Narcolepsy is a heritable central nervous system disorder that is a common cause of sleep disturbance.

Common symptoms include:

  • Sleep attacks
  • Cataplexy
  • Hypnotic-like hallucinations
  • Sleep paralysis
  • Disturbed nocturnal sleep with resultant insomnia

Narcolepsy 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;

  1. Cataplexy, characterized by sudden muscle weakness and partial or complete collapse during excitement or anticipation e.g. telling a joke or catching a fish.
  2. 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.

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.

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.


Symptoms - Sleep  

Having hypersomnolence


Current Smoker

See the link between Current Smoker and Hypersomnolence.



A vaccine used to combat the swine flu pandemic has been linked to the sleep disorder narcolepsy in some 800 children and teens across Europe. The case has sparked debate over the risk of immunization and the potentially greater threat of anti-vaccine

The European Centre for Disease Prevention and Control (ECDC) studied the effects of the Pandemrix vaccine in eight European countries after higher incidences of narcolepsy were reported among children given the vaccine during the 2009-2010 H1N1 swine flu pandemic, AFP reports.

Sweden and Finland have both seen a rise in the sleep condition since the vaccine was first used on children. The governments of both countries stressed their citizens were vaccinated with Pandemrix, which was the only vaccine used in both countries at the time.

In Sweden, nearly 200 children aged four to 19, developed narcolepsy after receiving the vaccine during that period, while in Finland the number was 79.

One such child, 14-year-old Emelie Olsson, told Reuters about the crippling effects narcolepsy had had on her life: “In the beginning I didn’t really want to live any more, but now I have learned to handle things better,” she said.

Narcolepsy is a neurological sleep disorder that causes people to fall asleep uncontrollably, makes sufferers feel excessively drowsy, and in more extreme cases brings on hallucinations, sleep paralysis, and cataplexy – a sudden loss of muscle strength.

Strong emotions can often bring on cataplexy in narcoleptics, and for Emelie, fun is the emotional trigger.

“I can’t laugh or joke about with my friends anymore, because when I do I get cataplexies and collapse.”

Research has found that some people are born with a variant in a gene known as HLA, meaning they have low hypocretin, a neurotransmitter that regulates arousal, wakefulness, and appetite.

Around 25 percent of Europeans have this genetic vulnerability, leaving them susceptible to narcolepsy.

Emelie was found to have 15 percent the normal amount of hypocretin, which is reflective of people suffering from the sleep disorder.

Scientists have subsequently begun investigating a connection between those with the HLA variant and the immunological AS03 adjuvant added to Pandemrix to stimulate the immune system‘s response to the target antigen.

Some have argued that AS03, its boosting effect or even the H1N1 flu itself may have trigged the onset of narcolepsy, which is now believed to be an autoimmune disease.

Angus Nicoll, a flu expert at the ECDC, says genetics might play a part, but external factors are likely to have brought on the cases of narcolepsy as well.

“Yes, there’s a genetic predisposition to this condition, but that alone cannot explain these cases,” he said. “There was also something to do with receiving this specific vaccination. Whether it was the vaccine plus the genetic disposition alone or a third factor as well – like another infection – we simply do not know yet,” he told Reuters. [European report links child Swine flu vaccine to narcolepsy,, Jan 23, 2013]


Symptoms - Muscular  

Momentary muscle weakness

An important symptom of narcolepsy is cataplexy, a momentary loss of muscle control that ranges from feelings of muscle weakness to feelings of paralysis. A cataplectic attack usually occurs during times of stress, but may also strike after an emotional outburst such as laughter, sadness, fear, anticipation, excitement, surprise or anger. A joke or moment of frustration with a young child can send a person with narcolepsy into cataplexy. These attacks can be as short as 30 seconds or as long as 30 minutes.



Conventional Drugs / Information

Xyrem has been approved by the FDA for narcolepsy drug treatment, but with tight restrictions on its use. In high doses, it can cause dependence in over time. In addition very serious side effects, including seizures, coma, respiratory arrest, and death have been reported in people who abused it.

Another narcolepsy drug treatment is Selegiline (Eldepryl, Movergan), also known as deprenyl. It is an antioxidant drug that blocks monoamine oxidase B, an enzyme that degrades dopamine and may play a role in narcolepsy drug treatment. It has adverse interactions with nearly every antidepressant, some very serious. Patients suffering from depression should discuss all narcolepsy treatment options with their physician.

People taking any monoamine oxidase inhibitor are at risk for high blood pressure if they consume tyramine-containing foods or beverages, including aged cheeses, most red wines, vermouth, dried meats and fish, canned figs, fava beans, and concentrated yeast products.

Antidepressants have been very useful in narcolepsy drug treatment. They can be effective controlling symptoms of narcolepsy, particularly cataplexy.

Tricyclic Antidepressants. The tricyclic antidepressants protriptyline (Vivactil), clomipramine (Anafranil), imipramine (Janimine, Tofranil), and viloxazine appear to suppress REM sleep and may be added to the stimulant regimen in severe cases. These antidepressants do not cause sedation and are useful in managing cataplexy, sleep paralysis, and hypnagogic hallucinations (the hallucinations that occur between sleep and wakefulness).

Selective serotonin reuptake inhibitors (SSRIs) may also be helpful in combination with stimulants for narcolepsy drug treatment. For example, fluoxetine (Prozac), the standard SSRI, and citalopram (Celexa), another SSRI, have been reported to be effective in treating cataplexy that does not respond to standard narcolepsy treatments.


GHB (Gamma-Hydroxybutyrate)

Several independent investigators have reported beneficial effects in narcolepsy with GHB but only 2 double-blind studies have been published (Scrima et al, 1989 and 1990; Lammers et al., 1993). Based on these two reports, there is little doubt that the drug is helpful to narcoleptic patients. Several other independent investigators have confirmed the findings. The most consistent and least controversial effects are improved cataplexy and improved nocturnal sleep disruption with GHB treatment (Scrima et al., 1990; Broughton andMamelak, 1980: Bedard et al., 1990). Further investigations would be needed to confirm a possible beneficial effect for daytime sleepiness. Importantly, GHB anti-cataplectic effects are clearly mediated by a different mode of action when compared to those produced by antidepressant compounds. As such, patients who do not tolerate classical antidepressant treatment because of side effects, tolerance or contraindications would not have any other choice if GHB were not available to them. Medical use in the treatment of narcolepsy is usually 50mg/Kg per day.

A form of gamma hydroxybutyrate (GHB), marketed under Xyrem, was approved for treatment of narcolepsy. GHB deepens sleep and has been shown to prevent many of the daytime problems associated with narcolepsy.

Lab Tests/Rule-Outs  

Tests, General Diagnostic


Nocturnal polysomnography remains an important part of the evaluation process in the diagnosis of sleep disorders.

Multiple Sleep Latency Test

Once a “normal” night’s sleep has been confirmed and other causes of excessive daytime sleepiness, such as obstructive sleep apnea (OSA) and periodic limb movement disorder (PLMD), have been excluded, a multiple sleep latency test (MSLT) is performed, usually the morning after polysomnography. The MSLT is a similar test, but it measures fewer parameters. The MSLT measures EEG, EOG, chin EMG, and usually heart rate. The patient attempts to take four to five 20-minute naps (depending on the protocol) every 2 hours throughout the day. After these naps, the time it takes the patient to fall asleep (sleep latency) is averaged. Sleep latency usually fluctuates in narcolepsy patients, where it may lengthen, but will most often remain shorter than normal latency.

Cerebrospinal fluid (CSF) hypocretin-1 assessment

It has been found that many (about 90% of narcolepsy-cataplexy subjects) patients with narcolepsy have very low or undetectable levels of hypocretin-1/orexin A in the cerebrospinal fluid.


Weak or unproven link
Proven definite or direct link
Very strongly or absolutely counter-indicative
Likely to help
Highly recommended



A cause of daytime sleepiness due to an inherited disorder of the control of dreaming sleep. It should be differentiated from sleep apnea, periodic leg movements and other rarer causes of daytime sleepiness.

Nervous System

A system in the body that is comprised of the brain, spinal cord, nerves, ganglia and parts of the receptor organs that receive and interpret stimuli and transmit impulses to effector organs.


An abrupt temporary loss of voluntary muscular function and tone, sometimes evoked by an emotional stimulus such as laughter, pleasure, anger, or excitement.


A false or distorted perception of objects or events, including sensations of sight, sound, taste, smell or touch, typically accompanied by a powerful belief in their reality.


Cessation of breathing.


Literally: innocent; not malignant. Often used to refer to cells that are not cancerous.


Usually Chronic illness: Illness extending over a long period of time.


Pertaining to the lungs.


An important supervisory center in the brain regulating many body functions. Despite its importance in maintaining homeostasis, the hypothalamus in humans accounts for only 1/300 of total brain weight, and is about the size of an almond.

Autoimmune Disease

One of a large group of diseases in which the immune system turns against the body's own cells, tissues and organs, leading to chronic and often deadly conditions. Examples include multiple sclerosis, rheumatoid arthritis, systemic lupus, Bright's disease and diabetes.


Chemicals in the brain that aid in the transmission of nerve impulses. Various Neurotransmitters are responsible for different functions including controlling mood and muscle movement and inhibiting or causing the sensation of pain.

Pellagra and Vitamin Niacinamide Deficiency

Pellagra, This patient sought medical attentio...
Image via Wikipedia
Pellagra is a disease condition caused by vitamin B3 or niacinamide deficiency. It is characterized by the 3 Ds- dermatitis, diarrhea and dementia. Historically, pellagra was described as early as 1735 by Don Gasper Casal, a Spanish court physician. He named this condition pellagra meaning rough skin due to the predominant finding of scaly, rough skin among the peasants of certain parts of Spain where, poverty was rampant and prevented these patients from having adequate intake of the vitamin in their diet. This condition was especially common in the regions of Europe where maize was the staple diet. The link between pellagra and vitamin niacinamide was discovered much later in the USA, almost 2 centuries later. Pellagra can be either primary or secondary Primary pellagra is caused by deficiency of vitamin B3 or niacin in the diet. Secondary pellagra is the condition resulting from deficiency of tryptophan (an essential amino acid) in the diet. Tryptophan is essential because it is a precursor for the synthesis of niacinamide. Even if this amino acid is consumed in sufficient quantities any process that interferes with its conversion to vitamin B3 can cause a deficiency of vitamin B3. The reason so many suffered from pellagra in the past is that maize was the staple crop in large parts of Europe and USA. Maize is deficient in both tryptophan and Niacin in its unfortified form. This discovery caused maize to subsequently to be marketed in a fortified form (with niacin), a practice that is prevalent today. Clinical features As stated previously, pellagra is characterized by diarrhea, dementia and dermatitis. The first clinical presentation is almost always that of Gastro-intestinal symptoms. Almost always the first symptom is that of mucosal atrophy, with the changes being visible on the tongue as redness with a smooth featureless appearance of the surface. This is the result of atrophy of the papillae of the tongue. Some of the first symptoms of pellagra include malaise, apathy, weakness, and lassitude. The gastro-intestinal symptoms include malabsorption and failure to thrive. Irritable bowel syndrome can also be a sign of pellagra with diarrhea a main symptom. The skin disease in pellagra usually affects the parts of the body that are exposed to sunlight. The skin becomes rough and scaly with reddening in the early stages. The histopathological features include vascular dilatation, proliferation of endothelial lining, perivascular lymphocytic infiltration, and hyperkeratinization and subsequent atrophy of the epidermis. The skin also becomes dark (hyperpigmentation) and thickened with presence of bullae or fluid filled vesicles on the surface. Many patients complain of a burning sensation of the affected skin. The nervous system is also affected with degenerative changes seen in the neurons (nerve cells). The nervous system changes result in anxiety, delusions, hallucinations, headaches, insomnia, and stupor. The end stage is a condition called dementia wherein the brain undergoes atrophy. Still untreated, pellagra can cause death as a result of the inability of the body to supply sufficient energy for the vital body functions due to depletion of the substances required for this function. Also see vitamin niacinamide - a full description.

Immune System

A complex that protects the body from disease organisms and other foreign bodies. The system includes the humoral immune response and the cell-mediated response. The immune system also protects the body from invasion by making local barriers and inflammation.


A substance, usually protein or protein-sugar complex in nature, which, being foreign to the bloodstream or tissues of an animal, stimulates the formation of specific blood serum antibodies and white blood cell activity. Re-exposure to similar antigen will reactivate the white blood cells and antibody programmed against this specific antigen.

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