Diseases of the Nervous System
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
Changes in myelin sheaths are easily recognizable features in a wide range of disease processes. In destructive lesions following infarcts, myelin sheaths are broken down and dissolved in the destroyed tissue parallel with the loss of neural and glial structures. When axons are lost, the corresponding myelin sheaths are also destroyed in both the central and peripheral nervous systems such as in Wallerian degeneration. Several toxic and metabolic changes affect primarily myelin sheaths, mainly Schwann cells; widespread demyelination occurs in areas of chronic cerebral edema and following exposure to carbon monoxide.59,92,238,252 In these disorders, the demyelinating process is secondary to other factors. Peripheral nerves show multiple foci of demyelination in many toxic and metabolic neuropathies, while axons remain relatively intact and are interspersed between normal myelinated and remyelinated segments. Chronic uremia and diabetes mellitus are connected with primary demyelination of the peripheral nerves. Diphteria toxin also affects primarily the peripheral myelin and Schwann cells. Myelin formation is defective in the developing brain in various inherited diseases of inborn errors of metabolism. In primary demyelinating disease, one or more components of the myelin sheath are selectively destroyed. In the latter groups, there is little or no damage to the neurons or axons and time integrity is maintained.
Neuroinfectious Diseases
Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw in Hankey's Clinical Neurology, 2020
Potential chronic neurologic complications of COVID-19Cognitive function. Approximately one-third of hospitalized COVID-19 patients with severe clinical features who are subsequently discharged have deficits in executive function.4 The long-term outcomes for these patients are not clear. It also is unknown whether these patients are at risk for the development of a progressive dementia similar to that observed in HIV/AIDS.29Demyelinating disease. In experimental animal models, coronaviruses initiate the formation of CNS demyelinating lesions similar to those seen in multiple sclerosis.30 At this point in time, there has not been a reported increase in MS-like diseases in patients who have recovered from COVID-19. However, assessment of the long-term impact of COVID-19 on the development of neurologic and autoimmune diseases will require clinical monitoring over several years.
Autoimmunity and Immune Pathological Aspects of Virus Disease
Irun R. Cohen in Perspectives on Autoimmunity, 2020
Immune reactions against self-constituents play an important role in the pathogenesis of several diseases affecting man and animals. Some of these disorders are clearly associated with a virus infection. In other cases, a viral etiology is suspected based on circumstantial evidence. One of the most enigmatic and challenging diseases of the latter type is multiple sclerosis. The hallmark of this disease consists of demyelinating lesions associated with inflammatory lymphoid cells affecting selected areas of the CNS. It is not known which mechanisms trigger and perpetuate autoimmune reactions against brain tissue. A variety of demyelinating diseases are clearly induced by a virus infection; some of them are accompanied by autoimmune responses. Some neurological disorders of unknown etiology are associated with autoantibodies and may be triggered by a viral infection. At least in animal systems, viruses can be associated with systemic lupus erythematosus, one form of diabetes, myocarditis, nephritis, and polyarthritis, all syndromes involving a variety of autoimmune phenomena. For extensive and detailed information the reader is referred to several books covering the addressed topics.1-6
Are electrophysiological and oligodendrocyte alterations an element in the development of multiple sclerosis at the same time as or before the immune response?
Published in International Journal of Neuroscience, 2021
Genaro Gabriel Ortiz, Mario A. Mireles-Ramírez, Fermín P. Pacheco-Moisés, Luis J. Ramírez-Jirano, Oscar K. Bitzer-Quintero, Daniela L. C. Delgado-Lara, L. Javier Flores-Alvarado, Miriam A. Mora-Navarro, Miguel Huerta, Blanca M. G. Torres-Mendoza
Multiple Sclerosis (MS) is defined as an inflammatory disease of the white matter (myelin). The central nervous system is mediated by autoreactive clones of T cells that would act against antigens (autoantigens) of myelin, causing their destruction, which would condition the symptomatology and appearance of the dysfunction. Multiple sclerosis is considered a disease mediated by helper T lymphocytes (CD4), but this fact, far from being proven, presents too much evidence that puts it in doubt as to the primary mechanism of the disease [1–3]. The disorder is diagnosed most often between 20 and 40 years of age but can be seen at any age. Multiple sclerosis is caused by damage to the myelin sheath, which is the protective covering that surrounds neurons. Damage to the nerve is caused by inflammation that occurs when the body's immune cells attack the nervous system, which can occur along any area of the brain, the optic nerve, or the spinal cord (among others). The clinical picture of MS is a consequence of the anatomopathological lesions observed in the central nervous system: inflammation, demyelination, axonal degeneration and gliosis, and their electrophysiological consequences such as conduction blocks, axonal hyperexcitability, and the generation of ectopic potentials [4–7]. There is no simple explanation with the most classic theories, and it is suggested that it is a demyelinating disease almost exclusively (Table 1).
Primary central nervous system lymphoma with no enhancement initially and no significant progression over a long term: a case report and review of the literature
Published in International Journal of Neuroscience, 2019
Ning-ning Hu, Man-man Zhang, Yan-yan Chen, Bei-lei Zhu
The patient was diagnosed as central nervous system demyelinating disease. Brain biopsy was suggested for the first time to exclude primary central nervous system lymphoma but was declined by the patient’s families. After quitting smoking, controlling blood glucose and blood pressure, and receiving antiplatelet, anxiolytic, and sleep-improving therapy, the patient’s symptoms improved substantially. Half a month later, re-examination of the cranial MRI indicated that the lesion was subsided than before, so hormone therapy was not administrated to the patient. A third cranial MRI scan was performed in June 2017, from which further subsidence of old lesions was suggested, while newly developed lesions were spotted in the left parietal lobe (Figure 1). The diagnosis of demyelinating disease seemed to be further supported. However, no special treatment was given as there was no complaint from the patient.
Neuropsychiatric manifestations in primary Sjogren syndrome
Published in Expert Review of Clinical Immunology, 2022
Simone Appenzeller, Samuel de Oliveira Andrade, Mariana Freschi Bombini, Samara Rosa Sepresse, Fabiano Reis, Marcondes C. França
Definitions for neuropsychiatric manifestations, including a minimal set of investigation and attribution criteria, are the first step toward a standardization. Positive experience has been made in other autoimmune diseases, such as systemic lupus erythematosus. Therefore, we consider that an international, multidisciplinary study could significantly contribute and make an important step toward diagnostic and/or classification criteria for neuropsychiatric manifestations in pSS. So far, these have been classified as PNS, CNS (Diffuse, focal, and spinal cord involvement), and ANS. Some manifestations, such as demyelinating disease, have to be differentiated from multiple sclerosis and neuromyelitis optica. Definition criteria and attribution could significantly impact future studies allowing comparisons of different cohorts and validation of biomarkers.
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