Hippocampal Sclerosis (original) (raw)
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Hippocampal sclerosis revisited
Brain and Development, 1998
Studies dating back more than 150 years reported a relationship between hippocampal sclerosis and epilepsy. Retrospective studies of patients who underwent temporal lobectomy for intractable partial epilepsy found a relationship between a history of early childhood convulsions, hippocampal sclerosis, and the development of temporal lobe epilepsy. Many believe that febrile seizures lead to hippocampal damage and this in turn predisposes the patient to the development of temporal lobe epilepsy. Studies in adult rats have shown that seizures can lead to hippocampal damage and unprovoked recurrent seizures. However, many questions remain as to the relevance of early childhood seizures to hippocampal sclerosis and temporal lobe epilepsy. Human prospective epidemiologic studies have not shown a relationship between early childhood seizures and temporal lobe epilepsy. Recent MRI studies in humans suggest that a preexisting hippocampal lesion may predispose infants to experience febrile seizures, later on hippocampal sclerosis, and possibly temporal lobe epilepsy may occur. Unlike the studies in adult rats, normal immature rats with seizures have not been shown to develop hippocampal damage or unprovoked seizures in adulthood. Furthermore, animal studies reveal that preexisting brain abnormalities can predispose to hippocampal damage following seizures early in life. This paper reviews evidence for and against the view that early childhood convulsions, hippocampal sclerosis, and temporal lobe epilepsy are related, while also exploring clinical and animal studies on how seizures can lead to hippocampal damage, and how this can result in temporal lobe epilepsy. By better understanding the cause and effect relationship between early childhood seizures and hippocampal injury in normal and abnormal brains specific treatments can be developed that target the pathogenesis of epilepsy.
Hippocampus, hippocampal sclerosis and epilepsy
Pharmacological Reports, 2013
Hippocampal sclerosis (HS) is considered one of the major pathogenic factors of drug-resistant temporal lobe epilepsy. HS is characterized by selective loss of pyramidal neurons -especially of sectors CA1 and CA3 of the hippocampus -pathological proliferation of interneuron networks, and severe glia reaction. These changes occur in the course of long-term and complex epileptogenesis. The authors, on the basis of a review of the literature and own experience, present the pathomechanisms leading to hippocampal sclerosis and epileptogenesis, including various morphological and functional elements of this structure of the brain and pharmacological possibilities of preventing these processes.
Hippocampal sclerosis-Origins and imaging
Epilepsia, 2012
The association between hippocampal sclerosis (HS) and epilepsy has been known for almost two centuries. For many years, HS was studied in postmortem series; however, since the mid-20th century, surgical specimens from temporal lobe resections have provided important new knowledge. HS is the most common pathology underlying drug-resistant mesial temporal lobe epilepsy (MTLE), a syndrome with a characteristic history and seizure semiology. In the early 1990s, it was recognized that magnetic resonance imaging (MRI) could detect HS. The standard MRI protocol for temporal lobe abnormalities uses coronal slices perpendicular to the long axis of the hippocampus. The MRI features of HS include reduced hippocampal volume, increased signal intensity on T 2 -weighted imaging, and disturbed internal architecture. The histopathologic diagnosis of HS is usually straightforward, with neuronal loss and chronic fibrillary gliosis centered on the pyramidal cell layer. There are several patterns or subtypes of HS recognized from surgical series based on qualitative or quantified assessments of regional neuronal loss. The pathologic changes of HS include granule cell dispersion, mossy fiber sprouting, and alterations to interneurons. There may also be more extensive sclerosis of adjacent structures in the medial temporal lobe, including the amygdala and parahippocampal gyrus. Subtle cortical neuropathologies may accompany HS. The revised classification of dysplasias in epilepsy denotes these as focal cortical dysplasias type IIIa. Sometimes, HS occurs with a second lesion, either in the temporal lobe or extratemporal, most often ipsilateral to the HS. HS on preoperative MRI strongly predicts good seizure outcome following temporal lobe resection (TLR). If adequate MRI shows no structural correlate in patients with MTLE, functional imaging studies are valuable, especially if they are in agreement with ictal electroencephalography (EEG) findings. Focal hypometabolism on 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) ipsilateral to the symptomatic temporal lobe predicts a good surgical outcome; the added value of 11 C-Flumazenil-PET (FMZ-PET) and proton magnetic resonance spectroscopy (MRS) is less clear. Surgical methods have evolved, particularly resecting less tissue, aiming to preserve function without compromising seizure outcome. Around two thirds of patients operated for MTLE with HS obtain seizure freedom. However, the best surgical approach to optimize seizure outcome remains controversial.
Hippocampal Sclerosis: Causes and Prevention
Seminars in Neurology, 2015
The importance of the hippocampus as a cause of epilepsy was first recognized in 1825, when Bouchet and Cazauvielh described the pathology of 18 autopsied patients in a thesis that attempted to establish the relationship between epilepsy, "l'épilepsie," and insanity, "l'aliénation mentale." 1 Later, Sommer (1880) described in detail the neuropathological finding of hippocampal sclerosis in the brains of patients with chronic epilepsy. 2 He noted gliosis and pyramidal cell loss in predominantly the CA1 region of the hippocampus; he proposed that these lesions were the cause of the epilepsy. Hippocampal sclerosis is now recognized as one of the main causes of focal epilepsy and is present in approximately 10% of adults with new-onset focal epilepsy. 3 Moreover, hippocampal sclerosis often causes refractory epilepsy and is the sole pathology in about a third of all surgical resections for epilepsy and is an associated pathology (so-called dual pathology) in approximately 5%. 4 However, the hippocampus has a twofold interest in epilepsy, as it also is an area of the brain that is particularly susceptible to damage by seizures (and other brain insults). This dichotomous role of hippocampal damage as the cause and result of seizures stems possibly from its physiological role in memory formation and neuronal plasticity. 5 Hippocampal Sclerosis Is More than One Condition Hippocampal sclerosis can have more than one cause, and often the cause is a complex interplay between genetic background and environmental insults (see below). However, hippocampal sclerosis is not even one neuropathological entity. 6 Indeed, older systems of grading the severity of cell loss in hippocampal sclerosis 7 have been superseded by a system that recognizes that it is not just the severity of cell
Hippocampal sclerosis in temporal lobe epilepsy demonstrated by magnetic resonance imaging
Annals of Neurology, 1991
The value of magnetic resonance imaging in the detection of hippocampal sclerosis has been controversial. We studied 10 patients aged 22.5 f 6.0 years with intractable temporal lobe epilepsy selected because of a history of a prolonged childhood convulsion, which is characteristic of a group of patients in whom hippocampal sclerosis is a constant finding. All 10 patients showed reduction in size of one hippocampus associated with increased signal intensity on T2weighted magnetic resonance images. These changes were reliably detected on coronal spin-echo images, perpendicular to the long axis of the hippocampus. Appreciation of the normal imaging anatomy of the hippocampus allowed correct interpretation of the relative changes in signal intensities of the hippocampus and adjacent temporal horn on sequential echo images. The side of the abnormal hippocampus on magnetic resonance imaging accorded with the electroencephalographic localization in all 10 patients, and with the lateralization of the early convulsions in all 6 patients where this was known. Temporal lobectomy was performed in all 10 patients. Hippocampal sclerosis was confirmed in the 3 patients in whom hippocampal tissue was available for histological examination. The value of this technique was reinforced by the excellent postoperative results, with 80% being seizure free at a mean follow-up time of 33 f 4 months.
The diagnosis of hippocampal sclerosis: Other techniques
Magnetic Resonance Imaging, 1995
Pathologically, hippocampal sclerosis (HS) is characterized by neuronal loss and gliosis affecting particularly the pyramidal neurons of CAl, CA3, and CA4 with relative sparing of the CA2 neurons. This can be identified in vivo with magnetic resonance (MR) imaging techniques that can reveal both morphological and signal abnormalities. The morphological changes are atrophy and loss of the normal internal architecture of the hippocampus as seen in coronal section. There is also T1-and Tz-weighted signal abnormality in the hippocampus. Quantitative techniques are very good at measuring any single one of these features, but the spectrum of HS includes cases in which a single feature can occasionally be misleading. Also, quantitation focuses entirely on the hippocampus, and it is becoming clear that HS may exist in the presence of other brain pathology that may affect proper management of the patient. Therefore, quantitative measures should always be interpreted in the context of optimlsed imaging sequences and visual inspection. For routine clinical purposes, the relative reliance on quantltatlon (hippocampal volume or Tz measurements) depends entirely on the yield of visual inspection in any institution. This, in turn, depends on whether optimised imaging is performed and on the familiarity of the reporting specialist with the MRI features of HS. A technique which approaches 95100% compared with pathology is essential in any epilepsy centre, and optimized visual analysis can achieve this. There are some cases where quantitation of a single feature can be misleading, so visual analysis should always be performed, and complements any quantitative study.
Turkish neurosurgery, 2020
AIM Hippocampal sclerosis (HS) is the most common neuropathological finding in patients undergoing surgery for drug-resistant temporal lobe epilepsy. Approximately 60-90% of patients operated for HS live without a seizure. In 2013, the International League Against Epilepsy (ILAE) reported a new classification based on specific cell losses in Hippocampal Sclerosis. We aimed to investigate the relationship between clinical features and prognosis of the HS cases and ILAE histopathology classification. MATERIAL AND METHODS A hundred patients with refractory epilepsy who were operated with the diagnosis of the Mesial Temporal Lobe Epilepsy were included in the study. Socio-demographic characteristics, clinical and family histories, post-operative ILAE and Engel epilepsy scores and diagnostic tests were recorded. At the same time, all of the pathological specimens were classified according to the new semi-quantitative ILAE classification. A significant statistical relationship was investi...