title: Hypoplasia or occlusion of the ipsilateral cranial venous drainage is associated with early fatal edema of middle cerebral artery infarction.
abstract: OBJECTIVE
  Thrombosis of the cerebral venous sinus may cause venous congestion, cerebral edema, and infarction. The role of cerebrovenous disorders in arterial ischemic stroke is unknown. The objective of this study was to examine the contribution of ipsilateral cranial venous abnormalities to the development of cerebral edema in middle cerebral artery infarction.
  
  
  METHODS
  This is a retrospective study of consecutive patients with large middle cerebral artery infarction admitted to our neurocritical care unit from January 2007 to October 2008. Medical records, laboratory data, and imaging of cerebral edema and cranial venous sinuses were analyzed.
  
  
  RESULTS
  Of the 14 patients identified to have large middle cerebral artery infarction and images of cranial venous drainages, 5 (35.7%) had fatal edema with clinical signs of transtentorial herniation. Four of the 5 patients developed fatal edema within 48 hours of ictus and were found to have abnormal ipsilateral cranial venous drainage, including atresia of the transverse sinus (one), occlusion of the internal jugular vein (one), and hypoplasia of the transverse sinus and internal jugular vein (2). The fifth patient had symmetrical bilateral cranial venous drainages and fatal edema at Day 5. Of the 9 patients with nonmalignant middle cerebral artery infarction, all had ipsilateral dominant or symmetrical bilateral venous drainages.
  
  
  CONCLUSIONS
  In this small case series, we demonstrated that only the patients with hypoplasia or occlusion of the ipsilateral cranial venous drainage developed early fatal edema after large middle cerebral artery infarction. Our results suggest a role of cranial venous outflow abnormalities in the development of brain edema after arterial ischemic stroke.
authors.affiliation: Department of Neurological Surgery and Neurology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-8855, USA. Wengui.Yu@UTSouthwestern.edu
authors.forename: Wengui
authors.initials: W
authors.lastname: Yu
authors.forename: Joanna
authors.initials: J
authors.lastname: Rives
authors.forename: Babu
authors.initials: B
authors.lastname: Welch
authors.forename: Jonathan
authors.initials: J
authors.lastname: White
authors.forename: Edward
authors.initials: E
authors.lastname: Stehel
authors.forename: Duke
authors.initials: D
authors.lastname: Samson
mesh_terms: D000208:Acute Disease / Q000401:mortality; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001929:Brain Edema / Q000401:mortality* / Q000503:physiopathology; D020520:Brain Infarction / Q000401:mortality* / Q000503:physiopathology; D020785:Central Nervous System Vascular Malformations / Q000175:diagnosis / Q000401:mortality* / Q000503:physiopathology; D002533:Cerebral Angiography; D002550:Cerebral Veins / Q000002:abnormalities / Q000473:pathology* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D015897:Comorbidity; D003392:Cranial Sinuses / Q000002:abnormalities / Q000473:pathology / Q000503:physiopathology; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D006940:Hyperemia / Q000401:mortality* / Q000503:physiopathology; D015994:Incidence; D020244:Infarction, Middle Cerebral Artery / Q000401:mortality* / Q000503:physiopathology; D018810:Magnetic Resonance Angiography; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012851:Sinus Thrombosis, Intracranial / Q000401:mortality / Q000503:physiopathology; D013997:Time Factors; D014057:Tomography, X-Ray Computed