The lacune, often used interchangeably with the definition of a stroke of small vessel atherosclerotic etiology, is traditionally based on a size definition of no greater than 15 mm. It is a classic feature of cerebral small vessel disease. However, despite its prolific use in the stroke literature, the exact characteristics and morphological features of a lacune are not well defined. Here, the authors analyzed the shape of incident lacunes in CADASIL, a genetically inherited small vessel arteriopathy, to better define the lacune’s morphological features.
Get With the Guidelines (GWTG) Participation is Associated with Improved Clinical Outcomes in Medicare Ischemic Stroke Patients
Early Appearance of Spot Sign on CT Perfusion Associated with Hematoma Expansion and Poor Outcome in Small Retrospective Study
Intracerebral hemorrhage (ICH) causes a significant amount of stroke-related morbidity and mortality. Of the various prognostic factors in ICH, hematoma expansion (HE) is one of the few potentially modifiable ones and as such has been a topic of increasing research. Unfortunately, large-scale randomized controlled trials aimed at preventing hematoma expansion have not shown robust results, possibly owing to the limited ability of clinicians to predict which patients are at greatest risk. The “spot sign,” a radiographic sign representing the leakage of contrast with a hematoma on CT scan has recently become a topic of extensive study with respect to its ability to predict hematoma expansion. As described previously, a recently published meta-analysis suggested that the sensitivity and positive predictive value of the spot sign was related to the time from ictus to scan acquisition and may not adequately predict HE when it is detected. Additionally, other studies have shown that using CT perfusion (CTP) improves the detection rate of the spot sign. Wang et al. sought to explore the relationship between spot sign characteristics on CTP (including number, timing, and maximum density) to evaluate the relationship between these characteristics and the risk of HE as well as clinical outcome.
Kuroki T, Tanaka R, Shimada Y, Yamashiro K, Ueno Y, Shimura H, et al. Exendin-4 Inhibits Matrix Metalloproteinase-9 Activation and Reduces Infarct Growth After Focal Cerebral Ischemia in Hyperglycemic Mice. Stroke. 2016
Hyperglycemia exacerbates acute brain injury and leads to worse outcomes in patients with ischemic stroke. In animal models of acute ischemic stroke, hyperglycemia is associated with increased infarct volume, increased blood-brain–barrier permeability, and hemorrhagic transformation. In order to avoid hyperlgycemia-induced brain injury, normoglycemia is recommended, and typically attained via use of insulin. Unfortunately, up to now, insulin has failed to show improvement in short-term outcomes in human studies and hypoglycemia, a not uncommon consequence of exogenous insulin is associated with further brain injury. Exendin-4 is an agonist of Glucagon-like peptide-1 (a hormone secreted by the small intestines) that mitigates hyperglycemia in diabetes and has a low risk of hypoglycemia. In addition, exendin-4 has shown been shown to reduce oxidative stress and inflammation.
Recent and Regular Use of Cocaine Significantly Increases Odds of IS in a Case-Control Study of Young Adults
Cuomo O, Pignataro G, Sirabella R, Molinaro P, Anzilotti S, Scorziello A, et al. Sumoylation of LYS590 of NCX3 f-Loop by SUMO1Participates in Brain Neuroprotection Induced byIschemic Preconditioning. Stroke. 2016
Small ubiquitin-like modifier (SUMO) conjugation, or sumoylation, is a post-translational modification of various proteins similar to ubiquination, and has been noted in stress conditions including anoxia, hypothermia, and hypoxia. Changes in sumolyation patterns have been reported after brain ischemia, where it is thought to be possibly protective. To this end, the authors here attempt to further elucidate a possible mechanism underlying the role of sumoylation of the transmembrane protein NCX3, which is thought to be an effector of neuroprotection in ischemic mouse models.
- First, that SUMO1 conjugation does increase at various times points following induced ischemia via transient middle cerebral artery occlusion (tMCAO) (at 5 and 24 hours), after preconditioning (at 3, 5, 24, and 72 hours) and when preconditioning was combined with tMCAO (at 5 hours).
- Second, using immunohistochemical stains, the authors identified NCX and SUMO1 colocalization to the neuronal cell bodies in the primary cortical neurons, with a probable sumoylation site in the NCX f-loop of the antiporter.
- Third, in SUMO1 knockdown mouse models, NCX3 expression decreased 72 hours after tMCAO and after preconditioning + tMCAO and displayed a significant increase in ischemic volume after tMCAO at 24 and 72 hours after tMCAO induction.
Identifying targets for neuroprotection seems to be the next frontier in the world of stroke research. This takes us one step closer to characterizing the mechanisms underlying the possible neuroprotectant effect of ischemic preconditioning, whereby targeting either sumoylation of NCX, or regulation of NCX itself, may lead to the development of better neuroprotectants.
Limitations are noted, especially in the in vitro model, due to needing to keep the three cell types in different media (ECs in one, PCs and astrocytes in another); so the possibility exists that if they were mixed we would see different effects. This is compensated by the in vivo model, however. Overall, this is an important study demonstrating a critical link and setting the foundation for future diagnostic and therapeutic advances in cerebrovascular and neurodegenerative disorders.
Collateral Circulation Status as Assessed by MR-Perfusion Modulates Relationship Between Time and Development of FLAIR Signal
Fluid-Attenuated Inversion Recovery eral Circulation. Stroke. 2016
The authors utilized clinical and neuroimaging data from the AXIS 2 trial, a multicenter Phase IIb placebo-controlled, randomized and double blinded trial investigating recombinant Granulocyte Colony Stimulating Factor in acute stroke. A total of 141 patients were included for analysis, excluding patients with incomplete imaging sequences, severe FLAIR lesions overlapping the acute lesion or in the contralateral hemisphere (as the contralateral hemisphere was used for FLAIR intensity measurement), or reperfused core. Quantitative relative FLAIR maps (rFLAIR) were calculated in a voxel-based manner using in house software. Collateral status assessed by HIR was dichotomized into “good” (n= 87, 61.7%) and “poor” (n= 54, 38.3%). Patients with poor collaterals had more severe stroke symptoms at baseline (NIHSS 14 vs NIHSS 11, p= 0.01), larger DWI lesion volumes (47.2 mL vs 14.6 mL, p= <0.01), and larger TMax > 6s perfusion volumes (91.5 mL vs 45.8 mL, p=0.01).