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1

Gorelick, Philip B. „Cerebrovascular Disease“. Nursing Clinics of North America 21, Nr. 2 (Juni 1986): 275–88. http://dx.doi.org/10.1016/s0029-6465(22)00416-9.

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2

Wolf, P. A., und J. C. Grotta. „Cerebrovascular Disease“. Circulation 102, Supplement 4 (14.11.2000): IV—75—IV—80. http://dx.doi.org/10.1161/01.cir.102.suppl_4.iv-75.

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3

Frost, Elizabeth A. M. „Cerebrovascular disease“. Current Opinion in Anaesthesiology 4, Nr. 5 (Oktober 1991): 639–44. http://dx.doi.org/10.1097/00001503-199110000-00002.

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4

Herrick, Ian A. „Cerebrovascular disease“. Current Opinion in Anaesthesiology 16, Nr. 3 (Juni 2003): 337–42. http://dx.doi.org/10.1097/00001503-200306000-00016.

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5

Caprio, Fan Z., und Farzaneh A. Sorond. „Cerebrovascular Disease“. Medical Clinics of North America 103, Nr. 2 (März 2019): 295–308. http://dx.doi.org/10.1016/j.mcna.2018.10.001.

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6

Holloway, R. G. „Cerebrovascular Disease“. Neurology 49, Nr. 4 (01.10.1997): 1192. http://dx.doi.org/10.1212/wnl.49.4.1192.

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7

Sacco, Ralph L., und Tatjana Rundek. „Cerebrovascular disease“. Current Opinion in Neurology 25, Nr. 1 (Februar 2012): 1–4. http://dx.doi.org/10.1097/wco.0b013e32834f89b1.

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8

Caplan, Louis R., D. Eric Searls und Fong Kwong Sonny Hon. „Cerebrovascular Disease“. Medical Clinics of North America 93, Nr. 2 (März 2009): 353–69. http://dx.doi.org/10.1016/j.mcna.2008.09.004.

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9

Bowsher, David, G. Vantrappen, David Mabey, Tom Treasure, KentL Woods, WilliamP Arend und David Bowsher. „CEREBROVASCULAR DISEASE“. Lancet 341, Nr. 8838 (Januar 1993): 156. http://dx.doi.org/10.1016/0140-6736(93)90015-9.

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10

Bonita, Ruth, und Robert Beaglehole. „CEREBROVASCULAR DISEASE“. Lancet 341, Nr. 8859 (Juni 1993): 1510–11. http://dx.doi.org/10.1016/0140-6736(93)90640-3.

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11

William, B. Thomas. „Cerebrovascular Disease“. Veterinary Clinics of North America: Small Animal Practice 26, Nr. 4 (Juli 1996): 925–43. http://dx.doi.org/10.1016/s0195-5616(96)50112-9.

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12

Riordan-Eva, Paul. „Cerebrovascular Disease“. Journal of Neuro-Ophthalmology 24, Nr. 2 (Juni 2004): 180–81. http://dx.doi.org/10.1097/00041327-200406000-00019.

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13

Findlay, J. Max. „Cerebrovascular Disease“. Neurosurgery 41, Nr. 4 (01.10.1997): 987–88. http://dx.doi.org/10.1097/00006123-199710000-00051.

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14

Fujishima, Masatoshi, und Kenichiro Fujii. „Cerebrovascular Disease“. Clinical Science 87, Nr. 2 (01.08.1994): 119–20. http://dx.doi.org/10.1042/cs0870119.

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15

&NA;. „Cerebrovascular disease“. Current Opinion in Neurology 9, Nr. 1 (Februar 1996): B8. http://dx.doi.org/10.1097/00019052-199602000-00017.

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16

&NA;. „Cerebrovascular disease“. Current Opinion in Neurology 10, Nr. 1 (Februar 1997): B9. http://dx.doi.org/10.1097/00019052-199702000-00017.

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17

Rinck, Peter A. „Cerebrovascular Disease“. Radiology 171, Nr. 1 (April 1989): 170. http://dx.doi.org/10.1148/radiology.171.1.170.

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18

Harbaugh, Robert E. „Cerebrovascular Disease“. JAMA: The Journal of the American Medical Association 277, Nr. 24 (25.06.1997): 1980. http://dx.doi.org/10.1001/jama.1997.03540480080047.

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19

Wiseman, Stewart J., Stuart H. Ralston und Joanna M. Wardlaw. „Cerebrovascular Disease in Rheumatic Diseases“. Stroke 47, Nr. 4 (April 2016): 943–50. http://dx.doi.org/10.1161/strokeaha.115.012052.

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20

Squizzato, A., V. E. A. Gerdes, D. P. M. Brandjes, H. R. Büller und J. Stam. „Thyroid Diseases and Cerebrovascular Disease“. Stroke 36, Nr. 10 (Oktober 2005): 2302–10. http://dx.doi.org/10.1161/01.str.0000181772.78492.07.

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21

Moalla, K., E. Turki, I. Bouchhima, N. Bouzidi, M. Damak und C. Mhiri. „Cerebrovascular diseases complicating Crohn’s disease“. Journal of the Neurological Sciences 357 (Oktober 2015): e396. http://dx.doi.org/10.1016/j.jns.2015.08.1404.

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22

Shibata, Shobu. „Cerebrovascular occlusive disease“. Nosotchu 8, Nr. 2 (1986): 144–49. http://dx.doi.org/10.3995/jstroke.8.144.

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23

Uchiyama, Shinichiro. „5) Cerebrovascular Disease“. Nihon Naika Gakkai Zasshi 98, Nr. 9 (2009): 2200–2206. http://dx.doi.org/10.2169/naika.98.2200.

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24

Uchiyama, Shinichiro. „5) Cerebrovascular Disease“. Nihon Naika Gakkai Zasshi 98, Suppl (2009): 82b. http://dx.doi.org/10.2169/naika.98.82b.

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25

Kitagawa, Kazuo, und Saburo Kakoda. „3) Cerebrovascular Disease“. Nihon Naika Gakkai Zasshi 99, Nr. 9 (2010): 2104–9. http://dx.doi.org/10.2169/naika.99.2104.

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26

Kitagawa, Kazuo, und Saburo Sakoda. „3) Cerebrovascular Disease“. Nihon Naika Gakkai Zasshi 99, Suppl (2010): 72b. http://dx.doi.org/10.2169/naika.99.72b.

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27

Fine Olivarius, Bent. „OCCLUSIVE CEREBROVASCULAR DISEASE“. Acta Neurologica Scandinavica 43, S31 (29.01.2009): 79–91. http://dx.doi.org/10.1111/j.1600-0404.1967.tb02066.x.

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28

Maria, Bernard L. „Childhood Cerebrovascular Disease“. Journal of Child Neurology 26, Nr. 9 (11.08.2011): 1072–73. http://dx.doi.org/10.1177/0883073811408095.

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29

Hughes, T. A. T. „ISCHEMIC CEREBROVASCULAR DISEASE“. Brain 125, Nr. 12 (01.12.2002): 2782—a—2783. http://dx.doi.org/10.1093/brain/awf263.

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30

MacGowan, Daniel J. L., und Stephan A. Mayer. „Acute cerebrovascular disease“. Current Opinion in Critical Care 2, Nr. 2 (April 1996): 92–97. http://dx.doi.org/10.1097/00075198-199604000-00002.

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31

Perdue, Garland D. „Extracranial cerebrovascular disease“. Journal of Vascular Surgery 6, Nr. 2 (August 1987): 204. http://dx.doi.org/10.1016/s0741-5214(87)70066-4.

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32

Lee, Nora S., und H. Royden Jones. „Extracranial Cerebrovascular Disease“. Cardiology Clinics 9, Nr. 3 (August 1991): 523–34. http://dx.doi.org/10.1016/s0733-8651(18)30289-3.

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33

Phi, Ji Hoon, Kyu-Chang Wang, Byung-Kyu Cho und Seung-Ki Kim. „Pediatric cerebrovascular disease“. Korean Journal of Pediatrics 51, Nr. 12 (2008): 1282. http://dx.doi.org/10.3345/kjp.2008.51.12.1282.

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34

Riordan-Eva, Paul. „Imaging Cerebrovascular Disease“. Journal of Neuro-Ophthalmology 24, Nr. 3 (September 2004): 270. http://dx.doi.org/10.1097/00041327-200409000-00020.

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35

Murphy, Kieran. „Imaging cerebrovascular disease“. Annals of Neurology 55, Nr. 3 (2004): 453. http://dx.doi.org/10.1002/ana.20023.

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36

LILLEHEI, KEVIN O. „Occlusive Cerebrovascular Disease“. Archives of Surgery 123, Nr. 6 (01.06.1988): 786. http://dx.doi.org/10.1001/archsurg.1988.01400300132036.

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37

Martinez, Veline, Esteban Echeverri, Maria Alejandra Urbano, Laura Juliana Ballen und Guillermo Edinson Guzman. „Hemorrhagic Cerebrovascular Disease“. Revista Ciencias de la Salud 21, Nr. 3 (04.10.2023): 1–12. http://dx.doi.org/10.12804/revistas.urosario.edu.co/revsalud/a.12671.

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Introduction: Stroke is a major cause of morbidity and mortality worldwide, with hemorrhagic stroke being the deadliest form of acute stroke. Therefore, the cause of the event should be determined to direct the associated therapy and take preventive measures. Hyperhomocysteinemia has been described as a rare etiology of stroke. Although hyperhomocysteinemia has been associated with venous thrombotic events, altered endothelial function, and procoagulant states, its clinical role in stroke remains controversial. Case description: We present a case of a 60-year-old male patient with primary autoimmune hypothyroidism who presented with dysarthria, facial paresis, and left upper-limb monoparesis after sexual intercourse. A simple skull computed tomography scan showed hyperintensity in the right basal ganglion, indicating an acute hemorrhagic event. Etiological studies were performed, including ambulatory blood pressure monitoring, cerebral angiography, and transthoracic echocardiogram, which ruled out underlying vascular pathology. During follow-up, vitamin B12 deficiency and hyperhomocysteinemia were detected, without other blood biochemical profile alterations. Supplementation was initiated, and homocysteine levels gradually decreased, without new neurological deficits observed during follow-up. Conclusion: Quantification of homocysteine should be considered in patients with a cerebrovascular disease without apparent cause, as documenting hyperhomocysteinemia and correcting its underlying etiology are essential not only for providing appropriate management but also for preventing future events.
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38

Waters, Michael F. „Editorial: Cerebrovascular disease“. Current Opinion in Neurology 36, Nr. 2 (April 2023): 124. http://dx.doi.org/10.1097/wco.0000000000001140.

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39

Parfenov, V. A. „Ménière’s disease and chronic cerebrovascular diseases“. Meditsinskiy sovet = Medical Council, Nr. 19 (01.12.2021): 35–40. http://dx.doi.org/10.21518/2079-701x-2021-19-35-40.

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Ménière’s disease (MD) is an idiopathic inner ear disease, which is characterized by noise in the ears, periodic attacks of vertigo and the development of sensorineural hearing loss. MD is characterized by endolymphatic hydrops – an increase in the volume of endolymph that fills the membered labyrinth of the inner ear. Currently highlighted subtypes MD. The first subtype meets most often and is characterized by classical manifestations of MD. The second subtype is characterized by the development of sensorineural hearing loss, to which only after a long time are joined by the episodes of dizziness. The third subtype of MD includes family cases of the disease. The fourth and fifth subtypes of MD is observed in patients with migraine and autoimmune diseases. The diagnosis of definite MD is based on the 2 or more spontaneous episodes of vertigo with each lasting 20 minutes to 12 hours, low-to medium-frequency sensorineural hearing loss in one ear, fluctuating aural symptoms (fullness, hearing, tinnitus) located in the affected ear, and lack of data for other reasons for dizziness. There are no effective treatment for auditory disorders MD, therapy is aimed at preventing dizziness attacks. The first line of MD’s therapy includes a dietary salt restriction, the use of betahistine and diuretics. Betahistine (Betaserc) is usually used in a daily dose of 48 mg for 3–6 months to reduce the frequency of vertigo. For long-term treatment, it is convenient to use a betahistine modified-released (Betaserc Long) 48 mg, taken once a day. With the ineffectiveness of conservative therapy, other methods of therapy are possible: intratympanic administration of corticosteroids or gentamicin, labyrinthectomy or vestibular neurectomy. Unfortunately, many patients suffering from BM mistakenly makes a diagnosis of cerebrovascular disease, vertebrobasilar insufficiency, cervical osteochondrosis. Diagnostic errors are usually caused by the fact that the patients with MD are not conducted audiometry, vestibular tests, and the signs of cerebral microangiopathy identified when MRI brain are mistakenly regarded as confirmation of vascular dizziness genesis.
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40

Németh, Noémi, Dóra Endrei, Lilla Horváth, Diána Elmer, Tímea Csákvári, Róbert Pónusz, László Szapáry und Imre Boncz. „A cerebrovascularis betegségekből eredő, idő előtti halálozás egyenlőtlenségei Európában 1990 és 2014 között“. Orvosi Hetilap 162, Nr. 4 (24.01.2021): 144–52. http://dx.doi.org/10.1556/650.2021.31980.

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Összefoglaló. Bevezetés: A cerebrovascularis betegségek népegészségügyi szempontból jelentősek, világszerte a vezető halálokok között szerepelnek, és a rokkantság egyik fő okát képezik. Célkitűzés: Vizsgálatunk célja a cerebrovascularis betegségekből eredő, idő előtti halálozás hazai és nemzetközi adatainak elemzése régiónkénti bontásban a 45–59 éves korcsoportban. Módszerek: Retrospektív, kvantitatív elemzés keretében vizsgáltuk a cerebrovascularis betegségekből eredő, korspecifikus, 1990 és 2014 közötti halálozást az Egészségügyi Világszervezet (WHO) Európai Régióján belül kiválasztott nyugat-európai (n = 17), kelet-európai országokban (n = 10) és a volt Szovjetunió utódállamaiban (n = 15), 100 000 főre vetítve, a WHO Európai Halálozási Adatbázisának adatai alapján. Leíró statisztikai módszereket, idősoros kimutatást, Kruskal–Wallis-próbát alkalmaztunk. Eredmények: A cerebrovascularis betegségekből eredő, 100 000 főre vetített korspecifikus halálozás a nyugat-európai országokban volt a legalacsonyabb (férfiak: 1990: 35,14, 2014: 14,31; nők: 1990: 21,11, 2014: 8,76) és a Szovjetunió utódállamaiban a legmagasabb (férfiak: 1990: 134,19; 2014: 91,13; nők: 1990: 83,62, 2014: 41,83) (p<0,05). A kelet-európai és a nyugat-európai országok, valamint a nyugat-európai országok és a Szovjetunió utódállamainak korspecifikus, cerebrovascularis halálozása között szignifikáns különbséget találtunk mindkét nemben (1990, 2004, 2014: p<0,05). A cerebrovascularis betegségek korspecifikus standardizált halálozása 1990 és 2014 között a nyugat-európai országokban (férfiak: –59,28%, nők: –58,29%) csökkent a legnagyobb mértékben, melyet a vizsgált kelet-európai országok (férfiak: –54,14%, nők: –57,53%), majd a Szovjetunió utódállamai (férfiak: –32,09%, nők: –49,97%) követtek. Következtetések: A korspecifikus, cerebrovascularis halálozás a férfiak és a nők körében egyaránt csökkent az egyes régiókban. Magyarországon a nyugat-európai átlagnál jobban, 62,2%-kal csökkent a férfiak és 59,1%-kal a nők korai cerebrovascularis halálozása 1990 és 2014 között. Orv Hetil. 2021; 162(4): 144–152. Summary. Introduction: Cerebrovascular diseases are a significant public health concern, they are among the leading causes of death worldwide and one of the major causes of disability. Objective: Our aim was to analyse national and international data regarding premature, cerebrovascular disease mortality per region in the 45–59 age group. Methods: We performed a retrospective, quantitative analysis on age-specific, premature cerebrovascular disease mortality between 1990 and 2014 per 100 000 population on data derived from the World Health Organisation, European Mortality Database on Western European (n = 17), Eastern European (n = 10) countries, and countries of the former Soviet Union (n = 15). Descriptive statistics, time series analysis and Kruskal–Wallis test were performed. Results: Age-related, cerebrovascular disease mortality per 100 000 population was the lowest in Western European countries (males: 1990: 35.14, 2014: 14.31; females: 1990: 21.11, 2014: 8.76), and the highest in former Soviet Union countries (males: 1990: 134.19; 2014: 91.13; females: 1990: 83.62, 2014: 41.83) (p<0,05). Significant differences were found in age-specific, cerebrovascular disease mortality in both sexes between Eastern and Western European countries and former Soviet Union countries (1990, 2004, 2014: p<0.05). Between 1990 and 2014, age-specific, standardized cerebrovascular disease mortality showed the biggest decrease in Western European countries (males: –59.28%, females: –58.29%) followed by Eastern European (males: –54.14%, females: –57.53%) and former Soviet Union countries (males: –32.09%, females: –49.97%). Conclusions: Age-specific, cerebrovascular disease mortality decreased in both sexes in all regions analysed. Hungary was found to have seen a decrease above the Western European average, premature cerebrovascular mortality decreased by 62.2% in males and 59.1% in females between 1990 and 2014. Orv Hetil. 2021; 162(4): 144–152.
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Geng, Xiaokun, Ankush Chandra, ChristopherR Stone, WilliamA Li und Yuchuan Ding. „The cerebral circulation and cerebrovascular disease II: Pathogenesis of cerebrovascular disease“. Brain Circulation 3, Nr. 2 (2017): 57. http://dx.doi.org/10.4103/bc.bc_11_17.

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42

Nakai, Michikazu, Yoshitaka Iwanaga, Yoko Sumita, Shinichi Wada, Haruhiko Hiramatsu, Koji Iihara, Takahide Kohro et al. „Associations among cardiovascular and cerebrovascular diseases: Analysis of the nationwide claims-based JROAD-DPC dataset“. PLOS ONE 17, Nr. 3 (11.03.2022): e0264390. http://dx.doi.org/10.1371/journal.pone.0264390.

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Cardiovascular and cerebrovascular diseases are frequently interconnected due to underlying pathology involving atherosclerosis and thromboembolism. The aim of this study was to investigate the impact of clinical interactions among cardiovascular and cerebrovascular diseases on patient outcomes using a large-scale nationwide claims-based dataset. Cardiovascular diseases were defined as myocardial infarction, heart failure, atrial fibrillation, and aortic dissection. Cerebrovascular diseases were defined as cerebral infarction, intracerebral hemorrhage, and subarachnoid hemorrhage. This retrospective study included 2,736,986 inpatient records (1,800,255 patients) at 911 hospitals from 2015 to 2016 from Japanese registry of all cardiac and vascular disease-diagnostic procedure combination dataset. Interactions among comorbidities and complications, rehospitalization, and clinical outcomes including in-hospital mortality were investigated. Among hospitalization records that involved cardiovascular disease, 5.9% (32,686 records) had cerebrovascular disease as a comorbidity and 2.1% (11,362 records) included an incident cerebrovascular complication after hospitalization. Cerebrovascular disease as a comorbidity or complication was associated with higher in-hospital mortality than no cerebrovascular disease (adjusted odds ratio (OR) [95% confidence interval]: 1.10 [1.06–1.14], 2.02 [1.91–2.13], respectively). Among 367,904 hospitalization records that involved cerebrovascular disease, 17.7% (63,647 records) had cardiovascular disease listed as comorbidity and 3.3% (11,834 records) as a complication. Only cardiovascular disease as a complication was associated with higher in-hospital mortality (adjusted OR [95% confidence interval]: 1.29 [1.22–1.37]). In addition, in-hospital mortality during rehospitalization due to the other disease was significantly higher than mortality during the hospitalization due to the first disease. In conclusion, substantial associations were observed between cardiovascular and cerebrovascular disease in a large-scale nationwide claims-based dataset; these associations had a significant impact on clinical outcomes. More intensive prevention and management of cardiovascular and cerebrovascular disease might be crucial.
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43

Kumar, Aditya, und Louise McCullough. „Cerebrovascular disease in women“. Therapeutic Advances in Neurological Disorders 14 (Januar 2021): 175628642098523. http://dx.doi.org/10.1177/1756286420985237.

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Cerebrovascular disease is a major cause of morbidity, mortality, and disability in women. The spectrum of disease differs between men and women, with women being particularly vulnerable to certain conditions, especially during specific periods of life such as pregnancy. There are several unique risk factors for cerebrovascular disease in women, and the influence of some traditional risk factors for stroke is stronger in women. Moreover, disparities persist in representation of women in clinical trials, acute intervention, and stroke outcomes. In this review, we aimed to explore the epidemiology, etiologies, and management of cerebrovascular disease in women, highlighting some of these differences and the growing need for sex-specific management guidelines and health policies.
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44

URAKAMI, Katsuya, und Kenji NAKASHIMA. „Epidemiology of Cerebrovascular Disease“. Internal Medicine 37, Nr. 9 (1998): 720–21. http://dx.doi.org/10.2169/internalmedicine.37.720.

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45

Heros, Roberto C. „Sundt's Occlusive Cerebrovascular Disease“. Mayo Clinic Proceedings 70, Nr. 5 (Mai 1995): 508. http://dx.doi.org/10.4065/70.5.508.

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46

Nair, Prejna, und Dr Radhika Arjunkumar. „Periodontitis And Cerebrovascular Disease“. IOSR Journal of Dental and Medical Sciences 13, Nr. 2 (2014): 67–69. http://dx.doi.org/10.9790/0853-13236769.

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47

Narasimhan, Manisha, Raymond Schwartz und Glenda Halliday. „Parkinsonism and cerebrovascular disease“. Journal of the Neurological Sciences 433 (Februar 2022): 120011. http://dx.doi.org/10.1016/j.jns.2021.120011.

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48

Stevens, James. „Sleep and cerebrovascular disease“. Journal of the Neurological Sciences 429 (Oktober 2021): 117887. http://dx.doi.org/10.1016/j.jns.2021.117887.

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49

Suzuki, Hidenori, und Fumihiro Kawakita. „Periostin in cerebrovascular disease“. Neural Regeneration Research 15, Nr. 1 (2020): 63. http://dx.doi.org/10.4103/1673-5374.264456.

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Lee, Kwang Ho. „Diagnosis of Cerebrovascular Disease“. Journal of the Korean Medical Association 45, Nr. 12 (2002): 1432. http://dx.doi.org/10.5124/jkma.2002.45.12.1432.

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