BACKGROUND AND PURPOSE: Cortical spreading depression (CSD) has been much studied experimentally but never demonstrated unequivocally in human neocortex by direct electrophysiological recording. A similar phenomenon, peri-infarct depolarization, occurs in experimental models of stroke and causes the infarct to enlarge. Our current understanding of the mechanisms of deterioration in the days after major traumatic or ischemic brain injury in humans has not yielded any effective, novel drug treatment. This study sought clear evidence for the occurrence and propagation of CSD in the injured human brain. METHODS: In 14 patients undergoing neurosurgery after head injury or intracranial hemorrhage, we placed electrocorticographic (ECoG) electrodes near foci of damaged cortical tissue. RESULTS: Transient episodes of depressed ECoG activity that propagated across the cortex at rates in the range of 0.6 to 5.0 mm/min were observed in 5 patients; this rate of propagation is characteristic of CSD. We also observed, in 8 of the 14 patients, transient depressions of ECoG amplitude that appeared essentially simultaneous in all recording channels, without clear evidence of spread. CONCLUSIONS: These results indicate that CSD or similar events occur in the injured human brain and are more frequent than previously suggested. On the basis of these observations, we suggest that the related phenomenon, peri-infarct depolarization, is indeed likely to occur in boundary zones in the ischemic human cerebral cortex.
BACKGROUND AND PURPOSE: Cortical spreading depression (CSD) has been much studied experimentally but never demonstrated unequivocally in human neocortex by direct electrophysiological recording. A similar phenomenon, peri-infarct depolarization, occurs in experimental models of stroke and causes the infarct to enlarge. Our current understanding of the mechanisms of deterioration in the days after major traumatic or ischemic brain injury in humans has not yielded any effective, novel drug treatment. This study sought clear evidence for the occurrence and propagation of CSD in the injured human brain. METHODS: In 14 patients undergoing neurosurgery after head injury or intracranial hemorrhage, we placed electrocorticographic (ECoG) electrodes near foci of damaged cortical tissue. RESULTS: Transient episodes of depressed ECoG activity that propagated across the cortex at rates in the range of 0.6 to 5.0 mm/min were observed in 5 patients; this rate of propagation is characteristic of CSD. We also observed, in 8 of the 14 patients, transient depressions of ECoG amplitude that appeared essentially simultaneous in all recording channels, without clear evidence of spread. CONCLUSIONS: These results indicate that CSD or similar events occur in the injured human brain and are more frequent than previously suggested. On the basis of these observations, we suggest that the related phenomenon, peri-infarct depolarization, is indeed likely to occur in boundary zones in the ischemic human cerebral cortex.
Authors: Johannes Woitzik; Jens P Dreier; Nils Hecht; Ingo Fiss; Nora Sandow; Sebastian Major; Maren Winkler; Yuliya A Dahlem; Jerome Manville; Michael Diepers; Elke Muench; Hidetoshi Kasuya; Peter Schmiedek; Peter Vajkoczy Journal: J Cereb Blood Flow Metab Date: 2011-12-07 Impact factor: 6.200
Authors: Russell E Carter; Isamu Aiba; Robert M Dietz; Christian T Sheline; C William Shuttleworth Journal: J Cereb Blood Flow Metab Date: 2010-10-27 Impact factor: 6.200
Authors: Alois J Schiefecker; Mario Kofler; Max Gaasch; Ronny Beer; Iris Unterberger; Bettina Pfausler; Gregor Broessner; Peter Lackner; Paul Rhomberg; Elke Gizewski; Werner O Hackl; Miriam Mulino; Martin Ortler; Claudius Thome; Erich Schmutzhard; Raimund Helbok Journal: J Cereb Blood Flow Metab Date: 2017-04-24 Impact factor: 6.200