Pramiracetam belongs to a class of drugs referred to in scientific literature as "nootropics," derived from Greek and meaning “acting on or towards the mind." [1,2] Nootropics are sometimes referred to as, but are not entirely synonymous with, "smart drugs." Smart drugs are a popular term for any cognition-boosting substance or drug, whereas nootropics specifically include the drugs piracetam, oxiracetam, aniracetam, pramiracetam and phenylpiracetam, all of which have been used in humans. 
The following passage is excerpted from a review by Gouliaev and Senning entitled "Piracetam and other structurally similar nootropics," with especially relevant selections regarding mechanism of action, general effects and characteristics, and specific therapeutics, in bold:
"The piracetam-like nootropics are capable of achieving reversal of amnesia induced by, e.g., scopolamine, electroconvulsive shock and hypoxia. Protection against barbiturate intoxication is observed and some benefit in clinical studies with patients suffering from mild to moderate degrees of dementia has been demonstrated. No affinity for the alpha 1-, alpha 2-, beta-, muscarinic, 5-hydroxytryptamine-, dopamine, adenosine-A1-, mu-opiate, gamma-aminobutyric acid (GABA) (except for nefiracetam (GABAA)), benzodiazepine and glutamate receptors has been found. The racetams possess a very low toxicity and lack serious side effects. Increased turnover of different neurotransmitters has been observed as well as other biochemical findings, e.g., inhibition of enzymes such as prolylendopeptidase. So far, no generally accepted mechanism of action has, however, emerged. We believe that the effect of the racetams is due to a potentiation of already present neurotransmission and that much evidence points in the direction of a modulated ion flux by, e.g., potentiated calcium influx through non-L-type voltage-dependent calcium channels, potentiated sodium influx through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor gated channels or voltage-dependent channels or decreases in potassium efflux. Effects on carrier mediated ion transport are also possible." 
Auteri, et al, found that half-life of pramiracetam varied greatly (2-8 hours) between various healthy volunteers, although the half-life varied very little between repeated dosings given to any one volunteer. Half-life was no different between tablet form and pramiracetam in a solution, although absorption rate was notably faster with the solution. 
Corasaniti, et al, speculate based on data gathered through experiments on rats, that a documented increase in Nitric Oxide Synthase (20% increase when 300mg/kg were applied intraperitoneally - which, of course, translates to a much lesser dose in humans) in the cerebral cortex of rats may be at least partly responsible for the nootropic effects of the drug: "present data demonstrate that pramiracetam given alone or in combination with LiCl increases NOS activity in brain cortical homogenates of rats and this may contribute to the mechanisms underlying learning and memory improvement produced by this nootropic." 
The nootropics, and specifically pramiracetam, have been researched within the last decade extensively in the role of treating "(i) cognition/memory; (ii) epilepsy and seizure; (iii) neurodegenerative diseases; (iv) stroke/ischaemia; and (v) stress and anxiety."  According to Malykh and Sadaie, "pramiracetam reportedly improved cognitive deficits associated with traumatic brain injuries." 
Dziak et al found "memory deterioration, consecutive memory decline and as a result to professional and social dysadaptation" were improved in patients experiencing cerebrovascular pathology manifesting in chronic cerebral blood insufficiency and stroke consequences: "data obtained suggest statistically significant heterogeneous influence of the medicine on intensity of the evaluated symptoms." 
McLean et al found in a double-blind, placebo-controlled study that on "the safety and efficacy of 400 mg pramiracetam sulphate TID in treating memory and other cognitive problems of males who have sustained brain injuries," indications that "subject performance in measures of memory, especially delayed recall, evidenced clinically significant improvements after the administration of pramiracetam sulphate as compared to placebo." Very notably, "this improvement was maintained during an 18-month open-trial period on the medication as well as during a 1-month follow-up period after the pramiracetam was discontinued." 
The following excerpt from an abstract of a review by Mondadori et al serves as a conclusion to contextualize pramiracetam and its future research potential, potentially as regards particular symptomatic manifestations of cognitive disorders, diseases, and damage. Especially relevant lines are emboldened:
"The mechanism through which nootropics of the piracetam type (i.e., piracetam itself and its analogues oxiracetam, pramiracetam, and aniracetam) improve memory is still uncertain. Its elucidation will, however, not only mark an advance in the treatment of cognitive disorders, but also shed light on the basic processes of memory storage. Although the great majority of the findings available so far seem to suggest cholinergic mechanisms, divergent results are obtained whenever parallel experiments are performed with two or more of these compounds. More recent observations indicate that interactions with steroids take place. All four compounds are inactive in adrenalectomized laboratory animals; chemical blockade of the adrenal cortex with aminoglutethimide and pretreatment which epoxymexrenon, a potent mineralocorticoid antagonist, eradicated the memory-enhancing effect of all four substances." 
 Giurgea, C. (1973) "The nootropic approach to the pharmacology of the integrative activity of the brain" Cond. Reflex 8, 108-115.
 C. Giurgea, M. Salama (1977) "Nootropic drugs" Prog. Neuro-Pharmac.1, 235-47.
 Malykh AG, Sadaie MR. Piracetam and piracetam-like drugs: from basic science to novel clinical applications to CNS disorders. Drugs. 2010 Feb 12;70(3):287-312.
 Dziak LA, Golik VA, Miziakina EV. Experience in the application of pramistar, a new nootropic peparation, in the treatment of memory disorders in patients with cerebrovascular pathology [Trans. Russian] Lik Sprava. 2003 Dec;(8):67-72.
 Corasaniti MT, Paoletti AM, Palma E, Granato T, Navarra M, Nisticò G. Systemic administration of pramiracetam increases nitric oxide synthase activity in the cerebral cortex of the rat. Funct Neurol. 1995 May-Jun;10(3):151-5.
 Gouliaev AH, Senning A. Piracetam and other structurally related nootropics. Brain Res Brain Res Rev. 1994 May;19(2):180-222.
 Auteri A, Blardi P, Celasco G, Segre G, Urso R. Pharmacokinetics of pramiracetam in healthy volunteers after oral administration. Int J Clin Pharmacol Res. 1992;12(3):129-32.
 McLean A Jr, Cardenas DD, Burgess D, Gamzu E. Placebo-controlled study of pramiracetam in young males with memory and cognitive problems resulting from head injury and anoxia. Brain Inj. 1991 Oct-Dec;5(4):375-80.
 Mondadori C, Petschke F, Häusler A. The effects of nootropics on memory: new aspects for basic research. Pharmacopsychiatry. 1989 Oct;22 Suppl 2:102-6.
*The latter article is intended for educational / informational purposes only. THIS PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. Bodily introduction of any kind into humans or animals is strictly forbidden by law.