AbstractObjectiveStereotactic electroencephalography (SEEG) has been widely used to explore the epileptic network and localize the epileptic zone in patients with medically intractable epilepsy. Accurate anatomical labeling of SEEG electrode contacts is critically important for correctly interpreting epileptic activity. We present a method for automatically assigning anatomical labels to SEEG electrode contacts using a 3D‐segmented cortex and coregistered postoperative CT images.MethodStereotactic electroencephalography electrode contacts were spatially localized relative to the brain volume using a standard clinical procedure. Each contact was then assigned an anatomical label by clinical epilepsy fellows. Separately, each contact was automatically labeled by coregistering the subject's MRI to the USCBrain atlas using the BrainSuite software and assigning labels from the atlas based on contact locations. The results of both labeling methods were then compared, and a subsequent vetting of the anatomical labels was performed by expert review.ResultsAnatomical labeling agreement between the two methods for over 17 000 SEEG contacts was 82%. This agreement was consistent in patients with and without previous surgery (P = .852). Expert review of contacts in disagreement between the two methods resulted in agreement with the atlas based over manual labels in 48% of cases, agreement with manual over atlas‐based labels in 36% of cases, and disagreement with both methods in 16% of cases. Labels deemed incorrect by the expert review were then categorized as either in a region directly adjacent to the correct label or as a gross error, revealing a lower likelihood of gross error from the automated method.SignificanceThe method for semi‐automated atlas‐based anatomical labeling we describe here demonstrates potential to assist clinical workflow by reducing both analysis time and the likelihood of gross anatomical error. Additionally, it provides a convenient means of intersubject analysis by standardizing the anatomical labels applied to SEEG contact locations across subjects.

We analyzed volume and diffusivity measures of the corpus callosum (CC) in patients with temporal (TLE) and frontal (FLE) lobe epilepsy in comparison with healthy subjects. On high-resolution T1-weighted scans of 18 controls and 44 patients the volumes (cm(3)) of Witelson regions (WRs) and the entire CC were measured. The apparent diffusion coefficients (ADCs, 10(-5)mm(2)s(-1)) for the entire CC and three areas of interest were measured from co-registered ADC maps. The CC of patients with TLE and FLE, corrected for total brain volume, was smaller than that of controls. Patients' ADC values were higher than those of controls. Findings were significant for WR1, WR2, and WR6, the CC regions connecting the frontal and temporal lobes. Patients with FLE had smaller WR1 and higher ADC values; in patients with TLE, the findings were similar for WR6. Atrophy and increased diffusivity in subregions of the CC connecting homotopic contralateral cortical regions indicate anatomical abnormalities extending beyond the epileptogenic zone in FLE and TLE.

Imaging changes in patients with focal epilepsy are not only seen in areas where seizures arise but often also in remote locations. The mechanism for such changes is unknown. We aimed to investigate whether patients with temporal lobe epilepsy (TLE) have microstructural changes involving the posterior portion of the corpus callosum (CC), where it links the temporal lobes, using presurgical diffusion tensor imaging (DTI) sequences. Ten patients with medically intractable TLE (two mesial TLE, eight neocortical TLE) who had seizure-free surgical outcomes were compared with 10 healthy controls. The regions of interest were outlined at each Witelson region (WR). Fractional anisotropy (FA), apparent diffusion coefficient (ADC) and three principal diffusivity values (λ1, λ2, λ3) were determined in each WR. We performed tractography originating at each WR. In the TLE patients, the FA values were lower at the splenium of the corpus callosum (WR 7) compared to controls (p<0.05). Analysis of Eigen values in that location revealed that λ1 values were decreased while λ2 and λ3 values were increased (p<0.05). Tractography revealed the connection between both temporal lobes via WR 7. In conclusion, decreased FA values with decreased λ1 and increased λ2 and λ3 at the splenium of CC suggest that the pathologic changes, Wallerian degeneration, extend to the corpus callosum in TLE patients. Seizure-induced damage may cause secondary white matter degeneration along the tapetum and through the splenium of the corpus callosum, a potential pathway of spread in temporal lobe seizures.