Biomedical subjects
Publications and source records attributed to A Katsarkas.
A case is reviewed of bilateral temporal bone metastases from a carcinoma of the uterine cervix. The pertinent literature is reviewed and the temporal bone histology is described.
During attacks of paroxysmal positional vertigo in 12 patients, nystagmus in different gaze positions was observed visually and recorded by electronystagraphy (eyes open, fixating). Visually observed eye movement was similar in all cases, with oblique (upward and horizontal) and rotatory (clockwise during leftward movement) components in fast phase; rotation dominated on ipsilateral gaze (toward the lower ear) and oblique movement dominated on contralateral gaze. However, ENG recordings showed greater variability and were often inconsistent with visual observation; the horizontal component often reversed with change in gaze position, and dissociated eye movements, as well as down-beating nystagmus, were sometimes seen. More sophisticated measurement and strict attention to gaze position is required to resolve these discrepancies.
In most of our patients with paroxysmal positional vertigo, the paroxysm was usually short (less than 25 or 30 seconds). With the eyes deviated toward the lowermost ear, the observed nystagmus was rotatory-linear and the fast phases beat toward this ear. When the eyes were deviated to the opposite side, the fast phase of nystagmus was mainly upward linear-oblique. In a small number of patients, however, some unusual findings were observed: the nystagmus was the usual rotatory-linear, but the duration was much longer; or the nystagmus was purely horizontal; or the nystagmus was rotatory-linear, but the fast phases were in opposite direction to that usually observed. These data suggest that: the observed paroxysmal nystagmus seems compatible with excitation of the posterior or horizontal semicircular canal of the lowermost ear, or the superior canal of the uppermost ear; and singular nerve section is an appropriate treatment only if the observed paroxysmal nystagmus is compatible with excitation of a posterior semicircular canal.
Brief whole-body movements (+/- 5 to 170 degrees/s peak velocity; approximately equal to 0.5 s duration), applied during 1.44-s intervals of total darkness while subjects "looked" at a just-viewed target, were used to examine vestibulo-ocular function in 3 patients who had compensated to total unilateral loss of peripheral vestibular function. We found that the combined effects of slow-phase and saccadic eye movements both tended to keep the eyes stabilized on the unseen target. Compensatory slow-phases elicited during rapid head movements ipsilateral to (i.e., towards) the lesion were only about 60% as effective as those elicited during rapid contralateral movements. Compensatory gaze-correcting saccades tended to supplement deficient slow-phase movements, especially during rapid ipsilateral head movement. However, the gaze-correcting effect of saccades was only about half of the required for perfect stabilization. Thus, two functional vestibular deficits were observed during rapid ipsilateral head movements: (1) reduced slow-phase stabilization, and (2) reduced saccadic ability to adequately supplement the deficient slow phases. However, overall vestibular functional capability, as assessed by observation of the net effect of both slow phases and saccades, was much better than would be indicated by conventional observation of slow-phase movements alone.
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The vestibular system is a major contributor to postural control and the vestibular nuclei are closely connected to the limb spinal motor neurons. Acute loss of unilateral peripheral vestibular function results in, among others, postural instability which improves with time due to central compensatory processes. It has been shown, however, that a number of processes, such as sensorimotor restriction, drugs, and so forth, may affect the speed and the quality of compensation. Due to the difference of ipsilateral vs contralateral connectivity between the vestibular nuclei and the limb spinal motor neurons, and the peculiarities of compensatory processes, the ipsilateral may not compensate as well as the contralateral foot to lesion in patients who lost unilateral peripheral vestibular function. To explore this possibility, the sway, while standing on each foot, was recorded in normal subjects (N = 30) and compensated (except three) patients (N = 37) with loss of unilateral peripheral vestibular function and the percentage difference between the two sways was calculated. No difference was found between patients swaying more on the ipsilateral vs patients swaying more on the contralateral foot to lesion (p > .80). There was, however, a statistical difference between patients as a group vs normal subjects as a group (p = .005). These data suggest, although not evident in all patients of the group, that sway on the contralateral foot was less than the sway on the ipsilateral foot to lesion, as initially speculated. They may, however, signify that one foot compensates better than the other. This is a preliminary report and more testing is on-going to confirm these results.