{"title":"The retrolabyrinthine approach.","authors":"Per Cayé-Thomasen","doi":"10.1016/B978-0-12-824534-7.00020-2","DOIUrl":"https://doi.org/10.1016/B978-0-12-824534-7.00020-2","url":null,"abstract":"<p><p>The development, technique, results, and complications of the retrolabyrinthine/presigmoid approach to the cerebellopontine angle are described. This somewhat overlooked approach allows for potential preservation of hearing and vestibular function and can be applied to the removal of a variety of pathologies in the cerebellopontine angle, including meningiomas, vestibular schwannomas, arachnoid cysts, epidermoid cysts, and other rarer tumors, but is also an option for procedures such as vestibular neurectomy, trigeminal nerve decompression, and auditory brainstem implantation. The addition of contemporary neuromonitoring technology to the approach provides the option for near-real-time monitoring of hearing and facial nerve function during surgery, for overall outcome improvement. The addition of endoscopes to the minimally invasive procedure aids to the surgical field overview, to complete removal of pathology and to preservation of crucial anatomic structures.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"212 ","pages":"177-183"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238544","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}
{"title":"The cholinergic synapses.","authors":"Hermona Soreq, Adi Bar, Iddo Paldor","doi":"10.1016/B978-0-443-19088-9.00003-2","DOIUrl":"https://doi.org/10.1016/B978-0-443-19088-9.00003-2","url":null,"abstract":"<p><p>Acetylcholine (ACh) is a leading regulatory neurotransmitter in the nervous system, which functions both directly and as modulator of other neurotransmitters. It is found in the central and peripheral nervous system, as well as in the autonomic system-both sympathetic and parasympathetic. In the central nervous system (CNS), ACh functions not only as a neurotransmitter, but also as a modulator of cognitive functions, including long-term and short-term memory, limbic activation, and alertness. No process in the mammalian body can commence without its participation.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"211 ","pages":"23-35"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983360","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}
{"title":"Advanced sleep phase syndrome: Role of genetics and aging.","authors":"Rosalia Silvestri, Biancamaria Guarnieri","doi":"10.1016/B978-0-323-90918-1.00005-8","DOIUrl":"10.1016/B978-0-323-90918-1.00005-8","url":null,"abstract":"<p><p>Advanced sleep phase (ASP) is seldom brought to medical attention because many individuals easily adapt to their early chronotype, especially if it emerges before the age of 30 and is present in a first-degree relative. In this case, the disorder is considered familial (FASP) and is mostly discovered coincidentally in the presence of other sleep disorders, mainly obstructive sleep apnea syndrome (OSAS). The prevalence of FASP is currently estimated to be between 0.21% and 0.5%. Autosomal dominant mutations in circadian clock genes like PER2, CK1, PER3, CRY2, TIMELESS, and DEC2 have been linked to FASP, some with pleiotropic effects influencing other health aspects like migraine and depression. Early morning awakening is, instead, more common among older individuals, occurring in almost 4% of cases, without considering associated comorbidities. Advanced sleep-wake phase disorder (ASWPD) is characterized by a consistent and distressing anticipation of sleep-wake timing, affecting almost 1% of middle-aged individuals. On average, women have a shorter circadian period than men, making them more susceptible to ASWPD, albeit no significant gender discrepancies have been observed. Age-related alterations in circadian rhythms are exacerbated and compounded by neurodegenerative disorders, impacting the suprachiasmatic nucleus (SCN), sensitivity to light, and light responsiveness in those affected. Conflicting data has surfaced regarding the protective or detrimental effects of ASWPD in studies on aging, mild cognitive impairment (MCI), and diverse dementia conditions.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"61-70"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045407","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}
Maria Antonia Quera-Salva, Sarah Hartley, Karol Uscamaita
{"title":"Circadian rhythm disorders in the blind.","authors":"Maria Antonia Quera-Salva, Sarah Hartley, Karol Uscamaita","doi":"10.1016/B978-0-323-90918-1.00007-1","DOIUrl":"10.1016/B978-0-323-90918-1.00007-1","url":null,"abstract":"<p><p>Non-24-h sleep-wake disorder in blind patients without light perception is an orphan circadian rhythm sleep-wake disorder and is extremely rare in sighted people. Non-24-h sleep-wake disorder is characterized by insomnia and daytime sleepiness alternating with asymptomatic episodes. The frequency of symptomatic periods depends on the daily desynchronization of endogenous circadian pattern of each patient. Diagnosis requires anamnesis, a sleep diary, and actigraphy, if possible; in addition, repeated 24-h measures of circadian markers such as melatonin secretion are also required. Treatment consists of sleep hygiene, behavioral therapy, and melatonin/melatonin agonist administration. Melatonin treatment should start when the circadian rhythm of the patient is in phase with the solar cycle. Efficacy of treatment may be evident after weeks even months from the beginning. There is often a relapse when the medication is stopped.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"113-123"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046128","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}
{"title":"Foreword.","authors":"Michael J Aminoff, François Boller, Dick F Swaab","doi":"10.1016/B978-0-323-90918-1.09991-3","DOIUrl":"https://doi.org/10.1016/B978-0-323-90918-1.09991-3","url":null,"abstract":"","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"ix"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046313","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}
{"title":"Sleep and circadian rhythms modeling: From hypothalamic regulatory networks to cortical dynamics and behavior.","authors":"Svetlana Postnova, Paula Sanz-Leon","doi":"10.1016/B978-0-323-90918-1.00013-7","DOIUrl":"10.1016/B978-0-323-90918-1.00013-7","url":null,"abstract":"<p><p>Sleep and circadian rhythms are regulated by dynamic physiologic processes that operate across multiple spatial and temporal scales. These include, but are not limited to, genetic oscillators, clearance of waste products from the brain, dynamic interplay among brain regions, and propagation of local dynamics across the cortex. The combination of these processes, modulated by environmental cues, such as light-dark cycles and work schedules, represents a complex multiscale system that regulates sleep-wake cycles and brain dynamics. Physiology-based mathematical models have successfully explained the mechanisms underpinning dynamics at specific scales and are a useful tool to investigate interactions across multiple scales. They can help answer questions such as how do electroencephalographic (EEG) features relate to subthalamic neuron activity? Or how are local cortical dynamics regulated by the homeostatic and circadian mechanisms? In this chapter, we review two types of models that are well-positioned to consider such interactions. Part I of the chapter focuses on the subthalamic sleep regulatory networks and a model of arousal dynamics capable of predicting sleep, circadian rhythms, and cognitive outputs. Part II presents a model of corticothalamic circuits, capable of predicting spatial and temporal EEG features. We then discuss existing approaches and unsolved challenges in developing unified multiscale models.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"37-58"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046570","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}
Alexei Verkhratsky, Elly M Hol, Lot D de Witte, Eleonora Aronica
{"title":"General pathophysiology of neuroglia.","authors":"Alexei Verkhratsky, Elly M Hol, Lot D de Witte, Eleonora Aronica","doi":"10.1016/B978-0-443-19102-2.00013-2","DOIUrl":"10.1016/B978-0-443-19102-2.00013-2","url":null,"abstract":"<p><p>Neuroglia in the CNS, represented by astroglia, oligodendroglia, and microglia, are responsible for the homeostatic support and protection of the nervous tissue. Neuroglia are intimately involved in the pathogenesis of all neurologic diseases, and neuroglial changes to a large extent define the progression of these diseases and their neurologic outcome. In contrast to neurons, neuroglia are capable of mounting an evolutionary conserved response to pathology known as reactive gliosis. Reactive gliosis is initially protective and allostatic, and it is aimed at preserving the nervous tissue function and integrity. However, in many diseases, neuroglial cells undergo atrophy and functional asthenia, contributing to nervous tissue damage.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"210 ","pages":"3-7"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729779","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}
{"title":"Foreword.","authors":"Michael J Aminoff, François Boller, Dick F Swaab","doi":"10.1016/B978-0-443-19102-2.09999-3","DOIUrl":"https://doi.org/10.1016/B978-0-443-19102-2.09999-3","url":null,"abstract":"","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"210 ","pages":"ix"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729808","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}
Daniele Mattei, Dilansu Guneykaya, Bilge Ugursu, Alice Buonfiglioli
{"title":"From womb to world: The interplay between maternal immune activation, neuroglia, and neurodevelopment.","authors":"Daniele Mattei, Dilansu Guneykaya, Bilge Ugursu, Alice Buonfiglioli","doi":"10.1016/B978-0-443-19102-2.00028-4","DOIUrl":"10.1016/B978-0-443-19102-2.00028-4","url":null,"abstract":"<p><p>This chapter introduces and discusses maternal immune activation (MIA) as a contributing factor in increasing the risk of neurodevelopmental disorders, particularly in relation to its interactions with neuroglia. Here we first provide an overview of the neuroglia-astroglia, oligodendroglia, microglia, and radial glial cells-and their important role during early brain development and in adulthood. We then present and discuss MIA, followed by a critical overview of inflammatory molecules and temporal stages associated to maternal inflammation during pregnancy. We provide an overview of animal and human models used to mimic and study MIA. Furthermore, we review the possible interaction between MIA and neuroglia, focusing on the current advances in both modeling and therapeutics. Additionally, we discuss and provide preliminary and interesting insights into the most recent pandemic, COVID-19, and how the infection may be associated to MIA and increased risk for neurodevelopmental disorders. Finally, we provide a critical overview of challenges and future opportunities to study how MIA may contribute to higher risk of developing neurodevelopmental disorders.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"210 ","pages":"269-285"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729813","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}
{"title":"Neuroglia in anxiety disorders.","authors":"Robin E Bonomi, Robert Pietrzak, Kelly P Cosgrove","doi":"10.1016/B978-0-443-19102-2.00008-9","DOIUrl":"10.1016/B978-0-443-19102-2.00008-9","url":null,"abstract":"<p><p>Anxiety disorders are some of the most prevalent in the world and are extraordinarily debilitating to many individuals, costing millions in disability. One of the most disabling is posttraumatic stress disorder (Snijders et al., 2020). Understanding the pathophysiology of these illnesses further and the cell types involved will allow better targeting of treatments. Glial cells, encompassing microglia, astrocytes, and oligodendrocytes, play critical roles in the pathophysiology of PTSD and other anxiety illnesses. Each of these cell types interacts with aspects of neuro-epigenetics, neuroimmune, and neuronal signaling and may contribute to the pathophysiology of anxiety illnesses. This chapter covers the literature on the role of glial cells in the neurobiology and pathology of anxiety disorders, more specifically PTSD. PTSD is one of the most debilitating anxiety disorders and one of the most complicated from a neurobiologic perspective. This chapter also features a discussion surrounding the current state of treatment and some of the hypothesized mechanisms for novel treatments including tetrahydrocannabidiol and 3,4-methylenedioxymethamphetamine. Finally, thoughts on the future directions for precision treatment and pharmacologic development with a focus on neuroglia are undertaken.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"210 ","pages":"335-346"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729818","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}
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