Spreading depolarizations in patients with spontaneous intracerebral hemorrhage: Association with perihematomal edema progression

Abstract

Pathophysiologic mechanisms of secondary brain injury after intracerebral hemorrhage and in particular mechanisms of perihematomal-edema progression remain incompletely understood. Recently, the role of spreading depolarizations in secondary brain injury was established in ischemic stroke, subarachnoid hemorrhage and traumatic brain injury patients. Its role in intracerebral hemorrhage patients and in particular the association with perihematomal-edema is not known. A total of 27 comatose intracerebral hemorrhage patients in whom hematoma evacuation and subdural electrocorticography was performed were studied prospectively. Hematoma evacuation and subdural strip electrode placement was performed within the first 24 h in 18 patients (67%). Electrocorticography recordings started 3 h after surgery (IQR, 3-5 h) and lasted 157 h (median) per patient and 4876 h in all 27 patients. In 18 patients (67%), a total of 650 spreading depolarizations were observed. Spreading depolarizations were more common in the initial days with a peak incidence on day 2. Median electrocorticography depression time was longer than previously reported (14.7 min, IQR, 9-22 min). Postoperative perihematomal-edema progression (85% of patients) was significantly associated with occurrence of isolated and clustered spreading depolarizations. Monitoring of spreading depolarizations may help to better understand pathophysiologic mechanisms of secondary insults after intracerebral hemorrhage. Whether they may serve as target in the treatment of intracerebral hemorrhage deserves further research.

Low-Dose Lithium Stabilizes Human Endothelial Barrier by Decreasing MLC Phosphorylation and Universally Augments Cholinergic Vasorelaxation Capacity in a Direct Manner

“…In light of the clinical effectiveness of lithium in stroke, we have recently examined lithium-endothelium interactions (Bosche et al, 2013, 2016). Lithium treatment (Rajkowska, 2000; Lan et al, 2015) may be effective in both ischemic and hemorrhagic stroke, and even traumatic brain injury (Leeds et al, 2014; Gao et al, 2016) by improving disturbances in endothelial functions, such as: vascular or cerebrovascular autoregulation of blood flow, vasorelaxation capacity, and dynamic endothelial barrier permeability (Bosche et al, 2003, 2009, 2010; Gündüz et al, 2003; Butcher et al, 2004; Dohmen et al, 2007; Meisel et al, 2012; Renú et al, 2015; Helbok et al, 2016). …”

Antihyperthermic treatment decreases perihematomal hypodensity

“…29,30 A novel and promising hypothesis associated the presence and progression of PHHD with the existence of spreading depressions and isoelectric spreading depolarizations, although its association with episodes of metabolic derangement and ischemic lesions remains speculative. 31 It has also been postulated that upregulated microRNA-23a-3p in patients with ICH promotes the apoptosis of cerebral vascular endothelial cells by downregulating ZO-1, thus participating in the formation of PHHD after ICH. 32 The prognostic role of PHHD in ICH has been widely debated in the literature, with contradictory results.…”

Cilostazol decreases duration of spreading depolarization and spreading ischemia after aneurysmal subarachnoid hemorrhage

“…Among the adverse consequences of SD, spreading ischemia is important because it occurs during the neuronal depolarization phase and delays cortical repolarization. Thus, it prolongs the SD‐induced (1) intraneuronal Ca 2+ surge, (2) glutamate release, and (3) neuronal edema.…”