The perception of body verticality (subjective postural vertical, SPV) was assessed in normal subjects and in patients with peripheral and central vestibular lesions and the data were compared with conventional neuro-otological assessments. Subjects were seated with eyes closed in a motorized gimbal which executed cycles of tilt at low constant speed (1.5 degrees s-1), both in the frontal (roll) and sagittal (pitch) planes. Subjects indicated with a joystick when they entered and left verticality, thus defining a sector of subjective uprightness in each plane. The mean angle of tilt (identifying a bias of the SPV) and the width of the sector (defining sensitivity of the SPV) were then determined. In normal subjects, the angle of the "verticality' sector was 5.9 degrees for pitch and roll. Patients with bilateral absence of vestibular function, patients with vertigo, i.e. acute unilateral lesions, benign paroxysmal positional vertigo (BPPV) and Ménière's disease, and patients with positionally modulated up-/downbeat nystagmus all had enlarged sectors (i.e. loss in sensitivity). Mean sector angle in these groups ranged from 7.8 to 11 degrees and the abnormality was present both in pitch and roll, regardless of the direction of nystagmus or body sway. Patients with chronic unilateral peripheral vestibular lesions and those with position-independent vertical nystagmus had normal sensitivities. No significant bias of the SPV was found in any patient group, not even those with acute unilateral vestibular lesions who had marked tilts of the subjective visual vertical (SVV). Complementary experiments in normal subjects tested under galvanic vestibular or roll-plane optokinetic stimulation also failed to show biases of the SPV. In contrast, a significant bias in the SPV could be induced in normal subjects by asymmetric cycles of gimbals tilt, presumably by proprioceptive adaptation. The following conclusions can be drawn. (i) The perception of body verticality whilst seated is mainly dependent on proprioceptive/contact cues but these are susceptible to tilt-mediated adaptation. (ii) Vestibular input improves the sensitivity of the SPV, even in vestibular disorders, as long as the abnormality is stable. (iii) There can be marked dissociation between vestibulo-motor (ocular and postural) phenomena and the perception of body verticality, and between the SPV and SVV. (iv) The postural sway asymmetries in patients with peripheral and central vestibular lesions, like those induced by galvanic or optokinetic stimulation in normal subjects, are not consequences of changes of the SPV.
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.
Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease and is manifested as a movement disorder. A positive family history is the second most important risk factor for developing the illness, after age. Both autosomal dominant and recessive forms of the illness have been described. Recently deletions in a novel gene, parkin, have been associated with the autosomal recessive form of the illness in Japanese families. In this study, we demonstrate that deletions of exons 5, 6 and 7 of the parkin gene are present in two affected individuals of a Greek pedigree with early onset Parkinson's disease. However, no deletions were identified in a different branch of the same pedigree with three affected individuals. These results suggest that deletions in the parkin gene will be found in other families besides those of Japanese origin and that there must be at least one additional locus responsible for early onset autosomal recessive Parkinson's disease.
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