BACKGROUND AND PURPOSE: There is no conclusive experimental support that decompressive surgery in late stages of space-occupying cerebral infarction will improve outcome. We studied the effects of delayed decompressive surgery on the development of tissue damage, edema formation, and cerebral perfusion with different MRI techniques in a rat model of space-occupying cerebral infarction. METHODS: Permanent middle cerebral artery (MCA) occlusion was performed in 6 Fisher 344 rats. Decompressive surgery was performed 17 hours after the occlusion. Each animal was assessed before surgery and 2 and 4 hours after surgery by means, of diffusion-weighted T2-weighted, and flow-sensitive alternating inversion recovery perfusion-weighted MRI. Ischemic damage was also evaluated in hematoxylin-eosin-stained brain sections. RESULTS: Lesion volume as derived from apparent diffusion coefficient (ADC) maps decreased from 522+/-98 mm3 before to 405+/-100 mm3 (P=0.016) 4 hours after decompressive surgery, whereas lesion volume from T2 maps increased from 420+/-66 mm3 before to 510+/-92 mm3 (P=0.048) 4 hours after decompressive surgery. Midline shift decreased from 1.4+/-0.1 mm to 0.5+/-0.2 mm (P=0.001). Blood flow in the noninfarcted area of the ipsilateral hemisphere improved from 25+/-9 mL/min/100 g of tissue to 38+/-9 mL/min/100 g of tissue (P=0.035). Despite the pseudonormalization of ADC, irreversible damage was found in the entire MCA territory on histological evaluation. CONCLUSIONS: In rats with space-occupying cerebral infarction, delayed decompressive surgery leads to a decrease in lesion volume derived from ADC maps, which is probably because of an increase of extracellular water formation. There are no signs that this reflects rescue of ischemic tissue.
BACKGROUND AND PURPOSE: There is no conclusive experimental support that decompressive surgery in late stages of space-occupying cerebral infarction will improve outcome. We studied the effects of delayed decompressive surgery on the development of tissue damage, edema formation, and cerebral perfusion with different MRI techniques in a rat model of space-occupying cerebral infarction. METHODS: Permanent middle cerebral artery (MCA) occlusion was performed in 6 Fisher 344 rats. Decompressive surgery was performed 17 hours after the occlusion. Each animal was assessed before surgery and 2 and 4 hours after surgery by means, of diffusion-weighted T2-weighted, and flow-sensitive alternating inversion recovery perfusion-weighted MRI. Ischemic damage was also evaluated in hematoxylin-eosin-stained brain sections. RESULTS: Lesion volume as derived from apparent diffusion coefficient (ADC) maps decreased from 522+/-98 mm3 before to 405+/-100 mm3 (P=0.016) 4 hours after decompressive surgery, whereas lesion volume from T2 maps increased from 420+/-66 mm3 before to 510+/-92 mm3 (P=0.048) 4 hours after decompressive surgery. Midline shift decreased from 1.4+/-0.1 mm to 0.5+/-0.2 mm (P=0.001). Blood flow in the noninfarcted area of the ipsilateral hemisphere improved from 25+/-9 mL/min/100 g of tissue to 38+/-9 mL/min/100 g of tissue (P=0.035). Despite the pseudonormalization of ADC, irreversible damage was found in the entire MCA territory on histological evaluation. CONCLUSIONS: In rats with space-occupying cerebral infarction, delayed decompressive surgery leads to a decrease in lesion volume derived from ADC maps, which is probably because of an increase of extracellular water formation. There are no signs that this reflects rescue of ischemic tissue.
Authors: Eric Jüttler; Peter D Schellinger; Alfred Aschoff; Klaus Zweckberger; Andreas Unterberg; Werner Hacke Journal: Crit Care Date: 2007 Impact factor: 9.097