Fear memory in humans is consolidated over time independently of sleep.

Fear memories can be altered after acquisition by processes, such as fear memory consolidation or fear extinction, even without further exposure to the fear-eliciting stimuli, but factors contributing to these processes are not well understood. Sleep is known to consolidate, strengthen, and change newly acquired declarative and procedural memories. However, evidence on the role of time and sleep in the consolidation of fear memories is inconclusive. We used highly sensitive electrophysiological measures to examine the development of fear-conditioned responses over time and sleep in humans. We assessed event-related brain potentials (ERP) in 18 healthy, young individuals during fear conditioning before and after a 2-hour afternoon nap or a corresponding wake interval in a counterbalanced within-subject design. The procedure involved pairing a neutral tone (CS+) with a highly unpleasant sound. As a control, another neutral tone (CS-) was paired with a neutral sound. Fear responses were examined before the interval during a habituation phase and an acquisition phase as well as after the interval during an extinction phase and a reacquisition phase. Differential fear conditioning during acquisition was evidenced by a more negative slow ERP component (stimulus-preceding negativity) developing before the unconditioned stimulus (loud noise). This differential fear response was even stronger after the interval during reacquisition compared with initial acquisition, but this effect was similarly pronounced after sleep and wakefulness. These findings suggest that fear memories are consolidated over time, with this effect being independent of intervening sleep.

LPDs - «Linked to penumbra¼ discharges or EEG correlate of excitotoxicity: A review based hypothesis.

Periodic lateralized epileptiform discharges (PLEDs) or lateralized periodic discharges (LPDs) are a well-known variant of pathological EEG activity. However, the mechanisms underpinning the appearance of this pattern are not completely understood. The heterogeneity of the features derived from LPDs patterns, and the wide range of pathological conditions in which they occur, raise a question about the unifying mechanisms underlying these phenomena. This paper reassesses the current opinion surrounding LPDs which considers glutamate excitotoxicity to be the primary pathophysiological basis, and the penumbral region to be the main morphological substrate. Arguments in favour of this hypothesis are presented, with interpretations supported by evidence from recent literature involving clinical and experimental data. Presently, no single hypothesis places considerable emphasis on the pathochemical properties of LPDs, which are implicitly meaningful towards better understanding of the clinical significance of this pattern.