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Titlebook: Cerebellar Degenerations: Clinical Neurobiology; Andreas Plaitakis Book 1992 Springer-Verlag US 1992 anatomy.cortex.neurobiology.neurophys

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發(fā)表于 2025-3-21 16:18:59 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱Cerebellar Degenerations: Clinical Neurobiology
編輯Andreas Plaitakis
視頻videohttp://file.papertrans.cn/224/223272/223272.mp4
叢書名稱Foundations of Neurology
圖書封面Titlebook: Cerebellar Degenerations: Clinical Neurobiology;  Andreas Plaitakis Book 1992 Springer-Verlag US 1992 anatomy.cortex.neurobiology.neurophys
描述This book encompasses basic and clinical reports on the cerebellum and its primary atrophic disorders, the cerebellar degenerations. Rapid progress has been made in undestanding the organization and function of the cerebellum at the neuronal, synaptic, and molecular level. Of particular importance has been the identification of the chemical transmitters utilized by the cer- ebellar cellular systems. More than any other brain region, the cerebellum utilizes amino acids as its main excitatory and inhibitory neurotransmitters. Excitatory amino acid transmitters, in addition to serving neuronal com- munication, may also mediate trophic and toxic effects, and as such, they may playa role in neurodegenerative processes. The cerebellar degenerations were among the first human disorders with primary system atrophy to be studied clinically and pathologically. This field of clinical cerebellar sciences, no longer confined to the previously known descriptive level, is now advancing rapidly, propelled by rapid advances in neuroimaging, immunology, and molecular biology. The advent of CT, MRI, and PET has in recent years permitted the study of central nervous system alterations in living patien
出版日期Book 1992
關(guān)鍵詞anatomy; cortex; neurobiology; neurophysiology; neuroscience; physiology
版次1
doihttps://doi.org/10.1007/978-1-4615-3510-2
isbn_softcover978-1-4613-6557-0
isbn_ebook978-1-4615-3510-2Series ISSN 0924-8935
issn_series 0924-8935
copyrightSpringer-Verlag US 1992
The information of publication is updating

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Claudia Fahrenwald,Magdalena Fellnerd to the many and complex functions the amino acid is thought to serve in the nerve tissue [2]. Of these, the putative neurotransmitter role [1] has attracted much attention lately due to rapidly accumulating evidence that it may be involved in the pathogenesis of neurodegenerative disorders [3, 4].
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Oculomotor Abnormalities in Cerebellar Degenerationlation studies [3], as well as anatomical tracing techniques), have cast some light on this dilemma. Meanwhile, we can at least try to attribute specific oculomotor subfunctions and related eye-movement abnormalities to distinct parts of the cerebellum [for more recent reviews see 4–7].
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發(fā)表于 2025-3-22 16:12:58 | 只看該作者
Glutamate Dehydrogenase Deficiency in Cerebellar Degenerationsd to the many and complex functions the amino acid is thought to serve in the nerve tissue [2]. Of these, the putative neurotransmitter role [1] has attracted much attention lately due to rapidly accumulating evidence that it may be involved in the pathogenesis of neurodegenerative disorders [3, 4].
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0924-8935 rogress has been made in undestanding the organization and function of the cerebellum at the neuronal, synaptic, and molecular level. Of particular importance has been the identification of the chemical transmitters utilized by the cer- ebellar cellular systems. More than any other brain region, the
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發(fā)表于 2025-3-23 01:41:03 | 只看該作者
Presentation Forms and Multimodal Formats,the cerebellum in the coordination of movements, and Flourens (1842) and Luciani (1891) established functional compensation as a characteristic feature of cerebellar action. Sherrington (1897), L?wenthal and Horseley (1897), Fodera (1923), and Pollock and Davis (1923) recognized inhibition as another characteristic feature of cerebellar action.
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發(fā)表于 2025-3-23 06:18:50 | 只看該作者
Carolin Rotter,Christoph Bressleries occurring with extreme rarity (even limited to single families), while others show an appreciable prevalence rate in the general population and, as such, they represent the primary hereditary ataxias.
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