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Camptocormia (Bent spine syndrome)

Camptocormia presents as an abnormal flexion of thoracolumbar spine when standing. Flexion worsens while mobilizing, and wanes when supine.¹ Etiology is primarily idiopathic paravertebral muscle degradation. Secondary etiology includes Parkinson’s disease, dystonia, myotonic dystrophy, and medications (olanzapine and valproate).² The MRI aids in diagnosis with STIR imaging detecting acute edema and T1-weighted imaging demonstrating chronic fatty muscle degredation.³ Multimodal management focuses on analgesics, physiotherapy, and symptom improvement by addressing the underlying pathology or withdrawing medication. Self-perpetuating cycle progressively worsens muscle weakness and arthritic degeneration.²
 

References
1. Lenoir T, Guedj N, Boulu P, Guigui P, and Benoist M. Camptocormia: the bent spine syndrome, an update. European Spine Journal 2010:19;1229–1237.

2. Finsterer J, Strobl W. Presentation, Etiology, Diagnosis, and Management of Camptocormia. European Neurology 2010:64;1-8.                                                   

3. Margraf NG, Wrede A, Deuschl G, and Schulz-Schaeffer W J. Pathophysiological Concepts and Treatment of Camptocormia. Journal of Parkinson’s Disease 2016:6;485–501.

Submitted by Joshua Christy, Medical Student, Windsor University School of Medicine, and Faisal Khan, MD, DABSM, DABPN, Consultant Neurologist, Sugar Land Neurology and Sleep, Texas.

Joshua Christy and Dr. Khan report no disclosures.