Difference between revisions of "Camptocormia"

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[[File:Camptocormia.png|thumb|right|A patient with camptocormia]]
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'''Camptocormia''' also known as '''bent spine syndrome''' is a usually organic disorder characterised by marked flexion (greater than 45 degrees) of the thoracolumbar spine that increases during the day and completely disappears when supine.
  
'''Camptocormia''' is characterised by marked flexion of the thoracolumbar spine that increases during the day.
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==Terminology==
 
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The term comes from the Greek words "to bend" (kamptō) and "trunk" ("trunk").
==History==
 
First described by Earle in 1815 and by Brodie in 1837.
 
  
 
==Aetiology==
 
==Aetiology==
 
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There are two competing hypothesis, one is that it has a CNS cause, and the other that it has a PNS cause. In the CNS hypothesis the affected area is the striatum and its projections to the [[Spinal Cord Anatomy|reticulospinal tract]] or thalamus. In the PNS hypothesis there is myopathy of the antigravity spine extension muscles. It only rarely has a psychiatric origin.<ref>{{Cite journal|last=Finsterer|first=Josef|last2=Strobl|first2=Walter|date=2010|title=Presentation, etiology, diagnosis, and management of camptocormia|url=https://pubmed.ncbi.nlm.nih.gov/20634620|journal=European Neurology|volume=64|issue=1|pages=1–8|doi=10.1159/000314897|issn=1421-9913|pmid=20634620}}</ref>
*Parkinson's disease: the most common cause (two third).
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*Parkinson's disease: the most common cause, but usually only develops when the disease is severe.
 
*Other parkinsonian syndromes
 
*Other parkinsonian syndromes
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*Multisystem atrophy
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*Alzheimer's disease
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*Motor neuron disease
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*Myaesthenia
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*[[Chronic Inflammatory Demyelinating Polyneuropathy|Chronic inflammatory demyelinating polyneuropathy]]
 
*Dystonia
 
*Dystonia
 
*Vascular lenticular lesions
 
*Vascular lenticular lesions
*Muscular disorders
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*Primary or secondary myopathy
*Rheumatologic disorders.
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*[[Internal Disc Disruption|Lumbar disc herniation]]
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*[[Osteoarthritis]]
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*Spinal trauma
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*Paraneoplasia
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*Medication side effects (olanzapine, donepezil, valproate, systemic steroids)
  
 
==Epidemiology==
 
==Epidemiology==
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==Clinical Features==
 
==Clinical Features==
 
As the day goes on or during walking there is a progressive marked flexion of the thoracolumbar spine. It is relieved by sitting and lying supine. It can also be relieved volitionally by extending the trunk when the patient leans against a wall. There may be associated lateral deviation of the trunk. In two thirds of patients there is a lumbar or thoracolumbar scoliosis.<ref name=":0" />
 
As the day goes on or during walking there is a progressive marked flexion of the thoracolumbar spine. It is relieved by sitting and lying supine. It can also be relieved volitionally by extending the trunk when the patient leans against a wall. There may be associated lateral deviation of the trunk. In two thirds of patients there is a lumbar or thoracolumbar scoliosis.<ref name=":0" />
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== Treatment ==
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Treatment is usually unrewarding. Where possible treatment should be directed to the underlying cause.
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==Further Reading==
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{{PDF|Presentation Etiology Diagnosis and Management of Camptocormia - Finsterer 2010.pdf|Presentation, Aetiology, Diagnosis, and Management of Camptocormia - Finsterer 2010}}
  
 
==References==
 
==References==
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{{Reliable sources}}
 
{{Reliable sources}}
 
[[Category:General Spine]]
 
[[Category:General Spine]]
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[[Category:Neuromuscular Disorders]]

Latest revision as of 21:07, 29 March 2022

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A patient with camptocormia

Camptocormia also known as bent spine syndrome is a usually organic disorder characterised by marked flexion (greater than 45 degrees) of the thoracolumbar spine that increases during the day and completely disappears when supine.

Terminology

The term comes from the Greek words "to bend" (kamptō) and "trunk" ("trunk").

Aetiology

There are two competing hypothesis, one is that it has a CNS cause, and the other that it has a PNS cause. In the CNS hypothesis the affected area is the striatum and its projections to the reticulospinal tract or thalamus. In the PNS hypothesis there is myopathy of the antigravity spine extension muscles. It only rarely has a psychiatric origin.[1]

  • Parkinson's disease: the most common cause, but usually only develops when the disease is severe.
  • Other parkinsonian syndromes
  • Multisystem atrophy
  • Alzheimer's disease
  • Motor neuron disease
  • Myaesthenia
  • Chronic inflammatory demyelinating polyneuropathy
  • Dystonia
  • Vascular lenticular lesions
  • Primary or secondary myopathy
  • Lumbar disc herniation
  • Osteoarthritis
  • Spinal trauma
  • Paraneoplasia
  • Medication side effects (olanzapine, donepezil, valproate, systemic steroids)

Epidemiology

In those with Parkinson's disease and camptocormia there is a male predominance, older age, longer duration of disease, and autonomic symptoms.[2]

Clinical Features

As the day goes on or during walking there is a progressive marked flexion of the thoracolumbar spine. It is relieved by sitting and lying supine. It can also be relieved volitionally by extending the trunk when the patient leans against a wall. There may be associated lateral deviation of the trunk. In two thirds of patients there is a lumbar or thoracolumbar scoliosis.[2]

Treatment

Treatment is usually unrewarding. Where possible treatment should be directed to the underlying cause.

Further Reading

References

  1. Finsterer, Josef; Strobl, Walter (2010). "Presentation, etiology, diagnosis, and management of camptocormia". European Neurology. 64 (1): 1–8. doi:10.1159/000314897. ISSN 1421-9913. PMID 20634620.
  2. 2.0 2.1 Benatru, I.; Vaugoyeau, M.; Azulay, J.-P. (2008-12). "Postural disorders in Parkinson's disease". Neurophysiologie Clinique = Clinical Neurophysiology. 38 (6): 459–465. doi:10.1016/j.neucli.2008.07.006. ISSN 0987-7053. PMID 19026965. Check date values in: |date= (help)

Literature Review