Paul Manley Back Pain and RSI Clinic

Paul Manley, D.O. (ESO 1980), M.A.O.(Manip), Registered Osteomyologist
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Opening hours: 9am to 7pm. Tuesdays, Thursdays and Saturdays.

Enhanced Cranial Technique

The following is an abridged version of an article published by Bastyr University, Journal of Naturopathic Medicine ( Oregon ), The New Zealand Journal of Osteopathy and by Temple University (Philadelphia), Frontier Perspectives, all 1993-1995. Author: Paul Manley D.O. (ESO 1980)

In one way this short paper describes mechanisms by which infants may suffer in the short and the long term from cranial abormalities, in another, it alludes to methods of diagnosis and manual treatment which can provide relief from such problems.

Enhanced Cranial Manipulation (ECM) is a 'nuts and bolts' approach to cranial problems and represents a unique collection of manipulative techniques as applied to the cranium. This is in contrast to the esoteric approach fostered by the ubiquitous practitioners of Cranio-sacral therapy etc..

The object of ECM is to optimize the elastance co-efficient of the cranium. This is acheived via manual de-compression techniques applied directly to the cranium. Stimulation of the venous drainage by increasing the circulation of the scalp is also a beneficial by-product of treatment.

Figure 1
The sutures of the vault bones of the human cranium.

The techniques are appropriate for cranial and autonomic symptoms only. They are not used for fixing a 'low-back pain' for example, other, more efficient, traditional techniques can deal with such problems.

The following points must be considered when forming an understanding of the cranium in relation to its contents:

1. The cerebral capsule (bone and membrane) changes in degrees of resilience due to the changes in ICP therein. The vault bones only grow in response to internal expansive pressures as the brain grows.

2. Intra-cranial pressure ( ICP ) varies in response to the following:

a. The rate of cerebro-spinal fluid ( CSF ) production.
b. The rate of CSF drainage.
c. The elasticity of the cerebral capsule.
d. The degree of responsiveness of the neurohumoral mechanisms which react with ICP fluctuations.

3. Increased ICP, even of short duration, can compromise cerebral circulation especially in the region of the brain stem activational and regulatory areas.

4. The "elastic coefficient" or elasticity of the cerebral capsule exerts a damping or shock absorbing action on ICP variations, thus providing a buffer between the CSF and the CNS.

5. The lower the elasticity of the cranium, the higher the ICP rises.

Infant development of the cranium:

During the passage of the infant through the birth canal, the head deforms, causing overlap of the coronal, sagittal and lambdoidal sutures.

This overlapping usually disappears during the first three days of life. It is most pronounced in premature infants due to the wideness of the sutures but nonetheless appears consistently in the normal neonate.




Figure 2
Compression of the Superior Sagittal sinus due to
external pressure on the Occipital bone


Lambdoidal overlap and superior sagittal sinus ( SSS ) compression may be produced merely by laying the infant on its back, head resting on its occipital bone. The pressure on the occipital bone effectively blocks the SSS. The overlap is accentuated when the infant is supine for prolonged periods. The compression of the SSS produces slowing in the cerebral circulation time and diverts drainage into the deep venous system. Due to the thinness of these vein walls at this age, intracerebral hemorrhage can occur and is one of the major causes of death in infants, especially preterm.

The practitioner should be capable of adequately differentiating between potential contributary factors.

is a term which applies to the types of deformity affecting the shape and elastic function of the skull resulting from the premature closure of one or more sutures. This can occur in response to direct trauma such as forceps delivery, constant moulding pressures such as sleeping on the same side of the head, or from congenital or genetic origins.

Growth responses to premature suture closure.

Synostosis:premature suture closure

Figure 3

Growth responses to premature suture closure



Figure 3: Legend

Solid line ____ normal
Dotted line ..... premature closure
Dashed line - - - secondary compensation (expansion)

A: Normal
B: Sagittal synostosis
C: Unilateral coronal closure
D: Bilateral coronal closure



Figure 3 illustrates the various configurations most likely to occur. The synostotic patterns can persist into adulthood and may result in gross deformity or in sutural fixations. The incidence of mental and/or motor deficit is high with this pathology. This is due to the effect on the ICP either by hampering drainage of CSF or by decreased elasticity failing to allow for optimal ICP fluctuations. Palpation of Lambda (the junction of the parietal and occipital bones) in order to ascertain the prescence of overlap is very important. Ridging of the sagittal and frontal sutures is generally present and palpable in premature closure, even into adulthood.

Anterior fontanelle pressure change monitoring

Figure 4:

Changes of anterior fontanelle in relation to atmospheric pressure in the infant.

A: Anterior fontanelle convex.
B: Anterior fontanelle flat.
C: Anterior fontanelle concave.


The shape of the anterior fontanelle (Figure 4 ), whilst still patent (un-ossified), can be very revealing with regard to the ICP. Normally the ICP is increased (from atmospheric pressure as baseline) when the infant is in the horizontal position and the fontanelle shows as convex, whereas in the vertical position the ICP is normally sub­atmospheric and the fontanelle will be concave. Thus, when the ICP is raised and the infant is in the vertical position the fontanelle will be convex, i.e. a bump.

There are a few exceptional circumstances when this principle does not apply and in such cases the fontanelle remains flat. This maneuver can be used to determine whether the ICP is in the normal range when used as a part of the usual diagnostic procedures.



When assessing the appropriateness of treatment, aggravating factors, and prognosis, the following factors must be considered:

1. ICP increases instantly with crying, laughing, abnormal respiratory patterns, abdominal straining, agitation, increase intrathoracic pressure, raised central venous pressure and pain.

2. The pressure of encircling bands and constrictions to the neck can produce ICP rise, the bands of nasal cannulae, phototherapy patches, tight collars, etc.

Because ICP rise alters the ratios of the monoamine axis (5HT, noradrenaline and dopamine) in the brain stem activational systems, general symptoms are many and vary greatly in both type and severity.

The most obvious signs and symptoms are:

1. Sensorimotor and mental deprecation (i.e. listlessness, sleeplessness or lack of normal responsiveness, difficulty suckling, gripey and agitated).

In the adult, agitation, emotional volatility, personality changes, headaches, inability to concentrate, drowsiness can all be symptoms of the need to improve the elastic compliance of the cranium.

2. Apneic (cessation of breathing) attacks and convulsions.

3. Neurological deterioration indicative of severe brain stem compression (such as inability to perform ocular tracking or lack of standard reflexes).

Even lesser degrees of ICP derangement can, over time, fundamentally disrupt and cause delay to the sequences involved in the laying down of the vital CNS developmental programs. This maturing and myelinatiing process is the basis for maximal motor and cognitive development in all infants. Indications of severe ICP compression must be assessed by a pediatric neurologist before initiation of any treatment.


1. Compression of the superior sagittal sinus by neonatal calvarial moulding. Radiology. 1975;(115): 6359
2. Changes in Superior Sagittal Sinus Blood Velocities Due to Postural Alterations and Pressure on the Head of the Newborn Infant
Cowan, et al. Pediatrics 1985; 75:6 1038-1047

3. Intracranial pressure and obstructive sleep apnea. Chest, 1989 (95)2: 27983
4. Degeneration of neurons in the thalamic reticular nucleus follow­ing transient ischemia due to raised intracranial pressure: Excitogenic degeneration mediated via non NMDA receptors. Brain Research 1989; (501): 12943
5. Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation. J. Neurosurgery 1982 (56):6668
6. Intracranial compliance is timedependant. J. Neurosurgery 1987 20(3) :38995
7. A fast method of estimating the elasticity of the intracranial system. J. Neurosurgery 1977; (47): 1926

Copyright: 2006-Paul Manley

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Paul Manley Back Pain and RSI Clinic
46 Theobalds Rd, Holborn, London WC1X 8NW

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