Cortical tissue surrounding acute ischemic infarcts undergoes repetitive spontaneous depolarizations. It is unknown whether these events are episodes of spreading depression (SD) elicited by the elevated interstitial K⁺ ([K⁺]_e) in the ischemic core or whether they are evoked by transient decreases of the local blood flow. Electrophysiologically, depolarization caused by SD or by ischemia (ID) can be distinguished by their characteristic patterns of [K⁺]_e rise: During SD, [K⁺]_e rises abruptly, while in ID, this fast rate of increase is preceded by a slow rate lasting minutes. To characterize the depolarizations, we occluded the right middle cerebral artery (MCA) in rats and inserted two K⁺-sensitive microelectrodes into the cortex surrounding the evolving infarct. Repeated increases in [K⁺]_e arose spontaneously following MCA occlusion. [K⁺]_e increased during these transients from a resting level of 3–6 to 60 mM. One-third of these transient increases in [K⁺]_e were biphasic, consisting of a slow initial increase to 10–12 mM, which lasted for minutes, followed by an abrupt increase, a pattern characteristic of ID. The remaining two-thirds exhibited a steep monotonic increase in [K⁺]_e (>10 s), characteristic of SD. The duration of the transients was a function of the pattern of [K⁺]_e increase: ID-like transients lasted an average 10.7 ±5.1 min, whereas the duration of SD-like transients was 5.7 ± 3.4 min. Both types of K⁺ transients occurred in an apparently random fashion in individual animals. A K⁺ transient was never observed solely at one electrode. In 40% of the cases, the K⁺ transients occurred simultaneously at the two electrode sites, and in the remaining a temporal separation of 20–420 s was observed. Our data suggest that the majority of the spontaneous depolarizations evoked by focal ischemia are SD-like phenomena probably evoked by the high values of [K⁺]_e or glutamate in the ischemic focus, while the rest are elicited by independent foci of low blood flow within the ischemic border areas.