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The Window Pain

chronic-pain

The Window Pain


Yes.  That is what I said. 
No, it is not a typo. 
Ok, maybe a bad pun. But you did read it correctly.
During the Christmas holidays, I had spent some time with my extended family. During dinner one evening I was asked about “chronic pain”.  The concern was more about how to relieve chronic pain of peripheral neuropathology, a debilitating disorder with sensation of pins and needles affecting upper and lower limbs.  I shared how Gabapentin has been effective for such symptoms. However,  this medicine made her feel foggy and without much relief. 
The thin frame of this very kind woman, in her late sixties begged the question of likely complications from osteoporosis; a problem which she acknowledged having.  After we ruled out the possibility of anemia in her history, I shared how it is likely her symptoms were related to her bone loss, especially if other labs for metabolic issues of medication side effects were non-contributory. 
Chronic pain is a burden that is unrelenting. It seems to never to cease its invasion of comforts. It tends to be a constant disruption  during valued time with family and friends.  Even the efforts to hide the pain can become stressful alone. The attempts to quiet its torment often feeds upon the the very energy needed to prevent it; burdening the sufferer with more tension,  fatigue, headaches and emotional drain. It can cause depression and anxiety.  
Over the years I have worked with many patients burdened by chronic pain.  Medications seem to help many people initially, but limitations from tolerance, dosage safety and side effects seem to restrict effective long-term coverage.

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Today, I came across an article which seems to explain many unanswered questions surrounding chronic pain.  It seems to suggest how medication to treat pain becomes less effective over time due to incorrect targeting of pain.  Further, we are not taking into account how our bodies have a different kind of brain, separate from the one on our shoulders.  Sure, they have shared pathways in communication.  But there seems to exists a “pre-approved sharing of pain” that is learned locally in areas around the source site which is not targeted by our medicines.  The very fibres of dorsal root networks at the spinal cord level learn from its neighbours what to watch for after there is injury next door.  Pain therefore propagates over a greater surface area from the pain origin.  

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At first blush, this seems to resemble an exaggeration of the one suffering pain.  Yet, as the article discloses, there exists a growing level of sensitization and a lowering of the threshold from the pain origin in neighbouring nerve fibres.
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But what is most peculiar is how this threshold and spread of pain is permitted.  You may tend to think that these changes take place at a very local dermatone region alone.   Yet this article points out that a “long distance call” is placed by the site injured as a collect call to the brain.
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The call is made through the network of the thalmus (operator) which interacts with a “body home address (sensory cortex)” and transfers priority messages to key players in another map of local neighbours (Cingulate cortex).  
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Here, phone numbers are pulled before sending them a “Neighbourhood Alert Watch”, through direct calls to their phone poles at the spinal column level.  
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It is only at that phone pole level where a particular home is set on either a warning mode or normal mode. It seems like a lot of work to place long distance calls when crossing a neighbours yard for help would seem more practical.  
 
So, in order to really treat body pain effectively, new strategies will be considered for silencing the address lookup table in cingulate, as well as calming a neighbour who is easily panicked at the dorsal column level. Current strategies only address site specific pain. It does not target the “local pain sharing network “, nor does it calm an easily startled operator in the brain that is eager to rally your neighbours when local pain erupts.  Function specific neuroreceptors and application alternatives are considered.

 
Enjoy the article here. 
Tsagareli, M. (2013) Pain and memory: Do they share similar mechanisms?. World Journal of Neuroscience, 3, 39-48. doi: 10.4236/wjns.2013.31005.
 

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The Bridge that could not..

 

 

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I have heard it said “if you want friends, do not build walls, build bridges”. But if you have ever felt depressed or under stress, you may have noticed that you did not really feel very sociable.  In fact, you may remember that you avoided being around people. You may even recall how stress impaired your thinking and planning. We tend to become myopic, or near sighted and any task undertaken can seem very energy demanding.

I have been reading an article recently that explains how this experience is actually a part of a neurobiological process ; one that is common not only for times of stress and depression, but it also appears to have a common involvement in most dementias.

You see, the bridgework of social engagement is much like the bridgework that can be found between neurons of our brains.  This bridgework aligns neurons across the a signalling gap between downstream neurons.  The terminal end of one firing neuron (presynapse) communicates with the dendrite (postsynapse)  of the next neuron through a gap known as a synapse.

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The alignment of neurons is an important feature for effective communication downstream.  Researchers discovered a structure protein known as Nectin-3 that maintains this alignment to secure connections in place.  Now, what has been found is that when mice were placed in a stressful environment, there was a significant reduction in Nectin-3 in their brains.  This also correlated with the avoidance behaviour observed in these mice from the stress induced.  In order to be certain of this relationship, other experiments were designed to restore  fibronectin-3, which resulted in increased cognitive function and improved  socialization in mice.

When the scientist explored the mechanism behind nectin-3 reduction, an enzyme known as MMP-9 was identified.  During times of stress, high glutamate levels prompt the release of this enzyme which degrades  nectin-3 protein. I think of this as Military Police (MP) that lose their role as peacekeepers, causing mass chaos.

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Normally, this enzyme has an important role, probably in modifying memory like fine tuning a piano to the right tone.  However, stress clearly permits a runaway mechanism to hinder our social interaction and capacity to think clearly.

 

I invite you to read this article below.


Stress Management Makes Us Antisocial Due To Severed Synapses: New Finding Opens Window For Disorder Treatment

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If you find yourself avoiding human interaction when you’re stressed, be sure to thank an enzyme in your brain. greg westfall, CC BY 2.0

The people who can carry on amiable conversation while also fighting a war inside their heads are few and far between. When we get stressed, we shut down.We recede from the social sphere, if only to count to 10, before rejoining the group with a clearer frame of mind. But what, exactly, is going on between our ears when all this is happening?

New research from the Brain Mind Institute at École polytechnique fédérale de Lausanne (EPFL), in Switzerland, suggests the neural mechanism that makes stress a precursor to antisocial behavior happens at the synaptic level. Specifically, there is a disruption between a key enzyme and a set of proteinsnecessary for sociability. Keeping that relationship intact could open important doors for the treatment of psychiatric disorders.

There’s a type of protein whose main function in the brain is to keep neurons stuck together. They’re called adhesion proteins, and one in particular, the nectin-3 adhesion protein, has been found in prior research to play a vital role in the preservation of cognitive functions. In rats with chronic stress, researchers recently found nectin-3 levels were substantially lower.

In looking for possible causes of the decrease, the researchers ended up at the enzyme MMP-9, known for its role in protein degradation. What they found when they looked at MMP-9 activity in the brain was that during episodes of chronic stress, when the neurotransmitter glutamate is released, the receptors responsible for memory and synaptic plasticity activated MMP-9. Literally like scissors, the enzyme cut the nectin-3 proteins.

“When this happens, nectin-3 becomes unable to perform its role as a modulator of synaptic plasticity” explained lead author and Brain Mind Institute professor Carmen Sandi in a statement. The end result for the rats was decreased sociability, avoidant behavior, and impaired memory and understanding.

By contrast, when EPFL researchers and a team of Polish scientists tried to reverse the effect — in other words, boost sociability through nectin-3 restoration — they found in in vitro and in vivo models that these external treatments yielded positive effects. Cognitive skills improved and memory returned. “The identification of this mechanism is important because it suggests potential treatments for neuropsychiatric disorders related to chronic stress, particularly depression,” Sandi said.

The research is admittedly early for any clinical application. So far, no drugs have been developed using nectin-3 as their primary target. Sandi and her team hope the findings can be repeated in future studies. Given the success with MMP-9, they also hope to exploit its benefits for other neurological diseases, like amyotrophic lateral sclerosis or epilepsy.

“This result opens new research avenues on the still unknown consequences of chronic stress,” Sandi said.

Source: Sandi C, et al. Nature Communications. 2014.

 

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Managing Frustration

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Fetal Faces Hint at Mom’s Stress – ABC News

If these fetuses look flustered, it might be because they’re picking up on mom’s stress, according to a new study of 4D ultrasounds.

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Anxiety: Your brain in Knots.

Anxiety and the Brain: What is happening in the brain in that moment of feeling Anxious? How does it impact our body?  Here is a good summary from Pinterst.

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Implication of sperm RNAs in transgenerational inheritance of the effects of early trauma in mice : Nature Neuroscience : Nature Publishing Group

In this study, the authors show that the heritable behavioral and metabolic changes that are observed in rodents exposed to early life stress are mediated by changes in miRNA levels in the sperm of affected males. Injection of isolated RNA from the sperm of stressed males into donor fertilized oocytes is able to induce these phenotypic changes in the resulting offspring.

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