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Yu.i. Holovchenko - One of the best experts on this subject based on the ideXlab platform.
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Pathogenetic Aspects of Prevention of Fatigue in the Early Recovery Period after Ischemic Stroke in Patients with Metabolic Syndrome
INTERNATIONAL NEUROLOGICAL JOURNAL, 2016Co-Authors: T.i. Nasonova, O.i. Asaulenko, T.v. Kolosova, O.v. Klimenko, T.m. Slobodin, O.yu. Honchar, Yu.a. Buhaiov, O.v. Tyshkevych, I.v. Kurochkin, Yu.i. HolovchenkoAbstract:Aim of the study. To investigate clinical effectiveness and safety of Armadin® in the early recovery period after acute ischemic stroke, its impact on the restoration of impaired functions and stroke induced fatigue in the patients with metabolic syndrome. The study aimed to determine target Brain areas by MRI data in cognitive and emotional impairments in patients with ischemic stroke against the metabolic syndrome and to compare with the data of the patients without metabolic syndrome. Materials and methods. The basic group consisted of 28 patients aged from 44 to 79 years old (mean age 66.0 ± 4.2) in the early recovery period after ischemic stroke. The patients of the basic group received Armadin® besides standard treatment. The control group involved 16 patients in the early period after ischemic stroke aged from 54 to 76 years old (mean age 63.0 ± 3.8) that received standard therapy only. The patients’ condition was estimated by the NIHSS, Renkin scale, Barthel index. Cognitive and emotional status was assessed by HADS, MMSE. The quantitative estimation of post-stroke fatigue was performed using Fatigue assessment scale (FAS). MRI of Brain was conducted using Siemens MAGNETOM Avanto 1.5T. There were determined foci size and hippocampus index. Results. Stroke induced fatigue was in both groups: severity median value by FAS was 32.2 (Q1 = 16.5; Q3 = 51.5) in the basic group and 34.25 (Q1 = 14.5; Q3 = 48.5) in the control group before treatment. 95 % of the patients had clinically significant fatigue (FAS ≥ 22), about 20 % of the patients had depression signs. There was no statistically significant correlation between fatigue and depression. Fatigue Level by FAS was more intensive in female in comparison with males. After the therapy fatigue symptoms reduced in both groups, but the reduction was statistically significant in the group received Armadin®. Expressed improvement after the therapy by NIHSS and Barthel index was determined in the basic group. There was not determined the dependence between fatigue intensity by FAS and stroke severity by NIHSS. Cognitive parameters improved due to treatment in both groups. However in the basic group there was 5 % improvement and in the control there was 1 % improvement. MRI 1.5 T by Scheltens et al. method was performed in the patients with metabolic syndrome and without it. The patients with metabolic syndrome had significant reduction of hippocampus index right side and left side compared with the patients without metabolic syndrome: right side 0.50 [0.41; 0.54] vs 0.594 [0.58; 0.61] (p < 0.05). Discussion. Early diagnosis of stroke induced fatigue is of great importance for the patients with ischemic stroke. In our study fatigue was diagnosed in 95 % patients. The diversity with literature data could be likely connected with cluster in the patients with metabolic syndrome which took part in the study. A small subset of the participants disables concluding about metabolic syndrome influence on fatigue development. We must consider that fatigue could form without depression background and it requires specific treatment without antidepressant medications. Improvement of cognitive functions and asthenia reduction in the patients received Armadin® could be likely explained by the opportunity of the drug to elevate Dopamine Brain Level from one side, and succinate acid in its formula which increases GABA Brain Level due to neurochemical reaction, from the other side. So, the usage of this today antioxidant reduced asthenia and thereby improved quality of life of the patients. Hippocampus measurement demonstrated more intensive atrophy in the patients after ischemic stroke combined with metabolic syndrome compared with the patients without metabolic syndrome (P < 0.05). Metabolic cluster with underlying arterial hypertension, insulin resistance, dyslipidemia exc. might enhance hippocampus atrophy than each element severally determined in the patients with ischemic stroke and without metabolic syndrome. Conclusions. Armadin® usage in the early recovery period after ischemic stroke reduced fatigue signs in the patients with metabolic syndrome, improved functions by NIHSS and Barthel index.
T.i. Nasonova - One of the best experts on this subject based on the ideXlab platform.
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Pathogenetic Aspects of Prevention of Fatigue in the Early Recovery Period after Ischemic Stroke in Patients with Metabolic Syndrome
INTERNATIONAL NEUROLOGICAL JOURNAL, 2016Co-Authors: T.i. Nasonova, O.i. Asaulenko, T.v. Kolosova, O.v. Klimenko, T.m. Slobodin, O.yu. Honchar, Yu.a. Buhaiov, O.v. Tyshkevych, I.v. Kurochkin, Yu.i. HolovchenkoAbstract:Aim of the study. To investigate clinical effectiveness and safety of Armadin® in the early recovery period after acute ischemic stroke, its impact on the restoration of impaired functions and stroke induced fatigue in the patients with metabolic syndrome. The study aimed to determine target Brain areas by MRI data in cognitive and emotional impairments in patients with ischemic stroke against the metabolic syndrome and to compare with the data of the patients without metabolic syndrome. Materials and methods. The basic group consisted of 28 patients aged from 44 to 79 years old (mean age 66.0 ± 4.2) in the early recovery period after ischemic stroke. The patients of the basic group received Armadin® besides standard treatment. The control group involved 16 patients in the early period after ischemic stroke aged from 54 to 76 years old (mean age 63.0 ± 3.8) that received standard therapy only. The patients’ condition was estimated by the NIHSS, Renkin scale, Barthel index. Cognitive and emotional status was assessed by HADS, MMSE. The quantitative estimation of post-stroke fatigue was performed using Fatigue assessment scale (FAS). MRI of Brain was conducted using Siemens MAGNETOM Avanto 1.5T. There were determined foci size and hippocampus index. Results. Stroke induced fatigue was in both groups: severity median value by FAS was 32.2 (Q1 = 16.5; Q3 = 51.5) in the basic group and 34.25 (Q1 = 14.5; Q3 = 48.5) in the control group before treatment. 95 % of the patients had clinically significant fatigue (FAS ≥ 22), about 20 % of the patients had depression signs. There was no statistically significant correlation between fatigue and depression. Fatigue Level by FAS was more intensive in female in comparison with males. After the therapy fatigue symptoms reduced in both groups, but the reduction was statistically significant in the group received Armadin®. Expressed improvement after the therapy by NIHSS and Barthel index was determined in the basic group. There was not determined the dependence between fatigue intensity by FAS and stroke severity by NIHSS. Cognitive parameters improved due to treatment in both groups. However in the basic group there was 5 % improvement and in the control there was 1 % improvement. MRI 1.5 T by Scheltens et al. method was performed in the patients with metabolic syndrome and without it. The patients with metabolic syndrome had significant reduction of hippocampus index right side and left side compared with the patients without metabolic syndrome: right side 0.50 [0.41; 0.54] vs 0.594 [0.58; 0.61] (p < 0.05). Discussion. Early diagnosis of stroke induced fatigue is of great importance for the patients with ischemic stroke. In our study fatigue was diagnosed in 95 % patients. The diversity with literature data could be likely connected with cluster in the patients with metabolic syndrome which took part in the study. A small subset of the participants disables concluding about metabolic syndrome influence on fatigue development. We must consider that fatigue could form without depression background and it requires specific treatment without antidepressant medications. Improvement of cognitive functions and asthenia reduction in the patients received Armadin® could be likely explained by the opportunity of the drug to elevate Dopamine Brain Level from one side, and succinate acid in its formula which increases GABA Brain Level due to neurochemical reaction, from the other side. So, the usage of this today antioxidant reduced asthenia and thereby improved quality of life of the patients. Hippocampus measurement demonstrated more intensive atrophy in the patients after ischemic stroke combined with metabolic syndrome compared with the patients without metabolic syndrome (P < 0.05). Metabolic cluster with underlying arterial hypertension, insulin resistance, dyslipidemia exc. might enhance hippocampus atrophy than each element severally determined in the patients with ischemic stroke and without metabolic syndrome. Conclusions. Armadin® usage in the early recovery period after ischemic stroke reduced fatigue signs in the patients with metabolic syndrome, improved functions by NIHSS and Barthel index.
O.i. Asaulenko - One of the best experts on this subject based on the ideXlab platform.
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Pathogenetic Aspects of Prevention of Fatigue in the Early Recovery Period after Ischemic Stroke in Patients with Metabolic Syndrome
INTERNATIONAL NEUROLOGICAL JOURNAL, 2016Co-Authors: T.i. Nasonova, O.i. Asaulenko, T.v. Kolosova, O.v. Klimenko, T.m. Slobodin, O.yu. Honchar, Yu.a. Buhaiov, O.v. Tyshkevych, I.v. Kurochkin, Yu.i. HolovchenkoAbstract:Aim of the study. To investigate clinical effectiveness and safety of Armadin® in the early recovery period after acute ischemic stroke, its impact on the restoration of impaired functions and stroke induced fatigue in the patients with metabolic syndrome. The study aimed to determine target Brain areas by MRI data in cognitive and emotional impairments in patients with ischemic stroke against the metabolic syndrome and to compare with the data of the patients without metabolic syndrome. Materials and methods. The basic group consisted of 28 patients aged from 44 to 79 years old (mean age 66.0 ± 4.2) in the early recovery period after ischemic stroke. The patients of the basic group received Armadin® besides standard treatment. The control group involved 16 patients in the early period after ischemic stroke aged from 54 to 76 years old (mean age 63.0 ± 3.8) that received standard therapy only. The patients’ condition was estimated by the NIHSS, Renkin scale, Barthel index. Cognitive and emotional status was assessed by HADS, MMSE. The quantitative estimation of post-stroke fatigue was performed using Fatigue assessment scale (FAS). MRI of Brain was conducted using Siemens MAGNETOM Avanto 1.5T. There were determined foci size and hippocampus index. Results. Stroke induced fatigue was in both groups: severity median value by FAS was 32.2 (Q1 = 16.5; Q3 = 51.5) in the basic group and 34.25 (Q1 = 14.5; Q3 = 48.5) in the control group before treatment. 95 % of the patients had clinically significant fatigue (FAS ≥ 22), about 20 % of the patients had depression signs. There was no statistically significant correlation between fatigue and depression. Fatigue Level by FAS was more intensive in female in comparison with males. After the therapy fatigue symptoms reduced in both groups, but the reduction was statistically significant in the group received Armadin®. Expressed improvement after the therapy by NIHSS and Barthel index was determined in the basic group. There was not determined the dependence between fatigue intensity by FAS and stroke severity by NIHSS. Cognitive parameters improved due to treatment in both groups. However in the basic group there was 5 % improvement and in the control there was 1 % improvement. MRI 1.5 T by Scheltens et al. method was performed in the patients with metabolic syndrome and without it. The patients with metabolic syndrome had significant reduction of hippocampus index right side and left side compared with the patients without metabolic syndrome: right side 0.50 [0.41; 0.54] vs 0.594 [0.58; 0.61] (p < 0.05). Discussion. Early diagnosis of stroke induced fatigue is of great importance for the patients with ischemic stroke. In our study fatigue was diagnosed in 95 % patients. The diversity with literature data could be likely connected with cluster in the patients with metabolic syndrome which took part in the study. A small subset of the participants disables concluding about metabolic syndrome influence on fatigue development. We must consider that fatigue could form without depression background and it requires specific treatment without antidepressant medications. Improvement of cognitive functions and asthenia reduction in the patients received Armadin® could be likely explained by the opportunity of the drug to elevate Dopamine Brain Level from one side, and succinate acid in its formula which increases GABA Brain Level due to neurochemical reaction, from the other side. So, the usage of this today antioxidant reduced asthenia and thereby improved quality of life of the patients. Hippocampus measurement demonstrated more intensive atrophy in the patients after ischemic stroke combined with metabolic syndrome compared with the patients without metabolic syndrome (P < 0.05). Metabolic cluster with underlying arterial hypertension, insulin resistance, dyslipidemia exc. might enhance hippocampus atrophy than each element severally determined in the patients with ischemic stroke and without metabolic syndrome. Conclusions. Armadin® usage in the early recovery period after ischemic stroke reduced fatigue signs in the patients with metabolic syndrome, improved functions by NIHSS and Barthel index.
T.v. Kolosova - One of the best experts on this subject based on the ideXlab platform.
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Pathogenetic Aspects of Prevention of Fatigue in the Early Recovery Period after Ischemic Stroke in Patients with Metabolic Syndrome
INTERNATIONAL NEUROLOGICAL JOURNAL, 2016Co-Authors: T.i. Nasonova, O.i. Asaulenko, T.v. Kolosova, O.v. Klimenko, T.m. Slobodin, O.yu. Honchar, Yu.a. Buhaiov, O.v. Tyshkevych, I.v. Kurochkin, Yu.i. HolovchenkoAbstract:Aim of the study. To investigate clinical effectiveness and safety of Armadin® in the early recovery period after acute ischemic stroke, its impact on the restoration of impaired functions and stroke induced fatigue in the patients with metabolic syndrome. The study aimed to determine target Brain areas by MRI data in cognitive and emotional impairments in patients with ischemic stroke against the metabolic syndrome and to compare with the data of the patients without metabolic syndrome. Materials and methods. The basic group consisted of 28 patients aged from 44 to 79 years old (mean age 66.0 ± 4.2) in the early recovery period after ischemic stroke. The patients of the basic group received Armadin® besides standard treatment. The control group involved 16 patients in the early period after ischemic stroke aged from 54 to 76 years old (mean age 63.0 ± 3.8) that received standard therapy only. The patients’ condition was estimated by the NIHSS, Renkin scale, Barthel index. Cognitive and emotional status was assessed by HADS, MMSE. The quantitative estimation of post-stroke fatigue was performed using Fatigue assessment scale (FAS). MRI of Brain was conducted using Siemens MAGNETOM Avanto 1.5T. There were determined foci size and hippocampus index. Results. Stroke induced fatigue was in both groups: severity median value by FAS was 32.2 (Q1 = 16.5; Q3 = 51.5) in the basic group and 34.25 (Q1 = 14.5; Q3 = 48.5) in the control group before treatment. 95 % of the patients had clinically significant fatigue (FAS ≥ 22), about 20 % of the patients had depression signs. There was no statistically significant correlation between fatigue and depression. Fatigue Level by FAS was more intensive in female in comparison with males. After the therapy fatigue symptoms reduced in both groups, but the reduction was statistically significant in the group received Armadin®. Expressed improvement after the therapy by NIHSS and Barthel index was determined in the basic group. There was not determined the dependence between fatigue intensity by FAS and stroke severity by NIHSS. Cognitive parameters improved due to treatment in both groups. However in the basic group there was 5 % improvement and in the control there was 1 % improvement. MRI 1.5 T by Scheltens et al. method was performed in the patients with metabolic syndrome and without it. The patients with metabolic syndrome had significant reduction of hippocampus index right side and left side compared with the patients without metabolic syndrome: right side 0.50 [0.41; 0.54] vs 0.594 [0.58; 0.61] (p < 0.05). Discussion. Early diagnosis of stroke induced fatigue is of great importance for the patients with ischemic stroke. In our study fatigue was diagnosed in 95 % patients. The diversity with literature data could be likely connected with cluster in the patients with metabolic syndrome which took part in the study. A small subset of the participants disables concluding about metabolic syndrome influence on fatigue development. We must consider that fatigue could form without depression background and it requires specific treatment without antidepressant medications. Improvement of cognitive functions and asthenia reduction in the patients received Armadin® could be likely explained by the opportunity of the drug to elevate Dopamine Brain Level from one side, and succinate acid in its formula which increases GABA Brain Level due to neurochemical reaction, from the other side. So, the usage of this today antioxidant reduced asthenia and thereby improved quality of life of the patients. Hippocampus measurement demonstrated more intensive atrophy in the patients after ischemic stroke combined with metabolic syndrome compared with the patients without metabolic syndrome (P < 0.05). Metabolic cluster with underlying arterial hypertension, insulin resistance, dyslipidemia exc. might enhance hippocampus atrophy than each element severally determined in the patients with ischemic stroke and without metabolic syndrome. Conclusions. Armadin® usage in the early recovery period after ischemic stroke reduced fatigue signs in the patients with metabolic syndrome, improved functions by NIHSS and Barthel index.
O.v. Klimenko - One of the best experts on this subject based on the ideXlab platform.
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Pathogenetic Aspects of Prevention of Fatigue in the Early Recovery Period after Ischemic Stroke in Patients with Metabolic Syndrome
INTERNATIONAL NEUROLOGICAL JOURNAL, 2016Co-Authors: T.i. Nasonova, O.i. Asaulenko, T.v. Kolosova, O.v. Klimenko, T.m. Slobodin, O.yu. Honchar, Yu.a. Buhaiov, O.v. Tyshkevych, I.v. Kurochkin, Yu.i. HolovchenkoAbstract:Aim of the study. To investigate clinical effectiveness and safety of Armadin® in the early recovery period after acute ischemic stroke, its impact on the restoration of impaired functions and stroke induced fatigue in the patients with metabolic syndrome. The study aimed to determine target Brain areas by MRI data in cognitive and emotional impairments in patients with ischemic stroke against the metabolic syndrome and to compare with the data of the patients without metabolic syndrome. Materials and methods. The basic group consisted of 28 patients aged from 44 to 79 years old (mean age 66.0 ± 4.2) in the early recovery period after ischemic stroke. The patients of the basic group received Armadin® besides standard treatment. The control group involved 16 patients in the early period after ischemic stroke aged from 54 to 76 years old (mean age 63.0 ± 3.8) that received standard therapy only. The patients’ condition was estimated by the NIHSS, Renkin scale, Barthel index. Cognitive and emotional status was assessed by HADS, MMSE. The quantitative estimation of post-stroke fatigue was performed using Fatigue assessment scale (FAS). MRI of Brain was conducted using Siemens MAGNETOM Avanto 1.5T. There were determined foci size and hippocampus index. Results. Stroke induced fatigue was in both groups: severity median value by FAS was 32.2 (Q1 = 16.5; Q3 = 51.5) in the basic group and 34.25 (Q1 = 14.5; Q3 = 48.5) in the control group before treatment. 95 % of the patients had clinically significant fatigue (FAS ≥ 22), about 20 % of the patients had depression signs. There was no statistically significant correlation between fatigue and depression. Fatigue Level by FAS was more intensive in female in comparison with males. After the therapy fatigue symptoms reduced in both groups, but the reduction was statistically significant in the group received Armadin®. Expressed improvement after the therapy by NIHSS and Barthel index was determined in the basic group. There was not determined the dependence between fatigue intensity by FAS and stroke severity by NIHSS. Cognitive parameters improved due to treatment in both groups. However in the basic group there was 5 % improvement and in the control there was 1 % improvement. MRI 1.5 T by Scheltens et al. method was performed in the patients with metabolic syndrome and without it. The patients with metabolic syndrome had significant reduction of hippocampus index right side and left side compared with the patients without metabolic syndrome: right side 0.50 [0.41; 0.54] vs 0.594 [0.58; 0.61] (p < 0.05). Discussion. Early diagnosis of stroke induced fatigue is of great importance for the patients with ischemic stroke. In our study fatigue was diagnosed in 95 % patients. The diversity with literature data could be likely connected with cluster in the patients with metabolic syndrome which took part in the study. A small subset of the participants disables concluding about metabolic syndrome influence on fatigue development. We must consider that fatigue could form without depression background and it requires specific treatment without antidepressant medications. Improvement of cognitive functions and asthenia reduction in the patients received Armadin® could be likely explained by the opportunity of the drug to elevate Dopamine Brain Level from one side, and succinate acid in its formula which increases GABA Brain Level due to neurochemical reaction, from the other side. So, the usage of this today antioxidant reduced asthenia and thereby improved quality of life of the patients. Hippocampus measurement demonstrated more intensive atrophy in the patients after ischemic stroke combined with metabolic syndrome compared with the patients without metabolic syndrome (P < 0.05). Metabolic cluster with underlying arterial hypertension, insulin resistance, dyslipidemia exc. might enhance hippocampus atrophy than each element severally determined in the patients with ischemic stroke and without metabolic syndrome. Conclusions. Armadin® usage in the early recovery period after ischemic stroke reduced fatigue signs in the patients with metabolic syndrome, improved functions by NIHSS and Barthel index.