DECEMBER 2003
THE LAYERS OF CRANIAL DYSFUNCTION
AND THEIR SIGNIFICANCE IN TREATMENT
By Tracy S Gates. D.O., DIBAK
Introduction
Cranial faults are a complicated mixture of primary structural and metabolic dysfunctions, and dynamically varying compensatory mechanisms of the body’s adaptation to its environment.
Many of the faults which are diagnosed - and subsequently treated - in the clinic are merely transient manifestations of the body’s current mode of compensation to a less than perfect inner and/or outer environment.
If left untreated, these faults would merely self-correct or be surpassed by a differing set of presentations.
On the other hand, some cranial faults may be regarded as a much more primary dysfunction – constant and largely unchangeable without corrective intervention.
From a practitioner viewpoint, it is significant to establish a method to distinguish between these two types of dysfunction, since we may otherwise find ourselves in a situation of wasting precious treatment time in the correction of secondary adaptations that do not truly benefit from the input of manual correction.
Developmental background of Cranial Motion
Let us momentarily consider the impact of birth on cranial motion and dysfunction:
The movement of the baby through the cervix in labour
demands that the head moves in a series of specific directions.
There is, by necessity, an overlapping of the bones of the skull in this process and, if the birth is prolonged, the membranes attached to the skull can tear, and/or the bones of the skull can compress together.
Unresolved compressions left untreated will start to have an effect on the baby's musculo-skeletal and neurological systems after only four days post partum. (Frymann 1990).
During the early stages of labour, there is an overlap of one parietal over the other (usually the right over the left) at the sagittal suture.
At the same time, the occiput slips under the parietals at the lambdoidal suture. This has the effect of placing the parietals in internal rotation. Both temporal bones automatically get pulled into internal rotation in consequence. The effect is that the sphenobasilar joint (SBJ) falls into extension. This puts a stretch on the falx cerebri and tentorium cerebelli.
If excessive or prolonged, this stretch can lead to tears in the membranes and bleeding of the micro capillaries running through the membranes. Small amounts of bleeding can be sustained without excessive amounts of damage to the fragile structures of the neonate’s cranium.
If, during the process of descent in the first stage of labour, the baby remains static for any prolonged period of time, the force of the muscular contractions can lead to excessive moulding and tears to the membrane as described above. It would be at this point in time when medical staff would take a decision to aid the baby’s exit with intervention techniques.
Injury to the cranium sustained by forceps depends on the positioning. Either they will be cupped laterally over each side of the baby’s head, in which case this forces the parietals into a position of excessive internal rotation, often causing a compression overlap of the central sagittal suture. The temporal bones will also fall into a compressive internal rotation, impairing drainage mechanisms. This results in the typical ‘egghead’ shape witnessed in neonates after forceps delivery.
A: Sub-occipito-bregmatic diameter B: Occipito-frontal diameter
compressed compressed –
“Crash-helmet” moulding
Alternatively, the forceps can be placed on one frontal bone and the posterior aspect of the contralateral parietal bone. The resulting pressure of the forceps leads to a lateral strain pattern at the sphenobasilar joint. The result is a head in the shape of a parallelogram when viewed from above.
Either scenario will cause abnormal tension on the membranes within the skull, with some tearing if the pressure is marked.
Face presentations cause the force of the uterine contractions to be directed toward the front of the head, so that the head extends as it enters the pelvis.
Unless the chin is very far forward, forceps will always be necessary to expediate the delivery. At birth, the eyelids and lips are generally grossly oedematous and the face is congested and bruised. The sagittal suture is compressed and the occipito-frontal diameter is increased. Sucking is often difficult.
Brow presentation generally leads to posterior compression of the sagittal and lambdoidal sutures and a superior vertical strain of the SBJ.
Application of the ventouse presents a slightly different problem. The site of application is normally the posteriosuperior aspect of the parietal bone. The tractioning force on the bone causes a structural one-sided lesion, but can also lead to a tearing away of the cartilage from the membranous attachments often with a consequential concentrated site of bleeding.
The local haemorrhage can be sufficient merely to distort the membranous tension (which leads to altered activity of relevant cranial nerves), or in more severe cases, can cause a local focus sufficient to alter function of the underlying portion of the cortex. If there is localised bleeding sufficient to affect not only the cranial and membranous structures, but also cortical function, the clinical picture is not nearly so correctable by cranial techniques.
Often, the body’s own self-correcting mechanisms will dispense the focus without significant damage, and cranial treatment to correct the abnormal distortions structurally will aid such a recovery.
A baby born by Caesarian tends to have a total or partial compression of the SBJ, due to failure of the bones to mould and initiate a rhythmic flow of CSF.
The most common damage in the birth process is from distortion of the condylar parts of the occiput. Under normal circumstances, the occiput is crowded anteriorly and the squama rotated to one side and then the other. Tension on the membranes can hold the condyles in an abnormal position. The groove in the basiocciput becomes deepened and the pons and medulla become crowded. Associated SBJ dysfunction occurs with distortion of the vault, affecting the orbits and nasal fossae.
A slow delivery tends to cause a base in excess flexion with side-bending rotation.
Discussion
Many cranial techniques in AK rely on creating change in the osseous or fascial mobility. This is in contrast to perceived treatment using classical osteopathic techniques, which facilitates a sustained unwinding of the dura to remove the fibrous tethering found at the sites of abnormal tension. Correction of osseous dysfunction, which is present as part of a chronic and primary membranous distortion, is generally only temporary. The dysfunction will continue to recur until the cause of the soft tissue or dural membrane tension is identified and addressed.
However, in the newborn, this issue is academic since the dura has had little or no time to react and compensate to the bony, fascial or muscular dysfunction, so that AK techniques are an equally effective mode of treatment as the more classical osteopathic approach. On this basis, provided all lesions are found and treated, permanent correction should be easily achieved.
An estimated 9 out of 10 births result in some degree of cranial lesions (Frymann 1990). However, because the body is a self-correcting, self-maintaining mechanism, many of these lesion patterns will resolve spontaneously. This is primarily aided by the baby crying or sucking on the breast immediately after birth. Crying leads to an increase in intracranial pressure, driving the CSF flow with a greater force and vitality, increasing the fundamental flexion / extension motion at the SBJ and facilitating membranous release and consequential osseous lesion. Sucking creates a cephalad pressure on the intermaxillary suture, which in turn rocks the vomer and increases the motion of the sphenoid; to create the same ultimate result as crying.
This inherent self-correcting mechanism also explains why children escape long-term structural lesions from the many falls and bumps they endure in the process of learning to walk and exploring their environment. The natural reaction of the child whenever he /she suffers physical harm is to cry loudly and perhaps thumb-suck for comfort, thereby automatically effecting a correction before the intracranial membranes can adapt to a change of tension from osseous drag.
As the pressure of social behaviour forces us to supress our instinctive behaviour, we discontinue these basic reactions of crying and comfort-seeking; with the ultimate consequence of unresolved lesions within the craniosacral mechanism; and subsequent muscular, fascial and membranous compensation.
These lesions will become part of the dynamically changing compensatory mechanism referred to in the introduction.
If we extend the concept of the baby crying / thumb-sucking into the adult, we can achieve an effective and rapid way of evaluating the layers of cranial dysfunction. This is clinically significant since it displays which cranial faults are transient / compensatory (and therefore treatment will provide little or no clinical benefit to the patient); and which are more primary – maintained by membranous torsion – and are therefore consistently involved in the clinical picture.
I would like to refer to a small research study undertaken within my office. Ten patients were evaluated using AK screening for cranial faults, and the results recorded. The Group was then divided into two groups of five. Group One was treated with the techniques consistent with the faults diagnosed. Group Two were treated with respiratory techniques other than those found in diagnosis, as shown in the table below:
GROUP TWO /Diagnosis
/ TreatmentPatient 1 / Right temporal bulge / Inspiration assist (acc Gerz)
Patient 2 / Glabella / Temporal bulge
Patient 3 / Expiration assist / Parietal descent
Patient 4 / Internal frontal / Expiration assist
Patient 5 / Inspiration assist / Glabella
All 10 patients were re-evaluated after treatment and, within Group One, 4 out of 5 patients no longer showed to their previous faults. The startling discovery was that, within Group 2, also 4 out of 5 patients no longer showed to their previously diagnosed faults.
This was repeated with three other groups of 10 patients and the results consistently showed a comparable correction of diagnosed cranial faults between Group One and Two. In fact, in the second study, Group Two showed a 5 out of 5 improvement, whilst Group One (following the correct protocol) showed only a 3 out of 5 improvement!
So, in the words of Goodheart: What does this mean?
In these compensatory lesion patterns, cranial bones are merely the pawn in the struggle between muscle and membranes. Any respiratory input into the cranial mechanism that optimises the flexion/extension capacity of the SBJ will have a beneficial impact on cranial bone motion and often create enough input to allow the osseous fault to self correct.
A further research study was undertaken in which six patients were evaluated for strain patterns within the craniosacral mechanism, findings were monitored and the patients left untreated. They were re-evaluated one week later by a second practitioner who had no record of the previous week’s findings and these results were recorded.
The findings are tabled below:
WEEK ONE / WEEK TWOCRANIUM / PELVIS / CRANIUM / PELVIS
PATIENT 1 / Frontal fix, Cat II post L
Temporal bulge L / Frontal fix Cat II post L
Inspiration assist L
PATIENT 2 / Glabella Cat I L / Universal fault Cat I R
PATIENT 3 / SB compression Sacral fixation / SB compression Cat II R
PATIENT 4 / Expiration assist Cat II R / None Cat II R
PATIENT 5 / Internal frontal Cat II R
Temporal bulge R / Inspir. assist R Cat II L
PATIENT 6 / SB compression Sacral fixation
Pub sym fix. / Frontal fixation Iliac fixation
Conclusion
We can only ever, at best, make educated judgement and assumption of what we are actually doing in our treatment to affect craniosacral dysfunction and optimise cranial bone motion and CSF flow, since it is an internal pressurised system which cannot be evaluated from the outside without destroying the very nature of its function.
It is probably a reality that, in the treatment of craniosacral compensations, it is often not the specificity of the treatment we give that creates the change, so much as the generalised input of raised intracranial pressure to affect self-correction.
However, we must also constantly question whether a technique is valid merely because it changes a muscle test, or whether it is valid because it creates symptomatic and clinical improvement.
Many craniosacral adaptations are not, within themselves, symptomatic and, since they are transient and constantly changing, are not likely to cause clinical dysfunction.
We are therefore, in conclusion, probably wasting precious clinical hours for both ourselves and our patients in treating these faults.
On the basis of the previous discussions, I have devised a simple procedure to evaluate which of the faults are more primary in origin and genuinely require correction and which do not:
1) Evaluate the patient for the presence of cranial and pelvic faults and note which are present
2) Have the patient scream loudly or suck firmly and repeatedly on his /her thumb
3) Re-evaluate the patient for the presence of cranial and pelvic faults previously established.
4) Those faults no longer present may be regarded as transient and compensatory in nature and would not be worth treating.
5) Cranial faults still remaining may be regarded as more primary and fundamental to the structural and functional disturbances of the patient and require treatment.
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