вопрос по детскому здоровью (Негатив)
А можно мне вопрос по детскому здоровью сюда? (Форум то "Детское Здоровье", по- моему, не функционирует совсем)
ППЦНС -это понятно что такое, в общих чертах. Снижен тонус в ножках, и родовая травма в ШОП. Лечим, лечим с месяца, сейчас уже три, а изменений никаких. На ножки так и не встает, шея кривая(. Вопрос: насколько это все серьезно? Чем грозит в будущем?
Родня ужо замучила, к бабке вести и все тут)))))) пугают , что ребенок вообще на ноги не встанет. Короче такой вот негатив.
ППЦНС -это понятно что такое, в общих чертах. Снижен тонус в ножках, и родовая травма в ШОП. Лечим, лечим с месяца, сейчас уже три, а изменений никаких. На ножки так и не встает, шея кривая(. Вопрос: насколько это все серьезно? Чем грозит в будущем?
Родня ужо замучила, к бабке вести и все тут)))))) пугают , что ребенок вообще на ноги не встанет. Короче такой вот негатив.
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Larssen
Может быть, есть смысл сходить на приём ещё к одному невропатологу? Так-то, Вы только начали лечение. Два месяца - это не срок. Жаль, что по теме ничего добавить не могу.
[Сообщение изменено пользователем 15.01.2007 20:32]
[Сообщение изменено пользователем 15.01.2007 20:32]
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...или не к неврологу, а к неонатологу... А как и чем лечитесь?
А как и чем лечитесь?
В 1 месяц были у неонатолога. Прокололи курс кортексина. 1 мес стугерон, вит В12. курс массажа , электрофорез. Потом местный невролог пантекальцин выписал, четыре дня давали, четыре дня деть не спал.
Сейчас пьем пантоган, танакан ,нейромультивит, парафин на ШОП , поясница, тазобедренные суставы( у детя еще и дисплазия до кучи). Вот так и лечим)))
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Ну да ((( Ужасно... Попробуйте поменять неонатолога .(((
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Качественная ссылка, респект! )))
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[Сообщение изменено пользователем 01.05.2011 22:55]
В
Вивекананда
Прокололи курс кортексина. 1 мес стугерон, вит В12. курс массажа , электрофорез. Потом местный невролог пантекальцин выписал, четыре дня давали, четыре дня деть не спал.
Сейчас пьем пантоган, танакан ,нейромультивит, парафин на ШОП , поясница, тазобедренные суставы( у детя еще и дисплазия до кучи). Вот так и лечим)))
Сейчас пьем пантоган, танакан ,нейромультивит, парафин на ШОП , поясница, тазобедренные суставы( у детя еще и дисплазия до кучи). Вот так и лечим)))
http://forums.rusmedserv.com/showthread.php?t=2779...
Приводим список наиболее частых нерациональных назначений в детской практике.
1. Так называемые сосудистые препараты. К ним относят препараты различных групп (циннаризин, кавинтон, сермион и т.д.)
2. Препараты, содержащие гидролизаты аминокислот, нейропептидов и т.д. - церебролизин, актовегин, солкосерил, кортексин и т.п.
3. Так называемые «ноотропные» препараты, «улучшающие питание мозга»: пирацетам, аминалон, фенибут, пантогам, пикамилон и т.д.
4. Гомеопатические средства.
5. Разнообразные растительные препараты, включая хорошо знакомые населению валериану, пустырник, а также брусничный лист, медвежьи ушки и т.д.
[Сообщение изменено пользователем 15.01.2007 22:03]
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Лечение, похоже, назначено относительно правильно, но раз динамики нет, то встает вопрос - индивидуальный ли подход использовал Ваш невролог при назначении терапии?.
Из всех названных препаратов только ГиБи имеет хоть какое-то право на существование, поскольку одинаковое количество ссылок как "за" так и "против" в медлайне. Возможно, танакан - перспективен... ))) Возможно!
Остальное - немедленно на свалку всвязи с явной неэффективностью.
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JAMA. 2002 Aug 21;288(7):835-40.
Ginkgo for memory enhancement: a randomized controlled trial.
Solomon PR, Adams F, Silver A, Zimmer J, DeVeaux R.
Bronfman Science Center, Williams College, 33 Hoxsey St, Williamstown, MA 01267, USA. psolomon@williams.edu
CONTEXT: Several over-the-counter treatments are marketed as having the ability to improve memory, attention, and related cognitive functions in as little as 4 weeks. These claims, however, are generally not supported by well-controlled clinical studies. OBJECTIVE: To evaluate whether ginkgo, an over-the-counter agent marketed as enhancing memory, improves memory in elderly adults as measured by objective neuropsychological tests and subjective ratings. DESIGN: Six-week randomized, double-blind, placebo-controlled, parallel-group trial. SETTING AND PARTICIPANTS: Community-dwelling volunteer men (n = 98) and women (n = 132) older than 60 years with Mini-Mental State Examination scores greater than 26 and in generally good health were recruited by a US academic center via newspaper advertisements and enrolled over a 26-month period from July 1996 to September 1998. INTERVENTION: Participants were randomly assigned to receive ginkgo, 40 mg 3 times per day (n = 115), or matching placebo (n = 115). RESULTS: Two hundred three participants (88%) completed the protocol. Analysis of the modified intent-to-treat population (all 219 participants returning for evaluation) indicated that there were no significant differences between treatment groups on any outcome measure. Analysis of the fully evaluable population (the 203 who complied with treatment and returned for evaluation) also indicated no significant differences for any outcome measure. CONCLUSIONS: The results of this 6-week study indicate that ginkgo did not facilitate performance on standard neuropsychological tests of learning, memory, attention, and concentration or naming and verbal fluency in elderly adults without cognitive impairment. The ginkgo group also did not differ from the control group in terms of self-reported memory function or global rating by spouses, friends, and relatives. These data suggest that when taken following the manufacturer"s instructions, ginkgo provides no measurable benefit in memory or related cognitive function to adults with healthy cognitive function.
J Clin Epidemiol. 2003 Apr;56(4):367-76.
Ginkgo for elderly people with dementia and age-associated memory impairment: a randomized clinical trial.
van Dongen M, van Rossum E, Kessels A, Sielhorst H, Knipschild P.
Department of Epidemiology, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. mcjm.vandongen@epid.unimaas.nl
Preparations based on special extracts of the Ginkgo biloba tree are popular in various European countries. Previous studies have suggested the clinical efficacy of Ginkgo in patients with dementia, cerebral insufficiency, or related cognitive decline. However, most of these studies did not fulfill the current methodologic requirements. We assessed the efficacy of the G. biloba special extract EGb 761 in patients with dementia and age-associated memory impairment in relation to dose and duration of treatment. Our study was a 24-week, randomized, double-blind, placebo-controlled, parallel-group, multicenter trial. Study participants were elderly patients with dementia (Alzheimer disease or vascular dementia) or age-associated memory impairment (AAMI). A total of 214 participants, recruited from 39 homes for the elderly in the Netherlands, were randomly allocated to Ginkgo (either 240 mg/d or 160 mg/d) or placebo (0 mg/d). After 12 weeks, the subjects in the two Ginkgo groups were randomized to continued Ginkgo treatment or placebo treatment. Primary outcome measures in this study were the Syndrome Kurz Test (SKT; psychometric functioning), the Clinical Global Impression of change (CGI-2; psychopathology, assessed by nursing staff), and the Nuremberg Gerontopsychological Rating Scale for Activities of Daily Living (NAI-NAA; behavioral functioning). One hundred twenty-three patients received Ginkgo (n=79, 240 and 160 mg/d combined) or placebo (n=44) during the 24-week intervention period. We found no statistically significant differences in mean change of scores between Ginkgo and placebo. The differences were SKT: +0.4 (90% confidence interval [CI] -0.9-1.7); CGI-2: +0.1 (90% CI -0.3-0.4), and NAI-NAA: -0.4 (90% CI -1.9-1.2). A positive difference is in favor of Ginkgo. Neither the dementia subgroup (n=36) nor the AAMI subgroup (n=87) experienced a significant effect of Ginkgo treatment. There was no dose-effect relationship and no effect of prolonged Ginkgo treatment. The trial results do not support the view that Ginkgo is beneficial for patients with dementia or age-associated memory impairment.
Ginkgo for memory enhancement: a randomized controlled trial.
Solomon PR, Adams F, Silver A, Zimmer J, DeVeaux R.
Bronfman Science Center, Williams College, 33 Hoxsey St, Williamstown, MA 01267, USA. psolomon@williams.edu
CONTEXT: Several over-the-counter treatments are marketed as having the ability to improve memory, attention, and related cognitive functions in as little as 4 weeks. These claims, however, are generally not supported by well-controlled clinical studies. OBJECTIVE: To evaluate whether ginkgo, an over-the-counter agent marketed as enhancing memory, improves memory in elderly adults as measured by objective neuropsychological tests and subjective ratings. DESIGN: Six-week randomized, double-blind, placebo-controlled, parallel-group trial. SETTING AND PARTICIPANTS: Community-dwelling volunteer men (n = 98) and women (n = 132) older than 60 years with Mini-Mental State Examination scores greater than 26 and in generally good health were recruited by a US academic center via newspaper advertisements and enrolled over a 26-month period from July 1996 to September 1998. INTERVENTION: Participants were randomly assigned to receive ginkgo, 40 mg 3 times per day (n = 115), or matching placebo (n = 115). RESULTS: Two hundred three participants (88%) completed the protocol. Analysis of the modified intent-to-treat population (all 219 participants returning for evaluation) indicated that there were no significant differences between treatment groups on any outcome measure. Analysis of the fully evaluable population (the 203 who complied with treatment and returned for evaluation) also indicated no significant differences for any outcome measure. CONCLUSIONS: The results of this 6-week study indicate that ginkgo did not facilitate performance on standard neuropsychological tests of learning, memory, attention, and concentration or naming and verbal fluency in elderly adults without cognitive impairment. The ginkgo group also did not differ from the control group in terms of self-reported memory function or global rating by spouses, friends, and relatives. These data suggest that when taken following the manufacturer"s instructions, ginkgo provides no measurable benefit in memory or related cognitive function to adults with healthy cognitive function.
J Clin Epidemiol. 2003 Apr;56(4):367-76.
Ginkgo for elderly people with dementia and age-associated memory impairment: a randomized clinical trial.
van Dongen M, van Rossum E, Kessels A, Sielhorst H, Knipschild P.
Department of Epidemiology, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. mcjm.vandongen@epid.unimaas.nl
Preparations based on special extracts of the Ginkgo biloba tree are popular in various European countries. Previous studies have suggested the clinical efficacy of Ginkgo in patients with dementia, cerebral insufficiency, or related cognitive decline. However, most of these studies did not fulfill the current methodologic requirements. We assessed the efficacy of the G. biloba special extract EGb 761 in patients with dementia and age-associated memory impairment in relation to dose and duration of treatment. Our study was a 24-week, randomized, double-blind, placebo-controlled, parallel-group, multicenter trial. Study participants were elderly patients with dementia (Alzheimer disease or vascular dementia) or age-associated memory impairment (AAMI). A total of 214 participants, recruited from 39 homes for the elderly in the Netherlands, were randomly allocated to Ginkgo (either 240 mg/d or 160 mg/d) or placebo (0 mg/d). After 12 weeks, the subjects in the two Ginkgo groups were randomized to continued Ginkgo treatment or placebo treatment. Primary outcome measures in this study were the Syndrome Kurz Test (SKT; psychometric functioning), the Clinical Global Impression of change (CGI-2; psychopathology, assessed by nursing staff), and the Nuremberg Gerontopsychological Rating Scale for Activities of Daily Living (NAI-NAA; behavioral functioning). One hundred twenty-three patients received Ginkgo (n=79, 240 and 160 mg/d combined) or placebo (n=44) during the 24-week intervention period. We found no statistically significant differences in mean change of scores between Ginkgo and placebo. The differences were SKT: +0.4 (90% confidence interval [CI] -0.9-1.7); CGI-2: +0.1 (90% CI -0.3-0.4), and NAI-NAA: -0.4 (90% CI -1.9-1.2). A positive difference is in favor of Ginkgo. Neither the dementia subgroup (n=36) nor the AAMI subgroup (n=87) experienced a significant effect of Ginkgo treatment. There was no dose-effect relationship and no effect of prolonged Ginkgo treatment. The trial results do not support the view that Ginkgo is beneficial for patients with dementia or age-associated memory impairment.
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[Сообщение изменено пользователем 01.05.2011 22:55]
Консультировались у неонатолога и двух неврологов. В итоге ответ один- на ножки не встает и это им не нравится.
И как же теперь быть? Ведь на многое лечение ребенок реагирует не однозначно (кортексин, паракльцин, электрофорез вызывают рев, тремор рук , сучение ног), врачи не связывают данное обстоятельство с назначаемым лечением. Сегодня все отменила самостоятельно (первый день ребенок уснул как обычно), когда никак не лечим))).
Ссылка и правда дельная, только чего то я совсем расстерялась. Что ж делать то теперь? Как быть?
И как же теперь быть? Ведь на многое лечение ребенок реагирует не однозначно (кортексин, паракльцин, электрофорез вызывают рев, тремор рук , сучение ног), врачи не связывают данное обстоятельство с назначаемым лечением. Сегодня все отменила самостоятельно (первый день ребенок уснул как обычно), когда никак не лечим))).
Ссылка и правда дельная, только чего то я совсем расстерялась. Что ж делать то теперь? Как быть?
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[Сообщение изменено пользователем 01.05.2011 22:55]
а к какому невропатологу вы ходите? у нас покруче диагнозы, но такого лечения (за исключением массажа) нам не назначали пока.
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Найду.
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[Сообщение изменено пользователем 01.05.2011 22:56]
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Pentoxifylline, propentofylline and pentifylline for acute ischaemic stroke.
Bath PM, Bath FJ, Asplund K.
...Four trials tested pentoxifylline in 763 people...
...Early death (within four weeks) occurred in 34 of 408 patients given pentoxifylline compared with 49 of 385 given placebo (odds ratio 0.64, 95% confidence interval 0.41 to 1.02)...
...This non-significant trend to less deaths was due mainly to one pentoxifylline trial that found a highly significant reduction in early deaths. Two trials reported early death or disability and found a non-significant reduction (odds ratio 0.49, 95% confidence interval 0.20 to 1.20)...
Cardiol Rev. 2001 Jul-Aug;9(4):238-45.
Medical management of peripheral arterial disease.
Creager MA.
...Two drugs-pentoxifylline and cilostazol-currently are approved by the Food and Drug Administration for the treatment of patients with claudication. Meta-analyses have suggested that, compared with placebo, pentoxifylline improves maximal walking distance by approximately 20-25%. Cilostazol is a phosphodiesterase type 3 inhibitor. In clinical trials, cilostazol has consistently improved maximal walking distance as compared with placebo, with the range of improvement being approximately 40-60%...
Angiology. 2002 Jan-Feb;53 Suppl 1:S39-43.
Intermittent claudication in diabetics: treatment with exercise and pentoxifylline--a 6-month, controlled, randomized trial.
Belcaro G, Nicolaides AN, Griffin M, De Sanctis MT, Cesarone MR, Incandela L, Ippolito E, Pomante P, Geroulakos G, Ramaswami G.
Department of Biomedical Sciences, Chieti University and San Valentino Vascular Screening Project, Pe, Italy.
The aims of this study were to evaluate the effect of PXF (1600 mg daily) in diabetic patients with intermittent claudication. Of the 60 included patients, 53 completed the study (27 in the PXF group). There were seven dropouts. The groups were comparable for age, sex distribution, and total walking distance (TWD), and risk factors. There was an increase in TWD at 3 and 6 months in both groups (p<0.05) possibly due to exercise. However the increase (both absolute and percentage) in TWD was significantly larger in the PXF group. At 6 months, PXF produced a 292% increase in TWD (vs 180% produced by placebo) (p<0.02). The excess increase produced by PXF treatment was 112% at 6 months in comparison with placebo (p<0.02). Treatment was well tolerated. Between-group analysis favors PXF considering TWD, and results indicate good efficacy and tolerability.
Bath PM, Bath FJ, Asplund K.
...Four trials tested pentoxifylline in 763 people...
...Early death (within four weeks) occurred in 34 of 408 patients given pentoxifylline compared with 49 of 385 given placebo (odds ratio 0.64, 95% confidence interval 0.41 to 1.02)...
...This non-significant trend to less deaths was due mainly to one pentoxifylline trial that found a highly significant reduction in early deaths. Two trials reported early death or disability and found a non-significant reduction (odds ratio 0.49, 95% confidence interval 0.20 to 1.20)...
Cardiol Rev. 2001 Jul-Aug;9(4):238-45.
Medical management of peripheral arterial disease.
Creager MA.
...Two drugs-pentoxifylline and cilostazol-currently are approved by the Food and Drug Administration for the treatment of patients with claudication. Meta-analyses have suggested that, compared with placebo, pentoxifylline improves maximal walking distance by approximately 20-25%. Cilostazol is a phosphodiesterase type 3 inhibitor. In clinical trials, cilostazol has consistently improved maximal walking distance as compared with placebo, with the range of improvement being approximately 40-60%...
Angiology. 2002 Jan-Feb;53 Suppl 1:S39-43.
Intermittent claudication in diabetics: treatment with exercise and pentoxifylline--a 6-month, controlled, randomized trial.
Belcaro G, Nicolaides AN, Griffin M, De Sanctis MT, Cesarone MR, Incandela L, Ippolito E, Pomante P, Geroulakos G, Ramaswami G.
Department of Biomedical Sciences, Chieti University and San Valentino Vascular Screening Project, Pe, Italy.
The aims of this study were to evaluate the effect of PXF (1600 mg daily) in diabetic patients with intermittent claudication. Of the 60 included patients, 53 completed the study (27 in the PXF group). There were seven dropouts. The groups were comparable for age, sex distribution, and total walking distance (TWD), and risk factors. There was an increase in TWD at 3 and 6 months in both groups (p<0.05) possibly due to exercise. However the increase (both absolute and percentage) in TWD was significantly larger in the PXF group. At 6 months, PXF produced a 292% increase in TWD (vs 180% produced by placebo) (p<0.02). The excess increase produced by PXF treatment was 112% at 6 months in comparison with placebo (p<0.02). Treatment was well tolerated. Between-group analysis favors PXF considering TWD, and results indicate good efficacy and tolerability.
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Pentoxifylline, propentofylline and pentifylline for acute ischaemic stroke.
Bath PM, Bath FJ, Asplund K.
Division of Stroke Medicine, University of Nottingham, City Hospital Campus, Hucknall Road, Nottingham, Nottinghamshire, UK, NG5 1PB.
philip.bath@nottingham.ac.uk
BACKGROUND: Methylxanthine derivatives are vasodilators. They also inhibit platelet aggregation and thromboxane A2 synthesis, decrease the release of free radicals and may be neuroprotective. OBJECTIVES: The objective of this review was to assess the effect of intravenous or oral methylxanthines (pentoxifylline, propentofylline, or pentifylline) in patients with acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register, Medline (from 1965), Embase (from 1981), ISI (from 1981) and the Ottawa stroke trials registry. We contacted drug companies. SELECTION CRITERIA: Randomised trials comparing pentoxifylline, propentofylline or pentifylline with placebo or control in patients with definite or presumed acute ischaemic stroke. Trials were included if treatment was started within one week of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the inclusion criteria. Trial quality was assessed. MAIN RESULTS: Five trials were included. Four trials tested pentoxifylline in 763 people, and one tested propentofylline in 30 people. No trials of pentifylline were found. Early death (within four weeks) occurred in 34 of 408 patients given a methylxanthine drug compared with 49 of 385 given placebo (odds ratio 0.64, 95% confidence interval 0.41 to 1.02). This non-significant trend to less deaths was due mainly to one pentoxifylline trial that found a highly significant reduction in early deaths. Two trials reported early death or disability and found a non-significant reduction (odds ratio 0.49, 95% confidence interval 0.20 to 1.20). Late death (beyond four weeks) was reported in the propentofylline trial involving 30 patients, with no difference between treatment and placebo (odds ratio 0.70, 95% confidence interval 0.13 to 3.68). Data for neurological impairment and disability were not in a form suitable for analysis. Data on quality of life, stroke recurrence, thromboembolism and bleeding were not reported. REVIEWER"S CONCLUSIONS: There is not enough evidence to assess the effectiveness and safety of methylxanthines after acute ischaemic stroke.
Curr Pharm Des. 2002;8(2):125-38.
Design and study of piracetam-like nootropics, controversial members of the problematic class of cognition-enhancing drugs.
Gualtieri F, Manetti D, Romanelli MN, Ghelardini C.
Dipartimento di Scienze Farmaceutiche, Universita di Firenze, Via G. Capponi 9, I-50121, Firenze, Italy. fulvio.gualtieri@unifi.it
Cognition enhancers are drugs able to facilitate attentional abilities and acquisition, storage and retrieval of information, and to attenuate the impairment of cognitive functions associated with head traumas, stroke, age and age-related pathologies. Development of cognition enhancers is still a difficult task because of complexity of the brain functions, poor predictivity of animal tests and lengthy and expensive clinical trials. After the early serendipitous discovery of first generation cognition enhancers, current research is based on a variety of working hypotheses, derived from the progress of knowledge in the neurobiopathology of cognitive processes. Among other classes of drugs, piracetam-like cognition enhancers (nootropics) have never reached general acceptance, in spite of their excellent tolerability and safety.
Bath PM, Bath FJ, Asplund K.
Division of Stroke Medicine, University of Nottingham, City Hospital Campus, Hucknall Road, Nottingham, Nottinghamshire, UK, NG5 1PB.
philip.bath@nottingham.ac.uk
BACKGROUND: Methylxanthine derivatives are vasodilators. They also inhibit platelet aggregation and thromboxane A2 synthesis, decrease the release of free radicals and may be neuroprotective. OBJECTIVES: The objective of this review was to assess the effect of intravenous or oral methylxanthines (pentoxifylline, propentofylline, or pentifylline) in patients with acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register, Medline (from 1965), Embase (from 1981), ISI (from 1981) and the Ottawa stroke trials registry. We contacted drug companies. SELECTION CRITERIA: Randomised trials comparing pentoxifylline, propentofylline or pentifylline with placebo or control in patients with definite or presumed acute ischaemic stroke. Trials were included if treatment was started within one week of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the inclusion criteria. Trial quality was assessed. MAIN RESULTS: Five trials were included. Four trials tested pentoxifylline in 763 people, and one tested propentofylline in 30 people. No trials of pentifylline were found. Early death (within four weeks) occurred in 34 of 408 patients given a methylxanthine drug compared with 49 of 385 given placebo (odds ratio 0.64, 95% confidence interval 0.41 to 1.02). This non-significant trend to less deaths was due mainly to one pentoxifylline trial that found a highly significant reduction in early deaths. Two trials reported early death or disability and found a non-significant reduction (odds ratio 0.49, 95% confidence interval 0.20 to 1.20). Late death (beyond four weeks) was reported in the propentofylline trial involving 30 patients, with no difference between treatment and placebo (odds ratio 0.70, 95% confidence interval 0.13 to 3.68). Data for neurological impairment and disability were not in a form suitable for analysis. Data on quality of life, stroke recurrence, thromboembolism and bleeding were not reported. REVIEWER"S CONCLUSIONS: There is not enough evidence to assess the effectiveness and safety of methylxanthines after acute ischaemic stroke.
Curr Pharm Des. 2002;8(2):125-38.
Design and study of piracetam-like nootropics, controversial members of the problematic class of cognition-enhancing drugs.
Gualtieri F, Manetti D, Romanelli MN, Ghelardini C.
Dipartimento di Scienze Farmaceutiche, Universita di Firenze, Via G. Capponi 9, I-50121, Firenze, Italy. fulvio.gualtieri@unifi.it
Cognition enhancers are drugs able to facilitate attentional abilities and acquisition, storage and retrieval of information, and to attenuate the impairment of cognitive functions associated with head traumas, stroke, age and age-related pathologies. Development of cognition enhancers is still a difficult task because of complexity of the brain functions, poor predictivity of animal tests and lengthy and expensive clinical trials. After the early serendipitous discovery of first generation cognition enhancers, current research is based on a variety of working hypotheses, derived from the progress of knowledge in the neurobiopathology of cognitive processes. Among other classes of drugs, piracetam-like cognition enhancers (nootropics) have never reached general acceptance, in spite of their excellent tolerability and safety.
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Cochrane Database Syst Rev. 2002;(4):CD000419.
Piracetam for acute ischaemic stroke.
Ricci S, Celani MG, Cantisani AT, Righetti E.
Stroke Service, USL 2, Via Guerra 17, 06127 Perugia, Italy. istitaly@unipg.it
BACKGROUND: Piracetam has neuroprotective and antithrombotic effects which may help to reduce death and disability in people with acute stroke. OBJECTIVES: The objective of this review was to assess the effects of piracetam in acute presumed ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Review Group Trials Register (last searched April 2001). In addition we searched the Cochrane Controlled Trials Register (Cochrane Library 2001, issue 2), MEDLINE (1966-April 2001), EMBASE (1980-April 2001), and ISI Science Citation Index (1981- April 2001). We also handsearched 15 journals and contacted the manufacturer to identify further published and unpublished studies. SELECTION CRITERIA: Randomised trials comparing piracetam with control, with at least mortality reported and entry to the trial within approximately 48 hours of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers extracted data and assessed trial quality and this was checked by the other two reviewers. Study authors were contacted for missing information. MAIN RESULTS: Three trials involving 1002 people were included, with one trial contributing 93% of the data. Participants" ages ranged from 40 to 85, and both sexes were equally represented. Piracetam was associated with a statistically non significant increase in death at one month (approximately 31% increase, 95% confidence interval 81% increase to 5% reduction). This trend was no longer apparent in the large trial after correction for imbalance in stroke severity. Limited data showed no difference between the treatment and control groups for functional outcome, dependency or proportion of patients dead or dependent. Adverse effects were not reported. REVIEWER"S CONCLUSIONS: There is some suggestion (but no statistically significant result) of an unfavourable effect of piracetam on early death, but this may have been caused by baseline differences in stroke severity in the trials. There is not enough evidence to assess the effect of piracetam on dependency.
Cochrane Database Syst Rev. 2001;(2):CD001011.
Piracetam for dementia or cognitive impairment.
Flicker L, Grimley Evans G.
OBJECTIVES: To determine the clinical efficacy of piracetam for the features of dementia or cognitive impairment, classified according to the major subtypes of dementia: vascular, Alzheimer"s disease or mixed vascular and Alzheimer"s disease, or unclassified dementia, or cognitive impairment not fulfilling the criteria for dementia. SEARCH STRATEGY: The trials were identified from a search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 10 November 2000 using the term spiracetam, nootropic and 2-Oxo-1-pyrrolidine. In addition the pharmaceutical company responsible for marketing most of the piracetam worldwide, UCB Pharma, provided a comprehensive list of abstracts, which included many unpublished studies. As many of these unpublished, placebo-controlled studies will be reviewed as possible. SELECTION CRITERIA: All unconfounded trials specified as randomized in which treatment with piracetam was administered for more than a day and compared with placebo in patients with dementia of Alzheimer type, vascular dementia,or mixed vascular and Alzheimer"s disease, or unclassified dementia, or cognitive impairment not fulfilling the criteria for dementia. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers. Each study was independently verified as fulfilling the inclusion criteria. Studies were pooled if appropriate and possible, and the pooled odds ratios (95%CI) or the average differences (95%CI) were estimated. Where possible, intention-to-treat analyses were undertaken. Sensitivity analyses were performed to determine if successive elimination of those studies performing most poorly on these quality criteria changed the effect estimate. MAIN RESULTS: Unfortunately, many of the studies were of cross-over design and first-phase data were unavailable, or could not be extracted. Global Impression of Change was the only outcoeme for which there was a significant volume of evidence from the pooled data. There was evidence of heterogeneity in the results from the individual studies, chi-square test = 20.8 (df=5). Using a fixed effects model the odds ratio for improvement in the piracetam group compared with the placebo group was 3.55, [95% CI][2.45, 5.16]. If a random effects model was used the odds ratio was 3.47 [1.29, 9.30]. If one single-blind study was excluded, the fixed effects model yielded an odds ratio of 3.36 [2.29, 4.99] and if a random effects model was applied then the odds ratio was 2.89 [1.01, 8.24]. The evidence of effects on cognition and other measures, was inconclusive. REVIEWER"S CONCLUSIONS: At this stage the evidence available from the published literature does not support the use of piracetam in the treatment of people with dementia or cognitive impairment. Although effects were found on global impression of change, no benefit was shown by any of the more specific measures. There is a need for further evaluation of piracetam by : 1) Obtaining the data from the identified studies for an individual patient database review, 2) Performing a randomized trial of piracetam in patients with diagnoses made by currently accepted diagnostic criteria. The trial should extend over for a period of at least 6 months and preferably longer. Specific cognitive instruments which are sensitive to change, Clinician Global Impression of Change, levels of dependency and caregiver quality of life scales should also be incorporated in such a study.
Piracetam for acute ischaemic stroke.
Ricci S, Celani MG, Cantisani AT, Righetti E.
Stroke Service, USL 2, Via Guerra 17, 06127 Perugia, Italy. istitaly@unipg.it
BACKGROUND: Piracetam has neuroprotective and antithrombotic effects which may help to reduce death and disability in people with acute stroke. OBJECTIVES: The objective of this review was to assess the effects of piracetam in acute presumed ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Review Group Trials Register (last searched April 2001). In addition we searched the Cochrane Controlled Trials Register (Cochrane Library 2001, issue 2), MEDLINE (1966-April 2001), EMBASE (1980-April 2001), and ISI Science Citation Index (1981- April 2001). We also handsearched 15 journals and contacted the manufacturer to identify further published and unpublished studies. SELECTION CRITERIA: Randomised trials comparing piracetam with control, with at least mortality reported and entry to the trial within approximately 48 hours of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers extracted data and assessed trial quality and this was checked by the other two reviewers. Study authors were contacted for missing information. MAIN RESULTS: Three trials involving 1002 people were included, with one trial contributing 93% of the data. Participants" ages ranged from 40 to 85, and both sexes were equally represented. Piracetam was associated with a statistically non significant increase in death at one month (approximately 31% increase, 95% confidence interval 81% increase to 5% reduction). This trend was no longer apparent in the large trial after correction for imbalance in stroke severity. Limited data showed no difference between the treatment and control groups for functional outcome, dependency or proportion of patients dead or dependent. Adverse effects were not reported. REVIEWER"S CONCLUSIONS: There is some suggestion (but no statistically significant result) of an unfavourable effect of piracetam on early death, but this may have been caused by baseline differences in stroke severity in the trials. There is not enough evidence to assess the effect of piracetam on dependency.
Cochrane Database Syst Rev. 2001;(2):CD001011.
Piracetam for dementia or cognitive impairment.
Flicker L, Grimley Evans G.
OBJECTIVES: To determine the clinical efficacy of piracetam for the features of dementia or cognitive impairment, classified according to the major subtypes of dementia: vascular, Alzheimer"s disease or mixed vascular and Alzheimer"s disease, or unclassified dementia, or cognitive impairment not fulfilling the criteria for dementia. SEARCH STRATEGY: The trials were identified from a search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 10 November 2000 using the term spiracetam, nootropic and 2-Oxo-1-pyrrolidine. In addition the pharmaceutical company responsible for marketing most of the piracetam worldwide, UCB Pharma, provided a comprehensive list of abstracts, which included many unpublished studies. As many of these unpublished, placebo-controlled studies will be reviewed as possible. SELECTION CRITERIA: All unconfounded trials specified as randomized in which treatment with piracetam was administered for more than a day and compared with placebo in patients with dementia of Alzheimer type, vascular dementia,or mixed vascular and Alzheimer"s disease, or unclassified dementia, or cognitive impairment not fulfilling the criteria for dementia. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers. Each study was independently verified as fulfilling the inclusion criteria. Studies were pooled if appropriate and possible, and the pooled odds ratios (95%CI) or the average differences (95%CI) were estimated. Where possible, intention-to-treat analyses were undertaken. Sensitivity analyses were performed to determine if successive elimination of those studies performing most poorly on these quality criteria changed the effect estimate. MAIN RESULTS: Unfortunately, many of the studies were of cross-over design and first-phase data were unavailable, or could not be extracted. Global Impression of Change was the only outcoeme for which there was a significant volume of evidence from the pooled data. There was evidence of heterogeneity in the results from the individual studies, chi-square test = 20.8 (df=5). Using a fixed effects model the odds ratio for improvement in the piracetam group compared with the placebo group was 3.55, [95% CI][2.45, 5.16]. If a random effects model was used the odds ratio was 3.47 [1.29, 9.30]. If one single-blind study was excluded, the fixed effects model yielded an odds ratio of 3.36 [2.29, 4.99] and if a random effects model was applied then the odds ratio was 2.89 [1.01, 8.24]. The evidence of effects on cognition and other measures, was inconclusive. REVIEWER"S CONCLUSIONS: At this stage the evidence available from the published literature does not support the use of piracetam in the treatment of people with dementia or cognitive impairment. Although effects were found on global impression of change, no benefit was shown by any of the more specific measures. There is a need for further evaluation of piracetam by : 1) Obtaining the data from the identified studies for an individual patient database review, 2) Performing a randomized trial of piracetam in patients with diagnoses made by currently accepted diagnostic criteria. The trial should extend over for a period of at least 6 months and preferably longer. Specific cognitive instruments which are sensitive to change, Clinician Global Impression of Change, levels of dependency and caregiver quality of life scales should also be incorporated in such a study.
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Cochrane Database Syst Rev. 2003;(1):CD003119.
Vinpocetine for cognitive impairment and dementia.
Szatmari SZ, Whitehouse PJ.
BACKGROUND: Vinpocetine is a synthetic ethyl ester of apovincamine, a vinca alkaloid obtained from the leaves of the Lesser Periwinkle (Vinca minor) and discovered in the late 1960s. Although used in human treatment for over twenty years, it has not been approved by any regulatory body for the treatment of cognitive impairment. Basic sciences studies have been used to claim a variety of potentially important effects in the brain. However, despite these many proposed mechanisms and targets, the relevance of this basic science to clinical studies is unclear. OBJECTIVES: To assess the efficacy and safety of vinpocetine in the treatment of patients with cognitive impairment due to vascular disease, Alzheimer"s disease, mixed (vascular and Alzheimer"s disease) and other dementias. SEARCH STRATEGY: The Cochrane Dementia & Cognitive Improvement Group"s Specialized Register was searched using the terms vinpocetin*, cavinton, kavinton, Rgh-4405, Tcv-3B, "ethyl apovincaminate", vinRx, periwinkle, "myrtle vincapervinc" and cezayirmeneksesi. The manufacturers of vinpocetine were asked for information on trials of vinpocetine for dementia. In addition we tried to collect articles not listed in MEDLINE or other sources on the Internet (e.g. articles in Hungarian and Romanian). SELECTION CRITERIA: All human, unconfounded, double-blind, randomized trials in which treatment with vinpocetine was administered for more than a day and compared to control in patients with vascular dementia, Alzheimer"s dementia or mixed Alzheimer"s and vascular dementia and other dementias. Non-randomized trials were excluded. DATA COLLECTION AND ANALYSIS: Data were independently extracted by the two reviewers (SzSz and PW) and cross-checked. Data from "washout" periods were not used for the analysis. For continuous or ordinal variables, such as cognitive test results, the main outcomes of interest were the change in score from baseline. The categorical outcome of global impression was transformed to binary data (improved or not improved) as was the occurrence of adverse effects; here the endpoint itself was of interest the Peto method of the "typical odds ratio" was used. A test for heterogeneity of treatment effects between the trials was made if appropriate. Data synthesis and analysis were performed using the Cochrane Review Manager software (RevMan version 4.1). MAIN RESULTS: All identified studies were performed before the 1990s and used various terms and criteria for cognitive decline and dementia. The three studies included in the review involved a total of 583 people with dementia treated with vinpocetine or placebo. The reports of these studies did not make possible any differentiation of effects for degenerative or vascular dementia. The results show benefit associated with treatment with vinpocetine 30mg/day and 60 mg/day compared with placebo, but the number of patients treated for 6 months or more was small. Only one study extended treatment to one year. Adverse effects were inconsistently reported and without regard for relationship to dose. The available data do not demonstrate many problems of adverse effects but intention-to-treat data were not available for any of the trials. REVIEWER"S CONCLUSIONS: Although the basic science is interesting, the evidence for beneficial effect of vinpocetine on patients with dementia is inconclusive and does not support clinical use. The drug seems to have few adverse effects at the doses used in the studies. Large studies evaluating the use of vinpocetine for people suffering from well defined types of cognitive impairment are needed to explore possible efficacy of this treatment.
Cochrane Database Syst Rev. 2002;(4):CD000277.
Calcium antagonists for aneurysmal subarachnoid haemorrhage.
Rinkel GJ, Feigin VL, Algra A, Vermeulen M, van Gijn J.
BACKGROUND: Secondary ischaemia is a frequent cause of poor outcome in patients with subarachnoid haemorrhage. Its pathogenesis has not been elucidated yet, but may be related to vasospasm. Experimental studies have indicated that calcium antagonists can prevent or reverse vasospasm. Calcium antagonists have been studied in several trials, but data are conflicting. There is no overview concerning all available calcium antagonists. OBJECTIVES: To determine whether calcium antagonists improve outcome in patients with aneurysmal subarachnoid haemorrhage (SAH). SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched November 2001). In addition, we handsearched two Russian journals (1990-1995) and contacted trialists and pharmaceutical companies to identify further studies SELECTION CRITERIA: All completed, unconfounded, truly randomised controlled trials comparing any calcium antagonist with control, within ten days of SAH onset. Eleven trials that met the inclusion criteria were included in the overview. DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted the data and assessed trial quality. Trialists were contacted to obtain missing information MAIN RESULTS: We analysed 11 trials totaling 2804 randomised patients with subarachnoid haemorrhage (1376 in the treatment and 1428 in the control group). The drugs analysed were: nimodipine (eight trials, 1574 patients), nicardipine (two trials, 954 patients), and AT877 (one trial, 276 patients). In 92% of the patients aneurysms were confirmed by angiography or autopsy. Overall, calcium antagonists significantly reduced the risk of poor outcome after subarachnoid haemorrhage: relative risk (RR) 0.82 (95% CI 0.72 to 0.93); the absolute risk reduction was 5.1%, the corresponding number of patients needed to treat to prevent a single poor outcome event is 20. For oral nimodipine alone the RR was 0.69 (0.58 to 0.84). The RR of death on treatment with calcium antagonists was 0.94 (95% CI 0.80 to 1.10), that of ischaemic neurological deficits 0.67 (95% CI 0.59 to 0.76), and that of CT-scan documented cerebral infarction 0.80 (95% CI 0.71 to 0.89). REVIEWER"S CONCLUSIONS: Calcium antagonists reduce the proportion of patients with poor outcome and ischaemic neurological deficits after aneurysmal SAH. The results for "poor outcome" are statistically robust, but depend largely on one large trial with oral nimodipine; the evidence for nicardipine and AT877 is inconclusive. The evidence for nimodipine is not beyond every doubt, but given the potential benefits and modest risks associated with this treatment, against the background of a devastating natural history, oral nimodipine (60 mg every 4 hours) is indicated in patients with aneurysmal SAH. Intravenous administration of calcium antagonists cannot be recommended on the basis of the present evidence. For oral nimodipine uncertainty remains regarding the (dis)advantages in patients in poor clinical condition on admission or in patients with established cerebral ischaemia, the optimal dose and time window, the question whether other types of calcium antagonists offer better protection and the intermediate factors through which nimodipine exerts its beneficial effect after aneurysmal SAH.
--------------------------------------------------------------------------------
Cochrane Database Syst Rev. 2002;(4):CD000419.
Piracetam for acute ischaemic stroke.
Ricci S, Celani MG, Cantisani AT, Righetti E.
Stroke Service, USL 2, Via Guerra 17, 06127 Perugia, Italy. istitaly@unipg.it
BACKGROUND: Piracetam has neuroprotective and antithrombotic effects which may help to reduce death and disability in people with acute stroke. OBJECTIVES: The objective of this review was to assess the effects of piracetam in acute presumed ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Review Group Trials Register (last searched April 2001). In addition we searched the Cochrane Controlled Trials Register (Cochrane Library 2001, issue 2), MEDLINE (1966-April 2001), EMBASE (1980-April 2001), and ISI Science Citation Index (1981- April 2001). We also handsearched 15 journals and contacted the manufacturer to identify further published and unpublished studies. SELECTION CRITERIA: Randomised trials comparing piracetam with control, with at least mortality reported and entry to the trial within approximately 48 hours of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers extracted data and assessed trial quality and this was checked by the other two reviewers. Study authors were contacted for missing information. MAIN RESULTS: Three trials involving 1002 people were included, with one trial contributing 93% of the data. Participants" ages ranged from 40 to 85, and both sexes were equally represented. Piracetam was associated with a statistically non significant increase in death at one month (approximately 31% increase, 95% confidence interval 81% increase to 5% reduction). This trend was no longer apparent in the large trial after correction for imbalance in stroke severity. Limited data showed no difference between the treatment and control groups for functional outcome, dependency or proportion of patients dead or dependent. Adverse effects were not reported. REVIEWER"S CONCLUSIONS: There is some suggestion (but no statistically significant result) of an unfavourable effect of piracetam on early death, but this may have been caused by baseline differences in stroke severity in the trials. There is not enough evidence to assess the effect of piracetam on dependency.
Cochrane Database Syst Rev. 2001;(2):CD001011.
[Сообщение изменено пользователем 15.01.2007 23:08]
Vinpocetine for cognitive impairment and dementia.
Szatmari SZ, Whitehouse PJ.
BACKGROUND: Vinpocetine is a synthetic ethyl ester of apovincamine, a vinca alkaloid obtained from the leaves of the Lesser Periwinkle (Vinca minor) and discovered in the late 1960s. Although used in human treatment for over twenty years, it has not been approved by any regulatory body for the treatment of cognitive impairment. Basic sciences studies have been used to claim a variety of potentially important effects in the brain. However, despite these many proposed mechanisms and targets, the relevance of this basic science to clinical studies is unclear. OBJECTIVES: To assess the efficacy and safety of vinpocetine in the treatment of patients with cognitive impairment due to vascular disease, Alzheimer"s disease, mixed (vascular and Alzheimer"s disease) and other dementias. SEARCH STRATEGY: The Cochrane Dementia & Cognitive Improvement Group"s Specialized Register was searched using the terms vinpocetin*, cavinton, kavinton, Rgh-4405, Tcv-3B, "ethyl apovincaminate", vinRx, periwinkle, "myrtle vincapervinc" and cezayirmeneksesi. The manufacturers of vinpocetine were asked for information on trials of vinpocetine for dementia. In addition we tried to collect articles not listed in MEDLINE or other sources on the Internet (e.g. articles in Hungarian and Romanian). SELECTION CRITERIA: All human, unconfounded, double-blind, randomized trials in which treatment with vinpocetine was administered for more than a day and compared to control in patients with vascular dementia, Alzheimer"s dementia or mixed Alzheimer"s and vascular dementia and other dementias. Non-randomized trials were excluded. DATA COLLECTION AND ANALYSIS: Data were independently extracted by the two reviewers (SzSz and PW) and cross-checked. Data from "washout" periods were not used for the analysis. For continuous or ordinal variables, such as cognitive test results, the main outcomes of interest were the change in score from baseline. The categorical outcome of global impression was transformed to binary data (improved or not improved) as was the occurrence of adverse effects; here the endpoint itself was of interest the Peto method of the "typical odds ratio" was used. A test for heterogeneity of treatment effects between the trials was made if appropriate. Data synthesis and analysis were performed using the Cochrane Review Manager software (RevMan version 4.1). MAIN RESULTS: All identified studies were performed before the 1990s and used various terms and criteria for cognitive decline and dementia. The three studies included in the review involved a total of 583 people with dementia treated with vinpocetine or placebo. The reports of these studies did not make possible any differentiation of effects for degenerative or vascular dementia. The results show benefit associated with treatment with vinpocetine 30mg/day and 60 mg/day compared with placebo, but the number of patients treated for 6 months or more was small. Only one study extended treatment to one year. Adverse effects were inconsistently reported and without regard for relationship to dose. The available data do not demonstrate many problems of adverse effects but intention-to-treat data were not available for any of the trials. REVIEWER"S CONCLUSIONS: Although the basic science is interesting, the evidence for beneficial effect of vinpocetine on patients with dementia is inconclusive and does not support clinical use. The drug seems to have few adverse effects at the doses used in the studies. Large studies evaluating the use of vinpocetine for people suffering from well defined types of cognitive impairment are needed to explore possible efficacy of this treatment.
Cochrane Database Syst Rev. 2002;(4):CD000277.
Calcium antagonists for aneurysmal subarachnoid haemorrhage.
Rinkel GJ, Feigin VL, Algra A, Vermeulen M, van Gijn J.
BACKGROUND: Secondary ischaemia is a frequent cause of poor outcome in patients with subarachnoid haemorrhage. Its pathogenesis has not been elucidated yet, but may be related to vasospasm. Experimental studies have indicated that calcium antagonists can prevent or reverse vasospasm. Calcium antagonists have been studied in several trials, but data are conflicting. There is no overview concerning all available calcium antagonists. OBJECTIVES: To determine whether calcium antagonists improve outcome in patients with aneurysmal subarachnoid haemorrhage (SAH). SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched November 2001). In addition, we handsearched two Russian journals (1990-1995) and contacted trialists and pharmaceutical companies to identify further studies SELECTION CRITERIA: All completed, unconfounded, truly randomised controlled trials comparing any calcium antagonist with control, within ten days of SAH onset. Eleven trials that met the inclusion criteria were included in the overview. DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted the data and assessed trial quality. Trialists were contacted to obtain missing information MAIN RESULTS: We analysed 11 trials totaling 2804 randomised patients with subarachnoid haemorrhage (1376 in the treatment and 1428 in the control group). The drugs analysed were: nimodipine (eight trials, 1574 patients), nicardipine (two trials, 954 patients), and AT877 (one trial, 276 patients). In 92% of the patients aneurysms were confirmed by angiography or autopsy. Overall, calcium antagonists significantly reduced the risk of poor outcome after subarachnoid haemorrhage: relative risk (RR) 0.82 (95% CI 0.72 to 0.93); the absolute risk reduction was 5.1%, the corresponding number of patients needed to treat to prevent a single poor outcome event is 20. For oral nimodipine alone the RR was 0.69 (0.58 to 0.84). The RR of death on treatment with calcium antagonists was 0.94 (95% CI 0.80 to 1.10), that of ischaemic neurological deficits 0.67 (95% CI 0.59 to 0.76), and that of CT-scan documented cerebral infarction 0.80 (95% CI 0.71 to 0.89). REVIEWER"S CONCLUSIONS: Calcium antagonists reduce the proportion of patients with poor outcome and ischaemic neurological deficits after aneurysmal SAH. The results for "poor outcome" are statistically robust, but depend largely on one large trial with oral nimodipine; the evidence for nicardipine and AT877 is inconclusive. The evidence for nimodipine is not beyond every doubt, but given the potential benefits and modest risks associated with this treatment, against the background of a devastating natural history, oral nimodipine (60 mg every 4 hours) is indicated in patients with aneurysmal SAH. Intravenous administration of calcium antagonists cannot be recommended on the basis of the present evidence. For oral nimodipine uncertainty remains regarding the (dis)advantages in patients in poor clinical condition on admission or in patients with established cerebral ischaemia, the optimal dose and time window, the question whether other types of calcium antagonists offer better protection and the intermediate factors through which nimodipine exerts its beneficial effect after aneurysmal SAH.
--------------------------------------------------------------------------------
Cochrane Database Syst Rev. 2002;(4):CD000419.
Piracetam for acute ischaemic stroke.
Ricci S, Celani MG, Cantisani AT, Righetti E.
Stroke Service, USL 2, Via Guerra 17, 06127 Perugia, Italy. istitaly@unipg.it
BACKGROUND: Piracetam has neuroprotective and antithrombotic effects which may help to reduce death and disability in people with acute stroke. OBJECTIVES: The objective of this review was to assess the effects of piracetam in acute presumed ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Review Group Trials Register (last searched April 2001). In addition we searched the Cochrane Controlled Trials Register (Cochrane Library 2001, issue 2), MEDLINE (1966-April 2001), EMBASE (1980-April 2001), and ISI Science Citation Index (1981- April 2001). We also handsearched 15 journals and contacted the manufacturer to identify further published and unpublished studies. SELECTION CRITERIA: Randomised trials comparing piracetam with control, with at least mortality reported and entry to the trial within approximately 48 hours of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers extracted data and assessed trial quality and this was checked by the other two reviewers. Study authors were contacted for missing information. MAIN RESULTS: Three trials involving 1002 people were included, with one trial contributing 93% of the data. Participants" ages ranged from 40 to 85, and both sexes were equally represented. Piracetam was associated with a statistically non significant increase in death at one month (approximately 31% increase, 95% confidence interval 81% increase to 5% reduction). This trend was no longer apparent in the large trial after correction for imbalance in stroke severity. Limited data showed no difference between the treatment and control groups for functional outcome, dependency or proportion of patients dead or dependent. Adverse effects were not reported. REVIEWER"S CONCLUSIONS: There is some suggestion (but no statistically significant result) of an unfavourable effect of piracetam on early death, but this may have been caused by baseline differences in stroke severity in the trials. There is not enough evidence to assess the effect of piracetam on dependency.
Cochrane Database Syst Rev. 2001;(2):CD001011.
[Сообщение изменено пользователем 15.01.2007 23:08]
Ч
Чудеsная
Нам ортопед говорила, что эффект от массажа, параллельно с которым делают лечебные процедуры(парафин или эл-рэз) - заметен через 2 месяца. Вот так и лечимся, через каждые 2 месяца, так как после года это плохо лечится. Нельзя теперь давать большую нагрузку на ноги. А невропатолог и педиатр - не
направили вовремя к ортопеду. Пришлось вернуться к коляске да санкам, хотя с 10,5 месяцев, как пошла сама - так и ходили сами, врачи говорили, что больше ходить надо, а ортопед обратное сказал...позже намного.
Авторизуйтесь, чтобы принять участие в дискуссии.