OBJECTIVE To examine the aetiology of parkinsonian camptocormia, a non-fixed pathological forward bending of the trunk, by measuring trunk muscle activation and force regulation in Parkinson patients with (PD + CC) and… Click to show full abstract
OBJECTIVE To examine the aetiology of parkinsonian camptocormia, a non-fixed pathological forward bending of the trunk, by measuring trunk muscle activation and force regulation in Parkinson patients with (PD + CC) and without (PD) camptocormia matched for disease severity, and in age- and sex-matched healthy controls (HC). METHODS The isometric forces of trunk extension and flexion were measured in PD + CC, PD and HC. Neuromuscular efficiency (increase of extension force per increase of paravertebral muscle surface electromyography signal) and the ability to maintain a constant submaximal trunk extension force were examined. RESULTS Peak trunk extension force was significantly lower in PD + CC and PD than in HC, with PD + CC non-significantly weaker than PD. Compared with HC and with PD, the neuromuscular efficiency of trunk extension was significantly reduced in PD + CC. The variability of the force output (coefficient of variation) was significantly larger for PD + CC than for HC or PD. CONCLUSION The reduced neuromuscular efficiency of trunk extension separates PD + CC from PD. Moreover, control of the trunk extensor force is impaired in PD + CC. SIGNIFICANCE There is weakness and a force control deficit in parkinsonian camptocormia suggesting a disturbed sensory-motor integration, which may contribute to myopathic changes in the trunk extensor muscles.
               
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