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Assessment of visual processing functions and disorders
Published in John Ravenscroft, The Routledge Handbook of Visual Impairment, 2019
Miller, Pasik and Pasik (1980) reported on measurements of responses to gratings in superior colliculus: “Monkeys with total bilateral ablation of the striate cortex, however, retain a residual capacity for pattern discrimination and also can differentiate between a vertical and an oblique luminous bar” (p. 1510). This confirmed our guesses. Monkeys responded to gratings up to 4 cpd as did the boy with visual acuity 0.01. Apparently, humans also had this newly discovered pathway. Later it was called the tectopulvinar pathway going via superior colliculus in tectum and pulvinar nucleus in thalamus to MT/V5 (middle temporal visual area/visual area 5) and further into occipital and parietal lobes.
Pain in Neurological Disease
Published in John W. Scadding, Nicholas A. Losseff, Clinical Neurology, 2011
Other brain areas targeted for the treatment of intractable pain include the dorsomedian nucleus, which projects to the cingulum, the frontal lobes and limbic system, and the medial and lateral pulvinar nuclei. Lesions in these structures tend to produce only transient analgesia. Lesions of the frontothalamic projections and the frontal lobes themselves will lead to reduced suffering from pain, but are associated with a change in personality, although this may be mild.
Parallel Visual Pathways in a Dynamic System
Published in Jon H. Kaas, Christine E. Collins, The Primate Visual System, 2003
Vivien A. Casagrande, David W. Royal
Is this really the case? To answer this question we need to describe briefly the V1 output pathways, their connections, and their targets. As in all cortical areas, input to V1 terminates primarily in the middle layers (IV and III), whereas output to extrastriate cortical areas exits from the upper layers (II/III) and output to subcortical structures exits from the lower layers (V and VI). V1 in primates has a number of cortical and subcortical targets. There are four major cortical targets of V1: these include V2, V3, the dorsal medial area (DM)/V3a, and the middle temporal (MT) visual area with smaller projections to the dorsal lateral or fourth visual area (DL/V4) and contralateral V1 (at least along the vertical meridian representation).49 The bulk of the output from V1 goes to V2 and arises from cells in interblob columns in layer III5051 (see, however, Reference 52). This projection terminates primarily within the CO pale bands and CO thick bands of V2. A second projection arises from the CO-rich blobs of V1 and terminates in the CO-rich thin bands of V2.50,53 In macaque monkeys V3 receives the second largest projection from V1, which also arises from layer III and possibly IVB.54 Connections to area DM/V3a arise from CO blobs in layer III and cells below these compartments in IVB, which also project to MT.55-57 All these output cortical targets of V1 and additional higher-order visual areas provide major feedback projections to V1, which can directly impact the output cells in the superficial layers and also influence activity within the deeper layers of V1.58 The deeper layers of V1, layers V and VI, send axons back to the thalamus and to the midbrain and pons. Layer VI is unique in that cells in this layer send both direct and indirect (via the thalamic reticular nucleus) feedback to the LGN and provide major pathways for V1 to regulate its own input. Cells in layer VI also send axons to the visual sectors of the claustrum, which appears to modulate the responses of V1 neurons via feedback. Cells in layer V provide the major driving input to many cells in the pulvinar nucleus of the thalamus in monkeys; the pulvinar, in turn, provides input to a number of extrastriate areas, including V2, V3, DM/V3a, and MT, that also feed signals back to V1. In addition, cells in layer V send a major projection to the superficial layers of the superior colliculus and other midbrain areas such as the pretectum, as well as nuclei in the pons that are concerned with eye movements. Thus, V1 is in a position to inform these structures of its activities and be informed by them indirectly through connections with the LGN or through feedback from extrastriate areas (see Reference 59 for overview).
Thalamic neuromodulation in epilepsy: A primer for emerging circuit-based therapies
Published in Expert Review of Neurotherapeutics, 2023
Bryan Zheng, David D. Liu, Brian B Theyel, Hael Abdulrazeq, Anna R. Kimata, Peter M Lauro, Wael F. Asaad
Because classification schemes based primarily on local anatomy and histology do not capture the functional heterogeneity of individual thalamic nuclei, some modern thalamic classification systems are based on circuit topology[26]. Distinctions have been made based on (i) the characteristics of thalamocortical output – core versus matrix nuclei[27], (ii) input – first- versus higher-order nuclei[28], or (iii) both input and output[29]. For example (of [i]), the anterior nucleus of the thalamus (ANT) has been defined as a core nucleus because it provides focal projections as a node in the medial limbic circuit. The pulvinar nucleus, specifically the PuM, also possesses ‘core-like’ properties based on its distinct circuits involving the temporal lobe[24]. In contrast, matrix nuclei like the centromedian nucleus of the thalamus (CMT) are characterized by markedly more diffuse cortical projections[30]. Meanwhile, within the framework of the first- and higher-order nuclear scheme (ii): first-order nuclei receive ‘driver’ inputs from subcortical sites carrying primary sensory information (e.g. lateral geniculate nucleus [LGN] receives visual input from the retina), while higher-order nuclei (e.g. the pulvinar) receive driver inputs from cortical layer V and primarily participate in transthalamic cortico-cortical circuits[28]. This classification scheme is useful in that it highlights how the thalamus continues to be involved in information processing between areas of cortex in addition to modulating and relaying primary sensory information.
Photoaversion in inherited retinal diseases: clinical phenotypes, biological basis, and qualitative and quantitative assessment
Published in Ophthalmic Genetics, 2022
Serena Zaman, Thomas Kane, Mohamed Katta, Michalis Georgiou, Michel Michaelides
There may be value in examining melanopsin-dependent pathways independently. Panorgias et al. undertook fMRI imaging in a patient with idiopathic photophobia. This patient stated specifically that blue light exposure resulted in nausea and a general feeling of malaise and would cease immediately upon cessation of blue light exposure (49). Imaging was indicative of activity in the pulvinar nuclei which are known to receive ipRGC input.
Updated review on the link between cortical spreading depression and headache disorders
Published in Expert Review of Neurotherapeutics, 2021
Doga Vuralli, Hulya Karatas, Muge Yemisci, Hayrunnisa Bolay
Somatosensory temporal discrimination (STD), the ability to perceive two consecutive somatosensory stimuli as distinct, was evaluated in migraine patients and robust prolongation of STD thresholds was revealed during the migraine attacks whereas STD threshold values were within normal limits outside the migraine attacks [5,7]. STD prolongation was specific to migraine attacks and STD remained normal during tension type headache [7]. Disruption of somatosensory temporal discrimination suggested a dysfunction in central sensory processing. In a later study, short latency afferent inhibition (SAI) was evaluated in migraine patients during preictal, ictal, and interictal periods [163]. SAI assesses the integration of ascending somatosensory input through the thalamic relay neurons and descending motor output. Facilitation instead of inhibition was shown to occur in the sensorimotor cortex in response to conditioned stimulation with SAI paradigm during preictal period, several hours prior to the onset of migraine headache and during an attack in migraine without aura patients. Impairment in SAI indicated a disinhibition in the sensorimotor integration showing a possible involvement of higher order centers. Pulvinar nucleus of thalamus is an integration area for multiple sensory modalities [164]. CSD may lead to a dysfunction in the thalamocortical network and change the interplay between the cortical areas such as sensorimotor cortex or visual cortex and the pulvinar and may cause synchronous or sequential multisensory symptoms. Impairment in multiple sensory domains accompanying migraine headache can be related to the dysfunction of the thalamocortical network. Moreover, thalamocortical dysfunction leading to the activation of the trigeminal pain nucleus through central pathways could also play a role in the development of lateralized headache in migraine. SAI is also a noninvasive measurement of cholinergic function. Drug TMS studies revealed that acetylcholinesterase inhibitors increased while muscarinic antagonist scopolamine decreased SAI. Cognitive disorders with cholinergic dysfunction such as Alzheimer dementia and mild cognitive impairment [165,166] were also shown to be associated with decreased SAI. Decreased SAI during preictal and ictal periods in migraine shows that there is a disruption in cholinergic system in migraine.