Middle Cerebral Research Articles

Synergism of salvianolic acid B and ginsenoside Rg1 magnifies the therapeutic potency against ischemic stroke.

Even though considerable progress has been made to reduce insult, ischemic stroke is still a significant cause of mortality and morbidity in the world, and new therapeutic strategies are urgently needed. In the present study, the magnesium salt of salvianolic acid B (SalB) and ginsenoside Rg1 (Rg1) combination as a multicomponent strategy against stroke was evaluated. The synergistic effect of Sa1B and Rg1 was evaluated by Bliss independence analysis on the middle cerebral artery occlusion model. The infarct volume, neuroethology, cerebral structure, and neurocyte number were evaluated by 3,5-triphenyltetrazolium chloride staining, Longa score, Garcia score, hematoxylin-eosin staining, and Nissl staining, respectively. Metabolomics was used to search for potential biomarkers and explore the mechanism of Sa1B/Rg1. First, the superior effects of SalB/Rg1 than SalB or Rg1 at the same dose were evaluated. Compared with SalB ( P < 0.001) or Rg1 ( P < 0.01), SalB/Rg1 significantly decreased infarct volume through 3,5-triphenyltetrazolium chloride staining and protected the structural integrity of cortex and striatum. The superior effect of SalB/Rg1 on neurological behavior was also detected compared with SalB or Rg1 significantly. Accompanying behavioral improvement, a considerable increase of SalB/Rg1 on neurons detected by Nissl staining was found on the cortex compared with SalB ( P < 0.05) or Rg1 ( P < 0.01). Second, the synergistic effect between SalB and Rg1 was strictly verified by Bliss independence analysis ( P < 0.01) based on infarct volume. Finally, alleviation of cerebral metabolic disorders may be the possible mechanism of SalB/Rg1. Our study provided a multicomponent strategy against ischemic stroke, with not only dose reduction but also improved efficacy relative to single agents.

Anatomical investigation of the morphometry of the cerebral arteries using digital subtraction angiography in the Thai population.

The main purpose of this study was to investigate the dimensions of cerebral arteries in the Thai population using digital subtraction angiography (DSA), with a focus on the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). The research aimed to explore anatomical variations in diameters and lengths of these arteries across different sexes and age groups, which are crucial for cerebrovascular interventions. This retrospective study measured the diameters and lengths of the ACA, MCA, and PCA in 177 Thai patients with an average age of 47.6 years (range: 11-82 years) with normal cerebral angiograms. Digital subtraction angiography (DSA) was used for the measurements. The study found significant sex-based differences in the mean diameters of the left ACA (males: 2.12 ± 0.28mm, females: 1.92 ± 0.20mm; p < 0.01), right MCA (males: 2.50 ± 0.25mm, females: 2.31 ± 0.17mm; p < 0.01), and left MCA (males: 2.44 ± 0.19mm, females: 2.30 ± 0.17mm; p < 0.01) with males exhibiting larger diameters. The right ACA length was significantly longer in males (15.46 ± 1.74mm) compared to females (13.98 ± 1.92mm; p < 0.01). While no significant age-related differences were observed in diameters, a significant increase in length with age was noted for the left ACA in the ≥ 60 years group (13.61 ± 1.64mm) compared to the < 60 years group (12.63 ± 1.36mm; p < 0.01). Among others, significant correlations were found between the diameters of the left ACA and right MCA (r = 0.699; p < 0.01), and a strong correlation between left ACA length and left PCA diameter (r = 0.975; p < 0.01). The findings provide invaluable data for tailoring neurosurgical approaches and designing angiographic equipment for the Thai population, emphasizing the importance of considering anatomical variations in clinical practice. These results highlight the necessity for personalized medical care based on anatomical differences to improve cerebrovascular intervention outcomes.

Transcranial Doppler in 150 Congolese children with sickle cell disease

IntroductionSickle Cell Disease (SCD) ranks among the most prevalent genetic disorders globally. The incidence in sub-Saharan African countries has been estimated to be 230.000/y with a high prevalence (1%) in the Democratic Republic of Congo (DRC). Stroke is a significant complication of Sickle Cell Disease (SCD), and carries a high risk of disability and mortality. Transcranial Doppler (TCD) is currently the non-invasive exploration recommended for the prevention of stroke in young SCD patients.ObjectiveTo determine the prevalence of pathological TCD in a population of young Congolese SCA patients and to assess its association with hematological parameters.Population and methodsThis cross sectional study was carried out on 150 Congolese SS homozygous children between the ages 2–16 years old (mean age: 8.5 ± 4.0 years) in stable condition, and followed from January 1 to December 31, 2013. TCD was performed using the STOP I method in the main cerebral arteries. The risk of stroke was absent when the average maximum speed during a cycle (TAMMV) in middle cerebral artery (MCA) was &amp;lt; 170 cm/s, but present when TAMMV was borderline or conditional for values between 170 and 199 cm/s and pathological for values ≥ 200 cm/s.ResultsThe prevalence of pathological TCD was 4% while the conditional TCD prevalence was 10%. The Mean blood velocity in MCA was 114.0 cm/s. There was a significant difference in the means of WBC (p = 0.003), Hb (p &amp;lt; 0.001), Hct (p &amp;lt; 0.001), MCV (p = 0.005) parameters when comparing normal and at risk TCD (conditional and abnormal). However, no significant association was found for the categorical corresponding parametersConclusionGlobally, 14% of patients were at risk of stroke, hence the interest in integrating TCD in the routine monitoring of children with SCD in order to prevent overt stroke by implementing a chronic blood transfusion program or the use of hydroxycarbamide.

Using Doppler ultrasound to assess fetal cardiac function and pregnancy outcomes in obstetric antiphospholipid syndrome pregnancies: a case-control study.

This study aimed to evaluate fetal left ventricular function (LVF) in pregnant women with obstetric antiphospholipid syndrome (OAPS) by Doppler ultrasound and developed a clinical nomogram to predict adverse perinatal outcomes. In this prospective observational study, 105 pregnant women were enrolled and divided into the OAPS cohort (n = 60) and the control cohort (n = 45). Fetal cardiac function parameters were collected and compared between two cohorts. Univariate and multivariate analysis was conducted to select the risk factors associated with adverse perinatal outcomes, and a clinical nomogram was developed based on these selected risk factors. The predictive performance of corresponding indicators for adverse perinatal outcomes was evaluated using receiver operating characteristic (ROC) curve analysis. The OAPS cohort revealed an increase in the isovolumic relaxation time (IVRT) and myocardial performance index (MPI), a decrease in the ejection time (ET), middle cerebral artery pulsatility index (MCA-PI) and cerebroplacental ratio (CPR) compared to the control cohort. Through univariate and multivariate analysis, gravidity, CPR, and MPI were the risk factors associated with adverse perinatal outcomes. A model predicting adverse perinatal outcomes in OAPS pregnant women was constructed based on these three factors and visualized as a nomogram. The nomogram could accurately predict adverse perinatal outcomes with an area under the curve of 0.923 (95% CI: 0.858-0.982). This performance was better than evaluating individual factors such as MPI (0.825, 95% CI: 0.739-0.911) and CPR (0.816, 95% CI: 0.705-0.927) for efficacy. MPI can be used to assess fetal LVF and predict adverse perinatal outcomes. We developed a nomogram to predict adverse perinatal outcomes in OAPS women. This imaging-based evidence can provide timely clinical intervention, enabling personalized clinical decision-making.

The Neuroprotective Effects of Peripheral Nerve Microcurrent Stimulation Therapy in a Rat Model of Middle Cerebral Artery Occlusion.

This study investigated the neuroprotective effects of peripheral nerve microcurrent stimulation therapy in a rat model of middle cerebral artery occlusion (MCAO). Twenty 8-week-old male Sprague Dawley rats weighing 300-330 g were categorised into group A, serving as the healthy control; group B, including rats subjected to MCAO; group C, including rats receiving microcurrent therapy immediately after MCAO, which was continued for one week; and group D, including rats receiving microcurrent therapy one week before and one week after MCAO. A gross morphological analysis, behavioural motion analysis, histological examination, immunohistochemistry, and Western blotting were conducted. Microcurrent therapy significantly reduced ischaemic damage and pyramidal cells of the hippocampus CA1 region. Haematoxylin and eosin staining revealed infarction areas/viable pyramidal cell numbers of 0%/94.33, 28.53%/40.05, 17.32%/80.13, and 5.38%/91.34 in groups A, B, C, and D, respectively (p < 0.001). A behavioural analysis revealed that the total distances moved were 1945.24 cm, 767.85 cm, 1781.77 cm, and 2122.22 cm in groups A, B, C, and D, respectively (p < 0.05), and the mean speeds were 6.48 cm/s, 2.50 cm/s, 5.43 cm/s, and 6.82 cm/s, respectively (p < 0.05). Inflammatory markers (cluster of differentiation 68, interleukin-6, and tumour necrosis factor-α) significantly decreased in the treated groups (p < 0.001). Western blotting revealed reduced proinflammatory, oxidative stress, and apoptosis-related protein levels, along with increased angiogenic factors and mitogen-activated protein kinase (MAPK) pathway modulation in the treated groups. Peripheral nerve microcurrent stimulation therapy effectively mitigates ischaemic damage, promotes recovery, reduces inflammation, and modulates protein expression, emphasising its potential as a therapeutic strategy for ischaemic stroke.

Inhibition of Phosphodiesterase 4 Suppresses Neuronal Ferroptosis After Cerebral Ischemia/Reperfusion.

We have previously shown that inhibition of phosphodiesterase 4 (PDE4) protects against cerebral ischemia/reperfusion injury. However, it remains unclear whether and how PDE4 affects ferroptosis under cerebral ischemia/reperfusion conditions. In this study, we found that overexpression of PDE4B in HT-22 cells exacerbated the detrimental effects of oxygen-glucose deprivation/reoxygenation (OGD/R), including a decrease in cell viability and glutathione (GSH) levels and an increase in Fe2+ content. PDE4B knockdown mitigated the effects of OGD/R, as evidenced by decreased oxidative stress, lactate dehydrogenase (LDH) release, Fe2+ content, and nuclear receptor coactivator 4 (NCOA4) expression. PDE4B knockdown also enhanced the levels of GSH, ferroportin (FPN), and ferritin heavy chain 1 (FTH1). Consistently, inhibition of PDE4 by roflumilast (Roflu) produced similar effects as PDE4B knockdown. Roflu also ameliorated the morphology and membrane potential of the mitochondria. Glutathione peroxidase 4 (GPX4) knockdown blocked the effects of Roflu on cell viability and lipid peroxidation. Moreover, we found that nuclear factor erythroid 2-related factor 2 (Nrf-2) knockdown decreased GPX4 expression. In addition, Nrf-2 knockdown led to enhanced lipid peroxidation, LDH release, and iron levels, while the GSH and FPN levels decreased. More crucially, PDE4 inhibition decreased infarct volume, alleviated oxidative stress, and restored the expression levels of ferroptosis-associated proteins in middle cerebral artery occlusion/reperfusion (MCAO/R) rats. Interestingly, the GPX4 inhibitor RSL3 blocked the neuroprotective effects of Roflu in rats subjected to MCAO/R. Thus, PDE4 inhibition significantly inhibits neuronal ferroptosis by activating the Nrf-2/GPX4 pathway. These data indicate the existence of a novel mechanism underlying the neuroprotective effects of PDE4 inhibition.

Maternal vascular indices at 36 weeks' gestation in pregnancy with small or growth-restricted fetus.

To compare maternal vascular indices and hemodynamic parameters at 35-37 weeks' gestation in pregnancies complicated by delivery of a small-for-gestational-age (SGA) or growth-restricted (FGR) neonate. This was a prospective observational study of women with a singleton pregnancy attending for a routine hospital visit at 35 + 0 to 36 + 6 weeks' gestation. The visit included recording of maternal demographic characteristics, medical history, vascular indices and hemodynamic parameters, which were obtained using a non-invasive operator-independent device and included pulse-wave velocity, augmentation index, cardiac output, stroke volume, central systolic and diastolic blood pressure, total peripheral resistance and heart rate. Women with hypertensive disorders of pregnancy were excluded. SGA was diagnosed if birth weight was < 10th percentile. FGR was diagnosed if, in addition to birth weight < 10th percentile, at the 35-37-week scan, uterine artery or umbilical artery pulsatility index (PI) was > 95th percentile or fetal middle cerebral artery PI was < 5th percentile. Among the 6413 women included in the study, there were 605 (9.4%) cases of SGA, 133 (2.1%) cases of FGR and 5675 (88.5%) cases that were unaffected by SGA or FGR. Women with SGA or FGR, compared to unaffected pregnancies, had increased peripheral vascular resistance and reduced cardiac output. Central systolic and diastolic blood pressure were increased in the FGR group compared with the unaffected group. Aortic stiffness, as assessed by pulse-wave velocity, and augmentation index did not differ between affected and unaffected pregnancies. In the FGR group, compared with the SGA group, central systolic and diastolic blood pressure were higher, whereas heart rate was lower. SGA and FGR pregnancies exhibit deranged maternal hemodynamic responses compared with unaffected pregnancies. Pregnancies with FGR have higher central blood pressure compared to those with SGA, but it remains unclear whether these differences are driven by the size of the fetus or pathological fetal growth. © 2024 International Society of Ultrasound in Obstetrics and Gynecology.

Aortic isthmus flow reversal in fetal coarctation of the aorta and the associated factors.

The aim of this study was to investigate the presence of aortic isthmus flow reversal and its associated factors in fetuses with positive and false-positive coarctation of the aorta (CoA) compared with normal controls. Pregnant women with fetuses suspected of CoA and normal control were enrolled, and these women experienced prenatal ultrasound scan and followed up for 6 months after birth to confirm the presence of CoA. All the ultrasound parameters were analyzed. A total of 134 pregnant women were enrolled, with 43 CoA-positive fetuses and 91 CoA false-positive fetuses, and 334 matched pregnant women were enrolled in the control group. Aortic isthmus flow reversal occurred in 28 (65.1%) fetuses in the CoA-positive group, significantly (p < 0.05) more than in the false-positive (37 or 40.7%) or control group (64 or 19.2%). Aortic isthmus flow reversal was mostly in the full systole (n = 17 or 60.7%) or late systole and early-middle diastole (n = 10 or 35.7%) in the CoA-positive fetuses (n = 27 or 96.4%), significantly (p < 0.001) different from that in the false-positive or control group. The aortic isthmus flow reversal peak systolic velocity (PSV), flow volume, and ratio of reversed flow/forward flow were significantly (p < 0.05) increased in the CoA-positive and false-positive groups than in the control group. The aortic isthmus flow reversal incidence was significantly (p < 0.05) correlated with the middle cerebral artery (MCA) PSV in the total three groups or in the false-positive group but was significantly (p < 0001) negatively correlated with the MCA resistance index (RI) in the CoA-positive group. The incidence of the aortic isthmus flow reversal was significantly (p < 0.05) positively correlated with the umbilical artery (UA) RI in the false-positive group and with the UA RI in the total three groups. Independently associated factors for aortic isthmus flow reversal were isthmic flow volume/CCO (combined cardiac output) in the CoA-positive group. Reversal of flow in the aortic isthmus is much more common in true-positive cases of CoA as compared to controls, and isthmic flow reversal in the full systolic phase only suggests presence of CoA. The aortic isthmic reversed flow volume accounts for over half of the isthmic forward flow volume in the CoA-positive fetuses than in the normal controls.

Intracranial bypass for giant aneurysms treatment assessed by computational fluid dynamics (CFD) analysis

Unruptured giant intracranial aneurysms (GIA) are those with diameters of 25 mm or greater. As aneurysm size is correlated with rupture risk, GIA natural history is poor. Parent artery occlusion or trapping plus bypass revascularization should be considered to encourage intra-aneurysmal thrombosis when other treatment options are contraindicated. The mechanistic background of these methods is poorly studied. Thus, we assessed the potential of computational fluid dynamics (CFD) and fluid–structure interaction (FSI) analyses for clinical use in the preoperative stage. A CFD investigation in three patient-specific flexible models of whole arterial brain circulation was performed. A C6 ICA segment GIA model was created based on CT angiography. Two models were then constructed that simulated a virtual bypass in combination with proximal GIA occlusion, but with differing middle cerebral artery (MCA) recipient vessels for the anastomosis. FSI and CFD investigations were performed in three models to assess changes in flow pattern and haemodynamic parameters alternations (wall shear stress (WSS), oscillatory shear index (OSI), maximal time averaged WSS (TAWSS), and pressure). General flow splitting across the entire domain was affected by virtual bypass procedures, and any deficiency was partially compensated by a specific configuration of the circle of Willis. Following the implementation of bypass procedures, a reduction in haemodynamic parameters was observed within the aneurysm in both cases under analysis. In the case of the temporal MCA branch bypass, the decreases in the studied parameters were slightly greater than in the frontal MCA branch bypass. The reduction in the magnitude of the chosen area-averaged parameters (averaged over the aneurysm wall surface) was as follows: WSS 35.7%, OSI 19.0%, TAWSS 94.7%, and pressure 24.2%. FSI CFD investigation based on patient-specific anatomy models with subsequent stimulation of virtual proximal aneurysm occlusion in conjunction with bypass showed that this method creates a pro-thrombotic favourable environment whilst reducing intra-aneurysmal pressure leading to shrinking. MCA branch recipient selection for optimum haemodynamic conditions should be evaluated individually in the preoperative stage.

A comparison of the effects of nifedipine and indomethacin used in preterm labor tocolytic treatment on feto-maternal Doppler ultrasonography flow.

To compare the effects of nifedipine and indomethacin, used for tocolytic purposes in the treatment of preterm labor (PTL), on fetal-maternal Doppler blood flows and perinatal outcomes. Eighty pregnant women between weeks 24 and 32 of gestation who used nifedipine (n = 40) and indomethacin (n = 40) as tocolytic treatments due to PTL were prospectively and consecutively included in the study. Sociodemographic, obstetric, and laboratory and Doppler flow parameters were compared between the groups. Statistically significant differences were observed between the groups in terms of gestational age at delivery and birth weight, Doppler flows (umbilical artery (UA) Pulsatility Index (PI), and UA Resistance Index (RI)) at 12, 24, and 48 h, middle cerebral artery RI at 12 h, and ductus venosus (DV) PI and DV-RI at 12, 24, and 48 h (p < 0.05). The findings of this study showed that nifedipine and indomethacin used in the treatment of PTL had significant effects on UA-PI and UA-RI Doppler flows at 12, 24, and 24 h, MCA-RI Doppler flows at 12 h, and DV-PI and DV-RI Doppler flows at 12, 24, and 48 h. Further studies involving larger numbers of participants are now needed to support these results.

Myxomatous cause of multiple intracranial aneurysms and cognitive decline: a case report

BackgroundThe occurrence of cerebral aneurysm in a case of cardiac myxoma is rare with less than 60 cases reported worldwide. The course of management is still debatable given its rarity. We present a case of multiple intracranial aneurysms secondary to atrial myxoma in a young lady with a brief review of the literature.Case presentationA young lady in her late 30s with a history of right middle cerebral artery territory stroke eight years ago presented with gradually progressive symptoms in the form of holocranial headache, inattention and forgetfulness for the last few years. On neuroimaging, she was found to have multi-territorial lacunar infarcts and multiple intracranial artery aneurysms which was confirmed with a digital subtraction angiogram. A cardiac evaluation revealed a left atrial myxoma. The aetiology of subcortical cognitive decline and intracranial aneurysms was attributed to the myxoma with secondary myxomatous embolism. Other secondary causes were ruled out. She is being followed up medically after resection of the myxoma.ConclusionIntracranial aneurysms are rare complications of cardiac myxoma which may present before, concurrent or many years after diagnosis of the myxoma. Nonspecific neurological complaints occasionally are the ominous signs of intracranial aneurysms which mandate a low threshold for neuroimaging in a case of cardiac myxoma. Given the absence of definitive risk factors and unclear natural history, clinical and radiological follow-ups are critical.Learning PointsIntracranial aneurysms are rare complications of cardiac myxoma that may present before, concurrent or many years after diagnosis of the myxoma.Special attention must be given to nonspecific neurological complaints with a low threshold for neuroimaging in those with a prior history of cardiac myxoma.Given the absence of definitive risk factors and unclear natural history, clinical and radiological follow-up including conventional angiography and/or magnetic resonance imaging is critical.

Phillygenin attenuates cell apoptosis and microglia activation in cerebral ischaemia-reperfusion rats through activation of peroxisome proliferator-activated receptor γ.

Ischaemic stroke is a common condition that can lead to cerebral ischaemia-reperfusion injury. Phillygenin (PHI), a natural bioactive compound derived from Forsythia suspensa, has been shown to play a crucial role in regulating inflammation across various diseases. However, its specific regulatory effects in ischaemic stroke progression remain unclear. In this study, we established a middle cerebral artery occlusion (MCAO) rat model. Treatment with PHI (50 or 100 mg/kg) significantly reduced cerebral infarction in MCAO rats. PHI treatment also mitigated the increased inflammatory response observed in these rats. Additionally, PHI suppressed microglial activation by reducing iNOS expression, a marker of M1-type polarization of microglia, and attenuated increased brain tissue apoptosis in MCAO rats. Furthermore, PHI's anti-inflammatory effects in MCAO rats were abrogated upon co-administration with GW9662, a peroxisome proliferator-activated receptor γ (PPARγ) inhibitor. In summary, PHI attenuated microglial activation and apoptosis in cerebral ischaemia-reperfusion injury through PPARγ activation, suggesting its potential as a therapeutic agent for mitigating cerebral ischaemia-reperfusion injury.

Age-related brain-region-specific changes in diffusion anisotropy in subarachnoid space of young adults

The glymphatic system theory postulates that brain waste is removed through the cerebrospinal fluid (CSF) flow. According to this theory, CSF in the subarachnoid space (SAS) moves to the perivascular space around the penetrating arteries, flows into parenchyma to mix with interstitial fluid and brain waste, and then moves to the perivenous space to be flushed out of the brain. Despite the controversies about the glymphatic theory, it is clear that SAS plays a key role in waste clearance. For instance, the SAS around the middle cerebral artery is known to be highly involved in glymphatic influx. While diffusion tensor imaging has been used for studying the glymphatic system, there has been limited exploration of age-related changes in diffusion anisotropy within SAS and their regional variations. Given the narrow and heterogeneous morphology of SAS, the fractional anisotropy (FA) in diverse brain regions may be more relevant to glymphatic transport than mean diffusivity (MD). The goal of this study was to investigate FA in SAS to observe age-related changes across different brain regions and to interpret the results based on the glymphatic transport. We segmented SAS in the whole brain of 83 young adults and divided SAS into four cortical lobes. We demonstrated regional variations in FA and MD within SAS and an age-related decline in FA among young adults, indicating that diffusion within SAS becomes more isotropic with aging. These findings raise new questions about the factors influencing diffusion anisotropy within SAS, which are relevant to glymphatic transport.

Inner Mitochondrial Membrane Peptidase 2-Like Deletion Aggravates Mitochondrial Apoptosis and Inhibits Autophagy After Hyperglycemia Stroke.

This study investigated the effects of inner mitochondrial membrane peptidase 2-like (Immp2l) deletion on mitochondrial apoptosis and mitochondrial autophagy under hyperglycemic conditions. The middle cerebral artery occlusion (MCAO) model was established in wild-type (WT) mice and Immp2l+/- mice; animals were then exposed to hyperglycemic (induced using 1% streptozotocin) and normoglycemic conditions. Tissues were collected at various time points post-reperfusion. The production of reactive oxygen species (ROS) was assessed by fluorescent measurements, and mitochondrial membrane potential was evaluated using a JC-1 assay kit. Autophagy was analyzed by measuring LC3II/LC3I protein expression and Beclin 1 expression. Mitochondrial ultrastructure was examined through transmission electron microscopy (TEM); neuronal autophagosomes were also assessed. Immp2l mutation in a hyperglycemic environment exacerbated brain injury by increasing ROS production, compromising mitochondrial membrane potential, inducing apoptotic cascades, and impairing mitochondrial autophagy. These findings highlight the critical role of Immp2l in modulating the response to hyperglycemic cerebral ischemia-reperfusion (I/R) injury. Furthermore, the deficiency of Immp2l appears to contribute to increased oxidative stress, mitochondrial dysfunction, and cell death, thereby exacerbating brain injury. These data may provide new insights into therapeutic strategies for reducing the impact of diabetes on stroke outcomes.

Predictive value of follow-up infarct volume on functional outcomes in middle cerebral artery M2 segment vessel occlusion stroke treated with mechanical thrombectomy.

Medium vessel occlusion (MeVO) strokes, particularly affecting the M2 segment of the middle cerebral artery, represent a critical proportion of acute ischemic strokes, posing significant challenges in management and outcome prediction. The efficacy of mechanical thrombectomy (MT) in MeVO stroke may warrant reliable predictors of functional outcomes. This study aimed to investigate the prognostic value of follow-up infarct volume (FIV) for predicting 90-day functional outcomes in MeVO stroke patients undergoing MT. This multicenter, retrospective cohort study analyzed data from the Multicenter Analysis of primary Distal medium vessel occlusions: effect of Mechanical Thrombectomy (MAD-MT) registry, covering patients with acute ischemic stroke due to M2 segment occlusion treated with MT. We examined the relationship between 90-day functional outcomes, measured by the modified Rankin Scale (mRS), and follow-up infarct volume (FIV), assessed through CT or MRI within 12-36 h post-MT. Among 130 participants, specific FIV thresholds were identified with high specificity and sensitivity for predicting outcomes. A FIV ⩽5 ml was highly specific for predicting favorable and excellent outcomes. The optimal cut-off for both prognostications was identified at ⩽15 ml by the Youden Index, with significant reductions in the likelihood of favorable outcomes observed above a 40 ml threshold. Receiver Operator Curve (ROC) analyses confirmed FIV as a superior predictor of functional outcomes compared to traditional recanalization scores, such as final modified thrombolysis in cerebral infarction score (mTICI). Multivariable analysis further highlighted the inverse relationship between FIV and positive functional outcomes. FIV within 36 h post-MT serves as a potent predictor of 90-day functional outcomes in patients with M2 segment MeVO strokes. Establishing FIV thresholds may aid in the prognostication of stroke outcomes, suggesting a role for FIV in guiding post intervention treatment decisions and informing clinical practice. Future research should focus on validating these findings across diverse patient populations and exploring the integration of FIV measurements with other clinical and imaging markers to enhance outcome prediction accuracy.

Acute nicotine exposure attenuates neurological deficits, ischemic injury and brain inflammatory responses and restores hippocampal long-term potentiation in ischemic stroke followed by lipopolysaccharide-induced sepsis-like state

Ischemic stroke is followed by an increased susceptibility to bacterial infections, which exacerbate histological stroke outcome, neurological deficits and memory impairment due to increased neuroinflammation and neurotransmitter dysfunction. Pharmacological activation of nicotinic acetylcholine receptors was suggested to mitigate brain inflammatory responses in ischemic stroke. The functional responses associated with nicotinic acetylcholine receptor activation were unknown. In this study, male NMRI mice subjected to transient intraluminal middle cerebral artery occlusion (MCAO) were intraperitoneally exposed to vehicle treatment or Escherichia coli lipopolysaccharide (LPS; 4 mg/kg)-induced sepsis-like state 24 h post-MCAO, followed by intraperitoneal administration of vehicle or nicotine (0.5 mg/kg) 30 min later. Over 96 h, rectal temperature, neurological deficits, spontaneous locomotor activity, working memory, ischemic injury, synaptic plasticity, and brain inflammatory responses were evaluated by temperature measurement, behavioral analysis, infarct volumetry, electrophysiological recordings, and polymerase-chain reaction analysis. LPS-induced sepsis induced hypothermia, increased general and focal neurological deficits, reduced spontaneous exploration behavior, reduced working memory, and increased infarct volume post-MCAO. Additional treatment with nicotine attenuated LPS-induced hypothermia, reduced neurological deficits, restored exploration behavior, restored working memory, and reduced infarct volume. Local field potential recordings revealed that LPS-induced sepsis decreased long-term potentiation (LTP) in the dentate gyrus post-MCAO, whereas concomitant nicotine exposure restored LTP in the contralateral dentate gyrus. LPS-induced sepsis increased microglial/ macrophage Iba-1 mRNA and astrocytic GFAP mRNA levels post-MCAO, whereas add-on nicotine treatment reduced astrocytic GFAP mRNA. Taken together, these findings indicate that acute nicotine exposure enhances functional stroke recovery. Future studies will have to evaluate the effects of (1) chronic nicotine exposure, a clinically relevant vascular risk factor, and (2) the cessation of nicotine exposure, which is widely recommended post-stroke, but might have detrimental effects in the early stroke recovery phase.

Exploring arterial anatomy of the internal capsule: an analysis of the deep vascular structures and related white matter pathways.

The internal capsule is supplied by perforators originating from the internal carotid artery, middle cerebral artery, anterior choroidal artery and anterior cerebral artery. The aim of this study is to examine the vascular anatomy of the internal capsule, along with its related white matter anatomy, in order to prevent potential risks and complications during surgical interventions. Twenty injected hemispheres prepared according to the Klingler method were dissected. Dissections were photographed at each stage. The findings obtained from the dissections were illustrated to make them more understandable. Additionally, the origins of the arteries involved in the vascularization of the internal capsule, their distances to bifurcations, and variations in supplying territories have been thoroughly examined. The insular cortex and the branches of the middle cerebral artery on the insula and operculum were observed. Following decortication of the insular cortex, the extreme capsule, claustrum, external capsule, putamen and globus pallidus structures were exposed. The internal capsule is shown together with the lenticulostriate arteries running on the anterior, genu and posterior limbs. Perforators supplying the internal capsule originated from the middle cerebral artery, anterior cerebral artery, internal carotid artery and anterior choroidal artery. The internal capsule's vascular supply varied, with the medial lenticulostriate arteries (MLA) and lateral lenticulostriate arteries (LLA) being the primary arteries. The anterior limb was most often supplied by the MLA, while the LLA and anterior choroidal artery dominated the genu and posterior limb. The recurrent artery of Heubner originated mostly from the A2 segment. The distance from the ICA bifurcation to the origin of the first LLA on M1 is 9.55 ± 2.32mm, and to the first MLA on A1 is 5.35 ± 1.84mm. MLA branching from A1 and proximal A2 ranged from 5 to 9, while LLA originating from the MCA ranged from 7 to 12. This study provides comprehensive understanding of the arterial supply to the internal capsule by combining white matter dissection. The insights gained from this study can help surgeons plan and execute procedures including oncological, psychosurgical, and vascular more accurately and safely. The illustrations derived from the dissections serve as valuable educational material for young neurosurgeons and other medical professionals.

B - 8 Preemie-Pediatric Left Middle Cerebral Arterial Cerebrovascular Accident and Comorbid Focal Left Central Epilepsy: a Case Study

Abstract Objective Literature regarding neurocognitive functioning in pediatric middle cerebral arterial (MCA) is limited. The aim of this study was to enhance the field’s knowledge and understanding of the presentation and impact of preemie-pediatric left MCA in utero with comorbid left-brain epilepsy in overall neurocognitive and behavioral functioning. Method The subject is a 12-year-old left-handed male with history of previously described events. The purpose of this evaluation was to determine current levels of neurocognitive and behavioral functioning as it relates to his medical history, treatment planning, and prognosis. Data collection was part of a pre-surgical consult to reduce epileptic activity. Results Results suggest overall cognitive functioning fell within the average range. However, relative difficulties in areas of attention and executive functioning were indicated. While all other domains were grossly intact, his profile indicates strengths in visual compared to verbal memory. Interestingly, the patient performed better on verbal tasks after a delay both with and without cuing. This suggests the presentation of a unique trait of pediatric epilepsy in that due to slowed processing speed as seen on the WISC, this patient is likely to remember more information over time. His academic achievements also fell within age-expectations. Conclusions This study impresses the importance of prompt neuropsychological evaluation in providing insight to the patient’s impairments and contribute to adaptive neurocognitive functioning moving forward. While idiopathic, this case demonstrates the need for continued research in pediatric-infantile infarct and provides the opportunity to improve the field’s understanding of the interpretation of similar cases.

Do changes in cerebral blood flow modulate the amplitudes of P300 during cognitive task?

A single session of aerobic or resistance training transiently enhances cognitive function, making it a valuable strategy for dementia prevention in the older people. Despite its acknowledged benefits, the precise mechanism behind exercise-induced cognitive improvement remains controversial. In the present study, we investigated the impact of altered cerebral blood flow (CBF) on brain neural activity originating from motor executive and inhibitory processing using electroencephalographic event-related potentials (EEG-ERPs). Sixteen healthy subjects participated in four sessions, with EEG-ERPs measured during somatosensory Go/No-go tasks. The sessions were conducted under four distinct respiratory conditions presented in random order: normal breathing (NB) and rapid breathing (RB) with room air, normal breathing with hypercapnic gas (5% CO2, 21% O2, and balanced N2) (NB+Gas), and rapid breathing with the same gas (RB+Gas). Changes in CBF were evaluated based on the middle cerebral artery mean blood velocity (MCA Vmean) using transcranial Doppler. PETCO2 was decreased under the RB condition but increased under the NB+Gas condition, thereby decreasing and increasing MCA Vmean, respectively. Under the NB+Gas condition, MCA Vmean significantly increased, but it had no effect on either the executive or inhibitory function. In contrast, the reduction in MCA Vmean induced by RB decreased the peak amplitudes of Go-P300 and No-go-P300. However, even under the RB+Gas condition while MCA Vmean increased, the peak amplitudes of both also decreased. These findings suggest that neither increases nor decreases in CBF affected cognitive function.

Evaluation of Middle Cerebral Artery Culprit Plaque Inflammation in Ischemic Stroke Using CAIPIRINHA-Dixon-TWIST Dynamic Contrast-Enhanced Magnetic Resonance Imaging.

Middle cerebral artery (MCA) plaques are a leading cause of ischemic stroke (IS). Plaque inflammation is crucial for plaque stability and urgently needs quantitative detection. To explore the utility of Controlled Aliasing in Parallel Imaging Results in Higher Acceleration (CAIPIRINHA)-Dixon-Time-resolved angiography With Interleaved Stochastic Trajectories (TWIST) (CDT) dynamic contrast-enhanced MRI (DCE-MRI) for evaluating MCA culprit plaque inflammation changes over stroke time and with diabetes mellitus (DM). Prospective. Ninety-four patients (51.6 ± 12.23 years, 32 females, 23 DM) with acute IS (AIS; N = 43) and non-acute IS (non-AIS; 14 days < stroke time ≤ 3 months; N = 51). 3-T, CDT DCE-MRI and three-dimensional (3D) Sampling Perfection with Application optimized Contrast using different flip angle Evolution (3D-SPACE) T1-weighted imaging (T1WI). Stroke time (from initial IS symptoms to MRI) and DM were registered. For 94 MCA culprit plaques, Ktrans from CDT DCE-MRI and enhancement ratio (ER) from 3D-SPACE T1WI were compared between groups with and without AIS and DM. Shapiro-Wilk test, Bland-Altman analysis, Passing and Bablok test, independent t-test, Mann-Whitney U test, Chi-squared test, Fisher's exact test, receiver operating characteristics (ROC) with the area under the curve (AUC), DeLong's test, and Spearman rank correlation test with the P-value significance level of 0.05. Ktrans and ER of MCA culprit plaques were significantly higher in AIS than non-AIS patients (Ktrans = 0.098 s-1 vs. 0.037 s-1; ER = 0.86 vs. 0.55). Ktrans showed better AUC for distinguishing AIS from non-AIS patients (0.87 vs. 0.75) and stronger negative correlation with stroke time than ER (r = -0.60 vs. -0.34). DM patients had significantly higher Ktrans and ER than non-DM patients in IS and AIS groups. Imaging by CDT DCE-MRI may allow to quantitatively evaluate MCA culprit plaques over stroke time and DM. 2 TECHNICAL EFFICACY: Stage 2.