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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
Ascending reticular activating system: wakefulness (Figure 28.10; Table 28.1). Location: brainstem, lateral/posterior hypothalamus, basal forebrain.The orexin- (also known as hypocretin) secreting neurons are key to maintenance of wakefulness. (Figure 28.11) These neurons have wide-ranging activating projections to the wake promoting brain, and inhibitory to sleep promoting regions, such as the ventrolateral preoptic (VLPO) nucleus (see below).
Organ Transplants and Criteria for Death
Published in David Lamb, Organ Transplants and Ethics, 2020
The significance of brainstem criteria can be appreciated with reference to its contribution to the continuous function of the organism as a whole. In its upper part the brainstem contains crucial centres for generating the capacity for consciousness. Thus whilst extensive damage to the cortex, from trauma or anoxia, may not cause permanent unconsciousness, there is one functional unit without whose activity consciousness cannot exist. This is the ascending reticular activating system, or ARAS, which is situated in the upper part of the brainstem. Acute, strategically situated bilateral lesions in the paramedian tegmental area of the rostral brainstem entail loss of the capacity for consciousness. In the lower part of the brainstem are mechanisms which control the respiratory centre. Thus lesions of critical areas in the lower part of the brainstem are associated with the permanent cessation of the ability to breathe which in turn deprives the heart and cerebral hemispheres of oxygen, causing them to cease functioning. It is death of the brainstem (which in practice is nearly always the result of a massive increase in intracranial pressure) which produces the crucial signs (apnoeic coma with absent brainstem reflexes) which doctors detect at the bedside, when they diagnose brain death.
Higher Brain, Whole Brain, and Lower Brain Formulations
Published in David Lamb, Death, Brain Death and Ethics, 2020
Whilst extensive damage to the cortex, from trauma or anoxia may not cause permanent unconsciousness there is one structure without which consciousness cannot exist. This is the ascending reticular activating system, or ARAS, which is situated in the brainstem. Strategically situated lesions in the parts of the brainstem known as the mesencephalic and pontine tegmentum produce irreversible coma. Moreover, since respiration is controlled by the brainstem, the total destruction of the brainstem will necessarily entail the permanent cessation of the body’s ability to breathe, which in turn deprives the heart and cerebral hemispheres of oxygen, causing them to cease functioning. Whole brain formulations of death recognise that survival of the brainstem is incompatible with a diagnosis of the death of the person as a whole. Survival of the brainstem is needed to generate a capacity for consciousness, and a capacity to breathe. One may survive in a vegetative state with an intact brainstem, but without brainstem function asystole is inevitable despite the most heroic resuscitative measures. In the United Kingdom, the Conference of Medical Royal Colleges and Their Faculties has focused on the brainstem. Pallis (1983a) has described brainstem death as the ‘physiological kernel’ of brain death. Destruction of the brainstem, it is held, precludes meaningful functioning of the brain as a whole.
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
The thalamus is likely key to the implementation of state transitions between levels or types of cortical arousal and can maintain those states through broad, course regulation of cortical activity[65–69]. This function is evident in various sleep stages and their distinct thalamocortical signatures. For example, the synchronous transition to ‘down’ states across multiple cortical regions during slow-wave sleep is likely mediated by the midline thalamus[70]. Here, the thalamus appears to be the critical link between brainstem regions involved in arousal, primarily the ascending reticular activating system (RAS), and the cortex. This network serves as a synchronous, broad modulator of cortical processing, and a potential regulator of sleep, alertness, and consciousness[71–73]. So, in addition to being the gatekeeper for specific information trying to gain access to cortex, modulatory projections via the thalamus enforce cortical compliance with brainstem-derived state signals.
¬Transcranial direct current stimulation improves sleep quality in patients with insomnia after traumatic brain injury
Published in Brain Injury, 2023
Babak Bakhshayesh Eghbali, Sara Ramezani, Sina Sedaghat Herfeh, Cyrus Emir Alavi, Kiomars Najafi, Pedram Esmaeeli Lipaei, Seddigheh Eslamparast Kordmahalleh, Vahid Hosseinpour Sarmadi, Naser Amini, Fatemeh Ramezani Kapourchali
Sleep-related brain substrates mainly include the ascending reticular activating system (ARAS), hypothalamic nuclei and their projections toward the cortex. The ARAS consists of a set of monoaminergic neurons with an inhibitory reciprocal effect on the ventrolateral preoptic (VLPO) nucleus and contributes to the awakening state. Pathologically, the lesions of VLPO nucleus bring about the disinhibition of ARAS and over-activation of thalamocortical projections, leading to a hyperarousal state in patients with TBI (21). It has also been suggested as a mechanism of primary insomnia with functional and anatomical changes in some brain regions including the dorsolateral prefrontal cortex (DLPFC) (21–23)where there is vulnerability to TBI (24–26). It is obvious that insomnia during the intermediate to chronicphase of TBI (27)prolongs neural regeneration and hampers the active participation of patients in the rehabilitation program and delays their functional recovery (28,29). Hence, it is a serious priority to remedy post-traumatic insomnia, especially during the chronic phase.
Making sleep easier: pharmacological interventions for insomnia
Published in Expert Opinion on Pharmacotherapy, 2018
Lukas Frase, Christoph Nissen, Dieter Riemann, Kai Spiegelhalder
To understand fundamental pharmacological principles of sleep medicine, basic physiological pathways of sleep regulation need to be highlighted. In their pivotal review, Saper and colleagues summarized current knowledge on the hypothalamic regulation of sleep and circadian brain rhythms [17]. During wakefulness, two major pathways set the brain in a responsive and alert state. Cholinergic cell groups in the laterodorsal and pedunculopontine tegmentum within the brain stem activate the relay and reticular nuclei of the thalamus [18]. Then cholinergic tonus sets the level of transmittance of this fundamental relay station between subcortical areas and the cortex [19]. In addition, thalamo-cortico-thalamic circuits play an important role in regulating consciousness and awareness by influencing cortical excitability levels [20]. Besides this cholinergic pathway, several monoaminergic hypothalamic cell groups comprise the ascending reticular activating system (ARAS [17]). The most important nuclei and dominant neurotransmitters are depicted in Figure 1.