Changes in connectivity after visual cortical brain damage underlie altered visual function.

Auditory and visual attention modulate motion processing in area MT+

We investigated the BOLD response of visual cortical and sub-cortical regions to fast drifting motion presented over wide fields, including the far periphery. Stimuli were sinusoidal gratings of 50% contrast moving at moderate and very high speeds (38 and 570 °/s), projected to a large field of view (~60°). Both stimuli generated strong and balanced responses in the lateral geniculate nucleus and the superior colliculus. In visual cortical areas, responses were evaluated at three different eccentricities: central 0–15°; peripheral 20–30°; and extreme peripheral 30–60°. “Ventral stream” areas (V2, V3, V4) preferred moderate-speeds in the central visual field, while motion area MT+ responded equally well to both speeds at all eccentricities. In all other areas and eccentricities BOLD responses were significant and equally strong for both types of moving stimuli. Support vector machine showed that the direction of the fast-speed motion could be successfully decoded from the BOLD response in all visual areas, suggesting that responses are mediated by motion mechanisms rather than being an unspecific preference for fast rate of flicker. The results show that the visual cortex responds to very fast motion, at speeds generated when we move our eyes rapidly, or when moving objects pass by closely.

A sudden change in the direction of motion is a particularly salient and relevant feature of visual information. Extensive research has identified cortical areas responsive to visual motion and characterized their sensitivity to different features of motion, such as directional specificity. However, relatively little is known about responses to sudden changes in direction. Electrophysiological data from animals and functional imaging data from humans suggest a number of brain areas responsive to motion, presumably working as a network. Temporal patterns of activity allow the same network to process information in different ways. The present study in humans sought to determine which motion-sensitive areas are involved in processing changes in the direction of motion and to characterize the temporal patterns of processing within this network of brain regions. To accomplish this, we used both magnetoencephalography (MEG) and functional magnetic resonance imaging (fMRI). The fMRI data were used as supplementary information in the localization of MEG sources. The change in the direction of visual motion was found to activate a number of areas, each displaying a different temporal behavior. The fMRI revealed motion-related activity in areas MT+ (the human homologue of monkey middle temporal area and possibly also other motion sensitive areas next to MT), a region near the posterior end of the superior temporal sulcus (pSTS), V3A, and V1/V2. The MEG data suggested additional frontal sources. An equivalent dipole model for the generators of MEG signals indicated activity in MT+, starting at 130 ms and peaking at 170 ms after the reversal of the direction of motion, and then again at approximately 260 ms. Frontal activity began 0-20 ms later than in MT+, and peaked approximately 180 ms. Both pSTS and FEF+ showed long-duration activity continuing over the latency range of 200-400 ms. MEG responses in the region of V3A and V1/V2 were relatively small, and peaked at longer latencies than the initial peak in MT+. These data revealed characteristic patterns of activity in this cortical network for processing sudden changes in the direction of visual motion.

Buildup of Choice-Predictive Activity in Human Motor Cortex during Perceptual Decision Making

Cortical Damage in Alzheimer’s Disease: Estimation in Medial and Lateral Aspects of the Cerebrum using an Improved Mapping Method based on Diffusion-Weighted Magnetic Resonance Imaging

Adaptive Surround Modulation in Cortical Area MT

In unequal alternating monocular exposure, each eye receives normal patterned input, but on alternate days and for unequal periods. This imbalance in stimulation produces a behavioral deficit for the less-experienced eye and alters the ability of that eye to activate cortical cells. To determine whether unequal alternating exposure also affects the sizes of cells in the lateral geniculate nucleus (LGN), we measured the cross-sectional areas of geniculate neurons in seven normally reared cats, 14 cats reared with equal alternating exposure, and 17 cats reared with unequal alternating exposure. We found that, in the LGNs of cats reared with unequal alternating monocular exposure, cells in layers that received their input from the less-experienced eye were smaller than those in layers that received their input from the more-experienced eye. This effect was restricted to the binocular segments of the nucleus, and the difference in cell size was a function of the imbalanced exposure, rather than the length of exposure per se. In control groups given balanced alternating exposure, cell size was not correlated with the length of daily exposure. In cats reared with unequal exposure, the change in cell size was greater in the nucleus ipsilateral to the less-experienced eye. Further, the size of the effect was correlated with the size of the imbalance imposed during rearing: Cats reared with a moderate imbalance (8 hours/day vs. 4 hours/day) showed less change in cell size than cats reared with a large imbalance (8 hours/day vs. 1 hour/day). These results are consistent with those of behavorial and physiological studies and strongly suggest (1) that unequal alternating monocular exposure affects the sizes of cells in the LGN by altering the normal competitive balance between the retinogeniculocortical pathways from the left and right eyes, and (2) that the contralateral pathway has some inherent advantage in this competition. We also found a slight shrinkage of cells in the LGNs of cats reared with equal alternating monocular exposure. Since this effect was restricted to the binocular segments of the nucleus, and was not related to the length of exposure given, it was probably caused by the imbalanced binocular competition that occurred during each day's monocular exposure.

The mechanisms of neuronal degeneration following traumatic head injury are not well understood and no adequate treatment is currently available for the prevention of traumatic brain damage in humans. Seven day old rat pups were subjected to mechanical percussion of the head. Cortical damage in infant rats was reduced by pre-treatment with the N-methyl-D-aspartate (NMDA) antagonists dizocilpine (MK-801) or 3-((+/-)-2-carboxypiperazin-4-yl)-propyl-I-phosphonate (CPP). The AMPA antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (f) quinoxaline (NBQX) did not significantly suppress cortical damage in infant rats. In adult rats, traumatic head injury leads to primary (at impact-cortex) and secondary (distant-hippocampus) damage to the brain. Morphometric analysis demonstrated that both cortical and hippocampal damage was mitigated by pre-treatment with either the NMDA antagonist CPP or the non-NMDA antagonist NBQX. Neither treatment prevented primary damage in the cortex when therapy was started after trauma. Delayed treatment of rats with NBQX, but not with CPP, beginning between 1 and 7 h after trauma prevented the hippocampal damage. No protection was seen when therapy with NBQX was started 10 h after trauma. These data indicate that NMDA antagonists may possess better neuroprotective properties against excitotoxic processes triggered by traumatic brain injury in young individuals whereas AMPA antagonists may be more beneficial in adults.

Chapter 5.14 - Exploring the pulvinar path to visual cortex

1. Luis H. Ospina, MD* 1. *Assistant Professor, Pediatric Ophthalmology and Neuro-ophthalmology, Ste-Justine Hospital, University de Montreal, Montreal, Quebec, Canada After completing this article, readers should be able to: 1. Recognize cortical visual impairment (CVI) as an important cause of pediatric visual loss. 2. Identify the most frequent causes of pediatric CVI and, more specifically, understand the role of hypoxia as a cause of central visual damage. 3. Describe the different patterns and implications for future vision of hypoxic central visual damage occurring in preterm compared with term babies. 4. Know the clinical signs suggestive of CVI in children. 5. Discuss the involvement of visual functions other than visual acuity (ie, cognitive visual aspects) in CVI and correlate them with the likely affected neuroanatomic substrates. 6. Explain the value of using a multidisciplinary approach in rehabilitating children who have CVI early in their development. Vision loss caused by central nervous system damage often is referred to as CVI but also may be referred to as cerebral visual impairment or neurologic visual impairment. These terms refer to the fact that the primary defect may not necessarily be limited to the striate (primary visual) cortex and may affect other areas subserving vision, such as the visual associative cortex, optic radiations, and visual attention pathways. Although it is not yet certain which of these three terms best describes the visual deficit, it is clear that use of the label cortical blindness must be abandoned. That term not only evokes negative connotations for the child and the family but is inaccurate because in almost every instance, some degree of residual vision remains, and visual improvement can occur. CVI has become the greatest cause of pediatric visual impairment in developed countries (1)(2)(3)(4)(5) and is becoming increasingly prevalent in developing nations. CVI is a problem of increasing frequency for two primary reasons. First, the progress in neonatal care has resulted in improved survival of …

<p>My dissertation focused on understanding how different areas of the brain coordinate in networks to drive higher cognitive functions, and how damage, changes the brain’s synchronized activity (or functional connectivity) in the short and long term. In this dissertation, I studied the functional connectivity of brain networks that are thought to underlie emotion and decision-making, and how these networks change in the face of neurological injury.</p><p>In my first set of experiments, I studied participants with chronic focal brain damage to determine how damage to brain areas which have been identified as important in emotion and decision-making behaviors (amygdala, ventromedial prefrontal cortex, & insula), affected connectivity of brain networks, and how changes in connectivity following damage to these areas related to emotion and decision-making behavior. Supporting my predictions, I found evidence that damage to the amygdala, ventromedial prefrontal cortex, and insula all result in significantly weaker connections between a network of areas important for assigning value to stimuli. Additionally, I found that stronger connectivity in this valuation network was significantly positively associated with performance on ratings of disgusted faces, while stronger connectivity in a network important for processing emotional salience was significantly positively correlated with decision-making performance.</p><p>In the second set of studies in this dissertation, I utilized a population of epilepsy patients who were undergoing brain surgery to treat their seizures to investigate how a brain network related to emotional salience changed from before to after surgery. This approach allowed me to study how the connectivity and associated behavior of this network changed from preoperative baseline, to the weeks and months after part of this network was removed. While I expected a decline in this network in the weeks following surgery, instead I found a significant positive correlation between preoperative and acute postoperative connectivity in a subset of this network. However, my hypothesis that there would be a significant increase in the connectivity of this network between acute and chronic postoperative epochs was supported. I only have partial evidence for a significant correlation between the change in salience network connectivity between preoperative and acute postoperative assessments and the associated change in decision-making behavior. This correlation was in the opposite direction of my hypothesis, with increased change in connectivity being positively associated with change in risk-taking behavior. I did not observe a significant correlation between the change in network connectivity and change in behavior across acute and chronic measurements.</p><p>These findings provide important insight on how measures of network connectivity can inform theories of neuroplasticity and reorganization following brain damage. Understanding how these networks change over time, and how changes in these networks relate to behavioral outcomes, are critical for the development and effective deployment of therapeutic interventions. Together, these studies provide a foundation for further study, demonstrating that these networks change over time with damage, and the residual network strength is associated with performance on measures of emotion and decision-making.</p>

The directional selectivity of the visual response properties was determined in 148 neurons, all located in area MT of three hemispheres of two macaque monkeys. The preferred direction of every neuron was obtained by analyzing the response obtained by a circular movement of the background while the monkeys fixated a stationary target. The distribution of the preferred directions was isotropic and showed no ipsiversive bias. MT neurons were excited in a directionally selective manner during the execution of optokinetic nystagmus, in a similar way to that produced by visual stimulation during fixation. The majority of neurons showed a sensitivity to the velocity of retinal image slip. Activity during the execution of optokinetic nystagmus could be traced back to residual retinal image slip in the direction of optokinetic stimulation. No dynamic effects of the neuronal activity during the build-up of eye velocity in early optokinetic nystagmus were observed. Obviously, the activity in area MT did not reflect the charging of the velocity storage mechanism. Accordingly, following the cessation of stimulation, the activity dropped to the level of spontaneous activity and did not parallel the execution of optokinetic afternystagmus. These results suggest that area MT is not part of the velocity storage mechanism and, furthermore, that the storage mechanism must be downstream of area MT in the processing of visual motion for the generation of the optokinetic nystagmus and afternystagmus.

We sought to better understand the neural representation of visual motion acceleration. A straightforward estimation of acceleration would involve calculating the rate of change of velocity, which itself would be calculated from change in position over time. As it is well-established that neurons in area MT encode velocity, the brain could thus indirectly estimate acceleration by calculating the change in MT’s velocity representations. An alternate mechanism, however, could operate more rapidly and directly. In this case, the brain could exploit interactions between MT’s standard motion encoding and idiosyncratic temporal dynamics of neural responses. Such direct decoding would thus exploit nonlinearities usually ignored in studies of MT coding. We tested between these two theories by measuring from ensembles of MT neurons while two male awake fixating macaques viewed linearly accelerating motion stimuli. Direct decoding of acceleration from MT was possible on faster time scales, and could be done with higher fidelity, than indirect decoding. Distinct motion acceleration information could thus be efficiently read out from rich and heterogeneous MT ensemble responses, regardless of the mechanisms that give rise to various forms of motion tuning that it exhibits. A similar analysis of activity in the medial superior temporal area (MST) did not suggest this later stage of motion processing has a more refined acceleration representation. Together, these results suggest that the brain may opportunistically exploit nonlinear idiosyncrasies of neural responses to efficiently extract behaviorally relevant information on fast time scales, instead of performing explicit calculation of some variables.

Nonspatially selective attention is based on the notion that specific features or objects in the visual environment are effectively prioritized in cortical visual processing. Feature-based attention (FBA), in particular, is a well-studied process that dynamically and selectively addresses neurons preferentially processing the attended feature attribute (e.g., leftward motion). In everyday life, however, behavior may require high sensitivity for an entire feature dimension (e.g., motion), but experimental evidence for a feature dimension-specific attentional modulation on a cellular level is lacking. Therefore, we investigated neuronal activity in macaque motion-selective mediotemporal area (MT) in an experimental setting requiring the monkeys to detect either a motion change or a color change. We hypothesized that neural activity in MT is enhanced when the task requires perceptual sensitivity to motion. In line with this, we found that mean firing rates were higher in the motion task and that response variability and latency were lower compared with values in the color task, despite identical visual stimulation. This task-specific, dimension-based modulation of motion processing emerged already in the absence of visual input, was independent of the relation between the attended and stimulating motion direction, and was accompanied by a spatially global reduction of neuronal variability. The results provide single-cell support for the hypothesis of a feature dimension-specific top-down signal emphasizing the processing of an entire feature class.NEW & NOTEWORTHY Cortical processing serving visual perception prioritizes information according to current task requirements. We provide evidence in favor of a dimension-based attentional mechanism addressing all neurons that process visual information in the task-relevant feature domain. Behavioral tasks required monkeys to attend either color or motion, causing modulations of response strength, variability, latency, and baseline activity of motion-selective monkey area MT neurons irrespective of the attended motion direction but specific to the attended feature dimension.

Cross-modal plasticity refers to the recruitment of cortical regions involved in the processing of one modality (e.g. vision) for processing other modalities (e.g. audition). The principles determining how and where cross-modal plasticity occurs remain poorly understood. Here, we investigate these principles by testing responses to auditory motion in visual motion area MT+ of congenitally blind and sighted individuals. Replicating previous reports, we find that MT+ as a whole shows a strong and selective responses to auditory motion in congenitally blind but not sighted individuals, suggesting that the emergence of this univariate response depends on experience. Importantly, however, multivoxel pattern analyses showed that MT+ contained information about different auditory motion conditions in both blind and sighted individuals. These results were specific to MT+ and not found in early visual cortex. Basic sensitivity to auditory motion in MT+ is thus experience-independent, which may be a basis for the region's strong cross-modal recruitment in congenital blindness.