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Eating seizures and distraction-arousal functions. A case study.

Reports of epileptic seizures evoked by eating are very scarce in the literature. A review of the reported cases suggests that various mechanisms may act as triggering factors in this form of reflex epilepsy. We studied a 17-year-old boy in whom the seizures precipitated by eating had been prevented by giving him some alerting stimuli during the meal. The attention-arousal coupling sustained by the meal seems to play a role in triggering the attacks.

Adolescent↗

Favorable outcome of epileptic blindness in children.

Acute blindness is a rare presentation of epileptic seizures, referring to loss of sight without loss of consciousness associated with electroencephalographic (EEG) epileptic discharges, mainly representing an ictal phase but also either pre- or postictal. We report a series of 14 children with documented epileptic blindness, describing the accompanying fits and thereafter the response to therapy to resolve the blindness and control associated seizures. All patients experienced episodes of acute complete visual obscuration lasting for 1 to 10 minutes. Seven patients hadaccompanying generalized seizures, with a photosensitive response recorded in three of them. All of these seven children were treated with valproic acid, regaining full vision, and six of them became seizure free. Three patients with acute blindness who had accompanying focal motor seizures and unilateral temporooccipital posterior epileptic discharges were treated with carbamazepine regained full vision and complete seizure control. Four additional children had the constellation of migrainous headaches, focal motor phenomena, and complete blindness, along with occipital discharges compatible with Gastaut syndrome, benign childhood epilepsy with occipital paroxysms. All four patients were started on carbamazepine and became asymptomatic. Our overall experience suggests that epileptic blindness in children is associated with a favorable outcome when promptly diagnosed and treated appropriately, resulting in complete resolution of blindness in all children and satisfactory control of seizures in most of them. We therefore recommend performing a prompt EEG in any child presenting with acute visual obscuration, even in the absence of other epileptic phenomena.

Acute Disease↗

[Electroencephalographic diagnosis of the idiopathic generalized epilepsies of childhood].

INTRODUCTION: The idiopathic generalized epilepsies of childhood form a heterogeneous group of epileptic syndromes, with certain clinical and electroencephalographic characteristics in common. From the onset, the seizures affect both cerebral hemispheres with generalized clinical expression and from the start there are bilateral electroencephalographic patterns during seizures. These epilepsies have no known causes, there is a genetic predisposition and relation to the age of onset. The electroencephalographic characteristics during and between seizures have points in common: the basal electroencephalographic activity is normal in all the epilepsies of this group, the paroxystic anomalies are generalized, synchronic and symmetrical, and are formed of bilateral discharges of spikes, multiple spikes, spikes and waves and multiple spikes and waves, with discharges at a frequency of 3 Hz or more. DEVELOPMENT: In this article we review the electroencephalographic characteristics during and between seizures of the idiopathic generalized epilepsies and epileptic syndromes of childhood, with particular emphasis on childhood absences, since we consider this to be the commonest and most representative of the idiopathic generalized epilepsies of infancy. CONCLUSIONS: We consider that the electroencephalographic aspects of epilepsies and the epileptic syndromes make up a factor of great importance as a help in confirmation in diagnosis.

Adolescent↗

Mesial temporal lobe epilepsy with focal photoparoxysmal response.

UNLABELLED: Intermittent photic stimulation (IPS) may produce epileptiform discharges and seizures, most of which are generalized. There are several cases of focal seizures of occipital origin induced by IPS and only five reported cases originating from the temporal lobe (TL). We report an unusual case of TL epilepsy, supported by electroclinical and neuroimaging data, with rhythmic focal TL discharges precipitated by photic stimulus. CASE REPORT: A 37 year old male with refractory epilepsy due to a right mesial temporal sclerosis presented a focal right TL photoparoxysmal response during IPS. A routine, interictal SPECT study obtained with injection of HMPAO, carried out during continuous pulses of the photic stimulus at 16 Hz, disclosed hyperperfusion over the right TL. Presurgical ictal studies demonstrated seizures arising from the same region. A temporal lobectomy rendered the patient seizure-free and further EEGs with IPS were normal. CONCLUSION: To our knowledge, this is the sixth case in medical literature showing evidence of photosensitivity associated with a TL lesion and it is the first in which photic stimulation induced a focal electrographic response of the involved TL. We hypothesize that in rare cases, photosensitivity may be related to a mesial TL lesion without occipital cortex involvement.

Adult↗

The origin of the focal spike in musicogenic epilepsy.

To clarify the pathogenesis of a typical case of musicogenic epilepsy, we examined interictal spikes using the dipole tracing method (DTM). The patient was a 49-year-old, right-handed Japanese man. He first experienced seizures at the age of 32 years; listening to his favorite piece of music frequently triggered them. His seizure type is partial (often complex, but sometimes simple). An interictal EEG examination revealed many focal spikes in F8 and T4. We estimated equivalent current dipoles (ECDs) using DTM. We performed one-dipole analyses on the peaks of the spikes using an EEG analyzer with a three-layer head model called the scalp-skull-brain (SSB) model. We analyzed the interictal EEG because there were no spikes during the seizure. The ECDs were located in the posterior transverse temporal gyrus. The characteristics in this patient not only bolstered arguments in favor of the role of the right temporal lobe in musicogenic epilepsy, but also showed that transverse temporal gyri, which are included in the auditory area, could play an important role in musicogenic epilepsy.

Electroencephalography↗

Synthesis and anticonvulsant properties of 3-(1,3,4-thiadiazol-2-yl) thiazolidin-4-ones.

A series of 2-substituted 3-(1,3,4-thiadiazol-2-yl)thiazolidin-4-ones were synthesized and evaluated for anticonvulsant activity in a genetic model of reflex epilepsy (sound-induced seizures in DBA/2 mice). The combination of preferred substituents in the 2-position coupled with the introduction of a mercapto group on the thiadiazole moiety led to a number of active compounds. The anticonvulsant activity of most derivatives is better than that of the clinically useful anticonvulsant sodium valproate and some of them appear to possess potencies in the same range as phenytoin and clobazam.

Acoustic Stimulation↗

Anticonvulsant action of the beta-carboline abecarnil: studies in rodents and baboon, Papio papio.

Abecarnil (ZK 112119; isopropyl-6-benzyloxy-4-methoxymethyl-beta-carboxylate) is a metabolically stable beta-carboline derivative with potent anxiolytic and few sedative and ataxic effects in rodents. The anticonvulsant and muscle relaxant actions of abecarnil have been evaluated in mice, rats, gerbils and baboons. Abecarnil raised the threshold for tonic electroconvulsions in mice after corneal but not after auricular application, had no effect on maximal electroshock-induced tonic convulsions triggered by either method, protected mice against the tonic hindlimb extension in PTZ-, picrotoxin- and 3-mercaptopropionate-induced seizures and blocked clonus after PTZ, DMCM (methyl-4-ethyl-6,7-dimethoxy-9H-pyrido-(3,4-b)-indol-3-carboxylate) and 3-mercaptopropionate. Abecarnil had no effect on convulsions induced by bicuculline and strychnine. Furthermore, abecarnil blocked kindled seizures after chronic administration of PTZ and FG 7142 (beta-carboline-3-carboxylic acid methylamide) and protected mice and rats against limbic convulsions induced by pilocarpine. Severity and afterdischarge duration of amygdala-kindled seizures were reduced in rats treated with abecarnil. Abecarnil also antagonized selectively convulsions induced by i.c.v. administration of kainate, but not those triggered by N-methyl-D-aspartate or quisqualate. In genetic models of reflex epilepsy, abecarnil was effective against sound-induced convulsions in DBA/2 mice, against air blast-induced generalized seizures in gerbils and against myoclonus in baboons Papio papio. The anticonvulsant effect of abecornil in a PTZ seizure model in mice was potentiated by ethosuximide, whereas no significant potentiation was found with diazepam, clonazepam, diphenylhydantoin, carbamazepine and phenobarbital. Electromyographic monitoring in a etorphine model of muscle rigidity in rats showed no or little muscle relaxant effect of abecarnil.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Kinesigenic choreoathetosis due to brain injury.

This uncommon paroxysmal movement disorder featuring attacks of dystonic spasm with athetoid posturing is usually of idiopathic nature, often familial and starting in childhood. There are a few reported examples due to cerebral pathology, and only four previous cases due to brain trauma. We report here a 21 year old man with left-sided motor spasms, choreoathetoid in type, which were clearly caused by a right frontal penetrating injury with contusion and haemorrhage. The attacks were relieved by phenytoin therapy. In this case, it seems that the post-traumatic paroxysmal kinesigenic choreoathetosis may be a form of reflex epilepsy.

Adult↗

Glutamate receptor GluR1 expression is altered selectively by chronic audiogenic seizures in the Frings mouse brain.

The audiogenic seizure-susceptible mouse, Frings, is genetically susceptible to sound-induced seizures and provides a reliable model of reflex epilepsy that lasts throughout the life span of the animal. We used immunohistochemistry to examine if the expression of the non-N-methyl-D-aspartate glutamate receptor (GluR) subunits GluR1, GluR2, or GluR3 were altered subsequent to multiple seizures. Following a regimen of one seizure per day for 3 weeks, GluR1 immunoreactivity, but not GluR2 or GluR3, was substantially elevated in the outer shell of the nucleus accumbens in 21 of 31 chronically seized Frings mice. No other brain regions such as the hippocampus exhibited any qualitative changes in expression of these subunits. In 9 of the 21 Frings mice exhibiting increased GluR1, but in none of the controls, bilateral structural lesions were observed in the lateral hypothalamus. These results support a model where highly localized changes in the expression of GluR1 occur in response to repeated audiogenic seizure.

Acoustic Stimulation↗

Cortical triggers in generalized reflex seizures and epilepsies.

Activation of specific cortical territories by sensory stimuli or of less restricted areas of the brain by cognitive stimuli is known to induce apparently generalized seizures in predisposed patients; this is clinically and electroencephalographically distinct from reflex triggering of partial seizures. Photosensitive patients may have seizures when exposed to environmental stimuli producing appropriate flickering light or geometric patterns. Some children with benign myoclonic epilepsy in infancy have seizures triggered by unexpected touch or noise. Seizures induced by thinking have been reported in response to non-verbal higher mental activity such as mental arithmetic. Praxis-induced seizures are triggered by similar mental activities accompanied by the use of the hands. Language-induced seizures are usually triggered by verbal higher mental activity. Functional imaging and other methods have contributed to understanding how these seizures arise. Patients with these generalized reflex seizures appear to have regions of cortical hyperexcitability overlapping or coinciding with areas physiologically activated during specific sensory stimulations and cognitive or motor activities. When these areas receive appropriate afferent volleys and a critical mass of cortex is activated, an epileptic activity is produced that ultimately involves cortico-reticular or cortico-cortical pathways resulting in a generalized or bilateral epileptic event.

Cerebral Cortex↗