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Visual-Evoked Potential in Neuro-Ophthalmology
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
The optic nerves form connection between retina and the brain. Light impulses stimulate the photoreceptors (rods and cones) which further synapse with the inner nuclear or bipolar layers; bipolar cells synapse further with the ganglion cell layer. The axons of the ganglion cell form the optic nerve. The two optic nerves joined at optic chiasma. The optic tract starts from the optic chiasma and terminates in the lateral geniculate body. The optic tract contains ipsilateral temporal and contralateral nasal retinal fibers. The fibers carrying impulses from upper part of retina terminate in the ventromedial segment and those from lower part terminate in the ventrolateral segment of geniculate body. The ipsilateral temporal and contralateral nasal retinal fibers terminate alternatively in six layers in lateral geniculate body. Lateral geniculate body neurons form optic radiation, which pass posteriorly to terminate in the striate cortex (area 17). The macular fibers occupy the larger portion of occipital lobe at the occipital pole in a wedge-shaped area. The upper half and lower half of the retinal fibers relay superior and inferior to the calcarine fissure, respectively (Figure 3B.1).
Consciousness, Sleep and Hypnosis, Meditation, and Psychoactive Drugs
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
In humans and mammals, the circadian rhythms are controlled by a tiny cluster of neurons in the medial hypothalamus called the suprachiasmatic nucleus (SCN), i.e., the master clock (Moore, 2007). Damage to the SCN in rats abolished their circadian rhythms of temperature, cortisol secretion, eating, drinking, and sleep–wakefulness. Keeping the circadian rhythms synchronized with one another and on a 24-hour schedule is also controlled by environmental time cues. The most important of these cues is bright light, especially sunlight. Light is detected by photoreceptors in the eye, and is communicated via the visual system to the SCN (which lies above the optic chiasm) in the hypothalamus (Berson, Dunn, & Takao, 2002; Drouyer, Rieux, Hut, & Cooper, 2007). A tuft of nerve fibers branches off from the main nerve and penetrates the hypothalamus above, forming synaptic connections with cells in the SCN. This pathway (the retinohypothalamic tract) allows a link between the outside world and the brain’s own clock (Blakemore, 1988). Information regarding light is also conveyed to the SCN indirectly through the intergeniculate leaflet of the lateral geniculate body.
Lateral geniculate body
Published in Fiona Rowe, Visual Fields via the Visual Pathway, 2016
The lateral geniculate body is in close proximity to the thalamus and pyramidal tracts. A lesion involving all structures can result in visual field loss along with contralateral hemiparesis and/or hemianaesthesia.
Efavirenz-Associated Retinal Toxicity Presenting with Night Vision Defects in Patients with Human Immunodeficiency Virus
Published in Ocular Immunology and Inflammation, 2020
Sridharan Sudharshan, Kolli Dileep Kumar, Muna Bhende, Jyotirmay Biswas, Poongulali Selvamuthu
All our patients presented with retinitis-pigmentosa-like symptoms, presenting with poor night vision and a recent history of initiation of HAART or a change in drug regime. Efavirenz was the common anti-retroviral drug that was added recently into their HAART regime in all patients. Literature reporting retinal toxicity with Efavirenz is very limited,12,13 with few studies on large cohort of patients even showing it to be safe even after prolonged use.14 Not all patients on efavirenz seem to experience visual function abnormalities. This wide inter-patient variability in efavirenz toxicity could possibly be due to variability in pharmacokinetics as a result of polymorphisms in the major metabolizing enzyme i.e. cytochrome P450 CYP2B6.15 Studies have reported histological changes in the lateral geniculate body in Wistar rats due to efavirenz which could possibly affect visual sensibilities.16
Measuring abnormal intrinsic brain activities in patients with retinal detachment using amplitude of low-frequency fluctuation: a resting-state fMRI study
Published in International Journal of Neuroscience, 2019
Hong-Hua Kang, Yong-Qiang Shu, Lin Yang, Pei-Wen Zhu, Dan Li, Qing-Hai Li, You-Lan Min, Lei Ye, Qiong Zhou, Yi Shao
As the anatomical region of the visual cortex, the occipital lobe takes a part in visual coding. And the primary visual cortex (V1) is an important part of the occipital lobe, which receives signals from the lateral geniculate body [23]. The V1 processed visual information with decorrelation and sparse coding [24]. In addition, the V1 is relevant to visuospatial integration [25,26]. The normal function of the retinal ganglion cells is of great importance in visual stimulation. The pathological mechanism of RD is when the retinal neuroepithelium separates from the pigment epithelium [27], which leads to the disruption in visual signals transferring. In RD patients of this study, we demonstrated significantly decreased ALFF in their right occipital lobe, and it indicates the dysfunction of the visual cortex. Thus, we speculated that the RD patients might associate with the impairment in visual cortex.
Optical coherence tomography in the investigation of systemic neurologic disease
Published in Clinical and Experimental Optometry, 2019
Sangeetha Srinivasan, Nathan Efron
A decrease in macular volume has been noted in patients with multiple sclerosis,2009 more so in the nasal portions,2010 which may corroborate with compromised retinal nerve fibre layer thickness in the temporal quadrant as reported in a previous study.2017 Evangelou et al.2001 examined the size distribution of neurons in the magnocellular and parvocellular layers of the lateral geniculate body, and axonal densities of the anterior visual pathway. They observed that the distribution of neuron size in the lateral geniculate body was correlated with axonal densities in the visual pathway. In addition, they observed there were no significant differences in neuronal size distribution between patients and controls in magnocellular layers. In parvocellular layers, cell sizes were smaller in those with multiple sclerosis compared with those of healthy controls, suggesting that smaller axons may be susceptible to damage from multiple sclerosis.2001