Sakowitz Oliver W, Kiening Karl L, Krajewski Kara L, Sarrafzadeh Asita S, Fabricius Martin, Strong Anthony J, Unterberg Andreas W, Dreier Jens P
Department of Neurosurgery, University of Heidelberg, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany.
Stroke. 2009 Aug;40(8):e519-22. doi: 10.1161/STROKEAHA.109.549303. Epub 2009 Jun 11.
Spreading depolarizations, characterized by large propagating, slow potential changes, have been demonstrated with electrocorticography in patients with cerebral hemorrhage and ischemic stroke. Whereas spreading depolarizations are harmless under normal conditions in animals, they cause or augment damage in the ischemic brain. A fraction of spreading depolarizations is abolished by N-methyl-d-aspartate receptor antagonists. Summary of Case- In 2 patients with severe acute brain injury (traumatic and spontaneous intracranial hemorrhage), spreading depolarizations were inhibited by the noncompetitive N-methyl-d-aspartate receptor antagonist ketamine. This restored electrocorticographic activity.
These anecdotal electrocorticographic findings suggest that ketamine has an inhibitory effect on spreading depolarizations in humans. This is of potential interest for future neuroprotective trials.
去极化扩散以大的传播性、缓慢的电位变化为特征,已通过皮层脑电图在脑出血和缺血性中风患者中得到证实。虽然在动物的正常情况下,去极化扩散是无害的,但它们会导致或加重缺血性脑损伤。一部分去极化扩散可被N-甲基-D-天冬氨酸受体拮抗剂消除。病例总结:在2例严重急性脑损伤(创伤性和自发性颅内出血)患者中,非竞争性N-甲基-D-天冬氨酸受体拮抗剂氯胺酮抑制了去极化扩散。这恢复了皮层脑电图活动。
这些皮层脑电图的个案发现表明,氯胺酮对人类的去极化扩散有抑制作用。这对于未来的神经保护试验具有潜在意义。