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

Anatomical data now strongly suggest that the common factor in curative ablative operations for the commonest (i.e. ammonshorn-sclerosis) form of temporal-lobe epilepsy is the cutting of the ipsilateral temporoammonic perforant path's "nozzle" where it leaves the entorhinal cortex to "spray" along the length of the ammonshorn. This substantially deafferences ipsilateral dentate granule-cells and hence the unsclerosed pyramidal neurons notably in "resistant sector" CA2, which are probably the source of the seizures. Stereo-chemoding of long-lasting (experimentally tested) chelates along the zone of peculiarly zinc-rich synapses of the mossy fibre system should block the commissural as well as the ipsilateral inputs to these residual neurons, to give higher percentage cures, and could probably be performed bilaterally (where indicated, in adults) without endangering memory function.
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PMID:Anatomical rationale of ablative surgery for temporal lobe seizures and dyscontrol: suggested stereo-chemode chelate-blockade alternative. 79 6

The regional distribution of radioactive ligand binding for different receptors of the gamma-aminobutyric acid A (GABAA)-benzodiazepine-picrotoxin chloride channel complex was measured on tissue section by autoradiography in brains taken from a genetic strain of Wistar rats with spontaneous absence-like seizures, the genetic absence epilepsy rats from Strasbourg (GAERS), and a control colony. The ligands employed included [3H]muscimol for high affinity GABA agonists sites; [3H]SR 95531 for the low-affinity GABA sites; [3H]flunitrazepam for the benzodiazepine sites; and [35S]t-butyl bicyclophosphorothionate (TBPS) for the picrotoxin site. There was no significant change between GAERS and control animals in [3H]flunitrazepam and [35S]TBPS binding. However, there was significantly decreased [3H]muscimol and [3H]SR 95531 binding in the CA2 region of the hippocampus of the GAERS. This was due to a decrease in Bmax of both [3H]muscimol and [3H]SR 95531 binding in the epileptic strain.
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PMID:The GABAA receptor complex in experimental absence seizures in rat: an autoradiographic study. 138 93

Fifty-nine patients with temporal-lobe epilepsy (28 left, 31 right) completed the Boston Naming Test (BNT), verbal subtests of the Wechsler Adult Intelligence Scale-Revised, and the Logical Memory Subtest of the Wechsler Memory Scale (WMS) before surgery. Performances by patients with left temporal seizure foci were significantly more impaired than those of patients with right seizure foci on the WMS Logical Memory subtest and the BNT. After surgical removal of the mesial temporal lobe structures, two blinded observers established volumetric cell densities for hippocampal subfields CA1, CA2, CA3, the hilar area, and the granule cell layer of area dentata. Statistically significant correlations existed only between percent retention scores and hippocampal neuron loss in CA3 and the hilar area for patients with left temporal seizure foci. None of the other dependent measures was significantly correlated with hippocampal neuron density in any subfield. These results support the hypothesis that certain verbal memory impairments are attributable to hippocampal damage specifically, and not to temporal lobe damage in general.
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PMID:Specificity in the correlation of verbal memory and hippocampal neuron loss: dissociation of memory, language, and verbal intellectual ability. 147 37

Magnetic resonance images (MRIs) were obtained from 25 patients with medically refractory epilepsy of temporal lobe origin (12 on the left, 13 on the right) and 14 right-handed control subjects. The hippocampi and temporal lobes were traced by computer on successive coronal images and the resulting measurements of area were summed for each region. The left and right hippocampi were symmetrical in the control subjects; however, for patients the hippocampus was smaller on the side of the seizure focus. Moreover, the left-right hippocampal ratio significantly differentiated the control subjects from each patient group. The left temporal lobe was significantly smaller than the right in control subjects. The epileptics' temporal lobes were smaller on the side of the seizure focus, compared to the temporal lobes in the control subjects. MRI hippocampal measurements were compared to hippocampal neuronal densities obtained postoperatively. Significant correlations were obtained between the ratio (side ipsilateral to focus/side contralateral to focus) of MRI hippocampal measurements and neuronal densities in all hippocampal subfields except CA2. Prior to surgery, patients were administered the Wechsler Memory Scale and the verbal Selective Reminding Test. Significant correlations existed between MRI measurements of the left hippocampus and the Wechsler logical memory percent retention scores and between the left temporal lobe measurements and the verbal Selective Reminding Test scores for patients with seizure foci in the left temporal lobe.
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PMID:Quantitative magnetic resonance imaging in temporal lobe epilepsy: relationship to neuropathology and neuropsychological function. 151 74

The authors examined hippocampal tissue removed during surgical procedures in 17 patients with intractable epilepsy who were found by preoperative magnetic resonance imaging or computerized tomography to have intra-axial masses in the temporal lobe. Neuronal densities in the cornu ammonis (CA) fields of the hippocampus and in the dentate granule cell layer were measured in hematoxylin and eosin-stained sections and were found to be lower compared to a group of 18 autopsy controls. The neuronal densities in all hippocampal fields except CA2 were related to the patient's age at seizure onset. Patients with an earlier onset of seizures had lower neuronal densities. With the exception of CA4, neuronal densities were not significantly related to the duration of the seizure disorder. Cell counts in all fields except CA2 were also related to the location of the lesion in the temporal lobe. Patients with mesial temporal lesions had lower neuronal counts. These results suggest increased vulnerability of hippocampal cytoarchitecture to proximal lesions with early ictal manifestation.
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PMID:Hippocampal pathology in patients with intractable seizures and temporal lobe masses. 156 34

Intrahippocampal injection of 1 nmol ouabain, a sodium/potassium (Na+,K(+)-)ATPase inhibitor, produced a necrotic lesion within 4 days, characterised by a massive invasion by foaming macrophages. A lower dose of ouabain (0.1 nmol) produced a more discrete lesion of all groups of neuronal perikarya in the hippocampus, with only a minimal degree of glial infiltration. The neuronal perikaryal death produced in the subicular, CA1 and CA2 regions was only partially decreased by intraperitoneal injections of the anticonvulsants diazepam and MK-801; these drugs were without effect in the CA3 or hilar interneuronal regions. At neither dose of ouabain was there any indication of neuronal loss in brain regions outside the hippocampus, typically produced by prolonged seizure activity. It is suggested that ouabain has a two-fold action, a release of toxic acidic amino acids and a prolonged depolarization of neurons leading to osmolysis or calcium necrosis.
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PMID:The neurotoxicity of ouabain, a sodium-potassium ATPase inhibitor, in the rat hippocampus. 170 75

The two forms of epileptic brain damage, that found in patients with chronic epilepsy (post-mortem or in an anterior temporal lobectomy specimen) and that occurring acutely after status epilepticus, have much in common but are not identical. Hippocampal lesions occurring acutely after status epilepticus show a high degree of selectivity for hilar interneurones, CA1 pyramidal neurones and CA3 pyramidal neurones. Hippocampal lesions in anterior temporal lobectomy specimens tend to involve the subfields less selectively with CA1 being only slightly more severely affected than dentate granule cells, CA3 and CA2 pyramidal neurones. The most severely damaged hippocampi may result from a combination of acute damage early in life (commonly from prolonged febrile convulsions) and cumulative damage associated with seizures. Less severe degrees of damage are probably a consequence of repeated seizures. The abnormal patterns of firing associated with epileptic activity are almost certainly responsible for cell death occurring acutely after status epilepticus; they may contribute to the progressive cell loss occurring in chronic epilepsy.
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PMID:Excitotoxicity and epileptic brain damage. 179 Jul 73

The intracarotid amobarbital sodium (Amytal) procedure (IAP) was performed for 46 patients with temporal lobe epilepsy (21 with left seizure foci; 25 with right seizure foci). After anteromedial temporal lobectomy, neuronal densities were established for hippocampal subfields CA1, CA2, and CA3; the hilum; and the dentate granule cell layer. Intracarotid amobarbital procedure memory results were related to CA3 neuronal loss only. Patients who did not demonstrate memory after injection contralateral to the seizure focus had significantly fewer cells in CA3 than patients who did. Additionally, a significant correlation was observed between the intracarotid amobarbital procedure memory examination raw score after injection contralateral to the seizure focus and CA3 cell density. Using chi 2 analysis, significant differences were documented in the frequency with which memory was demonstrated after injection contralateral to the seizure focus for groups of patients classified by degree of CA3 neuronal loss. This finding supports prior research showing subfield specificity in some memory processes.
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PMID:The neural substrate of memory impairment demonstrated by the intracarotid amobarbital procedure. 198 26

Thirty-five patients with medically refractory epilepsy localized to the temporal lobe (18 left, 17 right) completed the verbal Selective Reminding Test before surgery. Verbal memory impairments existed before surgery regardless of the lateralization of the seizure focus, but patients with left temporal seizure foci were significantly more impaired. After surgical removal of the mesial temporal lobe structures, 2 blinded observers established volumetric cell densities for hippocampal subfields CA1, CA2, CA3, the hilar area, and the granule cell layer of the area dentata. Statistically significant correlations existed between presurgical memory impairment and cell counts (in CA3 and the hilar area, only) for patients with left temporal seizure foci. These findings support the hippocampal model of memory and complement prior research documenting the memory impairments present after surgical removal of the mesial temporal structures.
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PMID:Verbal memory impairment correlates with hippocampal pyramidal cell density. 223 24

The behavioural effects of tetanus toxin, injected into the rostral hippocampus, have been studied in rats. A single dose (1000 mouse minimum lethal doses; n = 10) of the toxin produced tail rigidity, hunched back and sound- and touch-evoked stimuli, 48 hr after the injection in all rats treated and these culminated in generalized convulsions 5-7 days later. Seizures were also observed 4 days after the injection of 2000 MLDs (n = 10), whereas a dose of 500 MLDs (n = 10) was ineffective. Similarly, dose- and time-dependent lethal effects were observed. In comparison to the contralateral (untreated) hippocampus, tetanus toxin (1000 MLDs; n = 3) produced a statistically significantly reduction in the number of cells in the CA1 pyramidal cell layer of the injected side, 7 and 10 days after the injection. No changes were observed in other sectors (CA2 and CA3 areas) of the hippocampus. In conclusion, the present experiments have shown that the focal injection of tetanus toxin into the hippocampus produced dose- and time-dependent behavioural stimulation and lethal effects in rats.
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PMID:Behavioural and neuropathological effects produced by tetanus toxin injected into the hippocampus of rats. 227 11


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