Fluid Flow in the Head: a New Model for Cranial Osteopathy
Introduction
Osteopaths have been palpating movement at the cranium for over 100 years. Cranial osteopathy has gained much popularity as a treatment modality but emerging research may throw light on some of the clinical phenomena observed in practice.
Traditionally the view of the cranium is that of a rigid box. This rigid box has been viewed as enclosing the brain and all its fluids that independently do their own thing in their own way. One of the criticisms of cranial osteopathy is that it promotes impossible ranges of movement of the cranial bones and that this mobility is intricately linked to the physiology of the brain and its circulating fluids.
What is presented here is evidence representing a half way view. Intracranial movement has been shown to be intricate, associated with compression and tensile forces, that accommodate constant fluctuations in (1) extracranial forces e.g. mastication and (2) intracranial pressure. Intracranial pressure, producing intracranial movement, is associated with:
The movement of fluids including blood, cerebrospinal fluid (CSF) and Interstitial fluid (ISF).
The movement of brain tissue.
Determining the orientation of collagen fibers in the dura mater which has been associated with signalling mechanisms involving the brain and cranium.
The interplay of movement of all the fluids and brain tissue is mechanically far more dynamic than what is commonly perceived. This is for two reasons:
The Monro-Kellie hypothesis: a constant intracranial pressure has to be maintained. Therefore if so much fluid comes into the head (blood or CSF) an equal amount has to come out (blood, CSF or ISF).
Cranial compliance: the individual cranial bones don’t move much but they do ‘give’ being subject to compressive and tensile strains. If fluid spilled into the head and the cranial bones freely expanded (like inflating a balloon) the intracranial pressure wouldn’t change much as the volume of the head would expand to accommodate the increase fluid content. Obviously this doesn’t happen, whilst there is a bit of give in the cranium, there's not much. This tightly restricted movement means that when fluid enters the head intracranial pressure builds more rapidly which causes a rapid expulsion of fluid to maintain constant pressure. To illustrate how essential some movement in the cranial sutures are, no matter how small, restricting cranial compliance by placing external restraints on the head restricts this small but essential give in the cranium and is responsible for various physiological phenomena associated with this pressure sensitive system.
This intimate relationship between what happens internally and externally and the mechanical strain placed on the cranial sutures is the basis for this model of cranial osteopathy and the involuntary motion mechanism.
For this reason the article is divided into:
Forces at the sutures: analysis of compressive and tensile elements at the sutures. This is from intracranial and extracranial forces, including those associated with craniosacral techniques.
Meninges: anatomical review as a web like structure that runs from the cranium internally to the brain. Also a review of meningeal function as an independent signalling mechanism regulating homeostasis. This function is dependent upon collagen fibers that orientate themselves according to mechanical loads. Due to loads measured at the dura during craniosacral techniques could this affect the collagen fibers and intern its cellular signalling mechanisms?
Fluids: review of the physiology and intimate relationship between the movement of CSF, ISF and blood.
What can you feel at the head: a review of the close relationship of intracranial dynamics and what is palpated as the primary respiratory mechanism (PRM).
Appendix: Embryology: this illustrates the close developmental relationships of the different structures.
Forces at the cranial sutures
Sutures store energy associated with compressive and tensile strains.
Movement has been demonstrated at the sutures.
This movement accommodates external strain e.g. mastication and externally applied pressure associated with cranial osteopathy.
This movement accommodates internal strain i.e. it gives a bit on physiological increases in intracranial pressure.
Restricting this movement increases intracranial pressure and produces physiological changes.
Pritchard et al (1956) identified five layers at the sutures. In the middle zone was collagen fibers. These collagen fibers withstand compressile and tensile forces from:
(1) External strain producing movement at the sutures.
Muscle activity e.g. mastication increases compressive and tensile forces in different cranial sutures and can determine the orientation of the cranial sutures (Herring 2008 & Herring & Teng 2000 & Seimetz et al 2012).
(2) Internal strain producing movement at the sutures.
Expanding brain: When you inflate inside a balloon the outer skin gets pulled tight. Jin et al (2016) claimed as the brain expands and the dura inflates the bones get pushed further apart and this puts a tensile strain on the already pretensioned collagen in the cranial sutures.
Physiological changes in intracranial pressure: Seimetz et al (2012) reviewed the research associated with movement at the sutures and changes in intracranial pressure.
A review of all the research up to 2012 by Seimetz et al (2012) found cranial movement in adult post-mortem and living skulls. This movement was found to correspond to intracranial pressure and external forces likely to be used in cranial osteopathy.
Herring (2008) defined sutures as zones of flexibility and energy absorption that can undergo much greater deformations than the rigid bones of the skull. This enables them to reduce the amount of stress experienced by the surrounding bones (Wang et al 2014).
These forces occur during child birth, intracranial pressures (can be transmitted as mechanotrandusction by the dura mater), muscle activity, and traumatic impacts (Herring 2008).
External strain producing movement at the cranial sutures
The strain that sutures absorb determine their collagen fiber orientation as well as their pattern of bony interdigitation. For instance Herring (2008) reviewed research finding:
Increased jaw muscle force is associated with increased interdigitation and decreased tensile stiffness of the mouse sagittal suture.
Decrease jaw muscle force (in rats with a softer diet) leads to simpler, narrower, and sometimes obliterated facial sutures.
Nonmasticating (toothless) mice show similar changes in both facial and vault sutures, as well as poorly developed sutural ligaments.
Compressed sutures in pigs and fish are more highly interdigitated than tensed sutures.
However the simple model of a movement placing a suture under compression or tension was disputed by Herring and Teng (2000) who found the action of the masseter and temporalis in closing the jaw can produce simultaneous tension from the masseter and compression from the temporalis in the coronal suture.
Jaslow (1990) found sutures absorbed from 16% to 100% more energy during impact loading than did bone. This five-fold increase in energy absorption by the sutures was significantly correlated with increased sutural interdigitation. Bony interdigitation creates stiffness increasing its capacity for energy absorption showing a higher elastic moduli which is its most significant mechanical property (Herring 2008).
Jasinoski (2010) suggested randomly arranged sutural collagen fibres could optimise to an orientation most appropriate to withstand the predominant type of loading (compression and tension). The orientation of collagen fibers along with their proteoglycan and water content gives them energy-absorbing qualities (Herring 2008). This is because fluid is forced out of the sutural space and collagen fibers are rearranged depending on the rates of compression or tension.
Internal strain producing movement at the cranial sutures
Fluctuating intracranial pressure produces movement at the cranial sutures.
Restricting this movement at the cranial sutures produces systemic physiological symptoms.
Fluctutations in intracranial pressure has been associated with movement at the cranial bones (Seimetz et al 2012).
Heisey and Adams (1993) found movement of the cranial bones at their sutures an additional factor defining total cranial compliance. They found movement at the sagittal suture, along with a rotational movement of the parietal bones, with changes in intracranial pressure and found external restraints to the head restricts these movements.
Restricting these movements of the parietal bones at the sagittal suture by lateral head compression Adam et al (1992) caused sagittal suture closure, a small inward rotation of the parietal bones and resultant increased intraventricular pressure, transient apnea, and unstable systemic arterial blood pressure.
After removal of the applied force, the position of the parietal bones, heart rate, and respiratory rate returned close to normal. Conversely, the application of a downward force on the sagittal suture caused the parietal bones to move further apart and rotate outward, but did not result in any changes in intracranial pressure, heart rate, or respiratory rate.
Pitlyk et al (1985) found increasing intracranial pressure by intraspinal injections of saline produced a corresponding amount of cranial motion.
Heifetz and Weiss (1981) reported small cranial movements associated with increased intracranial pressure in two comatosed patients.
Meninges (Decimo et al 2012)
Meninges run continuously from the cranium to deep into the brain forming a lining for the perforating vasculature and parts of the brain.
Cranial suture development is dependent on the meninges.
The meninges form an independent signalling network essential to homeostasis.
Collagen fibers in the meninges orientate themselves according to mechanical strain.
The falx cerebri has been found to change length in response to craniosacral therapy techniques (on an embalmed cadaver). Movement of the cranial bones (and thus the dura) has been discussed under 'forces at the sutures'.
Could there be a link between mechanical strain, orientation of collagen fibers and homeostatic function?
The dura is intimately linked to (1) the cranium and (2) the brain. This is most evident embryologically:
(1) Cranium: The close relationship between the development of the cranial dura mater and the skull is evident as these layers are only clearly differentiated when the venous sinuses develop. This relationship continues postnataly when the bones of the cranium are still developing.
(2) Brain: the primitive meninges are necessary for the development of the whole forebrain and for the generation of the primitive brain vasculature (Decimo et al 2012).
Anatomically the meninges are split from external to internal: dura mater (periosteal & meningeal), arachnoid mater and pia mater.
(1) Dura mater (Adeeb et al 2012)
(1a) Periosteal layer forms the periosteal lining of the inner surface of the calvaria, to which it is strongly adherent, mainly at the base of the skull. At a young age the dura is also continuous with the sutural ligaments at the cranial sutures. When the sutures fuse, the dura becomes separated from them.
The periosteal layer is rich in blood vessels, nerves, and large collagenous bundles. These collagen fibers make this layer anisotropic. This means the mechanical behaviour of the periosteal layer depends on the orientation of its collagen fibres (Hamann et al 1998).
(1b) Meningeal layer: surrounds and supports the dural venous sinuses and is reflected in three infoldings, the first separating the two hemispheres of the cortex (falx cerebri), the second between the cerebellum and the occipital lobe (tentorium cerebelli and falx cerebelli) and the third covering the pituitary gland and the sella turcica.
Intracranial forces during embryological development have been postulated as determining the orientation of the collagen fibers in the dura mater (Hamann et al 1998). Consistent symmetric areas of collagen fiber distribution were shown in the temporal region (running parallel to the superior sagittal sinus) and the area extending laterally to the superior sagittal sinus. The frontal and dorsal regions however did not appear to have as many symmetrical regions. Could these asymmetries in the dorsal and frontal regions be due to variations in myofascial strains in these areas pulling on the underlying bones(?).
Obviously movement of the cranial bones will produce movement within the dura. As well as research suggesting movement of the adult cranial bones in response to intracranial pressure and cranial manipulative techniques (Seimetz et al 2012) Kostopoulos & Keramidas (1992) found changes in elongation of the falx cerebri during cranial techniques. These were for the frontal lift, 1.44 mm; for the parietal lift, 1.08 mm; for the sphenobasilar compression, -0.33 mm; for the sphenobasilar decompression, 0.28 mm.
(2) Arachnoid mater: send projections down from the arachnoid mater to line the major arteries in the subarachoid space.
(3) Pia mater: send projections up from the pia mater lining the major arteries in the subarachnoid space. The Pia Mater, with the Glilal Limitans also sends projections down to line the major arteries in the brain forming the outer layer of the perivascular space.
The Glila limitans, or the glial limiting membrane, is a thin barrier of astrocyte foot processes. Being the inner most layer it is associated with the parenchymal basal lamina surrounding the brain and spinal cord.
Collectively the arachnoid mater and pia mater are called the leptomeninges. As larger blood vessels develop they ‘drag’ the leptomeninges into the brain forming the perivascular space. The astrocytes that form the glia limitans also get dragged with the leptomeninges forming an outer sheath.
As the arteries change to arterioles and microvessles the pia mater disappears to leave the astroyctes that form the glia limitans. There is only a scant covering of plial cells around the veins (Zhang et al 1990).
The perivascular space represents a perilymphatic drainage channel connected to the meningeal interstitial spaces, thus permitting the exchange of fluids and cells between the brain and meninges (Decimo et al 2012).
Anatomically the meninges penetrate the brain deeply at every level:
Large projections between major brain structures.
Form perivascular spaces permitting the exchange of fluids and cells between the brain and meninges. Even in the smaller arterioles, capillaries and veins where the pia mater becomes non-existent the glial limitans still runs continuous with these blood vessels.
Stroma of the choroid plexus.
Meninges project between substructures e.g underneath the hippocampal formation where it’s continuous with the choroid plexus stroma.
Envelops the cerebrum and cerebellum extending into the sulci and fissures.
Forms the non-neural roof of the third ventricle, the lateral ventricle and the fourth ventricle.
This diffuse anatomical spread of the meninges throws light on its function to help with development of the CNS. The meninges have a distribution of protein exhibiting the potential to modulate stem cell homeostasis and cortical function (Decimo et al 2012).
These cells are proposed to communicate through intercellular signalling. This is thought to occur through anatomical and functional interactions between meningeal cells, meningeal-perivascular cells, ependymocytes and astrocytes.
This intercellular signalling in the dura is a possible mechanism for its role in ossification of cranial vault bones (Jin et al 2016) and keeping the suture as a flexible fibrous joint preventing it from being obliterated by bone Oppermann (2000).
This highlights a potential new role for leptomeninges in CNS repair in response to CNS injury and suggests the existence of a new stem cell niche in the meninges that participates in the reaction occurring in the parenchyma following injury (Decimo et al 2012).
The fluids: Cerebrospinal fluid (CSF), Interstitial Fluid (ISF) and Blood
Cerebrospinal fluid (CSF)
The production, movement and absorption of CSF is intimately associated with cardio-respiratory mechanisms.
These mechanisms work in fine concert and in a coordinated fashion.
This produces a defined movement of the brain.
CSF production
CSF is mainly produced in parenchymal capillaries of the brain and also in the spinal cord subarachnoid space and Choroid Plexus (Miyajima and Arai 2015). Yiming et al (2017) found 20% of all CSF originates from the brain's ISF.
CSF production has been found to be in response to pressure and concentration gradients. An increase intracranial pressure decreases CSF production just as an increase of osmotic pressure increases CSF production (Miyajima ans Arai 2015).
CSF flow (Miyajima and Arai 2015)
CSF occupies the subarachnoid space and ventricular system around or inside the brain parenchyma (Yiming et al 2017).
The traditional view of movement of CSF is a unidirectional flow of fluid. It was thought to be produced from the choroid plexus moving through the ventricles and along the cisterns and the subarachnoid space into the blood (via arachnoid villi and granulations in the walls of venous sinuses) and lymphatic systems (via the perineural subarachnoid compartments in the cranial nerves).
This directed flow of CSF is almost assumed as an independent movement of fluid trickling through the nervous system. However it has been shown to be driven by arterial systole-diastole, respiration and fluid transfer at the blood brain barrier and boarders between the CSF and ISF spaces. This renders more of a local mixing and diffusion of fluids rather than a trickle along a designated pathway.
This mixing, bidirectional flow and diffusion of CSF is dependent upon maintaining a constant pressure in the head. Put simply, to maintain constant pressure, if so much of one fluid comes in so much of another fluid must come out:
Arterial pulsation: an influx of arterial blood leads to an outflow of CSF (Greitz et al 1992).
Movement of the brain: In systole the arteries expand. This expansion creates a piston like effect squashing the CSF out of the brain and into the spinal cord (Greitz et al 1992). This venting of CSF into the spinal cord during systole may explain the funnel-shaped movement of the brain as if it were being pulled down by the spinal cord (Greitz et al 1992).
Forced inspiration leads to an increase venous flow out of the head and an increase CSF flow into the head. This upward movement of CSF on inspiration was noted from the middle thoracic spine all the way up to aqueduct in the ventricular system (Kulaczewski et al 2017).
Increased intracranial pressure decreases CSF production (Miyajima and Arai 2015).
Fluid movement is not only dependent on the gross movement of fluid coming in and out of the head. It also dependent on local to and fro movements of fluid in and around the brain. Brinker et al (2014) found aquaporins serving as channels in the transfer of fluid at the blood brain barrier and the cell membranes at the boarders between CSF and ISF spaces. This allowed for a continuous flow of bi-directional fluid exchange.
Absorption of CSF
The main drainage route of CSF is into the lymphatic circulation. Some CSF can be drained into the Arachnoid Villi and granulations of the walls of the venous sinus to the blood as a secondary pathway but only if there is an increased CSF hydrostatic pressure (Miyajima and Arai 2015).
It is estimated that at least 50% of CSF drains into lymphatics in some mammals but the proportion in humans is still unknown. CSF drains via larger lymphatic vessels to regional lymph nodes. Due to the larger diameter of the lymph vessels they can carrying antigen-presenting cells (Engelhardt et al 2016). These lymphatic pathways include:
Nasal lymphatics: via the cribriform plate of the ethmoid bone channels connect the subarachnoid space with lymphatic vessels in the nasal mucosa (Engelhardt 2016).
Dural lymphatics: Aspelund et al (2015) found, in the mouse, lymphatic vessels in the meninges underlying the cranium, adjacent to the dural blood vasculature. These dural lymphatics absorb the 'waste' from the mix of CSF and ISF that gets deposited from the brain parenchyma back into the CSF via the g-lymphatic system (refer ISF drainage pathways below). Through lymphatic vessels around the arteries, veins and cranial nerves (II, V, IX, X, XI) that exit the cranial base and the cribiform plate into the nasal mucosa they drain this 'waste' into the deep cerivcal lymph nodes. In human studies Visanji et al (2017) found dural lymphatics in the sagittal sinus. Engelhardt et al (2016) found in the mouse model lymphatic drainage along the sagittal sinus continued through the cribiform plate into the nasal mucosa.
Lymphatic vessels in perineural (subarachnoid) spaces: Koh et al (2005) found lymphatic drainage of the CSF along almost all of the cranial nerves including the olfactory, optic, trigeminal, acoustic, hypoglossal and vagus nerves. Although the eye doesn’t contain any lymphatics Hasuo and colleagues proposed CSF drainage from the subarachnoid space of the optic nerve through arachnoid granulations into the orbital connective tissue from which lymphatics were believed to transfer the fluid to the cervical lymph nodes. Engelhardt et al (2016) found lymphatic drainage along spinal nerve roots.
CSF is also absorbed from capillaries (Miyajima & Arai 2015):
Parenchymal capillaries: absorbs CSF from the cerebral ventricular walls into the brain parenchyma.
Spinal canal capillaries: absorbs CSF into the subarachnoid space. Arachnoid granulations have been shown to exist in the spinal subarachnoid space.
Interstitial Fluid (ISF) (Yiming Lei 2017)
Interstitial space is the space between neural cells and capillaries.
This space is filled with Interstitial fluid.
Interstitial fluid facilitates communication between nerves in the brain.
There is a common relation between production and drainage sites of CSF and ISF.
There is a growing trend for the relationship between ISF and CSF to be more intimate than once thought.
The brains interstitial space (ISS) is the space between neural cells and capillaries. It occupies 15% to 20% of the total brain volume. The ISS plays crucial roles in substance transport and signal transmission amongst neurons. This involves a number of roles in brain function, such as communication among neural cells, information processing and integration, and the coordinated response to changes in the external and internal environments of the brain.
The ISS is composed of ISF and ECM. The brain ISF bathes and surrounds neural cells providing a medium for nutrient supply, waste removal and intercellular communication.
ISF production, movement and absorbtion
ISF may originate from CSF, cell metabolism, the vascular system and from water generated from the oxidation of glucose to CO2 (Engelhardt et al 2016).
ISF moves through the extracellular spaces in the brain's and spinal cord parenchyma. These extracellular spaces are gaps that seperate the cells of the central nervous system. They interconnect, are filled with ISF and are in direct continuity with the basement membranes of the capillaries.
The flow of ISF through the ISS in the brain parenchyma doesn't flow globally but is restricted to certain divisions or territories. In other words the brain's ISS contains functional divisions based on ISF flow.
Movement of ISF comes mainly from diffusion (concentration gradients) and partially bulk flow (pressure gradients). These pressure gradients are suggested to be partially caused by arterial pulsations that drain ISF within the smooth muscle walls of the arteries directly into extracranial lymph nodes (Iliff et al 2013) (refer below).
Drainage of the ISF from the brain takes place through several routes. This results in ISF absorbing (1) directly into extracranial lymph nodes and (2) into the CSF in the subarachnoid space and then into extracranial lymph nodes.
(1) ISF drainage directly into extracranial lymphatic nodes by pressure gradients (bulk flow channels, Engelhardt et al 2016)
Intramural pathways: ISF drains within the smooth muscle walls of the artery. This pathway drains ISF directly from the brain parenchyma along the muscle wall of the artery by the arterial pumping action (pressure gradients). As the drainage of ISF along the artery occurs in the opposite direction to the flow of blood in the artery it has been proposed to be driven by a contary (reflection) wave (Engelhardt et al 2016). The contary wave travels in the reverse direction to the flow of blood. This intramural pathway drains along the arteries in the base of the skull and the neck. From here it leaves the arteries of the neck and drains directly into the adjacent deep cervical lymph nodes.
Interstitial fluid and solutes drain from the extracellular spaces in the brain parenchyma through gaps between astrocyte end feet. They enter channels in basement membranes of cerebral capillaries. From here it drains into basement membranes between smooth muscle cells in the tunica media of arterioles and arteries to the deep cervical lymph nodes. Due to their narrow restricted pathways they can’t carry antigen-presenting cells.
Bulk flow also occurs along white matter fiber tracts (Engelhardt et al 2016)
(2) Drainage of the ISF into the CSF by concentration gradients (diffusion) and then into extracranial lymph nodes
CSF is considered a reservoir for ISF and the ultimate site of removal of most waste products from the brain's ISF. Conversely 20% of CSF originates from the brain's ISF. The exchanges between ISF and CSF occur at the:
Wall of the ventricle through ependymal cells.
Surface of the brain and spinal cord via pia-glial membranes.
g-lymphatic system.
g-lymphatic system
CSF gets pumped along arterial perivascular pathways into the brain parenchyma.
This creates a mix of ISF-CSF in the brain parenchyma that gets drained from the brain along venous paravascular pathways.
This is a slower drainage route than intramural perivascular drainage (refer above, Engelhardt et al 2016).
In the g-lymphatic system CSF gets ‘pumped’ along perivascular spaces surrounding the cerebral arteries into the brain parenchyma. Once it’s mixed with ISF the metabolites get cleared via the perivascular channels surrounding large caliber draining veins. Fluid and tissue metabolites in this system appear to drain back into the CSF and may reach lymph nodes via the CSF. Iliff et al (2015) described this as a brain-wide perivascular pathway that supports the exchange of CSF and ISF.
Engelahrdt et al (2016) described the g-lymphatic system as being largely separate from the rapid, direct drainage of ISF from the brain parenchyma along the basement membranes in the walls of cerebral arteries (intramural perivascular drainage) to cervical lymph nodes. They described the exact relationship between the two systems as requiring further investigation.
Rassmussen et al (2018) found the g-lymphatic system is particulary active at draining the 'gunk' out of the brain at night. They found a single nights sleep deprivation results in an accumulation of Aβ in the human brain. Poor drainage of Aβ has been associated with Alzheimer's disease.
Blood
Movement of blood is part of the main driving force for circulation of CSF and ISF in the brain.
Palpation of the primary respiratory mechanism at the head has been shown to coincide with Traube-Hering-Mayer waves (the rhythmic rate of vasodilation and vasoconstriction in the arteries).
Interestingly the cranial rhythmic impulse palpated at the head by osteopaths has been linked to the circulation of blood (Nelson et al 2001) so holds a particular interest in this field.
The function of vasomotion in the circulation of fluids around the brain has already mentioned but will be summarised here. The driving force behind these vasomotor effects can be affected by internal carotid artery ligation (Iliff et al 2013).
Vasomotion drives CSF and ISF drainage circulation along paravascular arterial pathways (Iliff et al 2013).
Expansion of the arteries drives CSF out of the brain as well as being responsible for movement of the brain (Greitz et al 1992).
Arterial pulsation is partially responsible for the bulk flow movement of ISF through the brain parenchyma (Iliff et al 2013).
Strik et al (2002) found pulsation and flow of the CSF are closely linked to the changes in the cerebral blood flow induced by heartbeat and by respiration.
Traube-Hering-Mayer Waves
Traube Hering Mayer Waves is the cyclic variations in blood volume/pressure within the arteries and arterioles. This is the result of rhythmic variations in sympathetic nerve activity on vessel calibre (Scarr 2016). Essentially it measures the rhythmic rate of vasodilation and vasoconstriction of the arteries.
This rate is recorded as cycles per minute (cpm) or cycles per second (Hz), and is classified into three main groups:
a very-low frequency wave (0.00–0.18 cpm, 0.00–0.03 Hz).
Low-frequency (Mayer) wave (1.8 cpm–9.0 cpm, 0.03–0.15 Hz): associated with baroreflex activity.
Faster Traube-Hering wave (9.0–24.0 cpm, 0.15–0.4 Hz): associated with the respiratory cycle.
Although each group has traditionally implied a different mechanism of causation the differences between them are not clear cut (Scarr 2016).
Trabue-Hering-Mayer oscillations have been found to determine the flow of fluid (plasma) out of the capillaries into the extracellular matrix and its uptake into the venous and lymphatic system (Scarr 2016). Iliff (2013) described this as being central to the circulation of the g-lymphatic system determining circulation of CSF and ISF.
Strik et al (2002) found the pulsation and flow of CSF is closely linked to the changes in cerebral blood flow induced by the heartbeat and respiration. They attributed this though to mainly Mayer waves, although 'Mayer waves' is the new collective term for Traube-Hering-Mayer waves. The pivotal effects of vasomotion in driving all fluids around the brain, and in moving the brain, has already been summarised in the section above.
What can you feel at the head?
The head is jammed pack full of blood vessels, lymphatic vessles, blood, CSF, ISF and brain tissue. It all exhibits a continuous movement of fluids and tissue that has to work in perfect harmony to maintain an intracranial pressure within narrow parameters.
Interwoven amongst this mobile pressure sensitive complex are the meninges. Far from being a passive lattice work it is in fact mechanically sensitive. Much like a spiders web it picks up and transmits pressures and intertwines this with its own distinct homeostatic functions.
On the outer surface of all this lies the cranium. A solid box? More or less but it does give at the sutures to permit cranial compliance (Seimetz et al 2012). Whist the movement is small this does not mean it is not necessary.
Adam et al (1992) found lateral pressure to the parietal bones compressed the sagittal suture resulting in increase intraventricular pressure, transient apnea, and unstable systemic arterial blood pressure. Cranial manipulation involving the ‘lift’ techniques to the parietal and frontal bones have been shown to mechanically stretch the falx cerebri (Kostopoulos & Keramidas 1992).
Therefore it would seem for this pressure sensitive movement of fluid to occur the cranium may not necessarily move as in the traditional cranial osteopathic model but much like its underlying structures its sutures should be allowed to ‘breath’ and give a bit.
Interestingly the cranial rhythmic impulse that is commonly felt by osteopaths when palpating the cranium has been found to correlate with traube-hering-mayer oscillations (Nelson et al 2001) which the authors attributed to the mechanical effects of vasomotion controlling ICP, respiration and CSF flow.
This gives the impression of the intracranial contents almost trying to burst through the head and separate the cranial bones but with the sutures being pulled tight trying to resist this motion. That’s the dummy’s guide to the tensegrity model of cranial dynamics.
To further cranial treatment a whole body approach would be interesting to see. Posture, bite analysis, respiratory training, psychotherapeutic interventions, etc could all reduce myofascial strain around the sutures and affect autonomic tone determining blood pressure and lymphatic circulation.
If you own a clinic in an affluent area my advice is to offer this 'holistic' package. And if you can incorporate the terms ‘holistic’ and ‘fascia’ in your advertising that should be worth at least another £50 per treatment.
APPENDIX: Embryology
Skull and meninges is derived from the mesenchyme and neural crest
This embryological link maintains in the developing head anatomically (the dura mater attaches to skull) and functionally (the dura mater prevents ossification of sutures and possibly helps with the ossification of the cranium)
Dura acts mechanically to determine the shape of the brain. The expanding brain and developing skull places tension on the dura and this promotes signaling pathways in the dura effecting the development of the brain.
Embryology of the cranium and dura (Jin et al 2016)
The mesenchyme forming the bones of the skull is derived from the paraxial mesoderm and cranial neural crest. The neural crest provides the mesenchyme forming the frontal, sphenoid, squamous temporal bones as well as facial bone. Paraxial mesoderm provides the mesenchyme for the formation of the parietal, petrous temporal and occipital bones.
However, at the space of the two parietal bones, the neural crest also plays a significant role. A small line of the neural crest is derived from mesenchyme and remains between the two parietal bones and contributes to the signalling system that governs growth of the cranial vault at the sutures and to the development of the under lying meninges.
Mesenchyme differentiates into bone by two mechanisms:
(1) Intramembranous ossification: bone gets directly laid down into the mesenchyme.
(2) Endochondral ossification: the mesenchymal cells differentiate into cartilage, and this cartilage is later replaced by bone.
The cranial vault bones are formed by intramembranous ossification. While the bones that form the base of the skull are formed by endochondrial ossification.
Embryology of the cranial sutures and dura mater (Jin et al 2016)
The mesoderm and neural crest cells don’t just form the bones of the skull but also the meningeal mesenchyme that forms all three layers of the meninges.
It does this while the sutures are developing. The growing and expanding bone fronts both invade and recruit the intervening mesenchymal tissue into the advancing edges of the bone fronts. By this action the intervening bones separate the mesenchyme into an outer ectoperiosteal layer (to become the skull) and an inner dura mater.
The outer layer of the dura forms the inner periosteum of the skull and the inner dura layer forms the dural folds (falx and tentorium).
The dura mater also expresses osteogenic growth factors that may be required for ossification of cranial vault bones.
The dura covers the brain. This dural covering has reflections acting as partitions of the cranial cavity under the calvarium, adopting a course that follows the main direction of the sutures. The folds are the falx and tentorium.
They firmly attach the skull base at the crista galli, the cribriform plate, the lesser wings of the sphenoid and the petrous temporal crests.
The dura mater in conjunction with the falx cerebri and the tentorium cerebelli, come to define the zones where bone growth slows down and the coronal, lambdoid, and sagittal sutures develop.
Oppermann (2000) found the dura mater was not only crucial in keeping the suture a flexible fibrous joint preventing them from being obliterated by bone but it was needed to stabilise the suture. It's not until the third decade of life when the cranial vault sutures ossify and until the seventh or eighth decade of life for the facial complex.
Jin et al (2016) found these dural bands essential in determining the shape of the brain as without them it would expand into a perfect sphere.
The expanding brain, sending signals by means of the dura mater makes the cranium grow and expand by means of expanding the cartilaginous growth plates in the cranial base and making the sutures add more bone at their periphery in the cranial vault. Gagan et al (2007) found the cells of the dura mater not only have profound influence on cell migration and differentiation in the infant skull but also the brain.
Therefore the growing brain does not actually push the bones outward. Rather, each flat bone is suspended, with the existent traction forces, within a widespread sling of the collagenous fibers of the enlarging inner (meningeal) and outter (cutaneous) periosteal layers. As these membranes grow in an ectocranial direction ahead of the expanding brain, the bones are displaced with them. This draws all of them apart, and the tensile physiological forces thus created are believed to be the stimulus that triggers the bone producing response.
Embryology of the dura and brain
The mechanical and biochemical are not just related to the development of the skull but also the brain. The cells of the dura mater have a dynamic reciprocal influence on cell migration and differentiation in multiple regions of the embryonic and infant brain and skull (Gagan et al 2007)
References
Development and Growth of the Normal Cranial Vault : An Embryologic Review (2016). Sung-Won Jin, Ki-Bum Sim, M.D. and Sang-Dae Kim
Cranial sutures as intramembranous bone growth sites (2000). Lynne A. Opperman
Cellular dynamics and tissue interactions of the dura mater during head development (2007). Jeffrey R. Gagan, Sunil S. Tholpady, Roy C. Ogle
Clearing the mind: Implications of dural lymphatic vessels for brain function (2015). Jeffrey J. Iliff, Steven A. Goldman and Maiken Nedergaard
Integration of the subarachnoid space and lymphatics: Is it time to embrace a new concept of cerebrospinal fluid absorption? (2005). Lena Koh, Andrei Zakharov and Miles Johnston
The cranial dura mater: a review of its history, embryology and anatomy. Nimer Adeeb &Martin M. Mortazavi &R. Shane Tubbs
Interrelationships of the pia mater and the perivascular (Virchow-Robin) spaces in the human cerebrum (1990) E. T. ZHANG C. B. E. INMAN AND R. 0. WELLER
Meninges: from protective membrane to stem cell niche (2012). Ilaria Decimo, Guido Fumagalli, Valeria Berton, Mauro Krampera and Francesco Bifari
Pulsatile brain movement and associated hydrodynamics studied by magnetic resonance phase imaging. The Monro-Kellie doctrine revisited. (1992). Greitz D, Wirestam R, Franck A, Nordell B, Thomsen C, Ståhlberg F.
Evaluation of the Production and Absorption of Cerebrospinal Fluid (2015). Masakazu MIYAJIMA and Hajime ARAI
The brain interstitial system: Anatomy, modeling, in vivo measurement, and applications (2017). YimingLei Hongbin Han Fan Yuan Aqeel Javeed Yong Zhao
Cranial rhythmic impulse related to the Traube-Hering-Mayer oscillation: comparing laser-Doppler flowmetry and palpation (2001). KENNETH E. NELSON, DO; NICETTE SERGUEEF; CELIA M. LIPINSKI, MSII; ARINA R. CHAPMAN, MSII; THOMAS GLONEK,
Dural lymphatic vasculature in human superior saggital sinus: the brain drain (2017). N. Visanji, A. Lang, D. Munoz
Quantification of the collagen fibre architecture of human cranial dura mater (1998). Maria C.J. Imenez Hamann , Michael Sacks Theodore Malin
The cranial dura mater: a review of its history, embryology, and anatomy (2012). Adeeb N, Mortazavi MM, Tubbs RS, Cohen-Gadol AA.
Radiographic evidence of cranial bone mobility. (2002). Oleski SL, Smith GH, Crow WT.
An investigation of cranial motion through a review of biomechanically based skull deformation literature (2012). Christina N.Seimetz Andrew R.Kemper Stefan M.Duma
Changes in elongation of falx cerebri during craniosacral therapy techniques applied on the skull of an embalmed cadaver (1992). Kostopoulos DC, Keramidas G.
Noninvasive intracranial pressure monitoring (1985). P.J. Pitlyk, T.P. Piantanida, D.W. Ploege
Detection of skull expansion with increased intracranial pressure (1981). M.D. Heifetz, M. Weiss
Vascular, glial, and lymphatic immune gateways of the central nervous system (2016). Engelhardt B, Carare RO, Bechmann I, Flügel A, Laman JD, Weller RO.
The glymphatic pathway in neurological disorders (2018). Rasmussen MK, Mestre H, Nedergaard M.
