Sulforaphane (SFN) is a phytochemical found in cruciferous vegetables. It has been shown to have many protective effects against many diseases, including multiple types of cancer. SFN is a potent activator of the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response element (ARE) genetic pathway. Upregulation of Nrf2-ARE increases the availability of multiple antioxidants. A substantial amount of preclinical research regarding the ability of SFN to protect the nervous system from many diseases and toxins has been done, but only a few small human trials have been completed. Preclinical data suggest that SFN protects the nervous system through multiple mechanisms and may help reduce the risk of many diseases and reduce the burden of symptoms in existing conditions. This review focuses on the literature regarding the protective effects of SFN on the nervous system. A discussion of neuroprotective mechanisms is followed by a discussion of the protective effects elicited by SFN administration in a multitude of neurological diseases and toxin exposures. SFN is a promising neuroprotective phytochemical which needs further human trials to evaluate its efficacy in preventing and decreasing the burden of many neurological diseases.

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The advent of mechanical thrombectomy and increasing alteplase use have transformed the care of patients with acute ischemic stroke. Patients with major arterial occlusions with poor outcomes now have a chance of returning to independent living in more than half of the cases. However, many patients with these severe strokes suffer major disability despite these therapies. The search is ongoing for agents that can be combined with thrombectomy to achieve better recovery through halting infarct growth and mitigating injury after ischemic stroke. Several studies in animals and humans have demonstrated that therapeutic hypothermia (TH) offers potential to interrupt the ischemic cascade, reduce infarct volume, and improve functional independence. We performed a literature search to look up recent advances in the use of TH surrounding the science, efficacy, and feasibility of inducing TH in modern stroke treatments. While protocols remain controversial, there is a real opportunity to combine TH with the existing therapies to improve outcome in adults with acute ischemic stroke.

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Uric acid (UA) is a product of the catabolism of purine nucleotides, the principal constituents of DNA, RNA, and cellular energy stores, such as adenosine triphosphate. The main properties of UA include scavenging of hydroxyl radicals, superoxide anion, hydrogen peroxide, and peroxynitrite that make this compound to be the most potent antioxidant in the human plasma. As the result of two silencing mutations in the gene of the hepatic enzyme uricase which degrades UA to allantoin, humans have higher levels of UA than most mammals. However, these levels rapidly decrease following an acute ischemic stroke (AIS), and this decrement has been associated to worse stroke outcomes. This review highlights the safety and potential clinical value of UA therapy in AIS, particularly in patients more exposed to redox-mediated mechanism following the onset of ischemia, such as women, hyperglycemic patients, or patients treated with mechanical thrombectomy. The clinical findings are supported by preclinical data gathered in different laboratories, and in assorted animal species which include male and female individuals or animals harboring comorbidities frequently encountered in patients with AIS, such as hyperglycemia or hypertension. A remarkable finding in these studies is that UA targets its main effects in the brain vasculature since available evidence suggests that does not seem to cross the blood–brain barrier. Altogether, the available data with UA therapy extend the importance of vasculoprotection for effective neuroprotection at the bedside and reinforce the role of endothelial cells after brain ischemia for an increased survival of the whole neurovascular unit.

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Ischemic stroke is a leading cause of death and disability worldwide, but there are no effective, widely applicable stroke therapies. Systemic hypothermia is an international mainstay of postcardiac arrest care, and the neuroprotective benefits of systemic hypothermia following cerebral ischemia have been proven in clinical trials, but logistical issues hinder clinical acceptance. As a novel solution to these logistical issues, the application of local endovascular infusion of cold saline directly to the infarct site using a microcatheter has been put forth. In small animal models, the procedure has shown incredible neuroprotective promise on the biochemical, structural, and functional levels, and preliminary trials in large animals and humans have been similarly encouraging. In addition, the procedure would be relatively cost-effective and widely applicable. The administration of local endovascular hypothermia in humans is relatively simple, as this is a normal part of endovascular intervention for neuroendovascular surgeons. Therefore, it is expected that this new therapy could easily be added to an angiography suite. However, the neuroprotective efficacy in humans has yet to be determined, which is an end goal of researchers in the field. Given the potentially massive benefits, ease of induction, and cost-effective nature, it is likely that local endovascular hypothermia will become an integral part of endovascular treatment following ischemic stroke. This review outlines relevant research, discusses neuroprotective mechanisms, and discusses possibilities for future directions.

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According to the National Stroke Association, stroke is the leading cause of adult disability in the United States, where it is estimated that about 795,000 strokes occur on an annual basis. Minimizing the disability burden of a stroke routinely involves behavioral therapies such as physical and occupational therapy, as well as pharmacologic interventions. The positive effect of antidepressants on functional outcomes for patients with poststroke depression is well known and practiced. In the past 15 years, a growing body of evidence has demonstrated that antidepressant pharmacotherapy and selective serotonin reuptake inhibitors specifically have a role in the functional recovery from strokes even in the nondepressed population. The mechanisms by which antidepressants improve motor recovery following stroke are multifactorial, but it is clear that the process involves augmentation of cerebral blood flow, cortical excitation, and potentiation of neural growth factors all resulting in enhancement of neurogeneration. This review will examine the existing evidence and mechanisms behind antidepressant use for motor recovery in stroke patients and discuss the major human clinical trials that have been conducted surrounding this topic. The evidence clearly suggests that antidepressants have a positive impact on poststroke functional recovery regardless of the presence of depression, and although large-scale randomized, controlled trials are still ongoing, antidepressants are emerging as a promising pharmaceutical means of actively lessening the burden of disability following stroke.

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One of the complications of carotid artery stenting (CAS) is iatrogenic vasospasm caused by mechanical irritation of the blood vessel lumen by a guidewire, catheter, stent retriever, or distal protection devices. Although often self-limiting, the mechanical vasospasm can cause reduction in the cerebral blood flow and result in catastrophic ischemia, especially when undetected and persistent. Real-time cerebral oximetry with near-infrared spectroscopy (NIRS) could detect episodes of cerebral hypoxemia due to vasospasm and facilitate intervention for prevention of hypoxic brain injury during neuro-intervention procedures such as CAS. We present a case scenario where NIRS detected iatrogenic vasospasm even before the conventional tests could identify the event during CAS.

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Stroke is the leading cause of adult disability in the US. Rapid diagnosis and treatment of stroke, in addition to efficacious rehabilitation, is invaluable. The present review aims to report the recent improvements in hybrid operating rooms (hybrid ORs), and in the organization of Neurological intensive care unit (NICUs) and dedicated stroke wards (SWs), which contribute to enhanced stroke treatment. A PubMed literature review was conducted in addition to the collection of other online media releases regarding recent organizational advances in stroke care. PubMed keywords included but were not limited to “neurological intensive care unit,” “hybrid operating room,” and “stroke ward,” while all other online information regarding recent advances in the physical organization was selected and synthesized in accord with its relevance. The current research indicates that hybrid ORs facilitate surgical innovation and improved patient care through the colocation of advanced imaging modalities and surgical capabilities. Moreover, the recent reorganization of NICUs and SWs may lead to better-quality initial treatment and rehabilitation. The present review also considers the current ER triage protocol for stroke patients, and it concludes with relevant considerations relating to the role of the physical hospital structure and organization in stroke care.

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