The below comes from Mayo Clinic Proceedings. Best to Google Camptocormia and get full background. May not be your issue. Took me 15 years to find a Neurologist who diagnosed me within 2 minutes. Had visited Mayo at Jacksonville, neurologists, neurosurgeon, chiropractors, had stimulator implanted/removed, various injections, X-ray, MRI, physical therapist, acupuncture. Very common in Parkinson’s, which I don’t have. All symptoms go away when sitting/lying down. Got my back brace at Hangar Clinic in South Carolina, but I feel they are represented nationally. I have found the pictures (2) that I was able to include in my original comment but now I cannot bring them over. Just got it. Good luck.
Simon M. Glynn, MD, Sean J. Pittock, MD, Steven A. Vernino, MD, PhD
Mayo Clinic College of Medicine, Rochester, Minn
Article Info click to expand contents
To the Editor: Camptocormia, from the Greek words kormos (body) and kamptos (to bend), is a term used to describe extreme spinal flexion while standing that disappears in the horizontal position. The term was first used in 1914 by the French neurologist Souques to describe a syndrome affecting young soldiers during World War I.1 At that time, it was considered a form of conversion disorder rather than a disease of organic pathology.2 In the 1910s, definitive treatment for patients with refractory disease was the use of “électrothérapie persuasive” to the spine.3 The term camptocormia has recently reappeared in the medical literature in association with several clinical entities, including Parkinson disease (PD).4 We describe a patient who presented with this atypical manifestation of PD.
Report of a Case.—A 75-year-old man presented to our emergency department with severe, intractable back pain. Over the course of several years, he had leaned increasingly forward at the waist to relieve worsening back pain until he was nearly parallel to the floor (Figure 1, A). Although he was physically able to stand erect, this posture worsened his back pain. The pain did not respond to analgesics, including narcotics.
Figure thumbnail gr1
Patient with camptocormia on presentation (A) and at dismissal (B).
The patient appeared to be in severe distress, constantly shifting position from lying flat to standing with extreme flexion of the lower back and then returning to bed. He had reduced facial expression. Alternating movements of the upper extremities were slowed, more on the left than on the right. No tremor was noted. Strength, reflexes, and sensation were normal. Magnetic resonance imaging and plain films of the spine revealed no bony abnormalities and no abnormal signal in the paravertebral muscles that would suggest a muscle disorder.
Intravenous morphine was administered in the emergency department, without benefit. The patient was then given one 25/100-mg tablet of carbidopa/levodopa dissolved in carbonated soda (this method of administration provides a quicker peak response, about 20 minutes compared with 60-90 minutes for immediate-release carbidopa/levodopa in tablet form). Within 30 minutes, the patient reported complete resolution of his pain. His flexed posture disappeared, supporting the diagnosis of a painful axial dystonia in this patient (Figure 1, B). He was treated subsequently with carbidopa/levodopa, one 25/250-mg tablet 3 times a day, and extended-release carbidopa/levodopa (50/200 mg) at night. At follow-up 2 years later, the patient had no pain and ambulated well with a mildly stooped posture.
Discussion.—Abnormalities of posture represent one of the cardinal features of PD. Patients often have a characteristic posture with the head and body bent forward and the knees flexed. Historically, an extremely flexed posture as seen in our patient (camptocormia) has been associated with conversion disorder. Recently, this posture has been described in association with numerous neurologic disorders, including axial myopathy, motor neuron disease, and PD.4–6 Djaldetti et al5 described 8 patients with idiopathic PD who developed camptocormia, some of whom had hyperflexed posture as the presenting symptom. Some patients improved with levodopa therapy, while others did not. The pathogenesis of this posture is unclear, but it may represent a type of dystonia rather than rigidity because it resolves when the patient lies down. Dystonia is well described in PD, particularly in dopamine-deficient untreated patients or as an “off period” phenomenon, especially on awakening in the morning. A reported case of camptocormia in a PD patient that was treated successfully with use of pallidotomy6 reinforces the concept that camptocormia in PD may represent a type of dystonia.
Pain in PD is poorly understood and usually attributed to dystonia or rigidity. It may be so severe that it overshadows other characteristic features of PD. In addition, akathisia, a restlessness or compulsion to move, may be described by the patient as discomfort. These sensory complaints may precede the onset of the movement disorder and complicate the diagnosis, especially in younger patients.7,8
The coincident presentation of camptocormia and severe pain in our patient illustrates the protean early clinical manifestations of PD, which can be misleading to clinicians unfamiliar with these less common presentations. After other causes have been ruled out, treatment strategies for pain due to PD are the same as for motor symptoms but may be less effective. Importantly, although dystonic postures and dyskinesias may be caused by excess dopamine, clinicians should not assume that dystonia is always a peak-dose phenomenon. Rather, higher doses of levodopa or dopamine agonists may be needed to reduce rigidity and dystonia and relieve pain