Hippocampal Atrophy Is Associated with Altered Hippocampus–Posterior Cingulate Cortex Connectivity in Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

Shih, Yang-hsin; Tseng, Chen‐Te; Lin, Fa‐Hsuan; Liou, Horng-Huei; Tseng, Wen Yih I.

doi:10.3174/ajnr.a5039

Cited by 9 publications

(6 citation statements)

References 36 publications

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“…Notwithstanding the current view of focal epilepsy as a network disorder, there is increasing evidence for complex interactions between local function, structural pathology and whole-brain connectivity (Bernasconi, 2017). In temporal lobe epilepsy, numerous studies have shown decreased functional connectivity of the ipsilateral hippocampus (Bettus et al, 2009;Maccotta et al, 2013;Morgan et al, 2015), especially with the default mode network (Kucukboyaci et al, 2013), the severity of which scales with hippocampal pathology (Bernhardt et al, 2016;Shih et al, 2017). Conversely, in FCD, while individual analyses indicate altered local function and connectivity, as well as brain-wide alterations across patients (Stufflebeam et al, 2011;Lee et al, 2014;Besseling et al, 2016;Hong et al, 2017b;Jackson et al, 2017;Gupta et al, 2018), no study has so far tackled grouplevel connectivity from a lesion perspective and its relationship to the structural pathology.…”

Section: Discussionmentioning

confidence: 99%

A connectome-based mechanistic model of focal cortical dysplasia

Hong

Lee

Gill

et al. 2019

Brain

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Neuroimaging studies have consistently shown distributed brain anomalies in epilepsy syndromes associated with a focal structural lesion, particularly mesiotemporal sclerosis. Conversely, a system-level approach to focal cortical dysplasia has been rarely considered, likely due to methodological difficulties in addressing variable location and topography. Given the known heterogeneity in focal cortical dysplasia histopathology, we hypothesized that lesional connectivity consists of subtypes with distinct structural signatures. Furthermore, in light of mounting evidence for focal anomalies impacting whole-brain systems, we postulated that patterns of focal cortical dysplasia connectivity may exert differential downstream effects on global network topology. We studied a cohort of patients with histologically verified focal cortical dysplasia type II (n = 27), and age-and sex-matched healthy controls (n = 34). We subdivided each lesion into similarly sized parcels and computed their connectivity to large-scale canonical functional networks (or communities). We then dichotomized connectivity profiles of lesional parcels into those belonging to the same functional community as the focal cortical dysplasia (intra-community) and those adhering to other communities (inter-community). Applying hierarchical clustering to community-reconfigured connectome profiles identified three lesional classes with distinct patterns of functional connectivity: decreased intra-and inter-community connectivity, a selective decrease in intra-community connectivity, and increased intra-as well as inter-community connectivity. Hypo-connectivity classes were mainly composed of focal cortical dysplasia type IIB, while the hyperconnected lesions were type IIA. With respect to whole-brain networks, patients with hypoconnected focal cortical dysplasia and marked structural damage showed only mild imbalances, while those with hyperconnected subtle lesions had more pronounced topological alterations. Correcting for interictal epileptic discharges did not impact connectivity patterns. Multivariate structural equation analysis provided a mechanistic model of such complex, diverging interactions, whereby the focal cortical dysplasia structural makeup shapes its functional connectivity, which in turn modulates whole-brain network topology.

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Section: Discussionmentioning

confidence: 99%

A connectome-based mechanistic model of focal cortical dysplasia

Hong

Lee

Gill

et al. 2019

Brain

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“…Multiple causative factors have been implicated in the development of human mTLE/HS, including febrile seizures, brain trauma, inflammatory brain conditions, as well as genetic and epigenetic factors; it is likely that many cases may be multifactorial with regard to cause ( 15 – 19 ). Regardless of cause, the abnormal hippocampus is structurally and functionally connected to the adjacent mesial temporal lobe, and these structures are believed to develop an epileptic circuit ( 20 ). MRI can detect focal changes in brain architecture that can provide clues regarding etiology and treatment; this is visible as a change in the volume of a given region of the brain ( 14 ).…”

Section: Introductionmentioning

confidence: 99%

A Subset of Dogs with Presumptive Idiopathic Epilepsy Show Hippocampal Asymmetry: A Volumetric Comparison with Non-Epileptic Dogs Using MRI

et al. 2017

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MRI-acquired volumetric measurements from 100 dogs with presumptive idiopathic epilepsy (IE) and 41 non-epileptic (non-IE) dogs were used to determine if hippocampal asymmetry exists in the IE as compared to the non-IE dogs. MRI databases from three institutions were searched for dogs that underwent MRI of the brain and were determined to have IE and those that were considered non-IE dogs. Volumes of the right and left hippocampi were measured using Mimics® software. Median hippocampal volumes of IE and non-IE dogs were 0.47 and 0.53 cm3, respectively. There was no significant difference in overall hippocampal volume between IE and non-IE dogs; however, IE dogs had greater hippocampal asymmetry than non-IE dogs (P < 0.012). A threshold value of 1.16 from the hippocampal ratio had an 85% specificity for identifying IE-associated asymmetry. Thirty five percent of IE dogs had a hippocampal ratio >1.16. Asymmetry was not associated with any particular hemisphere (P = 0.67). Our study indicates that hippocampal asymmetry occurs in a subset of dogs with presumptive idiopathic/genetic epilepsy, suggesting a structural etiology to some cases of IE.

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“…Ictal propagation to the cingulate gyrus has frequently been observed among patients with temporallobe epilepsy [18].However,YCShih found in patients with left mesial temporal lobe epilepsy with hippocampal sclerosis, the left inferior cingulum bundle underwent degeneration in tandem with the left hippocampus volume, whereas intrinsic functional connectivity seems to react by compensating for the loss of connectivity. Their results suggested that increased intrinsic functional connectivity of the contralesional hippocampus was a compensatory response to decreased hippocampal connectivity on the lesion side [23].According to the hypothesis, we speculate that the PCG lesion and hippocampus functional connectivity decreased,but the contralesional PCG and hippocampus have extensive unctional connections. Fundamental to the original concept of the EZ was the idea of one or more regions of brain involved in the primary organization of the ictal discharge, rather than a ''focus''.Indeed, from the outset of SEEG development, the EZ was seen as a set of interconnected regional systems [24].…”

Section: Discussionmentioning

confidence: 59%

Electroclinical characteristics of seizures arising from the posterior cingulate cortex and surgical outcomes based on stereoelectroencephalography (SEEG)

Yan¹,

Wang²,

Deng³

et al. 2020

Preprint

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Background Seizures arising from the posterior cingulate cortex are rare, and few studies have to characterized the clinical presentation of such seizures within the anatomic context of the limbic network. We aimed to characterize the electrophysiological properties and clinical features of seizures arising from the PCC and surgical outcomes based on data from stereoelectroencephalography (SEEG).Methods The present retrospective study included 12 patients with medically intractable epilepsy, all diagnosed with posterior cingulate epilepsy via stereoelectroencephalography (SEEG) at Sanbo Hospital between 2014 and 2018.This retrospective analysis included clinical semiology, scalp EEG/SEEG findings and surgical outcomes of twelve intractable PCE patients.Results Six of the twelve patients reported auras, including vestibular responses (3/6),blurred vision (2/6), and fear and déjà vu(1/6). Clinical semiology included dialeptic seizures(3/12),automotor seizures(4/12) and complex motor behaviours(5/12).The classifications of scalp EEG varied, including bilateral regional posterior temporal-occipital discharges in eight cases, regional anterior-middle temporal discharges in two cases, and no epileptic discharge in two cases.In five patients, ictal onset occurred mainly in the tempo–parietal–occipital area.In ten patients, the seizure onset zone by SEEG occurred in the posterior cingulate gyrus, which spread to the medial temporal, precuneus, inferior parietal lobe and long insular gyrus. However, for the two patients with posterior cingulate lesions, the seizure onset zone was the contralateral hippocampal head that spread to the posterior cingulate lesion. One patient was seizure free after posterior cingulate gyrus lesion resection, but another had 50% fewer seizures by using SEEG-guided radiofrequency thermocoagulation. Nine patients who underwent epilepsy surgery were seizure-free(Engel IA: 7/9;EngelIB: 2/9).One patient showed a 30% reduction in seizures by using SEEG-guided radiofrequency thermocoagulation but not surgical resection.Conclusions Our findings indicate that the clinical characteristics of posterior cingulate epilepsy vary among patients, and recognition of a posterior cingulate focus is challenging, especially with MRI-negative epilepsies.Scalp EEG is of little use when attempting to localize posterior cingulate seizures.For patients with pharmacoresistant posterior cingulateepilepsy, favourable outcomes (Engel class I) could be observed by using SEEG.The SEEG findingsin PCE showed that the seizure onset zone and epileptogenic zone were a set of interconnected regional systems.Clinical trial registration Restrospective case reports do NOT need registration of clinical trials.

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Hippocampal Atrophy Is Associated with Altered Hippocampus–Posterior Cingulate Cortex Connectivity in Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

Cited by 9 publications

References 36 publications

A connectome-based mechanistic model of focal cortical dysplasia

A connectome-based mechanistic model of focal cortical dysplasia

A Subset of Dogs with Presumptive Idiopathic Epilepsy Show Hippocampal Asymmetry: A Volumetric Comparison with Non-Epileptic Dogs Using MRI

Electroclinical characteristics of seizures arising from the posterior cingulate cortex and surgical outcomes based on stereoelectroencephalography (SEEG)

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