Humans afflicted with narcolepsy suffer a variety of symptoms due to the dysregulation of the REM cycles.^3-5 These irregularities cause EDS, leading to uncontrollable urges to sleep known as sleep attacks even in active daily events. This sudden onset of sleep occurs primarily when participation level is low (watching television, reading, sitting in class, etc.).¹ While the regular REM cycle causes temporary inhibition of muscles during sleep, narcoleptics experience this temporary feeling of paralysis outside of sleep in processes known as sleep paralysis or cataplexy.^1,2,5 Hypnagogic hallucinations often occur in the transition between waking and sleeping, usually in the form of visual images but often in the shape of voices or bodily sensations.² These symptoms radically affect the normalcy of life for narcoleptic patients; unfortunately, treatment options are still limited. However, chosen wisely, treatment can dramatically increase the quality of life in patients with narcolepsy.

Treatments
Although the disorder was traditionally treated with amphetamines, the last decade has seen US Food and Drug Administration (FDA) approval of modafinil, the first drug therapy specifically approved to treat EDS caused by narcolepsy.^5-7 Modafinil is pharmacologically and clinically unrelated to amphetamines.^7,8 French pharmaceutical company Laboratoire L Lafon
originally developed modafinil and it quickly became the most often prescribed medication to treat EDS in narcolepsy patients.^4,5 Modafinil is a non-traditional stimulant whose mechanism of action is not yet entirely understood, although much has been discovered in recent years. Modafinil does not require the norepinephrine transporter or postsynaptic dopamine receptors. Modafinil does bind to the dopamine transporter (DAT), but with low affinity, which has led to the discussion of its relevance. ⁷ The high plasma concentration of modafinil appears to make up for its low affinity to DAT. However, modafinil is active in areas with both DAT and alpha-adrenergic receptors such as the basal forebrain, cerebral cortex, and the thalamus.^9,10 This may explain why modafinil is not useful for the cataplexy symptoms that often accompany narcolepsy, as regions that control muscle tone are not rich in DAT-bearing dopaminergic terminals. In summary, modafinil binds to DAT, which increases extracellular dopamine. Dopamine binds to alpha-adrenergic receptors, which activates downstream; this may cause an increase in dopamine and indirectly increase both histamine and glutamate, all of which may account for modafinil's wake-promoting properties.¹¹