Clot Burden Score and Early Ischemia Predict Intracranial Hemorrhage following Endovascular Therapy.

BACKGROUND AND PURPOSE: Intracranial hemorrhage is a known complication following endovascular thrombectomy. The radiologic characteristics of a CT scan may assist with hemorrhage risk stratification. We assessed the radiologic predictors of intracranial hemorrhage following endovascular therapy using data from the INTERRSeCT (Identifying New Approaches to Optimize Thrombus Characterization for Predicting Early Recanalization and Reperfusion With IV Alteplase and Other Treatments Using Serial CT Angiography) study. MATERIALS AND METHODS: Patients undergoing endovascular therapy underwent baseline imaging, postprocedural angiography, and 24-hour follow-up imaging. The primary outcome was any intracranial hemorrhage observed on follow-up imaging. The secondary outcome was symptomatic hemorrhage. We assessed the relationship between hemorrhage occurrence and baseline patient characteristics, clinical course, and imaging factors: baseline ASPECTS, thrombus location, residual flow grade, collateralization, and clot burden score. Multivariable logistic regression with backward selection was used to adjust for relevant covariates. RESULTS: Of the 199 enrolled patients who met the inclusion criteria, 46 (23%) had an intracranial hemorrhage at 24 hours. On multivariable analysis, postprocedural hemorrhage was associated with pretreatment ASPECTS (OR, 1.56 per point lost; 95% CI, 1.12-2.15), clot burden score (OR, 1.19 per point lost; 95% CI, 1.03-1.38), and ICA thrombus location (OR, 3.10; 95% CI, 1.07-8.91). In post hoc analysis, clot burden scores of ≤3 (sensitivity, 41%; specificity, 82%; OR, 3.12; 95% CI, 1.36-7.15) and pretreatment ASPECTS ≤ 7 (sensitivity, 48%; specificity, 82%; OR, 3.17; 95% CI, 1.35-7.45) robustly predicted hemorrhage. Residual flow grade and collateralization were not associated with hemorrhage occurrence. Symptomatic hemorrhage was observed in 4 patients. CONCLUSIONS: Radiologic factors, early ischemia on CT, and increased CTA clot burden are associated with an increased risk of intracranial hemorrhage in patients undergoing endovascular therapy.

Statin therapy does not affect the radiographic and clinical profile of patients with TIA and minor stroke.

BACKGROUND AND PURPOSE: Acute statin therapy improves neurologic outcome and diminishes infarct growth in animal models of stroke. Clinical studies suggest that premorbid and early statin use is associated with improved outcome after major stroke. We studied the association between statin therapy and radiographic and clinical outcomes in patients with high-risk TIA and minor stroke. MATERIALS AND METHODS: Patients with high-risk TIA and minor stroke (NIHSS ≤3) were prospectively enrolled within 24 hours of symptom onset. Patients were followed clinically for 3 months, and a subset had a repeat MR imaging at 90 days. RESULTS: Of 418 patients, 23% were prescribed statins before their stroke. Statins were continued in 20% and initiated in 42%. Patients on prior statin therapy were older and more hypertensive, treated with aspirin, and more likely to have symptomatic carotid disease compared with those not on statin. Adjusting for these differences, prior statin treatment was not associated with DWI positivity (adjusted OR = 1.3; 95% CI, 0.77-2.1; P = .32) or smaller median baseline infarct volume, 1.1 mL (interquartile range = 4) versus 1 mL (interquartile range = 2.5; P = .56). Early or continued treatment with statins did not improve the risk of clinical deterioration (adjusted OR = 0.66; 95% CI, 0.27-1.6; P = .35) or poor functional outcome at 3 months (adjusted OR = 0.66; 95% CI, 0.35-1.24; P = .19). CONCLUSIONS: Prestroke or early-stroke statin therapy was not associated with a reduction in the number of DWI lesions, infarct volume, or improved clinical or functional outcome at 3 months. The effect of acute statin treatment in patients with ischemic stroke/TIA remains unclear and needs further investigation.

Spontaneous limb movements and posturing secondary to acute basilar artery occlusion: a potentially devastating seizure mimic.

Basilar artery occlusion is a devastating but treatable form of ischaemic stroke with high morbidity and mortality rates. The diagnosis is often challenging due to considerable heterogeneity of clinical signs and symptoms. We report a case of an acute basilar artery occlusion presenting with decreased level of consciousness associated with rhythmic tonic movements of the four extremities, mimicking seizure activity. The patient was treated with intravenous thrombolysis and subsequently gained good recovery. Awareness of this entity is required to recognise this potentially treatable, but otherwise devastating seizure mimic.

DWI reversal is associated with small infarct volume in patients with TIA and minor stroke.

BACKGROUND AND PURPOSE: More than half of patients with TIA/minor stroke have ischemic lesions on early DWI, which represent irreversibly damaged tissue. The presence and volume of DWI lesions predict early deterioration in this population. We aimed to study the rate and implications of DWI reversal in patients with TIA/minor stroke. MATERIALS AND METHODS: Patients with TIA/minor stroke were prospectively enrolled and imaged within 24 hours of onset. Patients were followed for 3 months with repeat MR imaging either at day 30 or 90. Baseline DWI/PWI and follow-up FLAIR final infarct volumes were measured. RESULTS: Of 418 patients included, 55.5% had DWI and 37% had PWI (time-to-peak of the impulse response ≥2 seconds' delay) lesions at baseline. The median time from symptom onset to baseline and follow-up imaging was 13.4 (interquartile range, 12.7) and 78.73 hours (interquartile range, 60.2), respectively. DWI reversal occurred in 5.7% of patients. The median DWI lesion volume was significantly smaller in those with reversal (0.26 mL, interquartile range = 0.58 mL) compared with those without (1.29 mL, interquartile range = 3.6 mL, P = .002); 72.7% of DWI reversal occurred in cortically based lesions. Concurrent tissue hypoperfusion (time-to-peak of the impulse response ≥2 seconds) was seen in 36.4% of those with DWI reversal versus 62.4% without (P = .08). DWI reversal occurred in 3.3% of patients with penumbral patterns (time-to-peak of the impulse response ≥6 seconds - DWI) > 0 and in 6.8% of those without penumbral patterns (P = .3). The severity of hypoperfusion, defined as greater prolongation of time-to-peak of the impulse response (≥2, ≥4, ≥6, ≥8 seconds), did not affect the likelihood of DWI reversal (linear trend, P = .147). No patient with DWI reversal had an mRS score of ≥2 at 90 days versus 18.2% of those without reversal (P = .02). CONCLUSIONS: DWI reversal is uncommon in patients with TIA/minor stroke and is more likely to occur in those with smaller baseline lesions. DWI reversal should not have a significant effect on the accuracy of penumbra definition.

Therapeutic management of acute intracerebral haemorrhage.

Intracerebral haemorrhage (ICH) is a stroke resulting from spontaneous rupture of an intracranial vessel and is associated with high early mortality and long-term morbidity rates. With the exception of dedicated stroke units or neurocritical care, no surgical or medical intervention has been proven to effectively improve outcome following ICH. Pharmacotherapeutic considerations include optimal blood pressure control and the choice of antihypertensive agents. Acute haematoma expansion represents the most obvious acute treatment target. The use of haemostatic agents may have a role in ICH management; although it appears improved patient selection may be required before the use of these agents can be demonstrated clinically. In patients with anticoagulant-associated ICH, a number of therapeutic agents may be used to urgently reverse the coagulopathy, although further clinical trials are required. Recurrent bleeding and future thrombo-embolic event rates in patients who require anticoagulation following ICH risks are difficult to determine accurately, although risk stratification data are emerging. This article reviews the pathophysiology, natural history and the evidence supporting present therapeutic management practices for ICH. The authors' practice based on best available evidence is provided.