{"title":"Circadian pattern in restless legs syndrome.","authors":"Ambra Stefani","doi":"10.1016/B978-0-323-90918-1.00009-5","DOIUrl":"10.1016/B978-0-323-90918-1.00009-5","url":null,"abstract":"<p><p>This chapter provides an overview of circadian pattern in restless legs syndrome (RLS). Circadian variation of symptoms is a known feature of RLS. According to one of the five essential criteria for RLS diagnosis, symptoms \"only occur or are worse in the evening or at night than during the day.\" RLS symptoms are most pronounced in the evening and at night, with a relative improvement in the late sleep period or in the early morning. This unique feature helps differentiating RLS from other movement disorders. Although differentiating the circadian pattern of RLS manifestations from the worsening of RLS symptoms at rest is not always easy, the independency of these two features has been demonstrated in several studies. Mechanisms implicated in circadian variations of RLS include dopamine, iron, opioids, and genetic factors, which all interact with each other. Further insights on circadian fluctuations in patients with RLS derive from clinical studies reporting circadian variations in sensory processing and spinal excitability, as well as from studies showing circadian variations in cortical excitability, default mode network, and cognition in patients with RLS.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"206 ","pages":"105-111"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045882","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":"Cerebellar asymmetries.","authors":"Caroline Nettekoven, Jörn Diedrichsen","doi":"10.1016/B978-0-443-15646-5.00005-1","DOIUrl":"10.1016/B978-0-443-15646-5.00005-1","url":null,"abstract":"<p><p>The cerebellum is a subcortical structure tucked underneath the cerebrum that contains the majority of neurons in the brain, despite its small size. While it has received less attention in the study of brain asymmetries than the cerebrum, structural asymmetries in the cerebellum have been found in cerebellar volume that mirror cerebral asymmetries. Larger cerebellar structures have been reported on the right compared to the left, either for the whole cerebellar hemisphere or the anterior part of the cerebellum, with the latter accompanied by a left increase in the posterior cerebellum. Cerebellar asymmetries are considered evolutionary recent and have been observed prenatally and in early development. Both asymmetries in anterior-posterior divisions and specific lobules have been linked to handedness and cognitive abilities, in particular language. Functional lateralization in the cerebellum varies across motor and cognitive functions, with language activation predominantly localized in the right hemisphere, contralateral to cerebral activation. Meanwhile, working memory and executive functions are not lateralized to one hemisphere. New neuroimaging methods and resources, including a symmetric functional atlas of the cerebellum that enables precision mapping, open novel avenues for exploring cerebellar asymmetries and answering questions about the developmental timeline, relationships to behavior, and clinical relevance.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"208 ","pages":"369-378"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614607","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}
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":"10.1016/B978-0-323-90918-1.00003-4","url":null,"abstract":"<p><p>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.</p>","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}
{"title":"NGF-based cholinergic therapies in Alzheimer disease.","authors":"Sumonto Mitra, Ruchi Gera, Maria Eriksdotter","doi":"10.1016/B978-0-443-19088-9.00007-X","DOIUrl":"https://doi.org/10.1016/B978-0-443-19088-9.00007-X","url":null,"abstract":"<p><p>The cholinergic system is part of the parasympathetic nervous system, which works in tandem with the sympathetic and enteric nervous systems to maintain the physiologic functioning of our body. The neurotransmitter acetylcholine (ACh) facilitates cholinergic signaling pathways by activating specific cell surface receptors (nicotinic and muscarinic receptors). Altered cholinergic signaling has been implicated in several pathologic conditions. In this chapter, conditions where cholinergic modulation in the central nervous system occurs through the neurotrophin nerve growth factor (NGF) are addressed. NGF is the master regulator of several pathways, ultimately leading to cell survival, ACh production, regenerative signaling, and anti-inflammatory tone. NGF and cholinergic-related pathways have been reported to be severely affected in the case of Alzheimer disease (AD), the most common dementia disorder. In AD, the cholinergic nuclei of the basal forebrain are affected early during the AD continuum, resulting in cholinergic cell loss and hampered ACh production, which overall affects the propagation of cholinergic signals in other brain regions. Since the 1990s clinically relevant strategies to treat AD patients have been the drugs that enhance cholinergic signaling-termed cholinesterase inhibitors (ChEIs), however, other strategies in AD have been and are presently being assessed for clinical efficacy. Delivery of NGF to the basal forebrain is considered crucial to revive the cholinergic cell bodies, restore ACh production, and sustain cognitive function. This chapter provides a description of the relevance of NGF-based therapies targeted for AD treatment, technical approaches for NGF delivery to the brain, and the status of ongoing clinical studies are provided.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"211 ","pages":"123-135"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961710","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/B978-0-443-19104-6.09999-X","DOIUrl":"https://doi.org/10.1016/B978-0-443-19104-6.09999-X","url":null,"abstract":"","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"209 ","pages":"ix"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692078","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":"Gliotransmission in physiologic and pathologic conditions.","authors":"Eunji Cheong, C Justin Lee","doi":"10.1016/B978-0-443-19104-6.00003-6","DOIUrl":"10.1016/B978-0-443-19104-6.00003-6","url":null,"abstract":"<p><p>This chapter explores the roles of gliotransmission in physiologic and pathologic conditions, including psychiatric and neurologic disorders. Gliotransmission, facilitated by astrocytes through the release of gliotransmitters such as glutamate, d-serine, and GABA, regulates neuronal activity and synaptic transmission. Under physiologic conditions, astrocytic gliotransmission maintains the balance of tonic excitation and inhibition, influencing synaptic plasticity and cognitive functions. In psychiatric disorders, the chapter examines how dysregulated gliotransmission contributes to major depression and schizophrenia. In major depression, changes in astrocytic glutamate and adenosine signaling impact mood regulation and cognitive functions. Schizophrenia involves complex astrocyte-neuron interactions, with dysregulated astrocytic activity affecting synaptic function and contributing to symptoms. The chapter also delves into neurologic disorders. In Alzheimer disease, aberrant GABA release from reactive astrocytes impairs memory and cognitive functions. Parkinson disease features alterations in glutamatergic and GABAergic systems, affecting motor and nonmotor symptoms. Epilepsy involves a disruption in the balance between excitatory and inhibitory neurotransmission, with astrocytic GABA accumulation helping to maintain neuronal stability. Autism spectrum disorder (ASD) is linked to imbalances in glutamatergic and GABAergic neurotransmission, underlying sensory, cognitive, and social impairments. Overall, the chapter underscores the pivotal role of gliotransmission in maintaining neural homeostasis and highlights its potential as a therapeutic target in various disorders.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"209 ","pages":"93-116"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692079","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 autism spectrum disorders.","authors":"Vivi M Heine, Stephanie Dooves","doi":"10.1016/B978-0-443-19102-2.00006-5","DOIUrl":"10.1016/B978-0-443-19102-2.00006-5","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is characterized by difficulties in social interaction, communication, and repetitive behavior, typically diagnosed during early childhood and attributed to altered neuronal network connectivity. Several genetic and environmental risk factors contribute to ASD, including pre- or early life immune activation, which can trigger microglial and astroglial reactivity, impacting early neurodevelopment. In ASD, astrocytes show altered glutamate metabolism, directly influencing neuronal network activity, while microglia display impaired synaptic pruning, an essential developmental process for the refinement of neuronal connections. Additionally, reduced myelination in specific cortical and subcortical regions may affect brain connectivity in ASD, with white matter integrity correlating with the severity of the disorder, suggesting an important role for oligodendrocytes and myelin in ASD. This chapter provides an overview of current literature on the role of neuroglia cells in ASD, with a focus on immune activation, glutamate signaling, synaptic pruning, and myelination.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"210 ","pages":"303-311"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729823","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}
Alice Laurenge, Luis Jaime Castro-Vega, Gilles Huberfeld
{"title":"Reciprocal interactions between glioma and tissue-resident cells fueling tumor progression.","authors":"Alice Laurenge, Luis Jaime Castro-Vega, Gilles Huberfeld","doi":"10.1016/B978-0-443-19102-2.00007-7","DOIUrl":"10.1016/B978-0-443-19102-2.00007-7","url":null,"abstract":"<p><p>Gliomas are the most frequent primary brain tumor and are essentially incurable. While nondiffuse gliomas are circumscribed, diffuse gliomas display an aggressive behavior characterized by tumor cell migration over large distances into the brain parenchyma, thereby precluding curative surgical resection. Almost all diffuse gliomas progress and recur as higher grades and become resistant to standard-of-care treatments. It is being increasingly recognized that glioma cells establish functional interactions with cells residing in the tumor microenvironment. Of these, tumor-associated microglia and macrophages (TAMs) play critical roles in immunosuppression through modulation of the extracellular matrix, and the secretion of molecules such as cytokines, neurotrophic factors, and micro-RNAs (miRNAs). Conversely, glioma cell signals influence cell states and drive the metabolic reprogramming of TAMs. Similarly, emergent evidence indicates that neuronal activity influences glioma by released factors and by establishing functional synapses with glioma cells to promote tumor growth and invasion. Glioma cells also affect local neuronal activities and maintain connections through microtube gap junctions to amplify local effects. Here, we discuss the molecular mechanisms underlying bidirectional interactions between glioma cells and TAMs, as well as between glioma cells and neurons. A better understanding of these cellular cross talks is crucial for the development of novel therapeutic strategies for diffuse gliomas.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"210 ","pages":"177-190"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729885","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":"Gamma Knife radiosurgery for vestibular schwannomas.","authors":"Douglas Kondziolka, John G Golfinos","doi":"10.1016/B978-0-12-824534-7.00007-X","DOIUrl":"https://doi.org/10.1016/B978-0-12-824534-7.00007-X","url":null,"abstract":"<p><p>Gamma knife stereotactic radiosurgery is one of the most common procedures performed to manage patients with vestibular schwannoma. With a history that spans over 40 years, there has been continued evolution in radiosurgery technique and understanding of outcomes. The goal has always been to achieve long-term inactivation of tumor growth, commonly with tumor volumetric regression, and preservation of neurologic function. Challenges remain particularly pertaining to hearing preservation and other related symptoms such as those related to balance and tinnitus. Current discussions span a variety of topics including the importance of cochlear dose, the timing of the radiosurgery intervention as opposed to initial observation, the interpretation of imaging changes after radiosurgery, and the value of hearing augmentation strategies.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"212 ","pages":"259-266"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238251","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}
Simon K W Lloyd, Mathieu Trudel, Scott A Rutherford, Robert Behr
{"title":"Hearing rehabilitation in patients with vestibular schwannomas.","authors":"Simon K W Lloyd, Mathieu Trudel, Scott A Rutherford, Robert Behr","doi":"10.1016/B978-0-12-824534-7.00033-0","DOIUrl":"https://doi.org/10.1016/B978-0-12-824534-7.00033-0","url":null,"abstract":"<p><p>Hearing loss affects 95% of patients with vestibular schwannoma (VS), either because of the disease or its treatment. In untreated tumors, hearing loss is usually progressive but can be sudden and profound in up to 10%. In neurofibromatosis type 2-related schwannomatosis (NF2), where bilateral VS are almost universal, bilateral hearing loss has a greater impact on quality of life than any other factor. Hearing loss may result from vascular compromise of the cochlea, direct damage to the cochlear nerve by the tumor, direct growth of tumor into the cochlea, distortion of the cochlear nucleus by larger tumors, or the buildup of toxic metabolites in CSF, particularly at the fundus of the internal auditory canal. There are numerous means by which hearing can be rehabilitated. Hearing aids are helpful for those who have reasonable residual hearing although hearing distortion is common in VS patients and may limit the amount of benefit. If treatment of a tumor is required, then hearing preservation options such as stereotactic radiosurgery or hearing preservation surgery may be considered if the tumor is small- or medium-sized. However, hearing loss often progresses more quickly following stereotactic radiosurgery and the risk of losing hearing following hearing preservation surgery is as high as 60% depending on tumor size and the approach used. Patients with profound hearing loss often benefit from cochlear implantation as long as the cochlear nerve is intact and open-set speech discrimination is not uncommon. In patients in whom the cochlear nerve is no longer intact (usually following surgery for VS in NF2), auditory brainstem implantation is a viable option although auditory benefit is limited, mainly providing an aid to lip reading.</p>","PeriodicalId":12907,"journal":{"name":"Handbook of clinical neurology","volume":"212 ","pages":"381-394"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238308","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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