I have a young man with pelvic pain. He initially complained of groin and abdominal pain. Now he primarily has left pelvic pain (piriformis and left inner thigh).  The patient has huge lower rib cage flares, poor sitting posture and sensitivity in the left ilioguinal nerve above the inguinal ligament. My questions are: 1) How significant are the flares to the left pelvic pain? 2) What is the ideal treatment frequency to affect a change in the flares and how much change should we expect?

The ability for your patient to breathe and get his ribs down with his abdominals is related to his pelvic floor dysfunction.  They work together to support the “egg” that we are trying to re-establish in PRI.  I would work with your patient to re-establish his abdominals and mediastinum opening in supine, sitting, or sidelying.  Once he has lift scores of 2/5 I would get him in sidelying and inhibit his obturators to get more IR as this will lift his pelvic floor.  I would encourage activity that promotes AF IR/FA IR with hip extension on the left as he can tolerate with the correct inhalation and exhalation phase.

Rib flares are bony changes to the ribs secondary to torque…like a rib hump in scoliosis.  These flares won’t go away, however, you can still get the patient in anterior rib IR and a ZOA with abdominal control.

I have a patient who has an L1 compression fracture.  Primarily presents as a PEC with complaints of right low back pain.  The doctor does not want flexion but I feel I could still use PRI, because I am trying to decompress the spine.
My question is how should I progress with some of the exercises that involve thoracic/lumbar flexion?

I don’t think I would ‘pull’ on the anterior low spine by kicking in a psoas. Reciprocal Retro work might be a better way to incorporate some flexion with spinal rotation in a decompressed manner. Retro Walking or Retro Stair Descents – then progress to ascents. Standing Resisted Alternating Push Throughs with abs on and balloon activity on his side during Knee Toward Knee isometric to engage abs with contralateral adductor would be a good idea.

Am I correct to say that in the Left AIC pattern, the femur is positioned toward ER (from the oriented IR) secondary to the compensation of not tripping over your feet?  
Yes.  The Left AIC directs the pelvic ring clock-wise toward the right and that motion internally “orients” the left femur in the acetabulum until it compensates into ER to line up the foot, to line up the hinge of the knee joint, etc for forward ambulation.  The left psoas and iliacus are left hip ER muscles, but this ER compensation is primarily compensatory because their strongest influence is on the spine and the pelvis.

I don’t understand why abduction is compensatory when the femur is already positioned in abduction.
There is very limited actual left hip abduction from the direct influence of the Left AIC until the left leg has to deal with the ground and position itself to coordinate forward gait activities.  It is then that the left hip ends up so abducted and ER (relative to the resting neutral state of the left hip).  i.e. if an astronaut were floating upside down in space and the Left AIC actively influenced the pelvic girdle, it would not necessarily put the left hip in a state of abduction.  If that same muscle chain is active when he lands on earth and attempts to walk, it would.

Could you elaborate for me (why they do not have a left rib hump)? 
You are accurate in noting that pelvis and spine orientation toward the right would result in left rotation of the thorax.  In order to understand the rib hump, you need to recognize what happens to the rib cage on each side when the thoracic spine segments counter rotate toward the left.  The ribs on the left will rotate into ER (inhalation) with the front of the ribs coming up and the back of the ribs coming down (no rib hump).  The ribs on the right will rotate into IR (exhalation) with the front of the ribs coming down and the back of the ribs coming up (here’s the rib hump).  This left rib ER and right rib IR happens concomitantly as the thoracic spine segments rotate left (see various references on basic rib kinematics when the thoracic spine rotates).  When this spinal rotation reverses, then the rib rotation on each side reverses and they are moving into the other half of the gait cycle across their thorax.

My colleague just came back from the Pelvic Floor Restoration course and she is trying to teach me some of what she learned.  I am stumped on the left obturator internus. I learned in Myokinematic Restoration that the left obturator is short, straight and weak. That made perfect sense to me. My colleague tells me that the left is now considered long and weak in the outlet. Help! I get the weak, but I can only picture short with AF ER, IP IR, and outlet adduction. Please help me understand how the obturator is long on the left.

“The obturator is short, straight and weak in the distal attachment site on the femur (transverse plane).”  This is correct!  In the pelvic floor course, the obturator is long and weak with the proximal attachment site in the frontal plane.  In the pelvic floor course we are looking at the obturators influence on the pelvic outlet in the frontal plane.  In left AF IR, the obturator is being repositioned in both planes in relationship to the femur and the pelvic outlet.  Therefore, it is lengthening distally on the femur and shortening proximally in the pelvic outlet.

Is there a way to do left hip repositioning in a seated or standing position?  I’ve had a couple of patient populations that the supine position doesn’t work—1) 2nd and 3rd trimester pregnancy and 2) geriatric patients who are for the most part wheelchair confined and can walk only short distances with a walker.  I think that PRI would really benefit them, but just not sure how to get them started with it.

Yes, we have several and here are a couple of popular ones:  The PRI Wall Squat with Balloon(2nd Edition Non-Manual Techniques CD-Rom) and the Seated Resisted Single Arm Pull Down 
with Adduction and Balloon (2nd Edition Non-Manual Techniques CD-Rom).  Hope this helps get you started!

I am looking for references that link tinnitus to suboptimal dental occlusion or absence of centric occlusion. I’d appreciate any leads, names of journals or websites, that I should be looking at. Has any of the PRC therapists been able to help people with tinnitus, alone or in collaboration with a dentist?

Tinnitus, or ringing in the ears, can be a very confusing and often poorly understood symptom.  Tinnitus and dizziness are the two most frequently asked about symptoms, both here in the clinic and through the internet.  From the reading that I have done, it is thought to occur when the brain areas involved in hearing spontaneously increase their activity.  Therefore, it is associated with virtually all disorders of the auditory system.  It is not limited to ringing of the ears, but may be perceived as whistling, buzzing, humming, hissing, roaring, chirping or other related sounds. 

There appears to be three forms of tinnitus.  The last is more of an osteopathic thought process approach.  Nonetheless, I’d like to cover all three briefly in this response to a question received by a PRC therapist about the relationship between tinnitus and dental occlusion.  The first most common form of tinnitus according to James B. Snow Jr., a physician at the University of Pennsylvania, and former director of the National Institute on Deafness and other communication disorders, arises from damage to the inner ear, or cochlea, caused by exposure to high volumes of sound.  Dr. Snow also states that drugs such as aspirin, quinine and aminoglycoside antibiotics, cancer chemotherapeutics and other ototoxic agents, and infections and head injuries.  He goes on to state that if the inner ear is damaged, input decreases from the cochlea to the auditory centers of the brainstem, such as the dorso cochlear nucleus.  This input loss may lead to increased spontaneous activity in the nucleus neurons as a result of inhibition that has spontaneously been removed. 

The second most common form or theory of tinnitus is autonomic nervous system stimulation from increased neuromuscular tension.  Retraining therapy, a process that can take a long time, often two years or more, can help reduce this tension from the autonomic nervous system.  This process is called habituation of reaction.  Tinnitus then becomes quieter for longer periods of time and eventually or hopefully will disappear or become a natural part of the background noise or “sound of silence”.  This is sometimes referred to as habituation of perception.  This won’t happen if or while the tinnitus is still classified by the person experiencing it as a threat, negative experience, an undiagnosed symptom, or while the individual is under a lot of emotional stress.  Many tinnitus patients have hyperacousis or high degrees of sensitivity to external noise and therefore they seek and search for quiet environments to work in.  In this respect, according to information fromhttp://www.tinnitus.org, they are their own worst enemy.  Supposedly, if strong beliefs about the threatening nature of tinnitus are maintained, the survival style or condition response mechanisms in the subconscious brain insure that it is continuously monitored and therefore the condition itself will not improve.  Imaging studies confirm increased neural activity in the auditory cortices of those experiencing tinnitus.  Their brains also show increased activity in the limbic structures associated with emotional processing.  Other symptoms that sometimes appear alongside tinnitus, such as emotional distress, depression, dizziness, and insomnia, may have a common basis in some limbic structure such as a nucleus accumbens. 

In addition to the two most common forms of Tinnitus, that is damage to the inner ear and increased tension from the autonomic nervous system stimulation, I find that there is a very strong relationship between tinnitus and those who are experiencing temporal bone disorganization or temporalis overuse.  Clenchers, grinders, and trismus oriented individuals often experience tinnitus associated with hyperactivity of musculature that is attached directly to the temporal bone which houses the inner ear.  There does not appear to be a relationship between tinnitus and externally or internally rotated temporal bones at this time according to the literature, however, it does stand to reason that this third reason for tinnitus is strongly related to the position and orientation of a muscle called the tensor tympani muscle that inserts on the manubrium of the malleus bone and originates or attaches directly to the sphenoid bone and the temporal bone.  It lies in our auditory tube and its main action is to tense the tympanic membrane along with the stapedius muscle of the ear.  It also contains cerebellar input related to the ability to adapt to vision as well as hearing.  Since this muscle makes the tympanic membrane taught if it is put in a position where it is lengthened it can also influence its own innervation by the mandibular division of the trigeminal nerve.  It can have a direct impact on the external surface of the tympanic membrane. 

The external surface of the tympanic membrane is innervated by the oriculo temporal branch of the mandibular nerve and the oricular branch of the vagus nerve.  The internal surface of the membrane is supplied by the tympanic branch of the glossopharyngeal nerve.  Temporal and sphenoid orientation, therefore, can have a both direct and indirect impact on the autonomic nervous system, trigeminal innervation, and vagal activity.  Clinically, keeping the temporal innominates aligned, stable, and functioning in a reciprocal manner with respiration and mandibular activity is important to keep the tympanic membrane, tympanic cavity, and septum of the auditory muscular canal aligned.  Through manual or non-manual techniques using PRI principles and philosophy, I have been able to change the frequency and intensity of this irritant.  Many of these same patients also need to be evaluated by a dentist with a strong background in TMD and occlusion and it’s always helpful to work with a dentist who has a cranial-gnathic orthopedic mind.  Being familiar with the different lesions of the cranium that can occur with malocclusion is always helpful in restoring proper cranial symmetry with a bite. 

In addition to this I’ve also had success in working with optometrists, specifically COVD trained optometrists, who presently understands the autonomic nervous systems influence on accommodation and tension across the cranium as a result of vestibular constraint secondary to visual and spatial lack of integration.  Hopefully, this overview will help anyone working with a patient experiencing tinnitus.  Obviously, we’re excited that the physical and physiological implications associated with tinnitus, can be corrected or reduced using methodology that diminishes the asymmetrical issues at the temporal region as well as the hypersensitivity associated with torque placed on the temporal bone itself. 

I recently saw a patient with a diagnosis of severe CS arthritis with main complaints of numbness/tingling of her UE and ringing in her ears.  It appears that the intensity of the ringing in her ears is positively affected by the supine active sacro spheno flexion activity.  After this technique, the ringing is less intense.  She is now beginning to be able to control it with good diaphragmatic breathing in appropriate posture.  Can you help me better understand the physiology/anatomy of why this may be happening? 

The Supine Active Sacro-Spheno Flexion technique restores OA extension on the right, repositions the sphenoid in sagittal neutrality and in general, places the sphenoid in a state of flexion. The right temporal bone is then pulled into ER (external rotation) via the right styloid muscles. So, in essence the tensor tympanics in the temporal bones and the tensor veli palatins are re-set or repositioned to allow for normal malleus and inner ear function. Thanks for the question! 
Ron Hruska, MPA, PT

When testing for thoraco-lumbar flexion, my patient could easily touch the floor during the Standing Reach Test, however, she still maintained a very flat thoracic spine. I feel the movement was coming from her lumbar spine and hips. Can I still treat her with the exercises to improve thoracic flexion/inhibit extensors?

Your patient has a flat back with long hamstrings.  And yes, you can treat her with thoracic lumbar flexion activities (because this is always good for a flat back patient) as long as you don’t forget the need to target the hamstrings in a shortened state (maybe as a part of your standing BC activities) or with an activity like the Prone Reciprocal Hamstring Curls.

When treating a BC patient, why would we give the non-manual 90-90 Hip Lift with Right Arm Reach and Balloon (which includes R scapular protraction) if the right scapula is already in protraction?

You reach with the right arm during exhalation in 90-90 to treat the thorax (reposition the diaphragm toward the left ZOA, etc), not to do much of anything with the scapula.  But after you get a left ZOA, the next inhalation will externally rotate the right ribs and allow the scapula to return to more of a neutral position.  In other words, the airflow and rib rotation corrections will serve to reposition the scapula as the base of the scapula (rib cage) is corrected under the scapula.

The diaphragm is often referred to as a “postural muscle” when the Zone of Apposition is lost and the dome of the hemi-diaphragm lowers to the point of becoming tonically positioned with an ipsilateral anterior rib flare and hemilordosis.  Can you explain exactly why it is referred to as a postural muscle in this case?  I understand that it certainly becomes less of an effective respiratory muscle, but where exactly did that term come from?

The diaphragm is referred to as a “postural muscle” because without the ZOA the diaphragm becomes the primary stabilizer of the anterior spine.  The left abdominals are gone so the diaphragm takes over as a postural stabilizer.  The diaphragm is placed in a position at end range lumbar lordosis for lumbar-thoracic stability.

After taking the course, I still am a bit confused when it comes to putting together a home exercise program. I understand that there is a treatment hierarchy and I have been choosing exercises from the examples, but there are many other exercises. I feel like I don’t know the rational for choosing some of them.  Do you have any suggestions on how I can learn which of the exercises to choose?

Choosing the best exercises for the home exercise program is frequently a challenge.  You have to remember to stay focused on key AF IR principles and remember that not all exercise are of equal value.  It is easy to be tempted and think that having proficiency with more exercises makes you a better clinician, but the fact of the matter is that being good with a technique and staying focused on the right things is better than being mediocre with a lot of activities that you use at the wrong time in the wrong way.

I understand that when we want to reposition, we use the hamstrings. Why does it tell us on pages 46 & 47 of the Myokinematic Restoration manual that we use the bicep femoris (ER/EXT)? Don’t we want to use the medial hamstrings more since they are so weak? Or do we use the biceps because they ARE stronger?

You asked about biceps femoris and medial hamstrings.  The fact is that we want both.  The biceps femoris is positioned best to sagitally extend the hip (AF EXT) via the sacrotuberous ligament and the alignment of the biceps’ proximal tendon.  But when it comes to the much desired IR during hip extension, then you gotta love the medial hamstrings.  When you break it down a plane at a time, you have to focus on the best sagittal plane muscle first, but when you begin to integrate planes you have sagittal biceps together with sagittal and transverse medial hamstrings (these medial hamstrings are a functional mix between the biceps femoris and the ischial condylar adductor magnus).