Sleep Deprivation Can Lead To More Pain And Weakness

Today's post from brainlessblogger.blogspot.nl (see link below) looks at the effects of impaired sleep patterns on fibromyalgia patients. Fibromyalgia is also a neurological condition closely linked to other forms of neuropathy and many neuropathy patients are well aware that their problems getting quality sleep have an on-going effect on the rest of their lives. The article looks at studies that suggest that short-term sleep deprivation can lead to an increase in adrenalin production and the patient actually feeling better ('running on adrenalin'). However, long-term sleep impairment does lead to an increase in pain due to fatigue and a build up of over-worked neural activity. Neuropathy patients are often kept awake, or wakened, by the pain or tingling itself, leading to a vicious circle of symptoms that reduce the quality of life considerably. The conclusion is that good sleep is essential - no surprise there but if lack of quality sleep is a problem for you, it's worthwhile getting expert advice to achieve as much undisturbed sleep as is possible in your case.

sleep duration and fibromyalgia pain intensity
Tuesday, January 12, 2016

Insomnia, sleep disorders and impaired sleep have always been considered significant factors in regards to fibromyalgia syndrome and even explored as a cause to the syndrome. It is during deep sleep that people produce significant amounts of growth hormone which repair and maintain muscles. Therefore lack of deep sleep and interrupted sleep, which are predominate features with FM, have long been considered factors in pain intensity along with lack of overall time sleeping. Lack of sleep, therefore, must relate to pain levels. A recent study in the Journal of Pain, 2012, suggests this is not necessarily the case.


The Study


74 people with FM were asked to be a part of the University of Florida study and were observed over a 14 day time period. Given the small test group and time frame of the study we have to take these results with a grain of salt. In the study set up FM patients had a sleep diary where they would record how their sleep went and they also were to rate their pain levels every evening.

"For this study, a research team from the University of Florida hypothesized that decreased total sleep time would predict higher clinical pain in a sample of patients with fibromyalgia…Results of the analysis showed that four sleep measures evaluated in the study failed to significantly predict clinical pain. The authors noted that the effects of impaired sleep, such as fatigue and inactivity, may play more significant roles in clinical pain than measures of sleep duration or insomnia. Sciencedaily.com"

Why the results are surprising

These results are surprising because we would expect the opposite. Historically other studies have shown disruptive sleep patterns in people with chronic pain conditions will produce increased pain. Lack of sleep is in fact a factor that can produce pain in healthy people as well. Given the majority of FM patients have disrupted sleep one would expect the results to show decreased duration of sleep would increase pain the next day.

Why we cannot draw firm conclusions

The study is only of 74 people so this is not a large study and we cannot draw any conclusions from one small study. Secondly, the duration of the study itself was short, only over a span of two weeks, which given the nature of chronic pain and sleep disorders is hardly significant. A few days of less sleep can get someone, who regularly gets disrupted sleep, into a sleep deprivation state running on adrenaline. For the short term this will actually make them function fairly well on a pain basis. They will be in 'fight or flight' mode and not feel as much pain, or at least, not right away. However, accumulated sleep deprivation will cause the pain to build up such that we often see with FM the morning muscle pain being severe in the morning and becoming less severe as the day goes on. Ironically, also with short, disrupted sleep someone with FM may feel very alert in the morning because they have not actually gotten much sleep. They do not feel the pain from being in one position for a long period of time so there is no muscle aches from that. The lack of sleep, initially, makes them feel alert, energized and with no morning stiffness and pain. Whereas, longer durations of sleep are often still of poor quality leaving someone with FM still feeling groggy. They will often wake up with morning stiffness and pain from laying in one position for too long if they have managed to be asleep for any length of time. It is not necessarily duration that is a factor but quality. Therefore, it is not necessarily the case that decreasing the total sleep time would increase the pain the next day with someone with FM. Ten hours of poor quality sleep where the person woke up frequently and spent very little time in deep sleep cannot be compared to five solid good hours of sleep. Ten hours of poor quality sleep may leave the person feeling groggy, stiff and sore, while the five hours of restorative sleep may leave them feeling alert and well rested.

Nevertheless, FM patients suffer from poor quality sleep and, at times, other sleep disorders such as restless leg syndrome (RLS) or sleep apnea. Whether the duration of their sleep affects intensity or not certainly lack of sleep affects fatigue, mood and likely even overall health. It is vital with FM to try and maintain healthy sleep habits and a regular sleep cycle. Quality of sleep is just as important as quantity of sleep.

http://brainlessblogger.blogspot.com/2016/01/sleep-duration-and-fibromyalgia-pain.html

MIGRAINE WITH AURA MAY LEAD TO HEART ATTACK BLOOD CLOTS FOR WOMEN

Women who have migraines with aura, which are often visual disturbances such as flashing lights, may be more likely to have problems with their heart and blood vessels, and those on newer contraceptives may be at higher risk for blood clots, according to two studies released today that will be presented at the American Academy of Neurology's 65th Annual Meeting in San Diego, March 16 to 23, 2013.

The first study showed that migraine with aura is a strong contributor to the development of major cardiovascular events such as heart attack and stroke. The Women's Health Study involved 27,860 women, 1,435 of whom had migraine with aura. During the 15-year study, there were 1,030 cases of heart attack, stroke or death from a cardiovascular cause. The study examined the relative contribution of various vascular risk factors to these major cardiovascular events.

"After high blood pressure, migraine with aura was the second strongest single contributor to risk of heart attacks and strokes," said study author Tobias Kurth, MD, ScD, of INSERM, the French National Institute of Health and Medical Research in Bordeaux and Brigham and Women's Hospital in Boston. Kurth is also a Fellow of the American Academy of Neurology. "It came ahead of diabetes, current smoking, obesity, and family history of early heart disease."

Kurth cautioned that while people with migraine with aura have an increased risk, it does not mean that everyone with migraine with aura will have a heart attack or stroke. He said people with migraine with aura can reduce their risk in the same ways others can, such as not smoking, keeping blood pressure low and weight down and exercising.

The second study looked at women with migraine who take hormonal contraceptives and the occurrence of blood clots. The study involved women with migraine with and without aura who were taking both newer contraceptives such as the contraceptive patch and ring and older contraceptives. Of the 145,304 women who used the contraceptives, 2,691 had migraine with aura and 3,437 had migraine without aura.

Women with migraine with aura were more likely to have experienced blood clot complications such as deep vein thrombosis with all types of contraceptives than women with migraine without aura. For example, 7.6 percent of women with migraine with aura who used a newer generation combined hormonal contraceptive had deep vein thrombosis compared to 6.3 percent of women with migraine without aura, but the timing of the two events is not clear. The occurrence of blood clot complications was also higher in women with migraine who took contraceptives than women taking the contraceptives who did not have migraine.

"Women who have migraine with aura should be sure to include this information in their medical history and talk to their doctors about the possible higher risks of newer contraceptives, given their condition," said study author Shivang Joshi, MD, MPH, RPh, of Brigham and Women's Falkner Hospital in Boston and a member of the American Academy of Neurology.

Kurth's study was supported by the National Institutes of Health. Joshi's study was supported by the Graham Headache Center Research Fund.

Damaged Mitochondria Lead To Nerve Pain Repair Them And The Pain Goes Away!

Today's post from the ever-informative, sciencedaily.com (see link below) delves deep into the cellular behaviour of nerve cells but comes out with a potential benefit for us all in the future. If you feel this is all beyond you on a lazy Sunday morning, don't be put off; read on, because science daily nearly always delivers text that we can all follow. In this case it concerns the energy drivers of nerve cells and they are mitochondria. If the mitochondria are damaged or inhibited in some way then neuropathy is most often the result because if the neurons are deprived of the energy they generate then they just give up the ghost and start short-circuiting in the ways we feel every day. Basically, scientists have found that if the mitochondria are damaged, they can regenerate themselves if the protein that is blocking them, is disabled and that's apparently possible...in the ever-suffering mice in the test labs. Too molecular for you? Well yes but we must take heart that scientists are learning so much more every year and this is leading to improved treatments...however long it takes.

Mobilizing mitochondria may be key to regenerating damaged neurons 
Date:June 7, 2016 Source:Rockefeller University Press

Researchers at the National Institute of Neurological Disorders and Stroke have discovered that boosting the transport of mitochondria along neuronal axons enhances the ability of mouse nerve cells to repair themselves after injury. The study, "Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits," which has been published in The Journal of Cell Biology, suggests potential new strategies to stimulate the regrowth of human neurons damaged by injury or disease.

Neurons need large amounts of energy to extend their axons long distances through the body. This energy -- in the form of adenosine triphosphate (ATP) -- is provided by mitochondria, the cell's internal power plants. During development, mitochondria are transported up and down growing axons to generate ATP wherever it is needed. In adults, however, mitochondria become less mobile as mature neurons produce a protein called syntaphilin that anchors the mitochondria in place. Zu-Hang Sheng and colleagues at the National Institute of Neurological Disorders and Stroke wondered whether this decrease in mitochondrial transport might explain why adult neurons are typically unable to regrow after injury.

Sheng and his research fellow Bing Zhou, the first author of the study, initially found that when mature mouse axons are severed, nearby mitochondria are damaged and become unable to provide sufficient ATP to support injured nerve regeneration. However, when the researchers genetically removed syntaphilin from the nerve cells, mitochondrial transport was enhanced, allowing the damaged mitochondria to be replaced by healthy mitochondria capable of producing ATP. Syntaphilin-deficient mature neurons therefore regained the ability to regrow after injury, just like young neurons, and removing syntaphilin from adult mice facilitated the regeneration of their sciatic nerves after injury.

"Our in vivo and in vitro studies suggest that activating an intrinsic growth program requires the coordinated modulation of mitochondrial transport and recovery of energy deficits. Such combined approaches may represent a valid therapeutic strategy to facilitate regeneration in the central and peripheral nervous systems after injury or disease," Sheng says.

Story Source:

The above post is reprinted from materials provided by Rockefeller University Press. Note: Materials may be edited for content and length.

Journal Reference:
Bing Zhou, Panpan Yu, Mei-Yao Lin, Tao Sun, Yanmin Chen, Zu-Hang Sheng. Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits. The Journal of Cell Biology, 2016; jcb.201605101 DOI: 10.1083/jcb.20160510

 https://www.sciencedaily.com/releases/2016/06/160607151233.htm

Can Neuropathy Lead To Heart Failure

Today's post from healthline.com (see link below) may have you grabbing the phone to make a doctor's appointment straight away, so let's start with the disclaimer that the condition described in this article is very rare indeed! Not only that but heart failure due to neuropathy is only possible if you have autonomic neuropathy (you know, the sort that affects your involuntary functions, breathing, circulation, digestion, sexual function etc etc). The article (like so many) implies that this is only relevant for diabetes patients, which of course is not true (diabetes is the most common cause of neuropathy but there are 100 others!). Nevertheless, it does sound alarming and even logical that the nerve damage that affects so many bodily functions can also affect heart performance. If you have been diagnosed with autonomic neuropathy and are experiencing several of the symptoms associated with that form of neuropathy, you really need to make sure your doctor is aware of far reaching consequences and is taking the necessary steps to test for early warning signs. In this respect, you may need to take the discussion to him or her and not wait for the doctor to think of it. You may even need to be referred to a neurologist to check everything out but it's your body - if you're worried, you need to do something about it.

Ask D'Mine: When Neuropathy Can Kill
 
Written by Wil Dubois | Published on 09 May 2015

The prospect of diabetes complications can be scary indeed. In this week’s edition of our weekly diabetes advice column Ask D’Mine, our columnist Wil Dubois (himself a longtime type 1 who also works as a diabetes educator) offers some thoughts on killer neuropathy, following a troubling news report from overseas.

As our own Mike Hoskins read the news, he started worrying about what it could mean for his own life, so he’s reaching out to Wil himself today for some straight-up 411 on this topic.

Mike H, type 1 of DiabetesMine, writes:

Wil, I read an an article in a British newspaper recently, about a 41-year-old woman with type 1 who died one night while sleeping. She had been diagnosed a quarter-century ago, and was living with autonomic neuropathy. Her husband is quoted as saying she didn’t experience a heart attack or low blood sugar, which is what immediately came to my mind. Instead, a pathology report apparently confirmed that her autonomic neuropathy had “traveled to her chest and stopped her heart from beating in the night.”

WHAT?! I’ve been living with type 1 for many years now and am partially hypo unaware, so the thought of a severe hypo at night killing me is a big fear of mine. But I’ve never heard of this before! Yes, I’ve also lived with neuropathy in my feet and toes for about 10 years now... and I do realize there is more than one type of neuropathy. Still, should I be worried that this could happen to me??

Wil@Ask D’Mine replies: Advanced warning: This will be a downer of a column, filled with pain, despair, and death. We’re going to talk about an extreme complication of diabetes that’s rarely discussed, but may be frightingly more common than any of us wants to accept.

First, can neuropathy stop a beating heart? Yes. I’m sorry to say that it can. But to understand the mechanics behind the grim reaper’s scythe, you need to know a little more about how the heart beats and about the two flavors of neuropathy.

Oh God, where to start? I guess with the blue candle, which of course is a symbol in our D-community of lost loved ones. My condolences to British soccer player Stephen Reeves, the man who lost his T1 wife Louise (pictured) -- and on their wedding anniversary no less! As we say in this part of the world: Siento mucho, which translates to “I am so very sorry.”

Now on to neuropathy. Mike mentioned living with it in his feet and toes. We tend to use “neuropathy” almost like slang, but in most cases its proper name is diabetic peripheral neuropathy (DPN) because it’s the result of damage to the peripheral nerves. It’s caused by the corrosive effects of elevated blood sugars over time, and the best guess is that between 60 and 70% of all D-folks have some degree of peripheral neuropathy. In some people it causes a loss of sensation, and in others is causes phantom pain that ranges from hardly noticeable, to mildly annoying, to absolutely horrific.

DPN impacts us by hitting at how the brain communicates with our bodies through the so-called voluntary movements we make. If I reach out to take a drink of my cup of coffee, I’ve just used my voluntary nerves. I chose to make a movement and my brain sends messages, via assorted nerves, to the muscles in my arm, hand, and fingers to pick up the cup and move it to my mouth. It doesn’t take any particular degree of concentration to do this, but it does require conscious choice. It’s this voluntary system that’s damaged by peripheral neuropathy.

But that's not the only type of neuropathy, and the other type impacts all the things my brain controls in my body that I don't necessarily think about -- my lungs breathing, my stomach digesting, my sweat glads regulating temperature, and yes, my heart beating. That's run by what's called the autonomic nervous system, and that's what is impacted by Diabetic Autonomic Neuropathy -- or DAN as many in the medical profession call it.

DAN most commonly shows up as urinary or digestive issues, the inability to maintain body temperature, eye trouble, exercise intolerance, and crazy drops in blood pressure causing fainting spells. Oh yes, and “resting tachycardia,” when the heart rate explodes while doing nothing.

There’s more, too. Experts now speculate that “brittle” diabetes is caused by DAN, and even hypo unawareness may also be caused by DAN. Oh, grrrreat…

Hi, Dan, nice to meet you, you son of a bitch.

Can this get any worse?

Yes. A subset of DAN is known as CAN, or Cardiovascular Autonomic Neuropathy. This appears to be what got our D-sister in England. The nerves that ran her heart were damaged by her diabetes, ultimately leading to her heart simply not getting the message to keep beating. So it stopped.

Apparently, CAN is linked to a myriad of types of heart failure, with charmingly technical names like cardiac arrest, cardiac dysrhythmia, sudden cardiac death, painless silent ischemia, and the plain and simple “unexpected death.” Top cardiology experts are duking it out as to whether autonomic neuropathy is “causative” or merely a “contributing factor” but I’m not sure that really matters to us if it’s the bullet or the gun.

How common is this heart-stopper? That’s hard to say, and it depends on what group of PWDs you’re looking at, and what degree of automatic neuropathy you are testing for. In the best-case scenario, some established diabetes researchers think it affects only 2.5% of us. On the other hand, 90% of long-term type 1s on transplant lists have it. One large-scale study using heart-rate variability testing put the incidence at 25.3% of us T1s and 34.3% of our T2 cousins.

How serious is it? Well, don’t shoot the messenger, but if you have DAN, your risk of death is double that of D-folks who don’t have it. If you have CAN, your death risk is five times greater.

The onset of autonomic neuropathy and its deadlier subset are usually described as “slow and insidious,” and typically show up in the sixth decade of life. But not always, as another blue candle case study shows of one of our sisters who was only 26 years old when she succumbed to this complication.

So what is anyone doing about this? Well, interestingly, the American Diabetes Association recommends screening for DAN on diagnosis and annually thereafter for type 2s. For T1s, it suggests screening annually once you are five years post-diagnosis. These are the same intervals as for dilated eye exams, and for the same reason. Nerve damage takes some time to happen. With type 2s, the sugars have usually been elevated for a number of years prior to diagnosis, whereas type 1 comes on like a hurricane and at diagnosis the sugar hasn’t been out of whack long enough to have caused nerve damage.

Five years of diabetes is all it takes to cause damage.

Can it be treated? Not so much. It’s one of those treat-by-prevention kinds of complications, and the main thing is to do is to do your damnedest to control your blood sugar. That will help you avoid it, or keep it from getting worse if you already have it.

So what’s the take-away message from this depressing sermon? Should you be worried about this, Mike? Nah. I don’t think so.

First off, you could be the healthiest man in the world and a piece of Soviet-era space junk could fall out of the sky and squish you flat. Death comes to us all at some point. I think we should all do the best we can to keep as healthy as we can, but beyond that I think that worrying about the details is wasted energy.

To me, nothing changes with the new attention on autonomic neuropathy. As a person with diabetes I’ve known all along -- as should you -- that "heart stuff” will have a starring role on my death certificate. That’s the nature of diabetes. Now maybe there will be a new label for the same scythe of the grim reaper. Call it whatever type of heat failure you will, caused by neuropathy or something else, but in the end, does it really matter which?

Disclaimer: As mentioned way up above, this is not a medical advice column. We are PWDs freely and openly sharing the wisdom of our collected experiences — our been-there-done-that knowledge from the trenches. But we are not MDs, RNs, NPs, PAs, CDEs, or partridges in pear trees. Bottom line: we are only a small part of your total prescription. You still need the professional advice, treatment, and care of a licensed medical professional.

http://www.healthline.com/diabetesmine/ask-dmine-other-neuropathy-can-be-killer-complication#1