|
|
| |
 |
Reviews |
|
Int J Neuropsychopharmacol. 2004 Jul 1;:1-19.
Evidence-based pharmacotherapy of Alzheimers disease.
Evans JG, Wilcock G, Birks J.
Cochrane Dementia and Cognitive Improvement Group, University of Oxford, UK.
Dementia is an acquired global impairment of cognitive capacities. Approximately 5% of people aged over 65 yr are affected by dementia, and some 70% of cases are thought to be due primarily to Alzheimers disease. Descriptions of the clinical manifestations of Alzheimers disease have been increasingly refined in the last decade but there is no diagnostic test for what remains fundamentally a pathologically defined condition. At the present time interventions for Alzheimers disease are limited to those that modify the manifestations of the disease, and foremost amongst the candidates available are the cholinesterase inhibitors. The rationale for the use of cholinergic drugs for Alzheimers disease lies in enhancing the secretion of, or prolonging the half-life of, acetylcholine in the brain. Several potential compounds have been tested, but short half-lives and a high incidence of cholinergic and other adverse effects have eliminated most. Only three are widely licensed for use, donepezil, galantamine and rivastigmine. Their efficacy is relatively modest. These drugs have been tested in 32 randomized, placebo-controlled trials. The trials assess cognitive function primarily, and in addition they may assess global function, activities of daily living, quality of life and behavioural disturbance typically over 3 or 6 months. The performance of each drug is summarized in a Cochrane review, a systematic review carried out according to strict guidelines. There was a significant benefit in favour of treatment compared with placebo for cognition and activities of daily living, but withdrawals due to adverse events were significantly higher for treatment than placebo for all three drugs. There is little evidence from direct comparisons between the three drugs. There are several economic analyses of the cost-effectiveness of these drugs, but the findings cannot be considered robust owing to inadequate data. A range of other pharmacological treatments have been tested, including selegiline, piracetam, vitamin E, Ginkgo biloba, anti-inflammatory drugs and hormone replacement therapy, but, so far, Cochrane reviews have not established the efficacy of these interventions for Alzheimers disease. A Cochrane review of memantine shows benefits on cognitive and global function of the same order of magnitude as seen for the cholinesterase inhibitors. Memantine has been licensed in Europe for treatment of patients with moderately severe to severe Alzheimers disease.
|
Br J Pharmacol. 2004 Jun;142(3):594-608.
Piracetam and TRH analogues antagonise inhibition by barbiturates, diazepam, melatonin and galanin of human erythrocyte D-glucose transport.
Naftalin RJ, Cunningham P, Afzal-Ahmed I.
Physiology Division, Centre for Vascular Biology and Medicine, Kings College London, Guys Campus, New Hunts House, London SE1 1UL.
1 Nootropic drugs increase glucose uptake into anaesthetised brain and into Alzheimer's diseased brain. Thyrotropin-releasing hormone, TRH, which has a chemical structure similar to nootropics increases cerebellar uptake of glucose in murine rolling ataxia. This paper shows that nootropic drugs like piracetam (2-oxo 1 pyrrolidine acetamide) and levetiracetam and neuropeptides like TRH antagonise the inhibition of glucose transport by barbiturates, diazepam, melatonin and endogenous neuropeptide galanin in human erythrocytes in vitro. 2 The potencies of nootropic drugs in opposing scopolamine-induced memory loss correlate with their potencies in antagonising pentobarbital inhibition of erythrocyte glucose transport in vitro (P<0.01). Less potent nootropics, D-levetiracetam and D-pyroglutamate, have higher antagonist Ki's against pentobarbital inhibition of glucose transport than more potent L-stereoisomers (P<0.001). 3 Piracetam and TRH have no direct effects on net glucose transport, but competitively antagonise hypnotic drug inhibition of glucose transport. Other nootropics, like aniracetam and levetiracetam, while antagonising pentobarbital action, also inhibit glucose transport. Analeptics like bemigride and methamphetamine are more potent inhibitors of glucose transport than antagonists of hypnotic action on glucose transport. 4 There are similarities between amino-acid sequences in human glucose transport protein isoform 1 (GLUT1) and the benzodiazepine-binding domains of GABAA (gamma amino butyric acid) receptor subunits. Mapped on a 3D template of GLUT1, these homologies suggest that the site of diazepam and piracetam interaction is a pocket outside the central hydrophilic pore region. 5 Nootropic pyrrolidone antagonism of hypnotic drug inhibition of glucose transport in vitro may be an analogue of TRH antagonism of galanin-induced narcosis.
|
Pediatr Neurol. 2004 Apr;30(4):254-6.
Levetiracetam in the treatment of Lennox-Gastaut syndrome.
De Los Reyes EC, Sharp GB, Williams JP, Hale SE.
University of Arkansas for Medical Sciences, Arkansas Childrens Hospital, Little Rock, Arkansas, USA.
Lennox-Gastaut syndrome is an epileptic encephalopathy characterized by multiple seizure types, mental retardation, and a slow spike-and-wave pattern on electroencephalography. Medical intractability is common. We identified a case series of six patients diagnosed with Lennox-Gastaut syndrome in which levetiracetam was initiated as add-on therapy for the management of seizures. At follow-up, four patients experienced 100% reduction of their myoclonic seizures; two patients had greater than 50% reduction of their atonic seizures, and four patients experienced 100% reduction in their generalized tonic-clonic seizures. Tonic seizures were not responsive to treatment. The most common side effect was irritability; the most positive change involved alertness. In this small sample, levetiracetam appeared effective in reducing seizures in Lennox-Gastaut syndrome. This preliminary study is limited by its retrospective design and small number of patients, but positive findings warrant a larger scale, multicenter study.
|
Headache. 2004 Mar;44(3):238-43.
Efficacy and safety of levetiracetam in pediatric migraine.
Miller GS.
Pediatric Neurology Department, Hillcrest Healthcare System, Childrens Medical Center, Tulsa, Okla. 74104, USA.
BACKGROUND: Headache is a frequent occurrence among children and adolescents. Chronic headaches can be severe and disabling, and require prophylactic treatment; however, additional data on the use of prophylactic medications for migraine in children are needed. OBJECTIVE: To review the efficacy and safety of levetiracetam (Keppra) in pediatric patients with a history of recurrent headache. DESIGN/METHODS: Data from 19 pediatric patients were retrospectively reviewed. The initial dose of levetiracetam was usually 125 or 250 mg twice daily, but varied depending upon clinical judgment. RESULTS: Charts of 9 girls and 10 boys (mean age, 11.9 years) were reviewed. A variety of medications, including triptans, had been used before initiating treatment with levetiracetam. Mean headache frequency before treatment was 6.3 per month (standard deviation [SD], 3.8; confidence interval [CI], 4.4 to 8.1). Duration of headaches ranged from 0.25 to 8 years. Migraine (63.2%) and migraine with aura (15.8%) were the most common types of headache reported. Most patients (89.5%) had headaches that were severe. After treatment, the mean headache frequency decreased to 1.7 per month (SD, 2.7; CI, 0.4 to 3.0), representing a reduction compared with baseline (P <.0001). Levetiracetam eliminated headaches in 10 patients (52.6%), and 7 patients (36.8%) had less severe and less frequent headaches. Levetiracetam did not have an effect on headaches in 2 patients (10.5%). Mean duration of treatment with levetiracetam was 4.1 months. Doses ranged from 125 to 750 mg twice daily. Sixteen patients (84.2%) reported no side effects on levetiracetam. One patient experienced asthenia/somnolence and dizziness, and irritable, hyperactive, and hostile behavior led to discontinuation of levetiracetam in another patient. A third patient experienced irritability and moodiness that attenuated after 1 month of treatment and did not require discontinuation. CONCLUSIONS: In this small retrospective review, levetiracetam was found to be generally well tolerated and appears to be a promising candidate for additional evaluation in well-controlled clinical trials of pediatric patients with migraine.
|
Dement Geriatr Cogn Disord 2002;13(4):217-24.
Clinical efficacy of piracetam in cognitive impairment: a meta-analysis.
Waegemans T, Wilsher CR, Danniau A, Ferris SH, Kurz A, Winblad B.
Research and Development, UCB SA (Pharma Sector), Braine-lAlleud, Belgium.
A meta-analysis has been performed including nineteen double blind, placebo controlled studies with piracetam in patients suffering from dementia or cognitive impairment in the elderly. These studies had as common outcome measure a clinical global impression of change, a measure of clinically meaningful improvement. The meta-analysis of this global outcome followed the methodology set forward by the Cochrane Collaboration. This article describes the studies, the patient populations and the methods of data extraction. The results of the meta-analysis demonstrate a difference between those individuals treated with piracetam and those given placebo, both as significant odds ratio and as a favourable number needed to treat. While there may be problems in meta-analyses and the interpretation of the statistical results, the results of this analysis provide compelling evidence for the global efficacy of piracetam in a diverse group of older subjects with cognitive impairment.
|
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.
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.
|
J ECT. 2002 Sep;18(3):130-7.
Effect of piracetam on ECT-induced cognitive disturbances: a randomized, placebo-controlled, double-blind study.
Tang WK, Ungvari GS, Leung HC.
Department of Psychiatry, Chinese University of Hong Kong, Hong Kong, SAR, China.
Electroconvulsive therapy (ECT) is still the fastest, most effective, and frequently life-saving therapeutic intervention in several forms of depression and some other psychiatric disorders. Transient memory disturbances are frequent after ECT. A randomized, double-blind, placebo-controlled study was conducted to investigate the effects of piracetam on ECT-induced confusion and memory disturbances. Thirty-eight consecutively admitted patients with depressive illness or schizophrenia requiring ECT were given either piracetam or an identical-looking placebo during the period of ECT treatment and for 2 weeks afterward. Daily dosage of piracetam was 7.2 g, given orally for the first 2 weeks while patients underwent ECT (loading phase), followed by 4.8 g for the rest of the study period. Participants were evaluated by standardized clinical rating scales and cognitive psychologic tests 1 to 2 days before ECT, 1 day after their third and sixth ECT treatments, and 2 weeks after they had completed their ECT courses. Piracetam had no significant effect in preventing ECT-induced memory disturbances. All clinical ratings were consistently, albeit not significantly, better in the piracetam group, suggesting that piracetam may have augmented the effects of ECT.
|
Cochrane Database Syst Rev. 2001;(2):CD001011.
Piracetam for dementia or cognitive impairment.
Flicker L, Grimley Evans G.
Royal Perth Hospital, University of Western Australia, Box X2213 GPO, Perth, WA, Australia, 6847.
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 rated for methodological quality by assessment of blinding and loss before analysis as described by Jadad et al. (1996). 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.
|
Stroke. 2000 Sep;31(9):2112-6.
Piracetam improves activated blood flow and facilitates rehabilitation of poststroke aphasic patients.
Kessler J, Thiel A, Karbe H, Heiss WD.
Max-Planck-Institute for Neurological Research, Cologne, Germany.
BACKGROUND AND PURPOSE: In a prospective, double-blind, placebo-controlled study, it was investigated whether piracetam improves language recovery in poststroke aphasia assessed by neuropsychological tests and activation PET measurement of cerebral blood flow. METHODS: Twenty-four stroke patients with aphasia were randomly allocated to 2 groups: 12 patients received 2400 mg piracetam twice daily, 12 placebo. Before and at the end of the 6-week treatment period in which both groups received intensive speech therapy, the patients were examined neuropsychologically and studied with H(2)(15)O PET at rest and during activation with a word-repetition task. Blood flow was analyzed in 14 language-activated brain regions defined on reconstructed surface views from MRI coregistered to the PET images. RESULTS: Before treatment, both groups were comparable with respect to performance in language tasks and to type and severity of aphasia. In the piracetam group, increase of activation effect was significantly higher (P:<0.05) in the left transverse temporal gyrus, left triangular part of inferior frontal gyrus, and left posterior superior temporal gyrus after the treatment period compared with the initial measures. The placebo group showed an increase of activation effect only in the left vocalization area. In the test battery, the piracetam group improved in 6 language functions, the placebo group only in 3 subtests. CONCLUSIONS: Piracetam as an adjuvant to speech therapy improves recovery of various language functions, and this effect is accompanied by a significant increase of task-related flow activation in eloquent areas of the left hemisphere.
|
Orv Hetil. 2000 May 28;141(22):1189-93.
Cognitive enhancement effect of piracetam in patients with mild cognitive impairment and dementia.
Tariska P, Paksy A.
Memoria Klinika, Orszagos Pszichiatriai es Neurologiai Intezet, Budapest.
Effectiveness and tolerability of two piracetam-containing drugs were compared in the frame of an open, multicentre, Phase-IV, prospective study with group and self control carried out in 9 Hungarian centres in 1998. Patients with cognitive decline from Alzheimer's disease and/or cerebrovascular origin have received the drug, in the first 4 weeks in 4800, later 2400 mg daily doses. One hundred four patients finished the study. No relevant difference with statistically significant degree was registered between the two groups. Based on this fact in this study data of the 104 patients were examined together. Authors examined two problems. The first: on which cognitive function is more effective the drug. Five factors of the modified Mini-Mental State Examination were separated and compared. Nearly all of them significantly increased especially the factors of memory, and concentration-psychomotor speed. The second examined field: are there certain subgroups with prognostic value about the effectiveness of piracetam treatment. Neither the duration of the illness, nor etiologic diagnosis, severity of cognitive decline, or former treatment with piracetam did influence significantly the efficacy. In case of depressive symptoms such connection was established: the more pronounced the severity of these symptoms the higher improvement can be expected in cognitive functions. This was also stressed by the logistic regression analysis. Authors described an original evaluation method of the trail-making test, which could widen the application of this popular test in psychopharmacologic studies. Final conclusions: the cognitive enhancer effect of piracetam appeared in a few weeks. This treatment could be effective even in Alzheimer's disease, in case of more pronounced cognitive decline, longer duration of the illness, and in case of former piracetam treatment as well. The degree of cognitive improvement was most pronounced in patients with comorbid depressive symptoms.
|
J Neural Transm. 1999;106(7-8):757-61.
Piracetam reverses hippocampal membrane alterations in Alzheimers disease.
Eckert GP, Cairns NJ, Muller WE.
Department of Pharmacology, Biocenter, University of Frankfurt, Federal Republic of Germany.
The in vitro effects of piracetam treatment on the fluidity of membranes from the hippocampus of Alzheimer's Disease patients (AD) and non-demented controls were studied. Hippocampal membranes of AD patients showed a significant lower hydrocarbon core fluidity compared with membranes from elderly non-demented controls. Preincubation with piracetam enhanced the hydrocarbon core fluidity of hippocampal membranes from AD-patients as well as elderly controls in a concentration depending fashion, although the effect was more pronounced for the AD membranes. In the presence of piracetam, the difference of the membrane fluidity between AD and control membranes was not longer apparent.
|
J Clin Pharm Ther. 1999 Oct;24(5):369-74.
Piracetam in the treatment of schizophrenia: implications for the glutamate hypothesis of schizophrenia.
Noorbala AA, Akhondzadeh S, Davari-Ashtiani R, Amini-Nooshabadi H.
Roozbeh Psychiatric Hospital, Tehran University of Medical Sciences, Tehran, Iran.
OBJECTIVE: There is a growing interest in investigating the role of glutamate receptors in the pathophysiology of schizophrenia. Indeed, the hyperdopaminergic theory of schizophrenia can explain only the positive symptoms of schizophrenia, whereas the glutamate hypothesis may provide a more comprehensive view of the illness. We undertook a trial to investigate whether the combination of haloperidol with piracetam, a nootropic agent which modulates the glutamate receptor positively was more effective than haloperidol alone. METHODS: Thirty patients who met the DSM IV criteria for schizophrenia completed the study. Patients were allocated in a random fashion, 14 to haloperidol 30 mg/day plus piracetam 3200 mg/day and 16 to haloperidol 30 mg/day plus placebo. RESULTS: Although both protocols significantly decreased the score of the positive symptoms, the negative symptoms, the general psychopathological symptoms and the total score of PANSS scale over the trial period, the combination of haloperidol and piracetam showed a significant superiority over haloperidol alone in the treatment of schizophrenic patients. CONCLUSION: Piracetam, a member of the nootropic class of drugs and a positive modulator of glutamate receptor, may be of therapeutic benefit in treating schizophrenic patients in combination with typical neuroleptics. However, a larger study to confirm our results is warranted.
|
Zh Nevrol Psikhiatr Im S S Korsakova. 1997;97(10):29-34.
Nootropil in the treatment of disorders of the higher mental functions in patients with an ischemic stroke.
Burd GS, Gekht AB, Bogolepova AN, Buklina SB.
47 patients with acute ischemic stroke were treated with nootropil (pyracetam, UCB, Belgium) from the first day of the disease (12 g, intravenously, by drops during 2 weeks, then 4.8 g, per os) on the background of basic therapy. There was revealed increase of spontaneous activity, expressive and impulsive speech, audio- and speaking memory (especially delayed memory), tactile, acoustic and visual gnosis, space praxis. There was observed more pronounced positive dynamics of functions of damaged hemisphere in patients with localisation of ischemic focus in left hemisphere. Meanwhile restoration was slower when ischemic focus was localized in right hemisphere. Restoration of high mental functions occurred to be faster during nootropil treatment as compared with basic therapy only. The conclusion was made that nootropil can be prescribed for the patients with hemispheric ischemic stroke and especially for the patients with alterations of cerebral circulation in system of internal carotid artery including such disturbances on the background of insufficiency of circulation in vertebrobasilar system.
|
Klin Med (Mosk). 1989 May;67(5):36-8.
Experience using nootropil in patients with chronic ischemic heart disease.
Shubina TI, Zaitsev VP.
Course nootropil treatment was conducted in 34 IHD patients with neurotic and neurotic-like diseases. Dynamic changes in the psychic state were assessed by the clinical scale and the MMPI psychological test. Significant improvement or normalization of the psychic state was achieved in 58.8 per cent of the patients treated with nootropil. The best results were obtained in the treatment of asthenic states. Administration of nootropil had no influence on the incidence of angina pectoris attacks and produced no side effects.
|
Epilepsy Behav. 2004 Dec;5(6):878-83.
Levetiracetam for people with mental retardation and refractory epilepsy.
Kelly K, Stephen LJ, Brodie MJ.
Epilepsy Unit, Division of Cardiovascular and Medical Sciences, Western Infirmary, Glasgow G11 6NT, Scotland, UK.
Levetiracetam (LEV) is a novel antiepileptic drug (AED) with efficacy against a wide range of seizures types. The aim of this observational study was to assess its effectiveness in patients with mental retardation and refractory epilepsy. Sixty-four patients were started on adjunctive LEV after a 3-month baseline. LEV was initially dosed at 250 mg daily and increased by 250 mg every 2 weeks thereafter according to clinical response. Caregivers rated the patient's sleep, appetite, alertness, and behavior as poor (1), reasonable (2), or good (3) at each clinic visit. Patients were reviewed until one of four endpoints was reached: seizure freedom for at least 6 months, > or = 50% reduction in seizure frequency (responder) over a 6-month period, <50% reduction in seizure frequency (marginal effect) over a 6-month period, or LEV withdrawal due to lack of efficacy, adverse effects, or both. Twenty-four (38%) patients became seizure-free, 10 of whom were controlled on LEV 250 mg twice daily. An additional 18 (28%) patients were classified as responders, and 8 (12%) reported only marginal benefit from adjunctive LEV. Fourteen (22%) patients discontinued LEV (6 worsening seizures, 1 lack of efficacy, 7 adverse effects). Caregivers rated combined sleep, appetite, alertness, and behavior scores as "improved" at the end of follow-up (P<0.001). LEV improved seizure control in the majority of patients with mental retardation and may also have enhanced their quality of life.
|
Thromb Res. 1995 Jun 15;78(6):469-82.
The treatment of severe or recurrent deep venous thrombosis. Beneficial effect of the co-administration of antiplatelet agents with or without rheological effects, and anticoagulants.
Moriau M, Lavenne-Pardonge E, Crasborn L, von Frenckell R, Col-Debeys C.
Department of Internal Medicine, Haematology Division, Haemostasis and Thrombosis Unit, University of Louvain (UCL), St.-Luc University Clinics, Brussels, Belgium.
Deep venous thromboses can be divided into two groups according to their pathogenesis, anatomical features and differing responses to therapy. The first and most frequent consists of so-called simple venous thrombosis while the second group, which is less common, comprises severe or recurrent venous thrombosis characterised by a multifactorial pathogenesis, a mixed thrombus rich in platelets and by an incomplete response to both prophylactic and therapeutic treatment with anticoagulants (heparin or vitamin K antagonist). In a randomized, prospective blind study in patients with severe or recurrent venous thrombosis, which included 6 groups each of 100 patients, co-administration of anticoagulants with various types of antiplatelet agent, either with rheological effects (piracetam, buflomedil, pentoxifylline) or without them (dipyridamole), has shown a beneficial potentiating antithrombotic effect with those drugs possessing rheological effects and the absence of this effect with dipyridamole.
|
| |
|
Drug information |
|
| Brand name: Vinpotropile is a combination of Vinpocetine (with cerebro protecting properties) and Piracetam (with nootropic properties). Such combination synergize effects of Vinpocetine and Piracetam.
1. Pharmacology: Vinpocetine oxygenate and activate cerebral metabolism and it has several possible actions, including increasing cerebral blood flow and metabolism, anticonvulsant, cognition enhancement, neuroprotection and antioxidant. Vincamine, the parent compound of vinpocetine, is believed to be a cerebral vasodilator. Several mechanisms have been proposed for the possible actions of vinpocetine. Vinpocetine has been reported to have calcium-channel blocking activity, as well as voltage-gated sodium channel blocking activity. It has also been reported to inhibit the acetylcholine release evoked by excitatory amino acids and to protect neurons against excitotoxicity. In addition, vinpocetine has been shown to inhibit a cyclic GMP phosphodiesterase, and it is speculated that this inhibition enhances cyclic GMP levels in the vascular smooth muscle, leading to reduced resistance of cerebral vessels and increase of cerebral flow. In some studies, vinpocetine has demonstrated antioxidant activity equivalent to that of vitamin E. Piracetam is a smart-drug or nootropic. Nootropic means "acting on the mind". It is a term first used by Dr. Giurgea to describe a substance found to have useful effects in the treatment of memory loss, age related memory decline and lack of concentration etc. That substance was piracetam, not only was it beneficial, but it was also found to have so few side effects and contraindications that one biochemist described it; "as safe as salt!" Since then, nootropics have so-many beneficial affects on mental and memory capabilities, which they have come to be known as smart-drugs. One of the primary differences between nootropics and other "memory enhancers" is that nootropics have a beneficial effect upon the brain's Corpus Callosum. This area of the brain joins the two hemispheres, it links the logical side with creative side, hence ying and yang. This may be the major reason why "creative" individuals and "brain" workers find they can accomplish much more, when they are supplementing with nootropics.
2. Indications for usage: psychic or neurological symptoms of cerebral circulatory disturbances of various origins (post-apoplectic, post-traumatic or sclerotic) such as impaired memory, mobility disorders, vertigos and headaches.
Intermittent cerebrovascular insufficiency, vascular spasms, ischemic cerebral lesions, advanced cerebral arteriosclerosis.
Cerebro-vascular disease; degenerative cortical dementia (Alzheimer's disease);
Senile psychoorganic syndrome ("aging brain");
Cortical myoclonia; dyslexia of vascular and other origin; vestibulopathies;
Protection of the nervous tissue in a brain hypoxia; postoperative deliriums.
3. Indications limits, counter-indications: pregnancy, lactation.
4. Side effects: slight decrease in blood pressure, rarely tachycardia and extrasystole. Prolongs the excitability time of the ventricle (QT Time).
Caution! Before starting to take this medicine, it is vital that you should consult your doctor! Do not use it on your own initiative, without medical advice.
|
| |
|
Order now ! |
|
Dosage |
Packing |
Price |
Pay now |
Vinpocetine (5 mg), Piracetam (400 mg) |
50 tab |
USD 29.00 |
|
Vinpocetine (5 mg), Piracetam (400 mg) |
150 tab |
USD 79.00 |
|
|
|
| |
|  
|
|
