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JOURNAL ARTICLE
REVIEW
Causes of camptocormia.
PURPOSE: To identify and highlight the variable causes of camptocormia.
METHOD: Literature review.
RESULTS: Camptocormia (bent spine syndrome) is an acquired postural disease characterised by forward flexion of the thoraco-lumbar spine. Camptocormia leads to lumbar kyphosis and increases during walking or standing and completely disappears in supine position. Camptocormia is multicausal due to central or peripheral nervous system disease, idiopathic or due to some rare conditions. Camptocormia is most frequently associated with Parkinson's disease. Other causes include dystonia, multisystem atrophy, Alzheimer's disease, myopathy, motor neuron disease, myasthenia or chronic inflammatory demyelinating polyneuropathy. Rare causes include adverse reactions of drugs, disc herniation, arthritis, spinal trauma, paraneoplastic disorder, or psychiatric disease (more rarely than previously thought). Camptocormia is diagnosed upon clinical investigations, imaging of the cerebrum or spine, electromyography or muscle biopsy. Treatment is limited on supportive conservative measures, to withdrawal of causative drugs, electroconvulsive therapy, surgical correction or deep brain stimulation and effective only in single patients.
CONCLUSIONS: Camptocormia is organic in the vast majority of the cases due to neurological disease, or rarely drugs, trauma, orthopedic abnormalities or idiopathic.
METHOD: Literature review.
RESULTS: Camptocormia (bent spine syndrome) is an acquired postural disease characterised by forward flexion of the thoraco-lumbar spine. Camptocormia leads to lumbar kyphosis and increases during walking or standing and completely disappears in supine position. Camptocormia is multicausal due to central or peripheral nervous system disease, idiopathic or due to some rare conditions. Camptocormia is most frequently associated with Parkinson's disease. Other causes include dystonia, multisystem atrophy, Alzheimer's disease, myopathy, motor neuron disease, myasthenia or chronic inflammatory demyelinating polyneuropathy. Rare causes include adverse reactions of drugs, disc herniation, arthritis, spinal trauma, paraneoplastic disorder, or psychiatric disease (more rarely than previously thought). Camptocormia is diagnosed upon clinical investigations, imaging of the cerebrum or spine, electromyography or muscle biopsy. Treatment is limited on supportive conservative measures, to withdrawal of causative drugs, electroconvulsive therapy, surgical correction or deep brain stimulation and effective only in single patients.
CONCLUSIONS: Camptocormia is organic in the vast majority of the cases due to neurological disease, or rarely drugs, trauma, orthopedic abnormalities or idiopathic.
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