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An introduction is presented in which the editor discusses various papers within the issue on topics including biomedical engineering, computational biology and the role of ontologies in biology.

Eye movements in response to high-acceleration head rotations (thrusts) in the horizontal plane from patients with unilateral (UVD) or bilateral vestibular loss (BVD) were recorded. The rapid, gaze-position corrections (GPCs) that appeared when vestibulo-ocular reflex (VOR) slow phases were under-compensatory were characterized. For comparison, eye movements from normal subjects who were asked to generate saccades in the direction opposite head rotation (in the same direction as slow phases) were recorded. This normal-subject model produced responses with spatial and temporal characteristics similar to those from GPCs in patients as follows: When head rotations were generated actively, compared with passively, gaze-position errors and corresponding GPCs were smaller and occurred earlier. During passively generated head thrusts, GPCs still occurred when head rotations were made in total darkness, though their accuracy decreased as the requirement for maintaining gaze on a specific location in space was relaxed. Time of onset of GPCs was not rigidly tied to head kinematics (peak velocity or peak acceleration). Speeds of GPCs, however, were lower than speeds of similar-sized, headfixed saccades. Finally, during passive and active head thrusts in patients, sustained, high-frequency (20 to 30 Hz) oscillations that appeared as tiny saccades were occasionally observed, one immediately following the other, resembling a compensatory slow-phase response. Taken together, the results suggest that one strategy for overcoming a VOR deficit is to enlist the saccadic system to produce an oculomotor response that is required to compensate for head rotation. This response may come in the form of high-velocity GPCs or smaller-amplitude oscillations. [ABSTRACT FROM AUTHOR]

The 3-dimensional angular vestibulo-ocular reflexes (AVOR) elicited by rapid rotary head thrusts were studied in 17 subjects with unilateral Ménière's disease before and 2–10 weeks after treatment with intratympanic gentamicin and in 13 subjects after surgical unilateral vestibular destruction (SUVD). Each head thrust was in the horizontal plane or in either diagonal plane of the vertical semicircular canals, so that each head thrust effectively stimulated only one pair of canals. The AVOR gains (eye velocity/head velocity during the 30 ms before peak head velocity) for the head thrusts exciting each individual canal were averaged and taken as a measure of the function of that canal. Prior to intratympanic gentamicin, gains for head thrusts that excited canals on the affected side were 0.91 ± 0.20 (horizontal canal, HC), 0.78 ± 0.20 (anterior canal, AC), and 0.83 ± 0.10 (posterior canal, PC). The asymmetries between these gain values and those for head thrusts that excited the contralateral canals were <2%. In contrast, caloric asymmetries averaged 40% ± 32%. Intratympanic gentamicin resulted in decreased gains attributable to each canal on the treated side: 0.40 ± 0.12 (HC), 0.35 ± 0.14 (AC), 0.31 ± 0.14 (PC) (p <0.01). However, the gains attributable to contralateral canals dropped only slightly, resulting in marked asymmetries between gains for excitation of ipsilateral canals versus their contralateral mates: HC: 34% ± 12%, AC: 24% ± 25%, and PC: 42% ± 13%. There was no difference in the AVOR gain for excitation of the ipsilateral HC after gentamicin in patients who received a single intratympanic injection (0.39 ± 0.11, n = 12) in comparison to those who received 2–3 injections (0.42 ± 0.15, n = 5, p = 0.7). Gain decreases attributed to the gentamicin-treated HC and AC were not as severe as those observed after SUVD. This finding suggests that intratympanic gentamicin causes a partial vestibular lesion that may involve preservation of spontaneous discharge and/or rotational sensitivity of afferents. [ABSTRACT FROM AUTHOR]

Presents a study which examined the functionality of the vestibulo-collic reflex and the cervico-collic reflex during head and neck movements caused by perturbations of the trunk. Formalism of the neuromechanical model; Examinations of the main components of the head movement control; Conclusions of the study.

In this article, the author reflects on the integration of biocomputational models in biomedical research. She says that biocomputational modeling improves interdisciplinary research and training. She further opines that biomedical engineers need to accelerate the process of integrating mathematical models into biomedical research.