Narcolepsy is not a common disorder, with best estimates finding it affects only about .025–.05% of the population. Nonetheless, it is a vital disorder for school psychologists to be familiar with on the basis that its symptoms frequently first occur during childhood and adolescence. If undiagnosed, this disorder causes significant distress and disadvantage to the student as well as frustration and difficulty for school staff. It is surprising that narcolepsy has received almost no attention in the school psychology literature. This article provides school psychologists with an overview of the central features, causes, diagnosis and treatment of narcolepsy in young people. It then outlines school management of the disorder, with specific consideration of the role of the school psychologist.

The narcoleptic syndrome in its most specific way is characterized by a set of clinical symptoms, including cataplexy, irresistable sleep episodes, hypnagogic hallucinations and sleepparalysis; the syndrome has been defined by the association of excessive day-time somnolence and REM-sleep abnormalities. In principle, anamnestic information is sufficient to establish the clinical diagnosis, although neuro-physiological and biochemical data(CSF monoamine metabolites and HLA-typology) are sometimes needed to support the diagnostic procedure. Treatment of excessive daytime somnolence is still primarily based upon CNS stimulants, while treatment of cataplexy and related symptoms rests on antidepressants with a primarily serotonergic mode of action.

The medications used to treat narcolepsy are targeted toward alleviating symptoms such as excessive sleepiness and cataplexy. The cause of this neurological sleep disorder is still not completely clear, though a destruction of hypocretin/orexin neurons has been implicated. The destruction of these neurons is linked to inactivity of neurotransmitters including histamine, norepinephrine, acetylcholine, and serotonin, causing a disturbance in the sleep/wake cycles of narcoleptic patients. Stimulants and MAOIs have traditionally been used to counteract excessive daytime sleepiness and sleep attacks by inhibiting the breakdown of catecholamines. Newer drugs, called wake-promoting agents, have recently become first-line agents due to their better side-effect profile, efficacy, and lesser potential for abuse. These agents similarly inhibit reuptake of dopamine, but have a novel mechanism of action, as they have been found to increase neuronal activity in the tuberomamillary nucleus and in orexin neurons. Sodium oxybate, a sodium salt of gamma-hydroxybutyrate (GHB), is another class that is used to treat many symptoms of narcolepsy, and is the only U.S. Food and Drug Administration (FDA)-approved medication for cataplexy. It has a different mechanism of action than either stimulants or wake-promoting agents, as it binds to its own unique receptor. Antidepressants, like selective serotonin re-uptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs), have also been used, as similar to stimulants, they inhibit reuptake of specific catecholamines. In this article, we seek to review the mechanisms behind these classes of drugs in relation to the proposed pathophysiology of narcolepsy. Appropriate clinical strategies will be discussed, including specific combinations of medications that have been shown to be effective.