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

Furusawa, Yoshihiko; Hanakawa, Takashi; Mukai, Yukinori; Aihara, Yuki; Taminato, Tomoya; Iawata, Yasuyuki; Takei, Toshinobu; Sakamoto, Takashi; Murata, Miho

doi:10.1016/j.parkreldis.2015.02.027

Cited by 23 publications

(26 citation statements)

References 17 publications

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“…These results imply that anteflexion of PD patients is caused not only by the breakdown of the anterior column, but also by other factors, such as disproportionate muscle tension of body trunk or spinal column. Degeneration of psoas major muscle and quadrate muscle may manifest with anteflexion in PD patients [6,9,10]. In our study, there were no significant differences in the area and thickness of muscle of body trunk or spinal column.…”

Section: Anteflexion Vs Non-anteflexioncontrasting

confidence: 45%

“…In our study, abdominal oblique muscle and transverse abdominal muscle in improved C7SVA group were thicker than those in non-improved group. Camptocormia may be improved by the combination of lidocaine injection into external oblique muscle and rehabilitation [10,11]. Maintenance of the thickness of abdominal oblique muscle and transverse abdominal muscle by exercise may contribute to positive outcomes for PD patients with anteflexion receiving STN-DBS.…”

Section: Improvement Of Anteflexion After Stn-dbsmentioning

confidence: 99%

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Characteristics and prognostic factors of Parkinson's disease patients with abnormal postures subjected to subthalamic nucleus deep brain stimulation

Okazaki

Sasaki

Yasuhara

et al. 2018

Parkinsonism & Related Disorders

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Section: Anteflexion Vs Non-anteflexioncontrasting

confidence: 45%

Section: Improvement Of Anteflexion After Stn-dbsmentioning

confidence: 99%

Characteristics and prognostic factors of Parkinson's disease patients with abnormal postures subjected to subthalamic nucleus deep brain stimulation

Okazaki

Sasaki

Yasuhara

et al. 2018

Parkinsonism & Related Disorders

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“…Camptocormia in PD patients worsens with activities or walking, as seen in dystonia, and all patients in this study had these characteristics. Furusawa et al [13] reported that the onset of camptocormia preceded the appearance of abnormalities in the external oblique on surface electromyography in patients with camptocormia, and posture improved following injections of lidocaine to the external oblique muscle. The effect of repeated trans-spinal magnetic stimulation (rTMS) was transient, and rTMS can stimulate the efferent pathway, so efferent stimulation rather than afferent block is important in improving camptocormia [12] .…”

Section: Discussionmentioning

confidence: 99%

Treatment of Mild Camptocormia with Selegiline in Patients with Parkinson's Disease

Yoritaka

Mori

2016

Eur Neurol

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Background: Camptocormia in Parkinson's disease (PD) is unresponsive to various therapies and induced difficulties in their day-to-day life. Objective: This study, an open trial, was aimed at assessing the efficacy of selegiline in the treatment of mild camptocormia in PD patients. Methods: Participants were administered 5 mg of selegiline for the first 8 weeks and 7.5 mg for the second 8 weeks. Results: As primary endpoints, the degree of thoracolumbar anteflexion decreased from 23.2° (mean) (11.8° (SD)) at baseline to 18.3° (7.1°) at 16 weeks, and the area of postural sway measured using a Gravicorder increased. However, the differences were not significant. Thoracolumbar anteflexion improved in 60% of the participants. Conclusions: In this study, 60% of the participants showed an improvement in anteflexion of the thoracolumbar spine with selegiline, but the change in the degree of anteflexion was 5°, which was not statistically significant. Participants with significant improvement in thoracolumbar anteflexion had an increased postural sway. This change was induced by a decrease in truncal muscle tonus or change in the center of gravity. This study combined the study of anteflexion and stability, and provides information on the treatment of short-term or mild camptocormia.

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“…However, almost none of the patients showed a bending angle below 30° after treatment. Treatment with lidocaine shows only limited improvement, so far, but further investigation is needed [137]. …”

Section: Treatment Options For Camptocormiamentioning

confidence: 99%

Pathophysiological Concepts and Treatment of Camptocormia

Margraf

Wrede

Deuschl

et al. 2016

JPD

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Camptocormia is a disabling pathological, non-fixed, forward bending of the trunk. The clinical definition using only the bending angle is insufficient; it should include the subjectively perceived inability to stand upright, occurrence of back pain, typical individual complaints, and need for walking aids and compensatory signs (e.g. back-swept wing sign). Due to the heterogeneous etiologies of camptocormia a broad diagnostic approach is necessary. Camptocormia is most frequently encountered in movement disorders (PD and dystonia) and muscles diseases (myositis and myopathy, mainly facio-scapulo-humeral muscular dystrophy (FSHD)). The main diagnostic aim is to discover the etiology by looking for signs of the underlying disease in the neurological examination, EMG, muscle MRI and possibly biopsy. PD and probably myositic camptocormia can be divided into an acute and a chronic stage according to the duration of camptocormia and the findings in the short time inversion recovery (STIR) and T1 sequences of paravertebral muscle MRI. There is no established treatment of camptocormia resulting from any etiology. Case series suggest that deep brain stimulation (DBS) of the subthalamic nucleus (STN-DBS) is effective in the acute but not the chronic stage of PD camptocormia. In chronic stages with degenerated muscles, treatment options are limited to orthoses, walking aids, physiotherapy and pain therapy. In acute myositic camptocormia an escalation strategy with different immunosuppressive drugs is recommended. In dystonic camptocormia, as in dystonia in general, case reports have shown botulinum toxin and DBS of the globus pallidus internus (GPi-DBS) to be effective. Camptocormia in connection with primary myopathies should be treated according to the underlying illness.

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

Cited by 23 publications

References 17 publications

Characteristics and prognostic factors of Parkinson's disease patients with abnormal postures subjected to subthalamic nucleus deep brain stimulation

Characteristics and prognostic factors of Parkinson's disease patients with abnormal postures subjected to subthalamic nucleus deep brain stimulation

Treatment of Mild Camptocormia with Selegiline in Patients with Parkinson's Disease

Pathophysiological Concepts and Treatment of Camptocormia

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