Hippocampal sclerosis revisited

Fisher, Paul D.; Sperber, Ellen F.; Moshé, Solomon L.

doi:10.1016/s0387-7604(98)00069-2

Cited by 100 publications

(65 citation statements)

References 94 publications

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“…Neuroprotection. Because hippocampal damage has long been thought to be critically involved in the development of TLE, one potentially promising strategy for antiepileptogenesis is administration of neuroprotective drugs after a brain insult (Fisher et al, 1998;Willmore, 2005;Walker, 2007;Acharya et al, 2008). Such a strategy is reasonable because at least part of the brain damage develops after the initial insult, as a result of delayed ("programmed") types of cell death (Fujikawa, 2005).…”

Section: Novel Approaches For Antiepileptogenesis In Post-status Epilmentioning

confidence: 99%

Prevention or Modification of Epileptogenesis after Brain Insults: Experimental Approaches and Translational Research

Löscher¹,

Brandt²

2010

Pharmacol Rev

360

366

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Section: Novel Approaches For Antiepileptogenesis In Post-status Epilmentioning

confidence: 99%

Prevention or Modification of Epileptogenesis after Brain Insults: Experimental Approaches and Translational Research

Löscher¹,

Brandt²

2010

Pharmacol Rev

360

366

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“…Recent studies report a series of reorganizational changes in the dentate gyrus that result in hyperexcitable dentate granular neurons. 8 The subicular region of the sclerotic hippocampus is remarkable in that it does not show significant neuronal loss, 84,85 although more subtle changes in receptor expression and synaptic inputs may occur. This is quite different from other neurological disorders involving the hippocampus, such as Alzheimer's disease, schizophrenia, and so forth, where the subiculum shows significant neuronal injury.…”

Section: What Role Do Astrocytes Play In the Hippocampal Seizure Focus?mentioning

confidence: 99%

Astrocytes and Epilepsy

2010

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Summary: Astrocytes form a significant constituent of seizure foci in the human brain. For a long time it was believed that astrocytes play a significant role in the causation of seizures. With the increase in our understanding of the unique biology of these cells, their precise role in seizure foci is receiving renewed attention. This article reviews the information now available on the role of astrocytes in the hippocampal seizure focus in patients with temporal lobe epilepsy with hippocampal sclerosis. Our intent is to try to integrate the available data. Astrocytes at seizure foci seem to not be a homogeneous population of cells, and in addition to typical glial fibrillary acidic protein, positive reactive astrocytes also include a population of neuron glia-2-like cells The astrocytes in sclerotic hippocampi differ from those in nonsclerotic hippocampi in their membrane physiology, having elevated Naϩ channels and reduced inwardly rectifying potassium ion channels, and some having the capacity to generate action potentials. They also have reduced glutamine synthetase and increased glutamate dehydrogenase activity. The molecular interface between the astrocyte and microvasculature is also changed. The astrocytes are also associated with increased expression of many molecules normally concerned with immune and inflammatory functions. A speculative mechanism postulates that neuron glia-2-like cells may be involved in creating a high glutamate environment, whereas the function of more typical reactive astrocytes contribute to maintain high extracellular Kϩ levels; both factors contributing to the hyperexcitability of subicular neurons to generate epileptiform activity. The functions of the astrocyte vascular interface may be more critical to the processes involved in epileptogenesis.

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“…The TLE is epitomized by the progressive expansion of spontaneous recurrent motor seizures (SRMS) that arise from the limbic system regions, especially the hippocampus (Engel, 1998;French et al, 1993). The TLE with hippocampal sclerosis, one of the most prevailing types of partial seizure disorders (Engel, 1998;Wieser and Hane, 2004), is generally linked to an initial precipitating event such as febrile convulsions, head trauma, status epilepticus (SE) or encephalitis (Harvey et al, 1997;Fisher et al, 1998;Cendes, 2004). The hippocampal sclerosis is characterized by pervasive neuronal loss in the dentate hilus and the CA1 and CA3 subfields, deviant mossy fiber sprouting into the dentate supragranular layer and deeply diminished dentate neurogenesis (Sutula et al, 1989;Dalby and Mody, 2001;Buckmaster et al, 2002;Hattiangady et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Strategies for promoting anti-seizure effects of hippocampal fetal cells grafted into the hippocampus of rats exhibiting chronic temporal lobe epilepsy

Rao

Hattiangady

Kiranmai

et al. 2007

Neurobiology of Disease

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Efficacy of hippocampal fetal cell (HFC) grafting for restraining spontaneous recurrent motor seizures (SRMS) in chronic temporal lobe epilepsy (TLE) is unknown.We investigated both survival and anti-seizure effects of 5′-bromodeoxyuridine (BrdU) labeled embryonic day 19 (E19) HFC grafts pretreated with different neurotrophic factors and a caspase inhibitor. Grafts were placed bilaterally into the hippocampi of F344 rats exhibiting kainate (KA) induced chronic TLE, where the frequency of SRMS varied from 3.0 to 3.5 seizures/8-h duration. The first group received standard (untreated) HFC grafts, the second group received HFC grafts pretreated and transplanted with brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and caspase inhibitor Ac-YVAD-cmk (BNC-treated HFC grafts), the third group received HFC grafts pretreated and transplanted with fibroblast growth factor-2 (FGF-2) and caspase inhibitor Ac-YVAD-cmk (FC-treated HFC grafts), and the fourth group served as epilepsy-only controls. Epileptic rats receiving standard HFC grafts exhibited 119%increase in the frequency of SRMS at 2 months post-grafting consistent with 125% increase in seizure frequency observed in epilepsyonly controls during the same period. However, in epileptic rats receiving HFC grafts treated with BNC or FC, the frequency of SRMS was 33-39%less than their pre-transplant scores and 73-76% less than rats receiving standard HFC grafts or epilepsy-only rats. The yield of surviving neurons was equivalent to 30%of injected cells in standard HFC grafts, 57% in HFC grafts treated with BNC and 98% in HFC grafts treated with FC. Thus, standard HFC grafts survive poorly in the chronically epileptic hippocampus and fail to restrain the progression of chronic TLE. In contrast, HFCs treated and grafted with BNC or FC survive robustly in the chronically epileptic hippocampus, considerably reduce the frequency of SRMS and blunt the progression of chronic TLE.

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Hippocampal sclerosis revisited

Cited by 100 publications

References 94 publications

Prevention or Modification of Epileptogenesis after Brain Insults: Experimental Approaches and Translational Research

Prevention or Modification of Epileptogenesis after Brain Insults: Experimental Approaches and Translational Research

Astrocytes and Epilepsy

Strategies for promoting anti-seizure effects of hippocampal fetal cells grafted into the hippocampus of rats exhibiting chronic temporal lobe epilepsy

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