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Falling Down on the Job - Narcolepsy and Its Effect on People

Jon Stolee

Augustana University College

 

A paper submitted to Dr. Jayne Gackenbach as part of the course requirements for Psy 473 (Sleep and Dreams), April, 1997

 

For most people, the distinction between being awake and being asleep is clearly marked by when we go to bed and when we get up in the morning. Some people, however, suffer from a rather bizarre disorder in which elements of sleep creep into their waking life during the day. These attacks may involve drowsiness and the urge to sleep, or more dramatic events such as loss of body muscle tone, paralysis, or hallucinations. This paper will investigate the symptoms of the disorder these people suffer from, narcolepsy, and examine what the causes and treatments for it may be.

Narcolepsy is defined as sudden and irresistible episodes of sleeping during the day, even after an adequate night’s sleep (NHLBI, 1997; Barlow & Durand, 1995). Such sleep attacks can occur with or without warning, often at inopportune times (NHLBI, 1997), proving highly dangerous if the narcoleptic is driving or operating machinery (Findley et al, 1995)! Attacks can occur repeatedly in a single day (NHLBI, 1997). Narcoleptics also tend to suffer from general daytime drowsiness for prolonged periods of time (NHLBI, 1997).

According to the DSM-IV, in order to diagnose narcolepsy it is essential to determine that the individual’s disturbance is not due to the effect of a drug, medication, or other medical condition (Barlow & Durand, 1995).

Along with the primary symptom of daytime sleep attacks, a narcoleptic also experiences one or more of the following symptoms: cataplexy, sleep paralysis, and hypnagogic or hypnopompic hallucinations (Barlow & Durand, 1995; NHLBI, 1997). Only 20% to 25% of narcoleptics experience all of these symptoms (NHLBI, 1997).

Cataplexy involves the sudden loss of muscle tone while awake and conscious. This event can range is severity from the neck going limp or face muscles sagging through to complete collapse of the main body muscles (NHLBI, 1997). For reasons that are unclear, cataplexy may be triggered by emotions such as anger, fear, or happiness (NHLBI, 1997), and can last from a few seconds to a few minutes (Barlow & Durand, 1995).

Sleep paralysis and hypnagogic or hypnopompic hallucinations are both considered intrusions of Rapid Eye Movement (REM) sleep into the period when the person is passing from sleep to waking or from waking to sleep (Barlow & Durand, 1995).

Sleep paralysis is the term for the frightening experience of waking up but being unable to move or talk (Barlow & Durand, 1995; NHLBI, 1997). The paralysis is likely caused by the same switch mechanism which paralyses the body during REM sleep to prevent the sleeper from acting out the dreams going on inside his or her head (Barlow & Durand, 1995).

Hypnagogic and hypnopompic hallucinations are vivid, dream-like experiences that occur while the individual is either drifting off to sleep (the hypnagogic state) or coming out of sleep (the hypnopompic state) (Barlow & Durand, 1995; NHLBI, 1997). Often these hallucinations are very frightening (NHLBI, 1997). It is suspected that such hallucinations, along with sleep paralysis, may be behind many reports from people who sincerely believe that they have been abducted by aliens in the night (Barlow & Durand, 1995).

Narcolepsy is as common in America as Parkinson’s disease and Multiple Sclerosis are, having a prevalence of up to one in 1000 people (Mitler, 1990; NHLBI, 1997). It is found in both men and women of all ages, most commonly being first noticed during the teen years and early adulthood (NHLBI, 1997). One of the particularly frustrating things about narcolepsy is that it can take a long time for it to be diagnosed. Often it is mistaken for depression, epilepsy, or the side effects of medication (NHLBI, 1997). In one case, a man suffered for 23 years with recurrent episodes of unconsciousness, and it took 22 hospital stays before the doctors figured out that he was suffering from narcolepsy (Frey, 1991).

Narcolepsy is diagnosed and studied using two types of testing. A polysomnogram involves continuous monitoring of muscle and nerve functions through the night, much like an ongoing polygraph test without the questioning. Narcoleptics tend to fall asleep quickly, enter into REM sleep early, and awaken frequently during the night (NHLBI, 1997). The second test, called the multiple sleep latency test (MSLT), gives the subject the opportunity to sleep at two hour intervals through the normal waking day. They are observed for how far they fall asleep and how long it takes to reach the different stages of sleep. Narcoleptics tend to nod off quickly and begin REM sooner than normals during these naps (NHLBI, 1997).

For obvious reasons, these symptoms can create chaos and anguish in the personal, social, and professional lives of narcoleptics. Falling asleep or feeling drowsy while at work can make it difficult to keep a job, unless the sufferer has a particularly flexible and understanding boss. Personal issues may develop around being "different" and suffering the embarrassment of collapsing in public, especially if the sufferer is in the formative teenage years. Others may assume from their lethargic behaviour that the narcoleptic is lazy, hostile, or unmotivated (NHLBI, 1997). Narcoleptics, if they drive, are likely to have more accidents than other people (Findley et al., 1995; NHLBI, 1997). These debilitating consequences of the disorder have fuelled the scientific search for the cause of narcolepsy and for effective treatments to eliminate its symptoms.

The cause or causes of narcolepsy are as yet not known for certain. There are, however, several factors which have been identified as likely contributors to the disease, and which are the subject of ongoing research.

The clearest factor in the cause of narcolepsy appears to be heredity. Eight to twelve percent of people with narcolepsy have a close relative with the disease (NHLBI, 1997). It has been shown that narcoleptics almost all carry a particular genetic trait, that being the presence of human leucocyte antigen DR2 (abbreviated HLA-DR2) in their white blood cells (Barlow & Durand, 1995). In itself this antigen is likely not the cause of narcolepsy, but it is a marker of other nearby genetic material that is also shared by most narcoleptics. This indicates the strong likelihood that there is a genetic component to the development of narcolepsy. However, studies of monozygotic twins have indicated that the role of genetics is not absolute. Of the twelve known monozygotic twin pairs with at least one affected individual, in only three cases do both twins suffer from the disorder. The other nine pairs have one twin with the disorder and one without (Partinen et al, 1994).

A second area of research is into the role dopamine may play in narcolepsy. Administration of L-dopa, a precursor molecules of dopamine, to narcoleptic patients has been shown to improve their vigilance (Boivin & Montplaisir, 1991). Administration of the amino acid L-tyrosine, also a precursor to dopamine, has in preliminary investigation shown similar results (Roufs, 1990). If these findings are confirmed, researchers may conclude that dopamine levels are involved in the disorder.

Another suggestion has been that narcolepsy may be an autoimmune disease (Mignot et al., 1995). This theory is based on the fact that association with human leukocyte antigen "is a hallmark of most autoimmune diseases" (Mignot et al., 1995). However, no evidence for the connection to autoimmune abnormality has yet been found (Mignot et al., 1995).

Narcolepsy may also be caused by trauma to the brain. Lesions in the vicinity of the third ventricle have been shown to cause symptoms of narcolepsy (Clavelou, 1995). Also, there have been cases of narcolepsy developing in people after suffering closed head wounds (Lankford et al., 1994). It may be that narcolepsy is dormant in people genetically at risk for it, and that such trauma causes the person to become symptomatic (Lankford et al., 1994), or it may be that narcoleptic symptoms developing after a brain trauma are the result of damage to an area of the brain and are unrelated to the causes of common narcolepsy which develops without a head trauma.

A further factor may be the life situation of the individual. A limited study has found that narcoleptic subjects experienced more life stress during the year prior to the onset of the disorder than did control subjects (Orellana et al., 1994).

It appears at this point, then, that narcolepsy follows on the diathesis-stress model of illness. That is, there is a genetic characteristic in some people which makes them vulnerable to developing the disorder if certain environmental stressors come into play during their lifetime. The interaction between genetics and environment appears to be the best way to explain the different factors which have been identified as playing a role in narcolepsy. The mechanism by which narcolepsy is mediated likely involves the brain’s dopamine system.

Treatment currently available for sleepiness and cataplexy is as yet usually unable to offer complete control over symptoms (NHLBI, 1997).

The main treatment for sleepiness (somnolence) is in the form of stimulant drugs (NHLBI, 1997). The more effective of these are methylphenidate and dextroamphetamine (Mitler et al., 1990). Caffeine is neither effective nor recommended (NHLBI, 1997). Cataplexy and other symptoms related to REM intrusion are controlled with antidepressants and other medications that suppress REM sleep (NHLBI, 1997).

Lifestyle changes are also important to living with narcolepsy. Several scheduled naps through the day, lasting ten to fifteen minutes each, help to keep the individual alert (NHLBI, 1997; Garma & Marchand, 1994). Avoiding simple sugars in the diet has been shown to improve alertness in some subjects (Garma & Marchand, 1994).

It is also very important to have the social support and understanding of family and colleagues in order for a narcoleptic to lead a full and healthy life (NHLBI, 1997). Proper education of the people around the patient from day to day regarding the symptoms of the disorder can help to avoid misunderstanding and resentment.

Narcolepsy, with its unwelcome and incapacitating symptoms is a disorder that can rob individuals of their confidence, dignity, and ability to function as a normal person in the modern world. Fortunately, the medical and psychological community is developing ways to combat the symptoms of the disorder, and as its causes gradually become more fully understood, our ability to counters its symptoms should improve to the point where narcolepsy will someday soon be a fully treatable disease.

References

(Note: Medline resources were accessed through the services of http://www.avicenna.com)

Barlow, D.H., & Durand, V.M. (1995). Abnormal Psychology - An Integrative Approach. Pacific Grove: Brooks/Cole Publishing Company.

Boivin, D.B., & Montplaisir, J. (1991). The effects of L-dopa on excessive daytime sleepiness in narcolepsy. Neurology, vol. 41, no. 8, p.1267-9, as abstracted by Medline database, MedlineBack90 Medlars UID 91326252.

Clavelou, P. (1995). Narcolepsy associated with arteriovenous malformation of the diencephalon. Sleep, vol 18, no. 3, p. 202-5, as abstracted by Medline database, Medlars UID 95334650.

Garma, L., & Marchand, F. (1994). Non-pharmacological approaches to the treatment of narcolepsy. Sleep, vol. 17, no. 8, suppl, p.S97-102, as abstracted by Medline database, Medlars UID 95215725.

Findley, L., et al (1995). Vigilance and automobile accidents in patients with sleep apnea or narcolepsy. Chest, vol. 108, no. 3, p. 619-24, as abstracted by Medline database,Medlars UID 95385395.

Frey, H.R. (1991). Narcolepsy -- undiagnosed for 23 years. Schwiz Med Wochenschr, vol 121, no. 36, p.1289-92, as abstracted by Medline database, MedlineBack90 Medlars UID 920022426.

Lankford, D.A., et al. (1994). Posttraumatic narcolepsy in mild to moderate closed head injury. Sleep, vol. 17, no. 8, suppl, p. S25-8, as abstracted by Medline database, Medlars UID 95215713.

Mignot, E., et al. (1995). Narcolepsy and immunity. Adv Neuroimmunology, vol. 5, no. 1, p.23-37, as abstracted by Medline database, Medlars UID 95316267.

Mitler, M.M., et al. (1990). Narcolepsy. Journal of Clinical Neurophysiology, vol.7, no.1, p.93-118, as abstracted by Medline database, MedlineBack90, Medlars UID 90154302.

National Heart, Lung, and Blood Institute (NHLBI). (1997). Narcolepsy. Internet material from http://www.nhlbi.nih.gov/nhlbi/sleep/gp/narcolep.htm, retrieved 3/31/97.

Orellana, C., et al. (1994). Life events in the year preceding the onset of narcolepsy. Sleep, vol. 17, no. 8, suppl. p. S50-3, as abstracted by Medline database, Medlars UID 95215717.

Partinen, M., et al. (1994). Twin studies in narcolepsy. Sleep, vol. 17, no. 8, suppl, p. S13-6, as abstracted by Medline database, Medlars UID 95215710.

Roufs, J.B. (1990) L-tyrosine in the treatment of narcolepsy. Med Hypotheses, vol. 33, no 4, p. 269-73, as abstracted by Medline database, MedlineBack90, Medlars UID 91218707.

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