The emphasis on cognition in psychiatry and neurology has inspired interest in novel pharmacotherapies for cognitive dysfunction, and modafinil has emerged as a promising candidate. Modafinil possesses many of the wake-promoting effects of amphetamine but lacks the elevations in extracellular monoamines seen with this drug, and is less likely to be associated with abuse potential or cardiovascular side effects.

Boosts Brain Power

A number of studies indicate that modafinil 200mg australia enhances cognitive function in both narcolepsy and healthy controls. In one fMRI study, modafinil treatment of medication-free narcolepsy patients (titrated from 100-400 mg/day over 3 weeks) was associated with improved performance on the Pauli Test and decreased c-Fos activation in frontal and anterior cingulate cortices, suggesting that its effects are not limited to arousal or early sensory processes.

Similarly, modafinil enhances working memory in normal adults in a sleep-deprived context. A single dose of 200 mg modafinil was associated with improved digit span and visual recognition memory, and improved spatial planning and SSRT, suggesting improvements in both the maintenance and manipulation of working memory processes. Modafinil also enhanced vigilance in the wakefulness test and reduced interference during a simulated night shift (Turner et al, 2003).

The behavioral effects of modafinil may be related to its modulation of central neurotransmitter systems. For example, in a series of experiments with macaques, modafinil caused increased firing of dopamine D1 receptors in prefrontal cortex neurons involved in spatial working memory. Furthermore, dopamine D1 receptors in the tuberomammillary nucleus are involved in working memory performance and are inhibited by modafinil (Beracochea et al, 2001). In addition, the learning curve of a sequential alternation task is sensitive to damage to the anterior cingulate cortex and mediodorsal thalamus, which both show c-Fos activation after modafinil administration.

Boosts Focus

Modafinil (Modalert 200 mg) can help people who suffer from narcolepsy or sleep disturbances due to shift work. It has been shown to improve wakefulness in these patients without affecting their normal sleep cycles or having adverse effects on the heart and blood pressure. The drug also has a lower liability to dependence than amphetamine-like stimulants, although it has been shown in animal studies to induce cocaine-like discriminative stimulus and reinforcing effects when administered in very high doses.

In a series of human studies, modafinil has been found to boost performance on cognitive tasks such as Letter-Number Span and Timed Up-and-Go (TOVA). These benefits appear to be mediated through the LC/NE system and may be associated with an increase in dopamine levels. Interestingly, modafinil has been found to augment pupillary dilation parameters in a way that is consistent with arousal.

Modafinil does not interact with many drugs, but it is important to avoid taking the medication with phenobarbital (Bayer) and carbamazepine (Tegretol). It may also reduce the effectiveness of methylphenidate (Ritalin). Some sedatives, such as benzodiazepines, may decrease the effects of modafinil. It is also not recommended to take the medication with antidepressants or antipsychotics. Adverse reactions reported with the use of this medication include headache, nausea, vomiting, stomach upset, jitteriness, nervousness, depression, anxiety, and chest pain.

Boosts Energy

Modafinil (2-[(phenylmethyl) sulfinyl] acetamide), sold under the brand name Provigil, is an FDA-approved drug for treating excessive sleepiness in people with narcolepsy, shift work sleep disorder, and obstructive sleep apnea/hypopnea syndrome. It is a central nervous system stimulant that exerts its effects through a combination of mechanisms that involve noradrenergic (specifically, the norepinephrine transporter), dopaminergic (including the DAT), and GABAergic systems.

Like many traditional stimulants, modafinil causes euphoric effects that can alter thinking, mood, and feelings in some people, but it is less likely to result in intense pleasure, addiction, and high perceived reward associated with the abuse of other psychoactive drugs. Moreover, it does not cause a pounding heartbeat, high blood pressure, and rapid breathing often seen with amphetamines at typical clinical doses.

In studies with seasoned substance abusers, modafinil was found to be generally well-tolerated and did not induce craving or the desire for more of the drug. Furthermore, it does not increase adrenergic stimulation or raise blood pressure as much as amphetamines at similar doses and is more effective than caffeine in reducing fatigue.

Boosts Memory

With a relative lack of abuse potential and a lower risk of adverse cardiovascular effects, modafinil is becoming increasingly attractive as a clinical agent for medical and psychiatric conditions currently treated with stimulants. For example, several studies have shown the efficacy of modafinil in fatigue syndromes, narcolepsy, and attention deficit hyperactivity disorder (ADHD).

Studies of cognitive functioning suggest that modafinil enhances performance on both simple and complex cognitive tasks. For example, in a sleep-deprived condition modafinil increases digit span, visual recognition memory, spatial planning, and SSRT compared to placebo, suggesting improved working memory capacity and inhibition of prepotent responding (Turner et al, 2004b).

Moreover, an experiment in which participants with schizophrenia were administered either modafinil or dextroamphetamine after overnight sleep deprivation found that both medications improved performance on the WCST and the ED shift task – indicating enhancement of fronto-cortical loops that are modulated by ascending dopamine systems.

In another study using fMRI, eight healthy volunteers were administered a single dose of modafinil or methylphenidate and performed a delayed response task. fMRI results indicated that modafinil augmented cortical activity in the lateral prefrontal cortex (BA 46) and the right superior temporal gyrus, which are involved in the control of inhibitory processes (Thomas RJ and Kwong, 2006). In contrast, methylphenidate did not enhance BA 46 activity or inhibit the cis-flupenthixol-mediated decrease in go-trial RT, indicating a differential modulation by these two compounds.