title: Intravenous immunoglobulin reduces infarct volume but not edema formation in acute stroke.
abstract: OBJECTIVE
  Intravenous immunoglobulin (IVIG) is used for treatment of immunodeficiencies and autoimmune disorders. Recently, IVIG has also been shown to reduce infarct size in acute stroke. Since edema treatment can provide secondary neuroprotective effects, we conducted the present study to evaluate whether edema reduction is the underlying cause of the neuroprotective properties of IVIG in experimental stroke.
  
  
  METHODS
  Male Wistar rats received either IVIG or placebo and were subjected to temporary middle cerebral artery occlusion. 24 h after temporary middle cerebral artery occlusion, clinical evaluation and 7.0T magnetic resonance imaging were performed. Ischemic lesion volume was determined on high-resolution T(2) images. T(2) relaxation time and midline shift assessed on magnetic resonance imaging as well as brain water content detected by the wet/dry method after 24 h were measured to quantify edema formation.
  
  
  RESULTS
  Pretreatment with IVIG leads to a statistically significant reduction of the ischemic lesion volume by 42% after 24 h, as compared to placebo treatment (p < 0.05). All three methods for quantifying edema formation indicated no differences between IVIG-treated and untreated animals (p > 0.05).
  
  
  CONCLUSIONS
  These results suggest that the neuroprotective effect of IVIG is not an indirect result of edema reduction, but is caused by direct neuronal protection. Application of IVIG is a promising treatment concept for acute stroke. To further investigate this neuroprotective effect, studies on the efficacy, the safety profile and on the underlying mechanisms are required.
authors.affiliation: Department of Neurology, University Hospital Cologne, Cologne, Germany.
authors.forename: Maureen
authors.initials: M
authors.lastname: Walberer
authors.forename: Max
authors.initials: M
authors.lastname: Nedelmann
authors.forename: Nouha
authors.initials: N
authors.lastname: Ritschel
authors.forename: Clemens
authors.initials: C
authors.lastname: Mueller
authors.forename: Marlene
authors.initials: M
authors.lastname: Tschernatsch
authors.forename: Erwin
authors.initials: E
authors.lastname: Stolz
authors.forename: Georg
authors.initials: G
authors.lastname: Bachmann
authors.forename: Franz
authors.initials: F
authors.lastname: Blaes
authors.forename: Tibo
authors.initials: T
authors.lastname: Gerriets
mesh_terms: D000208:Acute Disease; D000818:Animals; D001834:Body Water / Q000378:metabolism; D001921:Brain / Q000098:blood supply / Q000187:drug effects* / Q000473:pathology; D001929:Brain Edema / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D019610:Cytoprotection / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D018450:Disease Progression; D016756:Immunoglobulins, Intravenous / Q000494:pharmacology* / Q000627:therapeutic use; D007155:Immunologic Factors / Q000494:pharmacology; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D020521:Stroke / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D016896:Treatment Outcome
chemical_list: D016756:Immunoglobulins, Intravenous; D007155:Immunologic Factors; D018696:Neuroprotective Agents