The Original

OMM Board Review

John D. Capobianco, D.O., F.A.A.O.

General Practice of Osteopathic Medicine, Sea Cliff, NY

Copyright 1986, 87, 92, 93, 94, 95, 98, 99, 2000, 2001, 2002, 2003, 2005
16th printing: March, 2013. All rights reserved. This book is protected by copyright. No
part of this book may be reproduced in any form or by any means, including
photocopying, or utilization by any information storage and retrieval system without
written permission from the copyright owner.

HISTORY

1828 AT Still born

1874 Osteopathy founded "...I flung to the breeze the banner of Osteopathy."
1892 1st class at American School of Osteopathy
1896 Vermont first state to license D.O.'s
1910 Flexner report
1917 AT Still dies
1918 Spanish influenza pandemic; osteopathy dramatically reduces
morbidity/mortality
1962 D.O.'s exchange degrees for M.D. in California
1973 Mississippi last state to license D.O.'s
1974 California Supreme Court: Resume licensure of D.O.’s
2001 Louisiana accepts COMLEX

OSTEOPATHIC PRINCIPLES

1. The body is a unit. Mind, body, spirit.

2. It has its own self-protecting and regulating mechanisms.
3. Structure and function are reciprocally related.
4. The body has the capacity to defend and repair itself.
5. When adaptability is disrupted, disease may ensue.

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The following chart is reproduced from: Kuchera, ML, Kuchera, WA: Osteopathic Principles and Practice, Revised
2nd edition, 1994, Guyton, Medical Physiology, Eighth Edition, 1991

AUTONOMICS
Sympathetic vs. Parasympathetic Response
Hyposympathetonia=Hyperparasympathetonia
Hypoparasympathetonia=Hypersympathetonia

Organ Sympathetic Parasympathetic

Pupil Dilation Constriction/accomodation

Ciliary Muscle Relax (far) Constriction (near vision)
Lacrimal Gland Vasoconstriction Secretory
Mucus Glands Vasoconstriction Secretory
Salivary Glands Vasoconstriction Secretory
Blood Vessels (skin) Vasoconstriction ---------
Pilomotor Muscles Contraction ---------
Sweat Glands Secretory ---------
Common Carotid Artery Vasoconstriction ---------
Mucous Glands (Phx-Larx) Vasoconstriction Secretory
Thyroid Gland Vasoconstriction --------
Heart Excitation Inhibition
Bronchial Glands Inhibitory Secretory
Bronchial Muscles Relaxation Contraction
Upper body vasculature Vasoconstriction --------
Stomach Inhibition Motor and secretion
Liver Glycogenolysis Glycogen Synthesis
Spleen Vasoconstriction --------
Gallbladder & ducts Relaxation Contraction
Pancreas Inhibition Secretory
Kidney Vasoconstriction --------
Adrenal Medulla Adrenaline --------
Secretion
Intestinal Tract Dec. Peristalsis Inc. Peristalsis
Rectal Sphincter Contraction Relaxation
Vesicle Sphincter Contraction Relaxation
Vesicle body Relaxation Constriction
Uterine Body Constriction Relaxation
Uterine Cervix Relaxation Constriction
Male Reproductive Organ Ejaculation Erection
Ovary and Testes Vasoconstriction (unknown)

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 Sympathetics Thoracolumbar outflow (T1-L2)
(Composite according to Kuchera)

Head/Neck T1-4
Thyroid T1-4
Mammary T1-6
Esophagus (lower 2/3rds) T1-6
Trachea/bronchi T1-6
Heart T1-6 (T2 on left is most common area of
somatic dysfunction for MI)
Lung T1-6
Pleura of lung (visceral) T1-6
Pleura of lung (parietal) T1-11
Abdominal Viscera T5-L2
Stomach T5-9 (left)
Duodenum T5-9
Liver T5-9
Gall bladder T5 (right)
Gall bladder (ducts) T6 (right)
Pancreas T7 (right-head, left-tail)
Spleen T7 (left)
Small intestine to right colon T10-11
Left colon to rectum to pelvic organs T12-L2
Appendix T10 (if not presented with T10 as an
option go with T12) (Appendicitis--Right
twelfth rib tip is tender)
Ovary-/teste T10-11
Adrenals T10-11
Kidney T10-11
Upper ureter T10-11
Lower ureter T12-L1
Cisterna Chyli T11
Pelvic Viscera T12-L2
Uterus T12-L2
Prostate T12-L2
Bladder T12-L2
Upper extremity T2-8
Lower extremity T11-L2

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 Sympathetic Innervation of the GI tract (Kuchera)

Greater Splanchnic Nerve Stomach, Liver (T5-9) Celiac Ganglion

(T5-9) Pancreas,
duodenum

Lesser Splanchnic Nerve Small intestine (T10-11) Superior Mesenteric

(T10-11) Rt. Colon (12) Ganglion

Least Splanchnic Nerve Left Colon (T12-L2) Inferior Mesenteric

(T12) & Pelvic Organs Ganglion
Lumbar Splanchnic Nerve
(L1-L2)

Parasympathetics--cranial and sacral areas

CN III Pupil (constriction and accomodation)

CN VII/IX Lacrimal/salivary glands (secretomotor) sinuses and eustachian tube
CN IX/X Carotid body/sinus (blood pressure regulation & C0 2 /0 2 tension)
CN X Vagus nerve (thorax. abdomen &- pelvis)
Mnemonic 1973 (X. IX. VII. III):
Left and right vagus nerves terminate at the doudenum and
Midtransverse colon respectively. The right one is longer!
S2-S4 Left colon and pelvis via pelvic splanchnic nerve

Parasympathetic Innervation

Nucleus/Plexus Cranial Nerve Ganglia End Organs

Edinger-Westphal Oculomotor III Ciliary Eye , Accomodation

Superior Salivatory Facial VII Pterygo- Submandibular/Sublingual

Palatine & gland, Lacrimal/palatine
Submandibular glands

Inferior Salivatory Glossopharyngeal IX Otic Parotid

Dorsal Motor & Vagus X Nodosum Respiration, heart

Nucleus Ambiguous GI, Liver, Pancreas,kidney

Pelvic Splanchnic Pelvic, GU Tract

Descending Colon &
Rectum

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Buzz words for vagus: Dysfunction of the vagus is reflected to OM, OA, AA, C1
& C2. Vagal viscerosomatic reflex from the lungs may be seen as a dysfunction
of the OM. Reason for this is probably due to the ganglion nodosum, which is
anterior to C2. All organs from the thyroid and below except (?) mammary
glands, (?) ovaries and (?) testes. Innervates GI tract up to the middle transverse
(right) colon. ALWAYS LOOK AT THE OCCIPUT, SUBOCCIPITAL, C1 OR C2
AREA FOR PARASYMPATHETIC VISCEROSOMATIC REFLEX BECAUSE OF
CLOSE PROXIMITY OF VAGUS (GANGLIA NODOSUM) TO THIS REGION.
Don’t forget that the SUPERIOR CERVICAL GANGLION is in the area of C2/3
and thusly may exhibit tissue texture changes as a result of viscerosomatic
reflexes from the head/neck and heart!

In inferior wall MI: There are many cholinergic fibers located in the inferior wall
of the myocardium. Viscerosomatic reflex will be to the suboccipital region. The
anterior wall MI viscerosomatic reflex is to T1-T7, predominantly T2.

Upper respiratory tract: Sympathetics produce epithelial hyperplasia resulting

in an increase in the number of goblet cells in relation to the ciliated cells
(increased goblet to ciliated cell ratio). Due to this, there is an increase in mucus
production and thickening of the secretions. Parasympathetic stimulation
produces the opposite. There is increased ciliated to goblet cell ratio. This helps
the sweeping mechanism by the thinning of secretions.

PUD: This disease is related to an excessive vagal type of syndrome.

Viscerosomatic reflex due to PUD will also be to the OA/OM region. Be aware of
pepsin and acid production secreted by parasympathetic overstimulation.
Hypersympathetic tone decreases mucosal barriers!

Post–Op ileus: Under sympathetic stimulation the intestines contract. During

surgery there is an acute disruption of the intestinal system, which goes into
shock. Sympathetic override inhibits peristalsis leading to post-op ileus. Rib
raising is an effective treatment to tone down the sympathetic gain to the
intestines.

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Clinical Notes:
♦ Pelvic splanchnic (S2-S4) vs. Sacroiliac joint (S1-S3)
♦ Pelvic splanchnics (S2-S4) innervate from left colon down to genital
cavernous tissue except adrenals.
♦ Note: No parasympathetic innervation to the extremities.
♦ Right vagus (AKA Posterior vagal trunk) gives rise to the celiac branch
and the left vagus (AKA Anterior vagal trunk) gives rise to the hepatic
branch.
♦ The right vagus innervates the Ascending colon and the 1st 2/3 of the
Transverse colon. The left vagus innervates the liver and part of the
duodenum. Therefore the right vagus is longer than the left vagus.
♦ Rt. Vagus innervates the SA node: Hyperparasympathetic stimulation can
cause bradyarrhythmias.
♦ Rt. Sympathetic fibers innervate the SA node: Hypersympathetic
stimulation may lead to supraventricular arrhythmias.
♦ Lt. Vagus innervates the AV node: Hyperparasympathetic stimulation can
cause heart block.
♦ Lt. Sympathetic fibers innervate the AV node: Hypersympathetic activity
may lead to malignant dysrhythmias (ventricular tachycardia and
ventricular fibrillation).
♦ Sympathetics to the head and neck come from T1 to T4. Travel up to the
Superior Cervical Ganglia at the level of C1 to C3, follows the arterial
supply and goes through the Sphenopalatine Ganglion without synapsing
continuing on to the eyes, nasal mucosa, etc.
♦ Sphenopalatine ganglion is basically a parasympathetic mechanism
mainly from CN VII. Covers throat, sinuses, ears and others.
♦ Greater petrosal nerve carries parasympathetic fibers.
♦ Deep petrosal nerve carries sympathetic fibers.
♦ Hering-Breuer Reflex: Mediated by the 10th cranial nerve occurs when
the air sacs are filled with fluid. The respiratory centers receive confusing
information. The vagus sends signals to decrease diaphragmatic
excursion since the air sacs are filled. Concurrently, the carotid body (CN
IX) perceives the need for more oxygen and sends signals to increase the
diaphragmatic rate. The result of these signals is rapid and shallow
breathing.
♦ The carotid sinus senses changes in blood pressure.
♦ The carotid body senses changes in the partial pressure of dissolved O2
in the blood. Both the sinus and body are innervated by CN IX.

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 Autonomics Big Picture

Sympathetics
Head/Neck/Heart/Lungs: T1-4 (6)
Upper GI: T5-9
Lower GI/Pelvis: T10-L2
Remember: the sympathetics technically terminate at the ganglion impar,
just anterior to the coccyx.

Parasympathetics
Head/Neck: CN III, VII, IX, X
Chest/Upper GI: CN X
Lower GI/Pelvis: S2-4

NEUROLOGIC (PROPRIOCEPTIVE) REFLEXES

Muscle Energy: (Golgi tendon organ reflex). (Direct method). A pull on the tendon
sends signal from the Golgi tendon organ to spinal cord. At the spinal cord level
inhibitory interneurons synapse with alpha motor neurons causing a reflex relaxation of
the muscle. When tension on a tendon becomes extreme the inhibitory effect from the
organ can become so great it causes a sudden relaxation of the entire muscle. Golgi
tendon organs respond to rate and changes in muscle tension. Summary: Activation of
large myelinated group 1b afferent fibers from tendon insertion reflexively inhibits alpha
motor neuron to muscle spindle. Buzz: Golgi, alpha motor neurons, tension/force,
direct technique. Primary source: Kuchera and Kuchera, OPP

Counterstrain: Decrease gamma gain: "...stop inappropriate proprioceptor activity...

shortening the muscle that contains the malfunctioning muscle spindle by applying a
mild strain to its antagonist." (Jones) This is an indirect technique that employs the
Muscle spindle reflex. This reflex responds to rate and changes of intrafusal fiber
length. Hypershortening the extrafusal fibers by bringing the origin and insertion of the
muscle mass closer together, decreases the length of the intrafusal fibers and relaxes
them. This relaxation phase is followed by a slow return to neutral in order to allow the
CNS to reset the gamma gain activity in the spindle to a new lower level. The end result
of counterstrain on the muscle spindle fibers is a turning down of the gamma gain.
Remember: Position of ease, slow return after 90 seconds. Red herrings: C3 posterior
put into flexion. C4 anterior put into extension, inion put into flexion, lower pole L5 put
into flexion. Anterior C7 and C8 represent the lateral and medial portions of the SCM
muscle. Otherwise SARA for C-spine. CS of these point treats the SCM by shortening
the muscle. Know the C.S. tx for piriformis spasm: Flexion, external rotation and
abduction. Know the spot is half way b/t the PSIS and gr. Trochanter. Key words:
proprioceptor, gamma gain. Note: FPR also employs the muscle spindle reflex. Primary
source: Kuchera and Kuchera, OPP

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HVLA: Can involve both the Golgi tendon organ and muscle spindle reflex. HVLA may
produce changes in muscle tension and length of muscle spindles.
1. Thrust activation initiates so much afferent input into the CNS, causing the
CNS to turn down the gamma gain to the muscle spindles, which relaxes the
tight muscle mass.
2. During a thrust the tension on the tight muscle firmly pulls on the tendon.
This activates the Golgi tendon receptors, which in turn causes a reflex
relaxation to that tight muscle.
3. The stretch of the extrafusal fibers of the tight muscle pulls on the Golgi
tendon receptors, which will cause a reflex activation to inhibit the contraction
of the same muscle.
4. HVLA of 1/8” to 1/4” of forceful stretching of a contracted muscle may
produce such a barrage of afferent impulses from the spindles to the CNS
causing the CNS to respond by sending inhibitory impulses to the gamma
gain cell bodies. This turns down the gamma gain activity to the spindles,
thus relaxing the muscle mass via a central inhibitory reflex. Know
“Articulatory Technique”, which is “low-velocity, moderate amplitude. You will
go through the barrier with both techniques, and even get a “pop”. Kuchera
and Kuchera, OPP
5. Still Technique: Place dysfunction into position of EASE first, then into
BARRIER. This would translate into Indirect, then Direct engagement. The
barrier may resultant in a “pop”. Compression may also be used.
6. PINS=Progessive Inhibition of Neural Structure. Locate sensitive point at
beginning of connecting structure (ligament, muscle, etc) and analyze that
structure. Find another less sensitive structure and apply inhibition for about
30 seconds. The less sensitive structure is the “endpoint”. Keep locating less
sensitive points about 2-3cm towards less sensitive point. Reassess status of
dysfunction. (Still and PINS technique as per Dowling, An Osteopathic
Approach to Diagnosis and Treatment, Third Edition, 2005.

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 CHAPMAN’S REFLEXES

Chapman’s reflexes are a system of reflex points originally used by Frank Chapman,
D.O. Most importantly, they are diagnosed as viscerosomatic reflexes. These reflexes,
or “gangliform contractions” present as predictable anterior and posterior fascial tissue
texture abnormalities assumed to be reflections of visceral dysfunction or pathology
(viscerosomatic reflexes). A given reflex is associated with the same viscus;
Chapman’s reflexes are manifested by palpatory findings of plaque-like changes of
stringiness of the involved tissues (1).

The Chapman's reflexes follow sympathetic afferent pathways and therefore are
manifest along the dermatome, sclerotome and myotome segmental lines. Chapman’s
reflexes are neurologic, lymphatic and myofascial reflexes that indicate increased
functional activity of the sympathetic nervous system. They do not reflect the
parasympathetic nervous system.

These reflexes in the thoracic area are palpated anteriorly in the intercostal spaces via
sympathetic fibers of intercostal nerves. The heart reflex is located at the 2nd intercostal
space and posteriorly at T2, which is a major innervation of the heart. The reflex for the
bronchus, thyroid and esophagus is also at the anterior 2nd intercostal space. (BETH)

The Chapman’s reflexes for the colon are located on the lateral thigh along the Iliotibial
band and Tensor fascia lata. Also, in this same area are the reflexes for the broad
ligament of the uterus and prostate. It is important for the student to realize that the
colon reflexes are mapped out by fixing the cecum and rectosigmoid area and “flipping
over” the transverse colon over the right and left thighs. For example, the reflex for the
cecum is located at the Rt. Greater Trochanter, the splenic flexure is at the left knee; the
sigmoid colon lay at the Lt. Greater Trochanter.

Ex. Disorder in middle ear and sinuses will increase sympathetic tone to clavicle and
first rib anteriorly and C2 posteriorly. Again, Chapman’s reflexes follow classic
viscerosomatic patterns. An argument can be made stating: treatment of Chapman’s
reflexes are mediated via somatovisceral reflexes.

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10
11
 OTHER TREATMENT MODALITIES
• Effleurage: Form of lymphatic stroking, distal to proximal
• Petrissage: Grasp, lift and twist skin to break superficial fascial adhesions.
• Tapotement: Striking belly of muscle with hypothenar eminence to increase
blood flow and tone

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 SOMATIC DYSFUNCTION
Somatic dysfunction: Is an impaired or altered function of related components of the
somatic (body framework) system; skeletal, arthrodial and myofascial structures, and
related vascular, lymphatic and neural elements (1). Somatic dysfunction is treatable by
using osteopathic manipulative medicine. Mnemonic: SAM VLN. Remember TART
(Tissue texture changes, Asymmetry, Restricted motion & Tenderness). “Sensitivity
changes” may be substituted for tenderness. The other mneumonc STAR may be used
which signifies Sensitivity, Tissue Texture Change, Asymmetry and Restricted Motion.

Acute:
• Increase temperature (blood flow from kinins, etc).
• Increase moisture (sudomotor from sympathetics).
• Increased bogginess (edema from leakage of vessels and stagnant lymph)
Increased tenderness (nociceptor firing in tissues).
• Erythema (vascular response, redness lasts more than 15-30 seconds).

Chronic:
• Decreased temperature (cool, decreased blood supply from ongoing
sympathetonia).
• Dryness (sustained sympathetic tone "burns out" sweat glands and
decreases sudomotors).
• Blanching in response to erythema streaking (sympathetics vasoconstrict
blood vessels).
• Ropy, stringy soft tissues.

ERYTHEMA TEST
Acute: A positive red reflex sign due to release of substance P and other biochemical
neuropeptides, kinins, etc., into soft tissues causing dilation of capillaries and
inflammation. Redness shouldn't last > 30 sec.

Chronic: There is a blanching response due to excess vasoconstriction from

sympathetic override.

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 BARRIERS
Restrictive Barrier: A functional limit within the anatomic range of motion, which
abnormally diminishes the normal physiologic range (1). (Between normal midline range
and physiologic barrier). AKA: Somatic dysfunction.

Physiologic Barrier: The limit of active motion; can be altered to increase range of
active motion by warm-up activity (1).

Anatomic Barrier: The limit of motion imposed by anatomic structure; the limit of
passive motion (1). (End point of ligament, fascia, muscle, etc. Beyond these joint is
disrupted).

Pathologic Barrier: 1. Restrictive barrier; 2. Permanent restriction of joint motion

associated with pathological change of tissues (ex. Contracture, osteophytes) (1).

Elastic Barrier: The range between the physiologic and anatomic barrier of motion in
which passive ligamentous stretching occurs before tissue disruption (1). Similar to
“anatomic barrier”.

FRYETTE'S RULES
Note: Fryette’s rules apply to the Thoracic and Lumbar spinal regions only. Recent research has disputed that
sidebending and rotation occur to the same side in the cervical spine for the type II rule (American Academy of
Osteopathy Journal, Fall, 2002, p17-32).

Law/Type I: NEUTRAL
• Sidebending and rotation to opposite sides.
• Involves more than one segment (usually 3 or more) = group curve.
• Dysfunction greatest in neutral (N) position.
• Long restrictors maintain lesion (erector spinae).
• Compensatory/gradual onset.

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 • Treat after Type II.
• Example: T3-L1 N SBI Rr: To treat put patient into RI SBr N (for muscle energy).
• A functional or structural scoliosis fit this model.
• Functional: Due to muscle spasms
• Structural: Congential, bony abnormality.
• Most common occurrence in scoliosis is sacral base unleveling.

Law/Type II: NON-NEUTRAL

• Sidebending and rotation to same side.

• Single segment.
• Dysfunction greatest in either flexion or extension.
• Short restrictors maintain lesion (rotatores brevis & intertransversarii muscles.)
• Abrupt/traumatic (found at apex, beginning or end of group curve).
• Treat first.
• Example: T8 F SBl Rl: To treat put patient into Rr SBr E (for muscle energy).
• Recent research shown to disprove type II dysfunctions in the cervical spine.

Law III:
• Named by Dr. CR Nelson in 1948: Initiation of motion in one plane MODIFIES
motion in all other planes.

RULE OF THREES FOR THORACIC SPINE

A. T1-3 Spinous process of segment is with its transverse process
B. T4-6 Spinous process of segment is half way, to t-process of segment
below
C. T7-9 Spinous process of seg. is at level with t-process of seg. below
D. T10 Like "C"
E. T11 Like "B"
F. T12 Like "A"

FACILITATION/SENSITIZATION
1. The maintenance of a pool of neurons (e.g. premotor, motorneurons or
preganglionic sympathetic neurons in one or more segments of the spinal cord)
in a state of partial or subthreshold excitation; in this state, less stimulation is
required to trigger the discharge of impulses (1).
2. Facilitation may be due to sustained increase in afferent input, or changes within
the affected neurons themselves of their chemical environment. Once
established facilitation can be sustained by normal CNS activity (1).
3. Synapses in the cord that have low threshold are easily triggered by impulses of
sublevel intensity. Visceral afferent and somatic propioceptor bombardment to
the cord from visceral or somatic disease produces facilitation. These facilitated
segments will then fire sympathetic outburst to related organ and soma

15
 structures when other visceral or somatic impulses pass through that region of
the cord. This inappropriate sympathetic bombardment of visceral and somatic
tissue will have detrimental effects to these tissues and the body in general.

DERMATOMES
C5 Clavicles
C6 Thumb
C7 Middle finger
C8 Ring/Little Finger
C5-C6 Ball of shoulder (deltoid)
C5-C7 Lateral Arm (C5 for lateral upper arm, C6 for lateral forearm)
C8-T1 Medial Inner Arm
T4 Nipple
T7 Xyphoid
T10 Umbilicus
T12 Groin
L4 Innermost foot
L5 Dorsum of foot
S1 Outermost foot
L4-L5 Medial Foot
L3-L4 Knee
L5, S1-S2 Posterior/Outer Thigh
L1-L4 Anterior/Inner Thigh
S1-S5 Perineum

T1 – In MI, T1 is probably the connection to viscerosensory pain referral to

the inner arm.

Viscerosensory vs. viscerosomatic = pain vs. tissue texture changes

Pain: In general, pain including and above the uterine fundus is mediated by the
sympathetics. Pain below (including the cervix but not the the gonads) are mediated by
the parasympathetics. For a more complete discussion of pain, see section, “PAIN”.

Perineum (S1-S5), very important when assessing for Cauda Equina Syndrome. Patient
with large central disc herniation will have trouble with urinary or bowel retention.

ANATOMIC LEVELS
T2-Sternal notch
T4-Angle of Louis
T9-Xyphoid
L3-Umbilicus

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 KEY REFLEXES
L4 Patella (knee jerk)
L5 None (test strength of great toe dorsiflexion-extensor hallucis longus-- and
heel walking)
S1 Achilles (ankle jerk/toe walking)
C5 Biceps
C6 Brachioradialis
C7 Triceps
V1 Corneal blink
V2 Sneeze
V3 Jaw jerk
IX Gag/carotid
X Cough
L1-2 Cremesteric

CRANIAL
Founded in 1899 by Dr. A.T. Still's student. William Gardner Sutherland. D.O., D.Sc.

Five phenomena:
1. The fluctuation of the cerebrospinal fluid (or potency of the Tide)
2. The motility of the brain and spinal cord (alternating shape of CNS)
3. The mobility of the intracranial and intraspinal membranes (reciprocal tension
membranes) DURA MATER
4. The articular mobility of the cranial bones-- joint/suture motion
5. The involuntary movement of the sacrum between the ilium (via the dural
membranes to S2). NOTE: This is NOT voluntary. It exists along the respiratory
axis of S2, the superior pole of the sacroiliac joint. Craniosacral
flexion=counternutation.

#’s 1 and 2 are thought to be the "motive power" behind #’s 3-5

The five phenomena make up the Primary Respiratory Mechanism.

Note: Most cranial dysfunctions are named in relation to the position of the sphenoid
bone.

Flexion: Increase in transverse diameter, decrease in longitudinal and A-P

diameters. Flexion refers to midline structures such as the sphenoid. Normal
motion occurs about two parallel horizontal axes, one thru the zygomatic process
of the temporal and thru the body of the sphenoid. The other axis is for the
occiput; it travels thru a point located bt the mastoid process and Asterion and
goes above the foramen magnum out the other side. BERT and sloping forehead

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Extension: Decrease in transverse diameter, increase in longitudinal and A-P
diameters. Extension refers to midline structures such as the occiput. The axes
are obviously the same as described above. ERNIE and vertical forehead

Torsion: Twisting of articulation of sphenoid and occiput, the sphenobasilar

synchondrosis. Name lesion for side of higher greater wing of the sphenoid.
Greater wing of the sphenoid is superior on the right and a low occiput on the
right = Rt. Torsion. This pattern occurs about an a-p axis, from nasion to
opisthion.

Sidebending/Rotation: Bending of articulation of sphenoid and occiput, the

SBS; the low greater wing of sphenoid is on same side as low occiput, head
fuller, convex, on this side and named for this convex side (of low sphenoid and
low occiput). Mnemonic: "Down and Out in Beverly- Hills". Greater wing and
occiput both inferior on the right and convex (fuller) on the right = Rt.
Sidebending/Rotation. This pattern occurs about the same a-p axis above in
addition to two parallel vertical axes coming up through the foramen magnum
and body of sphenoid.

Lateral Strain: Sphenoid shifted to either right or left of occiput. Sphenoid

shifted to the right in relation to the occiput = Rt. Lateral Strain. Traditionally
named for which side the basisphenoid shifts towards, however, recently
contested by some to be defined as to the direction opposite the sphenoid is
shifted towards. It’s really an intellectual argument because they are both
incorrect according to Magoun's Osteopathy in the Cranial Field. He contends
that the greater wing of the sphenoid actually shifts ANTERIORLY in a right
lateral strain and ANTERIORLY in a left lateral strain. The classic example is a
child with a parallelogram head. This occurs about the same two parallel
vertical axes of sidebending/rotation. This time the bones are moving in the
same direction (mother nature loves contralaterality!).

Vertical Strain: Sphenoid shifted up or down in relation to the occiput. If

sphenoid is shifted upward, for example from a punch to the bottom of the chin
upward, then it’s a superior vertical strain. If shifted downward, it's an inferior
vertical shear. When palpating in an A/P direction along the frontal bone and
there is a dip at the coronal suture = anterior cranium is superior = Superior
vertical strain. If anterior cranium (dividing line being the coronal suture) is
inferior = Inferior vertical strain. This occurs about the two physiologic axes of
the sphenoid and occiput (thru the zygomatic processes of the temporal bones
and the asterion in the area of the occiput {an axis that lies above the foramen
magnum). If the sphenoid is in extension=inferior vertical strain. If sphenoid is
high=superior vertical strain.

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 A hit with a bat on head anterior to the coronal suture or a fall on the tailbone
may result in an Inferior vertical strain. The later is possible since there is a
change in the relation of the sphenoid and the occiput. Caution: do not name the
lesion for the position of the occiput.

Compression: A-P compression at sphenobasilar symphysis, worst lesion:

overall decreased cranial motion. Described as a "bowling ball " head.

Bones:
• 22 cranial bones.
• 28 if you count the ossicles (3 in each temporal bone).
• 8 neurocranial bones (occiput, temporal (2), ethmoid, parietals (2), sphenoid and
frontal).
• 14 viscerocranial bones (facial).
• 7 orbital bones (frontal, zygoma. maxilla, sphenoid, lacrimal, ethmoid and
palatine). KNOW THESE SEVEN BONES OF THE ORBIT!
• 29 bones in the cranium (incl. Hyoid and Ossicles)
• 79 articulations in the face
• 43 articulations in the cranium
• Compare: 55 articulation in the foot
• Compare: 26 bones in the foot (not including the sesamoids)
• The skull has about 142 articulations. (79 face, 43 neurocranium)
• Basilar bones are occiput (except interparietal portion), petrous temporals,
sphenoid (except tip of greater wing) and ethmoid and are all formed in cartilage.
The nasal cartilage, septum and inferior conchae are also formed in cartilage.
• Vault bones are frontal, parietals, and temporals (include tip of greater wing of
sphenoid and interparietal occiput). All formed in membrane and are
accommodative to the basilar bones. The facial bones are for the most part
formed from membrane. All facial bones have the potential to have sinuses.

Sphenobasilar synchondrosis:

Major joint in cranium, formed in cartilaginous tissue, becomes cancellous bone around
the age of 25 and maintains pliability, flexibility thereafter.

19
Cranial Motion:

There are several wave form motions described in the cranial concept. The one for the
national boards is described as 8-14 cycles/minute. A cycle = 1 inhalation & 1
exhalation. Two other tides of note: One every 2.5 times per minute and one occurs six
times per minute. These latter two tidal motions are usually not included on the boards.
Clinical correlation: Depressed patient’s have decreased PRM.

Cranial amplitude is quantitative 1/10 – 10/10. The latter being healthiest

Inhalation phase of the primary respiratory mechanism (PRM) = flexion of

midline structures, (i.e. sphenoid, occiput, sacrum) and external rotation of paired
structures (i.e. temporal bones, femur, etc.).

Exhalation phase of PRM = extension of midline structures and internal rotation

of paired structures.

The “Breath of Life” is the “Tide” and not necessarily confined to the body. So, do not
confuse the CRI (cranial rhythmic impulse) with Tidal Movement. This level of palpation
most likely will not be on the boards.

Occiput, ethmoid and vomer all rotate (circumducts) in the same direction in flexion and
extension. Sphenoid rotates (circumducts) in opposite direction.

20
Cranial Landmarks:

• Pterion: Overlapping of frontal, parietal, sphenoid and the temporal. Area of

anterior branch of middle meningeal artery.
• Asterion: Meeting of parietal, temporal and occiput.
• Opisthion: Dorsal aspect of foramen magnum.
• Basion: Ventral aspect of foramen magnum.
• Nasion: Meeting of frontal and nasal bones.
• Glabella: Bump on distal frontal bone, above nasion.
• Bregma: Meeting of coronal and sagittal sutures.
• SS pivot point: Sphenosquamous point where temporal overlaps the sphenoid
superior to joint and sphenoid overlaps temporal below point.
• Sutherland's Fulcrum: Area of straight sinus (junction of three sickles of dura
mater); automatic shifting suspension fulcrum “…point of rest on which a lever
moves and from which it gets its power..." (Magoun)
• Reid’s Line: Extends from lower border of orbit thru the external auditory
meatus. Brain lies above this line.

Beveling: External bevel: Suture is on the external surface of the bone. If a bone
is externally beveled it is overlapped by another bone.
Internal bevel: Suture is on the internal surface of the bone. If a bone is
internally beveled then it overlaps another bone.

Example: At the occipitomastoid suture the Temporal has internal

beveling and the Occiput has external beveling. In this case the Temporal
overlaps the Occiput; therefore during a CV4 (compression of the fourth
ventricle) you have to place your thenars on the occiput, NOT
TEMPORAL.

Note: Above the SS pivot point the temporal overlaps the sphenoid and
below this point the sphenoid overlaps the temporal.

The beveling concept gives an indication of how certain treatment would work. When
treating a patient with a CV4 the occiput is compressed since it is overridden by the
temporals.

21
Sutures: Examples:

Serrate-Sagittal; allows rocking

Squamous-Temporoparietal; allows gliding
Harmonic-Lacrimoethmoid; allows shearing
Squamoserrate-combination, ie, Lamboidal and Coronal sutures

The Three Articulations between the Temporal and Occipital Bones:

1. Condylosquamomastoid Pivot: Rocking motion
2. Jugular Process: occiput drives the temporal
3. Petrobasilar: Tongue and groove & Hinge/Glide motion
4. Combination of all three equals “wobble”

The Major Attachments of the Dura (Reciprocal Tension Membrane):

1. Posterior pole:
2. Lateral pole:
3. Anterior Superior pole:
4. Anterior Inferior pole:
5. Inferior pole:
Occipital bone
Petrous portion of the Temporal bone
Cribiform and Crista Galli of the Ethmoid
Clinoid processes of the Sphenoid
S2 at the superior transverse axis of the
Sacrum CORE LINK/RTM

Flow of CSF:
Lateral ventricles  Interventricular foramen of Monroe  3rd ventricle  Aqueduct
of Sylvius  4th ventricle  through Midline foramen of Magendie or lateral to
foramen of Luschka  subarachnoid space  brain and spinal cord
(M=Midline=Megendie: L=Lateral=Luschka)

Venous flow:
♦ Superior Sagittal sinus  Rt. Transverse sinus
♦ Inferior Sagittal sinus  Lt. Transverse sinus
♦ Transverse sinus  Sigmoid sinus  Internal Jugular Vein which courses along
with CN IX, X & XI and exit through Jugular Foramen which is between two
bones, the occiput and temporal.
♦ Great vein of Galen together with the Inferior Sagittal sinus  Straight sinus
Confluence of Sinus
♦ Cavernous sinus empties into the Inferior and Superior Petrosal sinuses. Inferior
Petrosal sinus  Sigmoid sinus and the Superior Petrosal sinus  Transverse
sinus.
♦ The venous sinuses lie between the two layers of dura. These veins lack smooth
muscle, elastic fibers and valves. They depend on the mobility of the dura for
drainage.

22
Techniques:

CV4 (compression of the fourth ventricle): Generalized technique, used in any

instance except acute head trauma. Operator places thenar eminences medial to
mastoid processes: encourage extension phase by holding the occiput towards
you (very gently!) or away from the flexion phase. You are harnessing the
"Potency of the Tide." Pronounced effect on total body physiology. For example:
The medulla is on the floor of the fourth ventricle; if you work with the CSF to
alter this respiratory center you can in turn effect a change in the
thoracoabdominal diaphragm and hence increase lymphatic flow from the
cisterna chyli/thoracic duct via the aortic hiatus in the diaphragm (level of T12).

Sphenopalatine Ganglion: It hangs in its respective fossa via the second

division of CN V, but it is supplied by the greater petrosal nerve, a branch of the
geniculate ganglion of CN VII. To treat: Go to maxillary ridge near pterygoid plate
and gently inhibit to effect a decrease in goblet to ciliary cell ratio and lessen
thickened secretions of the nasopharynx (especially the Eustachian tube). You
palpate the lateral pterygoid muscle when you do this technique.

Condylar Decompression: Takes the occiput posteriorly to free up the

hypoglossal canal (CN XII) and the articulation with the temporal. Indicated for
the infant with suckling disorder. May also help CN 9, 10, and 11 in addition to
freeing up the jugular venous drainage.

V-Spread: “Peace Sign” around occipitomastoid suture. Frees up the

temporal bone in addition to opening up venous flow along the sigmoid sinuses.

Venous Sinus Decompression: Begin at the inion, then proceed to the

occipital, transverse, sagittal and metopic sinuses. Frees up venous flow.
Indicated for headache.

Galbreath Technique: Involves opening up Eustachian tube for otitis media.

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 CRANIAL NERVE ENTRAPMENTS
Cranial Nerve Entrapment Neuropathy
I Olfactory Anosmia
II Optic Visual Acuity/Field ,
III Oculomotor Eye deviation - down and out: [(CN III innervates all
muscles EXCEPT Lateral rectus (CN 6) and Superior Oblique (CN 4)]
Pupils not constricting (via Edinger-Westphal
Nucleus)/ptosis of lid, poor accomodation
IV Trochear Eye deviation - slight upward. Diplopia,esp look down
V Trigeminal* Anesthesia of the face, paralysis of muscles of
mastication, Trigeminal Neuralgia (V2)-Stabbing pain
VI Abducens Eye deviation - inward, strabismus
VII Facial Bells Palsy, Decreased Tears/Taste to anterior
2/3 of tongue, salivation, dysphagia
VIII Vestibulocochlear Decrease hearing, vertigo, Meniere's disease.
Always think of temporal bone dysfunction when it comes to “hearing changes”.
IX Glossopharyngeal Decreased swallowing, speech difficulty, inc gag
X Vagus Anesthesia of External auditory meatus; cough.
Circulation/Respiration changes
Digestion, swallowing
Swallowing/Speaking; inc gag, cough
XI Accessory Shoulder shrugs, diff turn to normal side, swallowing
Torticollis (SCM) (SCM also innerverated by C2/3)
XII Hypoglossal Tongue: trouble suckling;dysphagia, dysarthria

*Trigeminal neuralgia (tic douloureux) most commonly occurs in V2 distribution.

-V1 exits via the Superior Orbital Fissure
-V2 exits via Foramen Rotundum
-V3 exits via Foramen Ovale

24
 PELVIS AND SACRUM
♦ Standing flexion Test provides information on laterality or iliosacral dysfunction. The
seated flexion test provides information only on sacroiliac dysfunction, not on
laterality, except to say that the side of the (+) seated flexion test is opposite the axis
(named) or the same side as the inferior pole of the axis = piriformis spasm. The
seated flexion test lacks specificity but is useful for determination of sacral shear vs.
unilateral sacral extensions.

♦ Example of Innominate diagnosis:

Lt ASIS - Superior Lt ASIS - Inferior
Lt PSIS - Inferior Lt PSIS - Inferior
Lt Pubic Bone - Superior Lt Pubic Bone Inferior
(+) Rt Standing Flexion Test (+) Rt Standing Flexion Test
Dx = Rt Innominate Anterior Rotation Dx = Rt Innominate Superior Shear

Distance from ASIS to umbilicus is greater on the right, with a positive standing
flexion test on right=right outflare innominate. Distance from ASIS to umbilicus is
less on right than on left, standing flexion test positive on the right=right inflare
innominate. Same as above but positive standing flexion test on the left=left
outflare innominate.
♦ The axis in a sacral torsion is named for the superior pole of the axis. Name axis
AFTER rotation. The seated flexion test although realistically is not specific is
academically on the side opposite the named axis. It also determines whether you
have a sacral shear vs. a unilateral extension (deep sulcus and ILA post/inf same
side).
♦ The “stork test” is positive for INNOMINATE or iliosacral dysfunction: Operator
palpates PSIS, pt bends knee (one side) and you see if PSIS comes posteriorly. If it
does NOT, then a restriction or dysfunction of the INNOMINATE/iliosacral is noted.
♦ The “Sphinx test” just has the patient prone, in “TV watching position” to induce
lumbar extension. It would make a “backward sacral dysfunction” worse. A forward
sacral dysfunction would be more symmetrical. Same as Backward Bending Test.
♦ For sacral torsion remember that L5 is rotated opposite to the rotation of the sacral
rotation. If the same think “sacral rotation”.
♦ Superior transverse axis of the sacrum corresponds to Respiratory motion/
craniosacral. Middle transverse axis for sacroiliac motion and the inferior transverse
axis for iliosacral motion. For all of these axes motion occurs through S2 except the
last one which lies in the area of S3.
♦ A question regarding a restricted ILA is referring to a posterior/inferior ILA
♦ Anterior Superior ILA on the Rt = Posterior Inferior ILA on the Lt
♦ Counternutation of the Sacrum = Base is posterior = Craniosacral Flexion = Postural
extension. All operate on different areas of the SI.

25
♦ Nutation of the Sacrum = Base is anterior (nods) = Craniosacral Extension =
Postural flexion. Different axes as above.
♦ In the birthing process, as the baby comes down the birth canal the sacral base 1st
moves posteriorly in counternutation and 2nd as the baby comes further down the
apex of the sacrum moves posteriorly in nutation. As the baby comes into the pelvic
inlet the ilia flare out and pubic symphysis adducts. The opposite occurs when the
baby exits the pelvic outlet.
♦ Pelvic Side Shift Test: Pelvis shifts easier to side opposite short leg and psoas
spasm. Same side as piriformis spasm.
♦ Respiratory/craniosacral motion occurs about a superior transverse axis.
♦ Sacral flexion and extension occurs about a middle transverse axis.
♦ Walking, iliosacral motion and pubic motion occur about an inferior transverse axis.
♦ All three occur in the area of S2, roughly the superior, middle joints except the
inferior pole which is located in the area of S3. (remember the SI is S1-3)

Sacral Dysfunctions

Torsion: By definition deep sacral sulcus opposite from side of inferior lateral angle
(ILA) being posterior-inferior. Of course L5 is rotated opposite sacral rotation. The
sacrum moves about an oblique axis. Should have concomitant somatic dysfunction of
the lumbar region (with lumbar or lumbars rotated to the opposite side of the sacral
rotation). Torsions either forward (left on left. right on right) or backward (right on left,
left on right). Most common: Left on left forward sacral torsion. Note: L5 must be
rotated in the opposite direction as the sacrum to be a torsion. Also, the seated flexion
test is generally positive on the side opposite the axis because the inferior pole of the
axis is fixed by a piriformis spasm. The superior pole of the axis is fixed by a quadratus
lumborum spasm. The KEY to determining whether you have a “forward” vs. a
“backward” sacrum is the LUMBAR SPRING TEST; if positive then the sacrum is
backward (bc the lumbars are kyphotic and thusly not physiologic). If you have a
normal or accentuated lumbar angle (avg. 30 degrees) then you will have a Forward
Sacrum because the base of the sacrum goes forward with lumbar extension/lordosis.

Sacral Rotation: Means L5 is rotated in SAME direction as sacrum.

Sacral Torsion: L5 rotated opposite sacrum

26
Flexion/Extension lesions: Remember flexion/extension in the muscle energy model
is opposite the cranial model. That is the postural and respiratory models are not to be
confused. Both have an axis in the S2 region, but then, are called "middle transverse"
for the postural, muscle energy model and "superior transverse" for the respiratory
cranial model. If a deep sacral sulcus is on the same side of the ILA being posterior-
inferior it is a unilateral sacral flexion lesion or sacral shear. For example: Deep sulcus
and posterior-inferior ILA on the left = left unilateral sacral flexion lesion or left sacral
shear. If both sulci deep = bilateral sacral flexion. If both sulci, shallow = bilateral sacral
extension. If the there is a unilateral shallow sulcus with a anterior/superior ILA with an
ipsilateral positive seated flexion test then it is a “unilateral sacral extension” dysfunction
(antishear). Most common USFL/shear is on left. Mnemonic: United States Football
League. You can also have a bilateral sacral flexion or extension lesion (postural
model) whereby the sacral sulci are either deep or shallow bilaterally.

The fifth lumbar: Is key to the latest version of sacral dysfunction: If L5 is rotated
opposite to the sacrum you most likely have a sacral torsion. If L5 is rotated in the
same direction then it is a sacral rotation.

Spring test: Used to distinguish whether you have a backward v. forward sacral torsion.
If the lumbars are taut, kyphotic, tense and do not spring well on compression in the
prone position = positive spring test. Also,if the lumbosacral angle of Ferguson is less
than 25 degrees it constitutes a backward sacral “something”. If the LS angle is greater
than 35 degrees it constitutes a hyperlordosis of the LS spine (Forward sacral
something). If the lumbars retain natural lordosis and are flexible = negative spring test.
Positive = backward torsion. Negative = forward torsion.

27
Nomenclature: Name Rotation on Axis. Mnemonic: Rheumatoid Arthritis

DEEP
SULCUS

Note: in the above the Seated Flexion Test was positive on the Left. If it were
positive on the right then you would have a “Right Unilateral Extension” sacrum.

Note: Spring test equivocal or negative and positive with shear.

Note: + seated flexion test is opposite the axis in a torsion and ipsilateral in
a shear.
Note: Sacrotuberous ligament taut on side of posterior inferior ILA and posterior
innominate.

28
Muscle Energy Treatment of Sacrum:
Forward sacral torsion: In any torsion whether it's forward or backward always lie the
patient on the involved axis. If left axis, lie on left side, etc. etc. For forward torsion, lie in
the lateral Sims's position, that is their chest is forward on the table. Have patient flex
both legs and attempt to bring both ankles toward the ceiling against your isometric
resistance. Muscle energy activates the Golgi tendon reflex (changes in muscle
tension).

Backward sacral torsion: Patient in lateral recumbent position that is their back is
towards the table. Have patient straighten out bottom leg on table, straighten upper leg
with the hip semi-flexed and attempt to bring their ankle/knee towards the ceiling
against your isometric resistance.

Sacral shear (unilateral sacral flexion): Patient prone. You place thenar or
hypothenar eminence on their ILA and push cephalad and anteriorly as they inhale.
Remember, the lumbar curves increase with exhalation, decrease with inhalation. The
mechanism for a sacral shear is the same as for an innominate shear (superior or
inferior), such as a “misstep”.

Unilateral Extension sacrum: Place thenar or hypothenar on sacral base and push
down with exhalation.

Sacral Rotations: Essential L5 is rotated in the same direction as the sacrum.

Summary:

FST: Negative spring, deep sulcus opposite post/inf ILA: lat. Sims's (forward on
table 2 legs)
BST: Positive spring, deep sulcus opposite post/inf ILA: lat. recumbent (back on
table, one leg).
USF/shear: Negative spring, deep sulcus ipsilateral to post/inf ILA; prone
position.

Primary ligaments of sacrum: Anterior, Interosseous and Posterior sacroiliac

ligaments. The long dorsal sacroiliac ligament promotes a posterior sacral base.

Accessory ligaments of sacrum: Sacrospinous, Sacrotuberous and iliolumbar

ligaments. The sacrotuberous ligament promotes a forward sacral base.

Romboid of Michaelis: Diamond from PSIS to spine of L5. Then from PSIS to
tip of sacrum. Deviation indicates possible malalignment of sacrum.

29
 Sciatic nerves leaves the pelvis via the greater sciatic foramen.

Note: Sacrotuberous ligament is taut with a post/inf ILA or posteriorly rotated

innominate.

Note: Iliolumbar ligament attaches from the transverse processes of L4/5 to the
PSIS/iliac crest. Dysfunction here can refer pain to groin and simulate "hernia"
symptoms. Occurs on side of lumbar convexity.

Sacral motion during vaginal delivery: Counternutation = base going in

extension or backward about the middle transverse axis. Nutation (nodding) =
base going in flexion or forward about the middle transverse axis. At zero
station (and negative 3, 2 and 1 leading to it) the sacrum is counternutated
(sacral base posterior). The opposite is true for plus one-three stations.

THE MANY DIAPHRAGMS OF THE BODY

Tentorium cerebelli: One of four reduplications of cranial dura. Dura mater lying
transversely on posterior cranial fossa separating cerebellum from cortex. Area of
automatic shifting suspension fulcrum (Sutherland’s Fulcrum in the “area of the straight
sinus”). Is pierced by the midbrain.

Sibson's fascia: Thoracic inlet, measures 4 by 2 inches, attaches C7-TI around first rib
to manubrium, also attaches to cupula of lung. Comprised of fascia from the scalenes
and the longus colli muscles. Thoracic Duct travels up through and down through this
diaphragm before entering into the venous circulation (junction of the left internal jugular
and subclavian veins). The right (minor) duct empties into the region of the
brachiocephalic vein. NOTE: OMT third edition by Saverese et al. mistakenly notes the
left duct as “minor” on it’s illustration.

Thoracoabdominal: 60% motive force for inhalation. Innervated by C3-5 somatic

nerves. Hiatus for vena cava is T8, esophagus is T10 and aorta (and thoracic duct) is
T12. Influences Cisterna Chyli at level of L2 Attached to the lower six vertebra and
ribs and upper three lumbars.

Pelvic: Comprised of two muscles, levator ani and coccygeus. Somatic and
parasympathetic innervation by the cord segments S2-4 (pudendal and pelvic
splanchnics respectively).

Popliteal fossa: Fascial pathways for lymph from the leg. The fascia of the hamstrings
attach and become contiguous with the sacrotuberous ligament.

Medial longitudinal arch of foot: Navicular and plantar fascia supportive and stress
bearers.

30
 THORACIC INLET VS. THORACIC OUTLET
Thoracic Inlet: Structures coming from the head, neck and upper extremity enter the
thorax through the thoracic inlet. It is the opening for the pharyngeal structures into the
thorax and is one of the many diaphragms of the body.

Keep in mind that these diaphragms assist in maintaining the intracavitary pressures
(intrathoracic {-}, pharyngeal {+} and abdominal/pelvic {+}). The maintenance of these
pressure gradients is vital for fluid movement.

The thoracic duct travels up through the thoracic inlet to the level of C7, then reenters
the thoracic cavity through the thoracic inlet to empty into the venous system.

Buzz words for the thoracic inlet: Sibson's fascia and suprapleural membrane. These
keep the pharyngeal structures from being "sucked" into the thorax by the negative
pressure in the thoracic cavity.

Thoracic Inlet

Structures Functional Anatomic

Apices of the lungs T1, T2, T3, T4 Manubrium
Trachea Ribs 1 & 2 Ribs 1 & T1
Esophagus Manubrium
Brachiocephalic veins
Vagus
Cervical symphathetics
Phrenic Nerve
Thoracic Duct

Thoracic inlet assessment: This is used to assess the dimension of thoracic inlet
torsion. Example:
 If the left coracoclavicular angle is anterior or more convex = right
coracoclavicular angle is deep = Thoracic inlet is rotated to the
right.
 If left rib is elevated = Thoracic inlet is sidebent to the right.
 Rotation is assessed by the coracoclavicular angle or infraclavicular
fossa. Sidebending is determined by an elevated 1st rib.
ALWAYS TREAT THORACIC INLET BEFORE LYMPHATIC
DRAINAGE: DON’T “MUDDY THE WATER’S”.

31
Thoracic Outlet: Structures leave the thorax through the thoracic outlet mainly to the
upper extremities.

Thoracic Outlet

Clavicle
1st rib
Neurovascular Bundle

Downward displacement of the clavicle onto the 1st rib may cause compression of the
neurovascular bundle resulting in thoracic outlet syndrome. Compression of the
subclavian artery and brachial plexus may occur: (1) As these structures pass through
the triangle formed by the 1st rib and the anterior and medial scalenes; (2) As the
neurovascular bundle passes between the pectoralis minor near its attachment to the
coracoid process and the rib cage. The subclavian artery, brachial plexus and
sympathetics leave bt the anterior and medial scalenes. The subclavian vein exits
anterior to the anterior scalene muscle.

32
 COMMON COMPENSATORY PATTERN OF ZINK
Dr. Zink described patterns of fascia, which alternated direction at certain anatomical
junctions (OA [occipitoatlantal], Thoracic Inlet, Thoracolumbar area, Lumbosacral area).
It is also called the “Respiratory/Circulatory Model”. These junctions coincide with
diaphragms of the body. According to Dr. Zink the alternating fascial patterns are the
body’s response to provide postural compensation, most importantly from the effects of
gravity. Most common pattern is L, R, L, R.

• OA-- Rotated to left.

• Thoracic inlet-- Rotated (and side-bent) to right
• Thoracolumbar junction-- Rotated to left
• Lumbosacral junction-- Rotated to right

Note: This is the most compensatory (physiologic) pattern of fascial directions. As long
as it alternates L-R-L-R (80%) or R-L-R-L (20%) this is good. Very dysfunctional to have
R-L-L-R or R-R-R-R, etc.

33
 Lymphatics
“We strike at the source of life and death when we go to the lymphatics.” (1, p68)
(A.T. Still, The Philosophy and Mechanical Principles of Osteopathy, pg 68)

“What we meet with in all diseases is dead blood, stagnant lymph, and albumen in a semi-vital or
dead and decomposing condition all through the lymphatics and other parts of the body, brain,
lungs, kidneys, liver and fascia.” (2, p71)
(Webster, GV: Sage Sayings of A.T. Still, Reprinted 1991, American Academy of Osteopathy,
p71)
Note: Primary information for this chapter is derived from: Wallace, et al, Foundations for
Osteopathic Medicine; Kuchera and Kuchera, Osteopathic Considerations in Systemic
Dysfunction; Dowling, An Osteopathic Approach to Diagnosis and Treatment; and Willard, et al,
Foundations for Osteopathic Medicine. Proceeds from this section have been given to the
Undergraduate American Academy of Osteopathy, (UAAO).
I. Overview:

The right upper extremity, the right hemicranium (including the head and face), and the
heart and the lobes of the lung (except the left upper lobe) drain into the right (minor)
lymphatic duct (3, p943). Lymph from remainder of the body traverses Sibson’s fascia of
the thoracic-inlet up to the level of C7 before turning around and emptying into the left
(major) duct. The right (minor) duct only traverses the thoracic duct once (4, p86, 210)

The lymphatic drainage into the right (minor) duct is variable; it usually drains into the
right brachiocephalic vein or the junction of the right internal jugular and subclavian
veins.

The lymphatic drainage into the left (main) duct is more consistent: it drains into the
junction of the left internal jugular and subclavian veins.

34
 Therefore, lymphatic drainage from an infection of the right first toe would drain into the
left (major) lymphatic duct. A left maxillary sinus infection would drain into the right
(minor) duct, as would extracellular fluid resulting from lymphedema of the right upper
extremity.

II. Anatomicophysiologic Relationships:

Lymphatics are tubes lined with endothelial cells which drain the interstitium and viscera
in general (5, p1605). Lymphoid tissues are aggregates of lymphocytes and other
immune cells (5, p1605). Not all lymphoid tissues (for example, lymph nodes) are
connected to lymphatic capillaries. Not all lymphatics are connected to the lymphoid
tissue. The thyroid, esophagus and the coronary and triangular ligaments of the liver
bypass lymphoid tissue and drain directly into the lymphatic duct. (5, p1605).
Traditionally, the superficial skin, deep portions of the peripheral nerves, the
endomysium of muscles, and bones were thought not to have lymphatic vessels.
However, they have prelymphatics, the Haversian canals being an example. Two-thirds
of the lymphatic fluid is produced by the liver and intestines (6, p180) Also, the
cerebrospinal fluid is the de facto lymph of the central nervous system.

The lymphatic duct extends approximately 18 inches from the cisterna chyli below the
diaphragm (at the level of L2), through the aortic hiatus (at the level of T12) into the neck
for about 3 centimeters before draining into the left (main) duct. (4, p86).

Embryologically, the lymphatic system is developed by the third month in utero and the
lymph vessels are closely related to the development of the venous system. However, the
lymph vessels have more valves than do the veins. These valves are also semilunar (5,
p1605). The terminal lymphatic capillary has a “flap valve” which allows fluid to enter
in addition to anchoring filaments into the surrounding connective tissue (fascia).
Interstitial fluid may also enter the terminal lymphatic vessel via micropinocytosis (5,
p1605). All of these factors conspire to keep the fluid in and propel it proximally to
lymph nodes and into the central circulation.

Ordinarily, the lymphatic return to the heart in a day’s time is equal to the “entire volume
of serum of the body” (4, p39). Approximately 10-20% of extracellular tissue fluid is
carried from the interstitium to the blood circulation. This translates into at least 3 liters
of fluid per day (5 p1605; 3, p944).

III. Factors Influencing Lymphatic Fluid Movement:

The lymphatics relieve the body’s excess fluids and wastes by both intrinsic and extrinsic
forces. Osteopathic manipulative treatment as well as exercise would be an example of
the latter. The lymphatics cleanse the body of immune complexes, bacteria, viruses, salts
and 50% of the plasma proteins. Substances found in the lymph include amino acids,

35
 glycerol and glucose (7, p256). Vital to one’s nutritional state, the intestinal lymphatics
absorb long chain fats, chylomicrons, and cholesterol (3, pp944-945). Lymph also
contains clotting factors. The main cell found in lymph are lymphocytes. Hence, the
lymph is essential for bringing particulate matter to both immune cells (for example
lymphocytes) and lymphoid tissue (for example, nodes) (3, pp943-944). It is important to
realize that the lymphatic capillary is under the same sympathetic influences as are other
vasculature. The sympathetics constrict the lymphatic capillaries. Initially, this will lead
to an increase in perstalsis of the lymph vessel. Sustained, inappropriate symppathetic
tone (hypersympathetonia) may however decrease the overall movement of lymphatic
fluids. Although there are cholinergic fibers in the lymphatics, little is known of the
parasympathetic influence upon the lymph movement. Nitric oxide vasodilates the
lymphatics (Willard, 2004). The sympathetic control to the lymphatic duct is
topographically innervated by the intercostal nerves . The cisterna chyli is innervated by
T11. (8, p120)

Factors allowing extracellular fluid to enter the lymphatic capillary. According to

Guyton (6, p182):

1. Increased capillary pressure.

2. Decreased plasma colloidal osmotic pressure.
3. Increased protein in the interstitium.
4. Increased capillary permeability
The interstitium is normally –6.3mmHg and flows at a rate of 120cc/hr. An increase to
0mmHg will increase lymph flow twenty-fold (3, p945).
Factors increasing interstitial pressure that correlate to numbers 1-4 above are according
to Wallace, et al (3, p945):
1. Systemic hypertension.
2. Cirrhosis.
3. Hypoalbuminemia associated with starvation.
4. Toxins such as rattlesnake poisoning.

Factors allowing lymph to move into the central circulation are according to Gray’s
Anatomy (5, p1606):

1. Smooth muscle contraction of the vessel.

2. Pulsation of adjacent arteries.
3. Contraction of the muscles.
4. Respiratory movement to increase negative intrathoracic pressure

36
III. Osteopathic Diagnosis for Lymphatic Dysfunction (4, p206). According to Drs. Kuchera
this includes but is not limited to the following:

1. Supraclavicular fullness and bogginess resulting from lymphatic

congestion of the head and neck. Eg., sinusitis.
2. Posterior axillary fold fullness and bogginess resulting from lymphatic
congestion of the arm. Eg., post-mastectomy lymphedema.
3. Epigastric area fullness and bogginess resulting from organ congestion of
the chest or abdomen. Eg., cirrhosis.
4. Inguinal area fullness and bogginess resulting from lymphatic congestion
of the lower extremity. Eg., infection.
5. Popliteal area fullness and bogginess resulting from lymphatic congestion
of the leg. Eg., thrombophlebitis.
6. Achilles tendon fullness and bogginess resulting from lymphatic
congestion of the ankle or foot. Eg., sprained anterior talofibular
ligament.
Additionally, other many areas of dysfunction may be apparent. Some of these
include:

7. Tense pelvic diaphragm (levator ani and coccygeus muscles)

8. Restricted thoracic cage motion (7, p258)
9. Viscerosomatic tissue texture changes (Chapman’s reflexes) from
lymphatic congestion of any organ.
10. Increased lumbar lordosis with resultant flattened diaphragm.
11. Torsioned thoracic-inlet.
12. Cranial base strain, particularly along the attachments of the
tentorium cerebelli (occiput, parietals, temporals, sphenoid or ethmoid).

V. Osteopathic Treatment for Lymphatic Dysfunction. This includes

but is not limited to the following:

1. Chapman’s reflexes. For example, lymphatic congestion of the bronchus,

upper or lower lung may involve a gangliform contraction of the second,
third or fourth intercostal space along the parasternal border respectively
anteriorly or a rubbery nodule (it feels like a classic viscerosomatic reflex)
between the spinous and transverse processes of T2, T3 or T4
respectively. There are about 100 recorded Chapman’s reflexes in the
body.
2. Thoracic Pump (of Miller). This facilitates increased rib cage motion in
addition to mobilizing total lymphatic fluid movement.
3. Lymphatic Pump (of Dalrymple). Again, this encourages total body
lymphatic movement and is particularly useful for the pediatric patient.
4. Osteopathy in the Cranial Field. This will decrease dural strains of what is
considered the uppermost diaphragm of the body, the tentorium cerebelli
and the reciprocal tension membrane in general. This will also increase
venous return from the head by undoing strains at the occipital and

37
 temporal regions which make up the jugular foramen. In addition, the
CSF not only is considered the lymphatic fluid of the brain but also drains
directly into the facial and spinal lymphatics.
5. Muscle Energy or any treatment to the Thoracic-Inlet. Remember
Sibson’s fascia is made up of the connective tissues of the scalenes and
longus colli muscle and is traversed by the both thoracic ducts.
6. Rib raising. This will increase thoracic motion by lessened somatic
dysfunction of the spine, ribs and sternomanubrial-clavicular complex.
Also, normalization of the parathoracic sympathetic ganglia are achieved
by rib raising.
7. Splenic/Liver Pump. This facilitates bringing toxins and other antigens
into close contact with the macrophages of the liver (Kupffer cells) and
allows the spleen to screen and remove damaged cells form the circulation
(3, p957, 7, p258).
8. Facial Sinus Pressure/Galbreath Technique. This includes direct
“stroking” of the frontal, nasal, maxillary and zygomatic bones and/or
TMJ in order to facilitate lymph movement toward the jugulodigastric
node (just anterior to the TMJ) and eventually distally to the thoracic
ducts. This is useful in sinus congestion or otitis media.
9. Anterior Cervical Mobilization. Basically, gentle translatory (right to left,
vice versa) motion of the hyoid, thyroid, cricoid and trachea will also
encourage lymphatic drainage of the head, neck and throat.
10. Extremity Pump (of Wales). Involves effleurage wave-like motions of the
arms and legs in order to move lymph proximally to the axillae and groin
respectively before terminating into the thoracic ducts.

VI. Indications for lymphatic treatment include. According to Wallace, et al,

this list includes but is not limited to the following:

1. Upper respiratory infections such as sinusitis, otitis, pharyngitis.

2. Bronchitis, pneumonia, asthma, COPD, atalectasis.
3. Post myocardial infarction, congestive heart failure,
myoepipercarditis.
4. Mastitis, lymphedema
5. Gastrointestinal disorders such as hiatal hernia, Crohn’s or colitis.
6. Cirrhosis, chronic hepatitis, pancreatitis, nephrotic syndrome (9,
pp24-28).
7. Premenstrual syndrome, uterine fibroma, endometriosis, cystitis.
8. Disorders of the extremities including tendinitis, joint swelling
from infection or trauma, ezcema or psorasis.

VII. Contraindications to lymphatic treatment. This includes but is not limited

to the following:

38
 The distinction between relative contraindication and contraindications to
lymphatic technique are unfortunately not well deliniated. In fact, the
term “absolute contraindications” is not generally used when it comes to
lymphatic treatment. Here is an attempt to shed some clarity on the
situation. Remember, treat each patient on an individual basis. The
following lists are mostly extrapolated from Wallace et al (3, pp955-964)
and Dowling (7, p260).
Relative contraindications to treatment of the lymphatics include:

1. osseous fractures.
2. Bacterial infections with a temperature greater than 102 degrees
Fahrenheit.
3. Abscess or localized infection.
4. Osteoporosis (with thoracic pump).
5. Certain stages of carcinoma, although this fact has not been
demonstrated. Dowling argues that a case can be made for the
delivery of cancerous cells to the body’s immune system for
clearance and destruction (7, p260).

Contraindications to the treatment of the lymphatics include according to

Wallace, et al, but is not limited to the following:

1. Rib raising and thoracic pump contraindications include

fractures/dislocations of the thoracic cage, lymphatic malignancy
or a decreased ability to cough.
2. Pedal pump or abdominal pump contraindications include
fracture/dislocation of the thoracic cage, recent trauma or surgery
to the abdominal viscera or a full stomach.
3. Liver and spleen pump contraindications include thoracic cage
bony fractures or dislocations, lymphatic malignancy, recent
trauma or surgery to the viscera, acute hepatitis or infectious
mononucleosis.

References:
1. Still, AT, The Philosophy and Mechanical Principles of Osteopathy, 1892,
Osteopathic Enterprises, Kirksville, MO, 1986.
2. Webster, GV, Sage Sayings of A.T. Still, reprinted 1991, American
Academy of Osteopathy.
3. Wallace, E, McPartland, JM, Jones III, JM, Kuchera, WA and Buser, BR,
Lymphatic Manipulative Technique in Foundations for Osteopathic
Medicine, Ward, RC, Editor, Williams and Wilkins, Baltimore, MD, 1997.
4. Kuchera, ML, Kuchera, WA, Osteopathic Considerations in Systemic
Dysfunction, Revised Second Edition, Greyden Press, Columbus, Ohio,
1994.
5. Gray’s Anatomy, 38th Edition, Churchill Livingston, New York Edinburgh
London Tokyo Madrid and Melbourne, 1995.

39
 6. Guyton, AC, Textbook of Medical Physiology, 8th Edition, WB Saunders
Company, Philadelphia, PA, 1991.
7. Dowling, DJ, Evaluation of the Thorax in An Osteopathic Approach to
Diagnosis and Treatment, Second Edition, DiGiovanna and Schiowitz,
Eds., Lippincott-Raven, Philadelphia, PA, 1997.
8. Willard, FH, Mokler, DJ, Morgane, PJ, Neuroendocrine-Immune System
and Homeostasis in Foundations for Osteopathic Medicine, Ward, RC,
Editor, Williams and Wilkins, Baltimore, MD, 1997.
9. Rivera-Martinez, S, Capobianco, JD, Osteopathic treatment of
nephrotic syndrome, American Academy of Osteopathy Journal, Volume
11, number 3, Fall, 2001, A publication of the AAO, Indianapolis, IN, pp24-
28

SPINAL CORD/COLUMN
Facets of cervical spine are oblique.
Facets of thoracic spine are coronal.
Facets of lumbar spine are sagittal.

Cervical spine:

OA = flexion/extension (50%), 45 degrees each

AA = rotation (50%), 45 degrees each
C2-7 = increasing sidebending as you proceed distally. Joints of Luschka are lateral
ridges along the superior aspect of the vertebral body that prevents sideslipping,
sidebending of the cervical spine.

Spinal cord:

Ends at L1-2 vertebral level (L3 in infant)

Thirty-one pairs of nerve roots (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal)

SCIATIC NERVE
• Comprised of L4-L5 and S1-S3
• Peroneal portion pierces belly of Piriformis 10% of population. Most often exits
inferior to muscle and 0.5% exits superiad to muscle.

40
 • “Sciatica” is a lay term to describe a syndrome of chemical irritation of the nerve
bundle, usually related to piriformis spasm, in which pain does not extend below
the knee.
• Note: “Psoas syndrome” usually involves contralateral piriformis spasm.
• Common peroneal nerve called the “common fibular nerve” or “fibularis”. Injured
when a bumper of a car comes into contact with your knee. A posterior fibular
head can cause impingement of the fibularis nerve and cause foot drop.

MUSCULOSKELETAL PATHOLOGY
Herniated Disk
Herniated intervertebral disk (herniated nucleus pulposus): A posterior-lateral herniation
of the nucleus pulposus through the posterior longitudinal ligament. This is because the
PLL is the most weakest ligament, reduced in size to 50%. Most common between L4-5
and L5-S1 vertebral segments. Specifically, however, the fifth lumbar disk (btw L5-S1) is
the most commonly herniated. An L4-5 disk impinges the L5 root. L5-S1 disk impinges
an S1 root. This is because the pedicle “spares” and diverts the upper nerve out
laterally, away from the bulging disk. Remember, “herniation” is the extreme of “bulge”
or “protrusion”. A “sequestered” herniated nucleus pulposus is the most refractory
entity. The disk is not pain sensitive. All the surrounding structures are, however.

Lower extremity radiculopathies are mainly from L5-S1. Which nerve gets impinged in a
disc herniation at L5-S1? L5 or S1? The nerve root that is affected is S1. Herniations
affect the nerve root of the lower vertebral level. (See Netter’s plate no. 149).

Spondylolisthesis
♦ Most common type is isthmic spondylolisthesis (Type IIA). It is also the most
common cause of lower back pain in the pediatric population.
♦ Spondylolisthesis is a primary defect of the pars interarticularis.
♦ Anterior slippage of one vertebra on its subjacent vertebra. Most commonly L5
slips forward on S1.
♦ Most commonly occurs in the general population of < 50 y.o.
♦ The affected children will have an exaggerated lumbar lordosis, high gluteal
crease line (flattened, heart shaped buttocks) and tight hamstrings. The
hamstrings innervation is between L5-S1 nerve roots. The nerve roots are not
necessarily impinged but they are affected and cause somatosomatic reflex.
♦ Again, most common spasm is to the hamstrings!
♦ A Scotty dog seen on X Ray is a sign for spondylolysis:
Collar: Microfracture between the superior and inferior articular
facets
Eye: Pedicle
Hind leg: Spinous process
Fore leg: Inferior articular facet
Nose: Transverse process

41
Spondylolysis: Defect in the posterior neural arch (pars interarticularis which is at the
junction of the superior and inferior articular facets): usually bilateral; postulated as
microfractures sustained over time; gives rise (usually) to...spondylolisthesis.

Spondylitis: Inflammatory arthritis of the spine begins at sacroiliac, joint and ascends
up spine then extremities, males, 15-30 years old.

Spondylosis: Basically arthritis, degenerative, calcium build-up at the vertebral level.

Also means degeneration of the disk. Leads to spinal stenosis.

Spinal stenosis: Result of DJD/disk degeneration; spinal foramen closes due to

calcium build up and compromises spinal cord (normal AP diameter of canal is 1.2-1.5
cm). Gives rise to “pseudoclaudication" in which radicular symptoms are worse in
lumbar extension, for example, standing or walking. Symptoms are better with lumbar
flexion, for example sitting. "Pseudo" because true aortic-iliac plaque stenosis would
give leg pain/paresthesias that are relieved by simple rest, i.e. standing, which would
not relieve cord compromise (spinal stenosis).

L5: Best answer for the vertebra with “the most common congenital malformations”.

Diagnositic Tests:
• Sitting flexion: Tests sacroiliac dysfunction
• Standing flexion: Tests iliosacral dysfunction
• Trendelenberg: Tests strength of gluteus medius on the same side as the weight
bearing leg. Greater than 15 degree pelvic drop = (+).
• Hip Drop: Tests lumbar sidebending capability on opposite side to genuflexed
knee.
• Lachman: Tests anterior and posterior Collateral ligament laxity/rupture with knee
semi-flexed
• Allen (modified): Tests ulnar and radial collateral circulation of the hand
• Finkelstein's: De Quervain’s tenosynovitis of the wrist. Caused by inflammation
and overuse of the abductor pollicis longus and extensor pollicis brevis tendons
at the radial side of the wrist.
• Straight leg raising: Puts tension on the sciatic nerve epineurium from a disk
impingement.
• Patrick’s or FABERE test. Makes number four with lower extremity in the supine
position. Restriction in flexion, abduction, external rotation and extension
indicates degenerative (osteo) arthritis of hip.

42
 RIBS
Pump handle: Ribs 1-5; larger "spinotransverse angle", favors motion about a
transverse axis.
Bucket handle: Ribs 6-10, smaller "spinotransverse angle", favors motion about an AP
axis.

Treatment involving muscle energy:

• Rib 1: use anterior and middle scalenes
• Rib 2: use posterior scalenes
• Ribs 3-5 (6): use pectoralis minor
• Ribs 6-9: use serratus anterior
• Ribs 10-11: use latissimus dorsi
• Rib 12: use quadratus lumborum

Inhalation restrictions: Equals "exhalation somatic dysfunction", the rib is caught

expired, held down. Clinical example: Pneumonia or congestive heart failure. Cough
produces inhalation restriction/exhalation somatic dysfunction. “Restriction” is opposite
to “Dysfunction”.

Note: TREAT UPPER RIB IN RIB GROUP HELD DOWN

Exhalation restrictions: Equals "inhalation somatic dysfunction", the rib is caught

inspired, held up. Treatment involving respiratory cooperation will have operator
increasing thorax flexion for pump handle ribs and increasing thoracic sidebending for
bucket handle ribs as patient exhales. Clinical examples: Asthma or COPD.

Note: TREAT LOWER RIB IN GROUP HELD UP

Ribs 11 & 12:

Eleventh and Twelfth rib motion is caliper or pincer like motion. Inhalation will move
these ribs up, out and posteriorly. Exhalation will move them down, in and anteriorly.
The latissimus dorsi pulls the 11th and 12th ribs up, while the quadratus lumborum pulls
the 12th rib down.

43
 UPPER EXTREMITY
Shoulder has seven articulations (five true and two false): The costovertebral joint of the
first rib, the costosternal joint of first rib, the sternoclavicular, acromioclavicular and the
glenohumeral joints are all true shoulder joints. The scapulothoracic and suprahumeral
joints are false shoulder joints.

Rotator cuff: Mnemonic: SITS muscles for Supraspinatus, infraspinatus, teres minor
and subscapularis. Does little rotation, however, stabilizes and maintains glenohumeral
joint function, especially holding head of humerus in glenoid fossa and gliding it
inferiorly during abduction. (Kuchera). The teres major is NOT a rotator cuff muscle; it
is a medial rotator and adductor and helps latissiumus w/ extension. Supraspinatous is
the most commonly torn rotator cuff.

SITS: C5 somatic nerve

Falling forward on outstretched hand will tear infraspinatus and teres minor and
dislocate the humerus posteriorly. (Kuchera) Additionally, it will facilitate a posterior
radial head dysfunction at the elbow. Pronation=posterior radial head. Also, lateral cord
of brachial plexus compromised against coracoid process leading to paralysis or paresis
of cuff muscles.

Rotator cuff tear: Most common tendon torn is supraspinatus. Test: Jobe or Drop Arm.
common after age 40 due to lifetime of Gravitational stress on tendon with resultant
weaker arterial supply to muscle. Also, repeated wear and tear bt acromion and
humerus lead to weakness of muscle.

Spencer techniques for shoulder: (for glenohumeral motion restrictions)

1) Extension “Every
2) Flexion Fine
3) Circumduction Cartoonist
4) Circumduction with traction Creates, then
5) Abduction/adduction Abounds
6) Internal rotation/external rotation In Red
7) Abduction with traction Abs tracts”

44
 • New guidelines add ADDuction and EXTernal rotation to no’s 5 and 6 above.

Elbow dysfunction: Hyperpronation of forearm such as a forward fail onto the palm
creates a posterior radial head lesion. Tx: Hypersupinated, extend and thrust radial
head anteriorly.

Elbow dysfunction: Hypersupination injury, such as falling backward and landing on

the palm creates an anterior radial head. Tx: Hyperpronated, flex and thrust radiaI head
posteriorly.

Remember: Pronation = posterior radial head. Supination = anterior radial head

“ADD SOUP”= adduction of the elbow (olecranon points towards the body) with
supination and abduction of the elbow (olecranon points away from the body)
occurs with pronation.

Reciprocal motion of forearm: Abduction of distal ulnar causes medial glide of

olecranon and adduction of wrist joint with resulting distal glide of proximal radial head.
This creates a “carrying angle” which is greater in females (10-15 v. 5 degrees for men).
A decrease in carrying angle is called a “gunstock deformity” or cubitus varus.

Wrist dysfunction: Restricted extension due to ventral glide of proximal carpal bones
(scaphoid, lunate and triquetral) is most common. Lunate usual trouble maker, esp in
“carpal tunnel syndrome” or median nerve impingement. The true wrist joint is the
articulation of the radial with the scaphoid (navicular), lunate and triquetrial bones.
Carpometacarpal joint of thumb: Saddle shape, great motion (except axial rotation),
therefore susceptible to somatic dysfunction. Is the first and most common joint
involved with degenerative (osteo) arthritis.

Other carpometacarpal joints: Somatic dysfunction with dorsal glide.

Note: Gliding motions, which are considered minor motions, are the major area of
somatic dysfunction in the extremities.

45
 LOWER EXTREMITY
Femur: 1/3 length of human body. Has four axes: A-P (abduction 55, adduction 35),
transverse (flexion 85-130, extension 35), anatomical longitudinal (along shaft of femur),
and functional longitudinal (internal & external rotation: from line imagined from ASIS to
patella).

Note: Internal rotation of femur equals a relatively shortening of the leg.

(Kuchera)

Note: External rotation of the femur equals a relatively lengthening of the leg.
(Kuchera)

Knee dysfunction: Due to restricted gliding motions. Remember 6 glides: Posterior,

anterior, medial, lateral and anterior-medial (increased with knee flexion) and posterior-
lateral (increased with knee extension).

Usual somatic dysfunction of the knee are anteromedial, medial and posterior glide.
(Kuchera)

Anterior cruciate ligament: Keeps tibia from gliding anteriorly on femur. (Lachman's
test)

Posterior cruciate ligament: Keeps tibia from gliding posteriorly on femur.

Fibular head: Reciprocity of Proximal and distal fibula: Dorsiflexion of the ankle will
carry the proximal fibula anterior, lateral and superior. Plantar flexion (as part of a
supination/inversion or “sprained” ankle will do the opposite (fibular head posterior,
medial and inferior). PMI/ALS. This is the basis for direct (HVLA/ME) of a posterior
fibula head.

• Opposite occurs with internal rotation of tibia and inversion of ankle.

46
 • Plantar flexion of the ankle tends to create a posterior fibular head
• Dorsiflexion of the ankle tends to create an anterior fibular head
• Joint configuration of proximal tiblofibula joint is oblique therefore
glide is actually posterior-medially, or anterior-laterally. These are
coupled with inferior and superior glide respectively.

 HVLA treatment for posterior fibular head therefore involves thrusting the
proximal fibula head both anteriorly and laterally while flexing the knee,
externally rotating the tibia and everting the ankle to engage and
breakthrough restrictive glide barrier. Muscle energy is set up the same
(even though the standard literature has the pt in the inverted position, it is
incorrect and will be updated in the future to reflect the physiological motion
of the lower extremity).

 Usual somatic dysfunction of ankle joint occurs in plantar flexion when the
talus glides anteriorly, that is ankle is restricted in dorsiflexion and the talus is
restricted in posterior glide. (Kuchera)

 HVLA treatment for anterior talus/posterior tibia is "tug" thrust with ankle
locked out in dorsiflexion.

 An “anterior talus”= “posterior tibia”: “posterior talus”= “anterior tibia”

 Somatic dysfunction of the navicular bone is plantar glide plus internal

rotation (about an AP axis) of its plantar surface. (Kuchera)

 Somatic dysfunction of the cuboid bone is plantar glide plus external rotation
(about an AP axis) of its plantar surface. (Kuchera)

 Somatic dysfunction of cuneiforms is plantar glide.

 The second metatarsal/tarsal articulation is the LEAST mobile of any. This is

why “march” or stress fractures occur there.

 A long second toe in relation to a big toe is call Morton’s toe.

 Morton’s neuroma is a ganglion of nerve tissue bt the third and fourth toes.

 HVLA treatment for navicular, cuboid and cuneiform is "Hiss Whip Maneuver".
You literally whip the tarsals dorsally with thrust contact on plantar surface of
foot.

 Note: Again, somatic dysfunction of the extremities tends to involve a

restriction in gliding motion.

47
  Note: To paraphrase Dr. Korr: In any disease process there will be hypersympathetic tone. If you have
a sustained injury in the extremities and develop, say, reflex sympathetic dystrophy, you must treat the
cord levels that supply sympathetics to the extremities. Thoracic cord segments T2-8 supply the upper
extremity; thoracic cord segments T11-L2 supply the lower extremity.

SUPINATION INJURY OF THE ANKLE

Most common form of strain/sprain of the ankle is supination injury.
Supination of the ankle involves:
♦ Inversion
♦ Plantarflexion
♦ Adduction

Biomechanics of Supination injury of the Ankle

Structures Motion
Talus Moves anteriorly
Calcaneus Everts
Fibular head Moves posteriorly
Innominate (via Biceps Femoris) Rotates posteriorly
Sacrum Superior oblique axis,
usually on the same side of
the somatic dysfunction
Tibia Anterior medial glide/external rotation
Femur Internal Rotation
Navicular Plantar/Medial glide
Cuboid Plantar/Lateral glide

Pronation of the ankle involves:

♦ Eversion
♦ Dorsiflexion
♦ Abduction

Inversion sprain affects the anterior talofibular ligament. An eversion sprain affects the
deltoid ligament.

48
Ligaments most commonly affected in an ankle sprain are the anterior talofibular,
calcaneofibular and posterior talofibular (in this order).

SHORT LEG SYNDROME

Heilig formula:

Lift required (L) = Sacral base unleveling in inches (SBU)

Duration (D) + Compensation (C)

Duration: 1 = 1 to 10 years
2 = 10 to 30 years
3 = > 30 years

Compensation: 0 = Sidebending only

1 = Rotation toward the convexity
2 = wedging, altered facets

Example: 50 y.o. patient with a 1/4" SBU for the past 31 yrs with a compensation of
rotation toward the convexity, similar to that of a Type I group curve, with no major
spinal deformities (no zygopaphyseal or facet deformity, no wedging of the vertebra).

SBU = 1/4 " = 1/16"

Duration (3) + Compensation (1)

♦ If structural short leg (congenital, etc) the ASIS will be low and the medial
malleoli high on the side of the short leg.
♦ Functional compensation (due to sacral torsion, etc) the ASIS will be higher on
the side of the higher malleoli. A higher ASIS in posterior rotation of the
Innominate can be related to short leg only if it is compensated.
♦ Any sacral base unleveling of greater than 5 mm should be addressed
♦ Dropped sacral base will result in a short leg. May use lift therapy to correct the
short leg. Use Heilig to determine the lift required.
♦ The side of SBU is the side where the lumbar convexity will be found. This is
where the body begins to compensate.

49
♦ The final analysis for a heel lift will be different by a 50 to 75% less than the
original x-ray findings. This is due to x-ray distortion of bone size.
♦ Pelvis rotates and sideshifts towards the long leg side
♦ There is an increase in the lumbosacral angle of 2 to 3 degrees
♦ The shoulder will be low on the opposite side of the SBU
♦ Fragile/Acute pain/Aged, osteoporosis: 1/16" q 2 wk. Do not start with more than
1/16"
♦ Patient is stable: 1/8" q 2 wk
♦ Sudden loss (Acute fracture): restore full amount/length, this is to prevent
compensation by the body.
♦ Up to1/4” replaceable heel lift can be used inside the shoe
♦ Up to1/2" total heel lift can be placed between the heel of the patient’s foot and
the floor. This can be 1/4" inside the shoe & 1/4" to the heel of shoe. Not more
than 1/4” of the total heel lift can be placed inside the shoe.
♦ If an increase beyond a 1/2” heel lift must be added then use an anterior half
sole. Ex: If heel had been lifted 1/2” and an increase of 1/4” was required: 1/4”
would be added to the heel and 1/4” to the anterior half sole.
♦ Heel lift rotates pelvis opposite side
♦ Sole lift rotate pelvis same side
♦ Therefore if lift > 1/2" need half sole ON CONTRALATERAL SIDE.
♦ Lift therapy will elevate the lower extremity and sacral base and also rotate the
pelvis to the opposite side. This rotation of the pelvis needs to be addressed
when the lift is > 1/4". In this case you need an anterior half sole to help bring
back the pelvis to midline.

50
 PSOAS SPASM
♦ A psoas spasm will give you a non-neutral (Type II, usually flexion but may be
extension) somatic dysfunction at L1 and L2.
♦ The psoas originates from T12-L5 and inserts into the lesser trochanter of the femur
♦ Somatic nerves to the psoas are T12-L3. A psoas spasm can cause a contralateral
piriformis spasm leading to a piriformis syndrome with pain referral to the L2 range.
The nerve supply to the piriformis is S2.
♦ A spasm of the piriformis will be the cause of an Inferior pole in a sacral torsion. The
spasm anchors the inferior pole of the oblique axis. Sidebending of the lumbar spine
will anchor the superior pole of the oblique axis (usually via the quadratus
lumborum).
♦ The psoas can go into spasm in a patient that is passing a renal stone through the
ureters. Psoas spasm may also affect ureteral function since the ureters descend
on the fascia of the psoas. The upper ureter is innervated by T10-11. The lower,
T12-L1.

RANGE OF MOTION BY REGION

Region Range of Motion Muscles

Cervical Flexion - 45 degrees SCM/Scaleni

Extension - 90 degrees Trapezius/Spleni/Erector Spinae
Sidebending - 45 degrees SCM/Scaleni/Spleni/ES
Rotation - 90 degrees SCM/Scaleni/ES/Spleni
*SCM & Scaleni rotate opposite
Thoracolumbar Flexion - 45 degrees Rectus Abdominis/psoas
Extension - 45 degrees Erector Spinae
Sidebending - 45 degrees ABS/ES/Quadratus Lumborum/psoas
Rotation - 45 degrees Obliques/ES

REMEMBER: Range of motion only comprises 1/4th of somatic dysfunction!!!

T.A.R.T. Try to alleviate and improve the others.

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 SPECIFIC MUSCLE ACTIONS

Muscle Action
Suboccipital muscles Extends and rotates head to same side
Intertranversarii Bends column to same side
Rotatores Brevis Rotates column to opposite side
Splenius Extends, sidebends & rotates to same side
Trapezius Extends & sidebends toward; rotates away
Semispinalis Extend and rotate to opposite side
Longissimus Extends, sidebends & rotates to same side

Postural muscles: Antigravity. Cross weight bearing joints. If overused

tend to cause “spasm” in muscle.

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 Phasic muscles: Not involved w/ posture; more “voluntary” movements.
Overuse tends to cause “fatique” or weakness in muscle.

GATE THEORY OF WALL AND MELZACK

According to this theory, the substantia gelatinosa acts as a gating mechanism for the
control of afferent input to the spinothalamic neurons. The activity in pain carrying slow,
small unmyelinated C fibers keep the gates open and activation of fast, large myelinated
A alpha and A beta (nonnociceptive receptors) closes the gate. Impulses carried by the
larger faster fibers are thought to cause synaptic inhibition of the tracts carrying pain
perception (C and A delta fibers). Under this gate control theory, on the basis of all
afferent stimuli, the neurons of the spinal cord would decide whether or not a particular
event should be reported to the brain as being painful.

The spray and stretch technique for the treatment of trigger points is believed to act
through this theory. The vapocoolant or TENS unit activates nonnociceptive receptors
which report centrally via fast fibers. The afferent volley conveyed through these fast
fibers blocks the trigger point nociceptive impulses transmitted by slow fibers at the
substantia gelatinosum (lamina 5). This allows the operator to stretch the muscle
containing the trigger point without pain or reflex spasm. Adapted from Marieb/Mallatt
and Kuchera/Kuchera and Barr/Kiernan. Again, nociceptors=A delta fibers (also
classified as B-afferents or III nerves). A-afferents are non-nociceptors. When you
shake your hand after hitting your thumb with a hammer you are activated A-afferents
(non-painful receptors) to overcome A delta and C fibers (fast and slow pai

Coolant Spray (or TENS) Deep pain is blocked

Muscles can be stretched

and reset Gate is blocked (dorsal horn)

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 PAIN

PAIN
Fast fibers ascend the cord via the neospinothalamic tracts (acute). Slow fibers ascend
the cord via the paleospinothalamic tracts (chronic).

The fibers enter the dorsal horn, may ascend or descend a few segments, synapse at
the substantia gelatinosa which precedes the posterior grey matter, then cross over the
cord to ascend ultimately to among other areas the thalamus (and periaquaductal grey
matter of the ventricles) and cortex.

Pain from the viscera is transmitted via the sympathetic nerves. Exceptions include the
cervix, upper vagina, bladder trigone, prostate and the esophagus, trachea, and main
bronchi, which transmit pain via the parasympathetics (2). Remember, however, that
there are no parasympathetic fibers in the extremities. Autonomic mediated pain from
an extremity (reflex sympathetic dystrophy) is the result of sympathetic activation and
During inflammation of an organ, the appendix for example, pain is first recorded in the
“visceral layer” which obviously refers pain to the embryological origin (around the
umbilicus) then inflames the “parietal layer” (and peritoneum) which stimulates the
somatic nerves which are dermatomally related, in this instance to the right lower
quadrant of the abdominal wall. Thusly the pain of appendicitis “moves” because of
different neural activation; first the visceral then somatic. In addition, the organs are
insensitive to burning, cutting, heat and cold but are sensitive to traction, distension,
anoxia or contractions (2). Pain from the uterus is T10-L2. Pain from the perineum is
via the pudendal somatic nerve, S2-4. The Percutaneous Reflex of Morley is
“somatic pain located directly over an inflamed organ. It is produced by direct irritation
of the parietal peritoneum and abdominal wall. It is responsible for rebound tenderness
and abdominal guarding associated with severe abdominal pain. “ (Source:
Foundations, second edition, 2003).
Pain insensitive structures may include the parenchyma of the brain, hyaline and
articular cartilage and the nucleus pulposus.
Pain is initiated by potassium, serotonin, substance P, cytokines, bradykinins,
kinins, prostanoids/prostaglandins (edema, inflammation) which activate the B-afferent
(unmyelinated or thinly myelinated, slower fibers) into the dorsal horn. They may
facilitate WDRN (wide dynamic range neurons) at the substantial gelatosa (lamina II).
Faster nociceptors such as A delta fibers transmit sharp, acute pain. They are thinly
myelinated and classified as class III neurons. C fibers transmit dull pain and are
classified as IV fibers. C fibers are unmyelinated. Class I and II neurons are non-
nociceptive. N-methyl-D-aspartate receptors are pain receptors. GABA is inhibitory to
pain.

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NERVE ENTRAPMENT SYNDROMES

Nerve Entrapment Site

Median carpal tunnel, transverse carpal ligament

Ulnar cubital tunnel, tunnel of Guyon

Radial supinator muscle

Brachial thoracic outlet, pectoralis minor

Sciatic piriformis muscle

Common Peroneal posterior fibular head (“foot-slap”)

Posterior tibial tarsal tunnel (medial ankle)

Lateral femoral cutane. inguinal ligament (meralgia paresthetica)

(source: Foundations, second edition, 2003)

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 FIBROMYALGIA
Pathogenesis and Clinical Presentation: Largely unknown. Look for a preceding
traumatic event. Abnormal levels of serotonin and norepinephrine and substance P.
Disturbances of stage 4 (non-rapid eye movement, non-REM) sleep. Female, pain,
stiffness and fatique. Total body pain for greater than 3 months in at least 11 of 18
areas:
1. Occiput, suboccipital mm
2. Low cervical, anterior intertransverse process space C5-7
3. Trapezius
4. Suprapinatus
5. Second rib at costochondral junction
6. Lateral epicondyle
7. Gluteals
8. Greater trochanter
9. Knee (medial knee fat pad)

Note: 9 areas bilaterally equals 18 total. You need at least 11 of the above (bilaterals
count for two areas) to secure a diagnosis of Fibromylagia. In addition, axial spinal pain
is important as having pain in 3 of the four quadrants of the body; ie, “my right arm, back
and both lower extremities hurt all the time.”

Treatment includes OMT, Tricyclics, SSRI’s, Cognitive Behavioral Therapy,

Cardiofitness

Restless Leg Syndrome: Akathisia. 5% of population, mostly elderly. Sensation is of

deep ache, “crawling sensation”, worst w/ rest, sleep (major cause of insomnia), better
w/ motion. Associated w/ Iron, Vitamin B, Calcium, K+ deficiency, excess caffeine,
sedative drug withdrawal and neuroleptic medication. Also associated w/ SSRI usage.
Familial. Pharmocologic treatment may include Carbidop/L-dopa combinations.

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 MISCELLANEOUS INFORMATION
♦ 1st rib: most dysfunctions are of exhalation restriction. Rib is stuck up.
♦ In a question regarding scoliosis that only refers to the side of the convexity of the
curve, this will indicate the side of the rotation. Sibebending will be opposite.
Ex: convexity to the right = rotated right, sidebent left.
♦ Piriformis tenderpoint for counterstrain is line bisecting PSIS/ILA and between the
greater trochanter. The psoas attaches to the lesser trochanter.
♦ L5 nerve root supplies motor innervation to the extensor hallicus longus.
♦ Muscles of the Pelvic Diaphragm = Levator Ani and Coccygeus. The innervation is
from S2-S4
♦ The first rib that you feel below the tip of the scapula is the 8th rib. Important
landmark for pleurocentesis. The tip of the scapula is at the level of the seventh
spinous and eighth transverse processes.
♦ Motion occurs perpendicular (ninety degrees) to an axis.
♦ There are about 206 bones in the human adult body. (just in case you’re on TV)

Law’s:

Wolff’s: Bone forms along lines of bodily stress

Hooke’s: Deformation proportional to stress
Newton’s 3rd: Force by first body exerted on second body equal in magnitude and
opposite in direction to the force exerted by the second body on the first body.
Sherrington’s: Contraction of one muscle relaxes antagonist. Also, Every spinal nerve
invades a specific region of skin, although fibers from other nerves may supply that area
too.
Head’s: When a pain stimulus is applied to an organ of low sensitivity an adjacent area
(soma) of high sensitivity will feel it. Pain finds it own level.
Cross Extensor Reflex: Someone steps on a nail and the opposite leg moves in flexion.
Can be used therapeutically to relax contralateral antagonist muscles.

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 Applied, Clinical and Surgical Anatomy:
The tunnel of Guyon transmits the ulnar nerve and artery. It is formed by a ligament
attaching the hook of the hamate with the pisiform bone.
Erb-Duchenne paralysis: C5-6 roots, upper trunk injury, "waiter's tip" hand.
Klumpke paralysis: T1 root, Lower trunk roots, caused by prolonged/abrupt upward
position of arm, breech delivery, apical lung tumor, scalene syndrome, cervical ribs.
Klumpkes="claw hand".
Also, may involve stellate ganglion=”Horner’s syndrome”.
"Crutch palsy/"saturday night palsy": Posterior cord, radial nerve, wrist drop.
Scalene syndrome (thoracic outlet): Lower trunk, lesion bt anterior and middle
scalenes. Causes medial arm and hand symptoms such as paresthesias and atropy.
Winged Scapula: Long thoracic nerve of Bell, C5-7, serratus anterior.
Dupuytren's contracture: thickening of the palmer fascia, affects the ulnar (4th and
fifth) fingers in a state of flexion. May see lesion/dysfunction of T1.
Nursemaid's elbow: posterior displacement of the underdeveloped proximal radial
head from the orbicular/annular ligament of the elbow. Caused by "yanking" on little
Janey's or Johnny's hand while crossing the street. Treatment involves supination and
flexion of the elbow.
KNOW that an "upslipped innominate/ilium"=superior innominate shear.
"Downslipped inn/ilium"=inf. inn. shear.
Also, IMPORTANT: for innominate/ilium: KNOW "outflare" v. "inflare". Use standing
flexion test (or leg lengthening/shortening test whereby pt. is supine and you flex,
externally rotate and extend leg and compare to opposite side to see whether there is a
movement (neg) or lack of motion (pos.) movement of the malleoli). In the "flares" you
determine which side is dysfunction (standing flexion/or leg length test--see above):
then you measure the umbilicus to ASIS. If one side greater than the other=outflare
(only name this side for the positive standing flexion test/leg length test). If the other
side is less distance=inflare ,Seated flexion test is only for SACRUM.
Speaking of sacrum: the "sacral compression" test gives you the same info as a seated
flexion test. The operator places her thenar/hypothenar eminence on the lateral aspect
of the sacrum/SI joint and presses anteriorly. A resistance=positive test=same as
seated flexion=same side as INFERIOR POLE OF THE AXIS (or, opposite axis).
Remember, a sacral torsion by definition means deep sulcus opposite a posterior-
inferior ILA. Torsions occur about an OBLIQUE axis. Use seated flexion/compression
test to determine which side the axis is on. Remember, if the seated
flexion/compression test is opposite a deep sulcus you have a BACKWARD sacral
torsion. If seated flexion/compression test is opposite a shallow sulcus=FORWARD
sacral torsion. A torsion also means that the lumbars or L5 are rotated OPPOSITE the
sacrum.

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A sacral rotation means that the sacrum rotates to the same side as the lumbars.
Determining whether you have a kyphotic v. lordotic lumbar spine (LUMBAR SPRING
TEST) is key to naming it backward v. forward sacral dysfunction.
The occipitoatlantal joints in NEITHER a type I or II mechanism exclusively. It involves
flexion/extension PLUS sidebending/rotation AWAY. The ligament that allows SB and
Rotation to occur opposite is the "lateral atlanto-occipital ligament".
The odontoid process of the axis (C2) is held to the anterior arch of the atlas via
the"transverse ligament". It allows SLIGHT flexion of C1 on C2. The odontoid (dens) is
very fragile in Down's syndrome and rheumatoid arthritis; HVLA is contraindicated in
these syndromes.
The pisiform, patella and fabella are sesamoid bones. The fabella, a sesamoid in the
hamstrings often seen on X-ray as an anatomic variant of normal.
The transverse ligament of the dens is called the cruciform ligament.
The lunate is anteriorly displaced when causing carpal tunnel syndrome.
The web space bt the thumb and index finger is supplied by the radial nerve.
Treatment of muscle energy involves an initial position of barrier/restriction. The pt.
pushes into the freedom. You go further through the barrier. The Still technique
involves going into the freedom (dysfunction named), then moving into the barrier.
Batson's plexus is in the epidural space. It's a pathway for pelvic cancer to spread.
The pia becomes the filum terminale.
The lateral (long) thoracic artery is the major artery to the breast. The internal thoracic
(mammary) artery is a minor supplier to the breast. It can be a collateral supply to the
heart, however.
The axillary nodes are the major drainage for the breast.
The scaphoid bone has an arterial supply distally, which makes for avascular necrosis
secondary to fracture.
The median (anterior) antecubital vein is for phlebotomy.
Know the SITS muscles. They do NOT incl the teres major. They include the
supraspinatus, infraspinatus, teres minor and subscapularis. The "stabilize" more than
rotate the glenohumeral bone. The latissimus is medial rotator, adductor and extender
of the shoulder. It's supply is C6-8.
Sacralization of L5 means L5 (trans. process) fuses with the sacrum. ( Batwing)
Lumbarization of S1 looks like an L6 bc S1 is separated from the sacrum.
The nucleus pulposus is a remnant of the NOTOCHORD.
31 pairs of spinal nerves. C8 exits bt C7 and T1.
Dura mater ends as coccygeal ligament.
The ganglion impar is anterior to the coccyx. It's the terminus of the sympathetic
nervous system.
Accomodation is a parasympathetic mechanism (CNIII)
Insertions onto the gr. trochanter: Piriformis/sup/inf gemelli, obtur ext/int and quad
femoris.
Lat cutan. fem. nerve (L2) innervates the outer/lateral thigh: entrapment leads to
Meralgia Paresthetica
What passes thru Hunter's canal (hiatus)? It contains the femoral artery, femoral vein,
saphenous nerve and nerve to vastus medialis. Site of femoral artery stenosis and
popliteal aneurysm.

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The tarsal tunnel is a condensation of crural fascia bt the med. malleolus and
calcaneus. It contains the tibialis post. muscle, flexor dig. longus muscle, post. tibial
artery and nerve, and flexor hallucis longus muscle. TOM/DICK ANd HARRY.
Sural nerve S2 can be harvested for use elsewhere. It's unnecessary.
The seasmoids of the great toe lie in the flexor hallucis longus muscle.
Spring lig. of foot is bt sustent tali of calcaneus and navicular. Supports the talus.
Vomeronasal organ of Jacobson is in the nasal septum, superior to the vestibule. It
may be used to sense phermones.
CN XI innervates the traps and scm muscles
Afferent limb of blink=CNV Efferent limb of blink=CNVII
Eye winks=orbicularis oculi=CNVII
Innervation to ear includes: CNV, VII, VIII, IX, and X. Also sensory from somatic
nerves C2, C3.
Muscles in spasm in “TMJ” syndrome: Masseter, medial pterygoid and temporalis.
The medial pterygoid muscle attaches to the tensor veli palatine and allows the
Eustachian tube to open. A low pitched tinnitus indicates an “externally rotated
temporal bone”. A “high pitched tinnitus” indicates an internally rotated temporal bone.
Most common temporal finding in TMJ: Externally rotated temporal bone.
Schlemm's canal is in the angle of the anterior chamber. Blockage of this (sinus
venosum sclerae) leads to glaucoma (ischemia).
Semicircular canals are suspended by perilymph.
Organ of Corti is suspended in endolymph (vibrations).
The infrahyoid mm.s are innervated by the ansa cervicalis (C1-3).
Branchial Arch: First, CNV, Second, CNVII, Third, CNIX, Fourth, CNX, Sixth, CNX
also. The whereabouts of the fifth arch is questionable.
20 deciduous teeth. 32 permanent. Enamel of teeth are derived from brain.
Platsyma=CNVII
Inferior (recurrent) laryngeal nerve=CNX, trapped by lig. arteriosum. Goes to intrinsic
mm. of larynx, except cricothyroid mm.
Emergency (field) tracheotomy=go thru the cricothryoid membrane.
"Flashing lights"=retinal detachment or scintillating scotoma of migraine.
Halos=digitalis toxicity or glaucoma.

REFERENCES
1. Kuchera WA. Glossary of osteopathic terminology. In: Ward RC, ed. Foundations for
Osteopathic Medicine. Baltimore, MD: Williams and Wilkins 1997, p. 1127-1140
2. Ellis, Harold, Feldman, Stanley. Anatomy for Anaesthetists, 6th Edition, 1993,
Blackwell Scientific Publications

PRIMARY SOURCES:
1. Kuchera and Kuchera, Osteopathic Principles in Practice, Revised 2nd edition,
1994
2. Kuchera and Kuchera, Osteopathic Considerations in Systemic Dysfunction,
Second Edition, 1994

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SECONDARY SOURCE:
1. Goroll, AH, Mulley, AG: Primary Care Medicine, Fourth edition, 2000

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