Dilatation of the Lateral Ventricles as a Common Brain Lesion in Epilepsy

Thom, Douglas A.

doi:10.1097/00005053-191711000-00004

Cited by 4 publications

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“…In 1917, Thom was the first to note ventricle enlargement in individuals with epilepsy; he reported lateral ventricle dilation following postmortem examinations of patients with idiopathic epilepsy (Thom, 1917). But over the decades, interest in the ventricular system has never matched that seen in other disorders.…”

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confidence: 99%

Ventricular enlargement in new-onset pediatric epilepsies

et al. 2011

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Summary Purpose To examine baseline and prospective (2-year) changes in third, fourth, and lateral ventricle volumes in children with new-onset idiopathic epilepsies and controls (age 8–18 years). Methods Structural magnetic resonance imaging (MRI) were collected from children with idiopathic generalized epilepsy (IGE, n = 29), idiopathic localization-related epilepsy (ILRE, n = 30), and healthy controls (HCs, n = 49). Volumes of the third, fourth, and lateral ventricles were derived and compared across groups, followed by shape analyses, to identify specific regions of ventricular abnormality. Of the initial cohort, a consecutive sample of 71 children returned 2 years later for reimaging and determination of progressive changes in the ventricular system. Key Findings At baseline, children with new-onset IGE had significantly larger lateral and third ventricle volumes relative to the HC group. In addition, lateral ventricle enlargement in IGE was significantly greater compared to new-onset ILRE. Shape analysis of the lateral ventricles revealed that volume expansion in IGE was selective for the anterior horn, a region surrounded by the lateral and medial frontal lobes as well as basal ganglia. These abnormalities did not progress over a 2-year interval. Significance Abnormalities in brain development prior to onset and diagnosis of epilepsy are evident and reflected in expansion of the ventricular system, especially among children with IGE. These abnormalities appear to represent an antecedent and possibly static finding given the lack of progressive ventricular expansion over the 2-year interval following diagnosis and treatment.

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confidence: 99%

Ventricular enlargement in new-onset pediatric epilepsies

et al. 2011

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“…Hippocampal scarring and/or gliosis is often observed in animal models of TLE as well as in humans, where it leads to hippocampal atrophy [46][47][48][49]. Hippocampal atrophy in TLE patients has been observed using MRI T 2 weighted scans where the ventricles adjacent to the hippocampus expand along with a reduction of hippocampal size [50][51][52]. We created epileptic rats as previously described, and performed T 2 weighted MRI eight weeks post KA in order to record their ventricular volumes prior to Thiamet-G treatment.…”

Section: Chronic Inhibition Of Oga Activity Increased Hippocampal Atrmentioning

confidence: 99%

Human and rodent temporal lobe epilepsy is characterized by changes in O-GlcNAc homeostasis that can be reversed to dampen epileptiform activity

Sánchez

Parrish

Rich

et al. 2019

Neurobiology of Disease

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Temporal Lobe Epilepsy (TLE) is frequently associated with changes in protein composition and post-translational modifications (PTM) that exacerbate the disorder. O-linked-β-N-acetyl glucosamine (O-GlcNAc) is a PTM occurring at serine/threonine residues that is derived from and closely associated with metabolic substrates. The enzymes O-GlcNActransferase (OGT) and O-GlcNAcase (OGA) mediate the addition and removal, respectively, of the O-GlcNAc modification. The goal of this study was to characterize OGT/OGA and protein O-GlcNAcylation in the epileptic hippocampus and to determine and whether direct manipulation of these proteins and PTM's alter epileptiform activity. We observed reduced global and protein specific O-GlcNAcylation and OGT expression in the kainate rat model of TLE and in human TLE hippocampal tissue. Inhibiting OGA with Thiamet-G elevated protein O-GlcNAcylation, and decreased both seizure duration and epileptic spike events, suggesting that OGA may be a therapeutic target for seizure control. These findings suggest that loss of O-GlcNAc homeostasis in the kainate model and in human TLE can be reversed via targeting of O-GlcNAc related pathways.

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“…Thom, 1917, was the first to report dilatations in the LV and cortical lesion in epilepsy patients in post‐mortem examinations. The relations between the volumes of the brain ventricles and various types of epileptic seizures has been reported (Betting et al, 2006a,b; Kalnin et al, 2008; Jackson et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…Increase of cerebral ventricular volumes and cortical atrophy have been associated with various neurological and psychiatric disorders (Moriguchi, 1981;Wright et al, 2000), including dementia (Carmichael et al, 2007), Alzheimer's disease (Nestor et al, 2008), mesiotemporal epilepsy (Lehericy et al, 1995), bipolar disorder (Edmiston et al, 2011), multiple sclerosis (Dalton et al, 2006) and autism (Palmen et al, 2005). Thom, 1917, was the first to report dilatations in the LV and cortical lesion in epilepsy patients in post-mortem examinations. The relations between the volumes of the brain ventricles and various types of epileptic seizures has been reported (Betting et al, 2006a,b;Kalnin et al, 2008;Jackson et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Comparison of cerebral ventricular volumes and cortical thicknesses in normal rats and Genetic Absence Epilepsy (GAERS): A developmental study

Kirazlı

Bay

Çakmak

et al. 2018

Intl J of Devlp Neuroscience

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Ventricular enlargement and cortical atrophy have been associated with various central nervous system diseases. The aim of the present study was to measure the volumes of the lateral (LV) and third (3V) ventricles and to determine the cortical thickness for the motor (MCx), somatosensory (SSCx), visual (VCx) and auditory (AuCx) cortex and the striatum of Wistar rats, in a developmental series at 10, 20, 30, and 60 days postnatal, and to compare them with similar data from genetic absence epilepsy rats from Strasbourg (GAERS). Serial sections were taken from the brains of Wistar and GAERS animals and were Nissl stained. Photographs were taken from specific sections of the brain for measurements of ventricular volume, cortical and striatal thickness. The image-j computer program was used for the volume and thickness measurements. The data was statistically analyzed by 3-way ANOVA using SPSS 15. Comparison of the measurements of GAERS and Wistar animals showed no statistically significant differences at any of the developmental stages regarding the ventricular (LV and 3V) volumes. However, at P60 and P30 of the MCx, P30 of the SSCx, P20 of the VCx and AuCx showed a significantly thinner cortical thickness in the GAERS than in the Wistar animals. The striatal measurements showed significant decrease in thickness of the striatum at P30 and P60. Further, brain size measurements (between the two temporal poles) showed significant decrease in the size at P30 and P60 of GAERS animals. The presence of thinner cortical and striatal thicknesses and smaller brain size in GAERS animals may suggests that these changes could be involved in the mechanism of epileptogenicity or be a result of the epileptogenicity.

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Dilatation of the Lateral Ventricles as a Common Brain Lesion in Epilepsy

Cited by 4 publications

References 0 publications

Ventricular enlargement in new-onset pediatric epilepsies

Ventricular enlargement in new-onset pediatric epilepsies

Human and rodent temporal lobe epilepsy is characterized by changes in O-GlcNAc homeostasis that can be reversed to dampen epileptiform activity

Comparison of cerebral ventricular volumes and cortical thicknesses in normal rats and Genetic Absence Epilepsy (GAERS): A developmental study

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