Long-term effect of repeated lidocaine injections into the external oblique for upper camptocormia in Parkinson's disease

Mechanism of camptocormia in Parkinson's disease analyzed by tilt table-EMG recording

“…In a previous study, we categorized camptocormia into upper and lower types and demonstrated an improvement in posture in PD patients with upper camptocormia (UC) following lidocaine injection into the external oblique muscle (EO), but not the internal oblique or rectus abdominis muscle [4]. We also reported that repeated lidocaine injections prolonged this effect up to 90 days, suggesting that it could be a potential therapeutic option for UC [5]. Furthermore, the results also suggested that abnormal contraction of the EO is a possible pathophysiological mechanism of UC.…”

“…UC was defined as abnormal truncal flexion (flexion angle >40 ) at a point between the lower thoracic and upper lumbar vertebrae, whereas LC was defined as abnormal truncal flexion at the hip joint [4]. The flexion angle was measured using the method reported previously [5]. The angle of lateral truncal deviation, which was defined as the angle formed between a parallel line to the ground and a line linking both acromions, was also measured.…”

“…Lidocaine (5 ml of 1% xylocaine ® , Astrazeneca, Japan) was injected into bilateral EO under ultrasound guidance in patients with UC in whom bilateral muscle discharge or no discharge in the EO was noted [5]. Furthermore, lidocaine (10 ml) was injected in the EO ipsilateral to the side of muscle discharge if patients had unilateral muscle discharge.…”

“…This muscle was selected because it is a major hip flexor muscle. Each injection was repeated for 4 or 5 days as reported previously [5] and the Data are mean ± SD. No statistically significant differences were noted for all other unmarked data.…”

In-Home Posture Evaluation and Visual Feedback Training to Improve Posture with a Kinect-Based System in Parkinson’s Disease

“…Mechanisms underlying the development of the postural abnormalities in PD are not well understood, but a number of possible mechanisms, such as dystonia, rigidity, drugs, myopathy, skeletal and soft tissue changes, and proprioceptive disintegration have been proposed [1]. There is insufficient evidence to support the effectiveness of the adjustment of antiparkinson medications [2,3], deep brain stimulation [4][5][6], botulinum toxin or Lidocaine injections [7,8], and orthosis and physiotherapy [9][10][11][12].…”