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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A detailed study was made of the pathology of specimens removed by hemispherectomy for the treatment of intractable epilepsy in children with unilateral middle cerebral artery stroke. Neuropathological criteria were used to differentiate strokes that occurred in early intrauterine development (before 28 weeks gestational age) from those occurring in the last trimester, at birth, or after birth: 19 children had early strokes and 21 late. There was no difference in seizure history or occurrence of febrile convulsions in these two groups. Hippocampal tissue was available in 20 patients; pathology in the hippocampus, remote from the infarcted area, showed a marked difference between early-onset and late-onset groups. Hippocampal sclerosis was uncommon in children with early-onset strokes but developed in most of the children whose strokes were of later origin. However, hippocampal sclerosis was more closely related to a clinical history of a late initial precipitating insult irrespective of infarct timing. These findings demonstrate the changing vulnerability of the developing brain and show that hippocampal pathology is more closely related to the timing of an insult than seizure history or the occurrence of febrile convulsions.
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PMID:Stroke in the developing brain and intractable epilepsy: effect of timing on hippocampal sclerosis. 1294 24

Hippocampal sclerosis represents a common structural basis of temporal lobe epilepsy. However, the etiological factors and mechanisms leading to its development still remain unexplained. In our study, we present neuropathological findings in the resected hippocampus and the pole of the temporal lobe in 15 patients with hippocampal sclerosis. "Initial precipitating injuries" that are thought to cause the development of hippocampal sclerosis (febrile seizures in early childhood, head injury or meningoencephalitis) were present in the history of 12 patients. In the remaining 3 cases, no predisposing factors were found. Attention was paid to the histopathological identification of disturbed neuronal migration and differentiation in the temporal lobe. These defects were observed in 7 cases; in three of these, no predisposing factors were stated in the patients' histories. We suggest that in these cases, hippocampal sclerosis arises due to previously undetected disorders of cortical development. A latent neocortical malformation may also contribute to the development of hippocampal sclerosis in patients with an initial precipitating injury in anamnensis. Histopathological examination of resected epileptic brain tissue can provide insights into the individual pathogenesis of epileptic disorders, especially by the detection of microscopic disorders of cortical development.
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PMID:[Microscopic disorders of cortical development of the brain and its etiopathogenic importance for detection in patients with temporal epilepsy associated with hippocampal sclerosis]. 1466 30

0.5-1% of the population suffers from epilepsy, while another 5% undergoes diagnostic evaluations due to the possibility of epilepsy. In the case of suspected epileptic seizures we face the following questions: Is it an epileptic seizure? The main and most frequent differential-diagnostic problems are the psychogenic non-epileptic seizures ("pseudo-seizures") and the convulsive syncope, which is often caused by heart disorders. Is it epilepsy? After an unprovoked seizure, the information on recurrence risk is an important question. The reoccurrence is more possible if a known etiological factor is present or the EEG shows epileptiform discharges. After an isolated epileptic seizure, the EEG is specific to epilepsy in 30-50% of cases. The EEG should take place within 24 hours postictally. If the EEG shows no epileptiform potentials, a sleep-EEG is required. What is the cause of seizures? Hippocampal sclerosis, benign tumors, and malformations of the cortical development are the most frequent causes of the focal epilepsy. Three potentially life-threatening conditions may cause chronic epilepsy: vascular malformations, tumors, and neuroinfections. The diagnosis in theses cases can usually be achieved by MRI, therefore, MRI is obligatory in all epilepsies starting in adulthood. The presence of epileptogenic lesion has a prognostic significance in treatment. If the MRI shows a circumscribed lesion then the pharmacological treatment will likely to be unsuccessful, while surgery may result in seizure freedom. The new and quantitative MRI techniques, such as volumetry, T2-relaxometry, MR-spectroscopy, and functional MRI play a growing role in the epilepsy diagnosis.
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PMID:[Diagnosis of epilepsy]. 1526 91

Hippocampal sclerosis describes a pattern of neuronal loss and gliosis involving the medial temporal structures most often encountered in patients with epilepsy. It is still a matter for debate as to whether this lesion is acquired during the course of the patient's seizure history or is present at the outset. Early febrile seizures, episodes of status epilepticus as well as repetitive brief seizures may all contribute to the evolution of hippocampal sclerosis. In addition, genetic factors and developmental abnormalities of the hippocampus may both increase vulnerability to seizures and hippocampal injury. Recent human studies have addressed neuropathological changes in young adults and children undergoing surgery for refractory seizures with hippocampal sclerosis. Post-mortem examination, however, provides the opportunity to evaluate the effect of a lifetime of seizures on both left and right hippocampi, and the presence of any co-existing malformation. Post-mortem stereological analysis of 28 patients with poorly controlled seizures has confirmed a subgroup with absence of significant hippocampal neuronal loss despite decades of generalized seizures, including status epilepticus. The presence of granule cell dispersion correlated to the severity of hippocampal neuronal loss. Furthermore, in patients with confirmed hippocampal sclerosis at post-mortem examination, stereological assessment of the neocortex failed to confirm significant white matter neuronal heterotopia that might indicate an underlying developmental abnormality. In conclusion, seizures do not invariably lead to hippocampal injury and white matter heterotopia is not invariably associated with hippocampal sclerosis.
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PMID:Quantitative post-mortem study of the hippocampus in chronic epilepsy: seizures do not inevitably cause neuronal loss. 1575 32

The aim of this study was to describe magnetic resonance imaging (MRI) findings in patients with medically intractable epilepsy and to compare different magnetic resonance (MR) sequences in order to establish a dedicated and shorter scan time imaging protocol of choice. One hundred and twenty patients with seizures that were refractory to medical treatment were assessed by MRI with spin-echo (SE) T1, fast spin-echo (FSE) T2, fluid-attenuated inversion recovery (FLAIR), inversion recovery (IR) and contrast-enhanced T1 SE sequences. Pathological scans were acquired in 78 patients. Hippocampal sclerosis was detected in 30 patients (25%), cerebral, tumoral, mass lesions in 12 patients (10%), vascular malformations in nine patients (7.5%), cortical infarcts in eight patients (6.7%), cerebral infections in four patients (4.2%) and developmental disorders in 15 patients (12.5%). The most common location of the lesions was the temporal lobe (60%). Coronal, thin (slice thickness 4-5 mm) images have proven to be the most useful in the assessment of the hippocampus. FLAIR and IR are particularly useful in the detection of lesions abutting cerebrospinal fluid (CSF) spaces and developmental disorders, respectively, while T1 SE sequences before and after the intravenous administration of gadolinium offer great facility in identifying space-occupying lesions and infections. MRI is the most important diagnostic tool for the assessment of epileptogenic foci, thus playing the primary role in indicating the type of treatment to be applied.
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PMID:Magnetic resonance imaging in 120 patients with intractable partial seizures: a preoperative assessment. 1583 12

Hippocampal sclerosis (HS) is one of the most common pathologies in medically intractable temporal lobe intractable epilepsy. Significant hippocampal volume loss has also been found in patients with chronic depression. Depression is common in chronic epilepsy populations, but the effects of this comorbidity on hippocampal volume are unknown. We examined the hippocampal volumes of 87 patients (n=31 right hippocampal sclerosis, RHS; n=56 left hippocampal sclerosis, LHS). Each subject completed the Hospital Anxiety and Depression Scale (HADS). In the group as a whole, 13 subjects (15%) recorded moderate or severe levels of depression. Depression was more common in the LHS group with 1 in 5 scoring in the moderate or severe range on the HADS (n=11). Depression scores were not significantly correlated with quantitative measures of hippocampal volume in the LHS group. However, higher degrees of hippocampal symmetry were associated with higher levels of depression in the RHS group. This suggests that the left hippocampus may be smaller in depressed patients with RHS, although our numbers were too small to confirm this statistically. Our results suggest that the depression may influence left hippocampal volume in patients with right hippocampal sclerosis. We conclude that the neuroradiological characteristics of patients with epilepsy and chronic depression deserve further examination.
Seizure 2005 Sep
PMID:Epilepsy & depression: the effects of comorbidity on hippocampal volume--a pilot study. 1609 26

Hippocampal sclerosis is often associated with macroscopic or microscopic dysplasia in the temporal neocortex (TN). The relevance of such a dual pathology with regard to epileptogenesis is unclear. This study investigates the role of both pathologies in the generation of ictal and interictal activity. Ictal (113 seizures) and interictal data from invasive EEG recordings with simultaneous depth electrodes in the hippocampus and subdural electrodes over the TN were analysed retrospectively in 12 patients with variable degrees of hippocampal sclerosis and different types of histologically confirmed temporal cortical dysplasia [all male, age at epilepsy onset <1-29 years (mean 9.6 years), age when invasive recordings were performed 6-50 years (mean 28.2 years)]. Of the seizures 41.3% arose from the amygdala/hippocampus complex (AHC), 34.7% from the TN, 22% were simultaneously recorded from AHC and TN (indeterminate seizure onset), and 2% from other regions. In three patients, seizure onset was recorded only from the AHC. In patients with severe hippocampal sclerosis only 12% of the seizures arose from the TN, whereas in patients with mild hippocampal sclerosis 58% arose from the TN. The type of cortical dysplasia, however, did not predict seizure onset in the AHC or TN. Propagation time from the TN to the AHC tended to be shorter (mean 7.4 s) than vice versa (mean 13.7 s). The most common initial ictal patterns in the AHC were rhythmic beta activity (<25 Hz) and repetitive sharp waves, and in the TN were fast activity (>25 Hz) and repetitive sharp waves. The interictal patterns over the TN were similar to those seen over extratemporal focal cortical dysplasias. Simultaneous recordings from the hippocampus and the TN strongly suggest that dysplastic tissue in the TN is often epileptogenic. The quantitative contribution of the hippocampus to seizure generation corresponded with the degree of hippocampal pathology, whereas different subtypes of cortical dysplasia did not affect its relative contribution to seizure generation and even mild forms of dysplasia were epileptogenic.
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PMID:Epileptogenicity of cortical dysplasia in temporal lobe dual pathology: an electrophysiological study with invasive recordings. 1631 23

Hippocampal sclerosis is the most common abnormality associated with medial temporal lobe epilepsy (MTLE). Converging evidence supports that hippocampal sclerosis progresses with time. However, it is unclear whether extrahippocampal atrophy in patients with MTLE, similarly to hippocampal sclerosis, is an unremitting progressive process. In this article, we investigate the relationship between duration of epilepsy and gray matter concentration reduction in patients with MTLE within and outside the hippocampus. We employed a voxel-based morphometry study of MRI of the entire brain of 36 patients with drug refractory MTLE and 49 neurologically healthy age-matched controls. We performed a voxel-based parametric and nonparametric investigation of the association between gray matter concentration, age and duration of epilepsy. We complemented the investigation by extracting the gray matter concentration of regions of interest (ROIs) within the limbic system, and we investigated the association between the gray matter concentration on the ROIs and duration of epilepsy. Patients with MTLE exhibited gray matter concentration reduction that is negatively correlated with the duration of epilepsy within the ipsilateral hippocampus, temporal lobes as well as extratemporal limbic structures that are closely connected with the hippocampus. In conclusion, longer duration of refractory epilepsy was associated with a more intense hippocampal and extrahippocampal atrophy in patients with MTLE. The mechanism of progressive neuronal damage in MTLE may be related to active seizure activity within a limbic network, and early seizure control may prevent further brain atrophy in patients with refractory MTLE.
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PMID:Gray matter atrophy associated with duration of temporal lobe epilepsy. 1687 43

Hippocampal sclerosis (HS) is a pathologic term used to describe severe loss of neurons and reactive gliosis without cystic cavitation in the CA1 sector of the hippocampus. In late life, HS is associated with hippocampal atrophy, severe amnesia, and slowly progressive dementia without clinical seizure activity. HS is difficult to distinguish clinically from Alzheimer's disease and is often diagnosed postmortem. In autopsy series, HS may be found without significant other pathology (2%-4% of cases), but it occurs frequently in combination with other vascular and neurodegenerative disorders (12%-20% of cases). HS is found bilaterally in 50% of cases and unilaterally in 50% of cases, with similar predilection for the right versus left hemisphere. The pathogenesis of HS is unknown and may be multifactorial in origin, possibly due to anoxic/ischemic injury or TDP-43-related neurodegeneration. Little is known about the prevention and treatment of late-life HS, although circumstantial evidence suggests the importance of identifying and treating vascular risk factors.
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PMID:Understanding hippocampal sclerosis in the elderly: epidemiology, characterization, and diagnostic issues. 1871 71

Hippocampal sclerosis (HS) continues to be the most common pathology identified in patients with refractory temporal lobe epilepsy undergoing surgery. Wilhelm Sommer described this characteristic pattern of neuronal loss over 120 years ago through his post-mortem studies on patients with epilepsy. Neuropathological post-mortem studies in the 20th century proceeded to contribute significantly to the understanding of this disease process, with regard to the varying patterns of HS and involvement of adjacent limbic structures. From studies of surgical temporal lobe specimens from the 1950s onwards it was recognized that an early cerebral injury could act as the precipitant for the sclerosis and epilepsy. Modern neuropathological studies have focused on aspects of neuronal injury, loss of specific neuronal groups and cellular reorganization to address mechanisms of epileptogenesis and the enigma of how specific hippocampal neuronal vulnerabilities and glial proliferation are both the effect and the cause of seizures.
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PMID:Hippocampal sclerosis: progress since Sommer. 1876 61


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