Neuronal deactivation explains decreased cerebellar blood flow in response to focal cerebral ischemia or suppressed neocortical function.

Functional neuroimaging in humans with acute brain damage often reveals decreases in blood flow and metabolism in areas unaffected by the lesion. This phenomenon, termed diaschisis, is presumably caused by disruption of afferent excitatory input from the lesioned area to other brain regions. By characterizing its neurophysiological basis, we used cerebellar diaschisis to study the relationship between electrical activity and blood flow during decreased neuronal activity. Here we show that focal cerebral ischemia in rats causes diaschisis in the cerebellar cortex characterized by pronounced decreases in Purkinje cell spiking activity and small decreases in cerebellar blood flow. The findings were explained by decreased excitatory input to the cerebellar cortex, i.e., deactivation, as cerebellar neuronal excitability and vascular reactivity were preserved. Functional ablation of the cerebral cortex by either spreading depression or tetrodotoxin reproduced the changes in cerebellar function with complete recovery of Purkinje cell activity and cerebellar blood flow concomitant with recovery of neocortical function. Decreases of activity involving the contralateral frontal cortex produced the largest decrease in cerebellar electrical activity and blood flow. Our data suggest that deactivation explains the decreases in blood flow and metabolism in cerebellar diaschisis observed in human neuroimaging studies. Decreases in spiking activity were 3-7 times larger than the respective decreases in flow. Therefore, under pathological conditions, neuroimaging methods based on hemodynamic signals may only show small changes, although the underlying decrease in neuronal activity is much larger.