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PubMed2000

A double-blind, placebo-controlled investigation of the efficacy of modafinil for sustaining the alertness and performance of aviators: a helicopter simulator study.

RATIONALE: In 1998, the FDA approved modafinil for treating excessive daytime sleepiness in narcoleptics, and this has raised questions about the appropriateness of this compound for enhancing alertness in sleep-deprived controls. This study explored the efficacy of modafinil for maintaining the performance of volunteers required to accomplish highly demanding tasks despite sleep loss. OBJECTIVE: The principal objective was to determine whether prophylactic doses of modafinil would attenuate decrements in aviator performance and arousal throughout 2 days and 1 night without sleep. METHODS: Six pilots were exposed to two 40-h periods of continuous wakefulness. In one, three 200-mg doses of modafinil were given and in the other, matching placebos were administered. Helicopter simulator flights, resting EEGs, and Profile of Mood States (POMS) questionnaires were evaluated. RESULTS: Modafinil attenuated sleep deprivation effects on four of six flight maneuvers, reduced slow-wave EEG activity, and lessened self-reported problems with mood and alertness in comparison to placebo. The most noticeable benefits occurred between 0330 and 1130 hours, when the combined impact of sleep loss and the circadian trough was most severe. The most frequently observed drug side effects were vertigo, nausea, and dizziness. These could have been related to: 1) the motion-based testing, 2) the use of a simulator rather than an actual aircraft (i.e., "simulator sickness"), and/or 3) the administration of more than 400 mg modafinil. CONCLUSIONS: Modafinil is a promising countermeasure for sleep loss in normals; however, additional studies aimed at reducing side effects are needed before it should be used in aviators.

Adult↗
PubMed1991

Effect of modafinil on pancreatic exocrine secretion in the rat. A comparison with methadone.

Modafinil is a recently developed drug which increases wakefulness in several animal species and in man, an effect involving, at least in part, central adrenoceptors. In the present experiments, the effect of modafinil was studied on a model of neurally stimulated secretion, pancreatic secretion induced by 2-deoxyglucose (2DG) in the rat, and compared with that of the mu-opiate methadone. Modafinil induced a dose-related inhibition of 2DG-stimulated pancreatic secretion, reaching more than 80% after 250 mg/kg i.p. The modafinil effect was suppressed by idazoxan or by large doses of prazosin but not by naloxone. In addition modafinil (250 mg/kg i.p.) did not change the pancreatic response to electrical vagal stimulation. Methadone also potently suppressed 2DG-stimulated pancreatic secretion, but in contrast to modafinil, the methadone effect was blocked by naloxone, but not by the adrenoceptor antagonists idazoxan, prazosin and propranolol. It is concluded that modafinil decreases centrally 2DG-stimulated pancreatic secretion through a pathway involving alpha 1- and alpha 2-adrenoceptors, without an interaction with opiate receptors.

Adrenergic alpha-Antagonists↗
PubMed2004

Modafinil improves cognition and response inhibition in adult attention-deficit/hyperactivity disorder.

BACKGROUND: Modafinil, a novel cognitive enhancer, has a clinical profile similar to conventional stimulants such as methylphenidate, despite a seemingly different mechanism of action. Modafinil selectively improves neuropsychological task performance in healthy volunteers, possibly through improved inhibitory control. We examined whether modafinil induced similar improvements in adults with attention-deficit/hyperactivity disorder. METHODS: Twenty patients with a DSM-IV diagnosis of attention-deficit/hyperactivity disorder were entered into a double-blind, randomized, placebo-controlled crossover study using a single 200 mg dose of modafinil. RESULTS: Modafinil produced a similar pattern of cognitive enhancement to that observed in healthy adults, with improvements on tests of short-term memory span, visual memory, spatial planning, and stop-signal motor inhibition. On several measures, increased accuracy was accompanied by slowed response latency. This alteration in the speed-accuracy trade-off may indicate that modafinil increases the ability to "reflect" on problems coupled with decreased impulsive responding. Improvements were also seen in sustained attention, which was unaffected in healthy subjects. CONCLUSIONS: If these benefits are shown to be maintained with chronic administration, modafinil may have potential as an important therapy for attention-deficit/hyperactivity disorder with a similar effect to stimulants such as methylphenidate in improving stop-signal response inhibition but without the side effects commonly experienced with amphetamine-like drugs.

Adult↗
PubMed2006

Modafinil inhibits rat midbrain dopaminergic neurons through D2-like receptors.

Modafinil is a well-tolerated medication for excessive sleepiness, attention-deficit disorder, cocaine dependence and as an adjunct to antidepressants with low propensity for abuse. We investigated the modafinil action on identified dopaminergic and GABAergic neurons in the ventral tegmental area (VTA) and substantia nigra (SN) of rat brain slices. Modafinil (20 microM) inhibited the firing of dopaminergic, but not GABAergic neurons. This inhibition was maintained in the presence of tetrodotoxin and was accompanied by hyperpolarization. Sulpiride (10 microM), a D2-receptor antagonist, but not prazosine (20 microM, an alpha1-adrenoreceptor blocker) abolished the modafinil action. Inhibition of dopamine reuptake with a low dose of nomifensine (1 microM) reduced the firing of DA neurons in a sulpiride-dependent manner and blunted the effect of modafinil. On acutely isolated neurons, modafinil evoked D2-receptor-mediated outward currents in tyrosine-hydroxylase positive cells, identified by single-cell RT-PCR, which reversed polarity near the K(+) equilibrium potential and were unchanged in the presence of nomifensine. Thus modafinil directly inhibits DA neurons through D2 receptors.

Action Potentials↗
PubMed2006

Modafinil-induced modulation of working memory and plasma corticosterone in chronically-stressed mice.

The original aims of our study were to investigate the dose-effect relationship of modafinil administration on working memory performance, in parallel with the measurement of plasma corticosterone in chronically-stressed mice, as compared to control mice. Memory performance was evaluated by spontaneous alternation in a T-maze. Vehicle or modafinil (8, 16 or 32 mg/kg) were administered after or without chronic stress (immobilization and exposure to light) for 15 min/day over a period of consecutive 14 days. Immediately after behavioral testing, blood was sampled to measure plasma corticosterone levels. Under non-stress conditions, corticosterone significantly increased with 16 and 32 mg/kg modafinil administration. Interestingly, optimal working memory performance was revealed at the 16 mg/kg dose. Moreover, no correlation was evidenced between working memory performance and plasma corticosterone level in modafinil-treated animals. Under stress conditions, corticosterone level was lowered at 8 mg/kg and remained unchanged at 16 and 32 mg/kg modafinil. An optimal working memory performance was evidenced at 8 mg/kg, which indicated a decrease in the efficiency threshold of modafinil under stress. Furthermore, an inverse correlation emerged between working memory performance and corticosterone level. Our study evidenced for the first time the interaction between stress and memory, in the emotional modulation of working memory performance, as a function of the administered dose of modafinil.

Animals↗
PubMed2004

Modafinil treatment in patients with seasonal affective disorder/winter depression: an open-label pilot study.

BACKGROUND: Hypersomnia is a cardinal symptom of seasonal affective disorder/winter depression. This open-label pilot study assessed modafinil, a novel wake-promoting agent, as treatment for seasonal affective disorder/winter depression. METHODS: Total daily modafinil dose was 100 mg (all patients week 1), and 100 mg or 200 mg split dose (weeks 2-8). Efficacy assessments (weeks 1, 2, 5, and 8) included the Structured Interview Guide for the Hamilton Depression (HAM-D) Rating Scale, Seasonal Affective Disorder Version (SIGH-SAD), Montgomery-Asberg Depression Rating Scale (MADRS), Clinical Global Impression of Change (CGI-C), Fatigue Severity Scale (FSS), and Epworth Sleepiness Scale (ESS). RESULTS: Thirteen patients (11 women; mean age, 41 years) were enrolled, 12 were evaluable for efficacy (100 mg dose, five patients; 200 mg dose, seven patients), and nine completed treatment. Modafinil significantly improved winter depression as shown by reductions from baseline in mean SIGH-SAD at week 1 (P<0.01) through week 8 (P<0.001 weeks 2-8) and MADRS total scores from week 2 through week 8 (P<0.01 for all). At week 8, mean SIGH-SAD total score was 17.1 (versus 37.2 at baseline, P<0.001), and mean MADRS total score was 13.3 (versus 26.9 at baseline, P<0.01). Modafinil significantly improved overall clinical condition at all time points (P<0.001). The response rate was 67% on the SIGH-SAD (29 item), HAM-D (21 item), and MADRS, and 100% on eight atypical SIGH-SAD items. Modafinil significantly reduced fatigue (FSS) and improved wakefulness (ESS) from weeks 2 through 8 (P<0.01). Modafinil was well tolerated. LIMITATIONS: This was an open-label, single site study. CONCLUSIONS: Modafinil may be an effective and well-tolerated treatment in patients with seasonal affective disorder/winter depression.

Adult↗
PubMed2003

Modafinil increases histamine release in the anterior hypothalamus of rats.

Modafinil, (RS)-2-(Diphenylmethylsulfinyl)acetamide, is a well known wake promoting drug used for the treatment of narcolepsy. We investigated the effect of modafinil on the hypothalamic histamine release in the anesthetized rat using in vivo microdialysis. Modafinil (150 mg/kg, i.p.) increased histamine release by 150% of the basal release. The intracerebroventricular (i.c.v.) injection of modafinil (1 nmol) also increased histamine release, however, when modafinil (1 nmol) was injected directly into the tuberomammillary nucleus, a limited region where cell bodies of the histaminergic neurons are located, histamine release was not altered. These observations suggest that modafinil may promote waking via the activation of the histaminergic system, although it does not appear to be a direct pharmacological target of modafinil.

Animals↗
PubMed1999

Determination of the D- and L-enantiomers of modafinil in human plasma utilizing liquid-liquid extraction and high-performance liquid chromatography.

Modafinil, DL-2-[(diphenylmethyl)sulfinyl]acetamide (Provigil), which is chiral at its sulfur atom, is a novel wake-promoting agent currently being developed as the racemate in the United States by Cephalon, Inc. In order to characterize the pharmacokinetic properties of each enantiomer, a stereospecific high-performance liquid chromatography (HPLC) method has been developed for simultaneous determination of D- and L-modafinil in human plasma. The analytes are extracted from plasma into a mixture of hexane-methylene chloride-triethylamine (55:45:2, v/v/v) and then resolved on an EM Separations ChiraDex beta-cyclodextrin column at 12 degrees C using an isocratic mobile phase of 0.020 M, pH 3.0 phosphate buffer-acetonitrile (84:14, v/v). D- and L-modafinil, and the internal standard, 3,3-diphenylpropylamine, are monitored by UV detection at 225 nm. The two major circulating metabolites, modafinil acid and modafinil sulfone, have been shown not to interfere with the assay. Using 0.200 ml of plasma for extraction, the quantifiable range of the assay is 0.100 to 15.0 microg/ml for each enantiomer. The utility of the assay for the characterization of D- and L-modafinil pharmacokinetics in humans after single and multiple oral doses of racemic modafinil has been demonstrated.

Benzhydryl Compounds↗
PubMed1999

The vigilance promoting drug modafinil increases extracellular glutamate levels in the medial preoptic area and the posterior hypothalamus of the conscious rat: prevention by local GABAA receptor blockade.

The effects of modafinil on glutamatergic and GABAergic transmission in the rat medial preoptic area (MPA) and posterior hypothalamus (PH), are analysed. Modafinil (30-300 mg/kg) increased glutamate and decreased GABA levels in the MPA and PH. Local perfusion with the GABAA agonist muscimol (10 microM), reduced, while the GABAA antagonist bicuculline (1 microM and 10 microM) increased glutamate levels. The modafinil (100 mg/kg)-induced increase of glutamate levels was antagonized by local perfusion with bicuculline (1 microM). When glutamate levels were increased by the local perfusion with the glutamate uptake inhibitor L-trans-PDC (0.5 mM), modafinil produced an additional enhancement of glutamate levels. Modafinil (1-33 microM) failed to affect [3H]glutamate uptake in hypothalamic synaptosomes and slices. These findings show that modafinil increases glutamate and decreases GABA levels in MPA and PH. The evidence that bicuculline counteracts the modafinil-induced increase of glutamate levels strengthens the evidence for an inhibitory GABA/glutamate interaction in the above regions controlling the sleep-wakefulness cycle.

Amino Acids↗
PubMed2006

Modafinil augmentation of SSRI therapy in patients with major depressive disorder and excessive sleepiness and fatigue: a 12-week, open-label, extension study.

INTRODUCTION: Many patients with major depressive disorder (MDD) treated with selective serotonin reuptake inhibitors have residual symptoms (eg, persistent fatigue, excessive sleepiness) despite an overall antidepressant response. Placebo-controlled studies indicate that modafinil, a wake-promoting agent, may relieve residual symptoms. METHODS: This 12-week, open-label, dose titration, extension study followed an 8-week placebo-controlled study of modafinil augmentation in patients with MDD. The dose was 100-400 mg/day. The median stable dose was 300 mg/day. Assessments were the Epworth Sleepiness Scale, Brief Fatigue Inventory, Clinical Global Impression of Improvement scale, 17-item Hamilton Rating Scale for Depression, and Montgomery-Asberg Depression Rating Scale. RESULTS: Of the 245 patients treated, 194 completed the study; 70% reported Clinical Global Impression of Improvement scale responses of "much improved" or "very much improved" between open-label baseline and final visit (previous randomized modafinil group: 74%; placebo group: 66%). When data were analyzed for four subsets of patients (former modafinil responders, placebo responders, modafinil nonresponders, and placebo nonresponders), improvements in scores on all outcome measures were at least twice as great among former modafinil and placebo nonresponders compared with responders. Most common adverse events were headache (18%), nausea (9%), and dizziness (7%); all were generally mild to moderate in severity. CONCLUSION: Twelve weeks of modafinil augmentation relieved excessive sleepiness, reduced fatigue, and improved patients' overall clinical condition, including mood.

Adolescent↗
PubMed1998

Effect of modafinil on plasma melatonin, cortisol and growth hormone rhythms, rectal temperature and performance in healthy subjects during a 36 h sleep deprivation.

Modafinil is an alerting substance which has been used successfully to treat narcolepsy. Nothing is known about its effect on hormone secretions. For this purpose, eight healthy young men were enrolled in a double blind trial to test the effects of modafinil on daily plasma melatonin, cortisol and growth hormone (GH) rhythms. Blood was sampled for hormone assays, every hour during the daytime and every 30 min during the nighttime. In addition, rectal temperature and mental performances were determined during the study which comprised 3 sessions, two weeks apart: a 24 h control session including a night with sleep (S1) and two 48 h sessions S2 and S3 with a sleep-deprived night (N1) followed by a recovery night (N2). Modafinil (300 mg x 2) or placebo were randomly attributed during N1 at 22 h and 8 h. As expected, performance was improved after modafinil administration and body temperature was maintained or increased. Plasma melatonin and cortisol profiles were similar after modafinil and placebo administration. The levels observed during the recovery and the control nights (N2) displayed no difference. For GH, during both sleep deprived nights, secretion was dramatically reduced compared with the control one, although the number of secretory episodes was unchanged. These data show that the alerting property of modafinil is not related to an alteration of hormone profiles and suggest that the acute modafinil administration is devoid of short-term side-effects.

Adult↗
PubMed1999

Functional magnetic resonance imaging neuroactivation studies in normal subjects and subjects with the narcoleptic syndrome. Actions of modafinil.

Functional magnetic resonance imaging (fMRI) can be used to detect regional brain responses to changes in sensory stimuli. We have used fMRI to determine the amount of visual and auditory cortical activation in 12 normal subjects and 12 subjects with the narcoleptic syndrome, using a multiplexed visual and auditory stimulation paradigm. In both normal and narcoleptic subjects, mean cortical activation levels during the presentation of periodic visual and auditory stimulation showed no appreciable differences with either age or sex. Normal subjects showed higher levels of visual activation at 10:00 hours than 15:00 hours, with a reverse pattern in narcoleptic subjects (P = 0.007). The group differences in spatial extent of cortical activation between control and narcoleptic subjects were small and statistically insignificant. The alerting action, and imaging response, to a single oral dose of the sleep-preventing drug modafinil 400 mg were then determined and compared with placebo in both the 12 normal (8 given modafinil, 4 placebo) and 12 narcoleptic subjects (8 modafinil, 4 placebo). Modafinil caused an increase in self-reported levels of alertness in 7 of 8 narcoleptic subjects, but there was no significant difference between mean pretreatment and post-treatment activation levels as determined by fMRI for either normal or narcoleptic syndrome subjects given modafinil. However, in the modafinil-treated group of 8 normal and 8 narcoleptic subjects, there was a clock time independent correlation between the initial level of activation as determined by the pretreatment scan and the post-treatment change in activation (visual, P = 0.002; and auditory, P = 0.001). No correlation was observed in placebo-treated subjects (P = 0.99 and 0.77, respectively). Although limited by the small number of subjects, and the lack of an objective measure of alertness, the findings of this study suggest that low cortical activation levels in both normal and narcoleptic subjects are increased following the administration of modafinil. Functional magnetic resonance imaging may be a valuable addition to established studies of attention.

Acoustic Stimulation↗
PubMed1996

Potential brain neuronal targets for amphetamine-, methylphenidate-, and modafinil-induced wakefulness, evidenced by c-fos immunocytochemistry in the cat.

Much experimental and clinical data suggest that the pharmacological profile of modafinil, a newly discovered waking substance, differs from those of amphetamine and methylphenidate, two classical psychostimulants. The brain targets on which modafinil acts to induce wakefulness, however, remain unknown. A double-blind study using the protooncogene c-fos as experimental marker in the cat was, therefore, carried out to identify the potential target neurons of modafinil and compare them with those for amphetamine and methylphenidate. Cats were sacrificed after a single oral administration of amphetamine, methylphenidate, or modafinil at equivalent doses for wake induction (1, 2.5, or 5 mg/kg, respectively) and brain sections examined for Fos by immunocytochemistry. Administration of either amphetamine or methylphenidate evoked Fos-like immunoreactivity in a large number of neurons in the striatum and whole cortex, especially in the caudate nucleus and mediofrontal cortex, which are known to be dopaminergic targets. In contrast, administration of modafinil resulted in the labeling of few cells in these structures, but did induce marked Fos labeling in neurons of the anterior hypothalamic nucleus and adjacent areas. These results provide evidence for the potential brain targets of modafinil, which differ from those of amphetamine or methylphenidate, and suggest that modafinil induces wakefulness by mechanisms distinct from those of the two stimulants.

Amphetamine↗
PubMedDate not supplied

Modafinil-associated weight loss in a clozapine-treated schizoaffective disorder patient.

BACKGROUND: We report a case of weight loss associated with modafinil-initiation in a clozapine-treated man with schizoaffective disorder. METHODS: To report the impact of modafinil, a wake promoting agent that lacks the unwanted side affects brought on by many psychostimulants, on weight in a clozapine-treated patient. RESULTS: Modafinil was initiated, and over the course of 1 year, Mr. B. experienced a weight loss of 40 lbs (from 280 lbs to 240 lbs) and a reduction in body mass index (BMI) of 5.08 Kg/m2 (from 35.52 Kg/m2 to 30.44 Kg/m2). After 3 years on the combination of clozapine and modafinil, his weight stabilized at 230 lbs (BMI = 29.59 Kg/m2). A 30-lb weight gain over a 6-month period occurred following discontinuation of modafinil. Reinstitution of modafinil resulted in a 10-lb. weight loss over a 6-week period. CONCLUSIONS: Modafinil treatment resulted in a significant weight loss in this patient, possibly due to reducing clozapine-associated fatigue. Randomized placebo-controlled trials are necessary to evaluate the safety and efficacy of modafinilfor clozapine-associated weight gain.

Adult↗
PubMed1999

Health-related quality of life effects of modafinil for treatment of narcolepsy.

OBJECTIVE: To evaluate the burden of illness of narcolepsy and assess the health-related quality-of-life (HQL) effects of oral modafinil, a wake-promoting therapy for excessive daytime sleepiness associated with narcolepsy. METHODS: Subjects with narcolepsy enrolled in a nine-week, placebo-controlled, double-blind study and were randomized to placebo, modafinil 200 mg, or modafinil 400 mg. After the study, consenting subjects received modafinil in a 40-week open-label extension. A self-administered HQL questionnaire consisting of the 36-Item Short Form Health Survey (SF-36) and supplemental narcolepsy-specific scales was given to subjects at baseline, study endpoint, and several open-label timepoints. RESULTS: 481 subjects completed a baseline and double-blind endpoint HQL assessment. Compared to population norms, baseline HQL scores reflected substantial burden in vitality, social functioning, and performing usual activities. At study endpoint, subjects in the 400 mg modafinil group had significantly higher scores than placebo for 10 of the 17 HQL scales. The 400 mg modafinil group had more energy, fewer difficulties performing usual activities, fewer interferences with social activities, improved psychological well-being and higher productivity, attention and self-esteem compared to placebo subjects (p<.05). The positive treatment effects were sustained over the open-label extension. CONCLUSION: Modafinil significantly improves health-related quality of life in narcolepsy.

Adult↗
PubMed2004

The effects of modafinil and cognitive behavior therapy on sleep continuity in patients with primary insomnia.

BACKGROUND: Daytime fatigue, if not frank sleepiness, is a common symptom among patients with insomnia, one that is exacerbated during acute treatment with cognitive behavior therapy (CBT). The present study was undertaken to assess whether modafinil could be used to reduce daytime fatigue, sleepiness, or both in patients with primary insomnia and whether the pharmacologic augmentation of wakefulness might produce improved sleep by itself or in combination with CBT. METHODS: 30 subjects with primary insomnia were enrolled in this study and were randomly assigned to 1 of 3 treatment conditions: (1) placebo plus CBT, (2) 100 mg modafinil plus CBT, or (3) 100 mg modafinil plus a contact control (monitor-only condition). Subjects were continuously monitored with sleep diaries from study intake until study end (10 weeks) and were evaluated on a weekly basis for changes in sleepiness. RESULTS: The mean age of the group was 41.3 years (SD, 13.4), and 70.4% of subjects were women. All 3 groups exhibited mean sleep latency and wake after sleep-onset times that were more than 30 minutes in duration. The mean pretreatment sleep profiles did not significantly differ. Modafinil, when administered alone, did not significantly affect the patients' sleep profiles. A trend, however, was evident for improved sleep latency. Modafinil, as an adjunct to CBT, tended to (1) reduce daytime sleepiness as measured by the Epworth Sleepiness Scale and (2) enhance compliance with CBT. With respect to the latter, subjects in the modafinil plus CBT group more reliably adhered to the prescribed phase delay in bedtime than did the placebo plus CBT group. DISCUSSION: These data suggest that modafinil may be used to diminish the negative side effects of CBT (increased daytime sleepiness) and may increase subject compliance with therapy. Whether enhanced daytime function mediates the change in adherence and whether reduced sleepiness and enhanced compliance translate to less patient attrition in the clinical setting remain to be evaluated.

Adult↗
PubMedDate not supplied

Benefits of adjunct modafinil in an open-label, pilot study in patients with schizophrenia.

Patients with schizophrenia experience cognitive impairments associated with hypofunctioning of the frontal cortex. Modafinil, a novel wake-promoting agent, works through the sleep-wake centers of the brain to activate the cortex. This 4-week, open-label, pilot study evaluated adjunct modafinil in patients with schizophrenia or schizoaffective disorder. Eleven patients received once-daily oral doses of modafinil (100 mg/day, days 1-14; 100 or 200 mg/day, days 15-28) in addition to antipsychotic therapy. Modafinil significantly improved patients' global functioning as assessed by a blinded clinician (week 2, P = 0.026; week 4, P = 0.012) and the investigator (week 3, P = 0.035). Modafinil significantly improved overall clinical condition, with 64% and 82% of patients rated as clinically improved at week 4 by a blinded clinician and the investigator respectively. Eighty-nine percent of patients considered themselves to be clinically improved. Modafinil significantly improved fatigue (P = 0.025, week 3) and tended to improve cognitive functioning scores. Control of positive symptoms was well maintained. Treatment-emergent adverse events included dry mouth (n = 2) and hallucinations (n = 2). One patient discontinued the study because of hallucinations that were considered to be possibly related to inadequate antipsychotic therapy. Although preliminary, these results suggest modafinil may be an effective and well-tolerated adjunct treatment that improves global functioning and clinical condition, and reduces fatigue in patients with schizophrenia or schizoaffective disorder. Additional controlled studies are warranted.

Adult↗
PubMed2002

Acute behavioral and physiological effects of modafinil in drug abusers.

Modafinil, a novel stimulant, is effective in the treatment of excessive daytime sleepiness associated with narcolepsy. It is biochemically and pharmacologically distinct from prototypical stimulants such as D-amphetamine, cocaine, and methylphenidate. The present experiment was designed to assess the acute behavioral effects of oral modafinil, cocaine, and placebo in participants (n=9) with recent histories of cocaine use (i.e. positive urine for cocaine or benzoylecgonine during the initial screening interview). Drug effects were assessed with a battery of self-reported drug-effect questionnaires, performance measures, and physiological indices. Cocaine, but not modafinil, produced stimulant-like self-reported drug effects (e.g. increased ratings of High and Stimulated). Modafinil and cocaine dose-dependently increased heart rate and blood pressure. The results of the present study suggest that modafinil has minimal abuse potential, but should be viewed cautiously because of the relatively small sample size. Future studies should further characterize the abuse potential of modafinil using other behavioral arrangements, such as drug discrimination or drug self-administration. A full characterization of the abuse potential of modafinil will become important as the use of this drug increases.

Adult↗