[Prevention of contrast-induced nephropathy]. / Prévention de la néphropathie aux produits de contraste iodés.

Contrast-induced nephropathy (CIN) is a renal complication occurring after the administration of iodinated contrast agents routinely used in medical imaging. CIN causes acute renal failure of varying severity. The pathophysiology of CIN is probably multifactorial: it involves (i) renal vasoconstriction inducing tissue hypoxia, and (ii) a possible direct toxicity of iodine derivatives leading to tubular inflammation and necrosis. Several risk factors are associated with CIN, some related to the procedure itself, others to the patient's co-morbid profile. In particular, the pre-existence of chronic renal failure, dehydration, congestive heart failure, diabetes or hypotension has been associated with an increased risk of CIN, as summarized in the Mehran score. Prevention of CIN relies essentially on adequate i.v. hydration before and after the procedure, and on the administration of the lowest possible volumes of contrast. In patients at high risk of CIN, the use of metformin and non-steroidal anti-inflammatory drugs is contraindicated at the time of contrast medium i.v. injection. In these patients, renal function assessment after 3-7 days post imaging is required.

La néphropathie aux produits de contraste iodés (NPCI) est une complication rénale survenant après l'administration de certains agents de contraste utilisés en imagerie médicale. La NPCI cause une insuffisance rénale aiguë de gravité variable. La physiopathologie de la NPCI est probablement multifactorielle : elle implique (i) une vasoconstriction rénale induisant une hypoxie tissulaire et (ii) une possible toxicité directe des dérivés iodés entraînant inflammation et nécrose tubulaire. Plusieurs facteurs de risque sont associés à la NPCI, liés tantôt à la procédure elle-même, tantôt aux comorbidités du patient. La préexistence d'une insuffisance rénale chronique, d'une déshydratation, d'une insuffisance cardiaque congestive, d'un diabète ou d'une hypotension artérielle a, notamment, été associée à un risque accru de NPCI, tel que résumé dans le score de Mehran. La prévention de la NPCI repose essentiellement sur une hydratation i.v. adéquate avant et après la procédure, ainsi que sur l'administration de volumes de contraste aussi faibles que possible. Chez les patients à haut risque de NPCI, l'utilisation de metformine et/ou d'anti-inflammatoires non stéroïdiens concomitante à l'injection de PCI est formellement contre-indiquée, et la vérification de la fonction rénale à J3-J7 après l'examen radiologique est requise.

Spinal cord involvement in progressive multifocal leukoencephalopathy and immune reconstitution inflammatory syndrome.

Progressive multifocal leukoencephalopathy (PML) is an opportunistic infectious demyelinating disease of the central nervous system caused by JC polyomavirus predominantly affecting immunocompromised individuals. Nowadays, HIV, hematological malignancies and iatrogenic immune suppression account for most PML cases. For unknown reasons, spinal cord is classically protected from PML lesions. Here, we report the course of a patient harboring spinal cord lesions in the context of PML with immune reconstitution inflammatory syndrome and review the eight other cases reported in the literature so far. Then, we discuss the evolving spectrum of PML over recent years, potentially making its diagnosis more challenging.

[How do I investigate... the vulnerability of a carotid artery plaque in 2024]. / Comment j'explore la vulnérablilité d'une plaque carotidienne en 2024.

Carotid artery atherosclerosis is one of the leading causes of stroke. Even though the association between the risk of stroke and the level of morphological stenosis of a carotid plaque has been known for a long time, growing evidence has since proven necessary to assess the composition of the plaque itself to identify vulnerability predictors. These vulnerable plaques, even more if non-stenosing, may be responsible for a significant - but hard to quantify - proportion of strokes so far classified cryptogenic. As a matter of fact, plaque composition may escape detection and characterisation with classical imaging. Several biomarkers associated with its vulnerability to destabilization and with the risk of stroke such as intraplaque hemorrhage and inflammation are now routinely assessable. After a few pathophysiological reminders and a critical reading of the historical literature concerning carotid artery atherosclerosis management, we will review in this article the imaging techniques that can be used in the routine work-up of a carotid atherosclerotic plaque, with a focus on vessel wall magnetic resonance imaging and contrast enhanced ultrasonography.

L'athérosclérose carotidienne est une des causes les plus fréquentes d'accident ischémique cérébral (AIC). Si la dangerosité d'une plaque d'athérome est historiquement vue uniquement à travers le prisme de la sténose qu'elle engendre, l'évolution des connaissances nous pousse à considérer sa composition à la recherche de facteurs de vulnérabilité. Ces plaques à risque, a fortiori «non sténosantes¼, sont responsables d'une proportion difficilement quantifiable, mais probablement non négligeable d'AIC jusqu'ici considérés cryptogéniques. En effet, ces critères échappent pour beaucoup aux méthodes d'imagerie traditionnelle. Plusieurs propriétés associées à la vulnérabilité de la plaque et au risque d'AIC, principalement l'hémorragie intra-plaque et l'inflammation, sont désormais accessibles en pratique courante. Après quelques rappels physiopathologiques et une lecture critique de la littérature historique de la prise en charge de l'athérome carotidien, nous passerons en revue les différentes techniques d'imagerie utilisables en routine dans la mise au point de la plaque d'athérosclérose, avec un focus pratique sur l'imagerie pariétale vasculaire par résonance magnétique et, dans une moindre mesure, par échographie de contraste.

The dural vascular plexus in subdural hematoma: Illustration through a case of dural arteriovenous fistula.

Background: The initiation of chronic subdural hematoma (cSDH) is traditionally explained by rupture of bridging veins. Recent descriptions of the embryology and anatomy of the meninges and their vascularization, however, point to the dural vascular plexus (DVP) as a plausible origin of cSDH. This dural plexus is supplied by meningeal arteries. Their endovascular occlusion is efficient in cSDH treatment. Dural arteriovenous fistulae (dAVF) may also present with subdural hematoma. Case Description: A 65-year-old female patient presented with parietal parasagittal dAVF and bilateral cSDH requiring surgical disconnection followed by complete clinical and imaging resolution of dAVF and cSDH. Conclusion: In common cSDH, pressure in the DVP may be normal and subdural bleeding may occur due to mechanical traction on the DVP. In the setting of dAVF, it may be the increase in pressure due to the fistula, within the DVP, that causes subdural hematoma. The DVP, supplied by meningeal arteries, thus not only allows for convergent pathophysiological explanation of subdural bleeding in both cSDH and dAVF but may also be the actual target of the emergent endovascular treatment of cSDH trough meningeal artery embolization.

Killing Two Birds With One Stone: Effective Control of Both Non-Small Cell Lung Cancer and Progressive Multifocal Leukoencephalopathy With Atezolizumab, A Case Report.

Treating patients with cancer complicated by severe opportunistic infections is particularly challenging since classical cancer treatments, such as chemotherapy, often induce profound immune suppression and, as a result, may favor infection progression. Little is known about the potential place of immune checkpoint inhibitors in these complex situations. Here, we report a 66-year-old man who was concomitantly diagnosed with non-small cell lung cancer and progressive multifocal leukoencephalopathy. The patient was treated with anti-PD-L1 antibody atezolizumab, which allowed effective control of both lung cancer and progressive multifocal leukoencephalopathy, as demonstrated by the patient's remarkable neurologic clinical improvement, JC viral load reduction in his cerebrospinal fluid, regression of the brain lesions visualized through MRI, and the strict radiological stability of his cancer. In parallel, treatment with atezolizumab was associated with biological evidence of T-cell reinvigoration. Hence, our data suggest that immune checkpoint inhibitors may constitute a treatment option for patients with cancer complicated by severe opportunistic infections.

E3 ubiquitin ligases and cerebral cortex development in health and disease.

Cerebral cortex development involves the sequential progression of biological steps driven by molecular pathways whose tight regulation often relies on ubiquitination. Ubiquitination is a posttranslational modification involved in all aspects of cellular homeostasis through the attachment of a ubiquitin (Ub) moiety on proteins. Over the past years, an increasing amount of research has highlighted the crucial role played by Ub ligases in every step of cortical development and whose impairment often leads to various neurodevelopmental disorders. In this review, we focus on the key contributions of E3 Ub ligases for the progression of the different steps of corticogenesis, as well as the pathological consequences of their mutations, often resulting in malformations of cortical development. Finally, we discuss some promising therapeutic strategies for these diseases based on recent advances in the field.

Multimodal imaging of a patient with RAB39B mutation.

Mutations in RAB39B gene have been linked to intellectual deficiency associated with parkinsonism, also referred as to Waisman syndrome. As it appears to be a very rare cause of Parkinson Disease (PD), with only few cases described in the literature, the typical clinical and radiological features are yet to be determined. In this article, we report and illustrate multimodal brain imaging by computed tomography, magnetic resonance imaging, transcranial ultrasound (US), dopamine transporter single photon emission computed tomography and [18F]-fluorodeoxyglucose positron emission tomography ([18F]FDG-PET) in a 37-year-old man with PD features and mild mental retardation harboring a new RAB39B mutation. We then propose a comparison with data previously published regarding neuroimaging in this condition and present a summary of previous imaging reports. If our patient's results partly support previously described radiological features, they also highlight potential new characteristics of this rare syndrome. To the best of our knowledge, [18F]FDG-PET and transcranial US have never been reported before in this condition. This is therefore the first multimodal brain imaging description of a patient presenting RAB39B mutation.

Conventional and advanced imaging throughout the cycle of care of gliomas.

Although imaging of gliomas has evolved tremendously over the last decades, published techniques and protocols are not always implemented into clinical practice. Furthermore, most of the published literature focuses on specific timepoints in glioma management. This article reviews the current literature on conventional and advanced imaging techniques and chronologically outlines their practical relevance for the clinical management of gliomas throughout the cycle of care. Relevant articles were located through the Pubmed/Medline database and included in this review. Interpretation of conventional and advanced imaging techniques is crucial along the entire process of glioma care, from diagnosis to follow-up. In addition to the described currently existing techniques, we expect deep learning or machine learning approaches to assist each step of glioma management through tumor segmentation, radiogenomics, prognostication, and characterization of pseudoprogression. Thorough knowledge of the specific performance, possibilities, and limitations of each imaging modality is key for their adequate use in glioma management.

Mechanical Thrombectomy for Acute Ischemic Stroke Amid the COVID-19 Outbreak: Decreased Activity, and Increased Care Delays.

BACKGROUND AND PURPOSE: The efficiency of prehospital care chain response and the adequacy of hospital resources are challenged amid the coronavirus disease 2019 (COVID-19) outbreak, with suspected consequences for patients with ischemic stroke eligible for mechanical thrombectomy (MT). METHODS: We conducted a prospective national-level data collection of patients treated with MT, ranging 45 days across epidemic containment measures instatement, and of patients treated during the same calendar period in 2019. The primary end point was the variation of patients receiving MT during the epidemic period. Secondary end points included care delays between onset, imaging, and groin puncture. To analyze the primary end point, we used a Poisson regression model. We then analyzed the correlation between the number of MTs and the number of COVID-19 cases hospitalizations, using the Pearson correlation coefficient (compared with the null value). RESULTS: A total of 1513 patients were included at 32 centers, in all French administrative regions. There was a 21% significant decrease (0.79; [95%CI, 0.76-0.82]; P<0.001) in MT case volumes during the epidemic period, and a significant increase in delays between imaging and groin puncture, overall (mean 144.9±SD 86.8 minutes versus 126.2±70.9; P<0.001 in 2019) and in transferred patients (mean 182.6±SD 82.0 minutes versus 153.25±67; P<0.001). After the instatement of strict epidemic mitigation measures, there was a significant negative correlation between the number of hospitalizations for COVID and the number of MT cases (R2 -0.51; P=0.04). Patients treated during the COVID outbreak were less likely to receive intravenous thrombolysis and to have unwitnessed strokes (both P<0.05). CONCLUSIONS: Our study showed a significant decrease in patients treated with MTs during the first stages of the COVID epidemic in France and alarming indicators of lengthened care delays. These findings prompt immediate consideration of local and regional stroke networks preparedness in the varying contexts of COVID-19 pandemic evolution.

Image in transplantation surgery: median arcuate ligament in liver transplantation.

Low inserted median arcuate ligament (MAL) may cause extrinsic coeliac trunk compression and MAL syndrome (association of post-prandial epigastric pain, weight loss and nausea or vomiting). In liver transplantation (LT), liver graft arterial supply depends on the recipient's hepatic artery, as the gastro-duodenal artery has generally been ligated. A decreased graft arterial flow caused by coeliac trunk stenosis might induce hepatic artery thrombosis leading to graft loss. In this short report, the authors describe LT procedure during which recipient's hepatic artery pressure was dramatically decreased after ligature of the gastro-duodenal artery. Dissection and division of the MAL allowed to restore an excellent blood flow through the hepatic artery. This report reminds how important it is to be able to recognize and how to manage a stenosing MAL in LT.

Mutations in the HECT domain of NEDD4L lead to AKT-mTOR pathway deregulation and cause periventricular nodular heterotopia.

Neurodevelopmental disorders with periventricular nodular heterotopia (PNH) are etiologically heterogeneous, and their genetic causes remain in many cases unknown. Here we show that missense mutations in NEDD4L mapping to the HECT domain of the encoded E3 ubiquitin ligase lead to PNH associated with toe syndactyly, cleft palate and neurodevelopmental delay. Cellular and expression data showed sensitivity of PNH-associated mutants to proteasome degradation. Moreover, an in utero electroporation approach showed that PNH-related mutants and excess wild-type NEDD4L affect neurogenesis, neuronal positioning and terminal translocation. Further investigations, including rapamycin-based experiments, found differential deregulation of pathways involved. Excess wild-type NEDD4L leads to disruption of Dab1 and mTORC1 pathways, while PNH-related mutations are associated with deregulation of mTORC1 and AKT activities. Altogether, these data provide insights into the critical role of NEDD4L in the regulation of mTOR pathways and their contributions in cortical development.