Treatment of Camptocormia in Parkinson's Disease
There is no established effective treatment for camptocormia in Parkinson's disease, but a trial of physical therapy with back extensor strengthening exercises combined with a CASH (cruciform anterior spinal hyperextension) brace represents the most reasonable first-line approach, as pharmacological and surgical interventions have shown limited or no benefit. 1
Understanding Camptocormia
Camptocormia is an axial postural deformity characterized by abnormal thoracolumbar spinal flexion of at least 45° that occurs during standing and walking, but resolves when lying supine or sitting. 1 The prevalence in Parkinson's disease ranges from 3% to 18%, typically occurring in patients with longer disease duration and greater disease burden. 2, 1
Treatment Approach Algorithm
First-Line: Conservative Management
Physical therapy with back extensor strengthening exercises combined with a CASH brace should be attempted first. 3 This approach demonstrated effective correction of camptocormia in at least one documented case with patient satisfaction regarding the amount of correction provided. 3 The brace can be modified through follow-ups for proper application with minimal discomfort. 3
Second-Line: Botulinum Toxin (Limited Evidence)
If conservative measures fail and the patient has predominantly thoracic-level flexion, botulinum toxin injection into the bilateral external oblique muscles may be considered, though evidence is extremely limited. 4
- Onabotulinum toxin A (75-90 units per side) injected bilaterally into the external oblique muscle under ultrasound guidance showed significant attenuation of camptocormia angle at 2 weeks in a small prospective study of 6 PD patients. 4
- The median camptocormia angle improved from 38° to 18° (p = 0.028). 4
- Subjective relief occurred in only 4 of 6 patients, and repeated injections were needed to maintain amelioration. 4
Avoid injection into the iliopsoas muscle, as this approach failed to show relevant or lasting improvement in posture and caused mild hip flexion weakness at higher doses (500-1,500 MU per side). 5
Pharmacological Optimization
Optimize levodopa therapy, as camptocormia is associated with PD disease burden. 6
- Administer levodopa at least 30 minutes before meals to maximize absorption. 7, 6
- Consider protein redistribution diet (low-protein breakfast and lunch, normal protein at dinner) to improve motor function and increase "ON" time. 7, 6
- Monitor for vitamin B12 and folate levels, as levodopa can cause hyperhomocysteinemia. 7, 6
Surgical Consideration: Deep Brain Stimulation
Deep brain stimulation may be considered for advanced motor complications, though specific evidence for camptocormia treatment is lacking. 6
- Either STN or GPi targets can be selected for motor symptoms. 8, 6
- If cognitive concerns exist, prefer GPi over STN. 8, 6
- If depression risk is significant, consider GPi over STN. 8, 6
Critical Caveats
The evidence base for camptocormia treatment is extremely weak. 1 Most interventions have shown poor and variable responses between studies. 2 The pathogenesis remains debated, with both central and peripheral mechanisms potentially contributing. 1
Botulinum toxin results are inconsistent and depend heavily on injection site selection. 5, 4 The iliopsoas approach has been definitively shown to be ineffective. 5 The external oblique approach shows promise but requires further validation with longer follow-up and larger sample sizes. 4
Physical therapy and bracing remain the safest initial approach with at least one documented success, minimal risk, and potential for patient satisfaction. 3