Fig. 6: An integrated scenario.
From: Sleep-like cortical dynamics during wakefulness and their network effects following brain injury
A schematic illustration of the vision encompassing a key role of cortical bistability in the aftermath of brain injury. A The primary structural lesion (black shade) critically deprives perilesional areas of lateral excitation and/or ascending activating influences (green arrows). The ensuing shift of the excitation/inhibition balance and/or the enhancement of adaptation mechanisms (possibly facilitated by hypoperfusion and inflammation) lead to the local expression of sleep-like cortical bistability (graded blue shade) during wakefulness. The alternation between Up- and Down-states in the affected neuronal population is reflected in slow waves during wakefulness in the scalp EEG. Bistability and slow waves can then propagate either by disfacilitation of distant targets or through chains of connected circuits and disrupt neuronal activity in distant areas (blue shades of different intensity in cortical areas distant from the structural damage connected by red arrows). In this specific example, involving the network illustrated in ref. 107, the network-level intrusion of bistability during wakefulness and the resulting disruption of neuronal interactions over the right intraparietal sulcus and right frontal eye field contributes to behavioral deficits (hemispatial neglect, i.e. an attentional bias towards the right hemispace), which are not fully accounted for by the structural damage alone (located over the right temporo-parietal junction). B While structural damage and disconnections are likely to persist, bistability and its network consequences are potentially reversible, leading to a progressive recovery of function over time (t0–t1).
