Muscle mass as a modifier of stress response in acute ischemic stroke patients.

Stroke triggers a systemic inflammatory response over the ensuing days after the cerebral insult. The age and comorbidities of the stroke population make them a vulnerable population for low muscle mass and sarcopenia, the latter being another clinical condition that is closely associated with inflammation, as shown by increased levels of pro-inflammatory biomarkers, including neutrophil-to-lymphocyte ratio (NLR). In this study, we evaluated the relationship between post-stroke NLR changes and muscle mass in a prospective cohort of acute ischemic stroke patients (n = 102) enrolled in the Muscle Assessment in Stroke Study Turkey (MASS-TR). Admission lumbar computed tomography images were used to determine the cross-sectional muscle area of skeletal muscles at L3 vertebra level and calculate the skeletal muscle index (SMI). The median (IQR) SMI was 44.7 (39.1-52.5) cm2/m2, and the NLR at admission and follow-up were 4.2 (3.0-10.5) and 9.4 (5.7-16.2), respectively. While there was no relationship between SMI and admission NLR, a significant inverse correlation was observed between SMI and follow-up NLR (r = - 0.26; P = 0.007). Lower SMI remained significantly associated (P = 0.036) with higher follow-up NLR levels in multivariate analysis. Our findings highlight the importance of muscle mass as a novel factor related to the level of post-stroke stress response.

Carotid Artery Perivascular Adipose Tissue Density and Response to Intravenous Tissue Plasminogen Activator in Acute Ischemic Stroke.

The importance of Carotid Artery Perivascular Adipose Tissue Density (CAPATd), a parameter that can be readily evaluated on emergency computed tomographic angiography (CTA), in acute stroke has not been adequately clarified. We created exploratory logistic regression models to detect the interaction between the effect of CAPATd and intravenous (IV) tissue plasminogen activator (tPA) in 174 patients (mean age 71 ± 14 years, 94 women) with acute ischemic stroke treated with IV-tPA alone. The CAPATd-average mean (-60.6 ± 18.7 vs -89.8 ± 25.3 Hounsfield units (HU), P = .002) and CAPATd-maximum (14.8 ± 68.9 vs -20.5 ± 39.8 HU, P = .020) values were higher on the ipsilateral side of carotid artery stenosis >60%. CAPATd-maximum ipsilateral emerged as an independent predictor for both modified Rankin's Score 0-2 (52%) [exp(ß) = .984] and mRS 0-1 outcome (32%) [exp(ß) = .828] in addition to admission National Institutes of Health Stroke Scale, age and carotid plaque burden. CAPATd-maximum ipsilateral was acceptably accurate (Area under the Receiver operating characteristic Curve was .607, P = .0109 for mRS 0-2 and .613, P = .0102 for mRS 0-1). Ipsilateral CAPATd ≥ -25 HU predicted both mRS >3 and mRS >2 with usable sensitivity (59.8% and 66.07%) and specificity (63.6% and 59.68%). In conclusion, higher maximum CAPATd measured on emergency CTA indicates poorer functional prognosis in acute stroke patients treated with IV-tPA.

Hybrid PET/MRI with Flutemetamol and FDG in Alzheimer's Disease Clinical Continuum.

AIMS: We aimed to investigate the interaction between ß -amyloid (Aß) accumulation and cerebral glucose metabolism, cerebral perfusion, and cerebral structural changes in the Alzheimer's disease (AD) clinical continuum. BACKGROUND: Utility of positron emission tomography (PET) / magnetic resonance imaging (MRI) hybrid imaging for diagnostic categorization of the AD clinical continuum including subjective cognitive decline (SCD), amnestic mild cognitive impairment (aMCI) and Alzheimer's disease dementia (ADD) has not been fully crystallized. OBJECTIVE: To evaluate the interaction between Aß accumulation and cerebral glucose metabolism, cerebral perfusion, and cerebral structural changes such as cortex thickness or cerebral white matter disease burden and to detect the discriminative yields of these imaging modalities in the AD clinical continuum. METHODS: Fifty patients (20 women and 30 men; median age: 64 years) with clinical SCD (n=11), aMCI (n=17) and ADD (n=22) underwent PET/MRI with [18F]-fluoro-D-glucose (FDG) and [18F]- Flutemetamol in addition to cerebral blood flow (CBF) and quantitative structural imaging along with detailed cognitive assessment. RESULTS: High Aß deposition (increased temporal [18F]-Flutemetamol standardized uptake value ratio (SUVr) and centiloid score), low glucose metabolism (decreased temporal lobe and posterior cingulate [18F]-FDG SUVr), low parietal CBF and right hemispheric cortical thickness were independent predictors of low cognitive test performance. CONCLUSION: Integrated use of structural, metabolic, molecular (Aß) and perfusion (CBF) parameters contribute to the discrimination of SCD, aMCI, and ADD.

Vagus Nerve Stimulation in Ischemic Stroke.

PURPOSE OF REVIEW: Vagus nerve stimulation (VNS) has emerged as a potential therapeutic approach for neurological and psychiatric disorders. In recent years, there has been increasing interest in VNS for treating ischemic stroke. This review discusses the evidence supporting VNS as a treatment option for ischemic stroke and elucidates its underlying mechanisms. RECENT FINDINGS: Preclinical studies investigating VNS in stroke models have shown reduced infarct volumes and improved neurological deficits. Additionally, VNS has been found to reduce reperfusion injury. VNS may promote neuroprotection by reducing inflammation, enhancing cerebral blood flow, and modulating the release of neurotransmitters. Additionally, VNS may stimulate neuroplasticity, thereby facilitating post-stroke recovery. The Food and Drug Administration has approved invasive VNS (iVNS) combined with rehabilitation for ischemic stroke patients with moderate to severe upper limb deficits. However, iVNS is not feasible in acute stroke due to its time-sensitive nature. Non-invasive VNS (nVNS) may be an alternative approach for treating ischemic stroke. While the evidence from preclinical studies and clinical trials of nVNS is promising, the mechanisms through which VNS exerts its beneficial effects on ischemic stroke are still being elucidated. Therefore, further research is needed to better understand the efficacy and underlying mechanisms of nVNS in ischemic stroke. Moreover, large-scale randomized clinical trials are necessary to determine the optimal nVNS protocols, assess its long-term effects on stroke recovery and outcomes, and identify the potential benefits of combining nVNS with other rehabilitation strategies.

Stroke-Related Visceral Alterations: A Voxel-Based Neuroanatomic Localization Study.

OBJECTIVE: Functional and morphologic changes in extracranial organs can occur after acute brain injury. The neuroanatomic correlates of such changes are not fully known. Herein, we tested the hypothesis that brain infarcts are associated with cardiac and systemic abnormalities (CSAs) in a regionally specific manner. METHODS: We generated voxelwise p value maps of brain infarcts for poststroke plasma cardiac troponin T (cTnT) elevation, QTc prolongation, in-hospital infection, and acute stress hyperglycemia (ASH) in 1,208 acute ischemic stroke patients prospectively recruited into the Heart-Brain Interactions Study. We examined the relationship between infarct location and CSAs using a permutation-based approach and identified clusters of contiguous voxels associated with p < 0.05. RESULTS: cTnT elevation not attributable to a known cardiac reason was detected in 5.5%, QTc prolongation in the absence of a known provoker in 21.2%, ASH in 33.9%, and poststroke infection in 13.6%. We identified significant, spatially segregated voxel clusters for each CSA. The clusters for troponin elevation and QTc prolongation mapped to the right hemisphere. There were 3 clusters for ASH, the largest of which was in the left hemisphere. We found 2 clusters for poststroke infection, one associated with pneumonia in the left and one with urinary tract infection in the right hemisphere. The relationship between infarct location and CSAs persisted after adjusting for infarct volume. INTERPRETATION: Our results show that there are discrete regions of brain infarcts associated with CSAs. This information could be used to bootstrap toward new markers for better differentiation between neurogenic and non-neurogenic mechanisms of poststroke CSAs. ANN NEUROL 2023;94:1155-1163.

Impact of Cerebral Microbleeds in Stroke Patients with Atrial Fibrillation.

OBJECTIVES: Cerebral microbleeds are associated with the risks of ischemic stroke and intracranial hemorrhage, causing clinical dilemmas for antithrombotic treatment decisions. We aimed to evaluate the risks of intracranial hemorrhage and ischemic stroke associated with microbleeds in patients with atrial fibrillation treated with vitamin K antagonists, direct oral anticoagulants, antiplatelets, and combination therapy (i.e. concurrent oral anticoagulant and antiplatelet). METHODS: We included patients with documented atrial fibrillation from the pooled individual patient data analysis by the Microbleeds International Collaborative Network. Risks of subsequent intracranial hemorrhage and ischemic stroke were compared between patients with and without microbleeds, stratified by antithrombotic use. RESULTS: A total of 7,839 patients were included. The presence of microbleeds was associated with an increased relative risk of intracranial hemorrhage (adjusted hazard ratio [aHR] = 2.74, 95% confidence interval = 1.76-4.26) and ischemic stroke (aHR = 1.29, 95% confidence interval = 1.04-1.59). For the entire cohort, the absolute incidence of ischemic stroke was higher than intracranial hemorrhage regardless of microbleed burden. However, for the subgroup of patients taking combination of anticoagulant and antiplatelet therapy, the absolute risk of intracranial hemorrhage exceeded that of ischemic stroke in those with 2 to 4 microbleeds (25 vs 12 per 1,000 patient-years) and ≥ 11 microbleeds (94 vs 48 per 1,000 patient-years). INTERPRETATION: Patients with atrial fibrillation and high burden of microbleeds receiving combination therapy have a tendency of higher rate of intracranial hemorrhage than ischemic stroke, with potential for net harm. Further studies are needed to help optimize stroke preventive strategies in this high-risk group. ANN NEUROL 2023;94:61-74.

Acute stroke in familial Mediterranean fever: An analysis of 23 new cases and systematic review of the literature.

OBJECTIVE: The nature of neurovascular involvement in cases of familial Mediterranean fever (FMF) has not been adequately clarified. METHODS AND PATIENTS: Clinical features, infarct topography, vascular status, and stroke etiology were prospectively determined in 35 acute neurovascular events that occurred in 23 FMF patients. Clinicoradiological features were compared with an age- and gender-matched control group of 115 acute stroke patients. Characteristics of additional FMF and acute stroke cases (6 episodes in 6 patients) identified from a systematic literature review (PROSPERO registration no: CRD420212264820) were also analyzed. RESULTS: There were 27 acute ischemic stroke episodes in 19 patients, 7 transient ischemic attack episodes in 3 patients, and 1 patient with a single episode of parietal hematoma in our cohort. Twenty (74%) ischemic stroke episodes in 12 patients were cryptogenic. Ten of these 12 cases had a previous FMF diagnosis and were taking colchicine. There was no significant difference in the FMF group in terms of the presence of vascular risk factors and angiography-documented disease in comparison to controls. Cerebral distal artery involvement was significantly prevalent in FMF (78% vs 45%, P = .002). Especially, midbrain central deep perforating territory involvement was higher (30% vs 1%, P < .001). The long-term prognosis (median 8.5 years) under antiplatelet agents and colchicine is favorable. DISCUSSION: The acute stroke phenotype in FMF cases is herein described for the first time. Several clinicoradiological features such as thrombotic lacunar infarcts located in the central mesencephalon seem so typical that we recommend searching for FMF mutations in geographic regions where FMF is common.

Determinants of in-hospital muscle loss in acute ischemic stroke - Results of the Muscle Assessment in Stroke Study (MASS).

BACKGROUND & AIMS: There is a change in the mass and composition of paretic and non-paretic skeletal muscles in the chronic phase of stroke. The multi-center, prospective, and observational Muscle Assessment in Stroke Study (MASS) was performed to evaluate the degree of muscle loss during the in-hospital acute stroke setting and determine factors contributing to this loss. METHODS: Acute dysphagic ischemic stroke patients (n = 107) admitted to neuro-intensive care units were evaluated by computed tomography on days 1 and 14 after admission to determine the cross-sectional muscle area (CSMA) at the level of the mid-humerus, mid-thigh, and third lumbar vertebra. The percentage change in CSMA and variables associated with this change were evaluated by univariate and multivariate analyses. RESULTS: There were significant reductions in CSMA in all the muscle groups analyzed; the most prominent change was observed in the arms (both: 14.2 ± 10.7%; paretic: 17.7 ± 11.6%; non-paretic: 10.1 ± 12.5%), followed by the muscles in the legs (both: 12.4 ± 8.7%; paretic: 12.9 ± 9.9%; non-paretic: 12.0 ± 9.3%) and L3-vertebra level (5.6 ± 9.8%) (P < 0.001 for all). Higher calorie (r = -0.378, P < 0.001) or protein (r = -0.352, P < 0.001) intake was negatively associated with the decrease in CSMA of upper extremities. A substantial protein (≥0.4 g/kg/d) or calorie (≥5 kcal/kg/d) gap between targeted or actual intake was related to a larger decrease in CSMA in all the anatomic regions (P ≤ 0.05 for all). Other significant predictors of muscle loss included history of diabetes mellitus, male sex, higher BMI, in-hospital infections, and the necessity for invasive mechanical ventilation. CONCLUSIONS: There is a considerable degree of loss in the global muscle mass in acute ischemic stroke patients over a two-week period. Along with several factors, falling significantly behind the daily protein or calorie targets was related to the decrease in the muscle area. TRIAL REGISTRATION INFORMATION: clinicaltrials.gov identifier NCT03825419.

Clinical pharmacist's contribution to treatment adherence and quality of life in patients with stroke.

PRIMARY OBJECTIVE: The optimal treatment adherence rate among patients with stroke is low. This study aims to determine the effect of clinical pharmacists' intervention on treatment adherence and quality of life (QOL) in patients with first-ever stroke. RESEARCH DESIGN: This open, controlled, prospective and interventional study was conducted sequentially at two different university hospitals for 3 months. Patients in the intervention group (IG) were provided with clinical pharmacist-led education whereas the control group (CG) only received routine care. METHODS AND PROCEDURES: Treatment adherence and QOL were assessed on discharge day, and in months 1 and 3 after discharge. Morisky Green Levine Adherence Scale and Stroke Specific Quality of Life Scale were employed to evaluate treatment adherence and QOL, respectively. MAIN OUTCOMES AND RESULTS: Changes in treatment adherence score were higher between discharge day, 1st and 3rd months after discharge in IG than CG (p < 0.001). Regarding 'energy' and 'work/productivity' domains, patients' scores in IG were higher than those from CG at months 1 and 3 after discharge (p < 0.05). CONCLUSION: Clinical pharmacist-led education improves treatment adherence in patients with first-ever stroke. The clinical pharmacist might be integrated into the multidisciplinary team to improve QOL and treatment adherence.

Cerebral vasomotor reactivity across the continuum of subjective cognitive impairment, amnestic mild cognitive impairment and probable Alzheimer's dementia: A transcranial Doppler and PET/MRI study.

Cerebrovascular dysfunction has been suggested as a physiomarker of Alzheimer's disease (AD)-associated neuronal degeneration, but the underlying mechanisms are still debated. Herein cerebral vasomotor reactivity (VMR, breath-hold index: BHI), metabolic activity (lobar SUVs, FDG PET MRI), amyloid load (Centiloid score, Flutemetamol PET MRI), hemispheric cortical thickness, white matter lesion load and cerebral blood flow (ASL) were studied in 43 consecutive subjects (mean age: 64 years, female 13), diagnosed with subjective cognitive impairment (SCI, n = 10), amnestic mild cognitive impairment (aMCI, n = 15), and probable Alzheimer's dementia (AD, n = 18). BHI was significantly reduced in AD and aMCI patients compared to SCI subjects. A highly significant inverse correlation was found between BHI and the centiloid score (r = -0.648, p < 0.001). There was moderate positive correlation between BHI and frontal, temporal and parietal FDG SUV and ASL values, and a borderline negative correlation with age and white matter lesion volume. The link between amyloid burden and VMR was independent and strong in linear regression models where all these parameters were included (ß from -0.580 to -0.476, p < 0.001). In conclusion, our study confirms the negative association of cerebral amyloid accumulation and vasomotor reactivity in Alzheimer's disease with the most direct data to date in humans.

Admission chest CT findings and risk assessment for stroke-associated pneumonia.

INTRODUCTION: Stroke-associated pneumonia (SAP) is a significant cause of morbidity and mortality after stroke. Various factors, including dysphagia and stroke severity, are closely related to SAP risk; however, the contribution of the baseline pulmonary parenchymal status to this interplay is an understudied field. Herein, we evaluated the prognostic performance of admission chest computed tomography (CT) findings in predicting SAP. METHODS: We evaluated admission chest CT images, acquired as part of a COVID-19-related institutional policy, in a consecutive series of acute ischemic stroke patients. The pulmonary opacity load at baseline was quantified using automated volumetry and visual scoring algorithms. The relationship between pulmonary opacities with risk of pneumonia within 7 days of symptom onset (i.e., SAP) was evaluated by bivariate and multivariate analyses. RESULTS: Twenty-three percent of patients in our cohort (n = 100) were diagnosed with SAP. Patients with SAP were more likely to have atrial fibrillation, COPD, severe neurological deficits, and dysphagia. The visual opacity score on chest CT was significantly higher among patients who developed SAP (p = 0.014), while no such relationship was observed in terms of absolute or relative opacity volume. In multivariate analyses, admission stroke severity, presence of dysphagia and a visual opacity score of ≥ 3 (OR 6.37, 95% CI 1.61-25.16; p = 0.008) remained significantly associated with SAP risk. CONCLUSIONS: Pulmonary opacity burden, as evaluated on admission chest CT, is significantly associated with development of pneumonia within initial days of stroke. This association is independent of other well-known predisposing factors for SAP, including age, stroke severity, and presence of dysphagia.

Frequency and Types of Complications Encountered in Patients With Nonconvulsive Status Epilepticus in the Neurological ICU: Impact on Outcome.

Objectives. The frequency and types of complications in patients with nonconvulsive status epilepticus (NCSE) who are followed up in the intensive care unit (ICU), and the impact of these complications on outcome are not well-known. We investigated the complications and their effects on prognosis in NCSE patients. Methods. After reviewing the video-EEG monitoring (VEEGM) reports of all the consecutive patients who were followed up in our ICU between 2009 and 2019, we identified two groups of patients: 1-patients with NCSE (study group) and 2-patients who underwent VEEGM for possible NCSE but did not have ictal recordings (no-NCSE group). Electronic health records were reviewed to identify demographic and clinical data, duration of ICU care, medical and surgical complications, pharmacologic treatment, and outcome. These parameters were compared statistically between the groups. We also investigated the parameters affecting prognosis at discharge. Results. Thirty-two patients with NCSE comprised the study group. Infection developed in 84%. More than half were intubated, had tracheostomy or percutaneous endoscopic gastrostomy application. Refractory NCSE was associated with significantly more frequent complications and worse outcome. There was a higher tendency of infections in the study group (P = .059). Higher organ failure scores and prolonged stay in ICU predicted worse outcome (P < .05). Conclusion. The frequency of complications in patients with NCSE who are cared for in the ICU is considerable. Most of the complications are similar to the other patients in ICU, except for the higher frequency of infections. Increased physician awareness about modifiable parameters and timely interventions might help improve prognosis.

Assessment of safety and feasibility of non-invasive vagus nerve stimulation for treatment of acute stroke.

BACKGROUND: Non-invasive vagus nerve stimulation (nVNS) using a hand-held stimulator placed on the neck is an FDA-approved treatment for primary headache disorders. The safety of nVNS is unknown in stroke patients. OBJECTIVE: To assess the safety and feasibility of nVNS for the acute treatment of stroke. METHODS: TR-VENUS (clinicaltrials.gov identifier NCT03733431) was a randomized, sham-controlled, open-label, multicenter trial conducted in patients with acute ischemic stroke (IS) or intracerebral hemorrhage (ICH). Patients were randomly assigned to standard-dose nVNS, high-dose nVNS, or sham stimulation. The primary endpoint was a composite safety outcome defined as bradycardia or reduction in mean arterial blood pressure during treatment or progression of neurological or death within 24 h of treatment. The feasibility endpoints were the proportion of eligible subjects receiving nVNS within 6 h of symptom onset and the proportion completing all pre-specified treatment doses. Efficacy assessments included infarct growth from baseline to 24 h after treatment. RESULTS: Sixty-nine patients (61 IS, 8 ICH) completed the study. The composite safety outcome was achieved in 32.0% in sham and 47.7% in nVNS group (p = 0.203). Treatment was initiated in all but two randomized patients. All dosed subjects received 100% of prespecified stimulations. A non-significant reduction in infarct growth was observed in the high-dose nVNS group (184.2% in sham vs. 63.3% in high-dose nVNS; p = 0.109). CONCLUSIONS: The results of this study suggest that nVNS may be safe and feasible in the setting of acute stroke. These findings support further development of nVNS as a potential treatment for acute ischemic stroke.

Multimodal assessment of intensive care unit-acquired weakness in severe stroke patients.

BACKGROUND: Intensive care unit-acquired weakness (ICUAW) defines generalized muscle weakness seen in critically ill patients in the absence of other causative factors. Herein, we aimed to evaluate ICUAW in stroke patients by electrodiagnostic testing, histopathology, and assessment of respiratory complex activities (RCA), to define the frequency of ICUAW in this patient group, and to reach new parameters for early prediction and diagnosis. METHODS: We prospectively recruited twenty-four severe acute stroke patients during a sixteen-month period. In addition to serial nerve conduction studies (NCS), we performed muscle biopsy and RCA analysis on the non-paretic side when ICUAW developed. Patients undergoing orthopedic surgery without metabolic and neuromuscular diseases constituted the control group for RCA. Survival and longitudinal data were analyzed by joint modeling to determine the relationship between electrophysiological parameters and ICUAW diagnosis. RESULTS: Eight patients (33%) developed ICUAW, and six of them within the first two weeks. Extensor digitorum brevis, abductor digiti minimi (ADM), rectus femoris and vastus medialis (VM) compound muscle action potential (CMAP) amplitudes showed a significant decrease in the ICUAW group. VM CMAP amplitude (BIC = 358.1574) and ADM CMAP duration (BIC = 361.1028) were the best-correlated parameters with ICUAW diagnosis. The most informative electrophysiological findings during the entire study were obtained within the first 11 days. Muscle biopsies revealed varying degrees of type 2 fiber atrophy. Complex I (p = 0.003) and IV (p = 0.018) activities decreased in patients with ICUAW compared to controls. CONCLUSION: VM CMAP amplitude and ADM CMAP duration correlate well with ICUAW diagnosis, and may aid in the early diagnosis.

The Role of Non-Vitamin K Antagonist Oral Anticoagulants (NOACs) in Atrial Fibrillation: Treatment Management Based on Patient and Drug Characteristics.

Data from Turkey revealed that atrial fibrillation patient percentage under adequate anti- coagulation in Turkey is less than that in other countries due to multiple parameters such as treatment adherence problems, failure to follow guideline recommendations, negative perspective on the use of new drugs, drug costs, and payment conditions. The aim of this article is to provide physicians with a compiled resource that focuses on the differences between non-vitamin K antagonist oral anticoagulants and heterogeneity of atrial fibrilla- tion patients by reviewing the global and national data from a multidisciplinary perspective and provide guidance on the choice of non-vitamin K antagonist oral anticoagulants in atrial fibrillation patients. A gastroenterologist, 2 neurologists, and 11 cardiologists from university and training and research hospitals in Turkey who are experienced in atrial fibrillation and non-vitamin K antagonist oral anticoagulant treatments gathered in 3 separate meetings to identify the review topics and evaluate the outcomes of the systematic literature search. Based on the pharmacological characteristics, clinical studies, and real-world data compari- sons, it has been revealed that non-vitamin K antagonist oral anticoagulants are not similar. Thromboembolism and bleeding risks, renal and hepatic functions, coexisting conditions, and concomitant drug usage have been shown to affect the levels of benefits gained from non-vitamin K antagonist oral anticoagulant in atrial fibrillation patients. Although Turkish patients with atrial fibrillation have been observed to be younger, they are more likely to have coexisting cardiovascular conditions compared to the atrial fibrillation patients in other countries. Selection of an appropriate non-vitamin K antagonist oral anticoagulant in line with the available evidence and recent guidelines will provide substantial benefits to atrial fibrillation patients.

Comparison of early- and late-phase CT angiography findings in brain death.

BACKGROUND: Late-phase images on computed tomography angiography (CTA), traditionally used for assessing cerebral circulatory arrest in brain death, suffer from suboptimal diagnostic yield due to stasis filling. Herein, we assessed contrast filling in individual intracranial arteries and veins in the early and late phases of CTA in patients with clinically confirmed brain death. METHODS: Contrast opacification within 28 arterial/venous segments was evaluated in both phases of CTA in 79 patients. This information was combined with reports in the literature to calculate prevalence of contrast filling in different intracranial vessels. Additionally, diagnostic sensitivity of 4-point, 7-point, and 10-point scores defined for brain death were compared among ratings based on early, late, and both phases (arteries rated on early, veins rated on late phase) of imaging. RESULTS: The median (IQR) number of vessel segments with contrast opacification was 0 (0-2) in early phase and 6 (0-10) in late phase. All segments showed increased prevalence of opacification when evaluated in late phase (p < 0.05). The M4 segments of MCA, internal cerebral veins, and vein of Galen had the lowest percentage of opacification in both phases. The sensitivity of 4-, 7-, and 10-point scoring algorithms increased from 59-91% to 94-99% when ratings were performed using early-phase images rather than based solely on late-phase images. CONCLUSIONS: The incorporation of early-phase images might be considered as a strategy to improve the sensitivity of CTA as an ancillary test in confirming brain death, especially in patients without missing or questionable elements in clinical examination.

Apparent diffusion coefficient signature of ischemic tissue predicts neurological progression in isolated pontine infarcts.

Background: Early neurological deterioration is encountered in up to a third of patients with isolated pontine infarcts. A limited number of clinical and imaging features have been suggested as predictors of neurological progression in this setting. In this study, we assessed whether quantitative apparent diffusion coefficient (ADC) measurements within the ischemic pontine region could be used as a radiomic feature to forecast clinical deterioration. Methods: We calculated the mean ADC value of ischemic voxels within the ischemic region and normalized them to the contralateral non-ischemic tissue (relative ADC, rADC) in patients with isolated pontine infarcts. This imaging signature was then compared among patients with neurological progression (n = 21) and a propensity matched cohort of non-progressors (n = 42), together with other clinical and imaging features in bivariate and multivariate statistical models. Results: The rADCmean was significantly lower among patients with progression (p = 0.008). Female gender and extension of the ischemic lesion to the ventral pontine surface were other features significantly associated with progression. The association between rADCmean and progression persisted in multivariate models with an odds ratio of 13.7 (95% CI 2.6-72.8; p = 0.002) for progression among patients with rADCmean ≤ 0.67 in their ischemic tissue. The probability for worsening was 80% among patients who had an ischemic lesion extending to the ventral pontine surface with a mean rADC ≤ 0.67. Conclusion: The mean rADC value within the ischemic lesion is closely related with early neurological deterioration in patients with isolated pontine infarcts.

Cortical Subarachnoid Hemorrhage in Behcet's Disease.

OBJECTIVE: Cortical subarachnoid hemorrhage (cSAH) can be resulted from by a wide variety of causes. A cSAH probably associated with Behcet's disease is herein reported for the first time. CASE REPORT: A 58-year-old male with stable Behcet's disease evaluated for sudden onset headache. Emergency computed tomography disclosed cSAH in the left frontal sulci. A ruptured middle cerebral artery cortical branch aneurysm was found. Surprisingly, this aneurysm obliterated completely after diagnostic catheter angiography. CONCLUSION: This case highlights three important points; First, non-mycotic (non-infectious) distal cerebral artery aneurysms may rarely cause cSAH. Second, distal dissecting aneurysms may rarely become obliterated after diagnostic cerebral angiography. Third, such aneurysms may be one of the long-term consequences of vascular inflammation in Behçet's disease.

Incidental DWI Lesions in Patients with Recent Small Subcortical Infarctions.

OBJECTIVES: Incidental acute ischemic lesions distinct from the primary neurological insult are identified on diffusion-weighted imaging (DWI) in a number of conditions where cerebral microvascular pathology plays a central role. Another major manifestation of cerebral small vessel disease (CSVD) is ischemic stroke named as recent small subcortical infarction (RSSI). In this study, we sought to identify the prevalence and predictors of incidental DWI lesions in patients with RSSI. MATERIALS AND METHODS: We retrospectively analyzed a consecutive series of acute ischemic stroke patients with DWI evidence of acute lesions solely localized to perforator artery territories. Images were evaluated for the presence of additional acute or subacute subcortical DWI lesions, apart from the symptomatic lesion. Clinical features including vascular risk factor burden, together with imaging markers of chronic CSVD, were compared among patients with and without incidental acute or subacute lesions. RESULTS: Among 396 patients with no alternate stroke etiology additional incidental subcortical DWI bright lesions were identified in 74 (19%) cases. These lesions were primarily localized in the corona radiata, or centrum semiovale. Patients with incidental DWI lesions were more likely to have a history of hypertension, a higher white matter hyperintensities burden in the periventricular and subcortical region, higher perivascular spaces burden in the basal ganglia, multiple cerebral microbleeds, and multiple chronic lacunes. Presence of multiple chronic lacunes (OR 5.98, 95% CI 3.18-11.24) and ≥2 vascular risk factors (OR 2.03, 95% CI 1.05-3.91) stood out as features significantly associated with incidental DWI lesions in multivariate analysis. CONCLUSIONS: Our study shows that acute or subacute ischemic lesions can be incidentally detected in approximately one-fifth of patients with RSSI. This observation suggests that the course of CSVD might be more active, temporally and spatially, in a distinct subgroup of RSSI patients, specifically those with a higher chronic lacune and vascular risk factor burden.