene therapy for Duchenne muscular dystrophy: the EMBARK phase 3 randomized trial. Nat Med, 2025.PMID 39385046