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Cortical Abnormalities (cortical + abnormality)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Involvement of the thalamocortical network in TLE with and without mesiotemporal sclerosis

EPILEPSIA, Issue 8 2010
Susanne G. Mueller
Summary Purpose:, The thalamus plays an important role in seizure propagation in temporal lobe epilepsy (TLE). This study investigated how structural abnormalities in the focus, ipsilateral thalamus and extrafocal cortical structures relate to each other in TLE with mesiotemporal sclerosis (TLE-MTS) and without hippocampal sclerosis (TLE-no). Methods:, T1 and high-resolution T2 images were acquired on a 4T magnet in 29 controls, 15 TLE-MTS cases, and 14 TLE-no. Thalamus volumes were obtained by warping a labeled atlas onto each subject's brain. Deformation-based morphometry was used to identify regions of thalamic volume loss and FreeSurfer for cortical thickness measurements. CA1 volumes were obtained from high-resolution T2 images. Multiple regression analysis and correlation analyses for voxel- and vertex-based analyses were performed in SPM2 and FreeSurfer. Results:, TLE-MTS had bilateral volume loss in the anterior thalamus, which was correlated with CA1 volume and cortical thinning in the mesiotemporal lobe. TLE-no had less severe volume loss in the dorsal lateral nucleus, which was correlated with thinning in the mesiotemporal region but not with extratemporal thinning. Discussion:, The findings suggest that seizure propagation from the presumed epileptogenic focus or regions close to it into the thalamus occurs in TLE-MTS and TLE-no and results in circumscribed neuronal loss in the thalamus. However, seizure spread beyond the thalamus seems not to be responsible for the extensive extratemporal cortical abnormalities in TLE. [source]

Neuroimaging and Neurophysiology of Periodic Lateralized Epileptiform Discharges: Observations and Hypotheses

EPILEPSIA, Issue 7 2007
Giridhar P. Kalamangalam
Summary:,Purpose: We assessed neuroimaging lesion type and distribution in patients with periodic lateralized epileptiform discharges (PLEDs), with a view to identifying electrographic differences between PLEDs associated with differing lesion locations. Our observations led us to consider a conceptual synthesis between PLEDs and periodic complexes (PCs). Methods: Retrospective review of acute neuroimaging results (CT/MRI) on patients identified to have EEG PLEDs, for the period 1999,2003 (n = 106). Blinded classification of original EEG recordings. Results: Neuroimaging abnormalities were classified as acute or chronic cortical, or acute or chronic subcortical. Seven out of 106 scans were classified nonlesional. Overall ,70% of scans had cortical abnormalities, whether acute or chronic; ,23% had subcortical abnormalities. "Cortical" PLEDs were significantly longer in duration (p < 0.05) and more variable in morphology (p < 0.01) than "subcortical" PLEDs. Conclusions: Structural brain disease commonly, but not invariably, underlies PLEDs; lesion type is spatiotemporally variable. Cortical and subcortical PLEDs have distinct EEG signatures. There is evidence that these may relate to mechanisms for other pathological large-scale oscillatory brain synchronies (e.g., PCs). [source]

Selective chronic stress-induced in vivo ERK1/2 hyperphosphorylation in medial prefrontocortical dendrites: implications for stress-related cortical pathology?

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2002
A. Trentani
Abstract Stress has been shown to affect brain structural plasticity, promote long-term changes in multiple neurotransmitter systems and cause neuronal atrophy. However, the mechanisms involved in these stress-related neural alterations are still poorly understood. Mitogen-activated protein kinase (MAPK) cascades play a crucial role in the transduction of neurotrophic signal from the cell surface to the nucleus and are implicated in the modulation of synaptic plasticity and neuronal survival. An intriguing possibility is that stress might influence brain plasticity through its effects on selective members of such intracellular signalling cascades responsible for the transduction of neurotrophin signals. Here, we have investigated the effects of stress on the expression of three members of the MAPK/extracellular-regulated kinase (ERK) pathway such as phospho-ERK1, phospho-ERK2 and phospho-cAMP/calcium-responsive element-binding protein (CREB) in the adult rat brain. Male rats were subjected to mild footshocks and the patterns of protein expression were analysed after 21 consecutive days of stress. We found that chronic stress induced a pronounced and persistent ERK1/2 hyperphosphorylation in dendrites of the higher prefrontocortical layers (II and III) and a reduction of phospho-CREB expression in several cortical and subcortical regions. We hypothesized that defects in ERK signalling regulation combined with a reduced phospho-CREB activity may be a crucial mechanism by which sustained stress may induce atrophy of selective subpopulations of vulnerable cortical neurons and/or distal dendrites. Thus, ERK-mediated cortical abnormalities may represent a specific path by which chronic stress affects the functioning of cortical structures and causes selective neural network defects. [source]

The Neuropathology of Autism

BRAIN PATHOLOGY, Issue 4 2007
Manuel F. Casanova MD
Autism is a brain disorder characterized by abnormalities in how a person relates and communicates to others. Both post-mortem and neuroimaging studies indicate the presence of increased brain volume and, in some cases, an altered gray/white matter ratio. Contrary to established gross findings there is no recognized microscopic pathology to autism. Early studies provided multiple leads none of which have been validated. Clinicopathological associations have been difficult to sustain when considering possible variables such as use of medications, seizures, mental retardation and agonal/pre-agonal conditions. Research findings suggest widespread cortical abnormalities, lack of a vascular component and an intact blood,brain barrier. Many of the previously mentioned findings can be explained in terms of a mini-columnopathy. The significance of future controlled studies should be judged based on their explanatory powers; that is, how well do they relate to brain growth abnormalities and/or provide useful clinicopathological correlates. [source]