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1. Happi Ngankou E, Gory B, Marnat G, et al. Thrombectomy complications in large vessel occlusions: incidence, predictors, and clinical impact in the ETIS Registry. Stroke 2021;52:e764–68

This study is a retrospective analysis of 4029 stroke patients with anterior large vessel occlusions treated with thrombectomy between January 2015 and May 2020 in 18 centers. The authors systematically collected procedural data, incidence of embolic complications, perforations and dissections, clinical outcome at 90 days, and hemorrhagic complications.

Procedural complications occurred in 7.99%, and embolus to a new territory (ENT) was the most frequent (5.2%). Predictors of embolus to a new territory were terminal carotid/tandem occlusion and an increased total number of passes. ENTs were associated to worse clinical outcomes, increased mortality, and symptomatic intracerebral hemorrhage. Perforations occurred in 1.69%.  Predictors of perforations were terminal carotid/tandem occlusions (39.7% versus 27.6%). 40.7% of patients died at 90 days, and the overall rate of poor outcome was 74.6% in case of perforation. Dissections occurred in 1.46% and were more common in younger patients. Dissections did not affect the clinical outcome at 90 days. Besides dissection, complications were independent of the thrombectomy technique.

Whereas dissection did not affect clinical outcome, embolus to a new territory and perforations have a substantial negative clinical effect. ENTs and perforations were related to terminal carotid/tandem occlusions and an increased number of passes for ENTs, but the thrombectomy technique had no impact on procedural complications.

2 tables, 1 figure, no imaging

2. Visser MJ, Yang JY-M, Calamante F, et al. Automated perfusion-diffusion magnetic resonance imaging in childhood arterial ischemic stroke. Stroke 2021;52:32 96–3304

Recent studies using automated perfusion imaging software have identified adults most likely to benefit from reperfusion therapies in extended time windows. The time course of penumbral tissue is poorly characterized in childhood arterial ischemic stroke (AIS). The authors explored the feasibility of using automated perfusion-diffusion imaging software to characterize penumbra in childhood AIS.

Diffusion-weighted imaging and dynamic susceptibility contrast perfusion magnetic resonance imaging performed within 72 hours of symptom onset were acquired in 29 children in this cohort study. Perfusion-diffusion mismatch was estimated using RAPID software. Ischemic core was defined as ADC <620×10−6 mm2/s and hypoperfusion as Tmax >6 seconds. Favorable mismatch profile was defined as core volume <70 mL, mismatch volume ≥15 mL, and a mismatch ratio ≥1.8. Patients had 26 unilateral middle cerebral artery and 3 unilateral cerebellar infarcts.

Most cases had cryptogenic (n=11) or focal cerebral arteriopathy (n=9) causes. Median time-to-imaging was 13.7 hours. RAPID detected an ischemic core in 19 (66%) patients. In the remaining cases, the mean apparent diffusion coefficient values were mostly higher than the threshold as the majority of these presentations were delayed (median >21 hours) and infarct volumes were small (<3.5 mL). Overall, 3 children, imaged at 3.75, 11, and 23.5 hours had favorable mismatch profiles.

The majority of children had unilateral subcortical middle cerebral artery infarcts. Twelve children had vascular occlusion on MR angiography, which included 5 with large anterior vessel occlusion (internal carotid artery or M1), 5 children with M2 occlusions, and 2 children with posterior circulation occlusions. All 3 children who had mismatch had a large vessel occlusion, one of whom received intravenous alteplase. A further 9 children had vascular stenoses and 8 had normal vascular imaging. Focal cerebral arteriopathy was the most common identifiable cause (31%). The cause of stroke was undetermined in 41%. The median stroke volume for the entire sample was 12.6 mL. Eighteen participants required general anesthetic before their imaging scans.

This study demonstrates it is feasible to rapidly assess perfusion-diffusion mismatch in childhood AIS using automated software. Favorable mismatch profiles, using adult-based parameters, persisted beyond the standard 4.5 hours window for thrombolysis, suggesting potential therapeutic benefit of RAPID use.

3 figures, 2 tables

3. van der Kamp LT, Rinkel GJE, Verbaan D, et al. Risk of rupture after intracranial aneurysm growth. JAMA Neurol 2021;78:12 28–35

To determine the absolute risk of rupture of an aneurysm after detection of growth during follow-up and to develop a prediction model for rupture. Individual patient data were obtained from 15 international cohorts. Patients 18 years and older who had follow-up imaging for at least 1 untreated unruptured intracranial aneurysm with growth detected at follow-up imaging and with 1 day or longer of follow-up after growth were included. Fusiform or arteriovenous malformation-related aneurysms were excluded. Of the 5166 eligible patients who had follow-up imaging for intracranial aneurysms, 4827 were excluded because no aneurysm growth was detected, and 27 were excluded because they had less than 1 day follow-up after detection of growth. All included aneurysms had growth, defined as 1mm or greater increase in 1 direction at follow-up imaging.

A total of 312 patients were included (71% women; mean age,61 years) with 329 aneurysms with growth. During 864 aneurysm-years of follow-up, 25 (7.6%) of these aneurysms ruptured. The absolute risk of rupture after growth was 2.9% at 6 months, 4.3% at 1 year, and 6.0% at 2 years. In multivariable analyses, predictors of rupture were size (7mm or larger), shape (irregular), and site (middle cerebral artery; anterior cerebral artery, posterior communicating artery, or posterior circulation). In the triple-S prediction model based on 3 independent predictors of rupture (size, site, and shape), the 1-year risk of rupture ranged from 2.1% to 10.6%.

The authors state that the implications for clinical practice from the study are that preventive endovascular or neurosurgical aneurysm treatment should be reconsidered as soon as aneurysm growth is detected. In such instances of aneurysm growth, the triple-S prediction model can be used by physicians and patients as a starting point for discussing the pros and cons of preventive aneurysm treatment. If it is decided to continue follow-up imaging, it seems reasonable to repeat imaging at a short interval, but actual data on the optimal time interval are lacking and should be gathered in future studies.

4. Liotta EM. Management of cerebral edema, brain compression, and intracranial pressure. Continuum (Minneap Minn) 2021;27:11 72–1200

Cerebral edema and brain compression should be treated in a tiered approach after the patient demonstrates a symptomatic indication to start treatment. All patients with acute brain injury should be treated with standard measures to optimize intracranial compliance and minimize risk of ICP elevation. When ICP monitors are used, therapies should target maintaining ICP at 22 mm Hg or less. Evidence exists that serial clinical examination and neuroimaging may be a reasonable alternative to ICP monitoring; however, clinical trials in progress may demonstrate advantages to advanced monitoring techniques. Early decompressive craniectomy and hypothermia are not neuroprotective in traumatic brain injury and should be reserved for situations refractory to initial medical interventions. Medical therapies that acutely lower plasma osmolality may lead to neurologic deterioration from osmotic cerebral edema, and patients with acute brain injury and renal or liver failure are at elevated risk.

This is an extensive review, and appropriately clinical in orientation, with some minor imaging examples.  However, the section on potential new therapies was also interesting, particularly the section on the glymphatic system.

The precise processes by which glymphatic function might contribute to cerebral edema formation are yet to be fully delineated, but several lines of evidence suggest a critical role. Recently, CSF was demonstrated to be the source of fluid influx responsible for early brain swelling after ischemic stroke. In a mouse model of ischemic stroke, accelerated CSF influx into the brain parenchyma along perivascular spaces was observed within minutes of stroke. This CSF influx followed the wave of spreading depolarization that occurred with the loss of ionic gradients during cellular death and appeared to be the result of parenchymal and pial arteriole vasoconstriction precipitated by the spreading depolarization. Interestingly, the magnitude of CSF influx was reduced in AQP4-deficient mice. The authors acknowledged that this process would not completely explain cerebral edema formation after ischemic stroke but proposed that it could also contribute to cerebral edema formation in other diseases in which spreading depolarizations have been observed, such as subarachnoid hemorrhage, intracerebral hemorrhage, and TBI. Glymphatic dysfunction in clearing t