Brain, Vol. 124, No. 2, 413-426,
February 2001
© 2001 Oxford University Press
Adaptive changes of saccadic eye–head coordination resulting from altered head posture in torticollis spasmodicus
1 Department of Neurology, University of Freiburg and 2 Sektion Neurophysiology, University of Ulm, Germany
Correspondence to:
Professor Dr T. Mergner, Neurologische Klinik, Neurozentrum, Breisacher Strasse 64, D-79106 Freiburg, Germany E-mail: mergner{at}uni-freiburg.de
We asked whether and how the abnormal head posture in torticollis patients affects saccadic gaze shifts and impairs the associated head movements. We wanted to learn to what extent observed changes directly result from the disease or reflect compensatory mechanisms, secondary to the altered head posture. We compared the results of patients with those of normal subjects. When patients viewed a centric target, their heads were a priori deviated in the direction of the torticollis, with orbital eye position showing a compensatory offset in the opposite direction. These abnormal eye and head positions were re-established when patients returned from an eccentric gaze position by means of a centripetal gaze shift, independently of its direction and magnitude, unlike in normal subjects who always recentred eyes and head. In normal subjects the share of the head in the total gaze shift amounted to about 70%, whereas in patients it contributed only 30%, necessitating correspondingly larger orbital eye displacements and eccentricities. Moreover, patients' head movements were asymmetric; they were larger when gaze was shifted into, or returned from the hemifield contralateral to the torticollis direction compared with gaze shifts in the ipsilateral hemifield. The eyes displayed a reversed asymmetry. Patients showed a significant increase in gaze latency and head versus eye delay as well as in the number of corrective saccades. However, head velocity was normal in four out of seven patients. Moreover, all patients made normal eye saccades (peak velocity, duration, gaze error), except for the increase in latency, which also occurred when gaze was shifted without head movements. Thus, patients' saccadic eye–head coordination showed abnormalities which mainly concerned the involved head movements. We suggest that the observed changes do not reflect a direct involvement of the disease upon the gaze shift mechanism, but can be interpreted as adaptive changes that compensate for the altered head posture. We formalized this view in the form of a dynamic model.
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