The recovery cycle of the human visual cortex in conditions of psychosensory rest and after i.v. administration of 250 and 500 mg of Cardiazol was studied in 10 normal subjects by means of the evoked photic potential. The evoked cortical responses were recorded from the scalp in bipolar derivation obtained by means of a CAT 400 B Mnemotron. Paired flashes were emitted at various intervals (20-30-40-50-70-80-100-120-150-170-200-230 msec). From the complex response obtained from the two flashes (R1 + R2), the response (R1) evoked by the first flash (conditioning flash) was subtracted, thus obtaining the response (R2) to the second flash (test flash). The ratio (R2/R1) between the amplitudes of waves III and VII of the two evoked responses so obtained was taken as the index of the state of cortical excitability in successive moments. Variations with respect to unity were then considered. If the ratio equals zero the cortex is not excitable further (R2 = 0), if less than one, excitability is reduced (R2 < R1), if greater than 1, it is increased (R2 > R1) and, finally, if it equals one, the cortex is in a condition of normal excitability (R2 = R1). The results obtained showed that the recovery cycle of the visual cortex in man in psychosensory res consists of: o (1) a period of absolute refractivity of 40 msec; (2) a period of supernormal facilitation lasting from 80 to 100 msec after stimulus with a maximum at 100 msec; (3) a period of subnormal excitability from 120 to 150 msec after the flash with a maximum at 150 msec; (4) the return to the state of normal excitability about 200 msec after the flash. I.v. administration of Cardiazol in doses of 250 and 500 mg provokes modifications in the evoked photic potential and in the cortical recovery cycle. The basal evoked response is increased in amplitude in its later components. The cortical recovery cycle has a shorter duration and is made up as follows: o (1) period of absolute refractivity 30 msec; (2) phase of supernormal excitability from 50 to 80 msec after the flash with a maximum at 80 msec; (3) phase of subnormal excitability between 100 and 120 msec with a maximum at 120 msec; (4) recovery of normal excitability at 150 msec after the stimulus. The described modifications are quite similar with 250 and 500 mg of i.v. Cardiazol. Both in basal conditions and during Cardiazol administration an increase in latencies and durations of waves III and VII of the evoked potential was noted in the period of maximum facilitation. Like supranormal excitability itself, it seems that these facts can be attributed to phenomena of spacial summation depending on the neuron contingent of the subliminal fringe excited by the second flash. In conclusion, the increase in cortical excitability produced by Cardiazol is pointed out. This also seems to predispose the cortex to respond to more frequent sensory stimuli by shortening the duration of the recovery cycle.