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Introduction: Neurological stroke is the most common cause of disability and leaves nearly 65% of survivors with sensory, motor and coordinative disabilities. At present, there are no therapies to prevent long-term neurological deficits after stroke. Many neuroprotective drugs are being tested with the aim to ensure these effects. Preclinical studies have shown a modulatory effect of cerebroprotein hydrolysate on synaptic remodeling and facilitated synaptic transmission. Material and methods: This was a hospital-based, open-label pilot study conducted in a tertiary care hospital of North India. All patients admitted with a diagnosis of stroke both ischemic and hemorrhagic, were included in the study. Patients were randomized into two groups. The test group was given cerebroprotein hydrolysate, along with standard treatment for stroke, whereas the other group was kept on standard treatment for stroke as per the latest guidelines, without cerebroprotein. Results: A total of 50 patients of stroke, admitted in a tertiary care center were included in the study. The mean age of the patients was 65.7 ± 11.86 years. Twenty-six (52%) were males and 24 (48%) were females. Out of the total 50 patients, 23 (46%) had ischemic stroke and 27 (54%) had hemorrhagic stroke. Twenty (40%) had diabetes, 37 (74%) had hypertension, 8 (16%) were known cases of coronary artery disease, 28 (56%) had dyslipidemia, 22 (44%) were smokers, 7 (14%) had a history of ethanol consumption and 13 (26%) were obese. Mean Barthel score at admission was 21.2 ± 11.3 and mean Rankin score at admission was 3.6 ± 1.37. Mean Barthel score at end of treatment was 53.9 ± 28.72 and mean Rankin score at end of treatment was 2.6 ± 1.65. The mean duration of admission was 6.8 ± 3.57 days. Conclusion: The current study highlights the role of cerebroprotein hydrolysate in improving the neurological scores and reducing hospital stay among patients hospitalized with stroke.
RESUMEN
Introduction: Neurological stroke is the most common cause of disability and leaves nearly 65% of survivors with sensory, motor and coordinative disabilities. At present, there are no therapies to prevent long-term neurological deficits after stroke. Many neuroprotective drugs are being tested with the aim to ensure these effects. Preclinical studies have shown a modulatory effect of cerebroprotein hydrolysate on synaptic remodeling and facilitated synaptic transmission. Material and methods: This was a hospital-based, open-label pilot study conducted in a tertiary care hospital of North India. All patients admitted with a diagnosis of stroke both ischemic and hemorrhagic, were included in the study. Patients were randomized into two groups. The test group was given cerebroprotein hydrolysate, along with standard treatment for stroke, whereas the other group was kept on standard treatment for stroke as per the latest guidelines, without cerebroprotein. Results: A total of 50 patients of stroke, admitted in a tertiary care center were included in the study. The mean age of the patients was 65.7 ± 11.86 years. Twenty-six (52%) were males and 24 (48%) were females. Out of the total 50 patients, 23 (46%) had ischemic stroke and 27 (54%) had hemorrhagic stroke. Twenty (40%) had diabetes, 37 (74%) had hypertension, 8 (16%) were known cases of coronary artery disease, 28 (56%) had dyslipidemia, 22 (44%) were smokers, 7 (14%) had a history of ethanol consumption and 13 (26%) were obese. Mean Barthel score at admission was 21.2 ± 11.3 and mean Rankin score at admission was 3.6 ± 1.37. Mean Barthel score at end of treatment was 53.9 ± 28.72 and mean Rankin score at end of treatment was 2.6 ± 1.65. The mean duration of admission was 6.8 ± 3.57 days. Conclusion: The current study highlights the role of cerebroprotein hydrolysate in improving the neurological scores and reducing hospital stay among patients hospitalized with stroke.
RESUMEN
Background: Stroke is a leading cause of death and disability worldwide acute ischaemic stroke accounts for 87% of strokes and mostly affects persons at the peak of their lives. Magnesium is known to have neuroprotective effects in ischemic stroke through a variety of mechanisms including decrease in glutamate release and inhibition of NMDA receptors and vasodilation. Previous studies on serum magnesium levels in stroke patients have shown variable results with many of them finding lower levels than in normal subjects. This study was undertaken to compare serum magnesium levels in patients of acute ischemic stroke with those of controls and also find a correlation if any between serum magnesium levels and neurological disability.Methods: This was a prospective non-interventional case-control study in which 50 patients of acute ischemic stroke in the age group of 20 to 80 years admitted in the department of Medicine Government Medical College Jammu from October 2019 to January 2020 were taken. Their serum magnesium levels were analysed within first 24 hours of admission and neurological disability was measured using modified Rankin Score. Serum magnesium levels were also estimated in 35 healthy controls for comparison.Results: Serum magnesium was lower in the study group (mean of 1.85±0.36) as compared to the control group (mean of 2.4±0.21) which was statistically significant (p value =0.001). Modified Rankin Score was 4 to 5 in 27 patients and 2 to 3 in 23 patients and it was negatively correlated with serum magnesium levels (r =-0.67).Conclusions: Ischemic stroke patients had lower serum magnesium levels as compared to healthy subjects in our study and also lower levels were seen in those with higher neurological disability.
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Objective To investigate the disease assessment and prognosis value of serum copeptin level in patients with acute cerebral infarction (ACI). Methods One hundred first diagnosed ACI patients were selected as ACI group. According to the National Institutes of Health stroke score (NIHSS), the ACI patients were divided into mild (NIHSS15 scores). Sixty cases of healthy subjects were selected as control group. The serum copeptin level was measured by double antibody sandwich enzyme linked immunosorbent assay method in control group and ACI group (onset within 24 h). The NIHSS, Alberta stroke program early CT score (ASPECTS) and modified Rankin score (mRS) onset within 24 h and 14 d were evaluated in patients with ACI, and the mRS 90 d and 180 d after ACI were evaluated. The neurological impairment was assessed by mRS 180 d after ACI, mRS ≤ 2 scores was good prognosis, ≥ 3 scores was poor prognosis. The correlation was analyzed. Results Among the 100 patients with ACI, mild was in 52 cases, moderate in 34 cases, and severe in 14 cases; good prognosis was in 79 cases and poor prognosis in 21 cases. The serum copeptin levels within 24 h of ACI in mild, moderate and severe patients of ACI group were significantly higher than that in control group:(4.82 ± 1.25), (6.39 ± 2.21) and (9.28 ± 3.82) pmol/L vs. (1.95 ± 0.28) pmol/L. The serum copeptin level within 24 h of ACI in moderate patients was significantly higher than that in mild patients, in severe patients was significantly higher than that in moderate patients, and there were statistical differences (P<0.05). Within 24 h of ACI , the ASPECTS in moderate and severe patients were significantly lower than that in mild patients:(10.02 ± 2.10) and (6.24 ± 3.05) scores vs. (12.16 ± 0.84) scores, in severe patients was significantly lower than that in moderate patients, and there were statistical differences (P<0.05). The NIHSS in moderate and severe patients were significantly higher than that in mild patients:(10.68 ± 3.14) and (16.20 ± 4.26) scores vs. (4.35 ± 1.52) scores, in severe patients was significantly higher than that in moderate patients, and there were statistical differences (P<0.05). The serum copeptin levels within 24 h of ACI and NIHSS in each time point in good prognosis patients were significantly lower than those in poor prognosis patients:(3.52 ± 1.26) pmol/L vs. (8.68 ± 3.06) pmol/L and (5.68 ± 2.11) scores vs. (15.36 ± 3.25) scores, (4.85 ± 1.86) scores vs. (12.60 ± 3.89) scores, (3.68 ± 1.21) scores vs. (6.35 ± 2.96) scores, (2.16 ± 0.75) scores vs. (5.21 ±1.96) scores, and the ASPECTS within 24 h of ACI was significantly higher than that in poor prognosis patients:(11.38 ± 2.21) scores vs. (7.86 ± 2.49) scores, and there were statistical differences (P<0.05). The single factor Logistic regression analysis results showed that the age, ASPECTS, NIHSS and serum copeptin level were the influencing factors of severity of illness in patients with ACI (OR = 1.21, 5.36, 5.61 and 6.62;95%CI 0.99-1.39, 3.34-9.21, 2.86-7.52 and 1.38-12.64;P=0.04, 0.01, 0.01 and 0.00), and the influencing factors of poor prognosis (OR=1.32, 5.21, 4.86 and 6.82;95%CI 0.84-1.43, 3.52-8.39, 2.62-5.35 and 2.67-11.85;P=0.04, 0.01, 0.01 and 0.00). ROC analysis results showed that the area under curve of NIHSS, serum copeptin level and ASPECTS in predicting poor prognosis in patients with ACI were 0.926, 0.863 and 0.624. In the mild, moderate and severe patients, the serum copeptin level was negative correlated with ASPECTS ( r=-0.682,-0.594 and-0.572;P<0.01), and the serum copeptin level was positively correlated with NIHSS ( r = 0.652, 0.614 and 0.586; P<0.01). Conclusions The serum copeptin level in patients with ACI is significantly elevated. The serum copeptin level is positively correlated with neurologic impairment severity and prognosis in patients with ACI, and it has important significance in evaluating pathogenetic condition and prognosis.