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Sleep–Wake Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Margaret Kay-Stacey, Eunice Torres-Rivera, Phyllis C. Zee
The discovery of the hypocretin/orexin in neurons in the lateral hypothalamus was crucial to the understanding of the pathogenesis of narcolepsy. In particular, ‘NT1 is caused by deficiencies in hypocretin signaling, which is most likely due to a selective loss of hypothalamic hypocretin-producing neurons'.2 Orexin neurons innervate tuberomammillary nucleus (TMN), basal forebrain, periaqueductal gray (PAG), dorsal raphe, and locus ceruleus (LC), which are areas that promote arousal and suppress REM.38 Orexin neurons also suppress REM sleep. Narcoleptics have dysregulated REM sleep which leads to poor circadian timing of REM sleep, rapid transitions into REM sleep, and disruption of REM sleep physiology.38 The etiology of the loss of the orexin neurons is not totally clear, but it is thought to be a T-cell–mediated autoimmune disease. In 2009–2010, there was a striking increase in the number of patients who developed NT1 after flu vaccination, Pandemrix. There was an 8- to 12-fold increase in NTI in children and adolescents as well as a 3- to 5-fold increase in adults.38, 39
Central Nervous System Effects of Essential Oil Compounds
Published in K. Hüsnü Can Başer, Gerhard Buchbauer, Handbook of Essential Oils, 2020
Elaine Elisabetsky, Domingos S. Nunes
Safranal 26 potentiated the effects of hypnotic and sub-hypnotic doses of pentobarbital in mice, shortening the latency for and increasing the duration of NREM sleep (Hosseinzadeh and Noraei, 2009). Safranal per se did not affect baseline sleep wave profiles (Liu et al., 2012). The analysis of c-fos expression suggested that safranal activated the sleep-promoting neurons in the ventrolateral preoptic area (critical for NREM sleep promotion), with consequent inhibition of the wakefulness-promoting neurons in the tuberomammillary nucleus.
Viscerosensory Processing in Nucleus Tractus Solitarii: Structural and Neurochemical Substrates
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
D.A. Ruggiero, V.M. Pickel, T.A. Milner, M. Anwar, K. Otake, E.P. Mtui, D. Park
Pontine afferents (not illustrated) derive principally from the nucleus of Kölliker-fuse and A5 area. Analysis of material from rhodamine microbead deposits revealed additional afferents from medial vestibular, pedunculopontine and raphe dorsalis nuclei, and periaqueductal gray. Labeling of the fastigial nucleus correlated with deposits centered on nucleus parasolitarius adjacent to NTS. Labeling of the nucleus locus ceruleus was sparse and inconsistent and correlated with deposits centered on the DMX and ventral strip. Hypothalamic afferents to NTS were distributed bilaterally and predominantly ipsilaterally. The data illustrated (Figure 2) were obtained from a similar injection of WGA-HRP centered immediately rostral to obex. In the mammillary region, compact columns were identified in the dorsolateral quadrant of the lateral hypothalamic area and a ventral locus adjacent to the tuberomammillary nucleus (Figure 2a,b). Smaller numbers of cells occupied supramammillary and perifornical nuclei. In the tuberal region, labeled soma formed a shell surrounding the compact division of the dorsomedial hypothalamic nucleus (Figure 2c). Paraventricular hypothalamic afferents derive from cells concentrated in the medial and lateral parvocellular divisions (Figure 2d,e). Labeled cells were also observed in the retrochiasmatic region, central amygdaloid nucleus (illustrated), bed nucleus of the stria terminalis, and insular and medial prefrontal cortex5 (not illustrated). Labeled cells were more numerous after injections that involved the DMX and ventral NTS or subjacent LTF.
Excessive daytime sleepiness after traumatic brain injury
Published in Brain Injury, 2020
Thomas Crichton, Rajiv Singh, Kessewa Abosi-Appeadu, Gary Dennis
Sleep-wake disturbances are a common feature of patient morbidity following traumatic brain injury (TBI). Excessive daytime sleepiness (EDS) is one of the most prevalent sleep-wake disturbances noted after trauma (1–3) and significantly affects quality of life, risk of accidents, and cognitive and social functioning in survivors of TBI (1,45–6). The pathophysiological mechanisms of post-traumatic EDS are not yet fully understood but are likely heterogeneous and multifactorial in nature. The hypothalamus, an important arousal-promoting center in the brain, is a common site of injury after TBI (7). Damage to the histaminergic tuberomammillary nucleus, hypocretin-producing neurons, and melanin-concentrating hormone-producing neurons of the hypothalamus have been proposed to contribute to EDS after TBI (1,8910–11). Additionally, common sequelae of TBI, such as pain and anxiety can impact nocturnal sleep. As disruption of nighttime sleep can negatively impact daytime wakefulness, other symptoms may contribute to daytime sleep tendency (12). However, it is important to note that reduced nocturnal sleep quality does not necessarily lead to EDS. Baumann et al. observed no significant differences in sleep hours per night, sleep efficiency, or sleep architecture in those with objective and subjective EDS, compared to those without (1).
Pitolisant for treating patients with narcolepsy
Published in Expert Review of Clinical Pharmacology, 2020
Narcolepsy is the disruption of the brain wake-promoting system [26]. The main cause of the disruption is the loss of wake-promoting orexinergic neurons in the lateral hypothalamus [27]. These orexinergic neurons intermingle with the histaminergic neurons located in the tuberomammillary nucleus of the hypothalamus, and both of them are necessary for the promotion and maintenance of wakefulness [28]. Histamine has an important role in the light/dark cycle in which histamine levels increase during wakefulness to decline to the baseline level during sleep [29,30]. Therefore, enhanced histamine levels due to H3 receptor (an inhibitory autoreceptor) blockade can improve wakefulness and vigilance [31,32]. Pitolisant is an H3 receptor antagonist/inverse agonist [33]. It can trigger a long-lasting activation of histaminergic neurons in the brain, thus promoting the release of histamine in the central nervous system [34,35], improving wakefulness, consequently decreasing EDS and cataplexy (Figure 2). Pitolisant also promotes the release of other wake-promoting neurotransmitters (dopamine, noradrenaline, and acetylcholine) in cerebral cortex [36]. Pitolisant binds to H3 receptors with a high affinity (Ki = 1nM), and has no appreciable binding to other histamine receptors (H1, H2, or H4 receptors; Ki > 10 μM) [37]. Preclinical studies showed that pitolisant enhanced cerebral Nτ-methylhistamine (a major extracellular metabolite of histamine) levels in rodent models [38,39]. Additionally, the activity of prefrontal cortical dopaminergic and cholinergic pathways was also increased by the intraperitoneal administration of pitolisant in rat [37,38].
Fifty years of experience with loxapine for the rapid non-coercive tranquilization of acute behavioral disturbances in schizophrenia patients, and beyond
Published in Expert Review of Neurotherapeutics, 2022
Philippe Nuss, Emmanuelle Corruble, Emmanuelle Baloche, Ricardo P. Garay, Pierre-Michel Llorca
Histaminergic neurons in the tuberomammillary nucleus of the posterior hypothalamus are the only source of neuronal histamine and project axons throughout the brain [118]. Furthermore, electrophysiologic studies in cats [13] suggest that loxapine may induce sedation by affecting polysynaptic-mediated responses in diencephalic and mesencephalic reticular formation neurons. Therefore, the potential direct actions of loxapine in these types of neurons deserve to be investigated in the near future.