Cortical spreading
depression (CSD) and depolarization waves are associated with dramatic failure of
brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke,
subarachnoid hemorrhage and traumatic
brain injury. The implications of these findings are widespread and suggest that intrinsic
brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or
brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the
brain extracellular microenvironment and to the level of
brain perfusion and in consequence
brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute
brain disorders in the
intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human
brain cortex caused by depolarization waves.
Relevant Topics in Medical Sciences