The Body-Self Neuromatrix

I am very happy to finally get to a discussion of the Body-Self Neuromatrix.  There is no doubt in my mind this will become an extremely important and influential theory.  I'll explain why in my summery.

This theory deserves our attention because it was developed by Ronald Melzac PhD.  Dr. Melzac established his credibility in the pain field as the developer of the Gate Control Theory.  The Gain Control Theory is now widely accepted and serves as the basis for most current research into pain.  That he has revolutionized such an important field not once but twice is very impressive.

To understand this theory I strongly suggest that the reader read a presentation by the author.

It is too important, and too complex, for me to adequately summarize, but I'll say the following:
It hypothesizes a widespread network of neurons that provide a scaffolding, or matrix.  One is born with the matrix, but it can be altered during ones life.  It involves parallel cyclical but communicating pathways.  It has several classes of inputs and outputs, but the function of the matrix is relatively simple.  It decides is homeostasis is lost.

As conceived by Melzac, there are three classes of inputs.  The first comes from the brain, and includes both tonic (slowly changing) and phasic inputs (more reactive).  Please see the chart below for examples.  The second group of inputs comes from the body.  The sub divisions are phasic cutaneous, tonic somatic, visceral inputs and visual, vestibular and other sensory inputs.  His third group of inputs is labeled "motivational-affective" and includes our endocrine milieu.
 Outputs include pain perception, action programs and stress-regulation programs.

One of the outputs discussed in the article I linked to above, but not listed in the diagram, is the suggestion that one of the outputs from the BSN goes to an area called the sentient neural hub.  Here, a continuous stream from the body-self neuromatrix is converted to continually changing stream of awareness.   Further, he suggests that the output from the BSN bifurcates, one goes to the sentient neural hub and another eventually activates spinal cord neurons for activity.

Among the wonderful attributes to this theory is that:

-it finally conceives of pain as a psychological phenomena that may or may not have a basis in the body: finally a theory describing the creation of pain that is congruent with the International Pain Societies definition of pain.

-the theory is not only a pain theory, but a theory of PTSD and anxiety as well.  We no longer have to wonder about the relationship of PTSD and pain: they are generated by the same mechanism.

-This theory continues the progression of pain theory from outside the body to now squarely in the central nervous system.

-We have, for the first time, a complete accounting for the factors that can increase our chances of having pain.  The BSN provides a basis upon which various medical and non medical interventions can be evaluated.  It provides a common ground for pain discussion between medical, surgical, psychological and non-medical interventions.  For the administrator, who much decide how to spend limited research funds, we now have a complete list of factors that cause chronic pain, PTSD and anxiety.  

-We also are forced by this model to acknowledge that pain does not exist in isolation.  The consequence of a loss of homeostasis are wide ranging.  With this model the clinician is forced to see that a chronic pain suffer is in danger in many different areas of his or her life.  We can see that every corner of a suffers life is at risk including his mental health, bone health, immune system, etc.  Now, more than ever, we can see the importance in aggressively helping those suffering with pain, PTSD, anxiety.

-The BSN theory also continues the historic trend from 'the sufferer as victim' to 'the sufferer as an active participant'.

Any good theory should raise questions and opportunities for further research.  This theory certainly does:

-Is it valid to conceive of the BSN as a machine which does not trigger an alarm till a certain threshold is met?
-The BSN is drawn fairly simply with inputs and outputs.  Can we add a concept of a positive feedback to the process?  That is, can the outputs from the BSN itself create conditions that irritate the BSN the next moment?
- Is it possible to calm, reassure or stabilize the BSN?  Can we make it more resistant to triggering the alarm?
- We have a list of inputs into the BSN.  These inputs can irritate, or promote the BSN to action.   Can these same inputs also stabilize the BSN?  It would seem to me that if we were interested in finding ways for humans to suffer less, research into this question should be a high priority.
- What input to the BSN is most influential?  Does the BSN preferentially look to one of these inputs to decide if homeostasis is lost?
-  Which of these inputs are most easily changed?
-  The BSN outputs vary in relative intensity.  But with chronic pain all outputs are stimulated.  Thus, chronic pain never occurs as an independent, isolated entity within the sufferer.  Is, then the concept of chronic pain too limiting?  Should it be obsolete?  What term shall we use for the sum the BSN outputs?

One of the great mistakes in modern medicine was to create and perpetuate the idea that the physician alone is responsible for providing health.   Chronic pain is the most dramatic example of this paternalism.  The result, all too often, is a patient addicted to our prescribed narcotics but still in pain.  The sufferers sole object in life is to constantly badger the physician for more pain medication, while in utter denial that they have any role in their pain.  If we have any chance to shift the responsibility to more balanced position, we must be able to give the patient the tools to help themselves.

The creation of pain is now in the brain.  The sufferer is now no longer a victim but an active participant.  We have a definition and a model of how pain (and PTSD) are created.  We have a list of opportunities to stabilize the BSN.  What tools can we give the patients to help themselves?

We have a huge cortex, a vast ability to think and a high degree of neuroplasticity.  We can leverage these tools to guide sufferers to relief.

PTSD, Meditation and the Alexander Technique

Again, this blog seeks to introduce Alexander Technique to the medical provider, and explore if the AT should be recommended.  The blog makes most sense reading from start to finish.  The last entry, "Conclusion" wraps it all up.

But I have more thoughts to share.  This essay was inspired by a talk given by Steven Dobscha, MD from Portland Oregon, an expert on PTSD.  He spoke recently on the connection between pain and PTSD.  He suggested that mindfulness meditation seems to hold the most promise for treating PTSD.  This essay is about the intersections of pain, the AT, meditation, the Body Self Neuromatrix and PTSD.

I will try to present in this essay why the AT might be effective in alleviating PTSD.  This is very important.  If there is no clear theoretical reason suggesting that the AT is effective in PTSD, then only a small pilot study is indicated.  It makes sense to be prudent in these days of limited funding.  However, if there is a firm theoretical basis explaining why the AT would be effective in the prevention and alleviation of PTSD then more serious, definitive research is indicated.

Pain, PTSD, meditation and the AT all intersect at the startle reflex.

The startle reflex is among the most deeply entrenched and ancient reflexes.  Wikipedia refers to it a brainstem reflectory reaction.  It does not involve higher brain participation.  And yet, the reflex can seem to be influenced.  A heightened startle reflex is part of the very definition of PTSD.  So significant past trauma has the potential to interfere with the startle reflex.  On the opposite side of the spectrum is the meditator.  There was an intriguing study that showed that a meditator with 40 yrs experience can alter the startle reflex.

Perhaps if we examine meditation we can gain some insight on how it influences the startle reflex.

In the study above, the meditator was an expert in two forms of meditation: "open presence" and "focused" meditation.  Open presence is when the meditator tries to prevent the mind from getting stuck on anything.  The goal is not to dwell on any concerns or thought, not get wrapped up in emotions, not to get too curious about sights or smells to the exclusion of other sensory input.  In open presence the meditator does not exclude or neglect anything in the realm of awareness.  In distinction, focused mediation brings the mind back to an object and, over time, it becomes more and more fixed on it.  Of course, one can choose any number of things to bring the mind to: a question or thought, the sensation of breathing, a candle flame, etc.  All of which might have different effects on the meditator.

One might think that these meditators are special people with superhuman abilities.  Maybe after 40 year of experience they are (I doubt it), but I'm sure they didn't start out like that.  We all start out the same: with plenty of doubts, fears, obsessive preoccupations, nagging pains: a huge variety of distractions from either an "open presence" or a "focused" meditation.
   In the "focused meditation" what do you do when you've been distracted?  It is a three step process.
1.  The first is to wake up and realize that, for example, you just spent the last 10 minutes thinking about chocolate chip cookies instead of your object.
2.  The next step is to stop the distraction.
3.  The third step is redirect the mind to the object.
Those who practice the "open presence" do without the third step, and just rely on the first and second step.

There are countless ancient and modern lectures, books and teachings to navigate these three steps.  The huge variety of teachings exist to support and encourage any person in any situation.  But all the teaching support the notion that these two forms of meditation are “mind only”.  There is no role for the body.   Here is the process in a nutshell:  The mind wanders off.  The mind realizes that the mind has wandered off.  The mind stops focusing on the distraction.  And, in the “focused meditation” the mind drags itself back to the object.

For the beginner, a long period of time will go by without any 'stopping'.  But as time goes on ones skills improve.  A good meditator will recognize and stop distractions hundreds of times in an hour.  The mind will not wander very far, nor be away for very long.  One begins to be extremely good about stopping and shepherding the mind.

How might meditation effect the startle reflex?  It would seem reasonable to divide the reflex into two parts.  The first is the immediate reflective response to the jarring stimulus.  Again, this is by definition reflexive and does not have any higher cortical participation.  I believe that is is similar to the reflexes studied by Rudolf Magnus, and would expect this reflex to work quite well in the deceribrate model.
   The second part is not the reflex per say, but the fallout.  It's the longer term response.  It a combination of the lingering response from the reflex plus our cortical participation.
    What kind of time frame are we talking about?
      According to the scholarly review paper reviewing the startle eye movement "The psychological significance of human startle eye-blink modification: a review by Diane L. Filion, Michael E. Dawson, and Anne M. Schell:
"Based on these observations, we have proposed that within this paradigm startle inhibition at
the 60 ms lead interval represents automatic, pre-attentive processes, whereas startle inhibition at 120 ms represents a combination of automatic and controlled attentional processes."
      So the startle reflex is quick, about 60ms.  What I am calling the startle response begins to come into play at roughly 120 ms.

    As I have said in previous entries, I am a big fan of the body-self neuromatrix theory.   If the reader is not familiar with this one might read my blog post on this theory, but it is a much better idea to read this paper by Melzack.  One of the many fascinating aspects of this theory is that it illuminates not just the creation of pain, but of PTSD, and anxiety: any loss of homeostasis.  I have stated in the past that I believe the utility of the body-self neuromatrix would be enhanced by conceiving of the process not as simply linear, but as cyclical: the outputs from the BSN quickly become inputs in the next cycle of the BSN.

So, how fast is one cycle of the BSN?  It would seem somewhere in the range of 0.12 seconds or about 8 cycles/second.
 
Using the theory of the BSN how is the startle response is influenced?  First there is the loud, unexpected sound.  There is a reflective brainstem response called the startle reflex which can be seen in the startle eye movement and changes to the head-neck-back relationship.  This loud sound also sends a dramatic input to the BSN via the phasic sensory-discriminative pathway.  A loss of homeostasis occurs and various outputs are produced.    On the next pass of the BSN, there is the input of sensation via the tonic and phasic somatic inputs.  These are muscular changes that are the characteristic pattern of fear.  In addition, there is influence of the activation of the sympathetic nervous system.  There is input to the BSN from the brain: both tonic inputs (such as underlying PTSD) and phasic brain inputs (such as the pre-conditioning provided by researchers).  The thoughts and beliefs, the somatic inputs and the changes in the endocrine milieu are potent irritants to the BSN and lower the threshold for loss of homeostasis when presented with a sudden noxious stimulus.

Stimulating the startle reflex is then a sounding blast into the BSN.  Geologist sometime set off underground explosions and then observe the reflective seismic repercussion.  Thus they can find gas and oil deposits.  Just so, the response to a loud sound can be a measure of the stability of the BSN.  A robust startle response would suggest instability of the BSN and a predisposition towards PTSD, anxiety, and chronic pain.  This explains, in part, the findings of this study of Emotion, attention, and the startle reflex which finds that the "startle response (an aversive reflex) is enhanced during a fear state and is diminished in a pleasant emotional context."

The expected startle reflex will be seen in any neurologically intact person.  A healthy subject will have a minimal startle response.  That is, they will quickly realize that there is no real danger.  The tonic and phasic inputs from the brain will be reassuring on all subsequent cycles of the BSN.  In addition, the tonic inputs from the body will be reassuring.  The phasic inputs - the contraction characteristic of the startle reflex - will still be irritating to the BSN.  The overall response then is basically healthy: it is mostly appropriate to the non threatening environment.

In someone suffering from underlying anxiety, fear or PTSD the startle response triggered in a benign environment will be inappropriate to the surroundings: abnormal and unhealthy.  This secondary response is heightened by obsession, perseveration, distraction; and muscular tension, trigger points, deformity, etc.   The response is driven more by habit than by conscious reasoning.  It is undesirable if we hope to respond appropriately to our environment.

  Just the opposite is seen in the meditator.  As I have said above, meditators are very, very good at 'stopping'.  The meditators are experts in stopping the inappropriate, undesired responses to stimuli - both external stimuli such as loud sounds, and internal stimuli from the sympathetic nervous system.    The meditators underlying tonic state of their body/mind might be so non responsive that it would be very difficult for scientist to see after 60ms.  Should there be some spill over and the BSN becomes unstable in the next few passes, the meditators phasic abilities to "stop" distractions quickly will interfere with continued habit based responses.

Finally, we can take a look at how the AT student operates during a startle provocation.  Like the meditator the AT student is also an expert in 'stopping'.
        FM Alexander had no experience in meditation and was unfamiliar with it’s jargon.  But his language does capture the essence of contemporary mindfulness meditation.  He speaks about stopping the tendency to focus on the endpoint of our efforts.  He called focusing on achieving our goal as “end-gaining”.  Honestly, although the words he chooses might be a bit refreshing, this first tool does not add anything substantive to mindfulness meditation.  Realizing that we are well ahead of ourselves and stopping that distraction is nothing new, but it is vitally important.  Alexander called this first tool “inhibition” and the AT technical term is "inhibition of end-gaining" where end-gaining - the grasping after some goal - is more important than the means by which one achieves the goal.  This is similar to the meditator who is experienced at stopping the response to a stimulus that threatens to distracts from their object of meditation.  The AT student is an expert at stopping the distraction from how one responds to stimuli to achieve an end.  For example, if the phone rings during meditation, the meditator will be distracted, realized they are distracted, say no to the distraction and return to the object.  The AT student will hear the ring and inhibit the initial impulse to reach across the desk to answer it.  Both meditation and the AT are similar up to this point.   In modern pop psychological terms, both meditation and the AT radically anchor one's attention in the present.

But there is more.  This "inhibition" is only one of the two tools that the AT teaches.  This second tool is employed in the "space" created by stopping.  With meditation, one realizes that there is distraction, then stops it.  The meditator then passively waits until there is another distraction.  The AT makes use of this space between stopping and another distraction.  It is in this space that the second AT tool is used.

The second tool is unique to the AT.  Once we have applied the first tool we can apply the second tool.  This tool is to muster energy, or intention, to direct the use of the body in such a way as to oppose the characteristic pattern seen in the startle reflex.  As opposed to the first tool, this “direction” tool his highly nuanced and extremely experiential, hence the need for lessons with a skilled teacher.

The use of 'direction' will change the tonic somatic inputs to the BSN.  It's a rather bold statement, but the science suggests this is true.   This is a nice summary of some of the research that has measured the tone in AT experts and with those with back pain.  This improved tonic somatic input leads to greater resilience of the BSN.

So in addition to the influence of meditation on the BSN, the AT provides an improved tonic somatic influence that provides a highly stabilizing influence to the BSN.

Before moving on, there is one more important distinction between the AT and mediation. Meditation is done on a cushion in a quiet room by people who spend quite a bit away from an otherwise productive activities.  Apart from time spent in lessons, the AT is practiced while in every day activities.

So the Alexander Technique starts with the same tools used in "open focused" meditation, but then it adds a unique perspective that has a great deal to offer.  It should be far more effective than meditation in alleviating PTSD and anxiety.  It is ‘body-based mindfulness’ or ‘meditation in activity’.

So we can see how both meditation and the AT will effect the late expression of the startle response.  But so what?  What has this got to do with PTSD or anxiety or pain?  PTSD is at heart an abnormal, irrational, response to stimuli.  PTSD is a habit.  Both the AT and meditation help to replace unconscious, habitual, irrational, pathologic responses to stimuli with  conscious reasoned responses.  Both the meditator and the AT student are highly trained at quickly interrupting the response.  In addition, the AT student is experienced in directing the use of the self ways from the characteristic pattern seen in the startle reflex and thus with improvement in the tonic state of the body/mind will further stabilize the BSN.

The AT is effective for chronic pain.  There is strong scientific evidence for this.  If we subscribe to the theory of the BSN, we can also conclude that the AT is also helpful for PTSD and anxiety as well.    I have described here the theoretical basis why the AT is effective in chronic pain, and why the AT should be highly effective in PTSD and anxiety as well.  With this theoretical understanding we can suggest the AT to patients and justify spending significant resources on testing the hypothesis.

A Very Short History of Pain Theory

A theoretical understanding of a disease process and a definition of the problem is fundamental and essential if we want to help patients.  Having some idea of the disease process can suggests useful therapies and fruitful lines of investigation.  Without this, we have no basis for discussion, no way to measure either the problem or the efficacy of our intervention.

Reviewing pain theory history might not meet these needs, but it might help to illuminate why there is a problem in defining pain.  We might be able to see if there is any trends or trajectories to pain theory that might suggest the future of pain theory.  We might also find the roots to erroneous assumptions - the origination of cultural biases that color our thinking but have gone unchallenged.

According to my very brief research, in very early times, pain was thought to be the effects of evil entering the body.  These ill effects entered the body, caused pain, and when they left pain resolved.

It does not seem that there was a consensus among the ancient Greeks: some thought pain was an emotion, others an imbalance of vital fluids.  The central pain center was thought to be located in the heart.

The next model suggested that pain is the result of God testing our beliefs or putting us on trial. The therapeutic intervention that was recommended was prayer to confirm our beliefs.

The next big revolution came with René Descartes who conceived of the body as a machine.  He created a division between body and mind.  He moved the pain center from the heart to the brain.  He suggested that pain was damage to the periphery that traveled via some sort of pathway to the brain where something like a bell would ring. The stronger the stimuli the louder the ring.

Throughout the 1800s there was debate about receptors.  It was first thought that there were dedicated pain receptors and transmitters.  The Intensive Theory suggested that any sensation could cause pain as long as it was adequately intense.  In 1943 the summation theory proposed that stimulation of peripheral fibers would have to exceed some threshold for the sensation to spill over and send a signal to the brain.  Another theory proposed that only certain patterns of stimulation are able to create pain.

 In 1953, it was observed that a signal carried from injury traveled on two types of nerves: one with a large diameter, one that was small.  The large diameter fibers carried touch, pressure and vibration and these were found to inhibit the signal carried by the thinner pain sensation carrying fibers.

The final theory is the Gate control presented in 1965 by Ronald Melzack and Patrick Wall, and I'm quoting heavily from wikipedia.  They proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord.  From there, transmission cells carry the pain signal up to the brain, but inhibitory interneurons impede transmission cell activity. Activity in both thin and large diameter fibers excites transmission cells. Thin fiber activity impedes the inhibitory cells (tending to allow the transmission cell to fire) and large diameter fiber activity excites the inhibitory cells (tending to inhibit transmission cell activity). So, if there is more large fiber (touch, pressure, vibration) activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. This is why we rub an injury.
    They pictured not only a signal traveling from the site of injury to the inhibitory and transmission cells and up the spinal cord to the brain, but also a signal traveling from the site of injury directly up the cord to the brain (bypassing the inhibitory and transmission cells) where, depending on the state of the brain, it may trigger a signal back down the spinal cord to modulate inhibitory cell activity (and so pain intensity).   For the first time, the brain itself is an active participant in the transmission of pain.

There are several points that I wish to make about pain theory:
- In reviewing the evolution of pain theory there is a trend to locate the processing of pain from outside the the human, to their periphery, to the spinal column and to the brain.

- There is a trend from ancient times to view the sufferer as a simple receptor for pain to more modern theories that suggest the sufferer to be an active participant in it's creation and modulation.  The sufferer was a passive victim, but is becoming more responsible for their own pain.

- New theories do not necessarily negate established theories.  Reality is actually a vast fog that is beyond our comprehension.  A theory describes a small part of it.  Most of us live quite content in the well described center, but a few will go to the edges.  Here they find unexplained phenomena and then develop a theory to explain the observation.  The function of a theory then is not so much to finally describe reality, but to widen our edges of knowledge and give others the opportunity to explore further.

And here are some lessons that we have learned from the study of pain so far:

- No pain center has yet been found.  Functional MRI imaging has found that the perception of pain is widespread throughout the brain.
- Destruction of pain pathways frequently do not yield long term pain relief.
- We have discovered "phantom pain".  This is pain in a body part that has been surgically removed and no longer exists.  Further, people can have pain and sensation in their bodies even after a verified sectioning of the spinal cord.  People can even have sensation and pain in a limb that was non existent at birth.

And how is pain presently defined?  In 1994 The International Pain Society defined pain as "An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. "    Perhaps it is simply a reflection of my lack of intelligence, I frankly do not understand this.  The Society also includes a paragraph to help explain their definition.  I won't quote the whole paragraph but two sentence stand out "This definition avoids tying pain to the stimulus. Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state, even though we may well appreciate that pain most often has a proximate physical cause."

All the above is a preface to a discussion of the most current theory, The Body-self Neuromatrix.

The Importance of Pain Theory

In my 14 years as a medical care provider, I have gone to more than my share of medical conferences.  I have attended conferences in primary care, emergency care, internal medicine, cardiology, urology and other specialties.  Uniformly, they are a blend of theory and practice.  One must have some grasp of the theory behind a disease process to make sense of the promises and pitfalls of the interventions.
 
So it was quite a surprise to me that at the annual conference of the Western Pain Society, very little was said about the definition of pain, and even less about the theories regarding it's pathophysiology.  It was as if I had gone to a conference on the common cold and the presenters simple talked about the need for hydration, the merits of antihistamines, the role of antipyretics, etc without any interest in talking about the cold as a viral infection.

If we are going to talk about how to alleviate pain, we must present our definition and explicitly state the theory of we are using in our discussion.  How else are we going to evaluate relative efficacy?  How else are we going to discuss the mechanism of action?

The primary care provider might not recognize the need to examine a definition and theoretical explanation.   Typically, we simply accept what the experts give us.   For example, with type 2 diabetes we uniformly assume these needs are met with the A1c and the idea of insulin resistance.  But chronic pain has no clear definition, no way to measure it, and no universally accepted pathophysiology.

The conference of the Western Pain Society left me with the feeling that the pain specialty is in confused disarray.  The realization that the medical profession is actively seeking the participation of non medical providers initially gave me some hope.  But then I realized that the reason we welcome others is that we have so little to offer that is safe and effective   The medical providers, and the patients, are desperate.

To understand the present state of pain theory, I'll briefly review a history of pain theory.

The Head Neck Back Relationship

I have mentioned that one explanation of the mechanism by which the AT helps with back pain is simply that it improves posture, balance and coordination.  This is done by teaching the student to stop interfering with their inherent reflexes.  But this explanation does not explain the full effect of the AT and does not adhere to modern pain theory.

To begin to have a more robust understanding of the AT, we need to look more closely at reflexs. Again, the reflexes of most importance are the righting reflex and the startle reflex.  The righting reflex begins after an activity has been performed and, if working correctly, brings us back to a neutral,  upright, poised, relaxed but ready position.  This reflex works by comparing the desired ideal upright position with the current sensory information.  These inputs include the somatosensory inputs from the neck which are rich with stretch receptors.
   These and other reflexes were investigated by Rudolph Magnus.  He now has one of them named after him.   Magnus was very clear about the pivotable role the head-neck-back (HNB) relationship plays in our reflexes.  So much so that his work is frequently summarized as "the head leads and the body follows."  The HNB relationship is central to guiding the cascade of movements seen in reflex behavior   This might suggest that the HNB relationship is some kind of control center.  Of course, it is not.  The HNB relationship is part of the peripheral, not central, nervous system and as such it controls nothing.  But it is enormously influential.
    Significant problems arrise should the brainstem be conditioned to replace a default upright and neutral reference posture with some other default state.  This happens as habits influence our reflexes.  We can even see this happening over time by viewing the old frontal and sagital photos of disrobed children as the progress through grade school.  It is very sad to see this.

FM Alexander, independently of Magnus but at about the same time, also concluded that the HNB relationship was of primary importance.  The work in the first few classes of the AT focuses on improving the use of the HNB relationship, replacing the unconscious use patterns with a new consciously directed ones.  Alexander found that once the HNB relationship is improved, other habits of use of the self (such a stuttering, taking the eye off the ball durring a golf swing, etc.) are easily delt with.
But the process of improving the use of the HNB pattern is not trivial.  The skilled hands of the AT teacher can bring the student into an improved relationship, and this typically produces a sense of lightness, ease and uprightness.  But at the same time it can also feel unfamiliar and even wrong.  Student will invariable fall into their old accustomed patterns quickly.  So students are taught to rely, not on what is felt to be right, but on the tools provided by the AT teacher.

The second reflex of concern is the startle reflex.  This is both a unique and central reflex.  It is also of great interest clinically.
     The Veterans Administration is very interested in post traumatic stress dissorder.  The DSM-IV definition of PTSD is a blend of historical, psychological and behavioural factors.  But also central to the diagnosis is one neurological finding: an elevated startle response.
    Wikipedia defines the startle reflex as a reflective response.  That is, the stimulation goes directly into the brainstem and the brainstem in turn stimulates the cranial nerves: blink and the shortening of the sterncleidomastoid and trapesius muscles.  The shortening of the HNB relationship is first postural change one sees on highspeed photos of the startle reflex.  One would not think such a reflectory reflex could by influenced, but indeed it seems to be.  On one extreem PTSD heightens the response, and on the other, meditation seems to inhibit the response.
    The link between PTSD and pain is well established, and multiple theories on the relationship exist.  These theories lack an understanding of the primacy of the startle response (and modern pain theory that I will discuss later).
    Repeated and/or extreem triggering of the startle reflex creates a chronic shortening of the HNB relationship.  This chronic tension produced by the effort to shorten the HNB relationship is the cause of the neck and back pain that is very commonly seen in PTSD sufferers.
   The effects of the startle reflex do not stop with the HNB relationship but extend in a characteristic fashion throughout the body.

Durring lessons in the Alexander Technique students are taught, in part, to direct the use of themselves against the characteristic pattern seen in the startle response.

It is to Alexanders credit that he found that improvement in the use of the HNB relationship will lead to a less reactive nervious system and a lessening of the "fear response".  This is quite remarkable since he knew nothing of theories regarding reflexes or PTSD.

In sum, the HNB relationship is important for the following reasons:
- It is the first region of the body to respond to the startle reflex
- The sensory apparatus gives the HNB relationship primary importance in deciding how to orienting the rest of the body and thus is very influential.
- the HNB relationship is the gateway through which the not only the startle reflex must pass to influence the entire organism, but also fear and anxiety.
- Our use of the HNB relationship can either amplify the startle response (and the emotions of fear and anxiety) or suppress the response.

The above is an introduction to the importance of the HNB relationship.  The argument will be fleshed out once modern pain theory is reviewed.