PMID- 19923854
OWN - NLM
STAT- MEDLINE
DCOM- 20100420
LR  - 20100122
IS  - 1423-0216 (Electronic)
IS  - 1021-7401 (Linking)
VI  - 17
IP  - 2
DP  - 2010
TI  - Intravenous immunoglobulin reduces infarct volume but not edema formation in 
      acute stroke.
PG  - 97-102
LID - 10.1159/000258692 [doi]
AB  - OBJECTIVES: 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). CONCLUSION: 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.
CI  - Copyright 2009 S. Karger AG, Basel.
FAU - Walberer, Maureen
AU  - Walberer M
AD  - Department of Neurology, University Hospital Cologne, Cologne, Germany.
FAU - Nedelmann, Max
AU  - Nedelmann M
FAU - Ritschel, Nouha
AU  - Ritschel N
FAU - Mueller, Clemens
AU  - Mueller C
FAU - Tschernatsch, Marlene
AU  - Tschernatsch M
FAU - Stolz, Erwin
AU  - Stolz E
FAU - Bachmann, Georg
AU  - Bachmann G
FAU - Blaes, Franz
AU  - Blaes F
FAU - Gerriets, Tibo
AU  - Gerriets T
LA  - eng
PT  - Journal Article
DEP - 20091117
PL  - Switzerland
TA  - Neuroimmunomodulation
JT  - Neuroimmunomodulation
JID - 9422763
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Immunologic Factors)
RN  - 0 (Neuroprotective Agents)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Body Water/metabolism
MH  - Brain/blood supply/*drug effects/pathology
MH  - Brain Edema/*drug therapy/immunology/physiopathology
MH  - Cytoprotection/drug effects/physiology
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Immunoglobulins, Intravenous/*pharmacology/therapeutic use
MH  - Immunologic Factors/pharmacology
MH  - Infarction, Middle Cerebral Artery/*drug therapy/immunology/physiopathology
MH  - Magnetic Resonance Imaging
MH  - Male
MH  - Neuroprotective Agents/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Stroke/*drug therapy/immunology/physiopathology
MH  - Treatment Outcome
EDAT- 2009/11/20 06:00
MHDA- 2010/04/21 06:00
CRDT- 2009/11/20 06:00
PHST- 2009/05/13 00:00 [received]
PHST- 2009/07/09 00:00 [accepted]
PHST- 2009/11/20 06:00 [entrez]
PHST- 2009/11/20 06:00 [pubmed]
PHST- 2010/04/21 06:00 [medline]
AID - 000258692 [pii]
AID - 10.1159/000258692 [doi]
PST - ppublish
SO  - Neuroimmunomodulation. 2010;17(2):97-102. doi: 10.1159/000258692. Epub 2009 Nov 
      17.