Cortical Lesions Research Articles

Predictors of early seizures after first acute stroke

Background and objective:
 There is a lack of local data regarding the frequency and predictors of early seizures after stroke. The objective of this study was to determine the frequency of early seizures after stroke and identify the predictors which lead to them after first acute stroke.
 Methods:
 This cross-sectional observational study was conducted in the Department of Neurology, Pakistan Institute of Medical Sciences, Islamabad from October 2021 to June 2022. A total of 310 consecutive eligible patients of acute stroke were recruited. Key inclusion criteria included any patient of >20 years of age with confirmed diagnosis of stroke on imaging, non-traumatic, with no history of seizures in past. Data was analyzed by SPSS version 23.0.
 Results: 
 The mean age of patients in the seizures group was 48.40 ± 20.9 years. Hypertension was the most common co-morbid present in 225 (76.5%) patients. Early seizures were found in 52 (16.8%) patients with 42 (80.76%) having seizures in first 24 hours of stroke (p value 0.001). On National Institute of Health Sciences Scale (NIHSS) score most patients 125 (40.3%) had moderate severity score i.e. score in between 7 to 25 (p value 0.05). Ischemic stroke was identified as the stroke variety with most of the early seizures i.e. 16 (30.76%) (p value 0.003).
 Conclusion: 
 Early seizures were not infrequent after acute stroke (16.77%) in our study. Early seizures were associated with younger age, cortical region lesion, ischemic stroke, followed by cerebral venous thrombosis. Higher NIHSS score and greater disability was associated with increased incidence of early seizures.

Neurologic Biomarkers, Neuroimaging, and Cognitive Function in Persistent Atrial Fibrillation: A Cross-Sectional Study.

The aim of this study was to evaluate the specific neurologic biomarkers, neuroimaging findings, and cognitive function in patients with persistent atrial fibrillation (AF) undergoing electrical cardioversion, compared to control subjects. This cross-sectional study included 25 patients with persistent AF undergoing electrical cardioversion and 16 age- and sex-matched control subjects. Plasma levels of glial fibrillary acidic protein (GFAP), neurofilament light protein (NFL), and ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), as well as parameters of neuroimaging and cognitive function, were compared between the groups. Neuroimaging was performed using the standard magnetic resonance imaging (MRI) protocol. Cognitive function was assessed using the Patient-Reported Outcomes Measurement Information System (PROMIS) Cognitive Function Index. Further analysis of neurologic biomarkers was performed based on the subsequent electrical cardioversion. There was no significant difference in GFAP (median of 24.7 vs. 28.7 pg/mL, p = 0.347), UCH-L1 (median of 112.8 vs. 117.7 pg/mL, p = 0.885), and NFL (median of 14.2 vs. 15.4 pg/mL, p = 0.886) levels between AF patients and control subjects. Similarly, neuroimaging showed no between-group difference in large cortical and non-cortical lesions (n = 2, 8.0% vs. n = 0, 0.0%, p = 0.246), small non-cortical lesions (n = 5, 20.0% vs. n = 5, 31.3%, p = 0.413), white matter hyperintensity (n = 23, 92.0% vs. n = 14, 87.5%, p = 0.636), and thromboembolic lesions (n = 0, 0.0% vs. n = 1, 6.3%, p = 0.206). Cognitive assessment did not show any between-group difference in the PROMIS index (52.2 ± 9.6 vs. 51.2 ± 6.2, p = 0.706). Finally, there were no significant dynamics in neurologic biomarkers following electrical cardioversion (p > 0.05). This hypothesis-generating study did not find a significant difference in neurologic biomarkers, neuroimaging findings, or cognitive function between patients with persistent AF and controls. The restoration of sinus rhythm was not significantly associated with a change in neurologic biomarkers. Further powered longitudinal studies are needed to re-assess these findings in an AF population.

Abstract TP179: Laterality Of Carotid Plaque Is Associated With Aortic Complicated Lesion In Embolic Stroke Of Undetermined Source

Background and Purpose: To compare clinical features including carotid ultrasound findings, especially carotid plaque features, between patients with and without aortic complicated lesion (ACL) in embolic stroke of undetermined source (ESUS). Methods: Patients were selected from a comprehensive stroke center between April 2013 and April 2022. Inclusion criteria were: 1) consecutive ischemic stroke patients 2) who fulfilled ESUS criteria based on NAVIGATE-ESUS trial, and 3) who underwent transesophageal echocardiogram (TEE), and 4) admitted 7 days from onset. We compared clinical features, including carotid ultrasound findings in common carotid artery and internal carotid artery such as carotid plaque thickness on the each side, maximum carotid plaque thickness and carotid plaque laterality ratio defined as maximum left carotid plaque thickness divided by maximum right carotid plaque thickness, between ESUS patients with ACL (ACL-ESUS) and without ACL (non ACL-ESUS). Results: We screened 2,066 consecutive ischemic stroke patients, including 177 ESUS patients (136 [77%] male, median age 64 years old). Of all, 35 patients had ACL (30 [86%] male, median age 71 years old, Figure A). ACL-ESUS showed older age (ACL-ESUS vs. non ACL-ESUS; 71 vs. 64 years old, p = 0.004), higher frequency of having carotid plaque more than 1.6mm ipsilateral to the infarct (82% vs. 53%, p = 0.013), higher frequency of having cortical lesion (46% vs. 26%, p = 0.023), and higher carotid plaque laterality ratio (1.18 vs. 1.00, p = 0.042). In multivariable analysis, demonstrating cortical lesion (OR 2.86, 95%CI 1.03-7.92, p = 0.043), carotid plaque laterality ratio (OR 2.75, 95%CI 1.03-7.32, p =0.043) were independently associated with ACL (Figure B). Conclusions: In ESUS patients, higher carotid plaque laterality ratio was associated with ACL, suggesting TEE should be conducted to reveal ACL in ESUS patients with left-dominant carotid plaque.

Diagnostic implications of neuroimaging in epilepsy and other seizure disorders.

Epilepsy is the most common neurological disorder that affects ~1-2% of the global population, leading to presentation in the emergency room. The neuroimaging modalities have an important application in diagnosing new onset unprovoked seizures and epilepsy. This article discusses the various neuroimaging modalities for diagnosing seizures and epilepsy and addresses that the MRI is the investigation of choice, and urgent imaging is more commonly done by computed tomography in patients with new-onset seizures. The goal of the article was to diagnose seizures and epilepsy for early intervention to prevent complications or damage to the brain. MRI detects even small cortical epileptogenic lesions, whereas computed tomography is used in screening, diagnosis, evaluation, and monitoring of the prognosis of seizures in children. Magnetic resonance spectroscopy provides biochemical measurements of reduced N-acetyl aspartate and increased creatinine and choline in dysfunctioning epileptic zones. Volumetric MRI is very sensitive and specific in determining seizures originating in extratemporal and extrahippocampal sites. Even though diffusion tensor magnetic resonance imaging has a limited role, it is used in specific pediatric patient groups with temporal lobe epilepsy. Functional radionuclide imaging modalities (positron emission tomography and single-photon emission computerized tomography) are increasingly significant for the identification of the epileptic region. Furthermore, the authors recommend the use of artificial intelligence and further research on imaging modalities for early diagnosis of seizures and epilepsy.

Evidence of motor resonance in stroke patients with severe upper limb function impairments.

For the past fifteen years, observation of actions has proved to be effective in the motor rehabilitation of stroke. Despite this, no evidence has ever been provided that this practice is able to activate the efferent motor system of a limb unable to perform the observed action due to stroke. In fact, transcranial magnetic stimulation cannot easily be used in these patients, and the fMRI evidence is inconclusive. This creates a logical problem, as the effectiveness of action observation in functional recovery is attributed to its ability to evoke action simulation, up to sub-threshold muscle activation (i.e., motor resonance), in healthy individuals. To provide the necessary proof-of-concept, patients with severe upper limb function impairments and matched control participants were submitted to a verified action prediction paradigm. They were asked to watch videos showing gripping movements towards a graspable or an ungraspable object, and to press a button the instant the agent touched the object. The presence of more accurate responses for the graspable object trials is considered an indirect evidence of motor resonance. Participants were required to perform the task in two sessions which differed in the hand used to respond. Despite the serious difficulty of movement, 8 out of 18 patients were able to perform the task with their impaired hand. We found that the responses given by the paretic hand showed a modulation of the action prediction time no different from that showed by the non-paretic hand, which, in turn, did not differ from that showed by the matched control participants. The present proof-of-concept study shows that action observation involves the efferent motor system even when the hand used to respond is unable to perform the observed action due to a cortical lesion, providing the missing evidence to support the already established use of Action Observation Training (AOT) in motor rehabilitation of stroke.

Explanatory Power and Prognostic Implications of Factors Associated with Troponin Elevation in Acute Ischemic Stroke.

We investigated the impact of comorbidity burden on troponin elevation, with separate consideration of neurological conditions, in patients with acute ischemic stroke (AIS). This prospective, observational cohort study consecutively enrolled patients with AIS for 2 years. Serum cardiac troponin I was repeatedly measured, and disease-related biomarkers were collected for diagnosis of preassigned comorbidities, including atrial fibrillation (AF), ischemic heart disease (IHD), myocardial hypertrophy (MH), heart failure (HF), renal insufficiency (RI), and active cancer. The severity of neurological deficits and insular cortical ischemic lesions were assessed as neurological conditions. Adjusted associations between these factors and troponin elevation were determined using a multivariate ordinal logistic regression model and area under the receiver operating characteristic curve (AUC). Cox proportional hazards model was used to determine the prognostic significance of comorbidity beyond neurological conditions. Among 1,092 patients (66.5±12.4 years, 63.3% male), 145 (13.3%) and 335 (30.7%) had elevated (≥0.040 ng/mL) and minimally-elevated (0.040-0.010 ng/mL) troponin, respectively. In the adjusted analysis, AF, MH, HF, RI, active cancer, and neurological deficits were associated with troponin elevation. The multivariate model with six comorbidities and two neurological conditions exhibited an AUC of 0.729 (95% confidence interval [CI], 0.698-0.759). In Cox regression, AF, IHD, and HF were associated with adverse cardio-cerebrovascular events, whereas HF and active cancer were associated with mortality. Troponin elevation in patients with AIS can be explained by the burden of comorbidities in combination with neurological status, which explains the prognostic significance of troponin assay.

T1 /T2 ratio from 3T MRI improves multiple sclerosis cortical lesion contrast.

Cortical demyelinated lesions are prevalent in multiple sclerosis (MS), associated with disability, and have recently been incorporated into MS diagnostic criteria. Presently, advanced and ultrahigh-field MRIs-not routinely available in clinical practice-are the most sensitive methods for detection of cortical lesions. Approaches utilizing MRI sequences obtainable in routine clinical practice remain an unmet need. We plan to assess the sensitivity of the ratio of T1 -weighted and T2 -weighted (T1 /T2 ) signal intensity for focal cortical lesions in comparison to other high-field imaging methods. 3-Tesla and 7-Tesla MRI collected from 10 adults with MS were included in the study. T1 /T2 images were calculated by dividing 3T T1 -weighted (T1 w) images by 3T T2 -weighted (T2 w) fluid-attenuated inversion recovery images for each participant. A total of 614 cortical lesions were identified using 7T T2 *w and T1 w images and corresponding voxels were assessed on registered 3T images. Signal intensities were compared across 3T imaging sequences, including T1 /T2 , T1 w, T2 w, and inversion recovery susceptibility-weighted imaging with enhanced T2 weighting (IR-SWIET) images. T1 /T2 images demonstrated a larger contrast between median lesional and nonlesional cortical signal intensity (median ratio=1.29, range: 1.19-1.38) when compared to T1 w (1.01, 0.97-1.10, p<.002), T2 w (1.17, 1.07-1.26, p<.002), and IR-SWIET (1.21, 1.01-1.29, p<.03). T1 /T2 images are sensitive to cortical lesions. Approaches incorporating T1 /T2 could improve the accessibility of cortical lesion detection in research settings and clinical practice.

An Interpretable Machine Learning Model to Predict Cortical Atrophy in Multiple Sclerosis

To date, the relationship between central hallmarks of multiple sclerosis (MS), such as white matter (WM)/cortical demyelinated lesions and cortical gray matter atrophy, remains unclear. We investigated the interplay between cortical atrophy and individual lesion-type patterns that have recently emerged as new radiological markers of MS disease progression. We employed a machine learning model to predict mean cortical thinning in whole-brain and single hemispheres in 150 cortical regions using demographic and lesion-related characteristics, evaluated via an ultrahigh field (7 Tesla) MRI. We found that (i) volume and rimless (i.e., without a "rim" of iron-laden immune cells) WM lesions, patient age, and volume of intracortical lesions have the most predictive power; (ii) WM lesions are more important for prediction when their load is small, while cortical lesion load becomes more important as it increases; (iii) WM lesions play a greater role in the progression of atrophy during the latest stages of the disease. Our results highlight the intricacy of MS pathology across the whole brain. In turn, this calls for multivariate statistical analyses and mechanistic modeling techniques to understand the etiopathogenesis of lesions.

Clinical characteristics of chronic rhinitis following stroke.

We previously observed that patients with stroke complained of rhinitis symptoms that developed following the occurrence of stroke. To investigate the relationship between chronic rhinitis (CR) and stroke. This retrospective study analyzed the medical records and questionnaires of patients with stroke who visited our outpatient clinic from June to December 2020. Stroke lesions were mainly classified as supratentorial, infratentorial, and supra/infratentorial lesions. Supratentorial lesions were further divided into cortex, subcortex, and mixed. Participants were screened for CR and were subsequently divided into the CR and non-CR groups. The Sino-Nasal Outcome Test questionnaire and a questionnaire on autonomic nervous system symptoms were administered to all patients. Clinically evaluated indicators were not significantly different between the two groups. The number of patients with lesions in both the cortex and subcortex was significantly higher in the CR group than in the non-CR group. The risk of CR was higher in male patients with stroke than their female counterparts; additionally, the risk of CR was higher in patients with stroke who had both cortical and subcortical lesions, as well as autonomic dysfunction. Individuals with subcortical stroke damage had a greater probability of developing CR. The risk was increased in men, as compared with that in women, when autonomic symptoms were present.

Priorities for research on neuromodulatory subcortical systems in Alzheimer's disease: Position paper from the NSS PIA of ISTAART.

The neuromodulatory subcortical system (NSS) nuclei are critical hubs for survival, hedonic tone, and homeostasis. Tau-associated NSS degeneration occurs early in Alzheimer's disease (AD) pathogenesis, long before the emergence of pathognomonic memory dysfunction and cortical lesions. Accumulating evidence supports the role of NSS dysfunction and degeneration in the behavioral and neuropsychiatric manifestations featured early in AD. Experimental studies even suggest that AD-associated NSS degeneration drives brain neuroinflammatory status and contributes to disease progression, including the exacerbation of cortical lesions. Given the important pathophysiologic and etiologic roles that involve the NSS in early AD stages, there is an urgent need to expand our understanding of the mechanisms underlying NSS vulnerability and more precisely detail the clinical progression of NSS changes in AD. Here, the NSS Professional Interest Area of the International Society to Advance Alzheimer's Research and Treatment highlights knowledge gaps about NSS within AD and provides recommendations for priorities specific to clinical research, biomarker development, modeling, and intervention. HIGHLIGHTS: Neuromodulatory nuclei degenerate in early Alzheimer's disease pathological stages. Alzheimer's pathophysiology is exacerbated by neuromodulatory nuclei degeneration. Neuromodulatory nuclei degeneration drives neuropsychiatric symptoms in dementia. Biomarkers of neuromodulatory integrity would be value-creating for dementia care. Neuromodulatory nuclei present strategic prospects for disease-modifying therapies.

Primary Renal Leiomyosarcoma: Case Report and Review of the Literature

Renal leiomyosarcoma is an extremely rare malignant tumor. On clinical presentation and radio imaging it is challenging to make an accurate preoperative diagnosis. In our case, a 59-year-old female presented with history of left-sided flank pain, intermittent hematuria and weight loss of 6 months duration. She was known case of hypertension and diabetes mellitus of 20 years and on regular treatment. On the abdomino-pelvis sonography showed an exophytic cortical mass lesion measuring 4.0 x 3.8 cm lesion. Magnetic resonance imaging abdomen and pelvis (plain) shows a well defined non encapsulated exophytic predominantly solid mass lesion measuring 4.3 x 4 x 4.5 cm is noted in the anterior cortex of left kidney at interpolar region. There was no evidence of any regionalor distant metastesis. Patient underwent left radical nephrectomy. On histopathology reported as renal leiomyosarcoma. Immuhistochemistry showed smooth muscle actin diffusely and desmin focally positive. We present this review of rare case of primary renal leiomyosarcoma for its clinical presentation, radiographic findings, and pathologic features.

Lesion-induced sprouting promotes neurophysiological integration of septal and entorhinal inputs to granule cells in the dentate gyrus of rats

Axonal sprouting of dentate gyrus (DG) afferents after entorhinal cortex (EC) lesion is a model preparation to assess lesion-induced functional reorganization in a denervated target structure. Following a unilateral EC lesion, the surviving contralateral entorhinal projection, termed the crossed temporodentate pathway (CTD), and the heterotypic septal input to the DG, the septodentate pathway (SD), undergo extensive axonal sprouting. We explored whether EC lesion alters the capacity of the SD pathway to influence CTD-evoked granule cell excitability in the DG. We recorded extracellular field excitatory postsynaptic potentials (fEPSPs) after CTD stimulation alone and paired SD-CTD stimulation. Male rats were given unilateral EC lesions or sham operations; evoked fEPSPs in the DG were recorded at 4-, 15-, and 90-days post-entorhinal lesion to assess functional reorganization of the CTD and SD pathways. We found significantly increased fEPSP amplitudes in cases with unilateral lesions compared to sham-operates at 15- and 90-days post lesion. Within each time point, paired SD-CTD stimulation resulted in significantly depressed fEPSP amplitudes compared to amplitudes evoked after CTD stimulation alone and this effect was solely seen in cases with EC lesion. In cases where granule cell discharge was observed, SD stimulation increased discharge amplitude elicited by the CTD stimulation at 90-days postlesion. These findings demonstrate that synaptic remodeling following unilateral cortical lesion results in a synergistic interaction between two established hippocampal afferents that is not seen in uninjured brains. This work may be important for models of neurodegenerative disease and neural injury that target these structures and associated hippocampal circuitry.

Myelin oligodendrocyte glycoprotein antibody-associated disease in children: Are there MRI predictors of relapse?

Background and PurposeMyelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is increasingly recognized in children. Some children have isolated disease while others relapse. The study evaluates clinical, demographic and imaging features children with positive anti-MOG antibodies comparing to previously reported findings and correlate patterns on MR imaging with a relapsing course in MOGAD. Material and methodsAll pediatrics patients with serum anti-MOG antibodies were reviewed. Demographic, clinical, and imaging data were evaluated. Patients with a relapsing course were compared to those with a single event. We assessed initial MR images of the brain, orbits and spine obtained at the onset of clinical symptoms, whether performed at our institution or elsewhere. ResultsThirty patients were included, fourteen with a single event and sixteen with more than one clinical event. The mean age was 8.1 years, with a mean follow-up of 58 months (range of 0.67 to 238 months). The relapsing patients had a mean of 3.5 relapses (range 2–12). 55% of patients had long segment optic nerve lesions, 53% of patients had cortical or peripheral white matter lesions, and 46% of patients had thalamic lesions. 43% of patients had spinal cord lesions, with 39% involving the central cord and 26% with long segment involvement. The imaging features between the groups were not statistically significant. ConclusionThere were no distinguishing features in relapsing versus non-relapsing patients. In the absence of any predictive characteristics for future relapse, patients should have regular clinical and imaging follow up.

Interrater reliability for the detection of cortical lesions on phase-sensitive inversion recovery magnetic resonance imaging in patients with multiple sclerosis.

To assess the reliability of phase-sensitive inversion recovery (PSIR) magnetic resonance imaging (MRI) and its accuracy for determining the topography of demyelinating cortical lesions in patients with multiple sclerosis (MS). This was a cross-sectional study conducted at a tertiary referral center for MS and other demyelinating disorders. We assessed the agreement among three raters for the detection and topographic classification of cortical lesions on fluid-attenuated inversion recovery (FLAIR) and PSIR sequences in patients with MS. We recruited 71 patients with MS. The PSIR sequences detected 50% more lesions than did the FLAIR sequences. For detecting cortical lesions, the level of interrater agreement was satisfactory, with a mean free-response kappa (κFR) coefficient of 0.60, whereas the mean κFR for the topographic reclassification of the lesions was 0.57. On PSIR sequences, the raters reclassified 366 lesions (20% of the lesions detected on FLAIR sequences), with excellent interrater agreement. There was a significant correlation between the total number of lesions detected on PSIR sequences and the Expanded Disability Status Scale score (ρ = 0.35; p < 0.001). It seems that PSIR sequences perform better than do FLAIR sequences, with clinically satisfactory interrater agreement, for the detection and topographic classification of cortical lesions. In our sample of patients with MS, the PSIR MRI findings were significantly associated with the disability status, which could influence decisions regarding the treatment of such patients.

Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis: an update.

Myelin oligodendrocyte glycoprotein-immunoglobulin G (IgG)-associated optic neuritis has been established as a new entity of immune-mediated optic neuropathy. Patients usually present with recurrent optic neuritis, often bilaterally with initially severe vision loss and optic disc edema. However, in contrast to aquaporin 4-IgG-seropositive neuromyelitis optica spectrum disorder, visual recovery tends to be more favorable, with good response to steroid treatment. Another important differential diagnosis of myelin oligodendrocyte glycoprotein-IgG--associated optic neuritis is multiple sclerosis. Close monitoring for signs of relapse and long-term immunosuppression may be considered to maintain optimal visual function. The diagnosis can be made on the basis of the presence of a specific, usually serological, antibody against myelin oligodendrocyte glycoprotein (IgG; cell-based assay), and a demyelinating event (optic neuritis, myelitis, brainstem syndrome, or cortical lesions with seizures). The clinical spectrum of this newly recognized inflammatory demyelinating disease is expanding rapidly. We briefly review the epidemiological characteristics, clinical manifestations, diagnostic considerations, and treatment options of myelin oligodendrocyte glycoprotein-IgG-associated optic neuritis.

Alterations in EGFR and PDGFRA are associated with the localization of contrast-enhancing lesions in glioblastoma.

Glioblastoma (GBM) is a malignant brain tumor, with radiological and genetic heterogeneity. We examined the association between radiological characteristics and driver gene alterations. We analyzed the driver genes of 124 patients with IDH wild-type GBM with contrast enhancement using magnetic resonance imaging. We used a next-generation sequencing panel to identify mutations in driver genes and matched them with radiological information. Contrast-enhancing lesion localization of GBMs was classified into 4 groups based on their relationship with the subventricular zone (SVZ) and cortex (Ctx). The cohort included 69 men (55.6%) and 55 women (44.4%) with a mean age of 66.4 ± 13.3 years. EGFR and PDGFRA alterations were detected in 28.2% and 22.6% of the patients, respectively. Contrast-enhancing lesion touching both the SVZ and Ctx was excluded because it was difficult to determine whether it originated from the SVZ or Ctx. Contrast-enhancing lesions touching the SVZ but not the Ctx had significantly worse overall survival than non-SVZ lesions (441 days vs. 897 days, P = .002). GBM touching only the Ctx had a better prognosis (901 days vs. 473 days, P < .001) than non-Ctx lesions and was associated with EGFR alteration (39.4% vs. 13.2%, P = .015). Multiple contrast lesions were predominant in PDGFRA alteration and RB1-wild type (P = .036 and P = .031, respectively). EGFR alteration was associated with cortical lesions. And PDGFRA alteration correlated with multiple lesions. Our results suggest that clarifying the association between driver genes and tumor localization may be useful in clinical practice, including prognosis prediction.

Motor rehabilitation of aphasic stroke patient: the possibility of Rood's approach.

Motor rehabilitation of aphasic stroke patient: the possibility of Rood's approach.

Post-Stroke Detection of Subclinical Paroxysmal Atrial Fibrillation in Patients With Embolic Stroke of Undetermined Source in the Real World Practice: The Empoli ESUS Atrial Fibrillation (E 2 AF) Study.

Subclinical paroxysmal atrial fibrillation (AF) is one of the main occult causative mechanisms of embolic stroke of undetermined source (ESUS). Aim of this study was to identify AF predictors, and to develop a score to predict the probability of AF detection in ESUS. We retrospectively analyzed ESUS patients undergoing 2-week external electrocardiographic monitoring. Patients with and without AF detection were compared. On the basis of multivariate analysis, predictors of AF were identified and used to develop a predictive score, which was then compared with other existing literature scores. Eighty-two patients, 48 females, mean age±SD 72±10 years, were included. In 36 patients (43.9%) AF was detected. The frequency of age 75 years or above and arterial hypertension, and the median CHA 2 DS 2 -VASc score were significantly higher in patients with AF compared with those without. National Institutes of Health Stroke Scale (NIHSS) score ≥8 was the only independent variable associated with AF detection. We derived the Empoli ESUS-AF (E 2 AF) score (NIHSS ≥8 5 points, arterial hypertension 3 points, age 75 years or above 2 points, age 65 to 74 years 1 point, history of coronary/peripheral artery disease 1 point, left atrial enlargement 1 point, posterior lesion 1 point, cortical or cortical-subcortical lesion 1 point), whose predictive power in detecting AF was good (area under the curve: 0.746, 95% confidence interval: 0.638-0.836) and higher than that of CHA 2 DS 2 -VASc and other scores. In our study NIHSS score ≥8 was the only independent predictor of post-ESUS-AF detection. The E 2 AF score appears to have a good predictive power for detecting AF. External validations are required.

Personalized maps of T1 relaxometry abnormalities provide correlates of disability in multiple sclerosis patients

Objectives and aimsQuantitative MRI (qMRI) has greatly improved the sensitivity and specificity of microstructural brain pathology in multiple sclerosis (MS) when compared to conventional MRI (cMRI). More than cMRI, qMRI also provides means to assess pathology within the normal-appearing and lesion tissue. In this work, we further developed a method providing personalized quantitative T1 (qT1) abnormality maps in individual MS patients by modeling the age dependence of qT1 alterations. In addition, we assessed the relationship between qT1 abnormality maps and patients’ disability, in order to evaluate the potential value of this measurement in clinical practice. MethodsWe included 119 MS patients (64 relapsing-remitting MS (RRMS), 34 secondary progressive MS (SPMS), 21 primary progressive MS (PPMS)), and 98 Healthy Controls (HC). All individuals underwent 3T MRI examinations, including Magnetization Prepared 2 Rapid Acquisition Gradient Echoes (MP2RAGE) for qT1 maps and High-Resolution 3D Fluid Attenuated Inversion Recovery (FLAIR) imaging. To calculate personalized qT1 abnormality maps, we compared qT1 in each brain voxel in MS patients to the average qT1 obtained in the same tissue (grey/white matter) and region of interest (ROI) in healthy controls, hereby providing individual voxel-based Z-score maps. The age dependence of qT1 in HC was modeled using linear polynomial regression. We computed the average qT1 Z-scores in white matter lesions (WMLs), normal-appearing white matter (NAWM), cortical grey matter lesions (GMcLs) and normal-appearing cortical grey matter (NAcGM). Lastly, a multiple linear regression (MLR) model with the backward selection including age, sex, disease duration, phenotype, lesion number, lesion volume and average Z-score (NAWM/NAcGM/WMLs/GMcLs) was used to assess the relationship between qT1 measures and clinical disability (evaluated with EDSS). ResultsThe average qT1 Z-score was higher in WMLs than in NAWM. (WMLs: 1.366 ± 0.409, NAWM: −0.133 ± 0.288, [mean ± SD], p < 0.001). The average Z-score in NAWM in RRMS patients was significantly lower than in PPMS patients (p = 0.010). The MLR model showed a strong association between average qT1 Z-scores in white matter lesions (WMLs) and EDSS (R2 = 0.549, β = 0.178, 97.5 % CI = 0.030 to 0.326, p = 0.019). Specifically, we measured a 26.9 % increase in EDSS per unit of qT1 Z-score in WMLs in RRMS patients (R2 = 0.099, β = 0.269, 97.5 % CI = 0.078 to 0.461, p = 0.007). ConclusionsWe showed that personalized qT1 abnormality maps in MS patients provide measures related to clinical disability, supporting the use of those maps in clinical practice.

Neurodynamic speech disorders in the acute ischemic stroke

To identify the features of the clinical picture and evaluate the dynamics of regression of neurodynamic speech disorders in comparison with cortical aphasia in patients with ischemic stroke (IS) in the carotid system. We examined 268 patients with a median age of 59 (54; 70) years in the acute period of IS in the dominant hemisphere with the presence of cortical aphasia or neurodynamic speech disorders. The degree of speech recovery was characterized by an increase in the score on the Speech Questionnaire (ΔSQ) from 1 to 21 days after the development of IS. The patients were divided into group 1 (n=148) with a low level of recovery (ΔSQ≤6) and group 2 (n=120) with a high level (ΔSQ >6). Of the 268 patients, cortical aphasia was detected in 171 (63.8%) patients, and neurodynamic speech disorders characterized by significant variability of symptoms over the course of hours and days were detected in 97 (36.2%) patients. In patients with cortical aphasia, the majority of patients (63.2%) were classified into group 1, and among patients with neurodynamic speech disorders - into group 2 (58.8%), which showed the stability of the regression dynamics of speech disorders (p=0.001). In patients with cortical lesions the impressive side of speech suffered more often - in this group patients with sensorimotor aphasia predominate. In the case of neurodynamic speech disorders, motor and sensorimotor disorders are observed with approximately the same frequency (p=0.002). In comparison with cortical aphasias, the sensory component of speech suffers to a lesser extent in neurodynamic speech disorders. Neurodynamic speech disorders generally recover faster and more fully.