Changes in temporal binding related to decreased vestibular input

2012 ◽  
Vol 25 (0) ◽  
pp. 107
Author(s):  
Nai-Yuan Nicholas Chang ◽  
Alex K. Malone ◽  
Timothy E. Hullar

Imbalance among patients with vestibular hypofunction has been related to inadequate compensatory eye movements in response to head movements. However, symptoms of imbalance might also occur due a temporal mismatch between vestibular and other balance-related sensory cues. This temporal mismatch could be reflected in a widened temporal binding window (TBW), or the length of time over which simultaneous sensory stimuli may be offset and still perceived as simultaneous. We hypothesized that decreased vestibular input would lead to a widening of the temporal binding window. We performed whole-body rotations about the earth-vertical axis following a sinusoidal trajectory at 0.5 Hz with a peak velocity of 60°/s in four normal subjects. Dichotic auditory clicks were presented through headphones at various phases relative to the rotations. Subjects were asked to indicate whether the cues were synchronous or asynchronous and the TBW was calculated. We then simulated decreased vestibular input by rotating at diminished peak velocities of 48, 24 and 12°/s in four normal subjects. TBW was calculated between ±1 SD away from the mean on the psychometric curve. We found that the TBW increases as amplitude of rotation decreases. Average TBW of 251 ms at 60°/s increased to 309 ms at 12°/s. This result leads to the novel conclusion that changes in temporal processing may be a mechanism for imbalance in patients with vestibular hypofunction.

2003 ◽  
Vol 13 (2-3) ◽  
pp. 65-77
Author(s):  
Laurence R. Young ◽  
Kathleen H. Sienko ◽  
Lisette E. Lyne ◽  
Heiko Hecht ◽  
Alan Natapoff

Head movements made while the whole body is rotating at unusually high angular velocities (here with supine body position about an earth-vertical axis) result in inappropriate eye movements, sensory illusions, disorientation, and frequently motion sickness. We investigated the acquisition and retention of sensory adaptation to cross-coupled components of the vestibulo-ocular reflex (VOR) by asking eight subjects to make headturns while being rotated at 23 rpm on two consecutive days, and again a week later. The dependent measures were inappropriate vertical VOR, subjective tilt, and motion sickness in response to 90° yaw out-of-plane head movements. Motion sickness was evaluated during and following exposure to rotation. Significant adaptation effects were found for the slow phase velocity of vertical nystagmus, the reported magnitude of the subjective tilt experienced during head turns, and motion-sickness scores. Retention of adaptation over a six-day rest period without rotation occurred, but was not complete for all measures. Adaptation of VOR was fully maintained while subjective tilt was only partially maintained and motion-sickness scores continued to decrease. Practical implications of these findings are discussed with particular emphasis on artificial gravity, which could be produced in weightlessness by means of a short-radius (2 m) rotator.


2018 ◽  
Vol 120 (4) ◽  
pp. 1572-1577 ◽  
Author(s):  
Corey S. Shayman ◽  
Jae-Hyun Seo ◽  
Yonghee Oh ◽  
Richard F. Lewis ◽  
Robert J. Peterka ◽  
...  

A single event can generate asynchronous sensory cues due to variable encoding, transmission, and processing delays. To be interpreted as being associated in time, these cues must occur within a limited time window, referred to as a “temporal binding window” (TBW). We investigated the hypothesis that vestibular deficits could disrupt temporal visual-vestibular integration by determining the relationships between vestibular threshold and TBW in participants with normal vestibular function and with vestibular hypofunction. Vestibular perceptual thresholds to yaw rotation were characterized and compared with the TBWs obtained from participants who judged whether a suprathreshold rotation occurred before or after a brief visual stimulus. Vestibular thresholds ranged from 0.7 to 16.5 deg/s and TBWs ranged from 13.8 to 395 ms. Among all participants, TBW and vestibular thresholds were well correlated ( R2 = 0.674, P < 0.001), with vestibular-deficient patients having higher thresholds and wider TBWs. Participants reported that the rotation onset needed to lead the light flash by an average of 80 ms for the visual and vestibular cues to be perceived as occurring simultaneously. The wide TBWs in vestibular-deficient participants compared with normal functioning participants indicate that peripheral sensory loss can lead to abnormal multisensory integration. A reduced ability to temporally combine sensory cues appropriately may provide a novel explanation for some symptoms reported by patients with vestibular deficits. Even among normal functioning participants, a high correlation between TBW and vestibular thresholds was observed, suggesting that these perceptual measurements are sensitive to small differences in vestibular function. NEW & NOTEWORTHY While spatial visual-vestibular integration has been well characterized, the temporal integration of these cues is not well understood. The relationship between sensitivity to whole body rotation and duration of the temporal window of visual-vestibular integration was examined using psychophysical techniques. These parameters were highly correlated for those with normal vestibular function and for patients with vestibular hypofunction. Reduced temporal integration performance in patients with vestibular hypofunction may explain some symptoms associated with vestibular loss.


1988 ◽  
Vol 60 (5) ◽  
pp. 1765-1778 ◽  
Author(s):  
J. Kasper ◽  
R. H. Schor ◽  
V. J. Wilson

1. We have studied the responses of neurons in the lateral and descending vestibular nuclei of decerebrate cats to stimulation of neck receptors, produced by rotating the body in vertical planes with the head stationary. The responses to such neck stimulation were compared with the responses to vestibular stimulation produced by whole-body tilt, described in the preceding paper. 2. After determining the optimal vertical plane of neck rotation (response vector orientation), the dynamics of the neck response were studied over a frequency range of 0.02-1 Hz. The majority of the neurons were excited by neck rotations that brought the chin toward the ipsilateral side; most neurons responded better to roll than to pitch rotations. The typical neck response showed a low-frequency phase lead of 30 degrees, increasing to 60 degrees at higher frequencies, and a gain that increased about threefold per decade. 3. Neck input was found in about one-half of the vestibular-responsive neurons tested with vertical rotations. The presence of a neck response was correlated with the predominant vestibular input to these neurons; neck input was most prevalent on neurons with vestibular vector orientations near roll and receiving convergent vestibular input, either input from both ipsilateral vertical semicircular canals, or from canals plus the otolith organs. 4. Neurons with both vestibular and neck responses tend to have the respective orientation vectors pointing in opposite directions, i.e., a head tilt that produces an excitatory vestibular response would produce an inhibitory neck response. In addition, the gain components of these responses were similar. These results suggest that during head movements on a stationary body, these opposing neck and vestibular inputs will cancel each other. 5. Cancellation was observed in 12 out of 27 neurons tested with head rotation in the mid-frequency range. For most of the remaining neurons, the response to such a combined stimulus was greatly attenuated: the vestibular and neck interaction was largely antagonistic. 6. Neck response dynamics were similar to those of the vestibular input in many neurons, permitting cancellation to take place over a wide range of stimulus frequencies. Another pattern of interaction, observed in some neurons with canal input, produced responses to head rotation that had a relatively constant gain and remained in phase with position over the entire frequency range; such neurons possibly code head position in space.


2012 ◽  
Vol 25 (0) ◽  
pp. 209
Author(s):  
Timothy E. Hullar ◽  
Alexander K. Malone ◽  
Spencer B. Smith ◽  
Nai-Yuan N. Chang

Little is known about vestibular-related timing processes in patients with disequilibrium. Patients with a history of migraine headaches often complain of significant motion sensitivity and long-term vague imbalance inconsistent with a peripheral vestibular disorder. Some of these people have episodic spells of severe vertigo termed ‘vestibular migraines’. Other patients have no history of migraine but do report significant motion sensitivity. Motion sensitivity has typically been explained as a mismatch between the amplitude of vestibular and other (typically visual) sensory inputs. Another possibility is that motion sensitive patients may suffer from a mismatch in the temporal integration of vestibular and other sensory inputs. Here, we compared the temporal binding window (TBW) of vestibular + auditory stimuli in normal subjects, subjects with motion sensitivity, and those with both migraine and motion sensitivity. We asked subjects undergoing earth-vertical sinusoidal rotations at 0.5 Hz, 128°/s to identify whether a metronome-like series of tone bursts was synchronous with their cyclic motion. We calculated the TBW as the range in time encompassing the middle 68% of the area under the psychometric curve. The TBW in normal subjects was 312 ± 135 ms (mean ± SD), in subjects with motion sensitivity was 454 ± 103 ms, and in subjects with migraine and motion sensitivity was 451 ± 124 ms. The TBW of normal subjects was significantly shorter than the other groups. Temporal errors in perception, as manifested by a prolongation of the TBW, are a plausible mechanism for imbalance in patients with migraine and motion sensitivity.


2003 ◽  
Vol 375 (3) ◽  
pp. 539-549 ◽  
Author(s):  
Lise MADSEN ◽  
Rasmus K. PETERSEN ◽  
Morten B. SØRENSEN ◽  
Claus JØRGENSEN ◽  
Philip HALLENBORG ◽  
...  

Adipocytes play a central role in whole-body energy homoeostasis. Complex regulatory transcriptional networks control adipogensis, with ligand-dependent activation of PPARγ (peroxisome proliferator-activated receptor γ) being a decisive factor. Yet the identity of endogenous ligands promoting adipocyte differentiation has not been established. Here we present a critical evaluation of the role of LOXs (lipoxygenases) during adipocyte differentiation of 3T3-L1 cells. We show that adipocyte differentiation of 3T3-L1 preadipocytes is inhibited by the general LOX inhibitor NDGA (nordihydroguaiaretic acid) and the 12/15-LOX selective inhibitor baicalein. Baicalein-mediated inhibition of adipocyte differentiation was rescued by administration of rosiglitazone. Treatment with baicalein during the first 4 days of the differentiation process prevented adipocyte differentiation; supplementation with rosiglitazone during the same period was sufficient to rescue adipogenesis. Accordingly, we demonstrate that adipogenic conversion of 3T3-L1 cells requires PPARγ ligands only during the first 4 days of the differentiation process. We show that the baicalein-sensitive synthesis of endogenous PPARγ ligand(s) increases rapidly upon induction of differentiation and reaches a maximum on days 3–4 of the adipocyte differentiation programme. The conventional platelet- and leucocyte-type 12(S)-LOXs and the novel eLOX-3 (epidermis-type LOX-3) are expressed in white and brown adipose tissue, whereas only eLOX-3 is clearly expressed in 3T3-L1 cells. We suggest that endogenous PPARγ ligand(s) promoting adipocyte differentiation are generated via a baicalein-sensitive pathway involving the novel eLOX-3.


2000 ◽  
Vol 10 (2) ◽  
pp. 75-86 ◽  
Author(s):  
Jacob J. Bloomberg ◽  
Lauren A. Merkle ◽  
Susan R. Barry ◽  
William P. Huebner ◽  
Helen S. Cohen ◽  
...  

The goal of the present study was to determine if adaptive modulation of vestibulo-ocular reflex (VOR) function is associated with commensurate alterations in manual target localization. To measure the effects of adapted VOR on manual responses we developed the Vestibular-Contingent Pointing Test (VCP). In the VCP test, subjects pointed to a remembered target following passive whole body rotation in the dark. In the first experiment, subjects performed VCP before and after wearing 0.5X minifying lenses that adaptively attenuate horizontal VOR gain. Results showed that adaptive reduction in horizontal VOR gain was accompanied by a commensurate change in VCP performance. In the second experiment, bilaterally labyrinthine deficient (LD) subjects were tested to confirm that vestibular cues were central to the spatial coding of both eye and hand movements during VCP. LD subjects performed significantly worse than normal subjects. These results demonstrate that adaptive change in VOR can lead to alterations in manual target localization.


2006 ◽  
Vol 16 (1-2) ◽  
pp. 29-33
Author(s):  
Kim R. Gottshall ◽  
Michael E. Hoffer ◽  
Helen S. Cohen ◽  
Robert J. Moore

Study design: Four groups, between-subjects study. Objectives: To investigate the effects of exercise on adaptation of normal subjects who had been artificially spatially disoriented. Background: Many patients referred for rehabilitation experience sensory changes, due to age or disease processes, and these changes affect motor skill. The best way to train patients to adapt to these changes and to improve their sensorimotor skills is unclear. Using normal subjects, we tested the hypothesis that active, planned head movement is needed to adapt to modified visual input. Methods and measures: Eighty male and female subjects who had normal balance on computerized dynamic posturography (CDP) and the dynamic gait index (DGI), were randomly assigned to four groups. All groups donned diagonally shift lenses and were again assessed with CDP and DGI. The four groups were then treated for 20 min. Group 1 (control group) viewed a video, Group 2 performed exercise that involved translating the entire body through space, but without separate, volitional head movement, Group 3 performed exercises which all incorporated volitional, planned head rotations, and Group 4 performed exercises that involved translating the body (as in Group 2) and incorporated volitional, planned head motion (as in Group 3). All subjects were post-tested with CDP and DGI, lenses were removed, and subjects were retested again with CDP and DGI. Results: The groups did not differ significantly on CDP scores but Groups 3 and 4 had significantly better DGI scores than Groups 1 and 2. Conclusions: Active head movement that is specifically planned as part of the exercise is more effective than passive attention or head movements that are not consciously planned, for adapting to sensorimotor change when it incorporates active use of the changed sensory modality, in this case head motion.


1995 ◽  
Vol 73 (4) ◽  
pp. 1632-1652 ◽  
Author(s):  
J. O. Phillips ◽  
L. Ling ◽  
A. F. Fuchs ◽  
C. Siebold ◽  
J. J. Plorde

1. We studied horizontal eye and head movements in three monkeys that were trained to direct their gaze (eye position in space) toward jumping targets while their heads were both fixed and free to rotate about a vertical axis. We considered all gaze movements that traveled > or = 80% of the distance to the new visual target. 2. The relative contributions and metrics of eye and head movements to the gaze shift varied considerably from animal to animal and even within animals. Head movements could be initiated early or late and could be large or small. The eye movements of some monkeys showed a consistent decrease in velocity as the head accelerated, whereas others did not. Although all gaze shifts were hypometric, they were more hypometric in some monkeys than in others. Nevertheless, certain features of the gaze shift were identifiable in all monkeys. To identify those we analyzed gaze, eye in head position, and head position, and their velocities at three points in time during the gaze shift: 1) when the eye had completed its initial rotation toward the target, 2) when the initial gaze shift had landed, and 3) when the head movement was finished. 3. For small gaze shifts (< 20 degrees) the initial gaze movement consisted entirely of an eye movement because the head did not move. As gaze shifts became larger, the eye movement contribution saturated at approximately 30 degrees and the head movement contributed increasingly to the initial gaze movement. For the largest gaze shifts, the eye usually began counterrolling or remained stable in the orbit before gaze landed. During the interval between eye and gaze end, the head alone carried gaze to completion. Finally, when the head movement landed, it was almost aimed at the target and the eye had returned to within 10 +/- 7 degrees, mean +/- SD, of straight ahead. Between the end of the gaze shift and the end of the head movement, gaze remained stable in space or a small correction saccade occurred. 4. Gaze movements < 20 degrees landed accurately on target whether the head was fixed or free. For larger target movements, both head-free and head-fixed gaze shifts became increasingly hypometric. Head-free gaze shifts were more accurate, on average, but also more variable. This suggests that gaze is controlled in a different way with the head free. For target amplitudes < 60 degrees, head position was hypometric but the error was rather constant at approximately 10 degrees.(ABSTRACT TRUNCATED AT 400 WORDS)


1993 ◽  
Vol 264 (5) ◽  
pp. E756-E762 ◽  
Author(s):  
P. Nuutila ◽  
J. Knuuti ◽  
U. Ruotsalainen ◽  
V. A. Koivisto ◽  
E. Eronen ◽  
...  

To determine the tissue localization of insulin resistance in type 1 diabetic patients, whole body and regional glucose uptake rates were determined under euglycemic hyperinsulinemic conditions. Leg, arm, and heart glucose uptake rates were measured using positron emission tomography-derived 2-deoxy-2-[18F]-fluoro-D-glucose kinetics and the three-compartment model described by Sokoloff et al. (L. Sokoloff, M. Reivich, C. Kennedy, M.C. DesRosiers, C.S. Patlak, K.D. Pettigrew, O. Sakurada, and M. Shinohara. J. Neurochem. 28: 897–916, 1977) in eight type 1 diabetic patients and eight matched normal subjects. Whole body glucose uptake was quantitated by the euglycemic insulin clamp technique. Whole body glucose uptake was approximately 31% lower in the diabetic patients (P < 0.01) than in the normal subjects, thus confirming the presence of whole body insulin resistance. The rate of glucose uptake was approximately 45% lower in leg muscle when measured in the femoral region (55 +/- 7 vs. 102 +/- 13 mumol.kg muscle-1.min-1, diabetic patients vs. normal subjects, P < 0.05) and approximately 27% lower in the arm muscles (66 +/- 4 vs. 90 +/- 13 mumol.kg muscle-1.min-1, respectively, P < 0.05), whereas no difference was observed in heart glucose uptake [789 +/- 80 vs. 763 +/- 58 mumol.kg muscle-1.min-1 not significant (NS)]. Whole body glucose uptake correlated with glucose uptake in femoral (r = 0.93, P < 0.005) and arm muscles (r = 0.66, P < 0.05) but not with glucose uptake in the heart (r = 0.04, NS). We conclude that insulin resistance in type 1 diabetic patients is localized to skeletal muscle, whereas heart glucose uptake is unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 251 (2) ◽  
pp. R398-R408 ◽  
Author(s):  
M. E. Wastney ◽  
R. L. Aamodt ◽  
W. F. Rumble ◽  
R. I. Henkin

Zinc metabolism was studied in 32 normal volunteers after oral (n = 25) or intravenous (n = 7) administration of 65Zn. Data were collected from the blood, urine, feces, whole body, and over the liver and thigh regions for 9 mo while the subjects consumed their regular diets (containing 10 mg Zn ion/day) and for an additional 9 mo while the subjects received an exogenous oral supplement of 100 mg Zn ion/day. Data from each subject were fitted by a compartmental model for zinc metabolism that was developed previously for patients with taste and smell dysfunction. These data from normal subjects were used to determine the absorption, distribution, and excretion of zinc and the mass of zinc in erythrocytes, liver, thigh, and whole body. By use of additional data obtained from the present study, the model was refined further such that a large compartment, which was previously determined to contain 90% of the body zinc, was subdivided into two compartments to represent zinc in muscle and bone. When oral zinc intake was increased 11-fold three new sites of regulation of zinc metabolism were identified in addition to the two sites previously defined in patients with taste and smell dysfunction (absorption of zinc from gut and excretion of zinc in urine). The three new sites are exchange of zinc with erythrocytes, release of zinc by muscle, and secretion of zinc into gut. Regulation at these five sites appears to maintain some tissue concentrations of zinc when dietary zinc increases.


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