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Saturday, June 17, 2023

Freethought

From Wikipedia, the free encyclopedia

Freethought (sometimes spelled free thought) is an epistemological viewpoint which holds that beliefs should not be formed on the basis of authority, tradition, revelation, or dogma, and that beliefs should instead be reached by other methods such as logic, reason, and empirical observation. According to the Oxford English Dictionary, a freethinker is "a person who forms their own ideas and opinions rather than accepting those of other people, especially in religious teaching." In some contemporary thought in particular, free thought is strongly tied with rejection of traditional social or religious belief systems. The cognitive application of free thought is known as "freethinking", and practitioners of free thought are known as "freethinkers". Modern freethinkers consider free thought to be a natural freedom from all negative and illusive thoughts acquired from society.

The term first came into use in the 17th century in order to refer to people who inquired into the basis of traditional beliefs which were often accepted unquestioningly. Today, freethinking is most closely linked with deism, secularism, humanism, anti-clericalism, and religious critique. The Oxford English Dictionary defines freethinking as, "The free exercise of reason in matters of religious belief, unrestrained by deference to authority; the adoption of the principles of a free-thinker." Freethinkers hold that knowledge should be grounded in facts, scientific inquiry, and logic. The skeptical application of science implies freedom from the intellectually limiting effects of confirmation bias, cognitive bias, conventional wisdom, popular culture, urban myth, prejudice, or sectarianism.

Definition

Atheist author Adam Lee defines free thought as thinking which is independent of revelation, tradition, established belief, and authority, and considers it as a "broader umbrella" than atheism "that embraces a rainbow of unorthodoxy, religious dissent, skepticism, and unconventional thinking."

The basic summarizing statement of the essay The Ethics of Belief by the 19th-century British mathematician and philosopher William Kingdon Clifford is: "It is wrong always, everywhere, and for anyone, to believe anything upon insufficient evidence."[9] The essay became a rallying cry for freethinkers when published in the 1870s, and has been described as a point when freethinkers grabbed the moral high ground. Clifford was himself an organizer of free thought gatherings, the driving force behind the Congress of Liberal Thinkers held in 1878.

Regarding religion, freethinkers typically hold that there is insufficient evidence to support the existence of supernatural phenomena. According to the Freedom from Religion Foundation, "No one can be a freethinker who demands conformity to a bible, creed, or messiah. To the freethinker, revelation and faith are invalid, and orthodoxy is no guarantee of truth." and "Freethinkers are convinced that religious claims have not withstood the tests of reason. Not only is there nothing to be gained by believing an untruth, but there is everything to lose when we sacrifice the indispensable tool of reason on the altar of superstition. Most freethinkers consider religion to be not only untrue, but harmful."

However, philosopher Bertrand Russell wrote the following in his 1944 essay The Value of Free Thought:

What makes a freethinker is not his beliefs but the way in which he holds them. If he holds them because his elders told him they were true when he was young, or if he holds them because if he did not he would be unhappy, his thought is not free; but if he holds them because, after careful thought he finds a balance of evidence in their favour, then his thought is free, however odd his conclusions may seem.

A freethinker, according to Russell, is not necessarily an atheist or an agnostic, as long as he or she satisfies this definition:

The person who is free in any respect is free from something; what is the free thinker free from? To be worthy of the name, he must be free of two things: the force of tradition, and the tyranny of his own passions. No one is completely free from either, but in the measure of a man's emancipation he deserves to be called a free thinker.

Fred Edwords, former executive of the American Humanist Association, suggests that by Russell's definition, liberal religionists who have challenged established orthodoxies can be considered freethinkers.

On the other hand, according to Bertrand Russell, atheists and/or agnostics are not necessarily freethinkers. As an example, he mentions Stalin, whom he compares to a "pope":

what I am concerned with is the doctrine of the modern Communistic Party, and of the Russian Government to which it owes allegiance. According to this doctrine, the world develops on the lines of a Plan called Dialectical Materialism, first discovered by Karl Marx, embodied in the practice of a great state by Lenin, and now expounded from day to day by a Church of which Stalin is the Pope. […] Free discussion is to be prevented wherever the power to do so exists; […] If this doctrine and this organization prevail, free inquiry will become as impossible as it was in the middle ages, and the world will relapse into bigotry and obscurantism.

In the 18th and 19th century, many thinkers regarded as freethinkers were deists, arguing that the nature of God can only be known from a study of nature rather than from religious revelation. In the 18th century, "deism" was as much of a 'dirty word' as "atheism", and deists were often stigmatized as either atheists or at least as freethinkers by their Christian opponents. Deists today regard themselves as freethinkers, but are now arguably less prominent in the free thought movement than atheists.

Characteristics

Among freethinkers, for a notion to be considered true it must be testable, verifiable, and logical. Many freethinkers tend to be humanists, who base morality on human needs and would find meaning in human compassion, social progress, art, personal happiness, love, and the furtherance of knowledge. Generally, freethinkers like to think for themselves, tend to be skeptical, respect critical thinking and reason, remain open to new concepts, and are sometimes proud of their own individuality. They would determine truth for themselves – based upon knowledge they gain, answers they receive, experiences they have and the balance they thus acquire. Freethinkers reject conformity for the sake of conformity, whereby they create their own beliefs by considering the way the world around them works and would possess the intellectual integrity and courage to think outside of accepted norms, which may or may not lead them to believe in some higher power.

Symbol

Tombstone detail of a freethinker, late 19th century. (Cemetery of Cullera, Spain).

The pansy serves as the long-established and enduring symbol of free thought; literature of the American Secular Union inaugurated its usage in the late 1800s. The reasoning behind the pansy as the symbol of free thought lies both in the flower's name and in its appearance. The pansy derives its name from the French word pensée, which means "thought". It allegedly received this name because the flower is perceived by some to bear resemblance to a human face, and in mid-to-late summer it nods forward as if deep in thought. In the 1880s, following examples set by freethinkers in France, Belgium, Spain and Sweden, it was proposed in the United States as "the symbol of religious liberty and freedom of conscience".

History

Pre-modern movement

Critical thought has flourished in the Hellenistic Mediterranean, in the repositories of knowledge and wisdom in Ireland and in the Iranian civilizations (for example in the era of Khayyam (1048–1131) and his unorthodox Sufi Rubaiyat poems). Later societies made advances on freedom of thought such as the Chinese (note for example the seafaring renaissance of the Southern Song dynasty of 1127–1279), on through heretical thinkers on esoteric alchemy or astrology, to the Renaissance and the Protestant Reformation pioneered by Martin Luther.

French physician and writer Rabelais celebrated "rabelaisian" freedom as well as good feasting and drinking (an expression and a symbol of freedom of the mind) in defiance of the hypocrisies of conformist orthodoxy in his utopian Thelema Abbey (from θέλημα: free "will"), the device of which was Do What Thou Wilt:

So had Gargantua established it. In all their rule and strictest tie of their order there was but this one clause to be observed, Do What Thou Wilt; because free people ... act virtuously and avoid vice. They call this honor.

When Rabelais's hero Pantagruel journeys to the "Oracle of The Div(in)e Bottle", he learns the lesson of life in one simple word: "Trinch!", Drink! Enjoy the simple life, learn wisdom and knowledge, as a free human. Beyond puns, irony, and satire, Gargantua's prologue-metaphor instructs the reader to "break the bone and suck out the substance-full marrow" ("la substantifique moëlle"), the core of wisdom.

Modern movements

The year 1600 is considered a landmark in the era of modern free thought. It was the year of the execution in Italy of Giordano Bruno, a former Dominican friar, by the Inquisition.

Australia

Prior to World War II, Australia had high rates of Protestantism and Catholicism. Post-war Australia has become a highly secularised country. Donald Horne, one of Australia's well-known public intellectuals, believed rising prosperity in post-war Australia influenced the decline in church-going and general lack of interest in religion. "Churches no longer matter very much to most Australians. If there is a happy eternal life it's for everyone ... For many Australians the pleasures of this life are sufficiently satisfying that religion offers nothing of great appeal", said Horne in his landmark work The Lucky Country (1964).

Belgium

The Université Libre de Bruxelles and the Vrije Universiteit Brussel, along with the two Circles of Free Inquiry (Dutch and French speaking), defend the freedom of critical thought, lay philosophy and ethics, while rejecting the argument of authority.

Canada

In 1873 a handful of secularists founded the earliest known secular organization in English Canada, the Toronto Freethought Association. Reorganized in 1877 and again in 1881, when it was renamed the Toronto Secular Society, the group formed the nucleus of the Canadian Secular Union, established in 1884 to bring together freethinkers from across the country.

A significant number of the early members appear to have come from the educated labour "aristocracy", including Alfred F. Jury, J. Ick Evans and J. I. Livingstone, all of whom were leading labour activists and secularists. The second president of the Toronto association, T. Phillips Thompson, became a central figure in the city's labour and social-reform movements during the 1880s and 1890s and arguably Canada's foremost late nineteenth-century labour intellectual. By the early 1880s scattered free thought organizations operated throughout southern Ontario and parts of Quebec, eliciting both urban and rural support.

The principal organ of the free thought movement in Canada was Secular Thought (Toronto, 1887–1911). Founded and edited during its first several years by English freethinker Charles Watts (1835–1906), it came under the editorship of Toronto printer and publisher James Spencer Ellis in 1891 when Watts returned to England. In 1968 the Humanist Association of Canada (HAC) formed to serve as an umbrella group for humanists, atheists, and freethinkers, and to champion social justice issues and oppose religious influence on public policy—most notably in the fight to make access to abortion free and legal in Canada.

England

The term freethinker emerged towards the end of the 17th century in England to describe those who stood in opposition to the institution of the Church, and the literal belief in the Bible. The beliefs of these individuals were centered on the concept that people could understand the world through consideration of nature. Such positions were formally documented for the first time in 1697 by William Molyneux in a widely publicized letter to John Locke, and more extensively in 1713, when Anthony Collins wrote his Discourse of Free-thinking, which gained substantial popularity. This essay attacks the clergy of all churches and it is a plea for deism.

The Freethinker magazine was first published in Britain in 1881; it continued in print until 2014, and still exists as a web-based publication.

France

In France, the concept first appeared in publication in 1765 when Denis Diderot, Jean le Rond d'Alembert, and Voltaire included an article on Liberté de penser in their Encyclopédie. The concept of free thought spread so widely that even places as remote as the Jotunheimen, in Norway, had well-known freethinkers such as Jo Gjende by the 19th century.

François-Jean Lefebvre de la Barre (1745–1766) was a young French nobleman, famous for having been tortured and beheaded before his body was burnt on a pyre along with Voltaire's Philosophical Dictionary. La Barre is often said to have been executed for not saluting a Roman Catholic religious procession, but the elements of the case were far more complex.

In France, Lefebvre de la Barre is widely regarded a symbol of the victims of Christian religious intolerance; La Barre along with Jean Calas and Pierre-Paul Sirven, was championed by Voltaire. A second replacement statue to de la Barre stands nearby the Basilica of the Sacred Heart of Jesus of Paris at the summit of the butte Montmartre (itself named from the Temple of Mars), the highest point in Paris and an 18th arrondissement street nearby the Sacré-Cœur is also named after Lefebvre de la Barre.

The 19th century saw the emergence of a specific notion of Libre-Pensée ("free thought"), with writer Victor Hugo as one of its major early proponents. French Freethinkers (Libre-Penseurs) associate freedom of thought, political anti-clericalism and socialist leanings. The main organisation referring to this tradition to this day is the Fédération nationale de la libre pensée, created in 1890.

Germany

In Germany, during the period 1815–1848 and before the March Revolution, the resistance of citizens against the dogma of the church increased. In 1844, under the influence of Johannes Ronge and Robert Blum, belief in the rights of man, tolerance among men, and humanism grew, and by 1859 they had established the Bund Freireligiöser Gemeinden Deutschlands (literally Union of Free Religious Communities of Germany), an association of persons who consider themselves to be religious without adhering to any established and institutionalized church or sacerdotal cult. This union still exists today, and is included as a member in the umbrella organization of free humanists. In 1881 in Frankfurt am Main, Ludwig Büchner established the Deutscher Freidenkerbund (German Freethinkers League) as the first German organization for atheists and agnostics. In 1892 the Freidenker-Gesellschaft and in 1906 the Deutscher Monistenbund were formed.

Free thought organizations developed the "Jugendweihe" (literally Youth consecration), a secular "confirmation" ceremony, and atheist funeral rites. The Union of Freethinkers for Cremation was founded in 1905, and the Central Union of German Proletariat Freethinker in 1908. The two groups merged in 1927, becoming the German Freethinking Association in 1930.

More "bourgeois" organizations declined after World War I, and "proletarian" free thought groups proliferated, becoming an organization of socialist parties. European socialist free thought groups formed the International of Proletarian Freethinkers (IPF) in 1925. Activists agitated for Germans to disaffiliate from their respective Church and for seculari-zation of elementary schools; between 1919–21 and 1930–32 more than 2.5 million Germans, for the most part supporters of the Social Democratic and Communist parties, gave up church membership. Conflict developed between radical forces including the Soviet League of the Militant Godless and Social Democratic forces in Western Europe led by Theodor Hartwig and Max Sievers. In 1930 the Soviet and allied delegations, following a walk-out, took over the IPF and excluded the former leaders. Following Hitler's rise to power in 1933, most free thought organizations were banned, though some right-wing groups that worked with so-called Völkische Bünde (literally "ethnic" associations with nationalist, xenophobic and very often racist ideology) were tolerated by the Nazis until the mid-1930s.

Ireland

In the 19th century, received opinion was scandalised by George Ensor (1769-1843). His Review of the Miracles, Prophecies, & Mysteries of the Old and New Testaments (1835) argued that, far from being a source of moral teaching, revealed religion and its divines regarded questions of morality as "incidental"--as a "mundane and merely philosophical" topic.

Netherlands

In the Netherlands, free thought has existed in organized form since the establishment of De Dageraad (now known as De Vrije Gedachte) in 1856. Among its most notable subscribing 19th century individuals were Johannes van Vloten, Multatuli, Adriaan Gerhard and Domela Nieuwenhuis.

In 2009, Frans van Dongen established the Atheist-Secular Party, which takes a considerably restrictive view of religion and public religious expressions.

Since the 19th century, free thought in the Netherlands has become more well known as a political phenomenon through at least three currents: liberal freethinking, conservative freethinking, and classical freethinking. In other words, parties which identify as freethinking tend to favor non-doctrinal, rational approaches to their preferred ideologies, and arose as secular alternatives to both clerically aligned parties as well as labor-aligned parties. Common themes among freethinking political parties are "freedom", "liberty", and "individualism".

Switzerland

With the introduction of cantonal church taxes in the 1870s, anti-clericals began to organise themselves. Around 1870, a "freethinkers club" was founded in Zürich. During the debate on the Zürich church law in 1883, professor Friedrich Salomon Vögelin and city council member Kunz proposed to separate church and state.

Turkey

In the last years of the Ottoman Empire, free thought made its voice heard by the works of distinguished people such as Ahmet Rıza, Tevfik Fikret, Abdullah Cevdet, Kılıçzade Hakkı, and Celal Nuri İleri. These intellectuals affected the early period of the Turkish Republic. Mustafa Kemal Atatürkfield marshal, revolutionary statesman, author, and founder of the secular Turkish nation state, serving as its first President from 1923 until his death in 1938– was the practitioner of their ideas. He made many reforms that modernized the country. Sources point out that Atatürk was a religious skeptic and a freethinker. He was a non-doctrinaire deist or an atheist, who was antireligious and anti-Islamic in general. According to Atatürk, the Turkish people do not know what Islam really is and do not read the Quran. People are influenced by Arabic sentences that they do not understand, and because of their customs they go to mosques. When the Turks read the Quran and think about it, they will leave Islam. Atatürk described Islam as the religion of the Arabs in his own work titled Vatandaş için Medeni Bilgiler by his own critical and nationalist views.

Association of Atheism (Ateizm Derneği), the first official atheist organisation in Middle East and Caucasus, was founded in 2014. It serves to support irreligious people and freethinkers in Turkey who are discriminated against based on their views. In 2018 it was reported in some media outlets that the Ateizm Derneği would close down because of the pressure on its members and attacks by pro-government media, but the association itself issued a clarification that this was not the case and that it was still active.

United States

The Free Thought movement first organized itself in the United States as the "Free Press Association" in 1827 in defense of George Houston, publisher of The Correspondent, an early journal of Biblical criticism in an era when blasphemy convictions were still possible. Houston had helped found an Owenite community at Haverstraw, New York in 1826–27. The short-lived Correspondent was superseded by the Free Enquirer, the official organ of Robert Owen's New Harmony community in Indiana, edited by Robert Dale Owen and by Fanny Wright between 1828 and 1832 in New York. During this time Robert Dale Owen sought to introduce the philosophic skepticism of the Free Thought movement into the Workingmen's Party in New York City. The Free Enquirer's annual civic celebrations of Paine's birthday after 1825 finally coalesced in 1836 in the first national Free Thinkers organization, the "United States Moral and Philosophical Society for the General Diffusion of Useful Knowledge". It was founded on August 1, 1836, at a national convention at the Lyceum in Saratoga Springs with Isaac S. Smith of Buffalo, New York, as president. Smith was also the 1836 Equal Rights Party's candidate for Governor of New York and had also been the Workingmen's Party candidate for Lt. Governor of New York in 1830. The Moral and Philosophical Society published The Beacon, edited by Gilbert Vale.

Driven by the revolutions of 1848 in the German states, the 19th century saw an immigration of German freethinkers and anti-clericalists to the United States (see Forty-Eighters). In the United States, they hoped to be able to live by their principles, without interference from government and church authorities.

Many Freethinkers settled in German immigrant strongholds, including St. Louis, Indianapolis, Wisconsin, and Texas, where they founded the town of Comfort, Texas, as well as others.

These groups of German Freethinkers referred to their organizations as Freie Gemeinden, or "free congregations". The first Freie Gemeinde was established in St. Louis in 1850. Others followed in Pennsylvania, California, Washington, D.C., New York, Illinois, Wisconsin, Texas, and other states.

Freethinkers tended to be liberal, espousing ideals such as racial, social, and sexual equality, and the abolition of slavery.

The "Golden Age of Freethought" in the US came in the late 1800s. The dominant organization was the National Liberal League which formed in 1876 in Philadelphia. This group re-formed itself in 1885 as the American Secular Union under the leadership of the eminent agnostic orator Robert G. Ingersoll. Following Ingersoll's death in 1899 the organization declined, in part due to lack of effective leadership.

Free thought in the United States declined in the early twentieth century. By the early twentieth century, most free thought congregations had disbanded or joined other mainstream churches. The longest continuously operating free thought congregation in America is the Free Congregation of Sauk County, Wisconsin, which was founded in 1852 and is still active as of 2020. It affiliated with the American Unitarian Association (now the Unitarian Universalist Association) in 1955. D. M. Bennett was the founder and publisher of The Truth Seeker in 1873, a radical free thought and reform American periodical.

German Freethinker settlements were located in:

Anarchism

Free thought influenced the development of anarchism in the United States of America. In the U.S.,

"free thought was a basically anti-Christian, anti-clerical movement, whose purpose was to make the individual politically and spiritually free to decide for himself on religious matters. A number of contributors to Liberty were prominent figures in both free thought and anarchism. The American individualist anarchist George MacDonald [(1857–1944)] was a co-editor of Freethought and, for a time, The Truth Seeker. E.C. Walker was co-editor of the freethought/free love journal Lucifer, the Light-Bearer."

"Many of the anarchists were ardent freethinkers; reprints from free thought papers such as Lucifer, the Light-Bearer, Freethought and The Truth Seeker appeared in Liberty...The church was viewed as a common ally of the state and as a repressive force in and of itself."

European tradition

In Europe, a similar development occurred in French and Spanish individualist anarchist circles:

"Anticlericalism, just as in the rest of the libertarian movement, in another of the frequent elements which will gain relevance related to the measure in which the (French) Republic begins to have conflicts with the church...Anti-clerical discourse, frequently called for by the French individualist André Lorulot [(1885-1963)], will have its impacts in Estudios (a Spanish individualist anarchist publication). There will be an attack on institutionalized religion for the responsibility that it had in the past on negative developments, for its irrationality which makes it a counterpoint of philosophical and scientific progress. There will be a criticism of proselytism and ideological manipulation which happens on both believers and agnostics".

These tendencies would continue in French individualist anarchism in the work and activism of Charles-Auguste Bontemps (1893-1981) and others. In the Spanish individualist anarchist magazines Ética and Iniciales

"there is a strong interest in publishing scientific news, usually linked to a certain atheist and anti-theist obsession, philosophy which will also work for pointing out the incompatibility between science and religion, faith, and reason. In this way there will be a lot of talk on Darwin's theories or on the negation of the existence of the soul".

In 1901 the Catalan anarchist and freethinker Francesc Ferrer i Guàrdia established "modern" or progressive schools in Barcelona in defiance of an educational system controlled by the Catholic Church. The schools had the stated goal to "educate the working class in a rational, secular and non-coercive setting". Fiercely anti-clerical, Ferrer believed in "freedom in education", education free from the authority of church and state. Ferrer's ideas, generally, formed the inspiration for a series of Modern Schools in the United States, Cuba, South America and London. The first of these started in New York City in 1911. Ferrer also inspired the Italian newspaper Università popolare, founded in 1901.

Kleine–Levin syndrome

From Wikipedia, the free encyclopedia

Kleine–Levin syndrome
Other names
  • Familial hibernation syndrome
  • Sleeping Beauty Syndrome
SpecialtyNeurology 

Kleine–Levin syndrome (KLS) is a rare neurological disorder characterized by persistent episodic hypersomnia accompanied by cognitive and behavioral changes. These changes may include disinhibition, sometimes manifested through hypersexuality, hyperphagia or emotional lability, and other symptoms, such as derealization. Patients generally experience recurrent episodes of the condition for more than a decade, which may return at a later age. Individual episodes generally last more than a week, sometimes lasting for months. The condition greatly affects the personal, professional, and social lives of those with KLS. The severity of symptoms and the course of the syndrome vary between those with KLS. Patients commonly have about 20 episodes over about a decade. Several months may elapse between episodes.

The onset of the condition usually follows a viral infection (72% of patients); several different viruses have been observed to trigger KLS. It is generally only diagnosed after similar conditions have been excluded; MRI, CT scans, lumbar puncture, and toxicology tests are used to rule out other possibilities. The syndrome's mechanism is not known, but the thalamus is thought to possibly play a role. SPECT has shown thalamic hypoperfusion in patients during episodes.

KLS is very rare, occurring at a rate of 1 in 500 000, which limits research into genetic factors. The condition primarily affects teenagers (81% of reported patients), with a bias towards males (68-72% of cases), though females can also be affected, and the age of onset varies. There is no known cure, and there is little evidence supporting drug treatment. Lithium has been reported to have limited effects in case reports, decreasing the length of episodes and duration between them in some patients. Stimulants have been shown to promote wakefulness during episodes, but they do not counteract cognitive symptoms or decrease the duration of episodes. The condition is named after Willi Kleine and Max Levin, who described cases of the disease in the early 20th century. It was added to the International Classification of Sleep Disorders in 1990.

Symptoms

Patients with Kleine–Levin syndrome (KLS) experience recurring episodes of prolonged sleep (hypersomnia). In most cases, patients sleep 15 to 21 hours a day during episodes. Excessive appetite (hyperphagia) and unusual cravings are present in half to two thirds of cases. About half of patients, mainly male patients, experience dramatically increased sexual urges (hypersexuality). Several other symptoms usually accompany the syndrome, including marked changes in mood and cognitive ability. Derealization and severe apathy are present in at least 80 percent of cases. About one third of patients experience hallucinations or delusions. Depression and anxiety occur less commonly; one study found them in about 25 percent of patients. Individuals usually cannot remember what happened during episodes. Repetitive behaviors and headaches are commonly reported. Some patients act very childlike during episodes, and communication skills and coordination sometimes worsen.

Sleep studies of KLS show varying results based on the amount of time the patient is observed. Slow wave sleep is often reduced at the beginning of episodes, and REM sleep is reduced near the end. Conversely, REM sleep is often normal at the beginning, and slow wave sleep is often normal by the conclusion. Stage two non-rapid eye movement sleep is often interrupted during KLS. Studies also show that stage one and three non-rapid eye movement sleep become more efficient when the episodes end. The Multiple Sleep Latency Test has yielded inconsistent results when given to KLS patients. In many cases, hours are spent in a withdrawn sleep-like state while awake during episodes. Most sleep studies have been performed while subject is near the end of their episodes. Some patients experience brief insomnia and become very happy and talkative after the episode ends.

The first time a patient experiences KLS, it usually occurs along with symptoms that are similar to those of the flu or encephalitis. In at least 75 percent of cases, symptoms occur after an airway infection or a fever. Viruses observed before the development of the condition include Epstein–Barr virus, varicella zoster virus, herpes zoster virus, influenza A virus subtypes, and adenovirus. Several days after symptoms first occur, patients become very tired. In cases that occur after an infection, KLS usually starts within three to five days for teenagers and fewer for children. In other cases, alcohol consumption, head injury, or international travel precede symptoms. Lifestyle habits, such as stress, alcohol abuse and lack of sleep and stress, have also been proposed as possible triggers. First episodes of KLS are preceded by a clear event in about 90 percent of cases. Recurrences generally do not have clear triggers; only about 15 percent have a precipitating event.

The condition generally disrupts the social lives and academic or professional obligations of those with KLS. Some patients also gain weight during episodes. The most severe cases cause a long-term impact on mood and cognitive attention. In rare cases, patients experience long-term memory problems.

In patients with KLS, MRI and CT scans show normal brain morphology. When SPECT is performed, hypoperfusion can often be observed in the brain, particularly in the thalamic and frontotemporal areas. The hypoperfusion is significantly diminished between episodes. Serum biology, c-reactive proteins and leptins, the hormonal pituitary axis, and protein in the cerebral spinal fluid (CSF) are normal in KLS patients.

Cause

It is not known what causes KLS, but several mechanisms have been proposed. One possible explanation is hypothalamic or circadian dysfunction. The thalamus probably plays a role in the out-of-control sleeping, and patients with diencephalic–hypothalamic dysfunction caused by tumors experience symptoms similar to those of KLS patients. Specifically, the medial temporal regions of the thalamus may be involved, although examinations of KLS patients have not consistently found abnormalities in this area. The temporal lobe also appears to play a role in the condition, possibly causing cognitive difficulties. The apathy and disinhibition found in some with KLS suggest that the condition may include frontal lobe dysfunction as well. The involvement of the thalamus, temporal lobe, and frontal lobe of the brain suggests that there is a multifocal, localized encephalopathy. There are also persistent subclinical abnormalities in some with KLS.

Another possible explanation concerns the metabolism of serotonin and dopamine. An imbalance in the neurotransmitter pathways of these chemicals could play a role. Viral infections have also been suggested as a possible cause. Evidence for their role includes lesions found in autopsies. CSF samples from KLS patients indicate that the condition has a different cause than influenza-associated encephalopathy. Triggers of KLS may also affect the blood-brain barrier, which could play a role in the condition. There is limited evidence of what role hypocretin may play, although it often influences hypersomnia.

Androgen might (indirectly) block melatonin receptors, possibly by means of vasodilation, and cause cholinergic abnormalities in some cases of Kleine–Levin syndrome.

Because KLS occurs at a much higher rate in Jews and in some families, it is likely that there is some genetic component in addition to environmental factors. Genetic studies hold promise for understanding the disease, but they have yielded inconsistent results and few patients are available for testing.

Epilepsy and depression do not appear to cause KLS. The condition's rapid onset after infections indicates that the immune system is not to blame.

One study has suggested a link to the gene LMOD3 on chromosome 3.

Diagnosis

KLS can be diagnosed when there is confusion, apathy, or derealization in addition to frequent bouts of extreme tiredness and prolonged sleep. The earliest it can be diagnosed is the second episode, this is not common. The condition is generally treated as a diagnosis of exclusion. Because KLS is rare, other conditions with similar symptoms are usually considered first.

MRIs can determine if the symptoms are caused by certain brain disorders, stroke, and multiple sclerosis. Lumbar puncture can determine if encephalitis is the cause. KLS must be differentiated from substance abuse by toxicology tests. The use of electroencephalography (EEG) can exclude temporal status epilepticus from consideration. EEGs are normal in about 70% of KLS patients, but background slowing may sometimes be detected. In addition, low-frequency high-amplitude waves can be observed during waking hours.

Initially, KLS appears similar to bipolar depression. Patients with frontal-lobe syndromes and Klüver–Bucy syndrome also display similar symptoms, but these conditions can be differentiated by the presence of brain lesions. KLS should also be distinguished from very rare cases of menstruation-caused hypersomnia.

Prevention

Lithium is the only drug that appears to have a preventive effect. In two studies of more than 100 patients, lithium helped prevent recurrence of symptoms in 20% to 40% of cases. The recommended blood level of lithium for KLS patients is 0.8–1.2 mEq/ml. It is not known if other mood stabilizers have an effect on the condition. Anti-depressants do not prevent recurrence.

Treatment

Several drug therapies have been used on patients with KLS, but none of them have been subject to randomized controlled trials. A 2016 Cochrane Review concluded that "No evidence indicates that pharmacological treatment for Kleine–Levin syndrome is effective and safe".

In several cases, stimulants, including modafinil, have been reported to have a limited effect on patients, often alleviating sleepiness. They can cause behavioral problems, but they may pose fewer issues if used in older patients with mild symptoms. In some case reports, lithium has been reported to decrease the length of episodes and the severity of their symptoms and to increase the time between episodes. It has been reported to be effective in about 25 to 60 percent of cases. Its use carries the risk of side effects in the thyroid or kidneys. Antipsychotics and benzodiazepines can help alleviate psychotic and anxiety related symptoms, respectively. Carbamazepine has been reported to be less effective than lithium but more effective than some drugs in its class. Electroconvulsive therapy is not effective and worsens symptoms.

KLS patients generally do not need to be admitted to hospitals. It is recommended that caregivers reassure them and encourage them to maintain sleep hygiene. It may also be necessary for patients to be prevented from putting themselves in dangerous situations, such as driving.

Prognosis

The frequency of KLS episodes can vary from attacks one week in length occurring twice a year to dozens of episodes that follow each other in close succession. The median duration of KLS episodes is about ten days, but some last several weeks or months. A study of 108 patients found an average of 19 episodes over the duration of the disease. Another study found a median of 3.5 months between episodes. Outside of episodes, there is no disturbance in patients' sleep patterns and they are generally asymptomatic. Patients do not experience the same symptoms in each episode.

About 80 percent of patients are adolescents when they first experience KLS. On some occasions though, its first occurrence comes in childhood or adulthood. In most adolescent-onset patients, symptoms cease by the time they are 30 years old. A French study of 108 patients found a median duration of 13 years, but a review of 186 cases found a median duration of 8 years. Unusually young or old patients and those who experience hypersexuality tend to have a more severe course. Patients who initially have frequent attacks generally see the disease cease earlier than others. The condition spontaneously resolves, and the patient is considered to be cured if there have been no symptoms for six years.

Epidemiology

Population-based studies of KLS have not been performed. Its prevalence is about 1 to 2 cases per million people, although recent studies conducted by a French research team point to a higher number of 3 per million people. It occurs most frequently among Jews in the US and Israel. First-degree relatives of people who have the syndrome are much more likely than the general population to have it, although only in about one percent of cases do family members contract it. About 68 to 72 percents of patients are male. Patients with the syndrome are more likely than the general population to have genetic disorders, and about a third of people with the syndrome encountered some form of birth difficulty. In a study of 186 older patients, about ten percent had preexisting psychiatric issues. One study found that about ten percent of patients had a neurological condition before KLS developed. The condition does not appear to occur most frequently in one season.

History

In 1815, there was a report of a young man who showed excessive appetite and prolonged sleep after experiencing a fever; this may have been an early description of the condition. Another case with similar symptoms was described by Brierre de Boismont in 1862.

Five patients with symptoms of persistent sleepiness were described in detail in 1925 by Willi Kleine, a neurologist from Frankfurt. This report was followed four years later by details of a similar case by New York-based psychiatrist Max Levin. In 1935, Levin published information about several more cases, including one described by Kleine. Levin noted that some patients displayed an intense appetite in addition to their persistent tiredness. MacDonald Critchley, who first wrote about the condition in 1942, described 11 cases he had examined and reviewed 15 other published cases in a 1962 publication. In the report, which included patients he had examined in the Royal Navy during World War II, he observed that irritability and depersonalization often occurred while patients were awake. He named the condition Kleine–Levin syndrome and noted four common traits: hypersexuality, adolescent onset, spontaneous resolution, and compulsive eating. He believed that the condition only affected males, but later studies showed some female patients. In the 1970s, several psychoanalytic and psychodynamic explanations for the condition were proposed. In 1980, a Hawaiian–Caucasian family was found in which nine family members had the condition.

Diagnostic criteria for KLS was established by Schmidt in 1990, and the International Classification of Sleep Disorders further refined them. KLS is classified as a sleep disorder, specifically one of recurrent hypersomnia. Before 2005, hyperphagia and hypersexuality were thought to occur in all cases. That was changed with the guidelines published that year, which noted that they did not always occur.

Insomnia

From Wikipedia, the free encyclopedia

Insomnia
Other namesSleeplessness, trouble sleeping
53-aspetti di vita quotidiana, insonnia, Taccuino Sanitatis,.jpg
Depiction of insomnia from the 14th century medical manuscript Tacuinum Sanitatis
Pronunciation
SpecialtyPsychiatry, sleep medicine
SymptomsTrouble sleeping, daytime sleepiness, low energy, irritability, depressed mood
ComplicationsMotor vehicle collisions
CausesUnknown, psychological stress, chronic pain, heart failure, hyperthyroidism, heartburn, restless leg syndrome, others
Diagnostic methodBased on symptoms, sleep study
Differential diagnosisDelayed sleep phase disorder, restless leg syndrome, sleep apnea, psychiatric disorder
TreatmentSleep hygiene, cognitive behavioral therapy, sleeping pills
Frequency~20%

Insomnia, also known as sleeplessness, is a sleep disorder in which people have trouble sleeping. They may have difficulty falling asleep, or staying asleep for as long as desired. Insomnia is typically followed by daytime sleepiness, low energy, irritability, and a depressed mood. It may result in an increased risk of motor vehicle collisions, as well as problems focusing and learning. Insomnia can be short term, lasting for days or weeks, or long term, lasting more than a month. The concept of the word insomnia has two possibilities: insomnia disorder and insomnia symptoms, and many abstracts of randomized controlled trials and systematic reviews often underreport on which of these two possibilities the word insomnia refers to.

Insomnia can occur independently or as a result of another problem. Conditions that can result in insomnia include psychological stress, chronic pain, heart failure, hyperthyroidism, heartburn, restless leg syndrome, menopause, certain medications, and drugs such as caffeine, nicotine, and alcohol. Other risk factors include working night shifts and sleep apnea. Diagnosis is based on sleep habits and an examination to look for underlying causes. A sleep study may be done to look for underlying sleep disorders. Screening may be done with two questions: "do you experience difficulty sleeping?" and "do you have difficulty falling or staying asleep?"

Although their efficacy as first line treatments is not unequivocally established, sleep hygiene and lifestyle changes are typically the first treatment for insomnia. Sleep hygiene includes a consistent bedtime, a quiet and dark room, exposure to sunlight during the day and regular exercise. Cognitive behavioral therapy may be added to this. While sleeping pills may help, they are sometimes associated with injuries, dementia, and addiction. These medications are not recommended for more than four or five weeks. The effectiveness and safety of alternative medicine is unclear.

Between 10% and 30% of adults have insomnia at any given point in time and up to half of people have insomnia in a given year. About 6% of people have insomnia that is not due to another problem and lasts for more than a month. People over the age of 65 are affected more often than younger people. Women are more often affected than males. Descriptions of insomnia occur at least as far back as ancient Greece.

Signs and symptoms

Potential complications of insomnia.

Symptoms of insomnia:

  • Difficulty falling asleep, including difficulty finding a comfortable sleeping position
  • Waking during the night, being unable to return to sleep and waking up early
  • Not able to focus on daily tasks, difficulty in remembering
  • Daytime sleepiness, irritability, depression or anxiety
  • Feeling tired or having low energy during the day
  • Trouble concentrating
  • Being irritable, acting aggressive or impulsive

Sleep onset insomnia is difficulty falling asleep at the beginning of the night, often a symptom of anxiety disorders. Delayed sleep phase disorder can be misdiagnosed as insomnia, as sleep onset is delayed to much later than normal while awakening spills over into daylight hours.

It is common for patients who have difficulty falling asleep to also have nocturnal awakenings with difficulty returning to sleep. Two-thirds of these patients wake up in the middle of the night, with more than half having trouble falling back to sleep after a middle-of-the-night awakening.

Early morning awakening is an awakening occurring earlier (more than 30 minutes) than desired with an inability to go back to sleep, and before total sleep time reaches 6.5 hours. Early morning awakening is often a characteristic of depression. Anxiety symptoms may well lead to insomnia. Some of these symptoms include tension, compulsive worrying about the future, feeling overstimulated, and overanalyzing past events.

Poor sleep quality

Poor sleep quality can occur as a result of, for example, restless legs, sleep apnea or major depression. Poor sleep quality is defined as the individual not reaching stage 3 or delta sleep which has restorative properties.

Major depression leads to alterations in the function of the hypothalamic–pituitary–adrenal axis, causing excessive release of cortisol which can lead to poor sleep quality.

Nocturnal polyuria, excessive night-time urination, can also result in a poor quality of sleep.

Subjectivity

Some cases of insomnia are not really insomnia in the traditional sense, because people experiencing sleep state misperception often sleep for a normal amount of time. The problem is that, despite sleeping for multiple hours each night and typically not experiencing significant daytime sleepiness or other symptoms of sleep loss, they do not feel like they have slept very much, if at all. Because their perception of their sleep is incomplete, they incorrectly believe it takes them an abnormally long time to fall asleep, and they underestimate how long they stay asleep.

Causes

While insomnia can be caused by a number of conditions, it can also occur without any identifiable cause. This is known as Primary Insomnia. Primary Insomnia may also have an initial identifiable cause, but continues after the cause is no longer present. For example, a bout of insomnia may be triggered by a stressful work or life event. However the condition may continue after the stressful event has been resolved. In such cases, the insomnia is usually perpetuated by the anxiety or fear caused by the sleeplessness itself, rather than any external factors.

Symptoms of insomnia can be caused by or be associated with:

Sleep studies using polysomnography have suggested that people who have sleep disruption have elevated night-time levels of circulating cortisol and adrenocorticotropic hormone. They also have an elevated metabolic rate, which does not occur in people who do not have insomnia but whose sleep is intentionally disrupted during a sleep study. Studies of brain metabolism using positron emission tomography (PET) scans indicate that people with insomnia have higher metabolic rates by night and by day. The question remains whether these changes are the causes or consequences of long-term insomnia.

Genetics

Heritability estimates of insomnia vary between 38% in males to 59% in females. A genome-wide association study (GWAS) identified 3 genomic loci and 7 genes that influence the risk of insomnia, and showed that insomnia is highly polygenic. In particular, a strong positive association was observed for the MEIS1 gene in both males and females. This study showed that the genetic architecture of insomnia strongly overlaps with psychiatric disorders and metabolic traits.

It has been hypothesized that epigenetics might also influence insomnia through a controlling process of both sleep regulation and brain-stress response having an impact as well on the brain plasticity.

Substance-induced

Alcohol-induced

Alcohol is often used as a form of self-treatment of insomnia to induce sleep. However, alcohol use to induce sleep can be a cause of insomnia. Long-term use of alcohol is associated with a decrease in NREM stage 3 and 4 sleep as well as suppression of REM sleep and REM sleep fragmentation. Frequent moving between sleep stages occurs with; awakenings due to headaches, the need to urinate, dehydration, and excessive sweating. Glutamine rebound also plays a role as when someone is drinking; alcohol inhibits glutamine, one of the body's natural stimulants. When the person stops drinking, the body tries to make up for lost time by producing more glutamine than it needs. The increase in glutamine levels stimulates the brain while the drinker is trying to sleep, keeping him/her from reaching the deepest levels of sleep. Stopping chronic alcohol use can also lead to severe insomnia with vivid dreams. During withdrawal, REM sleep is typically exaggerated as part of a rebound effect.

Benzodiazepine-induced

Like alcohol, benzodiazepines, such as alprazolam, clonazepam, lorazepam, and diazepam, are commonly used to treat insomnia in the short-term (both prescribed and self-medicated), but worsen sleep in the long-term. While benzodiazepines can put people to sleep (i.e., inhibit NREM stage 1 and 2 sleep), while asleep, the drugs disrupt sleep architecture: decreasing sleep time, delaying time to REM sleep, and decreasing deep slow-wave sleep (the most restorative part of sleep for both energy and mood).

Opioid-induced

Opioid medications such as hydrocodone, oxycodone, and morphine are used for insomnia that is associated with pain due to their analgesic properties and hypnotic effects. Opioids can fragment sleep and decrease REM and stage 2 sleep. By producing analgesia and sedation, opioids may be appropriate in carefully selected patients with pain-associated insomnia. However, dependence on opioids can lead to long-term sleep disturbances.

Risk factors

Insomnia affects people of all age groups but people in the following groups have a higher chance of acquiring insomnia:

  • Individuals older than 60
  • History of mental health disorder including depression, etc.
  • Emotional stress
  • Working late night shifts
  • Traveling through different time zones
  • Having chronic diseases such as diabetes, kidney disease, lung disease, Alzheimer's, or heart disease
  • Alcohol or drug use disorders
  • Gastrointestinal reflux disease
  • Heavy smoking
  • Work stress

Mechanism

Two main models exists as to the mechanism of insomnia, cognitive and physiological. The cognitive model suggests rumination and hyperarousal contribute to preventing a person from falling asleep and might lead to an episode of insomnia.

The physiological model is based upon three major findings in people with insomnia; firstly, increased urinary cortisol and catecholamines have been found suggesting increased activity of the HPA axis and arousal; second, increased global cerebral glucose utilization during wakefulness and NREM sleep in people with insomnia; and lastly, increased full body metabolism and heart rate in those with insomnia. All these findings taken together suggest a deregulation of the arousal system, cognitive system, and HPA axis all contributing to insomnia. However, it is unknown if the hyperarousal is a result of, or cause of insomnia. Altered levels of the inhibitory neurotransmitter GABA have been found, but the results have been inconsistent, and the implications of altered levels of such a ubiquitous neurotransmitter are unknown. Studies on whether insomnia is driven by circadian control over sleep or a wake dependent process have shown inconsistent results, but some literature suggests a deregulation of the circadian rhythm based on core temperature. Increased beta activity and decreased delta wave activity has been observed on electroencephalograms; however, the implication of this is unknown.

Around half of post-menopausal women experience sleep disturbances, and generally sleep disturbance is about twice as common in women as men; this appears to be due in part, but not completely, to changes in hormone levels, especially in and post-menopause.

Changes in sex hormones in both men and women as they age may account in part for increased prevalence of sleep disorders in older people.

Diagnosis

In medicine, insomnia is widely measured using the Athens insomnia scale. It is measured using eight different parameters related to sleep, finally represented as an overall scale which assesses an individual's sleep pattern.

A qualified sleep specialist should be consulted for the diagnosis of any sleep disorder so the appropriate measures can be taken. Past medical history and a physical examination need to be done to eliminate other conditions that could be the cause of insomnia. After all other conditions are ruled out a comprehensive sleep history should be taken. The sleep history should include sleep habits, medications (prescription and non-prescription), alcohol consumption, nicotine and caffeine intake, co-morbid illnesses, and sleep environment. A sleep diary can be used to keep track of the individual's sleep patterns. The diary should include time to bed, total sleep time, time to sleep onset, number of awakenings, use of medications, time of awakening, and subjective feelings in the morning. The sleep diary can be replaced or validated by the use of out-patient actigraphy for a week or more, using a non-invasive device that measures movement.

Workers who complain of insomnia should not routinely have polysomnography to screen for sleep disorders. This test may be indicated for patients with symptoms in addition to insomnia, including sleep apnea, obesity, a thick neck diameter, or high-risk fullness of the flesh in the oropharynx. Usually, the test is not needed to make a diagnosis, and insomnia especially for working people can often be treated by changing a job schedule to make time for sufficient sleep and by improving sleep hygiene.

Some patients may need to do an overnight sleep study to determine if insomnia is present. Such a study will commonly involve assessment tools including a polysomnogram and the multiple sleep latency test. Specialists in sleep medicine are qualified to diagnose disorders within the, according to the ICSD, 81 major sleep disorder diagnostic categories. Patients with some disorders, including delayed sleep phase disorder, are often mis-diagnosed with primary insomnia; when a person has trouble getting to sleep and awakening at desired times, but has a normal sleep pattern once asleep, a circadian rhythm disorder is a likely cause.

In many cases, insomnia is co-morbid with another disease, side-effects from medications, or a psychological problem. Approximately half of all diagnosed insomnia is related to psychiatric disorders. For those who have depression, "insomnia should be regarded as a co-morbid condition, rather than as a secondary one;" insomnia typically predates psychiatric symptoms. "In fact, it is possible that insomnia represents a significant risk for the development of a subsequent psychiatric disorder." Insomnia occurs in between 60% and 80% of people with depression. This may partly be due to treatment used for depression.

Determination of causation is not necessary for a diagnosis.

DSM-5 criteria

The DSM-5 criteria for insomnia include the following:

Predominant complaint of dissatisfaction with sleep quantity or quality, associated with one (or more) of the following symptoms:

  • Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep without caregiver intervention.)
  • Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to sleep after awakenings. (In children, this may manifest as difficulty returning to sleep without caregiver intervention.)
  • Early-morning awakening with inability to return to sleep.

In addition:

  • The sleep disturbance causes clinically significant distress or impairment in social, occupational, educational, academic, behavioral, or other important areas of functioning.
  • The sleep difficulty occurs at least three nights per week.
  • The sleep difficulty is present for at least three months.
  • The sleep difficulty occurs despite adequate opportunity for sleep.
  • The insomnia is not better explained by and does not occur exclusively during the course of another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep disorder, a circadian rhythm sleep-wake disorder, a parasomnia).
  • The insomnia is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication).

Types

Insomnia can be classified as transient, acute, or chronic.

  • Transient insomnia lasts for less than a week. It can be caused by another disorder, by changes in the sleep environment, by the timing of sleep, severe depression, or by stress. Its consequences – sleepiness and impaired psychomotor performance – are similar to those of sleep deprivation.
  • Acute insomnia is the inability to consistently sleep well for a period of less than a month. Insomnia is present when there is difficulty initiating or maintaining sleep or when the sleep that is obtained is non-refreshing or of poor quality. These problems occur despite adequate opportunity and circumstances for sleep and they must result in problems with daytime function. Acute insomnia is also known as short term insomnia or stress related insomnia.
  • Chronic insomnia lasts for longer than a month. It can be caused by another disorder, or it can be a primary disorder. Common causes of chronic insomnia include persistent stress, trauma, work schedules, poor sleep habits, medications, and other mental health disorders. People with high levels of stress hormones or shifts in the levels of cytokines are more likely than others to have chronic insomnia. Its effects can vary according to its causes. They might include muscular weariness, hallucinations, and/or mental fatigue.

Prevention

Prevention and treatment of insomnia may require a combination of cognitive behavioral therapy, medications, and lifestyle changes.

Among lifestyle practices, going to sleep and waking up at the same time each day can create a steady pattern which may help to prevent insomnia. Avoidance of vigorous exercise and caffeinated drinks a few hours before going to sleep is recommended, while exercise earlier in the day may be beneficial. Other practices to improve sleep hygiene may include:

  • Avoiding or limiting naps
  • Treating pain at bedtime
  • Avoiding large meals, beverages, alcohol, and nicotine before bedtime
  • Finding soothing ways to relax into sleep, including use of white noise
  • Making the bedroom suitable for sleep by keeping it dark, cool, and free of devices, such as clocks, cell phones, or televisions
  • Maintain regular exercise
  • Try relaxing activities before sleeping

Management

It is recommended to rule out medical and psychological causes before deciding on the treatment for insomnia. Cognitive behavioral therapy is generally the first line treatment once this has been done. It has been found to be effective for chronic insomnia. The beneficial effects, in contrast to those produced by medications, may last well beyond the stopping of therapy.

Medications have been used mainly to reduce symptoms in insomnia of short duration; their role in the management of chronic insomnia remains unclear. Several different types of medications may be used. Many doctors do not recommend relying on prescription sleeping pills for long-term use. It is also important to identify and treat other medical conditions that may be contributing to insomnia, such as depression, breathing problems, and chronic pain. As of 2022, many people with insomnia were reported as not receiving overall sufficient sleep or treatment for insomnia.

Non-medication based

Non-medication based strategies have comparable efficacy to hypnotic medication for insomnia and they may have longer lasting effects. Hypnotic medication is only recommended for short-term use because dependence with rebound withdrawal effects upon discontinuation or tolerance can develop.

Non medication based strategies provide long lasting improvements to insomnia and are recommended as a first line and long-term strategy of management. Behavioral sleep medicine (BSM) tries to address insomnia with non-pharmacological treatments. The BSM strategies used to address chronic insomnia include attention to sleep hygiene, stimulus control, behavioral interventions, sleep-restriction therapy, paradoxical intention, patient education, and relaxation therapy. Some examples are keeping a journal, restricting the time spent awake in bed, practicing relaxation techniques, and maintaining a regular sleep schedule and a wake-up time. Behavioral therapy can assist a patient in developing new sleep behaviors to improve sleep quality and consolidation. Behavioral therapy may include, learning healthy sleep habits to promote sleep relaxation, undergoing light therapy to help with worry-reduction strategies and regulating the circadian clock.

Music may improve insomnia in adults (see music and sleep). EEG biofeedback has demonstrated effectiveness in the treatment of insomnia with improvements in duration as well as quality of sleep. Self-help therapy (defined as a psychological therapy that can be worked through on one's own) may improve sleep quality for adults with insomnia to a small or moderate degree.

Stimulus control therapy is a treatment for patients who have conditioned themselves to associate the bed, or sleep in general, with a negative response. As stimulus control therapy involves taking steps to control the sleep environment, it is sometimes referred interchangeably with the concept of sleep hygiene. Examples of such environmental modifications include using the bed for sleep and sex only, not for activities such as reading or watching television; waking up at the same time every morning, including on weekends; going to bed only when sleepy and when there is a high likelihood that sleep will occur; leaving the bed and beginning an activity in another location if sleep does not occur in a reasonably brief period of time after getting into bed (commonly ~20 min); reducing the subjective effort and energy expended trying to fall asleep; avoiding exposure to bright light during night-time hours, and eliminating daytime naps.

A component of stimulus control therapy is sleep restriction, a technique that aims to match the time spent in bed with actual time spent asleep. This technique involves maintaining a strict sleep-wake schedule, sleeping only at certain times of the day and for specific amounts of time to induce mild sleep deprivation. Complete treatment usually lasts up to 3 weeks and involves making oneself sleep for only a minimum amount of time that they are actually capable of on average, and then, if capable (i.e. when sleep efficiency improves), slowly increasing this amount (~15 min) by going to bed earlier as the body attempts to reset its internal sleep clock. Bright light therapy may be effective for insomnia.

Paradoxical intention is a cognitive reframing technique where the insomniac, instead of attempting to fall asleep at night, makes every effort to stay awake (i.e. essentially stops trying to fall asleep). One theory that may explain the effectiveness of this method is that by not voluntarily making oneself go to sleep, it relieves the performance anxiety that arises from the need or requirement to fall asleep, which is meant to be a passive act. This technique has been shown to reduce sleep effort and performance anxiety and also lower subjective assessment of sleep-onset latency and overestimation of the sleep deficit (a quality found in many insomniacs).

Sleep hygiene

Sleep hygiene is a common term for all of the behaviors which relate to the promotion of good sleep. They include habits which provide a good foundation for sleep and help to prevent insomnia. However, sleep hygiene alone may not be adequate to address chronic insomnia. Sleep hygiene recommendations are typically included as one component of cognitive behavioral therapy for insomnia (CBT-I). Recommendations include reducing caffeine, nicotine, and alcohol consumption, maximizing the regularity and efficiency of sleep episodes, minimizing medication usage and daytime napping, the promotion of regular exercise, and the facilitation of a positive sleep environment. The creation of a positive sleep environment may also be helpful in reducing the symptoms of insomnia. On the other hand, a systematic review by the AASM concluded that clinicians should not prescribe sleep hygiene for insomnia due to the evidence of absence of its efficacy and potential delaying of adequate treatment, recommending instead that effective therapies such as CBT-i should be preferred.

Cognitive behavioral therapy

There is some evidence that cognitive behavioral therapy for insomnia (CBT-I) is superior in the long-term to benzodiazepines and the nonbenzodiazepines in the treatment and management of insomnia. In this therapy, patients are taught improved sleep habits and relieved of counter-productive assumptions about sleep. Common misconceptions and expectations that can be modified include:

  • Unrealistic sleep expectations.
  • Misconceptions about insomnia causes.
  • Amplifying the consequences of insomnia.
  • Performance anxiety after trying for so long to have a good night's sleep by controlling the sleep process.

Numerous studies have reported positive outcomes of combining cognitive behavioral therapy for insomnia treatment with treatments such as stimulus control and the relaxation therapies. Hypnotic medications are equally effective in the short-term treatment of insomnia, but their effects wear off over time due to tolerance. The effects of CBT-I have sustained and lasting effects on treating insomnia long after therapy has been discontinued. The addition of hypnotic medications with CBT-I adds no benefit in insomnia. The long lasting benefits of a course of CBT-I shows superiority over pharmacological hypnotic drugs. Even in the short term when compared to short-term hypnotic medication such as zolpidem, CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia.

Common forms of CBT-I treatments include stimulus control therapy, sleep restriction, sleep hygiene, improved sleeping environments, relaxation training, paradoxical intention, and biofeedback.

CBT is the well-accepted form of therapy for insomnia since it has no known adverse effects, whereas taking medications to alleviate insomnia symptoms have been shown to have adverse side effects. Nevertheless, the downside of CBT is that it may take a lot of time and motivation.

Acceptance and commitment therapy

Treatments based on the principles of acceptance and commitment therapy (ACT) and metacognition have emerged as alternative approaches to treating insomnia. ACT rejects the idea that behavioral changes can help insomniacs achieve better sleep, since they require "sleep efforts" - actions which create more "struggle" and arouse the nervous system, leading to hyperarousal. The ACT approach posits that acceptance of the negative feelings associated with insomnia can, in time, create the right conditions for sleep. Mindfulness practice is a key feature of this approach, although mindfulness is not practised to induce sleep (this in itself is a sleep effort to be avoided) but rather as a longer-term activity to help calm the nervous system and create the internal conditions from which sleep can emerge.

A key distinction between CBT-i and ACT lies in the divergent approaches to time spent awake in bed. Proponents of CBT-i advocate minimizing time spent awake in bed, on the basis that this creates cognitive association between being in bed and wakefulness. The ACT approach proposes that avoiding time in bed may increase the pressure to sleep and arouse the nervous system further.

Research has shown that "ACT has a significant effect on primary and comorbid insomnia and sleep quality, and ... can be used as an appropriate treatment method to control and improve insomnia".

Internet interventions

Despite the therapeutic effectiveness and proven success of CBT, treatment availability is significantly limited by a lack of trained clinicians, poor geographical distribution of knowledgeable professionals, and expense. One way to potentially overcome these barriers is to use the Internet to deliver treatment, making this effective intervention more accessible and less costly. The Internet has already become a critical source of health-care and medical information. Although the vast majority of health websites provide general information, there is growing research literature on the development and evaluation of Internet interventions.

These online programs are typically behaviorally-based treatments that have been operationalized and transformed for delivery via the Internet. They are usually highly structured; automated or human supported; based on effective face-to-face treatment; personalized to the user; interactive; enhanced by graphics, animations, audio, and possibly video; and tailored to provide follow-up and feedback.

There is good evidence for the use of computer based CBT for insomnia.

Medications

Many people with insomnia use sleeping tablets and other sedatives. In some places medications are prescribed in over 95% of cases. They, however, are a second line treatment. In 2019, the US Food and Drug Administration stated it is going to require warnings for eszopiclone, zaleplon, and zolpidem, due to concerns about serious injuries resulting from abnormal sleep behaviors, including sleepwalking or driving a vehicle while asleep.

The percentage of adults using a prescription sleep aid increases with age. During 2005–2010, about 4% of U.S. adults aged 20 and over reported that they took prescription sleep aids in the past 30 days. Rates of use were lowest among the youngest age group (those aged 20–39) at about 2%, increased to 6% among those aged 50–59, and reached 7% among those aged 80 and over. More adult women (5%) reported using prescription sleep aids than adult men (3%). Non-Hispanic white adults reported higher use of sleep aids (5%) than non-Hispanic black (3%) and Mexican-American (2%) adults. No difference was shown between non-Hispanic black adults and Mexican-American adults in use of prescription sleep aids.

Antihistamines

As an alternative to taking prescription drugs, some evidence shows that an average person seeking short-term help may find relief by taking over-the-counter antihistamines such as diphenhydramine or doxylamine. Diphenhydramine and doxylamine are widely used in nonprescription sleep aids. They are the most effective over-the-counter sedatives currently available, at least in much of Europe, Canada, Australia, and the United States, and are more sedating than some prescription hypnotics. Antihistamine effectiveness for sleep may decrease over time, and anticholinergic side-effects (such as dry mouth) may also be a drawback with these particular drugs. While addiction does not seem to be an issue with this class of drugs, they can induce dependence and rebound effects upon abrupt cessation of use. However, people whose insomnia is caused by restless legs syndrome may have worsened symptoms with antihistamines.

Antidepressants

While insomnia is a common symptom of depression, antidepressants are effective for treating sleep problems whether or not they are associated with depression. While all antidepressants help regulate sleep, some antidepressants, such as amitriptyline, doxepin, mirtazapine, trazodone, and trimipramine, can have an immediate sedative effect, and are prescribed to treat insomnia. Amitriptyline, doxepin, and trimipramine all have antihistaminergic, anticholinergic, antiadrenergic, and antiserotonergic properties, which contribute to both their therapeutic effects and side effect profiles, while mirtazapine's actions are primarily antihistaminergic and antiserotonergic and trazodone's effects are primarily antiadrenergic and antiserotonergic. Mirtazapine is known to decrease sleep latency (i.e., the time it takes to fall asleep), promoting sleep efficiency and increasing the total amount of sleeping time in people with both depression and insomnia.

Agomelatine, a melatonergic antidepressant with claimed sleep-improving qualities that does not cause daytime drowsiness, is approved for the treatment of depression though not sleep conditions in the European Union and Australia. After trials in the United States, its development for use there was discontinued in October 2011 by Novartis, who had bought the rights to market it there from the European pharmaceutical company Servier.

A 2018 Cochrane review found the safety of taking antidepressants for insomnia to be uncertain with no evidence supporting long term use.

Melatonin agonists

Melatonin receptor agonists such as melatonin and ramelteon are used in the treatment of insomnia. The evidence for melatonin in treating insomnia is generally poor. There is low-quality evidence that it may speed the onset of sleep by 6 minutes. Ramelteon does not appear to speed the onset of sleep or the amount of sleep a person gets.

Usage of melatonin as a treatment for insomnia in adults has increased from 0.4% between 1999 and 2000 to nearly 2.1% between 2017 and 2018.

Most melatonin agonists have not been tested for longitudinal side effects. Prolonged-release melatonin may improve quality of sleep in older people with minimal side effects.

Studies have also shown that children who are on the autism spectrum or have learning disabilities, attention-deficit hyperactivity disorder (ADHD) or related neurological diseases can benefit from the use of melatonin. This is because they often have trouble sleeping due to their disorders. For example, children with ADHD tend to have trouble falling asleep because of their hyperactivity and, as a result, tend to be tired during most of the day. Another cause of insomnia in children with ADHD is the use of stimulants used to treat their disorder. Children who have ADHD then, as well as the other disorders mentioned, may be given melatonin before bedtime in order to help them sleep.

Benzodiazepines

Normison (temazepam) is a benzodiazepine commonly prescribed for insomnia and other sleep disorders.

The most commonly used class of hypnotics for insomnia are the benzodiazepines. Benzodiazepines are not significantly better for insomnia than antidepressants. Chronic users of hypnotic medications for insomnia do not have better sleep than chronic insomniacs not taking medications. In fact, chronic users of hypnotic medications have more regular night-time awakenings than insomniacs not taking hypnotic medications. Many have concluded that these drugs cause an unjustifiable risk to the individual and to public health and lack evidence of long-term effectiveness. It is preferred that hypnotics be prescribed for only a few days at the lowest effective dose and avoided altogether wherever possible, especially in the elderly. Between 1993 and 2010, the prescribing of benzodiazepines to individuals with sleep disorders has decreased from 24% to 11% in the US, coinciding with the first release of nonbenzodiazepines.

The benzodiazepine and nonbenzodiazepine hypnotic medications also have a number of side-effects such as day time fatigue, motor vehicle crashes and other accidents, cognitive impairments, and falls and fractures. Elderly people are more sensitive to these side-effects. Some benzodiazepines have demonstrated effectiveness in sleep maintenance in the short term but in the longer term benzodiazepines can lead to tolerance, physical dependence, benzodiazepine withdrawal syndrome upon discontinuation, and long-term worsening of sleep, especially after consistent usage over long periods of time. Benzodiazepines, while inducing unconsciousness, actually worsen sleep as – like alcohol – they promote light sleep while decreasing time spent in deep sleep. A further problem is, with regular use of short-acting sleep aids for insomnia, daytime rebound anxiety can emerge. Although there is little evidence for benefit of benzodiazepines in insomnia compared to other treatments and evidence of major harm, prescriptions have continued to increase. This is likely due to their addictive nature, both due to misuse and because – through their rapid action, tolerance and withdrawal they can "trick" insomniacs into thinking they are helping with sleep. There is a general awareness that long-term use of benzodiazepines for insomnia in most people is inappropriate and that a gradual withdrawal is usually beneficial due to the adverse effects associated with the long-term use of benzodiazepines and is recommended whenever possible.

Benzodiazepines all bind unselectively to the GABAA receptor. Some theorize that certain benzodiazepines (hypnotic benzodiazepines) have significantly higher activity at the α1 subunit of the GABAA receptor compared to other benzodiazepines (for example, triazolam and temazepam have significantly higher activity at the α1 subunit compared to alprazolam and diazepam, making them superior sedative-hypnotics – alprazolam and diazepam, in turn, have higher activity at the α2 subunit compared to triazolam and temazepam, making them superior anxiolytic agents). Modulation of the α1 subunit is associated with sedation, motor impairment, respiratory depression, amnesia, ataxia, and reinforcing behavior (drug-seeking behavior). Modulation of the α2 subunit is associated with anxiolytic activity and disinhibition. For this reason, certain benzodiazepines may be better suited to treat insomnia than others.

Z-Drugs

Nonbenzodiazepine or Z-drug sedative–hypnotic drugs, such as zolpidem, zaleplon, zopiclone, and eszopiclone, are a class of hypnotic medications that are similar to benzodiazepines in their mechanism of action, and indicated for mild to moderate insomnia. Their effectiveness at improving time to sleeping is slight, and they have similar—though potentially less severe—side effect profiles compared to benzodiazepines. Prescribing of nonbenzodiazepines has seen a general increase since their initial release on the US market in 1992, from 2.3% in 1993 among individuals with sleep disorders to 13.7% in 2010.

Orexin antagonists

Orexin receptor antagonists are a more recently introduced class of sleep medications and include suvorexant, lemborexant, and daridorexant, all of which are FDA-approved for treatment of insomnia characterized by difficulties with sleep onset and/or sleep maintenance.

Antipsychotics

Certain atypical antipsychotics, particularly quetiapine, olanzapine, and risperidone, are used in the treatment of insomnia. However, while common, use of antipsychotics for this indication is not recommended as the evidence does not demonstrate a benefit, and the risk of adverse effects are significant. A major 2022 systematic review and network meta-analysis of medications for insomnia in adults found that quetiapine did not demonstrate any short-term benefits for insomnia. Some of the more serious adverse effects may also occur at the low doses used, such as dyslipidemia and neutropenia. Such concerns of risks at low doses are supported by Danish observational studies that showed an association of use of low-dose quetiapine (excluding prescriptions filled for tablet strengths >50 mg) with an increased risk of major cardiovascular events as compared to use of Z-drugs, with most of the risk being driven by cardiovascular death. Laboratory data from an unpublished analysis of the same cohort also support the lack of dose-dependency of metabolic side effects, as new use of low-dose quetiapine was associated with a risk of increased fasting triglycerides at 1-year follow-up. Concerns regarding side effects are greater in the elderly.

Other sedatives

Gabapentinoids like gabapentin and pregabalin have sleep-promoting effects but are not commonly used for treatment of insomnia. Gabapentin is not effective in helping alcohol related insomnia.

Barbiturates, while once used, are no longer recommended for insomnia due to the risk of addiction and other side effects.

Comparative effectiveness

A major systematic review and network meta-analysis of medications for the treatment of insomnia was published in 2022. It found a wide range of effect sizes (standardized mean difference (SMD)) in terms of efficacy for insomnia. The assessed medications included benzodiazepines (SMDs 0.58 to 0.83), Z-drugs (SMDs 0.03 to 0.63), sedative antidepressants and antihistamines (SMDs 0.30 to 0.55), quetiapine (SMD 0.07), orexin receptor antagonists (SMDs 0.23 to 0.44), and melatonin receptor agonists (SMDs 0.00 to 0.13). The certainty of evidence varied and ranged from high to very low depending on the medication. The meta-analysis concluded that the orexin antagonist lemborexant and the Z-drug eszopiclone had the best profiles overall in terms of efficacy, tolerability, and acceptability.

Alternative medicine

Herbal products, such as valerian, kava, chamomile, and lavender, have been used to treat insomnia. However, there is no quality evidence that they are effective and safe. The same is true for cannabis and cannabinoids. It is likewise unclear if acupuncture is useful in the treatment of insomnia.

Prognosis

Disability-adjusted life year for insomnia per 100,000 inhabitants in 2004.
  no data
  less than 25
  25–30.25
  30.25–36
  36–41.5
  41.5–47
  47–52.5
  52.5–58
  58–63.5
  63.5–69
  69–74.5
  74.5–80
  more than 80

A survey of 1.1 million residents in the United States found that those that reported sleeping about 7 hours per night had the lowest rates of mortality, whereas those that slept for fewer than 6 hours or more than 8 hours had higher mortality rates. Severe insomnia – sleeping less than 3.5 hours in women and 4.5 hours in men – is associated with a 15% increase in mortality, while getting 8.5 or more hours of sleep per night was associated with a 15% higher mortality rate.

With this technique, it is difficult to distinguish lack of sleep caused by a disorder which is also a cause of premature death, versus a disorder which causes a lack of sleep, and the lack of sleep causing premature death. Most of the increase in mortality from severe insomnia was discounted after controlling for associated disorders. After controlling for sleep duration and insomnia, use of sleeping pills was also found to be associated with an increased mortality rate.

The lowest mortality was seen in individuals who slept between six and a half and seven and a half hours per night. Even sleeping only 4.5 hours per night is associated with very little increase in mortality. Thus, mild to moderate insomnia for most people is associated with increased longevity and severe insomnia is associated only with a very small effect on mortality. It is unclear why sleeping longer than 7.5 hours is associated with excess mortality.

Epidemiology

Between 10% and 30% of adults have insomnia at any given point in time and up to half of people have insomnia in a given year, making it the most common sleep disorder. About 6% of people have insomnia that is not due to another problem and lasts for more than a month. People over the age of 65 are affected more often than younger people. Females are more often affected than males. Insomnia is 40% more common in women than in men.

There are higher rates of insomnia reported among university students compared to the general population.

Society and culture

The word insomnia is from Latin: in + somnus "without sleep" and -ia as a nominalizing suffix.

The popular press have published stories about people who supposedly never sleep, such as that of Thái Ngọc and Al Herpin. Horne writes "everybody sleeps and needs to do so", and generally this appears true. However, he also relates from contemporary accounts the case of Paul Kern, who was shot in wartime and then "never slept again" until his death in 1943. Kern appears to be a completely isolated, unique case.

Cellular automaton

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