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Introduction: The World Health Organization (WHO) definition of stroke is: “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular origin”. The pathological background for stroke may either be Thrombotic or hemorrhagic disturbances of the cerebral blood circulation. Thrombotic cerebral infarction results from the atherosclerotic obstruction of large cervical and cerebral arteries, with ischemia in all or part of the territory of the occluded artery. Hyperhomocysteinemia has been emerging as an independent risk factor for atherosclerosis. Several workers opined that moderately elevated plasma Homocysteine (Hcy) concentration might be an independent risk factor for cerebrovascular disease including stroke and transient ischaemic attack. Material and Methods: The study is a hospital based observational study was conducted in the Department of General Medicine at ACSR Government Medical College, Nellore from Dec 2022 to October 2023. 31 patients with thrombotic stroke(cases) and 31 subjects without thrombotic stroke (controls) and other comorbid conditions that affect serum homocysteine were included in the study. Venous blood samples were collected in tubes containing disodium EDTA. Homocysteine assay is based on the measurement of co-substrate conversion product. Results: In the present study, the mean age ± SD of cases was 55.03±14.51. The mean age of males was 51.68±13.45 and the mean age of females was 60.33±15.11. The mean age in control group was 51.22±13.77. The mean serum homocysteine level in the present study, in cases was 25.98±11.95. The mean homocysteine level in males was 7.83±14.29. The mean in females was 23.05±5.67. The mean homocysteine level in control group was 7.19±3.51. Mean homocysteine level of cerebral ischemic stroke females was 14.86 ± 5.34. The mean homocysteine level in controls was 7.428 ± 4.091. The mean homocysteine level in controls was 12.30± 4.68. The mean cholesterol of the cases was167.67±40.68. The mean LDL in the study was 89.74±27.38. The mean HDL was 38.48±10.92. Conclusions: Serum homocysteine levels were significantly higher in those patients with stroke when compared to those without stroke. Apparently, Serum homocysteine level is an independent risk factor for thrombotic stroke. [ABSTRACT FROM AUTHOR]

Background: sodium disorders are the most common and least understood in patients with acute brain injury due to the major role played by the central nervous system in regulating sodium and water homeostasis, which can lead to serious complications and adverse outcomes, including death. Objective: to determine the hypernatremia contribution to mortality in patients with neurological conditions in critical state. Methods: longitudinal analytical observational study on 55 patients who were admitted to the acute care units at the Arnaldo Milián Castro University Hospital, between October 2020 and May 2022, regardless of the plasma sodium value upon admission to the service, as well as during their stay in the critical care units. Univariate and bivariate statistical methods were used in data analysis. Results: the average age was 60 ± 16 years. The most relevant diagnoses were intraparenchymal hemorrhage (56.37%), head trauma, and ischemic stroke (both 30%). Plasma sodium concentrations showed significant differences (pX2= 0.000), with the highest average at 24 hours of admission (174.2 ± 133.6) and the lowest at the 5th day (102.9 ± 72.9). There was a significant correlation between plasma sodium concentrations at admission, 24h and 72h with the state at discharge. In the individual bivariate analysis by period, there was only a significant relationship after 24 hours. In this period, hypernatremia contributed 1.78 times more to mortality than in those who did not have elevated sodium (OR=1.78 with CI: 1,39-3,4). Conclusions: hypernatremia in critically ill patients with neurological conditions is associated with increased mortality. [ABSTRACT FROM AUTHOR]

Background: There is no consensus on the effect of opium on stroke yet. Some studies show the negative effects of opium on ischemic strokes. Here, we attempt to compare the volume of lesions in opium addict and non-addict patients with thrombotic stroke. Methods: This case-control study was conducted on patients with thrombotic stroke at Shafa Hospital in Kerman, Iran. The diagnosis was confirmed by clinical examinations, imaging, and laboratory tests. The volume of lesions was calculated by magnetic resonance imaging (MRI), and the data were analyzed by descriptive statistics, Mann-Whitney U test, Chi-square test, and linear regression analysis. Findings: A total of 60 patients were studied, 30 of whom were opium addicts and the rest were non-addicts. The mean volume of the lesion was 46.008350 ± 7.488990 (in the addict group) and 31.023335 ± 1.441570 (in the non-addict group), indicating a significant difference between the two groups (P = 0.005). Regression analysis results showed a significant relationship between the volume of stroke with opium addiction (P = 0.017), ischemic heart diseases (IHDs) (P = 0.006), hyperlipidemia (HLP) (P = 0.016), age (P = 0.035), and smoking (P = 0.044). Conclusion: The results of this study showed a higher volume of lesion in opium-addict patients compared to that in non-addicts as an indicator of stroke severity. [ABSTRACT FROM AUTHOR]

COVID-19 disease caused by the SARS coronavirus has caused significant morbidity and mortality around the world ever since it was first declared as a pandemic by the World Health Organization (WHO) in March 2020. Acute neurological manifestations of this disease have also started emerging and being recognized around the world and acute ischemic stroke (AIS) or thrombotic stroke is becoming one of the major neurological illnesses related to COVID-19. The management of AIS is time-critical and major advances in its management over the recent years, such as bridging thrombolysis and mechanical thrombectomy (MT), are multidisciplinary activities requiring robust coordination and management in the acute setting. All these advances are severely challenged in the COVID-19 pandemic where severe pressures exist on the clinical resources and logistics required to deliver an effective stroke service. This is further compromised by legal and preventive measures during this pandemic like local lockdowns. Reporting of minor or initial symptoms has also been compromised due to the fear of approaching healthcare settings which are perceived as high-risk zones to catch the infection. The purpose of this document is to highlight these challenges and provide a guiding framework for the management of AIS under three principles: (a) Delivering an effective service, (b) Preventing infections within the healthcare setting, and (c) Optimizing resource utilization. [ABSTRACT FROM AUTHOR]

Antiplatelet agents are effective for secondary prevention of ischemic stroke and can reduce the severity of first-ever ischemic stroke. However, it is uncertain if prophylactic antiplatelet therapy reduces the severity of recurrent ischemic stroke. The aim of this study was to determine the effect of preceding antiplatelet treatment on the severity of thrombotic stroke (TS) in patients with a prior history of stroke. From a prospective hospital registry of 1338 consecutive patients with acute ischemic stroke, we identified patients with a prior history of stroke who were admitted for cardioembolic stroke (CE); TS including large-artery atherosclerosis, small vessel occlusion, and branch atheromatous disease; or other cause or cryptogenic stroke (OCS). Cases in each subtype were categorized based on preceding medication: antiplatelet agents (AP) and none (N). Severity of stroke (National Institutes of Health Stroke Scale: NIHSS) on admission was compared between AP and N cases. The total cohort of 252 patients included 83 with CE, 102 with TS, and 67 with OCS. After excluding those with prior anticoagulants, the median NIHSS on admission was lower in AP cases than in N cases (3 vs. 5, p = 0.002). In multivariate analysis, preceding AP treatment was independently associated with minor stroke (NIHSS ≤4) on admission in CE group (OR 8.48, 95% CI 1.71–62.9, p = 0.008) and TS group (OR 4.24, 95% CI 1.44–13.4, p = 0.009). Preceding antiplatelet treatment in patients with a prior history of stroke may reduce the severity of subsequent thrombotic and cardiogenic stroke. • Effects of prior antiplatelet agents on thrombotic stroke severity were examined. • The subjects were patients with ischemic stroke and a prior history of stroke. • Prior antiplatelet use was independently associated with minor stroke on admission. • Prior antiplatelet agents may reduce the severity of subsequent ischemic stroke. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction and vascular injuries are the early processes in thrombogenesis leading to thrombotic stroke. These processes trigger platelet activation characterized by synthesis of Thromboxane A2, potent agonist in platelet aggregation. Acetosal (ASA) 100 mg usually given to thrombotic stroke patients exerts its pharmacological effect by inhibition of TxA2 synthesis, thus could prevent thrombus formation. Diabetes mellitus (DM) as risk factor of thrombotic stroke exhibits an increase in TxA2 synthesis. It is not known whether ASA 100 mg could inhibit TxA2 adequately in diabetic patients. This study aimed to analyze the differences of serum TxA2 level, which was measured by serum TxB2 level as stabile metabolite of TxA2, after taking ASA 100 mg in diabetic and non-diabetic thrombotic stroke patients. This prospective observational study was held in Neurology Department of Dr. Soetomo Hospital, Surabaya. Total 27 patients, consisted of 15 patients with DM and 12 patients with non-DM were enrolled. Serum TxB2 was measured before and after 5-7 days 100 mg ASA 100 administration. Mean value of serum TxB2 level before and after taking ASA was 16.43 ± 16.08 ng/mL and 2.93 ± 1.83 ng/mL in diabetic and 27.36 ± 21.04 ng/mL and 5.36 ± 4.06 ng/mL in non-diabetic group. Mean reduction of serum TxB2 level in diabetic and non-diabetic group was 13.49 ± 15.9 ng/mL and 22.00 ± 21.65 ng/mL. There were significant differences in serum TxB2 level after taking ASA 100 mg in diabetic and non-diabetic group but the mean reduction of serum TxB2 level were not significantly different. [ABSTRACT FROM AUTHOR]

Large cerebral infarctions have high morbidity and mortality. Patients with large cerebral infarctions may have recurrent ischemia as high as 8.1% within 7 days; highest among other types of strokes. Data regarding risk factors for large cerebral infarction in Asian populations are still scant. All adult (age ≥15 years old) patients with the diagnosis of thrombotic ischemic stroke who were treated at Srinagarind Hospital, Khon Kaen University, Thailand from January 2012 to December 2013 were studied. Large cerebral infarctions are defined by clinical criteria of having cerebral cortical impairment, brain stem or cerebellar dysfunction with infarction sizes of more than 1.5 cm. The association of various stroke risk factors and large infarction strokes were calculated using multiple logistic regression analysis. There were 276 thrombotic stroke patients who met the study criteria; classified as large cerebral infarctions in 59 patients (21.38%) and small cerebral infarctions in 217 patients (78.62%). Baseline characteristics and risk factors for stroke were comparable between both groups. The large cerebral infarction group had a significantly larger proportions of right internal carotid artery stenosis, plaques on the left side, left internal carotid artery stenosis, and internal carotid artery stenosis at any side than the small cerebral infarction group. Among various stroke risk factors, only internal carotid artery stenosis at any side was the only significant factor associated with large cerebral infarction with an adjusted odds ratio of 11.14 (95% CI: 3.46, 35.82). In conclusion, significant internal carotid artery stenosis is associated with large cerebral infarction. [ABSTRACT FROM AUTHOR]

Background: Cerebrovascular disease (CVD) and coronary heart disease (CHD) cause 40%-50% of deaths in developed countries with CVD causing 10%-1 2% of deaths. Though increased Lipoprotein (a) is a risk factor in developing CHD, its role is poorly defined in etiopathogenesis of CVD. Aims: To find the association of lipoprotein (a) and lipid profile in thrombotic stroke patients after acute phase. Settings and Design: The study was conducted at Kasturba Medical College, Manipal. Twenty one cases of thrombotic stroke and 18 cases of age and sex matched controls were taken for the study. Informed consent was taken from both case and control. Materials and Methods: Overnight fasting sample was collected from both case and control. Serum was separated and parameters such as total cholesterol, triglycerides, high density lipoproteins-C, low density lipoprotein-C, lipoprotein (a), fasting blood sugars were estimated. Statistical analysis: Data were analyzed by SPSS software, Students t-test, standard deviation (SD), and standard error of mean (SEM), P-value <0.05 is considered to be significant. Results: In this study, we found no statistical significant differences in serum lipid and lipoprotein (a) profile between controls and thrombotic stroke patients. Conclusions: Highest frequency (38%) of stroke was found in the age group of 7080 years. There were other associated risk factors such as diabetes in five cases (24%), hypertension in nine cases (43%), and family history of stroke in four cases. However, further studies are required to evaluate the importance of serum Lp(a) estimation in the assessment as a risk factor for thrombotic stroke. [ABSTRACT FROM AUTHOR]

The object of this study was to assess the influence of oral contraceptives (OCs) on the risk of cerebral thromboembolic attacks (CTA) including thrombotic stroke and transitory cerebral ischemic attacks. A 5-year case-control study including all Danish hospitals was conducted. All women 15–44 years old suffering a first ever CTA during the period January 1, 1994 to December 31, 1998, were included. Controls were selected annually, 600 per year in 1994–1995, 1200 per year 1996–1998. Response rates for cases and controls were 88% and 90%, respectively. After exclusion of nonvalid diagnoses, pregnant women, and women with previous thrombotic diseases, 626 cases and 4054 controls were available for analysis.A multivariate matched analysis was performed. Controls were matched to cases within 1-year age bands. Adjustments were made for the following potential confounders: year, length of OC use, smoking, hypertension, migraine, family CTA, and years of schooling. There were 212 and 1208 current users of OCs among cases and controls, respectively.The risk of CTA among current users of OCs decreased significantly with decreasing estrogen dose (nonusers reference): OCs with 50 μg, 30–40 μg, 20 μg ethinyl estradiol (EE) and progestin-only pills implied adjusted odds ratios (ORs) (95% CI) of 4.5 (2.6–7.7), 1.6 (1.3–2.0), 1.7 (1.0–3.1), and 1.0 (0.3–3.0), respectively. Current users of OCs with second- (levonorgestrel or norgestimate) and third- (desogestrel or gestodene) generation progestins combined with 20–30 μg EE had ORs of CTA of 2.2 (1.6–3.0) and 1.4 (1.0–1.9), respectively. After correction for differences in estrogen dose, the third- to second-generation risk ratio was 0.6 (0.4–0.9; p = 0.01).In conclusion, high dose OCs and OCs with second-generation progestins were associated with the risk of CTA. The risk increased 2.5 times with estrogen dose increasing from 20 to 50 μg EE, and users of low-dose OCs with second-generation progestins had a 61% higher risk-association of CTA than users of OCs with third-generation progestins. [Copyright &y& Elsevier]

Platelet membrane glycoprotein polymorphisms are candidate risk factors for thrombosis, but epidemiological data are conflicting. Thus, demonstration of a genotype-dependent alteration in function is desirable to resolve these inconsistencies. We investigated in vivo platelet activation in acute thrombosis and related this to platelet genotype. Frequencies of the 1b and 2b alleles of the HPA 1a/1b and HPA 2a/2b platelet glycoprotein polymorphisms were determined in 150 (52 men/98 women, mean age 58·3 years) patients with atherothrombotic stroke, and the influence of genotype on markers of platelet activation was assessed. Platelet P-selectin (CD62P) expression and fibrinogen binding was measured using whole blood flow cytometry within 24 h of stroke and 3 months later in 77 patients who provided a repeat blood sample. Results were compared with matched controls. Neither the 1b allele [allele frequency 0·11 vs. 0·13, odds ratio (OR) confidence interval (CI) 0·8 (0·5–1·3)] nor the 2b allele [0·09 vs. 0·07, OR (CI) 1·4 (0·8–2·4)] was significantly over-represented in patients. Increased numbers of activated platelets were found following stroke (acute mean P-selectin expression 0·64% vs. control 0·35%, P < 0·001; acute mean fibrinogen binding 1·6% vs. control 0·9%, P < 0·001). Activation persisted in the convalescent phase (P < 0·001 and P = 0·005 vs. controls for P-selectin and fibrinogen respectively). Expression of P-selectin and fibrinogen was not influenced by either the HPA 1a/1b genotype (P > 0·95 for each marker, Scheffe's test) or the 2a/2b genotype (P > 0·95 for each). Although persisting platelet activation is seen in atherothrombotic stroke, it is independent of HPA 1a/1b and 2a/2b genotypes. These data suggest an underlying prothrombotic state, but do not support the polymorphisms studied as risk factors for thrombotic stroke in this... [ABSTRACT FROM AUTHOR]