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Physiology of the Pain System
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
The brain does not merely witness the nociceptive signal. It actively participates in constructing the nociceptive signal. The spinothalamic tract ultimately communicates with higher nociception processing centers within the brain. The lateral thalamic nuclei, SI, and SII somatosensory cortices play a sensory discriminative role. The medial thalamic nuclei, and anterior and medial cingulate cortices interpret the emotional significance of the stimuli via the limbic system. The insula, cerebellum, and prefrontal cortex contribute to memory and fear avoidance behaviors. The lentiform nucleus, and cerebellum are involved in reflexive motor responsiveness.2
The Pineal Gland and Melatonin
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Jerry Vriend, Nancy A.M. Alexiuk
In lower vertebrates, specific 125 I-melatonin binding is much more extensive than in mammals. In the chick (Gallus domesticus), goldfish (Carassius auratus), frog (Rana pipiens), and lizard (Anolis carolinensis), I-melatonin binding can be found throughout the brain. The most intense labeling in radioautographic preparations occurs in areas that receive primary or secondary visual input (optic tectum, lateral thalamic nuclei, SCN, corpus geniculatum, and interpeduncular nuclei) and in tracts associated with the visual system (optic nerve, optic chiasm, optic tract).474–477 These findings have led to the conclusion that melatonin binding sites may be associated with visual processing. Specific 125I-melatonin binding has also been reported in the inner plexiform layer of the retina in chicks,478 as well as in rabbits.479 In the chicken retina, there appears to be a correlation between melatonin binding and the ability of melatonin to reduce calcium-dependent dopamine release.480
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Finally, the authors of the sixth text are inconsistent in this regard. On p. 301, 370, and 495, Crosby, Humphrey, and Lauer (1962) use the terms “inferior thalamic peduncle” and “inferior thalamic radiations” interchangeably. They do not define “posterior thalamic peduncle” and “posterior thalamic radiations” identically, however. They describe the former as interrelating “the occipital and the parietal regions of the cortex with the lateral thalamic nuclei, with the pulvinar, and with the superior colliculus” (p. 396). The latter, however, is described as connecting Brodmann areas 18 and 19—i.e., occipital cortex only—with not only the pulvinar and the superior colliculus, but also the pretectal nucleus, the ipsilateral red nucleus and substantia nigra, and the contralateral abducens nucleus (Table 2B on p. 397).
Cerebellar degeneration in primary lateral sclerosis: an under-recognized facet of PLS
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2022
Eoin Finegan, We Fong Siah, Stacey Li Hi Shing, Rangariroyashe H. Chipika, Orla Hardiman, Peter Bede
The analyses of white matter diffusion metrics highlight the involvement of the cerebellar peduncles. The superior, middle, and inferior cerebellar peduncles provide the structural connection between the cerebellum and the brainstem. Our region-of-interest diffusivity analyses confirmed increased RD in the bilateral superior and inferior cerebellar peduncles and FA reductions in the inferior cerebellar peduncles. Additionally, our voxelwise analyses detected radial diffusivity alterations in the middle cerebellar peduncles. The superior cerebellar peduncles are the primary output tracts of the cerebellum connecting the cerebellar nuclei to the contralateral cortex via the ventral lateral nuclei, although they also contain spinocerebellar afferents (54,55). It is noteworthy, that the ventral lateral thalamic nuclei have previously been found to be affected in PLS (56,57). Superior cerebellar peduncle involvement has been described in a previous study of 3 PLS patients, in whom significantly lower FA was recorded in comparison with controls (58). Cerebellar peduncle white matter abnormalities have been consistently reported in ALS (59–61) and linked to impaired cerebro-cerebellar connectivity, including projections to the primary and supplementary motor cortices (59). MCP integrity changes have also been consistently described in ALS (59,62). The involvement of the MCP has been demonstrated in PLS patients and has been linked to pseudobulbar affect (PBA), supporting the concept of cerebellar deafferentation in the pathogenesis of PBA (35).
Burst and high frequency stimulation: underlying mechanism of action
Published in Expert Review of Medical Devices, 2018
Shaheen Ahmed, Thomas Yearwood, Dirk De Ridder, Sven Vanneste
At a systemic level, different pathways are responsible for processing different aspects of pain signals, as shown in Figure 2. A lateral pain system processes the discriminative components (location, intensity, and character) of the pain, mediated by the lateral thalamic nuclei and the somatosensory cortex. Concomitantly, a medial pain system involving the medial thalamic nuclei and the anterior cingulate cortex has been associated with the emotional and motivational aspects of pain, comprising such elements as the unpleasantness of the pain stimulus. In addition, a descending inhibition pain system involving the rostral and pregenual anterior cingulate cortices, with connections to the thalamus, the parahippocampal area, the periaqueductal gray, and the rostroventral part of the medulla oblongata. Imaging modalities such as functional magnetic resonance imaging demonstrate that tonic stimulation mainly modulates the lateral pain pathway, as visualized by blood-oxygen-level-dependent changes in the sensory thalamus and somatosensory cortices, but not in the dorsal anterior cingulate cortex or the insula [18]. A positron-emission tomography study further corroborated this hypothesis by demonstrating that activity increases in the thalamus contralateral to the painful limb as well as in the bilateral parietal association cortex, the anterior cingulate cortex, and prefrontal areas [19]. Hence, tonic stimulation only minimally modulates the medial pain system. Correlation analysis indicates that the amount of pain suppression is related to the activation of the pregenual anterior cingulate cortex and the dorsolateral prefrontal cortex, i.e. to the amount of mobilization of the descending pain inhibitory pathway [20].