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Legal row over wireless calling
A court is set to decide on a row between operator T-Mobile and wi-fi phone firm Truphone.
Truphone has accused T-Mobile of hindering its service by blocking calls made to numbers owned by the fledgling mobile operator.

To rectify the situation, Truphone has applied for an injunction to force T-Mobile to put the calls through.

In court documents T-Mobile said it had offered Truphone a deal to route its calls that had been rejected.

The Truphone service works by routing calls via wi-fi when handsets are within range of wireless hotspots the phone can connect to.

By using the wi-fi and the net Truphone hopes to cut mobile call costs, particularly those made to long distance numbers.

In its court documents, Truphone said T-Mobile was "abusing its dominant position" by not putting its numbers through.

In papers filed to the court by T-Mobile, the operator said a deal had been done over handling calls but Truphone had rejected it.

Truphone said it could not comment on the legal row while the case was ongoing. T-Mobile said it could not comment as it was in the middle of court proceedings.

The case was first heard on 11 July and a final decision is expected on 16 July.

In early 2007, Truphone has had wrangles with mobile phone firms that blocked some features on the Nokia N95 phone. Blocking the features limited the use customers could make of Truphone's service.


Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/technology/6897337.stm

Published: 2007/07/13 11:58:56 GMT

© BBC MMVII
 
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No price cut for Euro PS3 console

Sony boss on price cut
Sony is not cutting the price of the PlayStation 3 in Europe, but will offer free games and accessories instead.
There is also no word of plans for an 80GB version of the console in Europe.

Last week Sony said it would drop the US price of the 60GB PS3 by $100 (£50), and introduced a new 80GB version at the original price of $599 (£300).

In Europe gamers will get a "starter pack" at an unchanged price of £425 for the 60GB machine, with two games and two controllers included.

The new pack was announced at the E3 games conference in Santa Monica, in California. Sony says it is offering gamers £115 worth of added games and controller, for no extra charge.

But the firm could face criticism from gamers for deciding not to reduce the price of the 60GB PS3 and not announcing the 80GB machine.

Earlier this week, Jack Tretton, chief executive of Sony Computer Entertainment America, said he thought the US price cut would at least "double" the sales of PS3 in the country.

But in an interview with games website Gamesindustry.biz, David Reeves, president of Sony Computer Entertainment Europe, revealed that once the stock of 60GB machines was sold out in the US - probably by the end of July - the model would no longer be sold.
That would mean that US gamers would once again have to pay $599 for a full-spec console with features such as wi-fi, not available on the cheaper 20GB model.

In the UK, the PlayStation 3 remains £125 more expensive than the equivalent Xbox 360 bundle of console and games and £225 more expensive than the Nintendo Wii with two games.


What do you think about Sony's decision? You can contact BBC News and tell us your views by using the form below.

Will Sony be offering any kind of rebate or mail-in offer to those of us who bought our PS3s less than two weeks ago?
Tony Pincott, Sheffield

Even more annoying is that the EU version runs a PS2 emulator. This makes it cheaper to build/maintain than the US version and what's more the EU version can play fewer PS2 games (the more advanced ones) under emulation. Now that's something they won't advertise to the consumer. This is just another example of the EU being ripped off where ever possible. Buy a Wii, they are more fun by a long shot. Mark Doherty UK


Shame. I might have bought one otherwise. Looks like our house shall be going down the xbox route after all. Chris Godfrey, London

I personally feel like I've been snubbed by Sony, I bought every other playstation, but if they are going to charge me twice the price for the PS3 compared to what they offer in the US for a console with next to no games, I'll stick with my Wii and XBox 360 thanks. Stephen Bates, Derby

It's nice to hear that Sony are trying to claw back some of the customers that they alienated with the outrageous price of the console originally. However, they now run the risk of alienating the loyal customers who bought the console around the day of release, as I am certain that they will not be offered 2 games and an extra control pad. This annoys me somewhat, as Microsoft did offer something along these lines with the original Xbox, and they did make sure that ALL customers, new and existing received the benefits. David Higgins, Swindon

Do Sony actually want to sell any of these consoles? Huge delay on the initial unit, vast price increase on EU version with less hardware in it and glitchy software that makes PS2 games look horrid. And now price cuts for the already much cheaper US customers. Sorry Sony but each time I walk past any high street store your consoles are packed from floor to ceiling with an embarrassingly desperate "IN STOCK" sign next to it. Who on earth is making your marketing decisions here? David Newland, Hemel Hempstead


Europe and everyone else outside the U.S.A. gets the raw deal again! When will Sony learn that most of their key market 18-25 years do not have £425 to throw away on a games console that will have to come down eventually to compete successfully with Microsoft and Nintendo. This loyal Sony customer's support is drifting quickly towards buying a Wii as his next generation console. Richard Kendrick, Leeds

The arrogance of Sony is astonishing. They are taking European gamers for granted, so it is up to we Europeans to deliver the bloody nose they deserve. I have a son who wants a PS3 for Christmas but he may just find a different console in his set of gifts. Paul Valentine, Montrose, Scotland

Why does Sony keep shooting itself in the foot by annoying its large European Fan base? We seem to be the last and worst off with regards to everything PS3. If Sony still can't work out why they are not selling enough consoles I will spell it out for them, you can't expect us to fork out £400+ on a new machine when we are treated like dirt Jonathan Kay, London

Sony will see no rise in sales as long as this rip off continues. Americans can buy the superior Playstation 3 for £150 cheaper than European buyers. How can this price difference be defended? I for one will not buy the console even if they drop the price in the months to come as Sony have clearer shown their contempt for the European market with this blatant rip off. John Blair, Glasgow

The ps3 was for me a big disappointment. Having shelled out the best part of £500 pound on it. I found the games very boring and the launch range few in far between. I recently cut my losses and traded it in for the Wii. I think the Wii is winning the so called battle of the consoles. Sony were on top, but the over pricing and poor selection of games has dented the Playstation 3. Mark Kelly, East Kilbride

If Sony didn't have enough problems selling their console already due to alienating european customers they now hit us with another knockback. Seems like a much better idea just to import a console from the US instead. Dave Hamer, Thornbury

I think it's fair enough from Sony. They are testing the market to see which deal gives the greatest boost to sales - a price cut in the console or an equivalent games bundle. You can't use the console without the games, so you would end up having to buy them anyway. The only downside is that I'm guessing the choice of bundled games would not suit everyone's taste and therefore the price reduction will prove to be the better deal all round. Martin Randall, Wakefield


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Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/technology/6896261.stm

Published: 2007/07/13 00:38:51 GMT

© BBC MMVII
 
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Inside Microsoft's future kitchen
By Peter Price
BBC World Service's Digital Planet



Computing giant Microsoft is centring its plans for future growth less on the office and more on getting consumer-friendly devices into every room in our homes - at least if the projects on display at the country's research centre in Cambridge are anything to go by.
A "kitchen" at the centre is full of a whole range of the company's new designs - and few of them are suited to the office environment.

Instead, the focus is on something that would not look out of place next to the fridge or the sofa.

"Microsoft projects have traditionally been orientated towards the office and the personal computer; this is looking at the role that technology has in how families communicate and organise themselves," the Centre's managing director Frank Herbert told BBC World Service's Digital Planet programme.

"[It's] a world where you don't think of technology as a computer and something geeky - it's got to be much more approachable, much more engaging.

"[It's about] getting in touch with the emotional side of computing."

Thinking differently

Rather than being packed with hi-tech equipment, a number of the things on display in the kitchen appear deceptively simple - such as what at first glance looks like a basic Post-It notepad and a pen.

But researcher Lorna Brown says it is actually the future of text messaging - the key being the graphics tablet underneath the Post-It pad.


All the things in this space are meant to demonstrate how we can think differently about what the future might be
Richard Harper, senior researcher

"If I write on the pad, it recognises what I've written," she explains.
"Then I can gesture towards the name of someone I want to send it to, and it'll send the message to them."

Another device on display is the "bubble board" - a type of visual answering machine.

The prototype consists of a flat-screen display mounted within a wooden picture frame hanging on a wall - not much like a computer.

On it, pictures of friends bounce around - each one corresponding to a message left by that friend.

"All the things in this space are meant to demonstrate how we can think differently about what the future might be," explains Richard Harper, a senior researcher at the centre.

"When you look at most technology, it is designed first and foremost with the workplace in mind - and it's basically designed to focus on efficiency, allowing people to do things as quickly and efficiently as possible.

"Here at Cambridge, we don't really think that that's what homes are about. Often, homes are about inefficiency - you walk in your front door and you just want to kick back, watch some TV and relax. You're not in the same state of mind as you are in a workplace.

"So we've used this metaphor of the bubbles just to add a bit of delight for people - they bob around for people. It's deliberately designed to be playful and engaging, which is how we think a lot of homes should be."

Three Ways to Listen Digital Planet
Your guide to the digital world





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Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/technology/6895588.stm

Published: 2007/07/17 10:06:24 GMT

© BBC MMVII
 
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Wow!! dodm't notice it before but indeed a very informative thread. Good work, sir!!

Rep for you
 
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Wow!! dodm't notice it before but indeed a very informative thread. Good work, sir!!

Rep for you

thank you bushroda there is nothing more for a researcher then to be appreciated i thank you once again but there is a disappointment to my research well its not that i could not get some links but rather what i came across in the science & technology research departments specially regarding the health/mental sector of the human life yes you got it to live a healthy life and to get the strength to be in the cycle of life in the very best shape that we can to get the most of life. Sadly today along with new cures we are also discovering new diseases both in the physical & psychological dimensions of the human life two of them i will post one from the physical point for eg. a good day deserve a good night sleep you got but its when you don't have enough of it then one will have to do some research about "SLEEP APNEA" & the second findings have been in the psychological department a disorder that many of the new generations are faced with today but few only knows they have it while the rest live in an enormous amount of danger yes it is knows as the "BIPOLAR DISORDER" so lets start with "BIPOLAR DISORDER"
 
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WHAT IS A "BIPOLAR DISORDER" ?

Bipolar disorder
From Wikipedia, the free encyclopedia
Jump to: navigation, search
“Manic Depression” redirects here. For other uses, see Manic Depression (disambiguation).
Bipolar disorder
Classification & external resources ICD-10 F31.
ICD-9 296.80
OMIM 125480 309200
DiseasesDB 7812
MedlinePlus 001528
eMedicine med/229
MeSH D001714
Bipolar disorder is a psychiatric condition defined as recurrent episodes of significant disturbance in mood. These disturbances can occur on a spectrum that ranges from debilitating depression to unbridled mania. Individuals suffering from bipolar disorder typically experience fluid states of mania, hypomania or what is referred to as a mixed states in conjunction with depressive episodes. These clinical states typically alternate with a normal range of mood. The disorder has been subdivided into Bipolar I, Bipolar II-Rapid Cycling variant, and cyclothymia.

Also called Bipolar Affective Disorder until recently, the current name is of fairly recent origin and refers to the cycling between high and low episodes; it has replaced the older term Manic-depressive Illness coined by Emil Kraepelin (1856-1926) in the late 19th century.[3]

Onset of symptoms generally occurs in young adulthood. Diagnosis is based on the person's self-reported experiences, as well as observed behavior. Episodes of illness are associated with distress and disruption, and a relatively high risk of suicide.[1] Studies suggest that genetics, early environment, neurobiology, and psychological and social processes are important contributory factors. Current psychiatric research is focused on the role of neurobiology, but a clear organic cause has not been found. Bipolar disorder is usually treated with medications and/or therapy or counseling. The mainstay of medication are a number of drugs termed 'mood stabilizers', in particular lithium and sodium valproate ; these are a group of unrelated medications used to prevent relapses of further episodes. Neuroleptic medications, also termed 'antipsychotics', in particular olanzapine, are used in the treatment of manic episodes and in maintenance. The benefits of using antidepressants in depressive episodes is unclear. In serious cases where there is risk to self and others involuntary hospitalization may be necessary; these generally involve severe manic episodes with dangerous behaviour or depressive episodes with suicidal ideation. Hospital stays are less frequent and for shorter periods than they were in previous years.

Some studies have suggested a significant correlation between creativity and bipolar disorder. However, the relationship between the disorder and creativity is still very unclear.[2][3][4] One study indicated increased striving for, and sometimes obtaining, goals and achievements.[5]

Contents [hide]
1 History
2 Signs and symptoms
2.1 Classification
2.2 The depressive phase
2.3 Mania
2.4 Hypomania
2.5 Mixed state
2.6 Rapid cycling
2.7 Cognition
2.8 Creativity
3 Diagnosis
3.1 Diagnostic criteria
3.2 Delay in diagnosis
3.3 Children
4 Epidemiology
5 Etiology
5.1 Heritability or inheritance
5.2 Genetic research
6 Treatment
6.1 Medication
7 Research
7.1 Medical imaging
7.2 New treatments
8 Prognosis
8.1 Recurrence
8.2 Mortality
9 See also
10 References
10.1 Cited texts
11 Further reading
12 External links



History
Main article: History of bipolar disorder
Varying moods and energy levels have been a part of the human experience since time immemorial. The words "melancholia" (an old word for depression) and "mania" have their etymologies in Ancient Greek. The word melancholia is derived from melas/μελας, meaning "black", and chole/χολη, meaning "bile" or "gall",[6] indicative of the term’s origins in pre-Hippocratic humoral theories. Within the humoral theories, mania was viewed as arising from an excess of yellow bile, or a mixture of black and yellow bile. The linguistic origins of mania, however, are not so clear-cut. Several etymologies are proposed by the Roman physician Caelius Aurelianus, including the Greek word ‘ania’, meaning to produce great mental anguish, and ‘manos’, meaning relaxed or loose, which would contextually approximate to an excessive relaxing of the mind or soul (Angst and Marneros 2001). There are at least five other candidates, and part of the confusion surrounding the exact etymology of the word mania is its varied usage in the pre-Hippocratic poetry and mythologies (Angst and Marneros 2001).

The idea of a relationship between mania and melancholia can be traced back to at least the 2nd century AD[4]. Soranus of Ephesus (98-177 AD) described mania and melancholia as distinct diseases with separate etiologies[5]; however, he acknowledged that “many others consider melancholia a form of the disease of mania” (Cited in Mondimore 2005 p.49).

A clear understanding of bipolar disorder as a mental illness was recognized by early Chinese authors. The encyclopedist Gao Lian (c. 1583) describes the malady in his Eight Treatises on the Nurturing of Life (Ts'un-sheng pa-chien).[6]

The earliest written descriptions of a relationship between mania and melancholia are attributed to Aretaeus of Cappadocia. Aretaeus was an eclectic medical philosopher who lived in Alexandria somewhere between 30 and 150 AD (Roccatagliata 1986; Akiskal 1996). Aretaeus is recognized as having authored most of the surviving texts referring to a unified concept of manic-depressive illness, viewing both melancholia and mania as having a common origin in ‘black bile’ (Akiskal 1996; Marneros 2001).


Emil Kraepelin (1856–1926) refined the concept of psychosis.The contemporary psychiatric conceptualisation of manic-depressive illness is typically traced back to the 1850s. Marneros (2001) describes the concepts emerging out of this period as the “rebirth of bipolarity in the modern era”. On January 31, 1854, Jules Baillarger described to the French Imperial Academy of Medicine a biphasic mental illness causing recurrent oscillations between mania and depression. Two weeks later, on February 14, 1854, Jean-Pierre Falret presented a description to the Academy on what was essentially the same disorder. This illness was designated folie circulaire (‘circular insanity’) by Falret, and folie à double forme (‘dual-form insanity’) by Baillarger (Sedler 1983).

Emil Kraepelin (1856-1926), a German psychiatrist categorized and studied the natural course of untreated bipolar patients long before mood stabilizers were discovered. Describing these patients in 1902, he coined the term manic depressive psychosis. He noted in his patient observations that intervals of acute illness, manic or depressive, were generally punctuated by relatively symptom-free intervals in which the patient was able to function normally.[7]

After World War II, Dr. John Cade, an Australian psychiatrist, was investigating the effects of various compounds on veteran patients with manic depressive psychosis. In 1949 , Cade discovered that lithium carbonate could be used as a successful treatment of manic depressive psychosis.[8] Because there was a fear that table salt substitutes could lead to toxicity or death, Cade's findings did not immediately lead to treatments. In the 1950s, U.S. hospitals began experimenting with lithium on their patients. By the mid-'60s, reports started appearing in the medical literature regarding lithium's effectiveness. The U.S. Food and Drug Administration did not approve of lithium's use until 1970.[9]

The term "manic-depressive reaction" appeared in the first American Psychiatric Association Diagnostic Manual in 1952, influenced by the legacy of Adolf Meyer who had introduced the paradigm illness as a reaction of biogenetic factors to psychological and social influences.[10] Subclassification of bipolar disorder was first proposed by German psychiatrist Karl Leonhard in 1957; he was also the first to introduce the terms bipolar (for those with mania) and unipolar (for those with depressive episodes only).[11]

In 1968, both the newly revised classification systems ICD-8 and DSM-II termed the condition "manic-depressive illness" as biological thinking came to the fore.[12]

The current nosology, bipolar disorder, became popular only recently, and some individuals prefer the older term because it provides a better description of a continually changing multi-dimensional illness.[citation needed]


Signs and symptoms
Bipolar disorder is a cyclic illness where people periodically exhibit elevated (Manic) and depressive episodes. Most people will experience a number of episodes, averaging 0.4 to 0.7 a year with each lasting 3-6 months.[13][14] Late adolescence and early adulthood are peak years for the onset of the illness.[15][16] These are critical periods in a young adult's social and vocational development, and they can be severely disrupted by disease onset.


Classification
Bipolar disorder is commonly categorized as either Bipolar Type I, where an individual experiences full-blown mania, or Bipolar Type II, in which the hypomanic "highs" do not go to the extremes of mania. The latter is much more difficult to diagnose, since the hypomanic episodes may simply appear as a period of successful high productivity and is reported less frequently than a distressing depression. Psychosis can occur, particularly in manic periods. There are also 'rapid cycling' subtypes. Because there is so much variation in the severity and nature of mood-related problems, the concept of a bipolar spectrum is often employed, which includes cyclothymia. There is no consensus as to how many 'types' of bipolar disorder exist.[17] Many people with bipolar disorder experience severe anxiety and are very irritable (to the point of rage) when in a manic state, while others are euphoric and grandiose.


The depressive phase
Main article: Clinical Depression
Signs and symptoms of the depressive phase of bipolar disorder include: persistent feelings of sadness, anxiety, guilt, anger, isolation and/or hopelessness, disturbances in sleep and appetite, fatigue and loss of interest in usually enjoyed activities, problems concentrating, loneliness, self-loathing, apathy or indifference, depersonalization, loss of interest in sexual activity, shyness or social anxiety, irritability, chronic pain (with or without a known cause), lack of motivation, and morbid/suicidal ideation.[18]


Mania
Main article: Mania
Mania is generally characterized by a distinct period of an elevated, expansive or irritable mood state. People commonly experience an increase in energy and a decreased need for sleep. A person's speech may be pressured, with thoughts experienced as racing. Attention span is low and a person in a manic state may be easily distracted. People may feel they have been 'chosen', or are 'on a special mission', which are considered grandiose or delusional ideas. At more extreme phases, a person in a manic state can begin to experience psychosis, or a break with reality, where thinking is affected along with mood. In order to be diagnosed with mania according to DSM-IV, a person must experience this state of elevated or irritable mood as well as other symptoms for two or more weeks.


Hypomania
Main article: Hypomania
Hypomania is generally a less extreme state than mania, and people in the hypomanic phase generally experience less of the symptoms of mania than those in a full-blown manic episode. During an episode of Hypomania one might feel an uncontrollable impulse to laugh at things he or she does not normally find funny. The duration is usually also shorter than in mania. This is often a very 'artistic' state of the disorder, where there is a flight of ideas, extremely clever thinking, and an increase in energy.


Mixed state
Main article: Mixed state (psychiatry)
In the context of bipolar disorder, a mixed state is a condition during which symptoms of mania and clinical depression occur simultaneously (for example, agitation, anxiety, aggressiveness or belligerence, confusion, fatigue, impulsiveness, insomnia, irritability, morbid and/or suicidal ideation, panic, paranoia, persecutory delusions, pressured speech, racing thoughts, restlessness, and rage).[19]

Mixed episodes can be the most volatile of the bipolar states, as moods can easily and quickly be triggered or shifted.[citation needed] Suicide attempts, substance abuse, and self-mutilation may occur during this state.[citation needed]


Rapid cycling
Rapid cycling, defined as having four or more episodes per year, is found in a significant fraction of patients with bipolar disorder. It has been associated with greater disability or a worse prognosis, due to the confusing changeability and difficulty in establishing a stable state. Rapid cycling can be induced or made worse by antidepressants, unless there is adjunctive treatment with a mood stabilizer.[20][21]


Cognition
Recent studies have found that bipolar disorder involves certain cognitive deficits or impairments, even in states of remission.[22][23][24][25] Deborah Yurgelun-Todd of McLean Hospital in Belmont, Massachusetts has argued these deficits should be included as a core feature of bipolar disorder. According to McIntyre et al. (2006), "study results now press the point that neurocognitive deficits are a primary feature of BD; they are highly prevalent and persist in the absence of overt symptomatology. Although disparate neurocognitive abnormalities have been reported, disturbances in attention, visual memory, and executive function are most consistently reported."[26] However, in the April-June 2007 issue of the Journal of Psychiatric Research, Spanish researchers reported that people with bipolar 1 who have a history of psychotic symptoms do not necessarily experience an increase in cognitive impairment.[citation needed]


Creativity
Main article: Creativity and mental illness
A number of recent studies have observed a correlation between creativity and bipolar disorder,[2][3][4] although it is unclear in which direction the cause lies, or whether both conditions are caused by some third, unknown, factor. It has been hypothesized that temperament may be one such factor.


Diagnosis
Diagnosis is based on the self-reported experiences of the patient as well as abnormalities in behavior reported by family members, friends or co-workers, followed by secondary signs observed by a psychiatrist, social worker, clinical psychologist or other clinician in a clinical assessment. There is a list of criteria that must be met for someone to be so diagnosed. These depend on both the presence and duration of certain signs and symptoms.

An initial assessment includes a comprehensive history and physical examination by a physician. Although there are no biological tests which confirm bipolar disorder, tests are carried out to exclude medical illnesses which may rarely present with psychiatric symptoms. These include blood tests measuring TSH to exclude hypo- or hyperthyroidism, basic electrolytes and serum calcium to rule out a metabolic disturbance, full blood count including ESR to rule out a systemic infection or chronic disease, and serology to exclude syphilis or HIV infection; two commonly ordered investigations are EEG to exclude epilepsy, and a CT scan of the head to exclude brain lesions.[citation needed] There are several psychiatric illnesses which may present with similar symptoms; these include schizophrenia,[27] drug intoxication, brief drug-induced psychosis, schizophreniform disorder and borderline personality disorder.

The last is important as both diagnoses involve symptoms commonly known as "mood swings". In bipolar disorder, the term refers to the cyclic episodes of elevated and depressed mood which generally last weeks or months (notwithstanding Rapid Cycling variant of greater than four episodes a year). The term in borderline personality refers to the marked lability and reactivity of mood, known as emotional dysregulation, due to response to external psychosocial and intrapsychic stressors; these may arise or subside suddenly and dramatically and last for seconds, minutes, hours or days. A bipolar depression is generally more pervasive with sleep, appetite disturbance and nonreactive mood, whereas the mood in dysthymia of borderline personality remains markedly reactive and sleep disturbance not acute.[28]

The relationship between bipolar disorder and borderline personality disorder has been debated; some hold that the latter represents a subthreshold form of affective disorder,[29][30] while others maintain the distinctness, though noting they often coexist.[31][32]

Investigations are not generally repeated for relapse unless there is a specific medical indication. These may include serum BSL if olanzapine has previously been prescribed, lithium or valproate level to check compliance or toxicity with those medications, renal or thyroid function if lithium has been previously prescribed and taken regularly. Assessment and treatment are usually done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to self or others.[citation needed]

The most widely used criteria for diagnosing bipolar disorder are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, the current version being DSM-IV-TR, and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems, currently the ICD-10. The latter criteria are typically used in European countries while the DSM criteria are used in the USA or the rest of the world, as well as prevailing in research studies.


Diagnostic criteria
Main article: Current diagnostic criteria for bipolar disorder
Flux is the fundamental nature of bipolar disorder.[citation needed] Both within and between individuals with the illness, energy, mood, thought, sleep, and activity are among the continually changing biological markers of the disorder. The diagnostic subtypes of bipolar disorder are thus static descriptions—snapshots, perhaps—of an illness in continual change, with a great diversity of symptoms and varying degrees of severity. Individuals may stay in one subtype, or change into another, over the course of their illness. The DSM V, to be published in 2011 , will likely include further and more accurate sub-typing (Akiskal and Ghaemi, 2006).

There are currently four types of bipolar illness. The Diagnostic and Statistical Manual of Mental Disorders-IV-TR (DSM-IV-TR) details four categories of bipolar disorder, Bipolar I, Bipolar II, Cyclothymia, and Bipolar Disorder NOS (Not Otherwise Specified).

For a diagnosis of Bipolar I disorder according to the DSM-IV-TR, there requires one or more manic or mixed episodes. A depressive episode is not required for the diagnosis of Bipolar I disorder but it frequently occurs.

Bipolar II, which occurs more frequently is usually characterized by at least one episode of hypomania and at least one depression.

A diagnosis of Cyclothymic Disorder requires the presence of numerous hypomanic episodes, intermingled with depressive episodes that do not meet full criteria for major depressive episodes. The main idea here is that there is a low-grade cycling of mood which appears to the observer as a personality trait, but interferes with functioning.

If an individual clearly seems to be suffering from some type of bipolar disorder but does not meet the criteria for one of the subtypes above, he or she receives a diagnosis of Bipolar Disorder NOS (Not Otherwise Specified).

Although a patient will most likely be depressed when they first seek help, it is very important to find out from the patient or the patient's family or friends if a manic or hypomanic episode has ever been present, using careful questioning. This will prevent misdiagnosis of Depressive Disorder and avoids the use of an antidepressant which may trigger a "switch" to hypomania or mania or induce rapid cycling. Recent screening tools such as the Hypomanic Check List Questionnaire (HCL-32) have been developed to assist the quite often difficult detection of Bipolar II disorders.


Delay in diagnosis
The behavioral manifestations of bipolar disorder are often not understood by patients nor recognized by mental health professionals, so people may suffer unnecessarily for over 10 years in some cases before receiving proper treatment.[33]

That treatment lag is apparently not decreasing, even though there is now increased public awareness of this mental health condition in popular magazines and health websites. Recent TV specials, for example the BBC's The Secret Life of the Manic Depressive,[34] MTV's True Life: I'm Bipolar, talk shows, and public radio shows, and the greater willingness of public figures to discuss their own bipolar disorder, have focused on psychiatric conditions thereby further raising public awareness.

Despite this increased focus, individuals are still commonly misdiagnosed.[35]





Children
Main article: Bipolar disorder in children
Children with bipolar disorder do not often meet the strict DSM-IV definition. In pediatric cases, the cycling can occur very quickly (see section above on rapid cycling).[36]

Children with bipolar disorder tend to have rapid-cycling or mixed-cycling. Rapid cycling occurs when the cycles between depression and mania occur quickly, sometimes within the same day or the same hour. When the symptoms of both mania and depression occur simultaneously, mixed cycling occurs.

Often other psychiatric conditions are diagnosed in bipolar children. These other diagnoses may be concurrent problems, or they may be misdiagnosed as bipolar disorder. Depression, ADHD, ODD, schizophrenia, and Tourette syndrome are common comorbid conditions. Furthermore some children with histories of abuse or neglect may have Bipolar I Disorder. There is a high comborbidity between Reactive attachment disorder and Bipolar I Disorder with about 50% of children in the Child Welfare System who have Reactive Attachment Disorder also have Bipolar I Disorder[37]

Misdiagnosis can lead to incorrect medication.


Epidemiology
Clinical depression and bipolar disorder are currently classified as separate illnesses. Some researchers increasingly view them as part of an overlapping spectrum that also includes anxiety and psychosis.

According to Hagop Akiskal, M.D., at the one end of the spectrum is bipolar type schizoaffective disorder, and at the other end is unipolar depression (recurrent or not recurrent), with the anxiety disorders present across the spectrum. Also included in this view is premenstrual dysphoric disorder, postpartum depression, and postpartum psychosis. This view helps to explain why many people who have the illness do not have first-degree relatives with clear-cut "bipolar disorder", but who have family members with a history of these other disorders.

In a 2003 study, Hagop Akiskal M.D. and Lew Judd M.D. re-examined data from the landmark Epidemiologic Catchment Area study from two decades before.[38] The original study found that 0.8 percent of the population surveyed had experienced a manic episode at least once (the diagnostic threshold for bipolar I) and 0.5 a hypomanic episode (the diagnostic threshold for bipolar II).

By tabulating survey responses to include sub-threshold diagnostic criteria, such as one or two symptoms over a short time-period, the authors arrived at an additional 5.1 percent of the population, adding up to a total of 6.4 percent of the entire population who can be thought of as having a bipolar spectrum disorder. This and similar recent studies have been interpreted by some prominent bipolar disorders researchers as evidence for a much higher prevalence of bipolar conditions in the general population than previously thought.

However these re-analyses should be interpreted cautiously because of substantive as well as methodological study limitations. Indeed, prevalence studies of bipolar disorder are carried out by lay interviewers (that is, not by expert clinicians/psychiatrists who are more costly to employ) who follow fully structured/fixed interview schemes; responses to single items from such interviews may suffer limited validity.

Furthermore, a well-known statistical problem arises when ascertaining disorders and conditions with a relatively low population prevalence or base-rate, such as bipolar disorder: even assuming that lay interviews diagnoses are highly accurate in terms of sensitivity and specificity and their corresponding area under the ROC curve (that is, AUC, or area under the receiver operating characteristic curve), a condition with a relatively low prevalence or base-rate is bound to yield high false positive rates, which exceed false negative rates; in such a circumstance a limited positive predictive value, PPV, yields high false positive rates even in presence of a specificity which is very close to 100%.[39] To simplify, it can be said that a very small error applied over a very large number of individuals (that is, those who are *not affected* by the condition in the general population during their lifetime; for example, over 95%) produces a relevant, non-negligible number of subjects who are incorrectly classified as having the condition or any other condition which is the object of a survey study: these subjects are the so-called false positives; such reasoning applies to the 'false positive' but not the 'false negative' problem where we have an error applied over a relatively very small number of individuals to begin with (that is, those who are *affected* by the condition in the general population; for example, less than 5%). Hence, a very high percentage of subjects who seem to have a history of bipolar disorder at the interview are false positives for such a medical condition and apparently never suffered a fully clinical syndrome (that is, bipolar disorder type I): the population prevalence of bipolar disorder type I, which includes at least a lifetime manic episode, continues to be estimated at 1%.[40] "Mild-to-severe versions of bipolar disorder afflict nearly 4 percent of adults at some time in their lives."[41]

A different but related problem in evaluating the public health significance of psychiatric conditions has been highlighted by Robert Spitzer of Columbia University: fulfillment of diagnostic criteria and the resulting diagnosis do not necessarily imply need for treatment.[42] As a consequence, subjects who experience bipolar symptoms but not a full-blown, impairing bipolar syndrome should not be automatically considered as patients in need of treatment.

Recent studies have indicated that at least 50% of adult sufferers report manifestation of symptoms before the age of 17. Moreover, there is a growing consensus that bipolar disorder originates in childhood. In young children the illness is now referred to as pediatric bipolar disorder. Today about 0.5% of children under 18 are believed to have the condition. For children, the main concern is that bipolar disorder needs to be diagnosed correctly and treated properly because it can look like unipolar depression, ADHD, or conduct disorder. Young children, adolescents and adults each express the condition differently according to child and adolescent bipolar disorders expert Demitri Papolos M.D. and the Child and Adolescent Bipolar Foundation. There is, however, controversy about this last point[43]

Bipolar disorder manifests in late life as well. Some individuals with "hyperthymic" temperament (or "hypomanic" personality style) who experience depression in later life appear to have a form of bipolar disorder. Much more needs to be elucidated about late-life bipolar disorder.

Approximately 50% of children in the U.S. child welfare system who have reactive attachment disorder also have comorbid Bipolar I disorder according to research by John Alston, MD.


Etiology
According to the U.S. government's National Institute of Mental Health (NIMH), "There is no single cause for bipolar disorder—rather, many factors act together to produce the illness." "Because bipolar disorder tends to run in families, researchers have been searching for specific genes passed down through generations that may increase a person's chance of developing the illness." "In addition, findings from gene research suggest that bipolar disorder, like other mental illnesses, does not occur because of a single gene.".[44]

It is well established that bipolar disorder is a genetically influenced condition which can respond very well to medication (Johnson & Leahy, 2004; Miklowitz & Goldstein, 1997; Frank, 2005). (See treatment of bipolar disorder for a more detailed discussion of treatment.)

Psychological factors also play a strong role in both the psychopathology of the disorder and the psychotherapeutic factors aimed at alleviating core symptoms, recognizing episode triggers, reducing negative expressed emotion in relationships, recognizing prodromal symptoms before full-blown recurrence, and, practising the factors that lead to maintenance of remission (Lam et al, 1999; Johnson & Leahy, 2004; Basco & Rush, 2005; Miklowitz & Goldstein, 1997; Frank, 2005). Modern evidence based psychotherapies designed specifically for bipolar disorder when used in combination with standard medication treatment increase the time the individual stays well significantly longer than medications alone (Frank, 2005). These psychotherapies are interpersonal and social rhythm therapy for bipolar disorder, family focused therapy for bipolar disorder, psychoeducation, cognitive therapy for bipolar disorder, and prodrome detection. All except psychoeducation and prodrome detection are available as books.

Abnormalities in brain function have been related to feelings of anxiety and lower stress resilience. When faced with a very stressful, negative major life event, such as a failure in an important area, an individual may have his first major depression. Conversely, when an individual accomplishes a major achievement he may experience his first hypomanic or manic episode. Individuals with bipolar disorder tend to experience episode triggers involving either interpersonal or achievement-related life events. An example of interpersonal-life events include falling in love or, conversely, the death of a close friend. Achievement-related life events include acceptance into an elite graduate school or by contrast, being fired from work (Miklowitz & Goldstein, 1997). Childbirth can also trigger a postpartum psychosis for bipolar women, which can lead in the worse cases to infanticide.

The "kindling" theory[45] asserts that people who are genetically predisposed toward bipolar disorder can experience a series of stressful events, each of which lowers the threshold at which mood changes occur. Eventually, a mood episode can start (and becomes recurrent) by itself. Not all individuals experience subsequent mood episodes in the absence of positive or negative life events, however.

Individuals with late-adolescent/early adult onset of the disorder will very likely have experienced childhood anxiety and depression. Some argue that childhood-onset bipolar disorder should be treated early.

A family history of bipolar spectrum disorders can impart a genetic predisposition towards developing a bipolar spectrum disorder.[46] Since bipolar disorders are polygenic (involving many genes), there are apt to be many unipolar and bipolar disordered individuals in the same family pedigree. This is very often the case (Barondes, 1998). Anxiety disorders, clinical depression, eating disorders, premenstrual dysphoric disorder, postpartum depression, postpartum psychosis and/or schizophrenia may be part of the patient's family history and reflects a term called "genetic loading".

Bipolar disorder is not either environmental or physiological, it is multifactorial; that is, many genes and environmental factors conspire to create the disorder (Johnson & Leahy, 2004).

Since bipolar disorder is so heterogeneous, it is likely that people experience different pathways towards the illness (Miklowitz & Goldstein, 1997).

Recent research done in Japan indicates a hypothesis of dysfunctional mitochondria in the brain (Stork & Renshaw, 2005)


Heritability or inheritance
The disorder runs in families.[47] More than two-thirds of people with bipolar disorder have at least one close relative with the disorder or with unipolar major depression.

Studies seeking to identify the genetic basis of bipolar disorder indicate that susceptibility stems from multiple genes. Scientists are continuing their search for these genes, using advanced genetic analytic methods and large samples of families affected by the illness. The researchers are hopeful that identification of susceptibility genes for bipolar disorder, and the brain proteins they code for, will make it possible to develop better treatments and preventive interventions targeted at the underlying illness process.


Genetic research
There is increasing evidence for a genetic component in the causation of bipolar disorder, provided by a number of twin studies and gene linkage studies.

The monozygotic concordance rate for the disorder is 70%. This means that if a person has the disorder, an identical twin has a 70% likelihood of having the disorder as well. Dizygotic twins have a 23% concordance rate. These concordance rates are not universally replicated in the literature; recent studies have shown rates of around 40% for monozygotic and <10% for dizygotic twins (see Kieseppa, 2004[48] and Cardno, 1999[49]).

In 2003 , a group of American and Canadian researchers published a paper that used gene linkage techniques to identify a mutation in the GRK3 gene as a possible cause of up to 10% of cases of bipolar disorder. This gene is associated with a kinase enzyme called G protein receptor kinase 3, which appears to be involved in dopamine metabolism, and may provide a possible target for new drugs for bipolar disorder.[50]

A 2007 gene-linkage study by an international team coordinated by the NIMH has identified a number of genes as likely to be involved in the etiology of bipolar disorder, suggesting that bipolar disorder may be a polygenic disease. The researchers at NIMH have found a correlation between DGKH (diacylglycerol kinase eta) and bipolar disorder. The portion of the genome that encodes DGKH, a key protein in the lithium-sensitive phosphatidyl inositol pathway [51].


Treatment
Main article: Treatment of bipolar disorder
Currently, bipolar disorder cannot be cured, instead the emphasis of treatment is on effective management of acute episodes and prevention of further episodes by use of pharmacological and psychotherapeutic techniques.

Hospitalization may occur, especially with manic episodes. This can be voluntary or (if mental health legislation allows it) involuntary (called civil or involuntary commitment). Long-term inpatient stays are now less common due to deinstitutionalization, although can still occur.[52] Following (or in lieu of) a hospital admission, support services available can include drop-in centers, visits from members of a community mental health team or Assertive Community Treatment team, supported employment[53] and patient-led support groups.


Medication
The mainstay of treatment is a mood stabilizer medication; these comprise several unrelated compounds which have been shown to be effective in preventing relapses of manic, or in the one case, depressive episodes. The first known and current "gold standard" mood stabilizer is lithium,[54] while almost as widely used is sodium valproate,[55] originally used as an anticonvulsant. Other anticonvulsants used in bipolar disorder include carbamazepine, reportedly more effective in rapid cycling bipolar disorder, and lamotrigine, which is the first one to be shown to be of benefit in bipolar depression.[56]

Treatment of the agitation in acute manic episodes has often required the use of antipsychotic medications, such as chlorpromazine, olanzapine and thioridazine. More recently, olanzapine has been approved as an effective monotherapy for the maintenance of bipolar disorder.[57] A head-to-head randomized control trial in 2005 has also shown olanzapine monotherapy to be as effective and safe as lithium in prophylaxis.[58]

The use of antidepressants in bipolar disorder has been debated, with some studies reporting a worse outcome with their use. However mood stabilizers are of limited effectiveness in depressive episodes.


Research
Main article: Bipolar disorders research
The following studies are ongoing, and are recruiting volunteers:

The Maudsley Bipolar Twin Study, based at the Institute of Psychiatry in London is conducting research about the genetic basis of bipolar disorder using twin methodology. Currently recruiting volunteers: identical and non-identical twins pairs, where either one or both twins has a diagnosis of bipolar I or II.

The Maudsley Bipolar eMonitoring Project, another research study based at the Institute of Psychiatry in London, is conducting novel research on electronic monitoring methodologies (electronic mood diaries and actigraphy) for tracking bipolar symptom fluctuations in Bipolar individuals who are interested in self-managing their condition. The study is currently recruiting volunteers from all over the world (see Remote eMonitoring)


Medical imaging
Researchers are using advanced brain imaging techniques to examine brain function and structure in people with bipolar disorder, particularly using the functional MRI and positron emission tomography. An important area of neuroimaging research focuses on identifying and characterizing networks of interconnected nerve cells in the brain, interactions among which form the basis for normal and abnormal behaviors. Researchers hypothesize that abnormalities in the structure and/or function of certain brain circuits could underlie bipolar and other mood disorders, and studies have found anatomical differences in areas such as the prefrontal cortex[59] and hippocampus.

Better understanding of the neural circuits involved in regulating mood states, and genetic factors such as the cadherin gene FAT linked to bipolar disorder,[60] may influence the development of new and better treatments, and may ultimately aid in early diagnosis and even a cure


New treatments
In late 2003 , researchers at McLean Hospital found tentative evidence of improvements in mood during echo-planar magnetic resonance spectroscopic imaging (EP-MRSI), and attempts are being made to develop this into a form which can be evaluated as a possible treatment.[61][62]

NIMH has initiated a large-scale study at 20 sites across the United States to determine the most effective treatment strategies for people with bipolar disorder. This study, the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD), will follow patients and document their treatment outcome for 5-8 years. For more information, visit the Clinical Trials page of the NIMH Web site.[63]

Transcranial magnetic stimulation is another fairly new technique being studied.

Pharmaceutical research is extensive and ongoing, as seen at clinicaltrials.gov.


Prognosis
A good prognosis results from good treatment, which, in turn, results from an accurate diagnosis. Because bipolar disorder continues to have a high rate of both under-diagnosis and misdiagnosis, it is often difficult for individuals with the condition to receive timely and competent treatment.

Bipolar disorder can be a severely disabling medical condition. However, with appropriate treatment, many individuals with bipolar disorder can live full and satisfying lives. Persons with bipolar disorder are likely to have periods of normal or near normal functioning between episodes.

Ultimately one's prognosis depends on many factors, which are, in fact, under the individual's control: the right medicines; the right dose of each; a very informed patient; a good working relationship with a competent medical doctor; a competent, supportive, and warm therapist; a supportive family or significant other; and a balanced lifestyle including a regulated stress level, regular exercise and regular sleep and wake times.[citation needed]

There are obviously other factors that lead to a good prognosis, as well, such as being very aware of small changes in one's energy, mood, sleep and eating behaviors, as well as having a plan in conjunction with one's doctor for how to manage subtle changes that might indicate the beginning of a mood swing. Some people find that keeping a log of their moods can assist them in predicting changes.[citation needed]


Recurrence
Even when on medication, some people may still experience weaker episodes, or have a complete manic or depressive episode. In fact, a recent study found bipolar disorder to be "characterized by a low rate of recovery, a high rate of recurrence, and poor interepisodic functioning." Worse, the study confirmed the seriousness of the disorder as "the standardized all-cause mortality ratio among patients with BD is increased approximately 2-fold." Bipolar disorder is currently regarded "as possibly the most costly category of mental disorders in the United States."[64]

The following behaviors can lead to depressive or manic recurrence:

Discontinuing or lowering one's dose of medication, without consulting one's physician.
Being under- or over-medicated. Generally, taking a lower dosage of a mood stabilizer can lead to relapse into mania. Taking a lower dosage of an antidepressant, may cause the patient to relapse into depression, while higher doses can cause destabilization into mixed-states or mania.
Taking hard drugs—recreationally or not—such as cocaine, alcohol, amphetamines, or opiates. These can cause the condition to worsen.
An inconsistent sleep schedule can destabilize the illness. Too much sleep (possibly caused by medication) can lead to depression, while too little sleep can lead to mixed states or mania.
Caffeine can cause destabilization of mood toward irritability, dysphoria, and mania. Anecdotal evidence seems to suggest that lower dosages of caffeine can have effects ranging from anti-depressant to mania-inducing.
Inadequate stress management and poor lifestyle choices. If unmedicated, excessive stress can cause the individual to relapse. Medication raises the stress threshold somewhat, but too much stress still causes relapse.
Often bipolar individuals are subject to self-medication, the most common drugs being alcohol, and marijuana. Sometimes they may also turn to hard drugs. Studies show that tobacco smoking induces a calming effect on most bipolar people, and a very high percentage suffering from the disorder smoke. [7]
Recurrence can be managed by the sufferer with the help of a close friend, based on the occurrence of idiosyncratic prodromal events[65] That is, by noticing which moods, activities / behaviours or thinking process / thought content typically occur at the outset of their episodes. They can then take planned steps to slow or reverse the onset of illness, or take action to prevent the episode causing damage to important aspects of their life.[66]


Mortality
"Mortality studies have documented an increase in all-cause mortality in patients with BD. A newly established and rapidly growing database indicates that mortality due to chronic medical disorders (eg, cardiovascular disease) is the single largest cause of premature and excess deaths in BD. The standardized mortality ratio from suicide in BD is estimated to be approximately 18 to 25, further emphasizing the lethality of the disorder.".[67]

Although many people with bipolar disorder who attempt suicide never actually complete it, the annual average suicide rate in males and females with diagnosed bipolar disorder (0.4%) is 10 to more than 20 times that in the general population[68]

Individuals with bipolar disorder tend to become suicidal, especially during mixed states such as dysphoric mania and agitated depression.[citation needed] Persons suffering from Bipolar II have high rates of suicide compared to persons suffering from other mental health conditions, including Major Depression. Major Depressive episodes are part of the Bipolar II experience, and there is evidence that sufferers of this disorder spend proportionally much more of their life in the depressive phase of the illness than their counterparts with Bipolar I Disorder (Akiskal & Kessler, 2007).
http://en.wikipedia.org/wiki/Bipolar_disorder
 
.
What Is Sleep Apnea?

What Is Sleep Apnea?

Sleep apnea is a common disorder that can be very serious. In sleep apnea, your breathing stops or gets very shallow while you are sleeping. Each pause in breathing typically lasts 10 to 20 seconds or more. These pauses can occur 20 to 30 times or more an hour.

The most common type of sleep apnea is obstructive sleep apnea. During sleep, enough air cannot flow into your lungs through your mouth and nose even though you try to breathe. When this happens, the amount of oxygen in your blood may drop. Normal breaths then start again with a loud snort or choking sound.

When your sleep is upset throughout the night, you can be very sleepy during the day. With sleep apnea, your sleep is not restful because:

These brief episodes of increased airway resistance (and breathing pauses) occur many times.
You may have many brief drops in the oxygen levels in your blood.
You move out of deep sleep and into light sleep several times during the night, resulting in poor sleep quality.
People with sleep apnea often have loud snoring. However, not everyone who snores has sleep apnea. Some people with sleep apnea don&#8217;t know they snore.

Sleep apnea happens more often in people who are overweight, but even thin people can have it.
Most people don&#8217;t know they have sleep apnea. They don&#8217;t know that they are having problems breathing while they are sleeping.
A family member and/or bed partner may notice the signs of sleep apnea first.
Untreated sleep apnea can increase the chance of having high blood pressure and even a heart attack or stroke. Untreated sleep apnea can also increase the risk of diabetes and the risk for work-related accidents and driving accidents.
February 2006
http://www.nhlbi.nih.gov/health/dci/Diseases/SleepApnea/SleepApnea_WhatIs.html
 
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Sleep apnea
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Sleep apnea
Classification & external resources ICD-10 G47.3
ICD-9 327.23 confirmed diagnosis
Pickwickian syndrome
Classification & external resources ICD-10 E66.2
ICD-9 278.8
Sleep apnea, sleep apnoea or sleep apn&#339;a is a sleep disorder characterized by pauses in breathing during sleep. These episodes, called apneas (literally, "without breath"), each last long enough so one or more breaths are missed, and occur repeatedly throughout sleep. The standard definition of any apneic event includes a minimum 10 second interval between breaths, with either a neurological arousal (3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2), or a blood oxygen desaturation of 3-4 percent or greater, or both arousal and desaturation. Sleep apnea is diagnosed with an overnight sleep test called a polysomnogram.

Clinically significant levels of sleep apnea are defined as 5 events of any type or greater per hour of sleep time (from the polysomnogram). There are two distinct forms of sleep apnea: Central and Obstructive. Breathing is interrupted by the lack of effort in Central Sleep Apnea; in Obstructive Sleep Apnea, breathing is interrupted by a physical block to airflow despite effort. In Mixed Sleep Apnea, there is a transition from central to obstructive features during the events themselves.

Regardless of type, the individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). Symptoms may be present for years, even decades without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance. The definitive diagnosis of sleep apnea is made by polysomnography.

Contents [show]
1 Obstructive sleep apnea
1.1 Laboratory findings
1.1.1 Polysomnography
1.1.2 Home oximetry
1.2 Populations at risk
1.2.1 Adults
1.2.2 Children
1.2.3 Common signs and symptoms
1.2.4 Craniofacial syndromes
1.2.5 Pharyngeal flap surgery may cause obstructive sleep apnea
1.3 Treatment
1.3.1 Physical intervention
1.3.2 Pharmaceuticals
1.3.3 Neurostimulation
1.3.4 Surgical intervention
1.3.4.1 Special situation: surgery and anesthesia in patients with sleep apnea syndrome
1.3.5 Alternative treatments
2 Central sleep apnea
2.1 Laboratory findings
2.2 Clinical details
2.3 Mixed apnea and complex sleep apnea
2.4 Treatment
3 History
4 Symptoms, signs and sequelae
5 Notes
6 References
7 External links



[edit] Obstructive sleep apnea
Obstructive sleep apnea (OSA) is not only much more frequent than Central Sleep Apnea, it is a common condition in many parts of the world. If studied carefully in a sleep lab by polysomnography, approximately 1 in 5 American adults has at least mild OSA. [1] Since the muscle tone of the body ordinarily relaxes during sleep, and since, at the level of the throat, the human airway is composed of walls of soft tissue, which can collapse, it is easy to understand why breathing can be obstructed during sleep - particularly in the obese. Although many individuals experience episodes of obstructive sleep apnea at some point in life, a much smaller percentage of people are afflicted with chronic severe obstructive sleep apnea.

Normal sleep/wakefulness in adults has been given 6 distinct stages, numbered 1-4 and including REM sleep (Stage 5) and Wake. The deeper stages (3-4) are required for the physically restorative effects of sleep and in pre-adolescents are the focus of release for human growth hormone. Stages 2 and REM, which combined are 70&#37; of an average person's total sleep time, are more associated with mental recovery and maintenance. During REM sleep in particular, muscle tone of the throat and neck, as well as the vast majority of all skeletal muscles, is almost completely attenuated, allowing the tongue and soft palate/oropharynx to relax, and in the case of sleep apnea, to impede the flow of air to a degree ranging from light snoring to complete collapse. In the cases where airflow is reduced to a degree where blood oxygen levels fall, or the physical exertion to breathe is too great, neurological mechanisms trigger a sudden interruption of sleep, called a neurological arousal. These arousals may or may not result in complete awakening, but can have a significant negative effect on the restorative quality of sleep. In significant cases of obstructive sleep apnea, one consequence is sleep deprivation due to the repetitive disruption and recovery of sleep activity. This sleep interruption in stages 3 and 4 (also collectively called Slow-Wave Sleep), can interfere with normal growth patterns, healing, and immune response, especially in children and young adults.

Many people experience elements of obstructive sleep apnea for only a short period of time. This can be the result of an upper respiratory infection that causes nasal congestion, along with swelling of the throat, or tonsillitis that temporarily produces very enlarged tonsils. The Epstein-Barr virus, for example, is known to be able to dramatically increase the size of lymphoid tissue during acute infection, and obstructive sleep apnea is fairly common in acute cases of severe infectious mononucleosis. Temporary spells of obstructive sleep apnea syndrome may also occur in individuals who are under the influence of a drug (such as alcohol) that may relax their body tone excessively and interfere with normal arousal from sleep mechanisms.


[edit] Laboratory findings

[edit] Polysomnography

Two minute epoch representing continuous OSA. Click on this image for larger version.Results of polysomnography in obstructive sleep apnea show pauses in breathing. As in Central Apnea, pauses are followed by a relative decrease in blood oxygen and an increase in the blood carbon dioxide. Whereas in central sleep apnea the body's motions of breathing stop, in obstructive sleep apnea the chest not only continues to make the movements of inhalation, the movements typically become even more pronounced. Monitors for airflow at the nose and mouth show the dynamics of airflow[clarify], but efforts to breathe are not only present, they are often exaggerated. The chest muscles and diaphragm contract and the entire body may thrash and struggle.

Obstructive sleep apnea is the most common category of sleep-disordered breathing. The prevalence of OSA among the adult population in western Europe and North America has not been confidently established, but in the mid-1990s was estimated to be 3-4% of women and 6-7% of men. However, with the increasing trends in western societies toward obesity, OSA may be significantly under-reported, even as public and clinical awareness of the disorder increases.

An "event" can be either an apnea, characterised by complete cessation of airflow for at least 10 seconds, or a hypopnea in which airflow decreases by 50 percent for 10 seconds or decreases by 30 percent if there is an associated decrease in the oxygen saturation or an arousal from sleep (American Academy of Sleep Medicine Task Force, 1999). To grade the severity of sleep apnea the number of events per hour is reported as the apnea-hypopnea index (AHI). An AHI of less than 5 is considered normal. An AHI of 5-15 is mild; 15-30 is moderate and more than 30 events per hour characterizes severe sleep apnea.


[edit] Home oximetry
In patients who are at high likelihood of having OSA, a randomized controlled trial found that home oximetry may be adequate and easier to obtain than formal polysomnography[2]. High probability patients were indentified by Epworth Sleepiness Scale (ESS) of 10 or greater and a Sleep Apnea Clinical Score (SACS) of 15 or greater.[3]


[edit] Populations at risk
Individuals with decreased muscle tone, increased soft tissue around the airway, and structural features that give rise to a narrowed airway are at high risk for obstructive sleep apnea. Men, whose anatomy is typified by increased body mass in the torso and neck, are more typical sleep apnea sufferers, especially through middle age and older. Adult women suffer typically less frequently and to a lesser degree than men do, owing partially to physiology, but possibly to emerging links to levels of progesterone. Prevalence in post-menopausal women approaches that of men in the same age range.


[edit] Adults
In adults, the most typical individual with obstructive sleep apnea syndrome is obese, with particular heaviness at the face and neck. The hallmark symptom of obstructive sleep apnea syndrome in adults is excessive daytime sleepiness. Typically, an adult or adolescent with severe long-standing obstructive sleep apnea will fall asleep for very brief periods in the course of usual daytime activities if given any opportunity to sit or rest. This behavior may be quite dramatic, sometimes occurring during conversations with others at social gatherings.


[edit] Children
Although this so called "hyper-somnolence" (excessive sleepiness) may also occur in children, it is not at all typical of younger children with sleep apnea. Toddlers and young children with severe obstructive sleep apnea instead ordinarily behave as if "over-tired" or "hyper". Adults and children with very severe obstructive sleep apnea also differ in typical body habitus. Adults are generally heavy, with particularly short and heavy necks. Young children, on the other hand, are generally not only thin but may have "failure to thrive", where growth is reduced. Poor growth occurs for two reasons: the work of breathing is high enough so that calories are burned at high rates even at rest, and the nose and throat are so obstructed that eating is both tasteless and physically uncomfortable. Obstructive sleep apnea in children, unlike adults, is almost always caused by obstructive tonsils and adenoids and is usually cured with tonsillectomy and adenoidectomy.

Never forget that this problem can also be caused by excessive weight. The symptoms are more like the symptoms adults feel; restlessness, exhaustion, and more.


[edit] Common signs and symptoms
(The signs and symptoms that follow apply to both adults and children suffering with sleep apnea)

Additional signs of obstructive sleep apnea include restless sleep, and loud snoring (with periods of silence followed by gasps). Other symptoms are non-specific: morning headaches, trouble concentrating, irritability, forgetfulness, mood or behavior changes, decreased sex drive, increased heart rate, anxiety, depression, increased frequency of urination, nocturia (getting up during the night to urinate), esophageal reflux and heavy sweating at night.

The most serious consequence of obstructive sleep apnea is to the heart. In severe and prolonged cases, there are increases in pulmonary pressures that are transmitted to the right side of the heart. This can result in a severe form of congestive heart failure (cor pulmonale).


[edit] Craniofacial syndromes
There are patterns of unusual facial features that occur in recognizable syndromes. Some of these craniofacial syndromes are genetic, others are from unknown causes. In many craniofacial syndromes, the features that are unusual involve the nose, mouth and jaw, or resting muscle tone, and put the individual at risk for obstructive sleep apnea syndrome.

Down Syndrome is one such syndrome. In this chromosomal abnormality, several features combine to make the presence of obstructive sleep apnea more likely. The specific features in Down Syndrome that predispose to obstructive sleep apnea include: relatively low muscle tone, narrow nasopharynx, and large tongue. Obesity and enlarged tonsils and adenoids, conditions that occur commonly in the western population, are much more likely to be obstructive in a person with these features than without them. Obstructive Sleep Apnea does occur even more frequently in people with Down Syndrome than in the general population. A little over 50% of all people with Down Syndrome suffer from obstructive sleep apnea (de Miguel-D&#237;ez, et al 2003), and some physicians advocate routine testing of this group (Shott, et al 2006).

In other craniofacial syndromes, the abnormal feature may actually improve the airway- but its correction may put the person at risk for obstructive sleep apnea after surgery, when it is modified. Cleft palate syndromes are such an example. During the newborn period, all humans are obligate nasal breathers. The palate is both the roof of the mouth and the floor of the nose. Having an open palate may make feeding difficult, but generally does not interfere with breathing, in fact - if the nose is very obstructed an open palate may relieve breathing. There are a number of clefting syndromes in which the open palate is not the only abnormal feature, additionally there is a narrow nasal passage - which may not be obvious. In such individuals, closure of the cleft palate- whether by surgery or by a temporary oral appliance, can cause the onset of obstruction.

Skeletal advancement in an effort to physically increase the pharyngeal airspace is often an option for craniofacial patients with upper airway obstruction and small lower jaws (mandibles). These syndromes include Treacher Collins Syndrome and Pierre Robin Sequence. Mandibular advancement surgery is often just one of the modifications needed to improve the airway, others may include reduction of the tongue, tonsillectomy or modified uvulopalatoplasty.


[edit] Pharyngeal flap surgery may cause obstructive sleep apnea
Obstructive sleep apnea is a serious complication that seems to be most frequently associated with pharyngeal flap surgery, compared to other procedures for treatment of velopharyngeal inadequacy (VPI).[4] In OSA, recurrent interruptions of respiration during sleep are associated with temporary airway obstruction. Following pharyngeal flap surgery, depending on size and position, the flap itself may have an &#8220;obturator&#8221; or obstructive effect within the pharynx during sleep, blocking ports of airflow and hindering effective respiration.[5][6] There have been documented instances of severe airway obstruction, and reports of post-operative OSA continue to increase as healthcare professionals (i.e. physicians, speech language pathologists) become more educated about this possible dangerous condition.[7] Subsequently, in clinical practice, concerns of OSA have matched or exceeded interest in speech outcomes following pharyngeal flap surgery.

The surgical treatment for velopalatal insufficiency may cause obstructive sleep apnea syndrome. When velopalatal insufficiency is present, air leaks into the nasopharynx even when the soft palate should close off the nose. A simple test for this condition can be made by placing a tiny mirror at the nose, and asking the subject to say "P". This p sound, a plosive, is normally produced with the nasal airway closed off - all air comes out of the pursed lips, none from the nose. If it is impossible to say the sound without fogging a nasal mirror, there is an air leak - reasonable evidence of poor palatal closure. Speech is often unclear due to inability to pronounce certain sounds. One of the surgical treatments for velopalatal insufficiency involves tailoring the tissue from the back of the throat and using it to purposefully cause partial obstruction of the opening of the nasopharynx. This may actually cause obstructive sleep apnea syndrome in susceptible individuals, particularly in the days following surgery, when swelling occurs (see below: Special Situation: Anesthesia and Surgery)

AHI Rating
<5 Normal
5-15 Mild
15-30 Moderate
>30 Severe

[edit] Treatment
There are a variety of treatments for obstructive sleep apnea, depending on an individual&#8217;s medical history, the severity of the disorder and, most importantly, the specific cause of the obstruction.

In acute infectious mononucleosis, for example, although the airway may be severely obstructed in the first 2 weeks of the illness, the presence of lymphoid tissue (suddenly enlarged tonsils and adenoids) blocking the throat is usually only temporary. A course of anti-inflammatory steroids such as prednisone (or another kind of glucocorticoid drug) is often given to reduce this lymphoid tissue. Although the effects of the steroids are short term, in most affected individuals, the tonsillar and adenoidal enlargement are also short term, and will be reduced on its own by the time a brief course of steroids is completed. In unusual cases where the enlarged lymphoid tissue persists after resolution of the acute stage of the Epstein-Barr infection, or in which medical treatment with anti-inflammatory steroids does not adequately relieve breathing, tonsillectomy and adenoidectomy may be urgently required.

Most children with obstructive sleep apnea have the problem on the basis of chronically enlarged tonsils and adenoids. In these children, tonsillectomy and adenoidectomy is curative. The operation may be far from trivial, however, in the worst cases, in which growth is reduced and abnormalities of the right heart may have developed. Even in these extreme cases, however, the surgery tends to cure not only the apnea and upper airway obstruction - but to allow subsequent normal growth and development. Once the high end-expiratory pressures are relieved, the cardiovascular complications reverse themselves. The postoperative period in these children requires special precautions (see surgery and obstructive sleep apnea syndrome below).

The treatment for obstructive sleep apnea in the case of adults with poor oropharyngeal airways secondary to heavy upper body type is varied. Unfortunately, in this most common type of obstructive sleep apnea, unlike some of the cases discussed above, reliable cures are not the rule.

Some treatments involve lifestyle changes, such as avoiding alcohol and medications that relax the central nervous system (for example, sedatives and muscle relaxants), losing weight, and quitting smoking. Some people are helped by special pillows or devices that keep them from sleeping on their backs, or oral appliances to keep the airway open during sleep. If these conservative methods are inadequate, doctors often recommend continuous positive airway pressure (CPAP), in which a face mask is attached to a tube and a machine that blows pressurized air into the mask and through the airway to keep it open. There are also surgical procedures that can be used to remove and tighten tissue and widen the airway, but the success rate is not high. Some individuals may need a combination of therapies to successfully treat their sleep apnea.


[edit] Physical intervention
The most widely used current therapeutic intervention is positive airway pressure whereby a breathing machine pumps a controlled stream of air through a mask worn over the nose, mouth, or both. The additional pressure splints or holds open the relaxed muscles, just as air in a balloon inflates it. There are several variants:

(CPAP), or continuous positive airway pressure, in which a controlled air compressor generates an airstream at a constant pressure. This pressure is prescribed by the patient's physician, based on an overnight test or titration. Newer CPAP models are available which slightly reduce pressure upon exhalation to increase patient comfort and compliance. CPAP is the most common treatment for obstructive sleep apnea.
(VPAP), or variable positive airway pressure, also known as bilevel or BiPAP, uses an electronic circuit to monitor the patient's breathing, and provides two different pressures, a higher one during inhalation and a lower pressure during exhalation. This system is more expensive, and is sometimes used with patients who have other coexisting respiratory problems and/or who find breathing out against an increased pressure to be uncomfortable or disruptive to their sleep.
(APAP), or automatic positive airway pressure, is the newest form of such treatment. An APAP machine incorporates pressure sensors and a computer which continuously monitors the patient's breathing performance. It adjusts pressure continuously, increasing it when the user is attempting to breathe but cannot, and decreasing it when the pressure is higher than necessary. Although FDA approved, these devices are still considered experimental by many, and are not covered by most insurance plans.
A second type of physical intervention, a Mandibular advancement splint (MAS), is sometimes prescribed for mild or moderate sleep apnea sufferers. The device is a mouthguard similar to those used in sports to protect the teeth. For apnea patients, it is designed to hold the lower jaw slightly down and forward relative to the natural, relaxed position. This position holds the tongue farther away from the back of the airway, and may be enough to relieve apnea or improve breathing for some patients. The FDA accepts only 16 oral appliances for the treatment of sleep apnea. A listing is available at their website

Oral appliance therapy is less effective than CPAP, but is more 'user friendly'. Side-effects are common, but rarely is the patient aware of them.


[edit] Pharmaceuticals
There are no effective drug-based treatment for obstructive sleep apnea.

Oral administration of the methylxanthine theophylline (chemically similar to caffeine) can reduce the number of episodes of apnea, but can also produce side effects such as palpitations and insomnia. Theophylline is generally ineffective in adults with OSA, but is sometimes used to treat Central Sleep Apnea (see below), and infants and children with apnea.

When other treatments do not completely treat the OSA, drugs are sometimes prescribed to treat a patient's daytime sleepiness or somnolence. These range from stimulants such as amphetamines to modern anti-narcoleptic medicines. The anti-narcoleptic modafinil is seeing increased use in this role as of 2004.

In most cases, weight loss will reduce the number and severity of apnea episodes. In the morbidly obese, a major loss of weight (such as what occurs after bariatric surgery) can sometimes cure the condition.


[edit] Neurostimulation
This article or section needs to be updated.
Parts of this article or section have been identified as no longer being up to date.
Please update the article to reflect recent events, and remove this template when finished.


Many researchers believe that OSA is at root a neurological condition, in which nerves that control the tongue and soft palate fail to sufficiently stimulate those muscles, leading to over-relaxation and airway blockage. A few experiments and trial studies have explored the use of pacemakers and similar devices, programmed to detect breathing effort and deliver gentle electrical stimulation to the muscles of the tongue.

This is not a common mode of treatment for OSA patients as of 2004, but it is an active field of research.


[edit] Surgical intervention
A number of different surgeries are available to improve the size or tone of a patient's airway. For decades, tracheostomy was the only effective treatment for sleep apnea. It is used today only in rare, intractable cases that have withstood other attempts at treatment. Modern operations employ one or more of several options, tailored to each patient's needs. Long term success rates are low, resulting in most doctors favoring CPAP.

Nasal surgery, including turbinectomy (removal or reduction of a nasal turbinate), or straightening of the nasal septum, in patients with nasal obstruction or congestion which reduces airway pressure and complicates OSA.
Tonsilectomy and/or adenoidectomy in an attempt to increase the size of the airway.
Removal or reduction of parts of the soft palate and some or all of the uvula, such as uvulopalatopharyngoplasty (UPPP) or laser-assisted uvulopalatoplasty (LAUP). Modern variants of this procedure sometimes use radiofrequency waves to heat and remove tissue.
Reduction of the tongue base, either with laser excision or radiofrequency ablation.
Genioglossus Advancement, in which a small portion of the lower jaw that attaches to the tongue is moved forward, to pull the tongue away from the back of the airway.
Hyoid Suspension, in which the hyoid bone in the neck, another attachment point for tongue muscles, is pulled forward in front of the larynx.
Maxillomandibular advancement (MMA). A more invasive surgery usually only tried in difficult cases where other surgeries have not relieved the patient's OSA, or where an abnormal facial structure is suspected as a root cause. In MMA, the patient's upper and lower jaw are detached from the skull, moved forward, and reattached with pins and/or plates.
Pillar procedure, three small inserts are injected into the soft palate to offer support, potentially reducing snoring in mild to moderate sleep apnea[8]

[edit] Special situation: surgery and anesthesia in patients with sleep apnea syndrome
Many drugs and agents used during surgery to relieve pain and depress consciousness remain in the body at low amounts for hours or even days afterwards. In an individual with either Central, Obstructive or Mixed Sleep Apnea, these low doses may be enough to cause life-threatening irregularities in breathing.

Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.

Surgery on the mouth and throat, as well as dental surgery and procedures, can result in postoperative swelling of the lining of the mouth and other areas that affect the airway. Even when the surgical procedure is designed to improve the airway, such as tonsillectomy and adenoidectomy or tongue reduction - swelling may negate some of the effects in the immediate postoperative period.

Individuals with sleep apnea generally require more intensive monitoring after surgery for these reasons.


[edit] Alternative treatments
Breathing techniques, such as those used in Yoga or the Buteyko method may be of some use in treating sleep apnea. These breathing exercises encourage and strengthen nasal breathing, both during the day and nocturnally, which allows easier, deeper and more relaxed inhalation.


[edit] Central sleep apnea
In pure Central Sleep Apnea or Cheyne-Stokes Respiration, the brain's respiratory control centers are imbalanced during sleep. Blood levels of carbon dioxide, and the neurological feedback mechanism that monitors it do not react quickly enough to maintain an even respiratory rate, with the entire system cycling between apnea and hyperpnea, even during wakefulness. The sleeper stops breathing, and then starts again. There is no effort made to breathe during the pause in breathing: there are no chest movements and no struggling. After the episode of apnea, breathing may be faster (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases and absorb more oxygen.

While sleeping, a normal individual is "at rest", as far as cardiovascular workload is concerned. Breathing is regular in a healthy person during sleep, and oxygen levels and carbon dioxide levels in the bloodstream stay fairly constant. The respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. Any sudden drop in oxygen or excess of carbon dioxide (even if tiny) strongly stimulates the brain's respiratory centers to breathe. In central sleep apnea, the basic neurological controls for breathing rate malfunctions and fails to give the signal to inhale, causing the individual to miss one or more cycles of breathing. If the pause in breathing is long enough, the percentage of oxygen in the circulation will drop to a lower than normal level (hypoxia) and the concentration of carbon dioxide will build to a higher than normal level (hypercapnia). In turn, these conditions of hypoxia and hypercapnia will trigger additional effects on the body. Brain cells need constant oxygen to live; and, if the level of blood oxygen goes low enough for long enough, the terrible consequences of brain damage and even death will occur. Fortunately, Central Sleep Apnea is more often a chronic condition that causes much milder effects than sudden death. The exact effects of the condition will depend on how severe the apnea is, and the individual characteristics of the person having the apnea. Several examples are discussed below, and more about the nature of the condition is presented in the section on Clinical Details.

In any person, hypoxia and hypercapnia have certain common effects on the body. The heart rate will increase, unless there are such severe co-existing problems with the heart muscle itself or the autonomic nervous system that makes this compensatory increase impossible. The more translucent areas of the body will show a bluish or dusky cast from cyanosis, which is the change in hue that occurs due to lack of oxygen in the blood ("turning blue"). Overdoses of drugs that are respiratory depressants (such as heroin, and other opiates) kill by damping the activity of the brain's respiratory control centers. In Central Sleep Apnea, the effects of sleep alone can remove the brains' mandate for the body to breathe. Even in severe cases of central sleep apnea, the effects almost always result in pauses that make breathing irregular, rather than cause the total cessation of breathing.

Normal Respiratory Drive: After exhalation, the blood level of oxygen decreases and that of carbon dioxide increases. Exchange of gasses with a lungful of fresh air is necessary to replenish oxygen and rid the bloodstream of built-up carbon dioxide. How do the changing blood levels of oxygen and carbon dioxide result in a breath? In any healthy animal, including humans, oxygen and carbon dioxide receptors in the blood stream (called chemoreceptors) send nerve impulses to the brain, which then signals reflex opening of the larynx (so that the opening between the vocal cords enlarges) and movements of the rib cage muscles and diaphragm. These muscles expand the thorax (chest cavity) so that a partial vacuum is made within the lungs and air rushes in to fill it. The body inhales.
Physiologic effects of Central Apnea: During central apneas, the central respiratory drive is absent, and the brain does not respond to changing blood levels of the respiratory gases. No breath is taken despite the normal signals to inhale. The immediate effects of Central Sleep apnea on the body depend on how long the failure to breathe endures. At worst, central sleep apnea may cause sudden death. Short of death, drops in blood oxygen may trigger seizures- even in the absence of epilepsy. In people with epilepsy, the hypoxia caused by apnea may trigger seizures that had previously been well controlled by medications. In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery disease, a severe drop in blood oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction).With longstanding recurrent episodes of apnea, over months and years, increases in carbon dioxide levels may change the pH of the blood enough to cause a metabolic acidosis.

[edit] Laboratory findings
AHI Rating
<5 Normal
5-15 Mild
15-30 Moderate
>30 Severe
Polysomnography of sleep apnea shows pauses in breathing that are followed by drops in blood oxygen and increases in blood carbon dioxide. In adults, a pause must last 10 seconds to be scored as an apnea. However in young children, who normally breathe at a much faster rate than adults, the pause may be many seconds shorter and still be considered apnea. The cessation of airflow in central sleep apnea has an association with no physical attempts to breathe. On polysomnograms, there is an absence of rib cage and abdominal movements while airflow ceases at the nose and lips. Obstructive sleep apnea show pauses in breathing for at least 10 seconds causing a decrease in blood oxygen and associates with physical attempts to breathe.

Hypopneas in adults are defined as a 50% reduction in air flow for more than 10 s, followed by a 4% desaturation, and/or arousal. The Apnea- Hypopnea Index (AHI) is expressed as the number of apneas and hypopneas per hour of sleep.


[edit] Clinical details
Any individual, no matter how healthy, who is given enough of a central respiratory depressant drug will develop apnea on a central basis. Generally, drugs that are central respiratory depressants also have sedative effects, and so the individual taking a toxic dose of such a drug is likely to be asleep, or at least in an altered state of consciousness, when breathing becomes irregular. Alcohol is such a central respiratory depressant in large doses, so are opiates, barbiturates and many tranquilizers. Some individuals have abnormalities that predispose them to central sleep apnea. The treatment for the condition depends on its specific cause.

Similarly, in any person who has some form of sleep apnea (including obstructive sleep apnea), breathing irregularities during sleep can be dangerously aggravated by taking one of these drugs. Quantities that are normally considered safe may cause the person with chronic sleep apnea to stop breathing altogether. Should these individuals have general anesthesia, for example, they require prolonged monitoring after initial recovery, as compared to a person with no history of sleep apnea, because apnea is likely to occur with even low levels of the drugs in their system.

Premature infants with immature brains and reflex systems are at high risk for central sleep apnea syndrome, even if these babies are otherwise healthy. Fortunately, those premature babies who have the syndrome will generally outgrow it as they mature, providing they receive careful enough monitoring and supportive care during infancy to survive. Because of the propensity toward apnea, medications that can cause respiratory drive depression are either not given to premature infants, or given under careful monitoring, with equipment for resuscitation immediately available. Such precautions are routinely taken for premature infants after general anesthesia. Caffeine has been found to help reduce apnea in preterm infants and to aid in care after general anesthesia.[9]

Sudden Infant Death Syndrome (SIDS), a tragedy in which an apparently healthy baby dies in sleep, is sometimes caused by central sleep apnea. There are probably many causes of SIDS &#8212; central apnea is only one of them.

Congenital Central Hypoventilation Syndrome: This rare, inborn condition involves a specific gene, PHOX2B. This homeobox gene guides maturation of the autonomic nervous system, and loss-of-function mutations lead to the failure of the brain to effectively control breathing during sleep in patients with the syndrome. There may be a pattern of recognizable facial features among individuals affected with this syndrome.[1]

Once almost uniformly fatal, congenital hypoventilation ("abnormally low ventilation") syndrome is now treatable. The children who have it must have tracheotomies and access to mechanical ventilation on respirators while sleeping, but most do not need to use a respirator while awake. The use of a diaphragmatic pacemaker may offer an alternative for some patients. When pacemakers have enabled some children to sleep without the use of a mechanical respirator, reported cases still required the tracheotomy to remain in place, because the vocal cords did not move apart with inhalation. This form of central sleep apnea has been called Ondine's curse. Now that some children with the syndrome have grown up, there is particular need for their avoidance of adolescent behaviors, such as alcohol use, which can easily be lethal.[10]

Adults suffering from congestive heart failure are at risk for a form of central sleep apnea called Cheyne-Stokes respiration. This is periodic breathing with recurrent episodes of apnea alternating with episodes of rapid breathing. In those who have it, Cheyne-Stokes respirations occur while both awake and asleep. There is good evidence that replacement of the failed heart (heart transplant) cures central apnea in these patients. The use of some medications that are respiratory stimulants decrease the severity of apnea in some patients.

References

1) Macey PM. Macey KE. Woo MA. Keens TG. Harper RM. Aberrant neural responses to cold pressor challenges in congenital central hypoventilation syndrome.[see comment]. [Journal Article] Pediatric Research. 57(4):500-9, 2005 Apr. 2) Bradley TD. Floras JS. Sleep apnea and heart failure: Part II: central sleep apnea. [Review] [55 refs] [Journal Article. Review] Circulation. 107(13):1822-6, 2003 April 8. 3) Mansfield DR. Solin P. Roebuck T. Bergin P. Kaye DM. Naughton MT. The effect of successful heart transplant treatment of heart failure on central sleep apnea.[see comment]. [Journal Article] Chest. 124(5):1675-81, 2003 Nov. 4)Javaheri S. Acetazolamide improves central sleep apnea in heart failure: a double-blind, prospective study. [Clinical Trial. Journal Article. Randomized Controlled Trial] American Journal of Respiratory & Critical Care Medicine. 173(2):234-7, 2006 Jan 15.


[edit] Mixed apnea and complex sleep apnea
Some people with sleep apnea have a combination of both types. When obstructive sleep apnea syndrome is severe and longstanding, episodes of central apnea sometimes develop. The exact mechanism of the loss of central respiratory drive during sleep in OSA is unknown, but is most commonly related to acid-base and CO2 feedback malfunctions stemming from heart failure. There is a constellation of diseases and symptoms relating to body mass, cardiovascular, respiratory, and occasionally, neurological dysfunction that have a synergistic effect in sleep-disordered breathing. The presence of central sleep apnea without an obstructive component is a common result of chronic opiate use (or abuse), due to the characteristic respiratory depression caused by large doses of narcotics.

Complex Sleep Apnea has recently been described by researchers as a novel presentation of sleep apnea. Patients with complex sleep apnea exhibit OSA, but upon application of positive airway pressure, the patient exhibits persistent central sleep apnea. This central apnea is most commonly noted while on CPAP therapy, after the obstructive component has been eliminated. This has long been seen in sleep laboratories, and has historically been managed either by CPAP or BiLevel therapy. Adaptive servo-ventilation modes of therapy have been introduced to attempt to manage this complex sleep apnea. Studies have demonstrated marginally superior performance of the adaptive servo ventilators in treating cheyne stokes breathing, however, no longitudinal studies have yet been published, nor have any results been generated which suggest any differential outcomes versus standard CPAP therapy. At the AARC 2006 in Las Vegas, NV, researchers reported successful treatment of hundreds of patients on Adapt SV therapy, however these results have not been reported in peer reviewed publications as of July, 2007.

An important finding by Derniaka, et al., (Chest 2007, 132) suggests that transient central apnea produced during CPAP titration (the so called "Complex Sleep Apnea") is "... transient and self-limited." The central apneas may in fact be secondary to sleep fragmentation during the titration process. As of July 2007, there has been no alternate convincing evidence produced that these central sleep apnea events associated with CPAP therapy for obstructive sleep apnea are of any significant pathophysiologic import.


[edit] Treatment
One method of treating central sleep apnea is with a special kind of positive airway pressure machine providing additional pressure during inhalation, including a Spontaneous / Time (ST) feature. This machine will automatically deliver pressure to the patient if it fails to detect a certain minimum number of breaths per minute.

Another method is the use of dental appliances or devices, such as a Tongue Retaining Device, Mandibular Repositioning Splints or dental appliances, such as a mandibular repositioning splints or devices, or MORA (mandibular orthopedic repositioning appliance.)


[edit] History
The first reports of what is now called obstructive sleep apnea, in the medical literature date only from 1965, when it was independently described by French and German investigators. However, the clinical picture of this condition has long been recognized as a character trait, without an understanding of the disease process. The term &#8220;Pickwickian syndrome&#8221; that is sometimes used for the syndrome, was coined by the famous early 20th Century physician, William Osler, who must have been a reader of Charles Dickens. The description of Joe, "the fat boy" in Dicken's novel, The Pickwick Papers, is an accurate clinical picture of adult obstructive sleep apnea syndrome.

The early reports of obstructive sleep apnea in the medical literature described individuals who were very severely affected, often presenting with severe hypoxemia, hypercapnia and congestive heart failure. Tracheostomy was the recommended treatment and, though it could be life-saving, post-operative complications in the stoma were frequent in these very obese and short-necked individuals.

The management of obstructive sleep apnea was revolutionized with the introduction of continuous positive airway pressure (CPAP), first described in 1981 by Colin Sullivan and associates in Sydney, Australia. The first models were bulky and noisy but the design was rapidly improved and by the late 1980s CPAP was widely adopted. The availability of an effective treatment stimulated an aggressive search for affected individuals and led to the establishment of hundreds of specialized clinics dedicated to the diagnosis and treatment of sleep disorders. Though many types of sleep problems are recognized, the vast majority of patients attending these centers have sleep disordered breathing.


[edit] Symptoms, signs and sequelae
This section summarizes the clinical picture and consequences of obstructive sleep apnea syndrome.

As already mentioned, snoring is almost a uniform finding in an individual with this syndrome, but many people snore without having apnea. Snoring is the turbulent sound of air moving through the back of the mouth, nose and throat. The loudness of the snoring is not indicative of the severity of obstruction, however. If the upper airways are tremendously obstructed, there may not be enough air movement to make much sound. Even the loudest snoring does not mean that an individual has sleep apnea syndrome. The sign that is most suggestive of sleep apneas occurs if snoring stops. If it does, along with breath, while the persons' chest and body tries to breathe - that is literally a description of an event in obstructive sleep apnea syndrome. When breathing starts again, there is typically a deep gasp, and then the resumption of snoring.

Sometimes, elevated arterial pressure (commonly called high blood pressure) is a sequela of obstructive sleep apnea syndrome.[11] When high blood pressure is caused by OSA, it is distinctive in that, unlike most cases of high blood pressure (so-called essential hypertension), the readings do not drop significantly when the individual is sleeping.[12] Stroke is associated with obstructive sleep apnea.[13]. Sleep apnea sufferers also have a 30% higher risk of heart attack or death[14].
http://en.wikipedia.org/wiki/Sleep_apnea
 
.
12 Common Cancer Myths Debunked Jeanna Bryner
LiveScience Staff Writer
LiveScience.com
Thu Jul 26, 11:20 AM ET



Numerous Americans believe a score of scientifically unproven claims about cancer, with some people thinking shampoo and underwire bras cause tumors.


A nationally representative telephone survey by the American Cancer Society of nearly 1,000 U.S. adults who had never been diagnosed with cancer revealed a surprising number agreed with inaccurate or unlikely statements about cancer risk and prevention statements.


Individuals with lower education levels were more likely to believe the myths. And men were more likely than women to be duped.


1. The risk of dying from cancer in the United States is increasing.
67.7 percent true (9.8&#37; don't know) The remainder knew this was false


2. Living in a polluted city is a greater risk for lung cancer than smoking a pack of cigarettes a day.
38.7% true (18.8% don't know)


3. Some injuries can cause cancer later in life.
37.2% true (20.9% don't know)


4. Electronic devices, like cell phones, can cause cancer in the people who use them.
29.7% true (24.7% don't know)


5. What someone does as a young adult has little effect on their chance of getting cancer later in life.
24.8% true (7.1% don't know)


6. Long-time smokers cannot reduce their cancer risk by quitting smoking.
16.2% true (5.7% don't know)


7. People who smoke low-tar cigarettes have less chance of developing lung cancer than people who smoke regular cigarettes.
14.7% true (10.8% don't know)


8. Personal hygiene products, like shampoo, deodorant and antiperspirants, can cause cancer.
13.7% true (15.3% don't know)


9. Getting a mammogram, or using a special X-ray machine to detect breast cancer, can cause cancer of the breast.
10.2% true (16.1% don't know)


10. Getting a base tan or base coat at a tanning salon will provide protection from skin cancer when you go outside in the sun.
8.4% true (13.2% don't know)


11. Underwire bras can cause breast cancer.
6.2% true (30.9% don't know)


12. You cannot get skin cancer from using a tanning booth.
6.2% true (18.3% don't know)


The survey, reported in the Sept. 1 issue of the journal Cancer, reveals that communities most at risk for cancer were also the most likely to be misinformed.


Healthy behaviors depend partly on whether individuals can make an accurate assessment of risk factors for that disease. Unwarranted worry over unproven risk factors can distract attention from the valid risks, resulting in "risky" decisions," past research indicates.


"If people hold erroneous beliefs about risk factors for cancer they might not be making informed decisions for their behaviors," said lead study author Kevin Stein, of the American Cancer Society&#8217;s Behavioral Research Center in Atlanta.

The scientists say that individual beliefs are not the only determinants of health behavior, and other factors, such as access to health care and socioeconomic status, are also important.

However, beliefs can guide actions, they suggest. "People's attitudes and beliefs influence their behaviors," Stein told LiveScience.

For instance, misconceptions like the tobacco-related myths, which were relatively highly endorsed, can lead to risky behaviors.

"If you believe those statements [about smoking] then you can see why some people might engage in risky behavior like smoking," Stein said.

He added, "What we would like to do is to have people get accurate information and hold accurate beliefs about what are and what are not risk factors for cancer with the hope that will translate into healthy behavioral patterns."

10 Easy Paths to Self Destruction Can Men Get Breast Cancer? VOTE: Urban Legends Debunked
Original Story: 12 Common Cancer Myths Debunked
Visit LiveScience.com for more daily news, views and scientific inquiry with an original, provocative point of view. LiveScience reports amazing, real world breakthroughs, made simple and stimulating for people on the go. Check out our collection of Science, Animal and Dinosaur Pictures, Science Videos, Hot Topics, Trivia, Top 10s, Voting, Amazing Images, Reader Favorites, and more. Get cool gadgets at the new LiveScience Store, sign up for our free daily email newsletter and check out our RSS feeds today!





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Space computer 'sabotage' probe
Nasa is investigating the apparent sabotage of a computer due to be flown to the International Space Station on the Endeavour space shuttle next month.
The US space agency said the damage to wiring in a network box was intentional and obvious, but said it could be repaired before take-off on 7 August.

Nasa stressed that the lives of its astronauts had not been put at risk.

The discovery came as an independent health panel found astronauts had been allowed to fly after drinking alcohol.

The panel found that on two occasions Nasa astronauts had been allowed to fly despite warnings from flight surgeons and other astronauts that they were so drunk they posed a safety risk.

The panel was set up by Nasa to study health issues following the arrest on kidnapping and assault charges of the astronaut, Lisa Nowak.

Ms Nowak is accused of attacking her love rival, the girlfriend of a fellow astronaut.

The findings of the panel, which do not deal with Ms Nowak directly or mention any other astronaut by name, were reported by the trade journal, Aviation Week and Space Technology.

The official review into astronauts' medical and behavioural health is expected to be released by Nasa on Friday.

The agency has so far refused to comment on the allegations.

'Sub-contractor'

Nasa's Associate Administrator for Space Operations, William Gerstenmaier, said the apparent sabotage of a non-essential computer had been discovered earlier this month.


The damage is very obvious, easy to detect
William Gerstenmaier
Nasa Associate Administrator for Space Operations


"The damage is very obvious, easy to detect," he told reporters. "It's not a mystery to us."

Mr Gerstenmaier said wires had been found cut inside the unit before it had been loaded onto the shuttle.

The computer is designed to collect and relay data from sensors which detect vibrations and forces on the space station's external trusses.

"It's currently being investigated by the [Nasa] inspector general's office," he added.

The equipment had been supplied by a sub-contractor, he added.

Mr Gerstenmaier said engineers would try to repair the hardware before take-off in two weeks' time, but that the mission would not be delayed.

The damage is believed to be the first act of sabotage of flight equipment Nasa has discovered.

Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/americas/6918490.stm

Published: 2007/07/26 23:18:31 GMT

&#169; BBC MMVII
 
. .
Touch Bionics i-LIMB Hand
Watch the Touch Bionics i-LIMB Hand, the world's first bionic hand, in action. An interview with Juan Arredondo and Lindsay Block.
[YOUTUBE]
 
Last edited by a moderator:
. .
Google sidesteps mobile reports
Google has refused to deny mounting speculation that it is working to produce its own brand mobile phone.
Reports suggest that the web giant is developing a series of"GPhones", centred on its mobile services, such as search, e-mail and maps.

In a statement, Google said it was working with carriers, phone makers and content providers to "bring its services to users everywhere".

The firm would not say if its efforts included plans for a handset.

The Google statement said: "What our users and partners are telling us is that they want Google search and Google applications on mobile, and we are working hard every day to deliver that."

Reports circulate

Google has recently partnered with Apple to produce services, such as e-mail and maps, for its iPhone handset.

Eric Schmidt, Google's chief executive, said recently that more Google services for the iPhone would be rolled out.

Reports have circulated since last year that Google was working with mobile phone manufacturers to produce a handset.

The Wall Street Journal on Thursday said Google had invested "hundreds of millions of dollars" in the project and was involved in discussions with T-Mobile USA and Verizon Wireless.

The newspaper said the company was seeking to grab a bigger slice of the increasingly important mobile phone advertising market.

Market research firm eMarketer told the paper that the mobile ad industry would be worth $14bn (&#163;7bn) by 2011.

Last month, Google said it was interested in bidding for wireless spectrum licenses in the US, which could be the first step towards running its own mobile network.

Google said its interest was in ensuring that customers would be able to buy any mobile device to connect to the full capability of the internet.

At present, wireless carriers routinely try to restrict which models of cell phones that can be used on their networks.

They also often limit the software that can be downloaded onto them, such as ringtones, music or web browser software.



Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/technology/6929537.stm

Published: 2007/08/03 11:40:50 GMT

&#169; BBC MMVII
 
.
Warning of webmail wi-fi hijack
Using public wi-fi hotspots has got much riskier as security experts unveil tools that nab login data over the air.
Demonstrated at the Black Hat hacker conference in Las Vegas, the tools make it far easier to steal account details, said Robert Graham of Errata Security.

Identifying files called cookies are stolen in the attack which let hackers pose as their victim.

This gives attackers access to mail messages or the page someone maintains on sites such as MySpace or Facebook.

Hacker gathering

Prior to the demonstration, which involved the live hijacking of a Google mail account (GMail), many sites were thought to be safe because they encrypted the data swapped back and forth when people login.

However, Mr Graham carried out his attack on the unencrypted cookies, tiny text files, many sites use to identify people that regularly return.

The tools created by Mr Graham, called "Hamster" and "Ferret", watch the traffic flowing in and out of public wi-fi hotspots and let attackers grab cookies as they are passed back to people logging in to their webmail or social network account.

Using the cookie an attacker could pose as a victim and enjoy almost the same level of access to an account as its rightful owner.

There were some defences against the attack, said Mr Graham.

Attackers would be unable to change a password and take over an account as most sites ask people to re-enter their old password before letting them make changes.

Also, said Mr Graham, some webmail services, such as GMail, let people encrypt all the data passed back and forth as they deal with their mail.


Mr Graham revealed his findings during a presentation at the four-day Black Hat conference held in Las Vegas. The conference brings together security professionals around the world who swap information about the latest exploits and future vulnerabilities.

He said Errata would make the attack tools publicly available via the company's website for anyone to download.

Also at the conference David Thiel, of security firm iSec Partners, revealed that PC media players have significant vulnerabilities that could be exploited by hi-tech criminals.

The loopholes could be used to attach malicious programs to music or video downloads in order to hijack a PC.

He suggested that popular pages on social networking sites could be subverted by malicious hackers to add the booby-trapped media files.

"The potential for attack is pretty severe," he said.

Mr Thiel said the makers of the media players had been told about the problems and were working on fixes for them.


Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/technology/6929258.stm

Published: 2007/08/03 10:36:40 GMT

&#169; BBC MMVII
 
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