title: Subcortical injury is an independent predictor of worsening neurological deficits following awake craniotomy procedures.
abstract: BACKGROUND
  Tailored craniotomies for awake procedures limit cortical exposure. Recently we demonstrated that the identification of eloquent areas increased the risk of postoperative deficits. However, it was not clear whether the observed neurological deficits were caused by proximity of functional cortex to the tumor [cortical injury] or subcortical injury.
  
  
  OBJECTIVE
  We hypothesize that subcortical injury during tumor resection is an important predictor of postoperative neurological deficits compared to cortical injury.
  
  
  METHODS
  A retrospective review of 214 patients undergoing awake craniotomy was carried out in whom preoperative functional magnetic resonance imaging (fMRI) and cortical mapping (CM) were performed. A radiologist blinded to the clinical data reviewed and graded the postoperative changes on diffusion-weighted MR-imaging (DWI).
  
  
  RESULTS
  Of the 40 cases who developed new intraoperative neurological deficit, 36 (90%) occurred during subcortical dissection, 3 (7.5%) during both subcortical and cortical dissection, and 1 (2.5%) during cortical dissection. Neurological dysfunction acquired during subcortical dissection was an independent predictor of postoperative deficits both in the immediate postoperative period (P < .001) and at the 3-month follow-up (P < .001). Significant DWI restriction in the subcortical white matter was predictive of neurological deficits both immediately and at 3 months, P = .011 and P < .001, respectively. New or worsening deficits were seen in 38% of patients; however, at 3 months 13% had a mild persistent neurological deficit.
  
  
  CONCLUSIONS
  Subcortical injury with significant DWI changes result in postoperative neurological decline despite our efforts to preserve cortical areas of function. This underscores the importance of preserving subcortical fiber tracts during awake craniotomy procedures.
authors.affiliation: Department of Neurosurgery, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
authors.forename: Victoria T
authors.initials: VT
authors.lastname: Trinh
authors.forename: Daniel K
authors.initials: DK
authors.lastname: Fahim
authors.forename: Komal
authors.initials: K
authors.lastname: Shah
authors.forename: Sudhakar
authors.initials: S
authors.lastname: Tummala
authors.forename: Ian E
authors.initials: IE
authors.lastname: McCutcheon
authors.forename: Raymond
authors.initials: R
authors.lastname: Sawaya
authors.forename: Dima
authors.initials: D
authors.lastname: Suki
authors.forename: Sujit S
authors.initials: SS
authors.lastname: Prabhu
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001921:Brain / Q000473:pathology*; D001932:Brain Neoplasms / Q000601:surgery; D002540:Cerebral Cortex / Q000502:physiology; D003399:Craniotomy / Q000009:adverse effects*; D038524:Diffusion Magnetic Resonance Imaging; D004558:Electric Stimulation / Q000379:methods; D005260:Female; D005910:Glioma / Q000601:surgery; D006801:Humans; D008297:Male; D008875:Middle Aged; D009422:Nervous System Diseases / Q000175:diagnosis / Q000209:etiology*; D011183:Postoperative Complications / Q000473:pathology / Q000503:physiopathology*; D012189:Retrospective Studies; D014851:Wakefulness; D055815:Young Adult