No abstract

Background and Purpose— It has been hypothesized that in stroke patients, complete reperfusion (modified Thrombolysis in Cerebral Infarction; mTICI 3) after a single thrombectomy pass is a predictor for favorable outcome (modified Rankin Scale score, 0–2), but a true first-pass effect defined as improved clinical outcome after complete reperfusion with one versus multiple passes has not yet been specifically addressed in the literature. Methods— We compared clinical outcome of 164 consecutive patients with occlusions in the anterior circulation and known symptom onset, in whom we achieved complete reperfusion (mTICI 3), depending on whether complete reperfusion was achieved after a single thrombectomy pass (n=62) or multiple thrombectomy passes (n=102). To adjust for confounding factors such as prolonged time spans between symptom onset and reperfusion, additional administration of intra-arterial thrombolysis, and clot localization, we also compared clinical outcome of our first-pass group with a matched cohort (n=54) and a superselective subgroup of first-pass patients (only M1 occlusions, no additional intra-arterial thrombolysis; n=46) with its matched cohort (n=24). Results— Multivariable analysis of our cohort of 164 nonmatched patients revealed that there was a significant association between first-pass complete reperfusion and favorable clinical outcome ( P =0.013). This was confirmed in our case-control analyses ( P =0.010 and P =0.042). In our matched cohorts, favorable clinical outcome was seen almost twice as often if complete reperfusion was achieved after one pass (62% and 67% versus 36% and 37%), and odds for favorable outcome were 2.4 to 3.2× higher (CIs, 1.1–4.8 and 1.0–9.9). Conclusions— First-pass complete reperfusion is an independent factor for favorable outcome and should be aimed for in mechanical thrombectomy.

SAVE is fast and appears to be very effective in terms of first-pass complete reperfusion in patients with LVO.

IMPORTANCE Randomized clinical trials have shown the efficacy of thrombectomy of large intracranial vessel occlusions in adults; however, any association of therapy with clinical outcomes in children is unknown. OBJECTIVE To evaluate the use of endovascular recanalization in pediatric patients with arterial ischemic stroke. DESIGN, SETTING, AND PARTICIPANTS This retrospective, multicenter cohort study, conducted from January 1, 2000, to December 31, 2018, analyzed the databases from 27 stroke centers in Europe and the United States. Included were all pediatric patients (<18 years) with ischemic stroke who underwent endovascular recanalization. Median follow-up time was 16 months. EXPOSURES Endovascular recanalization. MAIN OUTCOMES AND MEASURES The decrease of the Pediatric National Institutes of Health Stroke Scale (PedNIHSS) score from admission to day 7 was the primary outcome (score range: 0 [no deficit] to 34 [maximum deficit]). Secondary clinical outcomes included the modified Rankin scale (mRS) (score range: 0 [no deficit] to 6 [death]) at 6 and 24 months and rate of complications. RESULTS Seventy-three children from 27 participating stroke centers were included. Median age was 11.3 years (interquartile range [IQR], 7.0-15.0); 37 patients (51%) were boys, and 36 patients (49%) were girls. Sixty-three children (86%) received treatment for anterior circulation occlusion and 10 patients (14%) received treatment for posterior circulation occlusion; 16 patients (22%) received concomitant intravenous thrombolysis. Neurologic outcome improved from a median PedNIHSS score of 14.0 (IQR, 9.2-20.0) at admission to 4.0 (IQR, 2.0-7.3) at day 7. Median mRS score was 1.0 (IQR, 0-1.6) at 6 months and 1.0 (IQR, 0-1.0) at 24 months. One patient (1%) developed a postinterventional bleeding complication and 4 patients (5%) developed transient peri-interventional vasospasm. The proportion of symptomatic intracerebral hemorrhage events in the HERMES meta-analysis of trials with adults was 2.79 (95% CI, 0.42-6.66) and in Save ChildS was 1.37 (95% CI, 0.03-7.40). CONCLUSIONS AND RELEVANCE The results of this study suggest that the safety profile of thrombectomy in childhood stroke does not differ from the safety profile in randomized clinical trials for adults; most of the treated children had favorable neurologic outcomes. This study may support clinicians' practice of off-label thrombectomy in childhood stroke in the absence of high-level evidence.

Cerebral cavernous malformations (CCM) are prevalent vascular malformations occurring in familial autosomal dominantly inherited or isolated forms. Once CCM are diagnosed by magnetic resonance imaging, the indication for genetic testing requires either a positive family history of cavernous lesions or clinical symptoms such as chronic headaches, epilepsy, neurological deficits, and hemorrhagic stroke or the occurrence of multiple lesions in an isolated case. Following these inclusion criteria, the mutation detection rates in a consecutive series of 105 probands were 87% for familial and 57% for isolated cases. Thirty-one novel mutations were identified with a slight shift towards proportionally more CCM3 mutations carriers than previously published (CCM1: 60%, CCM2: 18%, CCM3: 22%). In-frame deletions and exonic missense variants requiring functional analyses to establish their pathogenicity were rare: An in-frame deletion within the C-terminal FERM domain of CCM1 resulted in decreased protein expression and impaired binding to the transmembrane protein heart of glass (HEG1). Notably, 20% of index cases carrying a CCM mutation were below age 10 and 33% below age 18 when referred for genetic testing. Since fulminant disease courses during the first years of life were observed in CCM1 and CCM3 mutation carriers, predictive testing of minor siblings became an issue.

There is a broad consensus that MS represents more than an inflammatory disease: it harbors several characteristic aspects of a classical neurodegenerative disorder, i.e. damage to axons, synapses and nerve cell bodies. While the clinician is equipped with appropriate tools to dampen peripheral cell recruitment and, thus, is able to prevent immune-cell driven relapses, effective therapeutic options to prevent the simultaneously progressing neurodegeneration are still missing. Furthermore, while several sophisticated paraclinical methods exist to monitor the inflammatory-driven aspects of the disease, techniques to monitor progression of early neurodegeneration are still in their infancy and have not been convincingly validated. In this review article, we aim to elaborate why the thalamus with its multiple reciprocal connections is sensitive to pathological processes occurring in different brain regions, thus acting as a "barometer" for diffuse brain parenchymal damage in MS. The thalamus might be, thus, an ideal region of interest to test the effectiveness of new neuroprotective MS drugs. Especially, we will address underlying pathological mechanisms operant during thalamus degeneration in MS, such as trans-neuronal or Wallerian degeneration. Furthermore, we aim at giving an overview about different paraclinical methods used to estimate the extent of thalamic pathology in MS patients, and we discuss their limitations. Finally, thalamus involvement in different MS animal models will be described, and their relevance for the design of preclinical trials elaborated.

PCHD was not a risk factor for parenchymal haemorrhage in our series. The occurrence of PCHD was strongly related to the prior presence of infarction. PCHD was also a strong predictor for final infarction size.

ObjectiveTo study the diagnostic value of volume perfusion CT (VPCT) in patients with transient focal neurologic deficits following and during epileptic seizures, that mimic symptoms of stroke.MethodsA retrospective case-control study was performed on 159 patients who presented with a seizure and received an emergency VPCT within the first 3.5 hours of admission, after being misjudged to have an acute stroke. The reference test was a clinical-based, EEG-supported diagnostic algorithm for seizure.ResultsWe included 133 patients: 94 stroke-mimicking cases with postictal focal neurologic deficits (“Todd phenomenon,” n = 67) or ongoing seizure on hospital admission (“ictal patients,” n = 27), and 39 postictal controls without focal neurologic deficits. Patients with Todd phenomenon showed normal perfusion (64%), hypoperfusion (21%), and hyperperfusion (14%) on early VPCT. Ictal patients displayed more hyperperfusion compared to postictal patients (p = 0.015). Test sensitivity of hyperperfusion for ictal patients is 38% (95% confidence interval [CI] 20.7%–57.7%), specificity 86% (95% CI 77.3%–91.7%), positive predictive value is 42% (95% CI 27.5%–58.7%), and the negative predictive value 83% (95% CI 78.6%–86.9%). A cortical distribution was seen in all hyperperfusion scans, compared to a cortico-subcortical pattern in hypoperfusion (p < 0.001). A history of complex focal seizure and age were associated with hyperperfusion (p = 0.046 and 0.038, respectively).ConclusionVPCT can differentiate ictal stroke mimics with hyperperfusion from acute ischemic stroke, but not postictal patients who display perfusion patterns overlapping with ischemic stroke.Classification of evidenceThis study provides Class IV evidence that VPCT accurately differentiates ictal stroke mimics from acute ischemic stroke.