İNMEDE BEYİN ÖDEMİ VE KAFA İÇİ BASINÇ ARTIŞI: TÜRK BEYİN DAMAR HASTALIKLARI DERNEĞİ UZMAN GÖRÜŞÜ

Beyin ödemi inmeden sonra sık karşılaşılan bir sorundur. İntrakranial basınç artışı serebral perfüzyonu bozarak veserebral herniasyona yol açarak mortalite ve morbiditeyi artırır. İnme hastası takip eden nörologların, hangi inmedensonra beyin ödemi gelişeceğini kestirebilmesi, beyin ödemi gelişmemesi için önlemler alabilmesi, gelişirse intrakranialbasınç artışı ve serebral herniasyonu klinik ve radyolojik olarak tanıyabilmesi, ve önlenemezse beyin ödemi veintrakranial basınç artışını hızlı ve etkin şekilde tedavi edebilmesi gerekir. Bu uzman görüşü Türk Beyin DamarHastalıkları Derneği bünyesinde aktif olarak çalışan 60 uzmanın ortak görüşü ile hazırlanmış bir klinik rehberniteliğindedir

Blood-brain barrier leakage after transient cerebral ischemia

Acute ischemic stroke is a devastating disease leaving more than half of its victims disabled and causing nearly 5% of all deaths worldwide. In large ischemic strokes, a major cause of death is brain edema, which follows blood-brain barrier (BBB) leakage. The BBB ensures brain homeostasis in health and disease by limiting the entry of harmful blood-borne substances into the brain parenchyma. With a leaky BBB, the brain becomes devoid of protection from detrimental components of the circulating blood. The BBB leakage in animal models of ischemia reperfusion has long been considered to be biphasic; however, a considerable amount of discrepancies exist among the studies. Knowing exact temporal changes of the BBB permeability (BBBP) is important for the management of stroke patients. When the BBB is open, BBBP alleviating therapies would be effective, neuroprotective or neurorestorative drugs would be introduced, and if the BBB is closed these drugs would not enter the brain. Practical and reliable biomarkers of BBBP status are needed. Stanniocalcins (STCs) are widely expressed in the brain and STC-1 expression is elevated in pathologies, such as hypoxia and focal ischemia. Recent data suggest a neuroprotective role for STC-1 especially trough hypoxic preconditioning (HPC). No previous data associate STC-1 and the BBB. We systematically evaluated disruption of the BBB following ischemia-reperfusion in a rat model of transient focal ischemia via suture occlusion of the middle cerebral artery for 90 min. Firstly (I, II), animals were allocated to 15 groups after reperfusion (25 min to 5 weeks). Secondly (III), a group of animals were evaluated repeatedly from 2 h to 1 week after reperfusion. BBBP to both small (gadolinium) (I, II, III), and large (Evans blue) (I) molecules were quantified by magnetic resonance imaging and fluorescence, respectively. Lastly, the contribution of STC-1 to HPC and the BBB was explored using STC-1 deficient mice (STC-/-). (I, II, III) After transient ischemia, the BBB leakage was continuous. Leakage to Evans Blue persisted up to 3 weeks and to gadolinium up to 5 weeks. Evans blue leakage slightly decreased at 36 and 72 h, gadolinium leakage was lesser at 25 min, 3 and 4 weeks. (IV) In STC-/- mice, HPC was effective in reducing lesion size, but these mice scored worse than wild type littermates. BBBP to Evans blue was not increased in STC-/- mice; neither under normal conditions, nor after hypoxia. To conclude, transient focal ischemia in rats triggers a continuous BBB leakage lasting for several weeks. Until the final closure of the BBB, no earlier transient closure occurs. This finding indicates a long therapeutic window opportunity in respect to BBB passage of drugs to treat stroke. BBBP imaging method used in these studies may be easily translated to clinics. STC-1 is not obligatory for hypoxic preconditioning and is not a determining component of the BBB. Yet, STC-1 is important for preservation of neurological function after transient ischemia.Aivoinfarkti on vakava tauti jonka seurauksena yli puolet potilaista vammautuu ja tarvitsevat ulkopuolista apua. Maailmassa kaikesta kuolemista 5% johtuu aivoinfarktista. Kun kyseessä on laaja-alainen aivoinfarkti, tärkein kuoleman syy on veri-aivoesteen häiriö, joka johtaa nesteen siirtymiseen suonista aivokudokseen ja siten aivoturvotukseen. Aivoinfarktin eläinmalleissa aivoinfarktin jälkeinen veri-aivoesteenhäiriö on toistetusti osoitettu bifaasiseksi ilmiöksi, määrittäen että, este ensin avautuu, sitten sulkeutuu ja uudestaan avautuu. Kuitenkin, tutkimustuloksissa on merkittäviä eroja, lähinnä esteen avautumisen ajankohdat suuresti vaihtelevat. Väitöskirjatyössäni olen tutkinut aivoiskemian aiheuttamaa veri-aivoesteen vauriota systemaattisesti histologisin menetelmin ja magneettikuvausta käyttäen. Osatöissäni I-III rotille aiheutettiin aivoinfarkti ja veri-aivoesteen läpäisevyys tutkittiin 5-15 eri aikapisteessä. Menetelminä käytettiin eläinten ollessa elossa varjoaine (gadolinium, pieni molekyyli) -magneettikuvaus ja kokeiden lopetusvaiheessa Evans blue värjäys (iso molekyyli). Osajulkaisussa IV tutkittiin stanniokalsiini-1 (STC-1):n roolia veri-aivoesteen läpäisevyydessä ja hypoksia-esikäsittelyn jälkeen aivoinfarktista suojaamisessa (hypoxic preconditioning). Tätä varten käytettiin STC-1 poistogeenisiä hiiriä ja aivoinfarktimallia. Tutkimuksessa I-III todettiin veri-aivoesteen olevan jatkuvasti avoimena, toisin sanoen osoitimme häiriön olevan monofaasinen. Veri-aivoesteen lisääntynyt Evans blue-läpäisevyys on normalisoitunut 3 vko aivoinfarktin aiheuttamisen jälkeen ja gadolinium-läpäisevyys 5 vko jälkeen. Evans blue-läpäisevyys hieman väheni 36 ja 72 t infarktista, gadolinium läpäisi vähemmän 25 min sekä 3 ja 4 vko infarktista. STC-1 poistogeeniset hiiret pystyivät suojautumaan infarktista hypoksia-esikäsittelyn jälkeen, mutta olivat huonommassa neurologisessa tilassa kuin villityypin hiiret. Veri-aivoesteen vaurioitumisessa ei todettu eroja. Yhteenvetona, aivoinfarkti johtaa veri-aivoesteen jatkuvaan avautumiseen, joka kestää useita viikkoja. Ei paljastunut merkittäviä eroja läpäisevyydessä kunnes aivo-veriesteen toiminta lopulta korjaantui. Tulokset tulevat auttamaan veri-aivoesteen toimintahäiriön patofysiologian syvällisemmässä ymmärtämisessä ja siten saattavat auttaa kehittämään täsmähoitoja tähän vakavaan, aivohalvauspotilaiden henkeä uhkaavaan aivoturvotukseen. Väitöskirjani magneettikuvaukseen perustuva tutkimusmenetelmä voisi siirtää sellaisenaan kliiniseen käyttöön veri-aivoesteen läpäisevyyden tutkimiseksi aivoinfarkti potilailla

Diseases of the Brain, Head and Neck, Spine 2020–2023

This open access book offers an essential overview of brain, head and neck, and spine imaging. Over the last few years, there have been considerable advances in this area, driven by both clinical and technological developments. Written by leading international experts and teachers, the chapters are disease-oriented and cover all relevant imaging modalities, with a focus on magnetic resonance imaging and computed tomography. The book also includes a synopsis of pediatric imaging. IDKD books are rewritten (not merely updated) every four years, which means they offer a comprehensive review of the state-of-the-art in imaging. The book is clearly structured and features learning objectives, abstracts, subheadings, tables and take-home points, supported by design elements to help readers navigate the text. It will particularly appeal to general radiologists, radiology residents, and interventional radiologists who want to update their diagnostic expertise, as well as clinicians from other specialties who are interested in imaging for their patient care

The Brain-Heart Connection: Establishment of a Novel Rodent Model of Focal Insular Ischemic Stroke to Examine the Pathophysiology of Stroke-Induced Heart Injury

The neurological influence of ischemic stroke in the generation of stroke-induced heart injury (SIHI) has been acknowledged for several years. However, pathophysiological mechanisms remain uncertain. Clinically, it is hypothesized that stroke involving the insular cortex (IC) initiates SIHI, since the IC controls autonomic regulation of cardiovascular function. Yet, given the high prevalence of shared risk factors between ischemic stroke and cardiovascular disorders, mechanistic conclusions from clinical studies are largely speculative. We therefore sought to establish a novel rodent model of focal insular ischemic stroke, used to evaluate chronic outcomes of SIHI. Focal ischemic stroke was induced into the right or left IC of male Wistar rats, through stereotaxic injection of endothelin-1. Control groups received an injection of ibotenic acid, phosphate-buffered saline or no injection. Before euthanasia, rats were assessed for autonomic deficits in sensorimotor gating. At 28 days post-injection, rats with left IC damage displayed trends of impaired sensorimotor gating; compared to rats with right IC damage and control groups. Pathologically, all injured groups exhibited a chronic increase in microglia activation, present at the IC and remote white/grey matter regions. Furthermore, these groups expressed left atrial cardiac fibrosis. When correlated, a positive association between microglia activation and cardiac fibrosis was observed. With this novel model, we have identified several downstream consequences of IC ischemic stroke within the brain and heart; affirming the focal contribution of IC damage to SIHI. Taken together, these results provide insight into potential mechanisms of post-stroke cardiac damage, serving as future therapeutic targets for SIHI

Динаміка неврологічних та нейрофізіологічних порушень у хворих з головним болем та артеріальною гіпертензією у залежності від режиму харчування

Проведено клініко-параклінічне дослідження ефективності та безпеки застосування нефармакологічного методу інтервального харчування (ІХ, ще відомого за синонімами, як періодичне, короткострокове, лікувальне харчування, “intermittent fasting”) у 185 пацієнтів віком від 25 до 75 років (середній вік – 48,6 ±1,33 року) з артеріальною гіпертензією (АГ) та головним болем. У процесі добровільного застосування ІХ 43 пацієнта перервало участь у дослідженні, з них 31 - у 24- годинному та 12 - у 16-годинній схемі ІП. Таким чином, у групі дослідження залишилось 142 пацієнта середнім віком 49,26 ±1,33 рр., з них 69 чоловіків та 73 жінки. Дизайн дослідження відповідав ознакам відкритого (незасліпленого) клінічного інтервенційного продольного нерандомізованого дослідження з використанням контрольної групи, в якій не проводилось інтервенції. Наукове дослідження виконано в рамках теми кафедри неврології Дніпровського державного медичного університету (ДДМУ) (№ держреєстрації: 0119U104025). Chun Liu. Clinical characteristics of cephalalgia at patients with arterial hypertension during intermittent fasting. Dissertation for the degree of Doctor of Philosophy in the specialty 222 "Medicine" (22 "Health Care"). - Dnepr government medical university of Health Ministry of Ukraine". A clinical and paraclinical study of the effectiveness and safety of using a nonpharmacological method of intermittent fasting (IF, also known by synonyms as periodic, short-term, therapeutic nutrition, "intermittent fasting") in 185 patients aged 25 to 75 years (average age – 48,6 ±1,33 years) with arterial hypertension (AH) and headache was carried out. In the process of voluntary use of intermittent fasting, 43 patients discontinued participation in the study, 31 of them - in the 24-hour and 12 - in the 16-hour scheme of IF. Thus, 142 patients with an average age of 49,26 ±1,33 years remained in the study group, of which 69 were men and 73 were women. The study design conformed to the characteristics of an open (unblinded) clinical interventional longitudinal non-randomized study using a control group in which no intervention was carried out. The scientific research was provided on the base of the Department of Neurology of the Dnipro State Medical University (DSMU) (state registration number: 0119U104025)