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Reaching Out’s FREE Monthly Newsletter
MAY 2014 --- Volume 1, Issue 120
Editor’s Choice
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►Support Groups ►Advocacy ►Expressions & Stories ►Latest Information on Research & Treatments
Hope through Awareness – All Reaching Out Services are FREE
What’s in this issue?
Possible Clues to CFS Hyperalgesia vs Allodynia Cannabis Survey Important Links Fibromyalgia Cases
May be Autoimmune Coffee Break Members’ Page Vitamin D for FM Pain Editor’s Note
Possible Clues to Chronic Fatigue Syndrome
Inflammation may play a role, small study suggests
By Alan Mozes
Seeking better insight into chronic fatigue syndrome, a new brain scan investigation has pinpointed what could be the first evidence of a connection between
nerve cell inflammation and the onset of this debilitating and somewhat
mysterious illness, researchers say.
DETAILED and EASY to
understand information on the
causes of Fibromyalgia and
other autoimmune diseases –
and what you can do to get
HEALTHY again.
http://www.health-reports.com
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The finding stems from a small PET scan study, led by Yasuhito Nakatomi of the
RIKEN Center for Life Science Technologies in Hyogo, Japan. The study involved just nine patients with chronic fatigue
syndrome and 10 healthy participants.
However, the investigators believe that their initial results are the first to show that neuro-inflammation is a distinct
feature of chronic fatigue syndrome. This inflammation affects specific areas of the brain that are commonly linked with
the kind of fatigue, pain, depression, and thought-process difficulties long associated with the syndrome, the researchers
noted.
"While the results will need to be confirmed in larger studies, it is a very exciting finding," said Suzanne Vernon, scientific
director of the CFIDS (Chronic Fatigue and Immune Dysfunction Syndrome) Association of America. She was not involved
with the new study.
"This is the first time images of this type of brain inflammation have been seen in chronic fatigue syndrome," she added,
"and provides the evidence of the seriousness and debilitating
nature of this disease."
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The findings appeared online recently in advance of print
publication in the Journal of Nuclear Medicine.
The root cause of chronic fatigue syndrome is the subject of
much debate. While some health experts believe it is bacteria
driven, others think it's most probably brought on by a virus.
The syndrome -- which can take hold without warning -- is
typically characterized by extreme exhaustion, muscle and joint
pain, sleep difficulties and thinking problems. The result is often
an inability to perform even simple everyday tasks.
-Continued On Next Page-
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1
In the new study, all the participants first filled out questionnaires that asked them to indicate to what degree they were
experiencing any telltale signs of chronic fatigue syndrome.
Brain imaging was then conducted in key areas of the brain, including the cingulate cortex, hippocampus, amygdala,
thalamus, midbrain, and pons regions.
All signs of neuro-inflammation were then stacked up against chronic fatigue syndrome symptoms.
The result? While nerve cell inflammation was found to be "widespread" throughout the brains of chronic fatigue
syndrome patients, no such inflammation was observed among the healthy study participants.
Vernon said the study also found a graded relationship between levels of inflammation and the severity of disease.
"The higher the inflammation, the more severe the patients' symptoms," she noted.
The study authors further found that neuro-inflammation spiked in patterns that directly correlated with chronic fatigue
syndrome symptoms, ratcheting up in brain regions that are central to thought-processes typically impaired by the
condition.
That said, Nakatomi's team did not establish a direct cause-and-effect relationship between brain changes and chronic
fatigue syndrome. And the finding does not make clear whether such brain inflammation actually precedes the onset of the
condition or occurs as a result.
However, the authors suggested that their work should be viewed as a "proof of concept" that brain scanning could be a
useful way to screen for chronic fatigue syndrome, to both diagnose the disease and assess disease severity on a case-bycase basis.
Dr. Jim Pagel, an associate clinical professor at the University of Colorado Medical School System, said the study findings
make sense, and might be most helpful in the context of future research.
"There's no question that chronic fatigue syndrome is a real diagnosis. It's just a question as to how do you actually make
that diagnosis? What is the definition? What are the criteria?" said Pagel, who is also director of the Sleep Disorders Center
of Southern Colorado, in Pueblo, Colo.
"And for that I wouldn't say that this work ties PET scans to a clear method for diagnosis, or to any clear treatment
approach," he said.
"I really don't think this means that everybody should go out and get a PET scan to diagnose [chronic fatigue syndrome],"
Pagel said. "But at the same time, it doesn't surprise me at all there would be a potential level of nerve inflammation in
certain groupings of people with [the condition]. It certainly fits with what we know. And I think this finding will be useful
as the research continues."
http://www.webmd.com/chronic-fatigue-syndrome/news/20140502/brain-scans-spot-possible-clues-to-chronic-fatigue-syndrome
“Life is ten percent what happens to you and
ninety percent how you respond to it.”
-Lou Holtz
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2
2
What is Hyperalgesia?
What is Allodynia?
Two of the most commonly used terms in the pain research and medicine world are hyperalgesia and
allodynia. The word hyperalgesia means an increased response to a painful stimulus. The word allodynia
means a painful response to a normally innocuous stimulus.
Here is an example of hyperalgesia: if your arm was pricked by a pin and you said that it gave you 3 out of 10
pain this would be your baseline response. If an experimenter then gave you some injection (let’s say capsaicin
— the pungent ingredient in hot peppers) and then 30 minutes later pricked you with the pin again and you
reported 6 out of 10 pain this would be hyperalgesia. For hyperalgesia to occur it is important for the stimulus
to be painful to begin with. Remember that hyperalgesia is always an increased pain response to a noxious
stimulus.
Here is an example of allodynia: if an experimenter brushed your arm with a cotton bud (like a q-tip) you
would almost certainly say that the stimulus was not painful — 0 out of 10. If the experimenter then injected
your arm with capsaicin and brushed your arm again 30 minutes later you would likely report that it was
painful — let’s say 4 out of 10 pain. This is an allodynia, a painful response to an innocuous stimulus. In order
for allodynia to occur the stimulus MUST NOT normally be painful.
So now that we know what these word mean it is time to understand why they occur. First of all, there are a
variety of pain conditions where one of these conditions is present but not the other. This is because they are
mechanistically different. Sensory neurons that innervate your skin and visceral organs roughly fall into three
categories: 1) Rapidly adapting mechanotransducers. These are neurons that respond to touch and nonnoxious temperatures, they conduct action potentials (or nerve impulses) rapidly and they make a subset of
nerve fibers called A-beta fibers. 2) Proprioceptive neurons. These are neurons that tell you about the position
of your muscles, they also conduct action potentials rapidly and they comprise the other subset of nerve fibers
called A-beta fibers. 3) Nociceptors. These are pain sensing neurons that respond to painful mechanical or
thermal stimulation. They also comprise the class of neurons that respond to chemical irritants (like capsaicin).
They are lightly or unmyelinated so they conduct action potentials more slowly than A-beta fibers. They also
generally fail to adapt to stimulation so they keep firing until the stimulus is removed or escaped from. These
neurons fall into two classes, A-delta (the lightly myelinated ones) or C-fibers (the unmyelinated ones).
Neurons of all of these classes send a projection into the dorsal horn of the spinal cord where processing of
incoming sensory information first occurs (all you neuroscientists forget about A-betas and the dorsal
funiculus, they send a projection to lamina III as well where they synapse on interneurons that send
projections back into lamina I/II). This processing center in the dorsal horn of the spinal cord is commonly
referred to as “the gate” — a term that was spawned from Melzack and Wall’s famous gate theory of pain
control. These signals are then sent onto the brain where sensory perception occurs.
The physiological basis of hyperalgesia and allodynia lies in the distinction between the type of fibers that carry
the information evoked by the stimulus in the periphery.
-Continued on page 6-
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3
Survey: Fibromyalgia Patients Report
Subjective Relief From Cannabis
Fibromyalgia patients who have tried cannabis say that it is more likely to relieve their
symptoms than are conventional alternatives, according to the findings of an online survey of
over 1,300 subjects conducted by The National Pain Foundation and NationalPainReport.com.
Of those surveyed, 379 respondents reported having used cannabis therapeutically. Sixty-two
percent of them rated the substance to be "very effective" in the treatment of their
condition. Only five percent of said that cannabis did "not work at all."
By comparison, among those who had used the prescription drug Cymbalta, only eight
percent rated the drug as "very effective," and 60 percent said it did "not work at all." Among
those who had used Lyrica, ten percent said that drug was "very effective," versus 61 percent
who reported no relief. Among those who had used Savella, ten percent rated the drug as
effective, and 68 percent said it was ineffective.
Each of the three prescription drugs assessed in the survey is approved by the US Food and
Drug Administration for the treatment of fibromyalgia, a chronic pain syndrome characterized
by widespread musculoskeletal pain, fatigue and multiple tender points in the neck, spine,
shoulders and hips. An estimated five million Americans are afflicted by fibromyalgia, which is
often poorly controlled by standard pain medications.
Source: http://norml.org
Important Links
For a more complete list, please visit our web site at http://www.reaching-out.info. Remember, we offer FREE
advocacy services. If you need help with something and can’t find a link here or on our web site, please email me at
mailto:[email protected].
CFIDs Assoc. of America: http://www.cfids.org
National FM Assoc.: http://www.fmaware.org
American Academy of Pain: http://www.painmed.org
WebMD: http://www.webmd.com
IMMUNE SUPPORT: http://www.immunesupport.com
FM/CFS/ME Resources: http://fmcfsme.com/
Arthritis Foundation: http://www.arthritis.org
Am. Pain Society: http://www.ampainsoc.org
Needy Meds: http://www.needymeds.com
Social Security Admin.: http://www.ssa.gov
Good Doctor List: http://www.co-cure.org/Good-Doc.htm
Fibro Coalition: http://www.fibrocoalition.org
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4
Some Fibromyalgia Cases May be Autoimmune, Demyelinating
Adrienne Dellwo
Is fibromyalgia more like multiple sclerosis (MS) than we thought? A unique line of research is making it look that way. First, a few things
about MS. It's believed to be an autoimmune disease. Symptoms are caused by something called demyelination, which means destruction
of myelin.
Myelin is a specialized cell that covers some nerves and is necessary for them to function properly. It's similar to insulation on electrical
wires. A predominant theory is that, in MS, the immune system malfunctions and destroys the myelin sheath. Areas where the myelin is
destroyed are called lesions.
Fibromyalgia & Demyelination
The first study2 of fibromyalgia and demyelination came out in 2008, and the follow-up3 was just published this month.
The 2008 research suggested that a subset of fibromyalgia involved autoimmune deymyelination and polyneuropathy (pain from damaged
nerves.) It compared fibromyalgia to a neurological illness called chronic inflammatory demyelinating polyneuropathy, which is often
treated with intravenous immunoglobulin (IVIg.)
In fact, in that study, they used IVIg to treat people from this fibromyalgia subgroup. Granted, it was a small study and that was only 15
people, but researchers say those people had significantly less pain and tenderness plus improved strength, along with smaller
improvements in fatigue and stiffness.
This is a good example of how a preliminary study can have seemingly huge implications and yet have little or no impact. Yes, some
doctors have used IVIg on patients, but it's far from a widespread treatment and demyelination in fibromyalgia is almost never discussed.
Fast forward six years, and at last we have a follow-up study that appears to confirm the earlier findings as well as advancing them. It's
also supported by other work that's been done in the past few years.
Newer Findings
First, the researchers wanted to explore whether the demyelination of large fibers (bigger nerves,) found in the earlier study, is caused by
autoimmunity. Then, they also wanted to explore small fiber neuropathy, which has been suggested by other studies to be a part of
fibromyalgia.
Small fiber neuropathy is painful damage to structures in the of the skin, organs, and peripheral nerves that provide sensation and help
regulate automatic functions like heart rate and body temperature. Researchers were interested in it because it's known that small fiber
neuropathy is sometimes associated with demyelination lesions on large fibers.
They found indicators of small fiber neuropathy, including diminished feeling in the lower legs. Also tested were multiple markers of
immune activation and autoimmune activity. Researchers discovered high indicators of small fiber neuropathy and therefore large fiber
lesions, in the legs of people with fibromyalgia. They also found that these indicators, especially in the calf, appear to be linked to a marker
of immune activation (interleukine-2R.) They concluded that small fiber neuropathy likely contributes to our pain, and that some of our
pain comes from immune-system activity, such as autoimmunity.
In Context
This follow-up study comes at a time when the interest of the fibromyalgia research community appears to be shifting toward small fiber
neuropathy, inflammation, and possible autoimmunity. Taken in context, this work adds to the emerging picture that we do have damaged
nerves after all, that our peripheral nervous systems are definitely involved, and that autoimmunity or another aspect of immunity is at
work.
This was still a fairly small study, but the fact that it furthered earlier work and appears to gel with other recent research could mean that
it'll have a bigger impact than its predecessor. At the very least, it seems that this is a worthy line of study that should continue.
Going back to the similarities with MS, I have a couple of thoughts: 1-If fibromyalgia is a close cousin to MS, it could really up the
credibility. People know what MS is and they respect it. 2-Would MS treatments work for us? It would be great to see some of these
established medications investigated for fibromyalgia. 3-The similarity makes sense, since we both can have flares and remissions and our
symptoms are extremely similar.
http://www.chronicfatigue.about.com
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- Continued From Page 3 –
HYPERALGESIA:
Remember that hyperalgesia always involves a noxious stimulus, it just becomes more painful when hyperalgesia
is present. The noxious stimulus activates nociceptors in the periphery that then send the signal onto the spinal
cord. Hyperalgesia involves an amplification of the pain signal. This amplification can occur in the periphery (e.g.
the nociceptor is sensitized by an irritant, by inflammation or by disease) or in the spinal cord (via an amplification
of synaptic transmission between the nociceptor and the dorsal horn neuron that sends the signal to the brain) or
in both locations. There are some cases where the amplification is thought to occur in higher brain centers as well.
This can happen, for instance, after a stroke. We will talk more about mechanisms of amplification and there
promise for therapy in a later post.
ALLODYNIA:
Allodynia involves a noxious response to an innocuous stimulus (think putting on a shirt with a severe sunburn).
Because the stimulus is innocuous, and generally of the mechanical variety, it could be carried by rapidly adapting
mechanotransducers or by sensitized nociceptors. These two possibilities have been the focus of decades of
research both in humans and in animals. While there is evidence that the information can be carried by sensitized
nociceptors this is quite controversial. Our current understanding of allodynia suggests that nociceptor mechanical
thresholds do not change enough for them to carry information concerning light touch, brush or gentle vibration in
conditions where allodynia is present. Rather, it appears that rapidly adapting mechanotransducers (or A-beta
fibers) continue to be the sole carrier of this information in conditions where allodynia is present. The change that
causes allodynia occurs in the spinal cord. Through an unknown process, A-beta-fibers gain access to the
nociceptive channel. In normal conditions A-beta-fibers cannot activate dorsal horn neurons that respond only to
painful stimulation. In allodynic conditons, these same neurons begin to receive input from A-beta-fibers. This
allows for A-beta-mediated information to gain access to the nociceptive channel thereby stimulating the
perception of pain in the brain. Because allodynia can occur rapidly it is unlikely that this change is mediated by a
physical change in the connections of neurons in the dorsal horn (although this may occur over the longer term).
Rather, it appears that there are changes in the neurochemistry of the “gate” such that inhibitory
neurotransmission can switch to excitation. Because GABA (the primary inhibitory neurotransmitter in the brain)
can switch from inhibition to excitation (or vice-a-versa) in certain conditions (like epilepsy and during early neural
development) much current focus is on the role of GABA in allodynia.
In chronic pain conditions both allodynia and hyperalgesia are major problems for these patients. Small
movements, putting on or wearing clothes and even sitting or laying down can become very painful due to
allodynia. Patients are often able to avoid hyperalgesia but hyperalgesia can be so intense that it causes an
aversion to even the most mundane of activities for fear of triggering an attack. In the chronic pain patient both of
these conditions are extremely difficult to treat. Allodynia is notoriously resistant to opiate and NSAID analgesics
especially in conditions involving a peripheral neuropathy caused by injury or disease (like diabetes).
To wrap up:
Hyperalgesia is an increased response to a noxious stimulus. It is caused by sensitization of peripheral nociceptors
and/or by sensitization of central neurons that carry nociceptive information.
Allodynia is a painful response to a non-painful stimuli. It is caused by a change in the dorsal horn of the spinal
cord that gives non-noxious sensory information access to the nociceptive system causing innocuous stimuli to be
perceived as painful.
http://juniorprof.wordpress.com/2008/07/05/what-is-hyperalgesia-what-is-allodynia/
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AMIGO
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BOYFRIEND
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CONFIDE
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GOOD TIMES
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MEMBERS’ PAGE
These are all Linda N’s photos.
She has such talent. I look
forward to her sharing these
pictures on our Reaching Out
Facebook page. Sometimes a
beautiful picture can take away
our pain for a second. Thank you
so much Linda for sharing your
talent!
Vitamin D May Help Reduce Fibromyalgia Pain
A new report has yet another potential benefit of vitamin D. Vitamin D is known it as the sunshine vitamin. It takes about
15 minutes of outdoor sunlight to give you the vitamin D you need in a day. It may help fight pain and boost brain power!
This study found it may work against something called Fibromyalgia. Local 12's medical reporter, Liz Bonis, stopped out
at Great American Ball Park to tell you more. Fibromyalgia is a condition that doesn't have a cure and it causes pain to be
heightened if you touch a person even slightly. This report found those who have this condition also have lower levels of
vitamin D in the blood. That may make a difference in managing symptoms. Now vitamin D is in food and the sun, and if
you want you can ask your doctor to measure a level in the blood for vitamin D. This would tell you if you may need
supplements. If you do you may want to take vitamin D-3.
Read More at: http://www.local12.com/news/features/top-stories/stories/health-alert-vitamin-d-may-help-reducefibromyalgia-symptoms-11161.shtml
Happy May!
I hope you enjoy this issue of the newsletter.
I have been very tired this month and that seems to
be the consensus of many Outties. Weather changes,
etc. seem to play a part. I sure wish I had some great
advice to help anyone else struggling!
Do you have any thing to share for the Members
Page’s? Photos, art, poetry, etc? I would sure love to
share it with everyone!
Keep smiling and remember….
Reaching Out is run by survivors of Fibromyalgia and/or Chronic Fatigue Syndrome/ME. We are not doctors and encourage
everyone to check with their own doctor before starting any treatments, diets, medications, etc. that are mentioned in any
article. Reaching Out does not endorse or sponsor any doctors, supplements or treatment plans featured in our newsletter or
on our website.
If you need to contact the Editor for any reason, please do so by emailing
Cuz at mailto:[email protected] or by phone: 785-220-7969.
To subscribe to our e-newsletter and updates, visit
http://www.reaching-out.info or email me at mailto:[email protected].