Intracerebral hemorrhage markers on non-contrast computed tomography as predictors of the dynamic spot sign on CT perfusion and associations with hematoma expansion and outcome.

PURPOSE: To assess the association between non-contrast computed tomography (NCCT) hematoma markers and the dynamic spot sign on computed tomography perfusion (CTP), and their associations with hematoma expansion, clinical outcome, and in-hospital mortality. METHODS: Patients who presented with intracerebral hemorrhage (ICH) to a stroke center over an 18-month period and underwent baseline NCCT and CTP, and a follow-up NCCT within 24 h after the baseline scan were included. The initial and follow-up hematoma volumes were calculated. Two raters independently assessed the baseline NCCT for hematoma markers and concurrently assessed the CTP for the dynamic spot sign. Univariate and multivariate logistic regression analyses were performed to assess the association between the hematoma markers and the dynamic spot sign, adjusting for known ICH expansion predictors. RESULTS: Eighty-five patients were included in our study and 55 patients were suitable for expansion analysis. Heterogeneous density was the only NCCT hematoma marker to be associated with the dynamic spot sign after multivariate analysis (odds ratio, 58.61; 95% confidence interval, 9.13-376.05; P < 0.001). The dynamic spot sign was present in 22 patients (26%) and significantly predicted hematoma expansion (odds ratio, 36.6; 95% confidence interval, 2.51-534.2; P = 0.008). All patients with a spot sign had a swirl sign. A co-located hypodensity and spot sign was significantly associated with in-hospital mortality (odds ratio, 6.17; 95% confidence interval, 1.09-34.78; P = 0.039). CONCLUSION: Heterogeneous density and swirl sign are associated with the dynamic spot sign. The dynamic spot sign is a stronger predictor than NCCT hematoma markers of significant hematoma expansion. A co-located spot sign and hypodensity predicts in-hospital mortality.

Prevalence and Significance of Impaired Microvascular Tissue Reperfusion Despite Macrovascular Angiographic Reperfusion (No-Reflow).

BACKGROUND AND OBJECTIVES: The relevance of impaired microvascular tissue-level reperfusion despite complete upstream macrovascular angiographic reperfusion (no-reflow) in human stroke remains controversial. We investigated the prevalence and clinical-radiologic features of this phenomenon and its associations with outcomes in 3 international randomized controlled thrombectomy trials with prespecified follow-up perfusion imaging. METHODS: In a pooled analysis of the Extending the Time for Thrombolysis in Emergency Neurological Deficits-Intra-Arterial (EXTEND-IA; ClinicalTrials.gov NCT01492725), Tenecteplase Versus Alteplase Before Endovascular Therapy for Ischemic Stroke (EXTEND-IA TNK; NCT02388061), and Determining the Optimal Dose of Tenecteplase Before Endovascular Therapy for Ischaemic Stroke (EXTEND-IA TNK Part 2; NCT03340493) trials, patients undergoing thrombectomy with final angiographic expanded Treatment in Cerebral Infarction score of 2c to 3 score for anterior circulation large vessel occlusion and 24-hour follow-up CT or MRI perfusion imaging were included. No-reflow was defined as regions of visually demonstrable persistent hypoperfusion on relative cerebral blood volume or flow maps within the infarct and verified quantitatively by >15% asymmetry compared to a mirror homolog in the absence of carotid stenosis or reocclusion. RESULTS: Regions of no-reflow were identified in 33 of 130 patients (25.3%), encompassed a median of 60.2% (interquartile range 47.8%-70.7%) of the infarct volume, and involved both subcortical (n = 26 of 33, 78.8%) and cortical (n = 10 of 33, 30.3%) regions. Patients with no-reflow had a median 25.2% (interquartile range 16.4%-32.2%, p < 0.00001) relative cerebral blood volume interside reduction and 19.1% (interquartile range 3.9%-28.3%, p = 0.00011) relative cerebral blood flow reduction but similar mean transit time (median -3.3%, interquartile range -11.9% to 24.4%, p = 0.24) within the infarcted region. Baseline characteristics were similar between patients with and those without no-reflow. The presence of no-reflow was associated with hemorrhagic transformation (adjusted odds ratio [aOR] 1.79, 95% confidence interval [CI] 2.32-15.57, p = 0.0002), greater infarct growth (ß = 11.00, 95% CI 5.22-16.78, p = 0.00027), reduced NIH Stroke Scale score improvement at 24 hours (ß = -4.06, 95% CI 6.78-1.34, p = 0.004) and being dependent or dead at 90 days as assessed by the modified Rankin Scale (aOR 3.72, 95% CI 1.35-10.20, p = 0.011) in multivariable analysis. DISCUSSION: Cerebral no-reflow in humans is common, can be detected by its characteristic perfusion imaging profile using readily available sequences in the clinical setting, and is associated with posttreatment complications and being dependent or dead. Further studies evaluating the role of no-reflow in secondary injury after angiographic reperfusion are warranted. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that cerebral no-reflow on CT/MRI perfusion imaging at 24 hours is associated with posttreatment complications and poor 3-month functional outcome.

Tenecteplase vs Alteplase Before Endovascular Therapy in Basilar Artery Occlusion.

OBJECTIVE: To investigate the efficacy of tenecteplase (TNK), a genetically modified variant of alteplase with greater fibrin specificity and longer half-life than alteplase, prior to endovascular thrombectomy (EVT) in patients with basilar artery occlusion (BAO). METHODS: To determine whether TNK is associated with better reperfusion rates than alteplase prior to EVT in BAO, clinical and procedural data of consecutive patients with BAO from the Basilar Artery Treatment and Management (BATMAN) registry and the Tenecteplase vs Alteplase before Endovascular Therapy for Ischemic Stroke (EXTEND-IA TNK) trial were retrospectively analyzed. Reperfusion >50% or absence of retrievable thrombus at the time of the initial angiogram was evaluated. RESULTS: We included 110 patients with BAO treated with IV thrombolysis prior to EVT (mean age 69 [SD 14] years; median NIH Stroke Scale score 16 [interquartile range (IQR) 7-32]). Nineteen patients were thrombolysed with TNK (0.25 mg/kg or 0.40 mg/kg) and 91 with alteplase (0.9 mg/kg). Reperfusion >50% occurred in 26% (n = 5/19) of patients thrombolysed with TNK vs 7% (n = 6/91) thrombolysed with alteplase (risk ratio 4.0, 95% confidence interval 1.3-12; p = 0.02), despite shorter thrombolysis to arterial puncture time in the TNK-treated patients (48 [IQR 40-71] minutes) vs alteplase-treated patients (110 [IQR 51-185] minutes; p = 0.004). No difference in symptomatic intracranial hemorrhage was observed (0/19 [0%] TNK, 1/91 [1%] alteplase; p = 0.9). CONCLUSIONS: TNK may be associated with an increased rate of reperfusion in comparison with alteplase before EVT in BAO. Randomized controlled trials to compare TNK with alteplase in patients with BAO are warranted. CLINICALTRIALSGOV IDENTIFIERS: NCT02388061 and NCT03340493. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that TNK leads to higher reperfusion rates in comparison with alteplase prior to EVT in patients with BAO.

Stroke-like migraine attacks after radiation therapy syndrome: a case report and literature review.

Stroke-like migraine attacks after radiation therapy syndrome is a late complication of cranial radiation. It typically presents as reversible, unilateral cortical signs and symptoms such as confusion, hemiparesis, seizures, and headaches. Magnetic resonance imaging is also required for diagnosis, demonstrating cortical linear gadolinium enhancement. Typically, these magnetic resonance imaging findings resolve as patients experience partial or complete improvement in their symptoms and signs after a few weeks. Although a very rare condition, it is becoming increasingly observed as survival rates from brain tumors improve. In this report, we describe a typical case of stroke-like migraine attacks after radiation therapy syndrome and present a review of the literature.

Therapy of paraneoplastic disorders of the CNS.

Paraneoplastic neurological syndromes affecting the CNS are rare, presenting in less than 1% of all those with cancer. However, they account for significant disability and may respond to treatment. The pathogenesis of paraneoplastic neurological syndromes is presumed to relate to loss of self-tolerance spilling over from the immune attack on the underlying neoplasm. Testing for anti-neuronal antibodies is now available in most tertiary laboratories, enabling targeted therapies. While the evidence base for treatment is limited, the response to treatment can be largely determined based on the location of the target antigen; antibodies against cell surface antigens responding well to treatments targeting the humoral response. Intracellular antigen-target syndromes respond less well, but may theoretically respond best to T-cell based therapies. In both cases, aggressive tumor therapy is indicated.