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Query: UMLS:C0014547 (focal epilepsy)
 1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A detection of structural changes in the brain of epileptic patients is of importance to the choice of therapeutical management. Incidence and character of lesions in CT-scans of the skull were analysed in the random group of epileptic patients. Normal areas in CT-scans were prevailing in young patients. Atrophic lesions to the brain increased with the patients' age and duration of the disease. Normal results were obtained in post-traumatic epilepsy and that of unknown etiology similarly to atrophic lesions whereas localized lesions were found in all patients with cerebral tumors. Partial epilepsy, especially of short duration, was characterized by high incidence of localized lesions. Normal EEG records were rare in patients with localized lesions detected with CT-scans whereas normal CT-scans may be related to abnormal EEG record. Presence of the localized lesions in some patients and atrophic areas did not limit clinical results of monitored therapy. CT-scanning of the skull should be performed in case of all patients with epilepsy even if there are no significant changes in EEG records or clinical status.
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PMID:[Computerized tomography of the head in patients with epilepsy]. 281 64

The generation of focal cortical epilepsy as observed in human partial complex seizures is presumably due to enhanced physiologic responses or paroxysmal depolarization shifts (PDSs). However, the molecular mechanism that underlies these phenomena remains unknown. It could be due to a genetically determined error in a structural or regulatory protein or to posttranslational events that modulate membrane excitability. Since neither neuronal PDSs or interictal EEG spikes are sufficient to produce clinical epilepsy, the clinical expression of epilepsy may need the breakdown of neuronal or glial mechanisms that limit the spread of seizures. Hence, biochemical membrane studies of neurons and glia are necessary to understand the expression of human and experimental epilepsy. This chapter will review the role of glia in controlling neuronal excitability and neuron-glia relationships in experimental and human epilepsy. Data exploring the hypothesis that glial control of extracellular K+ or (K+)o is deficient in focal epilepsy induced by cold lesions will be reviewed. The role of glial carbonic anhydrase (CA) and glial control of putative amino acid transmitters in audiogenic epilepsy will be discussed. In the cold lesion, (K+)o activation constants of synaptosomal (Na+,K+)-ATPase are significantly decreased in the actively firing chronic focus, suggesting that the apparent affinity of the synaptosomal enzyme for K+ was increased within epileptic tissue that was actively firing. Interestingly, while sustained focal paroxysms could raise synaptosomal (Na+,K+)-ATPase, glial (Na+,K+)-ATPase and its activation by (K+)o remained decreased during sustained paroxysms in both acute and chronic lesions. Moreover, while the decrease of the absolute level of glial enzyme activity was less evident 45 days after lesion production, the poor response of glial enzyme to (K+)o never reversed to "normal" values. Hence, these experiments provided new information that glial (Na+,K+)-ATPase responds to K+ in a different manner when compared to synaptic enzyme. Glial ATPase and its activation by (K+)o remain decreased in either actively discharging acute lesions or in the indolent chronic foci. This could mean a reduction in the ability of glial membranes to maintain (K+)o homeostasis. As already suggested by Dichter, the impairment in glial control of elevated (K+)o could be mainly responsible for the transition of interictal discharges to ictal episodes, within the primary and the secondary foci.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuron-glia relationships in human and experimental epilepsy: a biochemical point of view. 287 19

This chapter reviews the chemical kindling model of epilepsy and speculates on its significance. Both human and experimental epilepsies are extremely heterogeneous, and it is unlikely that a single molecular or cellular mechanism can account for such a diversity of behavioral manifestations. Recent studies of chemical kindling favor the view that in this model, epilepsy is a property of neuronal networks that can take place in a structurally intact brain and does not depend on the presence of gross or microscopic brain damage. Kindling can be obtained by daily injections of nanomolar amounts of multiple muscarinic agonists in selective brain regions such as the amygdala and, once acquired, it is very persistent and frequently accompanied by spontaneous seizures. No evidence exists for creation of a novel pathway, and studies of seizure threshold suggest the need for a critical mass of neurons even on initial stimulation. The amounts of muscarinic agents injected are small enough to have little recordable effect initially, and the number of stimulations needed varies directly with the dose and inversely with the interstimulus interval. Carbachol kindling is inhibited by picomolar amounts of muscarinic antagonists, and the relative potencies of drugs on the kindling behavior in vivo parallel their affinity for muscarinic receptors in vitro. The (+) isomer of acetyl-beta-methylcholine, with good affinity for the muscarinic receptor, can induce kindling, whereas the (-) stereo isomer with poor affinity for the receptor cannot. No morphological differences are observed between animals injected with the (+) or the (-) isomer. These experiments suggest that the development of chronic focal epilepsy can take place in a structurally intact brain, be independent of the production of brain damage, and totally dependent on synaptic excitation. In other words, in this model, epilepsy may be a disease of cell-cell communication in which structurally normal neurons develop epileptiform responses as their interactions are modified through synaptic activation. A study of the relationships between carbachol and electrical kindling of the same site gave different results depending on the site of stimulation. In the amygdala, no interaction was found, but when both stimuli were aimed at the cholinoceptive hippocampal cells, a strong facilitation in both directions was observed. Thus, it appears that chemical and electrical kindling share similar mechanisms and that cross-facilitation depends on the existence of a common anatomy. The same anticonvulsants that block electrical kindling also inhibit chemical kindling.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Synaptic mechanisms in the kindled epileptic focus: a speculative synthesis. 287 22

The cellular phenomena underlying focal epilepsy are currently understood in the context of contemporary concepts of cellular and synaptic function. Interictal discharges appear to be due to a combination of synaptic events and intrinsic currents, the exact proportion of which in any given neuron may vary according to the anatomic and functional substrate involved in the epileptic discharge and the epileptogenic agent used in a given model. The transition to seizure appears to be due to simultaneous increments in excitatory influences and decrements in inhibitory processes--both related to frequency-dependent neuronal events. A variety of specific hypotheses have been proposed to account for the increased excitability that occurs during epileptiform activity. Although each of the proposed mechanisms is likely to contribute significantly to the epileptic process, no single hypothesis provides an exclusive unifying framework within which all kinds of focal epilepsy can be understood. The spread of epileptic activity throughout the brain, the development of primary generalized epilepsy, the existence of "gating" mechanisms in specific anatomic locations, and the extrapolation of hypotheses derived from simple models of focal epilepsy to explain more complex forms of human epilepsy, all are not yet fully understood.
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PMID:Cellular mechanisms of epilepsy: a status report. 303

Identical twins concordant for partial epilepsy, with onset at 8 and 11 years of age, are presented. Their course has been benign on anticonvulsant therapy. It is suggested that these cases of presumed genetic epilepsy support current concepts of cortical origin and genetic determinants in several subtypes of focal epilepsy of childhood.
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PMID:Partial seizures in monozygous twins. 308 20

The contemporary neuroanatomist has a number of available methods to analyze epileptic brain tissue. Many studies have utilized Nissl- and Golgi-stained preparations to determine that gliosis and neuronal loss occur at epileptic foci as well as a decrease in the dendritic spine density. These structural changes did not reveal any specific basic mechanism that may cause epileptic activity. In contrast, the relatively newer techniques in neurocytology provide functional data that relate to the physiology and chemistry of the brain tissue. The use of immunocytochemical, histochemical, and receptor ligand-binding autoradiographic methods have aided in the understanding of cellular neurochemistry in both normal and epileptic tissue. In addition, the use of intracellular horseradish peroxidase and recording and quantitative morphological methods at both light- and electron-microscopic levels has helped gain insights into the functional state of synapses and neurons. Together, these methods have been utilized to help unravel the mystery of epilepsy. Our laboratory has utilized immunocytochemical and quantitative light- and electron-microscopic methods to analyze four models of epilepsy; two resemble posttraumatic focal epilepsy, and the other two are genetic models of epilepsy. Our data indicate that a preferential loss of cortical GABAergic, inhibitory terminals occurs at posttraumatic epileptic foci. In contrast, the genetic models of epilepsy did not display a loss of GABAergic terminals. Instead, specific brain regions of epileptic animals had an increased number of GABAergic neurons and terminals. These data indicate that two different neuronal circuits may provide the anatomical substrate for epileptic activity: loss of inhibition and disinhibition.
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PMID:Contemporary methods in neurocytology and their application to the study of epilepsy. 308 36

Computed EEG Topography (CET) of 74 cases of epilepsy demonstrates the potential utility of this method beyond that of the analog EEG for the quantification and localization of regions of epileptogenesis. For the detection and localization of focal epilepsy, CET was equal to or better than the EEG in 77 p. 100 of cases and provided more evidence of focal abnormality in 8.5 p. 100. The topography of spectral power and of early and late, extravisual, components of the averaged evoked potential to flash were abnormal in the region of interictal spike activity.
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PMID:Computed EEG topography in epilepsy. 311 43

Intensive neuromonitoring of seizure surgery candidates, with its associated medication withdrawal, involves increased seizure susceptibility. This can cause a confusing array of seizure patterns. This problem was examined in the candidates for seizure surgery in the Austin Hospital Comprehensive Epilepsy Programme, emphasis being placed on focal seizures. Generalized seizures were very common. Eleven (15%) patients showed multiple focal seizure patterns. Seven patients showed temporal lobe seizures originating from either side separately. Three showed persistent frontal and temporal complex partial seizures. One patient showed 2 separate species of focal epilepsy. Whilst the simplest and most effective way out of this diagnostic problem was close consultation and video review with parent or spouse, this process was ineffective in 6 of 11 patients. In patients with bitemporal lobe epilepsy there was often little to distinguish the fit coming from one side from that coming from the other and often elements of the fit from either side were recognized by the relative. In all patients with frontal and temporal complex partial seizures, elements of the seizure had been seen previously and in only 1 was there any preponderance on neuromonitoring. Therefore it is suspected that the confusing seizure detail seen on intensive neuromonitoring may in fact exist in real life and render the clinical history suspect--a problem which can be avoided only by initial neuromonitoring.
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PMID:Intensive neuromonitoring for complex partial seizures: focal seizure pattern variability in surgical patients. 311 58

Psychiatric morbidity was assessed in a sample of 88 adult epileptic patients drawn from general practices in South London. Using the Clinical Interview Schedule, 48% emerged as psychiatric cases. When either total CIS score or caseness status was used for comparison, group differences were evident; patients with temporal lobe epilepsy and focal non-TLE did not differ, but each was significantly more impaired than those with primary generalised epilepsy. The groups also differed in their psychiatric symptom profiles. The results suggest that the increased prevalence of interictal psychopathology commonly associated with TLE may also be a feature of other forms of focal epilepsy.
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PMID:Relationship between interictal psychopathology and the type of epilepsy. Results of a survey in general practice. 311 98

In 150 consecutive cases of simple partial epilepsy significant CT abnormalities were found in 68%. The commonest lesion noted was a hypodense lesion on unenhanced scan, with a ring or disc-like enhancement on contrast scan, and surrounding hypodensity. This lesion was seen in 39 cases and was more common in patients below the age of 15 years and in those with shorter duration of fits (less than 6 months). Nineteen of these cases had focal signs, 16 showed focal slow activity on EEG and 17/39 had neither signs nor focal slowing on EEG. Ten cases with a ring or disc enhancing lesion had evidence of tuberculosis elsewhere in the body, three more had a past history of tuberculosis and four others had a history of close contact with a case of tuberculosis. After 3 months of antitubercular treatment, 23 out of 25 patients who were rescanned showed clearing of the lesion. The two who did not were operated upon, and the lesion was shown histologically to be a tuberculoma. Ten other cases have done well, but have not been rescanned. Only one case was not treated with antitubercular therapy. She developed fits, altered consciousness, and meningitis and recovered from this serious illness after starting antitubercular therapy. Though not histologically verified, it seems justified to conclude that in India a ring or disc enhancing lesion is the commonest accompaniment of focal epilepsy, and that at least one third (and probably more) of these lesions are tuberculomas.
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PMID:Focal epilepsy in India with special reference to lesions showing ring or disc-like enhancement on contrast computed tomography. 311 75


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