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import Article from "@/components/Article";
const ArticleCranialManipulation = () => {
return (
<Article
title="The Effect of Cranial Manipulation on the Traube-Hering-Mayer Oscillation as Measured by Laser-Doppler Flowmetry"
author=""
>
<h2>Source</h2>
<p>
Alternative Therapies, Nov/Dec 2002, Vol. 8 No. 6<br />
<a href="http://www.alternative-therapies.com/">
http://www.alternative-therapies.com/
</a>
</p>
<h2>Authors</h2>
<p>
Nicette Sergueff lectures throughout Europe on manual principles,
diagnosis, and treatment, and maintains a private practice in Corbas,
France. She is an assistant professor.
</p>
<p>
<em>Kenneth E. Nelson </em>is a professor, and Thomas Glonek is a
research professor in the Department of Osteopathic Manipulative
Medicine, Chicago College of Osteopathic Medicine, Midwestern
University, Downers Grove, Illinois.
</p>
<h2>Context</h2>
<p>
A correlation has been established between the Traube-Hering-Mayer
oscillation in blood-flow velocity, measured by laser-Dopper-flowmetry,
and the cranial rhythmic impulse.
</p>
<h2>Objective</h2>
<p>
To determine the effect of cranial manipulation on the
Traube-Hering-Mayer oscillation.
</p>
<h2>Design</h2>
<p>
Of 23 participants, 13 received a sham treatment and 10 received cranial
manipulation.
</p>
<h2>Setting</h2>
<p>
Osteopathic Manipulative Medicine Department, Midwestern University,
Downers Grove, Illinois.
</p>
<h2>Participants</h2>
<p>Healthy adult subjects of both sexes participated (N=23).</p>
<h2>Intervention</h2>
<p>
A laser-Doppler flowmetry probe was place on the left earlobe of each
subject to obtain a 5-min baseline blood flow velocity record. Cranial
manipulation, consisting of equilibration of the global cranial motion
patter and the craniocervical junction, was then applied for 10 to 20
minutes; the sham treatment was manipulation only.
</p>
<h2>Main Outcome Measure</h2>
<p>
Immediately following the procedures, a 5-min postreatment laser-Doppler
recording was acquired. For each cranial treatment subject, the 4 major
components of the blood-flow velocity record, the thermal (Mayer)
signal, the baro (Traube-Hering) signal, the respiratory signal, and the
cardiac signal, were analyzed, and the pretreatment and posttreatment
data were compared.
</p>
<h2>Results</h2>
<p>
The 10 participants who received cranial treatment showed a thermal
signal power decrease from 47.79 dB to 38.490 dB (P &lt; .001) and the
baro signal increased from 47.40 dB to 51.30 dB (P &lt; .021), while the
respiratory and cardiac signals did not change significantly (P &gt; .05
for both).
</p>
<h2>Conclusion</h2>
<p>
Cranial manipulation affects the blood-flow velocity oscillation in its
low-frequency Traube-Hering-Mayer components. Because these
low-frequency oscillations are mediated through parasympathetic and
sympathetic activity, it is concluded that cranial manipulation affects
the autonomic nervous system.
</p>
<h2>Introduction</h2>
<p>
Cranial manipulation is a form of broadly practiced alternative, manual
medicine. A fundamental component of cranial manipulation is the primary
respiratory mechanism (PRM).<sup>1</sup> It is described as an
oscillation that is palpable; the cranial rhythmic impulse (CRI)2 has an
agreed-upon frequency of 10-14 cycles per minute (cpm).<sup>2,3</sup>{" "}
The PRM/CRI is a subtle phenomenon that is readily palpable only by
experienced individuals, making its very existence subject to debate.{" "}
<sup>4,5</sup>
</p>
<p>
The Traube-Hering-Mayer (THM) wave is a complex oscillation in blood
pressure and blood-flow velocity. The Traube-Hering (TH) component of
this oscillation has a frequency of 6 to 10 cpm. Analysis of the TH was
first described in 1865, when Ludwig Traube reported the measurement of
a fluctuation in pulse pressure that occurred with a particular
frequency of respiration but persisted after respiration had been
arrested.<sup>6</sup> Fourier-transform analysis applied to blood
physiologic parameters shows that this fluctuation consists of 3
principal spectral peaks: the thermal or Mayer (M) wave (1.2-5.4 cmp),
the baro or TH wave (6.0-10.0 cpm), and the respiratory wave, which
shifts in frequency with changes in the respiratory rate.7 Multiple
authors have commeted on the similarity between the TH wave and the CRI.
<sup>8-11</sup>
</p>
<p>
By comparing cranial manipulation with laser-Doppler flowmetery, we have
demonstrated that the PRM/CRI is congruous with the TH component of the
THM oscillation in blood flow velocity.<sup>12</sup> A question,
therefore, logically arises: can cranial manipulation affect the THM
oscillation?
</p>
<h2>Method</h2>
<p>
Healthy adult subjects (both sexes, N=23, institutional review
board-approved informed consent obtained) were divided randomly into
cranial palpation (n=13) and cranial manipulation groups (n=10). A
laser-Doppler probe (BLF 21 Perfusion Monitor, Transonic Systems, Inc.
Ithaca, NY) was placed on the left earlobe of each subject. After the
subject was allowed to lie quietly on the examination table for 3
minutes of equilibration, a 5-minute baseline blood-flow velocity record
was obtained. Cranial manipulation or manipulation, with the physician
blinded to the flowmetry recording, was then performed for 10 to 20
minutes. Following palpation or treatment, a 5-minute postcontact
laser-Doppler recording was acquired. During this entire procedure, the
subject remained on the examination table, and the laser-Doppler probe
was not disturbed.
</p>
<p>
Cranial palpation (simply counting the CRI but without intervention) and
manipulation (therapeutic intervention) were performed while the
subjects were supine. The individual performing the procedure was seated
at the end of the examination table with hi or her forearms resting upon
it. The examiner’s palms conformed to the curvature of the subject’s
head, contacting the lateral aspect of the great wings of the sphenoid
bone and the temporal, occipital and parietal bones bilaterally. For
this study, similar contact pressure, firm, but light enough not to
ablate the sensation of the CRI, was employed for both palpation and
manipulation. Manipulation was directed at modulation of the rate,
rhythm, and amplitude of the CRI and perceived functional asymmetry
through equilibration of the craniocervical junction and global
anerioposterior cranial motion. Specific interventions were dictated by
the physical findings of the individual’s cranial pattern.
</p>
<h2>Results</h2>
<p>
For each subject, 4 component parts of the blood flow velocity record
were analyzed: the thermal (M) signal, the baro (TH) signal and the
respiratory signal of the THM, and the cardiac signal. The mean
precontact and postcontact data for each group were compared using the
paired-samples 2 tailed t statistic (see Table). After palpation only,
the thermal signal power decreased 3 dB (42.93 to 39.58 Db, P &lt;
.054), while the baro (39.83 to 40.10 dB, P &lt; .805), respiratory
(27.54 to 27.20 dB, P &lt; .715) and cardiac (37.92 to 37.14 dB, P &lt;
.511) signals did not change.
</p>
<p>
After cranial manipulation, the thermal signal power decreased 9 dB
(47.40 to 51.30 dB, P &lt; .021), while the respiratory (29.72 to 30.02
dB, P &lt; .747) and cardiac (41.11 to 40.70 dB, P &lt; .788) signals
did not change.
</p>
<p>
The 2 examples illustrated (see Figure), though visually exceptional,
illustrate the effects that can be obtained to varying degrees with any
subjecd, provided the treating physician possesses the requisite skill.
</p>
<h2>Comments</h2>
<p>
From the above data, we have drawn 3 conclusions. First, cranial
manipulation has an effect on low-frequency oscillations observed in
blood-flow velocity. It decreases the amplitude of the M wave and
increases the amplitude of the TH wave. Second, we conclude that cranial
manipulation affects the autonomic nervous system because it has been
demonstrated that the M an TH waves are mediated through parasympathetic
and sympathetic activity.7 Third, because palpation alone did not
greatly affect blood-flow velocity oscillations, we conclude that there
is a quantifiable difference between palpation and cranial treatment.
This conclusion suggests that palpation alone may be used as a sham
treatment in future research in the field of cranial manipulation.
</p>
<table>
<tbody>
<tr>
<td colSpan={8}>
<strong>
Traube-Hering-Mayer signal power comparison before and after
palpation only and cranial manipulation
</strong>
</td>
</tr>
<tr>
<td colSpan={2}></td>
<td colSpan={3}>
<strong>Palpation only n=13</strong>
</td>
<td colSpan={3}>
<strong>Cranial manipulation n=10</strong>
</td>
</tr>
<tr>
<td>
<strong>Signal</strong>
</td>
<td>
<strong>Doppler record segment</strong>
</td>
<td>
<strong>
Mean signal
<br />
power (dB)
</strong>
</td>
<td>
<strong>
Paired difference
<br />
before-after +/- SD
</strong>
</td>
<td>
<em>P</em>
</td>
<td>
<strong>
Mean signal
<br />
power (dB)
</strong>
</td>
<td>
<strong>
Paired difference
<br />
before-after +/- SD
</strong>
</td>
<td>
<em>P</em>
</td>
</tr>
<tr>
<td valign="top">
<strong>Thermal (M)</strong>
</td>
<td>
<strong>Before After</strong>
</td>
<td valign="top">
42.93
<br />
39.58
</td>
<td valign="top">3.36+/-5.69</td>
<td valign="top">.054</td>
<td valign="top">
47.79
<br />
38.49
</td>
<td valign="top">9.30+/-5.65</td>
<td valign="top">.001</td>
</tr>
<tr>
<td valign="top">
<strong>Baro (TH)</strong>
</td>
<td>
<strong>Before After</strong>
</td>
<td valign="top">
39.83
<br />
40.10
</td>
<td valign="top">-.27 +/-3.85</td>
<td>.805</td>
<td valign="top">
47.40
<br />
51.30
</td>
<td valign="top">-3.90+/-4.40</td>
<td valign="top">.021</td>
</tr>
<tr>
<td valign="top">
<strong>Resp.</strong>
</td>
<td>
<strong>Before After</strong>
</td>
<td valign="top">
27.54
<br />
27.20
</td>
<td valign="top">.34+/-3.23</td>
<td valign="top">.715</td>
<td valign="top">
29.72
<br />
30.02
</td>
<td valign="top">-.30+/-2.89</td>
<td valign="top">.747</td>
</tr>
<tr>
<td valign="top">
<strong>Cardiac</strong>
</td>
<td>
<strong>Before After</strong>
</td>
<td valign="top">
37.92
<br />
37.14
</td>
<td valign="top">.78+/-4.15</td>
<td valign="top">.511</td>
<td valign="top">
41.11
<br />
40.70
</td>
<td valign="top">.41+/-4.67</td>
<td valign="top">.788</td>
</tr>
</tbody>
</table>
<h2>References</h2>
<p>
1. Sutherland WG. The Cranial Bowl. Indianapolis, Ind: American Academy
of Osteopathy, 1986. (Original work published 1939).
</p>
<p>
2. Woods JM. Woods RH. A physical finding relating to psychiatric
disorders. J Am Osteopath Assoc. 1961;60:988-993.
</p>
<p>
3. Lay E. Cranial Feild. In: Ward RC, ed. Foundations for Osteopathic
Medicine. Baltimore, MD: Williams and Wilkins; 1997:901-913
</p>
<p>
4. Ferre JC. Barbin JY. The osteopathic cranical concept: fact or
fiction? Surg Radial Anat, 1991:13-65-179
</p>
<p>5. Norton JM. Dig on [Letter to the editor]. AAOJ. 2000;10(2):16:17</p>
<p>
6. Traube L. Uber periodische Thatigkeits-Aeusserungen des
vasomotorishen un Hemmungs-Nervenzentrums. Centralblatt fur die
medicinischen Wissenschaften 1865:56:881-885
</p>
<p>
7. Akselrod S. Gordon D. Madwed JB, Snidman NC, Shannon DC, Cohen RJ.
Hemodynamic regulation: investigation by spectral analysis. Am J
Physiol. 1985:249-H867-H875
</p>
<p>
8. Frymann VA. A study of the rhythmic motions of the living cranium. J
Am Ossteopath Assoc. 1971:70-928-945
</p>
<p>
9. Upledger JE. Vredevoogd JD. Craniosacral Therapy. Chicago, IL:
Eastland Press; 1983.
</p>
<p>
10. Geiger AJ. Letter to the editor. J Am Osteopath Assoc.
1992:92-1088-1093
</p>
<p>
11. McPartland JM, Mein EA. Entrainment and the cranial rhythmic
impulse. Altern Ther Health Med. 1997:3(1):40-45
</p>
<p>
12. Nelson KE, Sergueef N, Lipinski CL, Chapman A, Glonek T. The cranial
rhythmic impulse related to the Traube-Hering-Mayer oscillation:
comparing laser-Doppler flowmetry and palpation. J Am Osteopath Assoc.
2001:101(3):163-173
</p>
</Article>
);
};
export default ArticleCranialManipulation;

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import Article from "@/components/Article";
const ArticleIntervertebralDiscHerniation = () => {
return (
<Article
title="The Basics of Intervertebral Disk Herniation"
author="Brian Leonard, D.O."
>
<h1>Introduction</h1>
<p>
There are a great number of conditions and a variety of states of
illness that result in the symptom of “back/neck pain.” Back and neck
pain can be related to conditions ranging from muscle strains, somatic
dysfunction to nerve compression and anatomic anomalies.
</p>
<p>
The focus of this article is to discuss herniation of intervertebral
discs as a cause of pain. We will examine the pathophysiology and
biomechanics of disc degeneration and herniation as well as aspects of
the epidemiologic data. Lastly, it is important to mention the role that
manual/manipulative medicine plays with regard to this issue. While the
general principles of herniated discs may be applied to any level of the
spine, we will discuss each spinal level from cervical, thoracic, to
lumbar.
</p>
<h2>Anatomic Review</h2>
<p>
An intervertebral disc is formed of two elements: the nucleus pulposis
and the anulus fibrosis. The anulus fibrosis is composed of sequential
layers of fibrocartilage that envelope the nucleus pulposis. The nucleus
pulposis itself is formed of a proteoglycan and a water/gel substance
that is held loosely in place by a network of collagen and elastin
fibers. Together they form the intervertebral disc and serve to
distribute weight and force equally throughout the spine, even during
motions such as flexion and extension1. Blood vessels course along the
outer edge of the anulus fibrosis and thereby force the disc to obtain
its nutrient supply via osmosis. When the discs age, they are subject to
gradual degeneration as the water content decreases and the ability to
absorb impact diminishes. Degeneration begins on a microscopic level
around the age of skeletal maturation, or fifteen years of age. At this
time, cell densities begin to diminish, resulting in microstructural
tears and clefts (2).
</p>
<h2>Pathophysiology</h2>
<p>
The microstructural defects accumulate over time as a person ages and
the pulposis protrudes deeper into the anulus. These defects can result
in frank tears of the anulus. There are three main tears that have been
distinguished, these include:
</p>
<ul>
<li>circumferential tears or delaminations</li>
<li>peripheral rim tears</li>
<li>radial fissures</li>
</ul>
<p>
The circumferential tears represent shearing forces acting on the
interlaminar layers of the anulus fibrosis. The characteristic disc for
this type of tear is an older disc that has an advanced amount of
dessication and degeneration, retaining a limited ability to absorb
these stressors (3). The second type of tear, the peripheral rim tears,
are most frequently seen in the anterior portion of the disc and are
associated with bony outgrowths. Histologic data suggest that the actual
tears are a result of repeated microtrauma (4). Lastly, radial fissures
represent a grouping of tears that typically occur in a posterior or
posterolateral direction and are associated with degeneration of the
nucleus pulposis. These tears have been simulated in cadavers with
repeated cycles of sidebending and compression (5).
</p>
<p>
These variations of degeneration, dessication, and microstructural
defects seem to be common among studies reported in the current base of
literature. These tears, however, have not been shown to have a
correlation with the actual prolapse, or herniation, of the disc. The
tears and disc degeneration have been shown to be correlated only with
repetitive mechanical loading and cigarette smoking6 (as this inhibits
the body’s regulatory healing mechanisms in a vast number of ways). The
prolapse of the disc has been shown to correlate with heavy lifting.
That is to say, the degeneration of discs, and not the herniation,
appears to be a normal process of aging (1).
</p>
<h2>Epidemiology</h2>
<p>
For the discussion of rates of occurrence and particular mechanisms
associated with disc herniation, we will begin at the cervical level and
progress inferiorly to the thoracic and finish at the lumbar vertebrae.
</p>
<p>Cervical Disc Herniation</p>
<p>
Cervical radiculopathy, or pain in a pattern of the nerve root that is
compressed, is estimated to occur in 85 per 100,000 people in the
population. Most commonly affected regions include the seventh cervical
vertebra, C7, and the sixth cervical vertebra, C6, at rates of 60% and
25%, respectively (7). These radiculopathies in the cervical region are
commonly present in specific demographic groups. For instance, sudden
weight load on the neck while in either flexion or extension can be the
culprit. Also, in the elderly population, osteophyte formation can play
a role as previously mentioned. Sport-related injury can be more
insidious in nature, and can be attributed repetitive extension/rotation
while actively using postural muscles, as in swimming (7).
</p>
<p>Thoracic Disc Herniation</p>
<p>
Thoracic disc herniations appear to be less common than lumbar and
cervical herniations for a number of reasons. While they peak at the
third to fifth decade of life, similar to other herniations, estimates
place thoracic disc herniations only between 0.25% to 1% of all disc
herniations (10,11). One reason for decreased incidence, it is thought,
is the lesser degree of mobility in the thoracic spine due to the
presence of the rib cage. The articulation of the rib head with the
vertebral body naturally limits the amount of flexion, extension, and
sidebending. The majority of thoracic herniations occur below the level
of T7. Rib pairs 8-10 maintain a cartilaginous attachment to the
sternum, thus allowing more motion than vertebrae at higher levels. Rib
pairs 11 and 12 are known as “floating ribs” and do not maintain any
attachment to the sternum. This supports the theory that part of the
pathophysiology of herniated thoracic discs is directly related to the
ability of the segment to maintain a certain degree of flexability (12).
</p>
<p>Lumbar Disc Hernation</p>
<p>
Herniation of the nucleus pulposis of the lumbar disc is present more
commonly than the former two types. It is estimated that 95% of
herniated lumbar discs occur at the L4-L5 or L5-S1 level (13). Typical
presentation includes radicular pain that patients often describe as
shooting or stabbing pain that courses down the leg. There may also be
paresthesias present in the same distribution pattern. Often, the pain
is exacerbated by coughing, sneezing, straining, or standing for long
periods of time (14), as this increases the pressure on the disc and
therefore on the impinged nerve root. Pain is usually relieved by rest
and taking weight off of the prolapsed disc.
</p>
<p>Manual/Manipulative Medicine and Cervical Disc Herniation</p>
<p>
Considering the implications of nerve root impingement (including pain,
paresthesia, and decreased motor function) secondary to a herniated
disc, there is a natural concern regarding the safety of manual
manipulation of such an anomalous disc.
</p>
<p>
With regard to manipulation, a 2006 study was done to evaluate the
efficacy and safety of cervical manipulation in patients with spinal
cord compression and radiculopathy. The study incorporated a variety of
chiropractic techniques, including high-velocity, low-amplitude methods.
The conclusions drawn by the authors states, “The finding of cervical
spinal cord encroachment on magnetic resonance imaging, in and of
itself, should not necessarily be considered an absolute
contraindication to manipulation.” (8) The authors are specific in
mentioning exclusion criteria such as acute myelopathy or changes
indicating myelomalacia and make clear the message that special care and
astute clinical judgement need be exercised in cases of cervical
radiculopathy and pathologic segments.
</p>
<p>
A separate study suggests othewise, stating, “Cervical spinal
manipulation therapy may worsen preexisting cervical disc herniation or
cause disc herniation resulting in radiculopathy, myelopathy, or
vertebral artery compression.” (9) This study describes 22 case studies
and states in its conclusion a list of absolute contraindications
including patients with rheumatoid arthritis, acute fractures and
dislocations, os odontoideum, infection of bone, osseous malignancies,
or cervical myelopathy. These case studies included reports from
patients previously treated by chiropractors as well as osteopathic
physicians. The article puts forth the modality of surgical intervention
as the best treatment for certain cases of disc herniation and
radiculopathy.
</p>
<p>
With regard to the necessity of surgical intervention, let us consider a
2007 article from the Massachusetts Medical Society (15). The study
examines the outcomes of two groups of patients with herniated lumbar
discs who were randomly assigned to either a surgical intervention or
observation and symptom management. The study was inconclusive
statistically due to the high rate of crossover. That is, 40% of
patients assigned to the surgical intervention declined surgery because
their symptoms improved before any intervention could take place (with
observation alone). Conversely, 45% of patients referred to the
observation therapy, opted for surgical intervention due to worsening of
symptoms (15). Even though the study is scholastically inconclusive and
statistically insignificant, it does highlight the need for
individualized care.
</p>
<h2>Conclusion</h2>
<p>
As with any topic at the forefront of medicine, especially issues which
can be treated via different modalities and by different specialists,
there will be controversy, bias, and ever-emerging new evidence to
consider. This article demonstrates the basic science behind disc
degeneration leading to pathologic herniation. It also shows two sides
of a clinical debate to which there is no defined rule for treatment.
Patients, therefore, need to be evaluated and treated appropriately on
clinical grounds of their individual situation by a physician
well-versed in neuromusculoskeletal medicine to determine which specific
modality best suits the individual.
</p>
<h2>References:</h2>
<ol>
<li>
Michael A. Adams, PhD; Peter J. Roughley, PhD What is Intervertebral
Disc Degeneration, and What Causes It? Spine. 2006;31(18):2151-2161
</li>
<li>
Boos N, Weissbach S, Rohrbach H, et al. Classification of age-related
changes in lumbar intervertebral discs: 2002 Volvo Award in basic
science. Spine 2002;27:2631-44.
</li>
<li>
Goel VK, Monroe BT, Gilbertson LG, et al. Interlaminar shear stresses
and laminae separation in a disc. Finite element analysis of the L3-L4
motion segment subjected to axial compressive loads. Spine
1995;20:689-98.
</li>
<li>
Hilton RC, Ball J. Vertebral rim lesions in the dorsolumbar spine. Ann
Rheum Dis 1984;43:302-7
</li>
<li>
Adams MA, Bogduk N, Burton K, et al. The Biomechanics of Back Pain.
Edinburgh, UK: Churchill Livingstone; 2002
</li>
<li>
Battie MC, Videman T, Gill K, et al. 1991 Volvo Award in clinical
sciences. Smoking and lumbar intervertebral disc degeneration: An MRI
study of identical twins. Spine 1991;16:1015-21
</li>
<li>
Malanga, Gerard A MD Cervical Radiculopathy. Spine 2006 accessed via
emedicine
http://www.emedicine.com/sports/TOPIC21.HTM#section~AuthorsandEditors
</li>
<li>
Murphy, DR; Hurwitz, EL; Gregory AA. Manipulation in the presence of
cervical spinal cord compression: a case series. J Manipulative
Physiol Ther. 2006 Mar-Apr;29(3):236-44
</li>
<li>
David G. Malone, M.D., Nevan G. Baldwin, M.D., Frank J. Tomecek, M.D.,
Christopher M. Boxell, M.D., Steven E. Gaede, M.D., Christopher G.
Covington, M.D., Kenyon K. Kugler, M.D. Complications of Cervical
Spine Manipulation Therapy: 5-Year Retrospective Study in a
Single-Group Practice. Neurosurg Focus 13(6), 2002. © 2002 American
Association of Neurological Surgeons
</li>
<li>
Fisher, C., Noonan, V., Bishop, P., Boyd, M., Fairholm, D., Wing, P.,
et al. (2004). Outcome evaluation of the operative management of
lumbar disc herniation causing sciatica. Journal of Neurosurgery, 100,
317–324.
</li>
<li>
Strayer, Andrea J Lumbar Spine: Common Pathology and Intervention J
Neurosci Nurs. 2005;37(4):181-193
</li>
<li>
Thomas L. Schwenk, MD Is Surgery Necessary for Lumbar Disc Herniation?
Journal Watch. 2007;5(11) ©2007 Massachusetts Medical Society
</li>
</ol>
</Article>
);
};
export default ArticleIntervertebralDiscHerniation;

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import Article from "@/components/Article";
const ArticleNeuralBiologicalMechanisms = () => {
return (
<Article
title="Neural Biological Mechanisms"
author="Richard A. Feely, D.O., FAAO, FCA, FAAMA"
>
<p>
The goal of this article is to provide the clinician with information
and knowledge of known biological mechanisms involved in somatic
dysfunction.
</p>
<p>The reader will have the ability to describe:</p>
<ul>
<li>
The neural endocrine-immune network and its relationship to somatic
dysfunction
</li>
<li>How somatic dysfunction is endocrine-controlled and maintained</li>
<li>
Some of the known mechanisms of how somatic dysfunction is altered
biomechanically, biochemically, and bioenergetically
</li>
</ul>
<p>
The human body is a complex interdependent relationship of structure,
function, and mind. The body possesses complex homeostatic mechanisms
that maintain equilibrium for self-regulation and self-healing. These
homeostatic mechanisms represent an integrated network of messenger
molecules produced by cells in neural, endocrine, and immune systems.
Their signal coding and messenger molecules communicate through receptor
complexes located on cell membranes. The critical role of the nervous
system, especially the lymphatic, forebrain, and hypothalamus,
influences the output of the endocrine and immune systems.
</p>
<h2>Traditionally, the Immune and Nervous Systems</h2>
<p>
Traditionally, the immune and nervous systems were considered separate
and independent, each with its own cell types, cell functions, and
intercellular regulators. Altered function in each system was related to
the disease considered specific to that system. We now recognize not
only the interdependence and interlocking molecular organization but
also their extensive integration with the endocrine system. The
conceptual separations between the neural endocrine immune system
concerning structure, function, and communication have been discarded.
In their stead is a combination of multiple dimensional network
contributing to the functional unity of the body.
</p>
<p>
Today, we recognize this multifactorial nature is a result of the
following interactions of genetic, endocrine, nervous, immune, and
behavioral-emotional systems. This complex bi-directional interaction
occurs within the neural-endocrine-immune network. This network forms
the prime defense against disease and is responsible for the resistance
of infectious disease as well as cancer. The sensory information from
external and internal sources is tightly integrated with cognitive and
emotional processes which influence their neural endocrine immune
network through the hypothalamic-pituitary-adrenal axis.
</p>
<h2>Messengers</h2>
<p>
The basis for communication in the neural-endocrine-immune system is the
numerous messenger molecules that are released in the extracellular
fluid. These signal codes are small peptides, glycoproteins, amines, and
steroids. They express their activity through autocrine
(self-stimulating), paracrine (stimulates local tissue), synaptic, and
hormonal activity.
</p>
<h2>The Endocrine System</h2>
<p>
The endocrine system is described as using blood-borne messengers
operating over long distances by humoral transport. The neural system is
described as using chemical transmitters released into the neural
synaptic cleft, separating the pre and post-synaptic specialized nerve
cells. These common cellular mechanisms are bi-directional in
communication. Their similar molecular structure of many of the
messengers and the receptors are combined to transcend the traditional
borders that separate the neural, endocrine, and immune systems over the
years.
</p>
<p>
Monitoring the concentration of many of these extracellular messengers.
The central nervous system, particularly the limbic system and
hypothalamus, directly modulates the activity of the autonomic nervous
system and the endocrine systems. See The Network. Both of these systems
have extensive communication with the immune systems, thereby regulating
it under neural modulation as well. This combined action is
multi-dimensional and creates a compensatory reserve that enables the
body to mount an adaptive response to stressful conditions regardless of
their origin whether somatic, visceral, or psychogenic.
</p>
<h2>Stimuli-Somatic</h2>
<p>
Somatic, visceral, and emotional stimuli act as drivers capable of
influencing the activity via the hypothalamus, the spinal cord,
pituitary, to the autonomic nervous system, endocrine system, and immune
system, causing the general adaptive response. Noxious somatic stimuli
initiate protective reflexes providing the central nervous system with
warning signs. They influence the release of extracellular messengers
from the endocrine immune access system just described.
</p>
<p>
When activated by noxious stimuli such as rises from somatic
dysfunction, small capillary primary afferent fibers called alpha-gam
lambda and C-fibers, a-C-fibers or collectively referred to as (B
afferent system) from peripheral nociceptor endings, release neural
peptides such as substance P into the surrounding tissue thereby
initiating neurogenic inflammation.
</p>
<p>
The B afferent fibers systems represent a small subset of small
capillary primary afferent fibers with high threshold for activation
that are present in both somatic and visceral tissue. Central processes
of these fibers stimulate cells in the dorsal horn of the spinal cord.
Within the dorsal horn, the cells responding to the nociceptive input
initiate signals carried to the motor nuclei of the ventral horn to
alter the tonal muscles innervated by that particular spinal segment and
through the anterior lateral tract of the spinal cord which communicates
with the brain stem and the hypothalamus.
</p>
<p>
A significant result of the nociceptive input is increased activity in
the hypothalamic-pituitary-adrenal axis culminating in increased output
of norepinephrine from the sympathetic nervous system. This reflex can
be blocked by selectively eliminating the small capillary primary
afferent fibers. Capsaicin reduces the level of substance P in the
peripheral nervous system by destroying the small caliber primary
afferent fibers. This diminishes the hypothalamic response and reduces
the pituitary adrenal and autonomic responses to somatic stressors. The
neural-endocrine-immune network is affected by the output of the signals
from somatic dysfunction by initiating a compensatory shift in
extracellular messengers that then alters the function of the immune
system.
</p>
<p>
Collins and Strauss found that modulation of the sympathetic nervous
system plays an integral part in somatic pain and is a principal
mechanism of acupuncture’s action. The control of somatic sympathetic
vasomotor activity before and after the placement of acupuncture needles
resulted in pain relief by reducing sympathetic vasomotor activity.
</p>
<p>
Nakamura, et al. found that afferent pathways of diskogenic low back
pain are transmitted mainly by sympathetic afferent fibers in the L2
nerve root and after needle injection, pain dissipated.
</p>
<h2>Stimuli-Visceral</h2>
<p>
The visceral factors in the cervical, thoracic, abdominal, and pelvic
areas, as well as peripheral blood vessels, communicate with the brain
stem and spinal cord through an extensive complement of afferent fibers
also considered part of the B afferent system. The visceral afferent
fibers reach their target organs by coursing in the same nerves as the
efferent autonomic fibers. They follow the routes of the vascular
system. The visceral sensory fibers, typically small caliber and having
little or no myelin, have cell bodies located in the thoraco-lumbar
dorsal root ganglia and in ganglia of several cranial nerves. These
central processes, neurons, terminate in the superficial and deep
regions of the dorsal horn of the spinal cord.
</p>
<p>
Spinal trigeminal nucleus and solitary nucleus of the vagus. The
thoraco-abdominal and pelvic organs have extensive sensory innervations.
These afferent fibers travel to the central nervous system with efferent
autonomic fibers. These sensory fibers traveling in the parasympathetic
nerves such as the vagus carry non-noxious information for reflex
control of the organ. Those traveling with the sympathetic nerves such
as the greater splanchnic carry noxious information packets.
</p>
<p>
The neurons of the deeper portions of the dorsal horn receive extensive
convergence of information from the small caliber sensory axons arising
in both visceral and somatic sources.
</p>
<p>
A similar convergence of somatic and visceral input is seen in the
solitary nucleus of the vagus. Neurons responsive to both visceral and
somatic nociceptive stimuli are located in the spinal cord, brain stem,
hypothalamus, and thalamus. These dual response neurons provide an
explanation for the phenomenon of referred pain between visceral and
somatic sources.
</p>
<h2>Stimuli-Emotional</h2>
<p>
The emotional factors of the human effecting the neural endocrine immune
network arise largely from the limbic forebrain system and hypothalamus.
The major components of the limbic forebrain include large portions of
associated neocortex, which include the prefrontal area, the cingulate
cortex, the insular cortex, and the inferior medial aspect of the
temporal lobe. Hippocampal formation and the amygdala receive extensive
connections from the frontal parietal and cingulate associational areas
of the neocortex and in turn project to the hypothalamus from the fornix
and striaterminalis, influencing the hypophyseotropic and hypothalamic
nuclei.
</p>
<p>
This limbic forebrain areas exert considerable influence over the
pituitary gland as well as the autonomic nervous system affecting growth
hormone, ACTH, prolactin, and somatostatin. The limbic system also
increases the sympathetic output from the spinal cord. These alterations
in the neural-endocrine activity affect the metabolic processes of the
body, shifting peripheral tissue to a catabolic form of metabolism,
leading to marked changes in the function of the immune system,
including stress-induced suppression of immune function. These
conditions characterize the general adaptive response in life.
</p>
<p>
Highly stressful circumstances in life significantly alter the status of
the immune system. This can include the death of a loved one, caring for
a family member with chronic progressive disease, summer vacation,
change in lifestyle, divorce, new job, etc.
</p>
<p>
The regulation of the neural-endocrine-immune network increases
susceptibility to various disease states. Overproduction or
underproduction of extracellular messages in response to either external
or internal stimuli or as a secondary response to other
disease-dysfunctional processes result in dysfunction of many aspects of
the network. The aging process also alters the regulation of the network
and is associated with various disease-dysfunctional states.
</p>
<p>
Lundberg showed that psychosocial factors significantly associated with
back pain and shoulder problems were related to psychophysiological
stress levels, i.e., high psychophysiological stress levels and low work
satisfaction.
</p>
<p>
He also found that mental and physical stress was found to increase
physiological stress levels and muscular tension and that mental stress
is of importance for the development of musculoskeletal symptoms and
pain. In addition, mental stress is not only induced by high demands but
also by demands that are too low which happens in many repetitive and
monotonous work situations. Interestingly enough, women are more prone
than men to have somatic complaints with repetition and monotonous work.
</p>
<h2>The Network</h2>
<p>
<strong>SELECTED NEURAL REGULATORS</strong>
</p>
<ul>
<li>Catecholamines: Dopamine, Norepinephrine</li>
<li>Cholines: Acetylcholine</li>
<li>Indolamines: Serotonin</li>
<li>
Peptides: Substance P, Neuropeptide Y, Calcitonin gene-related,
Polypeptide, Enkaphalins, Endorphins, Neurotensin, Cholecystokinin,
Angiotensin II, Vasoactive intestinal polypeptide, Bombesin,
Adrenocorticotropin, Somatostatin, Corticotropin
</li>
<li>Amino Acids: Glutamate, Aspartate, GABA, Glycine</li>
<li>Dynorphin, Histamine</li>
<li>Purines: Adenosine</li>
</ul>
<h2>CELL TYPES OF THE IMMUNE SYSTEM</h2>
<ul>
<li>Thymocytes: Lymphoid Cells of the thymus</li>
<li>
T-Cells: Lymphoid cells that mature in the thymus & express the T-cell
receptor (TCR)
</li>
<li>
Helper T-Cells: Lymphoid cells responding to cell surface antigens by
secreting cytokines
</li>
<li>
Cytotoxic T-Cells: Lymphoid cells responding to the cell surface
antigens by lysing cell producing the antigen
</li>
<li>
B-Cells: Lymphoid cells that, when activated, are capable of producing
immunoglobulins
</li>
<li>
Natural Killer Cells: Lymphoid cells capable of killing tumor cells
and virus/infected cells
</li>
<li>
Neutrophils: Major Lymphoid cell of the acute inflammatory response
and effector cells of humoral immunity
</li>
<li>
Basophils: Effector cells of IgE-mediated immunity that secrete
histamine granules in response to IgE activation
</li>
<li>
Eosinophils: Lymphoid cells containing lysosomal granules that can
destroy parasites
</li>
</ul>
<h2>NON-LYMPHOID CELL TYPES</h2>
<ul>
<li>
Fibroblast: Connective tissue cell capable of secreting and
maintaining the collagenous fiber matrix
</li>
<li>
Endothelial Cell: Squamous cell lining of the inner aspect of the
vascular system
</li>
<li>
Mesangial Cells: Specialized mesenchymal cells found in the renal
glomerulus
</li>
<li>
Chromaffin Cell: Neural peptides secreting cell found in the adrenal
medulla
</li>
<li>
Enterochromaffin Cell: Neural peptides secreting cell found in the
lining of the gastrointestinal system
</li>
<li>
Hepatocyte Liver Cell: Liver cell capable of secreting the acute phase
proteins
</li>
<li>
Endometrial Cell: Epithelial cell lining the inner surface of the
uterus
</li>
<li>
Astrocyte: Neuroglial cell found in the central nervous system
involved in forming the blood-brain barrier
</li>
<li>
Oligodendrocyte: Neuroglial cell forming myelin sheath around axons in
the central nervous system
</li>
<li>
Osteoblast: Specialized mesenchymal cells capable of secreting the
osteomatrix for the formation of bones
</li>
<li>
Osteophyte: Connective tissue cell found in bone representing a mature
form of osteoblast
</li>
<li>
Reticular Cell: Endodermal cell creating a three-dimensional network
for lymphocytes in the thymus, spleen, and lymph nodes
</li>
</ul>
<h2>IMMUNOREGULATORS</h2>
<ul>
<li>Interleukins 1-7</li>
<li>Interferons alpha, beta, and gamma</li>
<li>Tumor necrosis factor, beta</li>
<li>Colony-stimulating factors:</li>
<ul>
<li>Granulocyte-stimulating factor</li>
<li>Macrophage-stimulating factor</li>
<li>Granulocyte macrophage-stimulating factor</li>
<li>Interleukin III</li>
<li>Leukemia inhibiting factor or neuroleukin</li>
</ul>
<li>Transforming factor, beta</li>
</ul>
<h2>
ENDOCRINE SUBSTANCES KNOWN TO INTERACT WITH THE NEURAL AND IMMUNE
SYSTEMS
</h2>
<ul>
<li>Pituitary</li>
<ul>
<li>Adrenal Corticotrophin-ACTH</li>
<li>Thyrotrophin-TSH</li>
<li>Growth hormone releasing factor-GRH</li>
<li>Somatostatin-SS-SS</li>
<li>Prolactin</li>
</ul>
<li>Adrenal Medullary Hormones</li>
<ul>
<li>Epinephrine</li>
<li>Norepinephrine</li>
</ul>
<li>Adrenal Cortical Hormones</li>
<ul>
<li>Cortisol</li>
<li>Corticosterone</li>
<li>Aldosterone</li>
</ul>
<li>Thyroid Hormones</li>
<ul>
<li>Thyroxine</li>
<li>Triiodothyronine</li>
</ul>
<li>Growth Hormones</li>
<ul>
<li>Somatotropin</li>
<li>Somatomammotropin</li>
<li>Somatomedin</li>
</ul>
<li>Thymus</li>
<ul>
<li>Thymulin</li>
<li>Thymosin</li>
<li>Thymopoietin</li>
<li>Thalmic factor X</li>
</ul>
<li>Others</li>
<ul>
<li>Estrogen</li>
<li>Testosterone</li>
<li>Insulin</li>
</ul>
</ul>
<h2>References</h2>
<ul>
<li>
Beal, Myron, D.O., FAAO, 1995-96 Yearbook, Osteopathic Vision,
American Academy of Osteopathy, 1996.
</li>
<li>
A.A. Buerger, Ph.D., Philip E. Greenman, D.O., Empirical Approaches to
the Validation of Spinal Manipulation, 1985, published by Charles C.
Thomas.
</li>
<li>
D. Thomas Collins, S. Strauss, “Somatic Sympathetic Vasomotor Changes
Documented by Medical Thermographic Imaging During Acupuncture
Analgesia“, Clinical Rheumatology, 1992, 55-59.
</li>
<li>
Richard G. Gillette, Ronald C. Kramis, William J. Roberts, ”
Sympathetic activation of cat spinal neurons responsive to noxious
stimulation of deep tissues in the low back“, Pain , 1994, 56, 31-42.
</li>
<li>
Ulf Lundberg, ” Methods and application of stress research“,
Technology and Health Care, 1995, 3-9.
</li>
<li>
Shin-Ichiro Nakamura, Kazuhisa Takahasi, Yuzuru Takahashi, Masatsune
Yamagata, Hideshige Moriya, ” The Afferent Pathways of Discogenic Low
Back Pain“, Bone and Joint Surgery, 1996, July; 78/B, 606-612.
</li>
<li>
Robert C. Ward, Foundations for Osteopathic Medicine, American
Osteopathic Association, 1997; Williams & Wilkins
</li>
</ul>
</Article>
);
};
export default ArticleNeuralBiologicalMechanisms;

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website/app/(pages)/articles/(content)/osteopathic-head-pain/page.tsx Normal file
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@ -0,0 +1,854 @@
import Article from "@/components/Article";
const ArticleOsteopathicHeadPain = () => {
return (
<Article title="Head Pain" author="Herbert C. Miller, D.O., FAAO">
<p>Reprinted with permission of the American Osteopathic Association.</p>
<p>
Pain has been defined in many ways, as the sensation “resulting from the
stimulation of specialized nerve endings,”‘ or, more poetically, as a
punishment or penalty, as for crime. Other definitions include acute
discomfort of body or mind, bodily or mental suffering or distress; a
distressing sensation, as in a particular part of the body, and trouble
experienced in doing something. (2) One’s concept of pain may be colored
by diverse circumstances or, in scientific language, feedback. Head pain
is usually interpreted by the clinician from the therapeutic point of
view, that is, in terms of measures that may stop in, rather than in
pathophysiologic terms.
</p>
<p>
When analyzing head pain, the physician often prefers to look at it as a
phenomenon or as the result of stimulation of specialized nerve endings.
In reality, pain may be an interpretation of bodily or mental distress.
Boshes and Arieff (3) stated:
</p>
<p>
Certain aspects of pain are predicated exclusively on a neural
substrate. Here the basis is an event or an alteration in the nervous
system per se, as contrasted to pain caused by malignant disease,
infected tissue, fractures or the like. Various divisions of the nervous
system may be implicated and a description of the disability or the
manner of posture and movement is often sufficient to enable the trained
observer to gain an impression as to whether the pain is genuine or
functional. Such involvement may be at the receptive, the conductive,
the perceptive or the apperceptive level, or combinations thereof.
</p>
<p>
This would appear to be a generally accepted concept, and yet head pain
often is described and interpreted on the basis of a symptom complex
rather than in terms of the anatomic and physiologic organization of the
central nervous system. It is the purpose of this paper to attempt to
describe some of the mechanisms involved in head pain and to provide
these mechanisms with an osteopathic orientation.
</p>
<h2>Neural Pathways</h2>
<p>
Most of the sensory nerve distribution to the head and face occurs
through the trigeminal nerve (Cr V) and fibers of cervical nerves C1,
C2, and C3 (Fig. 1.). Smith (4) stated:
</p>
<p>
The trigeminal fibers subserving pain have their neurons in the
trigeminal or semilunar ganglion which lies in a cave of the aura mater
in the middle cranial fossa just anterior to the apex of the petrous
temporal bone. The peripheral branches of the trigeminal nerve, . . .
the ophthalmic, maxillary, and mandibular nerves . . . supply a fairly
well defined cutaneous area and broadly speaking, the deep structures
underlying it. There is little overlap with the adjoining cutaneous
fields of the cervical nerves….
</p>
<p>
The glossopharyugeal nerve supplies common sensibility to the posterior
third of the tongue, the pharynx, soft palate, tonsils and fauces, the
auditory tube, the tympanic cavity and mastoid air cells, and the inner
lining of the eardrum. The vagus nerve . . . supplies the general
somatic afferent fibers to the posterior portion of the external
auditory canal, part of the eardrum, and the skin of the cranial surface
of the auricle adjoining the scalp.
</p>
<p>
The pain and temperature fibers of the glossopharyngeal and vagus nerves
relay to the nucleus of the descending trigeminal tract.
</p>
<p>
The cutaneous distribution of C I is not consistent. Larsell (5) said:
</p>
<p>
Occasionally it gives a cutaneous branch to the skin of the upper part
of the back of the neck and the lower part of the scalp.
</p>
<p>
The second cervical nerve chiefly supplies the area of the head and neck
adjoining the trigeminal territory, to which the third cervical nerve
contributes fibers. (4)
</p>
<p>Kimmel (5) stated:</p>
<p>
The nerve fibers supplying the cranial aura mater are derived from the
trigeminal nerve, the upper three cervical nerves, and the sympathetic
trunk. Nerve branches from the upper three cervical nerves and the
superior cervical ganglion supply the aura mater of the posterior
cranial fossa. The aural nerves derived from the three divisions of the
trigeminal nerve and from the sympathetic plexuses on the internal
carotid and middle meningeal arteries supply the remainder of the
cranial aura mater.
</p>
<p>
The first division of the trigeminal nerve supplies the aura mater in
the anterior cranial fossa, the diaphragm sellae, nearly all of the
cerebral falx, the tentorium cerebelli, part of the superior sagittal
sinus, the straight sinus, the superior wall of the transverse sinus,
and the terminal parts of the cerebral veins entering these sinuses.
</p>
<p>
The maxillary division of the trigeminal nerve supplies the aura mater,
covering the anterior part of the middle cranial fossa. Branches of the
third, or mandibular, division of the trigeminal nerve supply the aura
mater in the posterior and lateral parts of the middle cranial fossa and
the aura mater lining most of the calvaria. (6)
</p>
<p>
Perhaps the more important aspect of pain is that it is not a single
identifiable entity. It may be represented by vastly complicated and
intricate processes or by the mere experiencing of the touch of a sharp
object. The integration of actual pain reception and perception
represents an area of widely diverse opinion. On the basis of the
observation that successive surgical interruptions of peripheral nerves,
posterior roots, spinal cord, and thalamus, and ablations of portions of
the cerebral hemispheres, may all fail to give permanent relief from
pain, Gooddy (7) concluded that “any nervous pathways are potential
‘pain pathways.’ ”
</p>
<p>
Pain stimuli (or at least somatesthetic stimuli interpreted as pain)
arising from the spinal cord (C1, C2, and C3) pass principally to the
cuneate nucleus (homolateral), synapse, cross at this level, and ascend
to the ventrolateral nucleus of the thalamus.(8)
</p>
<p>Finneson (9) stated:</p>
<p>
The function of the thalamus is to pass impulses on to the
cerebralcortex, and it is presumed that these impulses are integrated by
the association nuclei in the thalamus before being relayed. The portion
of the thalamus that projects impulses to a specific cortical area
receives in return corticothalamic projection fibers from that area,
forming a circuit between thalamus and cortex.
</p>
<p>
Smith (4) said that pain fibers of the great auricular nerve synapse in
the substantia gelatinosa Rolandi, from which second order neurons
ascend in the lateral spinothalamic tract to the posteroventral nucleus
of the thalamus. He added:
</p>
<p>
Pain fibers from the trigeminal nerve have their cell bodies in the
semilunar ganglion…. Their central processes descend, as the spinal
tract of the trigeminal nerve, in the lateral brain stem from the upper
pons to the C-2 level of the cord or even somewhat lower, to terminate
in the associated spinal trigeminal nucleus which lies adjacent and deep
to the tract. The spinal tract and the spinal nucleus correspond to and
are continuous with the dorsolateral fasciculus of the cord and the
substantia gelatinosa respectively.
</p>
<p>
Pain afferents from the face, arriving via the trigeminal,
glossopharyngeal, and vagal routes, relay to the portion of the spinal
nucleus lying below the inferior limit of the fourth ventricle….
</p>
<p>
Second order neurons from the spinal trigeminal nucleus cross the
midline . . . at the ventral secondary tract to ascend on the medial
aspect of the lateral spinothalamic tract to gain the thalamus. There is
doubt as to the thalamic termination of these fibers. The classic view
is that the trigeminal lemniscus (combining the ventral and dorsal
secondary trigeminal tracts) projects to the medial portion (arcuate
nucleus) of the posteroventral nucleus of the thalamus…. From the
posteroventral nucleus of the thalamus, third order neurons pass in the
sensory radiation via the posterior limb of the internal capsule to the
somatic sensory area of the cortex in the lowest portion of the
postcentral areas (Brodmann’s areas 3. 1. 2) just above the fissure of
Sylvius. There is evidence of the face being represented bilaterally in
the thalamus and cortex…. It is likely that the thalamus is responsible
for the recognition of pain but that the perception of pain as a mental
event requires cortical participation-probably diffuse and generalized
cortical participation….
</p>
<p>
There is also evidence that pain pathways from both cord and medulla
relay bilaterally in the reticular formation of the brain stem and
ascend by slow, multisynaptic routes to the medial thalamic nuclei and
become part of the diffuse thalamic system. The latter system, which is
thought to control the general level and direction of attention. May
also be responsible for the affective coloring of pain.
</p>
<h2>Vascular Elements</h2>
<p>
The sensitiveness of the vascular elements has been discussed by Wolff
(11). His investigation showed consistent sensitiveness to compression,
stretching, and faradic stimulation in the arterial system. The great
venous sinuses were less sensitive than the arteries to these stimuli,
and the lesser sinuses and veins lost sensitiveness in proportion to
their distance from the greater sinuses.
</p>
<p>Crosby and associates (11) stated:</p>
<p>
The blood vessels of the head receive their preganglionic sympathetic
innervation from T-1 to T-2, but C-8 and T-3 and even T-4 may also
contribute. The axons pass out into the sympathetic chain and ascend to
synapse in the stellate and the superior cervical sympathetic ganglia.
The postganglionic fibers distribute from the superior cervical
sympathetic ganglion with the external and internal carotid arteries to
the head. The intracranial postganglionics follow along the internal
carotid artery to the circle of Willis and along branches of the
external carotid and distribute to the adventitia and the smooth muscle
of intracranial vessels, including arterioles of the pie mater, but not
to the blood vessels in the brain substance. Postganglionic fibers also
distribute to the middle meningeal artery. The plexuses along the common
carotid and the internal carotid are not continuous with those on the
external carotid, so that stripping the plexuses from the common and
internal carotids will not destroy the sympathetic supply to the blood
vessels of the face and the head. Postganglionic fibers from the
stellate ganglion ascend along the vertebral arteries and the basilar
artery….
</p>
<p>
A parasympathetic innervation to some of the blood vessels of the head
likewise has been demonstrated. Preganglionic parasympathetic fibers of
the facial nerve turn off in the region of the geniculate ganglion to
run in the great superficial petrosal nerve to the plexus on the
internal carotid artery. Postganglionic fibers from small clusters of
ganglion cells on the blood vessels distribute as vasodilators of the
vessels.
</p>
<p>
The vascular tone (sympathetic-parasympathetic influence) appears to be
mediated through the forebrain with connections in the hypothalamic
nuclei. Crosby and associates (11) wrote:
</p>
<p>
The pathways by which these impulses are discharged to hypothalamic and
midbrain segmental areas . . . constitute the various
cortico-hypo-thalamic . . . systems and the cortico-thalamo-hypothalamic
tracts by way of the dorsomedial thalarnic nucleus.
</p>
<p>
It seems probable, as others have suggested, that the cortical paths are
regulatory over the hypothalamic systems…. The pathways in general
provide for emotional accompaniments to cortically initiated motor
responses carried over pyramidal and extrapyramidal systems. . . .
Evidence has been forthcoming that pyramidal as well as extrapyramidal
systems carry corticofugal fibers for autonomic centers of the spinal
cord.
</p>
<p>
Before proceeding to a discussion of the types of stimuli that may be
interpreted as pain, the character of nerve endings present in the
meninges and associated structures of the head and neck should be
considered in order to clarify the types of stimuli that may give rise
to pain. Crosby and associates (11) wrote:
</p>
<p>
The sensory terminations in the aura have been studied by various
observers…. The nerve endings at the base of the skull are less numerous
than on the convexity. They are in the form of end-branches knob- or
club-shaped terminations, or are like balls of twine.
</p>
<p>
They reported that Meissner corpuscles are associated with the finest
tactile sensation. The Golgi-Mazzoni receptor is said to be a pressure
receptor, of similar function to the Pacini corpuscle. The Krause
corpuscle has been associated with discrimination of low temperatures.
It has been suggested (11) that it may function to distinguish cool
rather than cold. Ruffini end organs appear to serve in more than one
type of receptor. The larger Ruffini endings serve as pressure endings,
while smaller endings of this type are present in the subcutaneous
connective tissue and are regarded as receptors of warmth. (11) Golgi,
Meissner, and Pacini corpuscles have been described as receptors of
discrimination in joint motion. They are credited with reporting motion
characteristics in regard to rate of position change, direction of
motion, and force required to produce position change. (12)
</p>
<h2>Characteristics</h2>
<p>
Now that the involved circuitry has been described, pain itself may be
considered. Pain may result directly from factors originating outside
the body (a sharp object or excessive heat), from pathophysiologic
changes within the body (sustained muscle tension or a tumor) or from
abnormally mediated psychologic factor~ through autonomic response. Pain
may result from mechanical or psychologic stimulation or a combination
of these. It may be described, then, as a response to stimuli that
threaten tissue integrity or organizational integrity of the body unit.
</p>
<p>
Various authors have classified pain according to the particular portion
of the nervous system immediate!! Responsible for the transmission of
the stimulus to the central nervous system. As Boshes and Arieff (3)
said pain may be classified as being at the receptive, the conductive,
the perceptive, or the apperceptive level, at a combination of these.
</p>
<p>
Pain must be discerned as a local, projected, or referred phenomenon.
Localized pain is restricted to the immediate area of reception, as in
pain in a toot from an apical abscess. Projected pain in the head may be
exemplified by trigeminal neuralgia, which Magoun (13) stated is . . .
</p>
<p>
apparently due to restriction in the aural investiture of the root as
passes over the petrous ridge, in Meckel’s cave housing the ganglia or
in the sleeves around the three branches as they exist from the skull.
</p>
<p>
ain is projected at times over the entire hemiface served by the nerve.
Referred pain may be exemplified by reference to the face of thrombosis
of the posterior inferior cerebellar artery. (4)
</p>
<p>
Although these classifications of pain overlap to some degree, the use
of a combination of classification helps to explain various phenomena of
pain production. The Patient waiting for the attention of the dentist or
surgeon may suppress pain mentally and say, “It doesn’t hurt as it did
yesterday,” until the approach of the time for local anesthetic
preparation. Then a touch by any object may produce a unique response in
the area of attention. The apperceptive mechanisms, mediated through the
nuclei of the thalamus and modified through the cortifugal control
systems of the cerebellum, (14-17) plus the pituitary-adrenal
hyperfunction due to fear, cause pain uniquely individualized by the
patient’s level of apprehension. The cortifugal controls exerted through
the cerebellum modify the intensity of activity occurring both on a
motor level and through the thalamic nuclei. It appears that damage to
or suppression of the control system may be responsible for the
rigidity, hyperactivity, dysmetria, ataxia, and epileptiform activity
exhibited by patients with brain damage or trauma.(15)
</p>
<p>
Sutherland (18) described his observations and conclusions in reference
to stress mechanisms involving the aura mater and cranial sutures. The
observations of the various types of nerve endings in the leptomeninges
make the information supplied by stress on the aura mater and pie mater
available to the centers of perception, apperception, and motor
activity. It has been demonstrated (19) that the recurrent meningeal
nerves in the spinal area (especially the branches that enter through
the foremen magnum along with the internal carotid artery) are derived
from the sympathetic trunk and supply the aura mater lining the
posterior cranial fossa. This distribution makes available to this area
information from the outer layers of the cranial aura mater, which forms
the periosteum of the cranium, and the inner layer, which forms the
investing aura of the brain (the tentorium cerebelli, falx cerebri, and
falx cerebelli), and from the spinal cord meninges and supporting
ligaments.
</p>
<p>
Ray and Wolff (20) in 1940 studied the probable causes of headache or
head pain in relation to the aura mater from observations made on 30
patients during surgical procedures on the head; they concluded that the
pains result primarily from inflammation, traction, displacement, and
distention of pain-sensitive structures, of which cranial vascular
structures are most frequent and widely distributed. Unfortunately, they
failed to mention until Wolff’s later work (10) that the actual pain
sensitive nerve endings are located in the aura mater, the arachnoid,
and the pie mater supporting the vascular structures. These factors cast
new light on the observations of Sutherland, especially since the aura
mater on the internal surface of the cranium is continuous with the
periosteum of the head.
</p>
<p>
No studies have been published to support the possibility of a strain
gauge type of reporting across the sutures, but the observation of the
sensory distribution to the internal and external surfaces of the
cranial vault would appear to make such an arrangement feasible. (4, 6)
</p>
<p>
The information available indicates that essentially the same types of
stimuli elicit painful reactions whether they arise inside or outside
the cranium. Psychologic modification, through mechanisms mentioned, is
most likely to affect those areas of reception most easily observed
through the special senses, such as sight and hearing.
</p>
<p>
Since involvement of the special senses introduces the possibility of
modification of afferent stimuli by the limbic system, Aird (21) stated:
</p>
<p>
Neurophysiologic evidence has suggested that this portion of the nervous
system is concerned with smell, taste, and other special senses, the
gastrointestinal system and other autonomic functions, and behavioral
reactions.
</p>
<p>
This brings pain into the area of psychoneurophysiologic processes of
reception, conduction, and perception to the stage of apperception or
total integration of the process of interpreting pain, and a possible
introduction of the subject of pain threshold (which is beyond the scope
of this paper).
</p>
<p>
It should be mentioned that there are definite interrelations between
the cortifugal system, mentioned earlier, and the limbic system, which
as yet are not clearly defined.
</p>
<h2>Osteopathic Approach</h2>
<p>
The foregoing discussion has described the circuitry necessary for the
identification and response to head pain. Feedback mechanisms necessary
to establish a cybernetic model have been outlined. On the basis of this
description it should not be difficult for the knowledgeable physician
to apply therapeutic measures. The knowledgeable osteopathic physician
possesses the palpatory skills to intervene directly in the
pathophysiologic process. Pain in the head, through the mechanism
described, produces palpable reflex area or tissue response, in the
superficial tissues such as the skin, the muscle, and deep connective
tissues. By discriminatory palpation he can determine the relative
duration or stage of chronicity of the condition and apply therapy.
</p>
<p>
Hoover (22-25) has written extensively and descriptively in regard to
application of technique to the various ages or stages of the process
involved in stress. He described a functional technique as opposed to
structural technique. By this technique the physician may affect the
established cybernetic system by entering the system as an aid in
diminishing the stress system established. In this mode of treatment
enough force is exerted, through the various planes of motion of
accommodation of the tissue or articulation, to bring the structures
involved to a point of what Hoover called “dynamic reciprocal balance.”
(25) In this way the physician establishes a servocybernetic system
which allows the tissue or articulation to establish a new state of
equilibrium within the limits of its ability to accommodate
physiologically. Hoover (24) stated:
</p>
<p>
Treatment by functional technic depends upon and is directed by the
reaction of a part of the patient to demands for activity made upon that
part.
</p>
<p>
By the recruitment of the demonstrable changes in tissue and its
activity, it is possible for the palpating hand to discern the
cybernetic mechanisms involved in the origin of head pain.
</p>
<p>Harvey (25) stated:</p>
<p>
A basic cybernetic mechanism is “feedback.” This is the process of
transferring energy or information from the output of a circuit to its
input and is a generally accepted control mechanism in all types of
self-regulating systems that use closed-loop, negative feedback
networks.
</p>
<p>
I have not found active and passive joint motion palpation to be
sufficiently discriminating in the analysis of such cybernetic
mechanisms to allow me to enter into a servocybernetic relation with the
patient on a therapeutic level. After observation of several highly
skilled osteopathic physicians in their approaches to palpation and
treatment of a wide variety of pathophysiologic processes and syndromes,
a method of diagnostic palpation became apparent. As the newly found
method was used, its applications and uses began to reveal themselves,
and this continues. Articles (27, 28) have been published by two of the
highly skilled physicians whose work has been observed. The use of the
principles presented by these physicians allows one to determine the
area or areas of stress and the character of the assault involved and to
counteract their deleterious effects.
</p>
<p>
The previous discussion of mechanisms in the central nervous system
covered what is presently known of the circuitry involved in feedback
mechanisms of the human body in relation to head pain. After the
physician has determined the areas of stress and the character of the
assault, he bases his treatment on the counterbalancing of the stress
forces, that is, changing the characteristics of the input and feedback,
so as to create a servocybernetic system. Establishing controlled input
alters the level of control influence exerted by the negative feedback
network.
</p>
<p>
The completion of treatment for any particular time is signaled by
improved physiologic reaction of the tissues involved, that is, an
increase in activity in hyperactive tissue, and a synchronous motion
(internal or external rotation; flexion or extension) with the basal
respiratory cycle or primary respiratory mechanism, as defined by
Magoun. (13) This allows the patient to establish a new level of
homeostasis compatible with his or her ability at any particular time to
recover from the original assault.
</p>
<p>
Stress patterns of considerable duration complicated by numerous
overlying injuries have responded in a surprising manner to treatment
applied in this manner.
</p>
<h2>Case Report</h2>
<p>
A 44-year-old white woman was admitted to the hospital with a chief
complaint of severe headaches, which occurred in the left occipital area
and radiated to the left temporal bone and vertex of the skull. The
headaches were associated with nausea and vomiting. Their onset was
associated with an automobile accident that had occurred six years
before this admission. Following the accident hemianesthesia involving
the left arm, leg, and side of the face developed. At that time the
patient had been hospitalized for 22 days. Her condition improved with
bed rest, but she had not been freed of pain, and paresthesia of the
left arm, leg, and side of the face remained. She was unable to turn
from a supine position to a left lateral recumbent position. It was not
clear whether this was due to weakness, loss of proprioception, or loss
of motor control. The patient had spent a total of 66 days in the
hospital over the next two years for paresthesia of the left side of the
body and headache (hemicephalgia on the left). The patient said that she
had not been unconscious at the time of or after the accident. There was
no familial history of neurologic disease or headache.
</p>
<p>
During the six years after the accident the patient had received nearly
every know type of therapy for cephalgia and migraine, including
administration of narcotics and adrenocorticoids and trigger-point
injections.
</p>
<p>
The patient’s surgical history included appendectomy, cesarean section,
and total hysterectomy. Neurological examination did not demonstrate any
abnormality, and the cellular structure of the cerebrospinal fluid and
the chemical contents were not remarkable. The pressure of cerebrospinal
fluid was in the middle of the normal range, and the Queckenstedt test
did not show abnormality. Laboratory tests, including complete blood
count, measurement of fasting blood sugar an creatinine, urinalysis, and
the VDRL test for syphilis at the time of admission and discharge showed
no abnormality. X-ray examination at the time of admission showed what
appeared to be an articulation between the posterior tubercle of the
posterior arch of the atlas an the occiput, and a decrease of the normal
lordotic curvature of the cervical spine, that is, a reversal the normal
cervical curve.
</p>
<p>
After a week’s hospitalization, I was called in consultation, and my
examination elicited the following additional findings: decrease in
backward bending the cervical spine, decrease in mobility in all
direction through the occipito-atlanto-axial articulation flattening of
the cervical lordotic curvature, bilateral compression through the
sacroiliac articulation sphenobasilar compression of the cranial
mechanic, with vertical strain (spheroid high), side bending rotation,
with convexity to the left, and slight torsion on the right. The entire
paravertebral mass from occiput to sacrum was under extreme tension.
</p>
<p>
The findings were compatible with the following diagnosis: Spinal
ligamentous strain and sprat (spheroid high), left side bending
rotation, and right torsion of the cranial mechanism. Treatment was
directed at relieving the stress on the meninges an vascular channel
throughout the cranial sacral mechanism to reduce edema, muscle tensions
and spasm and to reduce the level of afferent CNS input to establish a
more physiologic level of function.
</p>
<p>
Both cranial treatment and fascial release technique were directed to
the sphenobasilar vertical strain suboccipital area, and sacrum because
of the hyperirritability of these tissues and their inability to react.
The patient was not treated again for 48 hours because of other demands
on the physician’s time. At the second treatment the tissue reaction was
much improved, an the patient could withstand deeper treatment to the
involved area without excessive pain or tissue reaction After this
treatment the patient’s cervical spine was reexamined
roentgenologically, and the films showed that the posterior arch of the
atlas was no longer in contact with the occiput and that there was
improvement in the cervical anteroposterior curvature. The patient’s
pain decreased over the next 24 hours, and she was released from the
hospital to be seen at my office within 48 hours. The patient was seen
twice a week for the next three weeks. At the end of this time the
patient had been free of pain for approximately 10 days, end that length
of time between treatments was extended to, a week.
</p>
<p>
As the patient’s tissue response improved, the interval between
treatments was lenghtened correspondingly, without recurrence of severe
headaches until her daughter, who had a congenital cardiac valvular
lesion, told her parents she was pregnant. Headaches recurred, but
responded well to treatment. They recurred frequently but were
terminated on the arrival for a normal healthy granddaughter. At the
time of this report the patient still was seen on occasion for
maintenance and preventive treatment
</p>
<h2>Treatment Discussion</h2>
<p>
The treatment of this patient was carried out according to the
principles already described.
</p>
<p>
After routine physical examination a thorough palpatory examination was
carried out. Palpation began at the sacral area. With the patient in the
supine position, her sacrum was cupped in the examiner’s left hand, with
the first finger extending over the right sacroiliac articulation to
make contact with the right iliolumbar ligament (lower portion). The
little finger was placed at the left sacroiliac articulation and the
second and third fingertips placed just lateral to the tip of the
spinous process of the fifth lumbar segment of the spine. Light
palpation demonstrated relatively little activity of the tissues. When
palpation was deepened it demonstrated a rigidity of the ligamentous
structures supporting the sacroiliac articulations both anteriorly and
posteriorly and extreme tension through the iliolumbar ligaments
bilaterally.
</p>
<p>
The examining procedure is as follows: Light palpation is carried out
with light contact with skin. The depth of palpation is increased by
establishing a fulcrum and gently increasing the tension or pressure
distal to the fulcrum so that the palpating hand may remain relaxed and
be used as a palpating instrument rather than attempting to constantly
monitor its own proprioceptive phenomena. The pressure is gently
increased until reaction is stimulated in the layer of tissue the
examiner wishes to palpate. The resulting tissue reaction will
demonstrate to the examiner the resultant force (the summation of the
various forces exerted at the time of injury) that elicited the
protective reaction of the tissues under examination.
</p>
<p>
The transition from examination to treatment is a matter of following
the resultant force to the point of dynamic reciprocal balance and
maintaining this balance until the tissues complete their accommodation.
This accommodation is accompanied with increased tissue relaxation, a
feeling of increased tissue vitality, and a longitudinal to-and-fro
motion corresponding to the primary respiratory cycle.
</p>
<p>
If continued force is applied to the injured tissues after the immediate
response, the ensuing fatigue may result in an adverse or excessive
reaction of the treated tissues, which appears to create a type of
kinesthetic shock (a dissociation of the proprioceptive motor feedback
mechanism resulting in a loss of coordinated, previously programmed or
learned motion patterns with an increase in sensitiveness and possibly
pain in the particular ligaments and connective tissues. This causes
gait or motion aberration that is not typical of the individual. This
usually occurs in a single member or limb or segment of such member or
limb.
</p>
<p>
Each area found to be involved in the total stress mechanism is treated
in a similar manner, the only differences being in the method of
application of the testing or treating forces to accommodate the
peculiarities of anatomic structure, of the region under study and
treatment. In the cervical area palpation is performed along the lateral
margin of the paravertebral mass that is located over the articular
pillar. This permits palpation of the paravertebral mass, the
periarticular ligaments, and the reaction of the musculature attached to
the anterior aspects of these vertebral segments. In palpation of the
cranium, the index finger approximates the lateral aspect of the great
wing of the spheroid; the second finger is placed posterior to the
sphenosquamal articulation; the third finger is placed at the
parietotemporo-occipital articulation (asterion), and the little finger
is placed on the occiput.
</p>
<p>
This contact is often altered to suit unusual injury patterns, but in
any case the application of treatment follows the same basic principles.
The fulcrum is usually established by crossing the thumbs. The flexor
pollicis longus muscle of each thumb is utilized to maintain good
contact and allow the hands to remain as relaxed as possible. Thus the
hands may be free to move within the demonstrated force mechanisms and
establish the dynamic reciprocal tension necessary to allow the tissues
to overcome injury force mechanisms. The mastering of this type of
therapeutic and diagnostic approach is not difficult but requires
studious concentration to avoid hindering the activity of the tissues,
so that they may reveal the stress patterns to which they have been
subjected. The physician must remain relaxed and observant so he may
participate in assisting the tissues to reach and maintain the point of
dynamic reciprocal tension.
</p>
<h2>Comments</h2>
<p>
The studies reviewed here demonstrated the possibility that pain may
arise from the neck and possibly lower levels. In many cases the
involvement of arthrodial articulations may require more stringent or
forceful modes of treatment than those described here. Hoover (22)
described the use of high velocity manipulation to accomplish a
“popping” of the joint so that the involved levels of discrimination
must rearrange their synaptic organization in response to shock produced
by the forceful articulatory motion. By this method a new level or at
least a different degree of function is established.
</p>
<p>
The little understood mechanisms of the central nervous system are
slowly revealing their intricacies through the devoted efforts of many
dedicated and curious researchers. These workers can divulge their
observations, but it becomes the responsibility of the physician to be
aware of their discoveries, analyze the information, and apply it
discreetly in clinical situations. The information presented here may
give the osteopathic physician a slightly different view and increase
the effectiveness of his application of osteopathic manipulative therapy
to his patient.
</p>
<p>
The neuroanatomy and physiology involved in head pain have been
discussed. Various types of input that may be characterized as pain have
been mentioned, and mechanisms involved in the apperception as pain have
been demonstrated. An attempt has been made to correlate the wide
varieties of osteopathic manipulative approach to the particular
situation in which pain is expressed in the head. A case history
exemplifying my approach to such problems has been presented and the
principles of treatment described.
</p>
<h2>References</h2>
<p>
Dorland’s illustrated medical dictionary. Ed. 24. W.B. Saunders Co.,
Philadelphia, 1965
</p>
<p>
1. Emery, H.G., and Brewster, K.G., editors: New century dictionary of
the English language. Appleton-Century-Crofts, Inc., New York, 1959
</p>
<p>
2. Boshes, B., and Arieff, A.J.: Clinical experience in the neurologic
substance of pain. Med Clin North Am 52:111-21, Jan 68
</p>
<p>3. Smith, B.H.: Anatomy of facial pain. Headache 9:7-13, Apr 69</p>
<p>
4. Larsell, O.: The nervous system. In Human anatomy. By H. Morris. Ed.
11, edited by J.P. Schaeffer. Blakiston Co., New York, 1953
</p>
<p>
5. Kimmel, D.L.: The nerves of the cranial aura mater and their
significance in aural headache and referred pain. Chicago Med Sch Quart
22:16-26, Fall 61
</p>
<p>6. Gooddy, W.: On the nature of pain. Brain 80:11831, 1957</p>
<p>
7. Netter, F.H.: Nervous system. Vol. 1. Ciba collection of medical
illustrations. Ciba Pharmaceutical Co., Summit, N.J., 1953
</p>
<p>
8. Finneson, B.E.: Diagnosis and management of pain syndromes. Ed. 2.
W.B. Saunders Co., Philadelphia, 1969
</p>
<p>
9. Wolff, H.G.: Headache and other headpain. Ed.2. Oxford University
Press, New York, 1963
</p>
<p>
10. Crosby, E.C., Humphrey, T., and Lauer, E.W.: Correlative anatomy of
the nervous system. Macmillan Co., New York, 1962
</p>
<p>
11. Korr, I.M., and Buzzell, K.A.: Personal communication to the author
</p>
<p>
12. Magoun, H.I.: Osteopathy in the cranial field. Ed.2. Journal
Printing Co., Kirksville, Mo., 1966
</p>
<p>
13. Steriade, M.: The cerebello-thalamo-cortical pathway. Ascending
(specific and unspecific) and corticofugal controls. Int J Neurol
7:177-200,1970
</p>
<p>
14. Gerstenbrand, F., et al.: Cerebellar symptoms as sequelae of
traumatic lesions of upper brain stem and cerebellum. Int J Neurol
7:271-82, 1970
</p>
<p>
15. Snider, R.S., Mitra, J., and Sudilovsky, A.: Cerebellar effects on
the cerebrum. A microelectrical analysis of somatosensory cortex. Int J
Neurol 7:141-51, 1970
</p>
<p>
16. Ito, M.: Neurophysiological aspects of the cerebellar motor control
system. Int J Neurol 7:162-76, 1970
</p>
</Article>
);
};
export default ArticleOsteopathicHeadPain;

465
website/app/(pages)/articles/(content)/the-trauma-of-birth/page.tsx Normal file
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@ -0,0 +1,465 @@
import Article from "@/components/Article";
const ArticleTheTraumaOfBirth = () => {
return (
<Article title="The Trauma of Birth" author="Viola M Fryman, D.O.">
<p>
The newborn skull is designed to provide maximum accommodation to the
forces of labor and minimum trauma to the developing brain. However,
injury to the head during birth is more common than many people realize.
</p>
<p>
In a study of 1,250 newborns I conducted a few years ago, it could be
demonstrated that severe visible trauma was inflicted on the head–either
before or during labor–in 10 percent of the infants. Membranous
articular strains, which could be detected by the physician proficient
in the diagnostic techniques of osteopathy in the cranial field, were
present in another 78 percent. Thus, nearly nine of every 10 infants in
the study had been affected. (1)
</p>
<p>
How important are these membranous articular strains to the physician? I
have found that common problems of the neonatal period–such as
difficulty in sucking, vomiting, nervous tension, and irregular
respiration–are frequently overcome just as soon as these strains are
corrected. Similar strains are encountered in school children who have
learning and behavior problems.
</p>
<p>
In a study of 100 children between the ages of five and 14 who were
having learning or behavioral difficulties, it was found that 79 had
been born after a long or difficult labor and had one or more of the
common symptoms of the neonatal period. Also, it is my impression that
many cases of childhood allergy can be traced to musculoskeletal strains
originating at the time of birth. (2) And vertebral scoliosis occurring
in childhood and adolescence is, in many instances, the consequence of
cranial scoliosis originating during birth. (3 ) Thus, recognition and
treatment of dysfunction of the craniosacral mechanism in the immediate
postnatal period represent one of the most, if not the most, important
phases of preventive medicine in the practice of osteopathic medicine.
</p>
<p>
To gain a clearer understanding of the origin and nature of these
membranous articular strains, it will be helpful to review the anatomic
features of the newborn skull and to note how they are affected by the
forces of labor.
</p>
<h2>Labor</h2>
<p>
As was mentioned above, the newborn skull is designed to provide maximum
accommodation to the forces of labor, minimum trauma to the infant’s
brain, and complete restoration to free mobility of all its parts once
the stress of labor is over.
</p>
<p>
Just before birth, the infant in utero is positioned for delivery by
presenting the smallest diameter of his head to the largest diameter of
the mother’s pelvis; this is the position of full fetal flexion. As
contractions continue, the infant is conducted by the inclination of the
maternal pelvic floor into the midline for delivery around the pubic
symphysis by a process of extension of the head.
</p>
<p>
This descent in full flexion, progressing to birth by extension of the
head, is of profound significance to the initiation of pulmonary
respiration. The respiratory activity associated with the vigorous vocal
activity of the newborn serves to expand the cranial mechanism and
restore the bones and membranes to their anatomic relationships
(permitting their free physiologic motion). Healthy sequential
development of the central nervous system within can then continue.
</p>
<p>
These ideal circumstances, however, seldom occur in our modern,
civilized world. Owing to such factors as poor nutrition of the mother,
structural inadequacies before and during pregnancy, drug abuse,
inadequate preparations for labor, and, sometimes, the mechanical or
artificial acceleration of labor by an impatient obstetrician, only a
relatively few infants are born without undue skein or cranial trauma.
</p>
<p>
Instead, structural inadequacies of the maternal pelvis may cause the
fetus to assume a degree of extension (and lateral cervical flexion)
greater than the ideal; the result will be a presentation of a portion
of the head greater than the minimum occipitobregmatic diameter. This
can range from a moderate extension to posterior occiput, to transverse
arrest, to brow presentation, or even to a complete extension in which
the face itself presents-a position in which vaginal delivery is
impossible. In such a circumstance, cesarean section will be necessary
if the baby is to survive.
</p>
<p>
But the compressive forces will have already traumatized the head as the
uterine contractions force it progressively towards the birth canal.
Prominence of the base of an anterior maternal sacrum may obstruct
descent of the head on one side, and such asynclitism can distort the
cranial mechanism. The presence of large twins, both striving to present
the head at the same time, may cause cranial stress to one or both even
before active labor begins. These are only a few of the mechanical
insults that may occur before birth.
</p>
<p>
So much for the passage of the infant into the birth canal. Now let us
consider the structure of the infant skull itself at the time of birth.
</p>
<h2>Anatomy</h2>
<p>
The vault of the newborn skull is a membranous structure. Plates of bone
are enveloped in two layers of membrane, which are in apposition at the
anterior and posterior fontanelles and sometimes at the pterion and
asterion. These plates of membranous bone are designed to telescope into
each other as the skull passes through the birth canal-the parietals
overriding the frontal at the coronal suture, and the occiput at the
lambdoid suture. The degree of this overriding is controlled and limited
by the investing aural membranes.
</p>
<p>
The bones of the base develop from the cartilaginous chondrocranium. At
birth, development is still incomplete.(4) The occipital bone is in four
parts, united by intraosseous articular cartilage. The spheroid is in
three parts, the temporal in two, the maxilla in two, the frontal
frequently in two.
</p>
<p>
The cranial suture is designed for a very small but vital degree of
motion.(5) How much greater is the potential motion of the bones of the
developing newborn skull! At this time each part of each of these bones
functions virtually as a separate bone, moving in relation to its other
parts.
</p>
<p>
Let us consider the occiput. It is most commonly the presenting part,
and therefore the part that may take the brunt of the trauma of labor.
The four developmental parts surround the foremen magnum. The base
articulates anteriorly with the base of the spheroid. Posterolaterally,
it articulates with the lateral masses. The hypoglossal nerve, which
innervates the muscles of the tongue, passes out of the skull between
the base and the lateral mass, through the intraosseous cartilage in the
space that will become the condylar canal. The occipital condyle, which
articulates with the atlas, spans the intraosseous cartilage; its
anteromedial third is found on the base, the posterolateral two-thirds
on the lateral mass.
</p>
<p>
Immediately anterolateral to this condylar area is the jugular foremen,
a space between the condylar part of the occiput and the petrous portion
of the temporal. This foremen gives passage not only to the jugular vein
but also to cranial nerves IX, X, and XI (glossopharyngeus, vague, and
accessorius, respectively). The vagus nerve provides innervation to the
gastrointestinal and cardiorespiratory systems.
</p>
<p>
The supraocciput formed in cartilage fuses with the membranous
interparietal bone to form the occipital squama. Compression transmitted
through the squama to the condylar part on one side may disturb the
function of the vagus and/or hypoglossal nerve, causing vomiting,
irregular respiration, and difficulty in sucking. If this compression is
transmitted further to the base, the relationship of the base of the
occiput to the base of the spheroid may be distorted, causing a lateral
strain of the sphenobasilar articulation and a parallelogram deformity
of the cranium(5) (Figure 1).
</p>
<p>
Figure 1. Lateral strain of the sphenobasilar articulation. Viewed from
above, the sphenobasilar symphysis has been strained (displaced), with
the basisphenoid moving to one side and the basiocciput to the other.
Both bones side-bend about parallel vertical axes in the same direction.
The lesion is named from the position of the basisphenoid: lateral
strain with the spheroid to the right, etc. (From Magoun, H.{" "}
<em>Osteopathy in the Cranial Field.)</em>
</p>
<p>
Bilateral condylar compression may cause a buckling type of strain of
the cranial base, producing a vertical strain between the occiput and
the spheroid at the sphenobasilar articulation. This may be associated
not only with vagal dysfunction but also with symptoms of tension,
spasticity, opisthotonic spasms, sleeplessness, and excessive crying due
to the irritation of the pyramidal tracts on the anterior and lateral
aspects of the brain stem in the foremen magnum. This should be
considered as a precursor of the spastic type of cerebral palsy.
</p>
<p>
The spheroid bone is in three parts at birth; the central body bears the
lesser wings, with the greater wings (from which the pterygoid process
subtends) on either side. The greater wing-pterygoid unit articulates
with the body by an intraosseous cartilage. This is situated immediately
beneath the cavernous sinus, through which pass cranial nerves III, IV,
and VI, innervating the extraocular muscles, and the ophthalmic division
of V, which is sensory to the orbit, upper face and scalp. The body of
the spheroid articulates with the base of the occiput posteriorly and is
therefore distorted by the lateral or vertical strains resulting from
condylar compression. Anteriorly the body carries the lesser wings,
which enter into the formation of the orbit. The orbit is approximately
pyramidal in shape; the apex is at the optic foremen-that is, the root
of the lesser wing at the body. Its anatomic integrity is dependent on
the relationship of the greater wing to the lesser wing, which is in
fact the relationship of the greater wingpterygoid unit to the body.
</p>
<p>
In the event of a lateral strain at the base due to unilateral condylar
compression of the occiput, the orbit will be distorted by rotation of
the base of the spheroid carrying the lesser wing anterior on one side
and posterior on the other. In the parallelogram head due to lateral
compression, the greater wing is compressed medially and carried forward
on one side and posterior on the other. In either event, lateral muscle
imbalance of the eyes is commonly found in varying degrees ranging from
mild esophoria or exophoria to severe strabismus.
</p>
<p>
The temporal bone is in two parts at the time of birth -the petromastoid
portion, developed in cartilage that projects obliquely between the
occiput and the greater wing of the spheroid to articulate at its apex
with the body of the spheroid, and the squamous portion, developed in
membrane the forms the greater part of the lower lateral wall of the
skull. The tympanic portion is not yet a bony canal but resembles a
horseshoe adherent to the inferior posterior aspect of the squama. These
two parts, the squamous and tympanic, unite just before birth. The
petromastoid portion contains the auditory and the vestibular apparatus.
</p>
<p>
The auditory apparatus consists of the bony eustachian tube emerging
between the petrous and squamous portions, from which the cartilaginous
tube extends to the fossa of Rosenmuller. The eustachian tube is
susceptible to distortion, which may impair hearing if lateral stress
compresses the squamous portion. Laterally the eustachian tube opens
into the middle ear, which, by the ossicular mechanism, transmits the
auditory vibrations received from the tympanic membrane to the internal
ear. The vestibular apparatus includes the semicircular canals,
precisely related to each other and geometrically balanced with those of
the opposite side. Distortion of the axis of the petrous portion may
disturb this delicate mechanism of equilibrium.
</p>
<p>
The maxilla develops in two parts-the premaxilla, which will give origin
to the incisor teeth, and the body, which carries the canine and all the
other upper teeth. Angulation between these two developmental parts of
the maxilla gives rise to malalignment and malocclusion in later years.
</p>
<p>
Thus far our consideration has been directed to certain structural
changes that may sometimes be visible and are always palpable following
various difficulties of labor. Radiologic techniques have been developed
to substantiate many of these palpatory observations and confirm their
persistence in childhood problems.(7)
</p>
<h2>Examination</h2>
<p>
The craniosacral mechanism of the newborn infant should be examined
within the first few days of life. There is probably no field of
osteopathic diagnosis where the injuction “if at first you don’t
succeed, try, try again” applies more than in the examination of the
newborn cranium. The mobility of the cranial mechanism is much greater
at this age than it is in the adult skull, although the range of motion
is of course much smaller. Dr. R. McFarlane Tilley used to speak of the
amplification mechanism within the human hand and brain, which permits
the perception of motion in the range of 0.0001 inch. It is this
perceptive mechanism that must be developed in order to make a
meaningful examination and to complete an adequate treatment program for
these infants.
</p>
<p>
Furthermore, one must learn to palpate motion within motion, for these
infants rarely lie absolutely still for an examination. One should first
consider the contours and articulations by passing the hands gently over
the surface. Look for asymmetry, bossing of the frontals or parietals,
grooves above the eyebrows, overlapping of one bone on the other at the
coronal or lambdoid suture, prominence and compression of the sagittal
or metopic suture, and depression of the pterion. Let the occiput rest
in the palm of the hand, and note unusual prominence of the
interparietal occiput or hard flattening of the supraocciput. Study the
relative size and position of the eyes and nostrils and the inclination
of the mouth. Examination for inherent motility will be facilitated if
the baby is nursing or sleeping. Here is a check list that may be
helpful:
</p>
<p>
1. Place the hands gently on the vault, with the index fingers on the
greater wing of the spheroid and the little fingers on the lateral
angles of the occiput. The other fingers lie comfortably between them.
Is your first palpatory impression that your two hands are symmetrical?
</p>
<p>
2. Are the index finger and the little finger of one hand cephalad or
superior to those of the other, as in a torsion strain. If so, the
spheroid and occiput will have rotated around an anteroposterior axis in
opposite directions, elevating the greater wing of the spheroid on one
side and the lateral angle of the occiput on the other (Figure 2).
</p>
<p>
Figure 2. Torsion strain. Torsion of the sphenobasilar symphysis occurs
about an axis running from the nasion (anterosuperior) to opisthion
(posteroinferior) at approximately right angles to the plane of the
sphenobasilar symphysis. In bottom view, a left torsion lesion is
diagrammed, with the greater wing and basisphenoid high on the left side
and the basiocciput and squama lower on that same side. (From Magoun, H.{" "}
<em>Osteopathy in the Cranial Field, </em>Second Edition. Kirksville,
Mo.: Journal Printing Company, 1966).
</p>
<p>
3. Are the index finger and little finger of one hand caudad or inferior
to those of the other hand, with a sense of fullness in the palm of the
inferior hand, as in a side-bending rotation strain. In this instance,
the spheroid and occiput have side-bent in opposite directions around
parallel vertical axes and rotated inferiorly into the convexity thus
created.
</p>
<p>
4. Is there a sensation that the index fingers on the greater wings are
directed towards one side, while the little fingers on the occiput are
carried to the other side? This is lateral strain (Figure 1). Owing to a
lateral force, the spheroid and the occiput have rotated in the same
direction around parallel vertical axes, causing a shearing strain at
the symphysis between them.
</p>
<p>
5. Are the two index fingers on the greater wings forward and downward
(caudad) as compared with the little fingers on the lateral angles?
Conversely, the index fingers may be superior (cephalad). These are
vertical strains (Figure 3 ). Both superior and inferior strains are
shown in the diagrams (superior on the left). The spheroid and the
occiput have rotated in the same direction around parallel transverse
axes, producing a vertical shearing strain at the sphenobasilar
articulation.
</p>
<p>
Figure 3. Vertical strains of the sphenobasilar symphysis. Viewed from
the side, the sphenobasilar symphysis has been strained or displaced
before ossification, with the basisphenoid moving cephalad (flexion) and
the basiocciput moving caudad (extension), or vice versa. Both bones
rotate about parallel transverse axes in the same direction. (From
Magoun, H. <em>Osteopathy in the Cranial Field </em>Second Edition.
Kirksville, Mo.: Journal Printing Company, 1966.
</p>
<p>
6. Is there a sense of hardness and tension under your hands, resembling
wood? This suggests a compression strain.
</p>
<p>
These palpatory observations of asymmetry are clues to the dysfunction
of this mechanism: But it is the nature of the inherent cranial rhythmic
impulse-its symmetry, rate, amplitude, and constancy of pattern- that is
important. If the inherent motion is distorted, impeded, limited, or
retarded, there are certainly membranous strains that need attention.
</p>
<p>
It is not possible to develop the necessary tactile skills in a few days
or during a brief course of instruction. But with assiduous application,
the sensitivity will be developed, and you will be able to make these
vital diagnoses at the age when they are most susceptible to correction.
</p>
<p>
7. With your index finger on the greater wing of the spheroid and your
little finger on the lateral angle of the occiput, be still and permit
the mechanism to convey its movement through your fingers and hands. Is
there rhythmic, symmetric expansion and contraction of{" "}
<strong>external and internal rotation </strong>of the bilateral vault
bones that accommodates the <strong>flexion and extension </strong>of
the spheroid and occiput? (This is transmitted to the index fingers as a
rhythmic downward and forward and then upward and backward cyclic
motion, while the little fingers also move downward and backward, then
upward and forward. ) Is the direction of motion that of the torsion,
side-bending rotation, vertical or lateral strains?
</p>
<p>
8. Cradle the occiput in the hands, and place the tip of the index
fingers on the mastoid process of the temporal bone bilaterally. (While
there is no bony mastoid process at birth, the attachment of the
sternomastoid muscle provides the palpatory landmark.) Is the sensation
that of symmetry, or does one fingertip seem posteromedial to the other?
If the tip of the mastoid is posteromedial (i.e., less prominent) the
temporal bone is externally rotated. If it is anterolateral (more
prominent), the temporal bone is internally rotated. This asymmetry of
the mastoid process is indicative of the position of the occiput, with
the internally rotated temporal bone or the prominent mastoid process
being associated with the elevated lateral angle of the occiput. Is one
temporal bone more anterior than the other without the medial or lateral
motion? This suggests a lateral strain of the sphenobasilar articulation
that has carried the head into a parallelogram distortion. Again, be
still, and observe the relative mobility of the two temporal bones.
</p>
<p>
9. Steadying the head with the two fingers gently on the frontal bone,
slip the other hand down and around the curve of the prominence of the
occiput. Two fingers are usually adequate. Note the tension of the
suboccipital muscles, and compare the two sides of the midline. Does one
of the two palpating fingers come in contact with the arch of the atlas
before the other? If it does, this is probably the side of condylar
compression, for the occiput will have rotated anteriorly on this side.
Be still, and observe the motility. Impaired motion on one side or both
will suggest, respectively, unilateral or bilateral condylar
compression.
</p>
<p>
10. By now the baby may have finished nursing and may even be asleep.
Now change your position, and sit at the infant’s right side, at the
level of his lower limbs. Steady the pelvis with the left hand while
placing two fingers of the right hand under the sacrum. Are the two
sides of the body symmetrical? Does the sacrum project into the hand at
the coccyx? Be still; observe the motion of the sacrum in relation to
the ilia. Is the motion symmetrical, around a transverse axis? Or do you
find a rotating motion superiorly on one side, around an anteroposterior
axis?
</p>
<p>
11. Place the hands under the lumbar spine, and note the presence of
lateral flexion producing a concavity to one side. Relate this to
lateral motion of the pelvis.
</p>
<p>
The treatment of the craniosacral mechanism cannot be learned solely
from the written word. The palpatory skills must be developed and
evaluated with supervised experience. But the treatment, in summary,
consists of finding the point of balanced membranous tension of the
mechanism, holding it, and permitting the inherent therapeutic force
within to normalize the body.
</p>
<p>
“The osteopath reasons that order and health are inseparable,” said Dr.
Andrew Taylor Still, “and that when order in all parts is found, disease
cannot prevail.” And as Dr. W. G. Sutherland reminded his students, as
the twig is bent, so the tree is inclined.
</p>
<p>
Give attention to those little bent twigs, so that they may grow into
handsome, healthy, happy generations for the future.
</p>
<h2>References</h2>
<p>
1. Frymann, V. M. Relation of disturbances of craniosacral mechanism to
symptomatology of the newborn: Study of 1,250 infants.{" "}
<em>J.A.O.A. 65 </em>(1966), 1059-1075.
</p>
<p>
2. Frymann, V. M. The osteopathic approach to the allergic patient.{" "}
<em>D.O. 10:7 </em>(1970), 159-164.
</p>
<p>
3. Cathie, A. Growth and nutrition of the body with special reference to
the head. <em>Yearbook of the Academy of Applied Osteopathy, </em>
1962,pp.149-153.
</p>
<p>
4. Crelin, E. S. <em>Anatomy of the Newborn: An Atlas. </em>
Philadelphia: Lea &amp; Febiger, 1969.
</p>
<p>
5. Pritchard, J. J., Scott, J. H., and Girgis, F. G. The structure and
development of cranial and facial sutures. <em>J. Anat. 90 </em>
(1956), 73-86.
</p>
<p>
6. Magoun, H. I. <em>Osteopathy in the Cranial Field, </em>Second
Edition. Kirksville, Mo.: Journal Printing Company, 1966, p. 133.
</p>
<p>
7. Greenman, P. E. Roentgen findings in the craniosacral mechanism.{" "}
<em>J.A. O.A. 70 </em>(1970), 60-71.
</p>
<p>
8. Still., A. T. <em>Philosophy of Osteopathy. </em>Ann Arbor, Mich.:
Edwards Brothers 1899
</p>
</Article>
);
};
export default ArticleTheTraumaOfBirth;

21
website/app/(pages)/articles/views/ArtsForDocs.tsx
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@ -1,7 +1,26 @@
import Link from "next/link";
const ArtsForDocs = () => {
return (
<section className="min-h-screen" id="artsfordocs">
ArtsForDocs
<div>
<h1>Osteopathy</h1>
<Link href="/articles/osteopathic-head-pain" className="block">
Head Pain
</Link>
<Link href="/articles/neural-biological-mechanisms" className="block">
Neural Biological Mechanisms
</Link>
<Link href="/articles/intervertebral-disc-herniation" className="block">
The Basics of Intervertebral Disc Herniation
</Link>
<Link href="/articles/cranial-manipulation" className="block">
Cranial Manipulation
</Link>
<Link href="/articles/the-trauma-of-birth" className="block">
The Trauma of Birth
</Link>
</div>
</section>
);
};