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Susan S. Spencer - One of the best experts on this subject based on the ideXlab platform.
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Localization-Related Epilepsy exhibits significant connectivity away from the seizure-onset area.
Neuroreport, 2009Co-Authors: Hitten P. Zaveri, Steven M. Pincus, Irina I. Goncharova, Robert B. Duckrow, Dennis D. Spencer, Susan S. SpencerAbstract:In Localization-Related Epilepsy, seizures are presumed to arise from a discrete cortical area. The control of seizures by Epilepsy surgery can be poor, however, even when there has been complete resection of the area identified by standard clinical procedures to give rise to seizures. We used a coherence-based measure of functional connectivity to test for network effects within and outside the seizure-onset area. Connectivity was evaluated from the background intracranial electroencephalogram of six unselected patients. We show significant nonzero connectivity not only for the seizure-onset area but also several centimeters from it, for example, for the beta-frequency band (P
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localization related Epilepsy exhibits significant connectivity away from the seizure onset area
Neuroreport, 2009Co-Authors: Hitten P. Zaveri, Steven M. Pincus, Irina I. Goncharova, Robert B. Duckrow, Dennis D. Spencer, Susan S. SpencerAbstract:In Localization-Related Epilepsy, seizures are presumed to arise from a discrete cortical area. The control of seizures by Epilepsy surgery can be poor, however, even when there has been complete resection of the area identified by standard clinical procedures to give rise to seizures. We used a coherence-based measure of functional connectivity to test for network effects within and outside the seizure-onset area. Connectivity was evaluated from the background intracranial electroencephalogram of six unselected patients. We show significant nonzero connectivity not only for the seizure-onset area but also several centimeters from it, for example, for the beta-frequency band (P<10(-5)), suggesting a nonlocal character to this disorder.
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how long does it take for partial Epilepsy to become intractable
Neurology, 2003Co-Authors: Anne T. Berg, Michael R Sperling, Barbara G. Vickrey, John T. Langfitt, Carl W. Bazil, Thaddeus S. Walczak, Steven V. Pacia, Shlomo Shinnar, Susan S. SpencerAbstract:Background: Much remains unknown about the natural history of intractable Localization-Related Epilepsy, including how long it typically takes before intractability becomes evident. This information could guide the design of future studies, resolve certain discrepancies in the literature, and provide more accurate information about long-term prognosis. Methods: Individuals evaluated for resective surgery for refractory Localization-Related Epilepsy were prospectively identified at the time of initial surgical evaluation at seven surgical centers (between 1996 and 2001). The latency time between onset of Epilepsy and failure of second medication and history of remission (≥1 year seizure-free) before surgical evaluation were examined with respect to age at onset, hippocampal atrophy, febrile seizures, and surgical site. Results: In the 333 patients included in the analysis, latency time was 9.1 years (range 0 to 48) and 26% reported a prior remission before surgery. A prior remission of ≥5 years was reported by 8.5% of study participants. Younger age at onset was strongly associated with longer latency time ( p p Conclusions: A substantial proportion of Localization-Related Epilepsy may not become clearly intractable for many years after onset. This is especially true of Epilepsy of childhood and early adolescent onset. If prospective studies confirm these findings and the underlying mechanisms behind these associations become understood, this raises the possibility of considering interventions that might interrupt such a process and some day prevent some forms of Epilepsy from becoming intractable.
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relationships between seizure severity and health related quality of life in refractory localization related Epilepsy
Epilepsia, 2000Co-Authors: Barbara G. Vickrey, Michael R Sperling, Anne T. Berg, John T. Langfitt, Carl W. Bazil, Thaddeus S. Walczak, Steven V. Pacia, Sehyun Kim, Shlomo Shinnar, Susan S. SpencerAbstract:Summary: Purpose: To evaluate relationships between self-report measures of seizure severity and health-related quality of life (HRQOL) in people with refractory Localization-Related Epilepsy. Methods: A sample of 340 adults enrolled in a seven-center, prospective study of resective Epilepsy surgery completed baseline questionnaires that included the Quality of Life in Epilepsy (QOLIE)-89 and a seven-item adaptation of the National Hospital Seizure Severity Scale. Associations between QOLIE-89 summary measures and both the total seizure severity scale score and individual seizure severity items were assessed, after adjustment for seizure frequency. Results: The seizure severity measure had adequate scale score variability and reliability in this sample. Correlations between individual items in the scale did not exceed 0.43. Product-moment partial correlations between the seizure severity scale and QOLIE-89 summary measures ranged from −0.17 to −0.29 (all p values <0.01). Of the seven seizure severity items, the average time before individuals perceived they were “really back to normal” after their seizures was broadly related to all domains of HRQOL (r values ranged from −0.16 to −0.30; p values <0.01). Severity of injury during seizures was the only other item having more than minimal associations with HRQOL, and it was selectively related to the physical health measure. Higher frequency of falls during seizures was modestly related to less employment. Conclusions: This seizure severity measure assesses constructs that are generally distinct from HRQOL, except for moderate and broad associations between HRQOL and patient's perceptions of the average duration of recovery time after seizures. Recovery time may potentially be a useful clinical indicator of seizure severity that reflects meaningful impairment of HRQOL in adults with frequent seizures.
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Driving in adults with refractory Localization-Related Epilepsy
Neurology, 2000Co-Authors: Anne T. Berg, Michael R Sperling, Barbara G. Vickrey, John T. Langfitt, Carl W. Bazil, Shlomo Shinnar, Thaddeus S. Walczak, Steven V. Pacia, Susan S. SpencerAbstract:Objective: To examine the frequency of driving an automobile and characteristics associated with driving in individuals with refractory Localization-Related Epilepsy. Background: Driving is generally restricted and monitored in people with Epilepsy. Little is known about the frequency of driving and subsequent accidents specifically in individuals with uncontrolled Epilepsy. Methods: In an ongoing, prospective, multicenter study of resective Epilepsy surgery, individuals were interviewed when they presented for surgical evaluation. Analyses were conducted using chi-square, t -tests, and multiple logistic regression. Results: Of 367 eligible participants, 115 (31.3%) had driven in the last year, most on at least a weekly basis. In a multivariable analysis, factors associated with an increased likelihood of driving were having a current license (OR = 10.71, p p = 0.003). Younger individuals were also more likely to drive. Lower levels of driving were found in women (OR = 0.31, p p p = 0.03) or part-time (OR = 0.15, p = 0.005). At some point in the past, 144 individuals experienced one or more seizures while driving, and 98 experienced at least one accident because of a seizure. Of those who had accidents, 94% reported property damage, 32% had an injury, and 20% caused injury to others. Conclusions: Despite restrictions, almost one third of individuals with refractory Epilepsy drive. Understanding why they do may help identify means of modifying this behavior or identifying services that, if provided, would help people with uncontrolled Epilepsy forego driving.
Kazuyoshi Watanabe - One of the best experts on this subject based on the ideXlab platform.
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phenytoin desensitization in a child with symptomatic localization related Epilepsy
Brain & Development, 2007Co-Authors: Kazuyoshi Watanabe, Tamiko Negoro, Akihisa Okumura, Seiko Itomi, Taketo IkutaAbstract:Abstract We reported a child with refractory partial seizures successfully managed by clinical desensitization to phenytoin. The patient had ischemic brain lesions due to cardiopulmonary arrest at 39 weeks of corrected age. He had complex partial seizures refractory to several antiepileptic drugs since 4 years of age. At 8 years 1 month of age, phenytoin was first administered. Fever and maculopapular rashes appeared at 10 days after phenytoin initiation, and then the drug was discontinued. At 8 years 8 months of age, desensitization was attempted because of refractoriness of seizures to drugs other than phenytoin. Desensitization was started at 1 mg daily, and then the dose was doubled every week. His seizures were controlled by 150 mg/day of phenytoin in combination with primidone. No problems have been observed during desensitization.
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Absence seizures in patients with Localization-Related Epilepsy.
Brain & development, 2003Co-Authors: Ayako Sofue, Tamiko Negoro, Akihisa Okumura, Fumio Hayakawa, Yoshiko Nakai, Naoko Toyota, Kazuyoshi WatanabeAbstract:We studied the clinical features of 12 patients with Localization-Related Epilepsy (LRE) associated with absence seizures (AS). AS did not appear in any patients before partial seizures (PS) were first observed. The interval between the onset of PS and AS ranged from 1 month to 7.2 years (mean 2.11 years). The duration of AS (mean 5 months) was short compared with that of PS (mean 3.8 years). Carbamazepine (CBZ) was used in seven patients at the onset of AS. It was discontinued in five but continued in the other two. AS was initially treated with valproate in ten patients. Three of them needed additional antiepileptic drugs: clonazepam in two patients and ethosuximide in one. All patients became free from AS after treatment for AS was started, whereas PS was relatively intractable. Generalized spike-and-waves were often observed before the onset of AS. The interval between the first appearance of generalized spike-and-waves and the onset of AS ranged from 1 to 53 months (mean 20 months). AS in patients with LRE will be relatively benign and transient, and will respond well to antiepileptic drugs.
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transient seizure remission in intractable localization related Epilepsy
Pediatric Neurology, 2000Co-Authors: Junko Takenaka, Kazuyoshi Watanabe, Kosaburo Aso, Akihisa Okumura, Tamiko NegoroAbstract:We sought to elucidate the clinical features of transient seizure remission in intractable cryptogenic or symptomatic Localization-Related Epilepsy of childhood onset. Transient seizure remission has been reported to occur in mesial temporal sclerosis or focal cortical dysplasia, but few reports have focused on this phenomenon. We retrospectively scrutinized the temporal profiles of seizure frequency of 99 patients with intractable Localization-Related Epilepsy by reviewing their medical charts. Ten patients (10%) had transient seizure remissions that lasted for 2 years or longer. When an appropriate antiepileptic agent was administered, seizure remission occurred within 1-18 months. Without any triggering factors, the seizures recurred abruptly in seven patients and gradually in three. Epileptiform discharges on electroencephalography disappeared during the transient remission in seven patients and reappeared in five of them after recurrence. After recurrence, no antiepileptic agent was able to control the seizures. In comparison with those without transient seizure remission, these 10 patients tended to have normal intelligence and a positive family history for Epilepsy. Transient seizure remission occurs in a variety of pathologic changes and may be a result of an interaction between the progressive nature of some types of epileptogenic foci and an effect of the antiepileptic drugs.
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Cryptogenic Localization-Related Epilepsy of neonatal onset.
Seizure, 1996Co-Authors: Jun Natsume, Kazuyoshi Watanabe, Tamiko Negoro, Kosaburo Aso, Keiko Kasai, Norihide Maeda, Takashi Ohki, Koichi HoriuchiAbstract:We report three patients with Localization-Related Epilepsy of neonatal onset. They exhibited favourable psychomotor development and had no cerebral lesions on neuroimaging studies despite the presence of intractable partial seizures of neonatal onset. Although rare, some cases of Epilepsy of neonatal onset may be cryptogenic, i.e. they belong to neither the symptomatic nor the idiopathic group.
Kazuichi Yagi - One of the best experts on this subject based on the ideXlab platform.
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Chronological progression of a language deficit appearing to be postictally reversible in a patient with symptomatic Localization-Related Epilepsy.
Psychiatry and clinical neurosciences, 2000Co-Authors: Tatsuya Kudo, Kazuichi YagiAbstract: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.
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Magnetoencephalographic Findings on Patients Having Symptomatic Localization‐Related Epilepsy with Dysembryoplastic Neuroepithelial Tumor as the Epileptogenic Lesion
Epilepsia, 2000Co-Authors: Kenjiro Fukao, Tadahiro Mihara, Kazumi Matsuda, Yutaka Watanabe, Hideaki Shiraishi, Koichiro Yamada, Tateki Fujiwara, Kazuichi YagiAbstract:Purpose: Dysembryoplastic neuroepithelial tumor (DNT) is one of the major pathologies that are related to the epileptogenicity in patients having symptomatic Localization-Related Epilepsy (SLE). Histopathological definition of DNT is as follows: (I) intracortical locations, (2) multinodular architecture, (3)heterogeneous cellular composition with astrocytes, oligodendrocytes, and neurons, and (4) foci of cortical dysplasia. There are many glial cells and very few neurons at the center of the MRI lesion of DNT, which shows low intensity in TI image and high in T2. This characteristic is in contrast with that of focal cortical dysplasia (FCD), with MRI lesions that show iso-intensity in TI image and high in T2, wherein are found many giant neurons pathologically. Epileptogenicity related to FCD is supposed to be intrinsic, that is, to exist within the MRI lesion, because of existence of these giant new rons. We have previously confirmed that spike-dipoles estimated by magnetoencephalography (MEG) in SLE patients with FCD are distributed within the MRI lesion, suggesting the intrinsic epileptogenicity of FCD. We, therefore, suppose that epileptogenicity related to DNT should exist in the foci of cortical dysplasia, which are rather distant from the center of the MRI lesion, and hypothesized that spike-dipoles in SLE patients with DNT would be distributed out of the center of the MRI lesion. This study was performed to test the hypothesis. Methods: Subjects of this study were composed of 1 I SLE patients who underwent surgical treatment and received good outcome for seizure reduction, and histopathological diagnosis of DNT was confirmed postoperatively. Three patients were female and 8 were male. Age at the MEG study ranged from I to 35 years. As to the epileptic syndrome, 3 were frontal lobe Epilepsy (FLE), 7 were temporal (TLE), and I patient was parietal (PLE). The lobe i n which DNT was found and from which the seizure was supposed to originate were the same in all of the patients. MEG measurement and dipole fitting of interictal spikes were performed using a 37+37-channel dual sensor system (Biomag-netic Technologies Inc.; San Diego, California, USA) preoperatively. Estimated spike-dipoles were overlaid on the preoperative MRI image, and the topographical relationship between spike-dipoles and MRI lesion was examined in each patient. Results: Estimated spike-dipoles were distributed at the marginal area around thc MRI lesion in all of the FLE patients and 20 of the TLE patients. In the PLE patient spike-dipoles were distributed at a rather distant area from the MRI lesion, although within the same lobe. Four of the TLE patients showed extended distribution of spike-dipoles around the MRI lesion. One patient with TLE was found to have DNT only after surgery. This patient's spike-dipoles were distributed in a pattern characteristic of the mesial type of TLE. Conclusions: Spike-dipoles estimated by MEC were distributed not within the MRI lesion but in a marginal area surrounding the lesion, or rather a distant area of the cortex in the majority of cases. This result supports our hypothesis that epileptogenicity of DNT exists not at the center of the lesion, but around its margin.
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the chronic hallucinatory paranoid state of symptomatic localization related Epilepsy studied by cctv eeg monitoring
Epilepsia, 1998Co-Authors: Tatsuya Kudo, Yasuyo Nomori, Michiyo Kageyama, Kouichi Hamada And And, Kazuichi YagiAbstract:Purpose: Because an epileptogenic zone is considered an important factor in the genesis of the hallucinatory–paranoid state of symptomatic Localization-Related Epilepsy, the epileptogenic zones of patients with chronic hallucinatory-paranoid states were studied. Methods: The 10 patients (P1-P10) studied were right-handed and had both symptomatic Localization-Related Epilepsy and chronic hallucinatory-paranoid states, without a family history of either psychosis or Epilepsy. Their average age was 30.3 years at examination, 11.5 years at the onset of Epilepsy, and 20.2 years at the onset of psychosis. The duration of the follow-up was 7.6 years the localizations of epileptogenic zones were investigated by seizure manifestations, and the findings from interictal and ictal EEG, computed tomography (CT), magnetic resonance imaging (MRI), single-proton-emission CT (SPECT), and electromyogram (EMG). Results: The patients had auditory hallucinations of voices speaking directly to them or in conversation with other voices, and also had delusions of reference and persecution and delusional perception and mood (“Wahnstimmung”). Four patients had a prefrontal syndrome, which appeared and deteroirated before the onset of psychosis, and showed attention deficits, hyperreactivity, puerilism, disinhibition of impulsive behavior, irritability, and paranoid tendencies (P1, P2, P3, and P4) in addition to euphoria (P1, P2, and P4) and moria (P1 and P2). PS had memory disturbances, anomia, and irritability, and both P6 and P10 had a state indistinguishable from the residual phase of schizophrenia, showing autism, bizarre behaviors, blunted affect, poverty of content of thought, and lack of volition, which progressed after the onset of psychosis. P1, P2, P3, P4, and P8 had seizures of frontal origin such as tonic posturing and complex gestural automatism. P5, P6, P7, P9, and P10 showed seizures of the temporal lobe origin such as au-tonomic signs, impairment of consciousness, and motionless staring. Interictal epileptogenic discharges were observed bilaterally in the frontal areas of P1, P2, P3, and P4, in the right or left temporal areas or both of P5, P6, P7, and P8, in the right of left frontotemporal areas of P9, and bilaterally in the temporofrontal or occipital areas of P10. The onset of ictal discharges seemed to be at the left frontal area of PI and P2, the central area of P3, the right temporal area of P6. the right or left frontotemporal areas of P9, and the right hemisphere or the left occipital area of P10. Organic lesions were observed in the left lateral (P1), left medial (P2), and medial (P4) parts of prefrontal lobe, in the right (P6 and P9) and left (P7) temporal lobes, and in multiple lobes (P10) consisting of the left temporal and the occipital lobes bilaterally. The epileptogenic zones were suggested to he in the prefrontal lobe of P1, P2, P3, and P4, the temporal lobe of P5, P6, and P7, either the temporal or the frontal lobe or the area extending over the temporal and frontal lobes of P8 and P9, and the temporal lobe or the area extending temporal to the occipital area of P10. Conclusions: The results suggest that the frontal and temporal lobes participate in the genesis of the seizures of patients with chronic hallucinatory–paranoid states. The hallucinatory–paranoid state is shared in common by patients with epileptogenic zones of both the temporal and frontal lobes, whereas changes in behavior and personality differ depending on whether the site of epileptogenic zones is in the temporal or frontal lobes.
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Effects of Playing Videogames on Paroxysmal Activities in Patients with Localization‐Related Epilepsy
Epilepsia, 1998Co-Authors: Takehisa Araki, Yushi Inoue, Tadahiro Mihara, Kazuichi YagiAbstract:Purpose: Although several articles suggested that videogames can induce seizures, little is known about the mechanism of videogame-induced seizures. We investigated the effects of playing videogames on paroxysmal activities in the patients who were undergoing invasive long-term EEG/video monitoring for surgical treatment. Methods: Twenty patients (mean age, 23.8 years) with Localization-Related Epilepsy who were undergoing invasive long-term EEG/video monitoring were investigated. Seven of them had frontal lobe Epilepsy, 12 had temporal lobe Epilepsy, and one had occipital lobe Epilepsy. None of them had either photosensitivity or a history of videogame-induced seizures. Subdural electrodes and depth electrodes were implanted (mean number of electrodes, 114.5) for surgical treatment. The recordings were made with a 64-channel EEG. EEG was recorded while sitting with open eyes for 1 h (control) and while playing videogames for 1 h. The number of interictal discharges (IIDs) in every electrode for 1 h were counted (Nippon Koden, Monitor Spike Detection). We investigated whether playing videogames induced an increase of IIDs of >50% or a decrease of IIDs of
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The Chronic Hallucinatory‐Paranoid State of Symptomatic Localization‐Related Epilepsy Studied by CCTV/EEG Monitoring
Epilepsia, 1998Co-Authors: Tatsuya Kudo, Yasuyo Nomori, Michiyo Kageyama, Kouichi Hamada. And And, Kazuichi YagiAbstract:Purpose: Because an epileptogenic zone is considered an important factor in the genesis of the hallucinatory–paranoid state of symptomatic Localization-Related Epilepsy, the epileptogenic zones of patients with chronic hallucinatory-paranoid states were studied. Methods: The 10 patients (P1-P10) studied were right-handed and had both symptomatic Localization-Related Epilepsy and chronic hallucinatory-paranoid states, without a family history of either psychosis or Epilepsy. Their average age was 30.3 years at examination, 11.5 years at the onset of Epilepsy, and 20.2 years at the onset of psychosis. The duration of the follow-up was 7.6 years the localizations of epileptogenic zones were investigated by seizure manifestations, and the findings from interictal and ictal EEG, computed tomography (CT), magnetic resonance imaging (MRI), single-proton-emission CT (SPECT), and electromyogram (EMG). Results: The patients had auditory hallucinations of voices speaking directly to them or in conversation with other voices, and also had delusions of reference and persecution and delusional perception and mood (“Wahnstimmung”). Four patients had a prefrontal syndrome, which appeared and deteroirated before the onset of psychosis, and showed attention deficits, hyperreactivity, puerilism, disinhibition of impulsive behavior, irritability, and paranoid tendencies (P1, P2, P3, and P4) in addition to euphoria (P1, P2, and P4) and moria (P1 and P2). PS had memory disturbances, anomia, and irritability, and both P6 and P10 had a state indistinguishable from the residual phase of schizophrenia, showing autism, bizarre behaviors, blunted affect, poverty of content of thought, and lack of volition, which progressed after the onset of psychosis. P1, P2, P3, P4, and P8 had seizures of frontal origin such as tonic posturing and complex gestural automatism. P5, P6, P7, P9, and P10 showed seizures of the temporal lobe origin such as au-tonomic signs, impairment of consciousness, and motionless staring. Interictal epileptogenic discharges were observed bilaterally in the frontal areas of P1, P2, P3, and P4, in the right or left temporal areas or both of P5, P6, P7, and P8, in the right of left frontotemporal areas of P9, and bilaterally in the temporofrontal or occipital areas of P10. The onset of ictal discharges seemed to be at the left frontal area of PI and P2, the central area of P3, the right temporal area of P6. the right or left frontotemporal areas of P9, and the right hemisphere or the left occipital area of P10. Organic lesions were observed in the left lateral (P1), left medial (P2), and medial (P4) parts of prefrontal lobe, in the right (P6 and P9) and left (P7) temporal lobes, and in multiple lobes (P10) consisting of the left temporal and the occipital lobes bilaterally. The epileptogenic zones were suggested to he in the prefrontal lobe of P1, P2, P3, and P4, the temporal lobe of P5, P6, and P7, either the temporal or the frontal lobe or the area extending over the temporal and frontal lobes of P8 and P9, and the temporal lobe or the area extending temporal to the occipital area of P10. Conclusions: The results suggest that the frontal and temporal lobes participate in the genesis of the seizures of patients with chronic hallucinatory–paranoid states. The hallucinatory–paranoid state is shared in common by patients with epileptogenic zones of both the temporal and frontal lobes, whereas changes in behavior and personality differ depending on whether the site of epileptogenic zones is in the temporal or frontal lobes.
John S. Duncan - One of the best experts on this subject based on the ideXlab platform.
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Multimodal MR imaging: functional, diffusion tensor, and chemical shift imaging in a patient with Localization-Related Epilepsy.
Epilepsia, 1999Co-Authors: K Krakow, Udo C. Wieshmann, Friedrich G. Woermann, Mark R. Symms, Mary A. Mclean, Louis Lemieux, Phillip Allen, Gareth J. Barker, David R. Fish, John S. DuncanAbstract:Summary: Purpose: To demonstrate the integration of complementary functional and structural data acquired with magnetic resonance imaging (MRI) in a patient with Localization-Related Epilepsy. Methods: We studied a patient with partial and secondarily generalized seizures and a hemiparesis due to a malformation of cortical development (MCD) in the right hemisphere by using EEG-triggered functional MRI (fMRI), diffusion tensor imaging (DTI), and chemical shift imaging (CSI). Results: fMRI revealed significant changes in regional blood oxygenation associated with interictal epileptiform discharges within the MCD. DTI showed a heterogeneous microstructure of the MCD with reduced fractional anisotropy, a high mean diffusivity, and displacement of myelinated tracts. CSI demonstrated low N-acetyl aspartate (NAA) concentrations in parts of the MCD. Conclusions: The applied MR methods described functional, microstructural, and biochemical characteristics of the epileptogenic tissue that cannot be obtained with other noninvasive means and thus improve the understanding of the pathophysiology of Epilepsy.
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A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed Localization-Related Epilepsy using MR-based cerebral T2 relaxation time measurements.
Epilepsy research, 1998Co-Authors: W. Van Paesschen, John S. Duncan, Alan ConnellyAbstract:Magnetic resonance (MR)-based T2 relaxation time measurement is a sensitive technique to detect neuropathological changes such as intramyelinic edema in vivo. To determine whether vigabatrin (VGB) causes an increase in T2 relaxation time in patients with newly diagnosed Localization-Related Epilepsy over 1 year. Patients with newly diagnosed Localization-Related Epilepsy who participated in a VGB-carbamazepine (CBZ) monotherapy trial were included. All were scanned on a 1.5 T Siemens SP63 Magnetom scanner. T2 maps of the brain were obtained at baseline and at follow-up 1 year later. Nine control subjects had repeated hippocampal T2 maps with a median interval of approximately 2 years. 23 patients (12 on VGB and 11 on CBZ) were included. There were no increased T2 relaxation times in the VGB treated group at follow-up and no significant differences between the two antiepileptic drug groups. There was a trend for the temporal and frontal white matter T2 relaxation times to be lower on follow-up in the patients compared to the control subjects. The findings do not suggest that intramyelinic edema occurs in patients taking monotherapy VGB for 1 year.
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A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed Localization-Related Epilepsy using MR-based cerebral T2 relaxation time measurements.
Epilepsy research, 1998Co-Authors: W. Van Paesschen, John S. Duncan, Alan ConnellyAbstract:Abstract Background: Magnetic resonance (MR)-based T2 relaxation time measurement is a sensitive technique to detect neuropathological changes such as intramyelinic edema in vivo. Objective: To determine whether vigabatrin (VGB) causes an increase in T2 relaxation time in patients with newly diagnosed Localization-Related Epilepsy over 1 year. Methods: Patients with newly diagnosed Localization-Related Epilepsy who participated in a VGB-carbamazepine (CBZ) monotherapy trial were included. All were scanned on a 1.5 T Siemens SP63 Magnetom scanner. T2 maps of the brain were obtained at baseline and at follow-up 1 year later. Nine control subjects had repeated hippocampal T2 maps with a median interval of ≈2 years. Results: 23 patients (12 on VGB and 11 on CBZ) were included. There were no increased T2 relaxation times in the VGB treated group at follow-up and no significant differences between the two antiepileptic drug groups. There was a trend for the temporal and frontal white matter T2 relaxation times to be lower on follow-up in the patients compared to the control subjects. Conclusion: The findings do not suggest that intramyelinic edema occurs in patients taking monotherapy VGB for 1 year.
Alan Connelly - One of the best experts on this subject based on the ideXlab platform.
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A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed Localization-Related Epilepsy using MR-based cerebral T2 relaxation time measurements.
Epilepsy research, 1998Co-Authors: W. Van Paesschen, John S. Duncan, Alan ConnellyAbstract:Magnetic resonance (MR)-based T2 relaxation time measurement is a sensitive technique to detect neuropathological changes such as intramyelinic edema in vivo. To determine whether vigabatrin (VGB) causes an increase in T2 relaxation time in patients with newly diagnosed Localization-Related Epilepsy over 1 year. Patients with newly diagnosed Localization-Related Epilepsy who participated in a VGB-carbamazepine (CBZ) monotherapy trial were included. All were scanned on a 1.5 T Siemens SP63 Magnetom scanner. T2 maps of the brain were obtained at baseline and at follow-up 1 year later. Nine control subjects had repeated hippocampal T2 maps with a median interval of approximately 2 years. 23 patients (12 on VGB and 11 on CBZ) were included. There were no increased T2 relaxation times in the VGB treated group at follow-up and no significant differences between the two antiepileptic drug groups. There was a trend for the temporal and frontal white matter T2 relaxation times to be lower on follow-up in the patients compared to the control subjects. The findings do not suggest that intramyelinic edema occurs in patients taking monotherapy VGB for 1 year.
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A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed Localization-Related Epilepsy using MR-based cerebral T2 relaxation time measurements.
Epilepsy research, 1998Co-Authors: W. Van Paesschen, John S. Duncan, Alan ConnellyAbstract:Abstract Background: Magnetic resonance (MR)-based T2 relaxation time measurement is a sensitive technique to detect neuropathological changes such as intramyelinic edema in vivo. Objective: To determine whether vigabatrin (VGB) causes an increase in T2 relaxation time in patients with newly diagnosed Localization-Related Epilepsy over 1 year. Methods: Patients with newly diagnosed Localization-Related Epilepsy who participated in a VGB-carbamazepine (CBZ) monotherapy trial were included. All were scanned on a 1.5 T Siemens SP63 Magnetom scanner. T2 maps of the brain were obtained at baseline and at follow-up 1 year later. Nine control subjects had repeated hippocampal T2 maps with a median interval of ≈2 years. Results: 23 patients (12 on VGB and 11 on CBZ) were included. There were no increased T2 relaxation times in the VGB treated group at follow-up and no significant differences between the two antiepileptic drug groups. There was a trend for the temporal and frontal white matter T2 relaxation times to be lower on follow-up in the patients compared to the control subjects. Conclusion: The findings do not suggest that intramyelinic edema occurs in patients taking monotherapy VGB for 1 year.
