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Cortical Visual Loss
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Striate cortex occupies the upper and lower banks of the calcarine fissure. The parieto-occipital fissure is its anterior boundary but its posterior limit is variable, extending over the first 1 or 2 centimeters of the posterior surface of the occipital lobe. It has a systematic retinotopic map of the contralateral visual field (26–29). Central vision is located posteriorly at the occipital pole and the far periphery is anterior near the parieto-occipital fissure, while the superior field is represented in the lower bank and the inferior field in the upper bank. As is the case throughout the visual system, there is far greater representation of the central than the peripheral field: over half of striate cortex is devoted to the central 10 degrees of vision (29, 30). The striate cortex is supplied mainly by the posterior cerebral artery, with a parieto-occipital branch supplying the upper bank and a posterior temporal branch supplying the lower bank. The occipital pole is a watershed between the calcarine branch of the posterior cerebral artery and the middle cerebral artery: individual cortical and vascular variation means central vision could be supplied by either artery (31).
Good times and bad times
Published in Patrick Rabbitt, The Aging Mind, 2019
A fascinating backstory as to how the suprachiasmatic nucleus is re-set by alternating light and dark is the discovery, by Russell Foster, that, among the light receptors in the retinae of our eyes, we have ganglion cells that are evidently responsive to light but contribute nothing to our conscious visual experience. Studies of completely retinally blind patients have found that they can tell, with undiminished accuracy, whether they are in the light or dark, although they angrily protest that they can see no light at all and are simply guessing. This version of retinal “blindsight” is another salutary example that consciousness is by no means the main business of the brain. It is paralleled by much more dramatically publicised evidence for “cortical blindsight”, found in some patients with damage to the striate cortex of their brains, who can fixate their gaze upon, point to and discriminate between different symbols that they vehemently claim that they cannot, consciously, see [13]. Some patients can respond to visual stimuli presented within their clinically absolute visual field defects that have been caused by partial destruction of striate cortex. These examples of discrimination without awareness are a salutary reminder that most of our brains’ computations about the nature of our phenomenal reality are successfully managed without bothering to keep the conscious mind informed.
Mortimer Mishkin (b. 1926) and Leslie Ungerleider (b. 1946)
Published in Andrew P. Wickens, Key Thinkers in Neuroscience, 2018
Nonetheless, it remained to be proven that damage to this pathway was the prime cause of the temporal lobe visual deficit, and Mishkin would do this in an ingenious study using serial lesioning. To begin, he unilaterally ablated the IT cortex. As expected, this produced no visual deficit since it was well established that a bilateral lesion was needed. He then removed the striate cortex in the opposite hemisphere. Again, this produced no deficit on a visual discrimination task (because the remaining striate cortex could still send visual input to the opposite-sided IT cortex). But in the final stage, Mishkin severed the corpus callosum, and this time observed a marked visual impairment. It was not only proof of a complex functional pathway between the striate and IT cortex but also that it was involved in higher order visual processing. A second major advance in understanding the IT cortex around this time was Mishkin’s discovery, made with Japanese researcher Eichii Iwai, that the IT cortex could be divided into two regions: an anterior region (TE) and a more posterior area (TEO). The former area was shown to play a more important role in mnemonic aspects such as recognising a recently seen object, whereas the latter area had a more important perceptual function with marked deficits shown on single pattern discrimination tasks.
Cognitive training in an everyday-like virtual reality enhances visual-spatial memory capacities in stroke survivors with visual field defects
Published in Topics in Stroke Rehabilitation, 2020
Lorenz B. Dehn, Martina Piefke, Max Toepper, Agnes Kohsik, Andreas Rogalewski, Eugen Dyck, Mario Botsch, Wolf-Rüdiger Schäbitz
Noteworthy, the majority of enhanced cognitive functions involved visual-spatial sub-functions. For example, the current paradigm required the participants to look in all directions in order to search and find specific products. Training of visual search might help to adapt the patients’ scanning strategies to their restricted visual field, thus targeting an efficient compensation of the visual field loss. Often hemianopia disrupts normal scanning patterns with patients exhibiting disorganized scan paths resulting in high rates of refixation and inaccurate saccades.34 It has therefore been proposed that the loss of reentrant pathways from higher visual areas to the damaged striate cortex may result in uncertainty about spatial locations across saccades.35 Since patients with hemianopia often show a series of small saccades with long latencies into their blind field, training is typically targeted to produce systematic horizontal or vertical scanning saccades into the blind field (oculomotor training).35,36 Such visual search training usually leads to an enlargement of the region in which subjects can successfully locate a target with eye movements (the visual search field) and to a reduction in response times.37,38 However, saccades and visual field size were not examined in the current work. Hence, these conclusions remain hypothetical.
Correlation between Ocular and Vestibular Abnormalities and Convergence Insufficiency in Post-Concussion Syndrome
Published in Neuro-Ophthalmology, 2020
Abdelbaset Suleiman, Brian J. Lithgow, Neda Anssari, Mehrangiz Ashiri, Zahra Moussavi, Behzad Mansouri
Recent primate studies on rhesus monkeys have shown that the pathways shown in Figure 1 are involved in controlling vergence (i.e., convergence and divergence). Convergence can occur voluntarily or in response to a near visual stimulus. In the latter, visual information originating from the retina reaches the primary visual cortex (striate cortex) through the lateral geniculate nucleus (LGN) of the thalamus; then, it projects to the extra-striate cortex, wherein it branches into two brain regions responsible for producing vergence eye movements: (1) The parietal cortex, which in turn sends fibres to the frontal eye field (FEF) areas in the frontal lobe, and the nucleus reticularis tegmenti pontis (NRTP) in the pons. It has been shown in human studies that acquired cerebral lesions, e.g., parietal lobe damage, can cause fusional convergence abnormality.38,39 Studies in patients who suffered from stroke have shown that damage to the NRTP in the pons caused vergence dysfunction as well40; (2) The supraoculomotor area (SOA) in the midbrain, which controls some of the actions of the medial recti muscles. Those are the main generators of convergence eye movements. It is important to note that in order for convergence to occur, eye abduction (i.e., rolling the eyes out) must be relaxed at the same time when adduction (i.e., rolling the eyes in) starts.
Neuroanatomy and Imaging Assessment in Traumatic Brain Injury
Published in Journal of Binocular Vision and Ocular Motility, 2020
Vergence function occurs via a distributed pathway. Projections from the striate cortex, medial temporal, medial superior temporal, and frontal eye fields all either directly or indirectly project into the supraocular motor area of the brainstem. Approximately 50% of patients with traumatic brain injury have trouble with vergence function whether it be convergence, accommodation, or a combination. Symptoms of convergence insufficiency include impaired near the point of convergence, double vision, and loss of place while reading. Accommodative insufficiency leads to decreased accommodative amplitudes with sore eyes, and words coming in and out of focus. Our hunter would have difficulty focusing on and keeping the duck single as it flew toward the boat.