actor associated with outcomes and mortality in COVID-19 patients includes cardiovascular and cerebrovascular comorbidities but the underlying mechanisms are still hypothetical 1. We report the case ...of a 73-year-old patient who developed within a week after the onset of respiratory symptoms related to SARS-CoV2 infection, an acute ischemic stroke (AIS) complicating a large floating thrombus within the common carotid artery. The patient has no specific past medical history, no treatment and no vascular risk factors. He presented at the emergency department on March 25th for the onset of fever and dry cough. Clinical evaluation was reassuring and the patient was discharged home. He was readmitted 7 days later for the acute onset of aphasia and right hemiparesis evolving for 9 hours. On admission, the patient was in respiratory distress, and neurological examination revealed a left middle cerebral artery (MCA) syndrome with a NIH stroke scale (NIHSS) of 10. Chest CT showed ground glass opacities typically reported in SARS-CoV2 infection, which was subsequently confirmed by real-time reverse transcriptase–polymerase chain reaction assay on a nasopharyngeal swab sample. Brain Computer Tomography (CT), CT angiography (CTA) and CT perfusion, performed on a 64-channel scanner (Optima, General Electric, USA), showed subtle cortical left frontal hypoattenuation with more extended surrounding hypoperfusion and distal occlusion of branch. CT perfusion was acquired before CTA, and both were performed using, for each, a 40 cc-bolus of iodine contrast injected at a 5 cc/sec rate (iobitridol 350, Guerbet, France), pushed by 40 cc of physiological serum. Cervical CTA also revealed a large intraluminal floating thrombus appended to a hypoattenuated non-stenosing plaque of the left common carotid artery wall. Dedicated wall imaging with 3 T MRI (Skyra, Siemens, Germany) and Doppler ultrasoonography confirmed the diagnosis of a large thrombus adherent to a thin atheromatous plaque. Of note, those examination disclosed no ulceration, plaque hemorrhage or circumferential gadolinium enhancement of the wall potentially suggestive of arteritis. Diffusion-Weighted Imaging performed 2 days later confirmed the diagnosis of multiple AIS with foci of hyperintensity scattered within left carotid territory.
After cerebral ischemia, events like neural plasticity and tissue reorganization intervene in lesioned and non-lesioned areas of the brain. These processes are tightly related to functional ...improvement and successful rehabilitation in patients. Plastic remodeling in the brain is associated with limited spontaneous functional recovery in patients. Improvement depends on the initial deficit, size, nature and localization of the infarction, together with the sex and age of the patient, all of them affecting the favorable outcome of reorganization and repair of damaged areas. A better understanding of cerebral plasticity is pivotal to design effective therapeutic strategies. Experimental models and clinical studies have fueled the current understanding of the cellular and molecular processes responsible for plastic remodeling. In this review, we describe the known mechanisms, in patients and animal models, underlying cerebral reorganization and contributing to functional recovery after ischemic stroke. We also discuss the manipulations and therapies that can stimulate neural plasticity. We finally explore a new topic in the field of ischemic stroke pathophysiology, namely the brain-gut axis.
Ultrasound characteristics of carotid web Fontaine, Louis; Guidolin, Brigitte; Viguier, Alain ...
Journal of neuroimaging,
September/October 2022, Volume:
32, Issue:
5
Journal Article
Peer reviewed
Open access
Background and Purpose
Carotid web (CaW) is a cause of recurrent ischemic stroke that remains underdiagnosed using Duplex ultrasound (DUS). Improved methods and description of its ultrasound's ...features could allow better detection of CaW. Ultrasound microflow imaging (MFI) is a blood flow imaging technique sensitive to slow flow that could increase CaW detection. This study aimed to describe ultrasound features of CaW using B‐mode imaging and MFI.
Methods
In a retrospective monocentric study, patients with CaW on CT angiography who underwent DUS examination of carotid arteries were included. DUS was performed by two nonblinded experienced neurosonologists. The specificity of CaW ultrasound features was evaluated using a group of patients with carotid atherosclerotic plaque (AP).
Results
Twenty‐four patients with CaW were included. Mean age (standard deviation) was 48 years (11). Seventeen (71%) were females. Fifteen (63%) CaWs were symptomatic. MFI was available for 22 patients. B‐mode imaging demonstrated the characteristic CaW appearance in 19/24 (79%) patients as a protruding triangular iso‐hypoechoic lesion on longitudinal view. CaW were detected on axial view in only 9/24 (38%) patients. MFI displayed slow blood flow above CaW during systole and allowed it delineation, appearing as a thin triangular endoluminal defect in 18/22 (82%) cases. Based on MFI and B‐mode, 21/22 (95%) CaWs were visible, including three CaWs only with MFI. These ultrasound features were not found among 24 patients with AP.
Conclusion
We report the ultrasound features from a series of 24 CaW. The use of MFI in addition to B‐mode imaging improved the detection rate of CaW.
Summary Background Carotid stenting is a potential alternative to carotid endarterectomy but whether this technique is as safe as surgery and whether the long-term protection against stroke is ...similar to that of surgery are unclear. We previously reported that in patients in the Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial, the rate of any stroke or death within 30 days after the procedure was higher with stenting than with endarterectomy. We now report the results up to 4 years. Methods In this follow-up study of a multicentre, randomised, open, assessor-blinded, non-inferiority trial, we compared outcome after stenting with outcome after endarterectomy in 527 patients who had carotid stenosis of at least 60% that had recently become symptomatic. The primary endpoint of the EVA-3S trial was the rate of any periprocedural stroke or death (ie, within 30 days after the procedure). The prespecified main secondary endpoint was a composite of any periprocedural stroke or death and any non-procedural ipsilateral stroke during up to 4 years of follow-up. Other trial outcomes were any stroke or periprocedural death, any stroke or death, and the above endpoints restricted to disabling or fatal strokes. This trial is registered with ClinicalTrials.gov , number NCT00190398. Findings 262 patients were randomly assigned to endarterectomy and 265 to stenting. The cumulative probability of periprocedural stroke or death and non-procedural ipsilateral stroke after 4 years of follow-up was higher with stenting than with endarterectomy (11·1% vs 6·2%, hazard ratio HR 1·97, 95% CI 1·06–3·67; p=0·03). The HR for periprocedural disabling stroke or death and non-procedural fatal or disabling ipsilateral stroke was 2·00 (0·75–5·33; p=0·17). A hazard function analysis showed the 4-year differences in the cumulative probabilities of outcomes between stenting and endarterectomy were largely accounted for by the higher periprocedural (within 30 days of the procedure) risk of stenting compared with endarterectomy. After the periprocedural period, the risk of ipsilateral stroke was low and similar in both treatment groups. For any stroke or periprocedural death, the HR was 1·77 (1·03–3·02; p=0·04). For any stroke or death, the HR was 1·39 (0·96–2·00; p=0·08). Interpretation The results of this study suggest that carotid stenting is as effective as carotid endarterectomy for middle-term prevention of ipsilateral stroke, but the safety of carotid stenting needs to be improved before it can be used as an alternative to carotid endarterectomy in patients with symptomatic carotid stenosis. Funding French Ministry of Health.
Background and Purpose- Convexity subarachnoid hemorrhage (cSAH) is an increasingly recognized presentation of cerebral amyloid angiopathy (CAA), usually revealed by transient symptoms, but data on ...its outcome are limited. We compared the risk of future intracerebral hemorrhage (ICH), cSAH, and death in patients with CAA after cSAH and after lobar ICH. Methods- Consecutive patients with probable CAA, based on the Boston criteria, presenting with cSAH (CAA-cSAH) or lobar ICH (CAA-ICH) were included. We obtained baseline clinical and magnetic resonance imaging data and follow-up information. Univariable and multivariable analyses were used to compare incidence rate for symptomatic ICH, symptomatic cSAH, and late-death (beyond 30 days) between patients with CAA-cSAH and CAA-ICH. Results- Among 105 patients (mean age, 76.7±7.5 years) enrolled, 44 participants presented with CAA-cSAH and 61 with CAA-ICH. The median follow-up was 22.2 months (interquartile range, 12.6-34.4). The symptomatic ICH rate (per person-year) was 10.5% (95% CI, 5.6-19.4) in patients with CAA-cSAH compared with 8.5% (95% CI, 4.4-16.4) in those with CAA-ICH (adjusted hazard ratio, 1.05; 95% CI, 0.32-3.43). The annual incidence rates of symptomatic cSAH (9.9% versus 3.8%; adjusted hazard ratio, 1.77; 95% CI, 0.43-7.28) and death (9.5% versus 17.8%; adjusted hazard ratio, 0.56; 95% CI, 0.22-1.43) were not significantly different between patients with CAA-cSAH and those with CAA-ICH. Conclusions- Patients with CAA-related cSAH have a poor outcome, with similar high risk of future ICH and long-term mortality than CAA patients after lobar ICH. Our findings may have important prognostic implication and guide management of patients with cSAH in CAA.
Background:
Leptomeningeal enhancement (LME) is a key feature of Susac syndrome (SuS) but is only occasionally depicted on post-contrast T1-weighted images (T1-WI).
Objective:
As post-contrast ...fluid-attenuated inversion recovery (FLAIR) may be more sensitive, our aim was to assess LME in SuS on this sequence.
Methods:
From 2010 to 2020, 20 patients with definite SuS diagnosis were retrospectively enrolled in this multicentre study. Two radiologists independently assessed the number of LME on post-contrast FLAIR and T1-WI acquisitions performed before any treatment. A chi-square test was used to compare both sequences and the interrater agreement was calculated.
Results:
Thirty-five magnetic resonance imagings (MRIs) were performed before treatment, including 19 post-contrast FLAIR images in 17 patients and 25 post-contrast T1-WI in 19 patients. In terms of patients, LME was observed on all post-contrast FLAIR, contrary to post-contrast T1-WI (17/17 (100%) vs. 15/19 (79%), p < 0.05). In terms of sequences, LME was observed on all post-contrast FLAIR, contrary to post-contrast T1-WI (19/19 (100%) vs. 16/25 (64%), p < 0.005). LME was disseminated at both supratentorial (19/19) and infratentorial (18/19) levels on post-contrast FLAIR, contrary to post-contrast T1-WI (3/25 and 9/25, respectively). Interrater agreement was excellent for post-contrast FLAIR (κ = 0.95) but only moderate for post-contrast T1-WI (κ = 0.61).
Conclusion:
LME was always observed and easily visible on post-contrast FLAIR images prior to SuS treatment. In association with other MRI features, it is highly indicative of SuS.
To describe the clinico-radiological features and long-term prognosis in patients with cerebral amyloid angiopathy-related inflammation (CAA-ri).
Twenty-eight CAA-ri patients were recruited ...retrospectively from 6 neurological centers. We recorded the clinico-radiological and biological data, at baseline and during follow-up. Baseline characteristics associated with relapse risk and prognosis were assessed.
Five patients had pathologically confirmed CAA-ri whereas 23 had probable (n = 21) or possible (n = 2) CAA-ri. The mean age was 72 years; main clinical symptoms included confusion (54%), hemiparesis (36%), and aphasia (29%). Cerebral MRI disclosed a brain parenchymal lesion (89%), which was usually multifocal (82%) and bilateral (89%). It was associated with gadolinium enhancement (84%), small ischemic lesions (39%), cortical superficial siderosis (CSS; 50%), and a high number of microbleeds (mean 240 ± 277). An isolated leptomeningeal involvement was observed in 3 patients with pathological confirmation. Despite a favorable initial evolution after treatment, we observed a 42% risk of relapse, mostly within the first year (83%). After a mean follow-up of 2 years, 29% died and 25% had a marked disability. Disseminated CSS was associated with death.
Despite an apparently favorable initial evolution, CAA-ri is characterized by a poor prognosis. Diagnostic criteria should consider patients with isolated leptomeningeal involvement.
Background and Purpose:
Whether patients with both lobar and deep cerebral microbleeds (mixed CMB) have advanced cerebral amyloid angiopathy (CAA), hypertensive angiopathy (HA) or both is uncertain. ...To get insight into the underlying small vessel disease (SVD) associated with mixed CMB, we explored its association with cortical superficial siderosis (cSS), a key marker of CAA and other MRI markers of SVD in patients with intracerebral hemorrhage (ICH).
Methods:
Of 425 consecutive patients with acute ICH who had received brain MRIs, 260 had ≥1 CMB and were included in the analysis. They were categorized as strictly lobar CMB (suggesting CAA), strictly deep CMB (suggesting HA) or mixed CMB. Clinical and imaging characteristics were compared (1) between the three CMB groups and (2) within mixed CMB patients according to the symptomatic ICH location.
Results:
Overall, 111 (26%) patients had mixed CMB. Compared to strictly lobar CMB (
n
= 111) and strictly deep CMB (
n
= 38), patients with mixed CMB had a more severe burden of lacune, white matter hyperintensities and CMB. cSS was observed in 24.3% of patients with mixed CMB compared to 44.1% in strictly lobar CMB and 10.5% in strictly deep CMB (
p
< 0.0001). Among patients with mixed CMB, 44 (39.6%) had a lobar symptomatic ICH and 67 (60.4%) had a non-lobar ICH. Patients with non-lobar ICH were more likely to have hypertension, whereas those with lobar ICH were more likely to have cSS and chronic lobar ICH and had higher ratio lobar CMB count/total CMB count.
Conclusions:
Mixed CMB is frequently encountered in patients with ICH and appears as a heterogeneous group, suggesting that both CAA and HA may be contributing to mixed CMB. Neuroimaging markers including ICH location, cSS, and CMB distribution may indicate the predominant underlying vasculopathy, with potential prognostic implications.
Acute ischaemic stroke represents the most common cause of new sudden neurological deficit, but other diseases mimicking stroke happen in about one-third of the cases. Magnetic resonance imaging ...(MRI) is the best technique to identify those ‘stroke mimics’. In this article, we propose a diagnostic approach of those stroke mimics on MRI according to an algorithm based on diffusion-weighted imaging (DWI), which can be abnormal or normal, followed by the results of other common additional MRI sequences, such as T2 with gradient recalled echo weighted imaging (T2-GRE) and fluid-attenuated inversion recovery (FLAIR). Analysis of the signal intensity of the parenchyma, the intracranial arteries and, overall, of the veins, is crucial on T2-GRE, while anatomic distribution of the parenchymal lesions is essential on FLAIR. Among stroke mimics with abnormal DWI, T2-GRE demonstrates obvious abnormalities in case of intracerebral haemorrhage or cerebral amyloid angiopathy, but this sequence also allows to propose alternative diagnoses when DWI is negative, such as in migraine aura or headaches with associated neurological deficits and lymphocytosis (HaNDL), in which cortical venous prominence is observed at the acute phase on T2-GRE. FLAIR is also of major interest when DWI is positive by better showing evocative distribution of cerebral lesions in case of seizure (involving the hippocampus, pulvinar and cortex), hypoglycaemia (bilateral lesions in the posterior limb of the internal capsules, corona radiata, striata or splenium of the corpus callosum) or in posterior reversible encephalopathy syndrome (PRES). Other real stroke mimics such as mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes (MELAS), Susac’s syndrome, brain tumour, demyelinating diseases and herpes simplex encephalitis are also included in our detailed and practical algorithm.
Key points
• About 30% of sudden neurological deficits are due to non-ischaemic causes.
• MRI is the best technique to identify stroke mimics.
• Our practical illustrated algorithm based on DWI helps to recognise stroke mimics.
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