When talking about breathing biochemically, the focus will be shifted toward oxygen delivery to the tissues and carbon dioxide removal. Maintaining these gases is a complex body task due to their constant fluctuations.
Looking at pH is a great way to get a glimpse of the the entire body. We know the pH scale runs from 1 to 14, with the physiological normal being between 7.35 and 7.45. If we have a value at 7.5 or above, our body goes into alkalosis. An example of this would be in the case of hyperventilation. If our pH drops to 7.3, we go into acidosis.
Carbon Dioxide (CO2)
CO2 determines blood acidity, and comes primarily from the mitochondria. It is the biological equivalent of smoke and ash.
CO2 levels can vary with exercise, as more is produced when we are training. However, pH stays balanced because oxygen demand increases. The opposite occurs when we are not exerting ourselves because CO2 is not produced as much.
Another example of changing CO2 levels is during breath holding. More is not necessarily produced, but CO2 levels rise because we are not exhaling it away. This rise is what we feel when we hold our breath.
Metabolic Alkalosis and Acidosis
Aberrant breathing can cause respiratory acidosis or alkalosis, but many physiological conditions can affect pH as well. These conditions can be differentiated by blood analysis. Some examples of metabolic acidosis include ketoacidosis and excessive diarrhea. Metabolic alkalosis can be induced by excessive vomiting or diuretic use.
The above changes can influence breathing and oxygen transport. If we are more acidic, more breathing will be necessary and oxygen will be more ready to dissociate from its carrier hemoglobin. The reverse occurs when we are in an alkaline state.
Breathing changes based on CO2 levels are regulated by two chemoreceptor types: medullary (central) and those in carotid and aortic bodies (peripheral). The medulla handles minute-to-minute adjustments while the peripheral receptors handle second-to-second adjustments.
Allergies, Diets, and Nutrition
It is not often discussed regarding how nutrition can affect breathing, but reading this book will make you think differently. Up to 10% of people with asthma may have a food allergy; especially if the asthma is poorly controlled. Even food intolerances can aggravate or trigger asthmatic attacks.
Elevated blood lactate levels have also been shown to induce panic attacks and hyperventilation in those prone to these states. The reason is lactate can create peripheral alkalosis by converting to bicarbonate.
Lactate matters because glucose has been shown to elevate lactate levels. So it may be fair to say that diets potentially high in sugar could influence panic and thus breathing disorders. Other substances such as alcohol and caffeine can also influence these levels.
That does not mean that glucose ought to be completely eliminated from the diet, as our brains utilize 20% of available glucose in the body at any given time. Therefore, as a way to see if glucose levels have an effect on breathing disorders, check to see if hyperventilation occurs relative to meal times.
Another unfortunate issue with hyperventilation is poor exercise tolerance. Carbonic acid levels increase with aerobic exercise; and lactic acid follows once the anaerobic threshold is crossed. Those who hyperventilate have smaller buffer zones for these acids due to less present bicarbonate.
This chapter’s goal is to cover both normal and abnormal breathing patterns. Often, breathing disorders can seem similar to serious disease when in reality the patient may not be getting an adequate breath. In fact, hyperventilation syndrome (HVS) and breathing pattern disorders (BPD) have the following incidence:
10% of general medicine practice patients have HVS/BPD as their primary diagnosis.
Female:male is about 2:1 to 7:1; most commonly in the 15-55 year age group.
Acute HVS only makes up about 1% of cases.
The normal resting breathing rates equate to around 10-14 breaths per minute, which moves around 3-5 liters of air per minute through the airways.
Not so Normal Breathing
HVS/BPD can be defined as a pattern of overbreathing where the depth and rate are greater than the body’s metabolic needs. In some cases, such as during exercise and organic disease, hyperventilation is an appropriate response. It is when these causes are not found that we attempt to affect these breathing patterns.
There are a large number of symptoms that may coincide with HVS, but none are absolutely diagnostic. Oftentimes these symptoms are exaggerated when one has a hyperventilatory episode. I will break the signs and symptoms into the following categories:
Numbness and tingling
Ataxia and tremor
Anxiety and panic
Detachment from reality
Impaired concentration, thinking, performance, and affect
Disturbance of sleep/nightmares
Chest pains and angina
Palpitations and arrhythmias
Lightheadedness and syncope
Breathlessness and inability to take a deep breath, often nocturnal
Sighing and yawning
Upper-chest breathing and use of accessory muscles in the neck
Chest wall tenderness
Two hand test; one on upper sternum and the other on upper abdomen – top hand moves more
Dry, unproductive cough and often clears the throat
Aching and stiffness due to hypertonicity
Cramps, carpopedal spasm and tetany
Lower chest and epigastric discomfort
Esophageal reflux and heartburn
Upper abdominal distension
Manneurism of air swallowing and belching
This is a Test
There are several special/lab tests that one can look at to help determine breathing disorders. Listed below are some of the more prominent tests performed:
Peak expiratory flow rate (PEFR)
Arterial blood gas
Think test – have the patient recall a painful experience in which they experienced their symptoms; if end-tidal CO2 drops 10 mmHG, then the patient likely has a HVS.
Breath holding time test – Those with HVS often have a hard time holding their breath no more than 10-12 seconds. 30 seconds is the dividing line between HVS and not.
Voluntary overbreathing to reproduce symptoms.
Other Breathing Issues
Hyperventilation can also occur as a secondary issue to other breathing dysfunctions. Two examples included obstructive and restrictive breathing disorders. You may also see those who have been in chronic pain may be especially prone to HVS/BPDs.
Breathing has been something I have been interested in very much since I first learned about its power from Bill Hartman and through the Postural Restoration Institute, and this excellent book is a great way to get a full overview.
The first chapter covers too much anatomy to go through every little detail in my short blog post. So study up. Here are the highlights.
Structure, Function, and You
In order to have favorable respiration, structure makes all the difference. Adequate thoracic, ribcage, and breathing muscle mobility must be restored and maintained in order to uptake a quality breath. This can be achieved via re-education and training.
Realize too that psychological distress can also play a huge role in how we breathe. Disorders such as anxiety and depression can have corresponding breathing dysfunctions. It may be the way the body responds to ensure survival.
Ergo, when attempting to change breathing patterns favorably, one must address both structural and psychological factors.
Homeostasis is the body’s process to normalize itself. If too many homeostatic-disrupting tasks are occurring at one time however—such as nutritional deficiencies and toxin ingestion—homeostatic function can become overwhelmed. This systematic stress can lead to breakdown and a switch to heterostasis, in which the body must be treated. We can restore homeostasis via the following:
Take away as many undesirable adaptive factors as possible.
Enhance, improve, and modulate defensive and repair processes.
Treat symptoms without further burdening the system.
A general rule of thumb when addressing these areas: The weaker a patient is, the lighter the intervention must be.
There are several benefits to having optimal respiratory function:
Allows gas exchange.
Enhanced cellular function so the brain, organs, and body tissues perform normally.
Permits normal speech.
Involved in non-verbal expression.
Assists in fluid movement.
Mobilizes the spine.
Enhances digestive function
Air takes a fascinating journey when it enters our body. It goes through the following passageway
The two breathing strategies we utilize are nose and mouth breathing. Nose breathing is slow and rhythmic; utilized for sleep, rest, and quiet activity. But when we need large air volumes, mouth breathing comes into play. Mouth breathing requires much less resistance compared to the nose, and involves intercostal and anterior neck muscle activity.
Regardless of which strategy is used to breathe, the following occurs at the diaphragmatic level:
Diaphragm descends during inhalation; pulling the central tendon down.
Abdominal viscera resist the diaphragm from descending.
This resistance fixes the central tendon, causing the ribs to displace laterally.
At the same time, the sternum moves superiorly and anteriorly.
The combination of the above two leads to thoracic cavity expansion.
Greater breath volumes lead to accessory muscle utilization.
Abdominal muscle tone allows for correct viscera position so an appropriate amount of central tendon resistance can occur.
At the gas exchange level, air travels via the following pathway:
Lung function can also be affected by fascial links throughout the body. There is a direct fascial connection from the base of the skull to the diaphragmatic apex. Thus, stress in one area along this pathway can affect areas along the same location. As an example, changes in cervical spine or diaphragm position can lead to changes in breathing patterns.
You can also see fascial connections between the diaphragm, cervical spine, and pleura. You can often see that the pleura can be affected with impairments in the prior regions. For example, there have been dissections in which degenerated lower cervical structures also have corresponding fibrotic change to the pleuropulmonary attachments.
Ain’t no Bones About it
From a spinal perspective, breathing has a large effect on joint mobility; namely in the frontal plane. Every time we inhale, the odd segments (C3, T7) become more mobile, with the even segments increasing mobility during exhalation. This effect decreases as we travel down to the lower thoracic segments. The exception for this mobility is the cervicocranial junction, in which all three planes become more mobile upon inhalation. Taking this phenomenon into account, it may be helpful to utilize breathing cycles during mobilizations depending on which segments you wish facilitate.
Neural Regulation and Breathing
The brain works on controlling respiration in order to maintain balanced concentrations of oxygen and carbon dioxide. Respiratory control centers are located in the brainstem via three primary nuclei groups:
Dorsal respiratory group – Found in the medulla. This area creates inspiratory movements and is responsible for the basic breathing rhythm.
Pneumotaxic center – Found in the superior part of the pons. This area controls the filling phase of breathing.
Ventral respiratory group – Found in the medulla. This area causes both inspiration and expiration. However, this area is inactive during quiet breathing.
While not a brain area, the Hering-Breuer reflex is an important neurological phenomenon. Located in the nerves of the bronchi and bronchioles, this reflex prevents lung overinflation via sending messages to the dorsal respiratory center via the vagus nerve.
Most of the above is in reference to quiet breathing. We can use a cortical overriding system via spinal neurons to respiratory muscles to consciously change breathing patterns.
This strategy is utilized in day-to-day activities such as speaking and singing. There is also some evidence that the cortex and thalamus drive some normal respiratory function. These areas are likely what we target and are likely originators for breathing pattern disorders (BPDs) and hyperventilation syndromes (HVSs).
You cannot talk breathing without mentioning the autonomic nervous system (ANS). There are two divisions of the ANS; the sympathetic (SNS) and parasympathetic (PNS) nervous systems. The SNS deals with flight, fight, or freeze responses; and its neurons connect to the head, neck, heart, larynx, trachea, bronchi, and lungs. So we can see a vast number of areas that are affected if the SNS is dominant.
The PNS, on the other hand, deals with visceral functions aka rest and digest. These areas govern the lungs, cranial, and pelvic regions.
There is also a third nervous system called the non-adrenergic noncholinergic (NANC) system, which contains inhibitory and stimulating fibers. The main neurotransmitter for this region is nitric oxide.
When inhibitory neurons in the NANC are active, smooth muscle relaxation and bronchodilation occur via calcium ions, with the opposite occurring via NANC’s stimulatory C fibers.
The Muscles of Respiration
The two thoracic-based muscle groups that influence respiration can be broken down into extrinsic and intrinsic. Extrinsic muscles position the torso; which influences shoulder, arm, neck, and head placement. As we learned previously, the position of these areas can influence breathing mechanics.
The intrinsic muscles predominately focus on moving thoracic vertebrae or the rib cage, and are the money muscles associated with respiration.
To get more specific, there are several muscles that work on inspiration. The king of course is the diaphragm, which provides 70-80% of the inhalation force. Other muscles that assist inspiration include lateral external intercostals, parasternal internal intercostals, scalenes, and levator costarum.
When we need an extra inspiratory kick for more demanding activities, we will often use accessory muscles to facilitate this process. These muscles include sternocleidomastoid (SCM), upper trapezius, pectoralis major and minor, serratus anterior, latissimus dorsi, serrratus posterior superior, iliocostalis thoracis, subclavius, and omohyoid.
We also have muscles that can perform exhalation, but understand that exhaling is primarily a passive process. We exhale based on elastic recoil from the lungs, diaphragm, pleura, and costal cartilages.
But sometimes you may want to utilize muscles to force an exhale. The guys for this would include interosseous internal intercostals, abdominal muscles, transversus thoracics, subcostales, iliocostalis lumborum, quadratus lumborum, serratus posterior inferior, and latissimus dorsi.
Piriformis syndrome often involves the fibular tract of the sciatic nerve. It has the capacity to create symptoms from the buttock down to the anterolateral leg. Testing the neurodynamics with a fibular nerve bias is essential.
To attempt to isolate this problem, we must best differentiate interface from neurodynamic components. Using Cyriax principles –palpation, contraction, and lengthening –can be beneficial in this regard. Keep in mind that below 70 degrees hip flexion the piriformis produces external rotation, and above 70 degrees it is an internal rotator.
When treating this problem, the goal is to change pressure between the piriformis muscle and the sciatic nerve.
Level 1a – Static opener
VID – KF, ER
Level 1b – Dynamic opener
VID – Passive ER
Level 2a – Closer mobilization using passive IR.
VID – Passive IR
Level 2b – We finish with a passive piriformis stretch
VID – Tailor stretch
If there is a neurodynamic component to things, slightly modify things by using sliders. We start things off with the same opener as the interface above. As the patient progresses, you can add proximal or distal components eventually finishing with a fibular nerve-based slump.
VID – Building the slump
To combine interface and neural treatments, contract-relax can be utilized.
Sciatic Nerve in the Thigh
Oftentimes with hamstring strains, sciatic nerve sensitivity can increase. The slump and straight leg raise tests can be utilized to help differentiate a pure hamstring issue from neural problems.
To treat this issue, sliders can be utilized, eventually working to a slump tensioner:
VID – PF at top for proximal dysfunction, DF at bottom for distal sliding…progress with spinal lateral flexion (done in slump
Knee and Thigh Pain
Implicating neurodynamic problems in this population is challenging, as these tests often show covert abnormal responses. These can be treated with simple sliders and tensioners. These are not in the Shacklock book, but are what I have been currently using.
VID of FS slider and tensioner
Here is an example of a slider and tensioner for fibular nerve impairments.
Both neck flexion and knee extension increase symptoms – Tension dysfunction.
The straight leg raise is another important test that can help determine the nervous system’s state.
The treatment parallels similar tactics as previous body areas. For reduced closing dysfunctions We start level 1 with static openers, progress to dynamic openers, then work to close.
For opening dysfunctions, we progress toward further opening/contralateral lateral flexion.
We treat these mechanisms based on which dysfunction is present. For cephalid sliding dysfunctions, we approach with distal to proximal progressions; and for caudad sliding dysfunction, we work proximal to distal
Tension dysfunctions are started with off-loading mvoements towards tensioners
Sometimes you can have interface dysfunctions that simultaneously have contradictory neurodynamic dysfunction. There are several instances of the case.
Reduced closing with distal sliding dysfunction – Treat by combining closing maneuvers while perform active knee extension.
Reduced closing with proximal sliding dysfunction – Address by closing maneuver with neck flexion.
Reduced closing with tension dysfunction – This is treated with adding closing components to tensioners
Reduced opening with distal sliding dysfunction – Here we add a dynamic opener along with leg movements.
Reduced opening with proximal sliding dysfunction – Same as above, only we add neck flexion instead of leg movements
Reduced opening with tension dysfunction – Basically a combination of the last two treatments.
The same techniques can be applied to mid-lumbar dysfunctions, this time utilizing the femoral slump:
And if all else fails, just watch this video (NSFW due to language).
Wow. That’s all that really needs to be said. I have had a great deal of exposure to PRI in the past, but I have only had one formal class under my belt. Needless to say, I was looking forward to learning more. James Anderson and the PRI folks did not disappoint.
Myokinematic Restoration was easily the best class I have taken all year.
It also helped having another like-minded group attending. You learn so much more when you are surrounded by friends. Here is the course low-down.
Disclaimer for the Uninitiated
I know there are a lot of misconceptions about PRI on the interwebz. Even though posture is in the name, PRI has little to do with posture in the traditional sense. We know posture does not cause pain, and PRI agrees with this notion. But it’s not like they can change the name of the organization now. What? Do you think Ron Hruska is Diddy or something?
After discussions with James and his mentioning this aloud in class, the target of PRI is the autonomic nervous system. Not posture, not pain, not pathoanatomy, but the brain. Essentially, they have figured out a window into the autonomic nervous system via peripheral assessment.
Moreover, PRI is not in the pain business, though many think this is the case. Hell, even in the home studies they mention pain quite a bit. But realize those were done in 2005. Would you like me to hold you to things you have said 8 years ago?
Throughout the entire two day course, pain was mentioned in two instances. The first time was this direct quote from James:
“ PRI does not treat pain.”
The second time was mentioned in the case of various pathologies, in which James put a disclaimer that PRI just puts these things in here per clinician requests.
What PRI treats is position, neutrality, a state of the autonomic nervous system that is shifted towards parasympathetic but can freely alternate between sympathetic and parasympathetic states.
So if PRI doesn’t treat pain why use it? I say because the autonomic nervous system influences pain states. The potentially indirect effects on pain when the autonomic nervous system is favorably influenced seem desirable. And from my own personal experience, for whatever that is worth, my limited understanding of PRI has netted me quite a bit of success with my patients. It also requires my patients to spend less time in the clinic since they do not require my hands; good news for everyone.
Back to the Basics
The basic PRI concepts rely on asymmetry. All body systems –neurological, respiratory, muscular, visual, etc.—are asymmetrical. This asymmetry cannot be changed, but we can strive to reduce one-sided dominance as best we can.
The side that is dominant in human beings is the right side. This lateralization is normal, but what we don’t want is the right to be overly biased. Too much right dominance essentially creates a low level left sided neglect.
Myokin’s utmost focus is on a polyarticular muscle chain known as the anterior interior chain (AIC), which is composed of the following muscles:
Diaphragm – king
Tensor fascia lata
You have two of these chains, a left and a right. For a variety of reasons, such as our asymmetrical build and left hemisphere/right sided dominance, the left AIC is more dominantly active compared to the right.
You can notice this dominance just by comparing right and left hemidiphragms:
Right has a larger diameter.
Right has a thicker & larger central tendon.
Right has a higher dome, and is better able to maintain this shape.
Right has more crural fibers and fascia.
The right crura attach 1-1.5 levels lower on the lumbar spine than the left.
Basically, the right diaphragm is built for success, whereas the left diaphragm is often more contracted, smaller, and less concentrically effective. This difference helps perpetuate a more active LAIC. The path of least resistance for you to have an effective breath is by activating these muscles.
Because the LAIC is the more dominant chain, this throws the body into an asymmetrical position. The left innominate is more anteriorly tilted and forwardly rotated with the right more posteriorly tilted and backwardly rotated. This position puts the right hip into internal rotation, adduction, and extension; and the left hip compensatorily into external rotation, abduction, and flexion.
Chains and Gait
These chains oppose each other during gait. For example, when you are standing on your right leg, your LAIC is active, causing the swing leg to further put weight on the right leg. You cannot fully use one chain unless the opposite chain is inhibited, so the RAIC is quite during this phase. Inhibition allows for alternating and reciprocal gait; the goal of PRI.
Realize that as long as you are in weight bearing, you are in a phase of gait. We can base this off of pelvic positioning. Since pelvic position can be altered with breathing, it is fair to say the every time you take a breath you are put into a phase of gait. Breathing and gait are one in the same.
To assess neutrality, many common tests already utilized in the therapy realm are used. The two big tests are:
Modified Ober’s test (adduction drop)
Modified Thomas test (extension drop)
With the LAIC pattern, you will see a positive Ober’s on the left but not on the right. This finding is due to either restriction from the anterior-inferior acetabular labral rim, transverse ligament, and piriformis muscle; or impact of the posteroinferior femoral neck on the posteroinferior rim of acetabulum that does not allow femoral adduction.
The Thomas test in this pattern can be either positive or negative. A positive Thomas correlates with the adduction drop due to the limited extension. A negative Thomas test, barring a positive Ober, would implicate iliofemoral and pubofemoral ligament laxity. If we think back to the position of the innominate, the left femur will have to externally rotate in order to face forward, which can stretch the anterior capsuloligamentous structures. Here is the same thing better explained by Bill Hartman:
You should also see limited right trunk rotation (unless there is iliolumbar ligament laxity), decreased left SLR (unless you have an overstretched hamstring), an apparent shorter left leg, and decreased left hip internal rotation and right hip external rotation.
PRI also has a test called the Hruska Adduction Lift test, which is used to assess acetabulofemoral control in a way that correlates with gait. The scope of this test and interpretations are too much to fully write about in a short summary, so perhaps when I get better understanding all the nuances, performance, and meaning I will post on this test further. Until then, PRI instructor Mike Cantrell wrote a great piece on the lift test here.
Taking the above tests, namely the adduction drop and lift test, the goal is to satisfy the following questions:
1) Can the person adduct? (adduction drop)
2) Can the person internally rotate on both sides? (Measurement, adduction lift)
3) Does the person have internal rotation strength on both sides? (adduction lift)
In order to inhibit the LAIC, there are several key muscles that are to be activated:
Left Hamstrings [sagittal repositioner]
Left anterior gluteus medius
Left ischiocondylar (hamstring portion; IC) adductor [frontal repositioner]
Left glute max (sagittal fibers)
Right adductor magnus
Right glute max (transverse fibers) [Transverse repositioner and the other key to maintaining neutrality].
Bilateral obturator interni (the key to maintaining neutrality)
Left abdominal obliques.
The goal is to influence the left hemidiaphragm away from its overly contracted state in order to allow better reciprocally alternating respiration, position, and gait.
Treating the LAIC
The LAIC patient has a positive adduction drop test and Thomas test. So the name of the game is to reposition and develop hole control. What hole control means is allowing the obturator and glute max to control the femur in the acetabulum to allow for reciprocal gait pattern.
For the LAIC, we want to activate the following muscles in the following order:
1) Biceps femoris in ER/extension
2&3) R Glute max & obturator & adductor magnus via ER
4) L Anterior glute med via IR
5) L IC adductor via IR
6) Medial hamstrings via IR
By performing the exercises in this order, we first reposition, then establish hole control, and then retrain the person to turn to the left side.
There are certain instances in which ligaments can get stretched out and become lax. This is where the concept of ligamentous muscle comes into play, in which muscles increase their tone to reinforce capsuloligamentous structures.
The theoretical reason this order is performed is because the IC adductor approximates the femur into the acetabulum, while the left anterior gluteus medius strangulates the joint by further driving internal rotation.
For a patho LAIC, we go for the following muscles in a slightly different order:
1) Biceps femoris to reposition
2) L IC adductor via IR
3) L anterior glute med via IR
4) R glute max via ER
5) R adductor magnus via ER
6) L medial hamstrings via IR
In this instance, we reposition, then build ligamentous muscle, and finish by establishing hole control.
If after a successful reposition you notice mobility changes in hip rotation, you may want to proceed in the following manner:
Decreased left IR (v Right): Stretch posterior capsule
Increased left ER (v right): go after L IC adductor and L anterior glute med
Increased right IR (v left): Kick in R glute max and R posterior glute med
Decreased right ER (v left): Stretch anterior & inferior capsule
Favorite James Quotes
“The diaphragm owns you.”
“If you don’t have position and throw in demand, someone else will do it.”
“I find it offensive when people say iliopsoas. We don’t call it the hamductor obturatoridiosus.”
“Screw PT school, subscribe to Oprah.”
“The whole body is in a phase of gait.”
“The problem is the brain and the diaphragm.”
“Nobody is Weak.”
“External rotation is worthless without internal rotation.”
“PRI is from start to finish brain therapy and parasympathetic awareness of the left side.”
I cannot recommend enough courses from PRI. I base this off of the methodology, effectiveness, and thought process. They appreciate the nervous system’s power just as much as anyone. Please check them out and tell ‘em Zac sent you.
When discussing TOS pathoneurodynamics, you must talk about breathing. The brachial plexus passes inferolaterally between the first rib and clavicle. When inhalation occurs, the plexus bowstrings over the first rib cephalidly. So breathing dysfunctions can contribute to one’s symptoms. Excessive scapular depression can also contribute because the clavicle approximates the plexus from above.
Clinically, TOS often presents as anteroinferior shoulder pain, with some cases passing distally along the course of the ulnar nerve. A resultant upper trapezius/levator scapula hyper or hypoactivity can occur that may affect the neural elements.
Treating the Interface
Level 1 – Static Opener with breathing
Level 2 – Static opener with rib mob during exhalation; progressing with scapular depression.
Level 3 – Rib depression with sliders and tensioners.
Pronator Tunnel Syndrome
This syndrome consists of pain in the anteromedial forearm region with or without pins and needles. Symptoms are usually provoked by repetitive activities such as squeezing, pulling through the elbow, and pronation movements.
From an interface perspective, pronator syndrome deals with excessive closing. So we will use openers to treat.
Level 1 – Static opener combining 60-90 degrees of elbow flexion with forearm pronation
Level 2 – Dynamic opener
Treating neural components depends on the present dysfunction. There are the following possible dysfunctions:
Distal sliding dysfunction – symptoms decrease with contralateral cervical flexion.
Proximal sliding dysfunction – Symptoms increase with contralateral cervical sidebend and finger flexion.
Tension dysfunction – Symptoms increase with contralateral cervical sidebend and finger extension.
We treat the distal sliding dysfunction by progression sliders from large to small distal movements, with the reverse occurring for proximal sliding dysfunctions:
Tension dysfunctions are going from anti-tension to tension mechanisms
You can also combine interfaces and neurodynamic treatment utilizing acupressure during a nerve mobilization:
Supinator Tunnel Syndrome
This syndrome involves anterolateral elbow and forearm pain with possibly pins and needles. There also can be isolated wrist dorsum pain. Symptoms are provoked by activities such as squeezing and pulling through elbow flexion and supination movements.
Interface treatment is very similar to that of pronator tunnel syndrome.
You can also have distal (improve with contralateral cervical sidebend) and proximal (worsen with contralateral cervical sidebend and wrist extension) sliding dysfunctions, which are treated in a similar fashion as the pronator tunnel syndrome. So too with tension dysfunction; the goal is to build up the test.
You can also perform neurodynamic massage over the supinator.
Carpal Tunnel Syndrome (CTS)
Treating CTS is an often underutilized area that can be of much benefit. We can mobilize the transverse ligament as an interface technique.
You can also treat the neural structures with different methods depending on the dysfunction.
Proximal sliding dysfunction – use a median nerve slider starting with distal components then adding proximal components
Distal sliding dysfunction – Use Median nerve test 1 and slowly add distal components.
The best slider for the median nerve is in fact the tensioner. This is because when you extend the wrist, the tendons and the nerve move in the same direction. Adding contralateral cervical sidebend slides the median nerve in the opposite direction of the tendons.
Tensioning dysfunction is just utilizing your basic tensioner.
You can tier your testing based on one’s dysfunctions, such as opening or closing, as well as using sensitizers for less severe problems.
Reduced Closing Dysfunction
Level 1a – Static opener to increase space and decrease pressure in the intervertebral foramen. In the picture below, we would open the right side by combining flexion, contralateral sidebend, and contralateral rotation.
Level 1b to 2b
Reduced Opening Dysfunctions
For these impairments, they are treated just the same as closing dysfunctions. The major difference is rationale. In closing dysfunction, the goal is to reduce stress on the nervous system. With opening dysfunctions, however, we are trying to improve the opening pattern.
Static openers will generally not be used because these treatments could potentially provoke symptoms.
The gentlest technique is the two-ended slider, in which an ipsilateral lateral glide and elbow extension are performed.
For tension dysfunctions, we go through the following progression:
The two main ways to treat interfaces involve opening and closing techniques. These treatments involve either sustained or dynamic components. We will discuss which techniques work best in terms of dysfunction classification.
– Reduced Closing Dysfunction – Given static openers early in this progression, continuing to increase frequency and duration. Eventually you move to more aggressive opening techniques, while finishing with closing maneuvers.
– Reduced Opening Dysfunction – Start with gentle opening techniques working to further increasing the range.
– Excessive Closing and Opening Dysfunctions – Work on improving motor control and stability.
How About Neural Dysfunctions
The main treatments are sliders and tensioners; each can be performed as one or two-ended. Sliders ought to be applied when pain is the key symptom. Sliding may milk the nerves of inflammation and increase blood flow. These techniques could also be used to treat a specific sliding dysfunction.
Sliders can be performed for 5 to 30 reps with 10 seconds to several minute breaks between sets. Increased symptoms such as heaviness, stretching, and tightness is okay, but pain should not occur afterwards. Typically sliders are performed in early stages, and in acute situations should occur away from the offending site.
Tensioners are reserved for higher level tension dysfunctions. The goal is to improve nerve viscoelasticity. Some symptoms are likely to be evoked, but this occurrence is okay as long as symptoms do not last. Tensioners are used in later-stage dysfunction.
With this test, the upper cervical tissues slide caudad, and the lower cephalid. The thoracic spine moves in a cephalid direction as well.
Normal responses ought to be upper thoracic pulling at end-range. Abnormal symptoms would include low back pain, headache, or lower limb symptoms.
Median Neurodynamic Test 1 (MNT1)
This test, also known as the base test, moves almost all nerves between the neck and hand.
Normal responses include symptoms distributed along the median nerve; to include anterior elbow pulling that extends to the first three digits. These symptoms change with contralateral lateral flexion and less often ipsilateral lateral flexion. Anterior shoulder stretching can also occur.
Ulnar Neurodynamic Test (UNT)
This test biases the ulnar nerve, brachial plexus, and potentially the lower cervical nerve roots.
Normal responses include stretching sensations along the entire limb, but most often in the ulnar nerve’s field.
Median Neurodynamic Test 2 (MNT2)
This version biases the lower cervical nerve roots, spinal nerves, brachial plexus, and median nerve.
Normal responses would be similar to MNT1.
Radial Neurodynamic Test (RNT)
This test looks predominately at radial nerve, as well as the nerve roots. It is uncertain if this test biases any particular nerve root.
Normal responses include lateral elbow/forearm pulling, stretch in the dorsal wrist.
Axillary Neurodynamic Test (ANT)
This test tenses the axillary nerve, though may not be specific.
Normal responses include posterolateral shoulder pulling with about 45-90 degrees of abducton.
Radial Sensory Neurodynamic Test (RSNT)
This test is used to rule out de Quervain’s disease as a neurodynamic problem.
Normal responses include intense pulling at the distal radial forearm.
Straight Leg Raise (SLR)
This test is performed with any posterior symptoms from the heel to the thoracic spine.
Active cervical flexion should not be used in this test because false results can occur from abdominal muscle contraction. This error may lead to posterior pelvic tilt, which reduces the hip flexion angle.
Normal response is pulling and stretching in the posterior thigh.
Tibial Neurodynamic Test (TNT)
This test is done for symptoms in the tibial nerve distribution.
Normal responses include stretching in the calf region that can go all the way to the plantar aspect of the foot.
Fibular Neurodynamic Test (FNT)
This test biases both the common and superficial fibular nerves.
Normal responses include stretching and pulling in the anterolateral leg and ankle and the foot dorsum.
Sural Neurodynamic Test (SNT)
This test biases the sural nerve, which can often be involved in a sprained ankle.
Normal responses include pulling in the posterolateral ankle region.
This test checks the peripheral and central nervous system, and can encompass symptoms from the head to the foot.
Normal responses vary depending on the sequence. Usually the movement performed earliest is where symptoms will occur.
Saphenous Neurodynamic Test (SAPHNT)
This test looks at medial knee, shin, and ankle.
Normal response is anterior thigh stretching.
Femoral Slump Test (FST) with Lateral Femoral Cutaneous Nerve and Obturator biases.
These movements bias the anterior-based nerve of the leg.
Shacklock normally performs the exam with the bottom leg in order to maximize gravity’s effects. The obturator can also be biased as such.
Normal responses includes pulling in the adductor region, anterior thigh, or lateral thigh depending on the bias.