Отправлено 27 Январь 2009 - 12:56
Есть, даже свежие. Но вот использовать не стоит.
Efficacy of piracetam in the treatment of tardive dyskinesia in schizophrenic patients: a randomized, double-blind, placebo-controlled crossover study. 2007 Jul;68(7):1031-7.Click here to read
Libov I, Miodownik C, Bersudsky Y, Dwolatzky T, Lerner V.
Division of Psychiatry, Ministry of Health, Be'er Sheva Mental Health Center; and the Faculty of Health Sciences, Ben-Gurion University of the Negev, Be'er-Sheva, Israel.
BACKGROUND: Piracetam is a potent antioxidant, a cerebral neuroprotector, a neuronal metabolic enhancer, and a brain integrative agent. More than 20 years ago, an intravenous preparation of piracetam demonstrated an improvement in the symptoms of tardive dyskinesia. The aim of our study was to reexamine the efficacy of piracetam in the treatment of tardive dyskinesia using an oral preparation. METHOD: The study was conducted at the Be'er Sheva Mental Health Center from May 2003 to December 2004 and involved a 9-week, double-blind, crossover, placebo-controlled trial assessing 40 DSM-IV schizophrenic and schizo-affective patients with DSM-IV-TR tardive dyskinesia. All study subjects received their usual antipsychotic treatment. Initially, subjects were randomly assigned to receive 4 weeks of treatment with either piracetam (4800 mg/day) or placebo. Thereafter, following a washout period of 1 week, they entered the crossover phase of the study for a further 4 weeks. The change in score of the Extrapyramidal Symptom Rating Scale from baseline to the study endpoint was the primary outcome measure. RESULTS: The mean decrease in score from baseline to endpoint in the clinical global impression subscale in patients treated with piracetam was 1.1 points compared to 0.1 points in the placebo group (p = .004). The mean decrease in the tardive parkinsonism subscale was 8.7 points in patients treated with piracetam and 0.6 points in those on placebo (p = .001). The mean decrease in the tardive dyskinesia subscale was 3.0 points in the piracetam group in contrast to deterioration of condition in the placebo group by -0.2 points (p = .003). CONCLUSION: Piracetam appears to be effective in reducing symptoms of tardive dyskinesia. The specific mechanism by which piracetam may attenuate symptoms of tardive dyskinesia needs to be further evaluated. CLINICAL TRIALS REGISTRATION: ClinicalTrials.gov identifier NCT00190008.
PMID: 17685739
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Curr Drug Targets CNS Neurol Disord. 2004 Jun;3(3):181-94.
AMPA receptor potentiators for the treatment of CNS disorders.
O'Neill MJ, Bleakman D, Zimmerman DM, Nisenbaum ES.
Eli Lilly and Co. Ltd., Lilly Research Centre, Erl Wood Manor, Windlesham, Surrey GU20 6PH, UK. Oneill_Michael_J@Lilly.com
Glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors mediate most of the excitatory neurotransmission in the mammalian central nervous system and also participate in forms of synaptic plasticity thought to underlie memory and learning, and the formation of neural networks during development. Molecular cloning techniques have shown that the AMPA receptor family is composed of four different subunits named GluR1-4 or GluRA-D (newly termed as Glu(A1)-Glu(A4)) and native AMPA receptors are most likely tetramers generated by the assembly of one or more of these subunits, yielding homomeric or heteromeric receptors. Additional complexity among AMPA receptors is conferred by alternative splicing of RNA for each subunit giving rise to flip and flop variants. Clinical and experimental data have suggested that positive modulation of AMPA receptors may be therapeutically effective in the treatment of cognitive deficits. Several classes of AMPA receptor potentiators have been reported, including pyrroliddones (piracetam, aniracetam), benzothiazides (cyclothiazide), benzylpiperidines (CX-516, CX-546) and more recently biarylpropylsulfonamides (LY392098, LY404187 and LY503430). These molecules enhance cognitive function in rodents, which appears to correlate with increased hippocampal activity. In addition, clinical studies have suggested that AMPA receptor modulators enhance cognitive function in elderly subjects, as well as patients suffering from neurological and psychiatric disorders. Several independent studies have suggested that AMPA receptors can increase BDNF expression by both calcium-dependent and independent pathways. For example, recent studies have shown that AMPA receptors interact with the protein tyrosine kinase, Lyn. Activation of Lyn can recruit the mitogen-activated protein kinase (MAPK) signalling pathway and increase the expression of BDNF. Therefore, in addition to directly enhancing glutamatergic synaptic transmission, AMPA receptor activation can increase the expression of BDNF in vitro and in vivo. This may account for activity of AMPA receptor potentiators in rodent models predictive of antidepressant activity (forced swim and tail suspension tests). The increase in neurotrophin expression also may contribute to the functional, neuroprotective and neurotrophic actions of LY404187 and LY503430 after infusion of 6-OHDA into the substantia nigra. In conclusion, several potent, selective and systemically active AMPA receptor potentiators have been reported. Data indicate that these molecules modulate glutamatergic transmission, enhance synaptic transmission, long-term potentiation (LTP) and increase neurotrophin expression. Therefore, these AMPA receptor potentiators offer an exciting new class of drugs with potential for treating (1) cognitive impairment associated with Alzheimer's disease and schizophrenia, (2) depression, (3) slowing the progression and potentially enhancing recovery from Parkinson's disease.
PMID: 15180479
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Miscellaneous treatments for neuroleptic-induced tardive dyskinesia.
Soares-Weiser KV, Joy C.
Department of Internal Medicine E, Rabin Medical Center, Beilison Campus, Petah Tikva, Israel, 49000. ksoares@netvision.net.il
BACKGROUND: Tardive dyskinesia is a disabling movement disorder associated with the prolonged use of neuroleptic medication. This review, one in a series examining the treatment of tardive dyskinesia, will cover miscellaneous treatments not covered elsewhere. OBJECTIVES: To determine whether the following interventions were associated with a reduction of neuroleptic induced tardive dyskinesia: botulin toxin, endorphin, essential fatty acid, EX11582A, ganglioside, insulin, lithium, naloxone, oestrogen, periactin, phenylalanine, piracetam, stepholidine, tryptophan, neurosurgery, or ECT. SEARCH STRATEGY: The initial search of Biological Abstracts (1982-1995), The Cochrane Schizophrenia Group's Register (January 1996), EMBASE (1980-1995), LILACS (1982-1996), MEDLINE (1966-1995) and PsycLIT (1974-1995) was updated by searching Cochrane Schizophrenia Group's Register in July 2002. References of all relevant studies were searched for further trial citations. Principal authors of trials were contacted. SELECTION CRITERIA: Studies were selected if they focused on people with schizophrenia or other chronic mental illnesses, with neuroleptic-induced tardive dyskinesia and compared the use of the interventions listed above versus placebo or no intervention. DATA COLLECTION AND ANALYSIS: Studies were reliably selected, quality assessed and data extracted. Data were excluded where more than 50% of participants in any group were lost to follow up. For binary outcomes a random effects risk ratio (RR) and its 95% confidence interval (CI) was calculated. Where possible, the weighted number needed to treat/harm statistic (NNT/H), and its 95% confidence interval (CI), was also calculated. For continuous outcomes, endpoint data were preferred to change data. Non-skewed data from valid scales were to have been synthesised using a weighted mean difference (WMD). MAIN RESULTS: Fifty-seven references describing 37 different trials were identified by the search strategy. Seven of these were included, 27 excluded, and three await assessment. Ceruletide was not clearly more effective than placebo (n=132, 2 RCTs, RR not any improvement in tardive dyskinesia 0.82 CI 0.6 to 1.1). This also applied to gamma-linolenic acid, although data were sparse (n=16, 1 RCT, RR no clinical improvement 1.00 CI 0.7 to 1.5), oestrogen (n=12, 1 RCT, RR no clinically important improvement 1.2 CI 0.8 to 1.7), and lithium (n=11, 1 RCT, RR no clinically important improvement 1.39 CI 0.6 to 3.1). Phenylalanine may even be detrimental (n=18, 1 RCT, MD AIMS score 4.40 CI 1.16 to 7.64). One small study (n=20) found that insulin was more likely to produce a clinical improvement in tardive dyskinesia than placebo (RR no clinical improvement 0.5 CI 0.3 to 0.9, NNT 2 CI 1 to 5). REVIEWER'S CONCLUSIONS: There is no strong evidence to support the everyday use of any of the agents included in this review. All results must be considered inconclusive and these compounds probably should only be used within the context of a well-designed evaluative study.
PMID: 12804390
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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. tangwk@cuhk.edu.hk
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.
PMID: 12394531
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Miscellaneous treatments for neuroleptic-induced tardive dyskinesia.
McGrath JJ, Soares KV.
Queensland Centre for Schizophrenia Research, Wolston Park Hospital, Brisbane, Queensland, Australia, Q4076. jjm@brain.wph.uq.oz.au
BACKGROUND: Tardive dyskinesia (TD) is a disabling movement disorder associated with the prolonged use of neuroleptic medication. This review, one in a series examining the treatment of tardive dyskinesia, will cover miscellaneous treatments not covered elsewhere. OBJECTIVES: The primary objective of this review was to determine whether the following interventions were associated with a reduction of TD in people with schizophrenia, or others chronic mental illnesses: botulin toxin, endorphin, estrogen, essential fatty acid, EX11582A, ganglioside, lithium, naloxone, periactin, phenylalanine, piracetam, stepholidine, tryptophan, neurosurgery, or ECT. SEARCH STRATEGY: Electronic searches of Biological Abstracts (1982-1995), Cochrane Schizophrenia Group's Register of trials (1995), EMBASE (1980-1995), LILACS (1982-1996), MEDLINE (1966-1995), PsycLIT (1974-1995), and SCISEARCH (1995) were undertaken. References of all identified studies were searched for further trial citations. Principal authors of trials were contacted. SELECTION CRITERIA: The inclusion criteria for all relevant randomised studies were that they should focus on people with schizophrenia or other chronic mental illnesses, with neuroleptic-induced TD and compare the use of the interventions listed above versus placebo or no intervention. DATA COLLECTION AND ANALYSIS: Forty references describing 31 different trials were identified by the search strategy. Of 31 trials, 15 trials were excluded, six trials were included, eight awaiting assessment and a further two trials are pending (awaiting translation, unable to locate). Data were independently extracted by each reviewer and the odds ratio or the average differences were estimated. The reviewers assumed that people who dropped out had no improvement. MAIN RESULTS: Data were available about the efficacy and safety of cerultide, essential fatty acids, estrogen, lithium and insulin. There was a significant improvement in TD associated with the use of insulin compared to placebo (OR = 0.04, 95%CI 0.01-0.24). No significant differences between the other compounds and placebo were identified. REVIEWER'S CONCLUSIONS: There is no strong evidence to support the use of any of the agents included in this review, however because of the small sample sizes, all results must be considered inconclusive. The association between low dose insulin and improvement of TD requires replication.
PMID: 10796325
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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
PMID: 10583700
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Piracetam in elderly psychiatric patients with mild diffuse cerebral impairment.
Chouinard G, Annable L, Ross-Chouinard A, Olivier M, Fontaine F.
In a 12-week double-blind study, piracetam at two dose levels (2.4 and 4.8 g/day) was compared to placebo in the treatment of 60 elderly psychiatric patients with mild diffuse cerebral impairment, but no signs of focal brain lesion. The psychiatric illness, schizophrenia or affective disorder, of patients selected was in remission at the time of the study. Monthly evaluations by the nurse revealed that piracetam improved overall functioning, particularly alertness, socialization, and cooperation, relative to the control group. Patients treated with 2.4 g/day piracetam also showed significant improvement in scores for the full IQ and the memory quotient on the Wechsler Adult Intelligence and Memory Scales; greater response was seen in those with lower initial scores. Piracetam at 4.8 g/day had a more rapid onset of action on behavioral variables than 2.4 g/day, but its therapeutic effect tended to diminish at 12 weeks, possibly as the result of overstimulation. Piracetam did not appear to interfere with concomitant psychotropic maintenance medication or affect the psychiatric illness itself.
PMID: 6415738
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Some effects of piracetam (UCB 6215, Nootropyl) on chronic schizophrenia.
Dimond SJ, Scammell RE, Pryce IG, Huws D, Gray C.
A study is described of effects of a nootropic drug on chronic schizophrenia. The nootropic drugs act on the central nervous system with the cerebral cortex as their target. Chronic schizophrenic patients on the drug showed improvement in object naming and in tests where the patient was required to indicate the number of times he had been tapped. Improvements were also noted in learning and memory tasks. In dichotic listening the patients showed a reduction in the amount of incorrect verbal responses produced. There were no improvements in symptom rating or social behaviour rating. These results suggest some cognitive improvement but little if any change in the disease state of the patient.
PMID: 116278
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Biological correlates of piracetam clinical effects in psychotic patients.
Kabes J, Erban L, Hanzlicek L, Skondia V.
The purpose of this controlled clinical trial was to demonstrate possible correlations between changes in bioenergetic metabolism and psychotropic drug administration in the treatment of functional psychosis. The study included twenty-six patients, eleven with schizophrenia, three with chronic atypical depression and twelve with drug-resistant endogenous depressions. All patients were kept on continuous psychotropic medication for at least 3 weeks before starting the trial, and piracetam was given additionally in a fixed dosage of 2400 mg daily; the same number of identical capsules was given during the pre- and post-treatment placebo periods. Psycho-pathological evaluation of the patients was by the BPRS; clinical and biochemical data were evaluated statistically by the analysis of regression. The results show that in schizophrenic patients an improvement was observed in those cases who had improved biochemically, i.e. where the ATP values had increased. In drug-resistant depressions there was a rapid and significant clinical improvement after piracetam co-administration, and this went in step with a significant rise in ATP levels.
PMID: 488520