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Cranio-sacral Motion - English
Journal of Bodywork & Movement TherapiesThe decrease of the cranial rhythmic impulse during maximal physical exertion: an argument for the hypothesis of venomotion?
ABSTRACT A new hypothesis for the explanation of the origin of the cranial rhythmic impulse (CRI) is based on the principle of venomotricity. Research on this physiological phenomenon was carried out on bats more than 100 years ago and showed an automatic rhythm of approximately 10 cycles per min (cpm).In this study we will attempt to discover whether a brief physical peak effort has an influence on the CRI. We will assume that there is, in the case of maximal exertion, a brief shift of the CO2/O2volume ratio (RER), which serves as a measure for the energy consumption within the blood vessels. In analogy with this physiological phenomenon we would expect a decrease of the CRI. Three examiners (twice) palpated the cranium and the sacrum for the CRI as well as the vena femoralis for local vasomotion (LVMvf) on a group of healthy subjects (n=15). The examiners changed places during the examination, both before and after the exertion test performed by the subject.
The study showed that the reproducibility of all measurements is exceptionally high and that there are no significant differences with respect to rhythm between the three measured locations on the body. The physical effort was determined by measuring the supplied physical strain within a certain time. The respiratory ratio (RER) was determined as the CO2/O2volume ratio in the bloodstream. Together with the values of lactic acid concentration these data were used as explanatory variables and compared to the outcome variables, i.e. the CRI of the cranium (CRI cranium), the CRI of the sacrum (CRI sacrum), cardiac pulse (CAP) and local vasomotion of the vena femoralis (LVMvf). It was found that for each of these research variables there was a significantly high difference associated with the exertion test. The experiment demonstrated that 20 min post-test, a maximal exertion test yields a significant decrease of the three measured rhythms of the CRI cranium, CRI sacrum and LVMvf, with an average reduction of 30%. This suggests that the common decrease probably points to a relation between 'CRI' and the decrease of O2concentration in the bloodstream. The CRI decreases after effort as a result of the simultaneously occurring reduced vasomotricity and does not show a proportional increase due to increased cardiac rhythm. As the three rhythms, CRI cranium, CRI sacrum and LVMvf, which were measured simultaneously, correspond both before and after the exertion test, and since all three rhythms decreased markedly following exertion, it is possible to hypothesize that venous vasomotricity is probably one of the forces behind CRI. Venomotricity is found in all the veins of the body, not only those in the cranium, for example in the vena porta, vena femoralis, vena poplitea, vena saphena magna etc. Copyright 2001 Harcourt Publishers Ltd
New hypothesis for the origin of cranio sacral motion
Farasyn Andre PhD PT, DO
SUMMARY. A new hypothesis for the origin of Cranio-Sacral Motion (CSM), has been formulated. The present concept is called in to question using arguments based on biomechanical studies of cerebro-spinal fluid pulsation waves, neural envelops and studies of those physiologic factors which influencevessel wall tonus. The difference between the rhythm of venomotion and the Cerebro-Spinal Fluid (CSF) is explained and a new hypothesis is put forwards: the CSM is probably the expression of Local Venomotion (LVM) and not of CSF pulsations or the consequences of it. The function of "rigidity" of the skull sutures is discussed, and finally, a suggestion is made for osteopathic normalisation of skull bone restrictions, using the patient's respiration as a powerfull and well controlled means of treatment.
IntroductionIn the early 20th century, W.G. Sutherland identified a rhythmic cranial motion, of obscure origin, with a rate of between 6 and l2 cycles per minute (cpm) . He named this motion the"primary respiratory mechanism" (1939) and sugested that rhythmical brain movement was responsible for cerebral ventricular and CSF fluctuations. Other researchers (Magoun, 1966; Upledger, 1981) proposed that this brain motility, or "Cranial Rhythmic Impulse", originates from the ventricular pumping actions themselves. An opinion concerning CRI, suggesting an 'entrainment model, has recently been put forward. (McPartiand, 1998).
Most manual therapists and osteopaths, employing cranial technics, who sense the physiological motions at the exocranium, have an interest in knowing exactly what they are palpating, and what lies behind the so called "cranio-sacral-motion" (Lippincott, 1949; Magoun, 1966; Frymann, 1971; Retzlaff et al., 1975; Mitchell, 1976; Roppel et al., 1978; Tettambel et al., 1978; Upledger, 1981; De Cock, 1982; Altieri, 1984; De Cock, 1988; Ferguson, 1991; Ferre et al., 1991; Norton, 1991; Rommeveaux, 1993; Chiatow, 1997; McPartiand & Mein, 1997).
CRANIO SACRAL MOTION AND CEREBROSPINAL FLUID PULSATION
Since many cranial osteopaths support the hypotheses that the origin of CSM is to be found in brain movement, or CSF motions, it is necessary to search what is known about CSF flow pulsation amplitudes in assessment of exocranial dynamics.
Magendie (1842) once found the dynamics of CSF in normal individuals has three characteristics :
• The existence of a slightly positive pressure, in comparison with the atmospheric pressure;
• CSF has the behaviour of rapid pulsations, cyclic and synchronous with the arterial pulse;
• There is also evidence of slower waves following the respiratory cycles. Most authors conclude that the configuration of CSF pulsations are recognised as essentially arterial in nature (O'Connell, 1943; Goldenshon, et al. 1951).
In the sixties, Bering pointed out that C.S.F. pulse pressure contributes to the intracranial pressure and that artedal pulsations occuring at the choroid plexus were transferred to the cerebral ventricles. Later investigators, (Du Boulay 1966) showed by means of pneumoencephalography, that CSF propulsion by the choroid plexus pulsations was of minimal.
Movements of the third ventricle, caused by the pulsations of the basal arteries, were noted to be of greater value. Those pulsations are probably partly the result of rhythmic fluid displacements of the expending brain tissues occuring at systole (ter Braak & de Viieger, 1962; Cserr, 1971; Martins et al., 1972; Wood, 1983;Herndon & Brumback, 1989; Schuller, 1993).
Some investigators (Hamit 1965) believed the pulsations of CSF depend on venous hydrodynamics. In case of congestive heart-failure, the pattern of intracranial CSF pulse wave is indeed purely venous, but under physiological conditions the intracranial CSF pulse wave is not primarily venous but arterial in origin (Martins et al., 1972; Hamer, 1977; Thomsen et al., 1990; Bhadelia et al., 1997, Ursino & Lodi, 1998).
The intracranial dynamics can be viewed as an interplay between the spatial requirements of four main components: arterial blood, capillary blood (brain volume), venous blood and CSF.
These components could be characterised, and the expansion of the arteries and the brain differentiated, by applying the Monro-Kellie (see: Box) doctrine to every moment of the cardiac cycle. The arterial expansion creates the prerequisites for the expansion of the brain by venting CSF to the spinal canal. The expansion of the brain is, in turn, responsible for compression of the ventricular system and hence for the intraventricular flow of CSF (Greitz et al., 1992).
HYPOTHESIS OF VASOMOTION
The so-called "cranial sacral motion", is possibly either an expression of a in general venous vessel wall pattern involving the vessels of the brain and those on sacral level, cyclically contracting at a rate of 6 to 12 cpm (Farasyn, 1986b; 1988; 1989).
It is necessary make a clear difference between something that causes rhythmic pulsation waves in CSF, and their consequences, passive brain squeezing by each systole, and on the other hand, the automatic rhythmic venomotions of the veins of the head.
The Norton's theory ( 1991) assumes that the sensation described as the cranial rhythmic impulse, is related to activation of slowly adapting cutaneous mechanoreceptors by tissue pressures of both the examiner and the subject. The sources of change in these pressures represents a complex interaction of at least four different physiologic rhythms : combined respiratory and cardiovascular rhythms of both examiner and subject.
The author wanted to explain the difference between venous cardiovascular rhythmic pattern of the subject & examiner suggested by Norton and the palpation of something totally different : venous vasomotion under the skull.
If CSF pulsations follow a physiological venous pattern, as is the case in some normal individuals, it suggests that the venous pattern is caused by cardiac contractions, and not by venous vessel wall contractions.
In other words, when palpating the exocranium, the so-called "cranial sacral motion" may be felt as an indirect expression of the characteristics of the venous vessel walls, at a rate of approximately 10 cpm, and not the CSF pulsations themselves.
Palpation of the great or small veins on the body demonstrate these same active characteristics of venous smooth muscle cell contraction at a rate of approximately 10 cpm.
The physiological behaviour of venous, venular and even arteriolar vessel wall require examination in relation to the concept of the cranial-sacral motion.
Arguments
In 1852, Jones described for the first time myogenic activity of bloodvessels by examination of periodic contractions of veins in the bat wing.
In the beginning of the 20th century, Bayliss proved that this behaviour is also common for arterial vessels and made a theoretical explanation for it.
In 1961 Funaki recorded, for the first time, with intracellular micro-electrode techniques, spike-discharges from venular smooth muscle fibre. The sum of trans-membrane potentials of smooth muscle fibre caused bursts of regular spike discharge, explaining the rhythmic and spontaneously "pace-maker” vascular activity.
Wiedeman (1963) demonstrated that injecting small volumes of physical solutions prolonged the duration of the contracting phase of venomotion. D'Argosa (1970) and Wiederhielm (1973) obtained, with micropunctures in the vascular bed of batwings, measurements of approximately 9.5 cpm.
Those vigorous contractions in muscular venules and veins in the batwing are present in other species too ( Holman et al. 1968; Wiederhielm & Weston, 1973; Morgan, 1983; Gustafsson et al., 1994).
Contractions of the smooth muscle cells of the venous wall cause active displacement of blood towards the heart, and, vasomotion contributes to the maintenance of blood fluidity in the microvessels (D'Argosa, 1970; Bevan et al., 1974; Muller-Schweinitzer & Sturmer, 1974; Vanhoutte, 1977; Siegel et al., 1980; Colantuoni et al., 1984; Folkow, 1984; Bumstock et al., 1986; Aggarwall et al., 1994; Davis et al., 1992; Gokina et al., 1996; Yuan et al., 1998).
The vessels wall of venules and veins are sensitive to: temperature-changes, extramural pressure (Mellander et al., 1964) and distension (Johanson & Mellander, 1975), but some local metabolic factors affect little the reactivity of venous smooth muscle, in contrast with the characteristics of the arteriolar one (Bayliss, 1902; Nicoll & Webb, 1946; Mellander et al., 1964; Wiederhielm, 1967; Mullier-Schweinitzer & Sturmer, 1974; Edwinsson et al., 1983; Colantoni et al., 1984; Vanhoutte & Rimele, 1984; Davis et al., 1992; Gustafsson et al., 1994; Aggarwal et al., 1 994; Gokina et al., 1996 ).
Pathological situations such as advanced diabetic mellitus (Bollinger et al., 1983), glucose concentrations (Linke & Betz, 1979; Morgan, 1983), 02 and carbon-di-oxide concentration, sympathoadrenergic activity (Bevan et al., 1974; Auer et al., 1981; Edvinsson et al., 1982) and some specific pharmacological agents (Altura, 1978) employed in neurology, anaesthesia and angiology (Thulesius et al., 1979; Xiu, 1983; Bumstock & Kennedy, 1986; Xiu & lntaglietta, 1986) all directly influence the vessel wall tonus and vasomotion.
Arterial vasomotion can play an important role in determination of oxygen distribution (Colantuoni et al., 1984; Folkow, 1984; Ragan et al., 1988). Laser-Doppler flowmetry and electromyography, used simultaneously for measuring skeletal blood perfusion, show vasomotion, i.e. rhythmic variations in blood flow with a frequency of 5-6 cpm-l (Larsson et al., 1993).
For many practitioners it is hard to accept the concept of "cranio-sacral motion" being noted simultaneously via contraction-waves of CSF, at both occipital and sacral level (Farasyn, 1986b; Ferre et al., 1991). Biomechanical studies of neurological envelope-displacement demonstrates elongation and displacement only if strong flexion or extension of the vertebral column occurs (Trolard, 1890; Reid, 1960; Decker, 1961: Kernig, 1969; Martins, 1972; Bourret & Louis, 1974; Breig, 1978; Louis, 1981; Williams et al., 1989).
CSF-fluctuations when passively induced are of such minor value that it is difficult to accept that they are responsible for the stronger displacement-movement noted at the sacral level.
As confirmed by some authors (Bourret & Louis, 1974; Decker, 1961; Troup, 1986), experiments demonstrated, even in neutral position, the sheath of the dura mater spinalis possesses pleats, suggesting that the tissues are relaxed.
Studies of Klein (1986), on cadavers, examining the biomechanical behaviour of the dura mater spinalis and spinal cord during flexion of the whole column, showed a downward slip in the upper cervical, an upward slip in the cervico dorsal and a downward movement in the lumbar area. There was no slipping in the area of C4 and Th6.
The author stated that it was hard to believe the cranio sacral system could work as it is proposed. One of the requirements for the mechanical expression of cranio-sacral motion would be sufficient tension of the spinal cord between sacrum and occiput, which seems to be absent.
Little rhythmic (real) respiratory displacement can be palpated on the sacrum of an individual in neutral position. It is also very difficult to palpate CSF-pulsations on the sacrum.
The small degree of flexion-extension of the sacrum at a rate of +/- 10 cpm, is probably caused by the venomotions of the Vena cava inferior bifurcation situated just anterior to it. Local venomotion associated with sacral motion is not only independent of, but also stronger than at occipital motion (Farasyn, 1988).
VENOMOTION: INDEPENDENT CONTRACTION WAVES
Veins and venules exhibit marked active vasomotion that sweeps centripetally as a peristaltic wave with the segment of any vessel between two valves forming an automatic responsive unit (Nicoll & Webb, 1946, 1955; D'Argosa, 1970; Siegel et al., 1980; Ragan et al., 1988, Larsson et al., 1993).
This means that veins coming from the head (without valves) and those coming from the limbs and trunk, demonstrate nearly the same frequency of vasocontriction, but have independent cycles. Palpation for only a brief time leads to a suggestion of the same frequency at both occipital and sacral level.
On the other hand, if palpation continues for more than 5 minutes, the contraction-wave which is noted is felt to occur independently at occipital and sacral levels. Just as it is possible to visualise venomotion influence at the sacral level, so can vasomotion of the Superior Sagittal Sinus, the great cerebral Vein, the straight Sinus, the Transverse Sinus and their confluence, posterior and inferior in the head be seen to influence motion in the cranium. It is possible, on the exocranium, to palpate these physiological pulsations independentally on the frontal and sagittal bones.
.
The laws of hydrodynamics suggest that the force of venomotion, in structures lying just under the skull, should be able to move, albeit slowly and with very small displacement ranges, the different bones of the skull (Farasyn, 1986b).
The existence of a cavernous nodule at the confluence between straight sinus and the great vein of Galen (Gray's Anatomy, 1973) can play possibly a role in CSM as it is suggested in Upledger’s pressurostat model (1981) . The validity of this has been difficult to accept because no muscular or elastic tissue components were found (Bergquist, 1974). Research may demonstrate that venomotion plays an active role in this hypothesised mechanism. The morphological organisation of cerebral veins, with a rich supply of collagenous material and only a few pericytes, supports the evidence of weak contractions, regularly observed in isolated vein preparations in vitro. These small contractions might however be of importance in vivo, since cerebral veins only have to constrict against a low pressure (Edvinsson et a]. 1983).
RIGIDITY OF THE SKULL
It is important to note that the rigidity of the skull of an adult serves particular needs and functions. Just as negative pressure exists in the thorax, produced by its osseous cage, pleura and a film of liquid, so in the head there exists an osseous box, different soft tissue layers and films liquid, between the periostium and the dura mater, assuring a negative pressure in sinus area of the head. This a perfect venous return is guaranteed by the pressure-gradient from a high (arterial) pressure to a low (venous) pressure system.
In support of this consider that :
• Young people under the age of about 11, do not yet have skull rigidity (Parsons, 1905; Ericson & Myrberg, 1973; Moss, 1975 ), and there is no negative pressure in the jugular vein system at this age (Hamit et al., 1965; Edvinsson et al., 1983).
• After ossification of the skull bones at the age of +/- 11, negative pressure is always present (normally) in the jugular vein system.
• Trepanation: the greater the surface of skull bone trepanation, the more the patient complains of headaches, possibly due to malfunction of vessel tonus, resulting from decreased negative pressure (Fodstad et al., 1984). On one hand, the function of bone structures may be necessary for impact protection by means of local absorption of kinetic energy (Moss, 1975; Dörheide & Hoyer, 1984; Spetzler et al., 1980), and relative rigidity may be a need for a normal, good working venous return in the head.
On the other hand, abnormal fixations of skull-bones can perhaps cause local decreased venous blood circulation potential, and could lead to increased circulation elswhere in compensation.
EXAMINATION OF PATIENTS
Suggested examination on a person lying supine:
Put one hand supine under the occipital bone and with your index-finger of the other hand, successively on a
- Facial Vein;
- External jugular Vein;
⁃ Anterior jugular Vein.
⁃
Put one hand under the occipital bone and with your other hand supine under L5-SI level.
Put one hand under L5-SI level and with the index-finger of the other hand on the Great Saphenous Vein, or if possible on the Common Femoral Vein. Put one hand under the occipital bone and the other under LS-SL level. Observe :
• the local force of venomotion;
• the greater the segmental distance the more obvious the independent rhythm the common frequency rate of 6 to 12 cpm. of venomotion;
• the force of contraction is greater at sacrat level than on occipital level : The sacral motions depends of the strong venomotion activity of the Vena cava inferior and Vena iliaca communis;
• the pulsations on occipital level are independent from those on sacral level; cranial rhythmic pulsations are the strongest at the level of the mastoid process, caused by the passage of the Vena jugularis interna.
Try also to palpate "ascending-descending" sensations of the liver or kidneys. Besides respiration and arterial pulsations, an apparently "intrinsic" force of swelling isto be felt each +/- 10 seconds, possibly caused by the rhythm of Vena Portal vasomotion.
In the concept of Cranial Rhythmic Motion, the rhythmic movements of +/- 10 cpm of "cranial bone mobility" is said to be palpable all over the body, but in the concept proposed by the author, the primary motor is local venomotion (LVM).
It is possible that arterioles take a part in these motion of CRM, but it is unknown in what degree.
The author hypothesises that the veins are responsible for palpated 'CRM' pulsations in the fascia, all over the body, even in organs.
Palpating for "CRM" by placing the hands, for example, on the legs of a patient, local venomotion may be noted rather than reflection of cranial motions.
TREATMENT FOR SUTURAL RIGIDITY
The "Local Venomotion" under the cranial bones, as described earlier, are necessary for diagnosis of "Cranio Sacral Motion" and is commonly employed therapeutically in classical cranial osteopathic treatment. If respiratory forces produce pressure within the cranial bowl these an be employed in treating cranial restrictions.
While for diagnosis of cranial bone mobility, the LVM is the best indicator of sutural restrictions of the skull, for treatment the force of respiration of the patient is more helpful. Asking the patient to inhale and exhale offers a greater degree of controllable force than the more subtile venous motion.
Following correction, employing respiration tools, palpation of LVM of cranial bones is necessary to check whether treatment has been successful.
In medical literature we could only find experimental studies concerning human arteriolar vasomotion. The only explanation we can give is that it is experimentally difficult to examine human venomotions: Flowmetry of venules and veins in vivo showed direct artefacts of cardioarteriolar rhythmic contraction waves. To make registrations of venomotions, researchers need a dissection's preparation of animal species. Only direct venomotion measurements in vivo where possible on batwings.
Recent literature of human evidence of arterioral vasomotion:
1. Experiments on segments of human basilar arteries with Caprate (C10) indicates that these lipids could influence directly vasomotion as vasodilators (White et aL, 1991);
2. Percutaneous measurement by Laser-Doppler flowmetry of human skeletal muscle microcirculation at varying levels of contraction force showed vasomotion, ie. rhythmic variations in the blood flow, with a frequency of 5-6 cpm-l (Larson et al., 1993);
3. Human pial arteries obtained during surgery frequently exhibit spontaneous periodic contractions. 53 segments from 38 patients were studied and spontaneous depolarisation reached levels of -40 to -35 mV. It was concluded that these periodic depolarisation and action potentials generation underlie the periodic spontaneous contractions of human pial arteries( Gokina et al., 1996).
We only can work out a theory based on clinical evidences concerning the relation between vasomotion and CSM but there are three mean problems: We have to prove:
1. the existence of human CRI;.
2. the existence of human venomotion in vivo;
3. the correlation between rhythmic venomotion and the rhythmic cranio sacral motion.
4.
CONCLUSION
It is proposed that the intrinsic movement of a cranial bones, fascia, organs, may be caused by local venomotion pulsation, the reflection of which we may palpate at the surface.
Arterial and venous vasomotoricity is to be found throughout the body, including the head where local venomotion is probably the prime motor ofcranio-sacral motion.
It remains to be demonstrate conclusively that factors such as temperature (fever), transmural-pressure (hydrocephalus), glucose concentration (diabetic patients), are able to change the patterns of venomotion and therefore of "Cranio Sacral motion".
The question is not to belief or not in CSM which exists as a measurable physiological phenomenon. The only problem is to explain the origin of it and this paper has offered a possible answer.
Note:
The Monro-Kellie doctrine: CSF& intracranial pressure:
The changes in intracranial pressure which occur following a change in one of the consistuent volumes within the skull are governed by the Monro-Kellie doctrine, stated in the late 18th century and describes how an increase in one of the constituent volumes must be reflected by a reciprocal decrease in another volume to avoid any change in pressure and that if this does not occur, there is a rapid rise in intracranial pressure. The development of cerebral dysfunction under some experimental conditions is independent of the rate of expansion and only dependent upon a critical volurne. This constancy of intracranial volume is the mean sense of the so-called "Monroe-Kellie doctrine".
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