Brain Circuits Underlying Narcolepsy

2021 ◽  
pp. 107385842110522
Author(s):  
Sara Katherine Pintwala ◽  
John Peever

Narcolepsy is a sleep disorder manifesting symptoms such as excessive daytime sleepiness and often cataplexy, a sudden and involuntary loss of muscle activity during wakefulness. The underlying neuropathological basis of narcolepsy is the loss of orexin neurons from the lateral hypothalamus. To date numerous animal models of narcolepsy have been produced in the laboratory, being invaluable tools for delineating the brain circuits of narcolepsy. This review will examine the evidence regarding the function of the orexin system, and how loss of this wake-promoting system manifests in excessive daytime sleepiness. This review will also outline the brain circuits controlling cataplexy, focusing on the contribution of orexin signaling loss in narcolepsy. Although our understanding of the brain circuits of narcolepsy has made great progress in recent years, much remains to be understood.

2021 ◽  
Vol 11 (12) ◽  
pp. 1574
Author(s):  
Maria P. Mogavero ◽  
Filomena I. I. Cosentino ◽  
Bartolo Lanuzza ◽  
Mariangela Tripodi ◽  
Giuseppe Lanza ◽  
...  

The objectives of this study were: (1) to identify subjects with hyperprolactinemia in a clinical sample of patients; (2) to compare the neurologic, psychiatric, and sleep conditions found in patients subgrouped by excessive daytime sleepiness (EDS) and hyperprolactinemia; and (3) to identify patients with hyperprolactinemia and EDS not supported by the presence of any other neurologic, psychiatric, or sleep disorder, or substance/medication use. A retrospective chart review of inpatients was carried out in order to identify all patients in whom the prolactin (PRL) serum levels were determined. A total of 130 subjects were retrieved: 55 had increased levels of PRL, while the remaining 75 participants had normal PRL levels. EDS was reported by 32 (58.2%) participants with increased PRL and 34 (45.3%) with normal PRL. Obstructive sleep apnea or other sleep or neurologic/psychiatric conditions could explain EDS in all participants with normal PRL. Among subjects with increased PRL, eight had no other neurologic/psychiatric or sleep disorder (or drug) potentially causing EDS; these participants, at polysomnography, had time in bed, sleep period time, and total sleep time longer than those with EDS associated to another condition. These findings can be considered as a preliminary indication of a role of hyperprolactinemia in EDS and represent a basis for future controlled studies able to test this hypothesis in a reliable, objective, and methodologically more appropriate way.


2019 ◽  
Vol 33 (12) ◽  
pp. 1475-1490
Author(s):  
Maria J Simon ◽  
Maria A Zafra ◽  
Amadeo Puerto

Background: Since the discovery of rewarding intracranial self-stimulation by Olds and Milner, extensive data have been published on the biological basis of reward. Although participation of the mesolimbic dopaminergic system is well documented, its precise role has not been fully elucidated, and some authors have proposed the involvement of other neural systems in processing specific aspects of reinforced behaviour. Aims and methods: We reviewed published data, including our own findings, on the rewarding effects induced by electrical stimulation of the lateral hypothalamus (LH) and of the external lateral parabrachial area (LPBe) – a brainstem region involved in processing the rewarding properties of natural and artificial substances – and compared its functional characteristics as observed in operant and non-operant behavioural procedures. Results: Brain circuits involved in the induction of preferences for stimuli associated with electrical stimulation of the LBPe appear to functionally and neurochemically differ from those activated by electrical stimulation of the LH. Interpretation: We discuss the possible involvement of the LPBe in processing emotional-affective aspects of the brain reward system.


Author(s):  
Mahya Shabani ◽  
Besharat Rahimi ◽  
Mohammad Mehdi Mehrabi Nejad ◽  
Reza Erfanian ◽  
Arezu Najafi

Coronavirus infectious disease 2019 (COVID-19) is confirmed to develop neurocognitive complications. In the present paper, we describe two patients with laboratory-confirmed COVID-19 and excessive daytime sleepiness. In the present study, we reported two laboratory-confirmed cases of COVID-19 with excessive daytime sleepiness. Patients had drowsiness and mild confusion on presentation. In both cases, CNS infections, including meningitis and encephalitis, were ruled out. Both patients’ symptoms remarkably improved following the therapeutic course indicating the direct effect of SARS-CoV2 in sleep modulating centers on the brain. COVID-19 should be considered in patients with excessive daytime sleepiness and drowsiness in the current outbreak.


2021 ◽  
Vol 27 (5) ◽  
pp. 488-498
Author(s):  
I. K. Ternovykh ◽  
T. M. Alekseeva ◽  
L. S. Korostovtseva ◽  
Yu. V. Sviryaev ◽  
Yu. V. Gavrilov

A number of studies have demonstrated a high incidence of sleep disturbances in patients with stroke. The paper reviews the variants of wakefulness disorders observed in ischemic stroke, taking into account the current terminology, as well as methods for their diagnosis. Currently, the origin of post-stroke hypersomnolence and its pathophysiology remain debatable. Various mechanisms including orexin ligand deficiency, degeneration of orexin neurons, as well as disruption of the links between the histaminergic and orexinergic systems are considered as links in the pathogenesis of hypersomnolence caused by ischemic stroke. The paper discusses the pathophysiology of hypersomnia and excessive daytime sleepiness in patients with ischemic stroke, demonstrates various points of view on the relationship of these pathological phenomena with ischemic stroke. A hypothesis on the compensatory nature of hypersomnia and excessive daytime sleepiness in acute ischemic stroke and their possible neuroprotective effect on the brain in patients with stroke is presented.


2019 ◽  
pp. 203-219
Author(s):  
Jaak Panksepp

Emotion in the brain generated by subcortical brain circuits provides the foundation for creativity. Creativity is ultimately a higher brain process that is grounded in a variety of primal affective states of mind, mainly of the emotional variety. Of these emotional systems, the brain’s SEEKING system, arises from the medial forebrain bundle, which connects many regions of the lower brainstem and midbrain to the many higher regions of the brain, with especially rich innervation of the medial frontal cortex. This system, often known for prompting curiosity and exploration and giving rewards, is probably the most important brain engine for creativity. Animals share this core, primary emotional system with humans, despite the evolution of massive neocortices that are distinct for human creativity. But there are no intrinsic urges for creativity in the cortex itself. From an affective neuroscience perspective, the study of the emotional system in animal models can significantly serve for understanding the motivational sources of creativity in humans.


SLEEP ◽  
2020 ◽  
Vol 43 (10) ◽  
Author(s):  
Daniel J Taylor ◽  
Kristi E Pruiksma ◽  
Willie Hale ◽  
Carmen P McLean ◽  
Laurie J Zandberg ◽  
...  

Abstract Study Objectives To examine sleep disorder symptom reports at baseline and posttreatment in a sample of active duty U.S. Army Soldiers receiving treatment for posttraumatic stress disorder (PTSD). Explore sleep-related predictors of outcomes. Methods Sleep was evaluated in 128 participants in a parent randomized clinical trial comparing Spaced formats of Prolonged Exposure (PE) or Present Centered Therapy and a Massed format of PE. In the current study, Spaced formats were combined and evaluated separately from Massed. Results At baseline, the average sleep duration was < 5 h per night on weekdays/workdays and < 6 h per night on weekends/off days. The majority of participants reported clinically significant insomnia, clinically significant nightmares, and probable sleep apnea and approximately half reported excessive daytime sleepiness at baseline. Insomnia and nightmares improved significantly from baseline to posttreatment in all groups, but many patients reported clinically significant insomnia (>70%) and nightmares (>38%) posttreatment. Excessive daytime sleepiness significantly improved only in the Massed group, but 40% continued to report clinically significant levels at posttreatment. Short sleep (Spaced only), clinically significant insomnia and nightmares, excessive daytime sleepiness, and probable sleep apnea (Massed only) at baseline predicted higher PTSD symptoms across treatment course. Short weekends/off days sleep predicted lower PTSD symptom improvement in the Spaced treatments. Conclusions Various sleep disorder symptoms were high at baseline, were largely unchanged with PTSD treatment, and were related to worse PTSD treatment outcomes. Studies are needed with objective sleep assessments and targeted sleep disorders treatments in PTSD patients. Clinical Trial Registration NCT01049516.


2019 ◽  
Vol 5 (3) ◽  
pp. 222-242 ◽  
Author(s):  
Nicole A. Crowley ◽  
Nigel C. Dao ◽  
Sarah N. Magee ◽  
Alexandre J. Bourcier ◽  
Emily G. Lowery-Gionta

Author(s):  
Dora A. Lozsadi

Epilepsy is the commonest serious chronic neurological condition, affecting 0.5% of the population in the UK. Subjective sleep disturbance and excessive daytime sleepiness are reported to be 50% more frequent in those with epilepsy than in controls. Causes are multiple. Both poor seizure control and nocturnal attacks are known to contribute to such sleep disorders. Epilepsy also increases the risk of associated sleep disorders, and additional neurological conditions, such as dementia, learning disability, and depression. These all affect sleep hygiene. Prescribed anti-epileptic drugs will further aggravate the problem. Side-effects will include drowsiness. Sedating benzodiazepines and barbiturates are considered worst offenders. Others affect sleep architecture to varying degrees and/or cause insomnia. While hyper-somnolence in patients with epilepsy will raise the possibility of any of the above issues, sleep deprivation is one of the commonest seizure triggers. This chapter will shed more light on the intricate relationship between sleep and epilepsy.


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