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Modafinil: A Review of Neurochemical Actions and Effects on Cognition | Neuropsychopharmacology

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Neuropharmacology 59, 9— Several studies of modafinil effects on cognition in healthy adults undergoing sleep deprivation or simulated night shifts have been reported see Wesensten, for review.

A few studies of cognition and functional neuroanatomy have been conducted in patients with narcolepsy Table 3. An fMRI study of narcolepsy patients and healthy controls found no within- or between-group differences in modafinil vs placebo effects on extent of activation across the whole brain in passive response to combined visual and auditory stimulation Ellis et al, This suggests that modafinil does not merely cause diffuse activation across the cortex, as might result from primary effects on arousal or early sensory processes.

Other studies have examined effects on scalp electrophysiology measures in narcolepsy patients. Whereas it is not entirely certain how to resolve this finding with the reported effects on the other EEG phenomena, it is possible that this last effect represents activation of brainstem centers with a diffuse cortical distribution, such as the monoamine nuclei, whose activity may be associated with widespread effects on other cortical electrical phenomena such as the other frequency bands.

This issue may be best resolved by testing modafinil effects either in animal models, where single-unit or multiunit activity can be compared to simultaneous scalp electrical activity, or in humans with both scalp EEG and whole-brain imaging by fMRI. Modafinil effects on cognition have been studied as well in psychiatric populations Table 3. This includes a study of 20 patients with stable chronic schizophrenia, in a double-blind, placebo controlled, single-dose crossover study Turner et al, b.

In this visual discrimination learning task developed as a WCST analog that could be performed by animalsthe ED shift is a form of attentional set-shifting mediated by fronto-cortical loops that are modulated by ascending DA systems.

This suggests a measure of specificity to patients with schizophrenia for enhancement of attentional set-shifting, a function strongly dependent in this task on lateral PFC Dias et al, The placebo-condition coefficient of variation was negatively associated with changes in both this behavioral measure and BA 46 neural activity, suggesting that those patients with worse baseline performance exhibited the strongest response to modafinil.

Two studies of add-on modafinil treatment Ans schizophrenia patients have failed to find significant differences Procigil placebo on behavioral cognitive measures. On the Letter-Number Span, within the modafinil group, d was approximately 0. These results suggest that the Provigil And Cognitive Function sample sizes 10 patients completing the study in each group conferred inadequate statistical power to detect Provitil differences on these measures. In addition, the modafinil group was Ad worse in performance Congitive baseline on most of the other cognitive measures, whereas the placebo group exhibited a significant response on the clinical measures.

The abstract does not indicate how many subjects completed the study. These studies appear to remain inconclusive regarding null findings with modafinil on cognitive dysfunction in schizophrenia and provide emphasis on the critical need for adequate statistical power in clinical trials study design.

The two doses were not directly compared for cognitive effects in this study. As indicated above, modafinil effects on cognition have also been studied in ADHD. The patients as a group showed slowed latencies together with increased accuracy on several measures, including the Delayed Match-to-Sample, Tower of London, and visual recognition memory tasks, suggesting that Provigil And Cognitive Function effects including shifting individuals on the speed—accuracy curve to Fuction performance.

In contrast, a 2-week study of 22 adult ADHD patients, where the modafinil-treated group Provkgil titrated over 4—7 days to an average dose of In these two latter studies, overall TOVA performance improved in the modafinil-treated group, whereas it declined from pre-treatment baseline in the placebo group. These studies show consistent evidence for the benefits of modafinil for cognitive function.

Studies in rodents indicate that modafinil can improve working memory performance in a dose- and delay-dependent manner, that the processing of contextual cues is also enhanced with modafinil, and that these effects may be augmented with sustained dosing regimens. In healthy humans with or without undergoing sleep deprivationworking memory, recognition memory, sustained attention, and other tasks dependent on cognitive control are enhanced with modafinil.

Some evidence suggests that the magnitude of modafinil effects in healthy adults may depend on underlying cognitive abilities. Among psychiatric populations, there is now consistent evidence that modafinil in well-tolerated dosing regimens improves attention and response inhibition in children and adolescents with ADHD; this benefit may be related to modafinil effects in modulating performance along the speed-accuracy curve for responsive individuals.

Among adult psychiatric patients, there is evidence that modafinil improves several prefrontal-dependent cognitive functions in schizophrenia, major depression, and adult ADHD. Some null findings have been reported in schizophrenia; however, these studies have significant limitations evident in their design. The range of clinical samples and cognitive functions that are subject to modafinil treatment study is expected to expand in the future.

The most highly elaborated model of catecholamine modulation of higher cognition has been developed for PFC dopamine in working memory, based primarily on studies of nonhuman primates. D1 receptors in the PFC are primarily found on the distal dendritic spines of pyramidal cells, often in conjunction with asymmetric, presumably glutamatergic synapses, and occasionally in triads which also include DA terminals Smiley and Goldman-Rakic, ; Smiley et al, ; Williams and Goldman-Rakic, This may represent a post-synaptic site where D1 receptors can gate glutamatergic transmission, as D1 activation not only directly excites pyramidal neurons, but enhances the responsiveness of the post-synaptic NMDA receptor on those cells as well Seamans and Yang, The facilitation of NMDA effects on intracellular calcium via calcyon—G q interactions has been proposed as one of the most important functions of DA in the PFC, by not only by supporting persistent delay-related activity, but also by influencing both short and long-term plasticity, gene expression, and neuroadaptation see discussion in Williams and Fhnction, A second major site in the PFC for the D1 receptor is at the glutamatergic terminals between neighboring Proviigil cells Gao et al, At this site, D1 receptor activation leads to the attenuation of recurrent excitation within cortical microcircuitry, probably by presynaptic inhibition of glutamate release Seamans and Functioon, This may have the effect of constraining the extent of local activation during cognitive processes.

This may serve to facilitate a feedforward inhibition that further restricts the extent of local circuit activity. Taken together, these three mechanisms of D1 receptor-mediated action in the PFC appear to potentiate intense focal activity, whereas dampening the responsiveness of the local surrounding circuitry that would otherwise compete with the presently active circuit Goldman-Rakic et al, The information processing consequences of these physiological effects may be as follows: in a scenario of increased afferent glutamatergic activity, Abd informs the PFC of both when to initiate persistent activity and Functioh the information content is, D1 receptor activation then adjusts the gain ie, the strength of the representation of the glutamate-encoded information in the PFC Seamans and Yang, This includes a depression of background PFC activity, which serves to make the self-sustained activity robust to noise eg, distractors Durstewitz and Seamans, NE is implicated as well in PFC-dependent cognitive functions.

In the Aston-Jones and Cohen Aston-Jones and Cohen, model, phasic LC activity is driven by the outcome of task-related decision processes signaled by descending projections from the ACC and orbitofrontal cortexProvigil And Cognitive Function subsequently adjusts the gain in target neurons via ascending projections back to PFC. During high accurate performance of visual target-detection tasks, monkeys exhibit LC activity characterized Fynction moderate tonic activity and additional phasic responses that are selectively observed to targets but not Cognnitive Aston-Jones et al, The phasic activity is not related to the sensory features or a specific reward associated Cognitivw the target stimuli, and is observed even if targets are presented on every trial.

In contrast, no phasic response to distractors is seen even if distractors are infrequent. Moreover, in reversal tasks, LC activity quickly re-sets to the new target and is extinguished to the new distractor; this precedes behavioral reversal PProvigil a single testing session Aston-Jones et al, Provigil And Cognitive Function This is considered adaptive in allowing the animal Procigil pursue alternative behaviors or cognitive processes Aston-Jones and Cohen, This reciprocal relationship between tonic and phasic modes of LC activity may be mediated by changes in the degree of electrotonic coupling between LC cells Aston-Jones and Cohen, ; Usher et al, It appears also that when levels of tonic LC activity are minimal, such as during sleep, grooming, and eating, that phasic responses are also less robust Aston-Jones and Bloom, This suggests that, as with other catecholamine-mediated phenomena, phasic LC activity may CCognitive related to tonic activity Provigil And Cognitive Function an inverted-U-shaped manner.

For individuals with excessively-low tonic LC activity, enhancements of both tonic and phasic LC activity may possibly be elicited in concert. Modafinil has consistently shown efficacy in measures of alertness in narcolepsy and shift-work sleep disorder. Two randomized, double-blind placebo-controlled studies with a total of patients conducted by the US Modfinil in Narcolepsy Multicenter Study Groupfound significant efficacy of modafinil for subjective and objective measures of wakefulness among patients with narcolepsy.

Similar results have been found in smaller double-blind, placebo-controlled studies Billiard et al, ; Broughton et al, In these studies and others, open-label Provigil And Cognitive Function have found modafinil to have long-term efficacy for sleepiness extending for as long as weeks, and to be well-tolerated, with no evidence of significant adverse events or abuse Besset et al, ; Hirshkowitz et al, ; Mitler et al, Modafinil has also shown efficacy for shift work sleep disorder, with a large randomized, double-blind placebo-controlled study showing improvements in sleep latency, vigilance, sleep-related function, and the rate of automobile accidents during the post-work commute Czeisler et al, Modafinil has also been evaluated for the treatment of fatigue and sedation in a number of other neurological and medical conditions, including multiple sclerosis, idiopathic Parkinson's disease, chronic fatigue syndrome, polio, HIV infection, Proviyil, obstructive sleep apnea, post-anaesthetic sedation, and fibromyalgia, Cgnitive generally favorable but somewhat mixed results see comprehensive summary of these studies in Ballon and Feifel, Remarkably, despite the importance of cognitive dysfunction in a range of neurological and medical illnesses, to our knowledge there have been no reports to date Provigio modafinil effects on cognition in these disorders.

PANSS scores were unchanged, indicating that positive symptoms were not exacerbated, and no serious adverse events were detected. Two studies of patients with major depression have been reported. In a week, open-label extension study of these depressed patients, with modafinil doses titrated following the initial 8-week placebo-controlled study cited above, the initial modafinil non-responders showed a significantly greater clinical response on all measures than the initial treatment-responsive group Thase et al, Among child and adolescent psychiatric disorders, modafinil has only been studied Provigil And Cognitive Function date in ADHD.

Throughout these clinical intervention studies, modafinil has been well tolerated. Nevertheless, case reports have appeared describing significant adverse events in routine clinical use of modafinil. One case report has appeared describing exacerbation of psychosis in a year-old inpatient, with schizophrenia and hypertension, after initiation of modafinil treatment Narendran et Funtion, The patient is reported to have stabilized within 2 weeks after discontinuation of modafinil including severity of positive psychotic symptoms with no other medication changes, Fknction there is no indication in the report of serious sequelae in the intervening period of worsened psychosis.

Whereas other single case reports have appeared describing adverse events in the treatment of psychiatric patients such as clozapine toxicity Dequardo,premature ventricular contractions Oskooilar,induced mania Vorspan et al, ; Wolf et al,and irritability and verbal aggression Ranjan and Chandra,these events have not been observed at a significant rate in modafinil-treated patients compared to placebo-treated patients in the clinical trials cited above.

Modafinil effects on anxiety have also been measured, in animal models and in humans. One study found that whereas amphetamine increased three measures of anxiety in mice, with increased latency of exploration of a white compartment, increased open-field thigmotaxis, and decreased time in the open arms of an elevated-plus maze, modafinil lacked these effects at doses that induce comparable effects on locomotor activity Simon et al, A study of wake-promoting effects in monkeys reported no significant observations of anxiety responses to modafinil after single Functioj repeated doses that increased nocturnal activity Hermant et al, Interestingly, in this study, both overall positive and negative affect was relatively increased on modafinil.

Two studies of obstructive sleep apnea patients reported on anxiety. In the second, rates of anxiety were 5. A study of 50 multiple sclerosis patients found three leading to drop out or dose reduction due to nervousness or restlessness Zifko et al, It does appear, therefore, that modafinil at clinically-effecive doses is associated with increased anxiety in healthy individuals and clinical populations, although it is unclear if this is dose-related.

Modafinil is an agent with a rapidly expanding list of off-label uses in neurology, medicine, and psychiatry. It appears to have multiple effects on Cognitige systems in the brain, including DAT and NET inhibition, and elevation of extracellular catecholamines, glutamate, serotonin, and HA, activation of the orexinergic system, and decreased GABA.

Alpha-adrenergic, D1 and D2 receptors in the brain mediate modafinil effects on waking and activity, and may also mediate the neurochemical effects on these other Provigil Class Medication systems. Modafinil is also significantly different from amphetamine in structure and profile of neurochemical and behavioral effects.

Intriguing preliminary evidence suggests that modafinil may be relatively selective for cortical over Functiin effects. In the clinical setting, modafinil shows efficacy in a number of neurological and psychiatric illnesses, with a significantly improved side-effect profile compared to amphetamine, including a relatively low liability to abuse. Equally important, there is now increasing evidence that modafinil can improve cognitive function, particularly working memory, episodic memory, and processes requiring cognitive control.

Studies in animal models and neuroimaging in humans suggest that these effects may be related to specific actions of modafinil in the frontal cortex. The remediation of cognitive dysfunction and related neural activity may in turn form the basis of the clinical efficacy of this agent, across a range of neuropsychiatric disorders.

Further investigation is necessary to confirm these initial findings, to identify specificity of these effects in the domains of neurochemistry, neuroanatomy, and cognition, and to evaluate other factors relevant to clinical use, such as the relationship of single-dose to sustained dosing regimens, and the relationship of pro-cognitive effects to clinical outcome.

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Review of ‘smart drug’ shows modafinil does enhance cognition

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Tiagabine, a gamma-amino-butyric acid transporter inhibitor impairs spatial learning of rats in the Morris water-maze. A Fuhction trial of modafinil for nicotine dependence. Substance use disorders in Iraq and Afghanistan veterans in VA healthcare, — Implications for screening, diagnosis and treatment.

Innervation of histaminergic tuberomammillary neurons by GABAergic and galaninergic neurons in the ventrolateral preoptic nucleus of the rat. Non-amphetaminic mechanism of stimulant locomotor effect of modafinil in mice. Experimental studies on the role of serotonin in cognition. Noradrenaline and attention lapses. Section II. The dopamine An. Int Rev Neurobiol. Section III.

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Inhibitory effects of the psychoactive drug modafinil on gamma-aminobutyric acid outflow from the cerebral cortex of the awake freely moving guinea-pig.

Possible involvement of 5-hydroxytryptamine mechanisms. Naunyn Schmiedebergs Arch Pharmacol. Modafinil and cortical gamma-aminobutyric acid outflow. Modulation Provigil And Cognitive Function 5-hydroxytryptamine neurotoxins. Efficacy of modafinil compared to dextroamphetamine for the treatment Cognitife attention deficit hyperactivity disorder in adults. Provivil Child Adolesc Psychopharmacol.

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Modafinil, sold under the brand name Provigil among others, is a medication to treat sleepiness due to narcolepsy, shift work sleep disorder, or .serp-item__passage{color:#} Researchers have found that modafinil boosts higher-order cognitive function without causing serious side effects. Modafinil, which has been primarily prescribed in the U.S. since Provigil is sometimes prescribed for off-label purposes in the treatment of ADHD, certain mood disorders, and as a cognitive enhancer or  Another review found that Modafinil was seen to mainly affect cognition by improving executive function (decision-making, problem-solving, mental control, self-regulation) especially when.

Effects of modafinil-induced wakefulness on glutamine synthetase regulation in the rat brain. Brain Res Mol Brain Res. A review of the use of modafinil for attention-deficit hyperactivity disorder. Expert Rev Neurother. Cognitive enhancing effects of modafinil in healthy volunteers.

Br J Pharmacol. Modafinil enhances thalamocortical activity by increasing neuronal electrotonic coupling. Functional alteration in frontolimbic systems relevant to moral judgment in cocaine-dependent subjects. Effects of modafinil on dopamine and dopamine transporters in the male human brain: clinical implications.

Subjective effects of modafinil, a new central adrenergic stimulant in healthy volunteers: a comparison with amphetamine, caffeine and placebo. European psychiatry. Assessment of modafinil on attentional processes in a five-choice serial reaction time test in the rat. Randomized clinical study of a histamine H3 receptor Provigil And Cognitive Function for the treatment of adults with attention-deficit hyperactivity disorder.

CNS Drugs. Effects of Provigil And Cognitive Function on cognitive performance and alertness during sleep deprivation. Curr Here Des. Prvigil of brain dopamine in food reward and reinforcement. Dopaminergic role in stimulant-induced wakefulness. Ann Neurol. Neurotransmitters and cognition. Evidence for the involvement of dopamine transporters in behavioral stimulant effects of modafinil.

Discrimination of subjective effects of cocaine mg PO. No significant cocaine-like subjective effect but MOD fully substituted for cocaine in 3 subjects.

Rush et al. MOD did not show significant induction of psychoactive effects. Subjective effects of amphetamine 15 mg PO caffeine mg PO Functioj placebo. No significant induction of amphetamine-like psychoactive effects. Warot et al.

For example, MOD-induced improvement of cognitive performance has been explored in. Background: Animal models and human studies have identified the potential of modafinil as a cognitive enhancing agent, independent of its effects on promoting.

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