Postural deficits in Huntington's disease are partly different from those in Parkinson's disease

Huntington's disease (HD) is characterized clinically by abnormal, involuntary movements (chorea) associated with psychiatric signs and progressive dementia. Motor disturbances involve both hyperkinetic motor signs (chorea) and a progressive, akinetic-rigid syndrome at more advanced stages. Clinical features of the disturbed stance and gait in HD were reported to resemble (see e.g. Delval A. et al., J Neurol 2006; 253: 73–80) those in Parkinson's disease (PD). Therefore, we studied postural control in subjects with manifest HD using a model based approach and compared the results to those of patients with PD.

Methods: We examined postural control in a total of 15 HD patients and compared the results to 16 PD patients and 15 age-matched healthy control subjects. We analyzed spontaneous sway using a factorial analysis and, in addition, exposed subjects to varying tilts of the support surface, using a pseudo-random waveform (PRTS, spectral bandwidth 0.05–10Hz).

Results: Spontaneous sway amplitude and velocity of HD patients were larger than those of both control subjects and PD patients. Primarily, this reflects the hyperkinetic motor signs (chorea). Additionally, HD corrective responses to externally-generated tilts of the support surface were more insufficient than those of PD patients, both in the presence and absence of visual cues. Unlike control subjects, both HD and PD patients suffer from a lack of flexibility when it comes to weighting the sensory information (visual, vestibular, proprioceptive) depending on the availability of external cues. However, HD patients, unlike PD patients, show a clearly larger overall time delay of their corrective response and, again unlike PD patients, display a passive stiffness in the normal range.

Conclusions: Whereas some parameters of HD patients' postural control mechanism resemble those of PD patients (insufficient error correction, lack of sensory reweighting), others are clearly different from PD patients (abnormally large time delay, normal passive stiffness), thus indicating that HD patients' postural control deficit is clearly distinguishable from that of PD patients. The parameters discussed here allowed us to fully characterize and simulate postural behavior of all three subject groups and to implement these behaviors on a humanoid robot developed in our laboratory.