Chapter

The Hippocampus in Neurological Disease

Thorsten Bartsch

in The Clinical Neurobiology of the Hippocampus

Published in print July 2012 | ISBN: 9780199592388
Published online September 2012 | e-ISBN: 9780199949922 | DOI: http://dx.doi.org/10.1093/acprof:oso/9780199592388.003.0011
The Hippocampus in Neurological Disease

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The hippocampus, and in particular the CA1 region, is vulnerable to metabolic stress. This affection can be observed in acute neurological disorders such as ischaemia, limbic encephalitis, hypoglycaemic encephalopathy, epilepsy, multiple sclerosis, and transient global amnesia. The basis of this regional susceptibility is, however, only partly understood but may include genetically-determined, glutamate-dependent, and calcium-mediated mechanisms of neuronal excitotoxicity and oxidative stress. Additionally, inflammatory responses and immunologically-mediated mechanisms may contribute to the response to acute metabolic stress but may also be involved in ageing and neurodegenerative disorders. The structure–function relationship of the hippocampus in pathological states can be monitored in vivo using magnetic resonance imaging (MRI). Here, the cellular and imaging correlates and pattern of hippocampal damage is reviewed in terms of studying the evolution and sequelae of hippocampal CA1 diffusion and ADC changes in acute neurological disorders. The evolution of diffusion changes over the course of the disease show that CA1 diffusion lesions can be most prominently detected within the first 3 days after the injury, frequently leading to a ‘delayed neuronal death’ of CA1 neurons. The cellular correlates of hippocampal damage, as reflected by MRI are incorporated into a pathophysiological framework highlighting the clinical neurobiology of the hippocampus.

Keywords: transient global amnesia; hippocampal stroke; hippocampus; limbic encephalitis; selective vulnerability; CA1; memory

Chapter.  16645 words.  Illustrated.

Subjects: Neuroscience

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