T2 hyperintense signal in patients with temporal lobe epilepsy with MRI signs of hippocampal sclerosis and in patients with temporal lobe epilepsy with normal MRI

Kubota, Bruno Y.; Coan, Ana Carolina; Yasuda, Clarissa L.; Cendes, Fernando

doi:10.1016/j.yebeh.2015.04.001

Cited by 10 publications

(10 citation statements)

References 19 publications

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“…Moreover, ictal fear, d ej a vu, and various sensations (cephalic, warm, or indescribably strange) are associated with an abnormal T2 relaxation on MRI imaging (Van Paesschen et al, 2001). A reduction in the white matter volume was also reported in temporal and extratemporal areas of TLE patients (Briellmann et al, 2007;Pell et al, 2008;Alhusaini et al, 2012;Kubota et al, 2015). Diffusion tensor imaging and functional MRI (fMRI) data further suggest that such white matter alterations in TLE include changes in the organization of amygdala face-processing networks because the integrity of the inferior longitudinal fasciculus (which connects anterior temporal and occipital lobes) as well as activation of the ipsilateral amygdala and occipital face-responsive region were both reduced (Riley et al, 2015).…”

Section: Amygdala Volume and Metabolismmentioning

confidence: 96%

Contribution of amygdala pathology to comorbid emotional disturbances in temporal lobe epilepsy

Yilmazer-Hanke

O’Loughlin

McDermott

2015

J of Neuroscience Research

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The amygdala contributes to the generation and propagation of epileptiform activity in temporal lobe epilepsy (TLE). Ictal symptoms such as fear, dreamy states (déjà vu, memory flashbacks, experiential hallucinations), epigastric auras, or sympathetic outflow with cardiovascular changes are often linked to a seizure focus in the amygdala. However, the amygdala may also play a role in comorbid anxiety, depression, and other psychiatric symptoms experienced in the interictal phase, especially in pharmacoresistant TLE. The few studies available on TLE-related alterations in surgical amygdala specimens indicate loss of both excitatory spiny projection neurons as well as interneurons in nuclei with a cortex-like architecture, which may influence mechanisms of feedforward and feedback inhibition. Studies of the human amygdala indicate global alterations in the density of AMPA/kainate, metabotropic glutamate, γ-aminobutyric acid type A (GABAA ), muscarinic M2 and M3, serotonergic 5-HT1A, and adrenergic α1 receptors. Also, amygdala GABAergic and neuropeptide Y (NPY) systems affected in human TLE are both involved in antiepileptic and anxiolytic effects. Experimental and human positron emission tomography studies indicate changes in amygdala serotonergic, NPY Y1 receptor, neurokinin, and opioid systems in emotional disturbances in TLE. Of particular interest is the reduction in amygdala volume in conjunction with ictal fear, seizure focus in the amygdala, and amygdala and hippocampal sclerosis in TLE patients. In contrast, patients with interictal depression often have an intact or even enlarged amygdala and a negative MRI associated with amygdala hypometabolism, which can be associated with limbic autoimmune encephalitis. These findings suggest a differential role of TLE-related amygdala changes in ictal and interictal emotional disturbances.

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Section: Amygdala Volume and Metabolismmentioning

confidence: 96%

Contribution of amygdala pathology to comorbid emotional disturbances in temporal lobe epilepsy

Yilmazer-Hanke

O’Loughlin

McDermott

2015

J of Neuroscience Research

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“…We performed a routine MRI protocol for epilepsy cases in a 3T Philips Achieva scanner, as previously described (21,22). Such protocol included T1-weighted 3D images, T1 and T2weighted images in the axial and coronal planes, fluid-attenuated inversion recovery (FLAIR) images, susceptibility weighted imaging (SWI), inversion recovery (IR) coronal imaging, and diffusion-weighted imaging (DWI).…”

Section: Mri Acquisition and Processingmentioning

confidence: 99%

“…We processed the T2-weighted multiecho coronal images of all individuals with the Aftervoxel software (http://http://www. liv.ic.unicamp.br/~bergo/aftervoxel) as previously documented (21). The region of interest (ROI) was defined using the postoperative T1-weighted image as a visual control to localize the surgical resected area.…”

Section: Relaxometrymentioning

confidence: 99%

Histopathological Correlations of Qualitative and Quantitative Temporopolar MRI Analyses in Patients With Hippocampal Sclerosis

et al. 2021

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Hippocampal sclerosis (HS) is a common cause of pharmacoresistant focal epilepsy. Here, we (1) performed a histological approach to the anterior temporal pole of patients with HS to evaluate cortical and white matter (WM) cell populations, alteration of myelin integrity and markers of neuronal activity, and (2) correlated microscopic data with magnetic resonance imaging (MRI) findings. Our aim was to contribute with the understanding of neuroimaging and pathophysiological mechanisms of temporal lobe epilepsy (TLE) associated with HS. We examined MRIs and surgical specimens from the anterior temporal pole from TLE-HS patients (n = 9) and compared them with 10 autopsy controls. MRIs from healthy volunteers (n = 13) were used as neuroimaging controls. Histological techniques were performed to assess oligodendrocytes, heterotopic neurons, cellular proliferative index, and myeloarchitecture integrity of the WM, as well as markers of acute (c-fos) and chronic (ΔFosB) activities of neocortical neurons. Microscopic data were compared with neuroimaging findings, including T2-weighted/FLAIR MRI temporopolar blurring and values of fractional anisotropy (FA) from diffusion-weighed imaging (DWI). We found a significant increase in WM oligodendrocyte number, both in hematoxylin and eosin, and in Olig2-stained sections. The frequencies of oligodendrocytes in perivascular spaces and around heterotopic neurons were significantly higher in patients with TLE–HS compared with controls. The percentage of 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase; a marker of myeloarchitecture integrity) immunopositive area in the WM was significantly higher in TLE-HS, as well as the numbers of c-fos- and ΔFosB-immunostained neocortical neurons. Additionally, we demonstrated a decrease in axonal bundle integrity on neuroimaging, with a significant reduction in the FA in the anterior temporal pole. No differences were detected between individuals with and without temporopolar blurring on visual MRI analysis, considering the number of oligodendroglial cells and percentage of WM CNPase-positive areas. Also, there was no relationship between T2 relaxometry and oligodendrocyte count. In conclusion, our histopathological data support the following: (1) the hypothesis that repetitive neocortical neuronal activity could induce changes in the WM cellular constitution and myelin remodeling in the anterior temporal pole from patients with TLE-HS, (2) that oligodendroglial hyperplasia is not related to temporal blurring or T2 signal intensity on MRI, and (3) that reduced FA is a marker of increase in Olig2-immunopositive cells in superficial temporopolar WM from patients with TLE-HS.

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“…6,7 The use of quantitative magnetic resonance imaging (MRI) techniques provides objective data and can be a useful tool for the understanding of the underlying mechanisms involved in hippocampal damage. [6][7][8][9][10][11][12][13][14][15] MRI features that characterize HS are HA, loss of hippocampal internal structures, and increased hippocampal T2 signal. [6][7][8] Previous studies have shown that reduced hippocampal volumes are associated with neuronal loss.…”

Section: Introductionmentioning

confidence: 99%

“…[6][7][8][9][10][11][12][13][14][15] MRI features that characterize HS are HA, loss of hippocampal internal structures, and increased hippocampal T2 signal. [6][7][8] Previous studies have shown that reduced hippocampal volumes are associated with neuronal loss. 6,8 The presence of hyperintense T2 signal in the hippocampus is more likely to reflect gliosis in hippocampal formation.…”

Section: Introductionmentioning

confidence: 99%

Abnormality in hippocampal signal intensity predicts atrophy in patients with systemic lupus erythematosus

Lapa

Pedro

Francischinelli

et al. 2016

Lupus

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Objectives To quantify signal abnormalities in the hippocampus (Hsig) of patients with systemic lupus erythematosus (SLE) and to determine if Hsig predict hippocampal atrophy (HA) in SLE. Methods We included all SLE patients and healthy age- and sex-matched individuals with two magnetic resonance imaging (MRI) scans performed with a minimum of 1 year interval. All individuals underwent a standardized neuropsychological evaluation. Individual results were converted into standard scores and compared to normative data. SLE patients were additionally assessed for disease activity (SLE Disease Activity Index (SLEDAI)), damage (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI)), and the presence of antiphospholipid antibodies. MRI was performed on an Elscint 2 T scanner and T1 inversion recovery and T2 coronal images were used for analysis. Volumetric (HV) and signal quantification (Hsig) were determined by standardized protocols. Results We included 54 SLE patients (48 women; mean age 32.2 ± 10.56 years). Hsig were found at study entry in 15 (45.5%) patients. Hsig in the body and tail of non-atrophic hippocampi correlated with progression of volume loss during the follow-up period ( r = 0.8, p < 0.001). The presence of Hsig in the head of atrophic hippocampi correlated with progression of HA ( r = 0.73, p = 0.005) during the same period. No correlation of Hsig and disease activity or prednisone dose was observed. Conclusion HA is frequently observed in SLE patients and volume loss is progressive in a subgroup of patients. The evaluation of Hsig is an easy tool to determine patients that may have progressive hippocampal volume loss and should be followed more closely with MRI and cognitive evaluation.

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T2 hyperintense signal in patients with temporal lobe epilepsy with MRI signs of hippocampal sclerosis and in patients with temporal lobe epilepsy with normal MRI

Cited by 10 publications

References 19 publications

Contribution of amygdala pathology to comorbid emotional disturbances in temporal lobe epilepsy

Contribution of amygdala pathology to comorbid emotional disturbances in temporal lobe epilepsy

Histopathological Correlations of Qualitative and Quantitative Temporopolar MRI Analyses in Patients With Hippocampal Sclerosis

Abnormality in hippocampal signal intensity predicts atrophy in patients with systemic lupus erythematosus

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