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Shen Build
Ability Sequence
Not Updated For Current Season
The masteries shown here are not yet updated for the current season, the guide author needs to set up the new masteries. As such, they will be different than the masteries you see in-game.
Shen - The Eye of Twilight
"Tanking guide to Shen, nothing special"
Know that above all else Shen is a support unit, the game is about teamwork and accomplishing tasks by using your teammates strength. So when you're playing Shen you have to remember that you are the tank! You are suppose to protect your allies and work together as a team to win the game. You have to help ganking, pushing, and saving your teammates. This guide will focus on keeping you alive, teaching you have to farm, gank, and tank. Before you start playing Shen you have to know that you're not suppose to strive for godhood, your job is to initiate and keep teammates out of harms way. Not to finish of enemy champions and get kills. This means that you sometimes die for your team, and never really get the chance to kill unless you are ganking. But the purpose of Shen is still to flip' out and kill people, so never let anyone get away. In otherwords, you have to be active and have some map awereness.
1. Very good tank
2. Great survivability
3. Never runs out of steam
1. Difficult to master
2. Restricted by energy
3. Constantly being nerfed
Acceptable Runes: Click here
Greater Quintessence: Fortitude, Swiftness
Greater Glyph: Shielding, Warding, Focus
Greater Seals: Evasion, Vitality, Regeneration
Greater Marks: Desolation, Alacrity, Vitality
Shen's Abilities: Click here
Shen is the first champion in the League of Legends to use energy to cast his abilities, rather than mana or health like most other champions. This system caps the maximum amount of energy Shen can have at 200 energy, and regenerates Shen's energy very rapidly (10 energy per second). This regeneration can be increased by getting an ancient golem buff (+1.5%).
Ki Strike
(Innate): Every 8 seconds, Shen's next attack deals bonus damage gained from 3.5% health. If a champion is hit there is a cooldown reduction of 2 second for all the abilities.
Ki Strike is one of your main damage output abilities, by focusing on health you will be able to harass and farm minions by combining it with Vorpal Blade and Shadow Dash if they are hard to catch. If you want to master Ki Strike you have to know it by heart, in other words you need to count those 8 seconds yourself, then use it to your advantage when you hit your enemy. Since this scales with 3.5% of your total health it is extremely beneficial to have a lot of early-game health for Shen, later on you can get up to 3000hp and if used right you can do some decent dps, but you're not a dps! Is, but is not? Something, a ****** would say.
Vorpal Blade
(Active): Shen deals magic damage to target unit. That unit becomes life tapped for 5 seconds, healing any champions who attack it over 3 seconds.
- Cooldown: 3 seconds
- Range: 475
- Cost: 70 / 65 / 60 / 55 / 50 Energy
- Damage: 50 / 95 / 140 / 185 / 230 (+0.65 per ability power)
- Life Tap: 10 / 20 / 30 / 40 / 50 health (+0.1 per ability power)
This will keep you in the lane for as long as you want, a good Shen can get back up from low health to medium health and from there on you can get back up to full if you can avoid getting harassed with proper use of Feint. Don't forget that you place this buff on some minion, which means that your lane-partner can hit it as well. This works well if he is ranged, otherwise it's tricky to pull off. Next up you have Vorpal Blade used as a farming tool combined with Ki strike, at level one you will need your minions to be 150hp, and at some point you can get a minion at full health by opening with Vorpal Blade and then hit it with Ki Strike. The same method can be used to harass enemy champions, this is not meant to kill them, it is meant to intimidate, annoy, and give you some space. Lastly, you can use it to finish of enemy champion that are running away with an obscenely long range.
(Active): Shen takes reduced damage for a few seconds.
- Cost: 45 Energy
- Range: 20
- Cooldown: 9 / 8 / 7 / 6 / 5 seconds
- Damage Blocked: 40 / 70 / 100 / 130 / 160 (+0.3 per ability power)
Probably one of the most boring and overlooked skill by all the new Shen players, but don't be fooled! This is what makes Shen able to tower-dive, avoid getting harassed, and get away with so little health. Nullifying damage: Activate Feint to block the damage from projectiles, launches, and enemies teleporting themselves to you. As soon as you see them casting something activate Feint, not a second later. DoT's and CC: If you get hit by a DoT like Ignite, Malefic Visions, Rune Prison, Dark Binding, you should activate Feint to avoid most of the damage. The same goes for whenever you are about to get stunned, activate Feint just before it hits. Don't spam Feint in the middle of a fight, 1v1's or when you are chasing! You should only use it to block CC, spells, and even auto-attacks when you are running away because you won't need more of your energy. The exception is when you are getting full focus and you know something bad is going to hit you.
Shadow Dash
(Active): Shen rapidly dashes to a target location, Taunting enemies he collides. Restores 50 Energy if you hit a champion.
- Cooldown: 10 seconds
- Range: Unknown
- Cost: 120 / 115 / 110 / 105 / 100 Energy
- Taunt Duration: 0.8 / 1.1 / 1.4 / 1.7 / 2 seconds
You dash for a short distance and taunt any nearby champion and minion you hit, this is a great skill but most of the time I see it used poorly. Most players use it as an escape mechanism to make the gap wider between Shen, and a pursuing opponent. Keep in mind that it costs 120/200 Energy! If you're running away you should use Feint, but if you fear getting CC'ed then you should use it to like Flash. The most basic use of Shadow Dash is to save a teammate, just dash into the crowd and keep them busy long enough for your teammate to escape. For starters, the common mistake is to use Shadow Dash to open up a fight, you have to be patient! "Wait for it!" should be your motto, it's best to use it to stun at the right moment. When they get 50-20% you can think about using it if you have teammates nearby. Otherwise you should just let to go, remember that you are the tank.
Stand United
(Active): Places a shield on both a target allied champion and Shen, absorbing damage for 7.5 seconds (Shen's shield absorbs half as much damage). After channeling for 2.5 seconds, Shen teleports to the target's location.
- Cost: 50 Energy
- Range: Global
- Cooldown: 180 / 150 / 120 seconds
- Damage Absorbed: 300 / 525 / 750 (+1 per ability power)
When first introduced this was one of the most ridicules ultimate in the game! I can't remember how many times I didn't get a kill because of a Shen who used his ultimate to save a teammate. Most of the time it's used to teleport, saving a teammate, and changing a 1v1 to a 1v2. This can also be used to get out of sticky situations by using it to teleport to any of your teammates [R + F2-5]. With great powers comes great responsibilities, in other words you have to keep an eye on your teammates all the time. But with Shen farming takes a lot of concentration so this can be difficult, unless you're a girl or just got a talent for multi-tasking. If you have communication it can often be advised that you tell them you can shield them if things turn out bad, or allow them to tower dive when they are going for the kill. Other than that you can always combine it with ultimates such as Crowstorm, Destiny, and Absolute Zero.
Summoner Spells: Click here
I mostly recommend defensive summoner spells, but if you like to be a little more aggressive then you could always use Ignite + Exhaust. But for Shen that's not really a priority at all, however you could always consider other spells such as Teleport and Exhaust as long as you get to upgrade them in your masteries.
Your Champion ignores unit collision and moves 32% faster for 14 seconds. Cooldown: 210
Ghost is currently one of the best summoner spells in League of Legends, since you are one of those more durable champions flash becomes rather dull in comparison. This allows you to charge in for the squishes, flee from a gank or whenever you're low in a teamfight, and catch up with someone fleeing. Just know when to use it, and when not to waste it. Whenever things turn out bad you should try to get away but as the tank you have to make sure everyone else makes it as well. You are only suppose to buy them time, if you know that your ally will only make it if you distract them then it'll be worth it.
Removes all debuffs from your champion and reduces the duration of subsequent stuns, slows, taunts, fears, snares, sleeps, and immobilizes by 50% for the next 3 seconds. Cooldown: 120
Cleanse is getting very popular, especially at level 30, mainly because people got tired of Ignite + Exhaust. The use of Cleanse has to be adapted to what champion you're playing, Shen, and what you can cleanse on your enemies team. Finally, we got what sort of situation you are in. For Shen it's mostly Ignite and Exhaust in the laning phase, Stun and Silence in Teamfights, and anything that can get you killed while fleeing. Then we have Blind if you're about to kill someone, but it's not always necessary if you only need a Vorpal Blade to kill your target.
Heal heals oneself for 140 + 20x level and every allied unit for half the amount. Cooldown: 270
Heal should only be taken if you're all new to League of Legends and if you have somewhat moderate or poor skills. Don't worry, you'll get better I promise. But first you should focus on learning all that you can and try to adapt to your current situation. In the lower levels of LoL you will see almost everyone using Heal, this is because it allows players to make up for mistakes and not die too easily. It's not all that scrubish, but it's not all that pro either. This goes for the old saying:"What's up with heal on tanks?" 500 out of 3000 health is not that much, I mean you have better options.
Grants invulnerability to all Allied Turrets and causes them to attack 100% faster for 7 seconds. While Fortify is ready to cast, you deal 9 bonus damage to minions. Cooldown: 300
If you are doing a pre-made and your team likes to have Fortify at their disposal then you should take it. Keep in mind that you have to push, to win! Not everyone knows this so in the lower ELO Fortify is by no means necessary, but if your enemies tend to backdoor or gather up for a push then Fortify can help delay them until everyone, or someone, gets there in time. You can also use this if your opponents towerdive to punish and possibly kill them before they get away.
Core Item build:Ruby Crystal will give you a lot of early-game health and since Vorpal Blade will fix regeneration you can stick with that. Frozen Mallet will allow you to more initiate ganks more effectively and keep enemies busy. The Aegis of the Legion will help out the rest of your team and fix a few weak spots, while Guardian Angel will make it seem hopeless to try and kill you. After that you can get Randuin's Omen for an AoE slow and attackspeed nerf, and it's also a lot easier to get away with the passive slow. Finally we got Banshee's Veil for late-game, it's really just to annoy but I doubt normal games will last that long.
Optional Items:At some point you will begin to rely less on a structured build, and more on your opponents, and what their builds are. But most of all your own preference and your own team. Like starting with a Doran's Shield to get a good start, and getting Spirit Visage for its increased healing effect which is nice if you got a healer on your team. The most common choice you have to make which depends on the enemy team are what shoes to buy: If you are up against a lot of physical dps champions 4/5 then I recommend taking Ninja Tabi. If your opponents got a hell of a lot of CC then I recommend taking Mercury's Treads because you can't cleanse everything. For late-game we got items like thornmail vs. physical dps and force of nature vs. magic dps.
Team Composition:
Before the game starts you have to make sure that you have a good team composition, it's important to have at least 2 or 3 ranged, 1 tank, 1 support, and a mix of physical dps and magical dps. Setup is the key, you wouldn't be playing Shen without it. Most of the time this is the kind of setup you get, but if you don't recall that in your own experience then you can always fix that in pre-mades. Shen is not the type of champion that goes mid lane, this is because he has a disadvantage when it comes to being ranged and most of all that he's not a carry. Who you are laning with doesn't really matter, but I would rather have a dps than a support by my side. Mostly because Shen can't kill all by himself so having a little extra dps is more helpful.
The Laning-phase:
Instead of going all into detail I figured it would be better to tell you your goals, what to do, and what not to do. But let's start out with a few techniques like Vorpal Blade + Ki Strike harassing, which is also the basic farming technique. All you need to do is toss a Vorpal blade and move up to your target and auto-attack it once, then retreat and use Feint to block anything if you suspect it. If you have problems reaching your target, like any ranged, then you can always use Shadow Dash and then use Vorpal + Auto-attack and then retreat with Feint. This will create a gap between you and give you some space, if you don't you might not get to last hit anything, so try to be a little aggressive but not so much that it gets you killed. When you reach level 4 there is a possibility you might get ganked from mid or from one of the other two lanes or a jungler perhaps. That is why you always have to keep an eye on the map yourself, you can't always depend on miss calls. If everyone or someone you might get you killed if you're not careful, then you should avoid taking unnecessary chances.
Ganks and Teamfights:
When you reach level 6 you should keep an eye on your allies health and make sure youre ready to throw down your ultimate. But don't lose focus, it's important to concentrate instead of mindlessly auto-attacking minions. Once you get a kill or two, and / or manage to bring the tower down in your lane you can leave the lane for good but you can always get back to it for pushing. Now there are two very important things about Shen that you have to know, the first one being Shen fights all the time! You've probably heard it before, but it has a different meaning other than a simple fact. The thing is that you can't be all passive when you're playing Shen, hell, not even when you're playing LoL in general. It's important to get out there and gank a little, get kills and support your allies, take some action! The second one is that you can't be all bloodthirsty and try to get a kill all by yourself, one thing that has been annoying me as Shen is that I can't go all over the place and try to get a kill. It just doesn't work like that; you have to keep your allies close, and your enemies closer.
Thanks for reading, please rate and leave a comment if you like.
(I have yet to master Shen, so like all my other builds I will update it)


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Oppo announced earlier this month that the N1 CyanogenMod edition device would be available for purchase starting on Dec. 24, and true to the company's word, the limited handset can now be had for $599 from the online OppoStyle store. In exchange for their hard-earned ducats, buyers of the N1 CyanogenMod edition will receive an Oppo N1 that's running CyanogenMod 10.2 out of the box as well as some stickers, a case that features CM and Oppo mascots Cid and Ollie as well as some special packaging. The N1 CyanogenMod edition comes with 16GB of storage.
Besides the fact that it comes with CyanogenMod 10.2 out of the box, the N1 CyanogenMod edition is the same as its standard Oppo N1 sibling. That means that it's rocking a 5.9-inch 1080p display on its face, a 13-megapixel camera that's capable of rotating 206 degrees up at the top of its frame and a combination of a 1.7GHz quad-core Snapdragon 600 processor, 2GB RAM and 3610mAh battery inside its body.
The CyanogenMod team today announced that as part of the N1 CM edition launch, it's releasing the device's factory images as well as the source code for the CM 10.2 software that it comes preloaded with. The code goodness doesn't end there, though, as the group is making the code for CyanogenMod 11 available for download as well.
The past few months have been big for CyanogenMod, including major events like the announcement of Cyanogen Inc. and the launch of the CyanogenMod Installer. The launch of this Oppo N1 CyanogenMod edition seems like a nice way to cap off both the team's streak of major events and the entire year of 2013. Now that the N1 CM edition is here with Google's CTS and CDD approval, it'll be interesting to see where CyanogenMod and the team behind it go in 2014. While we wait for the calendar to flip over and begin to reveal what's in store for CM, you can check out a video of the N1 CyanogenMod edition in action below. The device is available for purchase from Oppo's online store right here.

subset: commoncrawl


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Have an environmentally friendly vacation
1. Select an appropriate destination
- Look at eco-tourism options. Many travel companies now offer holidays which support sustainable development, do not impact negatively on the environment, and provide financial support to local communities.
2. Choose the best way to get there
3. Choose the right place to stay
4. Be responsible guest
- Choose reputable, conservation-minded tour operators and suppliers.
- Conserve water. Take showers rather than baths; use a refillable water container, sterilizing water when necessary rather than buying bottled water. Minimize your use of personal care products and detergents to wash linen, and reuse your hotel towels and bed linen.
- Limit energy use. This includes your use of air-conditioning and hot water. Turn off all lights and taps when you leave hotel rooms.
- Dispose of sanitary waste properly. Don't flush cotton buds, condoms, tampons and plastics down the toilet.
- Recycle and reduce. Recycle newspapers, magazines and your beverage containers (many can be returned for refunds), and reduce the number of bags, napkins and disposable cups you use when you eat fast food.
- Choose environmentally friendly transport. Rather than hiring a car, choose other ways to get around like taxis, trains or buses. In many places you can also rent bikes. And don't forget your feet!
- Avoid damaging recreational activities. Avoid sports which have a significant harmful impact on the environment, or choose more progressive establishments (e.g. golf courses which recycle water).


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Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a chronic, disabling illness that affects approximately 0.2% of the population. Non-restorative sleep despite sufficient or extended total sleep time is one of the major clinical diagnostic criteria; however, the underlying cause of this symptom is unknown. This review aims to provide a comprehensive overview of the literature examining sleep in CFS/ME and the issues surrounding the current research findings. Polysomnographic and other objective measures of sleep have observed few differences in sleep parameters between CFS/ME patients and healthy controls, although some discrepancies do exist. This lack of significant objective differences contrasts with the common subjective complaints of disturbed and unrefreshed sleep by CFS/ME patients. The emergence of new, more sensitive techniques that examine the microstructure of sleep are showing promise for detecting differences in sleep between patients and healthy individuals. There is preliminary evidence that alterations in sleep stage transitions and sleep instability, and other physiological mechanisms, such as heart rate variability and altered cortisol profiles, may be evident.
Future research investigating the etiology of non-restorative sleep in CFS/ME may also help us to undercover the causes of non-restorative sleep and fatigue in other medical conditions.
Jackson ML; Bruck D. Sleep abnormalities in chronic fatigue syndrome/myalgic encephalomyelitis: a review. J Clin Sleep Med 2012;8(6):719-728.
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a medically unexplained disabling illness, with prevalence estimates of between 0.007% and 2.8% of the general adult population.1–3 It is primarily characterized by persistent relapsing fatigue of at least 6 months in duration that reduces activity levels. Other key features of the disorder include post-exertion malaise of either physical or mental exertion, memory and concentration difficulties, muscle pain, headaches, tender lymph nodes, sore throat, and non-restorative sleep. Of direct relevance to the current review, patients often report daytime sleepiness, feeling unrefreshed upon waking despite sufficient or extended total sleep time, extended sleep including daytime napping, and other sleep-related symptoms, such as difficulty falling asleep and disturbed sleep.2,4,5 Since the late 1980s, research in the area of CFS/ME has begun to focus on examining and determining the cause of non-restorative sleep and sleep disturbance in CFS/ME, and how these symptoms may relate or contribute to patients' daytime fatigue. The current review aims to provide a comprehensive overview of these studies, describe where the field currently stands on this issue, and outline potential directions for future research.
Clusters of symptoms including chronic fatigue, cognitive and mood impairments, sleep difficulties and pain have been observed in clinical practice for centuries. A collection of symptoms similar to that of CFS/ME, including fatigue, depression, headache, impotence and neuralgia, were first reported in the 19th century.6 The diagnosis "neurasthenia" was popularized by American neurologist George Beard to describe this collection of symptoms.7 With increasing sophistication of psychiatric diagnoses over time, diagnosis of neurasthenia has declined, however, the symptoms described in these early patients closely match those we now recognize in CFS/ME today.
The name "chronic fatigue syndrome" was first suggested in 1988, and most commonly used by the medical and scientific community to describe the illness. However, the name CFS has been rejected by many patients, patient advocacy groups and some doctors as it undermines and trivializes the illness. Since 1969, myalgic encephalomyelitis (ME) has been included in the World Health Organization's International Classification of Diseases (ICD-10), and although is clinically distinct from CFS, the two terms are used interchangeably. Due to the stigma of the name "chronic fatigue syndrome," the illness is often referred to as CFS/ME.
It is important to make a distinction between CFS/ME and fibromyalgia (FM). FM is a chronic medical disorder characterized by widespread pain, a heighten pain response, and sleep disturbance,8 and is commonly comorbid with CFS/ME.9 Given the overlapping symptoms and lack of a diagnostic test, it is important for research studies to have clear criteria for distinguishing these two conditions. This review will focus on research that has specifically examined sleep in CFS/ME.
The first working case definition of chronic fatigue syndrome was introduced in 1988 by the United States Centers for Disease Control and Prevention (CDC).10 The development of a case definition allowed for a systematic and comprehensive approach to defining the etiology and pathophysiology of CFS/ME. These definitions, along with the 198811 and 199012 Australian definitions, and the 1991 Oxford, UK definition,13 have played an essential role in orienting clinical research, and facilitating consistency and homogeneity of samples across research studies. Although these initial criteria were considered quite restrictive, the diagnostic criteria did not specifically exclude a sleep disorder. As a result, early studies that examined the association between sleep complaints and functional disability in CFS/ME suggested that a primary sleep disorder may be the cause of unrefreshed sleep in some patients.
In 1994, a revision to the case definition and a set of research guidelines for use in studies of CFS patients was proposed by the Centers for Disease Control and Prevention.14 These guidelines (known as the Fukuda criteria) used more relaxed definitions than the 1988 criteria, requiring only four criteria beyond fatigue for diagnosis, and not excluding non-psychotic psychiatric disorders. Given that there is no laboratory test for diagnosing CFS/ME, and the etiology is typically unknown, CFS/ME was seen as a diagnosis of exclusion. This was reflected in the new criteria by specifically excluding comorbid conditions such as a treatable sleep disorder (e.g., obstructive sleep apnea [OSA] and narcolepsy) and other potential causes of fatigue (e.g., substance abuse, psychiatric disorder). Unrefreshing sleep was the only criteria relating to sleep, with other sleep disturbances not a criterion. Although alternative definitions have been proposed,15 the 1994 Fukuda criteria are considered the international accepted research definition. However, it was recognized that the Fukuda criteria and other broadly inclusive criteria15 do not adequately discriminate CFS/ME patients from those with other conditions such as major depressive disorder. Additionally, since the Fukuda criteria were primarily developed to inform clinical research excluding comorbid conditions, such as treatable sleep disorders, they may not be appropriate to use exclusively for clinical diagnoses, which are often more broadly defining.
In 2003, an Expert Medical Consensus Panel with extensive experience in the research and clinical management of CFS/ME developed the Canadian Clinical Case Definition.16 This document was created specifically to inform healthcare professionals. The Canadian Criteria has incorporated a larger spectrum of potential symptoms, aimed to assist recognition of the "interrelationships of each patient's symptoms and their coherence into a syndrome of related symptoms."16 This updated clinical definition captured, in addition to chronic fatigue, the issue of post-exertion malaise. These criteria also highlight mental fatigue (loss of cognitive function and alertness) as well as physical fatigue (lack of energy and strength). Sleep disturbance is recognized as a major feature of CFS/ME in the Canadian Criteria. Specifically, sleep and circadian rhythms disturbances are listed, including early, middle, and late insomnia, and reversed or abnormal diurnal and sleep rhythms. Further, periodic limb and restless legs syndrome are reported to accompany these other changes in sleep in many cases. These criteria also recognize the importance of ruling out a treatable sleep disorder, such as upper airway resistance syndrome and OSA.
Most recently, International Consensus Criteria (ICC) have been developed.17 The ICC build from the Canadian Criteria to identify the distinct characteristic patterns of symptom clusters of CFS/ME. These new definitions relaxed the requirement for symptoms to have persisted for at least 6 months, giving the physician more temporal control of when the diagnosis of CFS/ME can be made. Sleep disturbances were divided into two categories: disturbed sleep patterns, including insomnia, prolonged sleep including naps, frequent awakenings, and vivid dreams/nightmares; and unrefreshed sleep, including excessive daytime sleepiness.17 Importantly, these updated criteria serve to not only diagnose patients in the clinical setting, but to also assist in identifying patients for research studies.
The diagnostic overlap between CFS/ME and primary sleep disorders has been documented in a number of studies. Prior to the revision of the diagnostic criteria for CFS/ME in 1994, two studies reported that over half of their CFS/ME patients had a sleep disorder as assessed by overnight polysomnography (PSG).5,18 These sleep disorders include hypersomnia, sleep maintenance and sleep initiation insomnia, OSA, narcolepsy, and periodic limb movement disorder, as well as inadequate sleep hygiene. CFS/ME patients were found to have higher levels of fatigue and sleep disturbance than patients with multiple sclerosis5; those with a comorbid sleep disorder reported greater functional impairment.18 Since these studies included CFS/ME patients with a suspected sleep disorder who were attending the sleep clinic, rather than randomly selected or consecutive patients, these figures are mostly likely inflated.
Subsequent to the 1994 guideline revisions, Fossey et al. (2004) observed prevalence rates > 50% of ICSD-classified primary sleep disorders (OSA and movement disorders) in CFS/ME patients.19 Similarly, Le Bon and colleagues examined the prevalence of primary sleep disorders and objective sleepiness in CFS/ME and found that 46% of the 46 unselected patients who met Fukuda criteria for CFS/ME also presented with OSA (using a criterion of AHI > 5), and a further 5% presented with periodic limb movement disorder.20 On multiple sleep latency testing (MSLT), an objective measure of sleep propensity, 30% of the patients were classified as clinically sleepy. Objective (MSLT) and subjective (Stanford Sleepiness Scale) measures of sleepiness, however, were not associated with a subjective fatigue measure, suggesting that the fatigue experienced by CFS/ME patients is separate from the expression of sleepiness. Importantly, this study compared CFS/ME patients with and without a primary sleep disorder and found that they could not be separated on clinical presentation. The authors concluded that the symptoms of CFS/ME are clearly distinct from those of primary sleep disorders, and the illness is more than simply a somatic expression of an underlying sleep disorder or sleepiness.20
Larger population-based studies of CFS/ME patients have also provided some insight into the rates of sleep disorders in CFS/ME patients over time.15,21 Approximately 20% of CFS/ME patients in these studies were found to have either OSA or narcolepsy, with one study reporting that 20% of patients were given an alternative diagnosis of sleep disorder at 3-year follow-up.21 Subclinical levels of sleep disordered breathing have also been reported in some studies.15,22
From a clinical standpoint, early studies that examined prevalence of comorbid sleep disorders provide new insights into the syndrome and potential differential diagnoses and highlight the importance of considering a potential sleep disorder as a cause of unexplained fatigue.23 While there is overwhelming evidence of the distinction between CFS/ME and sleep disorders,24 some researchers argue that a diagnosis of OSA should not be an exclusion criterion for CFS/ME. It is argued that primary sleep disorders do not influence the core symptoms of CFS/ME and therefore should be considered a comorbid condition.25 Indeed, in clinical practice many physicians treat primary sleep disorders concurrently with CFS/ME rather than exclude these patients. CPAP therapy in CFS/ME patients with comorbid OSA has been found to improve some daytime features, such as cognitive and daytime sleepiness; however, the underlying fatigue state remains.25 The magnitude of OSA in CFS/ME also depends on what diagnostic threshold is used for OSA. Le Bon and colleagues acknowledge that if an AHI cutoff of 20/h was used in their study (rather than AHI < 5), OSA would only be prevalent in 11% of their CFS/ME sample (as opposed to nearly 50%).20 These figures are comparable to the prevalence of sleep disordered breathing in the general population.26 Thus it could be argued that primary sleep disorders are a comorbid condition that occur at a similar frequency in CFS/ME to the general population and are therefore not reflective of the disorder itself.
In addition to generalized joint and muscle myalgia, which are integral features of the diagnostic criteria, CFS/ME is also associated with comorbid pain conditions including irritable bowel syndrome and migraine headaches. Pain experienced by CFS/ME patients may also play a critical role in sleep disturbance. Studies of FM have found that both subjective sleep quality measures and phasic alpha sleep are associated with pain sensitivity.27 There is a potential bidirectional relationship between sleep and pain—pain disrupts sleep, and sleep disruption enhances pain. Firstly, pain causes disruption to sleeping pattern and increases sleep onset latency. Experimental manipulations of pain stimuli to the muscles during sleep have revealed decreased delta and increased alpha activity of the sleep EEG, and impaired sleep quality.28,29 CFS/ME patients are found to have more self-reported awakenings during sleep due to pain compared to depressed patients and healthy controls.32 On the other hand, sleep disturbance also leads to reduced pain thresholds during waking.30 Pain and fatigue symptoms, similar to those reported in CFS/ME and FM, have been induced in healthy individuals by disrupting SWS.30 Thus, it has been posited that the physiological arousals that are observed during sleep reflect a vigilant nocturnal state that contributes to daytime fatigue, pain, and hypersensitivity, and subjective feelings of non-restorative sleep. The influence of myalgic symptoms on sleep disturbance in CFS/ME has received little research attention to date.
Some patients with CFS/ME have comorbid psychiatric or somatoform illness, such as depressive disorder or fibromyalgia, which do not rule out a diagnosis of CFS/ME. Given that sleep disturbance is a common symptom of psychiatric conditions,31 it could be argued that sleep disturbance in CFS/ME is a secondary consequence of comorbid depression. Studies that have explored this potential link by comparing sleep study results of CFS/ME patients with and without a psychiatric comorbidity suggest that sleep disturbances are common in both subtypes, and therefore do not appear to be solely the result of underlying depression.4,32 All of these studies mentioned above have been critical for highlighting CFS/ME as an autonomous syndrome.
Table 1 presents studies that have compared sleep parameters of CFS/ME patients to healthy controls using polysomnography. Of 24 papers reviewed, only 15 used recognized diagnostic criteria for patient recruitment, and only these 15 are included in Table 1. Of these 15, only 10 reported that they excluded patients who were on medication or asked patients to withdraw from their medication for 2 weeks prior to the study.
Summary of literature investigating sleep, measured polysomnographically, in CFS/ME patients compared to healthy controls, using standard diagnostic criteria
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Studies examining traditional sleep parameters as measured by PSG have reported variable and nonspecific differences in sleep parameters between CFS/ME patients and controls. The reason for the discrepancy may be due in part to differences in selection criteria (e.g., medication status), the type of control group used, or characteristics of the recorded night (e.g., first night of recording only, home recordings), which also make comparisons between studies difficult. First night effects are apparent in CFS/ME patients who do not have a primary sleep disorder,33 and therefore studies that have only used one night of recording may not provide an accurate picture of the patient's typical sleep.
Reflecting the disturbed sleep reported by many CFS/ME patients, an increased number18,34,35 and duration18,34,36 of intermittent awakenings have been reported. However, using an adaptation night prior to the main sleep recording night, Reeves et al. found no difference in sleep efficiency between CFS/ME patients and controls.15 This study, however, enforced bed and wake times for both groups, and as such may not have captured true sleep efficiencies that the participants would typically experience. When patients and controls have been allowed to go to bed at their usual bed time, reduced total sleep time (TST) and sleep efficiency are observed in the CFS/ME group, both in single-night PSG recording in the laboratory,22,37,38 and in some,18,35 but not all36 at-home studies. Togo et al. (2008) examined this observation further by stratifying their patients into those who reported sleepiness upon waking, and those who reported more sleepiness in the evening. Using this distinction, they found that those who reported morning sleepiness had lower sleep efficiencies and more periods of interrupted sleep.38
Sleep onset latencies are often longer in CFS/ME patients compared to healthy control subjects, suggesting that some patients may have difficulties initiating sleep.4,37 It has been reported that CFS/ME patients may have differential parasympathetic activity at sleep onset, which may contribute to delayed sleep latency.39 This finding could also reflect poor sleep hygiene or extended sleep periods and napping, which may reduce sleep drive at night.
Actigraphy studies potentially provide a more ecologically valid assessment of TST, sleep efficiency, and sleep onset latency parameters, as measurements are made in a naturalistic setting where patients can follow their usual sleep routines. A study in children with CFS/ME reported that continuous sleep of > 10 h, measured with actigraphy, was not uncommon.40 Impaired daily sleep/wake rhythms and disturbed sleep were observed in those children who displayed an irregular sleep type. These studies can also examine whether changes in the circadian timing of sleep are evident, such as a delayed sleep phase. Most actigraphy studies to date have examined diurnal activity patterns in CFS/ME patients,41 and there are currently mixed findings relating to circadian rhythm disturbances.42,43
The sleep architecture of CFS/ME patients may differ from that of healthy individuals. Stage 3 sleep or slow wave sleep (SWS) is typically observed for approximately a fifth of the sleep period in young healthy individuals.55 A number of studies have reported reduced time in SWS in CFS/ME patients relative to controls4,38 and between monozygotic twins discordant for CFS/ME.41 These effects are independent of depression and FM.4,24
Alpha-delta sleep is an atypical electroencephalographic (EEG) pattern recorded during NREM sleep. In normal sleep, alpha activity is characteristic of drowsy wakefulness, and delta activity indicates restorative NREM sleep. Alpha-delta sleep was first observed during studies of sleep EEG of patients with psychiatric illness who presented with fatigue. The appearance of alpha-delta sleep, or alpha intrusions, during SWS has been reported in some early studies of CFS/ME patients.37,56 The appearance of alpha-delta sleep in these patients was initially thought to be the cause of non-restorative sleep. However, whether the patients in these studies had a "pure" diagnosis of CFS/ME or potentially some feature of FM is unclear. Later studies failed to find this phenomenon,51,57 and the role of alpha-delta sleep in the pathophysiology of CFS/ME has since been questioned.
The amount of SWS and slow wave activity (SWA; power density in the delta frequency) are determined by prior wakefulness. For example, SWS and SWA are found to increase following periods of sleep deprivation or restriction, when there is a build-up of homeostatic sleep pressure.58 As such, SWA during NREM sleep is often used as a marker of sleep homeostasis. A study by Armitage and colleagues exploited this phenomenon by exposing 13 monozygotic twins discordant for CFS/ME to a sleep delay schedule.49 After 2 baseline nights in the laboratory, a mild sleep challenge was imposed, involving a sleep delay of 4 hours, followed by a regular sleep length "recovery" period. Although no differences in SWA during baseline sleep were found, the CFS/ME twin expressed significantly less SWA in the first NREM period after the sleep delay. Additionally, the time course of dissipation of SWA across the night was altered in the CFS/ME twin. The authors concluded that CFS/ME is associated with impaired sleep homeostasis and basic sleep drive. Interestingly, the cytokine systems are intimately involved with sleep regulation; increased SWA also occurs in response to acute infection, with proinflammatory cytokines increasing SWS.59 Alteration in SWA may therefore be associated with the systemic inflammation found in CFS/ME.60 Further research examining SWA and immune dysfunction in CFS/ME would be valuable for understanding this potential link.
The distribution and amount of REM sleep in CFS/ME is not as clearly defined as that of SWS. Reduced REM sleep in CFS/ME patients is reported in some studies,35,38 whereas others have observed a higher percentage of REM sleep in CFS/ME relative to controls.37,45,61 When statistically controlling for medication use, no difference in REM sleep latency was observed between controls and CFS/ME patients,15 suggesting that medications used by these patients may play a role in some sleep architecture differences previously reported. Perhaps the clearest findings have been derived from twin studies, as described earlier. In these studies, no differences in REM sleep are observed between the CFS/ME twin and the healthy twin.51
To date, approximately 273 clinically diagnosed CFS/ME patients have been assessed using PSG, with less than half of these patients studied not using medication. Based on these limited data, there appear to be very few differences in sleep architecture or TST between CFS/ME patients and healthy individuals, with mixed findings for SWA and SWS. The distribution of SWS and the frequency of sleep stage transitions appear to differ between CFS/ME patients, healthy controls, and other sleep disorders. Of the 4 twin studies published, increased SWS and REM sleep are typically reported in the CFS twin, with evidence for an impaired sleep homeostatic response, but no differences on power spectral analysis were observed. Studies that have had utilized co-twin control methodology have the added benefit of controlling for many genetic and environmental factors that are typically not accounted for in either CFS/ME or sleep research, making for a more powerful and robust design.44
Based on these data, it appears that CFS/ME does not have a characteristic objective sleep disturbance found across all patients. As a result, some researchers have concluded that CFS/ME patients do not have abnormal sleep, and objective sleep measures do not account for subjective reports of non-restorative sleep. Studies using traditional PSG measures have been unable to shed light on a cause for the experience of non-restorative sleep.
While CFS/ME patients present with fatigue as their primary symptom, whether they also experience excessive daytime sleepiness is less clear cut. The consensus from a number of studies is that pathological sleepiness objectively measured using multiple sleep latency tests (MSLT) is not observed in CFS/ME patients.15,46,62 This is despite CFS/ME patients reporting higher levels of subjective sleepiness and poorer sleep quality than healthy controls.24,53,61
There are a few possible explanations for this discrepancy between objective and subjective sleepiness measures. Firstly, it has been suggested by some authors that CFS/ME patients have sleep quality misperception.15,61 Interestingly, poor self-rated health and depressive symptoms have been found to be associated with over reporting of sleep difficulties and underestimation of sleep efficiency.63 However, it is unlikely that this discord is truly a global phenomenon across all CFS/ME patients, and perhaps reflects more of a generalized issue among all patients experiencing sleep disturbance, such as insomnia.64 It may be that sleep disturbed individuals more closely monitor their sleep habits and patterns and are more in tune to changes in their sleep.
A second possibility is that the discrepancy reflects issues with definitions and measurement tools used to determine fatigue and sleepiness. Outside of the sleep arena, fatigue and sleepiness are ill-defined concepts with overlap in their definitions and are often used interchangeably. This can make it difficult for both patients and clinicians to correctly distinguish between the two states.65 Further, currently there is a lack of a clear and reliable subjective measure that differentiates the two states. One study examined whether current measures correctly distinguish between sleepiness and fatigue, by comparing CFS/ME and OSA patients whose primary symptom is daytime sleepiness.66 In this study, a clear distinction between subjective measures between the 2 patient groups was observed, with CFS/ME reporting the most fatigue and OSA patients reporting higher levels of sleepiness. However, there was some overlap in the levels of subjective sleepiness between the 2 groups, combined with the well-recognized discordance between objective and subjective sleepiness in the CFS/ME group. This study highlights the need for more precise tools and analyses for distinguishing these 2 states.
Another explanation for differences in objective and subjective measures of sleep in CFS/ME is that potential nocturnal neurophysiological disturbances that result in the non-restorative sensation following sleep in CFS/ME patients are not detected by traditional sleep variables or sleep stage distributions measures. More sensitive micro-analyses of the sleep EEG and other nocturnal parameters are currently being explored in this population.
While objective sleep parameters do not clearly predict subjective reports of sleep disturbance, other physiological measures may have more promise for detection of alterations in CFS/ME patients' sleep. Stage shifts4,34 and dynamic stage transitions50 have been shown to discriminate CFS/ME patients and healthy controls. The relative frequency of REM to NREM transition is lower in CFS/ME, while there are significantly more transitions from REM and stage 1 sleep to wakefulness.50 Normal continuation of sleep in stage 1 and REM is disrupted in CFS/ME, which may contribute to feelings of non-restorative sleep upon waking.
More recently, studies have utilized alternative methods for quantifying EEG in CFS/ME patients, which provide a more sensitive method for evaluation of sleep abnormalities. Power spectral analysis using fast Fourier transform (FFT) has been used in a few recent studies,51,52 with conflicting results. Decker reported differences in delta power, with reduced delta power observed in SWS and increased delta power during stage 1 and REM sleep in 35 CFS/ME patients relative to 40 healthy controls.52 Reductions in alpha power were observed most strongly during REM but were also seen in SWS and stage 2 in the CFS/ME subjects. The finding of attenuated delta power complements the reduced SWA reported previously following sleep delay,49 providing further evidence of an altered sleep homeostat in CFS/ME. In contrast, Armitage found no difference in any frequency band between twins discordant for CFS/ME.51 There is a clear need for future research utilizing this method of sleep EEG analysis to clarify these findings.
It is also plausible that CFS/ME patients may experience arousals during sleep that are not detected using traditional scoring methods.67 Supporting this idea, more microarousals have been observed in the sleep of CFS/ME patients than healthy control subjects.24,66 Recently, other methods of arousability or sleep instability have been developed and used in this population. Cyclic alternating pattern (CAP) is an EEG-derived measure of sleep instability, which is reflected as periodic EEG activity during NREM sleep.68,69 In contrast, periods of Non-CAP are indicative of consolidated sleep. CAP is somewhat distinct from typically measured arousals from sleep, both as a phenomenon and in terms of how they are scored.69 Clinical studies of insomniacs have found strong correlations between CAP rate (ratio of total CAP time to total NREM sleep time) and subjective reports of sleep quality.70 This measure may therefore provide a more specific marker of sleep quality that the arousal index derived from PSG. Only one study to date has examined CAP rate in CFS/ME patients.22 Despite having similar NREM sleep times, CFS/ME patients had higher CAP rates than matched controls, indicating higher NREM sleep instability in their CFS/ME patients. Abnormal CAP rate was also accompanied by an increase in slow wave delta power. Interestingly, there was no difference in arousal indices between the patient and control groups. A number of CFS/ME patients in this study, however, were found to have nasal cannula flow limitation, indicative of upper airway resistance syndrome (UARS), which may have influenced the findings. CAP has also been associated with UARS and other sleep related breathing disorders previously.71 Whether the higher CAP rate observed in CFS/ME patients was solely a result of UARS is unclear. Importantly, CAP was associated with both subjective fatigue and sleepiness ratings, as has been found previously in other sleep disordered populations.70
Taken together, these studies indicate that conventional sleep stage scoring methods use may not be sensitive enough to detect microstructural changes in CFS/ME patients. Consideration of these microstructure methods for analyzing the sleep EEG may provide a fruitful alternative for uncovering subtle differences during sleep in individuals reporting non-restorative sleep and daytime fatigue.
Autonomic activity alterations, such as hypotension and reduced heart rate variability (HRV), are a common feature of CFS/ME,72 and are a feature of the diagnostic criteria. In healthy individuals, autonomic nervous system dynamics also have characteristic profiles during sleep onset,73 and different sleep stages and depths of sleep.74 In some CFS/ME patients, the autonomic dysfunction observed during waking also transfers into sleep.75 HRV during sleep is consistently found to be significantly lower in CFS/ME patients compared to well-matched controls, reflecting a reduction in nocturnal parasympathetic activity.39,43,75,76 Decreased HRV is thought to reflect a persistent state of autonomic hypervigilance. The influence of daytime physical activity, however, should not be dismissed as a potential confounder. Regression analyses have also demonstrated that HRV is the best predictor of subjective sleep quality in CFS/ME patients in one study.39
Cardiopulmonary coupling (CPC) is another emerging technique, used as a measure of sleep quality and stability based solely on the electrocardiogram (ECG) signal.77 This technique records both heart rate (R-R interval) and respiration dynamics to generate a spectrogram of cardiopulmonary coupling. Based on this output, one can determine periods of high-frequency and low-frequency coupling, indicative of high and low sleep stability. CPC has been used to demonstrate sleep instability in sleep disordered populations,77 major depressive disorder,78 and fibromyalgia.79 There is preliminary evidence that sleep quality and stability measured by CPC is poor in CFS/ME patients, with reduced high-frequency coupling and increased low-frequency coupling.80 Studies utilizing such autonomic activity techniques indicate that autonomic measures during sleep may be a promising mechanism associated with non-restorative sleep in CFS/ME.43
Substantial research examining the pathophysiology of CFS/ME indicates that the hypothalamic-pituitary axis (HPA) may be implicated in this disorder.81,82 The HPA also plays an important role in sleep regulation.83 Dysregulation of the HPA has been examined using salivary cortisol profiling in a few studies.84–86 Morning cortisol levels upon awakening, recognized as an indicator of the HPA response to stress, were attenuated in CFS/ME patients compared to healthy controls,85 with this difference most evident in females with CFS/ME.84 Given that CFS/ME is 2 to 3 times more prevalent in women, it has been proposed that sex differences in hypocortisolism may explain the increased risk of CFS in women.84
Heightened IL-6 plasma levels have also been reported in CFS/ME patients,87 possibly reflecting the low levels of systemic inflammation associated with CFS/ME. However, whether increased levels of IL-6 in this study were directly related to CFS/ME or other confounders such as BMI and underlying sleep disorders is unclear. IL-6 has been implicated in the pathogenesis of psychological and physiological fatigue in healthy individuals,88 and has been reported in other patient groups that suffer debilitating fatigue, such as cancer patients.89 Of direct relevance to this review, altered levels of IL-6 are also associated with somnolence and chronic sleep restriction.59 It is plausible that a link between IL-6 or other inflammatory markers and sleep disturbance in CFS/ME exists; this remains an interesting hypothesis that warrants further investigation.
Neuroimaging studies have allowed researchers to examine the sleeping brain in healthy subjects. These techniques have also applied to clinical populations, including primary insomnia,90 OSA,91,92 and depression.93 Particularly in primary insomnia, functional neuroimaging studies during sleep have helped understand the neurophysiological underpinnings of sleep dysregulation in these patients. In line with the hyperarousal theory of primary insomnia, patients were found to have abnormally high regional brain activity during sleep compared to controls subjects.94 This is proposed as one of the mechanisms contributing to sleep state misperception and sleep disturbance found in such patients. A growing number of studies are using functional neuroimaging to examine CFS/ME patients during wake (see Lange95 for a review). These studies have typically observed altered neural activity during performance of a fatiguing cognitive task in CFS/ME patients relative to controls, in the absence of performance impairment, potentially reflecting greater perceived cognitive effort.96,97 Future studies may also benefit from examining neural function and cerebral blood flow in CFS/ME patients during sleep.
There are still many unanswered questions regarding the pathogenesis and nature of sleep disturbance and unrefreshed sleep in CFS/ME. Sleep disturbance may precipitate CFS/ME, may alter or complicate its course by worsening fatigue, pain, or mood, or may represent an independent factor unrelated to fatigue itself. With the development of new standardized criteria for diagnosing CFS/ME, more homogenous patient samples and comparability across studies will be afforded for future research. Standardized research designs with less ridged imposition of sleep-wake times, and control over medication use and symptoms and comorbid conditions (such as pain and depression) will assist in understanding the state of sleep in CFS/ME.
Non-restorative sleep has a fairly distinct subjective definition; however, the physiological markers that underlie this experience and the extent to which alterations in sleep relate to the experience of non-restorative sleep in these patients are relatively unknown. Does non-restorative sleep stem from hyperarousability, sleep hygiene, or circadian rhythm disturbance, or is it biologically driven in some other way? Is the nature of non-restorative sleep in CFS/ME similar to that experienced in other clinical conditions and by healthy individuals on occasion, or is it a heterogeneous phenomenon? There may also be other symptoms that CFS/ME patients experience that could cause non-restorative sleep, such as upper airway resistance syndrome, food intolerance, or immunological and metabolic changes. Emergence of new methods for analyzing the microstructure of sleep have allowed researchers to detect more subtle EEG changes in CFS/ME patients during sleep. Given that very little is known about the nature and cause of non-restorative sleep, these studies have opened up new avenues for investigating sleep disturbance and non-restorative sleep, not only in CFS/ME but other clinical conditions such as insomnia.
Having a clearer understanding about the pathophysiology of non-restorative sleep in CFS/ME may lead to better treatment options for patients. For example, one theory for the non-restorative sleep experienced in insomnia suggests that negative cognitions trigger autonomic arousal during wakefulness that transfers into sleep.98 Nocturnal arousal is often treated by reducing hyperarousability and cognitions during the day, using cognitive behavioral therapy99 or mindfulness based techniques,100 with the aim of reducing arousal at night. If a similar arousal phenomenon is found during sleep in CFS/ME, then insomnia-based treatments have the potential to be utilized in CFS/ME patients.
More precise tools and analyses for differentiating fatigue and sleepiness are needed. Distinguishing these two states remains a diagnostic challenge for clinicians. While there are validated objective and subjective measures of sleepiness, only subjective measures currently exist for assessing fatigue. Development of an objective measure of fatigue and a questionnaire that assesses both fatigue and sleepiness would be useful not only in the context of CFS/ME, but for assessing other disorders in which both sleepiness and fatigue are a feature. In addition, further research into the relationship between sleep and fatigue is greatly needed.
Patients commonly report improved sleep following some treatment regimes, such as graded exercise therapy and antibiotic treatment for imbalances in gut microbial flora. There are avenues for research into objective assessments of sleep before and after treatment, and to follow the time course of changes in sleep as patients' symptoms improve. Future studies are needed to explore the interaction of sleep homeostasis, SWA, and immune system activation in CFS/ME, given the changes in immune function that are observed in these patients.6
The issue surrounding possible sleep state misperception in CFS/ME raises the question of whether abnormalities in sleep associated with CFS/ME are similar to those found in other populations that experience sleep misperception, such as insomnia, or whether they are specific to CFS/ME. This also raises the question of whether CFS/ME patients report a bigger discrepancy between objective and subjective measures of sleep compared to other medical conditions, and is this relative to the experience of non-restorative sleep? Understanding the association between these two conditions may provide insight into the mechanisms of sleep misperception. Future studies will benefit by incorporating subjective, physiological and behavioral measures of sleep to gain a broader insight into the nature of sleep disturbance of CFS/ME.
Finally, CFS/ME may provide a unique insight into the link between non-restorative sleep and fatigue. Other clinical conditions also experience non-restorative sleep and fatigue, such as FM, narcolepsy, and coronary heart disease,101,102 as well as a high number of otherwise healthy individuals.103 It is plausible that there may be subgroups of such people with fatigue and non-restorative sleep with similar underlying symptoms and etiologies, or, alternatively, there may be a continuum of such symptoms with CFS/ME being at the upper end of the spectrum. Given the constellation of physiological and psychological symptoms characterizing CFS/ME, examining sleep and fatigue in CFS/ME patients may allow us to better understand the neurobiology and etiology of fatigue in other patient populations.
CFS/ME is a complex and severely debilitating condition. Non-restorative sleep, reduced sleep quality, and extended periods of sleep are commonly reported, however the basis of these symptoms are unclear. The heterogeneities associated with this disorder make it challenging for researchers to study and make cross-study comparisons difficult. While there is little evidence of sleep architecture differences between CFS/ME and healthy individuals, many patients subjectively report sleep disturbance and unrefreshed sleep, highlighting a potential disconnect between objective and subjective measures of sleep. There is preliminary evidence that alteration in sleep stage transitions and sleep instability, and other physiological mechanisms such as heart rate variability and altered cortisol profiles, may be implicated in the sleep difficulties of this population. Further research is required to investigate the cause of non-restorative sleep and fatigue in CFS/ME, which may aid understanding of this symptom in other medical conditions.
This was not an industry supported study. Dr. Bruck received industry support from Bioscreen Inc. over three years 2011–2013 for research involving Chronic Fatigue Syndrome patients. The other authors have indicated no financial conflicts of interest.
cyclical alternating pattern
United States Centers for Disease Control and Prevention
chronic fatigue syndrome
continuous positive airway pressure
cardiopulmonary coupling
excessive daytime sleepiness
fast Fourier transform
hypothalamic-pituitary axis
heart rate variability
International Consensus Criteria
International Classification of Diseases
International Classification of Sleep Disorders
interleukin 6
Major Depressive Disorder
myalgic encephalomyelitis
multiple sleep latency test
obstructive sleep apnea
Primary Insomnia
Pittsburgh Sleep Quality Index
stage 1 sleep
stage 2 sleep
Sleep Disorder Questionnaire
sleep efficiency
sleep latency
Stanford Sleepiness Scale
slow wave activity
slow wave sleep
time in bed
total sleep time
Work for this study was performed at Victoria University, Melbourne, Australia.
Jason LA, King CP, Frankenberry EL, et al., authors. Chronic fatigue syndrome: assessing symptoms and activity level. J Clin Psychol. 1999;55:411–24. [PubMed]
Afari N, Buchwald D, authors. Chronic fatigue syndrome: a review. Am J Psychiatry. 2003;160:221–36. [PubMed]
Ranjith G, author. Epidemiology of chronic fatigue syndrome. Occup Med. 2005;55:13–9
Fischler B, author. Review of clinical and psychobiological dimensions of the chronic fatigue syndrome: differentiation from depression and contribution of sleep dysfunctions. Sleep Med Rev. 1999;3:131–46. [PubMed]
Krupp LB, Jandorf L, Coyle PK, Mendelson WB, authors. Sleep disturbance in chronic fatigue syndrome. J Psychosom Res. 1993;37:325–31. [PubMed]
Lorusso L, Mikhaylova SV, Capelli E, Ferrari D, Ngonga GK, Ricevuti G, authors. Immunological aspects of chronic fatigue syndrome. Autoimmunity Rev. 2009;8:287–91
Beard G, author. Neurasthenia, or nervous exhaustion. Boston Med Surg J. 1869;80:217–20
Wolfe F, Smythe HA, Yunus MB, et al., authors. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Arthritis Rheum. 1990;33:160–72. [PubMed]
Friedberg F, Jason LA, authors. Chronic fatigue syndrome and fibromyalgia: Clinical assessment and treatment. J Clin Psychol. 2001;57:433–55. [PubMed]
Holmes GP, Kaplan JE, Gantz NM, et al., authors. Chronic fatigue syndrome: a working case definition. Ann Intern Med. 1988;108:387[PubMed]
Lloyd AR, Wakefield D, Boughton CR, Dwyer J, authors. What is myalgic encephalomyelitis? Lancet. 1988;8597:1286–7
Lloyd AR, Hickie I, Boughton CR, Spencer O, Wakefield D, authors. Prevalence of chronic fatigue syndrome in an Australian population. Med J Australia. 1990;153:522–8. [PubMed]
Sharpe MC, Archard LC, Banatvala JE, et al., authors. A report—chronic fatigue syndrome: guidelines for research. J Royal Soc Med. 1991;84:118
Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A, authors. The chronic fatigue syndrome: a comprehensive approach to its definition and study. Ann Intern Med. 1994;121:953–9. [PubMed]
Reeves WC, Heim C, Maloney EM, et al., authors. Sleep characteristics of persons with chronic fatigue syndrome and non-fatigued controls: results from a population-based study. BMC Neurol. 2006;6:41[PubMed Central][PubMed]
Carruthers BM, Jain AK, Meirleir KLD, et al., authors. Myalgic encephalomyelitis/chronic fatigue syndrome: clinical working case definition, diagnostic and treatment protocols. J Chronic Fatigue Syndr. 2003;11:7–116
Carruthers BM, van de Sande MI, De Meirleir KL, et al., authors. Myalgic encephalomyelitis: International Consensus Criteria. J Intern Med. 2011;270:327–38. [PubMed Central][PubMed]
Morriss RK, Sharpe M, Sharpley AL, Cowen PJ, Hawton K, Morris J, authors. Abnormalities of sleep in patients with the chronic fatigue syndrome. BMJ. 1993;306:1161–4. [PubMed Central][PubMed]
Fossey M, Libman E, Bailes S, et al., authors. Sleep quality and psychological adjustment in chronic fatigue syndrome. J Behav Med. 2004;27:581–605. [PubMed]
Le Bon O, Fischler B, Hoffmann G, et al., authors. How significant are primary sleep disorders and sleepiness in the chronic fatigue syndrome? Sleep Res. 2000;3:43–8
Nisenbaum R, Jones J, Unger E, Reyes M, Reeves W, authors. A population-based study of the clinical course of chronic fatigue syndrome. Health Qual Life Outcomes. 2003;1:49[PubMed Central][PubMed]
Guilleminault C, Poyares D, Da Rosa A, Kirisoglu C, Almeida T, Lopes MC, authors. Chronic fatigue, unrefreshing sleep and nocturnal polysomnography. Sleep Med. 2006;7:513–20. [PubMed]
Buchwald D, Pascualy R, Bombardier C, Kith P, authors. Sleep disorders in patients with chronic fatigue. Clin Infect Dis. 1994;18:S68–S72. [PubMed]
Neu D, Cappeliez B, Hoffmann G, Verbanck P, Linkowski P, Le Bon O, authors. High slow-wave sleep and low-light sleep: Chronic fatigue syndrome is not likely to be a primary sleep disorder. J Clin Neurophysiol. 2009;26:207–12. [PubMed]
Libman E, Creti L, Baltzan M, Rizzo D, Fichten CS, Bailes S, authors. Sleep apnea and psychological functioning in chronic fatigue syndrome. J Health Psychol. 2009;14:1251–67. [PubMed]
Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S, authors. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328:1230–5. [PubMed]
Osorio CD, Gallinaro AL, Lorenzi-Filho G, et al., authors. Sleep quality in patients with fibromyalgia using the Pittsburgh Sleep Quality Index. J Rheumatol. 2006;33:1863–5. [PubMed]
Lavigne G, Brousseau M, Kato T, et al., authors. Experimental pain perception remains equally active over all sleep stages. Pain. 2004;110:646–55. [PubMed]
Modofsky, H, authors. The significance, assessment, and management of nonrestorative sleep in fibromyalgia syndrome. CNS Spectrums. 2008;13:22–6
Older SA, Battafarano DF, Danning CL, authors. The effects of delta wave sleep interruption on pain thresholds and fibromyalgia-like symptoms in healthy subjects; correlations with insulin-like growth factor I. J Rheumatol. 1998;25:1180–6. [PubMed]
Benca RM, Obermeyer WH, Thisted RA, Gillin JC, authors. Sleep and psychiatric disorders: A meta-analysis. Arch Gen Psychiatry. 1992;49:651–68. [PubMed]
Morriss RK, Wearden AJ, Battersby L, authors. The relation of sleep difficulties to fatigue, mood and disability in chronic fatigue syndrome. J Psychosom Res. 1997;42:597–605. [PubMed]
Le Bon O, Minner P, Van Moorsel C, et al., authors. First-night effect in the chronic fatigue syndrome. Psychiatry Res. 2003;120:191–9. [PubMed]
Fischler B, Le Bon O, Hoffmann G, Cluydts R, Kaufman L, De Meirleir K, authors. Sleep anomalies in the chronic fatigue syndrome. Neuropsychobiology. 1997;35:115–22. [PubMed]
Stores G, Fry A, Crawford C, authors. Sleep abnormalities demonstrated by home polysomnography in teenagers with chronic fatigue syndrome. J Psychosom Res. 1998;45:85–91. [PubMed]
Sharpley A, Clements A, Hawton K, Sharpe M, authors. Do patients with pure chronic fatigue syndrome (neurasthenia) have abnormal sleep? Psychosom Med. 1997;59:592–6. [PubMed]
Whelton CL, Salit I, Moldofsky H, authors. Sleep, Epstein-Barr virus infection, musculoskeletal pain, and depressive symptoms in chronic fatigue syndrome. J Rheumatol. 1992;19:939[PubMed]
Togo F, Natelson BH, Cherniack N, FitzGibbons J, Garcon C, Rapoport DM, authors. Sleep structure and sleepiness in chronic fatigue syndrome with or without coexisting fibromyalgia. Arthiritis Res Ther. 2008;10:R56
Burton A, Rahman K, Kadota Y, Lloyd A, Vollmer-Conna U, authors. Reduced heart rate variability predicts poor sleep quality in a case-control study of chronic fatigue syndrome. Exp Brain Res. 2010;204:71–8. [PubMed]
Ohinata J, Suzuki N, Araki A, Takahashi S, Fujieda K, Tanaka H, authors. Actigraphic assessment of sleep disorders in children with chronic fatigue syndrome. Brain Dev. 2008;30:329–33. [PubMed]
Evering RMH, van Weering MGH, Groothuis-Oudshoorn KCGM, Vollenbroek-Hutten MMR, authors. Daily physical activity of patients with the chronic fatigue syndrome: a systematic review. Clin Rehabil. 2011;25:112–33. [PubMed]
Tryon WW, Jason L, Frankenberry E, Torres-Harding S, authors. Chronic fatigue syndrome impairs circadian rhythm of activity level. Physiol Behav. 2004;82:849–53. [PubMed]
Rahman K, Burton A, Galbraith S, Lloyd AR, Vollmer-Conna U, authors. Sleep-wake behavior in chronic fatigue syndrome. Sleep. 2011;34:671–8. [PubMed Central][PubMed]
Watson NF, Kapur V, Arguelles LM, et al., authors. Comparison of subjective and objective measures of insomnia in monozygotic twins discordant for chronic fatigue syndrome. Sleep. 2003;26:324–8. [PubMed]
Ball N, Buchwald DS, Schmidt D, Goldberg J, Ashton S, Armitage R, authors. Monozygotic twins discordant for chronic fatigue syndrome: Objective measures of sleep. J Psychosom Res. 2004;56:207–12. [PubMed]
Majer M, Jones J, Unger E, et al., authors. Perception versus polysomnographic assessment of sleep in CFS and non-fatigued control subjects: results from a population-based study. BMC Neurol. 2007;7:40[PubMed Central][PubMed]
Neu D, Mairesse O, Hoffmann G, et al., authors. Sleep quality perception in the chronic fatigue syndrome: correlations with sleep efficiency, affective symptoms and intensity of fatigue. Neuropsychobiology. 2007;56:40–6. [PubMed]
Le Bon O, Neu D, Valente F, Linkowski P, authors. Paradoxical NREMS distribution in "pure" chronic fatigue patients: a comparison with sleep apnea-hypopnea patients and healthy control subjects. J Chronic Fatigue Syndrome. 2007;14:2
Armitage R, Landis C, Hoffmann R, et al., authors. The impact of a 4-hour sleep delay on slow wave activity inb twins discordant for chronic fatigue syndrome. Sleep. 2007;30:657–62. [PubMed]
Kishi A, Struzik ZR, Natelson BH, Togo F, Yamamoto Y, authors. Dynamics of sleep stage transitions in healthy humans and patients with chronic fatigue syndrome. Am J Physiol. 2008;294:R1980–R7
Armitage R, Landis C, Hoffmann R, et al., authors. Power spectral analysis of sleep EEG in twins discordant for chronic fatigue syndrome. J Psychosom Res. 2009;66:51–7. [PubMed Central][PubMed]
Decker M, Tabassum H, Lin J-M, Reeves W, authors. Electroencephalographic correlates of chronic fatigue syndrome. Behav Brain Funct. 2009;5:1–8. [PubMed Central][PubMed]
Creti L, Libman E, Baltzan M, Rizzo D, Bailes S, Fichten CS, authors. Impaired sleep in chronic fatigue syndrome. J Health Psychol. 2010;15:596–607. [PubMed]
Kishi A, Natelson BH, Togo F, Struzik ZR, Rapoport DM, Yamamoto Y, authors. Sleep stage transitions in chronic fatigue syndrome patients with or without fibromyalgia. Engineering in Medicine and Biology Society (EMBC). Annual International Conference of the IEEE. 2010;5391–4
Van Cauter E, Leproult R, Plat L, authors. Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men. JAMA. 2000;284:861–8. [PubMed]
Manu P, Lane TJ, Matthews DA, Castriotta RJ, Watson RK, Abeles M, authors. Alpha-delta sleep in patients with a chief complaint of chronic fatigue. South Med J. 1994;87:465–70. [PubMed]
Flanigan MJ, Morehouse RL, Shapiro CM, authors. Determination of observer-rated alpha activity during sleep. Sleep. 1995;18:702–6. [PubMed]
Dijk D-J, Brunner DP, Beersma D, Borbely AA, authors. Electroencephalogram power density and slow wave sleep as a function of prior waking and circadian phase. Sleep. 1990;13:430–40. [PubMed]
Madje JA, Krueger JM, authors. Links between the innate immune system and sleep. J Allergy Clin Immunol. 2005;116:1188–98. [PubMed]
Majde JA, Krueger JM, authors; D'haenen H, editor. Neuroimmunology of sleep. Textbook of biological psychiatry. 2002. London: John Wiley – Sons, Ltd; p. 1247–57
Watson NF, Jacobsen C, Goldberg J, Kapur V, Buchwald DS, authors. Subjective and objective sleepiness in monozygotic twins discordant for chronic fatigue syndrome. Sleep. 2004;27:973–7. [PubMed]
Jackowska M, Dockray S, Hendrickx H, Steptoe A, authors. Psychosocial factors and sleep efficiency: discrepancies between subjective and objective evaluations of sleep. Psychosom Med. 2011;73:810–6. [PubMed]
Edinger JD, Krystal AD, authors. Subtyping primary insomnia: is sleep state misperception a distinct clinical entity? Sleep Med Rev. 2003;7:203–14. [PubMed]
Pigeon WR, Sateia MJ, Ferguson RJ, authors. Distinguishing between excessive daytime sleepiness and fatigue: Toward improved detection and treatment. J Psychosom Res. 2003;54:61–9. [PubMed]
Neu D, Hoffmann G, Moutrier R, Verbanck P, Linkowski P, Le Bon O, authors. Are patients with chronic fatigue syndrome just 'tired' or also 'sleepy'? J Sleep Res. 2008;17:427–31. [PubMed]
Rechtschaffen A, Kales A, authors. A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects. 1968. U.S. Government Printing Office: Public Health Service;
Terzano MG, Mancia D, Salati MR, Costani G, authors. The cyclic alternating pattern as a physiologic component of normal NREM sleep. Sleep. 1985;8:137–45. [PubMed]
Terzano MG, Parrino L, authors. Origin and significance of the cyclic alternating pattern (CAP). Sleep Med Rev. 2000;4:101–23. [PubMed]
Parrino L, Milioli G, De Paolis F, Grassi A, Terzano MG, authors. Paradoxical insomnia: The role of CAP and arousals in sleep misperception. Sleep Med. 2009;10:1139–45. [PubMed]
Guilleminault C, Lopes MC, Hagen CC, Da Rosa A, authors. The cyclic alternating pattern demonstrates increased sleep instability and correlates with fatigue and sleepiness in adults with upper airway resistance syndrome. Sleep. 2007;30:641–7. [PubMed]
Yamamoto Y, LaManca JJ, Natelson BH, authors. A measure of heart rate variability is sensitive to orthostatic challenge in women with chronic fatigue syndrome. Exp Biol Med. 2003;228:167–74
Shinar Z, Akselrod S, Dagan Y, Baharav A, authors. Autonomic changes during wake-sleep transition: A heart rate variability based approach. Auton Neurosci. 2006;130:17–27. [PubMed]
Trinder J, Kleiman J, Carrington M, et al., authors. Autonomic activity during human sleep as a function of time and sleep stage. J Sleep Res. 2001;10:253–64. [PubMed]
Boneva RS, Decker MJ, Maloney EM, et al., authors. Higher heart rate and reduced heart rate variability persist during sleep in chronic fatigue syndrome: A population-based study. Auton Neurosci. 2007;137:94–101. [PubMed]
Tajima S, Kuratsune H, Yamaguti K, et al., authors. Estimation of fatigue state in patient with CFS using actigraph and R-R interval power spectrum analysis. Jpn J Clin Med. 2007;65:1057–64
Thomas RJ, Mietus JE, Peng CK, Goldberger AL, authors. An electrocardiogram-based technique to assess cardiopulmonary coupling during sleep. Sleep. 2005;28:1151–61. [PubMed]
Yang AC, Yang C-H, Hong C-J, et al., authors. Sleep state instabilities in major depressive disorder: Detection and quantification with electrocardiogram-based cardiopulmonary coupling analysis. Psychophysiol. 2011;48:285–91
Thomas RJ, Mietus JE, Peng C-K, Goldberger AL, Crofford LJ, Chervin RD, authors. Impaired sleep quality in fibromyalgia: Detection and quantification with ECG-based cardiopulmonary coupling spectrograms. Sleep Med. 2010;11:497–8. [PubMed Central][PubMed]
Cunnington D, Buccella D, Bastiampillai S, Swieca J, authors. Sleep architecture and sleep stability in chronic fatigue syndrome. J Sleep Res. 2011;20:25
Demitrack M, Dale J, Straus S, et al., authors. Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. J Clin Endocrinol Metab. 1991;73:1224–34. [PubMed]
Di Giorgio A, Hudson M, Jerjes W, Cleare AJ, authors. 24-Hour pituitary and adrenal hormone profiles in Chronic Fatigue Syndrome. Psychosom Med. 2005;67:433–40. [PubMed]
Vgontzas A, Chrousos G, authors. Sleep, the hypothalamic-pituitary-adrenal axis, and cytokines: multiple interactions and disturbances in sleep disorders. Endocrinol Metab Clin North Am. 2002;31:15–36. [PubMed]
Nater UM, Maloney E, Boneva RS, et al., authors. Attenuated morning salivary cortisol concentrations in a population-based study of persons with chronic fatigue syndrome and well controls. J Clin Endocrinol Metab. 2008;93:703–9. [PubMed]
Roberts ADL, Wessely S, Chalder T, Papadopoulos A, Cleare AJ, authors. Salivary cortisol response to awakening in chronic fatigue syndrome. Br J Psychiatry. 2004;184:136–41. [PubMed]
Jerjes WK, Cleare AJ, Wessely S, Wood PJ, Taylor NF, authors. Diurnal patterns of salivary cortisol and cortisone output in chronic fatigue syndrome. J Affect Disord. 2005;87:299–304. [PubMed]
Nater UM, Youngblood LS, Jones JF, et al., authors. Alterations in diurnal salivary cortisol rhythm in a population-based sample of cases with chronic fatigue syndrome. Psychosom Med. 2008;70:298–305. [PubMed]
Singh A, Petrides JS, Gold PW, Chrousos GP, Deuster PA, authors. Differential hypothalamic-pituitary-adrenal axis reactivity to psychological and physical stress. J Clin Endocrinol Metab. 1999;84:1944–8. [PubMed]
Schubert C, Hong S, Natarajan L, Mills PJ, Dimsdale JE, authors. The association between fatigue and inflammatory marker levels in cancer patients: a quantitative review. Brain Behav Immunol. 2007;21:413–27
Smith MT, Perlis ML, Chengazi VU, et al., authors. Neuroimaging of NREM sleep in primary insomnia: a Tc-99-HMPAO single photon emission computed tomography study. Sleep. 2002;25:325–35. [PubMed]
Morrell MJ, Jackson ML, Twigg GL, et al., authors. Changes in brain morphology in patients with obstructive sleep apnoea. Thorax. 2010;65:908–14. [PubMed]
O'Donoghue FJ, Wellard RM, Rochford PD, et al., authors. Magnetic resonance spectroscopy and neurocognitive dysfunction in obstructive sleep apnea before and after CPAP treatment. Sleep. 2012;35:41–8. [PubMed Central][PubMed]
Nofzinger EA, Price JC, Meltzer CC, Buysee DJ, Villemagne VL, Miewald JM, authors. Towards a neurobiology of dysfunctional arousal in depression: the relationship between beta EEG power and regional cerebral glucose metabolism during NREM sleep. Psychiatry Res. 2000;98:71–91. [PubMed]
Nofzinger EA, Buysee DJ, Germaine A, Price JC, Miewald JM, Kupfer DJ, authors. Functional neuroimaging evidence for hyperarousal in insomnia. Am J Psychiatry. 2004;161:2126–8. [PubMed]
Lange G, Wang S, DeLuca J, Natelson BH, authors. Neuroimaging in chronic fatigue syndrome. Am J Med. 1998;105:50S–3S. [PubMed]
Cook DB, O'Connor PJ, Lange G, Steffener J, authors. Functional neuroimaging correlates of mental fatigue induced by cognition among chronic fatigue syndrome patients and controls. Neuroimage. 2007;36:108–22. [PubMed]
Schmaling KB, Lewis DH, Fiedelak JI, Mahurin R, Buchwald DS, authors. Single-photon emission computerized tomography and neurocognitive function in patients with chronic fatigue syndrome. Psychosom Med. 2003;65:129–36. [PubMed]
Harvey AG, author. A cognitive model of insomnia. Behav Res Ther. 2002;40:869–93. [PubMed]
Harvey AG, author. A cognitive theory and therapy for chronic insomnia. J Cogn Psychother. 2005;19:41–59
Lundh LG, author. The role of acceptance and mindfulness in the treatment of insomnia. J Cogn Psychother. 2005;19:29–39
Modofsky H, author. The significance, assessment, and management of nonrestorative sleep in fibromyalgia syndrome. Sleep Med. 2008;13:22–6
Droogleever Fortuyn HA, Fronczek R, Smitshoek M, et al., authors. Severe fatigue in narcolepsy with cataplexy. J Sleep Res. 2012;21:163–9. [PubMed]
Ohayon MM, author. Prevalence and correlates of nonrestorative sleep complaints. Arch Intern Med. 2005;165:35–41. [PubMed]


text: So, how can creating a poster for a Wilco or Nine Inch Nails show help us to better sell your product or service? The answer is simple: We get to push our creative boundaries. That freedom and opportunity to experiment means we're better prepared creatively when it comes to your projects. Here's a sampling of some of our favorite posters from over the years. To purchase posters or to see a complete archive of our poster designs, please visit the Poster Store.


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There was an expression in London that "The King is always right." Here we have the IRS that says almost the same thing. You may feel that you a have a bonafide case, but that is not always the way it turns out. Here is the sad story of a couple filing jointly and taking a tax deduction of over $25,000 in charitable contributions on their tax return. The majority of these payments were made by check to their church. The IRS sent them a letter of deficiency denying them this deduction. They bundled copies of these checks along with a statement from their church to support their claim. But the IRS did not accept this positive assertion from the church because it did not include the wording that "no goods or services" were provided for these contributions.
So the taxpayers requested the church officials to complete another acknowledgment of the contributions and indicate that there were no "goods or services" granted. After receipt, they forwarded this letter to the IRS and they were denied the deduction again. This time the refusal was centered on the fact it was not "contemporaneous" based on the Internal Revenue Code (section 170(f)(8)(A). That states that "no deduction shall be allowed for any contribution of $250. or more unless the taxpayer substantiates the donation by receiving written acceptance stating that the taxpayer did not receive any goods or services". This written acknowledgment meets the contemporaneous definition if it had been received before the taxpayer files the original return for the year of the contribution by the due date or a later date that includes extensions.
In this case the IRS claims the first acknowledgement from the church did not include the language "no goods or services" were provided for the contribution and the second letter failed the contemporaneous requirement.
The taxpayers took this case to tax court and conceded that they did not strictly comply with the statute. But they also claimed that they did substantially comply with statute. The court disagreed with the couple and stated that there is nothing in the statute that requires the IRS to look beyond the written acknowledgement when on the face of the letter the information was not properly presented. The decision rested on the premise that the requirements of this regulation was not clearly substantiated. This raises a question. What if there had been a letter received from the church before the original filing of the return was lost? Or misplaced? Would the IRS accept a letter from the church upon audit? After each donation of more than $250 would there have to be a letter received? Or can a year end all inclusive acknowledgment be acceptable?
Court dealings with IRS regulation
These kinds of decisions are causing much grief and consternation to tax practitioners with respect to dealing with the IRS. Many question what gives the IRS the power to interpret what the statutory language devised by Congress meant at the time of the legislation. Is it also allowed to have these regulations determined to be retroactive? The Supreme Court in an earlier case asked the following two questions regarding statutory language. Is it ambiguous, and if so is the regulation a reasonable interpretation of the law? If both questions can be answered with a yes, then the regulation will stand. Had a enough of regulations?
Observation: It is a mistake to believe that shorter hours and less work will produce a higher standard of living.
Edward J. Loughrey, CFE, EA, LPA can be reached at email@example.com or at 843-705-7258.


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The Victorian Society in America publishes an award-winning scholarly magazine, Nineteenth Century, twice per year, and the seasonal Victorian Quarterly newsletter, published four times per year. Back issues of our publications are available at a nominal price plus shipping while supplies last.
Nineteenth Century
The flagship publication of the Victorian Society in America is the respected Nineteenth Century, published in the Spring and Fall as a benefit to members.
It is devoted to the cultural and social history of the United States during the Victorian era, with regular features on Architecture, Fine arts, Decorative arts, Interior design, Life-style, Clothing, Photography, and more.
We encourage features on personalities, material culture, architecture, gardens, interior design, fine and decorative arts, and photography. Submitted manuscripts are reviewed by an editorial board. Click here for how to submit an article for consideration.
Nineteenth Century is accepting new advertisers. Please click here if you are interested in advertising in our publications.
Editor: Warren Ashworth
Consulting Editor: William Ayres
Book Review Editor: Karen Zukowski
Advertising Manager/Graphic Designer: Wendy Midgett
The Victorian Quarterly, published since 2009, is the current newsletter of the Society. It contains news of national and chapter events, exhibitions, symposia and books, as well as features on individual members and business partners. The current newsletter is available online, and·in hard copy for those without computer access.
Editor: Sue Verzella, Business Manager
The Victorian, a newsletter published by The Victorian Society in America from 1981 to 2008 focused on then-current activities and the latest news from the Society's local chapters. The Victorian listed nineteenth century exhibitions, lectures, trips, symposia, new books, grants, and educational opportunities within the United States. Back issues of The Victorian may be available at a nominal price plus shipping while supplies last.


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Car Recall
Honda Recalls 2012 Civic
- Recall addresses improperly seated driver's-side driveshaft
- Separation of driveshaft could cause a loss of power or result in a parked car rolling away
- Recall effort to begin on or around June 21
Honda has initiated a voluntary recall to address improper assembly of the driver's-side driveshaft on as many as 50,190 Civics. In a filing with the National Highway Traffic Safety Administration (NHTSA), the federal agency handling vehicle safety recalls, Honda says proper assembly of the driveshaft in some 2012 Civics was not completed because an assembly machine error was inconsistently remedied.
Driveshaft separation could cause a loss of power during driving. If a driveshaft separates on a parked car and the parking brake is not set, the vehicle could roll away, potentially causing injury or a crash.
The first claim of driveshaft separation on the new Civic was reported by a Honda dealer early this year. Since, the company has received 23 additional claims for the same issue but no reports of any related injuries or deaths.
Honda says that, to ensure proper assembly, the driveshaft must be seated and a retaining clip set. A machine error resulted in improperly seated driveshafts. Machine operators attempted to correct the issue, but the solution was not consistently effective.
While recall campaigns sometimes take more than a month from announcement to start, Honda is acting quickly to remedy this issue. Notification of customers is expected to begin around June 21. Honda dealers will inspect and, if necessary, replace the driver's-side driveshaft at no charge.
This is the second recall for the 2012 Honda Civic. The first, which began last month, addressed a misaligned O-ring in the fuel system on a small number of vehicles.
For more information, owners may call Honda Customer Service at 800-999-1009 and reference campaign S40. Alternately, check campaign ID 12V256000 on the NHTSA website safercar.gov, which lists all automotive recalls, or call NHTSA's vehicle safety hotline at 888-327-4236.
What it means to you: Honda will begin notifying owners of the campaign to remedy a potentially faulty driveshaft connection soon. In the meantime, always use your parking brake.


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Visually Cozy: 5 Warm Color Sofas
If you're looking for a way to add warmth to a room, but aren't ready to commit to a new paint color, consider adding a statement sofa in a vibrant, warm hue. Such pieces draw the eye and immediately switch the temperature of a space. Check out some of my favorites below, in a variety of colors and prices.
1. The Tetra Loveseat in lemongrass from CB2, on sale for $799. Depending on the styling of this sofa, the color can compliment either warm or cool tones, depending on your liking. Plus, certain light reflecting off of this yellow can even bring out cooler, green tones.
2. The super stylish Twilight Sleeper Sofa by Flemming Busk for Softline, available from Design Within Reach, on sale for $1615.00. Definitely an investment, this piece simplifies the concept of a pull-out sofa into a simple cylinder and rectangle.
3. Plushy and inviting, the Klyne sofa in saffron from Crate & Barrel offers a more traditional style, with a brightening twist. $1,199.
4. Bringing back this style of fainting sofa may change the entire feel of your room, but don't be afraid! The Antoinette Fainting Sofa from Urban Outfitters is elegant, yet tongue-in-cheek. $649.
5. Don't forget about this oldie but goodie: a great standby, the Klippan Loveseat in Granån red comes with removable and washable covers, so you can switch the color to your liking. $299 from IKEA.
(Images: as linked above).


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11w,0d. I woke up yesterday morning with the remains of a sore throat (more on how much sickness during pregnancy sucks at a later date)... and a baby bump. Here's why I'm delighted to actually look pregnant so early this time around…
I'm not going to lie—it feels like a bit of a relief to have some visual confirmation of this pregnancy. I continue to have all of the same symptoms I've been having: bigger boobs (requiring a shopping trip for new bras last week), mild but omnipresent morning sickness, and my husband's favorite—hormone-induced mood swings (we've had lots of crying around here). But I still have yet to see my midwives (I'm with a homebirth practice which starts seeing patients at 12 weeks), and I had my one and only ultrasound just shy of 6 weeks (when we saw the heartbeat after a doctor manually tilted my uterus for a better angle)—which means that for a crazy lady like me, I've had ample time to worry about all kinds of things going wrong.
And while I feel so strongly about the importance of women talking honestly about miscarriage and baby loss, right now it's kind of hard to hear others' stories—but it seems like now is the time that everyone wants to tell me about their loss. For example, a recent acquaintance (one so new I don't even know her last name) starting telling me about how much she enjoyed being pregnant—and then paused to reflect that part of her joy was likely because she'd miscarried a previous pregnancy at 3.5 months. Good friends (like the kind you'd think might call as they're peeing on the stick) have waited to reveal pregnancy news until the start of the second trimester or even halfway through a pregnancy because friends of theirs have had stillbirths in the third trimester and they're terrified of the same. And I still can't forget about a friend of a friend who delivered her stillborn baby on the day that was supposed to be her baby shower, after a seemingly normal and healthy pregnancy. I don't want anyone to keep quiet about their loss if they want to share, but I'm having a hard time separating their experiences from my own, especially since I too have miscarried, albeit quite early in a pregnancy.
All of which is to say that waking up yesterday morning to find that I actually look a little pregnant and not just bloated and puffy made me feel pretty good. I'm trying to tune out others' tales of loss and try to relax and even enjoy this pregnancy—but it really is a struggle for me right now, especially hearing stories of loss well beyond the typical first trimester miscarriages.
Did you feel like you had to tune out tales of miscarriage while you were pregnant? Were you ever afraid of losing your pregnancy?


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By: Ms Jen Cork, Category: Museullaneous, Date: 01 Jun 2011
We caught up with Dr Sandy Ingleby, manager of the mammals collection after she had collected the sperm whale jaw from Sydney's Newport Beach.
A few weeks ago a Sperm Whale carcass washed up on the rocks of Sydney's Newport Beach. Recently Dr Sandy Ingleby of the Australian Museum mammalogy collection discussed what this meant for the museum.
Following out first chat, Dr Ingleby went out and collected the specimen to start the process of integrating the jaw into the museums collection. Find out what she had to say.


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V.Group is a leading independent provider of global maritime services in the shipping, offshore, leisure and defence sector.
Baltic Group International (BGI)
Starting in 1990, BGI has earned a strong reputation in the market for the recruitment of marine personnel. Working with many of the world's most prestigious ship owners and operators, the brand provides stability and preferable working conditions to its seafarers.
Marine asset management is a central concept at ITM, and it provides a solid foundation for a continuous process covering the whole life-cycle of an asset, from design to construction, operations, maintenance and disposal.
MARCAS (Marine Contracting Association) is an association with 26 members that have aggregate volume agreements with 70 suppliers, providing best global rates, bringing together a combined purchasing volume for over 1,700 vessesls. Through this volume they are able to negotiate global contracts with suppliers based on best prices and service quality.
Marlins provide a diverse range of training products and services tailored to the needs of companies in the marine industry including the cruise and offshore sectors.
SeaTec Communications
SeaTec Communications supply communication, navigation and entertainment equipment and systems for the Merchant fleet including Cruise, Ferry and Yacht industries.
SeaTec provide products and services to meet the needs of the shipping, offshore, defence and energy renewable industries.
Seatec Repair Services
SeaTec Repair Services offer global footprint repair and installation services of qualified, skilled, and experienced riding squads to undertake various types of projects; whether at sea or at anchor, in ports or shipyards.
UMC International PLC
UMC provide a wide range of proven and affordable solutions for maintaining the integrity and performance of underwater equipment and fittings of vessels and offshore rigs.
V.Delta - a joint venture between V.Ships and the leading Finnish Engineering Company - is a one-stop-shop in ship conversions. Its portfolio ranges from feasibility studies to turn-key projects whereby clients are provided with a full range of services including project management, engineering, procurement, construction supervision, logistics and other related services.
V.Hospitality, a specialist unit promoting manning and hotel services to the global hospitality industry, focuses on two types of services - recruitment and hotel services
V.Ships Offshore
V.Ships Offshore is the marine operations division of V.Group, responsible for the management of assets deployed within the offshore oil, gas and renewable energy markets, from project inception to conclusion, catering for the management of all upstream asset classes.
V.Ships SMD encompasses a network of 18 ship management offices supported by the Divisional Team based in Glasgow. V.Ships offers technical, risk management, procurement and financial expertise and experience.
As well as providing a fully integrated insurance management and claims handling service to existing V.Ships' offices and their customers, V.Scope can offer the same service to third party clients.
V.Ships Agency
V.Ships Agency (VSA) provides worldwide ships agency services on behalf of owners, operators, charterers and managers, in and off port limits, for all types of vessels and cargos.
Oceanic Catering
Oceanic Catering is one of the world's largest specialist marine catering companies, which currently prepares approximately 40,000 meals daily for staff working on some 700 ships throughout the world. Its primary aim is to ensure that meals served are wholesome, well-balanced and ethnically suitable for consumers.
V.Ships Crew
The Manpower Management Services cluster encompasses the recruitment, deployment and management of deck and engine sea staff, as well as staff offering particular skills and expertise. Specialist support services - such as training, travel and payroll management - are also part of the cluster. Collectively, these complement technical management as key service offerings.
V.Ships Leisure
V.Ships Leisure is dedicated to the passenger shipping industry with services encompassing, technical management, hotel operation and catering, crew management, itinerary planning and port operation, Newbuilding and conversion project and supervision, consultancy and asset management.
V.Travel provides a complete travel management service for all those involved in the marine and offshore industry, from crew to corporate travel. The brand has the strength of a global player, supported by its local expertise and provided by it dedicated multilingual staff located throughout the world.