Successful Endovascular Management of Massive Pansinus Thrombosis: Case Report and Review of Literature.

Cerebral sinus venous thrombosis (CSVT) is a recognized cause of childhood and neonatal stroke. More than 50% of neonates have a poor outcome, and mortality is high. Coma is a predictor of death in neonatal CSVT. We present the case of a 9-day-old infant, who presented in coma and was treated successfully with a combination of mechanical thrombectomy using the MindFrame System via the right jugular vein, local infusion of recombinant tissue plasminogen activator and abciximab, as well as anticoagulation. In this case, aggressive thrombectomy and thrombolysis achieved complete neurologic restoration safely and quickly.

Vertebral Artery Sacrifice: Novel Strategy in Treatment of Vertebral Artery Loop.

BACKGROUND: We report a case of cervical radiculopathy caused by an anomalous vertebral artery (VA) and the efficacy of endovascular vertebral artery sacrifice. CASE DESCRIPTION: A 62-year-old woman was referred to neurosurgery because of an 8- to 9-year history of progressive left C6-7 radiculopathy refractory to other forms of treatment. Radiologic evaluation showed an abnormally tortuous loop of VA at V2 causing direct neurovascular compression at the C6-7 level. Initial attempts at microvascular decompression with posterior foraminotomy were unsuccessful due to strong adhesion between the VA and C7 nerve root. This was followed by an endovascular VA sacrifice relieving the patient's symptoms. CONCLUSIONS: Cervical root compression by an aberrant or anomalous extracranial VA is a rare cause of radiculopathy. Endovascular VA sacrifice provided symptom relief in our patient, when other options failed. To our knowledge, this is the first report of endovascular VA sacrifice for management of cervical radiculopathy due to VA loop.

A Case Series of 18 Patients Receiving Ticagrelor After Carotid Stenting.

PURPOSE: Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 receptor antagonist is often used to prevent thrombotic complications after endovascular stent placement. Most of the published experience surrounding DAPT after carotid stenting is with clopidogrel. Ticagrelor may be a promising alternative, especially in patients who may be considered nonresponders to clopidogrel. However, clinical outcomes utilizing DAPT with ticagrelor in a cohort with carotid stenting is lacking. In this case series, we describe our experience with systematic prescribing of ticagrelor after carotid stent placement in 18 patients. METHODS: A retrospective review of 18 patients prescribed ticagrelor who underwent carotid stenting between November 2015 and January 2017 was performed. All eligible patients were included in the review. The primary end point of interest was any ischemic stroke or death within 30 days following the procedure. Intracranial hemorrhage was a secondary end point. RESULTS AND CONCLUSIONS: No patients experienced the primary end point of ischemic stroke or death within 30 days. No intracranial hemorrhages were observed. The use of ticagrelor after carotid stenting may be a reasonable alternative to clopidogrel after carotid stent placement. Randomized trials to support our findings are needed.

Ticagrelor and Acetylsalicylic Acid after Placement of Pipeline Embolization Device for Cerebral Aneurysm: A Case Series.

BACKGROUND: Dual antiplatelet therapy with acetylsalicylic acid (ASA) and a P2Y12-receptor antagonist is often used to prevent thrombotic complications after placement of a Pipeline embolization device (PED) for cerebral aneurysm. Although clopidogrel is common in this setting, high rates of nonresponse to this drug have made ticagrelor a potentially attractive alternative. OBJECTIVE: To describe safety and efficacy outcomes for ticagrelor following PED placement, including measurement of platelet function. METHODS: A retrospective analysis of data was completed for patients who underwent PED placement for cerebral aneurysm at a single centre between November 2015 and March 2017, with subsequent prescription of ticagrelor and ASA as dual antiplatelet therapy. The primary end point was any ischemic stroke or death within 1 year after the procedure. Intracranial hemorrhage was a secondary end point. Additionally, measurement of and values for platelet reactivity units (PRUs) during receipt of ticagrelor and ASA were evaluated. RESULTS: A total of 29 patients were included in this retrospective study. One patient experienced ischemic stroke 226 days after placement of the PED. In addition, 3 patients died during the 1-year follow-up period for causes unrelated to stroke or bleeding complications. No cases of intracranial hemorrhage were observed. Samples for measurement of P2Y12 levels were drawn at the discretion of the neurointerventionalists, and the PRU value was measured at least once for 28 (97%) of the 29 patients. The mean number of PRU measurements per patient after initiation of ticagrelor was 2.1 (standard deviation [SD] 1). Mean PRU value after initiation of ticagrelor was 65 (SD 57). CONCLUSIONS: In this case series describing the use of ticagrelor and ASA as dual antiplatelet therapy after PED placement for cerebral aneurysm, there was just one ischemic stroke, which occurred after the dual antiplatelet therapy had been discontinued. Further prospective trials are needed to describe the utility of ticagrelor use after PED placement, as well as its dosing and monitoring.

CONTEXTE: Une bithérapie antiplaquettaire composée d'acide acétylsalicylique (AAS) et d'un inhibiteur du récepteur P2Y12 est fréquemment utilisée pour prévenir les complications thrombotiques après la mise en place d'un dispositif d'embolisation Pipeline pour traiter un anévrisme cérébral. Quoique le clopidogrel soit souvent utilisé dans ce contexte, des taux élevés d'absence de réponse à ce médicament ont fait du ticagrélor une solution de rechange potentiellement intéressante. OBJECTIF: Décrire les résultats relatifs à la sécurité et à l'efficacité du ticagrélor après la mise en place d'un dispositif d'embolisation, y compris l'analyse de la fonction plaquettaire. MÉTHODES: Une analyse rétrospective de données a été réalisée dans un seul centre entre novembre 2015 et mars 2017 à l'aide des dossiers médicaux de patients chez qui a été posé un dispositif d'embolisation Pipeline comme traitement pour un anévrisme cérébral et à qui a ensuite été prescrite une bithérapie antiplaquettaire de ticagrélor et d'AAS. Le critère d'évaluation principal était les cas d'infarctus cérébral ou de décès durant l'année suivant l'opération. Les cas d'hémorragie intracrânienne ont servi de critère d'évaluation secondaire. De plus, l'analyse a porté sur l'évaluation de la réactivité plaquettaire et sa quantification en unités de réaction au P2Y12 pendant la prise de ticagrélor et d'AAS. RÉSULTATS: Au total, 29 patients ont été admis à la présente étude rétrospective. Un patient a subi un infarctus cérébral 226 jours après la mise en place d'un dispositif d'embolisation Pipeline. De plus, 3 patients sont décédés au cours de la période de suivi d'un an en raison de causes sans lien avec des complications liées à un accident vasculaire cérébral ou à une hémorragie. Aucun cas d'hémorragie intracrânienne n'a été observé. Les échantillons destinés à la mesure des unités de réaction au P2Y12 ont été prélevés selon le jugement des neuro-intervenants et l'évaluation de la réactivité plaquettaire a été réalisée au moins une fois chez 28 (97 %) des 29 patients. Le nombre moyen de mesures des unités de réaction au P2Y12 par patient était de 2,1 (écart-type de 1). Après l'amorce d'un traitement par ticagrélor, le résultat moyen en unités de réaction au P2Y12 était de 65 (écart-type de 57). CONCLUSIONS: Dans la présente série de cas décrivant l'utilisation d'une bithérapie antiplaquettaire composée de ticagrélor et d'AAS après la mise en place d'un dispositif d'embolisation Pipeline comme traitement pour un anévrisme cérébral, seul un cas d'infarctus cérébral a été observé et il s'est produit après l'arrêt de la bithérapie antiplaquettaire. De plus amples études prospectives sont nécessaires pour décrire l'utilité et la posologie du ticagrélor ainsi que le suivi du traitement après la mise en place d'un dispositif d'embolisation Pipeline.

Novel solution for luminal access loss into the double-layered LVIS Blue™ construct.

We described a novel solution for a challenging case of double-layered LVIS Blue™ (LB) stent construct retraction into a large cavernous aneurysm. The double-layered LB stent construct was used as a flow diverter for treatment of a large cavernous aneurysm. Our solution comprised a balloon angioplasty and placement of balloon-mounted cardiac-stent construct through the side wall of the LB construct, with eventual placement of a Pipeline Flex inside of the final conduit.

Cerebral Granulomatous Inflammation Secondary to Hydrophilic Polymer Embolization Following Thrombectomy.

BACKGROUND Given the recent completion of multiple trials demonstrating the benefit of endovascular mechanical thrombectomy for select patients with proximal large artery occlusive ischemic strokes, there has been a large increase in the performance of these procedures. In the context of increased thrombectomy performance, there have also been increased reports of rare occurrences of granulomatous inflammatory response to the hydrophilic polymer which coat many of these interventional devices. CASE REPORT A 59-year-old female presented with a complete occlusion of her right proximal middle cerebral artery (MCA) and imaging showed a large area of penumbra. Cerebral angiogram and mechanical thrombectomy were successfully performed with reversal of clinical symptoms. Eight months following her stroke, she developed progressive recurrence of left-sided neurological deficits. After extensive workup culminating in tissue sampling, she was found to have developed granulomatous inflammation surrounding microscopic embolization of hydrophilic polymer, which is used to coat many interventional devices such as wires and catheters. The patient responded both clinically and radiographically to anti-inflammatory steroid therapy. CONCLUSIONS Recognizing the significant potential morbidity of a large vessel ischemic stroke and the expanded use of endovascular interventions aimed at staving off this disability, there are emerging and at times indolent complications from the use of hydrophilic polymer coated wires and catheters. This rare and potentially under-recognized complication should be considered in the differential for any patient with new neurological findings following cerebral intervention, especially given the consideration that this appears to a treatable complication.

Varicella-zoster virus activates inflammatory cytokines in human monocytes and macrophages via Toll-like receptor 2.

The pattern recognition receptor Toll-like receptor 2 (TLR2) has been implicated in the response to several human viruses, including herpes simplex viruses (types 1 and 2) and cytomegalovirus. We demonstrated that varicella-zoster virus (VZV) activates inflammatory cytokine responses via TLR2. VZV specifically induced interleukin-6 (IL-6) in human monocytes via TLR2-dependent activation of NF-kappaB, and small interfering RNA designed to suppress TLR2 mRNA reduced the IL-6 response to VZV in human monocyte-derived macrophages. Unlike other herpesviruses, the cytokine response to VZV was species specific. VZV did not induce cytokines in murine embryonic fibroblasts or in a mouse cell line, although VZV did activate NF-kappaB in a human cell line expressing a murine TLR2 construct. Together, these results suggest that TLR2 may play a role in the inflammatory response to VZV infection.

Nectin-1/HveC Mediates herpes simplex virus type 1 entry into primary human sensory neurons and fibroblasts.

Immunocytochemistry detects nectin-1/HveC, nectin-2/HveB, and HVEM/HveA on the surface of sensory neurons and fibroblasts grown as primary cultures from human dorsal root ganglia. Viral entry into these cultured cells was assayed by infection with a recombinant herpes simplex virus type 1 (HSV-1) expressing green fluorescent protein. Soluble, truncated nectin-1 polypeptide, as well as polyclonal and monoclonal antibodies against nectin-1, inhibited infection of neurons, whereas polypeptides and antibodies capable of inhibiting HSV-1 interaction with nectin-2 and herpesvirs entry mediator (HVEM) failed to prevent infection of neuronal cells. These results demonstrate that nectin-1 is the primary receptor for HSV-1 entry into human fetal neurons. Viral entry into fibroblasts was also reduced by soluble nectin-1 but not by soluble HVEM. However, in contrast to the results obtained with neurons, antibodies against receptors failed to inhibit entry into fibroblasts, indicating that unlike neurons, fibroblasts have multiple receptors or mechanisms for HSV-1 entry.

Varicella-zoster virus DNA in cells isolated from human trigeminal ganglia.

To determine the type of cell(s) that contain latent varicella-zoster virus (VZV) DNA, we prepared pure populations of neurons and satellite cells from trigeminal ganglia of 18 humans who had previously had a VZV infection. VZV DNA was present in 34 of 2,226 neurons (1.5%) and in none of 20,700 satellite cells. There was an average of 4.7 (range of 2 to 9) copies of VZV DNA per latently infected neuron. Latent VZV DNA was primarily present in large neurons, whereas the size distribution of herpes simplex virus DNA was markedly different.