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

A brief discussion of the manifestations of limbic lobe discharge as opposed to discharge in neocortical temporal lobe structures is given. The opinion is expressed that, apart from certain characteristic limbic auras, the manifestations of psychomotor epilepsy are those of inactivation of brain stem mechanisms subserving consciousness. A brief discussion of other manifestations of inactivation of brain stem mechanisms subserving various other functions, as seen in other clinical patterns of epileptic discharge, follows. Hippocampal sclerosis is put forth as the cause rather than the result of seizures in both the juvenile and the adult age groups. It is proposed that limbic lobe structures have a low threshold for initiating epileptic discharge when injured, are predisposed to injury and give rise to discharge which has preferential access to brain stem structures. It is stated that petit mal absences and psychomotor attacks are clinically indistinguishable. The further opinion is expressed that the 3 per second wave and spike EEG pattern associated with petit mal is an epiphenomenon dependent upon the maturational stage of development of the brain at the time when the causative lesion responsible for epilepsy is acquired. The view that the 3 per second wave and spike pattern is a direct correlate of the clinical manifestations of epilepsy, in those patients who show this pattern, is challenged. It is concluded that the pattern is the result of rostral brain stem discharge acting upon the cortex. The view is offered that two factors are necessary for the development of epilepsy: (1) an adequate pathological basis in the form of a cerebral lesion and (2) a greater or lesser predisposition toward inadequate biochemical mechanisms tending to check or control the spread of seizure discharge, the latter being in all probability at least partially genetically determined. It is concluded that triggering cortical foci exist in nearly all cases of epilepsy, though the participation of brain stem structures is essential to explain many of the clinical and EEG manifestations of the attack.
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PMID:The distinction between absence petit mal and psychomotor seizures. 82 98

We evaluated the ability of preoperative radiologic imaging to detect hippocampal sclerosis in 31 patients who underwent surgery for intractable epilepsy. Hippocampal sclerosis is commonly associated with surgically treatable temporal lobe epilepsy. It is pathologically described as neuronal cell loss with associated gliosis in the hippocampus. While previous reports have correlated imaging results with clinical or qualitative histologic findings, this study used quantitative pathologic criteria (neuronal cell density) to diagnosis hippocampal sclerosis. We focused our study on the 11 patients with cryptogenic temporal lobe epilepsy. Of these, nine had hippocampal sclerosis by pathologic criteria. MR findings included unilateral hippocampal atrophy, an increased signal in the hippocampus on long TR scans, and atrophy in the adjacent white matter and temporal lobe. Hippocampal atrophy was most frequently seen in the red nucleus plane on coronal scans, corresponding to the body of the hippocampus. We also compared hippocampal size on MR with neuronal density in surgical specimens of the 11 patients with cryptogenic temporal lobe epilepsy. A statistically significant correlation was found between MR size and neuronal density in CA3 and CA4 of the cornu ammonis and the granular cell layer of the hippocampus. Since temporal lobectomy eliminated seizures in seven of nine patients with hippocampal sclerosis, preoperative diagnosis by MR has important therapeutic consequences.
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PMID:Imaging findings in hippocampal sclerosis: correlation with pathology. 195 Sep 25

The value of magnetic resonance imaging in the detection of hippocampal sclerosis has been controversial. We studied 10 patients aged 22.5 +/- 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 T2-weighted 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 +/- 4 months.
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PMID:Hippocampal sclerosis in temporal lobe epilepsy demonstrated by magnetic resonance imaging. 201 85

Cognitive functions were examined before operation and 4 weeks after operation with respect to pathology in 40 patients who underwent temporal lobectomy for epilepsy. Hippocampal sclerosis was associated with febrile convulsions, an earlier onset of regular seizures, poorer preoperative intelligence and with a tendency towards greater cognitive improvement across the operation than found in patients with tumour-like malformations or non-specific pathology. Damage to the amygdala was associated with a poorer outcome for the retention in memory of verbal and non-verbal material. The absence of any specific abnormality in the resected tissue was not associated with a poorer cognitive outcome 4 weeks after the operation.
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PMID:Relationships between neuropathology and cognitive functioning in temporal lobectomy patients. 357 31

The relationship between hippocampal sclerosis, febrile seizures, and complex partial seizures in temporal lobe epilepsy continues to be the subject of great debate in the literature. Hippocampal sclerosis is reported infrequently in young children with temporal lobe epilepsy, a factor that has supported the theory that hippocampal sclerosis develops in later life during the course of recurrent complex partial seizures. In a blinded review of magnetic resonance imaging in 53 children, aged 2-17 years (mean: 10 years) with temporal lobe epilepsy, hippocampal sclerosis was diagnosed in 30 children (57%), concordant with ictal electroencephalographic lateralization in 93% and pathologic diagnosis in all children who had undergone surgery and had hippocampal tissue available for histologic examination. Fourteen of the children (47%) with hippocampal sclerosis were younger than 10 years of age, the youngest being 2 years. Thirty-four children (64%) had histories of neurologic insults prior to the onset of complex partial seizures, including idiopathic febrile seizures in 22. Hippocampal sclerosis was associated with a history of a neurologic insult prior to the onset of complex partial seizures (P < .001) and was not associated with age at onset of temporal lobe epilepsy, age at magnetic resonance imaging, duration of epilepsy, or presence of secondarily generalized seizures. These findings suggest that hippocampal sclerosis is underdiagnosed in children and is the cause and not the consequence of temporal lobe epilepsy.
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PMID:Febrile seizures and hippocampal sclerosis: frequent and related findings in intractable temporal lobe epilepsy of childhood. 761 85

Hippocampal sclerosis involves the selective loss of some hippocampal cell populations, in a process that may disturb the excitatory/inhibitory balance of the remaining cells and produce the epileptic focus. Endfolium sclerosis is the minimal common pathological change found in epileptic patients with hippocampal damage. This subtle lesion is characterized by extensive dentate hilar cell loss without a similarly severe loss of dentate granule cells or hippocampal pyramidal neurons. We attempted to reproduce endfolium sclerosis experimentally by producing dentate granule cell seizure discharges with focal electrical stimulation in anesthetized rats, thus avoiding generalized seizure activity and motor convulsions. With this model, dentate hilar neurons and CA3 pyramidal cells were selectively and irreversibly injured, replicating the pattern of human endfolium sclerosis, with hilar cell damage and survival of dentate granule cell layer GABA-containing basket cells. This results in permanent granule cell disinhibition and hyperexcitability. Excitatory deafferentation of GABAergic basket cells was probably secondary to the loss of hilar mossy cells that normally excite the GABA neurons, rendering these neurons dormant. I propose that endfolium sclerosis in humans represents a selective loss of intrinsically vulnerable dentate hilar cells that normally govern dentate granule cell excitability and that this process leads to epileptiform discharges.
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PMID:Hippocampal pathology and pathophysiology in temporal lobe epilepsy. 901 99

MRI has been applied to the investigation of epilepsy for 12 years. The principle role of MRI is in the definition of structural abnormalities that underly seizure disorders. Hippocampal sclerosis may be reliably identified, quantitative studies are useful for research and, in equivocal cases, for clinical purposes. A range of malformations of cortical development (MCD) may be determined. In patients with refractory partial seizures who are candidates for surgical treatment, a relevant abnormality is identifiable using MRI in 85%, it is likely that subtle MCD or gliosis accounts for the majority of the remainder. The proportion of cryptogenic cases will decrease with improvements in MRI hardware, signal acquisition techniques and post-processing methodologies. Functional MRI is used to identify the cerebral areas that are responsible for specific cognitive processes, and is of importance in planning resections close to eloquent cortical areas. Magnetic resonance spectroscopy (MRS) provides a means of investigating cerebral metabolites and some neurotransmitters, non-invasively. The concentrations of N-acetyl-aspartate (NAA), creatine and choline-containing compounds may be estimated using proton MRS. Reduction of the ratio of NAA/(creatine+choline) is a feature of cerebral regions that include epileptic foci. Cerebral concentrations of GABA and glutamate, and the effects of antiepileptic drugs on these, may be estimated. Concentrations of high energy phosphate compounds, inorganic phosphate and pH may be assessed using 31P-MRS. In general, epileptic foci are associated with an increase in pH, increased inorganic phosphate and decreased phosphate monoesters. Carbon-13 spectroscopy promises to be a useful method for investigating cerebral metabolism in vivo. PET may provide data on regional cerebral blood flow (rCBF), glucose metabolism and the binding of specific ligands to receptors. Correlation of functional and structural imaging data is necessary for adequate interpretation. The hallmark of an epileptic focus is an area of reduced glucose metabolism, identified using [18F]fluorodeoxyglucose (18FDG), that is commonly more extensive than the underlying anatomical abnormality. The clinical role of 18FDG-PET requires re-evaluation in the light of the advances in structural imaging with MRI. Specific ligands are used to investigate specific receptors. Benzodiazepine and opioid receptors have been studied most. Reduced benzodiazepine receptor binding is commonly seen at an epileptic focus, in a more restricted distribution than an area of hypometabolism. Focal increases and decreases in benzodiazepine receptor binding have been demonstrated in MCD in areas that appear normal on MRI, indicating the widespread nature of the abnormalities. It has been found that mu-opioid receptors are increased in temporal neocortex overlying mesial temporal epileptic foci. Dynamic studies of ligand-receptor binding are possible using PET, for example the release of cerebral endogenous opioids has been implied at the time of serial absences. The main use of single photon emission computed tomography (SPECT) is to produce images reflecting rCBF. Interictal studies alone are not reliable. A strength of SPECT is the ability to obtain images related to rCBF at the time of seizures. Concomitant video-EEG recording is necessary. Ictal scans need to be considered in comparison with an interictal scan and an MRI. Interpretation must be cautious, but may yield data that is useful in the investigation of patients for possible surgical treatment.
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PMID:Imaging and epilepsy. 911 80

Corpora amylacea have been reported in around 60% of hippocampal sclerosis specimens. The aim was to determine whether there are clinical and quantitative hippocampal MRI differences between hippocampal sclerosis with and without corpora amylacea. Corpora amylacea density was determined in 46 resected hippocampi of patients with temporal lobe epilepsy, using a three dimensional microscopical counting technique. Forty one hippocampi had hippocampal sclerosis. Twenty six of the 41 (63%) hippocampal sclerosis specimens contained corpora amylacea, which were found in highest numbers in the CA1 subregion of the hippocampus. Corpora amylacea density in the CA1 correlated inversely with the neuronal density in CA1. Hippocampal sclerosis with corpora amylacea had the same clinical and quantitative hippocampal MRI characteristics as hippocampal sclerosis without corpora amylacea, and did not affect seizure outcome after surgery adversely. In conclusion, formation of corpora amylacea seems to be a pathological response to neuronal cell loss in most hippocampal sclerosis specimens, with no clear clinical and quantitative hippocampal MRI correlates.
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PMID:Corpora amylacea in hippocampal sclerosis. 977 10

Two cases of intractable temporal lobe epilepsy associated with old intracerebral hemorrhage in the lateral temporal lobe were reported. Although preoperative magnetic resonance imaging (MRI) failed to reveal hippocampal atrophy with T2 hyperintensity, electrocorticographic (ECoG) recording with chronic invasive subdural electrodes indicated the mesial temporal lobe to be an ictal onset zone. After anterior temporal lobectomy involving the lesion and hippocampectomy, the patients became seizure-free. Hippocampal sclerosis, namely "dual pathology", was not noted on histological examination. Careful ECoG recording with chronic subdural electrodes is mandatory even when the preoperative MRI does not demonstrate the radiological hippocampal sclerosis.
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PMID:[Two cases of mesial temporal lobe epilepsy associated with old intracerebral hemorrhage in the lateral temporal lobe without "dual pathology"]. 962 60

This study compared temporal lobe epilepsy patients, along with kindled animals and self sustained limbic status epilepticus (SSLSE) rats for parallels in hippocampal AMPA and NMDA receptor subunit expression. Hippocampal sclerosis patients (HS), non-HS cases, and autopsies were studied for: hippocampal AMPA GluR1-3 and NMDAR1&2b mRNA levels using in situ hybridization: GluR1, GluR2/3, NMDAR1, and NMDAR2(a&b) immunoreactivity (IR); and neuron densities. Similarly, spontaneously seizing rats after SSLSE, kindled rats, and control animals were studied for: fascia dentata neuron densities: GluR1 and NMDAR2(a&b) IR; and neo-Timm's staining. In HS and non-HS cases, the mRNA hybridization densities per granule cell, as well as molecular layer IR, showed increased GluR1 (relative to GluR2/3) and increased NMDAR2b (relative to NMDAR1) compared to autopsies. Likewise, the molecular layer of SSLSE rats with spontaneous seizures demonstrated more neo-Timm's staining, and higher levels of GluR1 and NMDAR2(a&b) IR compared to kindled animals and controls. These results indicate that hippocampal AMPA and NMDA receptor subunit mRNAs and their proteins are differentially increased in association with spontaneous, but not kindled, seizures. Furthermore, there appears to be parallels in fascia dentata AMPA and NMDA receptor subunit expression between HS (and non-HS) epileptic patients and SSLSE rats. This finding supports the hypothesis that spontaneous seizures in humans and SSLSE rats involve differential alterations in hippocampal ionotrophic glutamate receptor subunits. Moreover, non-HS hippocampi were more like HS cases than hippocampi from kindled animals with respect to glutamate receptors; therefore, hippocampi from kindled rats do not accurately model human non-HS cases, despite some similarities in neuron densities and mossy fiber axon sprouting.
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PMID:Hippocampal AMPA and NMDA mRNA levels and subunit immunoreactivity in human temporal lobe epilepsy patients and a rodent model of chronic mesial limbic epilepsy. 976 17


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