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. 2010 Jul 28;30(30):10076–10085. doi: 10.1523/JNEUROSCI.6309-09.2010

Table 1.

Patient characteristics

Patient Sex Age at onset/surgery (years) n Duration of seizures (s) Electrodes Electrodes total/onset Seizure type (n) Onset activity Etiology Etiology (based on pathology) Lobe of involvement
A M 3/37 4 76, 63, 61, 134 Grids, strips, and depths 100/5 CPS + 2nd (4) Beta, alpha, delta Unknown No significant abnormalities Temporal (lateral)
B F 20/45 4 114, 102, 121, 142 Depths 65/5 CPS + 2nd (4) Delta Temporal lobe–MTS No pathology obtaineda Temporal (mesial)
C F 15/46 5 87, 93, 102, 100, 112 Grids, strips, and depths 122/5 CPS + 2nd (5) Beta, alpha, delta Cortical dysplasia Cortical dysplasia Temporo-parieto-occipital
D F 17/45 3 80, 82, 42 Depths 40/2 CPS + 2nd, CPS (2, 1) Beta, delta Possible post-infectious No pathology obtainedb Parieto-occipital
E M 7/22 2 87, 92 Grids, strips, and depths 124/4 CPS + 2nd (2) Delta Cortical dysplasia Cortical dysplasia Frontal (cingulate)
F F 14/28 4 331, 111, 84, 128 Grids, strips, and depths 94/22 CPS + 2nd, CPS, SPS (1, 1, 2) Delta Encephalitis Reactive gliosis Temporal (mesial)
G M 17/29 7 93, 137, 104, 134, 156, 179, 101 Depths 70/2 CPS, SPS (5, 2) Delta Traumatic brain injury Reactive gliosis Temporal (mesial)
H F 13/31 2 65, 90 Depths 34/4 CPS (2) Delta Temporal lobe–MTS No significant abnormalities Temporal (mesial)
I M 43/45 8 55, 57, 63, 49, 58, 199, 54, 90 Depths 64/4 CPS + 2nd, CPS, SPS (1, 1, 6) Alpha, delta Unknown No pathology obtaineda Temporal (mesial and lateral)
J M 14/19 4 82, 138, 123, 40 Grids, strips, and depths 80/3 SPS (4) Alpha, delta Temporal lobe–MTS Hippocampal sclerosis Temporo-parieto-occipital
K F 59/65 5 171, 121, 105, 224, 133 Depths 68/2 CPS, SPS (4, 1) Beta, alpha Unknown No pathology obtainedc Frontal (orbito-frontal)

Age at onset indicates the age at which seizures are first described by the patient. For each subject, n seizures were analyzed with durations listed in the fifth column. “Grids” and “strips” refer to surface (pial) electrode arrays that were also always accompanied by depth electrodes. “Depths” refer to patients who only received orthogonal placement of intraparenchymal arrays of electrodes. The total number of intracranial electrodes and the number of electrodes involved at seizure onset are listed for the dominant seizure type. All seizure types were complex partial seizures which had secondary generalization (CPS + 2nd), complex partial seizures without secondary generalization (CPS), or simple partial seizures (SPS); the number of each type of seizure for each patient is indicated. The frequency bands of maximum power at seizure onset were estimated using standard power spectrum analysis. Power spectra (Hann taper) were computed for 1 s of ECoG data immediately after clinical determination of seizure initiation and averaged over the onset electrodes. Beta, 15–30 Hz; alpha, 8–12 Hz; theta, 4–8 Hz; delta, 1–4 Hz. The etiology based on history, imaging, and seizure semiology refers to a diagnosis made by the clinical team with all available data before implantation of electrodes, surgical resection, and pathological examination of resected tissue. The etiology based on pathology comes directly from the clinical determination made by neuropathologists. The lobe of involvement was determined by examination of the seizure onsets on the intracranial recording electrodes. F, Female; M, male; MTS, mesial temporal sclerosis.

aBilateral onsets, no resection performed.

bEloquent cortex, no resection performed.

cPatient decided not to go forward with resection.