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Libros sobre el tema "Myelin sheath Diseases Diagnosis"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 30 de enero de 2023

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1

J, Valk y Valk J, eds. Magnetic resonance of myelin, myelination, and myelin disorders. 2a ed. Berlin: Springer, 1995.

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2

Knaap, Marjo S. van der., ed. Magnetic resonance of myelin, myelination, and myelin disorders. Berlin: Springer-Verlag, 1989.

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3

Marjo S. van der Knaap. Magnetic resonance of myelination and myelin disorders. 3a ed. Berlin: Springer, 2005.

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4

NATO Advanced Research Workshop on a Multidisciplinary Approach to Myelin Diseases (1986 Rome, Italy). A multidisciplinary approach to myelin diseases. New York: Plenum Press, 1987.

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5

D, Duncan I., Skoff R. P, Colman D y New York Academy of Sciences., eds. Myelination and dysmyelination. New York, N.Y: New York Academy of Sciences, 1990.

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6

Ay-ming, Wang, ed. Pediatric cranial MRI: An atlas of normal development. New York: Springer-Verlag, 1994.

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7

J, Vinken P. y Koetsier Johan C, eds. Demyelinating diseases. Amsterdam: Elsevier Science Publishers, 1985.

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8

Satellite Symposium on Myelination and Demyelination: Implications for Multiple Sclerosis (1987 Vancouver, B.C.). Myelination and demyelination: Implications for multiple sclerosis. New York: Plenum Press, 1989.

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9

(Susanne), Pitz S. y SpringerLink (Online service), eds. Primary Optic Nerve Sheath Meningioma. Berlin, Heidelberg: Springer-Verlag, 2008.

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10

Valk, Jacob y Marjo S. van der Knaap. Magnetic Resonance of Myelin, Myelination and Myelin Disorders. Springer London, Limited, 2013.

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11

Valk, Jacob y Marjo S. van der Knaap. Magnetic Resonance of Myelin, Myelination, and Myelin Disorders. Springer London, Limited, 2013.

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12

Valk, Jaap y Marjo S. van der Knaap. Magnetic Resonance of Myelination and Myelin Disorders. Springer London, Limited, 2005.

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13

Bisese, John H. y Ay-Ming Wang. Pediatric Cranial MRI: An Atlas of Normal Development. Springer, 2011.

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14

Bisese, John H. y Ay-Ming Wang. Pediatric Cranial MRI: An Atlas of Normal Development. Springer London, Limited, 2012.

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15

Crescenzi, G. Multidisciplinary Approach to Myelin Diseases. Springer London, Limited, 2013.

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16

Crescenzi, G. A Multidisciplinary Approach to Myelin Diseases. Springer, 2013.

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17

A Multidisciplinary Approach to Myelin Diseases. Springer, 1988.

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18

Salvati, S. Multidisciplinary Approach to Myelin Diseases II. Springer, 2012.

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19

S, Salvati, North Atlantic Treaty Organization. Scientific Affairs Division. y NATO Advanced Research Workshop on a Multidisciplinary Approach to Myelin Diseases (2nd : 1993 : Rome, Italy), eds. A Multidisciplinary approach to myelin diseases II. New York: Plenum Press, 1994.

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20

(Editor), Robert A. Lazzarini, John W. Griffin (Editor), Hans Lassman (Editor), Klaus-Armin Nave (Editor), Robert H. Miller (Editor) y Bruce D. Trapp (Editor), eds. Myelin Biology and Disorders. Elsevier Academic Press, 2004.

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21

Myelin biology and disorders. San Diego, Calif: Elsevier Academic Press, 2004.

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22

Pediatric Cranial MRI: An Atlas of Normal Development. Springer, 2011.

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23

Publications, ICON Health. Myelin - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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24

Brealey, David y Nicholas Hirsch. Diagnosis, assessment, and management of Guillain–Barré syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0246.

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The Guillain–Barré Syndrome describes a spectrum of acute inflammatory polyneuropathies and is the commonest cause of acute flaccid paralysis within the western world. The pathophysiology is complex and poorly understood, but appears to be an immune-mediated destruction of either the myelin sheath and/or the axons, predominantly of motor nerves. The clinical presentation is classically a rapid, ascending, flaccid paralysis, with minimal sensory deficit. This may ascend to involve respiratory or bulbar muscle function. These patients need careful monitoring and, if deteriorating, should be electively intubated and ventilated. Autonomic instability and sensory disturbance, including pain, is common. Treatment of the underlying condition relies upon immunomodulation with either intravenous immunoglobulin or plasma exchange. Supportive care is aimed at maintaining a safe airway, ventilatory support, and managing the complications of autonomic dysfunction and prolonged immobility. Mortality rates range up to 20%, but are significantly better in specialist neuromedical units. Survivors are often left with significant disability.
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25

Myelination and Demyelination: Implications for Multiple Sclerosis. Springer, 2011.

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26

Kim, Seung U. Myelination and Demyelination: Implications for Multiple Sclerosis. Springer, 1989.

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27

Kim, Seung U. Myelination and Demyelination: Implications for Multiple Sclerosis. Springer London, Limited, 2012.

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28

Kim, Seung U. Myelination and Demyelination: Implications for Multiple Sclerosis. Springer, 2011.

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29

Compston, Alastair. Multiple sclerosis and other demyelinating diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0871.

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The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.
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