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1
Perry, V. Hugh. Macrophages and the nervous system. Austin: R.G. Landes Co., 1994.
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2
M, Berry, e Logan Ann, eds. CNS injuries: Cellular responses and pharmacological strategies. Boca Raton: CRC Press, 1999.
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Parker, James N., e Philip M. Parker. Pantothenate kinase-associated neurodegeneration: A bibliography and dictionary for physicians, patients, and genome researchers [to Internet references]. San Diego, CA: ICON Health Publications, 2007.
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4
Venkatesan, Arun. Central Nervous System Whipple Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0169.
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Whipple disease (WD) is a multisystemic infection caused by the bacillus Tropheryma whipplei. Although the organism is ubiquitous in the environment, WD is rare. In affected individuals, the organism resides intracellularly within macrophages and can manipulate host immune responses to avoid clearance. Central nervous system (CNS) involvement can occur as a manifestation of classic WD, in the setting of a relapse of previously treated WD, or rarely as isolated nervous system infection. Diagnosis of CNS WD rests on polymerase chain reaction (PCR) and demonstration of periodic acid-Schiff (PAS) positive macrophages in tissue, and ef
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Letendre, Scott, Jennifer Iudicello, Beau Ances, Thomas D. Marcotte, Serena Spudich e Mary Ann Cohen. HIV-Associated Neurocognitive Disorders. Editado por Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding e Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0016.
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The human immunodeficiency virus (HIV) enters the central nervous system soon after infection; can infect glia and tissue macrophages in the brain; and can injure neurons, resulting in loss of dendrites. These and other processes underpin a syndrome of cognitive and motor impairment termed HIV-associated neurocognitive disorder (HAND). This chapter principally focuses on HAND, although delirium and other neurocognitive disorders are also discussed and should remain in the differential diagnosis of cognitive impairment in persons with HIV. A differential diagnosis of cognitive impairment in HIV also includes multimorbid conditions that can influence neurocognitive performance, such as metabolic syndrome, vascular disease, medication toxicity, and substance use disorders. When developing treatment recommendations for HAND, initiation of ART and treatment of multimorbid conditions and other neurocognitive disorders should be prioritized. It is important for clinicians to regularly monitor HIV patients for HAND and other neurocognitive disorders since cognitive impairment can affect activities of daily living; quality of life; adherence to risk reduction, medical care, and medication; and survival.
6
Berry, Martin. CNS Injuries: Cellular Responses and Pharmacological Strategies. Taylor & Francis Group, 2019.
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Berry, Martin. CNS Injuries: Cellular Responses and Pharmacological Strategies. Taylor & Francis Group, 2019.
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8
Berry, Martin. CNS Injuries: Cellular Responses and Pharmacological Strategies. Taylor & Francis Group, 2019.
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9
Berry, Martin, e Ann Logan. CNS Injuries: Cellular Responses and Pharmacological Strategies (Pharmacology & Toxicology (Crc Pr)). CRC, 1998.
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10
Berry, Martin. CNS Injuries: Cellular Responses and Pharmacological Strategies. Taylor & Francis Group, 2019.
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11
DeAngelis, Lisa M. Primary Central Nervous System Lymphoma. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0133.
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The lymphoid nature of PCNSL was established unequivocally by modern immunohistochemical techniques. PCNSL has been associated with a variety of congenital (Wiskott-Aldrich syndrome, ataxia-telangiectasia) and acquired (human immunodeficiency virus [HIV], renal transplant recipients) immunodeficiency states. PCNSL tends to be supratentorial, periventricular, and involve the deep structures such as the basal ganglia. The Epstein-Barr virus (EBV) plays an important role in initiating the development of PCNSL in immunocompromised patients includinig those with HIV infection. Leukoencephalopathy is a serious complication of effective PCNSL treatment, but apparent only when the patient is in a durable remission. Treatment utilizes chemotherapy with or without radiation, which can cause more cognitive disability than chemotherapy, and autologous stem cell therapy is under investigation in selected patients.
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Bicanic, Tihana, e Thomas S. Harrison. Fungal central nervous system infections. Editado por Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum e Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0022.
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Infections of the central nervous system (CNS) are amongst the most severe of all fungal infections. Cryptococcus neoformans is the commonest cause of adult meningitis in many countries with high HIV prevalence. C gattii is usually seen in the tropics in apparently immunocompetent patients. Meningitis is also caused by Candida in premature babies, and by the dimorphic fungi in endemic areas. CNS infections with Aspergillus, the mucormycetes, and less common moulds usually present as intracranial mass lesions in immunocompromised hosts. Early suspicion, prompt imaging, and appropriate samples for culture, histology, and antigen and molecular tests are all critical for early diagnosis. Organism-specific antifungal therapy relies largely on liposomal amphotericin B and voriconazole, with therapeutic drug monitoring for the latter. Amphotericin B plus flucytosine is recommended for cryptococcal meningitis. Management of underlying conditions is also critical. Targeted prophylaxis in highest risk groups and pre-emptive therapy for HIV-associated cryptococcosis hold promise for prevention and improved outcome.
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Adapa, Ram, e Anthony Absalom. Central nervous system physiology in anaesthetic practice. Editado por Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0006.
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How and where consciousness is generated and maintained remains an unsolved scientific mystery, and this has impeded progress in understanding anaesthesia. In recent years, however, significant progress has been made in understanding the neurobiology of anaesthetic-induced loss of consciousness. This has been made possible by advances in molecular biology techniques, which have helped shed light on the molecular mechanisms of action of the anaesthetic agents. In parallel, the development of neuroimaging techniques, such as functional magnetic resonance imaging and positron emission tomography, has also provided an enormous impetus. These techniques are providing new insights into the neural correlates of consciousness, and new insights into the alterations in neurophysiology associated with impaired consciousness caused by sleep, sedation, and anaesthesia. The information being gained from these studies on the neurobiology of impairments of attention, awareness, and memory will hopefully eventually not only lead to improvements in our understanding of consciousness and anaesthesia, but also to better clinical care. Understanding of memory functions during sedation and anaesthesia may, for example, lead to better strategies for preventing awareness with subsequent explicit recall of intraoperative events. Further, a better understanding of the neurobiology of anaesthetic-induced unconsciousness may inform future development of better anaesthetic agents, with a broader therapeutic index, and fewer unwanted effects.
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Amirian, E. Susan, Quinn T. Ostrom, Yanhong Liu, Jill Barnholtz-Sloan e Melissa L. Bondy. Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0056.
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Although brain and other nervous system tumors are relatively rare, constituting up to 4% of incident primary cancer diagnoses, they are often associated with high morbidity and mortality. Several etiologic factors have been examined in relation to nervous system tumors, with the majority of studies focusing on central nervous system tumors. Despite decades of research, the only established risk factors for brain tumors are family history and moderate to high levels of ionizing radiation exposure. Differences in study designs, case ascertainment, control selection, and accuracy of exposure assessment are challenges associated with studying risk factors for nervous system tumors, and may partly explain why the majority of risk for these tumors remains unexplained. There is now substantial evidence that gliomas are inversely associated with allergies and atopy and positively associated with taller height.
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Woldstad, Christopher, Michael Boska e Howard E. Gendelman. Neurological Complications of HIV in The Central Nervous System. Editado por Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding e Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0026.
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This chapter serves to highlight both the research advances made in understanding the effects of HIV on the nervous system and what lies ahead. Particular focus is given to both the effects HIV can play on the nervous system at the molecular and cellular levels and the comorbid conditions that affect neural function. Attention is also given to specific biomarkers to be used for increasing the effectiveness and availability of therapies. The pathogenesis of HIV-associated neurocognitive disorders (HAND) is comparable to that of several other neurodegenerative disorders, and their mechanistic similarities are also discussed in detail. With the introduction of antiretroviral therapy the life expectancy of persons with HIV has increased, with a concomitant decrease in the incidence of severe dementia. There has been a remarkable improvement in cognitive function with almost a complete reversal of associated symptoms of disease. Past and present disease manifestations and the implications for treatment are outlined in the chapter.
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Graham, Andrew, e Clare Galton. Nervous system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0018.
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Rheumatological conditions may be complicated by a variety of both central and peripheral nervous system disorder. Common complications such as entrapment neuropathies are familiar to rheumatologists but accurate diagnosis of less common neurological disorders may be challenging; careful clinical reasoning is essential, supplemented where necessary by imaging, neurophysiology, and other special investigations including cerebrospinal fluid examination. Complications vary according to the nature of background condition. In rheumatoid arthritis, neurological involvement is typically related to the mechanical consequences of advancing disease; the commonest complications are carpal tunnel syndrome and cervical myelopathy due to atlantoaxial subluxation. By contrast, neurological involvement in systemic lupus erythematosus (SLE) tends to occur earlier in the disease course, with a much wider range of manifestations. The management of stroke or seizures in SLE is not necessarily any different from that in the general population, unless complicated by the antiphospholipid syndrome. However, less common neurological syndromes may demand more specific investigation and treatment. For example, longitudinally extensive transverse myelitis and recurrent optic neuritis (neuromyelitis optica, or Devic's disease) is frequently associated with antibodies to aquaporin-4, and is highly likely to relapse unless treated vigorously with humoral immunosuppression. Nervous system involvement in vasculitis is common. Finally, not all neurological disorder in rheumatological disease is necessarily due to the underlying condition; neurological complications of disease-modifying therapy are increasingly recognized, in particular central and peripheral nervous system demyelination associated with TNF-α inhibitors.
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Gaitanis, John, Phillip L. Pearl e Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Editado por Donald L. Schomer e Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.
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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted energy metabolism (mitochondrial disorders, glucose transporter defect), neuronal toxicity (amino and organic acidopathies), impaired neuronal function (lysosomal and peroxisomal disorders), alteration of neurotransmitter systems (nonketotic hyperglycinemia), and vitamin and co-factor dependency (pyridoxine-dependent seizures). Environmental causes of perinatal brain injury often result in motor or intellectual impairment (cerebral palsy). Multiple proposed etiologies exist for autism, many focusing on synaptic development. This chapter reviews the EEG findings associated with this myriad of pathologies occurring in childhood.
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Mastroeni, Diego F. An Epigenetics Perspective on Diseases of the Central Nervous System. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0011.
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In the next two decades epigenetics could revolutionize understanding and treatment of diseases of the central nervous system. New research already demonstrates that manipulation of epigenetic mechanisms in vivo and in vitro can ameliorate a host of pathogenic processes associated with neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s (PD), amyotrophic lateral sclerosis (ALS), Huntington’s (HD), and multiple sclerosis (MS), among others. These advances have come relatively rapidly for a field that is still in its infancy compared to the much longer history of epigenetics in developmental biology. Epigenetic modifications are all-encompassing, from nucleotides to amino acids. They are capable of altering transcriptional to biochemical activity in a consistent manner across thousands of genes and hundreds of biologic pathways, yet they can do so differentially even in individuals or cells with identical gene codes. As such, epigenetic modifications are likely to touch on virtually all the mechanisms described in this book.
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Magalhaes, Eric, Angelo Polito, Andréa Polito e Tarek Sharshar. Sepsis-Associated Encephalopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0032.
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Brain dysfunction is a major complication of sepsis and is characterized by alteration of consciousness, ranging from delirium to coma and marked electroencephalographic changes. It reflects a constellation of dynamic biological mechanisms, including neurotransmitter imbalance, macro- and microcirculatory dysfunction resulting in ischaemia, endothelial activation, alteration of the blood-brain barrier impairment with passage of neurotoxic mediators, activation of microglial cells within the central nervous system, cumulatively resulting in a neuroinflammatory state. Sepsis-associated brain dysfunction is associated with increased mortality and long-term cognitive decline, whose mechanisms might include microglial activation, axonopathy, or cerebral microinfarction. There is no specific treatment, other than the management of the underlying septic source, correction of physiological and metabolic abnormalities, and limiting the use of medications with neurotoxic effects.
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Batchelor, Tracy T., Oussama Abla, Zhong-ping Chen, Dennis C. Shrieve e Samar Issa. Tumours of the haematopoietic system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0013.
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‘Tumours of the haematopoietic system’ examines the epidemiology, the pathogenesis, and the clinical features of adult and childhood primary central nervous system lymphomas (PCNSLs), extranodal forms of non-Hodgkin lymphoma, as well as the histiocytoses included in the World Health Organization (WHO) classification of central nervous system (CNS) tumours. It reviews these features in the most common PCNSL, primary central nervous system diffuse large B-cell lymphoma, as well as the other rare histopathological PCNSL variants including lymphomatoid granulomatosis, T-cell lymphoma, anaplastic large T-cell lymphoma, natural killer/T-cell lymphoma, low-grade lymphoma, mucosa-associated lymphoid tissue (MALT) of the dura, and Hodgkin lymphoma. The chapter also discusses clinical and anatomical PCNSL variants including vitreoretinal lymphoma, leptomeningeal lymphoma, intramedullary spinal cord lymphoma, intravascular lymphoma, and PCNSL in the immunocompromised host. It also reviews the CNS presentations of Langerhans cell histiocytosis and the following non-Langerhans cell histiocytoses: Erdheim–Chester disease, Rosai–Dorfman disease, juvenile xanthogranuloma, and histiocytic sarcoma. It is written for specialists and non-specialists managing these various conditions.
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Batchelor, Tracy, Joshua P. Klein, Andrés José María Ferreri e Lisa M. DeAngelis, eds. Oxford Textbook of Neurohaematology. Oxford University PressOxford, 2024. http://dx.doi.org/10.1093/med/9780198884903.001.0001.
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Abstract The Oxford Textbook of Neurohaematology is the first dedicated source of knowledge on the diverse neurological conditions associated with malignant and classical haematological diseases. The book is divided into three sections. In the first section, neurological conditions associated with malignant haematological diseases are covered. This section begins with chapters on primary haematological malignancies of the nervous system, including primary central nervous system lymphomas, vitreoretinal lymphoma, and other rare primary malignancies such as Hodgkin disease and lymphoproliferative disorders. Next, a chapter on histiocytic tumours of the central nervous system presents the neurological conditions associated with the Langerhans and non-Langerhans histiocytoses. This is followed by chapters covering the neurological complications of systemic myeloid and lymphoid malignancies. The second section of the book covers neurological complications of treatments used in the management of haematological malignancies such as chemotherapy, radiation, and immunotherapy, including chimeric antigen receptor T cells. The third and final section of the book features chapters on neurological complications associated with classical haematological diseases, including disorders of red blood cells (e.g. sickle cell anaemia), disorders of platelets and coagulation (e.g. immune thrombocytopenia), and disorders of white blood cells (e.g. hyperviscosity syndrome).
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Miller, Aaron E., e Teresa M. DeAngelis. Optic Neuritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0003.
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Optic neuritis (ON) is an ophthalmological syndrome commonly encountered in inflammatory and demyelinating diseases of the central nervous system. Here we review the cardinal clinical examination findings, the possible associated systemic diseases in which ON can manifest, and the recommended diagnostic evaluation and therapeutic measures.
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Misulis, Karl E., e E. Lee Murray. Developmental and Genetic Disorders. Editado por Karl E. Misulis e E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0037.
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There are innumerable developmental and genetic disorders associated with the brain and central nervous system. This chapter does not address conditions that primarily affect children because of the adult focus of this book. Instead, the chapter focuses on those disorders that are likely to come to the attention of the hospital neurologist.
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Elham, Bayat. Neurologic Manifestations of Hematological Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0193.
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A wide sprectum of hematologic disorders affect the central and peripheral nervous system. These disorders include porphyria, thrombotic thrombocytopenic purpura-hemolytic uremic syndromes, sickle cell disease, plasma cell dyscrasias, monoclonal gammopathy, primary systemic amyloidosis, primary systemic amyloidosis, Waldonstrom’s macroglobulinemia, myeloproliferative syndromes, cryoglobulinemia, and polycythemia vera. Some, like porphyria, cause both central and peripheral nervous system manifestations including sensory/motor peripheral neuropathy, dysautonomia, pain, seizures, and abdominal pain. Others such as sickle cell disease primarily affect the brain and cause both clinically apparent strokes associated with a vasculopathy of large intracranial blood vessels, as well as less obvious microstrokes that cause progressive cognitive decline if not treated.
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Wolf, David S. Neurofibromatosis Type 1. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0051.
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Neurofibromatosis type 1 is a common, autosomal dominant, monogenetic neurocutaneous disorder. It is characterized by café au lait spots, axillary and inguinal freckling, Lisch nodules, optic pathway gliomas, neurofibromas, and distinctive bony abnormalities. Also associated with this condition are other central nervous system tumors, scoliosis, hypertension, vascular abnormalities, and cognitive issues such as learning disabilities and attention deficit-hyperactivity disorder.
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Miller, Aaron E., e Teresa M. DeAngelis. Rheumatoid Arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0012.
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Rheumatoid arthritis (RA) is a systemic inflammatory disease that is characterized principally by a polyarthritis, but can result in several neurologic complications involving both the central and peripheral nervous system. In addition, several immunotherapies used to treat RA have been associated with neurological complications. In this chapter, we review the characteristic neurological sequelae of RA as well as the possible neurological consequences of its therapeutic regimens.
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Spaliaras, Joanne. Myelomeningocele. Editado por David E. Traul e Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0017.
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Spina bifida is a defect in which the vertebral arch of the spinal column is either incompletely formed or absent. Failure of closure of the neural tube during the third week of gestation leads to the constellation of defects observed in patients with meningomyelocele or open spina bifida. Myelomeningocele is the most common neural tube defect and the most severe birth defect compatible with long-term survival. It is associated with several characteristic central nervous system anomalies. Leak of cerebrospinal fluid (CSF) is commonly observed. The major indication for early operative repair (within 48 hours of delivery) is prevention of infection. Protection of the exposed neural tissue from trauma and drying is essential. An understanding of the pathophysiology and associated conditions of myelomeningocele helps guide anesthetic management of these patients.
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Chokroverty, Sudhansu, e Sushanth Bhat. Physiological changes in sleep. Editado por Sudhansu Chokroverty, Luigi Ferini-Strambi e Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0006.
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It is important for clinicians to be conversant with the physiological changes that occur in various organ systems during sleep, and the impact that sleep fragmentation and sleep deprivation have on the normal functioning of these systems. This chapter therefore strives to provide a brief overview of the physiological changes associated with sleep that occur in the central nervous system (CNS), the autonomic nervous system (ANS), the neuromuscular system, the respiratory system (including changes in the control of breathing during various stages of sleep) and cardiovascular systems, the gastrointestinal tract, the endocrine system, and the systems controlling thermoregulation and immune regulation. Additionally, the mechanisms underlying muscle hypotonia in sleep, as well as sleep-related changes in cerebral blood flow and cytokine function are discussed.
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Allison, Jacquelyn E., e Julie D. Dunlap. Myxedema Coma. Editado por Matthew D. McEvoy e Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0034.
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Thyroid hormones influence every metabolic function of the body. Inadequate amounts of circulating thyroid hormone cause dysfunction of two systems in particular that result in abnormal responses to anesthesia: the central nervous system and the cardiovascular system. Physiologic compensation for the slow onset of hypothyroidism can mask the degree of dysfunction and make diagnosis challenging. Stressors associated with surgery and anesthesia can aggravate coexisting hypothyroidism and trigger severe life-threatening hypothyroidism (myxedema). This chapter reviews the pathophysiology involved in hypothyroidism, identifies populations at risk for myxedema coma, and provides a stepwise treatment plan for these patients.
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Filippi, Massimo, e Maria A. Rocca. Multiple Sclerosis: White Matter versus Gray Matter Involvement (The Cause of Disability in MS). Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0083.
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The classic view of multiple sclerosis (MS) as a chronic, inflammatory-demyelinating condition affecting solely the white matter (WM) of the central nervous system (CNS) has been challenged by the demonstration, from pathologic and magnetic resonance imaging (MRI) studies, of an extensive and diffuse involvement of the gray matter (GM). This observation has driven the application of modern MR technology and methods of analysis to quantify the extent and distribution of damage to the different compartments of the CNS, with the ultimate goal of improving our understanding of the factors associated with the accumulation of clinical disability and cognitive impairment in these patients.
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Kuttikat, Anoop, e Nicholas Shenker. Fibromyalgia and chronic widespread pain syndromes—adult onset. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0160.
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Fibromyalgia syndrome (FMS) is characterized by chronic widespread pain, excessive fatigue, unrefreshing sleep, and other associated somatic symptoms. FMS is common in the general population with an estimated prevalence of 2-4% and is about six times more common in females than males. FMS causes significant individual and societal costs. The precise aetiology of FMS remains unclear. Dysfunctional pain processing within the central nervous system is the primary abnormality. FMS is a clinical diagnosis based on pattern recognition and it can coexist with other conditions. A multidisciplinary approach, incorporating patient education, physical therapies, psychological therapies, and pharmacotherapy, is effective in managing these patients.
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Hatef, Jeffrey, e Russell R. Lonser. Hemangioblastoma. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0007.
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Hemangioblastomas are benign central nervous system tumors that are found primarily (99%) in the cerebellum, brainstem, and spinal cord. They can occur sporadically (67% of cases) or in the context of the familial neoplasia syndrome, von Hippel-Lindau disease (VHL; 33%). These lesions often remain quiescent or grow in a saltatory pattern. When these tumors cause signs or symptoms, the signs or symptoms are often associated with peritumoral cyst formation. Whether the tumor occurs sporadically or in the context of VHL, complete resection is the treatment of choice when necessary. This chapter describes the clinical, imaging, and treatment features of this neoplasm.
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Elder, J. Bradley, e Ahmed Mohyeldin. Extramedullary Spinal Cord Tumors. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0021.
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Tumors of the spine that occur within the dura but outside of the spinal cord are characterized as intradural but extramedullary spine tumors. The vast majority of these tumors are benign. This chapter uses a case presentation to present diagnostic and management pearls for this anatomic category of central nervous system neoplasms. These tumors are typically diagnosed due to presenting symptoms including pain or neurologic symptoms that localize the tumor to a specific area of the spine. Management is typically surgical. Some types of tumors are associated with syndromes such as neurofibromatosis. This chapter also discusses potential pitfalls and complications and their management.
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Kanno, Hiroshi, e Joachim P. Steinbach. Familial tumour syndromes: von Hippel–Lindau disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0016.
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Von Hippel–Lindau (VHL) disease, an autosomal dominant familial tumour syndrome, is often associated with haemangioblastoma of the central nervous system. In the presence of oxygen, VHL protein serves to prevent the accumulation of hypoxia-inducible factor (HIF) protein by targeting it to the proteasomal pathway, while biallelic inactivation of the VHL gene blocks degradation of HIF and leads to constitutive activation of the HIF pathway although oxygen is present. HIF-target genes are involved in angiogenesis, proliferation, and metabolism enabling tumour growth. Haemangioblastoma is a highly vascularized, begin tumour commonly associated with a cyst, but it is linked with neurological morbidity and mortality based on its location and multiplicity. Haemangioblastoma in VHL is diagnosed according to symptoms and signs, past and family histories, laboratory data, neuroradiological findings, pathological findings, and genetic testing. Surgical treatment is usually the most recommended therapy for haemangioblastomas, and using well-defined microsurgical techniques, the majority can be resected safely.
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Tarsia, Paolo. Dyspnoea in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0083.
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Dyspnoea may be defined as a subjective experience of discomfort associated with breathing. Breathing discomfort arises as a result of complex interactions between signals relayed from the upper airways, the chest wall, the lungs, and the central nervous system. Integration of this information with higher brain centres provides further processing. The final aspects of the sensation of dyspnoea are influenced by contextual, environmental, behavioural, and cognitive factors. At least three qualitatively distinct sensations have been employed to describe discomfort in breathing—air hunger, increased effort of breathing, and chest tightness. Air hunger has been shown to be associated with stimulation of chemoreceptors. Increased effort of breathing may arise in clinical conditions that impair respiratory muscle performance through abnormal mechanical loads or when respiratory muscles are weakened (neuromuscular diseases). Chest tightness is often experienced by asthmatic patients during episodes of acute bronchoconstriction. Measurement of dyspnoea is essential in order to assess it adequately and monitor response to treatment. Dyspnoea assessment may be carried out thorough a number of different scales, questionnaires, or exercise tests. Strategies in controlling dyspnoea should not focus uniquely on decreasing dyspnoea intensity. Patients may profit from interventions that decrease the unpleasantness associated with breathlessness without necessarily affecting the intensity component of the symptom.
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Hancock, Laura M., Jared M. Bruce e Sharon G. Lynch. Multiple Sclerosis. Editado por C. Steven Richards e Michael W. O'Hara. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.020.
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Multiple sclerosis (MS) is a chronic disease that affects the central nervous system and can cause a wide variety of both physical and cognitive deficits. Mood disturbances are common, with as many as 50% of patients receiving a diagnosis of major depression during their lifetime. The risk of suicide is high and leaving depression untreated is associated with a host of additional MS symptoms. Depression in MS presents clinicians with unique challenges, as it is often difficult to distinguish from common neurological symptoms. The authors discuss recommended screening tools and therapeutic methods that can assist the clinician in successfully identifying and treating depression in MS.
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Tuddenham, Susan. Ehrlichia, Anaplasma, and Rickettsia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0051.
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Rickettsia, Ehrlichia, and Anaplasma are infections primarily transmitted by ticks (but, in the case of certain Rickettsial species, are transmitted by other vectors as well), which can cause an abrupt, febrile, and flu-like illness often associated with headache, nausea, vomiting, abdominal pain, rash, elevated liver function tests, and thrombocytopenia. Disease can be severe, particularly when patients are infected with Rickettsia rickettsii (Rocky Mountain Spotted Fever); patients may develop central nervous system involvement, shock, and multiorgan failure. Diagnostic tests are imperfect, and prompt empiric treatment should be initiated if disease is suspected. Doxycycline is the treatment of choice, and coinfection with other vector-borne pathogens may need to be considered.
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Vincent, Angela. Neuroimmunology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0015.
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This chapter relates to antibody-mediated disorders throughout the nervous system. Early papers recall how use of bungarotoxin, passive transfer experiments in mice, and clinical response to plasma exchange confirmed the role of acetylcholine receptor antibodies in myasthenia gravis. Cutting edge techniques subsequently discovered other key neuromuscular junctional proteins, including muscle-specific kinase an additional target for antibodies. Later papers report the link between brain inflammation and severe amnesia, paraneoplastic and non-paraneoplastic, and the identification of the first pathogenic antibodies to a central nervous system (CNS) receptor in Rasmussen’s syndrome. The first report of “Morvan’s syndrome” is followed by a single patient with antibodies immunoprecipitating potassium channels who improved remarkably with plasma exchange. Lastly, the patients in the 1920’s encephalitis lethargica epidemic described in detail by von Economo, exhibited many of the features now recognised as caused by antibodies to various CNS receptors and associated membrane proteins.
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Grant, Robert. Neurocutaneous syndromes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0235.
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This chapter describes several neurocutaneous syndromes, including tuberous sclerosis, neurofibromatosis, Sturge–Weber syndrome, Von-Hippel–Lindau disease and ataxia telangiectasia amongst others.Tuberous sclerosis, also known as Epiloia or Bournville’s Disease, is an autosomal dominant multisystem disease it usually presents in childhood with a characteristic facial rash, adenoma sebaceum, seizures, and sometimes learning difficulties. Central nervous system lesions in tuberous sclerosis are due to a developmental disorder of neurogenesis and neuronal migration. Other organs such as the heart and kidney are less commonly involved. The condition has very variable clinical expression and two-thirds of cases are thought to be new mutations, therefore it is important to examine and screen relatives. Management may involve many specialists and close co-operation between specialists is essential.The neurofibromatoses are autosomal-dominant neurocutaneous disorders that can be divided into ‘peripheral’ and ‘central’ types, although there is significant overlap. The characteristic features of neurofibromatosis type 1 are café au lait spots, neurofibromas, Lisch nodules, osseous lesions, macrocephaly, short stature and mental retardation, axillary freckling, and associations with several different types of tumours.Sturge–Weber syndrome involves a characteristic ‘port-wine’ facial naevus or angioma associated with an underlying leptomeningeal angioma or other vascular anomaly. It affects approximately 1/20 000 people. There can be seizures, low IQ, and underlying cerebral hemisphere atrophy as a result of chronic state of reduced perfusion and increased oxygen extraction. Patients may present with focal seizures which are generally resistant to anticonvulsant medication and can develop glaucoma.Von-Hippel– Lindau disease is one of the most common autosomal-dominant inherited genetic diseases that are associated with familial cancers. Von-Hippel–Lindau disease is characterized by certain types of central nervous system tumours, cerebellar and spinal haemangioblastomas, and retinal angiomas, in conjunction with bilateral renal cysts carcinomas or phaechromocytoma, or pancreatic cysts/islet cell tumours (Neumann and Wiestler 1991).Other neurocutaneous syndromes discussed include Hypomelanosis of Ito, Gorlin syndrome, Sjogren–Larsson syndrome, Proteus syndrome, Hemiatrophy and hemihypertrophy, Menke’s syndrome, Xeroderma pigmentosum and Cockayne’s syndrome.
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Colvin, Lesley A., e Marie T. Fallon. Pain physiology in anaesthetic practice. Editado por Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0009.
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The International Association for the Study of Pain defines pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’. A good understanding of the physiology of pain processing is important, with recent advances in basic science, functional neuroimaging, and clinical pain syndromes contributing to our understanding. It is also important to differentiate between nociception, the process of detecting noxious stimuli, and pain perception, which is a much more complex process, integrating biological, psychological, and social factors. The somatosensory nervous system, from peripheral nociceptors, to sensory nerves and spinal cord synapses has many potential sites for modulation, with ascending pathways to the brain, balanced by ‘top-down’ control from higher centres. Under certain circumstances, for example, after tissue injury from trauma or surgery, there will be continued nociceptive input, with resultant changes in the whole somatosensory nervous system that lead to development of chronic pain syndromes. In such cases, even when the original injury has healed, the pathophysiological changes in the nervous system itself lead to ongoing pain, with peripheral or central sensitization, or both. Additionally, in some chronic pain syndromes, for example, chronic widespread pain, it has been postulated that abnormalities in central processing may be the initiating factor, with some evidence for this from neuroimaging studies. Further work is needed to fully understand pain neurobiology in order to advance our management.
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Popova, Svetlana, Shannon Lange, Larry Burd e Jürgen Rehm. Burden and Social Cost of Fetal Alcohol Spectrum Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199935291.013.78.
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Damage to the central nervous system is a unifying concept for nearly all of the diagnoses that fall under the Fetal Alcohol Spectrum Disorders (FASD) umbrella. Thus, FASD are an important public health and social problem worldwide that consumes a large amount of resources, both economic and societal by imparting a large burden on society through such sectors as the healthcare system, mental health and substance abuse treatment services, foster care, the criminal justice system, and the long-term care of individuals with intellectual and physical disabilities. Existing estimates of the economic impact of FASD demonstrate significant cost implications on the individual, the family and society. Many of the costs associated with FASD can be reduced with the implementation of effective social policies and intervention programs.
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Watts, Richard A., e Eleana Ntatsaki. Miscellaneous vasculitides. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0137.
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The vasculitides are a group of relatively rare conditions with a broad spectrum of clinical presentations that can cause significant morbidity and mortality. Classification of the vasculitic syndromes is done according to the size of the vessels affected and also the presence of anti-neutrophil cytoplasmic antibodies (ANCA). Vasculitides can be either primary or secondary to an underlying systemic disease, malignancy, or infection. This chapter covers the spectrum of the secondary vasculitides; some of the non-ANCA-associated primary vasculitides and miscellaneous types of vasculitic syndromes. Secondary vasculitis can occur in the background of systemic rheumatic diseases such as rheumatoid arthritis, spondyloarthropathies, or other connective tissue diseases. Vasculitis can also present in relation to precipitants such as drugs (propylthiouracil, hydralazine, leucotriene antagonists) or vaccines. Infection (bacterial, mycobacterial, viral, and fungal) has been associated with vasculitis either as a trigger or as a consequence of iatrogenic immunosuppression. Infection-related vasculitis can affect all types and sizes of vessels. Certain forms of vasculitis such as cryoglobulinaemia are closely associated with viral infections and more specifically with HCV infection. There are forms of vasculitis, which appear to be isolated or localized to a single organ, or site (skin, gastrointestinal, genital, and primary central nervous system vasculitis) that may be histologically similar to systemic syndromes, but have a different prognosis. Other conditions that may mimic vasculitis and miscellaneous conditions such as Cogan's syndrome and relapsing polychondritis are also discussed.
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Soffietti, Riccardo, Hugues Duffau, Glenn Bauman e David Walker. Neuronal and mixed neuronal–glial tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0008.
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Neuronal and mixed neuronal-glial tumours are rare tumours of the central nervous system that occur more commonly in children. Despite a generally benign course, most tumours cause medically intractable seizures, and have been denominated as ‘long-term epilepsy-associated tumours’. The World Health Organization classification distinguishes nine histological variants: dysplastic gangliocytoma of the cerebellum/Lhermitte–Duclos disease, desmoplastic infantile astrocytoma and ganglioglioma, dysembryoplastic neuroepithelial tumour, gangliocytoma and ganglioglioma, central neurocytoma and extraventricular neurocytoma, cerebellar liponeurocytoma, papillary glioneuronal tumour, rosette-forming glioneuronal tumour of the fourth ventricle, and spinal paraganglioma. Early surgery with complete resection may significantly improve the likelihood of postoperative epilepsy freedom. Conformal radiotherapy can be considered in case of patients with incompletely resected symptomatic tumours, atypical or high-grade tumours, or in the case of multiple recurrences despite resections. The role of chemotherapy in these lesions remains poorly defined, while targeted therapies are now available to impact some molecular alterations.
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Young, Raymond. Infection in the Patient with Sickle Cell Anemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0060.
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This chapter provides a brief overview of the clinical manifestations of and management strategies for infectious complications in the immunocompromised sickle cell disease patient. The chapter discusses infections in various organ systems, including the respiratory tract, central nervous system, bone, hematopoietic cell lineage, and blood-borne infections. Differentiating infections from noninfectious processes that often have similar presentations in the sickle cell patient may at times be difficult, and clinicians managing sickle cell patients should be keenly aware of this fact. This chapter discusses the common bacterial pathogens associated with infection and a notable viral agent known to profoundly worsen anemia in the sickle cell host, parvovirus B19. Additionally, fundamental antimicrobial regimens and primary and secondary prophylactic strategies are included in this concise summary prepared for clinicians involved in the acute care management of the sickle cell patient.
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Messacar, Kevin, e Mark J. Abzug. Enterovirus and Parechovirus. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0003.
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Enteroviruses (EVs) comprise a genus in the Picornaviridae family. They are single-stranded RNA viruses and are common causes of human infection. Polioviruses, the prototypic EVs, were historically responsible for widespread outbreaks of paralytic poliomyelitis; now they are on the verge of global elimination through vaccination. More than 100 serotypes of nonpoliovirus EVs are described and are associated with a wide variety of diseases, ranging from respiratory infections, nonspecific febrile illnesses, herpangina, and hand-foot-and-mouth disease to meningitis, encephalitis, paralytic disease, myocarditis, chronic or disseminated infection in immunocompromised hosts (particularly those with defects in the humoral immune response), and severe disease in neonates. This chapter reviews disease manifestations during pregnancy and in neonates, with an emphasis on clinical presentation, diagnosis, and management. The newly emerging parechoviruses, important causes of central nervous system (CNS) disease, are also reviewed.
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Wingerchuk, Dean M. Neuromyelitis Optica Spectrum Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0023.
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Neuromyelitis optica (NMO) is an inflammatory demyelinating central nervous system disease. It has been classically defined as a monophasic, isolated co-occurrence of optic neuritis and transverse myelitis with uncertain relationship to multiple sclerosis. In the past decade, however, NMO has emerged as a distinct disorder associated with serum antibodies that target the astrocyte water channel aquaporin-4, distinguishing it from multiple sclerosis. The specificity of aquaporin-4 antibodies has led to appreciation of a wider spectrum of clinical and neuroimaging features, termed NMO spectrum disorders (NMOSD), than was encompassed by the classic NMO definition. Moreover, immunopathological studies have demonstrated that aquaporin-4 antibodies have pathogenic potential and that the disorder is a primary astrocytopathy with secondary demyelination. This chapter discusses the clinical definition and diagnosis of NMOSD and approaches to management, many informed by rapid advances in the understanding of NMO pathobiology.
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Bosworth, Brian P., Brian R. Landzberg e Elisa McEachern. Neurological Manifestations of Gastrointestinal and Hepatic Diseases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0190.
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Digestive diseases may have protean neurological manifestations, and should be considered during neurological evaluation of patients. Neurological manifestations of celiac disease (CD) may involve both central and peripheral nervous system, including syndromes of cerebellar and myoclonic ataxia, encephalopathy and dementia, seizures, CNS vasculitis and progressive multifocal leukoencephalopathy, peripheral neuropathy, and myopathy. Gluten sensitivity has been frequently implicated as a cause of neuropathy, with up to 49% of celiac disease patients experiencing some form of neuropathy and almost 40% meeting the criteria for peripheral neuropathy. Gluten ataxia is one of the most common neurological manifestations of celiac disease. Neurologic manifestations of inflammatory bowel disease (IBD) have long been recognized, with an incidence ranging from less than 1% to 35%. These manifestations may precede or, more commonly, follow a diagnosis of IBD. Hepatic encephalopathy, Wilson’s disease, and acute intermittent porphyria are examples of liver diseases associated with hepatic disorders.
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Fabbri, Chiara, e Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.
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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.
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Calandra-Buonaura, Giovanna, e Pietro Cortelli. Autonomic dysfunction and sleep disorders. Editado por Sudhansu Chokroverty, Luigi Ferini-Strambi e Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0029.
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Autonomic dysfunctions are frequently associated with sleep disorders, as the autonomic nervous system and sleep are closely related from anatomical, physiological, and neurochemical points of view. The autonomic dysfunctions described in this chapter may result from a common pathogenetic mechanism that affects both the autonomic and the sleep functions, as in fatal familial insomnia, or from a prevalent expression of a primary disorder of autonomic regulation during sleep, as in congenital central hypoventilation syndrome. Alternatively, the autonomic dysfunction may be mainly caused by the sleep disorder, as observed in obstructive sleep apnea syndrome, or the causal mechanism resulting in the association between the autonomic dysfunction and the sleep disorder has yet to be identified with certainty, as in narcolepsy with cataplexy and in REM sleep behavior disorder. The impact of the autonomic dysfunction on health and on patients’ quality of life is also reviewed.
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Gevirtz, Clifford M., Elizabeth Frost e Alan D. Kaye. Ultrarapid Opiate Detoxification. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190495756.003.0035.
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Extended opioid use results in physical dependence and neural adaptation. Opioid dependence treatment can be carried out with opioid receptor agonists, partial agonists, and antagonists. Conventional treatments have low success rates. Methadone and buprenorphine treatments involve substituting long-duration agonists for the opiate of abuse, essentially substituting one opiate for another. Rapid opiate detoxification is a 3-day process involving large amounts of an opiate antagonist. Both treatments have associated problems. Ultrarapid opiate detoxification (UROD) anesthetizes a patient and precipitates withdrawal while unconscious. It shortens withdrawal, avoiding much of the subjective withdrawal discomfort. Clonidine is critical to reduce catecholamine levels and mitigate central nervous system hyperarousal in acute withdrawal. A UROD advantage is that the withdrawal period is markedly shortened to 8 hours or less versus up to several months for conventional treatments. The patient is anesthetized during the acute withdrawal period and does not experience the unpleasant consequences of acute detoxification.