Handbook of clinical neurology最新文献_第2页

Circadian pattern in restless legs syndrome.

Handbook of clinical neurology Pub Date : 2025-01-01 DOI: 10.1016/B978-0-323-90918-1.00009-5

Ambra Stefani

引用次数: 0

Human sleep and immunity: The role of circadian patterns. 人类睡眠与免疫力：昼夜节律的作用

Handbook of clinical neurology Pub Date : 2025-01-01 DOI: 10.1016/B978-0-323-90918-1.00003-4

Renata Cristina Mendes Ferreira, Francieli S Ruiz, Marco Túlio de Mello

{"title":"Human sleep and immunity: The role of circadian patterns.","authors":"Renata Cristina Mendes Ferreira, Francieli S Ruiz, Marco Túlio de Mello","doi":"10.1016/B978-0-323-90918-1.00003-4","DOIUrl":"https://doi.org/10.1016/B978-0-323-90918-1.00003-4","url":null,"abstract":"It is well established that sleep promotes health and welfare. Literature data suggests that sleep is a recurrent resting state that performs multiple biological functions, such as memory consolidation and regulation of glucose, lipid metabolism, energy metabolism, eating behavior, and blood pressure, besides, regulating the immune system. These immunological functions depend on regular sleep and circadian rhythms, as both impact the magnitude of immune responses. Circadian rhythm is the 24-h internal clock in our brain that regulates cycles of alertness and sleepiness by responding to light changes in our environment. It encompasses physical and behavioral daily oscillations. Sleep deprivation and circadian misalignment affect immunity, and both have been related to adverse health effects and chronic diseases. Studies have shown that individuals with regular and consistent sleep patterns have a more effective immune response. Thus, understanding how sleep disturbance will affect the immune response is vital in developing interventions to prevent the health burden of irregular sleep patterns and circadian misalignment, favoring a homeostatic immune defense to microbial or inflammatory insults. Therefore, the scope of this chapter is to explore evidence that regular circadian rhythms and sleep patterns are needed for optimal resistance to infectious challenges.","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"93-103"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chronobiologic treatments for mood disorders.

Handbook of clinical neurology Pub Date : 2025-01-01 DOI: 10.1016/B978-0-323-90918-1.00011-3

Sara Dallaspezia, Francesco Benedetti

引用次数: 0

Irregular sleep-wake rhythm disorder: From the pathophysiologic perspective to the treatment. 睡眠-觉醒节律失调：从病理生理学角度看治疗。

Handbook of clinical neurology Pub Date : 2025-01-01 DOI: 10.1016/B978-0-323-90918-1.00006-X

Aleksandar Videnovic, Alice Cai

{"title":"Irregular sleep-wake rhythm disorder: From the pathophysiologic perspective to the treatment.","authors":"Aleksandar Videnovic, Alice Cai","doi":"10.1016/B978-0-323-90918-1.00006-X","DOIUrl":"https://doi.org/10.1016/B978-0-323-90918-1.00006-X","url":null,"abstract":"Irregular sleep-wake rhythm disorder (ISWRD) is an intrinsic circadian rhythm disorder caused by loss of the brain's circadian regulation, through changes of the input and/or output to the suprachiasmatic nucleus (SCN), or of the SCN itself. Although there are limited prevalence data for this rare disease, ISWRD is associated with neurodegenerative disorders, including the Alzheimer disease (AD) and the Parkinson disease (PD), which will become increasingly prevalent in an aging population. It additionally presents in childhood developmental disorders, psychiatric disorders, and traumatic brain injury (TBI). Patients present with unpredictable, short sleep periods over a 24-h period, with significant day-to-day and weekly variability. Symptoms manifest as insomnia and excessive daytime sleepiness. Sleep logs and actigraphy monitoring capture rest-activity patterns required for diagnosis. Treatment aims to enhance external circadian cues through timed light therapy, behavioral activity regimens, and melatonin, but efficacy remains quite limited. Pathophysiology of ISWRD in association with various diseases and their specific management are discussed. There is a need for further investigation of disease pathophysiology, development of widely applicable tools for diagnosis, and development of treatments.","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"71-87"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Shift work sleep disorder.

Handbook of clinical neurology Pub Date : 2025-01-01 DOI: 10.1016/B978-0-323-90918-1.00015-0

Claudia R C Moreno

引用次数: 0

Sleep-wake modulation and pathogenesis of Alzheimer disease: Suggestions for postponement and treatment.

Handbook of clinical neurology Pub Date : 2025-01-01 DOI: 10.1016/B978-0-323-90918-1.00001-0

Ya-Jing Liu, Dick F Swaab, Jiang-Ning Zhou

{"title":"Sleep-wake modulation and pathogenesis of Alzheimer disease: Suggestions for postponement and treatment.","authors":"Ya-Jing Liu, Dick F Swaab, Jiang-Ning Zhou","doi":"10.1016/B978-0-323-90918-1.00001-0","DOIUrl":"https://doi.org/10.1016/B978-0-323-90918-1.00001-0","url":null,"abstract":"Sleep-wake disorders are recognized as one of the earliest symptoms of Alzheimer disease (AD). Accumulating evidence has highlighted a significant association between sleep-wake disorders and AD pathogenesis, suggesting that sleep-wake modulation could be a promising approach for postponing AD onset. The suprachiasmatic nucleus (SCN) and the pineal hormone melatonin are major central modulating components of the circadian rhythm system. Cerebrospinal fluid (CSF) melatonin levels are dramatically decreased in AD. Interestingly, the number of neurofibrillary tangles in the hippocampus, which is one of the two major neuropathologic AD biomarkers, increases in parallel with the decrease in CSF melatonin levels. Furthermore, a decrease in salivary melatonin levels in middle-aged persons is a significant risk factor for the onset of the early stages of AD. Moreover, the disappearance of rhythmic fluctuations in melatonin may be one of the best biomarkers for AD diagnosis. Light therapy combined with melatonin supplementation is the recommended first-line treatment for sleep-wake disorders in AD patients and may be beneficial for ameliorating cognitive impairment. Sleep-wake cycle modulation based on AD risk gene presence is a promising early intervention for AD onset postponement.","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"211-229"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Circadian aspects in nonpharmacologic and pharmacologic treatment of insomnia.

Handbook of clinical neurology Pub Date : 2025-01-01 DOI: 10.1016/B978-0-323-90918-1.00010-1

Laura Palagini, Pierre-Alexis Geoffroy, Raffaele Manni, Angelo Gemignani

{"title":"Circadian aspects in nonpharmacologic and pharmacologic treatment of insomnia.","authors":"Laura Palagini, Pierre-Alexis Geoffroy, Raffaele Manni, Angelo Gemignani","doi":"10.1016/B978-0-323-90918-1.00010-1","DOIUrl":"https://doi.org/10.1016/B978-0-323-90918-1.00010-1","url":null,"abstract":"Insomnia disorder is a frequent sleep disorder leading to significant health and economic consequences. It has been proposed that individuals with insomnia may experience compromised deactivation systems of arousal, leading to a chronic state of hyperactivation of arousal known as hyperarousal, along with instability in the flip-flop system. Such disruptions may have a primarily impact on the sleep homeostatic drive process. Insomnia may indeed be associated with a disruption in the body's internal clock, known as chronodisruption. Despite the differentiation established in diagnostic nosology between insomnia disorder and circadian rhythm disorders, there is a significant body of evidence suggesting a complex interplay and frequent co-occurrence between these two conditions. In particular, circadian factors can predispose individuals to insomnia disorders, as well as precipitate and perpetuate their symptoms. Accordingly numerous pieces of evidence suggest that both pharmacologic and nonpharmacologic options for treating insomnia can have a resynchronization effect on circadian rhythms. The first-line treatment for chronic insomnia, according to current guidelines, is cognitive behavioral therapy for insomnia while pharmacologic interventions comprise of benzodiazepine receptor agonists also known as Z-drugs and short- to medium-acting benzodiazepines, melatonergic agonists such as ramelteon and melatonin 2mg prolonged release, and dual orexin receptor antagonists such as daridorexant, suvorexant, and lemborexant. At the same time, certain therapies recommended for circadian rhythm disorders can be utilized as adjunctive treatments for insomnia. Therefore, this chapter will discuss the circadian aspects of insomnia disorder and of its therapeutic approach. Furthermore, the effects of chronobiologic interventions, recommended for the treatment of circadian rhythm sleep-wake disorders, will be examined in individuals afflicted with chronic insomnia.","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"161-179"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Obstructive sleep apnea syndrome, orexin, and sleep-wake cycle: The link with the neurodegeneration.

Handbook of clinical neurology Pub Date : 2025-01-01 DOI: 10.1016/B978-0-323-90918-1.00014-9

Mariana Fernandes, Claudio Liguori

{"title":"Obstructive sleep apnea syndrome, orexin, and sleep-wake cycle: The link with the neurodegeneration.","authors":"Mariana Fernandes, Claudio Liguori","doi":"10.1016/B978-0-323-90918-1.00014-9","DOIUrl":"https://doi.org/10.1016/B978-0-323-90918-1.00014-9","url":null,"abstract":"Obstructive sleep apnea syndrome (OSAS) significantly affects the sleep-wake circadian rhythm through intermittent hypoxia and chronic sleep fragmentation. OSAS patients often experience excessive daytime sleepiness, frequent awakenings, and sleep fragmentation, leading to a disrupted circadian rhythm and altered sleep-wake cycle. These disruptions may exacerbate OSAS symptoms and contribute to neurodegenerative processes, particularly through the modulation of clock gene expression such as CLOCK, BMAL1, and PER. Emerging evidence connects OSAS to cognitive impairment and suggests that these changes may contribute to the development of neurodegenerative disorders such as Alzheimer disease, suggesting that OSAS could be a reversible risk factor for these conditions. Biomarkers, including melatonin and orexin, play crucial roles in understanding these mechanisms. In OSAS patients, melatonin, a marker of circadian rhythmicity, often shows altered secretion patterns that are not fully corrected by continuous positive airway pressure therapy. Orexin, which regulates the sleep-wake cycle, exhibits increased cerebrospinal fluid levels in OSAS patients, possibly due to compensatory mechanisms against sleep impairment and daytime sleepiness. These biomarkers highlight the intricate relationship between circadian rhythm disruptions and neurodegenerative risks in OSAS, emphasizing the need for further research and potential therapeutic strategies to mitigate these effects and improve patient outcomes.","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"141-160"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Disease-specific interventions using cell therapies for spinal cord disease/injury. 利用细胞疗法对脊髓疾病/损伤进行特定疾病干预。

Handbook of clinical neurology Pub Date : 2024-01-01 DOI: 10.1016/B978-0-323-90120-8.00007-1

Carl Moritz Zipser, Armin Curt

{"title":"Disease-specific interventions using cell therapies for spinal cord disease/injury.","authors":"Carl Moritz Zipser, Armin Curt","doi":"10.1016/B978-0-323-90120-8.00007-1","DOIUrl":"https://doi.org/10.1016/B978-0-323-90120-8.00007-1","url":null,"abstract":"Traumatic spinal cord injury (SCI) may occur across the lifespan and is of global relevance. Damage of the spinal cord results in para- or tetraplegia and is associated with neuropathic pain, spasticity, respiratory, and autonomic dysfunction (i.e., control of bladder-bowel function). While the acute surgical treatment aims at stabilizing the spine and decompressing the damaged spinal cord, SCI patients require neurorehabilitation to restore neural function and to compensate for any impairments including motor disability, pain treatment, and bladder/bowel management. However, the spinal cord has a limited capacity to regenerate and much of the disability may persist, depending on the initial lesion severity and level of injury. For this reason, and the lack of effective drug treatments, there is an emerging interest and urgent need in promoting axonal regeneration and remyelination after SCI through cell- and stem-cell based therapies. This review briefly summarizes the state-of the art management of acute SCI and its neurorehabilitation to critically appraise phase I/II trials from the last two decades that have investigated cell-based therapies (i.e., Schwann cells, macrophages, and olfactory ensheathing cells) and stem cell-based therapies (i.e., neural stem cells, mesenchymal, and hematopoietic stem cells). Recently, two large multicenter trials provided evidence for the safety and feasibility of neural stem cell transplantation into the injured cord, whilst two monocenter trials also showed this to be the case for the transplantation of Schwann cells into the posttraumatic cord cavity. These are milestone studies that will facilitate further interventional trials. However, the clinical adoption of such approaches remains unproven, as there is only limited encouraging data, often in single patients, and no proven trial evidence to support regulatory approval.","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"205 ","pages":"263-282"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pediatric inflammatory leukoencephalopathies. 小儿炎性白质脑病。

Handbook of clinical neurology Pub Date : 2024-01-01 DOI: 10.1016/B978-0-323-99209-1.00001-6

Omar Abdel-Mannan, Yael Hacohen

{"title":"Pediatric inflammatory leukoencephalopathies.","authors":"Omar Abdel-Mannan, Yael Hacohen","doi":"10.1016/B978-0-323-99209-1.00001-6","DOIUrl":"https://doi.org/10.1016/B978-0-323-99209-1.00001-6","url":null,"abstract":"Acquired demyelinating syndromes (ADS) represent acute neurologic illnesses characterized by deficits persisting for at least 24hours and involving the optic nerve, brain, or spinal cord, associated with regional areas of increased signal on T2-weighted images. In children, ADS may occur as a monophasic illness or as a relapsing condition, such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Almost all young people with MS have a relapsing-remitting course with clinical relapses. Important strides have been made in delineating MS from other ADS subtypes. Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and aquaporin 4-antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD) were once considered variants of MS; however, studies in the last decade have established that these are in fact distinct entities. Although there are clinical phenotypic overlaps between MOGAD, AQP4-NMOSD, and MS, cumulative biologic, clinical, and pathologic evidence allows discrimination between these conditions. There has been a rapid increase in the number of available disease-modifying therapies for MS and novel treatment strategies are starting to appear for both MOGAD and AQP4-NMOSD. Importantly, there are a number of both inflammatory and noninflammatory mimics of ADS in children with implications of management for these patients in terms of treatment.","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"204 ","pages":"369-398"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0