title: Intracranial EEG in temporal lobe epilepsy: location of seizure onset relates to degree of hippocampal pathology.
abstract: OBJECTIVE
  To determine whether the specific location of electrographic seizure onset in the temporal lobe is related to hippocampal pathology in temporal lobe epilepsy (TLE).
  
  
  METHODS
  Consecutive presurgical patients with scalp EEG-video evidence of TLE and no or mild hippocampal atrophy (HA) on magnetic resonance imaging (MRI) were prospectively studied by using depth and subdural strip electrode recordings to identify the site of the initial ictal discharge (IID). Thirty-four patients had either no or mild HA (HA- group). Four additional patients with moderate or marked HA (HA+ group) who required depth and strip electrodes served as a comparison group. Hippocampal pathology was assessed by MRI volumetrics and histopathologic grade of sclerosis (HS).
  
  
  RESULTS
  Thirty-eight patients were investigated. In the HA- group, 10 patients had lobar ictal EEG onsets in the hippocampus (HF), medial paleocortex (MPC), and lateral neocortex (LNC); eight cases had regional IIDs in both HF and MPC; 12 persons had IIDs completely outside the HF; three cases lacked depth electrodes, and only one case (3%) had an IID confined to the HF. By contrast, three (75%) of four HA+ cases had IIDs confined to the HF (p = 0.002). Similarly, in 12 patients with low-grade HS, IIDs confined to the HF area were seen significantly less often than in six cases with high-grade HS (p = 0.025).
  
  
  CONCLUSIONS
  In this study of a large number of patients with no to mild and a smaller group with moderate to marked HA and HS, the location of seizure onset in the temporal lobe was related to the degree of hippocampal pathology. Absence of HA and low-grade HS was each associated with IIDs in both the hippocampus and medial (with or without lateral) temporal cortex, or only the MPC or LNC. Marked HA and high-grade HS both were associated with IIDs restricted to the HF.
authors.affiliation: Epilepsy Center and Clinical Neurophysiology Laboratories, Swedish Neuroscience Institute, Seattle, Washington 98122, USA. david.vossler@swediah.org
authors.forename: David G
authors.initials: DG
authors.lastname: Vossler
authors.forename: Diana L
authors.initials: DL
authors.lastname: Kraemer
authors.forename: Alan M
authors.initials: AM
authors.lastname: Haltiner
authors.forename: Steven W
authors.initials: SW
authors.lastname: Rostad
authors.forename: Bent O
authors.initials: BO
authors.lastname: Kjos
authors.forename: Bradley J
authors.initials: BJ
authors.lastname: Davis
authors.forename: John D
authors.initials: JD
authors.lastname: Morgan
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Caylor
mesh_terms: D001284:Atrophy / Q000473:pathology; D004567:Electrodes, Implanted; D004569:Electroencephalography / Q000379:methods / Q000706:statistics & numerical data*; D004833:Epilepsy, Temporal Lobe / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology*; D006624:Hippocampus / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D019579:Neocortex / Q000503:physiopathology; D011446:Prospective Studies; D012720:Severity of Illness Index; D013702:Temporal Lobe / Q000473:pathology / Q000503:physiopathology*