Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014547 (focal epilepsy)
 1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spreading depression (SD) of EEG activity was elicited by microinjection (5 microliter) of 5% potassium chloride into the caudate nucleus (n = 7) or hippocampus (n = 3) during stereotactic brain surgery in patients with focal epilepsy. An electrode-cannula assembly for eliciting and recording the slow potential waves of SD is described. The parameters of SD in human brain are similar to those in lower mammals. Functional ablation by SD can be used as a diagnostic tool in neurosurgery.
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PMID:Functional ablation by spreading depression: possible use in human stereotactic neurosurgery. 9 40

The mechanisms of the anticonvulsant activity of cannabidiol (CBD) and the central excitation of delta 9-tetrahydrocannabinol (delta 9-THC) were investigated electrophysiologically with conscious, unrestrained cobalt epileptic rats. The well-known antiepileptics, trimethadione (TMO), ethosuximide (ESM), and phenytoin (PHT), were included as reference drugs. Direct measurements were made of spontaneously firing, epileptic potentials from a primary focus on the parietal cortex and convulsions were monitored visually. ESM and TMO decreased the frequency of focal potentials, but PHT and CBD exerted no such effect. Although CBD did not suppress the focal abnormality, it did abolish jaw and limb clonus; in contrast, delta 9-THC markedly increased the frequency of focal potentials, evoked generalized bursts of polyspikes, and produced frank convlusions. 11-OH-delta 9-THC, the major metabolite of delta 9-THC, displayed only one of the excitatory properties of the parent compound: production of bursts of polyspikes. In contrast to delta 9-THC and its 11-OH metabolite, CBD, even in very high doses, did not induce any excitatory effects or convulsions. The present study provides the first evidence that CBD exerts anticonvulsant activity against the motor manifestations of a focal epilepsy, and that the mechanism of the effect may involve a depression of seizure generation or spread in the CNS.
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PMID:The influence of cannabidiol and delta 9-tetrahydrocannabinol on cobalt epilepsy in rats. 11 6

We have described the occurrence in freely moving gerbils of slow potential changes (SPC) in two different models of experimental epilepsy: 1) maximal electroshock and 2) bilateral epileptic foci induced by penicillin. SPC is considered a by-product of epileptiform activity in both models and correlates to the SPC which occurs during spreading depression. In the first model there develops a cortical SPC simultaneous with a depression of EEG activity, although there is no propagation of the wave. We suggest that a non-propagated multifocal depression (MD) occurs in the MES model. In the model of focal epilepsy, all requirements are fulfilled, and the SPC is characterized as the one which occurs during spreading depression propagating with an average velocity of 8 mm/min.
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PMID:Cortical slow potential changes during convulsions induced by maximal electroshock or penicillin focus. 152 70

Penfield's observations in the 1930s provided the first systematic evidence of changes in regional cerebral blood flow (rCBF) associated with focal seizures. Further studies in humans and animals confirmed increases in cerebral blood flow and metabolism during generalised seizures, but the interictal, ictal, and postictal changes in focal epilepsy have begun to be elucidated in the last decade with the advent of in vivo imaging techniques such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) and, in the case of animal studies, of autoradiography. Most studies have been of temporal lobe epilepsy. Interictally, the characteristic finding has been reduced blood flow and/or metabolism in the affected temporal lobe, or more extensively in the ipsilateral hemisphere. The few studies to date of ictal or postictal changes have been of rCBF using SPECT. They show hyperperfusion of the whole temporal lobe ictally, hyperperfusion of the hippocampus, combined with hypoperfusion of lateral structures in the immediate postictal period. Later in the postictal period, hypoperfusion alone is seen. Studies of focal seizures in animals have shown hyperperfusion and hypermetabolism at the site of the focus often with widespread depression of both parameters in the ipsilateral neocortex. Limited studies of coupling between blood flow and metabolism in humans have suggested that flow during seizures is adequate for metabolic demand, although some animal studies have suggested localised areas of uncoupling. The results of modern in vivo imaging of ictal and postictal changes in blood flow and metabolism have correlated well with Penfield's observations, and these changes are now being used to help localise epileptic foci, allowing wider use of the surgical treatment he pioneered.
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PMID:Epilepsy, cerebral blood flow, and cerebral metabolic rate. 162 38

Penetration of cortical spreading depression (SD) into epileptic foci established in the cerebral cortex by penicillin or Metrazol and into electrically stimulated cortical regions was studied in anaesthetized rats. SD suppressed the activity of penicillin foci with low rates of interictal discharge (0.3 Hz) but did not invade more active foci (1 Hz) or foci triggered by electrical stimulation (1-3 Hz). Metrazol foci did not block SD propagation unless stimulated at 6-10 Hz. Repetitive direct cortical responses elicited by 0.05-0.1 msec pulses blocked SD propagation when applied at 6-10 Hz for 5-20 min. The SD blockade covered an area 3-5 mm in diameter around the bipolar stimulating electrodes. The block outlasted the stimulation for several minutes but was fully reversible. New stimulation reinstated the SD blockade after a shorter latency and at lower stimulus intensities and rates. Interaction of the blocked cortical area and SD resulted in anomalous SD propagation, characterized by reentry or circle waves, returning through or around the stimulated region to the recovered cortex. The dynamics of the onset and offset of blocking suggests that SD propagation is prevented by enhanced K+ reabsorption which rapidly removes the K+ ions penetrating the stimulated area from the SD wave front. The interactive phenomena, particularly SD circulation around an epileptic focus, may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy.
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PMID:Blockade of cortical spreading depression in electrically and chemically stimulated areas of cerebral cortex in rats. 615 12

The effects of delta 9-tetrahydrocannabinol (delta 9-THC), two of its metabolites, 8 beta-hydroxy-delta 9-THC and 11-hydroxy-delta 9-THC, and cannabidiol were comparatively studied by means of an iron-induced cortical focal epilepsy in conscious rats with chronically implanted electrodes. delta 9-Tetrahydrocannabinol produced depression of the spontaneously firing epileptic focus, excitatory behavior, generalized after-discharge-like bursts of epileptiform polyspikes and frank convulsions. The pharmacological profiles of the two metabolites differed from that of the parent compound: 11-Hydroxy-delta 9-THC did not precipitate convulsions, but it did elicit all the other effects of delta 9-THC; the 8 beta-hydroxy derivative, on the other hand, exerted only two delta 9-THC-like effects; that is, it evoked polyspike bursts and convulsions. In contrast, cannabidiol, even in large doses (100 mg/kg) was devoid of all the effects of delta 9-THC. Furthermore, pretreatment with cannabidiol markedly altered the responses to delta 9-THC in the following ways: focal depression was partially blocked, polyspike activity was enhanced and convulsions abolished. Phenytoin pretreatment elicited similar effects, but it failed to block the delta 9-THC-induced convulsions. In general, the cannabinoids exhibit a wide spectrum of CNS effects ranging from focal depression to convulsions; specifically, however, the pharmacological profile of each agent can differ markedly; for example, the convulsant properties of delta 9-THC are not a universal characteristic of this class of drugs.
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PMID:Central excitatory properties of delta 9-tetrahydrocannabinol and its metabolites in iron-induced epileptic rats. 627 53

A 13-year-old mentally retarded boy suffered from repeated vomiting attacks since infancy. Each episode lasted 2 to 10 days, and was precipitated by respiratory infection, exercise or stress. During an attack he became irritated, agitated and amnesic, but did not have headaches or seizures. Associated findings were transient elevation of serum creatine kinase (CK) (331-3381 IU/l), and of plasma ACTH and cortisol. The raised CK level was the result of muscle hypertonicity. Ictal EEGs showed delta activity in the front-temporal areas, and inter-ictal IMP-SPECT revealed hypoperfusion in both temporal regions. Unlike the periodic ACTH-ADH discharge syndrome, neither hypertension nor depression developed. These attacks were diagnosed as a migraine equivalent and were suppressed with phenytoin. From the EEG and SPECT findings, we concluded that the vomiting and behavioural changes were related to the paroxysmal vascular abnormality in the temporal regions, but it was not easy to make the distinction between migraine and focal epilepsy. Before a diagnosis of the periodic ACTH-ADH discharge syndrome is made, the possibility of migraine equivalent should be considered.
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PMID:Cyclic vomiting and elevation of creatine kinase associated with bitemporal hypoperfusion and EEG abnormalities: a migraine equivalent? 962 97

Depression is a frequent psychiatric symptom in epilepsy and has been related to epilepsy of temporal origin, especially of left-sided foci. No study differentiated the precise localization of the epileptogenic lesion within the temporal lobe. Regarding this issue, we evaluated depression assessed by the Beck Depression Inventory in 60 patients with temporal lobe epilepsy, with particular consideration of morphological abnormalities within the temporal lobe (mesial temporal sclerosis (MTS) versus neocortical lesions) and lateralization of the lesion. Multivariate analyses indicated significant higher depression scores in MTS independent of the lateralization of the lesion. Depression was a good indicator for MTS but not vice versa. Hence, MTS can be discussed as a predisposing factor for the development of mood disorders in focal epilepsy.
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PMID:Depression in patients with temporal lobe epilepsy is related to mesial temporal sclerosis. 1075

Interictal electroencephalography (EEG) potentials in focal epilepsies are sustained by synchronous paroxysmal membrane depolarization generated by assemblies of hyperexcitable neurons. It is currently believed that interictal spiking sets a condition that preludes to the onset of an ictal discharge. Such an assumption is based on little experimental evidence. Human pre-surgical studies and recordings in chronic and acute models of focal epilepsy showed that: (i) interictal spikes (IS) and ictal discharges are generated by different populations of neuron through different cellular and network mechanisms; (ii) the cortical region that generates IS (irritative area) does not coincide with the ictal-onset area; (iii) IS frequency does not increase before a seizure and is enhanced just after an ictal event; (iv) spike suppression is found to herald ictal discharges; and (v) enhancement of interictal spiking suppresses ictal events. Several experimental evidences indicate that the highly synchronous cellular discharge associated with an IS is generated by a multitude of mechanisms involving synaptic and non-synaptic communication between neurons. The synchronized neuronal discharge associated with a single IS induces and is followed by a profound and prolonged refractory period sustained by inhibitory potentials and by activity-dependent changes in the ionic composition of the extracellular space. Post-spike depression may be responsible for pacing interictal spiking periodicity commonly observed in both animal models and human focal epilepsies. It is proposed that the strong after-inhibition produced by IS protects against the occurrence of ictal discharges by maintaining a low level of excitation in a general condition of hyperexcitability determined by the primary epileptogenic dysfunction.
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PMID:Interictal spikes in focal epileptogenesis. 1116 21

Purpose. We sought to determine the prevalence of psychiatric conditions, particularly panic disorder, in epilepsy patients with ictal fear.Methods. A consecutive series of 12 patients with ictal fear underwent psychiatric evaluation, via either formal consultation with a psychiatrist or standardized interview using the Mini International Neuropsychiatric Interview; the latter was addended to create an instrument specifically for use in epilepsy patients (MINI-Epi).Results. Four of the twelve patients (33%) with ictal fear had a comorbid diagnosis of panic disorder. One of these developed panic attacks only after epilepsy surgery, and another worsened after surgery, while in the other two panic attacks were not related to any surgical procedure. Two patients had other anxiety disorders. Eight patients (67%) had current or past depression; this did not appear to be related to the presence of panic disorder.Conclusion. A specific comorbidity exists between focal epilepsy with ictal fear and panic disorder. Involvement of the amygdala in both temporal lobe epilepsy and panic disorder may underlie this. The predisposition to panic disorder in these patients may be exacerbated by anterior temporal lobectomy.
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PMID:Comorbidity of ictal fear and panic disorder. 1260 30


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