title: Three-dimensional hippocampal atrophy maps distinguish two common temporal lobe seizure-onset patterns.
abstract: OBJECTIVE
  Current evidence suggests that the mechanisms underlying depth electrode-recorded seizures beginning with hypersynchronous (HYP) onset patterns are functionally distinct from those giving rise to low-voltage fast (LVF) onset seizures. However, both groups have been associated with hippocampal atrophy (HA), indicating a need to clarify the anatomic correlates of each ictal onset type. We used three-dimensional (3D) hippocampal mapping to quantify HA and determine whether each onset group exhibited a unique distribution of atrophy consistent with the functional differences that distinguish the two onset morphologies.
  
  
  METHODS
  Sixteen nonconsecutive patients with medically refractory epilepsy were assigned to HYP or LVF groups according to ictal onset patterns recorded with intracranial depth electrodes. Using preimplant magnetic resonance imaging (MRI), levels of volumetrically defined HA were determined by comparison with matched controls, and the distribution of local atrophy was mapped onto 3D hippocampal surface models.
  
  
  RESULTS
  HYP and LVF groups exhibited significant and equivalent levels of HA ipsilateral to seizure onset. Patients with LVF onset seizures also showed significant contralateral volume reductions. On ipsilateral contour maps HYP patients exhibited an atrophy pattern consistent with classical hippocampal sclerosis (HS), whereas LVF atrophy was distributed more laterally and diffusely. Contralateral LVF maps also showed regions of subicular atrophy.
  
  
  CONCLUSIONS
  The HS-like distribution of atrophy and the restriction of HA to the ipsilateral hippocampus in HYP patients are consistent with focal hippocampal onsets, and suggest a mechanism utilizing intrahippocampal circuitry. In contrast, the bilateral distribution of nonspecific atrophy in the LVF group may reflect mechanisms involving both hippocampal and extrahippocampal networks.
authors.affiliation: Department of Neurobiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095-7169, USA.
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Ogren
authors.forename: Anatol
authors.initials: A
authors.lastname: Bragin
authors.forename: Charles L
authors.initials: CL
authors.lastname: Wilson
authors.forename: Gil D
authors.initials: GD
authors.lastname: Hoftman
authors.forename: Jack J
authors.initials: JJ
authors.lastname: Lin
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Dutton
authors.forename: Tony A
authors.initials: TA
authors.lastname: Fields
authors.forename: Arthur W
authors.initials: AW
authors.lastname: Toga
authors.forename: Paul M
authors.initials: PM
authors.lastname: Thompson
authors.forename: Jerome
authors.initials: J
authors.lastname: Engel
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Staba
mesh_terms: D000293:Adolescent; D000328:Adult; D017668:Age of Onset; D001284:Atrophy / Q000209:etiology / Q000473:pathology; D001931:Brain Mapping; D002648:Child; D004833:Epilepsy, Temporal Lobe / Q000145:classification* / Q000150:complications / Q000473:pathology*; D005260:Female; D006624:Hippocampus / Q000473:pathology*; D006801:Humans; D021621:Imaging, Three-Dimensional / Q000379:methods*; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D012640:Seizures / Q000145:classification / Q000209:etiology; D055815:Young Adult