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Journal articles on the topic 'Cerebrovascular disease Treatment Australia'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

De La Mata, Nicole Louise, Maria Alfaro-Ramirez, Patrick J. Kelly, Philip Masson, Rustam Al-Shahi Salman, and Angela C. Webster. "Absolute risk and risk factors for stroke mortality in patients with end-stage kidney disease (ESKD): population-based cohort study using data linkage." BMJ Open 9, no. 2 (February 2019): e026263. http://dx.doi.org/10.1136/bmjopen-2018-026263.

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IntroductionPeople with end-stage kidney disease (ESKD) have up to 30-fold higher risk of stroke than the general population.ObjectiveTo determine risk factors associated with stroke death in the ESKD population.MethodsWe identified all patients with incident ESKD in Australia (1980–2013) and New Zealand (1988–2012) from the Australian and New Zealand Dialysis and Transplant Registry (ANZDATA) registry. We ascertained underlying cause of death from data linkage with national death registries and risk factors from ANZDATA. Using a competing risks multivariable regression model, we estimated cumulative incidence of stroke and non-stroke deaths, and risk factors for stroke deaths (adjusted sub-HR, SHR).ResultsWe included 60 823 people with ESKD. There were 941 stroke deaths and 33 377 non-stroke deaths during 381 874 person-years of follow-up. Overall, the cumulative incidence of stroke death was 0.9% and non-stroke death was 36.8% 5 years after starting ESKD treatment. The risk of stroke death was higher at older ages (SHR 1.92, 95% CI 1.45 to 2.55), in females (SHR 1.41, 95% CI 1.21 to 1.64), in people with cerebrovascular disease (SHR 2.39, 95% CI 1.99 to 2.87), with ESKD caused by hypertensive/renovascular disease (SHR 1.39, 95% CI 1.09 to 1.78) or polycystic kidney disease (SHR 1.38, 95% CI 1.00 to 1.90), with earlier year of ESKD treatment initiation (SHR 1.93, 95% CI 1.56 to 2.39) and receiving dialysis (transplant vs haemodialysis SHR 0.27, 95% CI 0.09 to 0.84).ConclusionPatients with ESKD with higher risk of stroke death are older, women, with cerebrovascular disease, with hypertensive/renovascular or polycystic kidney disease cause of ESKD, with earlier year of ESKD treatment and receiving dialysis. These groups may benefit from targeted stroke prevention interventions.

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2

Georgieva, Dobrinka, Dobrinka Kalpachka, and Rossen Kalpachki. "Stroke and aphasia rehabilitation: A comparison of international guidelines." Logopedia Silesiana, no. 9 (December 29, 2020): 1–15. http://dx.doi.org/10.31261/logopediasilesiana.2020.09.19.

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Cerebrovascular diseases are the leading cause of morbidity and mortality worldwide. Unfortunately, Bulgaria leads most countries in its incidence of stroke. Furthermore, a substantial number of Bulgarian patients post-stroke present with persisting communication disorders, especially aphasia. The main purpose of the present study is to conduct an evidence-based theoretical review of leading international guidelines for treatment and rehabilitation of adult stroke patients. In particular, this theoretical overview compares the current Bulgarian guidelines with those developed by the United States of America, Europe, Australia, Canada, the United Kingdom, and New Zealand. The Bulgarian guidelines for the prevention, diagnosis, and treatment of cerebrovascular diseases strongly recommends pharmacological treatment, which is commensurate with international standards. Nationally, a range of different language tests are currently used in post-stroke aphasia.

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3

Donnelly, Kerry. "What's Etiology Got to Do With It?" Journal of the International Neuropsychological Society 12, no. 1 (January 2006): 153–54. http://dx.doi.org/10.1017/s135561770621021x.

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Cerebrovascular Disease, Cognitive Impairment and Dementia. John O'Brien, David Ames, Lars Gustafson, Marshal Folstein, and Edmond Chiu (Eds.). 2004. London: Martin Dunitz, 406 pp., $79.95 (HB).Cerebrovascular Disease, Cognitive Impairment and Dementiais the second edition ofCerebrovascular Disease and Dementia(2000). The new edition is over 160 pages longer than the earlier version, with several new chapters devoted to the pathophysiology of cerebrovascular disease [including provocative chapters on neurotransmitter changes in vascular dementia (VaD), the contributions of homocysteine and low vitamin B to VaD, and a good overview of hereditary forms of VaD], vascular mild cognitive impairment, noncognitive symptoms, and an expanded discussion of prevention and treatment. It is written for both clinical and scientific audiences. As in the first edition, there is a laudable comparative emphasis, with epidemiologic studies of vascular dementia in Europe, North America, Japan, and China. Indeed, the editors hail from the U.K, Australia, Sweden, and the U.S, and this affords the volume a useful global perspective. With five editors and 22 additional contributors, however, this book suffers a bit from the “too many cooks” syndrome. There is a good bit of redundancy. After the fifth or sixth description of classification criteria for vascular dementia, the reader begins to feel on the receiving end of some repetitive rehearsal therapy for her own dementia.

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Lazzarini, Peter A., Sheree E. Hurn, Suzanne S. Kuys, Maarten C. Kamp, Vanessa Ng, Courtney Thomas, Scott Jen, et al. "Foot Complications in a Representative Australian Inpatient Population." Journal of Diabetes Research 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/4138095.

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We investigated the prevalence and factors independently associated with foot complications in a representative inpatient population (adults admitted for any reason with and without diabetes). We analysed data from the Foot disease in inpatients study, a sample of 733 representative inpatients. Previous amputation, previous foot ulceration, peripheral arterial disease (PAD), peripheral neuropathy (PN), and foot deformity were the foot complications assessed. Sociodemographic, medical, and foot treatment history were collected. Overall, 46.0% had a foot complication with 23.9% having multiple; those with diabetes had higher prevalence of foot complications than those without diabetes (p<0.01). Previous amputation (4.1%) was independently associated with previous foot ulceration, foot deformity, cerebrovascular accident, and past surgeon treatment (p<0.01). Previous foot ulceration (9.8%) was associated with PN, PAD, past podiatry, and past nurse treatment (p<0.02). PAD (21.0%) was associated with older age, males, indigenous people, cancer, PN, and past surgeon treatment (p<0.02). PN (22.0%) was associated with older age, diabetes, mobility impairment, and PAD (p<0.05). Foot deformity (22.4%) was associated with older age, mobility impairment, past podiatry treatment, and PN (p<0.01). Nearly half of all inpatients had a foot complication. Those with foot complications were older, male, indigenous, had diabetes, cerebrovascular accident, mobility impairment, and other foot complications or past foot treatment.

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5

Sin Chin, Kai, Nawaf Yassi, Zina Hijazi, Victor Villemagne, Christopher Rowe, Colin L. Masters, and Rosie Watson. "316 - Lewy Body Study: An Australian longitudinal biomarker study of dementia with Lewy bodies." International Psychogeriatrics 32, S1 (October 2020): 74. http://dx.doi.org/10.1017/s1041610220002161.

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Background:Cerebral multi-morbidity is common in older people with dementia, including people with dementia with Lewy bodies (DLB). We describe the first Australian-based, longitudinal observational biomarker study of DLB.Aims:To investigate the frequency and influence of Alzheimer’s disease (AD) pathology (amyloid-β and tau) and cerebrovascular disease on clinical symptoms and disease outcome in DLB.Methods:The study will recruit 100 people with mild to moderate probable DLB, who will undergo comprehensive clinical and cognitive assessments. Scales targeting DLB-specific clinical features (such as cognitive fluctuations and rapid eye movement sleep behaviour disorder) are administered. Biomarker protocols incorporate blood sampling (including ApoE genotyping and systemic inflammatory markers), molecular imaging (amyloid-β [18F-NAV 4694], tau [18F-MK6240], VMAT2 [18F-AV133] PET scans), 3-tesla magnetic resonance imaging and optional lumbar puncture. Clinical assessments are completed 6 - monthly and imaging 18-monthly. Participants are also invited to register for post-mortem brain tissue donation.Results:Thirty participants with probable DLB have been enrolled to date (mean age 75.4 years, range 64-82; 87% male). All participants have mild to moderate cognitive impairment (mean MMSE 25, range 17-30). Approximately 64% of the participants were amyloid-β positive. Study procedure tolerability has been excellent with no adverse events reported.Conclusions:There is significant overlap of AD-related proteinopathies in people with DLB. Understanding the impact of multi-morbidity is essential in the development of effective treatment strategies. This study supports the feasibility of intensive, longitudinal biomarker studies in DLB in the Australian setting.

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6

Doerfler, Arnd, Wolfgang Becker, Isabel Wanke, Sophia Goericke, and Michael Forsting. "Endovascular treatment of cerebrovascular disease." Current Opinion in Neurology 17, no. 4 (August 2004): 481–87. http://dx.doi.org/10.1097/01.wco.0000137541.37480.96.

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7

Orito, Kimihiko, Masaru Hirohata, Yukihiko Nakamura, Yuusuke Uchiyama, Toshi Abe, and Motohiro Morioka. "7. Treatment of Cerebrovascular Disease." Japanese Journal of Radiological Technology 71, no. 6 (2015): 542–48. http://dx.doi.org/10.6009/jjrt.2015_jsrt_71.6.542.

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8

Hsu, Danny, Ibrahim Tohidi-Esfahani, Christina Brown, Scott Dunkley, Stephen Robert Larsen, Phoebe Joy Ho, Harry Iland, John Gibson, and Douglas E. Joshua. "Safety and Efficacy of CEEP (Cyclophosphamide, Epirubicin, Etoposide, Prednisolone) with or without Rituximab in Elderly Patients (>70) with Diffuse Large B-Cell Lymphoma (DLBL): A Retrospective Single Center Experience." Blood 118, no. 21 (November 18, 2011): 4957. http://dx.doi.org/10.1182/blood.v118.21.4957.4957.

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Abstract Abstract 4957 Background Over 40% of patients with the most common lymphoid malignancy worldwide, DLBL, are over the age of 70. Although R-CHOP is inarguably the mainstay of therapy for DLBL patients, a significant number of elderly patients do not tolerate the regimen due to underlying frailty and/or co-morbidities. Most elderly patients with significant co-morbidities have limited treatment options and are not offered anthracycline-containing chemotherapy due to concerns regarding toxicity. Here we describe our single center experience with CEEP, a lower intensity regimen for elderly patients with newly diagnosed or relapsed DLBL whom are deemed inappropriate for CHOP-based chemotherapy. Method All patients >70 years old (median 78.5, range 71 – 85) with histologically proven DLBL treated with CEEP ± Rituximab (R) at Royal Prince Alfred Hospital from 2000 to 2010 were retrospectively reviewed. Modified CEEP, Cyclophosphamide 300mg/m2 Day 1 (D1) and D15, Epirubicin 50mg/m2 D1 and D15, Etoposide 100mg/m2 D1 and D15, and Prednisolone 50mg D1-D5 (reduced dose from original CEEP protocol) was administered every 2 weeks. Rituximab 375mg/m2 (when approved for use in Australia) was administered every 28 days. As per institutional protocol, all patients received Bactrim prophylaxis for Pneumocystis. Baseline characteristics, Charlson Comorbidity Index, Revised International Prognostic Index (RIPI), the number of CEEP cycles, treatment response and toxicity from treatment were identified and reviewed. Results A total of 22 patients were identified, 10 were male. 15 received CEEP as initial therapy, and 7 for relapsed disease. 23% (n=5) had an ECOG score ≥ 2. 55% (n=12) had RIPI ≥ 3. All patients had a Charlson Comorbidity Index ≥ 2, with 23% (n=5) ≥ 5, which was considered sufficient to preclude conventional CHOP-based chemotherapy. Median cardiac ejection fraction was 62% (range 55 – 85%). 73% (n=16) received Rituximab and 50% (n=11) received primary GCSF prophylaxis. The median number of CEEP ± R cycles was 6 (range 2 – 9 cycles). 5% (n=1) required dose reduction and 9% (n=2) required delays in treatment due to haematological toxicity. Median follow-up was 10.0 months (range 1 – 92.7 months). At completion of therapy, complete responses (CR) were demonstrated in 10 patients (45%), with partial responses (PR) seen in 32% (n=7). 18% (n=4) demonstrated progressive disease (PD) despite therapy. Of the 7 patients with relapsed disease prior to CEEP ± R, CR was seen in 2 cases, both of whom had previous exposure to R-CVP (cyclophosphamide, vincristine, prednisolone) chemotherapy. At most recent follow up, 32% (n=7) have remained in CR with a median follow up period of 28.1 months (range 13 – 92.7 months), 36% (n=8) had disease progression, 9% (n=2) demonstrated stable residual disease, while 23% (n=5) have died. Of the 5 deaths, 3 were attributed to progressive DLBL. The other deaths were a result of complications following further salvage chemotherapy. Grade 3 – 4 haematological toxicity was observed in 72% (n=16) of patients. Febrile neutropenia occurred in 41% (n=9). Overall, 50% (n=11) required at least one re-admission to hospital. Non-haematological grade 3 – 4 toxicity was detected in 2 patients, one of whom suffered unstable angina in the setting of anaemia, the other an acute cerebrovascular event in the setting of new atrial flutter post-chemotherapy. Discussion Although limited by a small sample size, our retrospective single center experience demonstrates that CEEP ± R chemotherapy can be administered to elderly patients with significant co-morbidities. Our cohort was all aged >70, with medical co-morbidities leading to the unsuitability of conventional CHOP-based therapy. Whilst an overall response rate of 77% (CR + PR) was observed, on prolonged follow up, 32% of patients remained in CR. Significant haematological toxicity (72%) and infectious complications (41%) were observed, however no deaths were directly attributed to the chemotherapy. Future prospective studies are required to further evaluate the safety and efficacy of R-CEEP in the elderly. Disclosures: No relevant conflicts of interest to declare.

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9

AL-ROOMI, K. A., A. J. DOBSON, E. HALL, R. F. HELLER, and P. MAGNUS. "DECLINING MORTALITY FROM ISCHEMIC HEART DISEASE AND CEREBROVASCULAR DISEASE IN AUSTRALIA." American Journal of Epidemiology 129, no. 3 (March 1989): 503–10. http://dx.doi.org/10.1093/oxfordjournals.aje.a115161.

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10

Robertson, James. "Surgical Treatment of Cerebrovascular Occlusive Disease." Seminars in Neurology 6, no. 03 (September 1986): 316–23. http://dx.doi.org/10.1055/s-2008-1041476.

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11

Oczkowski, Wieslaw J., and Alexander G. G. Turpie. "14 Antithrombotic treatment of cerebrovascular disease." Baillière's Clinical Haematology 3, no. 3 (July 1990): 781–813. http://dx.doi.org/10.1016/s0950-3536(05)80028-9.

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12

Arustamyan, R. R., E. S. Lyashko, and V. N. Kuz’min. "Treatment of cerebrovascular disease during pregnancy." Problemy reproduktsii 22, no. 5 (2016): 36. http://dx.doi.org/10.17116/repro201622536-38.

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13

Ward, G., K. Jamrozik, and E. Stewart-Wynne. "Incidence and outcome of cerebrovascular disease in Perth, Western Australia." Stroke 19, no. 12 (December 1988): 1501–6. http://dx.doi.org/10.1161/01.str.19.12.1501.

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14

Luo, Yin, Yanting Wang, and Jie Fu. "Nanomaterials in Cerebrovascular Disease Diagnose and Treatment." Particle & Particle Systems Characterization 38, no. 5 (April 2, 2021): 2000311. http://dx.doi.org/10.1002/ppsc.202000311.

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15

Shchukin, I. A., A. V. Lebedeva, S. G. Burd, M. S. Fidler, R. K. Shikhkerimov, A. M. Ismailov, A. V. Bolotov, and M. Kh Belgusheva. "Chronic cerebrovascular disease: diagnosis and treatment questions." Consilium Medicum 18, no. 2 (2016): 85–94. http://dx.doi.org/10.26442/2075-1753_2016.2.85-94.

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16

Martin, David S. "Cerebrovascular Disease: Imaging and Interventional Treatment Options." Radiology 198, no. 2 (February 1996): 546. http://dx.doi.org/10.1148/radiology.198.2.546.

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17

Phatouros, Constantine C., Randall T. Higashida, Adel M. Malek, Philip M. Meyers, James E. Lefler, Christopher F. Dowd, and Van V. Halbach. "Endovascular Treatment of Noncarotid Extracranial Cerebrovascular Disease." Neurosurgery Clinics of North America 11, no. 2 (April 2000): 331–50. http://dx.doi.org/10.1016/s1042-3680(18)30136-0.

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18

Coon, Elizabeth A., Nicholas L. Zalewski, Ernest Matthew Hoffman, Ayalew Tefferi, and Kelly D. Flemming. "Nilotinib treatment-associated cerebrovascular disease and stroke." American Journal of Hematology 88, no. 6 (May 13, 2013): 534–35. http://dx.doi.org/10.1002/ajh.23442.

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19

Kai, Hisashi. "IV. Treatment for Hypertension Associated with Cerebrovascular Disease/Heart Disease." Nihon Naika Gakkai Zasshi 104, no. 2 (2015): 232–39. http://dx.doi.org/10.2169/naika.104.232.

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20

Colburn, Michael D., and Wesley S. Moore. "Pathology, natural history, and treatment of cerebrovascular disease." Current Opinion in Cardiology 6, no. 5 (October 1991): 757–61. http://dx.doi.org/10.1097/00001573-199110000-00015.

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21

Paranthaman, Raghu, and Robert C. Baldwin. "Treatment of psychiatric syndromes due to cerebrovascular disease." International Review of Psychiatry 18, no. 5 (January 2006): 453–70. http://dx.doi.org/10.1080/09540260600935462.

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22

Mcdowell, D. I., V. A. James, and M. Glasson. "SURGICAL TREATMENT OF EXTRACRANIAL CEREBROVASCULAR DISEASE: REGIONAL EXPERIENCE." ANZ Journal of Surgery 59, no. 7 (July 1989): 535–38. http://dx.doi.org/10.1111/j.1445-2197.1989.tb01626.x.

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23

Dougherty, Kathryn G., Anne Daleiden-Burns, Carol Kaden, Sergio Ramos, and Fayaz A. Shawl. "Percutaneous Techniques for the Treatment of Cerebrovascular Disease." Critical Care Nursing Quarterly 20, no. 4 (February 1998): 1–15. http://dx.doi.org/10.1097/00002727-199802000-00002.

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Dougherty, Kathryn G., Anne Daleiden-Burns, Carol Kaden, Sergio Ramos, and Fayaz A. Shawl. "Percutaneous Techniques for the Treatment of Cerebrovascular Disease." Critical Care Nursing Quarterly 20, no. 4 (February 1998): 1–15. http://dx.doi.org/10.1097/00002727-199820040-00002.

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25

Ramani, Subha, Susan Byrne-Logan, Karen M. Freund, Arlene Ash, Wei Yu, and Mark A. Moskowitz. "Gender Differences in the Treatment of Cerebrovascular Disease." Journal of the American Geriatrics Society 48, no. 7 (July 2000): 741–45. http://dx.doi.org/10.1111/j.1532-5415.2000.tb04747.x.

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26

Weisberg, Leon A. "Physician attitudes toward treatment options for cerebrovascular disease." Journal of Stroke and Cerebrovascular Diseases 5, no. 1 (January 1995): 12–19. http://dx.doi.org/10.1016/s1052-3057(10)80080-1.

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27

Ricci, Michael A. "Frontiers in Cerebrovascular Disease: Mechanisms, Diagnosis, and Treatment." Annals of Vascular Surgery 13, no. 3 (May 1999): 356. http://dx.doi.org/10.1016/s0890-5096(06)61779-2.

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28

Jellinger, K. A. "Frontiers in cerebrovascular disease. Mechanisms, diagnosis, and treatment." European Journal of Neurology 5, no. 3 (May 1998): 323–24. http://dx.doi.org/10.1046/j.1468-1331.1998.5303197.x.

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29

Couch, James R. "Antiplatelet therapy in the treatment of cerebrovascular disease." Clinical Cardiology 16, no. 10 (October 1993): 703–10. http://dx.doi.org/10.1002/clc.4960161004.

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Lin, Kailong, Liusheng Chen, Yang Wang, Yeqiang Xu, Guanliang Wang, Hongfang Li, Yicheng Pan, Lichun Ma, and Siyi He. "Endovascular treatment of cerebrovascular stenosis with stent for patients with ischemic cerebrovascular disease." Medicine 99, no. 47 (November 20, 2020): e23313. http://dx.doi.org/10.1097/md.0000000000023313.

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31

Zuckerman, Scott L., David B. Seder, Crystiana Tsujiura, Deborah Cushing, Holly Gallup, J. Mocco, Richard A. Hanel, and Robert D. Ecker. "Aspirin Allergy Desensitization in Cerebrovascular Disease." Interventional Neuroradiology 20, no. 1 (January 2014): 5–11. http://dx.doi.org/10.15274/inr-2014-10002.

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Aspirin (ASA) is the mainstay of treatment in cerebrovascular and systemic vascular disease. ASA hypersensitivity can pose a challenge to achieving optimum medical management prior to and after neurointerventional treatment. Desensitization to ASA is well described in the allergy and cardiovascular literature, but there are no similar discussions specific to neurointervention. The purpose of our study was to describe our experience with ASA hypersensitivity management and review the relevant literature. Two cases of patients with symptomatic cerebrovascular disease requiring neurointervention who were successfully desensitized to their ASA hypersensitivity prior to treatment are described. The subsequent literature is reviewed. Several ASA desensitization protocols exist and have been proven to successfully treat ASA hypersensitivity and allow for ASA therapy to be safely initiated. We describe several previously published protocols. ASA desensitization is a safe and simple way to manage ASA hypersensitivity. We provide comprehensive management guidelines for the neurointerventionalist engaging in ASA desensitization.

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32

Rothrock, John F., and Hans-Christoph Diener. "Headache secondary to cerebrovascular disease." Cephalalgia 41, no. 4 (March 18, 2021): 479–92. http://dx.doi.org/10.1177/0333102421999045.

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Objectives To discuss headache secondary to cerebrovascular disease. Background Headache is an important symptom in cerebrovascular diseases. In some conditions, headache is the leading symptom. Migraine is associated with an increased risk of stroke. Methods The authors undertook a literature search for the terms “headache” and “cerebrovascular diseases”. Results We report studies on headache in subarachnoidal hemorrhage, intracerebral hemorrhage, ischemic stroke, TIA, basilar artery thrombosis, cervical artery dissection, cerebellar stroke, arteritis and cerebral sinus venous thrombosis. In addition, we discuss migraine and stroke and thunderclap headache. Conclusions Headache is a leading symptom in many cerebrovascular diseases. Headache in combination with focal neurological deficits requires immediate diagnosis and treatment.

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Higashioka, Kazuhiko, Kenji Yoshida, Kensuke Oryoji, Kazuo Kamada, Shinichi Mizuki, Hiroshi Tsukamoto, Eisuke Yokota, and Koichi Akashi. "Successful Treatment of Lupus Cerebrovascular Disease with Mycophenolate Mofetil." Internal Medicine 54, no. 17 (2015): 2255–59. http://dx.doi.org/10.2169/internalmedicine.54.4582.

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Fedin, A. I., E. N. Saverskaya, and K. R. Badalyan. "Multimodal therapeutic strategies in the treatment of cerebrovascular disease." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 121, no. 12 (2021): 112. http://dx.doi.org/10.17116/jnevro2021121121112.

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Fujishima, Masatoshi. "Cerebrovascular Disease in the Elderly. Clinical Feature and Treatment." Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 36, no. 10 (1999): 681–89. http://dx.doi.org/10.3143/geriatrics.36.681.

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NISHIOKA, Hiroshi, Jo HARAOKA, Jiro AKIMOTO, Koichi HASEGAWA, Tadaharu FUKUDA, Masamichi HASUE, and Sachiro AZUMA. "Surgical Treatment of Cerebrovascular Disease with High Flow Bypass." Surgery for Cerebral Stroke 30, no. 1 (2002): 33–38. http://dx.doi.org/10.2335/scs.30.33.

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BILALOVA, RESEDA R., GULNARA Z. IBRAGIMOVA, ALBINA R. ZAYTSEVA, ELVIRA M. KOROLEVA, and ALIYA R. ISKHAKOVA. "COMBINED ACUTE CEREBROVASCULAR DISEASE AND MYOCARDIAL INFARCTION TREATMENT EXPERIENCE." Bulletin of Contemporary Clinical Medicine 11, no. 5 (2018): 16–22. http://dx.doi.org/10.20969/vskm.2018.11(5).16-22.

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38

Schindler, R. J. "Dementia with cerebrovascular disease: the benefits of early treatment." European Journal of Neurology 12, s3 (October 2005): 17–21. http://dx.doi.org/10.1111/j.1468-1331.2005.01323.x.

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39

Llinas, Rafael, and Louis R. Caplan. "Evidence-based treatment of patients with ischemic cerebrovascular disease." Neurologic Clinics 19, no. 1 (February 2001): 79–105. http://dx.doi.org/10.1016/s0733-8619(05)70006-2.

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Magnadottir, Hulda B., and Kimberly S. Harbaugh. "Anatomic Considerations in the Treatment of Extracranial Cerebrovascular Disease." Neurosurgery Clinics of North America 11, no. 2 (April 2000): 265–77. http://dx.doi.org/10.1016/s1042-3680(18)30131-1.

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Griessenauer, Christoph J., Paul Foreman, John P. Deveikis, and Mark R. Harrigan. "Endovascular Tools Available for the Treatment of Cerebrovascular Disease." Neurosurgery Clinics of North America 25, no. 3 (July 2014): 387–94. http://dx.doi.org/10.1016/j.nec.2014.04.001.

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42

Archila, Ricardo, and Antonieta Mahfoud. "Cerebrovascular disease in children and adolescents: Diagnosis and treatment." Pediatric Neurology 8, no. 5 (September 1992): 397. http://dx.doi.org/10.1016/0887-8994(92)90296-b.

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43

Lurie, L. "Real clinical practice." Infusion & Chemotherapy, no. 3.2 (December 15, 2020): 188–90. http://dx.doi.org/10.32902/2663-0338-2020-3.2-188-190.

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Background. Real clinical practice (RCP) exists in an evidence-based and regulatory framework, taking into account the social, political and economic situation in the country. Coronavirus pandemic (COVID-19) is the main challenge of modern RCP. Objective. To describe the modern features of the RCP. Materials and methods. Analysis of literature sources on this issue. Results and discussion. On December 31, 2019, WHO was informed about 27 cases of pneumonia of unknown origin. On January 1, 2020, the first WHO guidelines were issued. The COVID-19 outbreak was declared a health emergency on January 30 and a pandemic – on March 11. Experience with COVID-19 varies from country to country. In Germany, for example, pharmacies were allowed to produce disinfectants on their own, in Australia the telemedicine system was expanded, and in Poland a law was issued that provided the regulation of remote work, simplification of public procurement, and emergency pharmacy prescriptions. In Ukraine, the first information from the Ministry of Health on coronavirus was published on January 21. On February 19, a decision was made to procure medicines to combat COVID-19. On March 11, the export of personal protective equipment was banned, and on March 12, quarantine was imposed throughout Ukraine. On March 17, the first laws of Ukraine on combating the coronavirus were adopted. One in four patients who fell ill at the beginning of the outbreak was a health worker, which reduced the availability of medical care. The imposition of a pandemic on phase 2 of health care reform has limited health care and patients’ access to clinics and hospitals, and suspended planned hospitalizations and surgeries. Medicines without evidence were included in the COVID-19 National Treatment Protocol. An analysis of drug sales in pharmacies showed that quarantine had decreased the sales of cough and cold remedies, nasal irrigation solutions (due to a reduction in the number of socially transmitted diseases), and antidiarrheal drugs. Instead, sales of laxatives have increased (presumably due to changes in diet and limited physical activity). Sales of drugs for the treatment of sexually transmitted diseases also decreased. Quarantine in combination with the restriction of the availability of infusion therapy in the practice of the family doctor has led to a reduction in the appointment of parenteral drugs by half. In the absence of planned hospitalizations and surgeries, the volume of prescriptions for infusion drugs decreased by 13 %. There was a redistribution of drug consumption in favor of domestic drugs. “Yuria-Pharm” was in the top 3 among Ukrainian drug manufacturers. 6 out of 10 general leaders are domestic companies. “Yuria-Pharm” is a leader in blood substitutes and perfusion solutions prescribed by doctors of 16 specialties. The solutions were most often prescribed for pneumonia, mental and behavioral disorders caused by alcohol abuse, acute pancreatitis, cerebrovascular diseases, delivery, acute appendicitis, malignant tumors, insulin-dependent diabetes mellitus, chronic ischemic heart disease. For example, Tivortin (“Yuria-Pharm”) is most often prescribed by gynecologists, less often – by physicians / family doctors, neurologists, surgeons, cardiologists, anesthesiologists. In turn, Reosorbilact (“Yuria-Pharm”) is among the top 3 drugs administered by hospital doctors for the period 2014-2020. Repeated prescriptions for reimbursement were issued remotely, however, despite government programs, treatment in Ukraine still depends on the patient’s money. The National Health Service of Ukraine for 2021 proposed to increase the salaries of health care workers and reduce the catastrophic costs of medicines paid by patient on its own. At present, there is a need to transfer the results of clinical trials to the RCP, as the studies are conducted in specialized strictly controlled conditions, and the RCP allows to obtain more real results. There are several types of RCP studies: non-interventional, post-registration, marketing, pharmacoeconomic, and patient database and registry studies. Conclusions. 1. COVID-19 pandemic is the main challenge of modern RCP. 2. The imposition of a pandemic onto phase 2 of health care reform has limited health care and patients’ access to clinics and hospitals, and suspended planned hospitalizations and surgeries. 3. In the conditions of pandemic and quarantine there was a redistribution of drug consumption in favor of domestic drugs. 4. Reosorbilact (“Yuria-Pharm”) is among the top 3 drugs administered by hospital doctors for the period 2014-2020.

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Honjo, Kie, Sandra E. Black, and Nicolaas P. L. G. Verhoeff. "Alzheimer's Disease, Cerebrovascular Disease, and the β-amyloid Cascade." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 39, no. 6 (November 2012): 712–28. http://dx.doi.org/10.1017/s0317167100015547.

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Alzheimer's disease (AD), considered the commonest neurodegenerative cause of dementia, is associated with hallmark pathologies including extracellular amyloid-β protein (Aβ) deposition in extracellular senile plaques and vessels, and intraneuronal tau deposition as neurofibrillary tangles. Although AD is usually categorized as neurodegeneration distinct from cerebrovascular disease (CVD), studies have shown strong links between AD and CVD. There is evidence that vascular risk factors and CVD may accelerate Aβ 40-42 production/ aggregation/deposition and contribute to the pathology and symptomatology of AD. Aβ deposited along vessels also causes cerebral amyloid angiopathy. Amyloid imaging allowsin vivodetection of AD pathology, opening the way for prevention and early treatment, if disease-modifying therapies in the pipeline show safety and efficacy. In this review, we review the role of vascular factors and Aβ, underlining that vascular risk factor management may be important for AD prevention and treatment.

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Parfenov, V. A. "Ménière’s disease and chronic cerebrovascular diseases." Meditsinskiy sovet = Medical Council, no. 19 (December 1, 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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Yooprasert, Pimpimol, Monchai Siribamrungwong, Kamontip Chaikomon, and Kasemsuk Yothasamutr. "Interrelationship between Cerebrovascular Disease and Periodontitis." International Journal of Experimental Dental Science 4, no. 1 (2015): 47–52. http://dx.doi.org/10.5005/jp-journals-10029-1094.

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ABSTRACT Cerebrovascular disease (CVD) is the second most common cause of death and contributes to a high morbidity worldwide. The major etiology is an atherosclerosis. Many well-known risk factors, such as hypertension, dyslipidemia and diabetes, are defined as traditional risk factors. Treatment and control of traditional risk factors also improve both cardiovascular and cerebrovascular outcomes. To date, many studies reported an association between stroke and nontraditional risk factors, such as infectious diseases or inflammatory process. Periodontal disease (PD) is an infection of the gum and other toothsupporting structures, with an on going inflammatory process and affects a large number of populations worldwide. Current evidence demonstrated the local and systemic inflammatory effects in periodontitis induced an atherosclerosis. This review aims to provide the current knowledge on the association between periodontal disease and cerebrovascular disease. How to cite this article Chaikomon K, Yooprasert P, Yothasamutr K, Siribamrungwong M. Interrelationship between Cerebrovascular Disease and Periodontitis. Int J Experiment Dent Sci 2015;4(1):47-52.

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Badhwar, AmanPreet, Rebecca Brown, Danica B. Stanimirovic, Arsalan S. Haqqani, and Edith Hamel. "Proteomic differences in brain vessels of Alzheimer’s disease mice: Normalization by PPARγ agonist pioglitazone." Journal of Cerebral Blood Flow & Metabolism 37, no. 3 (July 20, 2016): 1120–36. http://dx.doi.org/10.1177/0271678x16655172.

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Cerebrovascular insufficiency appears years prior to clinical symptoms in Alzheimer’s disease. The soluble, highly toxic amyloid-β species, generated from the amyloidogenic processing of amyloid precursor protein, are known instigators of the chronic cerebrovascular insufficiency observed in both Alzheimer’s disease patients and transgenic mouse models. We have previously demonstrated that pioglitazone potently reverses cerebrovascular impairments in a mouse model of Alzheimer’s disease overexpressing amyloid-β. In this study, we sought to characterize the effects of amyloid-β overproduction on the cerebrovascular proteome; determine how pioglitazone treatment affected the altered proteome; and analyze the relationship between normalized protein levels and recovery of cerebrovascular function. Three-month-old wildtype and amyloid precursor protein mice were treated with pioglitazone- (20 mg/kg/day, 14 weeks) or control-diet. Cerebral arteries were surgically isolated, and extracted proteins analyzed by gel-free and gel-based mass spectrometry. 193 cerebrovascular proteins were abnormally expressed in amyloid precursor protein mice. Pioglitazone treatment rescued a third of these proteins, mainly those associated with oxidative stress, promotion of cerebrovascular vasocontractile tone, and vascular compliance. Our results demonstrate that amyloid-β overproduction perturbs the cerebrovascular proteome. Recovery of cerebrovascular function with pioglitazone is associated with normalized levels of key proteins in brain vessel function, suggesting that pioglitazone-responsive cerebrovascular proteins could be early biomarkers of Alzheimer’s disease.

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Fujishima, M., Y. Kiyohara, I. Kato, Y. Tanizaki, and Y. Saku. "Cerebrovascular Disease in the Elderly-Risk Factor, Treatment and Prognosis." Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 33, no. 9 (1996): 647–51. http://dx.doi.org/10.3143/geriatrics.33.647.

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SHIMBO, Matsuo. "Bobath Treatment for Patients with Cerebrovascular Disease and System Control." Rigakuryoho Kagaku 16, no. 1 (2001): 35–39. http://dx.doi.org/10.1589/rika.16.35.

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St-Amour, Isabelle, Benoit Aubé, Marie Rieux, and Francesca Cicchetti. "Targeting cerebrovascular impairments in Huntington's disease: a novel treatment perspective." Neurodegenerative Disease Management 5, no. 5 (October 2015): 389–93. http://dx.doi.org/10.2217/nmt.15.41.

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