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Misuse, Recreational Use, and Addiction in Relation to Prescription Medicines
Published in Ornella Corazza, Andres Roman-Urrestarazu, Handbook of Novel Psychoactive Substances, 2018
Francesco S. Bersani, Claudio Imperatori
In addition to amphetamines and methylphenidate, other medications are often misused as stimulants or cognitive enhancers. Piracetam is a cyclic derivative of GABA (Corazza, Bersani et al., 2014). Originally marketed in 1971, it has documented benefits in a diverse range of indications, including Alzheimer’s disease, age-associated memory impairment, vertigo, cortical myoclonus, dyslexia, neuropathic pain, and tardive dyskinesia (Corazza, Bersani et al., 2014). It is recently emerged that an increasing number of users purchase piracetam to enhance study- and work-related performances, as well as for pure recreational purposes (Corazza, Bersani et al., 2014). Similar evidence of misuse has been reported in relation to other stimulants, such as aniracetam and centrophenoxine (Schifano, Orsolini, Duccio Papanti, & Corkery, 2015).
Dementia and lower urinary tract dysfunction
Published in Jacques Corcos, David Ginsberg, Gilles Karsenty, Textbook of the Neurogenic Bladder, 2015
Cognitive impairment in patients with DLB also responded well to central cholinergic agents.27 In patients with mild-to-moderate dementia, decreased motivation can be treated with 200–300 mg/day of amantadine hydrochloride. However, it has not been determined whether these drugs could improve patients’ disability scale scores in toileting and functional incontinence. Aniracetam is a pyrrolidinone derivative and is thought to facilitate cholinergic neurotransmission. In an open study of 52 senile poststroke patients, some of whom had dementia, Kumon et al.88 found that 600 mg/day of aniracetam improved urinary and fecal incontinence in 46% patients.
Advances in the Prevention and Treatment of Age-Related Organic Memory Disorders
Published in José León-Carrión, Margaret J. Giannini, Behavioral Neurology in the Elderly, 2001
José León-Carrión, María Rosario Domínguez-Morales, Juan Manuel Barroso y Martín
Various authors have shown the effects of vinpocetine on memory. Nootropic effects of vinpocetine and its effects on memory were studied by DeNoble et al.42 They evaluated the abilities of vinpocetine, vincamine, aniracetan, and hydergine to prevent scopolamine-induced and hypoxia-induced impairment of passive avoidance retention (24 h) in rats. Results showed that vinpocetine, aniracetam, vincamine, and hydergine prevented memory disruption by scopolamine. Data support the view that vinpocetine has cognitive-activating ability as defined in models of both scopolamine-induced and hypoxia-induced memory impairment in rats. In another study, DeNoble43 found that vinpocetine has cognition-activating abilities as defined by an animal model of memory retrieval. Human studies are still needed to replicate results obtained with animals.
Effects of low-dose alcohol exposure in adolescence on subsequent alcohol drinking in adulthood in a rat model of depression
Published in The World Journal of Biological Psychiatry, 2021
Filip Siska, Petra Amchova, Daniela Kuruczova, Yousef Tizabi, Jana Ruda-Kucerova
Our finding that treatment with NBQX can transiently decrease alcohol intake in adulthood in OBX rats, confirms an important involvement of the glutamatergic system in alcohol intake, and its interaction with alcohol drinking and depressive-like phenotype (Gómez-Coronado et al. 2018). The involvement of glutamate and its receptors, particularly the ionotropic receptor groups composed of NMDA, AMPA and kainate receptors in alcohol addiction and withdrawal has been well documented (Kalivas 2000; Ayers-Ringler et al. 2016; Scofield et al. 2016; Márquez et al. 2017). Specifically, it has been shown that chronic alcohol exposure elevates the extracellular levels of glutamate in the mesolimbic dopaminergic pathway (Ding et al. 2012; Rao et al. 2015). Moreover, seizures associated with alcohol withdrawals are believed to be triggered by an increase in glutamate transmission, as they can be blocked by NMDA receptor antagonists (Nelson et al. 2005; Rao et al. 2015). In addition, both ketamine and NBQX can reduce alcohol intake in rodent models (Rezvani et al. 2017; Ruda-Kucerova et al. 2018). Cannady et al. (2013) have shown that promotion of alcohol drinking induced by aniracetam (selective positive modulator of AMPA receptors) can be reversed by DNQX, an AMPA receptor antagonist similar to NBQX (Cannady et al. 2013). Other studies using mixed AMPA/kainate receptor antagonists have revealed the potential of these substances in attenuating operant alcohol reinforcement (Stephens and Brown 1999) or cue-induced alcohol-seeking behaviour (Czachowski et al. 2012).
Pharmacological management of post-stroke depression: an update of the evidence and clinical guidance
Published in Expert Opinion on Pharmacotherapy, 2021
Janne Kaergaard Mortensen, Grethe Andersen
Neither the scientific statement on PSD from 2017 [7] nor the most recent Cochrane review from 2020 [8] recommends the use of any specific drug in the treatment of PSD. The Cochrane review includes 12 trials on different SSRIs (citalopram, fluoxetine, paroxetine and sertraline) and two trials on TCAs (amitriptyline and nortriptyline). Five trials (six comparisons) studies the antidepressants Deanxit (cyclic gamma aminobutyric acid compound), Aniracetam (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor modulator), reboxetine (a selective norepinephrine reuptake inhibitor/NARI), trazodone (serotonin receptor antagonist and serotonin reuptake inhibitor) and nefiracetam (cyclic gamma aminobutyric acid compound)). They did not identify any trials on mood stabilizers (e.g. lithium) or benzodiazepines. They identified one trial on the psychostimulant methylphenidate but it was not included due to the lack of separate outcome data on patients with depression at entry [24]. Another small RCT on methylphenidate including 21 patients from 1998 showed a significant reduction in depressive symptoms compared to placebo [25]. Given their cardiovascular risk profile and the risk of reversible vasoconstriction syndrome, and the fact that additional evidence of their efficacy comes from case reports [26] and open label trials [27], the scientific statement on PSD warrants further large-scale RCTs before it can be determined whether psychostimulants are effective in improving outcomes after stroke.
The unapproved drug centrophenoxine (meclofenoxate) in cognitive enhancement dietary supplements
Published in Clinical Toxicology, 2022
Pieter A. Cohen, Bharathi Avula, Ikhlas Khan
To our knowledge, our study is the first to quantify the unapproved drug centrophenoxine in dietary supplements. Our study adds centrophenoxine, a drug that may increase choline levels in the central nervous system, to several other prohibited drugs, including picamilon, phenibut, piracetam, omberacetam, tianeptine, and aniracetam, found in cognitive enhancement supplements sold in the US [1–4]. The FDA should warn consumers and manufacturers that centrophenoxine is an unapproved drug, and clinicians should advise patients that cognitive enhancement supplements may contain any one of a number of unapproved and prohibited drugs.