Deep comatose states are associated with discontinuous EEG consisting of bursts of activity on a suppressed background. When bursts can be triggered by external stimuli, these burst-suppression (BS) patterns are referred to as reactive. The current dogma is that the presence of a reactive BS has a more favorable outcome than a non-reactive BS; however, this dichotomy is entirely artificial. The prognostic value of BS reactivity remains poorly understood as there are no standardized quantification protocols. Here we investigated the reactivity of transient BS patterns induced by general anesthesia with chloral hydrate or isoflurane in adult male Wistar rats. Recordings were obtained from both hemispheres via implanted epidural electrodes. Constant intensity stimulation was carried out using super-bright LED monocular flashes or supramaximal electrical pulses to the tail nerves. The mean bursting frequency (BF) was calculated over 30-second epochs. Stimuli were delivered at 2-second intervals to minimize any peripheral cumulative effects. Reactivity was quantified as the change in BF during stimulation as compared to the epoch just prior to the first stimulus. For a wide range of anesthetic depths, stimulation induced a prompt increase in BF. Nevertheless, the increase was maximal during the first stimulation epoch and then it decreased to a plateau during the subsequent stimulation epochs. This accommodation of BS reactivity was independent of the anesthetic used and of stimulus type. Our data brings evidence that the reactivity of BS patterns depends on the stimulation history. To our knowledge this was not previously suspected and could account for the prognostic inconsistencies between studies evaluating BS reactivity using different stimulation frequencies and/or durations. We propose that for standardizing the BS reactivity measurement it is necessary to repeat the stimulus until the change in BF reaches its plateau.