Narcolepsy is a heritable central nervous system disorder that is a common cause of sleep disturbance.
Common symptoms include:
Sleep attacksCataplexyHypnotic-like hallucinationsSleep paralysisDisturbed nocturnal sleep with resultant insomniaNarcolepsy affects 0.03 to 0.06% of the population in western Europe and North America and is the second most common cause of disabling daytime sleepiness after sleep apnea. There is no difference in the prevalence of narcolepsy among men and women, but there may be a higher diagnostic rate in men. The disease typically emerges in the second decade of life and increases in severity through the third or fourth decade. No two people ever seem to experience narcolepsy in the same way. In fact, it can vary greatly at different periods of ones life. Symptoms may begin one at a time, but in later life the symptoms may begin all at once. It can stay the same or it can change for unknown reasons.
Narcoleptic patients suffer episodes of unwanted or unintended sleep. While these patients often experience excessive sleepiness and bouts of involuntary sleep, often called sleep attacks, they should be distinguished from the symptom of prolonged sleepiness. Narcoleptics also experience abnormal timing of rapid eye movement (REM) sleep associated with paralysis and hallucinations. Paralysis is due to the same central mechanisms which normally block muscle activity during REM sleep. Two distinct types of paralysis may occur;
Nonhereditary cases of narcolepsy are most common in humans, but the narcoleptic trait is also heritable. The risk for narcolepsy among the children of a patient with narcolepsy is several orders of magnitude greater than the risk observed in the general population.
- Cataplexy, characterized by sudden muscle weakness and partial or complete collapse during excitement or anticipation e.g. telling a joke or catching a fish.
- Sleep paralysis, an often frightening inability to move just before falling asleep. Sleep paralysis frequently is associated with hypnotic hallucinations; these also depend upon REM sleep mechanisms and occur as the patient falls asleep. Hypnotic hallucinations may range from benign to terrifying.
Narcolepsy seems to involve dysregulation of wakefulness and sleep rather than true hypersomnolence. Patients with narcolepsy do not sleep more than normal controls. However, they are prone to fall asleep throughout the day-night cycle, often at inappropriate times.
Diagnosis is based on the classical symptoms sleepiness, cataplexy, hypnotic hallucinations and sleep paralysis. Abnormal results on a Multiple Sleep Latency Test (MSLT) helps confirm a suspected diagnosis. The MSLT consists of four 20 minute opportunities to nap offered at two hour intervals throughout the day. Patients with narcolepsy fall asleep in approximately five minutes or less, and have two or more transitions into REM sleep during the four opportunities to nap. In contrast, normal subjects have an average sleep latency of 12 to 14 minutes and show no REM sleep on the MSLT.
There is no cure for narcolepsy, and a comprehensive approach to managing the excessive sleepiness is required. The symptoms of narcolepsy are usually controlled with stimulants and drugs which suppress REM sleep. Sound sleep hygiene, attention to other substances and drugs that may disrupt the sleep-wake cycle, and periodic reassessment of symptom severity and of the need for and adequacy of treatment modalities are other important aspects of management. Lifelong therapy frequently is required.
Patients with narcolepsy cannot perform psychomotor tasks or maintain alertness as well as normal controls, even when treated with psychostimulants and REM-sleep suppressing drugs. Review of multiple studies indicates that patients receiving the maximum recommended doses of stimulant medications rarely reach above 70 to 80 percent of normal control levels on tests of performance and alertness. Many authorities recommend a goal of obtaining maximum alertness at selected times of the day, for example during work or school hours and while driving, and using scheduled naps to help maintain alertness. Others recommend a goal of maximal or "normal" alertness throughout conventional waking hours. Unfortunately, most data indicate that although daytime sleep episodes can be reduced in most, they cannot be completely abolished in all patients.
Patients with narcolepsy face various psychosocial and work-related problems throughout their lives. As a result, patients with this disorder often experience progressive difficulty in meeting economic and social responsibilities throughout their lives. While the symptoms of narcolepsy do not tend to worsen with age, they do interact negatively with other age-related problems and medical conditions. For example, conditions such as chronic obstructive pulmonary disease, with its well-known capacity to disrupt sleep, can produce sleep deprivation and exacerbate the symptoms of narcolepsy.
Patients with narcolepsy have the additional burden of coping with misperceptions about the causes and the involuntary nature of the symptoms. Common misconceptions, even among healthcare providers, include beliefs that sleep attacks and cataplexy are manifestations of denial and avoidance, and that symptoms can be controlled with behavioral or psychotherapeutic techniques.
While there is no credible evidence to support such ideas, there is a role for psychologic intervention in the management of patients with narcolepsy. Such patients often benefit from participation in professionally supervised support groups that focus on coping skills and identification of community resources.
In the late 1990's, two new peptides, orexin A (hypocretin-a) and orexin B (hypocretin-2), were identified in the hypothalamus, which produce strong appetite-stimulating effects. Surprisingly enough, dogs with a modification of the orexin receptor also showed narcoleptic symptoms.
In the brains of patients suffering from narcolepsy very little orexin is produced. While the orexin A level of narcoleptic patients in plasma is normal, CSF levels of orexin A levels are quite low. This finding suggests that orexin might also be produced in CNS-independent sources, e.g. in the gut. It is tempting to speculate whether an autoimmune process attacking especially the orexin-producing cells in the hypothalamus might be a possible cause of the disease. This orexin system should play an important role in the development of new drugs for the treatment of narcolepsy or other disorders of excessive daytime sleepiness.[Neurology, 2001: 56: pp.1749-1751]
(NaturalNews January 27, 2014) A team of Swedish clinicians have clinically linked a 2009 swine flu vaccine to increased risk of narcolepsy in young adults, and a group of Danish researchers now understand how and why.
Pandemrix, an influenza vaccine unleashed in 2009, was widely administered to combat H1N1, or swine flu, in multiple countries. As reports of people experiencing sleep disturbances mounted, the vaccine manufacturer, GlaxoSmithKline, and organizations like the CDC scrambled to isolate the problem. But the manufacturer continues to pander, saying "Further research is needed to determine whether the observed risk is related to the vaccine, environmental effects, genetic factors, other factors or a combination of them."
But now Swedish clinicians are linking GlaxoSmithKline's 2009 Pandemrix vaccine to immune-related neurological diseases, including increased risk of developing narcolepsy in young adults.