Search Results (39)

Objective: The objectives of this study were to characterise induction-phase regional cerebral oxygen saturation (rSO₂)–mean arterial pressure (MAP) dynamics during near-infrared spectroscopy (NIRS)-guided selective carotid endarterectomy (CEA) and to examine whether the Awake→Intubated pressure–oxygenation pattern may represent an early adjunctive physiological signal of subsequent cross-clamp-related ipsilateral cerebral desaturation. Methods: In this retrospective observational cohort study, 322 consecutive elective CEAs managed with an NIRS-guided selective shunting protocol between October 2019 and February 2025 were analysed, after excluding patients considered for routine pre-emptive shunting because of contralateral internal carotid artery occlusion or ≥70% stenosis. Standardised MAP and bilateral rSO₂ values were extracted at the Awake, Intubated, and Clamp stages, defined as 3 min after carotid cross-clamping. Awake→Intubated ipsilateral ΔrSO₂/ΔMAP was evaluated as a continuous, exploratory pressure–oxygenation index, with MAP–rSO₂ directional change classified as concordant or discordant. Clamp-related desaturation was defined as a ≥20% ipsilateral rSO₂ decrease from Awake to Clamp. Discrimination and adjusted associations were evaluated using receiver operating characteristic analysis and multivariable logistic regression, respectively. Results: Clamp-related ≥20% ipsilateral rSO₂ desaturation occurred in 43 patients (13.4%). The Awake→Intubated ipsilateral ΔrSO₂/ΔMAP ratio differed significantly between patients with and without ≥20% desaturation and showed significant discrimination on receiver operating characteristic analysis, with an area under the curve (AUC) of 0.799 (95% confidence interval [CI] 0.723–0.876; p < 0.001). Concordant pressure–oxygenation change was more frequent among patients with ≥20% desaturation (31/43, 72.1%), whereas discordant change predominated among those without desaturation (228/279, 81.7%; p < 0.001). In multivariable analysis, Awake→Intubated ipsilateral ΔrSO₂/ΔMAP remained associated with clamp-related ≥20% desaturation after adjustment (adjusted odds ratio [OR] 1.63, 95% CI 1.15–2.33; p = 0.006), along with symptomatic presentation and 50–69% contralateral stenosis. Postoperative stroke occurred in 4/322 patients (1.2%), and no 30-day mortality occurred. Conclusions: During NIRS-guided selective CEA, induction-phase rSO₂–MAP dynamics were associated with subsequent cross-clamp-related ipsilateral cerebral desaturation. As the outcome was a NIRS-defined desaturation rather than an independent clinical, neurological, or imaging endpoint, these findings indicate association with a surrogate marker rather than prediction of clinically relevant cerebral ischaemia. The Awake→Intubated ΔrSO₂/ΔMAP ratio and directional pressure–oxygenation pattern may represent early adjunctive physiological signals associated with clamp-related desaturation. These findings are hypothesis-generating and require prospective validation with systematic multimodal monitoring. Full article

Objective: To test whether inpatient electrical muscle stimulation (EMS) using Russian current (5 kHz carrier, 50 Hz modulation; 4 s ON/6 s OFF) improves mobility and balance in elderly people with chronic cerebral ischaemia. Design: Prospective single-centre controlled observational pilot, embedded in routine inpatient rehabilitation; no concealed randomisation (EMS + standard care; sham EMS + standard care; standard care only (control)). Methods: A single-centre controlled observational study with three groups was conducted (EMS n = 27, control n = 10, sham n = 7) with 3–9 sessions over 2 weeks (20 min; quadriceps and calves). Pre/Post Outcomes: Tinetti (balance/gait), Rivermead Mobility Index, Timed Up and Go (TUG), ankle extensor maximal voluntary force (MVF), stabilography (statokinesiogram path length (L), mean velocity of COP (V), sway area (S), and myotonometry; ANOVA, α = 0.05). Ethics approval and informed consent were obtained. Between-group differences in change scores were evaluated descriptively, and no formal hypothesis-testing was planned. Results: EMS showed significant gains versus control/sham—higher Tinetti total and Rivermead scores, faster TUG, higher MVF, and improved stabilography in the eyes-closed condition (reduced L, V, and S), with good tolerability and no serious adverse events (SAEs). Conclusions: Short-course Russian-current EMS is feasible and associated with clinically meaningful improvements in balance, gait, and strength in elderly patients with chronic cerebral ischaemia; however, larger randomised trials are warranted. Full article

Background/Objectives: Patients with combined cardiovascular and cerebrovascular disease face poorer prognoses. Early, accurate assessment of the risk of cerebral ischaemic events (including transient ischaemic attacks (TIAs) and ischaemic strokes (ISs)) in patients with coronary artery disease (CAD) is therefore vital for clinical guidance. This study aims to develop a comprehensive risk assessment model for early warning in this population. Methods: In this study, we conducted a retrospective multicentre recruitment of CAD patients undergoing concurrent coronary CTA and cervical CTA (n = 326), with follow-up to observe the occurrence of cerebral ischaemic events. We performed an analysis of high-risk plaque (HRP) characteristics and subcomponent plaque in coronary and cervical arteries, measured the pericoronary fat attenuation index (FAI) and cervical perivascular fat density (PFD), and extracted corresponding radiomic features. Five models were constructed to identify the CAD patients who developed IS/TIA, respectively: Model 1—clinical characteristics; Model 2—coronary CTA parameters + Radscore_coronary; Model 3—cervical CTA parameters + Radscore_cervical; Model 4—Model 1 + Model 2; Model 5—Model 1 + Model 2 + Model 3. Results: In the cerebral ischaemia group, the prevalence of coronary and/or cervical HRP was higher than in the non-ischaemia group (28.0% vs. 26.1%, 57.0% vs. 44.0%, p = 0.02). Multivariate logistic regression confirmed that RCA FAI and PFD remained significant independent risk factors for IS/TIA (all p < 0.05). The model prediction results showed that progressively incorporating coronary and cerebral vascular risk factors into the clinical features gradually improved model performance (Model 4 vs. Model 5, AUC: 0.711 [0.645–0.777] vs. 0.821 [0.769–0.873]). Model 5 achieved a sensitivity of 0.788 [0.485–0.909] and specificity of 0.827 [0.385–0.923], demonstrating the best overall clinical benefit. Conclusions: RCA FAI and PFD are independent predictors of cerebral ischaemic events. By integrating clinical characteristics, coronary CTA and cervical CTA parameters, combined with Radscore_coronary and Radscore_cervical, the risk stratification capability for IS/TIA in CAD patients can be significantly enhanced. Full article

Background: Guidelines recommend patent foramen ovale (PFO) closure for secondary prevention after cryptogenic stroke in patients aged 18–65 years, but there is limited evidence to guide management of elderly adults. This research aims to assess the efficacy, safety and methodological quality of trials comparing secondary prevention PFO closure with medial therapy alone (MTA) in patients aged ≥ 60 years. Methods: A PubMed search identified four studies comparing PFO closure with MTA in elderly patients—PFOSK (South Korea), PT (Taiwan), DEFENSE (South Korea) and PFOG (Germany). Primary analyses evaluated study quality—patient selection, allocation, crossover and adherence. Secondary analyses compared recurrent cerebral ischaemia, mortality, new-onset atrial fibrillation (AF) and disability. Results: In 644 patients ≥ 60 years old, PFO closure was associated with a 45% (95% CI 0.35–0.86, p = 0.0091) reduction in recurrent cerebral ischaemia and an 85% (95% CI 0.05–0.49, p = 0.0016) reduction in mortality. Lower disability scores and increased incidence of new-onset AF (RR 2.15, 95% CI 1.07–4.32, p = 0.0306) was observed in closure groups. Study quality was limited by heterogeneity in medical regimens and closure protocols, crossover between treatment arms and imbalances in baseline characteristics, with closure groups generally younger and possessing larger shunt sizes. Conclusions: In patients aged ≥ 60 years, PFO closure appears to reduce the risk of the recurrence of ischaemic events and mortality, particularly in those with ‘high-risk’ PFO features. However, variability in study designs and low event rates limit certainty. Large, standardised trials are warranted to provide evidence for guideline recommendations in this population. Full article

Background: Gerstmann syndrome (GS) is characterised by the tetrad of agraphia, acalculia, finger agnosia, and right-left disorientation, which was first described by Josef Gerstmann in 1924 and is conventionally linked to lesions of the dominant angular gyrus. Contemporary neuroimaging and lesion mapping research indicates that a more dispersed parietal and occipito-temporal network may be involved. Bilateral parietal lobe infarcts are uncommon and usually arise from embolic events or small artery pathology, frequently resulting in multifocal cognitive and perceptual impairments. Method: This case report describes a 52-year-old male presented with acute confusion, perseverative speech, and an inability to follow commands. The neurological examination indicated the presence of the complete Gerstmann tetrad. The Magnetic Resonance Imaging (MRI brain) revealed bilateral parieto-occipital infarcts, with greater severity on the left, indicative of ischaemia in the territory of the posterior cerebral artery (PCA). The medical team provided supportive care and implemented secondary stroke prevention, leading to partial neurocognitive recovery over a period of three weeks. Results: This case highlights a rare presentation of Gerstmann syndrome due to bilateral parieto-occipital infarcts and emphasises that the syndrome can arise from bilateral or widespread parietal injury rather than lesions limited to the angular gyrus. Conclusions: The prompt identification of the Gerstmann constellation helps localise the lesion, enhances diagnostic accuracy, and aids in rehabilitation planning. Full article

Traumatic brain injuries (TBI) represent a leading cause of morbidity and mortality globally. Whilst clinical care has significantly improved in recent years, there is still significant scope to improve patient outcomes, particularly in relation to quality of life. However, there is a window of opportunity for clinical intervention, since most of the mortality and morbidity is associated with secondary injury processes that arise after the initial trauma. In the brain, as with any tissue, inflammation plays an important role in the response to injury. However, particularly with severe injuries, an excessive inflammatory response can have detrimental effects. Following TBI, inflammation can lead to the development of cerebral oedema and a rise in intracranial pressure. Without effective control, these processes can rapidly lead to patient deterioration. This narrative review focusses on the role of inflammation in TBI in order to examine the strategies that may help improve patient outcomes. Whilst there is clearly a relationship between the development of cerebral oedema, rising intracranial pressure (ICP), and poor patient prognosis, there are also discrepancies in terms of their impact on patient outcomes. In addition to causing a rise in ICP, this review examines in what other ways inflammation and the development of cerebral oedema may contribute to the injury process. The potential for these factors to impact upon microvascular function and reduce cerebral tissue perfusion and oxygenation is explored. In addition, the impact of TBI on glymphatic function is discussed. Following an evaluation of the potential injury processes, the scope for intervention and the development of novel therapeutic approaches is explored. Full article

Ischaemic stroke is the most prevalent stroke subtype, accounting for 80–90% of all cases worldwide, and remains a leading cause of morbidity and mortality. Its pathophysiology involves complex molecular cascades, with oxidative stress playing a central role. During cerebral ischaemia, reduced blood flow deprives neurons of essential oxygen and nutrients, triggering excitotoxicity, mitochondrial dysfunction, and excessive production of reactive oxygen and nitrogen species (RONS). Not only do these species damage cellular components, but they also activate inflammatory pathways, particularly those mediated by the transcription factor nuclear factor kappa-B (NF-κB). The pro-inflammatory milieu intensifies neuronal damage, compromises blood–brain barrier integrity, and exacerbates reperfusion-induced damage. Recent findings highlight the importance of the gut microbiota in modulating stroke outcomes, primarily through metabolic and immunological interactions along the gut–brain axis. Dysbiosis, characterised by reduced microbial diversity and an imbalance between beneficial and harmful strains, has been linked to increased systemic inflammation, oxidative stress, and worse prognoses. Specific gut-derived metabolites, including short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO), appear to either mitigate or intensify neuronal injury. SCFAs may strengthen the blood–brain barrier and temper inflammatory responses, whereas elevated TMAO levels may increase thrombotic risk. This narrative review consolidates both experimental and clinical data demonstrating the central role of oxidative stress in ischaemic stroke pathophysiology and explores the gut microbiota’s ability to modulate these damaging processes. Therapeutic strategies targeting oxidative pathways or rebalancing gut microbial composition, such as antioxidant supplementation, dietary modulation, probiotics, and faecal microbiota transplantation, present promising paradigms for stroke intervention. However, their widespread clinical implementation is hindered by a lack of large-scale, randomised trials. Future efforts should employ a multidisciplinary approach to elucidate the intricate mechanisms linking oxidative stress and gut dysbiosis to ischaemic stroke, thereby paving the way for novel, mechanism-based therapies for improved patient outcomes. Full article

Perioperative management of patients undergoing surgeries of the aortic arch is challenging. This cohort of patients has a high risk of poor neurological outcomes both as a consequence of the disease process as well as the methods employed during surgical management. Many strategies have been put forward to ameliorate these complications; however, maintaining cerebral and spinal cord perfusion and reducing metabolic oxygen demand is the core principle of these strategies. Moderate hypothermia and selective ante-grade perfusion are the most promising methods that provide the best conditions for the competing requirements of both the brain and spinal cord. Intraoperative and postoperative monitoring is essential for early detection and intervention in delayed spinal cord ischaemia and stroke. In this article we aim to discuss the current methods of neuroprotection and spinal cord protection in aortic arch surgery and stenting. Full article

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. Full article

Considering the variety of complications that arise after aneurysmal subarachnoid haemorrhage (aSAH) and the complex pathomechanism of delayed cerebral ischaemia (DCI), the task of predicting the outcome assumes a profound complexity. Therefore, there is a need to develop early predictive and decision-making models. This study explores the effect of serum biomarkers and clinical scales on patients’ outcomes and their interrelationship with DCI and systemic complications in aSAH. This was a retrospective analysis including aSAH patients admitted to the Wroclaw University Hospital (Wrocław, Poland) from 2011 to 2020. A good outcome was defined as a modified Rankin Scale (mRS) score of 0–2. The prediction of the development of DCI and poor outcome was conducted using logistic regression as a standard model (SM) and random forest as a machine learning method (ML). A cohort of 174 aSAH patients were included in the analysis. DCI was diagnosed in 79 (45%) patients. Significant differences between patients with poor vs. good outcome were determined from their levels of albumin (31 ± 7 vs. 35 ± 5 (g/L); p < 0.001), D-dimer (3.0 ± 4.5 vs. 1.5 ± 2.8 (ng/mL); p < 0.001), procalcitonin (0.2 ± 0.4 vs. 0.1 ± 0.1 (ng/mL); p < 0.001), and glucose (169 ± 69 vs. 137 ± 48 (nmol/L); p < 0.001). SM for DCI prediction included the Apache II scale (odds ratio [OD] 1.05; 95% confidence interval [CI] 1.00–1.09) and albumin level (OD 0.88; CI 0.82–0.95). ML demonstrated that low albumin level, high Apache II scale, increased D-dimer and procalcitonin levels had the highest predictive values for DCI. The integration of clinical parameters and scales with a panel of biomarkers may effectively facilitate the stratification of aSAH patients, identifying those at high risk of secondary complications and poor outcome. Full article

Adult mesenchymal stem cells are those obtained from the conformation of dental structures (DMSC), such as deciduous and permanent teeth and other surrounding tissues. Background: The self-renewal and differentiation capacities of these adult stem cells allow for great clinical potential. Because DMSC are cells of ectomesenchymal origin, they reveal a high capacity for complete regeneration of dental pulp, periodontal tissue, and other biomedical applications; their differentiation into other types of cells promotes repair in muscle tissue, cardiac, pancreatic, nervous, bone, cartilage, skin, and corneal tissues, among others, with a high predictability of success. Therefore, stem and progenitor cells, with their exosomes of dental origin and surrounding areas in the oral cavity due to their plasticity, are considered a fundamental pillar in medicine and regenerative dentistry. Tissue engineering (MSCs, scaffolds, and bioactive molecules) sustains and induces its multipotent and immunomodulatory effects. It is of vital importance to guarantee the safety and efficacy of the procedures designed for patients, and for this purpose, more clinical trials are needed to increase the efficacy of several pathologies. Conclusion: From a bioethical and transcendental anthropological point of view, the human person as a unique being facilitates better clinical and personalized therapy, given the higher prevalence of dental and chronic systemic diseases. Full article

Background: Prevention and treatment of haemodynamic instability and increased intracranial pressure (ICP) in patients with subarachnoid haemorrhage (SAH) is vital. This study aimed to evaluate the effects of protocolised cerebral perfusion pressure (CPP)-guided treatment on morbidity and functional outcome in patients admitted to the intensive care unit (ICU) with SAH. Methods: We performed a retrospective study comparing 37 patients who received standard haemodynamic treatment (control group) with 17 individuals (CPP-guided group) who were on the CPP-guided treatment aimed at maintaining CPP > 70 mmHg using both optimisations of ICP and mean arterial pressure (MAP). Results: MAP, cumulative crystalloid doses and fluid balance were similar in both groups. However, the incidence of delayed cerebral ischaemia was significantly lower in the CPP-guided group (14% vs. 64%, p < 0.01), and functional outcome as assessed by the Glasgow Outcome Scale at 30 days after SAH was improved (29.0% vs. 5.5%, p = 0.03). Conclusions: This preliminary analysis showed that implementing a CPP-guided treatment approach aimed at maintaining a CPP > 70 mmHg may reduce the occurrence of delayed cerebral ischaemia and improve functional outcomes in patients with SAH. This observation merits further prospective investigation of the use of CPP-guided treatment in patients with SAH. Full article

There is a growing prevalence of vascular cognitive impairment (VCI) worldwide, and most research has suggested that cerebral small vessel disease (CSVD) is the main contributor to VCI. Several potential physiopathologic mechanisms have been proven to be involved in the process of CSVD, such as blood-brain barrier damage, small vessels stiffening, venous collagenosis, cerebral blood flow reduction, white matter rarefaction, chronic ischaemia, neuroinflammation, myelin damage, and subsequent neurodegeneration. However, there still is a limited overall understanding of the sequence and the relative importance of these mechanisms. The glymphatic system (GS) and meningeal lymphatic vessels (mLVs) are the analogs of the lymphatic system in the central nervous system (CNS). As such, these systems play critical roles in regulating cerebrospinal fluid (CSF) and interstitial fluid (ISF) transport, waste clearance, and, potentially, neuroinflammation. Accumulating evidence has suggested that the glymphatic and meningeal lymphatic vessels played vital roles in animal models of CSVD and patients with CSVD. Given the complexity of CSVD, it was significant to understand the underlying interaction between glymphatic and meningeal lymphatic transport with CSVD. Here, we provide a novel framework based on new advances in main four aspects, including vascular risk factors, potential mechanisms, clinical subtypes, and cognition, which aims to explain how the glymphatic system and meningeal lymphatic vessels contribute to the progression of CSVD and proposes a comprehensive insight into the novel therapeutic strategy of CSVD. Full article

(1) Background: Alterations of blood flow volume in extracranial arteries may be related to the risk of occurrence of neurological symptoms. The aim of this study was the estimation of cerebral blood flow (CBF) in Doppler ultrasonography, as well as comparison of the flow volume in asymptomatic patients over 65 years old with ≥50%, and symptomatic patients with ≥70% internal carotid artery (ICA) stenosis, in order to assess whether the changes in the CBF correlates with the presence of neurological symptoms. (2) Methods: 308 patients over 65 years old were included in the retrospective cohort observational study: 154 asymptomatic with ≥50% ICA stenosis, 123 healthy volunteers, and 31 symptomatic referred for surgical treatment. The study group was split according to ICA stenosis (50–69%, 70–99% and occlusion). In all patients an extensive Doppler ultrasound examination with measurements of flow volume in common, internal, external carotid (ECA) and vertebral arteries (VA) was performed. (3) Results: Among asymptomatic (A) and symptomatic (S) patients with carotid stenosis 3 subgroups were identified: 57/154—37% (A) and 8/31—25.5% (S)—with significantly increased flow volume (CBF higher than reference range: average CBF + std. dev in the group of healthy volunteers), 67/154—43.5% (A) and 12/31—39% (S)—with similar to reference group flow volume (CBF within range average ± std.dev), and 30/154—19.5% (A) and 11/31—35.5% (S)—with decreased flow volume in extracranial arteries (flow lower than average-std.dev. in healthy volunteers). In symptomatic patients the percentage of patients with significant compensatory increased flow tends to raise with the severity of the stenosis, while simultaneous decline of number of patients with mild compensation (unchanged total CBF) is observed. The percentage of patients without compensation remains unchanged. In the group referred for surgical treatment (symptomatic, ≥70% ICA stenosis) the percentage of patients with flow compensation is twice as low as in the asymptomatic ones with similar degree of the ICA stenosis (8/31—25.8% vs. 26/53—49%, p = 0.04). Compensatory elevated flow was observed most frequently in ECA. (4) Conclusions: The presence of significant volumetric flow compensation has protective influence on developing ischaemic symptoms, including TIA or stroke. The assessment of cerebral inflow in Doppler ultrasonography may provide novel and easily accessible tool of identifying patients prone to cerebral ischaemia. The multivessel character of compensation with enhanced role of ECA justifies the importance of including this artery in the estimation of CBF. Full article

Ischaemic stroke involves the rapid onset of focal neurological dysfunction, most commonly due to an arterial blockage in a specific region of the brain. Stroke is a leading cause of death and common cause of disability, with over 17 million people worldwide suffering from a stroke each year. It is now well-documented that neuroinflammation and immune mediators play a key role in acute and long-term neuronal tissue damage and healing, not only in the infarct core but also in distal regions. Importantly, in these distal regions, termed sites of secondary neurodegeneration (SND), spikes in neuroinflammation may be seen sometime after the initial stroke onset, but prior to the presence of the neuronal tissue damage within these regions. However, it is key to acknowledge that, despite the mounting information describing neuroinflammation following ischaemic stroke, the exact mechanisms whereby inflammatory cells and their mediators drive stroke-induced neuroinflammation are still not fully understood. As a result, current anti-inflammatory treatments have failed to show efficacy in clinical trials. In this review we discuss the complexities of post-stroke neuroinflammation, specifically how it affects neuronal tissue and post-stroke outcome acutely, chronically, and in sites of SND. We then discuss current and previously assessed anti-inflammatory therapies, with a particular focus on how failed anti-inflammatories may be repurposed to target SND-associated neuroinflammation. Full article