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Stroke
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Approximately 35% of subarachnoid hemorrhage patients die after an initial aneurysmal hemorrhage. About 15% more will die within several weeks due to another rupture. After 6 months have passed, second ruptures occur in about 3% of cases annually. The prognosis is generally the worst when an aneurysm is the cause. Prognosis is better if the cause was an arteriovenous malformation. The best prognosis is when angiography finds no lesion because the source of bleeding is small and has already sealed. Even with the best treatments, most survivors of subarachnoid hemorrhage have neurologic damage.
Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
Focal lesions (usually basal ganglia–thalamus), hemidystonia: Trauma.Stroke.Arteriovenous malformation (AVM).Abscess.
Considerations regarding feasibility, safety, and efficacy of N-butyl cyanoacrylate (n-BCA) and Onyx embolization for the treatment of venous malformations
Published in Byung-Boong Lee, Peter Gloviczki, Francine Blei, Jovan N. Markovic, Vascular Malformations, 2019
Jovan N. Markovic, Cynthia K. Shortell
Embolization, either alone or followed by surgical excision, is a successfully used treatment modality in patients with high-flow vascular malformations (HFVMs).1, 2 Currently, limited data are available regarding the use of embolization in patients with venous malformations (VMs). Initially, embolization was mostly considered as a preoperative treatment adjunct to surgery. In contrast to sclerotherapy, where percutaneous, intraluminal injection of a sclerosing agent causes chemical injury and disruption of the endothelial lining with subsequent endoluminal obliteration of the treated vessel, embolization includes intraluminal placement of material and/or agents (such as coils, plugs, and/or embolization glues and liquids), through a catheter into the lumen of the vessel to seal off the site where malformation connects to the feeding and/or draining blood vessels and/or to occupy the lumen of a malformation and therefore reduce the portion of malformation that can be filled with blood.2 However, experience and data have shown that many arteriovenous malformations were successfully treated with embolization alone, and that surgical excision is primarily used for only well-localized lesions.3, 4
Neuroimaging in professional combat sports: consensus statement from the association of ringside physicians
Published in The Physician and Sportsmedicine, 2023
The CT is extremely sensitive in detecting the stigmata of acute TBI such as bleeding and bone pathology (craniofacial fractures, fractures of the orbits). It has the added advantage of widespread availability, short scan time, and low cost. The MRI is superior to a CT for detecting the stigmata of chronic TBI [1,6]. The ability of the MRI to detect hematomas improves over time as the composition of the blood changes [1,6]. The overwhelming majority of patients with mild brain injury frequently show no parenchymal abnormality on MRI [1,6]. However, coincidental structural brain abnormalities are found in about 2–3% of all studies, including meningiomas, coincidental, and non-pathologic anomalies, and small often unruptured cerebral aneurysms [1]. Small circle of Willis cerebral aneurysms are better visualized with CT or MR angiography. Large arteriovenous malformations (AVMs) can be readily identified on CT and MRI [7]. With reference to contact sports, relevant abnormalities include hemorrhagic cortical contusions, petechiae, or foci of altered signal that represent white matter shear injury (diffuse axonal injury) [1,5,6]. When petechiae resolve, they can leave a permanent hemosiderin deposition on the MRI [1]. While the MRI is superior to a CT in the detection of axonal injury, it is insensitive in detecting acute hemorrhage (oxy-Hgb and deoxy-Hgb) within 48–72 h after injury; emphasizing the value of CT without contrast in rapid triage of patients with acute TBI.
Thrombosed orbital arteriovenous malformation in a patient with lymphangioleiomyomatosis
Published in Orbit, 2022
Elzbieta Mechel, Ann Q. Tran, Andrea Tooley, Michael Kazim
Arteriovenous malformations are communications between arteries and veins, which bypass capillary vasculature, presumed to be developmental anomalies caused by failure of embryonic vasculature to differentiate.7 The pathophysiology of AVM formation remains unclear; however, numerous studies have looked at VEGF associations.8–10 VEGF has been implicated in the pathophysiology of cerebral AVMs, histologically equivalent to orbital AVMs.8 Expression of VEGF receptors has been examined in orbital vascular lesions, including venous malformations, capillary hemangiomas, lymphatic malformations, and lymphaticovenous malformations.9 Despite their congenital origin, AVMs may manifest later in life under the stimulation of menarche, pregnancy, or trauma, drawing parallels to a similar phenomenon seen in LAM.10 Estrogen has been causally implicated due to its ability to stimulate VEGF production.10 Rapamycin, which can decrease cell proliferation and lymphangiogenesis, has been examined as treatment of cerebral and orbital AVMs, the same mechanisms which support its use in LAM.11,12 Although no association has been reported between AVMs and LAM to date, these two entities share behavioral similarities, in particular VEGF expression and estrogen sensitivity, warranting consideration that LAM disease may promote a microenvironment suitable for AVM growth.1,2,8–10
Surgical management and outcome of adult posterior cranial fossa and spinal hemangioblastoma: a 6-case series and literature review
Published in Neurological Research, 2020
Bruno Splavski, Blazej Zbytek, Kenan I. Arnautovic
Unlike Type 1 tumors, Types 2–4 are extremely vascularized tumors that enhance on MRI scans with contrast, contain flow voids in their enhancing parts, and may contain cysts of different sizes (Types 3 and 4). Surgical management must be planned in a similar manner as management of arteriovenous malformations due to their extreme tendency for hemorrhaging. Therefore, microsurgical technique has to be planned to circumscribe the tumor and carefully dissect, coagulate, and divide arterial feeders in a systematic fashion [27]. The venous drainage coagulation and interception must be left until the very end of the surgery following elimination of all arterial feeders. For Types 2–4 tumors, preoperative preparation of blood transfusion and close communication with anesthesia are of tremendous importance. Finally, gross total resection should be the goal since leaving tumor parts may lead to significant postoperative hemorrhage and poor clinical outcomes [25–27,33,53].