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Abstract To report the preliminary result of empiric embolization for angiographycally-negative lower gastrointestinal bleeding (LGIB) by using the pharmaco-induced vasospasm technique with or without the adjunctive use of intra-arterial multi-detector computed tomography (MDCT). 23 LGIB patients with positive MDCT findings but negative angiographic results underwent empiric pharmaco-induced vasospasm therapy. The presumed bleeding artery was semi-selectively catheterized, and a segment of bowel was temporarily spasmed with bolus injection of epinephrine and immediately followed by 4-h’ vasopressin infusion. The rebleeding, primary and overall clinical success rates were reported. MDCT showed 19 bleeders in the SMA territory and 4 bleeders in the IMA territory. Early rebleeding was found in 6 patients (26.1%): 2 local rebleeding, 3 from new-foci bleeding and 1 uncertain. Of the 10 small bowel bleeding patients, only 1 out of the 7 who underwent intra-arterial MDCT showed rebleeding, whereas 2 out of the 3 without intra-arterial MDCT rebled. No patients exhibited procedure-related major complications, including bowel ischemia and cardiopulmonary distress. The overall clinical success rate was 91.3% (21/23) with a 30-day mortality rate of 26.1% (2 of the 6 patients had early rebleeding). Empiric pharmaco-induced vasospasm therapy, when localized with/without adjunctive intra-arterial MDCT, seems to be a safe and effective method to treat angiographically-negative LGIB patients.

Aneurysmal subarachnoid hemorrhage (aSAH) is a critical condition with high in-hospital mortality rates. Delayed cerebral ischemia (DCI), a secondary complication associated with aSAH, can also contribute to morbidity and mortality. Although draining the hematoma from the subarachnoid space has been considered effective in preventing DCI, the placement of a drainage system could increase the risk of bacterial meningitis and ventriculitis. This study aimed to examine the association between meningitis following aSAH and the occurrence of DCI, focusing on the role of cerebral vasospasm. Patients who underwent endovascular coiling or surgical clipping for aSAH from April 2001 to March 2022 were included in this study, while those who did not undergo postoperative drainage were excluded. The patient's clinical characteristics, treatment modalities, and outcomes were then analyzed, after which logistic regression was used to assess the odds ratios (OR) for DCI. A total of 810 patients with aSAH were included in this study. Meningitis following aSAH was identified as an independent factor associated with DCI (odds ratio 5.0 [95% confidence intervals (CI) 2.3-11]). Other significant factors were female sex (odds ratio 1.5 [95% CI 0.89-2.5]) and surgical clipping (odds ratio 2.1 [95% CI 1.3-3.4]). This study demonstrated a significant association between meningitis following aSAH and the development of DCI, suggesting that the inflammatory environment associated with meningitis may contribute to cerebral vasospasm. Early recognition and treatment of meningitis in patients with aSAH could reduce the risk of DCI and improve patient outcomes.

BACKGROUND: Cerebral vasospasm is a serious sequela of traumatic brain injury (TBI) which leads to further neurologic injury subsequent to the initial trauma. The natural history and associated risk factors are not well understood. The objective of this study is to evaluate the clinical and radiographic characteristics of patients with TBI. METHODS: This is a descriptive case series of all patients with TBI who underwent cerebral angiogram for evaluation and rescue therapy for posttraumatic arterial vasospasm (PTV) between October 2017 and November 2019. The association of clinical and radiographic characteristics with cumulative severity of angiographic vasospasm was evaluated. The clinical characteristics comprised of age, sex, Glascow Coma Scale (GCS) and need for surgery. The radiographic characteristics were presence of subarachnoid hemorrhage (SAH), location of SAH, presence of contusion, presence of subdural hemorrhage (SDH), and presence of pseudoaneurysm. RESULTS: Twenty-two patients with PTV were identified requiring 69 cerebral angiograms (mean: 3.2; range: 1–9 angiograms per patient) during this period. The average age upon presentation was 40 years old, 81% of the patients were male sex, and the average GCS was 6.8. 67% of the patients underwent craniotomy or craniectomy. All patients had SAH, although only 60% had cisternal SAH. Parenchymal contusion was noted on 90% as well as SDH in 90%. The PTV was noted between 3 and 19 days after trauma. There was more vasospasm involving proximal arteries and higher severity of vasospasm in patients with cisternal SAH. Otherwise, there was no strong association between the clinical or radiographic characteristics and cumulative severity noted on the angiograms for each patient. CONCLUSION: Posttraumatic vasospasm can be detected as early as posttrauma day 3–19 in patients with TBI and SAH. The absence of cisternal SAH does not rule out the occurrence of the vasospasm during the course of treatment.

We present a unique case of transient global amnesia following intravenous administration of a non-ionic iodinated contrast agent for abdominal CT examination. Follow up MR imaging and MR angiography studies revealed hippocampal microinfarction and transient cerebral vasospasm. To our knowledge, this is the first reported case capturing arterial vasospasm following intravenous use of iodinated contrast. Medical professionals handling contrast agents should note the potential for these rare but serious adverse effects.

Subarachnoid hemorrhage (SAH) is a type of stroke caused by bleeding into the subarachnoid space. SAH is a medical emergency and requires prompt treatment to prevent complications such as seizures, stroke, or other brain damage. Treatment options may include surgery, medication, or a combination of both. 2-Cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO), a compound with anti-inflammatory and antioxidant properties, is currently being investigated as a potential treatment for various diseases, including chronic kidney disease and pulmonary arterial hypertension. In this study, the effects of CDDO on rats subjected to SAH were evaluated. Male Sprague-Dawley rats were divided into four groups (n = 6/group): (1) control group, (2) SAH group, (3) SAH + low-dose CDDO (10 mg/kg injected into the subarachnoid space at 24 h after SAH) group, and (4) SAH + high-dose CDDO (20 mg/kg) group. CDDO improved SAH-induced poor neurological outcomes and reduced vasospasm in the basal artery following SAH. It also decreased the SAH-induced expression of proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 in both the cerebrospinal fluid and serum samples as determined by ELISA. A Western blot analysis confirmed an increase in the p-NF-κB protein level after SAH, but it was significantly decreased with CDDO intervention. Immunofluorescence staining highlighted the proliferation of microglia and astrocytes as well as apoptosis of the neuronal cells after SAH, and treatment with CDDO markedly reduced the proliferation of these glial cells and apoptosis of the neuronal cells. The early administration of CDDO after SAH may effectively mitigate neuronal apoptosis and vasospasm by suppressing inflammation.

Post-liver transplant (LT) hepatic artery vasospasm is a vascular complication that is not well recognized and its incidence is not known. As a possible sequela to vasospasm, hepatic artery thrombosis is the second major cause of allograft failure after primary nonfunction and its reported incidence is 2.9% in adults and 8.3% in pediatric LT. Lacuna in knowledge regarding early hepatic artery vasospasm post-LT makes it a difficult condition to diagnose and treat, as the initial ischemic insult on graft can have devastating consequences. We report a case of pediatric progressive familial intrahepatic cholestasis type 3-related chronic liver disease who underwent cadaveric orthotopic LT and postoperatively developed fever, worsening hypotension, and elevated liver enzymes with an absence of arterial flow in intrahepatic branches on Doppler ultrasound. Suspecting early hepatic artery thrombosis, the patient was re-explored and the graft hepatic artery was found to be in a state of vasospasm. Following the infusion of intra-arterial papaverine, urokinase, and intravenous nicorandil, there was an improvement in blood flow. The patient responded well and was discharged on postoperative day 23 with normal liver enzymes.

A peripherally inserted central catheter (PICC) can provide long-term and safe intravenous access for cancer patients with chemotherapy and patients who need long-term infusion and parenteral nutrition. This paper reviews studies on causes and countermeasures of difficulties in PICC insertion under ultrasound guidance. Common actors influencing the PICC insertion includes vascular access selection, vasospasm, puncture position, puncture operator and so on. Targeted nursing interventions should be carried out to prevention risk factors and improve the success rate of PICC placement, therefore reducing the pain of patient during PICC insertion under ultrasound guidance. (经外周静脉置入中心静脉导管(PICC)具有安全、可靠、留置时间长、并发症少等优点, 在临床上得到了广泛应用, 特别适用于肿瘤化疗患者及需要长期输液、静脉高营养治疗的患者。本文对PICC置管过程中送管困难的原因及处理对策进行综述, PICC置管过程中送管困难的原因通常包括血管选择、血管痉挛、穿刺体位、操作者因素等, 护理人员应针对相关的因素开展预防及实施高效处理方法, 提高PICC置管的成功率, 减轻患者痛苦。)

Women are disproportionately affected by symptoms of angina with nonobstructive coronary arteries (ANOCA) which is associated with significant mortality and economic impact. Although distinct endotypes of ANOCA have been defined, it is underdiagnosed and is often incompletely characterized when identified. Patients are often unresponsive to traditional therapeutic options, which are typically antianginal, and the current ability to guide treatment modification by specific pathways is limited. Studies have associated specific genetic loci, transcriptomic features, and biomarkers with ANOCA. Such panomic data, in combination with known imaging and invasive diagnostic techniques, should be utilized to define more precise pathophysiologic subtypes of ANOCA in women, which will in turn help to identify targeted, effective therapies. A precision medicine-based approach to managing ANOCA incorporating these techniques in women has the potential to significantly improve their clinical care.

Background: The aim of this study was to assess the efficacy of indocyanine green (ICG) angiography during full endoscopic microvascular decompression for trigeminal neuralgia. Methods: We extracted retrospective data of patients who received ICG videoangiography during full endoscopic microvascular decompression for trigeminal neuralgia. Preoperative neurovascular contact was evaluated by three-dimensional (3D) fusion images using image analysis software Ziostation2 (ZIOSOFT, Tokyo, Japan) and Intraoperative ICG angiography was used in pre and post ICG injection to identify and assess blood flow in the offending vessel for adequate transposition planification and assess for immediate post transposition blood flow or vasospasm respectively. Patients were assessed the next morning for early signs of brainstem infarction and at one month follow up. Results: There were 44 patients. All patients had ICG videoangiography done during the procedure. The mean age was 65.5 and male female ratio 3.4:1. Some anatomical variants were identified during this procedure. Five patients (11.3%) had a trigeminocerebellar artery, three patients (6.8%) had a developed superior petrosal vein and one patient (2.2%) had dural adhesions with encasement of anterior inferior cerebellar artery. Among the 44 patients enrolled, 34 had transposition done and 10 had combined transposition either with neurolysis or Teflon interposition. The main offending vessel was Superior cerebellar artery (SCA) in 23 patients (67.6%). In 5 (14.7%) of 34 patients who underwent Transposition, vasospasm was seen and no complications were observed in all patients but 93.1% had good pain control in postoperative. Conclusion: ICG angiography in endoscopic microvascular decompression is safe and effective in depicting the offending vessel, its branches and some perforators and contributes significantly to the determination of treatment strategy.

Traumatic brain injury (TBI) is a common diagnosis requiring acute hospitalization. Long-term, TBI is a significant source of health and socioeconomic impact in the United States and globally. The goal of clinicians who manage TBI is to prevent secondary brain injury. In this population, post-traumatic cerebral infarction (PTCI) acutely after TBI is an important but under-recognized complication that is associated with negative functional outcomes. In this comprehensive review, we describe the incidence and pathophysiology of PTCI. We then discuss the diagnostic and treatment approaches for the most common etiologies of isolated PTCI, including brain herniation syndromes, cervical artery dissection, venous thrombosis, and post-traumatic vasospasm. In addition to these mechanisms, hypercoagulability and microcirculatory failure can also exacerbate ischemia. We aim to highlight the importance of this condition and future clinical research needs with the goal of improving patient outcomes after TBI.

Abstract Background Half of the sufferers of reversible cerebral vasoconstriction syndrome (RCVS) exhibit imaging-proven blood-brain barrier disruption. The pathogenesis of blood-brain barrier disruption in RCVS remains unclear and mechanism-specific intervention is lacking. We speculated that cerebrovascular dysregulation might be associated with blood-brain barrier disruption in RCVS. Hence, we aimed to evaluate whether the dynamic cerebral autoregulation is altered in patients with RCVS and could be associated with blood-brain barrier disruption. Methods A cross-sectional study was conducted from 2019 to 2021 at headache clinics of a national tertiary medical center. Dynamic cerebral autoregulation was evaluated in all participants. The capacity of the dynamic cerebral autoregulation to damp the systemic hemodynamic changes, i.e., phase shift and gain between the cerebral blood flow and blood pressure waveforms in the very-low- and low-frequency bands were calculated by transfer function analysis. The mean flow correlation index was also calculated. Patients with RCVS received 3-dimensional isotropic contrast-enhanced T2 fluid-attenuated inversion recovery imaging to visualize blood-brain barrier disruption. Results Forty-five patients with RCVS (41.9 ± 9.8 years old, 29 females) and 45 matched healthy controls (41.4 ± 12.5 years old, 29 females) completed the study. Nineteen of the patients had blood-brain barrier disruption. Compared to healthy controls, patients with RCVS had poorer dynamic cerebral autoregulation, indicated by higher gain in very-low-frequency band (left: 1.6 ± 0.7, p = 0.001; right: 1.5 ± 0.7, p = 0.003; healthy controls: 1.1 ± 0.4) and higher mean flow correlation index (left: 0.39 ± 0.20, p = 0.040; right: 0.40 ± 0.18, p = 0.017; healthy controls: 0.31 ± 0.17). Moreover, patients with RCVS with blood-brain barrier disruption had worse dynamic cerebral autoregulation, as compared to those without blood-brain barrier disruption, by having less phase shift in very-low- and low-frequency bands, and higher mean flow correlation index. Conclusions Dysfunctional dynamic cerebral autoregulation was observed in patients with RCVS, particularly in those with blood-brain barrier disruption. These findings suggest that impaired cerebral autoregulation plays a pivotal role in RCVS pathophysiology and may be relevant to complications associated with blood-brain barrier disruption by impaired capacity of maintaining stable cerebral blood flow under fluctuating blood pressure. Graphical Abstract

Background The rate of underlying ruptured aneurysms, complications, and their relevance to outcomes in “benign” perimesencephalic subarachnoid hemorrhage are not well known and underreported. Methods Retrospective analysis of patients with perimesencephalic subarachnoid hemorrhage from a large tertiary care center (2007–2022). Results Eighty‐one patients were included with mean age of 55.5 ± 10.3 years. An underlying ruptured aneurysm was diagnosed in 5 patients (6.2%); 3 (60%) had negative computed tomography angiography and they were detected only in digital subtraction angiography (2 on initial digital subtraction angiography and 1 on follow‐up digital subtraction angiography). The most common complication was vasospasm in 25/81 patients (31%), and the majority 21/25 (84%) were asymptomatic. Symptomatic vasospasm occurred at a significantly higher rate among patients with underlying aneurysm (40% versus 2.6%; P = 0.01). Hydrocephalus occurred in 10% of patients, all within 1 day, but at a higher rate in the aneurysmal group (40% versus 8%; P = 0.07). A total of 88% of patients had modified Rankin scale score 0–2 at discharge, but at a significantly higher rate in nonaneurysmal patients (91% versus 40%; P = 0.01). An underlying aneurysm, hydrocephalus, and symptomatic vasospasm were associated with poor functional status (odds ratio [OR] = 14.7 [2.1–104]; P = 0.007, OR = 22.6 [4.2–123.5]; P

Background: Methamphetamine is an illegal drug that poses serious public health concerns worldwide. Previous studies have demonstrated a strong association between methamphetamine abuse and non-lethal haemorrhagic stroke. Ischaemic stroke after methamphetamine intake is less common than haemorrhagic stroke. The present study investigated the clinical features and potential pathogenesis in a young methylamphetamine addict that presented with acute ischaemic stroke and reversible middle cerebral artery (MCA) occlusion. Methods: A retrospective data analysis was performed for the young methylamphetamine addict admitted to a hospital for acute ischaemic stroke followed by a literature review to explore the possible pathogenesis. Results: The patient had been receiving methamphetamine for past 2 years. His recurrent headache occurred half an hour after each consumption and was relieved within a few hours. The patient was admitted for acute ischaemic stroke. Urine toxicology screening was positive for methamphetamine. Magnetic resonance angiography revealed occlusion of the right MCA. After discontinuing medication and routine treatment, digital subtraction angiography revealed normal blood flow in the right MCA, indicating reversible MCA occlusion. Conclusion: For young patients with a stroke, a thorough investigation of the history of illicit drug use and toxicological screening of urine and serum samples should be performed. Young methamphetamine users need to be aware of the elevated risk of stroke as well as early signs and symptoms. Transient headaches in young methamphetamine users may be caused by cerebral vasospasms, suggesting the possibility of future catastrophic stroke events.

Objective: Cerebral vasospasm and the resultant delayed cerebral infarction is a significant source of mortality following aneurysmal SAH. Vasospasm is currently detected using invasive or expensive imaging at regular intervals in patients following SAH, thus posing a risk of complications following the procedure and financial burden on these patients. Currently, there is no blood-based test to detect vasospasm. Methods: PubMed, Web of Science, and Embase databases were systematically searched to retrieve studies related to cerebral vasospasm, aneurysm rupture, and biomarkers. The study search dated from 1997 to 2022. Data from eligible studies was extracted and then summarized. Results: Out of the 632 citations screened, only 217 abstracts were selected for further review. Out of those, only 59 full text articles met eligibility and another 13 were excluded. Conclusions: We summarize the current literature on the mechanism of cerebral vasospasm and delayed cerebral ischemia, specifically studies relating to inflammation, and provide a rationale and commentary on a hypothetical future bloodbased test to detect vasospasm. Efforts should be focused on clinical-translational approaches to create such a test to improve treatment timing and prediction of vasospasm to reduce the incidence of delayed cerebral infarction.

BackgroundSubarachnoid hemorrhage (SAH) is a life-threatening vascular condition without satisfactory treatment options. The secreted peptide adropin is highly expressed in the human brain and has neuroprotective effects in brain injury models, including actions involving the cerebrovasculature. Here, we report an endothelial nitric oxide synthase (eNOS)-dependent effect of synthetic adropin treatment that reverses the deleterious effects of SAH.MethodsWe tested the molecular, cellular, and physiological responses of cultured brain microvascular endothelial cells and two mouse models of SAH to treatment using synthetic adropin peptide or vehicle.ResultsSAH decreases adropin expression in cultured brain microvascular endothelial cells and in murine brain tissue. In two validated mouse SAH models, synthetic adropin reduced cerebral edema, preserved tight junction protein expression, and abolished microthrombosis at 1 day post-SAH. Adropin treatment also prevented delayed cerebral vasospasm, decreased neuronal apoptosis, and reduced sensorimotor deficits at seven days post-SAH. Delaying initial treatment of adropin until 24 h post-SAH preserved the beneficial effect of adropin in preventing vasospasm and sensorimotor deficits. Mechanistically, adropin treatment increased eNOS phosphorylation (Ser1179) at 1 & 7 days post-SAH. Treating eNOS−/− mice with adropin failed to prevent vasospasm or behavioral deficits, indicating a requirement of eNOS signaling.ConclusionsAdropin is an effective treatment for SAH, reducing cerebrovascular injury in both the acute (1 day) and delayed (7 days) phases. These findings establish the potential of adropin or adropin mimetics to improve outcomes following subarachnoid hemorrhage.

Abstract As a complication of subarachnoid hemorrhage (SAH), vasospasm substantially contributes to its morbidity and mortality. We aimed at analyzing predictors of outcome for these patients including the role of endovascular treatment (ET). Our database was screened for patients with SAH treated in our Neuro-ICU from 2009 to 2019. Clinical parameters including functional outcome (modified Rankin Scale, mRS of 0–2 or 3–6 at discharge and after a median follow-up of 18 months) and details about ET were gathered on 465 patients, 241 (52%) of whom experienced vasospasm. Descriptive analyses were performed to identify explanatory variables for the dichotomized mRS score. A logistic regression model was fitted on 241 patients with vasospasm including age, Hunt and Hess Score, extraventricular drainage (EVD), forced hypertension, ET and delayed cerebral ischemia (DCI). The model found a Hunt and Hess Score of 5 (OR = 0.043, p = 0.008), requirement of EVD (OR = 0.161, p

ABSTRACT Introduction and objectives: Invasive diagnosis of vasoreactivity and microvascular function may be useful to optimize the management of patients with signs and/or symptoms of myocardial ischemia in the absence of significant coronary stenosis (INOCA). We analyzed the prevalence of the different endotypes, as well as the concordance between 2 diagnostic methods based on thermodilution assessment. Methods: We prospectively included 60 patients with INOCA who underwent a vasoreactivity test with intracoronary acetylcholine, and measurement of absolute coronary blood flow (Q) and minimum microvascular resistance (R) using continuous thermodilution assessment. Finally, calculations of the coronary flow reserve (CFR) and index of microcirculatory resistance index (IMR) were made using the bolus thermodilution method considering CFR 435 UW was estimated as the optimal cut-off value to identify patients with IMR ≥ 25 with an area under the curve of 0.67 (95%CI, 0.51-0.82; P = .04). Conclusions: The invasive study of vasoreactivity and microcirculation was feasible and safe. Prevalence of vasospasm and microvascular dysfunction in patients with INOCA was high. The CFR/MRI/Q combined study allowed us to unmask a subtype of microvascular dysfunction characterized by an abnormally high coronary flow at baseline. The concordance seen between the microvascular resistance obtained by continuous thermodilution measurements and the reference method was low so future studies are justified to determine the usefulness of this technique.

Abstract Background Focal cerebral arteriopathy (FCA) is a clinically important disease that often causes progressive arteriopathy. We report a case of FCA with progressive arteriopathy due to arterial shrinkage of the outer diameter found on T2-weighted three-dimensional sampling perfection with application optimized contrasts using different flip angle evolutions (3D-SPACE) imaging. Case presentation The patient was a 9-year-old girl who developed right hemiparesis. Acute infarction was detected in the basal ganglia. Vascular images revealed stenosis from the distal internal carotid artery (ICA) to the middle cerebral artery (MCA). Intravenous heparin was administered for 8 days, and the symptoms improved. However, 29 days after onset, right hemiparesis transiently developed again and magnetic resonance angiography (MRA) showed progressive stenosis from the ICA to MCA, while 3D-SPACE showed similar shrinkage of the outer diameter. Aspirin was started, and there was no subsequent recurrence. After 12 months, MRA and 3D-SPACE showed improvement of stenosis and arterial shrinkage. Conclusions Given the time course, the change in the outer diameter was thought to be vasospasm. Thus, vasospasm may be one of the causes of progressive arteriopathy in FCA.

Aneurysmal subarachnoid hemorrhage (aSAH) is an emergency that needs prompt diagnosis and treatment with endovascular coiling or surgical clipping of the aneurysm to prevent re-bleeding. In addition to neurologic manifestations, aSAH can cause respiratory and cardiovascular complications. The prevention of hypoxemia and hypercarbia, control of intracranial pressure, and restoration of cerebral perfusion pressure should be the primary aims of early management. Secondarily, the most important causes of persistent neurological deficits and physical dependence in aSAH are vasospasm and delayed ischemia following bleeding. During that period, a focus on the detection, prevention, and treatment of vasospasm should be the rule. Transcranial Doppler allows detection and follow-up of vasospasm, especially in severe cases. Nimodipine is the only drug that has proven efficacy for treating vasospasm. Balloon angioplasty is performed in cases of resistance to medical treatment. Along with angioplasty, intra-arterial vasodilators can be administered. New diagnostic and therapeutic advances will hopefully improve outcomes in the near future.

BackgroundNimodipine improves outcomes following aneurysmal subarachnoid hemorrhage (aSAH). Guidelines recommend that all patients should receive a fixed-dose nimodipine for 21 days. However, studies reported variability of nimodipine concentrations in aSAH. It is not clear if reduced systemic exposure contributes to worsening outcomes. The aim of this study was to compare nimodipine systemic exposure in those who experienced poor outcomes to those who experienced favorable outcomes.MethodsThis was a pilot prospective observational study in 30 adult patients admitted to the University of Alberta Hospital with aSAH. Data were collected from the electronic health records following enrollment. Blood samples were collected around one nimodipine 60 mg dose at a steady state, and nimodipine [total, (+)-R and (−)-S enantiomers] plasma concentrations were determined. The poor outcome was defined as a modified Rankin Scale (mRS) score at 90 days of 3-6, while the favorable outcome was an mRS score of 0-2. The correlation between nimodipine concentrations and percent changes in mean arterial pressure (MAP) before and after nimodipine administration was also determined. Furthermore, covariates potentially associated with nimodipine exposure were explored.ResultsIn total, 20 (69%) participants had favorable outcomes and 9 (31%) had poor outcomes. Following the exclusion of those with delayed presentation (>96 h from aSAH onset), among those presented with the World Federation of Neurological Surgeons (WFNS) grade 3–5, nimodipine median (interquartile range) area under the concentration time curve (AUC0-3h) in those with favorable outcomes were 4-fold higher than in those with poor outcomes [136 (52–192) vs. 33 (23–39) ng.h/mL, respectively, value of p = 0.2]. On the other hand, among those presented with WFNS grade 1–2, nimodipine AUC0-3h in those with favorable outcomes were significantly lower than in those with poor outcomes [30 (28–36) vs. 172 (117–308) ng.h/mL, respectively, value of p = 0.03)]. (+)-R-nimodipine AUC0-3h in those who did not develop vasospasm were 4-fold significantly higher than those who had vasospasm (value of p = 0.047). (−)-S-nimodipine was significantly correlated with percentage MAP reduction. Similar results were obtained when the whole cohort was analyzed.ConclusionThe study was the first to investigate the potential association between nimodipine exposure following oral dosing and outcomes. In addition, it suggests differential effects of nimodipine enantiomers, shedding light on the potential utility of nimodipine enantiomers. Larger studies are needed.

Introduction: Massive traumatic subarachnoid hemorrhage (tSAH) is a rare but potentially life-threatening condition that can mimic the clinical presentation of aneurysmal subarachnoid hemorrhage (aSAH). The accurate differentiation between these two entities is crucial, as their management and prognoses significantly differ. Case presentation: We present a case of a 64-year-old male patient who presented to our emergency department after being involved in a motor vehicle collision. His radiological findings on a computed tomography (CT) scan were suggestive of aSAH based on its location, which showed massive SAH in bilateral sylvian fissures and the basal cisterns. There was no evidence of vasospasm. The patient later developed a stroke despite the use of Nimodipine. Conclusion: While traumatic subarachnoid hemorrhage mimicking aneurysmal subarachnoid hemorrhage is a recognized phenomenon, it is relatively uncommon. We present a case of massive tSAH complicated by a stroke with no evidence of aneurysm on cerebral angiogram, shedding light on the diagnostic challenges in differentiating tSAH from aSAH and emphasizing the importance of accurate diagnosis for appropriate management, in addition, we aim to remind the readers that trauma may be a cause for massive SAH and should prompt a medical SAH management plan.

Background: “New psychoactive substances” (NPS), has been described as a “growing global epidemic”. The aim of our study was to document acute and chronic lesions that can be induced by NPS from autopsy cases for which complete toxicological analyses (including hair analysis) have been performed, in order to better define the role of NPS in the mechanisms of death. Material and methods: A retrospective study was performed at the Department of Forensic Medicine and Pathology, jointly with the Department of Pharmacology and Toxicology. All records for forensic autopsy case within a 6-year period, from January 2016 to January 2021, were reviewed for the diagnosis “death associated with NPS”. Results and discussion: Twelve young male adults complied with the inclusion criteria. Lifestyles were dominated by drug addiction and homosexual context which could be anchored in a practice of ChemSex or even of “slamming”. In regard to autopsy findings, previous pathological state was dominated by cardiovascular and hepatic lesions possibly of toxic etiology. Causes and manners of death were, on the whole, quite heterogeneous; however, an accident as a manner of death was the most frequently observed. In terms of histological findings, the most notable lesions were: (1) cardiovascular (sequelae of myocardial infarction probably secondary to a vasospasm, accelerated atherosclerosis); (2) hepatic (steatohepatitis); (3) neurological (peri mortem convulsions); (4) renal (granular cylinders that may indicate rhabdomyolysis); (5) pulmonary (chronic instertitial inflammation); all of them may have had a toxic origin. In regard to toxicological findings, our case series was mostly subject to chronic consumption of synthetic cathinones, in particular 3-MMC; their involvement in the fatal determinism was retained in 7 cases. Tissue distribution was highlighted as increased in brain, explaining at least partially psychoactive effects of these NPS. Average cardio-femoral ratio of 3.78 suggested a cardiac tropism. A lethal concentration of mexedrone, measured at 640 ng/mL, was described for the first time. Conclusion: We provide autopsy data on NPS consumption habits in Ile-de-France, namely men who have sex with men in ChemSex. Macroscopic and microscopic lesions observed were cardiovascular, hepatic, neurological, renal and pulmonary. From a toxicological point of view, we collect additional data on toxic, even lethal concentrations of NPS. Concerning 3-MMC, calculated cardio-femoral ratio is positive; moreover, it is to our knowledge the first study that demonstrates its pharmacokinetic tissue distribution.

In lower extremity reconstruction, the recipient vessel often requires long-range mechanical dilation because of extensive vasospasm or plaque formation induced by concomitant atherosclerosis. While a forceps dilator can be used to manipulate and dilate vessels approximately 1 cm from their end, a DeBakey vascular dilator can dilate long-range vessels. The authors successfully performed free flap reconstruction of the lower extremity using the DeBakey vascular dilator. Of the two patients who underwent lower extremity reconstruction, one had extensive vasospasm, and the other had plaques in the recipient arteries. Irrigation with 4% lidocaine and dilation of the lumen with a forceps dilator were insufficient to restore the normal arterial blood flow. Instead, a DeBakey vascular dilator with a 1-mm diameter tip was gently inserted into the lumen. Then, to overcome vessel resistance, the dilator gently advanced approximately 10 cm to dilate the recipient artery. Normal arterial blood flow was gushed out after dilating the vessel lumen using a DeBakey vascular dilator. The vascular anastomosis was performed, and intravenous heparin 5000 IU was administered immediately after anastomosis. Prophylactic low-molecular-weight-heparin (Clexane, 1 mg/kg) was administered subcutaneously to both patients for 14 days. The reconstructed flap survived without necrosis in either patient.

Abstract Background Vasospasm is a grave complication of aneurysmal subarachnoid hemorrhage (SAH) with a significant rate of morbidity and mortality. Endovascular intra-arterial injection of Ca channel blocker agent (Nimodipine) may offer a promising solution in refractory vasospasm. Results During the period between April 2017 and May 2019, 120 patients who presented with SAH due to a ruptured intracranial aneurysm were admitted to the neurosurgery department at Alexandria University Hospitals. Among them, 30 patients developed refractory vasospasm and were subjected to endovascular super selective intraarterial injection of nimodipine. The angiographic improvement was excellent in three (10%), good in 14 (46%) and poor in the remaining 13 procedures (43%). Clinical improvement was achieved in 15 cases while 15 cases showed no improvement on Modified Rankin Scale. No cases deteriorated following the injection. Conclusions Endovascular chemical angioplasty using a ca channel blocker agent (Nimodipine) is a safe and efficient method for the treatment of refractory post aneurysmal SAH vasospasm. The quest is still needed for developing a better efficient agent to overcome the vasospasm dilemma.

Delayed cerebral ischemia (DCI) and cerebral vasospasm (VS) are rare but serious post-operative complications after surgery for pituitary macroadenomas; the mechanism of which are poorly understood. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a vasoactive neuropeptide expressed in pituitary adenomas and may play a role in DCI/VS. The aim of this case-control study was to investigate the association between tumor expression of PACAP and DCI/VS following pituitary surgery. Tumor tissue from five patients with DCI/VS following pituitary surgery and nine matched controls were evaluated for PACAP expression by immunohistochemistry. Nuclear PACAP expression was significantly elevated in patients with DCI/VS following pituitary surgery compared to controls (0.396 ± 0.0.16 a.u. vs 0.093 ± 0.04 a.u, p

Arterial vasospasm after microsurgery can cause severe obstruction of blood flow manifested as low tissue temperature, leading to tissue necrosis. The timely discovery and synchronized treatment become pivotal. In this study, a reversible, intelligent, responsive thermosensitive hydrogel system is constructed employing both the gel–sol transition and the sol–gel transition. The “reversible thermosensitive (RTS)” hydrogel loaded with verapamil hydrochloride is designed to dynamically and continuously regulate the extravascular microenvironment by inhibiting extracellular calcium influx. After accurate implantation and following in situ gelation, the RTS hydrogel reverses to the sol state causing massive drug release to inhibit vasospasm when the tissue temperature drops to the predetermined transition temperature. Subsequent restoration of the blood supply alleviates further tissue injury. Before the temperature drops, the RTS hydrogel maintains the gel state as a sustained-release reservoir to prevent vasospasm. The inhibition of calcium influx and vasospasm in vitro and in vivo is demonstrated using vascular smooth muscle cells, mice mesenteric arterial rings, and vascular ultrasonic Doppler detection. Subsequent animal experiments demonstrate that RTS hydrogel can promote tissue survival and alleviate tissue injury responding to temperature change. Therefore, this RTS hydrogel holds therapeutic potential for diseases requiring timely detection of temperature change.

One of the main causes of the dismal prognosis in patients who survive the initial bleeding after aneurysmal subarachnoidal hemorrhage is the delayed cerebral ischaemia caused by vasospasm. Studies suggest that cerebral magnesium and pH may potentially play a role in the pathophysiology of this adverse event. Using phosphorous magnetic resonance spectrocopy (31P-MRS), we calculated the cerebral magnesium (Mg) and pH levels in 13 patients who suffered from aSAH. The values between the group that developed clinically significant vasospasm (n = 7) and the group that did not (n = 6) were compared. The results of this study show significantly lower cerebral Mg levels (p = 0.019) and higher pH levels (p < 0.001) in the cumulative group (all brain voxels together) in patients who developed clinically significant vasospasm. Further clinical studies on a larger group of carefully selected patients are needed in order to predict clinically significant vasospasm.

Background. Acute subarachnoid haemorrhage (SAH) is a dangerous condition: roughly 50% of patients die within 30 days, nearly 25% develop significant neuropsychological and cognitive deficits, about 10% suffer from other complications, and only around 15% recover fully. One of the main causes of mortality is cerebral vasospasm (CVS), a cause of delayed cerebral ischaemia (DCI), which can lead to secondary cerebral infarction. Thus, early detection of CVS is crucial for improving patient outcomes. The aim of this study was to analyse the demographic and clinical (including complications) data of patients diagnosed with SAH, to evaluate the diagnostic methods, and to investigate the prevalence and treatment of complications. Materials and methods. This retrospective study included 102 patients diagnosed with spontaneous SAH, aged at least 18 years, who were treated in the Vilnius University Hospital Santaros Klinikos (VUL SK) in 2014-2017. The obtained VUL SK data were selected by the I60 ICD-10-CM code and depersonalized. Head computerized tomography (CT), CT angiography (CTA), digital subtraction angiography (DSA), transcranial color-coded duplex sonography (TCCS), and magnetic resonance angiography (MRA) were used to evaluate the cerebral arteries. Results. In 102 patients (mean age 58±16 years; 55% female), the most common cause of spontaneous SAH was ruptured aneurysm, the most common arterial sites were the middle cerebral artery (36%), anterior cerebral artery and/or communicating artery (together 33%), and internal carotid artery (20%). In-hospital mortality was as high as 21%. All patients underwent head CT, 78% CTA, 33% DSA, 8% TCCS, and 1% MRA. 71% patients experienced SAH complications: 66% acute, 27% chronic. The most common acute complications were cerebral oedema (34%), rebleeding (29%), and acute ischaemia (23%), the most common chronic complications hydrocephalus (11%), DCI (9%), and CVS (8%). Conclusions. CVS was diagnosed considerably less frequently in this study compared to other studies. While the diagnosis rates of ischaemia and hyponatremia were likewise significantly lower in this study compared to those in others, they are in line with the CVS diagnosis rate. Aside from the CVS and CVS-related complications, all the other SAH complications were roughly within the range of the other studies.

Intracranial aneurysms (IA) are the most common cerebral vascular pathologies. Their rupture leads to the most dangerous subtype of stroke—aneurysmal subarachnoid hemorrhage (aSAH), which may be followed by cerebral vasospasm and ischemic sequelae. Recently, an imbalance within the intestinal microbiota, referred to as dysbiosis, was suggested to play a role in the formation, progression, and rupture of IA. As no systematic review on this topic exists, considering the significance of this matter and a lack of effective prophylaxis against IA or cerebral vasospasm, we aim to sum up the current knowledge regarding their associations with intestinal microbiome, identify the gaps, and determine future prospects. Scientific databases were systematically and independently searched by two authors from inception to 1st May 2023 for original articles regarding the role of intestinal microbiota in intracranial aneurysmal growth, aSAH occurrence, as well as in cerebral vasospasm following aSAH. The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) checklist was followed in an abstraction process. The STROBE tool was applied to assess the risk of bias. This research was funded by the National Science Centre, Poland (grant number 2021/41/N/NZ2/00844). Of 302 records, four studies were included that fully met eligibility criteria. Studies reported (1) that the relative abundance of Hungatella hathewayi is a protective factor against aneurysm growth and rupture, resulting from the reduced inflammation and extracellular matrix remodeling in the cerebral arterial wall and from reduced metalloproteinase-mediated degradation of smooth muscle cells in cerebral vessels. (2) Relative abundance of Campylobacter ureolyticus is associated with aSAH. (3) No article has evaluated microbiota in relation to cerebral vasospasm following aSAH although there is an ongoing study. We concluded that intestinal microbiota might be a potential target for diagnostic and therapeutic tools to improve the management of cerebral aneurysms. However, more studies of prospective design are needed.

Bacterial meningitis is a serious, life-threatening infection of the meninges. Several radiological studies highlight prominent structural alterations occurring in the cerebral vasculature, leading to significant cerebrovascular consequences during bacterial meningitis. Beginning with reflexive arterial vasospasm , cerebrovascular disease during bacterial meningitis proceeds through a orderly sequence of arterial vasculitis with inflammatory cell infiltration, medial smooth muscle migration and proliferation, medial necrosis, adventitial fibrosis and eventual intimal stenosis. As such, this review focuses on changes occurring within cerebral arteries during disease progression, highlighting the various structural modifications occurring in the arterial vessels that contribute to disturbances in cerebral hemodynamics and, ultimately, cerebrovascular consequences during bacterial meningitis.

This study aimed to investigate the relationship between prescription drugs and the slow-flow phenomenon after drug-coated balloon angioplasty. Of 30 patients, five (17%) presented with the slow-flow phenomenon. Patients with the slow-flow phenomenon were significantly less commonly prescribed calcium channel blockers than those without the slow-flow phenomenon (P = 0.03). There was no intergroup difference in the prescription of angiotensin II receptor blockers and β-blockers. The clinical outcomes, including restenosis, thrombosis, target lesion revascularization, and death, did not differ between groups during the 10-month observation period.

Abstract Purpose The treatment of vasospasms during endovascular stroke treatment (EST) with intra-arterial nimodipine (NM) is routinely performed. However, the efficacy of resolving iatrogenic vasospasms during the angiographic intervention and the infarct development in follow-up imaging after EST has not been studied yet. Methods Retrospective single-center analysis of patients receiving EST for anterior circulation vessel occlusion between 01/2015 and 12/2021. The primary endpoint was ASPECTS in follow-up imaging. Secondary endpoints were the clinical outcome (combined endpoint NIHSS 24 h after EST and difference between modified Rankin Scale (mRS) before stroke and at discharge (delta mRS)) and intracranial hemorrhage (ICH) in follow-up imaging. Patients with vasospasms receiving NM (NM+) or not (NM-) were compared in univariate analysis. Results Vasospasms occurred in 79/1283 patients (6.2%), who consecutively received intra-arterial NM during EST. The targeted vasospasm angiographically resolved in 84% (66/79) under NM therapy. ASPECTS was lower in follow-up imaging after vasospasms and NM-treatment (NM – 7 (6–9), NM + 6 (4.5-8), p = 0.013) and the clinical outcome was worse (NIHSS 24 h after EST was higher in patients treated with NM (median, IQR; NM+: 14, 5–21 vs. NM-: 9, 3–18; p = 0.004), delta-mRS was higher in the NM + group (median, IQR; NM+: 3, 1–4 vs. NM-: 2, 1–2; p = 0.011)). Any ICH (NM+: 27/79, 34.2% vs. NM-: 356/1204, 29.6%; p = 0.386) and symptomatic ICH (NM+: 2/79, 2.5% vs. NM-: 21/1204, 1.7%; p = 0.609) was equally distributed between groups. Conclusion Intra-arterial nimodipine during EST resolves iatrogenic vasospasms efficiently during EST without increasing intracranial hemorrhage rates. However, patients with vasospasms and NM treatment show higher infarct growth resulting in lower ASPECTS in follow-up imaging.

Delayed cerebral vasospasms after subarachnoid hemorrhage (SAH) are a risk factor for poor prognosis after successful treatment of ruptured intracranial aneurysms. Different strategies to remove clots from the subarachnoid space and prevent vasospasms have different outcomes. Intrathecal urokinase infusion therapy combined with endovascular treatment (EVT) can reduce the incidence of symptomatic vasospasms. To analyze the relationship between symptomatic vasospasms and residual SAHs after urokinase infusion therapy, we retrospectively reviewed the records of 348 consecutive patients managed with EVT and intrathecal urokinase infusion therapy for aneurysmal SAH at our institution between 2010 and 2021. Among them, 163 patients met the study criteria and were classified into two groups according to the presence of residual SAH in the cisterns, Sylvian fissures, and frontal interhemispheric fissure. The incidence of symptomatic vasospasms and the clinical outcomes were assessed. In total, eight (5.0%) patients developed symptomatic vasospasms. Patients with symptomatic vasospasms had a significantly higher incidence of residual SAH in the Sylvian or frontal interhemispheric fissures than those without (P

Delayed cerebral ischemia (DCI) is a life-threatening complication of aneurysmal subarachnoid hemorrhage (aSAH). The vasoactive P450 eicosanoids 20-hydroxyeicosatretraenoate (20-HETE) and 14,15-epoxyeicosatrenoate (14,15-EET) are associated with the development of DCI and may play opposing roles in DCI risk. We hypothesized that the ratio of these opposing eicosanoids in cerebrospinal fluid (CSF) is associated with hemorrhage severity and the risk of developing DCI after aSAH. In a preclinical model, rats received intracisternal blood injections to approximate aSAH. Hemorrhage severity, cerebral blood flow (CBF), cortical spreading depolarizations were recorded, and CSF eicosanoid levels were quantified using mass spectrometry. In a parallel clinical study, CSF samples were collected and analyzed prospectively from subjects with aSAH and outcomes were tracked. Preclinically, rats with greater hemorrhage severity had impaired CBF and lower median 14,15-EET/20-HETE ratios compared to those with lesser or no hemorrhage. In aSAH patients, the CSF 14,15-EET/20-HETE ratio was negatively correlated with hemorrhage grade on imaging. Patients who developed DCI had lower median 14,15-EET/20-HETE ratios compared to those without DCI. The CSF 14,15-EET/20-HETE ratio correlates with hemorrhage severity and may reflect a mechanistic underpinning of microvascular dysfunction that contributes to DCI. These results suggest that vasoactive eicosanoids may be a therapeutic target in aSAH.

Abstract Background Cerebral vasospasm (CV) can contribute to significant morbidity in subarachnoid hemorrhage (SAH) patients. A key unknown is how CV induction is triggered following SAH. Methods Human aneurysmal blood and cerebral spinal fluid were collected for evaluation. To confirm mechanism, c57/bl6 wild type and c57/bl6 IL-6 female knockout (KO) mice were utilized with groups: saline injected, SAH, SAH + IL-6 blockade, SAH IL-6 KO, SAH IL-6 KO + IL-6 administration, SAH + p-STAT3 inhibition. Dual-labeled microglia/myeloid mice were used to show myeloid diapedesis. For SAH, 50 μm blood was collected from tail puncture and administered into basal cisterns. IL-6 blockade was given at various time points. Various markers of neuroinflammation were measured with western blot and immunohistochemistry. Cerebral blood flow was also measured. Vasospasm was measured via cardiac injection of India ink/gelatin. Turning test and Garcia’s modified SAH score were utilized. P

BackgroundVasospasm and cerebral ischemia after aneurysmal subarachnoid hemorrhage are associated with mortality and poor neurological outcomes. We studied the efficacy of all available strategies targeting vasospasm and cerebral ischemia on outcomes in a network meta-analysis.MethodsWe searched EMBASE and MEDLINE databases from 1 January 1990 and 28 November 2021 according to PRISMA guidelines. Randomized controlled trials and longitudinal studies were included. All curative or preventive strategies targeting vasospasm and/or cerebral ischemia were eligible. A network meta-analysis was performed to compare all interventions with one another in a primary (randomized controlled trials only) and a secondary analysis (both trials and longitudinal studies). Mortality by 3 months was the primary outcome. Secondary outcomes were vasospasm, neurological outcome by 3 months, and dichotomized as “good” or “poor” recovery according to each study definition.ResultsA total of 2,382 studies were screened which resulted in the selection of 192 clinical trials (92 (47.9%) and 100 cohorts (52.1%) and the inclusion of 41,299 patients. In randomized controlled studies, no strategy decreased mortality by 3 months. Statins (0.79 [0.62–1]), tirilazad (0.82 [0.69–0.97]), CSF drainage (0.47 [0.29–0.77]), and clazosentan (0.51 [0.36–0.71]) significantly decreased the incidence of vasospasm. Cilostazol was the only treatment associated with improved neurological outcomes by 3 months in the primary (OR 1.16, 95% CI [1.05–1.28]) and secondary analyses (OR 2.97, 95% CI [1.39–6.32]).DiscussionIn the modern era of subarachnoid hemorrhage, all strategies targeting vasospasm failed to decrease mortality. Cilostazol should be confirmed as a treatment to improve neurological outcomes. The link between vasospasm and neurological outcome appears questionable.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=116073, identifier: PROSPERO CRD42018116073.

Low-level blast (LLB) exposure can lead to alterations in neurological health, cerebral vasculature, and cerebral blood flow (CBF). The development of cognitive issues and behavioral abnormalities after LLB, or subconcussive blast exposure, is insidious due to the lack of acute symptoms. One major hallmark of LLB exposure is the initiation of neurovascular damage followed by the development of neurovascular dysfunction. Preclinical studies of LLB exposure demonstrate impairment to cerebral vasculature and the blood–brain barrier (BBB) at both early and long-term stages following LLB. Neuroimaging techniques, such as arterial spin labeling (ASL) using magnetic resonance imaging (MRI), have been utilized in clinical investigations to understand brain perfusion and CBF changes in response to cumulative LLB exposure. In this review, we summarize neuroimaging techniques that can further our understanding of the underlying mechanisms of blast-related neurotrauma, specifically after LLB. Neuroimaging related to cerebrovascular function can contribute to improved diagnostic and therapeutic strategies for LLB. As these same imaging modalities can capture the effects of LLB exposure in animal models, neuroimaging can serve as a gap-bridging diagnostic tool that permits a more extensive exploration of potential relationships between blast-induced changes in CBF and neurovascular health. Future research directions are suggested, including investigating chronic LLB effects on cerebral perfusion, exploring mechanisms of dysautoregulation after LLB, and measuring cerebrovascular reactivity (CVR) in preclinical LLB models.

Myocardial infarction without coronary artery obstruction, according to Russian authors, occurs from 4.1 to 10.3% of cases of all myocardial infarctions. Despite a fairly complete description of the term "acute myocardial infarction", there are often situations when the diagnosis may cause doubts and the cause of the condition cannot be found out. The article demonstrates a clinical case of a 26-year-old young man whose genesis of myocardial infarction after a detailed examination turned out to be unclear.

Background: Previous cohort studies focused on relative risk stratification among patients diagnosed with vasospastic angina, and it is unknown how much vasospasm accounts for the cause of out-of-hospital cardiac arrest, and whether prognosis differs. Methods: From a registry data collected from 65 hospitals in Korea, 863 subjects who survived hospital cardiac arrest were evaluated. The patients with insignificant coro-nary lesion, vasospasm, and obstructive lesion were each grouped as group I, group II, and group III, respectively. The primary and secondary outcomes were survival to hospital discharge and good neurological function at discharge defined as cerebral performance index 1. Results: At hospital discharge, 529 subjects (61.3%) survived. There was no significant difference in survival according to coronary angiographic findings (P =.133 and P =.357, group II and group III compared to group I), but the neurological outcome was significantly better in groups II and III (P =.046 and P =.022, groups II and III compared to group I). Two multivariate models were evaluated to adjust traditional risk factors and cardiac biomarkers. The presence of coronary artery vasospasm did not affect survival to hospital discharge (P = 0.060 and P =.162 for both models), but neurological function was significantly better (OR: 1.965, 95% CI: 1.048-3.684, P =.035, and OR: 1.706, 95% CI: 1.012-2.878, P =.045 for vasospasm, models I and II, respectively). Conclusions: Coronary vasospasm does not show better survival to hospital discharge, but shows better neurological outcomes. Aggressive coronary angiography and intensive medical treatment for adequate control of vasospasm should be emphasized to prevent and manage fatal events.

One of the common complications of non-traumatic subarachnoid hemorrhage (SAH) is delayed cerebral ischemia (DCI). Intrathecal (IT) administration of nicardipine, a calcium channel blocker (CCB), upon detection of large-artery cerebral vasospasm holds promise as a treatment that reduces the incidence of DCI. In this observational study, we prospectively employed a non-invasive optical modality called diffuse correlation spectroscopy (DCS) to quantify the acute microvascular cerebral blood flow (CBF) response to IT nicardipine (up to 90 min) in 20 patients with medium-high grade non-traumatic SAH. On average, CBF increased significantly with time post-administration. However, the CBF response was heterogeneous across subjects. A latent class mixture model was able to classify 19 out of 20 patients into two distinct classes of CBF response: patients in Class 1 (n = 6) showed no significant change in CBF, while patients in Class 2 (n = 13) showed a pronounced increase in CBF in response to nicardipine. The incidence of DCI was 5 out of 6 in Class 1 and 1 out of 13 in Class 2 (p < 0.001). These results suggest that the acute (

Vasospasm, initial neurological damage, rebleeding, and periprocedural complications are associated prognostic factors for clinical outcomes after aneurysmal subarachnoid hemorrhage (SAH). In this study, factors related to delayed ischemic neurological deficit (DIND) are evaluated using data from our institute for the last 18 years. Data from 2001 to 2018 of patients with aneurysmal SAH who underwent surgical clipping (SC) or endovascular coiling (EC) within 7 days of onset were retrospectively analyzed. Cases of mortality within 5 days after treatment were excluded. Multivariate analysis was used to identify the risk factors for DIND. In total, 840 cases of SAH were assessed; among these cases, 384 (45.7%) and 456 (54.3%) were treated with SC and EC, respectively. The frequency of DIND in the EC group was significantly less than that in the SC group (11.8% vs. 17.7%; p = 0.016). In the results of multivariate analysis, internal carotid artery (ICA) aneurysm and hemorrhagic complications were the risk factors for DIND. Cilostazol administration and EC were significant factors for vasospasm prevention after aneurysmal SAH (odds ratio of ICA aneurysm: 1.59, hemorrhagic complications: 1.76, SC: 1.51, and cilostazol administration: 0.51, respectively). Cilostazol administration was also a significant factor in patients who were treated with EC. ICA aneurysm, treatment strategy, hemorrhagic complications, and cilostazol administration were associated with DIND. Oral administration of cilostazol and avoiding hemorrhagic complications were effective in DIND prevention. If both treatments are available for ruptured aneurysms, clinicians should choose EC on the basis of its ability to prevent DIND.

Abstract Background Questions remain on the optimal management of subarachnoid hemorrhage (SAH) patients once they are admitted to the referring center, before and after the aneurysm treatment. To address these issues, we created a consensus of experts endorsed by the Italian Society of Anesthesia and Intensive Care (SIAARTI) to provide clinical guidance regarding this topic. Specifically, in this manuscript (part 2), we aim to provide a list of experts’ recommendations regarding the management of SAH patients in a center with neurosurgical/neuroendovascular facilities after aneurysm treatment. Methods A multidisciplinary consensus panel composed by 24 physicians selected for their established clinical and scientific expertise in the acute management of SAH patients with different specializations (anesthesia/intensive care, neurosurgery, and interventional neuroradiology) was created. A modified Delphi approach was adopted. Results A total of 33 statements were discussed, voted, and approved. Consensus was reached on 30 recommendations (28 strong and 2 weak). In 3 cases, where consensus could not be agreed upon, no recommendation was provided. Conclusions This consensus provides practical recommendations (and not mandatory standard of practice) to support clinician’s decision-making in the management of SAH patients in centers with neurosurgical/neuroendovascular facilities after aneurysm securing.

Hypothermia or cold therapy is the local or systemic application of cold for therapeutic purposes. Local application of cold is used to control inflammation: pain and swelling, hematoma and trismus reduction. Despite the frequent use of cooling in prosthodontic rehabilitation and in physical therapy, as evidenced by many reports in the literature, there is scientific documentation that suggests disadvantages of using this treatment in maxillofacial surgery and oral surgery. Also the clinical studies that have been carried out in maxillofacial surgery and oral surgery have been conducted in an empirical manner, which casts doubt on the results. In view of this, it is relevant to study the mechanisms of microcirculatory preconditioning and hypothermia. This physiological process is so interesting for the development of medical devices of controlled hardware hypothermia to prevent inflammatory symptoms at the stage of rehabilitation by targeting the vascular and cellular component of the inflammatory process in different areas of the human body. To date, the use of local hardware controlled hypothermia in various pathological conditions in humans is a topical trend in medicine. Microcirculatory bloodstream is directly related to temperature factors. Although there are concepts of vascular spasm or dilatation in the microcirculatory bloodstream during systemic hypothermia, there are no reliable data on the cellular and vascular reactions during local hypothermia. In this paper, a search for fundamental and current scientific work on the topic of cellular and vascular changes under the influence of hypothermia was conducted. The search for data revealed that the mechanisms of intracellular hypothermia are of particular interest for the development of therapeutic treatments after surgical interventions in areas with extensive blood supply. With this in mind, it is relevant to investigate several areas: the role of endothelium, glycocalyx and blood cells in microcirculatory-mediated preconditioning and intracellular hypothermia, and in the molecular mechanism that regulates these processes, whether they occur in the same way in all tissues.

A field biologist was bitten by a female Nikolsky’s viper (Vipera berus nikolskii) in Kharkiv Oblast, Ukraine. Two months later, the patient began to experience cold-induced vasospasm of the affected digit diagnosed as acquired Raynaud phenomenon. The patient had more than 30 occurrences during the single winter following the bite, but the signs and symptoms of Raynaud phenomenon disappeared with the end of winter. This report describes the case and puts it into context with the literature on the topic of toxin-induced peripheral vasospastic disorders and their potential importance in snakebite envenoming.

Circulating extracellular vesicles (EVs) may play a pathophysiological role in the onset of complications of subarachnoid hemorrhage (SAH), potentially contributing to the development of vasospasm (VP). In this study, we aimed to characterize circulating EVs in SAH patients and examine their effects on endothelial and smooth muscle cells (SMCs). In a total of 18 SAH patients, 10 with VP (VP), 8 without VP (NVP), and 5 healthy controls (HC), clinical variables were recorded at different time points. EVs isolated from plasma samples were characterized and used to stimulate human vascular endothelial cells (HUVECs) and SMCs. We found that EVs from SAH patients expressed markers of T-lymphocytes and platelets and had a larger size and a higher concentration compared to those from HC. Moreover, EVs from VP patients reduced cell viability and mitochondrial membrane potential in HUVECs and increased oxidants and nitric oxide (NO) release. Furthermore, EVs from SAH patients increased intracellular calcium levels in SMCs. Altogether, our findings reveal an altered pattern of circulating EVs in SAH patients, suggesting their pathogenic role in promoting endothelial damage and enhancing smooth muscle reactivity. These results have significant implications for the use of EVs as potential diagnostic/prognostic markers and therapeutic tools in SAH management.

Background: Both indocyanine green videoangiography (ICG-VA) and flowmetry were considered beneficial in preventing parent artery compromise during aneurysm surgery. However, the appropriate strategy that should be used remains controversial. The objective of the study is to assess the outcomes of aneurysm clipping through flowmetry or ICG-VA monitoring. Materials and Methods: This retrospective cohort study included 75 patients who underwent aneurysm clipping with vascular patency monitoring. In total, 42 patients underwent flowmetry monitoring and 33 ICG-VA monitoring. Preoperative disease severity and functional outcomes were assessed using the World Federation of Neurosurgical Societies (WFNS) grading system and the modified Rankin scale, respectively. Results: As compared with ICG-VA, flowmetry group had nonsignificant higher incidence of clip modification (31.7% vs. 18.2%, P = 0.29) and residual neck (22% vs. 10%, P = 0.218). Besides Fisher grade, flowmetry monitoring (Crude odds ratio [OR] = 0124, P = 0.015), young age, and anterior communicating artery location were the independent risk factors for vasospasm based on multivariate analysis. The incidence of parent artery compromise did not differ between both groups. Old age, poor preoperative WFNS grade, low Glasgow coma scale (GCS) score, left-side location, and long hospital stay were associated with poor functional outcomes in the univariate analysis. However, only the GCS score was considered a prognostic factor in the multivariate analysis (Adjusted OR = 0.03, P = 0.034). Conclusion: Both monitoring methods have similar functional outcomes. Although not influencing outcome, the flowmetry group has a higher incidence of angiographic vasospasm than the ICG-VA group. The vessel preparation for flowmetry monitoring is more complicated than that for ICG-VA; thus, we recommend ICG-VA for routine monitoring. Flowmetry may be applicable in distal aneurysms when hemodynamic insufficiency in a parent artery is suspected.

BackgroundMinority of acute myocardial infarctions (MI) are caused by a non-atherosclerotic occlusion of the coronary artery. We present a case report, where MI with ST-segment elevation was provoked by a vasospasm, which is a rare aetiological finding.Case presentation27-year-old male patient presented to the emergency department because of a sudden onset chest pain radiating to the left arm. The patient underwent percutaneous coronary intervention (PCI) to the right coronary artery (RCA) 3 months ago due to inferior wall MI, however, chest pain episodes kept on recurring at night throughout the whole period after the intervention. During current admission, initial electrocardiogram (ECG) demonstrated ST-segment elevation in leads II, III and aVF. Coronary angiogram revealed diffuse severe narrowing of the right coronary artery, which was relieved with intracoronary administration of nitrates and verapamil. After coronary angiogram patient was given oral long-acting nitrates and verapamil, however, during the following days nocturnal chest pain episodes reoccurred. It was decided to swap verapamil to diltiazem, which led to complete cessation of angina episodes. The patient was discharged in stable condition and symptom free. It was suspected that the first MI was of vasospastic origin, which likely led to unnecessary stenting.ConclusionsThis clinical case has demonstrated the challenges clinician could face in order to correctly diagnose vasospasm-induced MI because of its rare occurrence and highly variable presentation. We strongly suggest using intracoronary nitroglycerine during coronary angiography as a standard practice to avoid a potential diagnostic error and unnecessary stenting. Although, in some cases the reason behind coronary artery spasm (CAS) remains unclear, medical treatment can be very effective for CAS prevention.

Acute subdural hemorrhage caused by ruptured cerebral aneurysms is rare. Herein, we report an atypical case of subdural hemorrhage caused by ruptured anterior communicating artery aneurysm in a 49-year-old woman. Computed tomography revealed subarachnoid, intracerebral, and subdural hemorrhages. After the treatment with endovascular coiling significantly decreased the patient's subdural hemorrhage. However, the subdural hemorrhage revealed and became iso-attenuation compared with the white matter on the 11th day, and hypo-attenuation on the 19th day. On the 33rd day, this subdural hemorrhage completely resolved after discontinuation of dual antiplatelet therapy. Due to rapid changes in the radiologic features of SDH, frequent computed tomography scans at least once a week may be needed especially in patients who receive antiplatelet therapy during the vasospasm phase.