Isolated Middle Cerebral Artery Dissection with Atherosclerosis: a Case Report
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Endovascular Treatment of Stroke Caused by Carotid Artery Dissection
brain sciences Case Report Endovascular Treatment of Stroke Caused by Carotid Artery Dissection Grzegorz Meder 1,* , Milena Swito´ ´nska 2,3 , Piotr Płeszka 2, Violetta Palacz-Duda 2, Dorota Dzianott-Pabijan 4 and Paweł Sokal 3 1 Department of Interventional Radiology, Jan Biziel University Hospital No. 2, Ujejskiego 75 Street, 85-168 Bydgoszcz, Poland 2 Stroke Intervention Centre, Department of Neurosurgery and Neurology, Jan Biziel University Hospital No. 2, Ujejskiego 75 Street, 85-168 Bydgoszcz, Poland; [email protected] (M.S.);´ [email protected] (P.P.); [email protected] (V.P.-D.) 3 Department of Neurosurgery and Neurology, Faculty of Health Sciences, Nicolaus Copernicus University in Toru´n,Ludwik Rydygier Collegium Medicum, Ujejskiego 75 Street, 85-168 Bydgoszcz, Poland; [email protected] 4 Neurological Rehabilitation Ward Kuyavian-Pomeranian Pulmonology Centre, Meysnera 9 Street, 85-472 Bydgoszcz, Poland; [email protected] * Correspondence: [email protected]; Tel.: +48-52-3655-143; Fax: +48-52-3655-364 Received: 23 September 2020; Accepted: 27 October 2020; Published: 30 October 2020 Abstract: Ischemic stroke due to large vessel occlusion (LVO) is a devastating condition. Most LVOs are embolic in nature. Arterial dissection is responsible for only a small proportion of LVOs, is specific in nature and poses some challenges in treatment. We describe 3 cases where patients with stroke caused by carotid artery dissection were treated with mechanical thrombectomy and extensive stenting with good outcome. We believe that mechanical thrombectomy and stenting is a treatment of choice in these cases. Keywords: stroke; artery dissection; endovascular treatment; stenting; mechanical thrombectomy 1. -
TIA Vs CVA (STROKE)
Phone: 973.334.3443 Email: [email protected] NJPR.com TIA vs CVA (STROKE) What is the difference between a TIA and a stroke? Difference Between TIA and Stroke • Both TIA and stroke are due to poor blood supply to the brain. • Stroke is a medical emergency and it’s a life-threatening condition. • The symptoms of TIA and Stroke may be same but TIA symptoms will recover within 24 hours. TRANSIENT ISCHEMIC ATTACK ● Also known as: TIA, mini stroke 80 E. Ridgewood Avenue, 4th Floor Paramus, NJ 07652 TIA Causes ● A transient ischemic attack has the same origins as that of an ischemic stroke, the most common type of stroke. In an ischemic stroke, a clot blocks the blood supply to part of your brain. In a transient ischemic attack, unlike a stroke, the blockage is brief, and there is no permanent damage. ● The underlying cause of a TIA often is a buildup of cholesterol- containing fatty deposits called plaques (atherosclerosis) in an artery or one of its branches that supplies oxygen and nutrients to your brain. ● Plaques can decrease the blood flow through an artery or lead to the development of a clot. A blood clot moving to an artery that supplies your brain from another part of your body, most commonly from your heart, also may cause a TIA. CEREBROVASCULAR ACCIDENT/STROKE Page 2 When the brain’s blood supply is insufficient, a stroke occurs. Stroke symptoms (for example, slurring of speech or loss of function in an arm or leg) indicate a medical emergency. Without treatment, the brain cells quickly become impaired or die. -
Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives
International Journal of Molecular Sciences Review Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives Diji Kuriakose and Zhicheng Xiao * Development and Stem Cells Program, Monash Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC 3800, Australia; [email protected] * Correspondence: [email protected] Received: 29 September 2020; Accepted: 13 October 2020; Published: 15 October 2020 Abstract: Stroke is the second leading cause of death and a major contributor to disability worldwide. The prevalence of stroke is highest in developing countries, with ischemic stroke being the most common type. Considerable progress has been made in our understanding of the pathophysiology of stroke and the underlying mechanisms leading to ischemic insult. Stroke therapy primarily focuses on restoring blood flow to the brain and treating stroke-induced neurological damage. Lack of success in recent clinical trials has led to significant refinement of animal models, focus-driven study design and use of new technologies in stroke research. Simultaneously, despite progress in stroke management, post-stroke care exerts a substantial impact on families, the healthcare system and the economy. Improvements in pre-clinical and clinical care are likely to underpin successful stroke treatment, recovery, rehabilitation and prevention. In this review, we focus on the pathophysiology of stroke, major advances in the identification of therapeutic targets and recent trends in stroke research. Keywords: stroke; pathophysiology; treatment; neurological deficit; recovery; rehabilitation 1. Introduction Stroke is a neurological disorder characterized by blockage of blood vessels. Clots form in the brain and interrupt blood flow, clogging arteries and causing blood vessels to break, leading to bleeding. -
A Rare Intracerebral Collateral Circulation Pathway from the Contralateral Vertebral Artery to the Ipsilateral Posterior Inferior Cerebellar Artery-V4 Segment Steal
A Rare Intracerebral Collateral Circulation Pathway from the Contralateral Vertebral Artery to the Ipsilateral Posterior Inferior Cerebellar Artery-V4 Segment Steal Yang Liu Qiqihar Medical University Bian Yang Sixth Medical Center of PLA General Hospital https://orcid.org/0000-0002-4002-5646 Jianan Wang General Hospital of the PLA Rocket Force Xiongwei Zhang General Hospital of the PLA Rocket Force Yan Miao Sixth Medical Center of PLA General Hospital Kunyu Wang Sixth Medical Center of PLA General Hospital Chunyan Li Qiqihar Medical University Feng Qiu ( [email protected] ) Research article Keywords: Vertebral artery, Occlusive disease, Posterior Inferior cerebellar artery, Steal blood, Collateral circulation Posted Date: May 26th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-25705/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/12 Abstract Background: Interrupted blood ow during ischemia can be compensated through collateral circulation when a cerebral artery is severely stenotic or occluded. We suppose that potential collateral pathway may exist in patients with vertebral artery occlusive disease (VAOD) around V4 segment due to the ipsilateral posterior inferior cerebellar artery (PICA) is sometimes patented after VAOD in the V4 segment. Methods: We retrospectively examined the medical database of 60 patients with VAOD admitted to the Department of Neurology from the Sixth medical center of the Chinese People's Liberation Army General Hospital and the Second Aliated Hospital of Qiqihar Medical University from June 2018 to November 2019. The pathways which supplied PICA were investigated by digital subtraction angiography (DSA). Results: 18 patients were proximal to the exit point of the PICA among all 60 patients with VAOD in V4 segment cases, and 7 individuals (11.7%) had the collateral circulation pathway via the contralateral vertebral artery (VA) ® vertebrobasilar junction ® ipsilateral VA ® ipsilateral PICA in the DSA. -
Dissection Is Most Likely Due to Multiple Environmental and Genetic Risk Factors. Also, Recent Infections (Mainly Respiratory) H
Synapsea clinical resource SPRING 2017, VOL. 8, ISSUE 1 Vertebral and Carotid Artery Dissections The most important environmental risk factor appears to be Lucian Maidan, MD major or minor trauma caused by events such as chiropractic manipulation, yoga poses, coughing, and sneezing. Trauma Although only 10% of the 750,000 people who annually suff er produces an intimal tear through which blood enters the wall an ischemic stroke in the U.S. are younger than 50, those and forms an intramural hematoma. younger individuals have a higher mortality. Dissection of carotid arteries (CAD) and vertebral arteries (VAD) is second Clinical manifestations of a cervical artery dissection include only to cardioembolic strokes in young people, with an incidence both local signs and symptoms and ischemic and even estimated at up to three per 100,000 people for carotid artery hemorrhagic cerebral events. dissection and 1.5 per 100,000 for the vertebral arteries. Local manifestations of CAD include Horner syndrome The second most common lesion of the cervical arteries after (ipsilateral), neck pain, headache, tinnitus, facial pain, and atherosclerosis, dissection may be either spontaneous or cranial nerve palsies (IX to XII most commonly). secondary to major trauma. The majority of dissections occur Local manifestations of a VAD include severe occipital extracranially—only 10% are intracranial—and in 16% of cases headache, nuchal pain, cervical root involvement (most multiple arteries are involved. commonly C5-C6 level), and lower brainstem compression if the Dissection is most likely due to multiple environmental and dissection extends in the intradural space. genetic risk factors. Also, recent infections (mainly respiratory) Ischemic manifestations of CAD include stroke, most commonly have been associated with dissection. -
Phenotypic Features of Cerebral Autosomal-Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy Subjects with R544C Mutation
Print ISSN 1738-1495 / On-line ISSN 2384-0757 Dement Neurocogn Disord 2016;15(1):15-19 / http://dx.doi.org/10.12779/dnd.2016.15.1.15 DND ORIGINAL ARTICLE Phenotypic Features of Cerebral Autosomal-Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy Subjects with R544C Mutation Jung Seok Lee,1 KeunHyuk Ko,1 Jung-Hwan Oh,1 Joon Hyuk Park,2 Ho Kyu Lee3 Departments of 1Neurology, 2Psychiatry, and 3Radiology, Jeju National University Hospital, Jeju, Korea Background and Purpose Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most-common single gene disorder of cerebral small vessel disease. There is no definite evidence of genotype-phenotype correlation in CADASIL. However, recent studies have shown the unique phenotypic feature of NOTCH3 R544C mutation. Methods We investigated the phenotypic spectrum of NOTCH3 R544C mutation in 73 CADASIL patients in Jeju between April 2012 and January 2014. Results Of the 73 subjects from 60 unrelated families included in this study, 40 (55%) were men. The mean age of the subjects was 62.2± 12.2 (range 34–86 years). Cerebral infarction was the most frequent manifestation (37%), followed by cognitive impairment (32%), headache (17%), psychiatric symptom (16%), intracerebral hemorrhage (12%), transient ischemic attack (7%), and seizure (1%). The mean age of the subjects with ischemic or hemorrhagic episodes was 64.9±10.9 (range 41–86 years). A diagnosis of dementia was made in 12 subjects (16%). The mean age of the subjects with dementia was 75.6±6.5 (range 62–86 years). About 3% of subjects were unable to walk without assistance at assessment. -
Posttraumatic Cerebral Infarction Diagnosed by CT: Prevalence, Origin, and Outcome
355 Posttraumatic Cerebral Infarction Diagnosed by CT: Prevalence, Origin, and Outcome Stuart E. Mirvis1 Posttraumatic cerebral infarction is a recognized complication of craniocerebral Aizik L. Wolf 2 trauma, but its frequency, cause, and influence on mortality are not well defined. To Yuji Numaguchi1 ascertain this information, all cranial CT studies demonstrating posttraumatic cerebral Gregory Corradino2 infarction and performed during a 40-month period at our trauma center were reviewed. John N. Joslyn1 Posttraumatic cerebral infarction was diagnosed by CT within 24 hr of admission (10 patients) and up to 14 days after admission (mean, 3 days) in 25 (1.9%) of 1332 patients who required cranial CT for trauma during the period. Infarcts, in well-defined arterial distributions, were diagnosed either uni- or bilaterally in the posterior cerebral (17), proximal andjor distal anterior cerebral (11), middle cerebral (11), lenticulostriate/ thalamoperforating (nine), anterior choroidal (three), andjor vertebrobasilar (two) terri tories in 23 patients. Two other patients displayed atypical infarction patterns with sharply marginated cortical and subcortical low densities crossing typical vascular territories. CT findings suggested direct vascular compression due to mass effects from edema, contusion, and intra- or extraaxial hematoma as the cause of infarction in 24 patients; there was postmortem verification in five. In one patient, a skull-base fracture crossing the precavernous carotid canal led to occlusion of the internal carotid artery and ipsilateral cerebral infarction. Mortality in craniocerebral trauma with complicating posttraumatic cerebral infarction, 68% in this series, did not differ significantly from that in craniocerebral trauma patients without posttraumatic cerebral infarction when matched for admission Glasgow Coma Score results. -
Delayed Ischemic Neurological Deficit After Uneventful Elective Clipping
brain sciences Case Report Delayed Ischemic Neurological Deficit after Uneventful Elective Clipping of Unruptured Intracranial Aneurysms Petr Vachata 1,2,*, Jan Lodin 1, Aleš Hejˇcl 1, Filip Cihláˇr 3 and Martin Sameš 1 1 Department of Neurosurgery, J. E. PurkynˇeUniversity, Masaryk Hospital, EU 401 13 Ústí nad Labem, Czech Republic; [email protected] (J.L.); [email protected] (A.H.); [email protected] (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. PurkynˇeUniversity, Masaryk Hospital, EU 401 13 Ústí nad Labem, Czech Republic; fi[email protected] * Correspondence: [email protected]; Tel.: +420-736210076; Fax: +420-477112880 Received: 29 June 2020; Accepted: 27 July 2020; Published: 29 July 2020 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. Keywords: unruptured intracranial aneurysm; vasospasm; delayed ischemic neurological deficit 1. Introduction Cerebral vasospasm (CVS) frequently complicates the course of patients with subarachnoid hemorrhage (SAH) caused by ruptured intracranial aneurysms. -
Aortic Emergencies
Aortic Emergencies a,b, Kathleen Wittels, MD * KEYWORDS Aortic dissection Abdominal aortic aneurysm Thoracic aortic aneurysm Patients with aortic emergencies are some of the highest acuity patients that the Emergency Medicine (EM) physician encounters. These emergencies are divided into 2 primary groups: those related to aortic dissection and those related to an abdominal aortic aneurysm (AAA). Thoracic aortic aneurysms without dissection comprise a smaller subset of patients with aortic emergencies. Because there are varying presenting complaints, these diagnoses can be challenging to make, and a missed diagnosis often leads to significant morbidity and mortality. This article discusses the clinical presentations, available diagnostic tools, and treatment consid- erations of aortic dissection, AAA, and thoracic aortic aneurysm. AORTIC DISSECTION Causes and Risk Factors Acute aortic dissection occurs when there is a tear in the aortic intima, resulting in separation between the aortic intima and the aortic media. Blood flows into this space, creating the false lumen. The initial tear may propagate proximally and/or distally and affect any arteries branching from the aorta, resulting in varied clinical presentations. Because of this, as well as the relative infrequency of the diagnosis, aortic dissection is a diagnosis that can be challenging for the emergency physician. Several risk factors have been associated with aortic dissection.1 These include: Hypertension Stimulant use Trauma Genetic conditions including Marfan syndrome, Ehlers-Danlos syndrome, bicuspid aortic valve Inflammatory vasculitides including Takayesu arteritis, giant cell arteritis, and Behc¸et arteritis There is no funding support for this article, and the author has nothing to disclose. a Harvard Medical School, USA b Department of Emergency Medicine, Brigham and Women’s Hospital, 75 Francis Street, Neville House, Boston, MA 02115, USA * Department of Emergency Medicine, Brigham and Women’s Hospital, 75 Francis Street, Neville House, Boston, MA 02115. -
British Aneurysm Nimodipine Trial
Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial J D Pickard, G D Murray, R Illingworth, M D M Shaw, G M Teasdale, P M Foy, P R D Humphrey, D A Lang, R Nelson, P Richards, J Sinar, S Bailey, A Skene Abstract Conclusions-Oral nimodipine 60 mg four hourly Objective-To determine the efficacy of oral is well tolerated and reduces cerebral infarction and nimodipine in reducing cerebral infarction and improves outcome after subarachnoid haemorrhage. poor outcomes (death and severe disability) after subarachnoid haemorrhage. Wessex Neurological Introduction Centre, Southampton Design-Double blind, placebo controlled, General Hospital, randomised trial with three months of follow up and Despite advances that have reduced considerably Southampton S09 4XY intention to treat analysis. To have an 80% chance the risks of operation to secure a ruptured cerebral J D Pickard, MCHIR, with a significance level of 0-05 of detecting a 50% aneurysm the overall mortality and morbidity during professor ofclinical reduction in an incidence of cerebral infarction of the management of patients with subarachnoid neurological sciences 15% a minimum of 540 patients was required. haemorrhage who have survived and not been R Nelson, FRCS, senior Setting-Four regional neurosurgical units in the devastated by the initial ictus has not fallen dramatic- registrar in neurosurgery ally. This is mainly because such patients rebleed and S Bailey, RGN, Medical United Kingdom. Research Council research Patients-In all 554 patients were recruited have delayed cerebral ischaemia. The management sister between June 1985 and September 1987 out of dilemma remains the need to weigh the risk of a population of 1115 patients admitted with sub- precipitating cerebral ischaemia by operation against Medical Statistics Unit, arachnoid haemorrhage proved by the results of that of rebleeding while awaiting surgery. -
Transient Ischemic Attack: an Evidence-Based Update
January 2013 Transient Ischemic Attack: Volume 15, Number 1 An Evidence-Based Update Authors Matthew S. Siket, MD, MS Assistant Professor of Emergency Medicine, Alpert Medical School of Abstract Brown University, Providence, RI Jonathan Edlow, MD Professor of Medicine, Harvard Medical School; Vice Chair of Transient ischemic attack represents a medical emergency and Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, warns of an impending stroke in roughly one-third of patients MA who experience it. The risk of stroke is highest in the first 48 hours Peer Reviewers following a transient ischemic attack, and the initial evaluation Christopher Y. Hopkins, MD in the emergency department is the best opportunity to identify Assistant Professor of Emergency Medicine and Neurocritical Care, those at highest risk of stroke recurrence. The focus should be on University of Florida Health Science Center, Jacksonville, FL J. Stephen Huff, MD differentiating transient ischemic attack from stroke and common Associate Professor of Emergency Medicine and Neurology, University mimics. Accurate diagnosis is achieved by obtaining a history of of Virginia, Charlottesville, VA abrupt onset of negative symptoms of ischemic origin fitting a CME Objectives vascular territory, accompanied by a normal examination and the Upon completion of this article, you should be able to: absence of neuroimaging evidence of infarction. Transient isch- 1. Cite recent studies on TIA diagnosis and management and emic attacks rarely last longer than 1 hour, and the classic 24-hour practice their indications. time-based definition is no longer relevant. Once the diagnosis has 2. Using available resources, incorporate imaging-enhanced risk stratification tools in the early evaluation of TIA in the ED. -
Update in the Management of Type B Aortic Dissection
VMJ0010.1177/1358863X16642318Vascular MedicineNauta et al. 642318research-article2016 Review Vascular Medicine 1 –13 Update in the management © The Author(s) 2016 Reprints and permissions: of type B aortic dissection sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1358863X16642318 vmj.sagepub.com Foeke JH Nauta1,2, Santi Trimarchi1, Arnoud V Kamman1, Frans L Moll3, Joost A van Herwaarden3, Himanshu J Patel4, C Alberto Figueroa5, Kim A Eagle2 and James B Froehlich2 Abstract Stanford type B aortic dissection (TBAD) is a life-threatening aortic disease. The initial management goal is to prevent aortic rupture, propagation of the dissection, and symptoms by reducing the heart rate and blood pressure. Uncomplicated TBAD patients require prompt medical management to prevent aortic dilatation or rupture during subsequent follow-up. Complicated TBAD patients require immediate invasive management to prevent death or injury caused by rupture or malperfusion. Recent developments in diagnosis and management have reduced mortality related to TBAD considerably. In particular, the introduction of thoracic stent-grafts has shifted the management from surgical to endovascular repair, contributing to a fourfold increase in early survival in complicated TBAD. Furthermore, endovascular repair is now considered in some uncomplicated TBAD patients in addition to optimal medical therapy. For more challenging aortic dissection patients with involvement of the aortic arch, hybrid approaches, combining open and endovascular repair, have had promising results. Regardless of the chosen management strategy, strict antihypertensive control should be administered to all TBAD patients in addition to close imaging surveillance. Future developments in stent-graft design, medical therapy, surgical and hybrid techniques, imaging, and genetic screening may improve the outcomes of TBAD patients even further.