Use Of Piracetam Research Articles

Treatment Efficacy of Pharmacotherapies for Frontotemporal Dementia: A Network Meta-Analysis of Randomized Controlled Trials

The neuropsychiatric symptoms of frontotemporal dementia (FTD) have a profound negative impact on disease outcomes and care burden. Available pharmacotherapies might be supported by small-scale randomized controlled trials (RCTs); however, clinical recommendations might not be conclusive. We systematically searched several databases from inception to April 30, 2022, for RCTs of drug therapy in patients with FTD and neuropsychiatric symptoms (primary outcome). Secondary outcomes included changes in caregiver stress, daily interactive activities, cognitive function, and acceptability (adverse event or dropout rates). The network meta-analysis (NMA) procedure was performed under the frequency model, showing effect sizes as standardized mean differences (SMD) or odds ratios (OR) with 95% confidence intervals (95% CIs). Seven RCTs with 243 participants were included. Compared with placebo, high-dose oxytocin (72 international units) was associated with the greatest improvement in patients' neuropsychiatric symptoms (SMD=-1.17, 95% CIs=-2.25 to -0.08, z=-2.10, p=0.035). Piracetam significantly worsened neuropsychiatric symptoms (SMD=3.48, 95% CIs=1.58 to 5.37, z=3.60, p < 0.001) and caregiver stress (SMD=2.40, 95% CIs=0.80-4.01, z=2.94, p=0.003). Trazodone had significantly higher rates of adverse events (OR=9.53, 95% CIs=1.85-49.20, z=2.69, p=0.007). No pharmacological intervention significantly benefited cognitive function. This study provides the first NMA for clinical recommendation to support the use of high-dose oxytocin and caution regarding the use of piracetam for neuropsychiatric symptoms in patients with FTD.

A Comparative Study of the Effectiveness of Anticonvulscants in the Treatment of Tinnitus

Introduction: Tinnitus is defined perception of an audiological sensory impulse in the absence of any external force. There are various causes considered for the pathophysiology of tinnitus but none are established. Carbamazepine is a commonly used anti-epileptic drug that functions by depressing the CNS response to excitatory stimuli. Gamma aminobutyric acid (GABA) is the major inhibitory neurotransmitter throughout the central nervous system and is also expressed in the inner ear. Piracetam is a commonly used anti-epileptic that is known to increase cerebral blood flow and perfusion. Methods: A group of 80 patients were evaluated by taking a detailed history and a subjective assessment of the tinnitus using Tinnitus Handicap Inventory Questionnaire. The patients were followed up for 3 months and were assessed with Pure Tone Audiometry both pre and post treatment to evaluate which drug is better. The patients were randomized into 3 groups and one control group. Each group consisted of 20 patients. Results: The study consisted of 46 males and 34 females. A significant difference was seen when the results of group A and C were compared with p-value 0.00512, 0.00512 and 0.0083 and U value 0, 0 and 1 showing improvement from severe to moderate, moderate to mild and mild to normal. A comparison of group A and D showed a significant change from severe to moderate, moderate to mild and mild to normal with p-value 0.00512, 0.00512 and 0.0512 respectively and U values 0, 0 and 0 respectively. Conclusions: In our study, we concluded that use of Piracetam helps in reducing tinnitus and the treatment should continue as long it persists. Thus, Piracetam and Gabapentin are effective as a modality of treatment in suppressing tinnitus according to this study. We hope that our outcomes will be helpful for patients suffering from chronic tinnitus.

Актуальні питання нейрореабілітації в бійців ООС та в потерпілих мирної території після черепно-мозкової травми

Traumatic brain injury remains one of the most urgent problems of modern medicine, and its consequences are not only a medical, but also a socio-economic problem. Despite the study of clinical, structural-morphological, biochemical, neurophysiological, hemodynamic changes in patients who have suffered traumatic brain injury, it does not give up its leading position among the causes of disability in young and middleaged people, the most active in the labor and social sense of the population. An in-depth study of the distant period of traumatic brain injury is necessary, due to the high percentage of its consequences, and the lack of a correlation between the clinical symptoms of acute and distant periods of brain injury. Purpose of study. The purpose of the stydy is to learn about the effects of entrop and piracetam on structural and morthological, biochemical, neurophysiological, hemodynamical processes in brain to improve the results of an integrated treatment of a mild Traumatic Brain Injury (concussion) when ensuring rehabilitative measures in the remote period of time. Content. Inspected 82 civilians and 82 JFO combatants with mild TBI in the remote period of time. All patients were males. The dynamic of functioning brain state has been studied using the electroencephalography data. Cerebral blood flow has been studied using the ultrasonic dopplerography method and characteristic of the cognitive disorders by MMSE. Results. In the remote period of time the use of piracetam and entrop in the integrated treatment of patients with mild TMI has positively affected the EEG and cognitive functions trends. The study results have shown that the cerebral hemodynamic didn`t change sighnificantly after adding piracetam and entrop to the standart treatment protocol. These researches on patientsd by MMSE scale confirmed anti-amnestic focus of pharmacotherapeutic effect in both nootropic drugs (piracetam and enthrop) in aspect of impact on cognitive dissfunction. To summarize. Treatment of patients with mild TBI in remote period with usage of piracetam and entrop demonstrates the multimodal effect of these drugs on CNS, their great pharmaceutical potential and contributes to the effectiveness of neurorehabilitation measures, which improve quality of life of patients, who had brain injuries.

Experimental substantiation of the expediency of the combined use of piracetam and metformin for pharmacological correction of cognitive disorders in conditions of prolonged hyperglycemia

Experimental substantiation of the expediency of the combined use of piracetam and metformin for pharmacological correction of cognitive disorders in conditions of prolonged hyperglycemia

Piracetam attenuates binge eating disorder related symptoms in rats

Binge eating disorder (BED) is a stress-related disorder characterized by acute episodes of excessive food intake. Piracetam, a nootropic agent has been reported to show several other neuropharmacological properties. The present study, evaluated the pharmacological effect of piracetam (200 mg/kg i.p.) on BED in female rats, induced by free access to palatable cookies for 2 h on alternate days. BED was confirmed by an increase in binge eating behavior and weight gain. BED leads to anxiety, cognitive and memory deficits, as evaluated by EPM (Elevated plus maze), OFT (open field test), and Y-maze tests. Increased levels of plasma corticosterone (CORT), glutamate in nucleus accumbens (NAC), hypothalamus (HYP) and prefrontal cortex (PFC) indicate stress and excitotoxicity. Moreover, it was observed that the levels of dopamine were higher in NAC and PFC, and less in HYP which may be responsible for motivational behavior for palatable feeding and cognitive deficits. More surprisingly, feeding behaviour regulating hormones namelyleptin was increased and ghrelin level was decreased in BED. Further, level of acetylcholine which regulates cognitive behaviour was compromised in BED. Piracetam significantly decreased binge eating behavior and associated body weight and regulated the levels of concerned neurotransmitters in respective regions. However, piracetam did not alter normal feeding behavior in the fast-refed model. Further, piracetam showed brain region-specific decrease in vascular endothelial growth factor expression. Piracetam showed anxiolytic activity and also alleviated cognitive deficit observed in BED. Hence, preclinical evidence indicates the potential use of piracetam for the treatment of BED.

Pharmacokinetic Study of Piracetam in Focal Cerebral Ischemic Rats.

Cerebral ischemia affects hepatic enzymes and brain permeability extensively. Piracetam was investigated up to phase III of clinical trials and there is lack of data on brain penetration in cerebral ischemic condition. Thus, knowledge of the pharmacokinetics and brain penetration of piracetam during ischemic condition would aid to improve pharmacotherapeutics in ischemic stroke. Focal cerebral ischemia was induced by middle cerebral artery occlusion for 2h in male Wistar rats followed by reperfusion. After 24h of middle cerebral artery occlusion or 22h of reperfusion, piracetam was administered for pharmacokinetic, brain penetration, and pharmacological experiments. In pharmacokinetic study, blood samples were collected at different time points after 200-mg/kg (oral) and 75-mg/kg (intravenous) administration of piracetam through right external jugular vein cannulation. In brain penetration study, the cerebrospinal fluid, systemic blood, portal blood, and brain samples were collected at pre-designated time points after 200-mg/kg oral administration of piracetam. In a separate experiment, the pharmacological effect of the single oral dose of piracetam in middle cerebral artery occlusion was assessed at a dose of 200mg/kg. All the pharmacokinetic parameters of piracetam including area under curve (AUC0-24), maximum plasma concentration (C max), time to reach the maximum plasma concentration (t max), elimination half-life (t 1/2), volume of distribution (V z), total body clearance, mean residence time, and bioavailability were found to be similar in ischemic stroke condition except for brain penetration. Piracetam exposure (AUC0-2) in brain and CSF were found to be 2.4- and 3.1-fold higher, respectively, in ischemic stroke compared to control rats. Piracetam significantly reduced infarct volume by 35.77% caused by middle cerebral artery occlusion. There was no change in the pharmacokinetic parameters of piracetam in the ischemic stroke model except for brain penetration. This indicates that variables influencing brain penetration may not be limiting factors for use of piracetam in ischemic stroke.

Heroin-piracetam mixture: Suggested mechanisms of action and risks of misinterpretation for drug users.

Piracetam is a positive allosteric modulator of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor that has been frequently used in the treatment of cognitive disorders. Press and internet reports indicate that the use of piracetam, as a heroin adulterant, has spread rapidly in some countries, especially in Asia and Europe. Its use, as adulterant, is believed to produce more profound desirable effects, while decreasing hangover. Recent surveys demonstrated that piracetam protects neurons from heroin-induced apoptosis. The protective role of this adulterating substance may be related to restoration of beta-endorphin levels and to its neuroprotective effects. The aim of this paper is to review the relevant literature and suggest the main hypothetical mechanisms that justify its use as a heroin adulterant, try to understand if its use could help people who want to come off heroin by reducing withdrawal symptoms and, finally, give useful information that permit us to understand why drug trafficking organisations started to use piracetam as heroin adulterant.

Piracetam Attenuates LPS-Induced Neuroinflammation and Cognitive Impairment in Rats.

The present study was performed to investigate the effect of piracetam on neuroinflammation induced by lipopolysaccharide (LPS) and resulting changes in cognitive behavior. Neuroinflammation was induced by a single dose of LPS solution infused into each of the lateral cerebral ventricles in concentrations of 1μg/μl, at a rate of 1μl/min over a 5-min period, with a 5-min waiting period between the two infusions. Piracetam in doses of 50, 100, and 200mg/kg i.p. was administered 30min before LPS infusion and continued for 9days. On ninth day, the behavioral test for memory and anxiety was done followed by blood collection and microdissection of the hippocampus (HIP) and prefrontal cortex brain regions. Piracetam attenuated the LPS-induced decrease in coping strategy to novel environment indicating anxiolytic activity. It also reversed the LPS-induced changes in the known arm and novel arm entries in the Y-maze test indicating amelioration of spatial memory impairment. Further, piracetam moderated LPS-induced decrease in the mitochondrial complex enzyme activities (I, II, IV, and V) and mitochondrial membrane potential. It ameliorated changes in hippocampal lipid peroxidation and nitrite levels including the activity of superoxide dismutase. Piracetam region specifically ameliorated LPS-induced increase in the level of IL-6 in HIP indicating anti-neuroinflammatory effect. Further, piracetam reduced HIP Aβ (1-40) and increased blood Aβ level suggesting efflux of Aβ from HIP to blood. Therefore, the present study indicates preclinical evidence for the use of piracetam in the treatment of neuroinflammatory disorders.

Analgesic effect of piracetam on peripheral neuropathic pain induced by chronic constriction injury of sciatic nerve in rats.

Despite immense advances in the treatment strategies, management of neuropathic pain remains unsatisfactory. Piracetam is a prototype of nootropic drugs, used to improve cognitive impairment. The present study was designed to investigate the effect of piracetam on peripheral neuropathic pain in rats. Neuropathic pain was induced by the chronic constriction injury of the sciatic nerve. Following this, piracetam was intraperitoneally administered for 2weeks in doses of 50, 100 and 200mg/kg, and pain was assessed by employing the behavioural tests for thermal hyperalgesia (hot plate and tail flick tests) and cold allodynia (acetone test). After the induction of neuropathic pain, significant development of thermal hyperalgesia and cold allodynia was observed. The administration of piracetam (50mg/kg) did not have any significant effect on all the behavioural tests. Further, piracetam (100mg/kg) also had no effect on the hot plate and tail flick tests; however it significantly decreased the paw withdrawal duration in the acetone test. Piracetam in a dose of 200mg/kg significantly modulated neuropathic pain as observed from the increased hot plate and tail flick latencies, and decreased paw withdrawal duration (in acetone test). Therefore, the present study suggests the potential use of piracetam in the treatment of neuropathic pain, which merits further clinical investigation.

Ameliorative Impact of Piracetam on Cognitive Dysfunction Associated with Animal Model of Alzheimer's Disease

Most of the current evidence for the impact of piracetam on memory consolidation originates from animal and human studies. However, the exact mechanism that underlies memory improvement is yet to be determined. The effects of piracetam pre-treatment on scopolamine induced cognitive dysfunction was examined. In the elevated plus maze, piracetam administration protected against the deterioration of short-term and long-term memory in scopolamine treated rats. Molecular experiments from tissue homogenate of cerebral cortex and hippocampus indicated that the marked decrease of the reduced glutathione activity in scopolamine treated rats was prevented by the use of piracetam Taken together, the current study suggests that piracetam protects learning and memory impairment induced by scopolamine through restoring the anti-oxidant activity into the normal level.

In people with acute ischemic stroke, is there randomized controlled trial evidence to support the use of piracetam?

In people with acute ischemic stroke, is there randomized controlled trial evidence to support the use of piracetam?

Ginkgo Biloba Extract and Long-Term Cognitive Decline: A 20-Year Follow-Up Population-Based Study

BackgroundNumerous studies have looked at the potential benefits of various nootropic drugs such as Ginkgo biloba extract (EGb761®; Tanakan®) and piracetam (Nootropyl®) on age-related cognitive decline often leading to inconclusive results due to small sample sizes or insufficient follow-up duration. The present study assesses the association between intake of EGb761® and cognitive function of elderly adults over a 20-year period.Methods and FindingsThe data were gathered from the prospective community-based cohort study ‘Paquid’. Within the study sample of 3612 non-demented participants aged 65 and over at baseline, three groups were compared: 589 subjects reporting use of EGb761® at at least one of the ten assessment visits, 149 subjects reporting use of piracetam at one of the assessment visits and 2874 subjects not reporting use of either EGb761® or piracetam. Decline on MMSE, verbal fluency and visual memory over the 20-year follow-up was analysed with a multivariate mixed linear effects model. A significant difference in MMSE decline over the 20-year follow-up was observed in the EGb761® and piracetam treatment groups compared to the ‘neither treatment’ group. These effects were in opposite directions: the EGb761® group declined less rapidly than the ‘neither treatment’ group, whereas the piracetam group declined more rapidly (β = −0.6). Regarding verbal fluency and visual memory, no difference was observed between the EGb761® group and the ‘neither treatment’ group (respectively, β = 0.21 and β = −0.03), whereas the piracetam group declined more rapidly (respectively, β = −1.40 and β = −0.44). When comparing the EGb761® and piracetam groups directly, a different decline was observed for the three tests (respectively β = −1.07, β = −1.61 and β = −0.41).ConclusionCognitive decline in a non-demented elderly population was lower in subjects who reported using EGb761® than in those who did not. This effect may be a specific medication effect of EGb761®, since it was not observed for another nootropic medication, piracetam.

Piracetam treatment in patients with cognitive impairment

Piracetam is a cognitive-enhancing agent that is used for the treatment of cognitive impairments of various etiologies. Little is known about its side effect profile, especially in those with psychiatric illness. We herewith present two cases with cognitive impairment who had contrasting responses to piracetam. One of them with organic amnestic syndrome had significant improvement, whereas the other who had an organic personality change as well as a family history of mental illness had significant worsening of behavioral problems after piracetam was introduced. This report highlights the need for caution in the use of piracetam, especially in those with past or family history of psychiatric illness.

Piracetam for fetal distress in labour

Piracetam is thought to promote the metabolism of brain cells when they are hypoxic. It has been used to prevent adverse effects of fetal distress. The objective of this review was to assess the effects of piracetam for suspected fetal distress in labour on method of delivery and perinatal morbidity. We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (15 February 2012). Randomised trials of piracetam compared with placebo or no treatment for suspected fetal distress in labour. Both review authors assessed eligibility and trial quality. One study of 96 women was included. Piracetam compared with placebo was associated with a trend to reduced need for caesarean section (risk ratio 0.57, 95% confidence interval 0.32 to 1.03). There were no statistically significant differences between the piracetam and placebo group for neonatal morbidity (measured by neonatal respiratory distress) or Apgar score. There is not enough evidence to evaluate the use of piracetam for fetal distress in labour.

Vertigo in neurological practice (common problems of diagnosis and treatment)

Most patients with vertigo seek neurological advice. In spite of the availability of current examination techniques, a differential diagnosis of vertigo is not frequently made. The paper discusses the terminology and classification of vertigo and clinical methods for diagnosing central and peripheral vestibulopathies. It considers the common problems of management of patients with diseases of the central and peripheral vestibular systems, the use of piracetam and other drugs to stimulate rehabilitation.

Does long term use of piracetam improve speech disturbances due to ischemic cerebrovascular diseases?

Aphasia causes significant disability and handicap among stroke survivors. Language therapy is recommended for aphasic patients, but not always available. Piracetam, an old drug with novel properties, has been shown to have mild beneficial effects on post-stroke aphasia. In the current study, we investigated the effects of 6 months treatment with piracetam on aphasia following stroke. Thirty patients with first-ever ischemic strokes and related aphasia were enrolled in the study. The scores for the National Institutes of Health Stroke Scale (NIHSS), Barthel Index (BI), modified Rankin Scale (mRS), and Gülhane Aphasia Test were recorded. The patients were scheduled randomly to receive either 4.8 g piracetam daily or placebo treatment for 6 months. At the end of 24 weeks, clinical assessments and aphasia tests were repeated. The level of improvement in the clinical parameters and aphasia scores was compared between the two groups. All patients had large lesions and severe aphasia. No significant difference was observed between the piracetam and placebo groups regarding the improvements in the NIHSS, BI and mRS scores at the end of the treatment. The improvements observed in spontaneous speech, reading fluency, auditory comprehension, reading comprehension, repetition, and naming were not significantly different in the piracetam and placebo groups, the difference reached significance only for auditory comprehension in favor of piracetam at the end of the treatment. Piracetam is well-tolerated in patients with post-stroke aphasia. Piracetam taken orally in a daily dose of 4.8 g for 6 months has no clear beneficial effect on post-stroke language disorders.

VITEFFECT OF NOOTROPIC AND NEUROPROTECTOR PRODUCTS PROPERTIES OF ENERGY METABOLISM PROCESSES AND MANIFESTATIONS OF MITOCHONDRIAL DYSFUNCTION IN THE NEURONS OF THE MAIN BRAIN OF RATS WITH ALOXAN DIAMIN D STATUS IN ADOLSECENTS WITH TYPE 1 DIABETES MELLITUS

In experimental studies in rats with chronic alloxan-induced hyperglycemia, it was found that the use of piracetam for 20 days,&#x0D; pramiracetam and ginkgo biloba extract to varying degrees help to reduce the effects of mitochondrial dysfunction and energy deficiency in brain neurons. The basis of these mechanisms is the prevention of mitochondrial opening&#x0D; cyclosporine-A-sensitive pores, reduction of mitochondrial transmembrane potential and increase of synthesis of macroergic phosphates. The most important&#x0D; the effect under these conditions has pramiracetam.

A Systematic Review and Meta-Analysis of the Efficacy of Piracetam and Piracetam-Like Compounds in Experimental Stroke

Background/Objective: Piracetam was a candidate neuroprotective drug for acute stroke ineffective in clinical trial. Here we use systematic review and meta-analysis to describe the evidence supporting a protective effect of piracetam and its derivatives in animal models of stroke. Methods: We present a systematic review of reports describing the use of piracetam and its derivatives in animal models of focal ischaemia, where the outcome was measured as an infarct size or neurological score (Der Simonian and Laird random effects meta-analysis). Results: Only 2 studies, published 10 years after the first clinical trial of piracetam had been initiated, described its efficacy in animal models of stroke. A further 4 studies described the efficacy of related compounds. Piracetam and its derivatives improved the outcome by 30.2% (95% CI = 16.1–44.4). The median study quality was 4/10 (inter-quartile range = 4–6). Conclusion: Piracetam and its derivatives demonstrate neuroprotective efficacy in experimental stroke, but our findings raise concerns about the amount of available data, the quality of the studies and publication bias.

Pharmacotherapy of Aphasia

M efforts have been undertaken at helping patients with aphasia recover from their deficits by using various rehabilitation techniques. A number of studies have also been carried out to investigate the role of pharmacological agents in the treatment of aphasia. Aphasia can result from a variety of injuries to the brain, including trauma and stroke. However, most of the research has focused on stroke due to the focal nature of the lesions and the vascular territories resulting in a more homogeneous patient population for study. Therefore, any possible benefits for people with traumatic brain injury must be extrapolated from the studies on subjects with stroke. A number of drugs have been developed for the treatment of Alzheimer’s disease. The N-methyl-D-aspartic acid receptor antagonists have also demonstrated benefits in patients with vascular dementia on batteries of cognitive tests that prominently feature language,1 suggesting that benefits might also result for patients undergoing rehabilitation for aphasia. Studies with cholinesterase inhibitors have also demonstrated significant benefits in patients with vascular dementia, and specifically in the treatment of patients with aphasia.2,3 A derivative of gamma aminobutyric acid, piracetam, with reported benefits for cognition and memory, has also been examined in the treatment of patients with aphasia. Significant benefits have been observed in these patients a few weeks to 3 years after onset of aphasia, at a dose of 2.4 mg twice a day.4 Use of piracetam in aphasia is also associated with an increase in language task– related activation on functional neuroimaging.5 How-

Piracetam for Acute Ischemic Stroke

Piracetam is a drug which has been marketed in several countries for many years as a “nootropic” agent (that is, a drug which has metabolic activity on human brain), and for the treatment of myoclonus. Recently, a Cochrane review has been published on efficacy of piracetam on ameliorating language in aphasic stroke patients; the drug has been reconsidered for acute stroke treatment as well. The objective of this review was to assess the effects of piracetam in acute presumed ischemic stroke. Randomized trials comparing piracetam with control, with at least mortality reported and entry to the trial within ≈48 hours of stroke onset. Two reviewers (S.R., M.G.C.) extracted data and assessed trial quality, and this was checked by the other 2 …