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.

Few epidemiological studies have explored hallucinations’ prevalence and types in the general population. Ohayon et al. [1] have emphasized the high prevalence of hypnagogic and/or hypnopompic hallucinations present respectively in 37 and 12.5% of the 4972 subjects. The rate of hypnagogic hallucinations was related to age. Women were more likely to report such hallucinations. The most frequent type of hallucinations was unexpected, that is kinesthesic (feeling of falling in an abyss) but all types of hallucinations could be present. These hallucinations had no relationship to a specific pathology in more than 50% of the cases but were exclusively present at nighttime. In old age, visual hallucinations are the most frequent. In a cohort of old non-demented subjects, 17.4% of them had hallucinations and behavioural symptoms (anxious agitation or/and irritability).

Several neurological pathologies included sleep disorders and hallucinations. Narcolepsy and Parkinson disease (P.D.) will be only considered here. In narcolepsy, with or without cataplexy, hallucinations are now called “secondary” symptom, as they are incidental, reported in 35 to 66% of the patients.

Hypnagogic and hypnopompic hallucinations are most often visual but all types have been described, formed, without whole scenes but terrifying the patient who is often implicated in it and sometimes associated with sleep paralysis, especially during daytime when sleep occurs in REM. Are they pieces of dream? These hallucinations can be differentiated on a phenomenological basis from hallucinations in healthy subjects and from hallucinations in schizophrenia [2]. They have also some differences with hallucinations observed in P.D. [3].

In P.D. hallucinations affected 25% of the patients in long duration disease. They are mainly visual, or with sensation of a presence (person or animal), coexisting with delusions and anxiety. They are rarely only a side- effect of dopaminergic treatment but are often linked to daytime sleepiness with REM sleep attacks, described in this disease and to cognitive impairment.

We sought to investigate the risk of incident major depressive disorder (MDD) attributable to a range of sleep disorders in the Danish population. Data were obtained by linking longitudinal Danish population-based registers. A total of 65,739 individuals who had first onset of depression between 1995 and 2013 were selected as cases. For each case, a set of 20 controls of the same sex, birth month and year and who had not had depression by the date that the case was diagnosed were selected at random form the population (N = 1,307,580 in total). We examined whether there was an increased rate of prior sleep disorders in MDD cases compared to controls using conditional logistic regression. An increased risk of incident depression in cases was found for all sleep disorders analyzed. Highest incidence rate ratios (IRRs) were found for circadian rhythm disorders (IRR = 7.06 [2.78–17.91]) and insomnia of inorganic origin (IRR = 6.76 [4.37–10.46]). The lowest estimated IRR was for narcolepsy (IRR = 2.00 [1.26–3.17]). Those diagnosed with a sleep disorder in the last 6 months were at highest risk of developing depression compared to those with at least 1 year since diagnosis (3.10 vs. 2.36). Our results suggest that having any sleep disorder is a risk factor for incident depression. Depression screening should be considered for patients with sleep disorders, and where possible, long-term follow-up for mental health problems is advisable.

Memory complaints and altered states of consciousness with automatic behaviour of narcoleptic patients indicate cognitive dysfunctioning. Although more problems arise while performing attention tasks than memory tasks, the neuropsychological test inquiry doesn't indicate one particular neuropsychological function as consistently impaired. They often perform well because they compensate impaired wakefulness by an increased willingness to respond. Neurophysiological research indicates that the sometimes occurring cognitive dysfunction is associated with a waxing and waning between wakefulness and sleep. The increased psychopathology is partly a reflection of, partly a reaction to the symptoms. The impact of hypersomnia on psychosocial functioning is more important than that of epilepsy in epileptics. In severe cases smoking and driving should better be dissuaded.

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.