When it comes to patient education, there are four things that every patient wants to know:
1) What is wrong with me?
2) How long will it take to get better?
3) What can I do for it?
4) What can you (the clinician) do for it?
When we do educate, we must not forget that pain is a biopsychosocial phenomenon and multifactorial. The onion skin model below provides a good relationship analogy for this.
The first goal addressed in education is making the patient understand pain. Patients must realize that pain is the defender, not the offender. It is our body’s way to perceive a threat. Therefore, we must quell this fear before focusing on function. Here are some suggested ways to describe pain in non-threatening ways.
When obtaining pain information from our patients, this is something that we do not have to measure. Instead, it is important to look at variables associated with pain, namely.
3) Explore how patient’s classify their symptoms (e.g. my joints are worn out), and ask why they think the symptoms still persist.
4) Consequences of the pain.
5) Coping types.
6) How the patient relates to pain (do they get angry or play the blame game).
When determining treatment course, instead of focusing on the structure at fault, look at sensitivity and function. We treat pain mechanisms, not sources. The way to classify sensitivity is by determining if the patient’s symptoms are nociceptive, peripheral neuropathic, or central-dominant. When looking at function, we look at general, specific, and mental qualities.
The Three Types of Function/Dysfunction
1) General – What are physical activity levels and favorite activities? How do their goals relate to these components?
2) Specific – Objective findings. These impairments have a heavier focus in acute pain than chronic.
3) Mental – Fear, anxiety, coping, attitude.
Your patients may have problems in one or all of these areas to one degree or another, but the biggest question a clinician must ask is if these dysfunctions are adaptive or maladaptive to pain.
Poor Outcomes 101
There are several factors that contribute to poor outcomes, many of them involving mindsets towards pain.
Belief that back pain is harmful or potentially severely disabling.
Fear-avoidance behavior and decreased activity.
Low mood and social withdrawal.
Expecting passive treatments over active participation.
Why Perform a Physical Exam
There are three reasons why you should perform the ultimate manual therapy, a physical exam:
1) Movement is how you engage the patient, and they expect it.
2) Support/reject subjective findings.
3) Allows for reassessment of patient’s problem. It helps show how you may be able to help them.
All approaches (Maitland, Mckenzie, Mulligan) have myths. The common bond between them all is pain. Today we will look at building a clinical framework with pain as the cornerstone.
Evidence-Based Medicine (EBM)
EBM is defined as a conscientious, explicit, and judicious use of current best evidence in making patient care decisions. This concept is not merely reading researches articles, but it combines scientific evidence and clinical expertise. You have to know when to apply what.
2) Evidence suggests manual therapy improvements are more psychosocial than physical.
3) A disconnect between researcher and clinician.
The researcher thinks: “What does this work contribute to the literature?”
The clinician thinks: “What does this work do for my patient?”
The movement towards outcome-based therapy per EBM is also problematic for several reasons.
1) Clinicians begin to think statistical analysis becomes greater than any other form of knowledge rather than complimentary.
2) Research doesn’t take into account the inherent uncertainty and subjectivity in a clinical encounter.
3) Good evidence can lead to bad practice if applied in uncaring and unappealing environments.
4) Outcomes may be coming out too quickly, leading to research development stopping in certain areas.
Butler’s thoughts are summed up very nicely when he states it would be a sad day if meta-analyses have the final say instead of exposing clinical errors. However, the self-scrutiny and analysis is a good thing as long as it stops short of reducing clinician self-confidence. For confidence is what allows us to practice in uncertainty and maximize the placebo effect, our most powerful pain reliever. The uncertain conditions which we practice in are what Butler terms the Grey Zone. These typify most syndromes in which underlying pathoanatomy and physiology is unknown.
Clinical Reasoning Science
Clinical reasoning involves the merging of three areas: science, current therapies, and the clinician-patient relationship.
Butler also suggests that we need to shy away from thinking damaged structures and move towards movement dysfunction. We must realize that movement sensitivity does not involve the tissues only, but is a process that involves changes at a chemical and cellular level. When a movement becomes sensitive, changes occur in the ion channel, neurotransmitters, and nervous system. These changes are driven biopsychosocially.
Following this process, central processes are very much active in all types of pain. For example, acute pain depends on peripherally activated central processes. We must also look at recurrent pain, which is actually a chronic, central process as opposed frequent acute injuries.
Does that mean we need to be psychologists?
We must treat faulty movement patterns, but that does not mean we cannot take aspects from psychology, namely…
Output: Sympathetic, immune, and endocrine systems, potentially consciousness as well.
Step 4: Classify in terms of dysfunction.
General physical function/dysfunction: The patient’s main problems.
Specific physical function/dysfunction: Problems found by clinician that are related to patient’s problems.
Mental/psychological function/dysfunction: What the patient thinks/feels about his/her injury, the clinician, the treatment, and society’s approach to his/her disability. Distress fits in here.
Step 5: Make sense of dysfunction
One needs to determine if the dysfunction is maladaptive or adaptive. For example, limping after a sprained ankle would be an adaptive response to allow for tissue healing. Limping for the same sprained ankle 25 years later would be considered maladaptive. Often too we must realize that we accumulate dysfunction over time, and minor findings may not be relevant to a person’s complaints.
Step 6: Find your sources
In terms of dysfunction and mechanisms. You need to know where you would fire a magic bullet if you have it. This could be a particular manual therapy or even explaining pain to reduce the fear of movement.
Step 7: Know your contributing factors
This can include any factor related to the predisposition, development, and maintenance of a problem. These factors can include psychosocial, genetics, anthropometrics, and ergonomics.
Do no harm is first and foremost. When thinking manual therapy, use the least amount of force for maximum gain.
Step 10: Management
Realize and be comfortable knowing that chronic pain is something we may never cure, but it is something we can manage.
The Reasoning Process: Key Points
Reasoning is an evolving process throughout the treatment course that starts broad and moves toward refinement. This path occurs via the information gained from the patient assessment coupled with the clinician’s knowledge, understanding, and previous experience.
Most important, we must keep the patient as part of the reasoning process. Their hypothesis of their problem affects all reasoning categories and will alter as assessment and management proceed.
The intervention provided will affect the evolving concept of the problem, and the placebo effect can occur anywhere in the process. With that in mind, be mindful of any errors made during.
Neurodynamics is the study and relationship of nervous system mechanics and physiology. The testing protocols for neurodynamics assess the nervous system’s ability to lengthen, glide, and change amongst interfacing structures.
When discussing neurodynamics, it is important to think of the nervous system as a continuum. Mechanical, electrical, and chemical changes in one part of the nervous system affect other related parts.
Gross Movements and Dynamics
When having a nervous system, the following qualities, movements, and buffering capabilities are necessary:
Slide, glide, strain.
Elongate (think gymnasts) and return from elongated position.
Compress (ulnar nerve during elbow flexion).
Stength (kicking a field goal).
Neural Connective Tissue
These include the meninges, nerve root complex, and peripheral nerve structures. Broken down as follows:
Dura mater (outer, tougher)
Pia mater (inner, thinner)
Nerve root complex
Dorsal and ventral roots
Mesoneurium – Sheath that surrounds a nerve. Contracts like an accordion to glide along adjacent tissues. Can become fibrotic with injury.
Meningovertebral ligaments – anchor down to spinal canal, which could become symptomatic.
Rectus capitus posterior is connected to the dura mater between the occiput and atlas; helping the dura fold. Makes you wonder what you are truly doing when you release this structure.
The sympathetic trunk’s proximity to the spinal column makes it susceptible to increased loads with upper cross syndrome.
Meninges are one of the components that may be represented by bilateral receptive fields (see chapter II). This could lead to dorsal irritation felt over a wide, bilateral, nondermatomal region. Dural pain is truly nociceptive, and may occur far from the irritated location. The leptomeninges (arachnoid and pia maters) also have mechanoreceptors, which make it responsive to movement.
The peripheral nerve’s connective tissue sheath is also very sensitive, as it is loaded with free nerve endings and pacinian corpuscles. There are also unmyelinated nerve fibers which contain pain neuropeptides. This component may demonstrate the sheath’s role in neurogenic inflammation.
Space and fluid
There really is no space in the nervous system, as everything is filled up with something.
Axoplasm is the nervous system’s juice, as it carries materials such as ion channels and neurotransmitters throughout. Axoplasm flows at 100-400mm per day, but during ischemia or physical constriction it may decrease or even stop. This substance is also thixotropic, meaning that flow is improved the more movement occurs. This is one reason why poor prolonged postures such as sitting for too long can become uncomfortable.
Blood Thirsty Neurons.
The brain and spinal cord make up 2% of body mass, yet consume 20% of available O2 in blood.
Brain and Spinomedullary Angle
The brainstem and cranial nerves move as the body nerves, and even a mild brain injury (think whiplash) can be associated with chronic pain.
The spinal cord is arranged in folds and spirals which straighten as the cord elongates, with most stretching occurring at the cervical spine. This attribute allows for increased cord protection.
Symptoms may arise from either the neural container/mechanical interface or the nerve itself, so both must be checked.
The sequencing of movements also affects the system’s response. This concept is called tissue borrowing, in which the first movement tested becomes the greatest challenged by other movements. For example, if I move the wrist first in a neurodynamic test, then the nerve in that location would uptake the most tension.
It is also important to mention that when loading the system, accumulation is nonuniform. Depending on where movement comes from, the nerve may get pulled in that direction. For example, near the critical zone at T6, cervical flexion may pull cephalid, whereas knee extension may pull the cord cauded. Other reversal areas include C5-6 and L4-5. Symptoms often show up first at these areas.
When the nerve is stressed available blood flow is affected. A simple increase of 20-30mm Hg pressure can affect blood supply, and generally the longer a stimulus is applied also has an effect. This change can be evident in the various neurodynamic tests.
If a nerve is entrapped, forces do not dissipate as far, which leads to greater strain at affected site.
The best resting position for a nerve depends on the injury.
Central sensitization is a phenomenon that occurs in the dorsal horn, which can be best described via 4 different states:
1) Normal: Inputs = outputs; innocuous sensations are perceived as such.
2) Suppressed: Inputs that would hurt do not; think an athlete who injures himself but finishes the game.
3) Increased sensitivity: Pain system has lower activation threshold, leading to pain spreading and pain with light touch and gentle movement. This change occurs because A beta fibers begin taking over C fiber locations in the dorsal horn.
4) Maintained afferent barrage, CNS influences, and morphological changes: Long lasting changes in the dorsal horn from a persistent driver, such as…
A fiber phenotype changes.
Persistent DRG discharge.
Gene transcription change in dorsal horn neurons.
Inflamed dorsal horn or DRG
Maladaptive beliefs, fears, and attitudes.
Dorsal horn sprouting; A Beta fibers take over C fiber space.
Persistent glutamate activity.
The CNS has an endogenous pain control system which activates during injury threat, noxious cutaneous input, or expectations and learning. Such an example of this is when you go to a healthcare practitioner’s office and no longer hurt. Another example of when this system is activated is during aggressive manual therapy. Think about how good your body may feel after sustained pressure or even a needle to a trigger point.
Central Sensitization Patterns
Symptoms not in neat anatomical/dermatomal boundaries.
Original pain spreads.
Multiple areas: Either linked or get one pain, then the other.
Contralateral side may be painful, though not like the other side (mirror pain).
Clinicians end up chasing pain.
Sudden, unexpected stabs.
Patients call the pain “It.” For example, “It has a mind of its own.”
Ongoing pain perception past normal healing times.
Summation via repetitive activities (sitting at a computer).
Distorted stimulus/response relationship. May get pain 10 seconds or days after stimulus is applied.
Unpredictable response to treatment/input, but ends up being predictable (x may only work 2 days).
Every movement hurts, but not big ROM loss (Symptom instability).
“It hurts when I think about it.”
Can be cyclical.
Change in other systems.
Links to traumatic life events.
Miracle cures can work.
Likely in most syndromes (fibromyalgia, complex regional pain syndrome).
2) Do not focus on finding an anatomical pain source which can make matters worse.
3) False positive are frequent on testing when tissues may be healthy (Eg, positive straight leg raise may just be adding slightly noxious input that results in an increased afferent barrage).
4) The physical exam is best considered a sensitivity test.
Increased levels of norepinephrine (physical stress), epinephrine (mental stress), and cortisol (shut down nonessential systems to maintain homeostasis) are upregulated and contribute to, but do not cause, pain. High sympathetic states can lead to problems that include tissue degeneration, mood swings, slow tissue healing, and increased infection susceptibility in people with chronic pain. Tissue change is particularly evident because the sympathetic nervous system innervates and interacts with muscles, joints, skin, connective tissue, inflammatory chemicals, AIGS, and the DRG. The parasympathetic nervous system is also important to mention to our patients in terms of healing effects of sleep and relaxation.
When we discuss peripheral issues, we are not only talking about the pathoanatomical source, but pathobiological processes dominating the clinical picture. There are several instances in which the pathoanatomical model falls short:
Tissues do get injured, but we must not forget the nervous system’s intricate link to injury. When tissues are hurt, they repair but are unlikely to ever be the same again. To protect against further threat, the CNS has the ability to increase nerve sensitivity. This change happens only if the person decides consciously or subconsciously that there is a need for it, and does not occur in everyone. There are two ways in which this sensitivity develops;
Primary sensitivity: Increased sensitivity to input at the injury site.
Secondary sensitivity: Increased sensitivity to uninjured tissues around the injury.
All pain is neurogenic, operates in a continuum, and has many components.
NOC is tissue pain that occurs at a neuron’s end that is excited by mechanical, thermal, or chemical stimuli. It does not always match up with tissue health status. A normal nerve ending has a very high firing threshold, and nearly 1/3 will never fire. These are called silent nociceptors.
Looking at a chemical process such as inflammation shows us how these nerves fire. When acute inflammation begins, a chemical soup with a swelling broth enters the area. Inflammatory chemicals flood the area, lowering the nerve’s firing threshold and increasing its firing rate. This process makes movements painful. In a chronic inflammatory case, the body becomes depleted of inflammatory mediators, thus potentially leading to change in the sensory neuron’s properties.
The nervous system is also involved with inflammation. C fibers begin neurogenic inflammation by releasing substance P and CGRP. These chemicals flatten capillaries, which further encourage swelling. The spinal cord uses antidromic impulses (firing in an opposite direction along a nerve) to mediate inflammation, thus suggesting a central influence.
The sympathetic nervous system can affect inflammation by releasing catecholamines, which maintain or enhance pain. This gives us clinicians a way to affect the inflammatory response by targeting stress reduction.
There are two ways to classify NOC based on inflammatory response. It is much easier to do this than it is to find a structure at fault.
Fluids forced out of tissues.
Evident in prolonged/unusual postures
End of the day
Rapid ease with posture change
Poor anti-inflammatory response
Acute pain / tissue damage
Concordant signs (redness, swelling, temperature change, etc.)
Hints of an unhealthy nervous system
Peripheral Neuropathic Pain (PNP)
Butler lists several modern concepts of nerves.
1) Peripheral nerves are long, living, and responsive tissues.
2) The dorsal root ganglion is the peripheral nervous system’s brain.
3) Nerves are stable and take many mechanical forces during movement
4) Axons are highways that transmit pulses, which get modified but abnormal impulse generating sites (AIGS) in chronic pain.
5) A nerve’s connective tissue is innervated and capable of causing pain. Therefore healthy connective tissue = healthier nerve.
6) It is unlikely that nerve entrapment exists on its own. Stress response and central sensitization likely occur as well.
7) The immune system plays a role in PNP.
When a peripheral nerve segment becomes injured, it can begin to generate its own impulses. These sites can form just about anywhere in the nervous system, including the spinal cord and dorsal root ganglion. AIGS can only occur in sensory nerves, and are likely what neurodynamic tests affect. Here is a list of stimuli that can cause an AIGS to fire.
6) Spontaneously: You’ll notice this when people cannot give an aggravating activity or likely an innocuous unperceived incident.
7) Mechanical: if nerves do not slide or glide well, more force is placed on the AIGS. Moreover, scar tissue formation highly correlates with nerve root mechanosensitivity.
One very important point to make, and this goes for all injuries is that pain does not equal injury. There have been several cadaveric studies that demonstrate nerve damage or compression in people who never complained of pain.
– Dermatomal or cutaneous innervation field. Can be a localized part.
– Pain along a nerve trunk.
– Minor spot pain (trigger point – an AIG in a cutaneous nerve struggling with relationship to myofascia).
– Motor involvement.
– Burning, especially in cutaneous nerves.
– Diffuse cramping if it is a nerve that innervates muscle.
– Paresthesia in a peripheral neural zone.
– Evoked by nerve movement or surrounding tissue change.
– Mechanosensitivity beginning, during, or at stimulus release.
– DRG – More spontaneous.
– Linked to stressed states or inflammation.
– Antalgic postures.
– AIGS give weird symptoms like strings pulling, ants, and/or electrical feelings.
– AIGS may be silent for a few days after injury.
Ultimately, the goals of treating these conditions follow a 3 step approach with the overall goal being turning a firing nerve off.
1) Alter sympathetic and immune inputs – explain pain, make goals, and decrease fear.
2) Increase circulation – simple exercise
3) Decrease mechanical forces – posture, nervous system health, and altering temperature.
This treatment must be done as soon as possible, for if AIGS continue to fire, the CNS may upregulate and lead to central sensitization.
Here we develop a framework for understanding the nervous system with pain as the centerpiece. The nervous system is very much misunderstood as an input/output system:
Myth: Input/output system.
Reality: The nervous system is an active activity constructor. It evolves and learns rather than computes. It is also widely distributed without a master neuron pool for a particular sensation.
The nervous system is made up of two components, hardware and wetware.
Neurons make up the hardware. These components respond and keep a chemical history of many different inputs and outputs. This is true for each individual neuron, which allows each one to be ready to go when called upon. This hardware is one time when the part actual does equal the whole, as one neuron’s activity resembles the entire Central Nervous System’s (CNS) behavior.
The nervous system’s size is near-astronomical. There are approximately 100 billion neurons with 1014 synapses. This figure only factors in the functionally known nervous system components. If we throw in 103 nodes/centers (connected by 105 pathways) and the 10:1 glial cell:neuron ratio, and we have an incredibly dense system in place. A pinhead speck of brain tissue has 350 million connections.
This hardware is also very redundant, as very few neurons go straight from sensory organ to cortex. There are several feedback loops in place which allows for constant checking and rechecking.
Wetware includes the different neurotransmitters and neuromodulators. Examples include the following:
GABA – Inhibitor
Glutamate – excitor (2 types)
NMDA – Important in memory acquisition and long term sensitivity changes.
Acetylcholine – Works at the neuromuscular junction (NMJ); plays a key role in autonomic nervous system function.
Amines – There are 2 categories.
Catecholamines: Run from brainstem to CNS. They function under autonomic and endocrine circuits. These upregulate in post-traumatic stress disorder (PTSD). There are 3 types:
Serotonin: Inhibit sensory input. This chemical is often low in depressive disorders.
Even though neuron and brain behavior are mirrored, the same cannot be said between brain anatomy and chemistry. The wetware is very widespread and nonexclusive throughout the system. There are home bases for different components, but many brain areas are active when stimuli are applied.
Ion Channels 101
This brain activity is governed predominantly by ion channels. There are several types of ion channels, with the most common being…
Voltage gated: Affected by electrical charge (milliseconds).
Ligand/chemical gated: Affected by body chemicals (milliseconds).
Mechanically gated: Affected by stretch/pressure (milliseconds).
Metabolic-receptors: Slow-acting (several minutes) via G-proteins.
The longer an ion channel can stay open, the longer lasting change can occur. Therefore, targeting the G-proteins can lead to both large positive or negative consequences.
There are seven key points that Butler wishes to discuss regarding ions, which I have narrowed down to four:
1) Ion channels are a collection of proteins that bind into neurons. Their lifecycle occurs as follows:
Synthesized on ribosomes → transported in the axoplasm→ Inserted into axolemma→ form a plug with a hole through it→ open/close via stimuli
2) They are constantly changing and may only have a half-life of a few days. This allows for self-regulation.
3) They are not distributed evenly, which allow for salutatory conduction.
4) Ion channel number, kind, and activity at any one time represent the sensitivity needed for one’s survival.
For example, injury states lead dramatic changes in receptor numbers in various brain locations.
Peripheral nerves usually don’t have ion channels unless demyelination occurs, which can lead to a high channel density at the damaged site.
Next we must talk about action potentials and their all-or-none firing capabilities. This quality can lead to continual spiking, which ultimately depend on the person’s needs and nervous system health status. At times such as in sport, this firing can be advantageous. But if a nerve is injured, it may repeatedly fire when less aggressive stimuli are applied.
Now, let us apply these concepts to the neuromatrix, which is the entire network whose spatial distribution and synapses are determined genetically and by sensory inputs. If we take pain as an example, there may be a certain genetic bias toward a particular pain state. Looking at the nurture aspect of this matrix, all experiences in which this pain occurs further sculpt what future pain is like.
Parallel and Bilateral Processing
Initially, information from the environment was thought to occur in a serial fashion. You prick your finger, which sends inputs all the way up to the brain.
A→ B→ C→ D→E
However, more recent research has indicated that processing occurs in a parallel fashion, leading to great redundancies.
Parallel processing is why surgery for chronic pain usually fails. If we remove the D aspect of pain processing, B; C; and E will continue to get inputs from A.
Bilateral processing is also a recently discovered phenomenon, in which some neurons will react to stimuli from both sides of the body. This most often occurs in midline structures such as the trunk or mouth or with structures that work together such as the hands. This processing can also be seen with nociception, as ipsilateral nociception leads to bilateral brain activity.
The Brain and Movement
The cerebellum and basal ganglia are major players linking the brain and movement, as they facilitate motor program recall and movement-based thoughts. These areas are the movement planners. They play a role in motor imagery, as this modality has been shown to activate similar neural substrates as with motor performance.
The link between the brain and movement can by seeing how motor control and pain processing are related. It is fairly established that in the presence of pain, motor control is altered. Butler suggests that if motor control contributes to pain processing, then perhaps it can be disengaged from the pain experience.
Receptive fields and homunculi
Receptive fields are sensory surfaces which must be stimulated for a neuron to respond. Generally these fields are connected from first to third order neurons in increasing complexity and fiber fashion.
These receptive fields are somatotopically arranged throughout the entire nervous system, meaning adjacent body parts a represented in adjacent sites. This arrangement anatomically facilitates plasticity, and may allow neighboring parts to take over during an injury.
This arrangement plays a large role in neuroplasticity, which is defined as neuron function change throughout the lifespan. For example, if a neuron were to go silent, the surrounding neurons would invade that space. This phenomenon can be seen in people who have had amputations, as oftentimes they can often feel their phantom limbs by touching an adjacent somatotopic area, such as the face. Another example would be with tinnitus, which Butler describes as an auditory phantom phenomenon. These representations can be altered by overuse, lack of use, minor injuries, and cognitive changes.
Neuroplasticity is not a fixed process, however. Representations can become smudged, in which pain in one area will often spread to adjacent areas. So the idea of shoulder pain on one side spreading to the other is not so farfetched. This is very often seen in people with chronic pain.
1) Prior to any active or passive inputs, the nervous system must be primed prior by education; understanding; empathy; and skilled placebo.
2) Altering one process could affect things on the whole
a. E.g. resolving a workplace issue could affect tissue healing.
This book is an all-encompassing manual regarding neurodynamics. This concept is defined as the physical and related physiological abilities of the nervous system.
Before delving into neurodynamic nitty-gritty, a brief history of physical therapy is laid out via a very cool brachial plexus design (you have to get the book to see it). There are three different progressions in physical therapy history: manual therapy, exercise, and neurological manual therapy.
The first time PTs learned manipulation was in 1916 at St. Thomas Hospital in London. The thought process of the time, as well as most early manual therapy, was predominantly biomechanically joint-centric. Eventually, muscle and other tissues were targeted. These approaches were championed by Geoffrey Maitland’s signs and symptoms approach and Graves’ pathological model.
Concomitant with manual therapy has been exercise, which had moved from nonspecific (aerobics, tai chi) to specific movements a la Vladimir Janda and Shirley Sahrmann.
On the other side of orthopedic manual therapy were manual techniques from the likes of Bobath’s NDT and PNF. What is sad about these techniques is that they have not interacted much during manual therapy’s development. Butler makes arguably one of the most important statements in the book by saying our patients are ultimately all neurological. We will all meet at the brain.
Aside from various manual approaches, recent techniques have been developed including psychology, counseling, exercise physiology, and acupuncture. Butler feels these are nice adjuncts to the plan of care.
The key manual therapy points Butler wishes to make are as follows.
1) Manual therapy is young, slightly over 2 generations.
2) In this short time frame, rapid change has occurred.
3) Relies heavily on tissue, usually muscle or joint.
Neurodynamics is not a new approach. Tension tests were mentioned as early as 1929. Butler argues that all the tissue techniques that manual therapy advocates have unconsciously encouraged the nervous system to move.