Search Results (129)

Traumatic subarachnoid hemorrhage (tSAH) is a common complication of traumatic brain injury (TBI) and represents an important predictor of poor functional outcome. One of the most serious secondary complications is cerebral vasospasm. The pathophysiology of vasospasm is complex, involving the effects of blood breakdown products, inflammatory mediators, and direct mechanical injury to the cerebral vessels. Compared to aneurysmal subarachnoid hemorrhage (aSAH), vasospasm in tSAH typically occurs earlier, lasts for a shorter duration, and presents mostly with a milder clinical course. Due to its atypical clinical presentation and the presence of concurrent injuries, vasospasm is often not recognized in time and may manifest as neurological deterioration or new ischemic lesions on CT imaging. Timely recognition and appropriate management can significantly improve neurological outcomes. This paper presents key characteristics and differences between tSAH and aSAH, available diagnostic approaches, and treatment options, including nimodipine, milrinone, and stellate ganglion block. Owing to the lack of specific clinical guidelines for tSAH, current management strategies often rely on recommendations and experiences from aSAH. Further research is needed to better define risk factors for vasospasm following tSAH, optimize diagnostic pathways, and evaluate targeted treatment strategies. Full article

Background: This study aims to assess associations between occurrence of delayed cerebral ischemia (DCI) in spontaneous subarachnoid hemorrhage (SAH) and possible dysfunction of autonomic cardiovascular modulation compared to transcranial Doppler ultrasound (TCD). Methods: In this prospective observational study, 53 patients with spontaneous SAH were enrolled, and 17 patients met DCI criteria, i.e., new cerebral infarction > 72 h after SAH onset on follow-up CT scans. Autonomic modulation as well as TCD-frequencies were monitored within 24 h after SAH onset and then daily until day 10. From 5 min time-series of R–R-interval (RRI) and blood-pressure (BP) recordings, parameters of sympathetic, parasympathetic and total autonomic cardiovascular modulation were calculated, including time- and frequency-domain parameters. Data were compared between patients with and without DCI. Further subgroup analyses were performed according to functional outcome after 3 to 6 months (i.e., favorable outcome, modified Rankin Scale (mRS) ≤ 3 vs. unfavorable outcome, mRS > 3) regardless of DCI. Results: RRI and BP values as well as TCD frequencies did not differ between patients with and without DCI. Compared to No DCI patients, the cohort of DCI patients had significantly lower values of sympathetic modulation (RRI-LF powers, SBP-LF powers) on days 5 and 9 after SAH, significantly lower values of total autonomic modulation (RRI-SD, RRI-CV, RRI-total powers) and insignificantly lower values of parasympathetic modulation (RMSSDs, RRI-HF powers) on day 5 after SAH. Parameters of sympathetic, parasympathetic, and total autonomic modulation did not differ significantly between patients with favorable and unfavorable outcomes, but showed slightly lower values in the unfavorable outcome group. Yet, additionally calculated value of normalized RRI-LF and normalized RRI-HF powers, as well as LF/HF ratios were significantly different in the unfavorable outcome cohort. Conclusions: Not only within the acute phase, but also during the first days after disease onset, spontaneous SAH induces a decrease in sympathetic, parasympathetic and total autonomic cardiovascular modulation. In contrast to standard diagnostic evaluation for detecting clinically relevant vasospasms—i.e., TCD—autonomic dysfunction was associated with development of DCI and poor clinical outcome. Thus, assessment of heart rate variability may predict augmented risk of cardiovascular complications and may represent a promising adjunctive marker within multimodal neuromonitoring in SAH patients. Full article

Background: Hyperglycemia after aneurysmal subarachnoid hemorrhage (aSAH) is associated with poor outcome, but admission glucose may not reflect dynamic metabolic stress during neurocritical care. Unlike previous studies focused primarily on admission measurements, we evaluated longitudinal glycemic trajectories and repeated glucose–potassium ratio (GPR) assessment across multiple observation windows in relation to clinical outcomes after aSAH. Methods: This retrospective single-center cohort study included 199 consecutive adults with aSAH treated between 2014 and 2025. Serial glucose and potassium measurements obtained during intensive care unit (ICU) stay were used to calculate admission values, longitudinal means across predefined observation windows, glycemic variability, hyperglycemia burden, and GPR. Primary outcomes were 30-day mortality and poor functional outcome at discharge (modified Rankin Scale ≥ 3). Secondary outcomes included delayed cerebral ischemia (DCI), delayed neurological deterioration (DND), transcranial Doppler (TCD) vasospasm, neurological deficit at ICU discharge, and length of stay. Results: Thirty-day mortality occurred in 35 patients (17.6%). Longitudinal metabolic markers demonstrated stronger associations with outcomes than admission values. Mean 30-day GPR was independently associated with mortality (OR 2.56, 95% CI 1.66–4.16; p < 0.001) and poor functional outcome (OR 2.90, 95% CI 1.80–5.03; p < 0.001). Hyperglycemia burden was associated with mortality (OR 1.10 per additional hyperglycemic day, 95% CI 1.02–1.20; p = 0.020) and poor functional outcome (OR 1.39, 95% CI 1.19–1.71; p < 0.001). Early GPR during the early brain injury period was associated with DCI (OR 1.40, 95% CI 1.01–1.93; p = 0.043), whereas 30-day GPR was associated with DND (OR 1.47, 95% CI 1.08–2.07; p = 0.019). ICU-specific GPR was associated with neurological deficit at ICU discharge (OR 2.06, 95% CI 1.29–3.50; p = 0.004), but not with TCD-defined vasospasm. Addition of GPR improved mortality prediction compared with the clinical model alone (AUC 0.86 vs. 0.77; p = 0.002). Conclusions: Longitudinal metabolic dysregulation after aSAH is strongly associated with mortality and neurological outcomes. Persistent hyperglycemia and repeated GPR assessment provide prognostic information beyond admission glucose, with early abnormalities associated with DCI and sustained disturbances linked to mortality and disability. Full article

Objective: To evaluate whether ABO blood group is associated with venous thromboembolic events (VTEs), cerebral severe vasospasm (CSV), delayed cerebral ischemia (DCI), and clinical or cognitive outcomes after aneurysmal subarachnoid hemorrhage (aSAH). Materials and Methods: A retrospective observational two-center cohort study of collected registry data, including 169 patients treated between September 2021 and November 2025. Outcomes were compared across ABO subtypes using univariate testing and multivariable logistic regression. Results: No ABO subtype was independently associated with VTE (7.7%), CSV/DCI (21.9%), intracranial hemorrhage, or in-hospital mortality (all p > 0.05). Higher age (OR 1.08, 95% CI 1.031–1.144, p = 0.003) was independently associated with increased in-hospital mortality, whereas single peri-interventional antiplatelet therapy (PIAT) (OR 0.076, 95% CI 0.004–0.506, p = 0.029) was associated with lower in-hospital mortality. ABO blood group was not associated with functional outcome (mRS) or cognitive performance (MoCA) in this cohort. Conclusions: In this two-center retrospective cohort, no independent association between ABO blood group and early cerebrovascular complications, functional outcome, or cognitive outcome after aSAH was detected. These findings suggest that short-term prognosis may be more strongly influenced by established patient- and treatment-related factors, particularly age and single PIAT. Further studies with larger cohorts are warranted to clarify the potential effect of ABO blood group on outcomes after aSAH. Full article

Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening cerebrovascular condition characterized by a dynamic clinical course spanning distinct pathophysiological stages, including aneurysm rupture, early brain injury (EBI), delayed cerebral vasospasm, and long-term neurological outcome. Despite extensive research, no clinically applicable molecular biomarkers exist to predict disease trajectory across these stages. MicroRNAs (miRNAs), small non-coding RNA molecules detectable in blood and cerebrospinal fluid (CSF), have emerged as promising candidates due to their stability and close association with vascular, inflammatory, and neuronal processes. However, existing studies have largely evaluated miRNAs in isolation, without integrating findings into a unified temporal framework. This review provides a structured, translational synthesis of miRNA dynamics in aSAH and proposes a stage-specific conceptual model integrating prospective clinical evidence with the broader literature. Dual-biofluid profiling has identified miR-29a, miR-200a-3p, and miR-451a as robust rupture-associated biomarkers, with distinct compartment-specific expression patterns. CSF-based profiling has demonstrated that miR-221-3p, miR-9-3p, and miR-183-5p predict vasospasm within 24 h of hemorrhage, while miR-24 and miR-21-5p correlate with disease severity and poor outcome. Integrating these findings with the broader literature, we categorize miRNA signatures across four stages: rupture discrimination, early brain injury, vasospasm prediction, and outcome stratification. This stage-specific framework highlights the biological continuum linking endothelial injury, vascular dysfunction, and secondary brain damage. The proposed model provides a foundation for multi-marker biomarker development, prospective validation studies, and future precision medicine strategies in aSAH. Full article

Background/objectives: Aneurysmal subarachnoid hemorrhage (aSAH) is a neurosurgical emergency associated with cerebral vasospasm, representing an important complication. This study assessed the association between cerebrospinal fluid (CSF) interleukin-6 (IL-6) levels and cerebral vasospasm after aSAH. Methods: This prospective single-center observational study with repeated measurements included 56 patients among 74 screened patients with aSAH; 18 patients were excluded according to predefined exclusion criteria, including infection, unavailable CSF samples or requirement for CSF diversion within the first seven days of onset. The samples were obtained via lumbar puncture on post-hemorrhage days 3 and 7. IL-6 was quantified using an electrochemiluminescent immunoassay. Radiological vasospasm (RV) was assessed by computed tomography angiography, while clinical vasospasm (CCV) was defined as new neurological deterioration unexplained by other causes. Results: Median IL-6 levels were 423.5 pg/mL on day 3 and 726.0 pg/mL on day 7. Day 7 IL-6 levels were associated with RV (p = 0.045) and CCV (p = 0.010), while day 3 IL-6 was associated with CCV only (p = 0.035). Day 7 IL-6 showed modest discriminatory performance for CCV: AUC = 0.722, cut-off 460 pg/mL, sensitivity 75.0%, and specificity 68.8%; for RV: AUC = 0.659, cut-off 451 pg/mL, sensitivity 81.8%, and specificity 56.5%. Conclusions: Elevated CSF IL-6 levels were associated with cerebral vasospasm after aSAH, with a more consistent association observed for CCV than for RV; however, these findings are hypothesis-generating and require validation before clinical applicability can be determined. Full article

Background: Temporary arterial occlusion (TAO) is a key adjunct in microsurgical clipping of middle cerebral artery (MCA) aneurysms, but its safe duration and impact on perioperative ischemia—particularly in subarachnoid hemorrhage (SAH)—remain uncertain. Methods: A retrospective cohort of 245 patients undergoing microsurgical clipping of MCA aneurysms (154 incidental, 91 SAH) at a tertiary neurovascular center (2010–2020) was analyzed. TAO use, cumulative duration (>5, >8, >10, >15 min), number of applications, and occlusion site were extracted alongside clinical, radiographic, and outcome data. The primary endpoint was perioperative ischemia within 48 h; secondary endpoints included clinically relevant cerebral vasospasm (CVS), intraoperative rupture, and functional outcome (mRS) at discharge and 6 months. Multivariable logistic and ordinal regression models adjusted for demographic, aneurysmal, and treatment covariates. Results: TAO was used in 134 cases (54.7%; mean total duration 10.4 ± 8.7 min). In the overall cohort, TAO (presence or duration) was not independently associated with perioperative ischemia or CVS. In the SAH subgroup, cumulative TAO > 5 min conferred an approximately sixfold higher odds of ischemia (p = 0.012; OR 6.33), whereas no threshold was significant in incidental aneurysms. Female sex, M2 location, SAH at admission, and initial GCS < 9 independently predicted ischemia; female sex, higher ASA grade, larger size, irregular morphology, and SAH predicted CVS. SAH and aneurysm wall calcification were associated with worse 6-month mRS. Conclusions: TAO appears safe in elective clipping of incidental MCA aneurysms when applied judiciously, but cumulative durations beyond 5 min substantially increase ischemia risk in SAH patients. TAO management should therefore be individualized by rupture status, neurological grade, and aneurysm morphology rather than a single universal time limit. Full article

Aneurysmal subarachnoid hemorrhage (SAH) remains a devastating cerebrovascular disorder with high morbidity and mortality, despite advances in aneurysm securing and neurocritical care. Clinical outcomes are determined by early brain injury (EBI), delayed cerebral ischemia (DCI), hydrocephalus, and long-term cognitive impairment, extending beyond the traditional focus on large-vessel vasospasm alone. Emerging evidence identifies the dysfunction of the glymphatic system and meningeal lymphatic pathway, the brain’s primary clearance pathways, as a central and unifying mechanism linking acute hemorrhagic injury to delayed and chronic neurological sequelae. Following SAH, acute intracranial pressure elevation, subarachnoid blood clot burden, loss of arterial pulsatility, venous congestion, astrocytic aquaporin-4 perivascular depolarization, and neuroinflammation converge to suppress cerebrospinal fluid–interstitial fluid exchange and outflow in glymphatic system and subsequent meningeal lymphatic drainage. Persistent clearance failure promotes the retention of blood breakdown products, inflammatory mediators, and metabolic waste, amplifying microvascular dysfunction, cortical spreading depolarizations, blood–brain barrier disruption, and secondary ischemic injury. Importantly, accumulating data highlight venous pathology and meningeal lymphatic impairment as critical, yet underappreciated, contributors to delayed injury and post-SAH hydrocephalus. In this review, we synthesize the current knowledge of the physiological organization of glymphatic and meningeal lymphatic systems, delineate the mechanistic and molecular drivers of their dysfunction after SAH, and discuss clinical implications for EBI, DCI, hydrocephalus, and long-term cognitive outcomes. We further outline future directions, including translational imaging, biomarker development, and therapeutic strategies targeting clearance pathways, to advance disease-modifying approaches in SAH. Full article

Point-of-care ultrasonography (POCUS) has become an integral part of intensive and emergency care. Despite the widespread use and availability of multipurpose ultrasound devices, the regular assessment of intracranial circulatory conditions has not become a part of daily routine in multidisciplinary intensive care units. This brief narrative review aims to summarize the fundamental knowledge about the transcranial Doppler technique and the most significant clinical areas in which the method can provide valuable assistance in daily diagnostic and therapeutic decision-making. The authors searched the PubMed database for reviews, systematic reviews, and meta-analyses using the keywords “transcranial Doppler sonography; critical care; cerebral vasospasm; brain death diagnosis; non-invasive intracranial pressure monitoring”. We conclude that TCD is a simple, yet skilled, bedside method for assessing intracranial circulation. In everyday practice, it can be used to support clinical decision-making primarily in the areas of intracranial pressure monitoring, diagnosis and follow-up of cerebral vasospasm, and diagnosis of cerebral circulatory arrest. The study of cerebral hemodynamics should be an integral part of the increasingly widespread bedside ultrasound diagnostics in intensive care. Full article

Background: Cerebral vasospasm (CV) as a complication after aneurysmal subarachnoid hemorrhage (aSAH) is a major determinant of secondary vasospasm-associated ischemic infarction (SVS-I) and poor outcome. Data on the interplay among the onset of CV, SVS-I, and in-hospital mortality remain limited. Methods: We conducted a retrospective, single-center study including patients admitted with aSAH between January 2016 and May 2024 who developed treatment-relevant CV. The primary outcome was the rate of in-hospital mortality. The relationship between the onset of CV, demographics, imaging, and treatment data and the primary outcome was analyzed using logistic regression. A confounder-adjusted mediation analysis was performed to quantify the extent to which the effect of time to CV onset on in-hospital mortality was mediated by SVS-I. Results: A total of 165 patients with aSAH and treatment-relevant CV were included. The median age was 55 (IQR, 48–64), and 67.2% (111) were female. Of the included patients, 13.3% (22) died during hospitalization. In multivariable logistic regression analysis, earlier onset of treatment-relevant CV (adjusted odds ratio [aOR] 0.79; 95% CI, 0.66–0.95) and the occurrence of SVS-I (aOR 13.47; 95% CI, 2.78–65.3) were associated with the primary outcome. Mediation analysis indicated that SVS-I accounted for 28% of the effect of earlier onset of CV on in-hospital mortality. Conclusions: Twenty-eight percent of the effect of earlier onset of cerebral vasospasm on in-hospital mortality was mediated by secondary ischemic infarction. Targeting patients with early-onset vasospasm and the associated risk of infarction may reduce in-hospital mortality following aneurysmal subarachnoid hemorrhage. Full article

Background/Objectives: Subarachnoid hemorrhage (SAH) is frequently complicated by cerebral vasospasm (VS). Clazosentan has reduced VS in Japanese studies but shown inconsistent efficacy in Western trials. We hypothesized that clinical and pharmacologic interactions may influence its effectiveness. Methods: We analyzed the multicenter “Database of Cohort Study for Outcome of SAH In Japan” (DCI Japan) registry, prospectively collected from 2020 to 2023, to assess associations between clazosentan use, VS prevention, functional outcomes, and potential interactions in adults with aneurysmal SAH (aSAH) treated by surgical clipping or endovascular coiling within 4 days of onset. Outcomes included angiographic VS (AVS), symptomatic VS (SVS), cerebral infarction, and modified Rankin Scale (mRS) scores at discharge and at 6 months. Predictors and interactions were first screened using univariable analysis and Light Gradient Boosting Machine, then evaluated via multivariable logistic regression. Results: Among 544 patients (mean age 65.2 ± 14.2 years; 71.5% female), 34.0% received clazosentan. AVS, SVS, and cerebral infarction occurred in 20.6%, 16.0%, and 22.4%, respectively. Poor outcomes (mRS 3–6) were observed in 48.8% at discharge and 33.7% (137/406) at 6 months. Clazosentan use was associated with reduced odds of AVS (OR 0.27, 95% CI [0.11–0.69]), SVS (OR 0.15 [0.04–0.64]), and poor 6-month outcome (OR 0.08 [0.01–0.68]). A potential interaction with nicardipine was linked to higher odds of AVS (OR 1.85 [1.43–2.65]). Conclusions: Clazosentan was associated with reduced VS and improved 6-month outcomes after aSAH, although concomitant nicardipine may attenuate its prophylactic effectiveness against AVS. Full article

Background/Objectives: Delayed cerebral ischemia (DCI) is a major cause of poor outcome after aneurysmal subarachnoid hemorrhage (aSAH). Beyond large-vessel vasospasm, DCI reflects a systemic, multifactorial process involving inflammation, hematologic dysregulation, and organ dysfunction. Stroke-associated pneumonia (SAP), a frequent aSAH complication linked to stroke-induced immunodepression, may aggravate secondary ischemic injury. Unlike prior studies focusing on classical predictors alone, we included pneumonia and longitudinal respiratory parameters alongside inflammatory, hematologic, and renal markers. Using machine learning, this study aimed to identify predictors of DCI and functional outcome from routinely collected intensive care data. Methods: In this retrospective single-center study, 182 aSAH patients treated in a neurosurgical intensive care unit were included. Clinical data, SAP status, and longitudinal inflammatory, hematologic, renal, and respiratory parameters were extracted. DCI and functional outcome were assessed. Continuous variables were summarized as minimum, maximum, and mean values. Supervised machine learning models combining 12 feature selection methods and 12 classifiers were trained using five-fold cross-validation and evaluated by accuracy, F1-score, and AUC. Results: DCI occurred in 22% of patients, and SAP in 27%. The machine learning models achieved a mean accuracy of 59.7% (F1-score 58.8%, AUC 59.7%) for DCI prediction. No single dominant feature emerged; predictive patterns included leukocyte counts, CRP, erythrocyte indices, platelet variability, renal function, and oxygenation metrics. Functional outcome prediction performed moderately better (mean AUC 65.7%) and shared overlapping predictors. Conclusions: DCI reflects systemic instability in aSAH, with longitudinal inflammatory and respiratory variability outperforming static thresholds. Dynamic risk stratification may enable earlier detection of deterioration, supporting future time-series modeling and external validation. Full article

Background/Objectives: Delayed cerebral ischemia (DCI) represents a major cause of morbidity and mortality after aneurysmal subarachnoid haemorrhage (aSAH). Early identification of developing cerebral ischemia is essential for timely prevention of DCI. Near-infrared spectroscopy (NIRS) provides continuous, non-invasive bedside monitoring of regional cerebral oxygen saturation (rSO₂); however, its clinical value in patients with aSAH has not yet been fully established. The primary objective of this study was to investigate whether NIRS-detected rSO₂ desaturation can serve as an early indicator of cerebral vasospasm (CV) and predict the occurrence of DCI. Secondary objectives were to examine the associations between rSO₂ changes and other cerebral deterioration events, length of intensive care unit stay, functional outcome, and in-hospital mortality. Methods: This prospective, single-centre study included 30 patients with aSAH admitted to the intensive care unit (ICU) of Riga East University Hospital between January 2019 and January 2023. Bilateral frontal near-infrared spectroscopy (NIRS) monitoring (Covidien INVOS™ 5100C-PB) was initiated within 72 h after ictus and continued for up to 7 days. Cerebral desaturation was defined as a >20% reduction from baseline (BL) or an absolute regional cerebral oxygen saturation (rSO₂) value < 50% lasting ≥30 min. CV and DCI were diagnosed according to established clinical and radiological criteria. Receiver operating characteristic (ROC) analysis was performed to evaluate the sensitivity and specificity of rSO₂ thresholds for the detection of CV, DCI, and other cerebral deterioration events. Results: CV occurred in 10 patients (33%); however, only four cases were detected during the NIRS monitoring period. NIRS demonstrated very high sensitivity (97.5%) but extremely low specificity (6%) for the early detection of CV. In contrast, diagnostic accuracy for DCI was high. An absolute rSO₂ cut-off value of 52% yielded a sensitivity of 97.5% and a specificity of 95%, whereas a decrease of ≥26% from baseline (BL) demonstrated a sensitivity of 98% and a specificity of 93%. Significant rSO₂ reductions were also observed during aneurysm re-rupture, hydrocephalus, cerebral edema, and postoperative ischemia; however, the sensitivity of NIRS for detecting these events was negligible. Patients with ≥20% desaturation tended to have longer ICU stays, and lower mean rSO₂ values as well as greater desaturation were associated with poorer functional outcomes as assessed by the modified Rankin Scale. Patients who died exhibited more pronounced rSO₂ decreases and less recovery compared with survivors. Conclusions: In this cohort, NIRS demonstrated limited specificity for the early detection of CV but showed strong associations with DCI and neurological outcome. NIRS may be useful as a non-invasive adjunct to multimodal neuromonitoring rather than as a stand-alone diagnostic tool for cerebral vasospasm. Larger, prospective studies incorporating standardized imaging protocols and optimized rSO₂ thresholds are required to more clearly define the role of NIRS in the management of aSAH. Full article

The Middle Meningeal Artery (MMA) occupies a pivotal role in the pathophysiology of migraine, functioning as a vascular and neuroimmune interface that precipitates the characteristic pulsatile pain. The inhibition of this pathophysiological cascade has been investigated as a therapeutic strategy. However, fewer than a dozen centers globally have disseminated procedural or mechanistic data. Given the nascency of this field and the imperative for standardization, the present review synthesizes mechanistic and clinical evidence underpinning intra-arterial pharmacological modulation of the MMA for migraine management. Methods: A focused narrative review was undertaken, drawing upon select but influential studies from pioneering research groups investigating intra-arterial interventions targeting the MMA. The extant literature was thematically categorized and organized according to the loci of cascade interruption and their corresponding clinical outcomes. Results: Since 2009, intra-arterial therapies for severe headache syndromes have evolved, initially utilizing nimodipine for vasospasm-related headaches, progressing to verapamil for reversible cerebral vasoconstriction, and more recently, lidocaine for refractory or status migrainosus, occasionally in conjunction with MMA embolization. Contemporary research uses language that conceptualizes migraine as an immunologically mediated neurovascular disorder, as opposed to a purely vascular or neuronal entity. Recent investigations have identified interleukins such as Interleukin-1β, Tumor Necrosis Factor-α, and Interleukin-6 as critical amplifiers of trigeminovascular activation. Purinergic signaling through the P2X3 receptor and the P2Y13 receptor, in conjunction with pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal peptide pathways, has been implicated in the modulation of MMA excitability and neuropeptide release. The development of novel calcitonin gene-related peptide receptor antagonists, such as zavegepant, further substantiates the artery’s significance as a pharmacological target. Conclusions: These findings support a shift toward immune-modulating intra-arterial therapeutic strategies, with migraine interventions targeting cytokine and neuroimmune signaling within the MMA, rather than relying exclusively on vasodilatory mechanisms. Full article

Background/Objectives: Cerebral subarachnoid hemorrhage (SAH) from ruptured aneurysms poses significant morbidity and mortality risks. Among survivors, cerebral vasospasm can develop, increasing complications. This study investigates the relationship between blood parameters and the risk of vasospasm. Methods: We analyzed clinical data from patients with SAH—both with and without vasospasm—and healthy controls. Statistical analyses, including Spearman’s rank correlation and univariate analysis, were conducted. Results: Significant differences were observed between patients with and without vasospasm. Elevated white blood cell counts, a higher neutrophil-to-lymphocyte ratio, and lower platelet counts showed a significant association with symptomatic vasospasm. Younger age and female gender were associated with a higher risk. Conclusions: These preliminary findings highlight the importance of specific blood parameters and demographic factors in assessing the risk of cerebral vasospasm in SAH patients, supporting early risk stratification and monitoring to improve outcomes; however, these results require validation in larger cohorts. Full article