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PYRROLIDINONE DERIVATIVES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) The pyrrolidinone nootropics (agents which are believed to enhance learning and memory) are cyclic derivatives of gamma-butyric acid (GABA), although they have no significant affinity for GABA or benzodiazepine receptors. Piracetam appears to have anti-myoclonic properties.

Specific Substances

    A) ANIRACETAM
    1) 2-Pyrrolidinone, 1-(4-methoxybenzoyl)-
    2) 1-(4-Methoxybenzoyl)-2-pyrrolidinone
    3) 1-(p-Methoxybenzoyl)-2-pyrrolidinon
    4) 1-p-Anisoyl-2-pyrrolidinone
    5) Draganon
    6) Ro 13-5057
    7) Sarpul
    8) Molecular Formula: C12-H13-N-O3
    9) CAS 72432-10-1
    ETIRACETAM
    1) Etiracetam
    FASORACETAM
    1) Fasoracetam
    NEBRACETAM
    1) Nebracetam
    NEFIRACETAM
    1) Nefiracetam
    OXIRACETAM
    1) 1-Pyrrolidineacetamide, 4-hydroxy-2-oxo-
    2) 4-Hydroxy-2-oxo-1-pyrrolidineacetamide
    3) 4-Hydroxypiracetam
    4) CGP-21690E
    5) CT-848
    6) Hydroxypiracetam
    7) ISF 2522
    8) Molecular Formula: C6-H10-N2-O3
    9) CAS 62613-82-5
    PIRACETAM
    1) 1-Pyrrolidineacetamide, 2-oxo-
    2) 1-Acetamido-2-pyrrolidinone
    3) 2-Ketopyrrolidine-1-ylacetamide
    4) 2-Oxo-pyrrolidin-1-ylacetamide
    5) 2-Oxo-pyrrolidine acetamide
    6) 2-Pyrrolidinoneacetamide
    7) 2-Pyrrolidoneacetamide
    8) Cl-871
    9) Pyrrolidone acetamide
    10) UCB 6215
    11) Molecular Formula: C6-H10-N2-O2
    12) CAS 7491-74-9
    PRAMIRACETAM
    1) 1-Pyrrolidineacetamide, N-(2-(bis(1-methylethyl)
    2) amino)ethyl)-2-oxo-, sulfate
    3) Amacetam sulfate
    4) CI-879
    5) N-(2-(Bis(1-methylethyl)amino)ethyl)-2-oxo-1-
    6) pyrrolidineacetamide sulfate
    7) Pramiracetam sulfate
    8) Molecular Formula: C14-H27-N3-O2.H2-O4-S
    9) CAS 72869-16-0 (pramiracetam sulfate)
    10) CAS 68497-62-1 (pramiracetam)
    TENILSETAM
    1) Tenilsetam

Available Forms Sources

    A) FORMS
    1) Piracetam is available as 800 mg tablets (Prod Info Nootropil oral tablets, 2015).
    B) USES
    1) These drugs are classified as "nootropics", or cognitive-enhancing agents. With the exception of levetiracetam, they are used for therapy of cognitive disorders, such as Alzheimer's disease, organic brain syndrome, dementia, and dyslexia. Piracetam is also an orphan drug used for the treatment of myoclonus and neuroprotection after stroke (Shorvon, 2001).
    2) Piracetam is used in combination with other agents to treat patients suffering from myoclonus of cortical origin, irrespective of aetiology (Prod Info Nootropil oral tablets, 2015).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: These drugs are classified as "nootropics", or cognitive-enhancing agents. They are used for therapy of cognitive disorders, such as Alzheimer's disease, organic brain syndrome, dementia, and dyslexia.
    B) PHARMACOLOGY: The pyrrolidinone nootropics (agents which are believed to enhance learning and memory) are cyclic derivatives of gamma-butyric acid (GABA), although they have no significant affinity for GABA or benzodiazepine receptors. Piracetam appears to have anti-myoclonic properties.
    C) EPIDEMIOLOGY: Overdoses are rare.
    D) WITH THERAPEUTIC USE
    1) The following adverse effects have been reported following piracetam use: Pruritus, vesiculobullous rash or skin discoloration, nausea, gastric discomfort, abdominal pain, flatulence, inhibition of platelet aggregation, elevated liver enzymes, nervousness, irritability, hyperkinesia, somnolence, headache, asthenia, and coordination difficulties.
    E) WITH POISONING/EXPOSURE
    1) In general, overdose effects are anticipated to be an extension of adverse effects following therapeutic administration. Drowsiness has been reported in patients receiving very high doses of piracetam.
    0.2.20) REPRODUCTIVE
    A) There are no adequate or well-controlled studies of piracetam administration during pregnancy. Piracetam crossed the placental barrier. Do not administer piracetam to pregnant women unless clearly necessary and only when the potential maternal benefit outweighs the potential fetal risk. Piracetam is excreted in human breast milk. Do not administer piracetam to women who are breastfeeding. A decision should be made whether to discontinue piracetam or to discontinue nursing, taking into consideration the importance of the drug to the mother.

Laboratory Monitoring

    A) Plasma concentrations are not readily available or clinically useful in the management of overdose.
    B) Monitor vital signs, liver enzymes, CBC, and mental status following significant overdose.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Closely monitor neurologic function. Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    C) DECONTAMINATION
    1) PREHOSPITAL: Severe toxicity from a pyrrolidinone derivative is rare. Prehospital gastrointestinal decontamination is not recommended because of the potential for somnolence.
    2) HOSPITAL: Consider activated charcoal in a patient with a potentially toxic ingestion who is able to maintain airway or if airway is protected.
    D) AIRWAY MANAGEMENT
    1) Endotracheal intubation may be necessary if significant CNS depression develops.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION
    1) In studies, about 50% to 60% of piracetam dose was extracted by hemodialysis.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    2) OBSERVATION CRITERIA: Patients with a deliberate overdose, and those who are symptomatic, need to be monitored until they are clearly improving and clinically stable.
    3) ADMISSION CRITERIA: Patients with severe symptoms despite treatment should be admitted.
    4) CONSULT CRITERIA: Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    H) PITFALLS
    1) When managing a suspected overdose, the treating physician should be cognizant of the possibility of multi-drug involvement.
    I) DIFFERENTIAL DIAGNOSIS
    1) Includes other agents that may cause neurologic disorders and elevated liver enzymes.

Range Of Toxicity

    A) TOXICITY: Piracetam doses, up to 32 g/day, have been given with drowsiness as the dose-limiting factor.
    B) THERAPEUTIC DOSE: ANIRACETAM: 500 mg orally twice daily. PIRACETAM: Initial, 7.2 g increasing by 4.8 g every 3 to 4 days up to a maximum of 24 g in 2 or 3 sub-doses. PRAMIRACETAM: Oral doses of 600 mg twice daily or up to 4000 mg/day have been used.

Clinical Effects

Summary Of Exposure

    A) USES: These drugs are classified as "nootropics", or cognitive-enhancing agents. They are used for therapy of cognitive disorders, such as Alzheimer's disease, organic brain syndrome, dementia, and dyslexia.
    B) PHARMACOLOGY: The pyrrolidinone nootropics (agents which are believed to enhance learning and memory) are cyclic derivatives of gamma-butyric acid (GABA), although they have no significant affinity for GABA or benzodiazepine receptors. Piracetam appears to have anti-myoclonic properties.
    C) EPIDEMIOLOGY: Overdoses are rare.
    D) WITH THERAPEUTIC USE
    1) The following adverse effects have been reported following piracetam use: Pruritus, vesiculobullous rash or skin discoloration, nausea, gastric discomfort, abdominal pain, flatulence, inhibition of platelet aggregation, elevated liver enzymes, nervousness, irritability, hyperkinesia, somnolence, headache, asthenia, and coordination difficulties.
    E) WITH POISONING/EXPOSURE
    1) In general, overdose effects are anticipated to be an extension of adverse effects following therapeutic administration. Drowsiness has been reported in patients receiving very high doses of piracetam.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH THERAPEUTIC USE
    a) CNS effects appear to be the most commonly reported effects with this class of drugs. Most often reported, especially during the first 4 weeks of therapy, were somnolence, asthenia, and coordination difficulties. Piracetam has been reported to cause repeated episodes of confusion and lethargy (Sandyk & Gillman, 1985; Prod Info Nootropil oral tablets, 2015). With piracetam doses as high as 32 grams/day, somnolence was a dose-limiting factor (Shorvon, 2001).
    b) Nervousness, irritability, hyperkinesia, somnolence, and headache have been reported in children treated with oral piracetam (Prod Info Nootropil oral tablets, 2015; DiIanni et al, 1985; Wilsher et al, 1987a). However, the incidence of these effects is low (less than 3%). Depression was described in 1 dyslexic child during piracetam therapy, although a cause-effect relationship was not established (DiIanni et al, 1985).
    c) High doses of piracetam have been associated with hyperstimulation, sleep disturbances, and dizziness in some patients (Galizia, 1984).
    d) Piracetam 3 grams IV was associated with worsening of choreic movements in patients with Huntington's chorea in a double-blind study (Destee et al, 1984).
    e) Repeat episodes of confusion and lethargy were described in a 44-year-old epileptic man with memory dysfunction following intravenous infusions of piracetam. The patient received piracetam 4 g infused over 30 minutes weekly for 4 weeks; confusion and lethargy occurred within 30 minutes of each infusion and persisted for 2 hours. The reported lack of GABA-ergic activity of piracetam is questioned by the authors, who speculate that this effect may have accounted for the episodes of confusion in this patient (Sandyk & Gillman, 1985a).
    B) FEELING NERVOUS
    1) WITH THERAPEUTIC USE
    a) High doses of piracetam have been associated with hyperstimulation, sleep disturbances, and dizziness in some patients (Galizia, 1984a). Nervousness, irritability, and headache have been reported in children treated with oral piracetam (Prod Info Nootropil oral tablets, 2015; DiIanni et al, 1985; Wilsher et al, 1987).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) WITH THERAPEUTIC USE
    a) Nausea, gastric discomfort, abdominal pain, and flatulence have been described occasionally during piracetam therapy (Wilsher et al, 1987; Obeso et al, 1988) and pramiracetam therapy (Scarpazza et al, 1993).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH THERAPEUTIC USE
    a) Elevations of liver enzymes have been reported rarely with piracetam administration (Wilsher et al, 1987). A cause-effect relationship has not been established.

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) PLATELET ADHESION
    1) WITH THERAPEUTIC USE
    a) Piracetam has been reported to inhibit platelet aggregation and decrease blood viscosity at high doses (JEF Reynolds , 2000).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) WITH THERAPEUTIC USE
    a) Pruritus, vesiculobullous rash or skin discoloration have been reported following therapy with these agents (Sourander et al, 1987).

Reproductive

    3.20.1) SUMMARY
    A) There are no adequate or well-controlled studies of piracetam administration during pregnancy. Piracetam crossed the placental barrier. Do not administer piracetam to pregnant women unless clearly necessary and only when the potential maternal benefit outweighs the potential fetal risk. Piracetam is excreted in human breast milk. Do not administer piracetam to women who are breastfeeding. A decision should be made whether to discontinue piracetam or to discontinue nursing, taking into consideration the importance of the drug to the mother.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) PIRACETAM: In animal studies, no teratogenic effects were observed when animals received piracetam doses up to 4.8 g/kg/day (Prod Info Nootropil oral tablets, 2015).
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY CATEGORY
    1) PIRACETAM: There are no adequate or well-controlled studies of piracetam administration during pregnancy. Piracetam crossed the placental barrier. In studies, piracetam blood concentrations in the newborn was about 70% to 90% of maternal blood concentrations. Do not administer piracetam to pregnant women unless clearly necessary and only when the potential maternal benefit outweighs the potential fetal risk (Prod Info Nootropil oral tablets, 2015).
    B) ANIMAL STUDIES
    1) PIRACETAM: In animal studies, piracetam doses up to 2.7 g/kg/day did not produce direct or indirect harmful effects during pregnancy. It also did not produce embryonal/fetal development and parturition or postnatal development adverse effects (Prod Info Nootropil oral tablets, 2015).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) PIRACETAM: Piracetam is excreted in human breast milk. Do not administer piracetam to women who are breastfeeding. A decision should be made whether to discontinue piracetam or to discontinue nursing, taking into consideration the importance of the drug to the mother (Prod Info Nootropil oral tablets, 2015).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) PIRACETAM: In animal studies, piracetam doses up to 2.7 g/kg/day did not produce fertility or peri- or postnatal development adverse effects (Prod Info Nootropil oral tablets, 2015).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma concentrations are not readily available or clinically useful in the management of overdose.
    B) Monitor vital signs, liver enzymes, CBC, and mental status following significant overdose.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.

Methods

    A) CHROMATOGRAPHY
    1) A rapid, sensitive and reproducible gas chromatographic method is described for the quantitative evaluation of piracetam in human serum (Alebic-Kolbah & Hirsl-Starcevic, 1990).
    2) A gas-liquid chromatographic method, following solvent extraction, has been used for the quantitative determinations of pramiracetam in plasma and urine. An average precision of 5% is reported (Chang et al, 1985).
    3) Two different reversed-phase high performance liquid chromatography methods for the quantitative determination of aniracetam and its metabolites in human plasma have been described. The limits of quantification were 5 ng/mL using a 200 microliter plasma specimen and 50 ng/mL using a 0.5 mL plasma specimen, respectively (Guenzi & Zanetti, 1990).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with severe symptoms despite treatment should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a deliberate overdose, and those who are symptomatic, need to be monitored until they are clearly improving and clinically stable.

Monitoring

    A) Plasma concentrations are not readily available or clinically useful in the management of overdose.
    B) Monitor vital signs, liver enzymes, CBC, and mental status following significant overdose.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Severe toxicity from a pyrrolidinone derivative is rare. Prehospital gastrointestinal decontamination is not recommended because of the potential for somnolence.
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Closely monitor neurologic function. Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    B) MONITORING OF PATIENT
    1) Plasma concentrations are not readily available or clinically useful in the management of overdose.
    2) Monitor vital signs, liver enzymes, CBC, and mental status following significant overdose.
    3) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.

Enhanced Elimination

    A) HEMODIALYSIS
    1) In studies, about 50% to 60% of piracetam dose was extracted by hemodialysis (Prod Info Nootropil oral tablets, 2015).

Range Of Toxicity

Summary

    A) TOXICITY: Piracetam doses, up to 32 g/day, have been given with drowsiness as the dose-limiting factor.
    B) THERAPEUTIC DOSE: ANIRACETAM: 500 mg orally twice daily. PIRACETAM: Initial, 7.2 g increasing by 4.8 g every 3 to 4 days up to a maximum of 24 g in 2 or 3 sub-doses. PRAMIRACETAM: Oral doses of 600 mg twice daily or up to 4000 mg/day have been used.

Therapeutic Dose

    7.2.1) ADULT
    A) SPECIFIC SUBSTANCE
    1) ANIRACETAM: 500 mg twice orally daily has been used in the treatment of dementia as seen in Alzheimer disease (Sourander et al, 1987).
    2) OXIRACETAM has been withdrawn in the United States from phase II clinical studies due to lack of efficacy in patients with Alzheimer disease (JEF Reynolds , 2000). In one clinical trial, a dose of 800 mg twice daily for 12 weeks had been given (Maina et al, 1989).
    3) PIRACETAM: Initial, 7.2 g increasing by 4.8 g every 3 to 4 days up to a maximum of 24 g in 2 or 3 sub-doses (Prod Info Nootropil oral tablets, 2015).
    4) PRAMIRACETAM: Oral doses of 600 mg twice daily have been given for age-related memory impairment and senile dementia (JEF Reynolds , 2000; Scarpazza et al, 1993). Doses up to 4000 mg/day have been given in clinical trials, with no clear symptomatic benefit in Alzheimer disease patients (Parnetti, 1995).
    7.2.2) PEDIATRIC
    A) PIRACETAM
    1) Doses of 1.65 g ORALLY twice daily have been effective in children with dyslexia (Wilsher et al, 1987; DiIanni et al, 1985).

Maximum Tolerated Exposure

    A) PIRACETAM: Doses as high as 32 grams per day have been given for the treatment of cortical myoclonus. Drowsiness appears to be the dose-limiting step at these high doses (Shorvon, 2001).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ANIRACETAM
    1) LD50- (ORAL)MOUSE:
    a) 3648 mg/kg (RTECS, 2005)
    2) LD50- (SUBCUTANEOUS)MOUSE:
    a) >5 gm/kg (RTECS, 2005)
    3) LD50- (ORAL)RAT:
    a) 4500 mg/kg (RTECS, 2005)
    4) LD50- (SUBCUTANEOUS)RAT:
    a) >5 gm/kg (RTECS, 2005)
    B) OXIRACETAM
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) >10 gm/kg (RTECS, 2005)
    2) LD50- (INTRAPERITONEAL)RAT:
    a) >10 gm/kg (RTECS, 2005)
    C) PIRACETAM
    1) LD50- (ORAL)MOUSE:
    a) 2 gm/kg (RTECS, 2005)
    2) LD50- (SUBCUTANEOUS)MOUSE:
    a) >12 gm/kg (RTECS, 2005)
    D) PRAMIRACETAM
    1) LD50- (ORAL)MOUSE:
    a) 4355 mg/kg (RTECS, 2005)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) GABA: Although derivatives of GABA, these drugs do not appear to have an effect on GABAergic transmission in the central nervous system (Kraaier et al, 1989; Sourander et al, 1987). It is speculated that actions of these nootropic agents may at least in part be facilitated through improved cholinergic neuronal function (Shih & Pugsley, 1985; Pepeu & Spignoli, 1989; Scarpazza et al, 1993). This is supported by animal data demonstrating that aniracetam can prevent brain acetylcholine decreases and amnesia induced by scopolamine (Toide, 1989; Spignoli & Pepeu, 1987; Cumin et al, 1982; Pepeu & Spignoli, 1989). It was speculated that pramiracetam may increase synaptic acetylcholine content of subcortical areas which are closely related to memory functions (Scarpazza et al, 1993).
    1) There are striking differences between the drugs in this class, with no single predominant mode of action shared by the whole group. Most drugs in this class do influence cholinergic function. Most stimulate acetylcholine production and turnover, but with varying actions at both muscarinic and nicotinic receptors. Few drugs of this group have substantial action at GABA receptor sites. Generally, there are no significant effects on dopaminergic, serotonergic, or adrenergic transmission (except nebracetam), and no affinity is reported for the adenosine type I or mu-opioid receptors (Shorvon, 2001).
    2) Aniracetam has also been reported to prevent amnesia induced by hemicholinium, an agent which blocks high affinity choline uptake at presynaptic sites and reduces acetylcholine synthesis (Pepeu & Spignoli, 1989). Nootropic agents including piracetam and oxiracetam have been demonstrated to stimulate high affinity choline uptake in the hippocampus as well as stimulating acetylcholine utilization in cerebral cortex and hippocampus (Spignoli & Pepeu, 1987; Parnetti, 1995).
    B) NOOTROPIC: In human studies, aniracetam has been demonstrated to protect against hypoxia-induced electroencephalogram (EEG) changes and associated impairment of mental performance (Saletu & Grunberger, 1984; Saletu & Grunberger, 1985). Improvements in some psychometric parameters (reaction time shortening, tapping speed acceleration) attributed to aniracetam have been reported in geriatric patients (Saletu et al, 1980), and there is evidence of memory-enhancing effects of the drug in age-related brain deficits (Sourander et al, 1987).
    1) Electroencephalographic changes observed in geriatric patients following oral aniracetam have included a decrease of delta and theta activity, an increase in alpha activity and slow beta activity, and an acceleration of dominant frequency (Saletu et al, 1980).

Physicochemical

Physical Characteristics

    A) PIRACETAM is a water soluble, white powder (Shorvon, 2001).

Molecular Weight

    A) ANIRACETAM - 219.2 (JEF Reynolds , 2000)
    B) OXIRACETAM - 158.2 (JEF Reynolds , 2000)
    C) PIRACETAM - 142.2 (JEF Reynolds , 2000)
    D) PRAMIRACETAM SULFATE - 367.5 (JEF Reynolds , 2000)

References

General Bibliography

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    2) Chang T, Young RM, & Goulet JR: Pharmacokinetics of oral pramiracetam in normal volunteers. J Clin Pharmacol 1985; 25:291-295.
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