Background: Various CLASSIFICATION criteria of brain INFARCT are used in clinical trials and STROKE registries. The practical Iranian criteria (PIC) is designed for clinical practice. Methods: From March 2001 through March 2003, all consecutive STROKE patients admitted to Vali-e- Asr Hospital, Birjand, Khorasan, Iran were included in this prospective observational study. Patients underwent a standard battery of diagnostic investigations by a STROKE neurologist. Data on patients, demographics, clinical presentations, and diagnostic work-up were kept in a database. Two STROKE neurologists and a general practitioner independently reviewed the data of 20 randomly selected patients and classified patients according to the PIC CLASSIFICATION of STROKE topography and etiology. The PIC is designed by STROKE neurologists and approved in the University of Alberta, Canada. The degrees of interrater agreement were measured with unweighted k-statistics. Results: Among 302 STROKE patients, 20 patients (11 females, 9 males) were randomly selected. The three interrater agreement for topographic subtyping of the patients was 0.95%, k = 0.915 (0.662 – 1), P < 0.0001 and for etiologic diagnosis was 0.90 %; k = 0.9022 (0.753 – 1), P < 0.0001. STROKE neurologists agreed in topographic diagnosis for 20 out of the 20 cases (100%; k= 1; 95% CI, 1.0 to 1.0; P < 0.0001). The general practitioner arrived at the same topographic diagnosis for 19 out of the 20 cases (0.95%; k = 0.875; 95% CI, 0.638 to 1.0; P < 0.0001). STROKE neurologists agreed in etiologic diagnosis for 18 out of the 20 cases (0.90%; k = 0.855; 95% CI, 0.66 to 1.0; P < 0.0001). The general practitioner arrived at the same etiologic diagnosis for 18 out of the 18 cases that the two STROKE neurologists agreed (100%; k = 0.875; 95% CI, 1.0 to 1.0; P < 0.0001). Conclusion: The interrater agreement of PIC for topographic and etiologic CLASSIFICATION of brain INFARCT is much higher than the other CLASSIFICATION systems. The PIC could be useful in STROKE practice.

Background: STROKE vastly contributes to death and disability worldwide. Acute ischemic STROKE (AIS) is caused by a reduction in supply of blood to the brain. Accumulation of unnecessary intracellular serum calcium in AIS induces the cytotoxic actions that activates enzymes involved in cell death. The present investigation assessed the relationship of total serum calcium level (at admission) and initial diffusion weighted imaging (DWI) INFARCT volume and correlated with National Institute of Health STROKE Scale (NIHSS) scores. Methods: A hospital-based observational study was conducted on 74 consecutive patients identified with AIS fulfilling the inclusion criteria. NIHSS scores and serum ionized calcium were calculated in every patient and compared with DWI INFARCT volume for assessing correlation between these three. Statistical software R Version 4. 0. 2 and Microsoft Excel were used for statistical analysis. Results: Out of the 74 patients, most of them were in age group of 50-69 years, with a male preponderance (68. 9%). A significant association was noticed between diabetes and dyslipidemia with age (P=0. 01499). A strong negative correlation was observed between NIHSS scores (at admission & discharge) with ionized calcium, while a strong positive correlation was noticed between STROKE scores with INFARCT volume. A statistically significant negative correlation was recorded between serum calcium (on admission) and INFARCT size (r=-0. 851755, P=0. 0001). The mean of NIHSS scores on admission (8. 24±, 5. 19) has been remarkably higher when compared with NIHSS scores at discharge (5. 25±, 3. 89). Conclusion: In patients with AIS examined within 6-24 hours of symptoms onset, serum ionized calcium and volume of INFARCT on DWI showed inverse association. Serum calcium serves as a marker of severity and acts as prognostic factor in AIS.

Introduction: Nephrotic syndrome (NS) is characterized by swelling, proteinuria, hypoalbuminemia, or hyperlipidemia. The incidence of NS depends on the country and ethnicity and is highest in Asia than in Europe. Nephrotic syndrome can cause complications such as arterial thromboembolism (ATE) due to a hypercoagulable state. Case Presentation: We encountered a 9-year-old boy with NS and INFARCT STROKE, which was treated with corticosteroid and low molecular weight of heparin with clinical improvement. Conclusions: We recommend that all NS children with high platelet levels perform thromboelastography (TEG) examination and use prophylactic anticoagulation with monitoring of bleeding risk during therapy.

Background: The presence of C-reactive protein (CRP) during different stages of STROKE had been shown in several studies. There is still no definite document about the correlation of CRP level and size of INFARCT in STROKE. We studied the correlation of the acute level of CRP with size of INFARCT in STROKE.Methods: A total of 90 consecutive patients with acute STROKE admitted in Fatemeh Zahra University Hospital in Bushehr city were studied. Levels of CRP were measured at admission time and 48 hours later. Sizes of INFARCT and types of STROKE were determined with Computerized Tomography scanning. The excluded patients were those with infection, STROKE in brain stem, a delay more than 24 hours after attack of STROKE and Transient Ischemic Attacks. CRP level was measured quantitatively using ELISA method.Results: No correlation between the first CRP levels and variables of age, size of INFARCT and type of STROKE was detected. Size of INFARCT was correlated with the second CRP (r=0.41, P<0.001) and the difference in CRP levels (r=0.45, P<0.001). The CRP difference was significant in ischemic, hemorrhagic and territory INFARCTs (P<0.01). But there was no difference between the first and the second CRP in lacunar INFARCTs.Conclusion: We found no correlation between the CRP levels of the 24 first hours after acute STROKE with size of INFARCT in STROKE. But the increase of CRP levels which were measured in 48 hours after the STROKE had correlation with size of INFARCT irrespective of types of STROKE. More studies could reveal the cause and effect of CRP in size of INFARCT in STROKE.

Introduction: Recent studies demonstrated that cannabidiol had neuroprotective property.There is some evidence about effective role of cannabidiol in reduction of ischemic damages.It has been reported that INFARCT size is influenced by various factors after MCAO, including inflammatory factors. The aim of the present study was to evaluate the effect of cannabidiol on INFARCTion volume and correlation of INFARCT size with tumor necrosis factor receptor 1 (TNFR1), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-кB) expression.Methods: Using stereotaxic surgery, guide cannula was implanted in the right lateral ventricle.Cannabidiol (50, 100, and 200 ng/rat) was injected through ntracerebroventricular (i.c.v.) route for 5 consecutive days. Then, the rats underwent 60 minutes of right middle cerebral artery occlusion (MCAO). After 24 h reperfusion, the INFARCT volume in total, cortex, piriform cortex-amygdala (Pir-Amy), and striatum areas of hemisphere were assessed. The expression of inflammatory factors such as TNFR1 and NF-кB in these regions were also studied.Results: The present results indicate that in the MCAO-induced cerebral ischemia, administration of cannabidiol (100 and 200 ng/rat) causes a significant reduction in INFARCTion volume in comparison with the vehicle group. Also, there were significant correlations between decrease of regional INFARCT volume and TNFR1/NF-кB expression.Conclusion: The results of this study indicate that cannabidiol reduced cerebral INFARCTion possibly through diminishing TNFR1/NF-  ĸB-induced neurotoxicity in transient focal cerebral ischemia.

Silent Brain INFARCTs (SBI) are associated with an increased risk of subsequent STROKE. SBI are incidentally revealed by CT or MRI executed in STROKE patients. A prospective study was undertaken involving 200 consecutive patients aged >45 years with brain INFARCT admitted in University of Alberta Hospital, Canada (100 patients) and Valie-Asr Hospital, Iran (100 patients) in 2003. Patients were divided in age groups aged <65 and >65. All of the patients underwent brain CT.A STROKE neurologist with knowledge of STROKE history subsequently reviewed the scans and diagnosed SBI. The relations of race, gender and age groups with SBI were analyzed with chi-square and Fisher exact tests.SBI were present in 26.9% of patients aged <65 and 48.6% of patients aged >65. Canadian patients were significantly more preponderant to SBI in age group> 65 (p=0.013). The mean age of Canadian patients was significantly higher than Persians (p<0.001). Within a total of 200 patients the female gender was significantly more preponderant to SBI (p= 0.02) which was not related to age and race groups. Small vessel territory INFARCT was present in 87% of our patients with SBI. SBI are common in STROKE patients. The frequency of SBI is higher in female gender and the elderly.

Background and Objectives: Evidences suggest that acid ascorbic (AA) has antioxidative effects and STROKE patients with high levels of acide ascorbic (AA), show better behavioral outcomes. In this study, the neuroprotective effect of AA, was investigated 3 hours after embolic model of cerebral ischemia.Materials and Methods: In this experimental study, rats were assigned to vehicle, AA and sham-operation. STROKE was induced by embolizing a preformed clot into the right MCA. For measuring INFARCT volume, 48 h later, the brain was removed, sectioned and stained with triphenyltetrazolum chloride and analyzed by a commercial image processing software program. Behavioral tests including neurological deficits and sensory impairment were also applied at 24 and 48 hours after the embolization.Results: The INFARCT volume in control and AA groups was 29.41±2.6% and 9.52±1.57%, respectively. Compared to the control group, AA significantly decreased INFARCT volume (p<0.001). AA late therapy also improved neurological deficits (p<0.05) and sensory impairments (p<0.001) at 48 h after the STROKE.Conclusion: Our data showed that AA may have beneficial effects on treatment and management of STROKE. Further studies should be undertaken to clarify the neuroprotective effects of AA after STROKE.