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

Preparatory to craniotomy for the relief of medically refractory focal epilepsy, the lateralization of cerebral speech functions was determined by the Wada intracarotid Amytal test in 134 patients with clinical and radiologic evidence of an early left-hemisphere lesion. Their results were compared with those for 262 patients (140 right-handed, 122 left-handed), who were tested in a similar way. One-third of the patients with early lesions were still right-handed, and 81% of these right-handers were left-hemisphere dominant for speech. In the non-right-handers, speech was represented in the left cerebral hemisphere in nearly a third of the group, in the right hemisphere in half the group, and bilaterally in the remainder. Bilateral speech representation was demonstrated in 15% of the non-right-handers without early left-brain injury and in 19% of those with evidence of such early injury, whereas it was extremely rare in the right-handed groups. In addition, nearly half the patients with bilateral speech representation exhibited a complete or partial dissociation between errors of naming and errors in the repetition of verbal sequences after Amytal injection into left or right hemispheres. This points to the possibility of a functionally asymmetric participation of the two hemispheres in the language processes of some normal left-handers. The results of the Amytal speech tests in this series of patients point to locus of lesion as one of the critical determinants in the lateralization of cerebral speech processes after early left-brain injury. It is argued that in such cases the continuing dominance of the left hemisphere for speech in largely contingent upon the integrity of the frontal and parietal speech zones.
Ann N Y Acad Sci 1977 Sep 30
PMID:The role of early left-brain injury in determining lateralization of cerebral speech functions. 10 Nov 16

The controversial relations between migraine and vascular headache on one hand, epilepsy on the other hand are once more discussed: survey of the arguments for a more than fortuitous connexion, taken from literature and general experience. Critical analysis of the personal case material. Discussion of some specific groups of patients with various combinations of both syndromes: long antecedents of headaches, leading up to sporadic epileptic attacks, focal or generalized; clinical seizures under photic stimulation (10% of the cases with chronic headaches without organic lesions); headaches in the latency period of symptomatic epilepsy; cases of seeming transition between the two syndromes; headaches as a substitute, an aura or as a component of the epileptic seizure, with clearly distinctive features between generalized and focal epilepsy: in patients with bilateral EEG paroxysms, headaches are usually diffuse or bilateral, in those with epileptogenic foci, headaches, if consistently localized, are always reported to be homolateral to the focus. Considerations concerning pathogenesis include the familiar hypothesis of hypoxic discharges following migrainous vasoconstriction, as well as secondary vascular headaches induced by focal epileptic activity. Headaches caused by excessive discharges in the sensory representation areas (H. Jackson) must be rare. Whether increased neuronal activity in the hypothalamus may be responsible for the migraine syndrome (Herberg), possibly in connection with biogenic amines, remains in open question.
EEG EMG Z Elektroenzephalogr Elektromyogr Verwandte Geb 1977 Sep
PMID:[Epilepsy and headaches (author's transl)]. 41 Jun 25

Estimation of autospectra and coherence and phase spectra of seizure EEG, using the FFT technique, will cause "smearing" of the rapid dynamic changes which occur during the seizure. This is inherent to FFT spectral estimation, due to the averaging process which is necessary in order to get consistent spectral estimates. A different approach suggested in the present study is to carry out multivariate autoregressive modeling of the multichannel seizure EEG, combined with adaptive segmentation. In order to obtain good estimates in cases of short record length, the vectorial AR modeling was based on residual energy ratios. The method has been tested on multichannel seizure EEG recordings from rats with focal epilepsy, caused by intracerebral administration of Kainic acid, and in depth EEG recordings in patients with temporal lobe epilepsy.
IEEE Trans Biomed Eng 1992 Sep
PMID:On the tracking of rapid dynamic changes in seizure EEG. 147 24

Cerebral single photon emission computed tomography (SPECT), a method of functional brain imaging, measures cerebral blood flow and metabolism. This paper describes the imaging procedure and several cases where cerebral SPECT was of use in the differential diagnosis of medically ill patients who also presented with psychopathology. SPECT patterns in cerebrovascular disease, dementia, focal epilepsy, and AIDS are at present the best described and seem to be the most specific. Often changes in regional cerebral blood flow are seen before structural changes become apparent on CT or MRI. Cerebral SPECT can add valuable diagnostic information in assessing psychopathology in the medically ill and can often lead to changes in treatment.
Gen Hosp Psychiatry 1991 Sep
PMID:The role of SPECT brain imaging in assessing psychopathology in the medically ill. 174 99

Immunocytochemical localization of glutamic acid decarboxylase (GAD), the synthesizing enzyme for the neurotransmitter gamma-aminobutyric acid (GABA), has been used to study the time course of the decrease in putative GABAergic synaptic terminals that occurs in an alumina gel-induced model of focal epilepsy. Monkeys were studied at progressive intervals following unilateral application of alumina gel to sensorimotor cerebral cortex, and were categorized into 3 different experimental groups depending upon their clinical status. These groups respectively exhibited: (1) no abnormal bioelectrical (EEG and ECoG) activity; (2) abnormal bioelectrical activity, but no clinical seizures; and (3) both abnormal bioelectrical activity and clinical seizures. Normal and sham-operated monkeys were also studied. The amounts of GAD-positive terminal-like structures were determined on control and experimental sides of motor cortex (layer V) of all specimens with an image analysis system. This quantitative study revealed that monkeys from the 3 experimental groups showed reductions of GAD-positive terminals on the experimental cortical side, with greater losses occurring at progressively longer times following alumina gel implants. Statistical tests showed that there were no significant cortical side differences for the normal and sham groups, but that cortical side variations were significantly different for each of the 3 experimental groups. Conventional electron microscopy of an early experimental stage revealed degenerating axon terminals in layer V of motor cortex, as well as phagocytosis of degenerating material and astrogliosis. Similar findings were obtained from a chronically epileptic specimen, except that degenerating terminals were observed less often and fibrous astrocytic scarring was more prevalent, especially surrounding the somata of pyramidal neurons. The main conclusion drawn from the results of this investigation is that significant decreases of GAD-positive terminals occur prior to the onset of clinical seizures, and this is consistent with a causal role for a loss of GABAergic innervation in the development of seizure activity in this primate model of focal epilepsy.
Brain Res 1986 Sep 24
PMID:Time course of the reduction of GABA terminals in a model of focal epilepsy: a glutamic acid decarboxylase immunocytochemical study. 309 29

Twenty adult male Wistar rats were divided randomly into two groups (10 rats for LM, 10 rats for EM). The experimental rats were injected with convulsive dosage 3.8 microliters (19 micrograms) of coriaria lactone (CL) in the left cerebral motor cortex of the fore limb to induce acute focal epilepsy. The control rats were injected with normal saline of the same volume and at the same location. Motor cortex was cut coronally 2 hours after seizure and the layer V was studied morphometrically. Under x400 and x7000, take photos of focus, parafocus areas respectively for morphometric study. The number of neurons and neuroglias of layer V was counted in the LM photos. The number of presynaptic terminals of the neuropil was counted in the x7000 EM photos and the area fraction of each constitute in the neuropil was measured. The positive results demonstrated that the number of neurons and neuroglias in the focus and parafocus areas of the experimental animals was significantly lower than that in the control group, the side injected was lower than the other side and it was the lowest in the focus. The number and area fraction of the presynaptic terminals of the experimental rats at the focus neuropil decreased significantly, but the area fraction of neuroglial components increased significantly. The authors suggest that the convulsive dosage of CL may have toxic effect on some neurons and neuroglias and therefore to decrease the number of both types of cells and the number and area fraction of presynaptic terminals in the neuropil.(ABSTRACT TRUNCATED AT 250 WORDS)
Hua Xi Yi Ke Da Xue Xue Bao 1994 Sep
PMID:[Morphometric study of motor cortex in acute focal epilepsy rat induced by coriaria lactone]. 789 44

1. The regional cerebral blood flow was studied by SPECT in patients with partial epilepsy before and after 30 days of monotherapy with carbamazepine (CBZ). 2. Both a qualitative visual interpretation and a semiquantitative analysis of SPECT was performed. All patients underwent EEG, CT scan, and MRI studies. The CBZ serum concentrations were assayed. 3. After therapy, in three patients with focal epilepsy, both a crossed cerebral and cerebellar diaschisis were observed, with respect to the side of the epileptic focus in the opposite hemisphere. No morphologic changes were detected at MRI in the cerebral or cerebellar remote hypometabolic areas found at SPECT. 4. CBZ may have a depressant action on the corticopontocerebellar pathways and on the corticocallosal connections.
Prog Neuropsychopharmacol Biol Psychiatry 1995 Sep
PMID:Cerebral and cerebellar diaschisis following carbamazepine therapy. 853 26

Chronic focal epilepsy is associated with synaptic plasticity and growth of new connections. Brain-derived neurotrophic factor (BDNF) is associated with each of these processes in normal brain and shows acute up-regulation in models of generalized epilepsy. Here, using an experimental model of focal epilepsy, we show persistent up-regulation of BDNF mRNA, independent of that of other growth factors, in association with the development and persistence of chronic seizures. In situ hybridization histochemistry revealed that rats perfused within 2-3 days after seizure onset had widespread increases in BDNF mRNA levels in the neocortex. Rats perfused at later times, however, showed focal up-regulation of BDNF mRNA at the injection site and down-regulation in a surrounding cortical zone. Nerve growth factor and neurotrophin-3 mRNAs were not significantly altered. These reciprocal changes in BDNF gene expression in the epileptic focus and the cortical surround may contribute to plastic changes in epileptic neuronal circuits that accompany the transition from acute to chronic epilepsy. BDNF down-regulation in the surround is likely to be associated with the inhibitory surround that hampers seizure spread, but facilitates the persistence of a chronic epileptic focus.
Cereb Cortex 1998 Sep
PMID:Reciprocal up- and down-regulation of BDNF mRNA in tetanus toxin-induced epileptic focus and inhibitory surround in cerebral cortex. 975 12

The limbic/mesial temporal lobe epilepsy syndrome has been defined as a focal epilepsy, with the implication that there is a well defined focus of onset, traditionally centered around the hippocampus. The pathology of the hippocampus in this syndrome has been well described and a number of physiological abnormalities have been defined in this structure in animal models and humans with epilepsy. However, anatomical and physiological abnormalities have also been described in other limbic sites in this form of epilepsy. Previous studies have shown broadly synchronized or multifocal seizure onset within the limbic system of the animal models and human patients. We hypothesized that the epileptogenic circuit for the initiation of seizures was distributed throughout the limbic system with a possible central synchronizing process. In vitro studies showed that multiple limbic sites in epileptic animals (hippocampus, entorhinal cortex, piriform cortex and amygdala) have epileptiform changes with prolonged depolarizations and multiple superimposed action potentials. In vivo studies revealed that thalamic stimulation yields short latency excitatory responses in the entorhinal cortex and hippocampus. In addition, in epileptic animals, thalamic stimulation caused epileptiform responses in the hippocampus. Based on the findings of this study and on previous anatomy and physiology reports, we hypothesize that the process of seizure initiation involves broad circuit interactions involving multiple independent limbic structures, and that the midline thalamus may act as a physiological synchronizer. We offer a new proposal for the functional anatomy of limbic epilepsy that takes widespread hyperexcitability in the limbic system and the potential for thalamic synchronization into consideration.
Epilepsy Res 1998 Sep
PMID:Functional anatomy of limbic epilepsy: a proposal for central synchronization of a diffusely hyperexcitable network. 976 20

A 29-year-old man experienced intractable partial seizures as the initial manifestation of neurosyphilis. The diagnosis was made after the onset of dementia 9 months later. Both the epilepsy and dementia resolved with penicillin therapy. Syphilis should be considered in patients with adult-onset focal epilepsy, particularly if there is associated dementia. Treatment may be successful even when the diagnosis is delayed.
Epilepsia 1999 Sep
PMID:Intractable epilepsy as the initial manifestation of neurosyphilis. 1048 97


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