We have investigated how the abnormal head posture and motility in spasmodic torticollis interferes with ecological movements such as combined eye-to-foot whole-body reorientations to visual targets. Eight mildly affected patients and 10 controls voluntarily rotated eyes and body in response to illuminated targets of eccentricities up to ± 180°. The experimental protocol allowed separate evaluation of the effects of target location, visibility and predictability on movement parameters. Patients latencies of eye, head, trunk and foot motion were prolonged but showed a normal modification pattern when target location was predictable. Peak head-on-trunk displacement and velocity were reduced both ipsi- and contralaterally with respect to the direction of torticollis. Surprisingly, peak trunk velocity was also reduced, even more than in previously studied patients with Parkinsons disease. As a consequence, patients made short, hypometric gaze saccades and only exceptionally foveated initially nonvisible targets with a single large gaze shift (4 % of predictable trials as opposed to 30 % in controls). Foveation of distant targets was massively delayed by more than half a second on average. Spontaneous dystonic head movements did not interfere with the execution of voluntary gaze shifts. The results show that neck dystonia does not arise from gaze (head-eye) motor centres but the eye-to-foot turning synergy is seriously compromised. For the first time we identify significant secondary complications of torticollis such as trunk bradykinesia and foveation delays, likely to cause additional disability in patients. Eye movements per se are intact and compensate for the reduced head/trunk performance in an adaptive manner.
This prospective study investigated whether plasma ionized calcium concentration abnormalities and other electrolyte disturbances represent risk factors for the development of critical illness polyneuromyopathy (CIPNM) in ICU patients.
A 43-year-old man with infantile nystagmus syndrome complained of "head tremor" that would occur during attempted reading. Three-dimensional, combined eye and head recordings were performed with the magnetic search coil technique in two conditions: 1) looking straight-ahead under photopic conditions without a particular attentional focus and 2) reading a simple text held one meter away. A mainly vertical-horizontal spontaneous nystagmus was evident in both conditions, whereas head nodding emerged in the second condition. The head oscillated only in the vertical plane and concomitant analysis of eye and head displacement revealed a counterphase, compensatory pattern of the first harmonic of the INS waveform. This was verified by the significant negative peak of the crosscorrelogram at zero lag. Eye-in-space (gaze) displacement during nystagmic oscillations was thereby reduced suggesting a central adaptive behavior that may have evolved to partly compensate for the abnormal eye movements during reading.
We investigated whether turning problems in Parkinsons disease may be the result of abnormal horizontal multisegmental angular coordination. Ten mildly affected patients and controls stood upright and voluntarily reoriented eyes and body to illuminated targets of eccentricities up to ±180 degrees. The effects of target location, visibility, and predictability on movement parameters were evaluated. Patients latencies were normal. Control subjects foveated large eccentricity targets with a single gaze shift in approximately 30% of predictable trials. Patients rarely did so (10% of predictable trials) because of reduced head-in-space and trunk velocity. This resulted in massive foveation delays in patients-an average of half a second for displacements of 180 degrees. The covariation of eye, head, and trunk rotations was quantified statistically by means of principal components analysis. In both groups, the combined movement was initially stereotyped and two principal components accounted for nearly all data variance-the original three mechanical degrees of freedom (i.e., eye-head-trunk) are reduced to two kinematic degrees of freedom. However, in patients, the eye contributed more, and the head and trunk less, to the gaze shift than in control subjects. Although the eye-to-foot turning synergy is preserved in early-stage parkinsonism, quantitative differences are prominent, particularly a larger ocular (and smaller head-trunk) contribution in patients. Turning problems in Parkinsons disease do not result from inability to assemble multisegmental movements, as patients ability to control numerous degrees of freedom is preserved. However, trunk bradykinesia reduces the frequency of single-step gaze shifts, thus prolonging target acquisition time. Preserved eye motion compensates for trunk slowness.
Alexanders law states that the amplitude of the spontaneous nystagmus grows with increasing gaze in the direction of the fast phase. Using the search-coil method we employed head impulses at various eye-in-orbit azimuth angles to test (i) whether the normal vestibulo-ocular reflex (VOR) in the behaviorally relevant high-frequency range has intrinsic properties that could account for Alexanders law and (ii) whether such properties can also be shown in patients with unilateral vestibulopathy. We showed that the gain of the VOR remained unaffected by eye-in-orbit position in contols and in patients, both on ipsilesional and contralesional stimuli. These findings suggest that eye-in-orbit position does not directly modulate the activity in VOR pathways, neither during unbalanced but reciprocal (in controls), nor during unbalanced and nonreciprocal natural vestibular stimulation (in patients).
Shifting the direction of the line of sight in everyday life often involves rotations not only of the eyes and head but also of the trunk. Here, we investigated covariation patterns of eye-in-orbit, head-on-trunk and trunk-in-space angular horizontal displacements during whole-body rotations to targets of up to 180 degrees eccentricity performed by standing healthy human subjects. The spatial covariation was quantified statistically across various behavioral task conditions (unpredictable, memory driven predictable, visual feedback) and constraints (accuracy) by principal components (PC) analysis. Overall, the combined movement was stereotyped such that the first two PCs accounted for essentially the whole data variance of combined gaze transfers up to about 400 ms, suggesting that the three mechanical degrees of freedom under consideration are reduced to two kinematic degrees of freedom. Moreover, quantification of segment velocity variability across repetitions showed that velocities of eye-in-space and head-in-space (i.e. end-point velocity) were less variable than those of the elemental variables composing them. In contrast, three statistically significant PCs accounted for the covariation of the three segments during presumably vestibularly mediated nystagmic transfers, suggesting control by a separate driving circuit. We conclude that progression of the line of sight is initially stereotypic and fulfills criteria defining a motor synergy.
Displacements of the visual axis and multi-segmental (eye-to-foot) coordination in the yaw plane were studied in ten human subjects (Ss) during voluntary reorientations to illuminated targets of eccentricities up to 180 degrees . We also investigated how knowledge of target location modifies the movement pattern. Eccentric targets (outbound trials) elicited eye, head, trunk and foot movements at latencies ca. 0.5, 0.6, 0.7 and 1.1 s, respectively. Knowledge of target location (return trials) reduced latencies for foot and trunk (but not eye and head) thus eye, head and trunk moved more en bloc. In most trials, the initial gaze shift fell short of the target and more than 50% of the visual angle was covered by the sum of vestibular nystagmic fast phases and head-in-space displacement, until target fixation. This indicates that during large gaze shifts the anticompensatory role of the vestibulo-ocular reflex in target acquisition is prominent. During some predictable trials Ss acquired targets with a single large gaze shift, shortening target acquisition time by more than 200 ms. In these, gaze velocity (trunk-in-space + head-on-trunk + eye-in-orbit) remained often fairly constant for durations of up to 500 ms, suggesting that gaze velocity is a controlled parameter. Such pattern occurred during trunk mobilization, thus eye velocity co-varied with head-in-space rather than head-on-trunk velocity. Foot rotations were stereotyped and of constant frequency, suggesting they are generated by locomotor pattern generators. However, knowledge of target location reduced foot latencies indicating that local and supraspinal mechanisms interact for foot control. We propose that a single controller is responsible for the coupling of the multiple body segments and gaze velocity control during gaze shifts.
Muscle rigidity in PD (Parkinsons disease) patients represents an involuntary increase in muscle tone that stands out upon passive rotation of a joint. The pathophysiology of rigidity is still not well understood. We measured head-trunk torque in PD patients and normal controls during transient passive head rotations by means of servomotors under the instruction to the subjects to relax the neck muscles. We observed that rotation onset was followed by an initial rapid rise in resistive torque, similarly in both subject groups. It then leveled off or declined in controls. With PD patients, in contrast, the rise continued roughly proportional to head eccentricity almost until the end of the rotation. These observations led us to the hypothesis that the initial rise in torque represents reflexive head stabilization that normal subjects in the course of the rotational stimulus are able to suppress, whereas PD patients are less effective in doing so. The hypothesis was implemented into a dynamic control model of active and passive head rotation. Model simulations successfully reproduced the torque responses of normal subjects and PD patients in the present and previous studies.
These findings are in line with previous data on the horizontal vestibulo-ocular reflex (VOR) from this laboratory and suggest that eye position signals do not modulate natural vestibular responses. Hence, the Alexanders law (AL) phenomenon cannot be interpreted simply as a consequence of vestibular or oculomotor nuclei activity modulation with desired gaze.
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