H MRS) has been proposed as a lateralizing method for the presurgical evaluation of patients with medically intractable temporal lobe epilepsy (TLE). Studies have shown correlations between temporal lobe (TL) NAA and seizure frequency and TL NAA/Cr and the duration of epilepsy in patients with TLE. This latter finding may suggest that progressive neuronal dysfunction may occur in both temporal lobes in patients with TLE even when the seizures originate in only one temporal lobe. We analyzed our data in an attempt to find a possible correlation between extension of neuronal dysfunction based on NAA measures and duration of epilepsy.
The term hippocampal sclerosis was originally used to describe a shrunken and hardened hippocampus which histologically displayed neuronal loss and glial proliferation. These alterations are mainly located in the hilus of the dentate gyrus and in the CA1 and CA3 pyramidal cell layers but all hippocampal regions may show neuronal cell loss to varying degrees. A number of morphologic and cytochemical findings are associated with mesial temporal sclerosis especially within the dentate gyrus. These changes include selective loss of inhibitory interneurons abnormal sprouting of axons reorganization of neural transmitter receptors alterations in second messenger systems and hyperexcitability of the granule cells. Extrahippocampal pathology is also found at other temporal lobe structures. Frequent extrahippocampal pathology affects the amygdala first seen with neuronal cell loss and gliosis in the laterobasal complex. Surgical removal of this epileptogenic area can be curative or provide significant reduction in seizure frequency in the majority of individuals. Magnetic resonance imaging (MRI) is highly sensitive in detecting and locating mesial temporal sclerosis when a correct MRI temporal lobe protocol is used. The most important MRI findings atrophy and abnormal T2 signal allow us to detect mesial temporal sclerosis in the majority of the cases. Secondary MRI findings help in the diagnosis and lateralization of mesial temporal sclerosis in patients with subtle primary findings and in cases of bilateral hippocampal abnormalities. The development of advanced magnetic resonance (MR) techniques such as functional MR diffusion or transference of magnetization will lead to greater understanding of this pathology and will improve our diagnostic capacity.
The incidence and structural basis of nonlesional medial temporal lobe epilepsy (MTLE) without hippocampal atrophy (HA) is not known. Reports suggest that 5–15% of patients with hippocampal sclerosis (HS) do not have HA. We reviewed 57 patients with MTLE who underwent magnetic resonance imaging (MRI) volumetric studies anteromedial temporal lobectomy (TL) and quantitative cell counts of the resected hippocampus and who had at least 1 year of surgical follow-up. We compared demographic pathologic and outcome data among patients with and without HA. Ten of the 57 patients did not have HA. Nine of the 10 patients had depth EEG for localization of seizure onset because of discordance or insufficient localization. Five patients had pathologic evidence of HS. Longer duration of epilepsy correlated inversely with the presence of HA. Outcome was not significantly different between patients with and without HA. We conclude that the incidence of MTLE and HS without HA is 9%. Except for duration of epilepsy there were no differences in the clinical syndrome or surgical outcome of patients with and without HA.
The G1465A polymorphism in the gene of the GABA type B receptor subunit 1 (GABABR1) has been linked to the risk for temporal lobe epilepsy (TLE). However six replication studies did not show significant association between the G1465A GABABR1 gene variant and TLE. The authors examined this association in a sample of 102 patients with mesial TLE with hippocampal sclerosis (MTLE-HS) and 71 controls. The genotype distribution varied significantly between patients and controls. Heterozygous carriers of the A-allele had a 10-fold increase in risk for MTLE-HS (OR 10.01; 95% CI 3.98–25.18 p = 3.788E−08).
Figure 6. (A) Coronal T2-weighted image shows left hippocampal sclerosis with diminished size high signal intensity and loss of internal features. Compare with normal right hippocampus in which a dark line (arrows) is clearly within it and probably corresponds to the stratum lacunosum. (B) Coronal view from positron emission tomography obtained during interictal period shows decreased metabolism throughout the corresponding temporal lobe. As a general rule the abnormality on metabolic studies is always more extensive than that seen on anatomical studies. (Color version of figure is available online.)
Figure 11. (A) Lateral radiograph clearly shows position of subdural grid in the patient with epileptic discharges in the right frontal cortex and in whom the MRI study identified a possible discreet lesion. (B) Axial T2-weighted image shows the possible cortical malformation (thick arrow). Note the cerebral cortex neighboring the lesion is swollen. The presence of the subdural grid (thin arrows) does not produce any significant artifact. The subdural fluid collection over the grid was judged to be not clinically significant. Resection of the lesion confirmed a balloon cell type dysplasia and the patient did well.
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