Effects Of Modafinil Research Articles

Effects of modafinil and R-modafinil on brain stimulation reward thresholds: implications for their use in the treatment of psychostimulant dependence.

Modafinil and its enantiomer R-modafinil are approved for the treatment of various sleep disorders, and may also be efficacious in the treatment of psychostimulant abuse. However, the ability of modafinil and R-modafinil to alter brain reward function has not yet been assessed. This study assessed the effects of modafinil and R-modafinil on brain reward function using the intracranial self-stimulation (ICSS) paradigm. Male Sprague-Dawley rats were trained to respond for ICSS using current-intensity threshold determination procedures. Changes in ICSS thresholds were then assessed following administration of modafinil and R-modafinil (50, 100, and 150 mg/kg), or cocaine (2.5 - 20 mg/kg) as a positive control. ICSS thresholds were reduced by modafinil at the 150 mg/kg dose, as well as by cocaine at the 10 and 20 mg/kg doses. R-modafinil only produced non-significant trends towards reducing ICSS thresholds. Modafinil and R-modafinil have limited effects on brain reward function in otherwise drug-naïve subjects. Additional assessments of these effects in the context of psychostimulant dependence are needed.

Pharmacological interventions for sleepiness and sleep disturbances caused by shift work.

Shift work results in sleep-wake disturbances, which cause sleepiness during night shifts and reduce sleep length and quality in daytime sleep after the night shift. In its serious form it is also called shift work sleep disorder. Various pharmacological products are used to ameliorate symptoms of sleepiness or poor sleep length and quality. To evaluate the effects of pharmacological interventions to reduce sleepiness or to improve alertness at work and decrease sleep disturbances whilst of work, or both, in workers undertaking shift work. We searched CENTRAL, MEDLINE, EMBASE, PubMed and PsycINFO up to 20 September 2013 and ClinicalTrials.gov up to July 2013. We also screened reference lists of included trials and relevant reviews. We included all eligible randomised controlled trials (RCTs), including cross-over RCTs, of pharmacological products among workers who were engaged in shift work (including night shifts) in their present jobs and who may or may not have had sleep problems. Primary outcomes were sleep length and sleep quality while of work, alertness and sleepiness, or fatigue at work. Two authors independently selected studies, extracted data and assessed risk of bias in included trials. We performed meta-analyses where appropriate. We included 15 randomised placebo-controlled trials with 718 participants. Nine trials evaluated the effect of melatonin and two the effect of hypnotics for improving sleep problems. One trial assessed the effect of modafinil, two of armodafinil and one examined caffeine plus naps to decrease sleepiness or to increase alertness.

Cerebrospinal fluid kynurenic acid and depressive symptoms in HIV-infected individuals

Aims: While the mechanisms underlying the therapeutic efficacy of (±)-Modafinil (MOD) are not fully understood, actions at the dopamine (DA) transporter (DAT) appear to be involved.With some exceptions, DAT blockers administered in combination potentiate the behavioral and reinforcing effects of psychostimulants (PSY) like cocaine (COC). That potentiation is related to increased accumbens (ACC) DA levels. However, recent clinical studies suggested efficacy ofMOD in treating PSY abuse, suggesting a potential reduction of COC use in PSY abusers rather than a potentiation. Methods: Effects of MOD and COC, were tested alone and in combination, on microdialysate ACC DA levels in rats (n=48), and mice (n=60), self-administration (SA) (n=12) in rats, and subjective effects (n=12) in mice trained to discriminate COC. Results: MOD alone (0.03–10mg/kg i.v.) did not maintain SA above vehicle levels when substituted for COC, but at those doses increased DA levels dose-dependently. MOD pretreatments (10–32mg/kg i.p., 5min prior) also dose-dependently (p<0.05) potentiated COC SA, but microdialysis studies showed no significant enhancement of the effects of COC (0.03–3.0mg/kg i.v.) on stimulation of DA levels in ACC in excess of those produced by COC alone. In mice, MOD alone (10–100mg/kg) produced COClike subjective effects and potentiated the subjective effects of low COC doses (p<0.05). In mice, MOD elicited significant (p<0.05) increases in DA levels without significant differences between ACC shell and core, distinguishing MOD from PSYs abused by humans. Conclusions: MOD alone has a reduced PSY profile compared to COC. Our preclinical results suggest it might enhance reinforcing effects when taken in combination with sub-threshold doses of COC, independently from stimulation of DA levels. Based on clinical reports, these effects suggest a basis for use of MOD as a substitution agonist therapy for PSY abuse. Studies are in progress to better address the mechanisms underlying these effects. Financial support: NIDA/IRP.

Antidepressant-like effect of modafinil in mice: Evidence for the involvement of the dopaminergic neurotransmission

BackgroundModafinil is a wake-promoting agent that provides wide ranges of neurological effects. There is evidence that it can produce antidepressant effects. This study investigated the antidepressant effect of modafinil in the tail suspension (TST) in mice. MethodsDifferent doses of modafinil was intraperitoneally (ip) administrated and then animals were subjected to TST and/or open field test (OFT). Moreover, the implication of the dopaminergic neurotransmission in modafinil's antidepressant effect was studied. For this purpose, animals were pretreated with haloperidol (non-selective dopamine receptor antagonist), or SCH23390 and sulpiride (the dopamine D1 and D2 receptor antagonist, respectively), then were assessed by TST. The possible effect of sub-effective dose of modafinil in combination with sub-therapeutic doses of standard antidepressants was also evaluated in separate groups. ResultsModafinil (75mg/kg, ip) produced antidepressant effect in TST, as compared to a control group, without any alterations in ambulation in OFT. Pretreatment of mice with haloperidol (0.2mg/kg, ip) and sulpride (50mg/kg, ip) blocked the anti-immobility effect of modafinil (75mg/kg, ip). We also found that the administration of SCH23390 (0.05mg/kg, sc) couldn’t antagonize the antidepressant effects of modafinil. In addition, a sub-effective dose of modafinil (50mg/kg, ip) potentiated the sub-effective doses of standard antidepressants including of bupropion (1mg/kg, ip), fluoxetine (1mg/kg, ip) and imipramine (0.1mg/kg, ip) and reduced immobility time in TST. ConclusionResults show that modafinil induced an antidepressant property in TST and this effect apparently was mediated through interaction with the dopaminergic (D2 receptors) system.

PC-FACS

PC-FACS

Modafinil increases the latency of response in the Hayling Sentence Completion Test in healthy volunteers: a randomised controlled trial.

BackgroundModafinil is a medication licensed for the treatment of narcolepsy. However, it has been reported that healthy individuals without wakefulness disorders are using modafinil off-label to enhance cognitive functioning. Although some studies have reported that modafinil improves cognitive task performance in healthy volunteers, numerous other studies have failed to detect cognitive enhancing effects of modafinil on several well-established neuropsychological tasks. Interestingly, several clinical and preclinical studies have found that improved cognitive task performance by modafinil is accompanied by slower response times. This observation raises the question as to whether this slowing of response time in healthy volunteers is a necessary and sufficient condition for cognitive enhancement with modafinil. The aim of the current experiment was to explore this question by investigating the effects of modafinil on the Hayling Sentence Completion Test (HSCT).MethodologySixty-four healthy volunteers received either a single dose (200 mg) of modafinil (n = 32) or placebo (n = 32) in a randomized, double-blind, placebo-controlled, parallel group study in which the principal outcome measures were response latencies on the response initiation and response inhibition sections of the HSCT.Principal FindingsParticipants dosed with modafinil had significantly longer mean response latencies on the HSCT for both the response initiation and response inhibition compared to participants dosed with placebo. However, participants in both groups made a similar number of errors on each of these measures, indicating that modafinil did not enhance the accuracy of performance of the task relative to placebo.ConclusionsThis study demonstrated that administration of single 200 mg doses of modafinil to healthy individuals increased the latency of responses in the performance of the HSCT, a task that is highly sensitive to prefrontal executive function, without enhancing accuracy of performance. This finding may provide important clues to defining the limitations of modafinil as a putative cognitive enhancer.Trial RegistrationClinicalTrials.gov NCT02051153

Effectiveness of Modafinil on Fatigue in Chronic Hepatitis C

Introduction: Objective: To assess the efficacy of modafinil on fatigue in patients with Chronic Hepatitis C. Background: Hepatitis C Virus (HCV) is present in about 8% of the veteran population. Fatigue accompanies HCV infection in 53%-67% of patients and is sufficiently severe enough to impair activity in 17%. Modafinil is a unique wake-promoting agent that has been found to be effective in the treatment of fatigue in patients with multiple sclerosis. Methods: Patients aged 18-65 years with a diagnosis of HCV and mean score >27 on the fatigue severity scale (FSS) were eligible for the randomized double-blind placebo controlled trial. Exclusion criteria included hemoglobin <12, total bilirubin >2, uncontrolled diabetes with HBA1c >8, congestive heart failure with EF <35%, malignancy, or pregnancy. Patients received either placebo or 100 mg of modafinil for 2 weeks. Efficacy was evaluated with self-rating scales: fatigue severity scale (FSS) [score= 9-63], Epworth sleep scale (ESS) [score=0-24], and CES-D depression scale [score=0-60]. Change scores were calculated as pre-score minus post-score. Adverse events were also recorded. The independent samples t-test was used to compare groups on change scores. Results: Of the 25 patients enrolled, 4 were lost to follow-up. Eleven patients received modafinil and 10 received placebo. Ten patients in each group completed all outcome measures. No significant improvement in fatigue, sleep, or depression was demonstrated. FSS decreased 7.4 for the modafinil group (pre=50.2, post=42.8) vs. 6.4 for the placebo group (pre=48.9, post 42.5) [p=0.87]. ESS decreased 2.5 for the modafinil group (pre=12.3, post=9.8) vs. 0.8 for the placebo group (pre=10.9, post 10.1) [p=0.38]. CES-D decreased 5.35 for the modafinil group (pre=24.0, post=18.65) vs. 1.9 for the placebo group (pre=25.4, post 23.5) [p=0.36]. Serious adverse events were not found. The most common adverse events were headache and nausea. Conclusion: While 100 mg modafinil daily did not improve fatigue, sleep, or depression compared to placebo, our study was an exploratory study with limited power (n=10 for each group). We showed the feasibility of such a study (i.e., low dropout rate and no serious adverse events) and recommend a future investigation with a larger sample to determine the effectiveness of modafinil to reduce fatigue in HCV patients. The lack of improvement in fatigue in the modafinil group may have also been due to lower dose of modafinil used.

Differential effects of environment-induced changes in body temperature on modafinil's actions against methamphetamine-induced striatal toxicity in mice.

Methamphetamine (METH) exposure can produce hyperthermia that might lead to toxicity and death. Modafinil is a wake-promoting compound that is also been prescribed off-label to treat METH dependence. Modafinil has shown neuroprotective properties against METH harmful effects in animal models. The goal of the present study was to test if the prevention of hyperthermia might play a role on the neuroprotective actions of modafinil against METH toxicity using various ambient temperatures. METH was administered to female C57BL/6 mice in a binge regimen: 4×5mg/kg, 2h apart; modafinil (90mg/kg) was injected twice, 1h before first and fourth METH injections. Drugs were given at cold ambient temperature (14°C) or hot ambient temperature (29°C). Body temperature was measured during treatments. Brains were dissected out 6days after treatments and processed for tyrosine hydroxylase (TH), dopamine transporter (DAT), GFAP and c-Fos immunohistochemistry. Exposure to hot ambient temperature exacerbated METH toxicity evidenced by striatal reductions in TH and DAT and increased GFAP immmunoreactivity. Modafinil counteracted reductions in TH and DAT, but failed to block astroglial activation. At both ambient temperatures tested modafinil did induce increments in GFAP, but the magnitude was significantly lower than the one induced by METH. Both drugs induced increases in c-Fos positive nuclei; modafinil did not block this effect. Our results suggest that protective effects of modafinil against METH-induced neurotoxicity may be dependent, in part, to its hypothermic effects. Nevertheless, modafinil maintained some protective properties on METH-induced alterations in the striatum at different ambient temperatures.

P.6.d.012 Effects of methylphenidate and MDMA (ecstasy) on appraisal of erotic stimuli

The aim of the present study was to compare the behavioral effects of modafinil, an atypical psychostimulatory acting and cognitive-function improving drug, with the effects of the psychostimulants methamphetamine (MET) and MDMA (3,4-methylenedioxymethamphetamine, or “ecstasy”) in a model of mouse agonistic behavior. This model enables the observation of ethologically well-defined sociable, timid, aggressive, and locomotor behavioral acts and postures. Singly-housed male mice (isolates) were separated into 4 groups. The observations were performed in 4 sessions, 1 week apart. In each interaction, singly-housed mice were paired with non-aggressive group-housed partners for 4 min in a neutral environment. The isolates received, in a Latin square design, either a) a vehicle or modafinil at doses 2.0, 10.0, or 50.0 mg/kg; or b) a vehicle or MET at doses 1.0, 5.0, or 10.0 mg/kg; or c) a vehicle or MDMA at doses 2.5, 10.0, or 30.0 mg/kg. The isolates were categorized as timid or aggressive according to their behavior in the control interaction (vehicle pre-treatment). Elements of locomotor, sociable, aggressive, and timid behavior were evaluated (one-way ANOVA).In the aggressive mice, no change in the sum of aggressive behavior was measured following modafinil administration, while both methamphetamine and MDMA produced dose-dependent inhibition of aggression (p < 0.01). The substantial difference in the tested drug effects on agonistic behavior was an increased occurrence of sociable acts (p < 0.01) accompanied by a simultaneous increase of timid acts (p < 0.01) recorded after MDMA, but not after modafinil or methamphetamine administration. In the timid mice, at least some doses of modafinil decreased timidity (p < 0.01) and increased aggression (p < 0.01) with no effect on sociability. Administration of MDMA increased timid activities (p < 0.01). Both MDMA and MET decreased sociability (p < 0.01).

The Effects of Modafinil on Convergent and Divergent Thinking of Creativity: A Randomized Controlled Trial

AbstractModafinil is a drug licensed for the treatment of narcolepsy and sleep apnea. Recently, modafinil has been reported to be used as a pharmacological cognitive enhancer by healthy individuals with no psychiatric disorders. This paper reports on a study that investigated the effects of modafinil on divergent and convergent thinking tasks of creativity. Sixty‐four healthy male (n = 31) and female (n = 33) volunteers participated in a randomized double‐blind placebo‐controlled parallel group design study. For the convergent thinking tasks, modafinil had no significant main effect on the Group Embedded Figures Task and the Remote Associates Task (RAT). However, a median split analysis showed that modafinil participants low in creativity personality trait had significantly higher RAT scores (Mean [M] = 6.85, SD = 3.39; 95% confidence interval [95% CI]: 5.53–8.2) than those high in creativity personality trait (M = 4.27, SD = 3.0; 95% CI: 2.4–6.0). For the divergent thinking tasks, relative to placebo (M = 1.195, SD = 0.28; 95% CI: 1.0–1.3), modafinil (M = 0.77, SD = 0.37; 95% CI: 0.63–0.92) significantly reduced the performance of flexibility scores and marginally reduced the elaboration scores as measured by the Abbreviated Torrance Test for Adults (ATTA). Overall, participants on modafinil (M = 6.3, SD = 2.6; 95% CI: 5.3–7.4) had significantly lower ATTA scores relative to participants on placebo (M = 9.5, SD = 2.3; 95% CI: 8.6–10.4). These results indicate that modafinil might reduce divergent thinking of creativity in healthy individuals. They suggest that, rather than being a more general cognitive enhancer, modafinil might have negative and subtle effects on creativity. However, the results are from a small‐scale trial, which tested a small number of participants. Therefore, the results need to be interpreted with caution. A replication with a large sample of participants is recommended.

Pharmacological interventions for sleepiness and sleep disturbances caused by shift work.

Shift work results in sleep-wake disturbances, which cause sleepiness during night shifts and reduce sleep length and quality in daytime sleep after the night shift. In its serious form it is also called shift work sleep disorder. Various pharmacological products are used to ameliorate symptoms of sleepiness or poor sleep length and quality. To evaluate the effects of pharmacological interventions to reduce sleepiness or to improve alertness at work and decrease sleep disturbances whilst off work, or both, in workers undertaking shift work in their present job and to assess their cost-effectiveness. We searched CENTRAL, MEDLINE, EMBASE, PubMed and PsycINFO up to 20 September 2013 and ClinicalTrials.gov up to July 2013. We also screened reference lists of included trials and relevant reviews. We included all eligible randomised controlled trials (RCTs), including cross-over RCTs, of pharmacological products among workers who were engaged in shift work (including night shifts) in their present jobs and who may or may not have had sleep problems. Primary outcomes were sleep length and sleep quality while off work, alertness and sleepiness, or fatigue at work. Two authors independently selected studies, extracted data and assessed risk of bias in included trials. We performed meta-analyses where appropriate. We included 15 randomised placebo-controlled trials with 718 participants. Nine trials evaluated the effect of melatonin and two the effect of hypnotics for improving sleep problems. One trial assessed the effect of modafinil, two of armodafinil and one examined caffeine plus naps to decrease sleepiness or to increase alertness.Melatonin (1 to 10 mg) after the night shift may increase sleep length during daytime sleep (mean difference (MD) 24 minutes, 95% confidence interval (CI) 9.8 to 38.9; seven trials, 263 participants, low quality evidence) and night-time sleep (MD 17 minutes, 95% CI 3.71 to 30.22; three trials, 234 participants, low quality evidence) compared to placebo. We did not find a dose-response effect. Melatonin may lead to similar sleep latency times as placebo (MD 0.37minutes, 95% CI - 1.55 to 2.29; five trials, 74 participants, low quality evidence).Hypnotic medication, zopiclone, did not result in significantly longer daytime sleep length compared to placebo in one low quality trial and we could not use the data from the study on lormetazepam.Armodafinil taken before the night shift probably reduces sleepiness by one point on the Karolinska Sleepiness Scale (KSS) (MD -0.99, 95% CI -1.32 to -0.67; range 1 to 10; two trials, 572 participants, moderate quality evidence) and increases alertness by 50 ms in a simple reaction time test (MD -50.0, 95% CI -85.5 to -15.5) at three months' follow-up in shift work sleep disorder patients. Modafinil probably has similar effects on sleepiness (KSS) (MD -0.90, 95% CI -1.45 to -0.35; one trial, 183 participants, moderate quality evidence) and alertness in the psychomotor vigilance test in the same patient group. Post-marketing, severe skin reactions have been reported. Adverse effects reported by trial participants were headache, nausea and a rise in blood pressure. There were no trials in non-patient shift workers.Based on one trial, caffeine plus pre-shift naps taken before the night shift decreased sleepiness (KSS) (MD -0.63, 95% CI -1.09 to -0.17).We judged most trials to have a low risk of bias even though the randomisation method and allocation concealment were often not described. There is low quality evidence that melatonin improves sleep length after a night shift but not other sleep quality parameters. Both modafinil and armodafinil increase alertness and reduce sleepiness to some extent in employees who suffer from shift work sleep disorder but they are associated with adverse events. Caffeine plus naps reduces sleepiness during the night shift, but the quality of evidence is low. Based on one low quality trial, hypnotics did not improve sleep length and quality after a night shift.We need more and better quality trials on the beneficial and adverse effects and costs of all pharmacological agents that induce sleep or promote alertness in shift workers both with and without a diagnosis of shift work sleep disorder. We also need systematic reviews of their adverse effects.

High resolution mapping of modafinil induced changes in glutamate level in rat brain.

Modafinil is marketed in the United States for the treatment of narcolepsy and daytime somnolence due to shift-work or sleep apnea. Investigations of this drug in the treatment of cocaine and nicotine dependence in addition to disorders of executive function are also underway. Modafinil has been known to increase glutamate levels in rat brain models. Proton magnetic resonance spectroscopy (1HMRS) has been commonly used to detect the glutamate (Glu) changes in vivo. In this study, we used a recently described glutamate chemical exchange saturation transfer (GluCEST) imaging technique to measure Modafinil induced regional Glu changes in rat brain and compared the results with Glu concentration measured by single voxel 1HMRS. No increases in either GluCEST maps or 1HMRS were observed after Modafinil injection over a period of 5 hours. However, a significant increase in GluCEST (19±4.4%) was observed 24 hours post Modafinil administration, which is consistent with results from previous biochemical studies. This change was not consistently seen with 1HMRS. GluCEST mapping allows regional cerebral Glu changes to be measured and may provide a useful clinical biomarker of Modafinil effects for the management of patients with sleep disorders and addiction.

Modafinil effects on middle-frequency oscillatory power during rule selection in schizophrenia.

Control-related cognitive processes such as rule selection are associated with cortical oscillations in the theta, alpha and, beta ranges, and modulated by catecholamine neurotransmission. Thus, a potential strategy for improving cognitive control deficits in schizophrenia would be to use pro-catecholamine pharmacological agents to augment these control-related oscillations. In a double-blind, placebo-controlled (within-subjects) study, we tested the effects of adjunctive single-dose modafinil 200 mg on rule-related 4-30 Hz oscillations in 23 stable schizophrenia patients, using EEG during cognitive control task performance. EEG data underwent time-frequency decomposition with Morlet wavelets to determine the power of 4-30 Hz oscillations. Modafinil (relative to placebo) enhanced oscillatory power associated with high-control rule selection in theta, alpha, and beta ranges, with modest effects during rule maintenance. Modafinil treatment in schizophrenia augments middle-frequency cortical oscillatory power associated with rule selection, and may subserve diverse subcomponent processes in proactive cognitive control.

Drug use among patients at public clinics treating sexually transmitted infections (STI)

Drug use among patients at public clinics treating sexually transmitted infections (STI)

Subjective and reinforcing effects of modafinil in rats

Subjective and reinforcing effects of modafinil in rats

Chronic administration of modafinil induces hyperalgesia in mice: Reversal by l-NG-nitro-arginine methyl ester and 7-nitroindazole

Modafinil [2-((diphenylmethyl) sulfinyl) acetamide] is a central nervous system stimulant. It has received considerable attention as a potential psychotropic agent in several psychiatric disorders. The current study was carried out to investigate the effect of modafinil after acute administration on animal models of pain in mice. Also, this study evaluated the effect of l-NG-nitroarginine methyl ester (l-NAME), 7-nitroindazole (7-NI) and naloxone following chronic administration of modafinil. Modafinil was administered in the doses of 50, 100 or 200mg/kg once in acute study and it showed significantly increased tail-flick latency (tfl) and paw-licking latency. In formalin test modafinil (100mg/kg) significantly reduced licking/biting time in both early and late phases in comparison to control. In chronic study, modafinil 100mg/kg administered for 10 days, produced a progressive decrease in the reaction time (i.e., tfl/paw-licking latency) in comparison to day 1 values which started building up from day 4 and fully established at day 6, indicating hyperalgesic response. Prior administration of 7-NI (on day 7) and l-NAME (on day 10) prevented the hyperalgesic response while naloxone on day 10 did not have a significant effect on modafinil-induced hyperalgesia. These results demonstrate that modafinil has a potential role in pain as it exhibited antinociceptive effect after acute administration in a dose-dependent manner and on chronic administration it caused hyperalgesia. This hyperalgesia is reversed by nitric oxide synthase inhibitors, suggesting the possibility of involvement of nitric oxide pathway. Further studies are required to evaluate the role of modafinil in clinical pain.

Evaluation of the Effect of Modafinil on Cognitive Functions in Patients with Idiopathic Hypersomnia with P300 (P5.296)

Evaluation of the Effect of Modafinil on Cognitive Functions in Patients with Idiopathic Hypersomnia with P300 (P5.296)

Behavioral Effects of Modafinil and Nicotine, Alone and in Combination, in Tobacco-Deprived Young Adult Smokers

Behavioral Effects of Modafinil and Nicotine, Alone and in Combination, in Tobacco-Deprived Young Adult Smokers

A Placebo Controlled Trial on Add-on Modafinil on the Anti-psychotic Treatment Emergent Hyperglycemia and Hyperlipidemia.

Modafinil is non stimulant drug which is marketed for mainly Narcolepsy and daytime drowsiness. The clinical experience and Summary of Product Characteristics (SPC) of the drug also mentions Anorexia as one of the side effects. Anorexia can have a direct impact on the carbohydrate and fat intake, which may, in turn, regulate antipsychotic induced dyslipidemia and Hyperglycaemia.Aim:To compare the effects of Modafinil- ADDON with Placebo add on with olanzapine, Clozapine and Risperidone in drug naive subjects and people who were started on the drugs within 15days of assessment.Materials and Methods:Randomized, Double blind, Placebo controlled study, which was conducted at two centres, one at department of Psychiatry, S.V Medical College, Tirupati and the other at Asha hospitals, Hyderabad. Seventy two patient were randomised, sixty three patients have completed the total study period of three months. The dose of Modafinil was 200 mgs constantly as Flexible doses of Olanzapine, Clozapine and Risperidone as per clinical need was given. A baseline, three week and twelve week assessments of Fasting blood Glucose and fasting Serum cholesterol were made and the groups were compared on these parameters.Results:From baseline to week 3 there was a significant raise in Fasting serum cholesterol followed by a fall from week 3 to week 12 in the Modafinil addon group, though it could not be considered a drug for hypercholesteremia like Statins in controlling hyperlipidaemia. The implications of these findings were discussed.

Neural substrates of impulsive decision making modulated by modafinil in alcohol-dependent patients.

Impulsive decision making is a hallmark of frequently occurring addiction disorders including alcohol dependence (AD). Therefore, ameliorating impulsive decision making is a promising target for the treatment of AD. Previous studies have shown that modafinil enhances cognitive control functions in various psychiatric disorders. However, the effects of modafinil on delay discounting and its underlying neural correlates have not been investigated as yet. The aim of the current study was to investigate the effects of modafinil on neural correlates of impulsive decision making in abstinent AD patients and healthy control (HC) subjects. A randomized, double-blind, placebo-controlled, within-subjects cross-over study using functional magnetic resonance imaging (fMRI) was conducted in 14 AD patients and 16 HC subjects. All subjects participated in two fMRI sessions in which they either received a single dose of placebo or 200mg of modafinil 2h before the session. During fMRI, subjects completed a delay-discounting task to measure impulsive decision making. Modafinil improved impulsive decision making in AD pateints, which was accompanied by enhanced recruitment of frontoparietal regions and reduced activation of the ventromedial prefrontal cortex. Moreover, modafinil-induced enhancement of functional connectivity between the superior frontal gyrus and ventral striatum was specifically associated with improvement in impulsive decision making. These findings indicate that modafinil can improve impulsive decision making in AD patients through an enhanced coupling of prefrontal control regions and brain regions coding the subjective value of rewards. Therefore, the current study supports the implementation of modafinil in future clinical trials for AD.