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BACKGROUND: Sympathetic-mediated vasoconstriction from the superior cervical ganglion (SCG) is a significant contributor to cerebral vasospasm. Inhibition of the SCG has been shown to improve cerebral blood flow and reverse cerebral vasospasm in swine models. We evaluated the efficacy of a novel minimally invasive endovascular approach to target and pharmacologically inhibit the SCG, using a Micro-Infusion Device for transmural drug delivery. METHODS: Eight SCGs in four Yorkshire swine were surgically identified. After confirming appropriate sympathetic-mediated intracranial vasoconstriction response with SCG stimulation, an endovascular Micro-Infusion Device was used for transmural targeting of the SCG and delivery of 1.5-2 mL of 1% lidocaine-contrast mixture to the perivascular space. Digital subtraction angiography was obtained at: (1) baseline; (2) with SCG stimulation; and (3) after lidocaine delivery to the SCG using the Micro-Infusion Device with concurrent SCG stimulation. Vessel diameters were measured and compared. RESULTS: Endovascular transmural delivery of lidocaine to the SCG and carotid perivascular tissue using the Micro-Infusion Device successfully inhibited sympathetic-mediated vasoconstriction response. Measured vessel diameters after lidocaine delivery were comparable to baseline despite SCG stimulation. CONCLUSION: A novel endovascular technique of transmural delivery of lidocaine to the SCG and carotid artery perivascular tissues successfully inhibits the sympathetic input to the cerebral vasculature and modulates sympathetic-mediated cerebral vasospasm. These results suggest promising steps towards translation to potential clinical use for patients suffering from cerebral vasospasm.

BACKGROUND: Cerebral vasospasm (CV) is a feared complication which occurs after 20-40% of subarachnoid haemorrhage (SAH). It is standard practice to admit patients with SAH to intensive care for an extended period of resource-intensive monitoring. We used machine learning to predict CV requiring verapamil (CVRV) in the largest and only multi-center study to date. METHODS: Patients with SAH admitted to UCLA from 2013 to 2022 and a validation cohort from VUMC from 2018 to 2023 were included. For each patient, 172 unique intensive care unit (ICU) variables were extracted through the primary endpoint, namely first verapamil administration or no verapamil. At each institution, a light gradient boosting machine (LightGBM) was trained using five-fold cross validation to predict the primary endpoint at various hospitalization timepoints. FINDINGS: A total of 1750 patients were included from UCLA, 125 receiving verapamil. LightGBM achieved an area under the ROC (AUC) of 0.88 > 1 week in advance and ruled out 8% of non-verapamil patients with zero false negatives. Our models predicted no CVRV vs CVRV within three days vs CVRV after three days with AUCs = 0.88, 0.83, and 0.88, respectively. From VUMC, 1654 patients were included, 75 receiving verapamil. VUMC predictions averaged within 0.01 AUC points of UCLA predictions. INTERPRETATION: We present an accurate and early predictor of CVRV using machine learning with multi-center validation. This represents a significant step towards optimized clinical management and resource allocation in patients with SAH. FUNDING: Robert E. Freundlich is supported by National Center for Advancing Translational Sciences federal grant UL1TR002243 and National Heart, Lung, and Blood Institute federal grant K23HL148640; these funders did not play any role in this study. The National Institutes of Health supports Vanderbilt University Medical Center which indirectly supported these research efforts. Neither this study nor any other authors personally received financial support for the research presented in this manuscript. No support from pharmaceutical companies was received.

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.

Background and Purpose Methods Results Conclusion Vasospasm is a common iatrogenic event during mechanical thrombectomy (MT). In such circumstances, intra‐arterial nimodipine administration is occasionally considered. However, its use in the treatment of iatrogenic vasospasm during MT has been poorly studied. We investigated the impact of iatrogenic vasospasm treated with intra‐arterial nimodipine on outcomes after MT for large vessel occlusion stroke.We conducted a retrospective analysis of the multicenter observational registry Endovascular Treatment in Ischemic Stroke (ETIS). Consecutive patients treated with MT between January 2015 and December 2022 were included. Patients treated with medical treatment alone, without MT, were excluded. We also excluded patients who received another in situ vasodilator molecule during the procedure. Outcomes were compared according to the occurrence of cervical and/or intracranial arterial vasospasm requiring intraoperative use of in situ nimodipine based on operator's decision, using a propensity score approach. The primary outcome was a modified Rankin Scale (mRS) score of 0–2 at 90 days. Secondary outcomes included excellent outcome (mRS score 0–1), final recanalization, mortality, intracranial hemorrhage and procedural complications. Secondary analyses were performed according to the vasospasm location (intracranial or cervical).Among 13,678 patients in the registry during the study period, 434 received intra‐arterial nimodipine for the treatment of MT‐related vasospasm. In the main analysis, comparable odds of favorable outcome were observed, whereas excellent outcome was significantly less frequent in the group with vasospasm requiring nimodipine (adjusted odds ratio [aOR] 0.78, 95% confidence interval [CI] 0.63–0.97). Perfect recanalization, defined as a final modified Thrombolysis In Cerebral Infarction score of 3 (aOR 0.63, 95% CI 0.42–0.93), was also rarer in the vasospasm group. Intracranial vasospasm treated with nimodipine was significantly associated with worse clinical outcome (aOR 0.64, 95% CI 0.45–0.92), in contrast to the cervical location (aOR 1.37, 95% CI 0.54–3.08).Arterial vasospasm occurring during the MT procedure and requiring intra‐arterial nimodipine administration was associated with worse outcomes, especially in case of intracranial vasospasm. Although this study cannot formally differentiate whether the negative consequences were due to the vasospasm itself, or nimodipine administration or both, there might be an important signal toward a substantial clinical impact of iatrogenic vasospasm during MT. [ABSTRACT FROM AUTHOR]

Teratomas account for 18–20% of all intracranial germ cell tumors and mostly occur in the pineal region with only a few cases of pediatric sellar and suprasellar teratomas described in the literature. Here, we present a case of a child with an intracranial mature teratoma with pancreatic features causing vasospasm and subsequent stroke, found to be positive for CDKN2A—an independent variant associated with malignancy and small vessel disease leading to stroke. [ABSTRACT FROM AUTHOR]

The Circle of Willis (CoW) is a ring-like network of blood vessels that perfuses the brain. Flow in the collateral pathways that connect major arterial inputs in the CoW change dynamically in response to vessel narrowing or occlusion. Vasospasm is an involuntary constriction of blood vessels following subarachnoid hemorrhage (SAH), which can lead to stroke. This study investigated interactions between localization of vasospasm in the CoW, vasospasm severity, anatomical variations, and changes in collateral flow directions. Patient-specific computational fluid dynamics (CFD) simulations were created for 25 vasospasm patients. Computed tomographic angiography scans were segmented capturing the anatomical variation and stenosis due to vasospasm. Transcranial Doppler ultrasound measurements of velocity were used to define boundary conditions. Digital subtraction angiography was analyzed to determine the directions and magnitudes of collateral flows as well as vasospasm severity in each vessel. Percent changes in resistance and viscous dissipation were analyzed to quantify vasospasm severity and localization of vasospasm in a specific region of the CoW. Angiographic severity correlated well with percent changes in resistance and viscous dissipation across all cerebral vessels. Changes in flow direction were observed in collateral pathways of some patients with localized vasospasm, while no significant changes in flow direction were observed in others. CFD simulations can be leveraged to quantify the localization and severity of vasospasm in SAH patients. These factors as well as anatomical variation may lead to changes in collateral flow directions. Future work could relate localization and vasospasm severity to clinical outcomes like the development of infarct. [ABSTRACT FROM AUTHOR]

Re-rupture of untreated intracranial aneurysm is a potentially life-threatening condition. Despite tremendous advances in the diagnosis and treatment of intracranial aneurysms, such events are not rare and continue to pose a management dilemma. In this study, we examined the clinical, radiological and treatment details of patients who underwent microsurgical clipping for re-rupture of previously untreated intracranial aneurysms. Re ruptures were categorized as early and late re ruptures (< or > 7 days of inter ictus interval respectively). Modified Rankin Score (mRS) was used for functional outcome assessment and logistic regression analysis was used to test the predictors of long-term outcome. Re-ruptured intracranial aneurysms comprised 5% (n = 32/637) of the aneurysm clippings done at our center in this time span. The mean mRS score at discharge and at last follow-up were 3 and 3.04 respectively. Twenty-four (75%) patients were alive at a mean follow-up of 36 months. Early re-ruptures were associated with worse mean mRS scores at discharge (3.9 vs 2.5, p = 0.03) including the perioperative deaths (n = 4, 12.5%). The functional status at discharge and a poor preoperative clinical grade predicted a poor long-term outcome. Therefore, the long-term outcomes are primarily dependent on the short-term outcomes and to a lesser extent, the clinical grade at presentation. Those presenting with poor preoperative clinical grade, especially in the setting of an early re rupture, have a very poor prognosis and do not benefit from surgery. [ABSTRACT FROM AUTHOR]

The association between patient age and cerebral arterial vasospasm (CVS) and delayed cerebral ischemia (DCI) risk following aneurysmal subarachnoid hemorrhage (aSAH) remains unclear. This study aims to assess the role of age on aSAH-related complications. Single-center retrospective study comprising aSAH patients treated between January 2009 and March 2023. Age was analyzed as continuous and categorical variables (<60 yrs vs. ≥60 yrs and by decade). Outcomes of interest included radiographic CVS, DCI, cerebral infarction, in-hospital mortality, length-of-stay (LOS), ventriculoperitoneal shunt placement, and modified Rankin Scale (mRS) scores at discharge and 3-month follow-up. Nine hundred and twenty-five aSAH patients were included. Most (n = 598; 64.6%) were <60 yrs old (46 ± 9.1 yrs). CVS likelihood was lower in the older cohort (aOR = 0.56 [0.38–0.82]). Patients ≥60 yrs had higher mortality rates (aOR = 2.24 [1.12–4.47]) and worse mRS scores at discharge (aOR = 2.66 [1.91–3.72]) and 3-month follow-up (aOR = 2.19 [1.44–3.32]). Advanced age did not have a significant effect on DCI or cerebral infarction risk. Higher in-hospital mortality was documented with increasing age (P < 0.001). A significant interaction between CVS and age for the outcome of DCI was documented, with a stronger positive effect on poor outcomes (i.e., higher odds of DCI) among patients aged <60 years compared to those aged ≥60. There is an inverse relationship between patient age and CVS incidence following aSAH. Nonetheless, patients ≥60 yrs had comparable DCI rates, higher in-hospital mortality, and worse functional outcomes than their younger counterparts. Routine screening and reliance on radiographic CVS as primary marker for aSAH-related complications should be reconsidered, particularly in older patients. [ABSTRACT FROM AUTHOR]

Eugenol has various curative properties. It affects the dilatation of cerebral arteries through voltage-dependent Ca2+ channel inhibition. This study is the first to explore the impact of eugenol on neuroprotection and vasospasm in an experimental subarachnoid hemorrhage (SAH) model. Twenty-four adult male Sprague-Dawley rats were indiscriminately separated into 3 groups: the control group (n = 8), the SAH group (n = 8), and the eugenol group (n = 8). A double-bleeding method was used. The eugenol group received intracisternal eugenol (Sigma-Aldrich, St. Louis, MO, USA) at 30 μg/20 μl after induction of SAH. On the day 7, all groups were euthanized. Measurements were taken for basilar artery wall thickness, lumen diameter, serum endothelin-1 (ET-1), and caspase-3 levels. The eugenol group exhibited significantly lower wall thickness, ET-1, oxidative stress index, and caspase-3 levels compared to the SAH group. In comparison to the control group, the eugenol group showed a higher oxidative stress index along with higher ET-1 and caspase-3 levels, but these differences were not statistically significant. Wall thickness was significantly higher in the eugenol group than in the control group. This study represents the first literature exploration of intrathecal eugenol's impact on vasospasm induced after experimental SAH. Administration of intrathecal eugenol demonstrates a positive effect on the treatment of experimental vasospasm as well as on the reduction of oxidative stress and apoptosis. [ABSTRACT FROM AUTHOR]

• Vasospasm contributes to delayed ischemic neurologic deficits and is associated with aneurysmal subarachnoid hemorrhage. • Traumatic brain injury is the leading cause of subarachnoid hemorrhage. • Traumatic subarachnoid hemorrhage and vasospasm are easily detected with CT angiogram of the head. • Traumatic subarachnoid hemorrhage may result in traumatic brain injury from vasospasm and delayed cerebral ischemia. To determine the incidence of vasospasm in traumatic brain injury patients with traumatic subarachnoid hemorrhage. IRB approval was obtained for this retrospective chart review. An institutional trauma database was queried for adult patients with traumatic brain injury (TBI) and traumatic subarachnoid hemorrhage (tSAH) seen on CT head obtained within 20 days. The presence of vasospasm on CTA was determined by radiology report. Association between categorical background characteristics and intracranial vasospasm was assessed by the chi-square test and association between a continuous variables and intracranial vasospasm was assessed by a paired t -test. 1142 patients with traumatic SAH were identified from the trauma database. 792 patients were excluded: 142 for age <18, 632 did not have CT angiography, and 18 had non-traumatic SAH. 350 patients were analyzed, of which 28 (8 %) had vasospasm. Traumatic vasospasm was associated with higher-grade TBI based on Cochran-Armitage trend test (p < 0.05). Vasospasm patients had longer length of stay in the ICU (mean days 13.64 vs 7.24, P < 0.001), and had a higher incidence of death (39.29 % vs 20.81 %), although this did not reach statistical significance. Intracranial vasospasm, specifically in patients with tSAH, is associated with more severe TBI and longer stays in the ICU. Our incidence is smaller compared to other studies likely due to the retrospective nature and the infrequency of obtaining CT angiography after initial presentation. Prospective studies are warranted as the incidence is significant and may represent a point of intervention for TBI. [ABSTRACT FROM AUTHOR]

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.

• The FROUNT inhibitor, Disulfiram, suppressed inflammatory cell infiltration. • Disulfiram suppressed microglia activation after subarachnoid hemorrhage in animals. • Disulfiram suppressed the death after experimental subarachnoid hemorrhage. • Disulfiram prevented the neuronal death after experimental subarachnoid hemorrhage. • Disulfiram prevented the vasospasm after experimental subarachnoid haemorrhage. Subarachnoid hemorrhage due to rupture of intracranial aneurysms has a poor outcome, making this disease being the social problem. Inflammation evoked by the increase in intracranial pressure and the clot in the subarachnoid space after the onset of SAH exacerbates neuronal death and vasospasm, resulting in the poor outcome and severe aftereffects. Here, FROUNT mediates CCR2 and CCR5 signaling as an intracellular molecule binding to these chemoattractant receptors which facilitate the migration of inflammatory cells, such as macrophages, in situ to trigger inflammation there. Animal model of subarachnoid hemorrhage was established in rats through intrathecal injection of autologous blood. The effect of the FROUNT inhibitor, disulfiram, on survival rate, neuronal death in hippocampus or vasospasm was then examined. The intrathecal administration of disulfiram significantly suppressed the infiltration of CD68-positive macrophages and myeloperoxidase-positive neutrophils toward the clot in the cistern in situ. In this condition, disulfiram ameliorated the death of animals after the onset of subarachnoid hemorrhage in rats. In addition, disulfiram suppressed both the two major events after subarachnoid hemorrhage, the neuronal death in hippocampus and vasospasm. The pharmacological inhibition of CCR2 and CCR5 signaling by disulfiram could thus be the therapeutic strategy to improve the outcome of subarachnoid hemorrhage. [ABSTRACT FROM AUTHOR]

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.

Background: Patients with aneurysmal subarachnoid hemorrhage (aSAH) who survive the rupture are at risk for delayed neurologic deficits and cerebral infarction. The ideal method(s) of surveillance for cerebral vasospasm, and the link between radiographic vasospasm and delayed neurologic deficits, remain controversial. We instituted a postbleed day 7 angiography protocol with the stated goals of identification of vasospasm, improving neurologic outcomes, and possibly lowering cost of care. Methods: We conducted a quality improvement project in which we retrospectively analyzed consecutive cases of aSAH from a single institution over a 5-year period. Patients were excluded if they did not receive treatment for their aneurysm or were < 18 years of age. We analyzed demographic and outcome information for patients managed by protocolled angiography versus those who were managed by as-needed endovascular rescue therapy. Statistical tests were performed comparing means and proportions in both cohorts, as appropriate. Results: In total, 223 patients were identified who met inclusion criteria. In total, 157 patients were identified in the protocolled day 7 angiography group, and 66 were in the nonprotocolled angiography group. Demographics were similar between the day 7 angiogram and medical management cohorts, except for a higher mean age among the latter group (p = 0.016). The protocolled angiography group underwent a significantly greater number of angiograms (p < 0.001) and had a significantly higher cost of hospitalization ($240,327 vs. $205,719, p = 0.03), with no significant difference in rate of cerebral infarction, length of intensive care unit stay, length of hospital stay, discharge location, or discharge modified Rankin Score. Conclusions: This cohort comparison analysis draws into question the practice of protocolized cerebral angiography in patients with aSAH. [ABSTRACT FROM AUTHOR]

Aneurysmal subarachnoid haemorrhage (aSAH) is a rare yet profoundly debilitating condition associated with high global case fatality and morbidity rates. The key determinants of functional outcome include early brain injury, rebleeding of the ruptured aneurysm and delayed cerebral ischaemia. The only effective way to reduce the risk of rebleeding is to secure the ruptured aneurysm quickly. Prompt diagnosis, transfer to specialized centers, and meticulous management in the intensive care unit (ICU) significantly improved the prognosis of aSAH. Recently, multimodality monitoring with specific interventions to correct pathophysiological imbalances has been proposed. Vigilance extends beyond intracranial concerns to encompass systemic respiratory and haemodynamic monitoring, as derangements in these systems can precipitate secondary brain damage. Challenges persist in treating aSAH patients, exacerbated by a paucity of robust clinical evidence, with many interventions showing no benefit when tested in rigorous clinical trials. Given the growing body of literature in this field and the issuance of contemporary guidelines, our objective is to furnish an updated review of essential principles of ICU management for this patient population. Our review will discuss the epidemiology, initial stabilization, treatment strategies, long-term prognostic factors, the identification and management of post-aSAH complications. We aim to offer practical clinical guidance to intensivists, grounded in current evidence and expert clinical experience, while adhering to a concise format. [ABSTRACT FROM AUTHOR]

Background: Delayed cerebral ischaemia (DCI) is a major cause of morbidity and mortality after aneurysmal subarachnoid haemorrhage (aSAH). Chemical angioplasty (CA) and transluminal balloon angioplasty (TBA) are used to treat patients with refractory vasospasm causing DCI. Multi-modal monitoring including brain tissue oxygenation (PbtO2) is routinely used at this centre for early detection and management of DCI following aSAH. In this single-centre pilot study, we are comparing these two treatment modalities and their effects on PbtO2. Methods: Retrospective case series of patients with DCI who had PbtO2 monitoring as part of their multimodality monitoring and underwent either CA or TBA combined with CA. PbtO2 values were recorded from intra-parenchymal Raumedic NEUROVENT-PTO® probes. Data were continuously collected and downloaded as second-by-second data. Comparisons were made between pre-angioplasty PbtO2 and post-angioplasty PbtO2 median values (4 h before angioplasty, 4 h after and 12 h after). Results: There were immediate significant improvements in PbtO2 at the start of intervention in both groups. PbtO2 then increased by 13 mmHg in the CA group and 15 mmHg in the TBA plus CA group in the first 4 h post-intervention. This improvement in PbtO2 was sustained for the TBA plus CA group but not the CA group. Conclusion: Combined balloon plus chemical angioplasty results in more sustained improvement in brain tissue oxygenation compared with chemical angioplasty alone. Our findings suggest that PbtO2 is a useful tool for monitoring the response to angioplasty in vasospasm. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: The present work aimed to determine whether a relationship exists between inflammatory parameters and the development of vasospasm (VS) and Takotsubo cardiomyopathy (TTC), as well as clinical outcome, in patients suffering from spontaneous subarachnoid hemorrhage (SAH). Methods: In this study, the authors processed the prospectively collected laboratory and clinical data of spontaneous SAH patients admitted to the neurointensive care unit between March 2015 and October 2023. The highest values of neutrophils (NEUpeak), monocytes (MONOpeak), neutrophil-to-lymphocyte ratio (NLRpeak), and CRP (CRPpeak) during the initial 7 days were correlated with the occurrence of VS and TTC, and with the outcome measures at day 30 after onset. Results: Data were collected from 175 SAH patients. Based on ROC analysis, for the development of VS, MONOpeak was the most accurate indicator (AUC: 0.619, optimal cut-off: 1.45 G/L). TTC with severe left ventricular dysfunction (ejection fraction < 40%) was indicated most sensitively by NEUpeak (ROC: 0.763, optimal cut-off: 12.34 G/L). Both for GOS and Barthel Index at day 30, CRPpeak was the best predictor for the outcome (GOS: ROC: 0.846, optimal cut-off: 78.33 mg/L and Barthel Index: ROC: 0.819, optimal cut-off: 78.33 mg/L). Conclusions: Laboratory parameters referring to inflammation during the initial 7 days after SAH correlate with the development of VS and TTC, and thus may predict functional outcome. [ABSTRACT FROM AUTHOR]

Background: For primary Raynaud phenomenon (PRP), an otherwise unexplained vasospastic disposition is assumed. To test the hypothesis of an additional involvement of distinct ultrastructural microvascular alterations, we compared the nailfold capillary pattern of patients with PRP and healthy controls. Methods: A total of 120 patients with PRP (with a median duration of vasospastic symptoms of 60 [IQR: 3–120] months) were compared against 125 controls. In both groups, nailfold capillaroscopy was performed to record the presence of dilatations, capillary edema, tortuous capillaries, ramifications, hemorrhages, and reduced capillary density and to determine a semiquantitative rating score. Further, the capacity of finger skin rewarming was investigated by performing infrared thermography in combination with cold provocation. Results: Unspecific morphologic alterations were found in both, PRP, such as controls, whereby the risk for PRP was four times as high in the presence of capillary dilations (CI: 2.3–7.6) and five times as high if capillary density was reduced (CI: 1.9–13.5). Capillary density correlated with thermoregulatory capacity in both hands in the PRP group, but not in controls. In addition, a negative correlation between the microangiopathy score and the percentage degree of rewarming in both hands was found for patients with PRP only. Conclusion: We found specific differences within the microvascular architecture between patients with PRP and controls. As a conclusion, PRP may not be an entirely benign vasospastic phenomenon, but might be associated with subtle microcirculatory vasculopathy. In addition, we suggest that the implementation of a scoring system might serve as guidance in the diagnostic process at least of patients with long-standing PRP. [ABSTRACT FROM AUTHOR]

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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.

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。)

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.

AbstractBackgroundMethods/case reportResultsConclusionsWatershed infarcts (WIs) are a distinct type of stroke with a varying clinical presentation that affects the border areas between the territories of two cerebral arteries and are typically associated with hemodynamic impairment and internal carotid artery stenosis. However, there is a paucity of data concerning its association with the history of recreational substance and drug abuse.This case report presents a unique instance of bilateral internal watershed infarcts in a 23-year-old male with a history of polysubstance abuse, including methadone and cocaine. The patient’s presentation included confusion, lower limb weakness, and systemic complications such as acute liver injury and myonecrosis, underlying the complexity of the clinical scenario.The investigation revealed no evidence of arterial stenosis or thrombosis, leading to the conclusion that the infarctions were likely precipitated by a total loss of consciousness due to substance abuse-related cerebral hypoperfusion and vasoconstriction. Methadone and cocaine, both implicated in vasoconstriction, lowering the seizure threshold and contributing to QTc prolongation, thus leading to loss of consciousness, were identified as potential triggers for the episode.In the young adult population, it is important to consider drug abuse as an etiological trigger for watershed infarcts, whereas the multi-system involvement and atypical presentation highlight the need for a comprehensive approach. [ABSTRACT FROM AUTHOR]

Subarachnoid hemorrhage often leads to poor outcomes owing to vasospasm, even after successful aneurysm treatment. Clazosentan, an endothelin receptor inhibitor, has been proven to be an effective treatment for vasospasms in a Japanese randomized controlled trial. However, its efficacy in older patients (≥ 75 years old) and those with World Federation of Neurosurgical Societies (WFNS) grade V has not been demonstrated. We retrospectively evaluated the efficacy of clazosentan in older patients and those with WFNS grade V, using real-world data. Patients with subarachnoid hemorrhage treated before and after the introduction of clazosentan were retrospectively evaluated. The patients were categorized into two groups (clazosentan era versus pre-clazosentan era), in which vasospasm management and outcomes were compared. Vasospasms were managed with fasudil hydrochloride-based (pre-clazosentan era) or clazosentan-based treatment (clazosentan era). Seventy-eight patients were included in this study: the clazosentan era (n = 32) and pre-clazosentan era (n = 46). Overall, clazosentan significantly reduced clinical vasospasms (clazosentan era: 31.3% versus pre-clazosentan era: 60.9%, p = 0.01), delayed cerebral ischemia (DCI) (9.4% versus 39.1%, p = 0.004), and vasospasm-related morbidity and mortality (M/M) (3.1% versus 19.6%, p = 0.03). In subgroup analysis of older patients or those with WFNS grade V, no significant difference was observed in clinical outcomes, although both DCI and vasospasm-related M/M were lower in the clazosentan era. Clazosentan was more effective than fasudil-based management in preventing DCI and reducing vasospasm-related M/M. Clazosentan could be used safely in older patients and those with WFNS grade V, although clinical outcomes in these patients were comparable to those of conventional treatment. [ABSTRACT FROM AUTHOR]

Traumatic subarachnoid hemorrhage (tSAH) is frequently comorbid with traumatic brain injury (TBI) and may induce secondary injury through vascular changes such as vasospasm and subsequent delayed cerebral ischemia (DCI). While aneurysmal SAH is well studied regarding vasospasm and DCI, less is known regarding tSAH and the prevalence of vasospasm and DCI, the consequences of vasospasm in this setting, when treatment is indicated, and which management strategies should be implemented. In this article, a systematic review of the literature that was conducted for cases of symptomatic vasospasm in patients with TBI is reported, association with tSAH is reported, risk factors for vasospasm and DCI are summarized, and commonalities in diagnosis and management are discussed. Clinical characteristics and treatment outcomes of 38 cases across 20 studies were identified in which patients with TBI with vasospasm underwent medical or endovascular management. Of the patients with data available for each category, the average age was 48.7 ± 20.3 years (n = 31), the Glasgow Coma Scale score at presentation was 10.6 ± 4.5 (n = 35), and 100% had tSAH (n = 29). Symptomatic vasospasm indicative of DCI was diagnosed on average at postinjury day 8.4 ± 3.0 days (n = 30). Of the patients, 56.6% (n = 30) had a new ischemic change associated with vasospasm confirming DCI. Treatment strategies are discussed, with 11 of 12 endovascularly treated and 19 of 26 medically treated patients surviving to discharge. tSAH is associated with vasospasm and DCI in moderate and severe TBI, and patients with clinical and radiographic evidence of symptomatic vasospasm and subsequent DCI may benefit from endovascular or medical management strategies. [ABSTRACT FROM AUTHOR]

The objective of this study was to establish an animal model of arteriosclerosis for assessing vasospasm and to investigate the relationship between arteriosclerosis and vasospasm. Twelve-week-old male Sprague–Dawley rats were fed a diet supplemented with adenine and vitamin D (adenine/vitD). Body weight, blood, and femoral artery histopathology were assessed at 2, 4, and 6 weeks. Change in the femoral artery was examined by transmission electron microscope (TEM). Vasospasm was induced by administering epinephrine extravascularly into the femoral artery and released by the treatment with lidocaine as a vasodilator. During this period, the extravascular diameter and blood flow were measured. The rats in the adenine/vitD group developed renal dysfunction, uremia, hyperphosphatemia, and elevated serum alkaline phosphatase. Histological and TEM analyses of the femoral arteries in the treated rats revealed the degeneration of elastic fibers and extensive calcification of the tunica media and intima. Vascular smooth muscles were degenerated and osteoblasts were developed, resulting in calcified arteriosclerosis. Vasospasm in arteriosclerotic arteries was detected; however, vasodilation as well as an increase in the blood flow was not observed. This study revealed the development of vasospasm in the femoral arteries of the arteriosclerotic rats and, a conventional vasodilator did not release the vasospasm. [ABSTRACT FROM AUTHOR]

Point-of-care brain ultrasound and transcranial doppler or color-coded doppler is being increasingly used as an essential diagnostic and monitoring tool at the bedside of critically ill neonates and children. Brain ultrasound has already established as a cornerstone of daily practice in the management of the critically ill newborn for diagnosis and follow-up of the most common brain diseases, considering the easiness to insonate the brain through transfontanellar window. In critically ill children, doppler based techniques are used to assess cerebral hemodynamics in acute brain injury and recommended for screening patients suffering from sickle cell disease at risk for stroke. However, more evidence is needed regarding the accuracy of doppler based techniques for non-invasive estimation of cerebral perfusion pressure and intracranial pressure, as well as regarding the accuracy of brain ultrasound for diagnosis and monitoring of acute brain parenchyma alterations in children. This review is aimed at providing a comprehensive overview for clinicians of the technical, anatomical, and physiological basics for brain ultrasonography and transcranial doppler or color-coded doppler, and of the current status and future perspectives of their clinical applications in critically ill neonates and children. Conclusion: In critically ill neonates, brain ultrasound for diagnosis and follow-up of the most common cerebral pathologies of the neonatal period may be considered the standard of care. Data are needed about the possible role of doppler techniques for the assessment of cerebral perfusion and vasoreactivity of the critically ill neonate with open fontanelles. In pediatric critical care, doppler based techniques should be routinely adopted to assess and monitor cerebral hemodynamics. New technologies and more evidence are needed to improve the accuracy of brain ultrasound for the assessment of brain parenchyma of critically ill children with fibrous fontanelles. What is Known: • In critically ill neonates, brain ultrasound for early diagnosis and follow-up of the most common cerebral and neurovascular pathologies of the neonatal period is a cornerstone of daily practice. In critically ill children, doppler-based techniques are more routinely used to assess cerebral hemodynamics and autoregulation after acute brain injury and to screen patients at risk for vasospasm or stroke (e.g., sickle cell diseases, right-to-left shunts). What is New: • In critically ill neonates, research is currently focusing on the use of novel high frequency probes, even higher than 10 MHz, especially for extremely preterm babies. Furthermore, data are needed about the role of doppler based techniques for the assessment of cerebral perfusion and vasoreactivity of the critically ill neonate with open fontanelles, also integrated with a non-invasive assessment of brain oxygenation. In pediatric critical care, new technologies should be developed to improve the accuracy of brain ultrasound for the assessment of brain parenchyma of critically ill children with fibrous fontanelles. Furthermore, large multicenter studies are needed to clarify role and accuracy of doppler-based techniques to assess cerebral perfusion pressure and its changes after treatment interventions. [ABSTRACT FROM AUTHOR]

Ischemic heart disease (IHD) is the leading cause of morbidity and mortality in both genders; however, young women fare the worst, likely reflecting the more complex spectrum of IHD in women when compared to men. Substantial sex-based differences exist in the underlying risk factors, risk enhancers, presentation, diagnosis, and pathophysiology of IHD that are mainly attributed to the influence of female sex hormones. This article reviews the spectrum of IHD including obstructive epicardial coronary artery disease (CAD), myocardial infarction with no obstructive coronary artery disease, ischemia with no obstructive coronary artery disease, spontaneous coronary artery dissection, coronary microvascular dysfunction, vasospastic angina, and coronary thrombosis/embolism that occur in women throughout various stages of their life cycle. We aim to update clinicians on the diagnosis and management of these various types of IHD and highlight where further randomized controlled studies are needed to determine optimal treatment and inform guideline-directed medical therapy. [ABSTRACT FROM AUTHOR]

Stellate ganglion block (SGB) may have protective effects in patients at risk of vasospasm following subarachnoid hemorrhage (SAH) due to reduced sympathetic activity. However, the safety and clinical outcomes of SGB in this scenario are not definitively known. The objective was to evaluate the safety, clinical outcomes, and cerebral blood flow velocity in patients submitted to SGB or cervical sympathectomy with SAH. Following Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines, a systematic review and meta-analysis of studies investigating SGB or cervical sympathectomy use in SAH were conducted. PubMed, Cochrane Library, and Embase were evaluated. Patients with mRS from 0 to 2, GOS from 4 to 5, or symptom resolution were considered favorable clinical outcomes. Related mortality was defined as death by vasospasm or delayed cerebral ischemia. The analysis included 8 studies comprising 182 patients. Only 2 studies employed SGB prophylactically. The results revealed favorable outcomes in 52% of patients (95% CI: 37%–65%). The overall incidence of complications was 2% (95% CI: 0% –26%). The mortality rate was 13% (95% CI: 7%–21%), with a vasospasm-related mortality rate of 11% (95% CI: 2%–20%). A decrease of cerebral blood flow velocity was reported in 4 studies. The notable reduction in cerebral blood flow velocity following SGB, alongside positive outcomes and a low occurrence of mortality and complications, highlights its significance as a therapeutic intervention for vasospasm following SAH. While the number of studies evaluating SGB as a preventive measure is limited, the promising results emphasize the importance of future research. [ABSTRACT FROM AUTHOR]

Subarachnoid hemorrhage (SAH) is a cerebrovascular disorder with significant mortality and morbidity. Neural injury in SAH is mediated through a variety of pathophysiological processes. Currently available treatments are either nonspecific in targeting the basic pathophysiological mechanisms that result in neural damage in SAH, or merely focus on vasospasm. Ferroptosis is a type of programmed iron dependent cell death, which has received attention due to its possible role in neural injury in SAH. Herein, we review how intracellular iron overload mediates the production of reactive free radicals and lipid peroxidation through a variety of biochemical pathways in SAH. This in turn results in induction of ferroptosis, as well as exacerbation of vasospasm. We also discuss several therapeutic agents that have been shown to inhibit ferroptosis through targeting different steps of the process. Such agents have proven effective in ameliorating vasospasm, neural damage, and neurobehavioral outcomes in animal models of SAH. Human studies to test the safety and efficacy of intrathecal or parenteral administration of the inhibitors of ferroptosis in improving outcomes of SAH patients are warranted. There are currently a few ongoing clinical trials pursuing this therapeutic concept, the results of which will be critical to determine the value of ferroptosis as a novel therapeutic target in SAH. [ABSTRACT FROM AUTHOR]

Purpose: Aneurysmal subarachnoid hemorrhage (aSAH) is associated with high morbidity and mortality, which is largely attributable to secondary complications such as vasospasm and subsequent delayed cerebral ischemia. Transcranial Doppler (TCD) is recommended for the screening of vasospasm; however, technicians are not always available. We aimed to see how feasible and reliable bedside transcranial point‐of‐care ultrasound (POCUS) color‐coded duplex sonography was compared with formal non‐imaging TCD in measuring velocities and in diagnosing vasospasm. Methods: This was a prospective observational study that took place in the neuroscience intensive care unit at a single academic medical center. Patients with aSAH who were undergoing formal TCDs were scanned on days 2–10 of their admission by physicians of ranging ultrasound experience. Absolute velocities were compared as well as the diagnosis of vasospasm via POCUS and formal TCDs. Results: A total of 226 bedside ultrasound exams were performed and compared with 126 formal TCD studies. Sonographic windows were obtained in 89.4% of patients. Scans took 6.6 minutes to complete on average by the advanced group versus 14.5 minutes in the beginner. Correlation ranged from.52 in the beginner group to.65 in the advanced. When good quality of images obtained at a depth of 4–5 cm were reviewed, correlation of mean velocities increased to.96. Overall sensitivity for diagnosing vasospasm was 75%, with a specificity of 99% and negative predictive value of 99%. Conclusion: Overall, POCUS TCD cannot replace a formal study performed by expert sonographers. An abbreviated POCUS scan can be performed quickly, however, particularly with more experienced operators. POCUS TCD can also feasibly detect vasospasm, and accurate velocities can be obtained by those with all levels of ultrasound experience. Care must be taken on image interpretation that velocities are obtained at an appropriate depth to ensure appropriate insonation of the MCA as well as in optimal alignment with the vessel to obtain the most accurate velocities. [ABSTRACT FROM AUTHOR]

Background: Nimodipine 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. Methods: This 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. Results: In 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. Conclusion: The 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. [ABSTRACT FROM AUTHOR]

Vasospasm following an aneurysmal subarachnoid hemorrhage (SAH) causes serious neurological complications, despite surgical clipping of the aneurysm. Intrathecal urokinase (UK) infusion has been shown to effectively prevent symptomatic vasospasm in patients who have undergone endovascular obliteration of the ruptured aneurysms. To investigate whether intrathecal UK infusion can prevent symptomatic vasospasm in patients undergoing surgical or endovascular treatment. A total of 90 patients with severe aneurysmal SAH were enrolled and assigned to a surgical neck clipping (n = 56) or an endovascular coil embolization (n = 34) groups. After treatment, UK infusion from the lumbar drain was repeated in 32 patients in the surgical neck clipping group (group B) and all in the endovascular coil embolization group (group C) until complete resolution of the SAH was observed on computed tomography. The remaining 24 of the surgical neck clipping group, without UK infusion, were assigned to group A. Symptomatic vasospasm occurred in 7 (29.2%) patients in group A, 2 (6.3%) in group B, and none in group C (group A vs. group B [ P = 0.02]; group B vs. group C [ P = 0.14]). Excellent clinical outcomes (modified Rankin score, 0 or 1) were observed in 37.5%, 59.4%, and 76.5% of patients in group A, B, and C, respectively (group A vs. group B [ P = 0.11]). Clearance of SAH via intrathecal UK infusion significantly reduced symptomatic vasospasm in patients in both UK groups, resulting in better clinical outcomes. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: Cerebral vasospasm is a rare postoperative complication of transsphenoidal pituitary adenoma surgery with potentially severe consequences. These vasospasms generally have a delayed presentation at a mean of 8 postoperative days. We report an unusual case of hyperacute onset of cerebral vasospasm that occurred immediately after surgery. Case Description: A 38-year-old man underwent endoscopic transsphenoidal surgery for a nonfunctioning pituitary adenoma. The patient experienced mild subarachnoid hematoma during surgery. Three hours after surgery, he developed rightward conjugate eye deviation and complete paralysis of the left upper and lower extremities. Diagnostic imaging revealed cerebral vasospasm in both middle cerebral arteries, and symptoms improved after intra-arterial administration of fasudil hydrochloride. Conclusion: There is a need for prompt diagnosis and therapeutic intervention when typical symptoms of cerebral vasospasm, such as paralysis, occur at any time during the postoperative course. [ABSTRACT FROM AUTHOR]

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.

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