Yesterday I saw a patient for complex/persistent neck pain, we had a productive session and she was a joy to work with. She writes copy for science based journals and I was therefore able to introduce advanced material without the preamble required by lay members of the public.
As she was getting dressed she began talking about other therapies that had helped her and her family in the past and wondered aloud whether it might speed things up if she had some myofascial release or reiki. I have had countless similar conversations over the years with physicists,surgeons,GPs etc:, it is as if someone has flicked a switch and it fascinates me.
This morning I revisited this
THE PATIENT IN FRONT OF US: FROM GENES TO ENVIRONMENT Gifford 2000
my bolds
Imo it is useful to know as much as possible about the therapies which appeal to patients and if possible something about their history. Chances are they will stay with you anyway, science is currently flavour of the month and it's starting to show in patient feedback forms.
Climbing Brain Levels of Organisation from Genes to Consciousness
http://www.cell.com/trends/cognitive...613(17)30004-9
It makes me smile to think that Louis was thinking along these lines 17 years ago 
Update
04/04/2017
MiR-183 cluster scales mechanical pain sensitivity by regulating basal and neuropathic pain genes
http://science.sciencemag.org/conten...cience.aam7671
Abstract
Update 02/06/2017
Unexpected mechanism behind chronic nerve pain
https://www.sciencedaily.com/release...0601151906.htm
Today's follow up on the above paper by Science Direct.
Update 03/06/2017
As she was getting dressed she began talking about other therapies that had helped her and her family in the past and wondered aloud whether it might speed things up if she had some myofascial release or reiki. I have had countless similar conversations over the years with physicists,surgeons,GPs etc:, it is as if someone has flicked a switch and it fascinates me.
This morning I revisited this
THE PATIENT IN FRONT OF US: FROM GENES TO ENVIRONMENT Gifford 2000
No matter what you do to a patient, from whatever level you focus, changes in
gene expression will occur if the patient makes some changes. That every
practitioner is ultimately a gene therapist is a nice idea, is unifying, and is, as
far as I can see, quite rational. Also, if you are a patient you can be your own
gene manipulator if you get involved in self help. Every therapist could argue
(and perhaps one day soon should argue) that fundamental to their ‘technique’
or ‘input’ is the modulation of gene expression. I might be no different in my
influence as a physiotherapy practitioner from a healer, a medicine man, a
magnetic or copper arm band with healing properties, a session of Reiki, a
cranial manipulation, a grade II p-a on a zygapophyseal joint, a muscle
rebalance session, a McKenzie extension exercise, an education session that
changes the patient’s perspective on their pain to a less fearful one, a successful
rehabilitation session where a formerly feared movement is conquered, or a
positively negotiated arrangement with a patient’s employer that results in a
comfortable stress free return to work. Based on this type of logic it
seems unwise to criticise therapies that you find unusual/different/unorthodox.
If patients have improved in some way from a therapy, there must be a
mechanism underlying that improvement............
gene expression will occur if the patient makes some changes. That every
practitioner is ultimately a gene therapist is a nice idea, is unifying, and is, as
far as I can see, quite rational. Also, if you are a patient you can be your own
gene manipulator if you get involved in self help. Every therapist could argue
(and perhaps one day soon should argue) that fundamental to their ‘technique’
or ‘input’ is the modulation of gene expression. I might be no different in my
influence as a physiotherapy practitioner from a healer, a medicine man, a
magnetic or copper arm band with healing properties, a session of Reiki, a
cranial manipulation, a grade II p-a on a zygapophyseal joint, a muscle
rebalance session, a McKenzie extension exercise, an education session that
changes the patient’s perspective on their pain to a less fearful one, a successful
rehabilitation session where a formerly feared movement is conquered, or a
positively negotiated arrangement with a patient’s employer that results in a
comfortable stress free return to work. Based on this type of logic it
seems unwise to criticise therapies that you find unusual/different/unorthodox.
If patients have improved in some way from a therapy, there must be a
mechanism underlying that improvement............
Imo it is useful to know as much as possible about the therapies which appeal to patients and if possible something about their history. Chances are they will stay with you anyway, science is currently flavour of the month and it's starting to show in patient feedback forms.
Climbing Brain Levels of Organisation from Genes to Consciousness
http://www.cell.com/trends/cognitive...613(17)30004-9
Given the tremendous complexity of brain organisation, here I propose a strategy that dynamically links stages of brain organisation from genes to consciousness, at four privileged structural levels: genes; transcription factors (TFs)–gene networks; synaptic epigenesis; and long-range connectivity. These structures are viewed as nested and reciprocally inter-regulated, with a hierarchical organisation that proceeds on different timescales during the course of evolution and development. Interlevel bridging mechanisms include intrinsic variation-selection mechanisms, which offer a community of bottom-up and top-down models linking genes to consciousness in a stepwise manner.
Trends
The proposed approach is to nest the various intertwined structural and functional levels that compose the brain into a coherent and open ‘brain models community’ covering multiple timescales.
A critical bridging role between the gene and neuronal levels is assigned to regulatory proteins termed ‘TFs’.
TFs regulate disparate genes into coherent assemblies.
The impact of the environment on brain synaptogenesis is modelled as activity-dependent selective stabilisation pruning of synapses.
Long-range connectivity, subject to developmental shaping through interactions with the physical, social, and cultural environment, is proposed to form the bridge between neuronal microcircuitry and higher cognitive functions by globally integrating the underlying neural organisations.
A novel allosteric pharmacology of TFs is proposed for neuropsychiatric diseases.
Trends
The proposed approach is to nest the various intertwined structural and functional levels that compose the brain into a coherent and open ‘brain models community’ covering multiple timescales.
A critical bridging role between the gene and neuronal levels is assigned to regulatory proteins termed ‘TFs’.
TFs regulate disparate genes into coherent assemblies.
The impact of the environment on brain synaptogenesis is modelled as activity-dependent selective stabilisation pruning of synapses.
Long-range connectivity, subject to developmental shaping through interactions with the physical, social, and cultural environment, is proposed to form the bridge between neuronal microcircuitry and higher cognitive functions by globally integrating the underlying neural organisations.
A novel allosteric pharmacology of TFs is proposed for neuropsychiatric diseases.

Update
04/04/2017
MiR-183 cluster scales mechanical pain sensitivity by regulating basal and neuropathic pain genes
http://science.sciencemag.org/conten...cience.aam7671
Abstract
Nociception is protective and prevents tissue damage but can also facilitate chronic pain. Whether a general principle governs these two types of pain is unknown. Here we show that both basal mechanical and neuropathic pain are controlled by the microRNA-183 cluster in mice. This single cluster controls more than 80% of neuropathic pain–regulated genes and scales basal mechanical sensitivity and mechanical allodynia by regulating auxiliary voltage-gated calcium channel subunits α2δ-1 and α2δ-2. Basal sensitivity is controlled in nociceptors, and allodynia involves TrkB+ light-touch mechanoreceptors. These light-touch–sensitive neurons, which normally do not elicit pain, produce pain during neuropathy that is reversed by gabapentin. Thus, a single microRNA cluster continuously scales acute noxious mechanical sensitivity in nociceptive neurons and suppresses neuropathic pain transduction in a specific, light-touch–sensitive neuronal type recruited during mechanical allodynia.
Unexpected mechanism behind chronic nerve pain
https://www.sciencedaily.com/release...0601151906.htm
It has long been assumed that chronic nerve pain is caused by hypersensitivity in the neurons that transmit pain. Researchers now show that another kind of neuron that normally allows us to feel pleasant touch sensation can switch function and instead signal pain after nerve damage. The results can eventually lead to more effective pain treatments, say the researchers.
Severe, treatment-demanding chronic nerve pain is a common condition but the drugs available have, at best, only some efficacy. Since the mechanisms behind nerve pain are largely unknown, the pharmaceutical industry has encountered major setbacks in the development of new drugs.
It was previously assumed that certain sensory neurons only transmit pleasant tactile sensations, while other specializes to transmit pain. During chronic nerve pain, normal touch can cause pain, but how this happens has remained a mystery. Scientists at Karolinska Institutet have now discovered that a small RNA molecule (microRNA) in sensory neurons regulates how touch is perceived. Upon nerve damage, levels of this molecule drop in the sensory neurons, which results in raised levels of a specific ion channel that makes the nerve cells sensitive to pain.
"Our study shows that touch-sensitive nerves switch function and start producing pain, which can explain how hypersensitivity arises," says Professor Patrik Ernfors at Karolinska Institutet's Department of Medical Biochemistry and Biophysics. "MicroRNA regulation could also explain why people have such different pain thresholds."
The drug substance gabapentin is often used to treat nerve pain, even though the mechanism of action has not been known. The new study shows that gabapentin operates in the touch-sensitive neurons and blocks the ion channel that increases when microRNA levels decrease. Yet it is still around only half of all patients who respond positively to the treatment.
"Nerve pain is a complex condition with several underlying mechanisms," says Professor Ernfors. "What's interesting about our study is that we can show that the RNA molecule controls the regulation of 80 per cent of the genes that are known to be involved in nerve pain. My hope, therefore, is that microRNA-based drugs will one day be a possibility."
The research was primarily conducted on mice but also verified in tests on human tissue, where low microRNA levels could be linked to high levels of the specific ion channel and vice versa, suggesting that the mechanism is the same in humans.
"It's vital that we understand the mechanisms that lead to chronic nerve pain so that we can discover new methods of treatment," says Professor Ernfors. "The pharmaceutical companies have concentrated heavily on substances that target ion channels and receptors in pain neurons, but our results show that they might have been focusing on the wrong type of neuron."
It was previously assumed that certain sensory neurons only transmit pleasant tactile sensations, while other specializes to transmit pain. During chronic nerve pain, normal touch can cause pain, but how this happens has remained a mystery. Scientists at Karolinska Institutet have now discovered that a small RNA molecule (microRNA) in sensory neurons regulates how touch is perceived. Upon nerve damage, levels of this molecule drop in the sensory neurons, which results in raised levels of a specific ion channel that makes the nerve cells sensitive to pain.
"Our study shows that touch-sensitive nerves switch function and start producing pain, which can explain how hypersensitivity arises," says Professor Patrik Ernfors at Karolinska Institutet's Department of Medical Biochemistry and Biophysics. "MicroRNA regulation could also explain why people have such different pain thresholds."
The drug substance gabapentin is often used to treat nerve pain, even though the mechanism of action has not been known. The new study shows that gabapentin operates in the touch-sensitive neurons and blocks the ion channel that increases when microRNA levels decrease. Yet it is still around only half of all patients who respond positively to the treatment.
"Nerve pain is a complex condition with several underlying mechanisms," says Professor Ernfors. "What's interesting about our study is that we can show that the RNA molecule controls the regulation of 80 per cent of the genes that are known to be involved in nerve pain. My hope, therefore, is that microRNA-based drugs will one day be a possibility."
The research was primarily conducted on mice but also verified in tests on human tissue, where low microRNA levels could be linked to high levels of the specific ion channel and vice versa, suggesting that the mechanism is the same in humans.
"It's vital that we understand the mechanisms that lead to chronic nerve pain so that we can discover new methods of treatment," says Professor Ernfors. "The pharmaceutical companies have concentrated heavily on substances that target ion channels and receptors in pain neurons, but our results show that they might have been focusing on the wrong type of neuron."
Update 03/06/2017
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