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Mecklenburg

From Wikipedia, the free encyclopedia

For other uses, see Mecklenburg (disambiguation).

Coat of arms of Mecklenburg, featuring the typical bull

Mecklenburg, divided between Mecklenburg-Schwerin and Mecklenburg-Strelitz, from 1866 to 1934.

Mecklenburg (Low German: Mkelborg) is a historical region in northern Germany comprising the western and larger part of the federal-state Mecklenburg-Vorpommern. The largest cities of the region are Rostock, Schwerin, Neubrandenburg andWismar. The name Mecklenburg derives from a castle named "Mikilenburg" (Old Saxon: "big castle"), located between the cities ofSchwerin and Wismar. In Slavic language it was known as Veligrad which also means "big castle". It was the ancestral seat of the House of Mecklenburg and for a time divided into Mecklenburg-Schwerin and Mecklenburg-Strelitz among the same dynasty. Linguistically Mecklenburgers retain and use many features of Low German vocabulary or phonology. The adjective for the region is Mecklenburgian (German: mecklenburgisch), inhabitants are called Mecklenburgians (German:Mecklenburger).
Contents [hide] 1 Geography o 1.1 List of urban centers in Mecklenburg

2 History o o o 2.1 Early history 2.2 History, 16211933 2.3 History since 1934

3 Coat of arms of the duchies of Mecklenburg 4 Economy o 4.1 Tourism

5 Notable Mecklenburgers 6 See also 7 References 8 External links

Geography[edit]
Mecklenburg is known for its mostly flat countryside. Much of the terrain forms a morass, with ponds, marshes and fields as common features, with small forests interspersed. The terrain changes as one moves north towards the Baltic Sea. Under the peat of Mecklenburg are sometimes found deposits of ancient lava flows. Traditionally, at least in the countryside, the stone from these flows is cut and used in the construction of homes, often in joint use with cement, brick and wood, forming a unique look to the exterior of country houses. Mecklenburg has productive farming, but the land is most suitable for grazing purposes.

List of urban centers in Mecklenburg[edit]


See also: List of cities in Mecklenburg-Vorpommern

Mecklenburg in today'sadministrative borders

Town/ municipality Rostock Schwerin

District district-free city district-free city

Population
as of December 31, 2012

202,887 91,264 63,509 42,433 28,586 20,322 21,074 17,174 11,998 11,427 11,324 10,621 10,169 8733 7657

Neubrandenburg Mecklenburgische Seenplatte Wismar Gstrow Neustrelitz Nordwestmecklenburg Rostock Mecklenburgische Seenplatte

Waren (Mritz) Mecklenburgische Seenplatte Parchim Ludwigslust Bad Doberan Hagenow Grevesmhlen Boizenburg/Elbe Teterow Malchin Ludwigslust-Parchim Ludwigslust-Parchim Rostock Ludwigslust-Parchim Nordwestmecklenburg Ludwigslust-Parchim Rostock Mecklenburgische Seenplatte

History[edit]
Early history[edit]
Mecklenburg is the site of many prehistoric dolmen tombs. Its earliest organised inhabitants may have had Celtic origins. By no later than 100 BC the area had been populated by preChristian Germanic peoples. The traditional symbol of Mecklenburg, the grinning steer's head (Low German: Ossenkopp, lit.: 'oxen's head', with osse being a synonym for steer and bull in Middle Low German), with an attached hide, and a crown above, may have originated from this period.[citation needed] It represents what early peoples would have worn, i.e. a steers's head as a hat, with the hide hanging down the back to protect the neck from the sun, and overall as a way to instill fear in the enemy. From the 7th through the 12th centuries, the area of Mecklenburg was taken over by Western Slavic peoples, most notably the Obotrites and other tribes that Frankish sources referred to as "Wends". The 11th century founder of the Mecklenburgian dynasty of Dukes and later Grand Dukes, which lasted until 1918, was Nyklot of the Obotrites. In the late 12th century, Henry the Lion, Duke of the Saxons, conquered the region, subjugated its local lords, and Christianized its people, in a precursor to the Northern Crusades. From 12th to 14th century, large numbers of Germans and Flemings settled the area (Ostsiedlung), importing German law and improved agricultural techniques. TheWends who survived all warfare and devastation of the centuries before, including invasions of and expeditions into Saxony, Denmark and Liutizic areas as well as internal conflicts, were assimilated in the centuries thereafter. However, elements of certain names and words used in Mecklenburg speak to the lingering Slavic influence. An example would be the city of Schwerin, which was originally called Zuarin in Slavic. Another example is town of Bresegard, the 'gard' portion of the town name derives from the Slavic word 'grad', meaning city or town. Since the 12th century, the territory has remained stable and relatively independent of its neighbours; one of the few German territories for which this is true. During the reformation the Duke in Schwerin would convert to Protestantism and so would follow the Duchy of Mecklenburg.

Historical 7-field coat of arms, symbolizing the 7 lordships of Mecklenburg: The duchy of Mecklenburg, the princedoms (former dioceses) of Schwerin and Ratzeburg, the county of Schwerin and theHerrschaft of Rostock, Werle and Stargard.

History, 16211933[edit]
Like many German territories, Mecklenburg was sometimes partitioned and re-partitioned among different members of the ruling dynasty. In 1621 it was divided into the two duchies of MecklenburgSchwerin and Mecklenburg-Gstrow. With the extinction of the Gstrow line in 1701, the Gstrow

lands were redivided, part going to the Duke of Mecklenburg-Schwerin, and part going to the new line of Mecklenburg-Strelitz. In 1815, the two Mecklenburgian duchies were raised to Grand Duchies, and subsequently existed separately as such in Germany under enlightened but absolute rule (constitutions being granted on the eve of World War I) until the revolution of 1918. Life in Mecklenburg could be quite harsh. Practices such as having to ask for permission from the Grand Duke to get married, or having to apply for permission to emigrate, would linger late into the history of Mecklenburg (i.e. 1918), long after such practices had been abandoned in other German areas. Even as late as the later half of the 19th century the Grand Duke personally owned half of the countryside. The last Duke abdicated in 1918, as monarchies fell throughout Europe. The Duke's ruling house reigned in Mecklenburg uninterrupted (except for two years) from its incorporation into the Holy Roman Empire until 1918. From 1918 to 1933, the duchies were free states in the Weimar Republic. Traditionally Mecklenburg has always been one of the poorer German areas, and later the poorer of the provinces, or Lnder, within a unified Germany. The reasons for this may be varied, but one factor stands out: agriculturally the land is poor and can not produce at the same level as other parts of Germany. The two Mecklenburgs made attempts at being independent states after 1918, but eventually this failed as their dependence on the rest of the German lands became apparent.

History since 1934[edit]


After three centuries of partition, Mecklenburg was united in 1934 by the Nazi government. The Wehrmacht assigned Mecklenburg and Pomerania to Wehrkreis II under the command of General der Infanterie Werner Kienitz, with the headquarters at Stettin. Mecklenburg was assigned to an Area headquartered at Schwerin, which was responsible for military units in Schwerin; Rostock; Parchim; and Neustrelitz.

Mecklenburg regional flag

After World War II, the Soviet government occupying eastern Germany merged Mecklenburg with the smaller neighbouring region ofWestern Pomerania (German Vorpommern) to form the state of Mecklenburg-Vorpommern. Mecklenburg contributed about two-thirds of the geographical size of the new state and the majority of its population. Also, the new state became temporary or permanent home for lots of refugees expelled from former German territories seized by the Soviet Union and Poland after the war. The Soviets changed the name from "MecklenburgWestern Pomerania" to "Mecklenburg" in 1947. In 1952, the East German government ended the independent existence of Mecklenburg, creating 3 districts ("Bezirke") out of its territory: Rostock, Schwerin and Neubrandenburg. During German reunification in 1990, the state of Mecklenburg-Vorpommern was revived, and is now one of the 16 states of the Federal Republic of Germany.

Coat of arms of the duchies of Mecklenburg[edit]

The arms used by both duchies in the 19th century

The House of Mecklenburg was founded by Niklot, prince of the Obotrites, Chizzini and Circipani on the Baltic Sea, who died in 1160. His Christian progeny was recognized as prince of the Holy Roman Empire 1170 and Duke of Mecklenburg 8 July 1348. On 27 February 1658 the ducal house divided in two branches: Mecklenburg-Schwerin and Mecklenburg-Strelitz. The flag of both Mecklenburg duchies is traditionally made of the colours blue, yellow and red. The sequence however changed more than once in the past 300 years. In 1813 the duchies used yellowred-blue. 23 December 1863 for Schwerin and 4 January 1864 for Strelitz blue-yellow-red was ordered.[1] Mecklenburg-Schwerin however used white instead of yellow for flags on sea by law of 24 March 1855.[2] Siebmachers Wappenbuch gives therefore (?) blue-white-red for Schwerin and blue-yellow-red for Strelitz.[3] According to this source, the grand ducal house of Schwerin used a flag of 3.75 to 5.625 M with the middle arms on a white quadrant (1.75 M) in the middle. The middle arms show the shield of Mecklenburg as arranged in the 17th century. The county of Schwerin in the middle and in the quartering Mecklenburg (bull's head with hide), Rostock (griffin), principality of Schwerin (griffin surmounting green rectangle), Ratzeburg(cross surmounted by crown), Stargard (arm with hand holding ring) and Wenden (bull's head). The shield is supported by a bull and a griffin and surmounted by a royal crown. The dukes of Strelitz used according to Siebmachers the blue-yellow-red flag with just the (oval) shield of Mecklenburg in the yellow band. Strhl in 1897 and Bulgaria,[4] show another arrangement: The grand-duke of Mecklenburg-Schwerin flows a flag (4:5) with the arms of the figures from the shield of arms. The former Schwerin standard with the white quadrant is now ascribed to the grand dukes of Strelitz. Strhl mentions a flag for the grand ducal house by law of 23 December 1863 with the middle arms in the yellow band. And he mentions a special sea flag, the same but with a white middle band. 'Berhmte Fahnen' shows furthermore a standard for grand duchess Alexandra of MecklenburgSchwerin, princess of Hannover (18821963), showing her shield and that of Mecklenburg joined by the order of the Wendic Crown in a white oval. On sea the yellow band in her flag was of course

white. The princes (dukes) of Mecklenburg-Schwerin had according to this source their own standard, showing the griffin of Rostock.

Economy[edit]
Tourism[edit]
Mecklenburg faces a huge increase in tourism since German reunification in 1990, particularly with its beaches and seaside resorts at the Baltic Sea (Warnemnde, Boltenhagen,Heiligendamm, Khlungsborn, Rerik and others), the Mecklenburg Lakeland (Mecklenburgische Seenplatte), the Mecklenburg Switzerland (Mecklenburgische Schweiz) with its pristine nature, the old Hanseatic towns of Rostock and Wismar (World Heritage) well known for their medieval Brick Gothic buildings, and the former royal residences of Schwerin,Gstrow, Ludwigslust and Neustrelitz.

Notable Mecklenburgers[edit]

Gebhard Leberecht von Blcher, Prussian army leader Jan Ullrich, cyclist Gottlob Frege, logician Siegfried Marcus, automobile pioneer Heinrich Schliemann, classical archaeologist Johannes Gillhoff, teacher, author of book on Mecklenburg emigrants to the USA Fritz Reuter, poet and novelist Ludwig Jacoby, (18131874), born in Altstrelitz, an author and Methodist clergyman, commissioned as a missionary to St. Louis, Missouri, by the founder of the German Methodist Church in America, William Nast (18071899). Jacoby founded the first Methodist Church West of the Mississippi River, originally known as Bethel Church, now known as Memorial United Methodist Church, in St. Louis in 1841.

Charlotte of Mecklenburg-Strelitz, (17441818), wife of George III of the United Kingdom and grandmother of Queen Victoria. Charlotte, North Carolina, USA and the county in which it lies were named in her honour, as was Charlottesville, Virginia, USA.

See also[edit]

Mecklenburg-Vorpommern Duchy of Mecklenburg-Schwerin Duchy of Mecklenburg-Strelitz List of Dukes and Grand Dukes of Mecklenburg Mecklenburg County, North Carolina Mecklenburg County, Virginia

References[edit]
1. Jump up^ (Strhl, Deutsche Wappenrolle, Stuttgart, 1897, p. 89) 2. Jump up^ (Strhl, 86) 3. Jump up^ Siebmachers Wappenbuch (Nurenberg, 1878) 4. Jump up^ Berhmte Fahnen Deutscher Geschichte (Dresden, 1922)

External links[edit]
Media related to Mecklenburg at Wikimedia Commons

Government portal of Mecklenburg-Western Pomerania "Mecklenburg". Catholic Encyclopedia. New York: Robert Appleton Company. 1913. Chisholm, Hugh, ed. (1911). "Mecklenburg". Encyclopdia Britannica (11th ed.). Cambridge University Press.
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V T E

Lower Saxon Circle (15001806) of the Holy Roman Emp



Ecclesiastical

Bremen1 Halberstadt1 Hildesheim Lbeck Magdeburg1 Ratzeburg2 Schwerin1 Bremen3 Brunswick and Lunenburg Blankenburg4 Calenberg5 Celle5 Grubenhagen6 Hanover7

Secular

Cities
1

Wolfenbttel Holstein Glckstadt Gottorp8 Pinneberg9 Mecklenburg Gstrow10 Schwerin Strelitz11 Rantzau12 Regenstein Saxe-Lauenburg5 Bremen Goslar Hamburg Lbeck Mhlhausen Nordhausen until 1701.
3

until 1648.

from 1648.

until 1731.

until 1705.

until 1596.

from 1708.

until 1773.

until 1640.

10

until 1695.

11

from 1

RhenishWestphalian, Franconian, (Lower) Saxon Circles est. 1512: Austrian, Burgundian, Upper Saxon, Electoral Rhenish
Coordinates: 53.61265N 12.42960E

Unenc

Categories:

States of the Holy Roman Empire Geography of Mecklenburg-Vorpommern Regions of Germany History of Mecklenburg Mecklenburg

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or b

Lubrication

From Wikipedia, the free encyclopedia

Lubrication of the ship steam engine crankshaft. The two bottles of lubricant are attached to the piston and move while the engine is operating.

Lubrication is the process, or technique employed to reduce wear of one or both surfaces in close proximity, and moving relative to each other, by interposing a substance called lubricant between the surfaces to carry or to help carry the load (pressure generated) between the opposing surfaces. The interposed lubricant film can be a solid, (e.g. graphite, MoS2)[1] a solid/liquid dispersion, a liquid, a liquid-liquid dispersion (a grease) or, exceptionally, a gas.

In the most common case the applied load is carried by pressure generated within the fluid due to the frictional viscous resistance to motion of the lubricating fluid between the surfaces. Lubrication can also describe the phenomenon where such reduction of wear occurs without human intervention (hydroplaning on a road). The science of friction, lubrication and wear is called tribology. Adequate lubrication allows smooth continuous operation of equipment, with only mild wear, and without excessive stresses or seizures atbearings. When lubrication breaks down, metal or other components can rub destructively over each other, causing destructive damage, heat, and failure.
Contents [hide] 1 The regimes of lubrication 2 See also 3 References 4 External links

The regimes of lubrication[edit]


As the load increases on the contacting surfaces three distinct situations can be observed with respect to the mode of lubrication, which are called regimes of lubrication:

Fluid film lubrication is the lubrication regime in which through viscous forces the load is fully supported by the lubricant within the space or gap between the parts in motion relative to one another (the lubricated conjunction) and solidsolid contact is avoided.[2]

Hydrostatic lubrication is when an external pressure is applied to the lubricant in the bearing, to maintain the fluid lubricant film where it would otherwise be squeezed out.

Hydrodynamic lubrication is where the motion of the contacting surfaces, and the exact design of the bearing is used to pump lubricant around the bearing to maintain the lubricating film. This design of bearing may wear when started, stopped or reversed, as the lubricant film breaks down.

Elastohydrodynamic lubrication: Mostly for nonconforming surfaces or higher load conditions, the bodies suffer elastic strains at the contact. Such strain creates a load-bearing area, which provides an almost parallel gap for the fluid to flow through. Much as in hydrodynamic lubrication, the motion of the contacting bodies generates a flow induced pressure, which acts as the bearing force over the contact area. In such high pressure regimes, the viscosity of the fluid may rise considerably. At full elastohydrodynamic lubrication the generated lubricant film completely separates the surfaces. Contact between raised solid features, or asperities, can occur, leading to a mixed-lubrication or boundary lubrication regime.

Boundary lubrication (also called boundary film lubrication): The bodies come into closer contact at their asperities; the heat developed by the local pressures causes a condition which is called stick-slip and some asperities break off. At the elevated temperature and pressure conditions chemically reactive constituents of the lubricant react with the contact surface forming a highly resistant tenacious layer, or film on the moving solid surfaces (boundary film) which is capable of supporting the load and major wear or breakdown is avoided. Boundary lubrication is also defined as that regime in which the load is carried by the surface asperities rather than by the lubricant.[3]

Besides supporting the load the lubricant may have to perform other functions as well, for instance it may cool the contact areas and remove wear products. While carrying out these functions the lubricant is constantly replaced from the contact areas either by the relative movement (hydrodynamics) or by externally induced forces. Lubrication is required for correct operation of mechanical systems pistons, pumps, cams, bearings, turbines, cutting tools etc. where without lubrication the pressure between the surfaces in close proximity would generate enough heat for rapid surface damage which in a coarsened condition may literally weld the surfaces together, causing seizure. In some applications, such as piston engines, the film between the piston and the cylinder wall also seals the combustion chamber, preventing combustion gases from escaping into the crankcase.

See also[edit]
This section is empty. You can help
by adding to it. (March 2013)

References[edit]
Lubrication Science in Persian
1. Jump up^ http://www.engineersedge.com/lubrication/applications_solid_lubrication.htm 14k 2. Jump up^ San Andrs. L. "Introduction to pump rotordynamics, Part i. Introduction to hydrodynamic lubrication". ("MEEN626 Lubrication Theory Class:Syllabus FALL2006"). [1] (11 Dec 2007) 3. Jump up^ Bosman R. and Schipper D.J. Microscopic Mild Wear in the Boundary Lubrication regime. Laboratory for Surface Technology and Tribology, Faculty of Engineering Technology, University of Twente, P.O. Box 217, NL 7500 AE Enschede, The Netherlands.

External links[edit]
Wikimedia Commons has media related to Lubrication.

Look up lubrication in Wiktionary, the free dictionary.

Different Lubrication Techniques used in Oil & Gas machinery Machinery Lubrication magazine International Council for Machinery Lubrication

Engineers Edge Categories:

Lubrication Tribology Lubricants

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1. y stress. Its consequences sleepiness and impaired psychomotor performance are similar to those of sleep deprivation.[13] 2. 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.[14] Acute insomnia is also known as short term insomnia or stress related insomnia.[15] 3. Chronic insomnia lasts for longer than a month. It can be caused by another disorder, or it can be a primary disorder. People with high levels of stress hormones or shifts in the levels of cytokines are more likely to have chronic insomnia.[16] Its effects can vary according to its causes. They might include muscular fatigue, hallucinations, and/or mental fatigue. Chronic insomnia can cause double vision.[13]

Patterns of insomnia[edit]
Symptoms of insomnia
[17]

difficulty falling asleep, including difficulty finding a comfortable sleeping position waking during the night and being unable to return to sleep feeling unrefreshed upon waking Daytime sleepiness, irritability or anxiety

Sleep-onset insomnia is difficulty falling asleep at the beginning of the night, often a symptom ofanxiety disorders. Delayed sleep phase disorder can be misdiagnosed as insomnia as it causes a delayed period of sleep, spilling over into daylight hours.[18]

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 middle of the night, with more than half having trouble falling back to sleep after a middle of the night awakening.[19] 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.[20]

Poor sleep quality[edit]


Poor sleep quality can occur as a result of, for example, restless legs, sleep apnea or major depression. Poor sleep quality is caused by 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 nighttime urination, can be very disturbing to sleep.[21]

Subjective insomnia[edit]
Main article: Sleep state misperception Some cases of insomnia are not really insomnia in the traditional sense. People experiencing sleep state misperception often sleep for normal durations, yet severely overestimate the time taken to fall asleep. They may believe they slept for only four hours while they, in fact, slept a full eight hours.

Causes and comorbidity[edit]

Potential complications of insomnia.

[22]

Symptoms of insomnia can be caused by or be co-morbid with:

Use of psychoactive drugs (such as stimulants), including certain medications, herbs, caffeine, nicotine, cocaine,amphetamines, methylphenidate, aripipra zole, MDMA, modafinil, or excessive alcohol intake.[23]

Withdrawal from anti-anxiety drugs such as benzodiazepines or pain-relievers such as opioids.[23]

Use of fluoroquinolone antibiotic drugs is associated with more severe and chronic types of insomnia.[24]

Restless legs syndrome, which can cause sleep onset insomnia due to the discomforting sensations felt and the need to move the legs or other body parts to relieve these sensations.[25]

Periodic limb movement disorder (PLMD), which occurs during sleep and can cause arousals of which the sleeper is unaware.[26] Pain[27] An injury or condition that causes pain can preclude an individual from finding a comfortable position in which to fall asleep, and can in addition cause awakening. Hormone shifts such as those that precede menstruation and those during menopause.[25] Life events such as fear, stress, anxiety, emotional or mental tension, work problems, financial stress, birth of a child and bereavement.[25] Gastrointestinal issues such as heartburn or constipation.[28] Mental disorders such as bipolar disorder, clinical depression, generalized anxiety disorder, post traumatic stress disorder, schizophrenia, obsessive compulsive disorder, anddementia.[29] or ADHD[30]

Disturbances of the circadian rhythm, such as shift work and jet lag, can cause an inability to sleep at some times of the day and excessive sleepiness at other times of the day. Chronic circadian rhythm disorders are characterized by similar symptoms.[23]

Certain neurological disorders, brain lesions, or a history of traumatic brain injury.[31] Medical conditions such as hyperthyroidism and rheumatoid arthritis.[32] Abuse of over-the counter or prescription sleep aids (sedative or depressant drugs) can produce rebound insomnia.[23] Poor sleep hygiene, e.g., noise or over-consumption of caffeine[23] A rare genetic condition can cause a prion-based, permanent and eventually fatal form of insomnia called fatal familial insomnia.[33]

Physical exercise. Exercise-induced insomnia is common in athletes in the form of prolonged sleep onset latency.[34]

Sleep studies using polysomnography have suggested that people who have sleep disruption have elevated nighttime 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 longterm insomnia.[32]

Steroid hormones and insomnia[edit]


Studies have been conducted with steroid hormones and insomnia. Changes in levels of cortisol, progesterone in the female cycle, or estrogen during menopause are correlated with

increased occurrences of insomnia. Those with differing levels of cortisol often have long-term insomnia, where estrogen is onset insomnia catalyzed by menopause, andprogesterone is temporary insomnia within the monthly female cycle. Cortisol[edit] Cortisol is typically thought of as the stress hormone in humans, but it is also the awakening hormone.[35] Analyzing saliva samples taken in the morning has shown that patients with insomnia wake up with significantly lower cortisol levels when compared to a control group with regular sleeping patterns.[36] Further studies have revealed that those with lower levels of cortisol upon awakening also have poorer memory consolidation in comparison to those with normal levels of cortisol.[37] Studies support that larger amounts ofcortisol released in the evening occurs in primary insomnia. In this case, drugs related to calming mood disorders or anxiety, such as antidepressants, would regulate the cortisol levels and help prevent insomnia.[38] Estrogen[edit] Many postmenopausal women have reported changes in sleep patterns since entering menopause that reflect symptoms of insomnia. This could occur because of the lower levels of estrogen. Lower estrogen levels can cause hot flashes, change in stress reactions, or overall change in the sleep cycle, which all could contribute to insomnia. Estrogen treatment as well as estrogen-progesterone combination supplements as a hormone replacement therapy can help regulate menopausal womens sleep cycle again.[39] Progesterone[edit] Low levels of progesterone throughout the female menstruation cycle, but primarily near the end of the luteal phase, have also been known to correlate with insomnia as well as aggressive behavior, irritability, and depressed mood in women.[40] Around 67% of women have problems with insomnia right before or during their menstrual cycle.[41] Lower levels of progesterone can, like estrogen, correlate with insomnia in menopausal women.[39] A common misperception is that the amount of sleep required decreases as a person ages. The ability to sleep for long periods, rather than the need for sleep, appears to be lost as people get older. Some elderly insomniacs toss and turn in bed and occasionally fall off the bed at night, diminishing the amount of sleep they receive.[42]

Risk factors[edit]
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 Travelling through different time zones[1]

Diagnosis[edit]
Specialists in sleep medicine are qualified to diagnose the many different sleep disorders. Patients with various disorders, including delayed sleep phase syndrome, are often mis-diagnosed with primary insomnia. When a person has trouble getting to sleep, 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.[43] In depression in many cases "insomnia should be regarded as a co-morbid condition, rather than as a secondary one;" insomnia typically predates psychiatric symptoms.[43] "In fact, it is possible that insomnia represents a significant risk for the development of a subsequent psychiatric disorder."[2] Knowledge of causation is not necessary for a diagnosis.[43]

Treatment[edit]
It is important to identify or rule out medical and psychological causes before deciding on the treatment for insomnia.[44] Cognitive behavioral therapy (CBT) "has been found to be as effective as prescription medications are for short-term treatment of chronic insomnia. Moreover, there are indications that the beneficial effects of CBT, in contrast to those produced by medications, may last well beyond the termination of active treatment."[45] Pharmacological treatments have been used mainly to reduce symptoms in acute insomnia; their role in the management of chronic insomnia remains unclear.[7] Several different types of medications are also effective for treating insomnia. However, 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.[46]

Non-pharmacological[edit]
Non-pharmacological 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.[47] Non pharmacological strategies provide long lasting improvements to insomnia and are recommended as a first line and long term strategy of management. The strategies include attention to sleep hygiene, stimulus control, behavioral interventions, sleep-restriction therapy, paradoxical intention, patient education and relaxation therapy.[48] Reducing the temperature of blood flowing to the brain slows the brain's metabolic rate thereby reducing insomnia.[49] Some examples are keeping a journal, restricting the time spending awake in bed, practicing relaxation techniques, and maintaining a regular sleep schedule and a wake-up time.[46] 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 regularizing the biological clock.[46] EEG biofeedback has demonstrated effectiveness in the treatment of insomnia with improvements in duration as well as quality of sleep.[50] 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 or 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 result 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 nighttime hours, and eliminating daytime naps.[51] 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, which is often used to help early morning wakers reset their natural sleep cycle, can also be used with sleep restriction therapy to reinforce a new wake schedule. Although applying this technique with consistency is difficult, it can have a positive effect on insomnia in motivated patients. 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).[52] Meditation has been recommended for the treatment of insomnia. The meditation teacher Siddhrtha Gautama, 'The Buddha', is recorded as having recommended the practice of 'loving-kindness' meditation, or mett bhvan as a way to produce relaxation and thereby, sound sleep putting it first in a list of the benefits of that meditation.[53] More recently, studies have concluded that: a mindfulness practice reduced mental and bodily restlessness before sleep and the subjective symptoms of insomnia;[54] and that mindfulness-based cognitive behavioural therapy reduced restlessness, sleep effort and dysfunctional sleep-related thoughts[55] including worry.[56] Cognitive behavioral therapy[edit] Main article: Cognitive behavioural therapy for insomnia There is some evidence that cognitive behavioural therapy for insomnia is superior in the long-term to benzodiazepines and the nonbenzodiazepines in the treatment and management of insomnia.[57] In this therapy, patients are taught improved sleep habits and relieved of counterproductive assumptions about sleep. Common misconceptions and expectations that can be modified include: (1) unrealistic sleep expectations (e.g., I need to have 8 hours of sleep each night), (2) misconceptions about insomnia causes (e.g., I have a chemical imbalance causing my insomnia), (3) amplifying the consequences of insomnia (e.g., I cannot do anything after a bad night's sleep), and (4) 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.[58][59] 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 (Ambien), CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia.[60] Metacognition is also a recent trend in approach to behaviour therapy of insomnia.[61] Prevention[edit] Insomnia can be short-term or long-term. Prevention of the sleep disorder may include maintaining a consistent sleeping schedule, such as waking up and sleeping at the same time. Also, one should avoid caffeinated drinks during the 8 hours before sleeping time. While exercise is essential and can aid the process of sleeping, it is important to not exercise right before bedtime, therefore creating a calm environment. Lastly, one's bed should only be for sleep and possibly sexual intercourse. These are some of the points included in sleep hygiene. Going to sleep and waking up at the same time every day can create a steady pattern, which may help against insomnia.[1]

Internet interventions[edit] 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.[62] 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.[63] Although the vast majority of health websites provide general information,[63][64] there is growing research literature on the development and evaluation of Internet interventions.[65][66] 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.[66] A number of Internet interventions for insomnia have been developed[67] and a few of them have been evaluated as part of scientific research trials. A paper published in 2012 reviewed the related literature[68] and found good evidence for the use of Internet interventions for insomnia.

Medications[edit]
Many insomniacs rely on sleeping tablets and other sedatives to get rest. In some places medications are prescribed to over 95% of insomniac cases.[69] The percentage of adults using a prescription sleep aid increases with age. During 20052010, about 4% of U.S. adults aged 20 and over reported that they took prescription sleep aids in the past 30 days. Prevalence of use was lowest among the youngest age group (those aged 2039) at about 2%, increased to 6% among those aged 5059, and reached 7% among those aged 80 and over. More adult women (5.0%) reported using prescription sleep aids than adult men (3.1%). Non-Hispanic white adults reported higher use of sleep aids (4.7%) than non-Hispanic black (2.5%) and Mexican-American (2.0%) adults. No difference was shown between non-Hispanic black adults and Mexican-American adults in use of prescription sleep aids.[70] As an alternative to taking prescription drugs, some evidence shows that an average person seeking short-term help may find relief from taking over-thecounter antihistamines such as diphenhydramine or doxylamine.[71] Certain classes of sedatives such as benzodiazepines and newer nonbenzodiazepine drugs can also cause physical dependence, which manifests in withdrawal symptoms if the drug is not carefully tapered down. The benzodiazepine and nonbenzodiazepine hypnotic medications also have a number of sideeffects such as day time fatigue, motor vehicle crashes, cognitive impairments and falls and fractures. Elderly people are more sensitive to these side-effects.[72] The non-benzodiazepines zolpidem and zaleplon have not adequately demonstrated effectiveness in sleep maintenance. Some benzodiazepines have demonstrated effectiveness in sleep maintenance in the short term but in the longer term are associated with tolerance and dependence. Drugs that may prove more effective and safer than existing drugs for insomnia are in development.[73] Benzodiazepines and nonbenzodiazepines have similar efficacy that is not significantly more than for antidepressants.[74] Benzodiazepines did not have a significant tendency for more adverse drug reactions.[74] 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 nighttime awakenings than insomniacs not taking hypnotic medications.[75] A further review of the literature regarding benzodiazepine hypnotic as well as the nonbenzodiazepines concluded that these drugs cause an unjustifiable risk to the individual and to public health and lack evidence of long-term effectiveness. The risks include dependence, accidents, and other adverse effects. Gradual discontinuation of hypnotics in long-term users leads to improved health without worsening

of sleep. It is preferred that hypnotics be prescribed for only a few days at the lowest effective dose and avoided altogether wherever possible in the elderly.[76] Antihistamines[edit] The antihistamine diphenhydramine is widely used in nonprescription sleep aids such as Benadryl. The antihistamine doxylamine is used in nonprescription sleep aids such as Unisom (USA) and Unisom 2 (Canada). In some countries, including Australia, it is marketed under the names Restavit and Dozile. It is the most effective over-the-counter sedative currently available in the United States, and is more sedating than some prescription hypnotics.[77] While the two drugs mentioned above are available over the counter in most countries, the effectiveness of these agents may decrease over time, and the incidence of next-day sedation is higher than for most of the newer prescription drugs.[citation needed] Anticholinergic side-effects may also be a draw back of 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. Benzodiazepines[edit]

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

[78]

The most commonly used class of hypnotics prescribed for insomnia are the benzodiazepines. Benzodiazepines all bind unselectively to the GABAA receptor.[74] But certain benzodiazepines (hypnotic benzodiazepines) have significantly higher activity at the 1 subunit of the GABAA receptor compared to other benzodiazepines (for example, triazolam and temazepam have significantly higher activity at the 1subunit compared to alprazolam and diazepam, making them superior sedative-hypnotics alprazolam and diazepam in turn have higher activity at the 2 subunit compared to triazolam and temazepam, making them superior anxiolytic agents). Modulation of the 1 subunit is associated with sedation, motor-impairment, respiratory depression, amnesia, ataxia, and reinforcing behavior (drug-seeking behavior). Modulation of the 2 subunit is associated with anxiolytic activity and disinhibition. For this reason, certain benzodiazepines are better suited to treat insomnia than others. Hypnotic benzodiazepines include drugs such as temazepam, flunitrazepam, triazolam, flurazepam,midazolam, nitrazepam, and quazepam. These drugs can lead to tolerance, physical dependence, and the benzodiazepine withdrawal syndrome upon discontinuation, especially after consistent usage over long periods of time. Benzodiazepines, while inducing unconsciousness, actually worsen sleep as they promote light sleep while decreasing time spent in deep sleep.[79] A further problem is, with regular use of shortacting sleep aids for insomnia, daytime rebound anxiety can emerge.[80] Benzodiazepines can help to initiate sleep and increase sleep time, but they also decrease deep sleep and increase light sleep. Although there is little evidence for benefit of benzodiazepines in insomnia and evidence of major harm, prescriptions have continued to increase.[81] 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.[82][83] Non-benzodiazepines[edit]

Nonbenzodiazepine sedative-hypnotic drugs, such as zolpidem, zaleplon, zopiclone, and eszopiclone, are a class hypnotic medications indicated for mild to moderate insomnia. Their effectiveness at improving time to sleeping is slight.[84] However, there are controversies over whether these non-benzodiazepine drugs are superior to benzodiazepines. These drugs appear to cause both psychological dependence and physical dependence, though less than traditional benzodiazepines and can also cause the same memory and cognitive disturbances along with morning sedation.[citation needed] Antidepressants[edit] Some antidepressants such as amitriptyline, doxepin, mirtazapine, and trazodone can have a sedative effect, and are prescribed to treat insomnia.[85] Amitriptyline and doxepin both have antihistaminergic, anticholinergic, and antiadrenergic properties, which contribute to their sideeffect profile, while mirtazapines side-effects are primarily antihistaminergic, and trazadones sideeffects are primarily antiadrenergic. Some also alter sleep architecture. As with benzodiazepines, the use of antidepressants in the treatment of insomnia can lead to withdrawal effects; withdrawal may induce rebound insomnia. Mirtazapine is known to decrease sleep latency, promoting sleep efficiency and increasing the total amount of sleeping time in people with both depression and insomnia.[86][87] Agomelatine is a novel melatonergic antidepressant with sleep-improving qualities and does not cause daytime drowsiness.[88] Melatonin[edit] Melatonin is a hormone synthesized by the pineal gland, secreted through the bloodstream in the dark or commonly at nighttime, in order to control the sleep cycle.[89] Evidence for ramelteon looks promising.[90] It and tasimelteon, increase sleep time due to a melatonin rhythm shift with no apparent negative effectives next day.[89][91] Although thus far there has been little evidence of abuse, but most melatonin drugs have not been highly tested for longitudinal side effects because of the lack of approval, except for Ramelteon, from the Food and Drug Administration, concluding that all the risks are not known at this time.[91] It is recommended that people who take melatonin take it at night right before going to bed.[92][93] Studies have also shown that children with Autism spectrum disorders, learning disabilities, Attention-Deficit Hyperactivity Disorder (ADHD) and other 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. Children who have ADHD then, as well as the other disorders mentioned, are given melatonin before bedtime in order to help them sleep. The sleep cycle regulates for these children when given the melatonin supplement.[94] Alcohol[edit] Main article: Alcohol use and sleep 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.[95] 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.[96]

Other[edit] 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.[27] However, dependence on opioids can lead to suffering from long time disturbance in sleep.[97] The use of antipsychotics for insomnia, while common, is not recommended as the evidence does not demonstrate a benefit and the risk of adverse effects is significant.[98][99]Concerns regarding side effects is greater in the elderly.[100]

Alternative medicine[edit]
Some insomniacs use herbs such as valerian, chamomile, lavender, cannabis, hops, Withania somnifera, and passion-flower. Purified valerian extract has undergone multiple studies and appears to be modestly effective.[101][102][103] L-Arginine L-aspartate, S-adenosyl-L-homocysteine, and delta sleep-inducing peptide (DSIP) may be also helpful in alleviating insomnia.[104] A 1973 study published in Psychopharmacologia found that orally administered THC significantly reduced sleep latency and frequency of sleep interruptions in 9 healthy subjects. A 20 mg dose of THC was found to be most effective, reducing sleep latency by over an hour on average.[105] A 2010 study published in Anesthesia and Analgesia found that synthetic THC was more effective than the antidepressant amitriptyline at improving sleep quality in patients with fibromylagia.[106]

Epidemiology[edit]

Disability-adjusted life year for insomnia per 100,000 inhabitants in 2002. no data less than 25 2530.25 30.2536 3641.5 41.547 4752.5 52.558 5863.5 63.569 6974.5 74.580 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. Getting 8.5 or more hours of sleep per night increased the mortality rate by 15%. Severe insomnia sleeping less than 3.5 hours in women and 4.5 hours in men also led to a 15% increase in mortality. However, most of the increase in mortality from severe insomnia was discounted after controlling for co-morbid disorders. After controlling for sleep duration and insomnia, use of sleeping pills was also found to be associated with an increasedmortality rate.[107] 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.[107] As long as a patient refrains from using sleeping pills, there is little to no increase in mortality associated with insomnia, but there does appear to be an increase in longevity. This is reassuring for patients with insomnia in that, despite the sometimes-unpleasantness of insomnia, insomnia itself appears to be associated with increased longevity.[107] It is unclear why sleeping longer than 7.5 hours is associated with excess mortality.[107] Insomnia is 40% more common in women than in men.[108]

Prevalence[edit]
The National Sleep Foundation's 2002 Sleep in America poll showed that 58% of adults in the U.S. experienced symptoms of insomnia a few nights a week or more.[109] Although insomnia was the most common sleep problem among about one half of older adults (48%), they were less likely to experience frequent symptoms of insomnia than their younger counterparts (45% vs. 62%), and their symptoms were more likely to be associated with medical conditions, according to the poll of adults between the ages of 55 and 84.[109] As explained by Thomas Roth,[2] estimates of the prevalence of insomnia depend on the criteria used as well as the population studied. About 30% of adults report at least one of the symptoms of insomnia. When daytime impairment is added as a criterion, the prevalence is about 10%. Primary insomnia persisting for at least one month yields estimates of 6%.

Society[edit]
The topic of insomnia is discussed in many cultural contexts.[110][111]

See also[edit]

Al Herpin, American insomniac, known as the "Man Who Never Slept" Actigraphy Fatal familial insomnia Hypnophobia Sleep deprivation Thai Ngoc, Vietnamese insomniac, claimed to be awake for 33 years

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