Effect of local brain retraction on local cerebral blood flow and neural function. Experimental study

Abstract

Changes in N1 amplitude of somatosensory evoked potential (SEP) with median nerve stimulation, cortical blood flow (CoBF) by a hydrogen clearance method, and histology were studied during brain retraction with graded local compression pressure (LCP) in 56 dogs. Local brain compression was applied with a brain spatula on the primary somatosensory cortex after right frontotemporal craniectomy and opening of the dura. In the first experiment, cerebral perfusion pressure (CPP) was reduced by three different methods, namely, exsanguination, infusion of saline solution into the cisterne magna, and continuous local brain compression. CPP was reduced by a 10 mmHg step every 30 minutes. Continuous local brain compression decreased both N1 amplitude and CoBF more markedly than did the other two methods. N1 amplitude decreased as soon as the local compression was started, and was reduced to 50% at 50 mmHg of LCP (CPP, 90-100 mmHg), and became null when LCP was elevated over 90 mmHg (CPP, below 60 mmHg). CoBF was significantly reduced at 110 mmHg of CPP. This suggests that immediate and severe neural dysfunction in local brain compression was due not only to destruction of the neural architecture by brain distortion but also to disturbance of cerebral circulation. As the second experimental step, intermittent local compressions with initial pressures of 20, 40, 60, and 80 mmHg was performed. Local compressions were applied four times for 30 minutes duration with five minute intermissions. At the initial levels of 40 mmHg of LCP, and higher the more the compressions were repeated or the higher the LCP was raised, the more both N1 amplitude and CoBF decreased. At 60 and 80 mmHg of LCP, N1 amplitude decreased significantly to 35% and 11% during compression and remained reduced to 70% and 35% at two hours after decompression, respectively. When the N1 amplitude was reduced more than 50% during compression, it remained suppressed to 55% 2 hours after decompression. In these dogs, histological study of the compressed area showed cortical microhemorrhage and edema. This study suggests that LCP over 40 mmHg and/or reduction of N1 amplitude by greater than 50% during brain retraction produce postoperative neuronal dysfunction and histological changes.