Neuroanatomy and Pathology of Sporadic Parkinson's Disease: Advances in Anatomy, Embryology and Cell Biology, cartea 201
Autor Heiko Braak, Kelly Del Tredicien Limba Engleză Paperback – 3 dec 2008
Against the background of the normal morphology and anatomy, the authors analyze the pathoanatomy of sPD in the nervous system at various neuropathological stages and summarize the potential functional consequences of the lesions.
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Specificații
ISBN-13: 9783540798491
ISBN-10: 3540798498
Pagini: 130
Ilustrații: VII, 119 p. 29 illus. in color.
Dimensiuni: 155 x 235 x 10 mm
Greutate: 0.25 kg
Ediția:2009
Editura: Springer Berlin, Heidelberg
Colecția Springer
Seria Advances in Anatomy, Embryology and Cell Biology
Locul publicării:Berlin, Heidelberg, Germany
ISBN-10: 3540798498
Pagini: 130
Ilustrații: VII, 119 p. 29 illus. in color.
Dimensiuni: 155 x 235 x 10 mm
Greutate: 0.25 kg
Ediția:2009
Editura: Springer Berlin, Heidelberg
Colecția Springer
Seria Advances in Anatomy, Embryology and Cell Biology
Locul publicării:Berlin, Heidelberg, Germany
Public țintă
ResearchCuprins
Prologue.- Morphology of Lewy Pathology.- The Evolving Distribution Pattern of Lewy Pathology Associated with sPD Renders Neuropathological Staging Possible.- Stage 1.- Stage 2.- Stage 3.- Stage 4.- Stages 5 and 6.- The Progression of the Cortical Lesions Mimics the Pattern of Myelination in Reverse Order.- The Staging Hypothesis: Assumptions, Challenges, Potential.
Textul de pe ultima copertă
The proteinopathy sporadic Parkinson’s disease (sPD) is the second most frequent degenerative disorder of the human nervous system after Alzheimer’s disease. The a -synuclein inclusion body pathology (Lewy pathology) associated with sPD is distributed throughout the central, peripheral, and enteric nervous systems. The resulting nonrandom neuronal dysfunction and, in some regions, neuronal loss is reflected by a distinctive topographic distribution pattern of the Lewy pathology that, in the brain, has been staged. Except for olfactory structures and spinal cord constituents of the pain system, sensory components of the nervous system remain uninvolved or virtually intact. The most disease-related damage revolves around motor areas – particularly around superordinate centers of the limbic and visceromotor systems as well as portions of the somatomotor system. Vulnerable regions are interconnected anatomically and susceptible nerve cell types are not neurotransmitter-dependent.
Not all clinical symptoms emerging in the course of sPD can be explained by a lack of dopamine in the nigrostriatal system. These include autonomic dysfunction, pain, hyp- or anosmia, excessive daytime sleepiness, REM sleep behavioral disorder, depression, anxiety, cognitive decline, and dementia. Against the background of the normal morphology and anatomy, the authors analyze the pathoanatomy of sPD in the nervous system at various neuropathological stages and summarize the potential functional consequences of the lesions.
Not all clinical symptoms emerging in the course of sPD can be explained by a lack of dopamine in the nigrostriatal system. These include autonomic dysfunction, pain, hyp- or anosmia, excessive daytime sleepiness, REM sleep behavioral disorder, depression, anxiety, cognitive decline, and dementia. Against the background of the normal morphology and anatomy, the authors analyze the pathoanatomy of sPD in the nervous system at various neuropathological stages and summarize the potential functional consequences of the lesions.