This technique is truly unique. Its mechanism of action is simple and well documented in fluid dynamics. The condition it tests for and treats is ubiquitous in vertebrates.

Most of our body components are poroelastic and therefore contain extracellular fluid. By  squeezing these tissues, the fluid will move out of the area; more scientifically, by decreasing the volume the pressure increases which in turn causes the fluid to move into a lower pressure area. The mechanism of action is just that. Tissues from bone to skin, blood vessels to nerves, and lungs to prostate all behave in the same manner. The volume is decreased by manual therapy procedures such as traction, compression and torque.

As mentioned earlier hypoxia and an increased interstitial fluid pressure is being associated with more and more pathologies. These can range from tendinosis to cancer, ischemic stroke to inflammatory bowel disorder, and low back pain to dementia. We test for and treat elevated interstitial fluid pressure as a result of edema. I behoove the practitioner to understand these diseases. I’m at the computer constantly investigating new findings regarding a patient’s complaint. Here’s a generic pathogenesis.

Tissues react to stress by producing proteoglycans. The proteoglycans are in the extracellular matrix, they absorb water through osmosis and by being hydrophilic. The pressure now rises. The original stressor could be mechanical, chemical, thermal, light, noise, pain, or psychological. The stressor may have been a one-time event or may be ongoing. Once the pressure is elevated, symptoms and disability ensue.

In testing the patient, we load tissues using the mechanism of action explained above and look for a response.

The patients’ responses mean everything. Only they can give a case history, say where the problem is and whether the test is affecting the correct tissues, and give feedback during the procedure.

To sum up, we have a simple mechanism of action to test for and treat a pathology that presents itself in many ways. The presenting problem may seem very intricate but by testing in the above logical manner, you will not get lost and will have a specific direction to move in.

The head and neck are incredibly complicated, so much so that medical specialities only involve one or two aspects of it. Consider fields such as ophthalmology, dentistry, oral facial surgery, psychiatry and speech pathology. How can a short seminar possibly address all these areas? There is so much research coming out every month, how can one keep up with it? When is the therapist crossing the line defining their scope of practice and can that line even be seen? In this section, I will answer those questions by using two examples.

Hopefully, these will help you discover the enormity of your profession.

In the first example, the patient presents with an ongoing post concussive syndrome since being knocked out five years ago. The symptoms include tinnitus and vertigo. Over that time, various medical exams and imaging studies have all come up negative. Massage, physio, chiro, counselling, and exercise therapy have all had little effect. Your examination of the patient reveals no red flags and is generally unremarkable. The one noticeable finding is tenderness in the left temporal bone. Could this problem be a result of increased pressure and a lack of blood supply? How would I check for that and if so, how would I treat it? Time for hypothesis testing: a lack of blood flow to certain soft tissues within the cranium may be the cause, specifically that area involving the eighth cranial nerve and inner ear. Which tissue has an elevated pressure: the brain, any of the structures in the middle and inner ear, or the temporal bone? My big clue in this case is the sensitive temporal bone. Is it tender due to exceedingly high intraosseous pressure? I know transcortical vessels in the temporal bone feed directly into the brain. If blood flow here is compromised it is likely there will be effects to the brain, CNVIII and the ear. I also know by flexing the temporal bone the intraosseous pressure will be increased. Lacunar-canalicular fluid should then drain. To test this hypothesis, the temporal bone is flexed by squeezing the patient’s cranium at that level.

The testing starts off light as pressure is slowly increased within the patient’s tolerance. This procedure lasts about 60 seconds and is repeated two to three times. The patient is giving constant feedback during the entire procedure. In this case, outcome measures would include less tenderness, a decrease in symptoms and an improvement in postural sway. If there is no change, look to something else.

Let’s deconstruct this scenario. The mechanism of action is always the same. There was a stressor, the temporal bone is tender, all previous tests were negative and previous treatments were ineffective. Therefore, is the disability of the pathology what we are interested in? Time to dive into the maze. What is the blood supply, nerve supply, shape and function of the temporal bone? How about the nerve supply to the vessels of the temporal bone?

To continue on with this example, here’s the general gross anatomy and blood supply.

The temporal bones are situated at the sides and base of the skull, and lateral to the temporal lobes of the cerebral cortex. They are overlaid by the sides of the head known as the temples, and house the structures of the ears. The lower seven cranial nerves and major vessels to and from the brain traverse the temporal bone. The temporal bone consists of four parts — squamous, mastoid, petrous and tympanic. The squamous part is the largest and most superiorly positioned relative to the rest of the bone. The zygomatic process is a long, arched process projecting from the lower region of the squamous part and it articulates with the zygomatic bone.

Posteroinferior to the squamous is the mastoid part. Fused with the squamous and mastoid parts and between the sphenoid and occipital bones lies the petrous part, which is shaped like a pyramid. The tympanic part is relatively small and lies inferior to the squamous part, anterior to the mastoid part, and superior to the styloid process. The styloid is a phallic shaped pillar directed inferiorly and anteromedially between the parotid gland and internal jugular vein. The arteries:

Stylo-mastoid from posterior: auricular enters the stylo-mastoid foramen. Tympanic from internal maxillary: it passes through the Glaserian fissure. Petrosal from middle meningeal: transmitted by the hiatus Fallopii. Tympanic from internal carotid whilst in the carotid canal. Auditory from the basilar: it enters the internal auditory meatus, and is distributed to the cochlea, vestibule, etc. You should have a working knowledge of this for more effective assessment and treatment. And this is just touching on it. What about the clefts, fissures, canals and foramen along with their content? What about the nerve supply to the blood vessels? It’s not only the sympathetics.

In the second example, the patient presents with tinnitus and vertigo which has been ongoing for three years after being rear-ended in a car accident. Again, imaging studies and various medical examinations were negative and treatments up to this point were ineffectual. No red flags during the examination. The one outstanding finding was a forward head posture along with an upper crossed syndrome. Could this problem be a result of increased pressure and a lack of blood supply? How would I check for that and how would I treat it? Time for hypothesis testing: The lack of blood supply would be in the area of the inner and middle ear. In this case, the actual pressure is elsewhere. The preganglionic sympathetic nerves supplying this area originate in the upper thoracic spinal cord. Misshaped upper thoracic vertebral bodies, discs and endplates are a result of gravity on a poor posture. That, coupled with the whiplash, may result in an aberrant sympathetic outflow causing a compromised blood flow around the inner ear as well as aberrant signals from the general visceral afferents. By applying the correct pressure to the upper thoracic spine fluid in the discs, endplates and vertebral bodies will be redistributed and normal morphology restored. Again, this procedure starts with little pressure and is gradually increased to the patient’s tolerance. Outcomes include improved posture, muscle balance and a decrease in symptoms.

Let’s deconstruct this scenario. The mechanism of action is always the same. Is the disability of the pathology what we are interested in? A mechanical stressor was evident, the patient does present with an upper crossed syndrome, previous tests were negative, and previous therapies were ineffective. Time to dive into the maze.

What is the relationship of the sympathetic nervous system to the inner ear? Does an upper crossed syndrome put the patient in a weakened position during a whiplash?

For example, here’s the course of the sympathetics from source to destination.

The central autonomic network is composed of both hypothalamic and extra-hypothalamic nuclei. Some of these sites regulate sympathetic outflow whereas others regulate parasympathetic outflow. This structure was first revealed in lesion studies that revealed multisynaptic connections descending from the hypothalamus and midbrain to preganglionic neurons in the brainstem and spinal cord. Similarly, connections from various limbic brain structures, most especially the amygdala, through the hypothalamus have been demonstrated.

The principal pathway of the hypothalamus in the central autonomic network is the dorsal longitudinal fasciculus (DLF). The DLF originates in the region of the paraventricular nucleus and descends along the most medial aspect of the third ventricle through the periaqueductal gray and mesencephalic reticular formation. The DLF continues caudally in the midline near the floor of the fourth ventricle until the closure of the open medulla where it becomes internalized near the central canal remnant. This position leaves the DLF in ideal position to innervate the periaqueductal gray, the parabrachial nucleus, the mesencephalic raphe nuclei, and the locus ceruleus rostrally and the dorsal motor nucleus of the vagus, the nucleus ambiguus and the medullary raphe more caudally. The centralized location of the DLF as it continues into the lower medulla and then the spinal cord renders it in perfect location to innervate the parasympathetic and sympathetic neurons of the intermediolateral spinal cord. As detailed above, the DLF projections are bilateral, though with an ipsilateral dominance due to several points of decussation. Afferent inputs from the periaqueductal gray, parabrachial nucleus, and the locus ceruleus ascend through the DLF to the hypothalamus.

Sympathetic nerves arise from near the middle of the spinal cord in the intermediolateral nucleus of the lateral grey column. They begin at the first thoracic vertebra of the vertebral column and are thought to extend to the second or third lumbar vertebra. Because its cells begin in the thoracic and lumbar regions of the spinal cord, the sympathetic nervous system is said to have a thoracolumbar outflow. Axons of these nerves leave the spinal cord through the anterior root. They pass near the spinal (sensory) ganglion, where they enter the anterior rami of the spinal nerves. However, unlike somatic innervation, they quickly separate out through white rami connectors (the shiny white sheaths of myelin around each axon) that connect to either the paravertebral (which lie near the vertebral column) or prevertebral (which lie near the aortic bifurcation) ganglia extending alongside the spinal column.

Presynaptic nerves’ axons terminate in either the paravertebral ganglia or prevertebral ganglia. There are four different paths an axon can take before reaching its terminal. In all cases, the axon enters the paravertebral ganglion at the level of its originating spinal nerve. After this, it can then either synapse in this ganglion, ascend or descend to a more superior or inferior paravertebral ganglion and synapse there, or descend to a prevertebral ganglion and synapse with the postsynaptic cell.

The postsynaptic cell then goes on to innervate the targeted end effector (i.e. gland, smooth muscle, etc.).

Because paravertebral and prevertebral ganglia are relatively close to the spinal cord, presynaptic neurons are generally much shorter than their postsynaptic counterparts, which must extend throughout the body to reach their destinations.

The cervical ganglia are paravertebral ganglia of the sympathetic nervous system. Preganglionic nerves from the thoracic spinal cord enter into the cervical ganglions and synapse with its postganglionic fibers or nerves. The cervical ganglion has three paravertebral ganglia:

• Superior cervical ganglion (largest) – Adjacent to C2 & C3; postganglionic axon projects to target: (heart, head, neck) via “hitchhiking” on the carotid arteries.
• Middle cervical ganglion (smallest) – Adjacent to C6; target: heart, neck.
• Inferior cervical ganglion – The inferior ganglion may be fused with the first thoracic ganglion to form a single structure, the stellate ganglion. – Adjacent to C7; target: heart, lower neck, arm, posterior cranial arteries.

The superior cervical ganglion (SCG) is the only ganglion in the sympathetic nervous system that innervates the head and neck. It is the largest and most rostral (superior) of the three cervical ganglia. The SCG innervates many organs, glands and parts of the carotid system in the head.

The SCG receives input from the ciliospinal center. The ciliospinal center is located between the C8 and T1 regions of the spinal cord within the intermediolateral column. The preganglionic fibers that innervate the SCG are the thoracic spinal nerves, which extend from the T1-T8 region of the ciliospinal center. These nerves enter the SCG through the cervical sympathetic nerve. A mature preganglionic axon can innervate anywhere from 50- 200 SCG cells. Postganglionic fibers then leave the SCG via the internal carotid nerve and the external carotid nerve. This pathway of SCG innervations is shown through stimulation of the cervical sympathetic nerve, which invokes action potentials in both the external and internal carotid nerves. These postganglionic fibers shift from multiple axon innervations of their targets to less profound multiple axon innervations or single axon innervations as the SCG neurons mature during postnatal development.

The SCG provides sympathetic innervations to structures within the head, including the pineal gland and blood vessels in the cranial muscles, the brain, the choroid plexus, the eyes, the lacrimal glands, the carotid body, the salivary glands, and the thyroid gland. The postganglionic axons of the SCG innervate the pineal gland and are involved in Circadian rhythm. This connection regulates production of the hormone melatonin, which regulates sleep and wake cycles; however, the influence of SCG neuron innervations of the pineal gland is not fully understood. The postganglionic axons of the SCG innervate the internal carotid artery and form the internal carotid plexus. The internal carotid plexus carries the postganglionic axons of the SCG to the eye, lacrimal gland, mucous membranes of the mouth, nose, and pharynx, and numerous blood vessels in the head. The postganglionic axons of the Superior cervical ganglion innervate the eye and lacrimal gland and cause vasoconstriction of the iris and sclera, pupillary dilation, widening of the palpebral fissure, and reduced production of tears. These responses are important during fight-or-flight response of the ANS. Dilation of the pupils allows for an increased clarity in vision, and inhibition of the lacrimal gland stops tear production allowing for unimpaired vision and redirection of energy elsewhere. The postganglionic axons of the SCG innervate blood vessels in the skin and cause the vessels to constrict. Constriction of the blood vessels causes a decrease in blood flow to the skin leading to paling of the skin and retention of body heat. This plays into the fight-or-flight response, decreasing blood flow to facial skin and redirecting the blood to more important areas like blood vessels in muscles. The SCG is connected with vestibular structures, including the neuroepithelium of the semicircular canals and otolith organs, providing a conceivable substrate for modulation of vestibulo-sympathetic reflexes.

As mentioned above, the internal carotid nerve hitch-hikes along the internal carotid artery, forming a network of nerves. Branches from the internal carotid plexus innervate structures in the eye, the pterygopalatine artery and the internal carotid artery itself. The external carotid nerve hitch-hikes along the common and external carotid arteries, forms a network of nerves and innervates the smooth muscle of the arteries. Nerve to pharyngeal plexus combines with branches from the vagus and glossopharyngeal nerves to form the pharyngeal plexus. Superior cardiac branch contributes to the cardiac plexus in the thorax. Nerves to cranial nerves II, III IV, VI and IX. Gray rami communicants distribute sympathetic fibres to the anterior rami of C1-C4.

The general visceral afferent fibers will follow a similar course.

Now consider the mechanical stress put on the lower cervical and upper thoracic spine in a rear-ender accident when the victim has a forward head posture. Unless the headrest is really moved forward it will have little effect on ameliorating the trauma. Upper thoracic preganglionic fibers, those ones going to the superior cervical ganglia will be involved. General visceral afferents in the area will also be affected due to trauma to holding elements of the upper thoracic and lower cervical spine. Do you see how it all fits in? Again, if your tests have no effect, move on to the next most likely hypothesis.