Head-free gaze shifts provide further insights into the role of the medial cerebellum in the control of primate saccadic eye movements.

This study examines how signals generated in the oculomotor cerebellum could be involved in the control of gaze shifts, which rapidly redirect the eyes from one object to another. Neurons in the caudal fastigial nucleus (cFN), the output of the oculomotor cerebellum, discharged when monkeys made horizontal head-unrestrained gaze shifts, composed of an eye saccade and a head movement. Eighty-seven percent of our neurons discharged a burst of spikes for both ipsiversive and contraversive gaze shifts. In both directions, burst end was much better timed with gaze end than was burst start with gaze start, was well correlated with eye end, and was poorly correlated with head end or the time of peak head velocity. Moreover, bursts accompanied all head-unrestrained gaze shifts whether the head moved or not. Therefore we conclude that the cFN is not part of the pathway that controls head movement. For contraversive gaze shifts, the early part of the burst was correlated with gaze acceleration. Thereafter, the burst of the neuronal population continued throughout the prolonged deceleration of large gaze shifts. For a majority of neurons, gaze duration was correlated with burst duration; for some, gaze amplitude was less well correlated with the number of spikes. Therefore we suggest that the population burst provides an acceleration boost for high acceleration (smaller) contraversive gaze shifts and helps maintain the drive required to extend the deceleration of large contraversive gaze shifts. In contrast, the ipsiversive population burst, which is less well correlated with gaze metrics but whose peak rate occurs before gaze end, seems responsible primarily for terminating the gaze shift.

Anterior canal neurons in cat vestibular nuclei have large phase leads during low frequency vertical axis pitch.

Vestibulo-ocular and second-order neurons in medial and superior vestibular nuclei of alert cats were identified by antidromic and orthodromic electrical stimulation, and their responses to whole body rotations were recorded in the dark. Neurons that had spatial sensitivity most closely aligned with the anterior canal (anterior canal neurons) were compared with neurons that had spatial sensitivity most closely aligned with the posterior canal (posterior canal neurons). Responses were recorded during low frequency earth-horizontal axis pitch rotations in the normal upright posture, and during earth-vertical axis pitch with the head and body lying on the left side. During upright pitch, response phases of anterior canal neurons slightly lagged those of posterior canal neurons or primary vestibular afferents, as previously reported. During on-side pitch, anterior canal neurons showed far greater phase leads with respect to head velocity than posterior canal neurons, primary vestibular afferents, or previously reported vestibulo-ocular reflex eye movements. These results provide challenges for vestibulo-ocular reflex models to incorporate central mechanisms for phase leads among the inputs to anterior canal neurons and to explain how the anterior canal neuron signals reported here combine with other signals to produce observed vestibulo-ocular reflex behavior.

Endovascular coiling for cerebral aneurysms.

Aneurysmal subarachnoid hemorrhage is an increasing problem in the United States, affecting approximately 30,000 people every year. Despite advances in the neurosurgical field, approximately 50% of patients die within the first month after hemorrhage. Traditionally, craniotomy with aneurysmal clipping has been employed to manage these patients, but endovascular embolization is moving to the forefront of treatment, particularly for high grade (IV to V) aneurysms. Patient selection is often based on age, aneurysm size, location, characteristics and presentation, and patient hemodynamics. Postprocedure management relies on skilled observers to determine those potential complications that may occur, including vasospasm, rupture, bleeding, or vessel occlusion. Advanced practice nurses have an obligation to be aware not only of the procedure and its management, but also of the potential complications and ongoing care of the patients and families as well.

Discharge patterns of cerebellar output neurons in the caudal fastigial nucleus during head-free gaze shifts in primates.

Lesion studies in both human and non-human primates indicate that the cerebellum is important for accurate and stereotyped saccadic eye movements. Based on single-unit recordings and pharmacological inactivations in head-fixed monkeys, we suggested that the caudal fastigial nucleus (CFN) provides the brainstem saccade generator with a burst that helps accelerate contraversive saccades and decelerate ipsiversive ones. Here we examine this suggestion during head-free gaze shifts where there can be a 10-fold difference in saccade duration. First, the timing of the burst does not depend on whether the gaze shift has a head component. When a family of either ipsiversive or contraversive gaze shifts with a variety of saccadic durations is aligned on gaze onset, the high-frequency burst in the associated rasters occurs progressively later as saccade duration increases. Realignment of the same rasters with the end of the saccade reveals a tight timing of burst end with saccade end for all 10 CFN burst neurons studied. The delayed bursts for contraversive saccades were unexpected based on the early burst illustrated in the published head-fixed data. One hypothesis is that the late activity helps terminate contraversive as well as ipsiversive gaze shifts. An alternative explanation is that the late CFN burst could still be used as an excitatory drive to promote the late reacceleration or prolonged velocity plateau that is present during large gaze shifts.

Timing of low frequency responses of anterior and posterior canal vestibulo-ocular neurons in alert cats.

The pitch vertical vestibulo-ocular reflex (VOR) is accurate and symmetrical when tested in the normal upright posture, where otolith organ and central velocity storage signals supplement the basic VOR mediated by the semicircular canals. However, when the animal and rotation axis are together repositioned by rolling 90 degrees to one side, head forward pitch rotations that excite the anterior semicircular canals elicit a more accurately timed VOR than do oppositely directed rotations that excite the posterior canals. This suggests that velocity storage of posterior canal signals is lost when the head is placed on its side. We recorded from 47 VOR relay neurons, second-order vestibulo-ocular neurons, of alert cats to test whether asymmetries are evident in the responses of neurons in the medial and superior vestibular nuclei during earth-horizontal axis rotations in the normal upright posture. Neurons were identified by antidromic responses to oculomotor nucleus stimulation and orthodromic responses to labyrinth stimulation, and were classified as having primarily anterior, posterior, or horizontal canal input based on response directionality. Neuronal response gains and phases were recorded during 0.5 Hz and 0.05 Hz sinusoidal oscillations in darkness. During 0.5 Hz rotations, anterior canal second-order vestibulo-ocular neurons responded approximately in phase with head velocity (mean phase re head position, +/- SE, 80 degrees +/- 3 degrees, n=18), as did posterior canal second-order vestibulo-ocular neurons (mean phase 81 degrees +/- 1 degree, n=25). Lowering the rotation frequency to 0.05 Hz resulted in only slight advances in response phases of individual anterior canal second-order vestibulo-ocular neurons (mean phase 86 degrees +/- 6 degrees, mean advance 7 degrees +/- 5 degrees, n=12). In contrast, posterior canal second-order vestibulo-ocular neurons behaved more like semicircular canal afferents, with responses markedly phase-advanced (mean advance 28 degrees +/- 5 degrees, n=14) by lowering rotation frequency to 0.05 Hz (mean phase 111 degrees +/- 5 degrees, n=14). In summary, low frequency responses of anterior and posterior canal second-order vestibulo-ocular neurons recorded during horizontal axis pitch correspond to the VOR they excite during vertical axis pitch. These results show that velocity storage is evident at anterior but not posterior canal second-order vestibulo-ocular neurons. We conclude that responses of posterior canal second-order vestibulo-ocular neurons are insufficient to explain the accurate low frequency VOR phase observed during backward head pitch in the upright posture, and that velocity storage or otolith signals required for VOR accuracy are carried by other neurons.