It has been hypothesized that head-unrestrained gaze shifts are controlled by an error signal produced by a feedback loop. It has also been hypothesized that the superior colliculus (SC) is within this feedback loop. If the feedback-to-SC hypothesis is valid, an unexpected mid-flight perturbation in gaze trajectory should be quickly followed by a concurrent change in the discharges of collicular saccade-related neurons. To verify this prediction experimentally, primate head movements were unexpectedly and briefly halted during head-unrestrained gaze shifts in the dark. Perturbed gaze shifts were composed of first a gaze saccade made when the head was immobilized by the head-brake, followed by a period where gaze was immobile, called a gaze plateau. The latter was composed of an initial period when the eyes and head were immobile, followed by a period wherein the head was released and the eyes counter-rotated to stabilize gaze. The plateau ended with a corrective gaze saccade to the goal location. In perturbed gaze shifts, there was widely distributed activity on the SC map during gaze plateaus, and there was no evidence that the initial motor program was aborted; the corrective gaze saccades were not "fresh" small stand-alone movements. Cells on the SC map responded at short latencies to head accelerations and associated gaze shift perturbations and carried a gaze position error (GPE = final - instantaneous gaze position) signal. As a large gaze shift progressed there was a caudo-rostral moving hill of activity on the SC map that encoded, not instantaneous veridical GPE, but a filtered version of it (time constant 100ms). Recordings from both the motor map and the so-called "fixation zone" in the rostral SC during perturbed head-unrestrained gaze shifts reveal gaze feedback control and a gaze feedback signal to the SC. However, these results do not prove that the SC is within the online gaze feedback loop, only that such a loop exists and that the collicular map is informed about its calculations.

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Summary Objective The purpose of this study was to describe the early vocalization skills in children with cleft lip and palate (CLP) at 6 and 12 months of age and compare these early vocalization measures to later speech and vocabulary development at 30 months of age. Methods The participants in the study included 13 children without cleft lip or palate (NCLP) who were typically developing and 13 children with CLP matched for age, gender and socioeconomic status. Standardized measures of cognition, language, hearing, and prelinguistic vocalization measures were administered at 6 and 12 months and speech production, and vocabulary measures were collected at 30 months of age. Results Group differences were observed in both receptive and expressive language development at 12 and 30 months of age. Group differences were observed in the frequency of babbling and Mean Babbling Level at 12 months and speech sound accuracy and vocabulary production at 30 months of age. Significant correlation coefficients were observed between babbling frequency at 6 months and consonant inventory size, vocabulary at 30 months for the children with clefts and PCC-R for noncleft children. Conclusions This study documented that young children with clefts have persistent vocalization and vocabulary deficits well beyond palate closure. Measures of babbling frequency, Mean Babbling Level and consonant inventories provide clinically effective means of identifying these early deficits. Additionally, these measures may provide a tool for monitoring the effects of early intervention programs that promote facilitation of sound and vocabulary development.

The two otolith organs (the saccule and utricle) are positioned perpendicular to each other and sense linear acceleration, head tilt, and gravity, with the primary role of providing input to the vestibulospinal reflex for postural stability. The vestibulospinal reflex serves to modulate posture via two descending pathways that aid in tonic contractions of the antigravity muscles in the arms and legs (lateral vestibulospinal tract) and activate neck motoneurons for the coordination of neck and eye movements (medial vestibulospinal tract). The lateral vestibulospinal tract receives the majority of its input from the otoliths and the cerebellum, whereas the medial vestibulospinal tract receives the majority of its input from the semicircular canals.

Background: The observation or measurement of eye movement can aid in the detection and localization of vestibular pathology due to the relationship between the function of the vestibular sensory receptors in the inner ear and the eye movements produced by the vestibulo-ocular reflex (VOR). The majority of bedside and laboratory tests of vestibular function involve the observation or measurement of horizontal eye movements (i.e., horizontal VOR) produced by stimuli that activate the horizontal semicircular canals (SCCs) and the superior vestibular nerve. The video head impulse test (vHIT) is a new clinical test of dynamic SCC function that uses a high-speed digital video camera to record head and eye movement during and immediately after passive head rotations. The SYNAPSYS Inc. vHIT device measures the “canal deficit” (deviation in gaze) during passive head impulses in the horizontal and diagonal (vertical) planes. There is, however, a paucity of data that has been reported using this device. Purpose: The purpose of this study was to obtain normative data and assess the test-retest reliability of the SYNAPSYS vHIT (version 2.0). Research Design: A prospective repeated measures design was utilized. Study Sample: Thirty young adults with normal hearing, normal caloric test results, and a negative history of vestibular disorder, neurological disease, open or closed head injury, or cervical spine injury participated in the study. Data Collection and Analysis: A single examiner manually rotated each participant’s head in the horizontal and diagonal planes in two directions (left and right in the horizontal plane; downward and upward in each diagonal plane) resulting in the stimulation of each of the six SCCs. Each participant returned for repeat testing to assess test-retest reliability. The effects of ear, session, and semicircular canal (horizontal, anterior, posterior) on the magnitude of canal deficit during the vHIT were assessed using repeated measures analysis of variance. Results: The mean canal deficit of the horizontal canals (8.3%) was significantly lower than the mean canal deficit of the anterior canals (16.5%) and the posterior canals (15.2%); there was no significant difference between the mean canal deficits of the anterior and posterior canals. The main effects of session and ear on canal deficit were not significant, and there were no significant interaction effects. There was no significant difference between the mean canal deficit for session 1 and session 2 for the horizontal, anterior, and posterior canals. The 95th percentiles for canal deficit were 19, 26, and 22% for the horizontal, anterior, and posterior SCCs, respectively. Conclusions: Testing of all six SCCs was completed in most participants in ∼10 min and was well-tolerated. The vHIT has some important advantages relative to more established laboratory tests of horizontal SCC function including the ability to assess the vertical SCCs, lower cost, shorter test time, greater portability, minimal space requirements, and increased patient comfort. Additional data, however, should be obtained from older participants with normal vestibular function and from patients with vestibular disorders. Within-subject comparisons between the results of the vHIT and the caloric and rotary chair tests will be important in determining the role of the vHIT in the vestibular test battery.

Otoacoustic emissions (OAEs) are generated in the cochlea in response to sound and are used clinically to separate ears with normal hearing from sensorineural hearing loss (SNHL). OAEs were elicited at ambient pressure by clicks (CEOAE) and wideband chirps (TEOAE) sweeping from low-to-high frequency with a sweep rate of either 187.6 Hz/ms (short chirps) or 58.2 Hz/ms (long chirps) and a bandwidth extending to 8 kHz. Chirps were presented at the same sound exposure level (SEL) as clicks, or + 6 dB relative to clicks. A total of 288 OAE waveforms were averaged for short chirps in ~1 minute compared to 120 waveforms for long chirps. Compared to clicks, the chirp has a lower crest factor, which allows it to be presented at an overall higher SEL without distortion. OAEs were elicited in 79 adults with normal hearing and 51 adults with mild-to-moderate SNHL. One-sixth octave OAE signal-to-noise ratios from 0.7 to 8.0 kHz were compared across stimulus types and conditions. The area under the receiver operating curve (AUC) was used to assess the accuracy of detecting SNHL. Average AUCs across 1/6th octave frequencies ranged from 0.90 to 0.89 for TEOAEs and were 0.87 for the CEOAE suggesting excellent test performance.

The left ventricle of the heart relaxes when it fills with blood and contracts to eject blood into circulation to meet the body’s metabolic demands. Dysfunction in either relaxation or contraction of the left ventricle can lead to heart failure. Transmural heterogeneity is thought to contribute to normal ventricular wall motion but it is not well understood how transmural modifications affect the failing left ventricle. The overall hypothesis of this dissertation is that normal left ventricles exhibit transmural heterogeneity in cellular level contractile properties and with aging and heart failure there are region-specific changes in cellular level contractile mechanisms. Age is the biggest risk factor associated with heart failure and therefore we investigated transmural changes in Ca2+ handling and contractile proteins in aging F344 rats before the onset of heart failure. We found that in 22-month old F344 rats there is a region-specific decrease in cardiac troponin I phosphorylation in the sub-epicardium that may contribute to slowed myocyte relaxation in the sub-epicardial cells of the same age. We then investigated the transmural patterns of contractile properties in myocardial tissue samples from patients with heart failure. Force and power output reduced most significantly in the samples from the mid-myocardial region when compared to sub-epicardium and sub-endocardium of the failing hearts. There was a region-specific increase in fibrosis is the mid-myocardium of the failing hearts. Myocardial power output was correlated with key sarcomeric proteins including cardiac troponin I, desmin and myosin light chain-1. The results in this dissertation reveal novel region-specific modifications in contractile properties in aging and heart failure. These transmural effects can potentially contribute to disruption in normal wall motion and lead to ventricular dysfunction.

Thesis (Ph.D. in Cell and Developmental Biology) -- University of Colorado at Denver and Health Sciences Center, 2005. / Typescript. Includes bibliographical references (leaves 139-155).