The objective of our study was to describe the clinical features of
camptocormia, an involuntary, marked flexion of the thoracolumbar spine in
idiopathic Parkinson's disease (PD) and to understand its etiology. In a prospective, cross-sectional study, we examined 15 patients with PD and
camptocormia using laboratory parameters, EMG, muscle magnetic resonance imaging, and biopsy of the paravertebral muscles. The clinical data were compared with a matched control group of PD patients without
camptocormia, and the biopsies were compared with muscles from age-matched autopsies. Almost all the patients (median age, 68.0 years; 7 women) with
camptocormia suffered from advanced PD.
Camptocormia occurred at a median of 9.0 years after the PD diagnosis. Compared with our clinical control group,
back pain was more frequent and less
dopa-sensitive in the patients with
camptocormia who suffered more often from additional diseases of the back. On EMG, we found mainly a myopathic pattern. The MRI of the paravertebral muscles showed localized changes ranging from
edema with contrast enhancement, which are considered to be early signs, to
atrophy and/or fatty degeneration, interpreted as late degenerative changes. Early signs were seen mainly during the first year and degenerative changes after 1.5 years. Biopsies revealed consistently myopathic changes and in some cases fatty degeneration. Clinical or electromyographic features favoring
dystonia were absent.
Camptocormia is a major disabling, non-fluctuating and
levodopa-resistant complication of advanced PD. The cause of
camptocormia in idiopathic PD is a focal
myopathy. Our findings suggest that the
myopathy has a progressive course, which finally leads to degeneration of the paravertebral muscles.