Relevant bibliographies by topics / Occipital lobe epilepsy – Research

Academic literature on the topic 'Occipital lobe epilepsy – Research'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Occipital lobe epilepsy – Research"

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Kaido, Takanobu, Tohru Hoshida, Toshiaki Taoka, and Toshisuke Sakaki. "Retinotopy with coordinates of lateral occipital cortex in humans." Journal of Neurosurgery 101, no. 1 (July 2004): 114–18. http://dx.doi.org/10.3171/jns.2004.101.1.0114.

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Object. The lateral occipital cortex in humans is known as the “extrastriate visual cortex.” It is, however, an unexplored field of research, and the anatomical nomenclature for its surface has still not been standardized. This study was designed to investigate whether the lateral occipital cortex in humans has retinotopic representation. Methods. Four right-handed patients with a diagnosis of intractable epilepsy from space-occupying lesions in the occipital lobe or epilepsy originating in the occipital lobe received permanently implanted subdural electrodes. Electrical cortical stimulation was applied directly applied to the brain through metal electrodes by using a biphasic stimulator. The location of each electrode was measured on a lateral skull x-ray study. Each patient considered a whiteboard with vertical and horizontal median lines. The patient was asked to look at the midpoint on the whiteboard. If a visual hallucination or illusion occurred, the patient recorded its outline, shape, color, location, and motion on white paper one tenth the size of, and with vertical and horizontal median lines similar to those on, the whiteboard. Polar angles and eccentricities of the midpoints of the phosphenes from the coordinate origin were measured on the paper. On stimulation of the lateral occipital lobe, 44 phosphenes occurred. All phosphenes were circular or dotted, with a diameter of approximately 1 cm, except one that was like a curtain in the peripheral end of the upper and lower visual fields on stimulation of the parietooccipital region. All phosphenes appeared in the visual field contralateral to the cerebral hemisphere stimulated. On stimulation of the lateral occipital lobe, 22 phosphenes moved centrifugally or toward a horizontal line. From three-dimensional scatterplots and contour maps of the polar angles and eccentricities in relation to the x-ray coordinates of the electrodes, one can infer that the lateral occipital cortex in humans has retinotopic representation. Conclusions. The authors found that phosphenes induced by electrical cortical stimulation of the lateral occipital cortex represent retinotopy. From these results one can assert that visual field representation with retinotopic relation exists in the extrastriate visual cortex.
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Alsemari, Abdulaziz, Faisal Al-Otaibi, Salah Baz, Ibrahim Althubaiti, Hisham Aldhalaan, David MacDonald, Tareq Abalkhail, et al. "Epilepsy Surgery Series: A Study of 502 Consecutive Patients from a Developing Country." Epilepsy Research and Treatment 2014 (January 30, 2014): 1–8. http://dx.doi.org/10.1155/2014/286801.

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Purpose. To review the postoperative seizure outcomes of patients that underwent surgery for epilepsy at King Faisal Specialist Hospital & Research Centre (KFSHRC). Methods. A descriptive retrospective study for 502 patients operated on for medically intractable epilepsy between 1998 and 2012. The surgical outcome was measured using the ILAE criteria. Results. The epilepsy surgery outcome for temporal lobe epilepsy surgery (ILAE classes 1, 2, and 3) at 12, 36, and 60 months is 79.6%, 74.2%, and 67%, respectively. The favorable 12- and 36-month outcomes for frontal lobe epilepsy surgery are 62% and 52%, respectively. For both parietal and occipital epilepsy lobe surgeries the 12- and 36-month outcomes are 67%. For multilobar epilepsy surgery, the 12- and 36-month outcomes are 65% and 50%, respectively. The 12- and 36-month outcomes for functional hemispherectomy epilepsy surgery are 64.2% and 63%, respectively. According to histopathology diagnosis, mesiotemporal sclerosis (MTS) and benign CNS tumors had the best favorable outcome after surgery at 1 year (77.27% and 84.3%, resp.,) and 3 years (76% and 75%, resp.,). The least favorable seizure-free outcome after 3 years occurred in cases with dual pathology (66.6%). Thirty-four epilepsy patients with normal magnetic resonance imaging (MRI) brain scans were surgically treated. The first- and third-year epilepsy surgery outcome of 17 temporal lobe surgeries were (53%) and (47%) seizure-free, respectively. The first- and third-year epilepsy surgery outcomes of 15 extratemporal epilepsy surgeries were (47%) and (33%) seizure-free. Conclusion. The best outcomes are achieved with temporal epilepsy surgery, mesial temporal sclerosis, and benign CNS tumor. The worst outcomes are from multilobar surgery, dual pathology, and normal MRI.
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Mushehian, Marianna, and Tetyana Litovchenko. "ANALYSIS OF PECULIARITIES OF EPILEPTIC SEIZURES AND STRUCTURAL DAMAGES OF BRAIN IN PATIENTS WITH ISCHEMIC STROKE." ScienceRise, no. 5 (October 31, 2020): 46–53. http://dx.doi.org/10.21303/2313-8416.2020.001454.

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The aim of the research: epilepsy on the background of ischemic stroke. Studied problem: improve of diagnosis of epilepsy on the background of ischemic stroke by establishing the clinical features of epileptic seizures and by detection of brain structural damages The main scientific results: a cross-sectional randomized cohort comparative study with retrospective and prospective stages was performed in 60 patients (men and women) with ischemic stroke aged 65 [57.0; 74.0] years, in 30 of which epileptic seizures were detected. The predominance of generalized single (66.7±38.5 %) variants was found in the structure of epileptic seizures in patients with acute cerebrovascular pathology. A higher frequency of generalized variants of seizures in patients over 60 years of age (maximum at 61–70 years, at descending – 71–80 years, over 80 years) has been revealed. The descending distribution of localization frequency of brain lesions (detected with MRI, CT) in patients with epileptic seizures after ischemic stroke is as follows: dilation of the subarachnoid space (93.3±24.1 %), dilation of the brain ventricles (83.3±34.0 %), subcortical ganglia (76.7±37.0 %), right hemisphere or temporal lobe (60.0±37.9 %), subcortex (56.7±37.3 %), frontal lobe (50.0±35.4 %), left hemisphere or diffuse-atrophic changes in the cortical region (43.3±32.6 %), temporal lobe (20.0±17.9 %), occipital lobe (16.7±15.2 %). The area of practical use of the research results: clinical medicine, especially neurology. Innovative technological product: methodology of diagnosis of epilepsy on the background of ischemic stroke. Scope of the innovative technological product: the evaluation of seizures and brain’s structural damages in patients with ischemic stroke with the development of epileptic seizures may be a means of improving the diagnosis of epilepsy on the background of cerebrovascular disease.
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Cascino, Gregory D. "Temporal Lobe Epilepsy: More than Hippocampal Pathology." Epilepsy Currents 5, no. 5 (September 2005): 187–89. http://dx.doi.org/10.1111/j.1535-7511.2005.00059.x.

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Voxel-based Morphometry of the Thalamus in Patients with Refractory Medial Temporal Lobe Epilepsy Bonilha L, Rorden C, Castellano G, Cendes F, Li LM Neuroimage 2005;25:1016–1021 Previous research has suggested that patients with refractory medial temporal lobe epilepsy (MTLE) show gray matter atrophy both within the temporal lobes and in the thalamus. However, these studies have not distinguished between different nuclei within the thalamus. We examined whether thalamic atrophy correlates with the nuclei's connections to other regions in the limbic system. T1-weighted MRI scans were obtained from 49 neurologically healthy control subjects and 43 patients diagnosed with chronic refractory MTLE that was unilateral in origin (as measured by ictal EEG and hippocampal atrophy observed on MRI). Measurements of gray matter concentration (GMC) were made by using automated segmentation algorithms. GMC was analyzed both voxel by voxel (preserving spatial precision) as well as using predefined regions of interest. Voxel-based morphometry revealed intense GMC reduction in the anterior portion relative to posterior thalami. Furthermore, thalamic atrophy was greater ipsilateral to the MTLE origin than on the contralateral side. Here we demonstrate that the thalamic atrophy is most intense in the thalamic nuclei that have strong connections with the limbic hippocampus. This finding suggests that thalamic atrophy reflects this region's anatomic and functional association with the limbic system rather than a general vulnerability to damage. Ipsilateral and Contralateral MRI Volumetric Abnormalities in Chronic Unilateral Temporal Lobe Epilepsy and Their Clinical Correlates Seidenberg M, Kelly KG, Parrish J, Geary E, Dow C, Rutecki P, Hermann B Epilepsia 2005;46:420–430 Purpose To assess the presence, extent, and clinical correlates of quantitative MR volumetric abnormalities in ipsilateral and contralateral hippocampus, and temporal and extratemporal lobe regions in unilateral temporal lobe epilepsy (TLE). Methods In total, 34 subjects with unilateral left ( n = 15) or right ( n = 19) TLE were compared with 65 healthy controls. Regions of interest included the ipsilateral and contralateral hippocampus as well as temporal, frontal, parietal, and occipital lobe gray and white matter. Clinical markers of neurodevelopmental insult (initial precipitating insult, early age of recurrent seizures) and chronicity of epilepsy (epilepsy duration, estimated number of lifetime generalized seizures) were related to MR volume abnormalities. Results Quantitative MR abnormalities extend beyond the ipsilateral hippocampus and temporal lobe with extratemporal (frontal and parietal lobe) reductions in cerebral white matter, especially ipsilateral but also contralateral to the side of seizure onset. Volumetric abnormalities in ipsilateral hippocampus and bilateral cerebral white matter are associated with factors related to both the onset and the chronicity of the patients’ epilepsy. Conclusions These cross-sectional findings support the view that volumetric abnormalities in chronic TLE are associated with a combination of neurodevelopmental and progressive effects, characterized by a prominent disruption in ipsilateral hippocampus and neural connectivity (i.e., white matter volume loss) that extends beyond the temporal lobe, affecting both ipsilateral and contralateral hemispheres. MR Volumetric Analysis of the Piriform Cortex and Cortical Amygdala in Drug-refractory Temporal Lobe Epilepsy Gonçalves Pereira PM, Insaustid R, Artacho-Pérulad E, Salmenperäe T, Kälviäinene R, Pitkänen A AJNR Am J Neuroradiol 2005;26:319–332 Purpose The assessment of patients with temporal lobe epilepsy (TLE) traditionally focuses on the hippocampal formation. These patients, however, may have structural abnormalities in other brain areas. Our purpose was to develop a method to measure the combined volume of the human piriform cortex and cortical amygdala (PCA) by using MRI and to investigate PCA atrophy. Methods The definition of anatomic landmarks on MRIs was based on histologic analysis of 23 autopsy control subjects. Thirty-nine adults with chronic TLE and 23 age-matched control subjects were studied. All underwent high-spatial-resolution MRI at 1.5 T, including a tilted T1-weighted 3D dataset. The PCA volumes were compared with the control values and further correlated with hippocampal, amygdale, and entorhinal cortex volumes. Results The normal volume was 530 ± 59 mm3 (422-644) (mean ± 1 SD [range]) on the right and 512 ± 60 mm3 (406-610) on the left PCA (no asymmetry, and no age or sex effect). The intraobserver and interobserver variability were 6% and 8%, respectively. In right TLE patients, the mean right PCA volume was 18% smaller than that in control subjects ( p < 0.001) and 15% smaller than in left TLE ( p < 0.001). In left TLE, the mean left PCA volume was 16% smaller than in control subjects ( p < 0.001) and 19% smaller than in right TLE ( p < 0.001). Overall, 18 (46%) of the 39 patients had a greater than 20% volume reduction in the ipsilateral PCA. Bilateral atrophy was found in 7 (18%) of 39. Patients with hippocampal volumes of at least 2 SDs below the control mean had an 18% reduction in the mean PCA volume compared with patients without hippocampal atrophy ( p < 0.001). Ipsilaterally, hippocampal ( r = 0.756, p < 0.01), amygdaloid ( r = 0.548, p < 0.01), and entorhinal ( r = 0.500, p < 0.01) volumes correlated with the PCA volumes. Conclusions The quantification of PCA volume with MRI showed that the PCA is extensively damaged in chronic TLE patients, particularly in those with hippocampal atrophy.
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Destina Yalçin, A., Asuman Kaymaz, and Hulki Forta. "Reflex occipital lobe epilepsy." Seizure 9, no. 6 (September 2000): 436–41. http://dx.doi.org/10.1053/seiz.2000.0424.

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Niedermeyer, E., Silvana Riggio, and Margarida Santiago. "Benign occipital lobe epilepsy." Journal of Epilepsy 1, no. 1 (January 1988): 3–11. http://dx.doi.org/10.1016/s0896-6974(88)80027-6.

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Kuzniecky, Ruben. "Symptomatic Occipital Lobe Epilepsy." Epilepsia 39, s4 (April 1998): S24—S31. http://dx.doi.org/10.1111/j.1528-1157.1998.tb05122.x.

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Lutskiy, M. A., M. V. Uvarova, V. P. Savinykh, and V. A. Bykova. "DIAGNOSIS OF OCCIPITAL LOBE EPILEPSY." Epilepsia and paroxyzmal conditions 9, no. 3 (January 1, 2017): 18–21. http://dx.doi.org/10.17749/2077-8333.2017.9.3.018-021.

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Guerrini, Renzo, Charlotte Dravet, Pierre Genton, Michelle Bureau, Paolo Bonanni, Anna Rita Ferrari, and Joseph Roger. "Idiopathic Photosensitive Occipital Lobe Epilepsy." Epilepsia 36, no. 9 (September 1995): 883–91. http://dx.doi.org/10.1111/j.1528-1157.1995.tb01631.x.

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Santangelo, Gabriella, Luigi Trojano, Carmine Vitale, Ilaria Improta, Irma Alineri, Roberta Meo, and Leonilda Bilo. "Cognitive dysfunctions in occipital lobe epilepsy compared to temporal lobe epilepsy." Journal of Neuropsychology 11, no. 2 (September 22, 2015): 277–90. http://dx.doi.org/10.1111/jnp.12085.

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Dissertations / Theses on the topic "Occipital lobe epilepsy – Research"

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Tian, Nan. "SLEEP-RELATED GENERALIZED TONIC SEIZURE AND HIGH FREQUENCY OSCILLATION (HFOs) IN A MESIAL TEMPORAL LOBE EPILEPSY MOUSE MODEL." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1277440218.

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Walpole, Pete. "An investigation into the implications of emotional intelligence and social cognition research for psychosocial problems associated with temporal lobe epilepsy." Thesis, University of Sheffield, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422171.

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Toprani, Sheela C. "MECHANISMS OF SEIZURE REDUCTION BY LOW FREQUENCY ELECTRICAL STIMULATION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1399474125.

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Eisenman, Daniel David. "Validation of a neuropsychological Wada procedure." 2005. http://edissertations.library.swmed.edu/pdf/EisenmanD081105/EisenmanDaniel.pdf.

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Wilson, Sarah Marie. "Involvement of Collapsin Response Mediator Protein 2 in Posttraumatic Sprouting in Acquired Epilepsy." Thesis, 2014. http://hdl.handle.net/1805/5604.

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Indiana University-Purdue University Indianapolis (IUPUI)
Posttraumatic epilepsy, the development of temporal lobe epilepsy (TLE) following traumatic brain injury, accounts for 20% of symptomatic epilepsy. Reorganization of mossy fibers within the hippocampus is a common pathological finding of TLE. Normal mossy fibers project into the CA3 region of the hippocampus where they form synapses with pyramidal cells. During TLE, mossy fibers are observed to innervate the inner molecular layer where they synapse onto the dendrites of other dentate granule cells, leading to the formation of recurrent excitatory circuits. To date, the molecular mechanisms contributing to mossy fiber sprouting are relatively unknown. Recent focus has centered on the involvement of tropomycin-related kinase receptor B (TrkB), which culminates in glycogen synthase kinase 3β (GSK3β) inactivation. As the neurite outgrowth promoting collapsin response mediator protein 2 (CRMP2) is rendered inactive by GSK3β phosphorylation, events leading to inactivation of GSK3β should therefore increase CRMP2 activity. To determine the involvement of CRMP2 in mossy fiber sprouting, I developed a novel tool ((S)-LCM) for selectively targeting the ability of CRMP2 to enhance tubulin polymerization. Using (S)-LCM, it was demonstrated that increased neurite outgrowth following GSK3β inactivation is CRMP2 dependent. Importantly, TBI led to a decrease in GSK3β-phosphorylated CRMP2 within 24 hours which was secondary to the inactivation of GSK3β. The loss of GSK3β-phosphorylated CRMP2 was maintained even at 4 weeks post-injury, despite the transience of GSK3β-inactivation. Based on previous work, it was hypothesized that activity-dependent mechanisms may be responsible for the sustained loss of CRMP2 phosphorylation. Activity-dependent regulation of GSK3β-phosphorylated CRMP2 levels was observed that was attributed to a loss of priming by cyclin dependent kinase 5 (CDK5), which is required for subsequent phosphorylation by GSK3β. It was confirmed that the loss of GSK3β-phosphorylated CRMP2 at 4 weeks post-injury was likely due to decreased phosphorylation by CDK5. As TBI resulted in a sustained increase in CRMP2 activity, I attempted to prevent mossy fiber sprouting by targeting CRMP2 in vivo following TBI. While (S)-LCM treatment dramatically reduced mossy fiber sprouting following TBI, it did not differ significantly from vehicle-treated animals. Therefore, the necessity of CRMP2 in mossy fiber sprouting following TBI remains unknown.
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Books on the topic "Occipital lobe epilepsy – Research"

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Wehner, Tim, Kanjana Unnwongse, and Beate Diehl. Focal epilepsy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0028.

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This chapter examines the neurophysiology of focal epilepsy. It discusses the principles of EEG source localization. This is followed by a presentation of nonspecific and epileptiform interictal EEG findings and ictal EEG patterns seen in focal epilepsy, along with normal EEG variants that may be mistaken for epileptiform features. Seizure semiologies and ictal and interictal EEG findings in mesial and neocortical temporal lobe epilepsy, orbitofrontal, dorsolateral, and mesial frontal epilepsy, insular epilepsy, and parietal and occipital epilepsy are presented with illustrative case discussions derived from patients investigated for resective epilepsy surgery. A brief discussion of prognosis and treatment strategies for focal epilepsy follows.
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Book chapters on the topic "Occipital lobe epilepsy – Research"

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Girvin, John P. "Occipital Lobe Resections." In Operative Techniques in Epilepsy, 239–43. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-10921-3_10.

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Panayiotopoulos, C. P. "Idiopathic Photosensitive Occipital Lobe Epilepsy." In Reflex seizures and related epileptic syndromes, 15–20. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-4042-9_2.

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Parmeggiani, Lucio, and Renzo Guerrini. "Idiopathic Photosensitive Occipital Lobe Epilepsy." In Atlas of Epilepsies, 1077–80. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84882-128-6_158.

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Damasceno, Benito. "Temporal Lobe Epilepsy." In Research on Cognition Disorders, 207–14. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-57267-9_19.

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Warrington, Elizabeth K. "Visual Deficits Associated with Occipital Lobe Lesions in Man." In Experimental Brain Research Supplementum, 247–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-662-09224-8_13.

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Qiu, Zhi-Jun, Hong-Yan Zhang, and Xin Tian. "Research of EEG from Patients with Temporal Lobe Epilepsy on Causal Analysis of Directional Transfer Functions." In Neural Information Processing, 337–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-24955-6_41.

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Werz, Mary Ann. "Occipital Lobe Epilepsy." In Epilepsy Syndromes, 109–16. Elsevier, 2010. http://dx.doi.org/10.1016/b978-1-4160-4833-6.00015-0.

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"Parieto-occipital lobe epilepsy." In Textbook of Epilepsy Surgery, 354–59. CRC Press, 2008. http://dx.doi.org/10.3109/9780203091708-45.

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Schwartzkroin, P. A., and H. Jurgen Wenzel. "TEMPORAL LOBE EPILEPSY | Genetic Determinants of Temporal Lobe Epilepsy." In Encyclopedia of Basic Epilepsy Research, 1361–65. Elsevier, 2009. http://dx.doi.org/10.1016/b978-012373961-2.00370-2.

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"7 Cortical Resection in Frontal, Parietal, and Occipital Lobe." In Operative Techniques in Epilepsy Surgery, edited by Gordon H. Baltuch and Jean-Guy Villemure. Stuttgart: Georg Thieme Verlag, 2009. http://dx.doi.org/10.1055/b-0034-56075.

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Conference papers on the topic "Occipital lobe epilepsy – Research"

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Hao, Jiaxin, Yuhai Xie, Qiangqiang Liu, Jiwen Xu, and Puming Zhang. "Localization of Epileptogenic Zone Based on Radiomics Features of 18F-FDG PET in Patients with Temporal Lobe Epilepsy**Research supported by the National Natural Science Foundation of China (No. 82071550)." In 2021 10th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2021. http://dx.doi.org/10.1109/ner49283.2021.9441427.

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