@article{10.11648/j.cnn.20261001.11,
  author = {Lehleng Agba and Kokou Mensah Guinhouya and Komla Nyinèvi Anayo and Adama Ephoevi-Ga and Komi Apetse and Vinyo Kumako and Damelan Kombaté and Komi Assogba and Mofou Belo and Agnon Ayelola Balogou},
  title = {Corticosteroid-Induced Myopathy in a 10-Year-Old: A Case from Kara (Togo)},
  journal = {Clinical Neurology and Neuroscience},
  volume = {10},
  number = {1},
  pages = {1-4},
  doi = {10.11648/j.cnn.20261001.11},
  url = {https://doi.org/10.11648/j.cnn.20261001.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cnn.20261001.11},
  abstract = {Introduction: Corticosteroid-induced myopathy (CIM) remains underdiagnosed, particularly in children. Its acute form can emerge rapidly after the initiation of corticosteroid therapy, sometimes within the first few days. Identification relies on a constellation of clinical-chronological and biological arguments, together with observation of the course after steroid withdrawal. We report an acute CIM in a 10-year-old girl from Kara (Togo) to illustrate a pragmatic diagnostic approach in a resource-limited setting. Case presentation: A 10-year-old schoolgirl referred for right-sided visual loss received an initial corticosteroid course with methylprednisolone 240 mg/day for 5 days, with partial improvement. Two weeks later, following a relapse, she received a second course of methylprednisolone 1 g/day for 5 days. Four days after completing this treatment, she developed diffuse myalgias and proximal weakness with inability to raise the lower limbs and walk. Beyond the clinical picture, laboratory tests showed creatine kinase (CK) 876 U/L (≈7.6× the upper limit of normal [ULN]) and aspartate aminotransferase (AST) ≈2.5× ULN, supporting a diagnosis of CIM. Other muscle enzymes were unavailable, as was electromyography. Management consisted of steroid withdrawal, analgesics and anti-inflammatory agents, and physiotherapy. Clinical improvement occurred within 72 hours; on day 7, CK was 430 U/L (≈3.7× ULN), followed by normalization to 97 U/L at 3 months, with complete functional recovery. Conclusion: This observation illustrates that early-onset proximal weakness occurring soon after corticosteroid pulses should prompt consideration of CIM, even in the absence of EMG. In resource-limited contexts, the trajectory of CK and the response to dechallenge are decisive elements that help optimize prognosis in a timely manner.},
 year = {2026}
}

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TY  - JOUR
T1  - Corticosteroid-Induced Myopathy in a 10-Year-Old: A Case from Kara (Togo)
AU  - Lehleng Agba
AU  - Kokou Mensah Guinhouya
AU  - Komla Nyinèvi Anayo
AU  - Adama Ephoevi-Ga
AU  - Komi Apetse
AU  - Vinyo Kumako
AU  - Damelan Kombaté
AU  - Komi Assogba
AU  - Mofou Belo
AU  - Agnon Ayelola Balogou
Y1  - 2026/01/16
PY  - 2026
N1  - https://doi.org/10.11648/j.cnn.20261001.11
DO  - 10.11648/j.cnn.20261001.11
T2  - Clinical Neurology and Neuroscience
JF  - Clinical Neurology and Neuroscience
JO  - Clinical Neurology and Neuroscience
SP  - 1
EP  - 4
PB  - Science Publishing Group
SN  - 2578-8930
UR  - https://doi.org/10.11648/j.cnn.20261001.11
AB  - Introduction: Corticosteroid-induced myopathy (CIM) remains underdiagnosed, particularly in children. Its acute form can emerge rapidly after the initiation of corticosteroid therapy, sometimes within the first few days. Identification relies on a constellation of clinical-chronological and biological arguments, together with observation of the course after steroid withdrawal. We report an acute CIM in a 10-year-old girl from Kara (Togo) to illustrate a pragmatic diagnostic approach in a resource-limited setting. Case presentation: A 10-year-old schoolgirl referred for right-sided visual loss received an initial corticosteroid course with methylprednisolone 240 mg/day for 5 days, with partial improvement. Two weeks later, following a relapse, she received a second course of methylprednisolone 1 g/day for 5 days. Four days after completing this treatment, she developed diffuse myalgias and proximal weakness with inability to raise the lower limbs and walk. Beyond the clinical picture, laboratory tests showed creatine kinase (CK) 876 U/L (≈7.6× the upper limit of normal [ULN]) and aspartate aminotransferase (AST) ≈2.5× ULN, supporting a diagnosis of CIM. Other muscle enzymes were unavailable, as was electromyography. Management consisted of steroid withdrawal, analgesics and anti-inflammatory agents, and physiotherapy. Clinical improvement occurred within 72 hours; on day 7, CK was 430 U/L (≈3.7× ULN), followed by normalization to 97 U/L at 3 months, with complete functional recovery. Conclusion: This observation illustrates that early-onset proximal weakness occurring soon after corticosteroid pulses should prompt consideration of CIM, even in the absence of EMG. In resource-limited contexts, the trajectory of CK and the response to dechallenge are decisive elements that help optimize prognosis in a timely manner.
VL  - 10
IS  - 1
ER  - 

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