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Verifi cation of the exact time of formation of hemorrhages in the human brain (HB) of traumatic (HTG) and non-traumatic (HNG) genesis makes it possible to signifi cantly narrow the circle of suspects in the case of a crime against human life.Aim of the work. Developing of forensic criteria for the diagnosis of the age of formation of hemorrhages of traumatic and non-traumatic genesis by light microscopy of histological sections of human brain.Materials and methods. For the study used stained histological specimens of the brain from 80 corpses with a known time of hemorrhage from 2 to 15 days, according to medical documents: in case of death from HNG – 30 histological specimens (1 group), death from HTG – 30 histological samples (group 2), brain preparations in case of death from coronary heart disease were selected for control – 20 samples (group 3).Results. Analyzing the available histopreparations, it was found that the corresponding time dependences of the age of hemorrhage are not linear, but on the contrary have fluctuations in their values – uneven appearance of pigment in HB with a gradual increase in time since the formation of hemorrhages of diff erent genesis.Conclusion. Histological examination of micropreparations of the substance of the brain, stained by the method of Pearls, is not eff ective for determining the age of hemorrhage., Верифікація точного часу утворення крововиливів у речовину головного мозку людини (РГМЛ) травматичного (КТҐ) та нетравматичного (КНҐ) ґенезів дає можливість значно звузити коло підозрюваних у разі скоєння злочину проти життя людини.Мета роботи. Розробка судово-медичних критеріїв діагностики давності утворення крововиливів травматичного та нетравматичного ґенезів методом світлової мікроскопії гістологічних зрізів речовини головного мозку людини.Матеріали та методи. Для дослідження використовувалися забарвлені за методом Перлса гістологічні препарати головного мозку 80 трупів з відомим часом утворення крововиливу від 2 до 15 діб, згідно з даними медичних документів: у випадку смерті від КНҐ – 30 гістологічних зразків (І група), смерті від КТҐ – 30 гістологічних зразків (ІІ група), для контролю були обрані препарати мозку у випадку смерті від ішемічної хвороби серця – 20 зразків (ІІІ група).Результати. Проаналізувавши наявні гістопрепарати, виявили, що відповідні часові залежності давності утворення крововиливів не лінійні, а, навпаки, мають коливання власних значень – нерівномірну появу пігменту в РГМЛ з поступовим збільшенням часу з моменту утворення крововиливів різного ґенезу.Висновок. Гістологічне дослідження мікропрепаратів речовини головного мозку, забарвлених за методом Перлса, не є ефективним для встановлення давності утворення крововиливів.

Objective: To analyze the imaging characteristics of hemorrhagic cerebral infarction (HI). Methods: The cases were selected from 220 patients with new cerebral infarction who were hospitalized in our hospital from March 2015 to February 2018, of which 34 cases were found with hemorrhagic cerebral infarction. All the selected cases met the criteria for "Diagnosis Points of Various Cerebrovascular Diseases" adopted by the Fourth National Cerebrovascular Diseases Academic Conference of the Chinese Medical Association in 1995, and were confirmed by cranial CT and/or GE1.5HDX MRI scans as Hemorrhagic cerebral infarction. Retrospectively analyze the clinical data, clinical manifestations, brain CT, GE1.5HDX magnetic resonance examination, and clinical data of 34 patients with HI, and analyze their short-term prognosis, HI occurrence time, type of bleeding, infarct area, incidence site, arteries The blood supply and imaging performance were analyzed by statistical X2 test to analyze the imaging characteristics of hemorrhagic cerebral infarction. Results: 1. 34 patients with HI in this group accounted for 15.45% of the cerebral infarction in the same period, including 16 males and 18 females. The ages ranged from 45 to 86 years, with an average of 68.09 ± 10.41 years. 2.34 cases of HI included cerebral embolism in 26 cases (76.47%), cerebral thrombosis in 7 cases (20.58%), lacunar infarction in 1 case (2.94%), cardiogenic cerebral embolism in 22 cases (64.71%), and history of atrial fibrillation. Fourteen patients (41.18%) and 24 patients with large infarction (70.59%). Conclusions: Embolization, occlusion, recanalization, and establishment of collateral circulation are closely related to the occurrence of HI. For patients with cardiogenic cerebral embolism and large-scale cerebral infarction, regardless of whether the clinical symptoms are exacerbated, attention should be paid to cerebral infarction.

Verification of the cause of death (CD) from ischemic cerebral infarction (ICI), hemorrhage of traumatic (GTG) and non-traumatic (GNG) genesis eliminates the violent origin of death. Very often it is difficult to diagnose the genesis of hemorrhage only macroscopically when performing an autopsy, so additional material should be selected for forensic histological examination. Aim of the work. To develop forensic criteria for the differentiation of ICI, GTG and GNG of the brain by light microscopy of histological sections of the human brain (HB). Material and methods. For the study were used native sections and stained histological specimens of HB from 110 corpses in the case of: death from ICI – 30 histological specimens (1 group), which were made of 30 speciments stained by the methods of Nissl and Spiel-Mayer; GNG – 30 histological samples (group 2) – 30 speciments, stained similarly to the previous group; GNG – 30 histological samples (group 3) – 30 speciments stained similarly to the previous group. Brain preparations in case of death from coronary heart disease were selected for control – 20 samples (4 groups) – 20 speciments stained by the methods of Nissl and Spiel-Mayer. Results. Analysis of the obtained data of histological examination of morphological changes of tissue elements of the human brain with different genesis of hemorrhage did not reveal stable relationships between changes in the structure of nervous tissue and the cause of hemorrhage. Conclusion. Given the nonspecificity of degenerative changes in the structural elements of the brain, depending on the genesis of hemorrhage, it can be concluded that morphological methods of histological preparations of the brain do not provide accurate and objective information about the genesis of hemorrhage., Верификация причины смерти (ПС) от ишемического инфаркта головного мозга (ИИГМ), кровоизлияний травматического (КТГ) и нетравматического (КНГ) генезов позволяет исключить насильственное происхождение смерти. Очень часто при проведении вскрытия эксперту трудно только макроскопически диагностировать генез кровоизлияния, поэтому следует дополнительно отобрать материал для судебно-гистологического исследования. Цель работы. Разработка судебно-медицинских критериев дифференциации ишемического инфаркта головного мозга, кровоизлияний травматического и нетравматического генезов мозга методом световой микроскопии гистологических срезов вещества головного мозга человека. Материалы и методы. Для исследования использовались нативные срезы и закрашенные гистологические препараты мозга от 110 трупов в случае: смерти от ИИГМ – 30 гистологических образцов (1 группа), из которых были изготовлены по 30 препаратов, окрашенных по методам Нисля и Шпиль-Майера; КНГ – 30 гистологических образцов (2 группа) – по 30 препаратов, закрашенных аналогично предыдущей группе; КТГ – 30 гистологических образцов (3 группа) – по 30 препаратов, окрашенных аналогично предыдущей группе. Для контроля были выбраны препараты мозга в случае смерти от ишемической болезни сердца – 20 образцов (4 группа) – по 20 препаратов, окрашенных по методам Ниссля и Шпиль-Майера. Результаты. Анализ полученных данных гистологического исследования морфологических изменений тканевых элементов вещества головного мозга человека с разным генезом образования кровоизлияний не выявил стабильных взаимосвязей между изменениями в структуре нервной ткани и причиной образования кровоизлияния. Вывод. Учитывая неспецифичность дегенеративных изменений структурных элементов вещества головного мозга в зависимости от генеза кровоизлияний, можно заключить, что морфологические методы исследования гистологических препаратов мозга не дают точной и объективной информации о генезе кровоизлияний., Верифікація причини смерті (ПС) від ішемічного інфаркту головного мозку (ІІГМ), крововиливів травматичного (КТҐ) та нетравматичного (КНҐ) ґенезів дозволяє виключити насильницьке походження смерті. Дуже часто при проведенні розтину експерту важко лишень макроскопічно діагностувати ґенез крововиливу, тому слід додатково відібрати матеріал для судово-гістологічного дослідження. Мета роботи. Розробка судово-медичних критеріїв диференціації ішемічного інфаркту головного мозку, крововиливів травматичного та нетравматичного ґенезів мозку методом світлової мікроскопії гістологічних зрізів речовини головного мозку людини. Матеріали та методи. Для дослідження використовувалися нативні зрізи та зафарбовані гістологічні препарати мозку від 110 трупів у випадку: смерті від ІІГМ – 30 гістологічних зразків (1 група), з яких були виготовлені по 30 препаратів, зафарбованих за методами Ніссля та Шпіль-Майєра; КНҐ – 30 гістологічних зразків (2 група) – по 30 препаратів, зафарбованих аналогічно до попередньої групи; КТҐ – 30 гістологічних зразків (3 група) – по 30 препаратів, зафарбованих аналогічно до попередньої групи. Для контролю були обрані препарати мозку у випадку смерті від ішемічної хвороби серця – 20 зразків (4 група) – по 20 препаратів, зафарбованих за методами Ніссля та Шпіль-Майєра. Результати. Аналіз отриманих даних гістологічного дослідження морфологічних змін тканинних елементів речовини головного мозку людини з різним генезом утворення крововиливів не виявив стабільних взаємозв’язків між змінами в структурі нервової тканини та причиною утворення крововиливу. Висновок. Враховуючи неспецифічність дегенеративних змін структурних елементів речовини головного мозку залежно від ґенезу крововиливів, можна зробити висновок, що морфологічні методи дослідження гістологічних препаратів мозку не дають точної й об’єктивної інформації щодо ґенезу крововиливів.

Direct oral anticoagulants (DOACs) are becoming increasingly prevalent in the general population for anticoagulation. However, rare adverse effects from these medications are still being discovered. Thrombocytopenia has previously been reported with these medications, but its clinical significance is still unknown. We present a patient who developed thrombocytopenia from apixaban and who subsequently developed a severe presentation of heparin-induced thrombocytopenia (HIT) from enoxaparin. This raises the possibility that thrombocytopenia from oral anticoagulants increases the likelihood of the development of heparin-induced thrombocytopenia.

Background Serum samples of patients with hemorrhagic cerebral infarction (HCI), cerebral infarction (CI), and healthy controls (HCs) were used to screen statistically different protein peaks as potential biomarkers and to establish a decision tree classification model. Methods The serum samples from clinically confirmed patients with HCI and CI from November 2018 to October 2019 were collected, along with those of HCs who visited our hospital during the same period. Surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) with CM10 ProteinChip was used to analyze the differences in serum protein expression profiles of 30 patients with HCI, 32 patients with CI, and 31 HCs in the training group, and a decision tree classification model was established. At the same time, the blind test group (18 patients with HCI, 21 patients with CI, and 17 HCs) was tested by a blind method. Results Model 1 was successfully established by software analysis with a mass-to-charge ratio of 3,495.2, 8,941.0, and 15,890.4 as a differential protein peak. The sensitivity, specificity, and accuracy of model 1 in distinguishing HCI from HCs were 86.8%, 87.1%, and 86.9%, respectively. After verification of model 1 by the blind test group, the results showed that the sensitivity, specificity, and accuracy were 88.9%, 94.1%, and 91.4%, respectively. The sensitivity, specificity, and accuracy of model 2 with a mass-to-charge ratio of 2,941.3 as a differential protein peak were 86.7%, 75.0%, and 80.6%, respectively. After verification of model 2 by the blind test group, the results showed that the sensitivity, specificity, and accuracy were 83.3%, 90.4%, and 87.2%, respectively. Conclusions Surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) and CM10 ProteinChip can be used to screen serum protein markers in patients with HCI. Mass-to-charge ratio of 3,495.2, 8,941.0, 15,890.4, and 2,941.3 may be potential protein biomarkers of HCI and used to distinguish HCI patients from HCs and CI.

The purpose of this study was to examine the frequency and characteristics of re-exacerbation of stroke symptoms within 24 hours after tissue plasminogen activator (t-PA) infusion.We studied consecutive stroke patients treated with t-PA within 3 hours of onset of symptoms admitted between October 2005 and March 2010. We divided patients into 4 groups: improvement (IM; improvement in National Institutes of Health Stroke Scale [NIHSS] ≥4 points), unchanged (UN; no change or decline in NIHSS4 points), exacerbation (EX; decline in NIHSS ≥4 points), and re-exacerbation (RE-EX; decline of NIHSS ≥4 points accompanied by re-exacerbation of neurologic symptoms in NIHSS ≥4 points). We compared clinical characteristics among the 4 groups.Two hundred twenty-two patients (135 men; median age 76 years) were enrolled. Sixteen of the 222 (7%) were in the RE-EX group. Small vessel disease (SVD), hemorrhagic cerebral infarction, and reocclusion were significantly more common among patients in the RE-EX group. SVD, hemorrhagic cerebral infarction, and reocclusion occurred in 44%, 25%, and 13% of patients in the RE-EX group, in 9%, 22%, and 0% of patients in the EX group, in 5%, 6%, and 0% of patients in the IM group, and in 17%, 14%, and 1% of patients in the UN group, respectively (P .001, P = .041, and P .001). Multivariate logistic regression analysis revealed that SVD was the only independent factor associated with re-exacerbation within 24 hours after t-PA infusion (odds ratio 3.52; 95% confidence interval [CI] 1.19-10.40; P = .023).Seven percent of patients re-exacerbated within 24 hours after intravenous infusion of t-PA. Re-exacerbation within 24 hours after t-PA infusion was strongly associated with SVD.

This study aimed to evaluate the early imaging characteristics of cerebral venous sinus thrombosis (CVST). A retrospective analysis was conducted of the clinical and imaging data of 62 patients with CVST diagnosed by magnetic resonance imaging (MRI) and/or digital subtraction angiography (DSA). In the 62 cases, MRI (1.5 T MRI) and magnetic resonance venography (MRV) examinations were conducted for 56 cases, and 54 of these were definitely diagnosed as CVST cases. Their MRI manifestations presented punctiform and sheet-like hemorrhagic cerebral infarction and extensive brain edema while partial cases presented cerebral ventricle dilation. In addition, MRI, MRV and DSA examinations were conducted synchronously for 2l cases. Among the 20 patients whose MRI and MRV examinations were positive, 19 cases were positive by DSA examination and the coincidence rate of the two was 95.00%. The clinical manifestations of CVST lack specificity. MRI combined with MRV examination is the preferred method of diagnosing CVST.

of initial NlHSSS >10 in the NINDS study (42%). PROACf II ended patient accrual August 24, 1998, and results may be available by this meeting. In the future, LIF reports must include documentation of the initial neurologic deficit, as measured by the NIHSSS, and outcomes as measured by the Barthel Index and Rankin Score, so relative comparison to NlNDS and ECASS data can be derived. Stratification for treatment based on initial NIHSSS or early imaging to document the area of infarction and potential major vessel occlu. sion is a concept that is being pursued. Documentation that LIF is superior to IV therapy in clinical benefit, with acceptable safety, awaits a comparison study of IV-tPA versus IA LIF or some other therapy that allows direct clot removal, with or without additional combination therapy.

症例は37歳の男性で1989年10月にネフローゼ症候群と診断されて治療を受けていた. その後腎機能の低下がみられ, 1992年7月から末期腎不全のために血液透析療法が開始された. 1994年10月に母親を提供者として生体腎移植を希望し当院へ転院してきた. 慢性腎不全の基礎疾患を知る目的で諸検査を施行した. その結果, 全身性エリテマトーデス (SLE) 由来の腎不全であると診断した. また同時にSLEの活動性が認められ, ステロイドパルス療法を含む副腎皮質ステロイド療法と免疫吸着療法を施行した. 血清補体価, 抗DNA抗体価はともに改善傾向がみられたが1994年12月外泊後に肺炎, 出血性脳梗塞を併発し17日後に死亡した. 剖検によって中大脳動脈のアスペルギルス塞栓による出血性脳梗塞を認めた. 一般的にSLE症例では脳血管障害の合併は少ないが, その中では閉塞性脳血管障害が約半数以上を占めている. 本症例のようにSLEに合併した中枢神経系アスペルギルス症の報告は特に少ないと思われたので, 文献的考察を加えて検討した.

We describe a 57-year-old woman, a heterozygote for Fabry disease who had multiple hemorrhagic cerebral infarctions. Her clinical course and radiological findings suggested cardiogenic cerebral embolus, but distinction from multiple cerebral infarction associated with Fabry disease seemed necessary. Our present case is reported with reference to the literature to introduce various types of stroke, which can develop in patients with Fabry disease.

Intraparenchymal hemorrhage in the full-term neonate rarely occurs more than 2 weeks after birth, and its definitive cause remains unclear. In the present report, a case of a patient with intraparenchymal hemorrhage occurring 33 days after birth is described. Histological examination of the brain tissue obtained during hematoma evacuation through craniotomy showed hemorrhagic infarction. Patent foramen ovale may have been present and this may have led to spontaneous paradoxical cerebral embolism followed by hemorrhagic infarction.

Using the thalamic infarction model in the dog, the protective effect of mannitol and/or artificial blood (perfluorochemicals) on hemorrhagic infarction was investigated. In mannitol-treated animals some protective effect was found, especially in cases in which mannitol was administered within 60 minutes following occlusion. Hemorrhagic infarction was not suppressed in any of the perfluorochemical-treated animals, but there was no hemorrhagic infarction in any of the animals treated with both mannitol and perfluorochemicals. The present results are thought to indicate that these drugs administered together are effective in the treatment of hemorrhagic cerebral infarction.

約30年の糖尿病歴がある55歳の慢性腎不全患老が急性心筋梗塞を発症し入院, 経過は良好であったが, 入院6日目左中大脳動脈領域の広範な脳梗塞, さらに消化管出血を併発し, 腎不全の急性増悪を認めた. 心機能の面から体外楯環が可能と考えられたため入院15日目血液透析を施行, 抗凝固剤はnafamostat mesilateを使用した. この初回の透析開始直後より意識が低下し, 頭部CTで上述の脳梗塞部に一致して, 広範囲の高吸収域と著明な脳浮腫を認め, 出血性梗塞が確認された. その翌日より腹膜透析に変更したが, 脳ヘルニアをきたし入院33日目死亡した.広範な脳梗塞の急性期に, 血液透析の際の抗凝固剤投与が誘因となって, 出血性梗塞を併発した可能性が推察された. また血液透析中は頭蓋内圧が亢進することから, 広範な脳梗塞を合供した腎不全患考の血液浄化法の選択として, 脳出血同様腹膜透析が適当であると考えられた.

Two patients with ischemic strokes, presumably due to embolism, developed spontaneous hemorrhagic cerebral infarctions which were detected by follow-up cranial computed tomography. Clinical deterioration was associated with hemorrhagic transformation in one patient. In each case, immediate anticoagulant therapy was considered but was deferred. Implications of the use of anticoagulant therapy in pediatric patients with acute embolic stroke are discussed.

A combined histological and radioautographical study was made to determine the mechanism for the selective localization of Hg-203-labelled Chlormerodrin in the brain of 13 cats with experimentally induced cerebral infarction. The presence of the radioactive tracer in the infarcted areas was noted within a few days after the onset of the lesions and was increased by hemorrhage into the tissues. The radioautograms revealed the radioactive material to be localized mostly within macrophages and in areas surrounding capillary proliferation. These two pathoanatomic processes associated with necrosis of the cerebral tissues most likely account for the abnormal accumulation of radionuclide tracer in brain scans of patients with cerebral infarction.

A polymorphonuclear pleocytosis of the cerebrospinal fluid is an occasional occurrence following hemorrhagic cerebral infarction. Because the peak of this neutrophilic reaction occurs 3 to 4 days after the event it is usually missed and not widely appreciated. We have described an example of this response in an attempt to alert physicians to an important differential diagnostic consideration when faced with a neutrophilic CSF pleocytosis.

A case of surgically proven left atrial myxoma presented with multiple episodes of cerebral infarctions, both ischemic and hemorrhagic, documented on serial CT and magnetic resonance (MR). Magnetic resonance studies showed, as well, dilated blood vessels in the hemorrhagic areas, proven by angiography to represent mycotic aneurysms. One of these lesions was surgically removed and confirmed to represent a combination of hematoma, infarction, myxomatous nodules, and underlying mycotic aneurysms, as shown on MR scans. This case demonstrates a known delayed neurologic complication of cardiac myxoma that can occur long after resection of the tumor.

Retinal arteriolar recanalization was studied by fluorescein angiographic and pathological studies in SHRSP. In SHRSP, severe hypertension seemed to aggravate hemorrhagic cerebral infarction. Pathologically retinal arteriolar recanalization of the obstructed vessels caused more severe damage to the peripheral vessels than obstruction of the retinal arterioles only.

Successful employment of anticoagulants in the treatment of thromboembolic disease outside the central nervous system is well documented and widely accepted. However, only in recent years has clinical support been given to utilization of these drugs when similar vascular lesions occur intracranially, and then only in selected cases in which damage is limited. Recently Siekert, Millikan, and Shick1listed only five currently accepted indications for use of anticoagulants in cerebrovascular disease. Encouraging results from the use of anticoagulants in the treatment of the syndromes of intermittent insufficiency of the basilar and carotid arterial systems have been reported in detail by Millikan and Siekert.2,3These authors subsequently described4the administration of anticoagulants to patients who had received clinical diagnoses of thrombosis in the vertebral-basilar system. In their series, there was a mortality of 10%, as compared with a mortality of 43% in a similar group of patients not

Introduction Almost every known central neurological syndrome has been reported as a complication of carbon monoxide poisoning. Hemorrhagic infarct has rarely been considered as an early manifestation of carbon monoxide poisoning. A case of cerebral hemorrhagic infarction is presented. Typical findings, neuropathology and the role of vascular injury are described. Case presentation The symptoms and clinical course of acute poisoning with carbon monoxide in a 7-year-old boy are described. To evaluate the possible causes, a brain computed tomography (CT) was performed that showed thick clot in the left medial temporal and parasellar area, left sylvian fissure(acute intravascular thrombus) accompanied by left diffuse frontotemporal hypodensity and midline shift. Four-vessel digital subtraction angiography two weeks after intoxication was not indicative of any vascular lesion. Conclusion Hemorrhagic infarction is a rare presentation of carbon monoxide poisoning. When found in a child, in addition to conservative treatment to reduce the neurocognitive squeal, other probable causes should be ruled out.