Camptocormia is defined as an abnormal, severe and involuntary forward flexion of the thoracolumbar spine, which becomes manifest during standing and walking and subsides in the recumbent position. It was originally described as a psychogenic disorder, particularly in soldiers involved in long-term trench service during World War 1. It is becoming increasingly recognized as a prominent and disabling phenomenon during the course of Parkinson's disease (PD). In our experience, there is no clear correlation between camptocormia and levodopa treatment. In a few patients, the abnormal posture improved and in others it was unaltered or even became worse following levodopa administration. In a minority of fluctuating patients, there was a temporary deterioration during the "off" periods, but in most, the severity of camptocormia was unchanged during the "on" and "off" phases. In some patients it is associated with back pains, whereas in others it is painless. It occurs in sporadic PD as well as in postencephalitic and parkin-gene mutation PD and in other parkinsonian syndromes such as MSA. The pathogenesis of this striking clinical sign is unknown. It is definitely not due to a primary vertebral disease causing kyphosis such as ankylosing spondylitis, as the bent spine disappears when the patient lies on his back. The muscles involved may be the abdominal, paravertebral or both. It may by due to a peculiar dystonia or to an extreme form of rigidity. Local myopathic changes were suggested as a possible cause, but these may rather be a secondary phenomenon. Treatment is currently unsatisfactory in most cases. Occasional patients may benefit from intramuscular botulinum toxin injections or from deep brain stimulation.