Intracranial Artery Calcifications Profile as a Predictor of Recanalization Failure in Endovascular Stroke Treatment.

BACKGROUND: Acute ischemic stroke with large or medium-vessel occlusion associated with intracranial artery calcification (IAC) is an infrequent phenomenon presumably associated with intracranial atherosclerotic disease. We aimed to characterize IAC and its impact on endovascular treatment outcomes. METHODS: We performed a retrospective cross-sectional study of consecutive patients with stroke treated with thrombectomy from January 2020 to July 2021 in our institution. We described IAC findings (length, density, and location pattern) on baseline noncontrast computed tomography. Patients were divided into 3 groups: IAC related to the occlusion location (symptomatic-IAC group), unrelated to the occlusion (asymptomatic-IAC group), and absence of any IAC (non-IAC group). We analyzed the association between the IAC profile and outcomes using logistic regression models. Intracranial angioplasty and stenting were considered rescue treatments. RESULTS: Of the 393 patients included, 26 (6.6%) patients presented a symptomatic-IAC, 77 (19.6%) patients an asymptomatic-IAC, and in 290 (73.8%) patients no IAC was observed. The rate of failed recanalization (expanded Thrombolysis in Cerebral Infarction 0-2a) before rescue treatment was higher in symptomatic-IAC (65.4%) than in asymptomatic-IAC (15.6%; P<0.001) or non-IAC (13.4%; P<0.001). Rescue procedures were more frequently performed in symptomatic-IAC (26.9%) than in asymptomatic-IAC (1.3%; P<0.001) and non-IAC (4.1%; P<0.001). After adjusting for identifiable clinical and radiological confounders, symptomatic-IAC emerged as an independent predictor of failed recanalization (odds ratio, 11.89 [95% CI, 3.94-35.91]; P<0.001), adoption of rescue procedures (odds ratio, 12.38 [95% CI, 2.22-69.09]; P=0.004), and poor functional outcome (90-day modified Rankin Scale score ≥3; odds ratio, 3.51 [95% CI, 1.02-12.00]; P=0.046). CONCLUSIONS: The presence of IAC related to the occlusion location is associated with worse angiographic and functional outcomes. Therefore, identification of symptomatic-IAC on baseline imaging may guide optimal endovascular treatment strategy, predicting the need for intracranial stenting and angioplasty.

Derivation and validation of three intracerebral hemorrhage expansion scores using different CT modalities.

OBJECTIVES: To derivate and validate three scores for the prediction of intracerebral hemorrhage (ICH) expansion depending on the use of non-contrast CT (NCCT), single-phase CTA, or multiphase CTA markers of hematoma expansion, and to evaluate the added value of single-phase and multiphase CTA over NCCT. METHODS: After prospectively deriving NCCT, single-phase CTA, and multiphase CTA hematoma expansion scores in 156 patients with ICH < 6 h, we validated them in 120 different patients. Discrimination and calibration of the three scores was assessed. Primary outcome was substantial hematoma expansion > 6 mL or > 33% at 24 h. RESULTS: The evaluation of single-phase and multiphase CTA markers gave a steadily increase in discrimination for substantial hematoma expansion over NCCT markers. The C-index (95% confidence interval) in derivation and validation cohorts was 0.69 (0.58-0.80) and 0.59 (0.46-0.72) for NCCT score, significantly lower than 0.75 ([0.64-0.87], p = 0.038) and 0.72 ([0.59-0.84], p = 0.016) for single-phase CTA score, and than 0.79 ([0.68-0.89], p = 0.033) and 0.73 ([0.62-0.85], p = 0.031) for multiphase CTA score, respectively. The three scores showed good calibration in both derivation and validation cohorts: NCCT (χ2 statistic 0.389, p = 0.533; and χ2 statistic 0.352, p = 0.553), single-phase CTA (χ2 statistic 2.052, p = 0.359; and χ2 statistic 2.230, p = 0.328), and multiphase CTA (χ2 statistic 0.559, p = 0.455; and χ2 statistic 0.020, p = 0.887) scores, respectively. CONCLUSION: This study shows the added prognostic value of more advanced CT modalities in acute ICH evaluation. NCCT, single-phase CTA, and multiphase CTA scores may help to refine the selection of patients at risk of expansion in different decision-making scenarios. KEY POINTS: • This study shows the added prognostic value of more advanced CT modalities in acute intracerebral hemorrhage evaluation. • The evaluation of single-phase and multiphase CTA markers provides a steadily increase in discrimination for intracerebral hemorrhage expansion over non-contrast CT markers. • Non-contrast CT, single-phase CTA, and multiphase CTA scores may help clinicians and researchers to refine the selection of patients at risk of intracerebral hemorrhage expansion in different decision-making scenarios.

Systematic CT perfusion acquisition in acute stroke increases vascular occlusion detection and thrombectomy rates.

BACKGROUND: In patients with stroke, current guidelines recommend non-invasive vascular imaging to identify intracranial vessel occlusions (VO) that may benefit from endovascular treatment (EVT). However, VO can be missed in CT angiography (CTA) readings. We aim to evaluate the impact of consistently including CT perfusion (CTP) in admission stroke imaging protocols. METHODS: From April to October 2020 all patients admitted with a suspected acute ischemic stroke underwent urgent non-contrast CT, CTA and CTP and were treated accordingly. Hypoperfusion areas defined by time-to-maximum of the tissue residue function (Tmax) >6 s, congruent with the clinical symptoms and a vascular territory, were considered VO (CTP-VO). In addition, two experienced neuroradiologists blinded to CTP but not to clinical symptoms retrospectively evaluated non-contrast CT and CTA to identify intracranial VO (CTA-VO). RESULTS: Of the 338 patients included in the analysis, 157 (46.5%) presented with CTP-VO (median Tmax >6s: 73 (29-127) mL). CTA-VO was identified in 83 (24.5%) of the cases. Overall CTA-VO sensitivity for the detection of CTP-VO was 50.3% and specificity was 97.8%. Higher hypoperfusion volume was associated with increased CTA-VO detection (OR 1.03; 95% CI 1.02 to 1.04). EVT was performed in 103 patients (30.5%; Tmax >6s: 102 (63-160) mL), representing 65.6% of all CTP-VO. Overall CTA-VO sensitivity for the detection of EVT-VO was 69.9% and specificity was 95.3%. Among patients who received EVT, the rate of false negative CTA-VO was 30.1% (Tmax >6s: 69 (46-99.5) mL). CONCLUSION: Systematically including CTP in acute stroke admission imaging protocols may increase the diagnosis of VO and rate of EVT.

Relationship between infarct size and serum uric acid levels during the acute phase of stroke.

INTRODUCTION: Uric acid has gained considerable attention as a potential neuroprotective agent in stroke during the last decades, however, its role in the pathophysiology of ischemic stroke remains poorly understood. A serial evaluation of uric acid levels during the acute phase of stroke and its association with infarct size on magnetic resonance imaging is lacking. METHODS: We present a cohort study of 31 patients with ischemic stroke who were not candidates for thrombolysis according to current criteria at the time. We performed daily measurements of serum uric acid and total antioxidant capacity of plasma during the first week after symptoms onset and 30 days after. Infarct size was determined in the acute phase by a DWI sequence and the final infarct size with a control MRI (FLAIR) at day 30. RESULTS: Uric acid significantly decreases between days 2 to 6 compared to day 1, after adjustment by sex, age and DWI at diagnosis, with a nadir value at 72h. A mixed model analysis showed a negative association between DWI at diagnosis and uric acid evolution during the first week after stroke. Moreover, multivariable linear regression of uric acid values during follow up on DWI volumes demonstrated that DWI volume at diagnosis is negatively associated with uric acid levels at day 3 and 4. There were no significant associations between total antioxidant capacity of plasma and DWI at diagnosis, or FLAIR at any point. DISCUSSION: Patients with larger infarcts exhibited a significant decrease in serum uric acid levels, accounting for a more prominent reactive oxygen species scavenging activity with subsequent consumption and decay of this antioxidant. The different kinetics of total antioxidant capacity of plasma and serum uric acid levels suggests a specific role of uric acid in the antioxidant response in ischemic stroke.

Trastornos del sueño en pacientes con Esclerosis Múltiple: Fisiopatología y clínica / Sleep disorders in patients with Multiple Sclerosis: Pathophysiology and clinic

Resumen Los pacientes con Esclerosis múltiples tienen mayor tasa de trastornos del sueño que la población general. Los trastornos del sueño más prevalentes son: somnolencia diurna, insomnio, síndrome de piernas inquietas, trastornos respiratorios del sueño y narcolepsia. Los principales factores involucrados en la calidad del sueño en estos pacientes son la nicturia, dolor inespecífico, depresión, efectos colaterales de las terapias, ubicación de las lesiones y severidad de la enfermedad. La presencia de estos trastornos contribuyen de forma significativa a la reducción en la calidad de vida y funcionalidad diurna. A pesar de su alta frecuencia, está demostrado que los trastornos del sueño en estos pacientes son subdiagnosticados. Esta revisión, busca hacer un repaso de los trastornos del sueño más frecuentes en pacientes con esclerosis múltiple, su fisiopatología y clínica.

Sleep disorders occur in multiple sclerosis patients at higher frequency than the general population. Among sleep disorders; daytime sleepiness, insomnia, restless legs syndrome, sleep disordered breathing and narcolepsy have all been reported to be more frequent in multiple sclerosis patients. Factors that influence the quality of sleep in this population include pain, nycturia, depression, medication effects, location of lesions, and disease severity. Sleep disorders have the potential to negatively impact overall health and quality of life in these patients. Sleep disorders in multiple sclerosis patients are known to be clinically underdiagnosed. High suspicion of this condition is pivotal to prompt diagnosis and treatment. The aim of this paper is to review pathophysiology and clinical aspect of the most frequent sleep disorders in multiples sclerosis patients.