Abstract
ObjectivePatients with temporal lobe epilepsy (TLE) with hippocampal sclerosis (HS) have diffuse subtle gray matter (GM) atrophy detectable by MRI quantification analyses. However, it is not clear whether the etiology and seizure frequency are associated with this atrophy. We aimed to evaluate the occurrence of GM atrophy and the influence of seizure frequency in patients with TLE and either normal MRI (TLE-NL) or MRI signs of HS (TLE-HS).MethodsWe evaluated a group of 172 consecutive patients with unilateral TLE-HS or TLE-NL as defined by hippocampal volumetry and signal quantification (122 TLE-HS and 50 TLE-NL) plus a group of 82 healthy individuals. Voxel-based morphometry was performed with VBM8/SPM8 in 3T MRIs. Patients with up to three complex partial seizures and no generalized tonic-clonic seizures in the previous year were considered to have infrequent seizures. Those who did not fulfill these criteria were considered to have frequent seizures.ResultsPatients with TLE-HS had more pronounced GM atrophy, including the ipsilateral mesial temporal structures, temporal lobe, bilateral thalami and pre/post-central gyri. Patients with TLE-NL had more subtle GM atrophy, including the ipsilateral orbitofrontal cortex, bilateral thalami and pre/post-central gyri. Both TLE-HS and TLE-NL showed increased GM volume in the contralateral pons. TLE-HS patients with frequent seizures had more pronounced GM atrophy in extra-temporal regions than TLE-HS with infrequent seizures. Patients with TLE-NL and infrequent seizures had no detectable GM atrophy. In both TLE-HS and TLE-NL, the duration of epilepsy correlated with GM atrophy in extra-hippocampal regions.ConclusionAlthough a diffuse network GM atrophy occurs in both TLE-HS and TLE-NL, this is strikingly more evident in TLE-HS and in patients with frequent seizures. These findings suggest that neocortical atrophy in TLE is related to the ongoing seizures and epilepsy duration, while thalamic atrophy is more probably related to the original epileptogenic process.
Highlights
The structural damage in patients with temporal lobe epilepsy (TLE) extends beyond the mesial temporal structures [1]
We demonstrated that a network of diffuse gray matter (GM) atrophy occurs in both TLE-hippocampal sclerosis (HS) and TLE and either normal MRI (TLE-NL) and that the atrophy in some regions is common to both groups, in TLE-NL there is no detectable atrophy in the mesial temporal structures
– GM atrophy in the mesial structures in TLE-HS and in bilateral thalamus in both TLE-HS and TLENL are related to the original epileptogenic process;
Summary
The structural damage in patients with temporal lobe epilepsy (TLE) extends beyond the mesial temporal structures [1]. This knowledge corroborates the hypothesis that TLE is a network disease [2]. Among patients with TLE, the phenotypic presentation, natural history and response to treatment vary significantly. 60– 70% of cases of TLE show MRI signs of hippocampal sclerosis (HS), a significant number of patients have normal MRIs [3]. Surgical specimens from drug-resistant MRI-negative TLE rarely show hippocampal cell loss compatible with HS [4,5], and this is considered a distinct entity from TLE-HS5
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