Cases reported "epilepsy, frontal lobe"

Filter by keywords:



Retrieving documents. Please wait...

1/115. Extremely acute phenytoin-induced peripheral neuropathy.

    PURPOSE: Peripheral neuropathy is a rare adverse effect associated with phenytoin (PHT), and it usually occurs after the prolonged use of PHT. Acute PHT-induced peripheral neuropathy is extremely rare. methods: An 18-year-old girl was admitted for the control of epilepsy. Just a few hours after the administration of PHT, she complained of distal lower-extremity paresthesia in a stocking distribution and motor weakness: the achilles tendon reflex was absent. RESULTS: Electrophysiological studies revealed slightly reduced sensory-conduction velocity and mild prolongation of distal latency in the lower extremities. After the discontinuation of PHT, these symptoms disappeared gradually, and sensory-conduction velocity and distal latency became normal. CONCLUSIONS: Although it has been reported that peripheral neuropathy occurred after treatment with PHT for a week, there has been no report of a patient such as ours, who developed peripheral neuropathy just a few hours after the initial administration of PHT. The underlying mechanism remains unknown; however, we should pay attention to such extremely acute peripheral neuropathy when using PHT. ( info)

2/115. Confirmation of two magnetoencephalographic epileptic foci by invasive monitoring from subdural electrodes in an adolescent with right frontocentral epilepsy.

    PURPOSE: To report our evaluation of interictal two epileptic spike fields on magnetoencephalography (MEG) by using invasive intracranial monitoring in a patient without lesion on magnetic resonance imaging (MRI). methods: A 15-year-old left-handed boy with a 9-year history of refractory simple partial seizures, secondarily generalized, and a normal MRI, was studied with MEG to define magnetic spike sources, followed by invasive intracranial monitoring with subdural electrodes to delineate the epileptogenic zone and eloquent function pursuant to focal cortical excision. RESULTS: MEG demonstrated two spike foci on the right middle frontal and inferior rolandic areas adjacent to the sensory area. Ictal recordings during prolonged invasive monitoring from subdural electrodes revealed two epileptogenic zones in the same locations as those defined by MEG. Focal cortical excision was performed of each epileptogenic zone. The patient has been seizure free for 24 months without neurologic deficit. CONCLUSIONS: Magnetic source imaging is a valuable adjunct in the planning of subdural grid placement in epilepsy surgery, particularly in patients in whom conventional imaging fails to reveal a lesion. ( info)

3/115. A case of startle epilepsy and SSMA seizures documented with subdural recordings.

    PURPOSE: To study the mechanisms of startle-induced supplementary sensorimotor area (SSMA) seizures. methods: We present a patient investigated with indwelling subdural grid electrodes covering both the SSMA and the dorsolateral frontal lobe. RESULTS: We found a simultaneous seizure onset in the right dorsolateral premotor cortex and the right SSMA. High-resolution magnetic resonance imaging (MRI) showed a small subcortical lesion adjacent to the right SSMA. The patient became seizure free after resection of the lesion and the ictal-onset zone. CONCLUSIONS: We conclude that an extended region of abnormally excitable tissue within the frontal lobe could facilitate the generation of startle-induced seizures. We speculate that a widespread epileptogenic zone could help to explain why some patients with SSMA or dorsolateral frontal lobe seizures are more likely to have startle-induced seizures. ( info)

4/115. Motiveless firesetting: implicating partial limbic seizure kindling by revived memories of fires in "Limbic Psychotic Trigger Reaction".

    23 unselected juvenile firesetters (M age 12.0 yr.) consisted of seven with schizophrenia, three with organic mental disorder, six with posttraumatic stress disorder, two with severe mental retardation, and two with conduct disorders. Three previously nondestructive boys (M age 11.0 yr.), all of them loners, did not fit such traditional diagnoses. Their fleeting (c. 20 min.) symptoms included flat affect, autonomic arousal, and delusions or hallucinations. It appeared that their motiveless, unplanned acts were each preceded by a chance encounter with an individualized stimulus which revived the three boys' repeatedly ruminated memories of intermittently experienced merely moderate stresses associated with fire, smoke, or matches. Such a sequence of events is characteristic of seizure kindling. One boy's abnormal EEG was congruent with seizures in the temporal lobe area, which includes the amygdala, i.e., that part of the limbic system particularly susceptible to seizure kindling. The three boys' consistent symptomatology was very similar to that reported for 17 men with bizarre homicidal acts implicating a kindled partial seizure called "Limbic Psychotic Trigger Reaction." In primates, too, similar partial nonconvulsive "behavioral seizures" with psychosis-like symptoms can be elicited through experiential kindling. ( info)

5/115. Circling seizures in a case with Wilson's disease.

    We report a case of Wilson's disease with circling seizures. Because of the existence of other types of frontal automatism and the EEG focus on the frontal regions, circling seizures of the patient were thought to originate from the frontal lobe. magnetic resonance imaging demonstrated large cavitary lesions on bilateral frontal lobes. The mechanisms of circling behavior are discussed in association with Wilson's disease. ( info)

6/115. Electroclinical picture of autosomal dominant nocturnal frontal lobe epilepsy in a Japanese family.

    PURPOSE: Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is the first described partial epilepsy syndrome known to be due to a single gene mutation. We found a first Japanese ADNFLE family with a novel mutation of the neuronal nicotinic acetylcholine receptor (nAChR) alpha4 subunit (CHRNA4) gene. The aim of this report is precisely to describe the electroclinical manifestations of ADNFLE in this family and to compare these findings with those of other families reported previously in the literature. methods: Three affected family members were investigated electroclinically by close clinical observation, interictal EEG, video-EEG monitoring, magnetic resonance imaging, and single-photon-emission tomography. Information about other affected family members was obtained from either the spouse or the parents. Mutations within the CHRNA4 gene were examined in seven family members. RESULTS: The clinical manifestations and diagnostic findings in the members of this family were consistent with ADNFLE. However, there were intrafamilial and interfamilial variations in clinical features. The seizures of the patients were brief tonic seizures, with hyperventilation in children and secondarily generalized tonic-clonic convulsions in adults. The onset of the children's seizures began in infancy and early childhood. The children's seizures were sometimes provoked by movement and sound stimulation, and did not respond to antiepileptic drugs. On the other hand, the adults' seizures disappeared spontaneously or were easily controlled with carbamazepine. Three children showed hyperactivity, and two children had mild mental retardation. All patients had impaired consciousness during their seizures and no auras. A novel missense mutation (c755C>T) in exon 5 of the CHRNA4 gene was found in four affected family members. CONCLUSIONS: The electroclinical pictures of a Japanese family with ADNFLE were basically the same as those of other families reported, but with slight differences. ADNFLE is probably not uncommon, and it is very likely that there are unidentified patients with this inherited disorder in japan. ( info)

7/115. Systematic approach to dipole localization of interictal EEG spikes in children with extratemporal lobe epilepsies.

    OBJECTIVES: To assess the reliability of dipole localization based on residual variances (RV), using equivalent current dipole analysis of interictal EEG spikes in children with extratemporal lobe epilepsy. methods: Four pediatric patients with extratemporal lobe epilepsy were studied. Digital EEG was recorded from 19 scalp electrodes. Computer programs for spike detection and clustering analysis were used to select spikes. Dipoles were calculated 5 times for each spike using different initial guesses by the moving dipole model. Standard deviation (SD) of the dipole positions was calculated at each time point in the 5 trials. RESULTS: We analyzed the dipoles at 1097 time points from 4 patients. Among 106 time points with RV < 2%, the SD was < 1 mm in 78 (74%), while in those with SD > 1 mm the dipole positions varied between 2.8 and 52.6 mm. Of dipoles with RV < 1%, 26 of 27 (96%) had an SD < 1 mm; the one dipole with SD > 1 mm varied within 2.5 mm. The dipole localizations with RV < 2% corresponded to the epileptogenic zones identified on intracranial invasive video EEG and intraoperative ECoG. CONCLUSIONS: The systematic approach of equivalent current dipole analysis using spike detection, clustering analysis, and an RV < 2% as a standard is useful for identifying extratemporal epileptic regions. ( info)

8/115. Secondary bilateral synchrony due to fronto-mesial lesions. An invasive recording study.

    frontal lobe epilepsies may present difficulties in focus localization in the pre-operative work-up for epilepsy surgery. This is specially true in patients with normal MRIs. We report on a 16 years-old girl that started with seizures by the age of 8 years. They were brief nocturnal episodes with automatisms such as bicycling and boxing. Seizure frequency ranged from 4-10 per night. scalp EEG showed few right frontal convexity spiking and intense secondary bilateral synchrony (SBS). High resolution MRI directed to the frontal lobes was normal. Ictal SPECT suggested a right fronto-lateral focus. Ictal video-EEG showed no focal onset. She was submitted to invasive recordings after subdural plates implantation. electrodes covered all the frontal convexity and mesial surface bilaterally. Ictal recordings disclosed stereotyped seizures starting from the right mesial frontal. Using a high-resolution tool to measure intra and interhemispheric latencies, the timing and direction of seizure spread from the right fronto-mesial region were studied. Motor strip mapping was performed by means of electrical stimulation. She was submitted to a right frontal lobe resection, 1.5 cm ahead of the motor strip and has been seizure free since surgery (8 months). Pathological examination found a 4 mm area of cortical dysplasia. Invasive studies are needed to allow adequate localization in patients with non-localizatory non-invasive work-up and may lead to excellent results in relation to seizures after surgery. ( info)

9/115. Drug-induced changes in cerebral glucose consumption in bifrontal epilepsy.

    PURPOSE: Positron emission tomography (PET) using 18F-radiolabeled deoxyglucose (18F-FDG) is a sensitive procedure for detection of epileptogenic foci. Although alterations in glucose consumption are not restricted to the area of seizure generation itself, the magnitude and extent of cerebral metabolic disturbances induced by epileptic discharges can be detected. Despite two decades of epilepsy research using 18F-FDG-PET, little is known about the metabolic changes during therapy of focal epilepsy. We report on a child with frontal epilepsy with severe glucose hypometabolism that was nearly completely normalized during drug therapy. methods: Interictal 18F-FDG-PET was performed at the onset of epilepsy and after optimized drug therapy in a 5-year-old boy with behavioral abnormalities and repetitive seizures of frontal origin with bifrontal interictal EEG slowing for 8 weeks. Both scans were anatomically matched; initial and intratherapeutic glucose metabolism were compared. RESULTS: In accordance with the epileptogenic focus as identified by EEG and ictal/interictal perfusion single-photon emission tomography (SPECT), bifrontal hypometabolism was depicted by 18F-FDG-PET. magnetic resonance imaging (MRI) was unremarkable. After dual-drug therapy (valproate, carbamazepine), the boy became seizure free, and his initial behavioral deficits disappeared. A control PET study after 3 months of therapy showed restored glucose consumption; the frontal EEG slowing was normalized. CONCLUSIONS: This case demonstrates that reduction of glucose metabolism in epileptogenic foci may be a result of reversible neuronal dysfunction that correlates with the electroclinical follow-up. ( info)

10/115. Chronological progression of a language deficit appearing to be postictally reversible in a patient with symptomatic localization-related epilepsy.

    A language deficit occurring interictally, with chronological progression, and postictally in a patient with symptomatic localization-related epilepsy, which began at 1.6 years of age, is reported. The patient was a 30-year-old right-handed man whose seizures seemed to originate from the left frontal lobe and to involve the left temporal lobe. The deficit in oral language consisted mainly of features of motor aphasia, including delayed initiation of speech with great effort, echolalic and palilalic tendencies, and word-finding difficulty, but he also showed features of sensory aphasia. Written language had agraphia observed in sensory aphasia, including well-formed letters, paraphasias, neologisms, and paragrammatism. Postictally, the language deficit appeared to be superficially reversible, and evolved from mutism through non-fluent jargon to the interictal level of language. Analysis of the patient's diaries from 10 to 26 years of age disclosed chronologically progressive deterioration of language with paragrammatism, showing an increase of grammatical errors, neologismus, literal and verbal paraphasias and misconstruction of sentences. The results suggest that localization-related epilepsy of presumably left frontal lobe origin causes not only a postictal language deficit but also a slowly progressive deficit of language function. ( info)
| Next ->


Leave a message about 'Epilepsy, Frontal Lobe'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.