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Epileptic Seizures (epileptic + seizures)

Distribution by Scientific Domains

Medical Sciences	84%
Life Sciences	12%
2 Other Domains	4%

Selected Abstracts

Epileptic Seizures Superimposed on Catatonic Stupor

EPILEPSIA, Issue 4 2006
Kazumasa Suzuki
Summary:,Purpose: Some patients with nonconvulsive status epilepticus are known to exhibit catatonic stupor. Thus it is necessary to rule out ictal catatonia by electroencephalography in patients with catatonic stupor. However, few reports are available on epileptic seizures superimposed on catatonic stupor. Methods: We report three cases of epileptic seizures superimposed on psychiatric catatonic stupor without a prominent predisposing factor, including high fever or encephalitis. None of the patients had a personal or family history of neurologic disease, including epilepsy. Results: In all three patients, catatonic stupor persisted after resolution of the epileptic seizures with administration of phenytoin. In two of the three patients, catatonic stupor resolved with electroconvulsive therapy, which caused no marked adverse effects. Conclusions: Because it is possible that catatonic stupor itself predisposes patients to the development of epileptic seizures, electroencephalographic examinations in patients with catatonic stupor are indispensable for early recognition not only of nonconvulsive status epilepticus but also of epileptic seizures superimposed on catatonic stupor. Electroconvulsive therapy deserves consideration when catatonic stupor persists after resolution of epileptic seizures. [source]

Epilepsy in Colombia: Epidemiologic Profile and Classification of Epileptic Seizures and Syndromes

EPILEPSIA, Issue 1 2006
Alberto Velez
Summary:,Purpose: A national study was performed in Colombia to determine the general and regional prevalence of epilepsy, clinical profiles, seizure types, and clinical syndromes. Methods: Based on the National Epidemiological Study of Neurological Diseases (EPINEURO), we evaluated and followed up for 1 year all the subjects with epilepsy from the National Sample. Clinical profiles were further assessed. Seizure types and epilepsy syndromes were established according to the international classifications. Results: General prevalence was found to be 11.3 per 1,000, with little variation among regions, except the eastern region, where prevalence was 23 per 1,000; prevalence for active epilepsy was 10.1 per 1,000. Women have a slightly greater (not statistically significant) risk. Most seizures are focal (partial), frequently with secondary generalization. The most frequent epilepsy syndrome encountered was partial symptomatic/cryptogenic (80%). Epilepsy onset in Colombia occurs most frequently in childhood. Conclusions: Prevalence rates of epilepsy in Colombia are similar to those reported in nations with comparable developmental status and have diminished over time. The study presents the distribution of seizures and syndromes. The most frequent types are focal syndromes. [source]

Epileptic Seizures and Epilepsy

EPILEPSIA, Issue 10 2005
S. Nizam Ahmed
No abstract is available for this article. [source]

On the Definition of Epileptic Seizures and Epilepsy

EPILEPSIA, Issue 10 2005
Juan Gomez-Alonso
No abstract is available for this article. [source]

Evidence for a Role of the Parafascicular Nucleus of the Thalamus in the Control of Epileptic Seizures by the Superior Colliculus

EPILEPSIA, Issue 1 2005
Karine Nail-Boucherie
Summary:,Purpose: The aim of this study was to investigate whether the nucleus parafascicularis (Pf) of the thalamus could be a relay of the control of epileptic seizures by the superior colliculus (SC). The Pf is one of the main ascending projections of the SC, the disinhibition of which has been shown to suppress seizures in different animal models and has been proposed as the main relay of the nigral control of epilepsy. Methods: Rats with genetic absence seizures (generalized absence epilepsy rat from Strasbourg or GAERS) were used in this study. The effect of bilateral microinjection of picrotoxin, a ,-aminobutyric acid (GABA) antagonist, in the SC on the glutamate and GABA extracellular concentration within the Pf was first investigated by using microdialysis. In a second experiment, the effect of direct activation of Pf neurons on the occurrence of absence seizures was examined with microinjection of low doses of kainate, a glutamate agonist. Results: Bilateral injection of picrotoxin (33 pmol/side) in the SC suppressed spike-and-wave discharges for 20 min. This treatment resulted in an increase of glutamate but not GABA levels in the Pf during the same time course. Bilateral injection of kainate (35 pmol/side) into the Pf significantly suppressed spike-and-wave discharges for 20 min, whereas such injections were without effects when at least one site was located outside the Pf. Conclusions: These data suggest that glutamatergic projections to the Pf could be involved in the control of seizures by the SC. Disinhibition of these neurons could lead to seizure suppression and may be involved in the nigral control of epilepsy. [source]

Hyperventilation and Epileptic Seizures

EPILEPSIA, Issue 12 2004
S. Nizam Ahmed
No abstract is available for this article. [source]

Heart Rate Changes and ECG Abnormalities During Epileptic Seizures: Prevalence and Definition of an Objective Clinical Sign

EPILEPSIA, Issue 8 2002
Maeike Zijlmans
Summary: ,Purpose: To determine the prevalence of heart rate changes and ECG abnormalities during epileptic seizures and to determine the timing of heart rate changes compared to the first electrographic and clinical signs. To assess the risk factors for the occurrence of ECG abnormalities. Methods: We analyzed retrospectively 281 seizures in 81 patients with intractable epilepsy who had prolonged video-EEG and two-channel ECG. The nature and timing of heart rate changes compared to the electrographic and clinical seizure onset was determined. The ictal period (including one minute preictally and three minutes postictally) was analyzed for cardiac arrhythmias, conduction and repolarization abnormalities. Risk factors for cardiac abnormalities were investigated using parametric and non-parametric statistics. Results: There was an increase in heart rate of at least 10 beats/minute in 73% of seizures (93% of patients) and this occurred most often around seizure onset. In 23% of seizures (49% of patients) the rate increase preceded both the electrographic and the clinical onset. ECG abnormalities were found in 26% of seizures (44% of patients). One patient had an asystole for 30 seconds. Long seizure duration increased the occurrence of ECG abnormalities. No other risk factor was found. Conclusions: Heart rate changes occur frequently and occur around the time or even before the earliest electrographic or clinical change. The change can clarify the timing of seizure onset and the specific rate pattern may be useful for seizure diagnosis and for automatic seizure detection. ECG abnormalities occur often and repeatedly in several seizures of the same patient. [source]

Epileptic Seizures after Treatment with Thiocolchicoside

EPILEPSIA, Issue 8 2001
Pier Luigi De Riu
Summary: ,Purpose: To report the occurrence of epileptic seizures in humans, closely related to the use of the centrally acting muscle relaxant thiocolchicoside. Methods: Description of three case histories. Results: Two patients, affected with complex-partial seizures, sometimes secondarily generalized, receiving antiepileptic therapy, were seizure free for 7 and 9 years, respectively. They had the reappearance of tonic,clonic seizures few days after the continued use of thiocolchicoside, at a cumulative dose of the drug of 52 mg and 76 mg, respectively. The third patient was brain damaged and without a history of seizures. He had a sudden, convulsive seizure a few minutes after 4 mg intramuscular thiocolchicoside. Conclusions: Our case histories indicate that thiocolchicoside has a powerful epileptogenic activity. This drug should be avoided in patients with epilepsy or acute brain injury and possible disruption of the blood,brain barrier. [source]

A Proposed Diagnostic Scheme for People with Epileptic Seizures and with Epilepsy: Report of the ILAE Task Force on Classification and Terminology

EPILEPSIA, Issue 6 2001
Jerome Engel Jr.
First page of article [source]

The Midline Thalamus: Alterations and a Potential Role in Limbic Epilepsy

EPILEPSIA, Issue 8 2001
Edward H. Bertram
Summary: ,Purpose: In limbic or mesial temporal lobe epilepsy, much attention has been given to specific regions or cell populations (e.g., the hippocampus or dentate granule cells). Epileptic seizures may involve broader changes in neural circuits, and evidence suggests that subcortical regions may play a role. In this study we examined the midline thalamic regions for involvement in limbic seizures, changes in anatomy and physiology, and the potential role for this region in limbic seizures and epilepsy Methods: Using two rat models for limbic epilepsy (hippocampal kindled and chronic spontaneous limbic epilepsy) we examined the midline thalamus for evidence of involvement in seizure activity, alterations in structure, changes in the basic in vitro physiology of the thalamic neurons. We also explored how this region may influence limbic seizures. Results: The midline thalamus was consistently involved with seizure activity from the onset, and there was significant neuronal loss in the medial dorsal and reuniens/rhomboid nuclei. In addition, thalamic neurons had changes in synaptically mediated and voltage-gated responses. Infusion of lidocaine into the midline thalamus significantly shortened afterdischarge duration. Conclusions: These observations suggest that this thalamic region is part of the neural circuitry of limbic epilepsy and may play a significant role in seizure modulation. Local neuronal changes can enhance the excitability of the thalamolimbic circuits. [source]

Neurologic manifestations of ulcerative colitis

EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2007
R. Scheid
Ulcerative colitis (UC) has traditionally been considered to be an inflammatory disease limited to the colonic mucosa. However, since it has been shown that UC is frequently accompanied by various extraintestinal disorders, there is increasing evidence that UC may also manifest in the nervous system. The following review focuses particularly on these possible manifestations of UC, both in the peripheral (PNS), and in the central nervous system (CNS). A systematic literature search according to the MEDLINE database was performed for this purpose. Although a reliable differentiation may clinically not always be possible, three major pathogenic entities can be differentiated: (i) cerebrovascular disease as a consequence of thrombosis and thromboembolism; (ii) systemic and cerebral vasculitis; (iii) probably immune mediated neuropathy and cerebral demyelination. With the exception of thromboembolism and sensorineural hearing loss, evidence for a causal relationship relies merely on single case reports or retrospective case series. Considering the CNS-manifestations, similarities between UC-associated disorders of the white matter and acute disseminated encephalomyelitis (ADEM) are obvious. Epileptic seizures, unspecified encephalopathies and confusional states are most likely epiphenomena that have to be regarded symptomatic rather than as own entities. A prospective study on the neurologic aspects of UC would be very welcome. [source]

Noninvasive dynamic imaging of seizures in epileptic patients

HUMAN BRAIN MAPPING, Issue 12 2009
Louise Tyvaert
Abstract Epileptic seizures are due to abnormal synchronized neuronal discharges. Techniques measuring electrical changes are commonly used to analyze seizures. Neuronal activity can be also defined by concomitant hemodynamic and metabolic changes. Simultaneous electroencephalogram (EEG)-functional MRI (fMRI) measures noninvasively with a high-spatial resolution BOLD changes during seizures in the whole brain. Until now, only a static image representing the whole seizure was provided. We report in 10 focal epilepsy patients a new approach to dynamic imaging of seizures including the BOLD time course of seizures and the identification of brain structures involved in seizure onset and discharge propagation. The first activation was observed in agreement with the expected location of the focus based on clinical and EEG data (three intracranial recordings), thus providing validity to this approach. The BOLD signal preceded ictal EEG changes in two cases. EEG-fMRI may detect changes in smaller and deeper structures than scalp EEG, which can only record activity form superficial cortical areas. This method allowed us to demonstrate that seizure onset zone was limited to one structure, thus supporting the concept of epileptic focus, but that a complex neuronal network was involved during propagation. Deactivations were also found during seizures, usually appearing after the first activation in areas close or distant to the activated regions. Deactivations may correspond to actively inhibited regions or to functional disconnection from normally active regions. This new noninvasive approach should open the study of seizure generation and propagation mechanisms in the whole brain to groups of patients with focal epilepsies. Hum Brain Mapp, 2009. © 2009 Wiley-Liss, Inc. [source]

Aromatic l -amino acid decarboxylase deficiency associated with epilepsy mimicking non-epileptic involuntary movements

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 11 2008
Susumu Ito MD
Aromatic l -amino acid decarboxylase (AADC) deficiency is a rare inborn error of neurotransmitter biosynthesis that leads to a combined deficiency of catecholamines and serotonin and is characterized by global developmental delay, involuntary movements, and autonomic dysfunction. We report the case of an 11-year-old male patient with AADC deficiency who also had epileptic spasms and generalized tonic seizures with asymmetrical features, in addition to frequent involuntary non-epileptic movements. The clinical manifestation of the epileptic attacks apparently resembled that of non-epileptic attacks. It was difficult to differentiate between both attacks without the help of an ictal electroencephalographic study. The epileptic attacks were finally controlled by appropriate antiepileptic drugs. Because an association with epileptic seizures is uncommon in AADC deficiency, some cases may have been regarded as involuntary non-epileptic movements. This indicates that the differentiation of epileptic attacks from non-epileptic ones is indispensable for the adequate treatment of patients with AADC deficiency. [source]

Ring chromosome 20 syndrome with intractable epilepsy

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 5 2005
Asude Alpman MD
Ring chromosome 20 (r[20]) syndrome is characterized by mild to moderate learning disability*, behavioural disorders, epilepsy, and various dysmorphic features. Although still considered rare, r(20) syndrome is being increasingly diagnosed. More than 30 cases have been described in the literature since 1976. Here we report an additional case of a 14-year-old male with r(20). He had moderate to severe learning disability and epileptic seizures manifesting at about 18 months of age. During the 13 years' follow-up period he showed intractable epileptic seizures, behavioural disorders, and mild dysmorphological features including microcephaly, strabismus, micrognathia, down-slanting eyelids, and ear abnormalities. Frequent episodes of atypical absence or non-convulsive status associated with electroencephalogram changes were seen in follow-up. He was treated with several classical and new antiepileptic drugs, including intravenous immunoglobulin, corticotropin, and vagal nerve stimulation, with unsuccessful control of seizures. Finally, surgical treatment (corpus callosotomy) was performed at the age of 13 years; severity of tonic seizures was diminished, but frequency was unchanged. Although his behavioural problems, e.g. hyperactivity, were mild in early childhood they became more severe when he was 11 years old. Aggressiveness, compulsiveness with self-injury, and panic attacks developed at the age of 13 years, and were more pronounced after callosotomy. This case report provides the first description of deterioration in psychological situation in patients with r(20) intractable epilepsy. The patient was diagnosed with r(20) syndrome after 13 years of clinical follow-up. Karyotype analysis should, therefore, be performed in every patient with intractable epilepsy of unknown aetiology. [source]

Familial partial epilepsy with variable foci: A new family with suggestion of linkage to chromosome 22q12

EPILEPSIA, Issue 9 2010
José Morales-Corraliza
Summary Familial partial epilepsy with variable foci (FPEVF) is an autosomal dominant form of partial epilepsy characterized by the presence of epileptic seizures originating from different cerebral lobes in different members of the same family. Linkage to chromosomes 22q12 and 2q36 has been reported, although only six families have been published. We studied a new FPEVF family including nine affected individuals. The phenotype in this family was similar to that previously described and consisted of nocturnal and daytime seizures with semiology suggesting a frontal lobe origin. A video-EEG (electroencephalography) recording of the proband's seizures is presented and revealed hyperkinetic seizures of frontal lobe origin preceded by left frontal spikes. We excluded linkage to chromosome 2q36 and found a suggestion of linkage to chromosome 22q12 with a lod score of 2.64 (, = 0) for marker D22S689. [source]

Evidence of shared genetic risk factors for migraine and rolandic epilepsy

EPILEPSIA, Issue 11 2009
Tara Clarke
Summary Purpose:, Evidence for a specific association between migraine and rolandic epilepsy (RE) has been conflicting. Children with migraine frequently have electroencephalographic (EEG) abnormalities, including rolandic discharges, and approximately 50% of siblings of patients with RE exhibit rolandic discharges. We assessed migraine risk in RE probands and their siblings. Methods:, We used cohort and reconstructed cohort designs to respectively assess the relative risk of migraine in 72 children with RE and their 88 siblings using International Classification of Headache Disorders (ICHD-2) criteria. Incidences were compared in 150 age and geographically matched nonepilepsy probands and their 188 siblings. We used a Cox proportional hazards model, using age as the time base, adjusting hazard ratios (HRs) for sex in the proband analysis, and for sex and proband migraine status in the sibling analysis. Results:, Prevalence of migraine in RE probands was 15% versus 7% in nonepilepsy probands, and in siblings of RE probands prevalence was 14% versus 4% in nonepilepsy siblings. The sex-adjusted HR of migraine for an RE proband was 2.46 [95% confidence interval (CI) 1.06,5.70]. The adjusted HR of having ,1 sibling with migraine in an RE family was 3.35 (95% CI 1.20,9.33), whereas the HR of any one sibling of a RE proband was 2.86 (95% CI 1.10,7.43). Discussion:, Migraine is strongly comorbid in RE and independently clusters in their siblings. These results suggest shared susceptibility to migraine and RE that is not directly mediated by epileptic seizures. Susceptibility gene variants for RE may be tested as risk factors for migraine. [source]

The effects of intracerebroventricular AM-251, a CB1-receptor antagonist, and ACEA, a CB1-receptor agonist, on penicillin-induced epileptiform activity in rats

EPILEPSIA, Issue 7 2009
Ramazan Kozan
Summary Purpose:, Several results support the conclusion that the cannabinoid system has a role in generation and cessation of epileptic seizures. The aim of this study was to evaluate the effects of intracerebroventricular AM-251 [N -(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide], a CB1-receptor antagonist, and ACEA (arachidonyl-2-chloroethylamide), a CB1-receptor agonist, on penicillin-induced epileptiform activity in rats. Methods:, In the first set of experiments, 30 min after penicillin injection, AM-251, at doses of 0.125, 0.25, 0.5, and 1 ,g, was administered intracerebroventricularly (i.c.v.). In the second set of experiments, 30 min after penicillin injection, ACEA, at doses of 2.5, 5, 7.5, and 15 ,g (i.c.v.), was administered. In the third set of experiments, AM-251, at doses of 0.125 and 0.25 ,g (i.c.v.), was administered 10 min before ACEA (7.5 ,g, i.c.v.) injection. Results:, ACEA, at a dose of 7.5 ,g, significantly decreased the frequency of penicillin-induced epileptiform activity without changing the amplitude. ACEA, at doses of 2.5, 5, and 15 ,g, had no impact on either frequency or amplitude of epileptiform activity. AM-251, at doses of 0.25 and 0.50 ,g, significantly increased the frequency of epileptiform activity. AM-251, at a dose of 0.25 ,g (i.c.v.), was the most effective in changing the frequency of penicillin-induced epileptiform activity, and it also caused status epilepticus,like activity. AM-251, at doses of 0.125 and 0.25 ,g, 10 min before ACEA (7.5 ,g), reversed the anticonvulsant action of ACEA. Discussion:, The results of the present study provide electrophysiologic evidence for the role of CB1 receptors in regulating the frequency of epileptiform activity in the model of penicillin-induced epilepsy. To elucidate the precise mechanism of cannabinoid action in the brain during seizure, more advanced electrophysiologic and neurochemical studies are required. [source]

Experimental epileptology before 1900

EPILEPSIA, Issue 3 2009
Mervyn J. Eadie
Summary The available English and other major Western European language literature was reviewed to assess the stage of development of experimental epileptology prior to the end of the 19th Century. The relevant investigations had been carried out in animals of various species employing a number of methods of evoking convulsive seizures, mainly mechanical, electrical or chemical stimulation or surgical removal of parts of the cerebral cortex. The studies had produced some conflicting data but (i) allowed the development of a number of reasonably satisfactory experimental models of convulsive epileptic seizures (ii) confirmed that such epileptic seizures arose from the cerebral cortex, and (iii) suggested that for local onset epileptic seizures to become generalised tonic-clonic ones, the opposite motor cortex and probably a brain stem, possibly pontine, centre needed to be involved. No generally acceptable animal model of chronic epilepsy had been developed, and the non-motor manifestations of epileptic seizures were still largely unexplored experimentally. Nevertheless, the pre-1900 investigations not only laid the foundations for the 20th Century expansion of experimental studies on epileptogenesis but also advanced the understanding of epileptic seizure production. [source]

Epileptiform synchronization in the cingulate cortex

EPILEPSIA, Issue 3 2009
Gabriella Panuccio
Summary Purpose:, The anterior cingulate cortex (ACC),which plays a role in pain, emotions and behavior,can generate epileptic seizures. To date, little is known on the neuronal mechanisms leading to epileptiform synchronization in this structure. Therefore, we investigated the role of excitatory and inhibitory synaptic transmission in epileptiform activity in this cortical area. In addition, since the ACC presents with a high density of opioid receptors, we studied the effect of opioid agonism on epileptiform synchronization in this brain region. Methods:, We used field and intracellular recordings in conjunction with pharmacological manipulations to characterize the epileptiform activity generated by the rat ACC in a brain slice preparation. Results:, Bath-application of the convulsant 4-aminopyridine (4AP, 50 ,M) induced both brief and prolonged periods of epileptiform synchronization resembling interictal- and ictal-like discharges, respectively. Interictal events could occur more frequently before the onset of ictal activity that was contributed by N -methyl- d -aspartate (NMDA) receptors. Mu-opioid receptor activation abolished 4AP-induced ictal events and markedly reduced the occurrence of the pharmacologically isolated GABAergic synchronous potentials. Ictal discharges were replaced by interictal events during GABAergic antagonism; this GABA-independent activity was influenced by subsequent mu-opioid agonist application. Conclusions:, Our results indicate that both glutamatergic and GABAergic signaling contribute to epileptiform synchronization leading to the generation of electrographic ictal events in the ACC. In addition, mu-opioid receptors appear to modulate both excitatory and inhibitory mechanisms, thus influencing epileptiform synchronization in the ACC. [source]

Seizures in multiple sclerosis

EPILEPSIA, Issue 6 2008
Marcus Koch
Summary Seizures have long been recognized to be part of the disease spectrum of multiple sclerosis (MS). While they occur in only a minority of patients with MS, epileptic seizures can have serious consequences. The treatment of MS can be epileptogenic, and antiepileptic treatment can conversely worsen the symptoms of MS. In this article we present an overview of the current literature on the epidemiology, clinical presentation, pathology, imaging, prognosis and treatment of epileptic seizures in MS. [source]

Clinical picture of EPM1-Unverricht-Lundborg disease

EPILEPSIA, Issue 4 2008
Reetta Kälviäinen
Summary Unverricht-Lundborg disease (ULD), progressive myoclonic epilepsy type 1 (EPM1, OMIM254800), is an autosomal recessively inherited neurodegenerative disorder characterized by age of onset from 6 to 16 years, stimulus-sensitive myoclonus, and tonic,clonic epileptic seizures. Some years after the onset ataxia, incoordination, intentional tremor, and dysarthria develop. Individuals with EPM1 are mentally alert but show emotional lability, depression, and mild decline in intellectual performance over time. The diagnosis of EPM1 can be confirmed by identifying disease-causing mutations in a cysteine protease inhibitor cystatin B (CSTB) gene. Symptomatic pharmacologic and rehabilitative management, including psychosocial support, are the mainstay of EPM1 patients' care. Valproic acid, the first drug of choice, diminishes myoclonus and the frequency of generalized seizures. Clonazepam and high-dose piracetam are used to treat myoclonus, whereas levetiracetam seems to be effective for both myoclonus and generalized seizures. There are a number of agents that aggravate clinical course of EPM1 such as phenytoin aggravating the associated neurologic symptoms or even accelerating cerebellar degeneration. Sodium channel blockers (carbamazepine, oxcarbazepine) and GABAergic drugs (tiagabine, vigabatrin) as well as gabapentin and pregabalin may aggravate myoclonus and myoclonic seizures. EPM1 patients need lifelong clinical follow-up, including evaluation of the drug-treatment and comprehensive rehabilitation. [source]

Dense array EEG: Methodology and new hypothesis on epilepsy syndromes

EPILEPSIA, Issue 2008
Mark D. Holmes
Summary Dense array EEG is a method of recording electroencephalography (EEG) with many more electrodes (up to 256) than is utilized with standard techniques that typically employ 19,21 scalp electrodes. The rationale for this approach is to enhance the spatial resolution of scalp EEG. In our research, dense array EEG is used in conjunction with a realistic model of head tissue conductivity and methods of electrographic source analysis to determine cerebral cortical localization of epileptiform discharges. In studies of patients with absence seizures, only localized cortical regions are involved during the attack. Typically, absences are accompanied by "wave,spike" complexes that show, both at the beginning and throughout the ictus, repetitive cycles of stereotyped, localized involvement of mainly mesial and orbital frontal cortex. Dense array EEG can also be used for long-term EEG video monitoring (LTM). We have used dense array EEG LTM to capture seizures in over 40 patients with medically refractory localization-related epilepsy, including both temporal and extra temporal cases, where standard LTM failed to reveal reliable ictal localization. One research goal is to test the validity of dense array LTM findings by comparison with invasive LTM and surgical outcome. Collection of a prospective series of surgical candidates who undergo both procedures is currently underway. Analysis of subjects with either generalized or localization-related seizures suggest that all seizures, including those traditionally classified as "generalized," propagate through discrete cortical networks. Furthermore, based on initial review of propagation patterns, we hypothesize that all epileptic seizures may be fundamentally corticothalamic or corticolimbic in nature. Dense array EEG may prove useful in noninvasive ictal localization, when standard methods fail. Future research will determine if the method will reduce the need for invasive EEG recordings, or assist in the appropriate placement of novel treatment devices. [source]

Seizure Outcome after Resection of Supratentorial Cavernous Malformations: A Study of 168 Patients

EPILEPSIA, Issue 3 2007
Christian R. Baumann
Summary:,Purpose: The optimal management of cerebral cavernous malformations (CCMs) with epileptic seizures is still a matter of debate. The aim of our study was to examine seizure outcome in the largest published series of surgically treated patients with epilepsy due to a supratentorial CCM, and to define predictors for good surgical outcome. Methods: We retrospectively studied 168 consecutive patients with a single supratentorial CCM and symptomatic epilepsy in a multicenter study. Pre- and postoperative clinical examinations, age at epilepsy onset, age at operation, type of symptoms due to the CCM (seizures, headache, hemorrhage, focal deficits), type and frequency of epileptic seizures, and the localization and size of the CCM were assessed. Seizure outcome was determined in the first, second, and third postoperative years. Results: The CCM was completely resected in all patients. More than two thirds of the patients were classified as seizure free in the first 3 postoperative years. Predictors for good seizure outcome were age older than 30 years at the time of surgery, mesiotemporal CCM localization, CCM size <1.5 cm, and the absence of secondarily generalized seizures. No mortality occurred in our series, but only mild postoperative neurologic deficits in 12 (7%) patients. Conclusions: Considering the natural history of CCMs, the favorable neurologic and seizure outcome, surgical resection of CCMs should be considered in all patients with supratentorial CCMs and concomitant epilepsy, irrespective of the presence or absence of predictors for a favorable seizure outcome. [source]

Autosomal Dominant Early-onset Cortical Myoclonus, Photic-induced Myoclonus, and Epilepsy in a Large Pedigree

EPILEPSIA, Issue 10 2006
Elena Gardella
Summary:,Purpose: Cortical tremor, a form of rhythmic cortical myoclonus (rhythmic CM), and epilepsy have been described in families with autosomal dominant inheritance. Linkage analyses revealed two putative loci on chromosome 2p and 8q. Clinical photosensitivity was not a prominent feature in such families. We describe a large Italian family with rhythmic CM, photosensitivity, and epilepsy. Methods: Twenty-three individuals of a five-generation family were studied. Linkage analyses for the loci on chromosome 2p11.1 and 8q23.3 were performed. Results: Of the 23 studied family members, 16 were affected. Rhythmic CM of childhood onset was present in all 16 individuals (onset ranging from 3 to 12 years), was associated with photic-induced myoclonic jerks in seven, and with epileptic seizures in six (onset ranging from 23 to 34 years). Five children of the V generation manifested also episodes of arousal with generalized tremor in early infancy ("tremulous arousals"). Jerk-locked back-averaging of rhythmic CM of six affected individuals, documented a premyoclonic EEG correlate. C-reflex at rest was present in two affected adults. Linkage analyses excluded mapping to the 2p11.1 and 8q23.3 loci. Conclusions: Clinical variability and severity of the phenotypes in this family are in line with those of previously described pedigrees with autosomal dominant cortical myoclonus and epilepsy. In this family, a progression of symptoms was found: rhythmic CM and tremulous arousals occurred in childhood, whereas visually induced manifestations and epileptic seizures occurred during adolescence,adulthood. Exclusion of linkage to the two known loci is consistent with genetic heterogeneity of such familial clustering of symptoms. [source]

Epileptic Seizures Superimposed on Catatonic Stupor

Victor Horsley's Contribution to Jacksonian Epileptology

EPILEPSIA, Issue 11 2005
Mervyn J. Eadie
Summary:,Purpose: To describe Victor Horsley's contribution to John Hughlings Jackson's understanding of the mechanisms involved in the generalization of convulsive epileptic seizures. Methods: I reviewed Horsley's writings and other relevant late 19th century medical literature. Results: Horsley's combination of strategically sited surgical lesions and cerebral cortex stimulation studies in experimental animals showed that, contrary to Hughlings Jackson's earlier belief, epileptic activity arising in one cerebral hemisphere had to spread to the contralateral hemisphere before bilateral convulsing could occur. Conclusions: On the basis of well-designed experiments, Horsley made a major contribution to the understanding of epileptic seizure propagation mechanisms. [source]

Nonepileptic Disorders Imitating Generalized Idiopathic Epilepsies

EPILEPSIA, Issue 2005
Natalio Fejerman
Summary:, Differential diagnosis between epileptic and nonepileptic paroxysmal disorders is fundamental not only to allow correct management of patients but also to avoid the burden of unnecessary antiepileptic medication. The focus of this chapter is limited to imitators of idiopathic generalized epilepsies (IGE) which are expressed through myoclonic, tonic,clonic, tonic, atonic, and absence seizures. Apparent losses of consciousness and drop attacks also have to be considered. Benign myoclonus of early infancy is the main nonepileptic disorder in the differential diagnosis of infantile spasms, but is not dealt with here because West syndrome is not an IGE. Hyperekplexia, metabolic disorders, hypnagogic myoclonus, and disturbed responsiveness caused by the use of drugs are listed in Table 1. Other conditions that may imitate more focal epileptic seizures are omitted. Benign neonatal sleep myoclonus, apnea and apparent life-threatening events in infants, cyanotic and pallid breath-holding spells, syncope, staring spells, psychogenic seizures, hyperventilation syndrome, and narcolepsy have been selected based on frequency or difficulties in differential diagnosis with the intention to cover the most conspicuous imitators of IGE in different ages. Table 1. Nonepileptic disorders imitating idiopathic generalized epilepsies [source]

Symptomatic Epilepsies Imitating Idiopathic Generalized Epilepsies

EPILEPSIA, Issue 2005
Hirokazu Oguni
Summary:, The diagnosis of idiopathic generalized epilepsies (IGEs) is not generally difficult if one follows the clinical and electroencephalogram (EEG) definitions of each subsyndrome that constitutes IGEs. In contrast, symptomatic epilepsies develop based on organic brain lesions and are easily diagnosed by the presence of developmental delay, neurologic abnormalities, and a characteristic seizure and EEG pattern. However, in clinical practice, it is sometimes difficult to differentiate IGEs from symptomatic epilepsies, especially when the clinical course from the onset of epilepsy is too short to exhibit typical clinical and EEG findings of either epilepsy type, or when patients with symptomatic epilepsies have atypical features that imitate the clinical characteristics of IGEs. The neurodegenerative or metabolic disorders at times start during the clinical course with epileptic seizures and later show typical neurologic abnormalities. The newly recognized metabolic disorder of glucose transporter type 1 deficiency syndrome (Glut-1 DS) may start with myoclonic seizures at an age of less than 1 year and imitate benign myoclonic epilepsy in infancy early in the clinical course. Progressive myoclonus epilepsies (PMEs) that develop at 1,4 years of age at times imitate epilepsy with myoclonic-astatic seizures with respect to the presence of astatic seizures and an epileptic encephalopathic EEG pattern. In addition, young children with focal cortical dysplasia may also have similar clinical and EEG patterns, although the latter may become localized after treatment. Approximately 15% of patients with juvenile myoclonic epilepsy (JME) are resistant to antiepileptic drugs (AEDs) and may require extensive study to make a differential diagnosis from symptomatic epilepsies. PMEs that develop during adolescence may imitate JME early in the clinical course; however, a detailed history and the differentiation between myoclonic seizures and myoclonus would help to distinguish both conditions. The diagnosis of IGEs is very demanding for patients with atypical features with regard to seizure type, EEG findings, and response to appropriate AEDs. [source]

Cerebral Damage in Epilepsy: A Population-based Longitudinal Quantitative MRI Study

EPILEPSIA, Issue 9 2005
Rebecca S. N. Liu
Summary:,Purpose: Whether cerebral damage results from epileptic seizures remains a contentious issue. We report on the first longitudinal community-based quantitative magnetic resonance imaging (MRI) study to investigate the effect of seizures on the hippocampus, cerebellum, and neocortex. Methods: One hundred seventy-nine patients with epilepsy (66 temporal lobe epilepsy, 51 extratemporal partial epilepsy, and 62 generalized epilepsy) and 90 control subjects underwent two MRI brain scans 3.5 years apart. Automated and manual measurement techniques identified changes in global and regional brain volumes and hippocampal T2 relaxation times. Results: Baseline hippocampal volumes were significantly reduced in patients with temporal lobe epilepsy and could be attributed to an antecedent neurologic insult. Rates of hippocampal, cerebral, and cerebellar atrophy were not syndrome specific and were similar in control and patient groups. Global and regional brain atrophy was determined primarily by age. A prior neurologic insult was associated with reduced hippocampal and cerebellar volumes and an increased rate of cerebellar atrophy. Significant atrophy of the hippocampus, neocortex, or cerebellum occurred in 17% of patients compared with 6.7% of control subjects. Patients with and without significant volume reduction were comparable in terms of seizure frequency, antiepileptic drug (AED) use, and epilepsy duration, with no identifiable risk factors for the development of atrophy. Conclusions: Overt structural cerebral damage is not an inevitable consequence of epileptic seizures. In general, brain volume reduction in epilepsy is the cumulative effect of an initial precipitating injury and age-related cerebral atrophy. Significant atrophy developed in individual patients, particularly those with temporal lobe and generalized epilepsy. Longer periods of observation may detect more subtle effects of seizures. [source]

Biting Behavior, Aggression, and Seizures

EPILEPSIA, Issue 5 2005
Carlo Alberto Tassinari
Summary:,Purpose: To describe the semiologic features of aggressive behaviors observed in human epileptic seizures with particular reference to the act of biting a conspecific. Methods: We analyzed the biting behavior (BB) and other aggressive gestures occurring in a group of 11 patients retrospectively selected from >1,000 patients subjected to video-EEG/SEEG monitoring for presurgical evaluation of drug-resistant seizures. Results: Patients displaying BB showed (a) a male sex predominance, (b) heterogeneous etiologies and lesion locations, and (c) seizures involving the frontotemporal regions of both hemispheres. The act of biting was a rapid motor action, lasting ,600 ms, occurring in the context of strong emotional arousal, fear, and anger, with various bodily gestures with aggressive connotation. BB was mainly a "reflexive" behavior, in that biting acts were evoked (both during and after seizures) by actions of people in close contact with the patient. The sole intrusion of the examiner's hand in the space near the patient's face was effective in triggering BB. Rarely, self-directed or object-directed biting acts were not triggered by external stimuli. Intracranial data (SEEG) obtained in one subject showed that the amygdala/hippocampal region plus the orbitomedial prefrontal cortex had to be involved by ictal activity to observe BB. Conclusions: Anatomic and electrophysiologic data in our patients suggest that a model of dual,temporal and frontal,dysfunction could account for the occurrence of ictal/postictal BB. Behavioral data suggest also that BB and related aggressive gestures can be considered as the emergence of instinctive behaviors with an adaptative significance of defense of the peripersonal space. [source]