Delayed decompressive surgery increases apparent diffusion coefficient and improves peri-infarct perfusion in rats with space-occupying cerebral infarction

• Published in: Stroke (1970) 2004-06, Vol.35 (6), p.1476-1481
• Main Authors: HOFMEIJER, J, SCHEPERS, J, VELDHUIS, W. B, NICOLAY, K, KAPPELLE, L. J, BÄR, P. R, VAN DER WORP, H. B
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Brain Edema - pathology; Cerebral Infarction - pathology; Cerebral Infarction - surgery; Cerebrovascular Circulation; Decompression, Surgical; Diffusion; Diffusion Magnetic Resonance Imaging; Magnetic Resonance Angiography; Male; Medical sciences; Neurology; Rats; Rats, Inbred F344; Time Factors; Treatment Outcome; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.STR.0000128415.31274.3a

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. 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. 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. 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.