scholarly journals USING TRANSCRANIAL MAGNETIC STIMULATION (TMS) TO PROBE EFFECTS OF VISUAL MOTION ADAPTATION ON PRIMARY VISUAL CORTEX (V1) EXCITABILITY IN BILATERAL VESTIBULAR FAILURE (BVF) PATIENTS

2015 ◽  
Vol 86 (11) ◽  
pp. e4.70-e4
Author(s):  
Hena Ahmad ◽  
Richard Roberts ◽  
Qadeer Arshad Arshad ◽  
Mitesh Patel ◽  
Adolfo Bronstein

Background and aimPatients with BVF report oscillopsia due to a defective vestibulo-ocular reflex causing retinal slip. No previous studies have probed visual cortical excitability using TMS and visual motion processing in these patients. We investigated the effects of visual motion adaptation on V1 cortical excitability in BVF patients and correlated this with psychophysical parameters.Methods12 BVF patients (7 males) aged 29–65 (mean=54.5) and 12 controls (6 males) aged 42–73 (mean=55) were recruited. Biphasic TMS pulses were applied at V1 and phosphene threshold (PT) was estimated. 3 measurement phases were (1) Stationary (2) Motion with optokinetic stimulation (OKS) Adaptation: OKS rightwards for 5 minutes 3) Post adaptation during viewing motion. All subjects completed questionnaires prior to the experiment. Results were analysed offline by calculating the probability of phosphene perception.ResultsBaseline phosphene thresholds were significantly higher in BVF patients (p=0.024) reflecting reduced visual cortical excitability. Lower oscillopsia scores correlated with reduced baseline V1 excitability (p=0.009).ConclusionsThis novel finding acts as a neurophysiological correlate for clinical observations of adaptive visual motion perception and is also correlated with psychophysical parameters. These results provide evidence for adaptive mechanisms leading to cortical plasticity following BVF.

2017 ◽  
Vol 117 (3) ◽  
pp. 903-909 ◽  
Author(s):  
Astrid J. A. Lubeck ◽  
Angelique Van Ombergen ◽  
Hena Ahmad ◽  
Jelte E. Bos ◽  
Floris L. Wuyts ◽  
...  

The objectives of this study were 1) to probe the effects of visual motion adaptation on early visual and V5/MT cortical excitability and 2) to investigate whether changes in cortical excitability following visual motion adaptation are related to the degree of visual dependency, i.e., an overreliance on visual cues compared with vestibular or proprioceptive cues. Participants were exposed to a roll motion visual stimulus before, during, and after visual motion adaptation. At these stages, 20 transcranial magnetic stimulation (TMS) pulses at phosphene threshold values were applied over early visual and V5/MT cortical areas from which the probability of eliciting a phosphene was calculated. Before and after adaptation, participants aligned the subjective visual vertical in front of the roll motion stimulus as a marker of visual dependency. During adaptation, early visual cortex excitability decreased whereas V5/MT excitability increased. After adaptation, both early visual and V5/MT excitability were increased. The roll motion-induced tilt of the subjective visual vertical (visual dependence) was not influenced by visual motion adaptation and did not correlate with phosphene threshold or visual cortex excitability. We conclude that early visual and V5/MT cortical excitability is differentially affected by visual motion adaptation. Furthermore, excitability in the early or late visual cortex is not associated with an increase in visual reliance during spatial orientation. Our findings complement earlier studies that have probed visual cortical excitability following motion adaptation and highlight the differential role of the early visual cortex and V5/MT in visual motion processing. NEW & NOTEWORTHY We examined the influence of visual motion adaptation on visual cortex excitability and found a differential effect in V1/V2 compared with V5/MT. Changes in visual excitability following motion adaptation were not related to the degree of an individual's visual dependency.


2013 ◽  
Vol 20 (1) ◽  
pp. 113-122 ◽  
Author(s):  
Yukari Takarae ◽  
Beatriz Luna ◽  
Nancy J. Minshew ◽  
John A. Sweeney

AbstractImpairments in visual motion perception and use of visual motion information to guide behavior have been reported in autism, but the brain alterations underlying these abnormalities are not well characterized. We performed functional magnetic resonance imaging (fMRI) studies to investigate neural correlates of impairments related to visual motion processing. Sixteen high-functioning individuals with autism and 14 age and IQ-matched typically developing individuals completed two fMRI tasks using passive viewing to examine bottom–up responses to visual motion and visual pursuit tracking to assess top–down modulation of visual motion processing during sensorimotor control. The autism group showed greater activation and faster hemodynamic decay in V5 during the passive viewing task and reduced frontal and V5 activation during visual pursuit. The observations of increased V5 activation and its faster decay during passive viewing suggest alterations in local V5 circuitries that may be associated with reduced GABAergic tone and inhibitory modulation. Reduced frontal and V5 activation during active pursuit suggest reduced top–down modulation of sensory processing. These results suggest that both local intrinsic abnormalities in V5 and more widely distributed network level abnormalities are associated with visual motion processing in autism. (JINS, 2014, 20, 113–122)


2014 ◽  
Vol 111 (1) ◽  
pp. 112-127 ◽  
Author(s):  
L. Thaler ◽  
J. L. Milne ◽  
S. R. Arnott ◽  
D. Kish ◽  
M. A. Goodale

We have shown in previous research (Thaler L, Arnott SR, Goodale MA. PLoS One 6: e20162, 2011) that motion processing through echolocation activates temporal-occipital cortex in blind echolocation experts. Here we investigated how neural substrates of echo-motion are related to neural substrates of auditory source-motion and visual-motion. Three blind echolocation experts and twelve sighted echolocation novices underwent functional MRI scanning while they listened to binaural recordings of moving or stationary echolocation or auditory source sounds located either in left or right space. Sighted participants' brain activity was also measured while they viewed moving or stationary visual stimuli. For each of the three modalities separately (echo, source, vision), we then identified motion-sensitive areas in temporal-occipital cortex and in the planum temporale. We then used a region of interest (ROI) analysis to investigate cross-modal responses, as well as laterality effects. In both sighted novices and blind experts, we found that temporal-occipital source-motion ROIs did not respond to echo-motion, and echo-motion ROIs did not respond to source-motion. This double-dissociation was absent in planum temporale ROIs. Furthermore, temporal-occipital echo-motion ROIs in blind, but not sighted, participants showed evidence for contralateral motion preference. Temporal-occipital source-motion ROIs did not show evidence for contralateral preference in either blind or sighted participants. Our data suggest a functional segregation of processing of auditory source-motion and echo-motion in human temporal-occipital cortex. Furthermore, the data suggest that the echo-motion response in blind experts may represent a reorganization rather than exaggeration of response observed in sighted novices. There is the possibility that this reorganization involves the recruitment of “visual” cortical areas.


1988 ◽  
Vol 60 (3) ◽  
pp. 940-965 ◽  
Author(s):  
M. R. Dursteler ◽  
R. H. Wurtz

1. Previous experiments have shown that punctate chemical lesions within the middle temporal area (MT) of the superior temporal sulcus (STS) produce deficits in the initiation and maintenance of pursuit eye movements (10, 34). The present experiments were designed to test the effect of such chemical lesions in an area within the STS to which MT projects, the medial superior temporal area (MST). 2. We injected ibotenic acid into localized regions of MST, and we observed two deficits in pursuit eye movements, a retinotopic deficit and a directional deficit. 3. The retinotopic deficit in pursuit initiation was characterized by the monkey's inability to match eye speed to target speed or to adjust the amplitude of the saccade made to acquire the target to compensate for target motion. This deficit was related to the initiation of pursuit to targets moving in any direction in the visual field contralateral to the side of the brain with the lesion. This deficit was similar to the deficit we found following damage to extrafoveal MT except that the affected area of the visual field frequently extended throughout the entire contralateral visual field tested. 4. The directional deficit in pursuit maintenance was characterized by a failure to match eye speed to target speed once the fovea had been brought near the moving target. This deficit occurred only when the target was moving toward the side of the lesion, regardless of whether the target began to move in the ipsilateral or contralateral visual field. There was no deficit in the amplitude of saccades made to acquire the target, or in the amplitude of the catch-up saccades made to compensate for the slowed pursuit. The directional deficit is similar to the one we described previously following chemical lesions of the foveal representation in the STS. 5. Retinotopic deficits resulted from any of our injections in MST. Directional deficits resulted from lesions limited to subregions within MST, particularly lesions that invaded the floor of the STS and the posterior bank of the STS just lateral to MT. Extensive damage to the densely myelinated area of the anterior bank or to the posterior parietal area on the dorsal lip of the anterior bank produced minimal directional deficits. 6. We conclude that damage to visual motion processing in MST underlies the retinotopic pursuit deficit just as it does in MT. MST appears to be a sequential step in visual motion processing that occurs before all of the visual motion information is transmitted to the brainstem areas related to pursuit.(ABSTRACT TRUNCATED AT 400 WORDS)


2018 ◽  
Author(s):  
Florian Herpich ◽  
Michael D Melnick ◽  
Sara Agosta ◽  
Krystel Huxlin ◽  
Duje Tadin ◽  
...  

Numerous behavioral studies have shown that visual function can improve with training, although perceptual refinements generally require weeks to months of training to attain. This, along with questions about long-term retention of learning, limits practical and clinical applications of many such paradigms. Here, we show for the first time that just 10 days of visual training coupled with transcranial random noise stimulation (tRNS) over visual areas causes dramatic improvements in visual motion perception. Relative to control conditions and anodal stimulation, tRNS-enhanced learning was at least twice as fast, and, crucially, it persisted for 6 months after the end of training and stimulation. Notably, tRNS also boosted learning in patients with chronic cortical blindness, leading to recovery of motion processing in the blind field after just 10 days of training, a period too short to elicit enhancements with training alone. In sum, our results reveal a remarkable enhancement of the capacity for long-lasting plastic and restorative changes when a neuromodulatory intervention is coupled with visual training.


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