No significant differences were promotion information observed in the thalamus or caudate. Within the L TLE group, only the hippocampus showed a trend toward lower volume in the ipsilateral vs. contralateral side. Discussion In this study we compared L TLE, NL TLE, IGE, and healthy controls using the same methodology and same 3 T scanner. Our study revealed that patients with TLE and IGE demonstrated similar tissue specific atrophies in the whole brain and white matter. After correcting for age and gender, normal brain volume, normal grey matter volume and normal white matter volume were lower in the epilepsy group compared to controls, but predominantly as a result of white matter volume loss. Our results in L TLE patients were similar to varying TLE study reports in relation to atrophy at various subcortical structures such as the hippocampus and basal ganglia.

The extent of atrophy noted in TLE patients suggests that the impact of temporal seizures is more widespread than the immediate temporal vicinity of the epileptogenic region. Furthermore, the bilateral distribution of tissue specific atrophy suggests that the neuronal atrophy extends to both hemispheres, regardless Inhibitors,Modulators,Libraries of the side of focal epileptic origin. Our results suggest that patients with chronic epilepsy, whether TLE or IGE, have chronic atrophy, mostly of white matter and of various subcortical deep grey matter structures particularly hippocampi and amygdale bilaterally. Altered white matter integrity has been reported in TLE, with association to cognitive and clinical profiles as measured on diffusion tensor imaging studies in the temporal, cerebellar and fronto parietal structures.

Extensive white matter tracts abnormalities on DTI were identified also in JME. Findings of ipsilateral thalamic hypometabolism on positron emission tomography studies have been described in patients with Inhibitors,Modulators,Libraries TLE, often attributed to a diaschisis effect. It has been postulated that hippocampal cell loss may result in decreased efferent synaptic activity to the thalamus and basal ganglia, causing decreased neuronal activity in these structures with consequent hypometabolism. It remains unknown whether Inhibitors,Modulators,Libraries the process of subcortical deep grey matter atrophy seen in volumetric studies is due to a similar mechanism to the ipsilateral hypometabolism seen in PET studies in TLE patients.

Several limitations in Inhibitors,Modulators,Libraries our study which may have impacted our results and statistical power should be acknowledged. Our study was retrospective, and included Inhibitors,Modulators,Libraries a relatively small patient sample. Consesquently this might have altered our ability to detect Tenatoprazole? subtle volume changes. In particular, we saw many intriguing statistical trends that should be investigated in a larger study. In addition, we performed a cross sectional evaluation, making it difficult to ascertain progressive developments. We also did not have sufficient power to analyze the impact of medication, which may have modified atrophy rates.