Search Results (92)

Background and Clinical Significance: Chronic subdural hematomas (cSDHs) present characteristic imaging findings, making the diagnosis straightforward. In rare cases, arachnoid cysts (ACs) may be associated with their formation. There is still no consensus regarding their treatment; Case Presentation: A young adult male presented with occipital headache. Neurological examination was normal. Laboratory investigations were within physiological limits. A CT scan revealed the presence of a Galassi Grade III temporo-parietal AC accompanied by a parietal epidural hematoma (EDH) on the right side. His medical history was significant for treated hypertension. There was no use of anticoagulants, antiplatelets, or history of trauma. Vascular pathology was excluded by MRA/MRV. He was discharged for home care and was readmitted 10 days later after a repeat CT scan. A brief cognitive assessment with the Mini-Mental State Examination (MMSE) revealed mild cognitive impairment. A burr-hole evacuation was performed, and a drainage catheter was left in place for 24 h. Intraoperative findings were consistent with a chronic subdural hematoma. The patient was discharged with complete resolution of symptoms. A follow-up CT scan performed one month postoperatively confirmed the favorable result. Cognitive functions were normal on follow-up; Conclusions: A SDH may mimic the characteristics of an EDH in the presence of an AC. The most common symptom is cephalalgia. Neurocognitive impairment may occur secondary to elevated intracranial pressure. A burr-hole hematoma evacuation may be sufficient. Further treatment should be considered only in the case of complications associated with ACs. Full article

Background: Intracranial hypertension is a critical complication of acute intracerebral hemorrhage (ICH), contributing to high early mortality and poor functional outcomes. Invasive intracranial pressure (ICP) monitoring remains the gold standard but carries procedural risks and is resource-intensive. This study evaluated the diagnostic and prognostic utility of optic nerve sheath diameter (ONSD) ultrasonography and transcranial Doppler (TCD)-derived pulsatility index (PI) as non-invasive ICP surrogates in patients with severe ICH. Methods: A prospective observational study was conducted in 42 patients with acute ICH who underwent concurrent invasive ICP monitoring and serial ONSD/PI measurements at 10 time points (T0–T9) between October 2021 and August 2024. Diagnostic performance was assessed using measurement-level receiver operating characteristic (ROC) curve analysis. Exploratory early mortality prediction was evaluated using random forest machine learning models incorporating ONSD, PI, age, and sex. Results: A total of 274 paired ONSD–PI–ICP measurements were obtained. Both ONSD and PI showed moderate positive correlations with invasive ICP (rho = 0.49 and 0.43, respectively; p < 0.001). ONSD demonstrated superior diagnostic accuracy for detecting ICP ≥ 20 mmHg (AUC = 0.83; optimal threshold: 5.88 mm; sensitivity: 81%; specificity: 82%) compared to PI (AUC = 0.75). In exploratory random forest analyses, the combined ONSD–PI model showed high apparent discrimination for elevated ICP detection (AUC = 0.98), while the model incorporating ONSD, PI, age, and sex showed promising but potentially optimistic discrimination for early mortality prediction (AUC = 0.95). These machine learning results should be interpreted cautiously because of the small sample size, repeated-measurement structure, measurement-level data partitioning, and limited number of early deaths. Conclusions: ONSD ultrasonography and TCD-derived PI showed promising performance as non-invasive ICP markers in severe acute ICH. However, because of the small sample size, repeated-measurement design, measurement-level analyses, and exploratory nature of the machine learning models, these findings require validation in larger external cohorts before routine clinical implementation. Full article

Elevated intracranial pressure (ICP) is a major determinant of secondary injury and mortality in severe traumatic brain injury (TBI), yet objective markers of decompressive craniectomy (DC) efficacy remain limited. Optic nerve sheath diameter (ONSD), measurable on computed tomography (CT), has emerged as a non-invasive surrogate of ICP. This study evaluated the relationship between perioperative ONSD changes and clinical and surgical parameters in patients undergoing DC. In this retrospective cohort study, 72 patients with severe TBI were included. ONSD was measured on preoperative and early postoperative CT, and the change (ΔONSD) was analyzed in relation to craniectomy surface area and outcomes. DC resulted in a significant reduction in ONSD (6.44 ± 0.88 mm vs. 5.55 ± 0.82 mm, p < 0.001). Larger craniectomy surface areas were associated with greater ΔONSD change (r = −0.31, p = 0.008). ΔONSD was independently associated with in-hospital mortality (OR = 0.12, p = 0.005), with larger reductions associated with improved survival. Additionally, ΔONSD was correlated with shorter hospital stay (ρ = −0.32, p = 0.007). These findings support ΔONSD as a practical imaging biomarker reflecting the physiological response to DC in severe TBI. 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

Background and Clinical Significance: Decompressive hemicraniectomy (DHC) is a life-saving intervention for malignant middle cerebral artery (MCA) infarction, but postoperative secondary injury mechanisms and functional outcome remain difficult to evaluate using intracranial pressure (ICP) alone. The pressure reactivity index (PRx), calculated as the moving correlation coefficient between ICP and mean arterial pressure (MAP), provides a measure of cerebral autoregulation. The utility of PRx monitoring in ischemic stroke, especially following DHC, remains uncertain. Case Presentation: We describe two patients presenting with acute ischemic stroke in the MCA territory who underwent DHC followed by postoperative ICP and PRx monitoring. Case 1 is a 40-year-old female with a left proximal MCA occlusion initially treated with endovascular thrombectomy (EVT) who required emergent DHC due to re-occlusion. Postoperatively, ICPs remained controlled, and PRx values were favorable (<0.2), indicating preserved cerebral autoregulation. She later showed moderate neurological improvement. Case 2 was a 68-year-old female with a left proximal MCA occlusion treated with EVT who developed worsening cerebral edema and midline shift, necessitating emergent DHC. Despite adequate ICP control, PRx values remained markedly elevated (0.45 to 0.73), consistent with impaired cerebral autoregulation, and her neurologic state remained poor at discharge. Conclusions: These contrasting cases suggest that PRx may provide physiologic information not reflected by ICP metrics alone post-DHC. PRx monitoring may provide complementary physiologic insight into postoperative autoregulatory status following DHC. Further investigation is warranted to define its role in individualized post-DHC management and prognostication in malignant ischemic stroke. Full article

Background/Objectives: Traumatic brain injury (TBI) is a leading cause of morbidity and mortality worldwide. Electrolyte disturbances are common in this patient cohort, with serum chloride frequently elevated. Chloride dysregulation may be associated with poor neurological outcomes through mechanisms including paradoxical gamma amino butyric acid receptor excitation, cytotoxic edema, and ferroptosis. The aim of this review was to evaluate the relationship between serum chloride levels and outcomes in patients with TBI. Methods: A literature review was performed to identify all potential studies that reported on serum chloride levels and TBI. All study types and patient groups were included. Studies were included if they reported on serum chloride measurements as well as outcomes such as mortality, surgical intervention, intracranial pressure, and neurological/functional outcome scores in patients with TBI. References and citations were also reviewed. Results: A small number of mostly retrospective studies with modest patient numbers demonstrate an association between high chloride levels and increased mortality in patients with TBI, with this relationship persisting independent of hypernatremia. Recent large, randomized trials showed that balanced crystalloid solutions, despite lower chloride content, may be associated with worse outcomes in TBI patients compared to saline. No studies directly correlated chloride levels with intracranial pressure measurements. Chloride level rather than total chloride load appears more strongly associated with adverse outcomes, with non-hypertonic saline sources contributing substantially to chloride burden. Mechanistic evidence links chloride channel dysregulation to ferroptosis and cytotoxic edema, with sex-specific patterns of transporter expression. Conclusions: Limited available evidence suggests that hyperchloremia is independently associated with increased mortality in TBI though causality remains unestablished. The findings regarding balanced solutions challenge conventional fluid management assumptions and highlight the complexity of chloride’s role in TBI pathophysiology. The absence of studies directly correlating chloride with intracranial pressure represents a critical evidence gap. Future studies with larger patient numbers, prospective designs, and multimodal neuromonitoring should further define these relationships to inform evidence-based chloride management strategies. Full article

Background/Objectives: Periprocedural blood pressure influences outcomes after endovascular treatment (EVT), but the impact of pulse pressure (PP) remains unclear. We assessed associations between intraprocedural PP and clinical and radiological outcomes after EVT. Methods: We retrospectively analyzed adults with acute ischemic stroke (AIS) due to proximal anterior circulation large vessel occlusion treated with EVT under general anesthesia. Non-invasive BP was recorded every 5 min during EVT. From these recordings, we derived baseline, maximal, minimal, and median PP, PP variability indices, and cumulative time above predefined PP thresholds. The primary endpoint was poor functional outcome at 90 days (modified Rankin Scale 3–6). Secondary endpoints were final infarct volume (FIV), malignant brain edema (MBE), symptomatic intracranial hemorrhage (sICH), and hemorrhagic transformation (HT). Multivariable regression models were adjusted for established prognostic factors. Results: In the 217 patients included, higher median PP during EVT independently predicted poor functional outcome, larger FIV, MBE, and HT, but not sICH. Longer duration of PP > 50 mmHg was independently associated with poor outcome, MBE, and HT. Among other hemodynamic variables, only a >40% mean arterial pressure (MAP) drop from baseline independently predicted poor outcome. Adding median PP to the baseline multivariable model modestly increased its discriminative ability and significantly improved model fit. Conclusions: In AIS patients with proximal anterior circulation large vessel occlusion treated with EVT under general anesthesia, higher intraprocedural PP and longer exposure to elevated PP are associated with worse functional and radiological outcomes, supporting PP as a potential hemodynamic target alongside avoidance of large MAP reductions. Full article

Cardiac disturbances are well-recognized in traumatic brain injury (TBI), but most involve supraventricular arrhythmias or repolarization abnormalities, while sinus arrest is rarely reported. We present a case of a 37-year-old man who developed recurrent, prolonged sinus arrest following severe TBI. He arrived intubated for airway protection after an assault, and imaging demonstrated an acute, depressed, comminuted right temporoparietal skull fracture scattered subarachnoid hemorrhage, and bilateral humeral head fractures with posterior shoulder subluxation. After craniotomy and placement of an external ventricular drain (EVD) for intracranial pressure (ICP) monitoring, the patient experienced multiple spontaneous sinus arrest episodes lasting up to 15 s despite normal metabolic, electrolyte, and toxicology evaluations. A transvenous pacemaker (TVP) was inserted to maintain adequate cardiac output and cerebral perfusion. As ICP improved, the sinus arrests resolved and the TVP was removed. This case highlights a rare neurocardiac manifestation of TBI, demonstrating that elevated ICP can precipitate profound conduction disturbances that may require temporary pacing to manage hemodynamics and prevent secondary brain injury. Full article

Background: Diffuse leptomeningeal glioneuronal tumors (DLGNT) are rare pediatric central nervous system tumors, first recognized in the 2016 WHO classification. Their clinical course is highly heterogeneous, and no international consensus treatment guidelines are currently available. This study aims to describe clinical characteristics, disease evolution, and management strategies for pediatric DLGNT patients, with a focus on aggressive forms. Methods: This retrospective, multicenter, international study (Belgium and France) included pediatric patients diagnosed with DLGNT between 1 February 2016 and 31 December 2024. Clinical, radiological, histopathological, molecular, and therapeutic data were collected. Findings were analyzed and contextualized through an extensive literature review. Results: Eleven patients were enrolled (median age: 8.2 years; median follow-up: 52 months). The median delay between the first MRI and definitive diagnosis was 6.5 months. Symptoms of intracranially elevated pressure were present in 55% of patients. Two-thirds of the patients presented with leptomeningeal dissemination at diagnosis. The primary tumor site could not be identified in two patients. A KIAA1549::BRAF transcript fusion was detected in 82% of cases, and chromosome 1q gain in 38%. All patients underwent surgery at diagnosis. The median number of therapeutic lines was four: 82% received chemotherapy (weekly vinblastine in 55%, vincristine/carboplatin regimen in 45%), 64% received MAPK pathway-targeted therapy, and 18% underwent radiotherapy. Five-year overall survival (OS) was 68.5%, and median progression-free survival (PFS) was 5.3 months after first-line therapy and 16.5 months after the second line. At the end of follow-up, only one patient achieved complete remission, and 78% of survivors presented with persistent neurological deficits. Conclusions: This study underscores the significant diagnostic delay, clinical heterogeneity, and absence of standardized therapeutic approaches in pediatric DLGNT patients. Conventional low-grade glioma chemotherapy constitutes the current treatment backbone, while MAPK pathway-targeted therapies show promising potential. Further studies and the establishment of an international registry are crucial to better characterize aggressive subtypes and optimize management strategies. Full article

In recent years, Transcranial Color Doppler (TCCD) has gained increasing recognition as a non-invasive neuromonitoring tool. However, there remains a strong tendency to view arterial TCCD as the ‘stethoscope for the brain,’ while the assessment of cerebral venous flow is still underrepresented in clinical protocols. This review aims to explore the emerging role of venous TCCD, particularly when combined with Internal Jugular Vein (IJV) ultrasound, in evaluating cerebral venous outflow in both critically ill and surgical patients. We conducted a narrative review of e-Pub articles from PubMed, MEDLINE, and Scopus, on the pathophysiological factors that impair cerebral venous drainage and their clinical implications in surgical and critical care settings. Based on this evidence, we developed two procedural algorithms that integrate established knowledge of cerebral venous hemodynamics with common clinical conditions affecting venous outflow, including internal jugular central venous catheter placement, mechanical ventilation, and pneumoperitoneum. The algorithms emphasize systematic monitoring of cerebral venous drainage, including assessment of internal jugular vein morphology and Rosenthal’s vein flow, to guide procedural optimization and minimize potential neurological complications. They were informed by validated frameworks, such as the RaCeVa protocol, and are illustrated through two representative clinical case scenarios. Cerebral venous congestion can be induced by multiple established risk factors, including mechanical ventilation, cardiovascular disease, elevated intra-abdominal pressure, the Trendelenburg position, and central venous catheterization. In selected patients, real-time venous TCCD monitoring, combined with IJV assessment, allows early detection of cerebral venous outflow impairment and guides timely hemodynamic and procedural adjustments in both surgical settings and critical care contexts. Venous TCCD neuromonitoring may help prevent intracranial hypertension and its consequent neurological complications. It can guide clinical decisions during procedures that may compromise cerebral venous drainage, such as mechanical ventilation, the placement of large-bore central venous catheters, or laparoscopic and robot-assisted surgeries. Further studies are warranted to validate this strategy and better define its role in specific high-risk clinical scenarios. Full article

Objective: Traumatic brain injury (TBI) represents a significant clinical problem, with the biomechanical mechanisms of striking from different blunt instruments remaining unclear. This study aims to quantitatively evaluate TBI severity under blunt strikes and to assess the effects of strike velocity and blunt instrument size on biomechanical responses to provide a finite element approach for investigating injury mechanisms and informing clinical diagnosis. Methods: A head finite element model incorporating an outer cortical-cancellous-inner cortical bone structure was developed and verified against a previous cadaveric impact study. Strike velocities and blunt instrument parameters, obtained from experiments in which a long bat (LB) and a short bat (SB) were used to strike a dummy head, were applied as the loading conditions in the finite element simulation. Kinetic energy (KE), internal energy (IE), impact force, von Mises stress on skull, intracranial pressure (ICP), and Head_3ms acceleration were analyzed as indicators of injury severity. Results: Simulated force and ICP responses agreed with cadaveric experimental data within a 9.8% error. With increasing strike velocity (10–30 m/s), KE, IE, impact force, ICP, and Head_3ms all rose, while von Mises stress evolved from localized to dispersed distribution. Head_3ms reached an injury threshold of 80 g at a strike velocity of 10 m/s, and ICP peaks for LB and SB exceeded the brain injury threshold (235 kPa, ≈1760 mmHg) at 12 m/s and 14 m/s, respectively. At the same velocity, LB generated higher KE, IE, impact force, ICP and Head_3ms than SB. At 30 m/s, LB generated 390 J KE and 29.0 kN peak force, which were 50.0% and 11.1% higher than those of SB (260 J, 26.1 kN). Conclusion: This study reveals that increasing strike velocity and employing a larger blunt instrument elevate biomechanical responses, resulting in von Mises stress transitioning from localized concentration to multipolar dispersion. Specifically, when striking the head with the LB at velocities exceeding 12 m/s or with the SB exceeding 14 m/s, the impacts indicate a severely life-threatening level. These findings deepen our understanding of the mechanisms of blunt TBI. The constructed and validated finite element model can be repeatedly used for computer simulations of TBI under various blunt striking conditions, providing a scientific basis for clinical diagnosis and surgical planning. Full article

Background/Objectives: Idiopathic intracranial hypertension (IIH) is an uncommon but clinically important cause of elevated intracranial pressure in children. Conventional MRI findings such as perioptic subarachnoid space (SAS) distension and posterior globe flattening are helpful but may lack sensitivity or specificity in certain cases. Diffusion tensor imaging (DTI), which quantifies white matter microstructure through metrics such as fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD), offers additional diagnostic potential, yet its role in pediatric IIH remains insufficiently defined. Methods: This retrospective case–control study included 26 pediatric patients with IIH and 26 age- and sex-matched controls who underwent brain MRI with DTI between 2010 and 2025. DTI parameters were measured in major white matter tracts, and conventional MRI findings associated with raised intracranial pressure were recorded. Associations between DTI metrics and conventional imaging markers were analyzed using standardized statistical tests. Results: Children with IIH demonstrated significantly reduced FA and increased MD and RD values in several key white matter regions, particularly within the optic radiation, splenium of the corpus callosum, and posterior limb of the internal capsule. FA values showed a negative correlation with perioptic SAS width, while RD and MD were positively correlated with posterior globe flattening and empty sella grade. Receiver operating characteristic analysis identified FA in the optic radiation as the strongest discriminator between IIH and controls (AUC = 0.83). Inter-observer reliability for FA measurements was excellent (ICC = 0.91). Conclusions: Pediatric IIH appears to be associated with pressure-related microstructural alterations in white matter, detectable through DTI. Among the diffusion metrics, FA demonstrated the strongest diagnostic potential and may serve as a complementary tool to conventional MRI. Validation in larger, prospective pediatric cohorts is required to establish its clinical utility. Full article

Optical coherence tomography (OCT) is a non-invasive imaging tool that is currently used in the evaluation and management of neuro-ophthalmic disorders. The detailed ability to visualize the optic nerve head, peripapillary retinal nerve fiber layer, and the macula, including the ganglion cell layer, allows for both qualitative and quantitative analysis of optic nerve diseases. This review covers the technical aspects of OCT and related imaging techniques in neuro-ophthalmology and discusses its use in common optic nerve head diseases such as optic disc drusen, optic disc coloboma, and elevated intracranial pressure. It also explores emerging OCT angiography applications in these disorders. Full article

Background: Severe traumatic brain injury (TBI) often leads to elevated intracranial pressure (ICP) that requires aggressive management. Inducing burst suppression with deep sedation is an established therapy for refractory intracranial hypertension. Traditionally, barbiturate coma has been used to achieve burst-suppression EEG in TBI patients, but alternative sedative agents (propofol, midazolam, ketamine, dexmedetomidine) are increasingly utilized in modern neurocritical care. This review compares barbiturates with these alternatives for inducing burst suppression in adult TBI, focusing on protocols, mechanisms, efficacy in controlling ICP, safety profiles, and impacts on neurological outcomes. Methods: A search of the literature was performed, including clinical trials, observational studies, and guidelines on deep sedation for ICP control in adult TBI. Studies comparing high-dose barbiturates to other sedatives (propofol, midazolam, ketamine, dexmedetomidine) in the context of burst suppression or severe TBI management were included. Data on sedative protocols (dosing and EEG targets), mechanisms of action, ICP-lowering efficacy, complications, and patient outcomes were extracted and analyzed qualitatively. Results: High-dose barbiturates (e.g., pentobarbital or thiopental) and propofol are both effective at inducing burst-suppression EEG and reducing ICP via cerebral metabolic suppression. Barbiturate coma remains a third-tier intervention reserved for ICP refractory to other treatments. Propofol infusion has become first-line for routine ICP control due to rapid titratability and shorter half-life, though it can also achieve burst suppression at high doses. Midazolam infusions provide sedation and seizure prophylaxis but yield less metabolic suppression and ICP reduction compared to barbiturates or propofol, and are associated with longer ventilation duration and delirium. Ketamine, once avoided for fear of raising ICP, has shown neutral or lowering effects on ICP when used in ventilated TBI patients, thanks to its analgesic properties and maintenance of blood pressure; however, ketamine alone does not reliably produce burst-suppression patterns. Dexmedetomidine offers sedative and anti-delirium benefits with minimal respiratory depression, but it is generally insufficient for deep burst-suppressive sedation and has only a modest effect on ICP. In comparative clinical evidence, propofol and barbiturates both effectively lower ICP, but neither has demonstrated clear improvement in long-term neurological outcome when used prophylactically. Early routine use of barbiturate coma may increase complications (hypotension, immunosuppression), and thus, current practice restricts it to refractory cases. Modern sedation protocols emphasize using the minimal necessary sedation to maintain ICP < 22 mmHg, with continuous EEG monitoring to titrate therapy to a burst-suppression target (commonly 2–5 bursts per minute) when deep coma is employed. Conclusions: In adult TBI patients with intracranial hypertension, propofol-based sedation is favored for first-line ICP control and can achieve burst suppression if needed, whereas high-dose barbiturates are reserved for ICP crises unresponsive to standard measures. Compared to barbiturates, alternative agents (propofol, midazolam, ketamine, dexmedetomidine) offer differing advantages: propofol provides potent, fast-acting metabolic suppression; midazolam adds anticonvulsant sedation for prolonged use at the cost of slower wake-up; ketamine supports hemodynamics and analgesia; dexmedetomidine aids lighter sedation and delirium control. The choice of agent is guided by the clinical scenario, balancing ICP reduction needs against side effect profiles. While all sedatives can transiently reduce ICP, careful monitoring and a tiered therapy approach are essential, as no sedative has conclusively improved long-term neurological outcomes in TBI. EEG monitoring for burst suppression and meticulous titration is required when employing barbiturate or propofol coma. Ongoing research into optimal combinations and protocols may further refine sedation strategies to improve safety and outcomes in severe TBI. Full article

Background/Objectives: Idiopathic intracranial hypertension (IIH) often features dural venous sinus stenosis; venous sinus stenting (VSS) improves venous outflow and intracranial pressure, but most stents are off-label, and few are engineered for intracranial venous anatomy. The aim was to synthesize animal models relevant to IIH/VSS, catalogue stents used clinically for VSS and summarize corresponding animal data, appraise current preclinical VSS research, and propose a pragmatic preclinical evaluation framework. Methods: We performed a targeted search (PubMed, Web of Science, Scopus; through to May 2025), dual-screened the records in Nested Knowledge, and extracted the model/device characteristics and outcomes as per the predefined criteria. Results: We identified 65 clinical VSS studies; most were retrospective and used off-label carotid/peripheral/biliary stents (Precise, Zilver, and Wallstent were the most frequent). Recent dedicated systems (River, BosStent) have limited animal evidence; VIVA has GLP porcine venous peripheral data demonstrating its patency, structural integrity, and benign healing outcomes. Rodent models reproduce obesity/androgen drivers with modest, sustained ICP elevation; large animal models show the technical feasibility of in sinus implantation, but no chronic focal venous stenosis model fully mirrors the IIH condition. Conclusions: Despite broad clinical uptake, the translational underpinnings of VSS in IIH remain incomplete: most devices lack intracranial venous-specific preclinical validation, and there is no existing animal model that recapitulates both IIH biology and focal sinus stenosis. Full article