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Piracetam

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Piracetam
Clinical data
Trade namesBreinox, Dinagen, Lucetam, Nootropil, Nootropyl, Oikamid, Piracetam and many others
AHFS/Drugs.comInternational Drug Names
Routes of
administration
Oral, parenteral and vaporized
ATC code
Legal status
Legal status
  • AU: S4 (Prescription only)
  • UK: POM (Prescription only)
  • US:
    Not FDA approved
Pharmacokinetic data
Bioavailability~100%
Elimination half-life4–5 hr
ExcretionUrinary
Identifiers
  • 2-(2-oxopyrrolidin-1-yl)acetamide
CAS Number
PubChem CID
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.028.466 Edit this at Wikidata
Chemical and physical data
FormulaC6H10N2O2
Molar mass142.16 g/mol g·mol−1
3D model (JSmol)
  • O=C1N(CC(=O)N)CCC1
  • InChI=1S/C6H10N2O2/c7-5(9)4-8-3-1-2-6(8)10/h1-4H2,(H2,7,9) checkY
  • Key:GMZVRMREEHBGGF-UHFFFAOYSA-N checkY
  (verify)

Piracetam (sold under many brand names) is a nootropic drug in the racetams group, with chemical name 2-oxo-1-pyrrolidine acetamide. It shares the same 2-oxo-pyrrolidone base structure with pyroglutamic acid. Piracetam is a cyclic derivative of GABA. In the United States, it is not approved by the US Food and Drug Administration for any medical use and it is not permitted to be sold as a dietary supplement.[1][2] In the UK, piracetam is prescribed by doctors for some conditions, mainly myoclonus,[3] but is used off-label for other indications.

Effects

A two-week regimen of piracetam was reported in 1976 to enhance verbal memory in healthy college students in a double-blind, placebo-controlled study.[4][non-primary source needed]

While reviews have been published supporting the use of piracetam in the treatment of a wide range of cognitive disorders,[5] a Cochrane review concluded that there was no such clinical use of piracetam justified based on the published evidence.[6]

A 2002 meta-analysis by UCB (company) concluded that piracetam had a therapeutic effect in older patients with cognitive impairment.[7]

In 2008, a working group of the British Academy of Medical Sciences noted that many of the clinical trials of piracetam for dementia were methodologically flawed.[8][9]

Several meta-reviews of literature on piracetam indicate that piracetam increases performance on a variety of cognitive tasks among dyslexic children,[medical citation needed] though this may reflect its enhancement of cross-hemispheric communication and of cognitive function in general, rather than a specific improvement in whatever causes dyslexia. Piracetam also seems to inhibit brain damage caused by a variety of factors including hypoxia and excessive alcohol consumption.[10][11][non-primary source needed]

Piracetam has been studied in an extensive number of clinical experiments, and has shown positive results in the treatment of post-stroke aphasia, epilepsy, cognitive decline following heart and brain surgery, dementia,[7] and myoclonus.[12][13] Its peripheral vascular effect has indicated its use for vertigo, dyslexia and, at one time, sickle cell anemia as well,[5] but a subsequent Cochrane review of the evidence found that it did not support piracetam's use in sickle cell crisis prevention.[14]

Piracetam possesses pronounced antihypoxic and antiarrhythmic effect; the latter is carried out by decreasing the rhythm rate and increasing the contraction amplitude. The animals treated with piracetam in a dose when its antiarrhythmic effects (300 mg/kg) exhibited a decrease of the membrane potential of erythrocytes as compared with control. Similar effects occurred in the animals treated with lidocaine. It can be concluded that in certain types of arrhythmias the use of piracetam restores the normal rhythm of contractions that is perhaps connected with its positive influence on metabolic processes in the myocardium.[15]

In animal studies piracetam appeared to have increased communication between the two hemispheres of the brain and increased activity of the corpus callosum.[16][17]

Mechanisms of action

Piracetam 800mg tablets.

Piracetam's mechanism of action, as with racetams in general, is not fully understood. The drug influences neuronal and vascular functions and influences cognitive function without acting as a sedative or stimulant.[5] Piracetam is a positive allosteric modulator of the AMPA receptor.[18] It is hypothesized to act on ion channels or ion carriers; thus leading to increased neuron excitability.[19] GABA brain metabolism and GABA receptors are not affected by piracetam.[citation needed] It has been found to increase blood flow and oxygen consumption in parts of the brain but this may be a side effect of increased brain activity rather than a primary effect or mechanism of action for the drug.[20]

Piracetam improves the function of the neurotransmitter acetylcholine via muscarinic cholinergic (ACh) receptors, which are implicated in memory processes.[21] Furthermore, piracetam may have an effect on NMDA glutamate receptors, which are involved with learning and memory processes. Piracetam is thought to increase cell membrane permeability.[21][22] Piracetam may exert its global effect on brain neurotransmission via modulation of ion channels (i.e., Na+, K+).[19] It has been found to increase oxygen consumption in the brain, apparently in connection to ATP metabolism, and increases the activity of adenylate kinase in rat brains.[23][24] Piracetam, while in the brain, appears to increase the synthesis of cytochrome b5,[25] which is a part of the electron transport mechanism in mitochondria. But in the brain, it also increases the permeability of the mitochondria of some intermediaries of the Krebs cycle.[23]

History

Piracetam was first synthesized in 1964 by scientists at the Belgian pharmaceutical company UCB led by Corneliu E. Giurgea; struck by its apparent ability to boost mental functioning in even healthy individuals and by its safety, Giurgea coined the term nootropic to describe it and other substances. Piracetam (trade name "Nootropil") was launched clinically by UCB in the early 1970s, and currently is in use in many European countries.[26]

Approval and usage

Piracetam is primarily used in Europe, Asia, and South America. In the United States, it is not approved by the US Food and Drug Administration for any medical use and it is not permitted to be sold as a dietary supplement. Piracetam is legal to import into the United Kingdom for personal use with or without prescription. P Piracetam has no DIN in Canada, and thus cannot be sold but can be imported for personal use in Canada.[citation needed] It has become popular as a cognitive enhancement drug among students.[27] It may even be possibly used for the treatment of childhood autism, a practice partially supported by clinical research.[28][non-primary source needed]

Aging

Piracetam appears to diminish some effects of aging in the brain of mice.[29][30][failed verification]

Piracetam appears to reduce accumulation of lipofuscin, a common symptom of aging and alcoholism, in the rat brain.[31]

Alcoholism

Piracetam appears to be effective in treating cognitive impairment in alcoholism.[32][33][34][35][36][37]

Alzheimer's and senile dementia

Once thought to be effective for improving cognition in Alzheimer's disease and senile dementia patients, the evidence is now seen as too inconsistent to support the use of piracetam for these conditions.[38]

Clotting, coagulation, vasospastic disorders

Piracetam is useful as a long-term treatment for clotting, coagulation, and vasospastic disorders such as Raynaud's phenomenon[39] and deep-vein thrombosis.[21][40] It is an extremely safe anti-thrombotic agent that operates through the novel mechanism of inhibiting platelet aggregation and enhancing blood-cell deformability.[21] Because traditional anti-thrombotic drugs operate through the separate mechanism of inhibiting clotting factors, co-administration of piracetam has been shown to highly complement the efficacy and safety of traditional Warfarin/Heparin anti-coagulation therapy.[41] The most effective treatment range for this use is a daily dose of 4.8 to 9.6 grams divided into three daily doses at 8 hours apart.[40] Piracetam was investigated as a complement or alternative to Warfarin as a safe and effective long-term treatment for recurring deep-vein thrombosis.[40]

Depression and anxiety

Some sources suggest that piracetam's overall effect on lowering depression and anxiety is higher than improving memory.[42] However, depression is reported to be an occasional adverse effect of piracetam.[43]

Stroke, ischemia and symptoms

Piracetam has been found to improve cognition after stroke, and reduce symptoms, such as aphasia.[44] It also improves cognition in cases of chronic ischemia.[45][46]

Developmental coordination disorder and dysgraphia

Due to its supposed effect on nerves and muscles it is sometimes prescribed as an aid to muscle or dexterity training, particularly in cases of agraphia and developmental coordination disorder. There has not been a specific study as to whether it is beneficial in this. Vinpocetine, another purported nootropic with which piracetam is indirectly synergistic, is confirmed to help with these conditions to a certain degree.[citation needed]

Schizophrenia

At least one study shows that, while piracetam positively affected the cognition of patients suffering from schizophrenia in the same way as it positively affected the cognition of others, the severity of subjects' schizophrenia remained unaffected, for better or worse.[47]

Preventive for breath-holding spells

Two articles support the use of piracetam as a prophylactic for severe cases of breath-holding spells. A 2008 study in the International Journal of Psychiatry Medicine supported the notion that piracetam was effective as a preventive, but did not use a control to evaluate results against normal recovery times from severe BHS.[48] A 1998 study by the Turkish ministry of health evaluated 76 children, half of them in a control group. Children in the experimental group were three times as, and almost completely likely, to exhibit "overall control" over their BHS, with BHS episodes dropping by 60% over two months.[49]

The 2008 study notes:

Breath holding spells (BHS) are apparently frightening events occurring in otherwise healthy children. Generally, no medical treatment is recommended and parental reassurance is believed to be enough, however, severe BHS can be very stressful for the parents and a pharmacological agent may be desired in some of these children.

Closed craniocerebral trauma

Piracetam has positive therapeutic effects on adolescents with closed craniocerebral trauma (CCT). Treatment with piracetam was initiated 1.5 to 5 years after trauma. Compared to controls, after one month of daily treatment with 1600–2400 mg of piracetam there were meaningful and statistically significant improvements in the higher mental functions (visual memory, attention and executive), motor functions (gait, balance and sequential limb movements) and in the rates of cognitive and motor operations.[50]

Dosage

For blood coagulation, clotting, and vasospastic disorders such as Raynaud's phenomenon or deep-vein thrombosis, the most effective treatment range is a daily oral dose of 4.8 to 9.6 grams divided into three daily doses at 8 hours apart.[21][39][40] The LD50 for oral consumption in humans has not been determined,[19] however the LD50 for mice is 5.6 g/kg for rats, and 20 g/kg for mice, indicating extremely low acute toxicity.[51]

Side effects

Piracetam has been found to have very few side effects, and those it has are typically "few, mild, and transient."[52] A large-scale, 12-week trial of high-dose piracetam found no adverse effects occurred in the group taking piracetam as compared to the placebo group.[53] Many other studies have likewise found piracetam to be well tolerated.[12][52][54]

Symptoms of general excitability, including anxiety, insomnia, irritability, headache, agitation, nervousness, tremor, and hyperkinesia, are occasionally reported.[43][55][56] Other reported side effects include somnolence, weight gain, clinical depression, weakness, increased libido, and hypersexuality.[43]

Lucid dreaming

Piracetam has become a popular supplement in the subculture of lucid dreaming. Its use has been largely made popular by a book published by Thomas Yuschak titled Advanced Lucid Dreaming: The Power of Supplements. Piracetam is not used directly to cause vivid dreams; it is even said to prevent them. The premise for its use is to counter the desensitization of acetylcholine receptors in the brain caused by taking another supplement, galantamine, which is said to cause stronger, more vivid dreaming experiences. Piracetam is taken immediately after having a lucid dream experience with galantamine. The lucid dreamer will then not take the supplement combination again until the galantamine has completely left their system (approximately 30 hours). Piracetam has a peak plasma time of 1.5 hours and an elimination half-life equal to 5 hours. For the purpose of lucid dreaming dosing is much lower than doses taken in clinical studies, averaging typically 2400 mg.

Availability

Piracetam is sold under a wide variety of brand names world wide. Popular trade names for piracetam in Europe are Nootropil and Lucetam, among many others. In Argentina, it is made by GlaxoSmithKline S.A. laboratories and sold under the trade name of Noostan (800 mg or 1200 mg). In Venezuela and Ecuador, piracetam is produced by Laboratorios Farma S.A. and sold under the brand name Breinox. In Mexico is produced by UCB de Mexico, and sold under the brand name of Nootropil. Other names include Nootropil in The United States, Europe, Brazil, Hong Kong, India, and Mexico; Lucetam, Oikamid, Smart, Geratam, and Biotropil in Europe and Brazil; Neurobasal in Colombia; Breinox in Ecuador and Venezuela; Noostan in Argentina; Stimulan in Egypt; and Nocetan in Latin America.

Notes

  1. ^ Inspections, Compliance, Enforcement, and Criminal Investigations
  2. ^ Enforcement Report - Week of March 20, 2013
  3. ^ "Nootropil". NetDoctor.co.uk. 8 July 2004. Retrieved 21 September 2009.
  4. ^ Dimond, SJ; Brouwers, EM (1976). "Increase in the power of human memory in normal man through the use of drugs". Psychopharmacology. 49 (3): 307–9. doi:10.1007/BF00426834. PMID 826948.
  5. ^ a b c Winblad, B (2005). "Piracetam: a review of pharmacological properties and clinical uses". CNS Drug Reviews. 11 (2): 169–82. doi:10.1111/j.1527-3458.2005.tb00268.x. PMID 16007238.
  6. ^ Template:Cite cochrane
  7. ^ a b Waegemans, T; Wilsher, CR; Danniau, A; Ferris, SH; Kurz, A; Winblad, B (2002). "Clinical efficacy of piracetam in cognitive impairment: a meta-analysis". Dementia and geriatric cognitive disorders. 13 (4): 217–24. doi:10.1159/000057700. PMID 12006732.
  8. ^ Horne G; et al. (May 2008). Brain science, addiction and drugs (PDF) (Report). Academy of Medical Sciences. p. 145. ISBN 1-903401-18-6. {{cite report}}: Explicit use of et al. in: |author= (help)
  9. ^ Talbot, Margaret (27 April 2009). "Brain Gain: The underground world of 'neuroenhancing' drugs". The New Yorker. Retrieved 21 September 2009.
  10. ^ Vaglenova, J; Vesselinov Petkov, V (2001). "Can nootropic drugs be effective against the impact of ethanol teratogenicity on cognitive performance?". European Neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 11 (1): 33–40. doi:10.1016/S0924-977X(00)00129-2. PMID 11226810.
  11. ^ Gabryel, B; Adamek, M; Pudełko, A; Małecki, A; Trzeciak, HI (2002). "Piracetam and vinpocetine exert cytoprotective activity and prevent apoptosis of astrocytes in vitro in hypoxia and reoxygenation". Neurotoxicology. 23 (1): 19–31. doi:10.1016/S0161-813X(02)00004-9. PMID 12164545.
  12. ^ a b Fedi, M; Reutens, D; Dubeau, F; Andermann, E; D'agostino, D; Andermann, F (2001). "Long-term efficacy and safety of piracetam in the treatment of progressive myoclonus epilepsy". Archives of neurology. 58 (5): 781–6. doi:10.1001/archneur.58.5.781. PMID 11346373.
  13. ^ Brown, P; Steiger, MJ; Thompson, PD; Rothwell, JC; Day, BL; Salama, M; Waegemans, T; Marsden, CD (1993). "Effectiveness of piracetam in cortical myoclonus". Movement disorders : official journal of the Movement Disorder Society. 8 (1): 63–8. doi:10.1002/mds.870080112. PMID 8419809.
  14. ^ Template:Cite Cochrane
  15. ^ Samvelian, VM; Malakian, MG; Badzhinian, SA (1990). "Nekotorye aspekty antiaritmicheskogo deĭstviia piratsetama". Farmakologiia i toksikologiia (in Russian). 53 (6): 22–3. PMID 2081561. {{cite journal}}: Unknown parameter |trans_title= ignored (|trans-title= suggested) (help)
  16. ^ Giurgea, CE; Moyersoons, FE (1972). "On the pharmacology of cortical evoked potentials". Archives internationales de pharmacodynamie et de therapie. 199 (1): 67–78. PMID 4342020.
  17. ^ Buresová, O; Bures, J (1976). "Piracetam-induced facilitation of interhemispheric transfer of visual information in rats". Psychopharmacologia. 46 (1): 93–102. doi:10.1007/BF00421555. PMID 1257371.
  18. ^ Ahmed, A; Oswald, R (2010). "Piracetam Defines a New Binding Site for Allosteric Modulators of α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors". Journal of Medicinal Chemistry. 53 (5): 2197–2203. doi:10.1021/jm901905j. PMC 2872987. PMID 20163115.
  19. ^ a b c Gouliaev, AH; Senning, A (1994). "Piracetam and other structurally related nootropics". Brain research. Brain research reviews. 19 (2): 180–222. doi:10.1016/0165-0173(94)90011-6. PMID 8061686.
  20. ^ Jordaan, B; Oliver, DW; Dormehl, IC; Hugo, N (1996). "Cerebral blood flow effects of piracetam, pentifylline, and nicotinic acid in the baboon model compared with the known effect of acetazolamide". Arzneimittel-Forschung. 46 (9): 844–7. PMID 8876930.
  21. ^ a b c d e Winnicka, K; Tomasiak, M; Bielawska, A (2005). "Piracetam--an old drug with novel properties?". Acta poloniae pharmaceutica. 62 (5): 405–9. PMID 16459490.
  22. ^ Müller, WE; Eckert, GP; Eckert, A (1999). "Piracetam: novelty in a unique mode of action". Pharmacopsychiatry. 32 Suppl 1: 2–9. doi:10.1055/s-2007-979230. PMID 10338102.
  23. ^ a b Grau, M; Montero, JL; Balasch, J (1987). "Effect of Piracetam on electrocorticogram and local cerebral glucose utilization in the rat". General pharmacology. 18 (2): 205–11. doi:10.1016/0306-3623(87)90252-7. PMID 3569848.
  24. ^ Nickolson, VJ; Wolthuis, OL (1976). "Effect of the acquisition-enhancing drug piracetam on rat cerebral energy metabolism. Comparison with naftidrofuryl and methamphetamine". Biochemical pharmacology. 25 (20): 2241–4. doi:10.1016/0006-2952(76)90004-6. PMID 985556.
  25. ^ Tacconi, MT; Wurtman, RJ (1986). "Piracetam: physiological disposition and mechanism of action". Advances in neurology. 43: 675–85. PMID 3946121.
  26. ^ S. D. Shorvon (2004). "Piracetam". In Simon D. Shorvon, David Fish, Emilio Perucca, W E Dodson (ed.). The treatment of epilepsy. Wiley–Blackwell. pp. 489–495. ISBN 978-0-632-06046-7.{{cite book}}: CS1 maint: multiple names: editors list (link)
  27. ^ Medew, Julia (1 October 2009). "Call for testing on 'smart drugs'". Fairfax Media. Retrieved 29 May 2014.
  28. ^ Akhondzadeh, S., et al. A double-blind placebo controlled trial of piracetam added to risperidone in patients with autistic disorder. Child Psychiatry and Human Development, Vol 39(3), Sep, 2008. pp. 237–245.
  29. ^ Pilch, H; Müller, WE (1988). "Piracetam elevates muscarinic cholinergic receptor density in the frontal cortex of aged but not of young mice". Psychopharmacology. 94 (1): 74–8. doi:10.1007/BF00735884. PMID 3126530.
  30. ^ Stoll, L; Schubert, T; Müller, WE (1992). "Age-related deficits of central muscarinic cholinergic receptor function in the mouse: partial restoration by chronic piracetam treatment". Neurobiology of Aging. 13 (1): 39–44. doi:10.1016/0197-4580(92)90006-J. PMID 1542379.
  31. ^ Paula-Barbosa, MM; Brandão, F; Pinho, MC; Andrade, JP; Madeira, MD; Cadete-Leite, A (1991). "The effects of piracetam on lipofuscin of the rat cerebellar and hippocampal neurons after long-term alcohol treatment and withdrawal: a quantitative study". Alcoholism, clinical and experimental research. 15 (5): 834–8. doi:10.1111/j.1530-0277.1991.tb00610.x. PMID 1755517.
  32. ^ Skondia, V; Kabes, J (1985). "Piracetam in alcoholic psychoses: a double-blind, crossover, placebo controlled study". The Journal of International Medical Research. 13 (3): 185–7. PMID 3891457.
  33. ^ Buranji, I; Skocilić, Z; Kozarić-Kovacić, D (1990). "Cognitive function in alcoholics in a double-blind study of piracetam". Lijecnicki vjesnik. 112 (3–4): 111–4. PMID 2204773.
  34. ^ Kalmár, S (2003). "Adjuvant therapy with parenteral piracetam in alcohol withdrawal delirium". Orvosi hetilap. 144 (19): 927–30. PMID 12809069.
  35. ^ Dencker, SJ; Wilhelmson, G; Carlsson, E; Bereen, FJ (1978). "Piracetam and chlormethiazole in acute alcohol withdrawal: a controlled clinical trial". The Journal of International Medical Research. 6 (5): 395–400. PMID 359384.
  36. ^ Meyer, JG; Forst, R; Meyer-Wahl, L (1946). "Course of alcoholic predelirium during treatment with piracetam: results of serial psychometric tests (author's transl)". Deutsche Medizinische Wochenschrift. 104 (25): 911–4. doi:10.1055/s-0028-1104013. PMID 446321.
  37. ^ Binder, S; Doddabela, P (1976). "The efficacy of Piracetam on the mental functional capacity of chronic alcoholics (author's transl)". Medizinische Klinik. 71 (17): 711–6. PMID 775275.
  38. ^ Template:Cite cochrane
  39. ^ a b Moriau, M; Lavenne-Pardonge, E; Crasborn, L; Von Frenckell, R; Col-Debeys, C (1993). "Treatment of the Raynaud's phenomenon with piracetam". Arzneimittel-Forschung. 43 (5): 526–35. PMID 8328997.
  40. ^ a b c d Moriau, M; Crasborn, L; Lavenne-Pardonge, E; Von Frenckell, R; Col-Debeys, C (1993). "Platelet anti-aggregant and rheological properties of piracetam. A pharmacodynamic study in normal subjects". Arzneimittel-Forschung. 43 (2): 110–8. PMID 8457235.
  41. ^ Moriau, M; Lavenne-Pardonge, E; Crasborn, L; Von Frenckell, R; Col-Debeys, C (1995). "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". Thrombosis research. 78 (6): 469–82. doi:10.1016/0049-3848(95)00081-2. PMID 15714749.
  42. ^ Malykh AG, Sadaie MR (February 2010). "Piracetam and piracetam-like drugs: from basic science to novel clinical applications to CNS disorders". Drugs. 70 (3): 287–312. doi:10.2165/11319230-000000000-00000. PMID 20166767.
  43. ^ a b c Nootropil®. Arzneimittel-Kompendium der Schweiz. 2013-09-12. Retrieved 2013-10-27.
  44. ^ Deberdt, W (1994). "Interaction between psychological and pharmacological treatment in cognitive impairment". Life Sciences. 55 (25–26): 2057–66. doi:10.1016/0024-3205(94)00386-6. PMID 7997065.
  45. ^ Herrschaft, H. (1989). "Effects and therapeutic efficacy of nootropic drugs in acute and chronic cerebral ischaemia in man". In Josef Krieglstein (ed.). Pharmacology of Cerebral Ischemia. Boca Raton: CRC Press. pp. 481–. ISBN 978-3-8047-1036-8. OCLC 20898140.[page needed]
  46. ^ Platt, D; Horn, J; Summa, JD; Schmitt-Rüth, R; Kauntz, J; Krönert, E (1993). "On the efficacy of piracetam in geriatric patients with acute cerebral ischemia: a clinically controlled double-blind study". Archives of gerontology and geriatrics. 16 (2): 149–64. doi:10.1016/0167-4943(93)90006-4. PMID 15374345.
  47. ^ Dimond, Stuart J.; Scammell, RE; Pryce, IG; Huws, D; Gray, C (1979). "Some effects of piracetam (UCB 6215 nootropyl) on chronic schizophrenia". Psychopharmacology. 64 (3): 341–8. doi:10.1007/BF00427522. PMID 116278.
  48. ^ Azam M, Bhatti N, Shahab N (2008). "Piracetam in severe breath holding spells". Int J Psychiatry Med. 38 (2): 195–201. doi:10.2190/PM.38.2.f. PMID 18724570.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Donma MM (January 1998). "Clinical efficacy of piracetam in treatment of breath-holding spells". Pediatr. Neurol. 18 (1): 41–5. doi:10.1016/S0887-8994(97)00153-7. PMID 9492090.
  50. ^ Zavadenko, NN; Guzilova, LS (2009). "Sequelae of closed craniocerebral trauma and the efficacy of piracetam in its treatment in adolescents". Neuroscience and Behavioral Physiology. 39 (4): 323–8. doi:10.1007/s11055-009-9146-2. PMID 19340573.
  51. ^ "Piracetam Material Safety Sheet" (PDF). Spectrum.
  52. ^ a b Koskiniemi, M; Van Vleymen, B; Hakamies, L; Lamusuo, S; Taalas, J (1998). "Piracetam relieves symptoms in progressive myoclonus epilepsy: a multicentre, randomised, double blind, crossover study comparing the efficacy and safety of three dosages of oral piracetam with placebo". Journal of neurology, neurosurgery, and psychiatry. 64 (3): 344–8. doi:10.1136/jnnp.64.3.344. PMC 2169975. PMID 9527146.
  53. ^ De Reuck, J; Van Vleymen, B (1999). "The clinical safety of high-dose piracetam--its use in the treatment of acute stroke". Pharmacopsychiatry. 32 Suppl 1: 33–7. doi:10.1055/s-2007-979234. PMID 10338106.
  54. ^ Giurgea, C.; Salama, M. (1977). "Nootropic drugs". Prog Neuro-Psychopharmacolgy. 1 (3–4): 235–247. doi:10.1016/0364-7722(77)90046-7.
  55. ^ Chouinard, G; Annable, L; Ross-Chouinard, A; Olivier, M; Fontaine, F (1983). "Piracetam in elderly psychiatric patients with mild diffuse cerebral impairment". Psychopharmacology. 81 (2): 100–6. doi:10.1007/BF00429000. PMID 6415738.
  56. ^ Hakkarainen, H; Hakamies, L (1978). "Piracetam in the treatment of post-concussional syndrome. A double-blind study". European neurology. 17 (1): 50–5. doi:10.1159/000114922. PMID 342247.

See also

  • Aniracetam
  • Brivaracetam—another analogue of Piracetam with the same additional side chain as Levetiracetam and a three carbon chain. It exhibits greater antiepileptic properties than Levetiracetam but with a somewhat smaller, although still high, therapeutic range. As of 2011, it is in 3rd stage pharmaceutical trials
  • Hydergine
  • Levetiracetam—an analogue of Piracetam bearing an additional CH3-CH2- sidechain and bearing antiepileptic pharmacological properties through a poorly understood mechanism probably related to its affinity for the vesicle protein SV2A
  • Oxiracetam
  • Pramiracetam

References


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