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      Delayed Ischemic Neurological Deficit after Uneventful Elective Clipping of Unruptured Intracranial Aneurysms

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          Abstract

          Cerebral vasospasm and subsequent delayed ischemic neurological deficit is a typical sequela of acute subarachnoid hemorrhage after aneurysm rupture. The occurrence of vasospasms after uncomplicated surgery of an unruptured aneurysm without history of suspected rupture is extremely rare. The pathogenesis and severity of cerebral vasospasms is typically correlated with the amount of blood breakdown products extravasated during subarachnoid hemorrhage. In rare cases, where vasospasms occur after unruptured aneurysm surgery, the pathogenesis is most likely multifactorial and unclear. We present two cases of vasospasms following uncomplicated clipping of middle cerebral artery (MCA) aneurysms and a review of literature. Early diagnosis and therapy of this rare complication are necessary to achieve optimal clinical outcomes.

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          Most cited references36

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          The International Cooperative Study on the Timing of Aneurysm Surgery. Part 1: Overall management results.

          The International Cooperative Study on the Timing of Aneurysm Surgery evaluated the results of surgical and medical management in 3521 patients between December, 1980, and July, 1983. At admission, 75% of patients were in good neurological condition and surgery was performed in 83%. At the 6-month evaluation, 26% of the patients had died and 58% exhibited a complete recovery. Vasospasm and rebleeding were the leading causes of morbidity and mortality in addition to the initial bleed. Predictors for mortality included the patient's decreased level of consciousness and increased age, thickness of the subarachnoid hemorrhage clot on computerized tomography, elevated blood pressure, preexisting medical illnesses, and basilar aneurysms. The results presented here document the status of management in the 1980's.
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            Subarachnoid hemorrhage: who dies, and why?

            Introduction Subarachnoid hemorrhage (SAH) is a devastating form of stroke. Causes and mechanisms of in-hospital death after SAH in the modern era of neurocritical care remain incompletely understood. Methods We studied 1200 consecutive SAH patients prospectively enrolled in the Columbia University SAH Outcomes Project between July 1996 and January 2009. Analysis was performed to identify predictors of in-hospital mortality. Results In-hospital mortality was 18 % (216/1200): 3 % for Hunt-Hess grade 1 or 2, 9 % for grade 3, 24 % for grade 4, and 71 % for grade 5. The most common adjudicated primary causes of death or neurological devastation leading to withdrawal of support were direct effects of the primary hemorrhage (55 %), aneurysm rebleeding (17 %), and medical complications (15 %). Among those who died, brain death was declared in 42 %, 50 % were do-not-resuscitate at the time of cardiac death (86 % of whom had life support actively withdrawn), and 8 % died despite full support. Admission predictors of mortality were age, loss of consciousness at ictus, admission Glasgow Coma Scale score, large aneurysm size, Acute Physiology and Chronic Health Evaluation II (APACHE II) physiologic subscore, and Modified Fisher Scale score. Hospital complications that further increased the risk of dying in multivariable analysis included rebleeding, global cerebral edema, hypernatremia, clinical signs of brain stem herniation, hypotension of less than 90 mm Hg treated with pressors, pulmonary edema, myocardial ischemia, and hepatic failure. Delayed cerebral ischemia, defined as deterioration or infarction from vasospasm, did not predict mortality. Conclusion Strategies directed toward minimizing early brain injury and aneurysm rebleeding, along with prevention and treatment of medical complication, hold the best promise for further reducing mortality after SAH. Electronic supplementary material The online version of this article (doi:10.1186/s13054-015-1036-0) contains supplementary material, which is available to authorized users.
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              Innervation of the feline cerebral vasculature by nerve fibers containing calcitonin gene-related peptide: trigeminal origin and co-existence with substance P.

              The presence of a population of nerve fibers containing immunoreactive calcitonin gene-related peptide (CGRP) has been demonstrated around cerebral arteries of the cat with immunocytochemistry and radioimmunoassay. CGRP immunoreactivity in the feline cerebral vasculature, as characterized by high-performance liquid chromatography, is similar to authentic rat CGRP. Numerous perikarya containing CGRP are present in the trigeminal ganglia, and surgical lesions of the trigeminal ganglia significantly reduce the levels of CGRP in the cerebral vasculature, suggesting that this cranial nerve is the principal origin of these cerebrovascular nerve fibers. As demonstrated by sequential immunocytochemistry, CGRP coexists with substance P both in the trigeminal ganglion and nerve fibers around cerebral blood vessels. The presence of CGRP in the cerebrovascular trigeminal innervation provides further versatility and complexity for this sensory afferent system putatively involved in the transmission of intracranial pain.
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                Author and article information

                Journal
                Brain Sci
                Brain Sci
                brainsci
                Brain Sciences
                MDPI
                2076-3425
                29 July 2020
                August 2020
                : 10
                : 8
                : 495
                Affiliations
                [1 ]Department of Neurosurgery, J. E. Purkyně University, Masaryk Hospital, EU 401 13 Ústí nad Labem, Czech Republic; jan.lodin@ 123456kzcr.eu (J.L.); ales.hejcl@ 123456kzcr.eu (A.H.); martin.sames@ 123456kzcr.eu (M.S.)
                [2 ]Department of Neurosurgery, University Hospital in Pilsen, The Faculty of Medicine in Pilsen, Charles University in Prague, 30605 Prague, Czech Republic
                [3 ]Department of Radiology, J. E. Purkyně University, Masaryk Hospital, EU 401 13 Ústí nad Labem, Czech Republic; filip.cihlar@ 123456kzcr.eu
                Author notes
                [* ]Correspondence: petr.vachata@ 123456kzcr.eu ; Tel.: +420-736210076; Fax: +420-477112880
                Author information
                https://orcid.org/0000-0001-8139-4707
                Article
                brainsci-10-00495
                10.3390/brainsci10080495
                7464283
                32751242
                5ccbc669-0358-4117-8fac-bac25c6ae1e3
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 29 June 2020
                : 27 July 2020
                Categories
                Case Report

                unruptured intracranial aneurysm,vasospasm,delayed ischemic neurological deficit

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