Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/21447
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dc.contributor.authorYıldız, Harun-
dc.date.accessioned2021-08-18T05:26:15Z-
dc.date.available2021-08-18T05:26:15Z-
dc.date.issued2005-03-
dc.identifier.citationHakyemez, B. vd. (2005). "Apparent diffusion coefficient measurements in the hippocampus and amygdala of patients with temporal lobe seizures and in healthy volunteers". Epilepsy & Behavior, 6(2), 250-256.en_US
dc.identifier.issn1525-5050-
dc.identifier.urihttps://doi.org/10.1016/j.yebeh.2004.12.008-
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S1525505004003725-
dc.identifier.urihttp://hdl.handle.net/11452/21447-
dc.description.abstractPurpose: The goals of this work were to measure the apparent diffusion coefficients (ADCs) for both hippocampus and amygdala of persons diagnosed with temporal lobe epilepsy (TLE) and unilateral hippocampus pathology on magnetic resonance imaging and to evaluate the sensitivity of diffusion-weighted (DW) images in determination of the lateralization of the epileptogenic focus. Methods: Thirteen cases with a TLE diagnosis and 21 healthy subjects were evaluated. Fluid-attenuated inversion recovery and T2W images of TLE cases revealed hippocampal volume loss and signal intensity changes. DW images were obtained by spin-echo echo-planar sequences vertical to the hippocampal axis. Qualitative and quantitative ADCs for left and right hippocampus and the amygdala of the controls and the patients were determined. Hippocampal ADCs were obtained independently at the head, body, and tail levels of the hippocampus. Statistical evaluation was conducted with Kruskal–Wallis and Mann–Whitney U tests. Predictive cutoff levels of hippocampal ADCs for identifying pathologic areas were established through receiver operating characteristic (ROC) curve analysis. Result On conventional images, 5 of 13 cases had right hippocampal pathology, and 8 of 13 cases had left hippocampal pathology. There were no bilateral hippocampal changes in signal intensity and no cases with bilateral atrophy. The amygdala was normal in all patients except one case of hyperintense signals. No statistical differences were found between the hippocampal and amygdaloid ADCs of the control subjects (P > 0.05). However, there was a significant difference between the ADCs for the side with hippocampal pathology and the ADCs for the contralateral side, and the control group (P < 0.001). No statistical difference was detected for the amygdala (P > 0.05). Hippocampal and amygdaloid ADCs of the contralateral lesion and the values of the control group were not statistically significantly different (P > 0.05). ROC curve analysis indicated 136 as the best cutoff level for hippocampal pathology. Conclusion DW trace images are insensitive in lateralization of hippocampal pathology; however, lateralization can be achieved through ADC measurements of the hippocampus. An increase in ADC on the affected side should be considered as indicating pathology. On the other hand, amygdaloid ADC values remain inaccurate.en_US
dc.language.isoenen_US
dc.publisherAcademic Press Inc Elsevier Scienceen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectEpilepsyen_US
dc.subjectDiffusion-weighted imagingen_US
dc.subjectAmygdalaen_US
dc.subjectHippocampusen_US
dc.subjectMagnetic resonanceen_US
dc.subjectWater diffusionen_US
dc.subjectSclerosisen_US
dc.subjectMRen_US
dc.subjectEpilepsyen_US
dc.subjectDiagnosisen_US
dc.subjectBehavioral sciencesen_US
dc.subjectPsychiatryen_US
dc.subjectNeurosciences & neurologyen_US
dc.titleApparent diffusion coefficient measurements in the hippocampus and amygdala of patients with temporal lobe seizures and in healthy volunteersen_US
dc.typeArticleen_US
dc.identifier.wos000227219000019tr_TR
dc.identifier.scopus2-s2.0-13844256296tr_TR
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Radyoloji Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Biyoistatistik Anabilim Dalı.tr_TR
dc.contributor.orcid0000-0002-3425-0740tr_TR
dc.contributor.orcid0000-0002-2382-290Xtr_TR
dc.identifier.startpage250tr_TR
dc.identifier.endpage256tr_TR
dc.identifier.volume6tr_TR
dc.identifier.issue2tr_TR
dc.relation.journalEpilepsy & Behavioren_US
dc.contributor.buuauthorHakyemez, Bahattin-
dc.contributor.buuauthorErdoğan, Cüneyt-
dc.contributor.buuauthorErcan, İlker-
dc.contributor.buuauthorParlak, Müfit-
dc.contributor.researcheridAAI-2318-2021tr_TR
dc.relation.collaborationYurt içitr_TR
dc.identifier.pubmed15710312tr_TR
dc.subject.wosBehavioral sciencesen_US
dc.subject.wosPsychiatryen_US
dc.subject.wosClinical neurologyen_US
dc.indexed.wosSCIEen_US
dc.indexed.scopusScopusen_US
dc.indexed.pubmedPubmeden_US
dc.wos.quartileQ2 (Clinical neurology)en_US
dc.wos.quartileQ3en_US
dc.subject.scopusTemporal Lobe Epilepsy; Sclerosis; Drug Resistant Epilepsyen_US
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