Ischemic stroke presents a major global economic and public health burden. Although recent advances in available endovascular therapies show improved functional outcome, a good number of stroke patients are either ineligible or do not have access to these treatments. Also, robust collateral flow during acute ischemic stroke independently predicts the success of endovascular therapies and the outcome of stroke. Hence, adjunctive therapies for cerebral blood flow (CBF) enhancement are urgently needed. A very clear overview of the pial collaterals and the role of genetics are presented in this review. We review available evidence and advancement for potential therapies aimed at improving CBF during acute ischemic stroke. We identified heme-free soluble guanylate cyclase activators; Sanguinate, remote ischemic perconditioning; Fasudil, S1P agonists; and stimulation of the sphenopalatine ganglion as promising potential CBF-enhancing therapeutics requiring further investigation. Additionally, we outline and discuss the critical steps required to advance research strategies for clinically translatable CBF-enhancing agents in the context of acute ischemic stroke models.
The supracondylar process is a rare but commonly reported anatomical variant of the humerus. Though it is usually asymptomatic, it can lead to serious symptoms. In this report, a lateral supracondylar process of the humerus was found. This is much rarer than a medial supracondylar process, and to our knowledge, it has not been reported previously. Surgeons and radiologists must account for supracondylar process variations to diagnose neurovascular pathology in the forearm accurately and quickly to optimize surgical outcomes. Here, we describe the origin and clinical importance of the supracondylar process variant.
Morphological variations of the foramen magnum (FM) have been demonstrated to have different shapes and sizes, according to sex, age, and ethnicity. In this report, an ancient Roman skull was found to have a unique anterior notching further specified as an anterior elongation of the FM. To our knowledge, this feature has not been previously reported. The FM is one of the most challenging neurosurgical regions due to both its deep location and proximity to vital structures. Therefore, physicians and surgeons must account for FM anatomical variations in order to properly diagnose craniocervical pathology, interpret radiological images, and optimize surgical outcomes. In this case report, we describe the possible embryology and clinical importance of an apparently rare FM variant.
Vascular dementia (VaD) is the second-most common form of dementia, accounting for 20% of all dementia cases. Although the pathobiology of VaD is poorly understood and lacks effective treatment, clinically relevant factors such as age and sex are rarely considered in preclinical modeling. This places efforts to develop future therapies at a severe disadvantage, as clinically relevant translation of underlying pathobiology may be lost. We reviewed common morphological and physiological outcomes in six major rodent models of VaD in a total of 258 full-text publications: 1) chronic cerebral hypoperfusion, 2) high fat diet, 3) diabetes, 4) hypertension, 5) carotid arterial calcification, and 6) and CADASIL (Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy), and evaluated translational features relevant to human pathophysiology with an analysis of timepoints of observed pathology and rodent sex and age. We found that all models of VaD shared common features of decreased CBF and upregulation of inflammatory signaling molecules such as TNF-α, IL-1β, and IL-6, and reactive oxygen species (ROS) such as SOD and NOX, consistent with clinical presentations of VaD. Only the carotid artery calcification model showed inconsistent evidence for brain endothelial tight junction loss, astrogliosis, and macrophage reactivity, in disagreement with other models. We conclude that improved translational insight may critically depend on 1) inclusion of a constellation of comorbidities in preclinical modeling instead of modeling each in isolation to better capture human disease pathogenesis, 2) increased use of middle-aged and aged preclinical rodent models which are sensitive to clinically relevant disease presentation in middle-age and elderly individuals, and 3) inclusion of female animals in disease models as sex is a relevant biological factor which may better define future therapeutic strategy in real-world populations.
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