Segmental Facilitation

Identifying Central Pain
Manifestations
2009 AAOMPT Annual Conference,
Washington DC
Richard Kring, DMT, DPT, PT,
FAAOMPT
Facilitated Segment
• Korr: “barriers having been lowered.”
• Korr and Upledger:
– Reduction in the stimulus threshold in a
particular spinal cord segment. When
becoming highly excitable, a smaller stimulus
will trigger excessive impulse firing in the
segment.
Segmental
Facilitation
OGI
Hair triggered
• Nerve roots: “hair triggered”.
• Hyperactive motor root joins the
sympathetic chain state of constant
over-activity. further increasing
facilitation.
Threshold Spill Over
A.D.L.
Threshold
+
EmV
Interneuron Pool In A
Facilitated Segment
Of The Spinal Cord
Threshold
EmV
+
Interneuron Pool In A
Normal Segment Of
The Spinal Cord
• Shower
• Hair
• Brush Teeth
• Dress
• Cook
• Reaching
=
Threshold
EmV
A.D.L. + Facilitated
Segment
A.D.L.
• Shower
• Hair
• Brush Teeth
• Dress
• Cook
• Reaching
=
Threshold
EmV
A.D.L. + Normal
Segment
1
Facilitated Segment
• Denslow:
T4
– Result of a sustained barrage of subthreshold
impulses into the segment of the cord with the
lesion.
T6
• A central excitatory state is established.
Segmental Facilitation
I. Korr & J Denslow:
Ascending and descending intersegmental
neurons
Sensory endings in Spinous Process
T8
Recording Electrodes
T10
Location
•
•
•
•
Areas of postural stress
Sites of trauma
Areas related to visceral problems.
Once a segment is facilitated, all of the
target structures (connective tissue,
muscle, bone, blood vessels, skin, sweat
glands, and internal organs) will be
affected.
• Must interrupt the self perpetuating cycle.
Segmental Facilitation
2 Segments Involved
3 Segments Involved
4 Segments Involved
Complete Reciprocity:
all segments facilitated with
stimulus to any one of them.
Denslow J, Korr I, Drems A. The collected papers of Irvin Korr. 1947
Spinal Muscles
Influence
•Pain isby:
not what occursMaintenance
at the periphery by:
Influenced
•Pain: what the brain perceives:
• psychic
• proprioceptors
indisputably modifiable by emotions and
• emotional
• suprasegmental
beliefs
sources
• traumatic
•Actual damage is neither necessary nor
• visceral and other
• bacterial
sufficient for the perception of pain
afferents.
• physical.
Anger, depression, anxiety, fear, and
other psychological variables can all
increase the perception of both acute
and chronic pain
Goff
Findings
• Palpable changes: muscle &
subcutaneous
• Decrease in joint mobility
• Fibrositis: tender tissues
• Sympathetic: changes in tissue texture,
sweat gland activity, and capillary blood
supply to skin.
• Increase in muscle electrical activity
2
Treatment
• Focus on: relaxing the muscles
• Mobilization
• Reducing
Osteopathic Lesion /
Somatic Dysfunction
– stasis and edema
– postural stress
– the number of signals from higher centers in the CNS.
• Must break the cycle and reduce the number of
signals from higher centers of the CNS.
Osteopathic Lesion
• Denslow: “ Impaired or altered function of
related components of the somatic
system: musculoskeletal, arthrodial, and
myofascial structures, and related
vascular, lymphatic, and neural elements
Or Korr:
• “chronic segmental facilitation, a localizing,
channelizing, and predisposing influence
in the bodily expression, mental or
emotional imbalance”
• Cole: Instigates, augments, and maintains
an alteration in function through reflex
activity of the nervous system, including
the ANS.
Definitions cont.
• Korr : sustaining factor in disease
• Establishes and maintains a vicious cycle
of irritation, inflammation, and pathological
process
Multiple factors influence the process:
• Psychic
• Emotional
• Traumatic
• Bacterial
• and physical.
• Same as FS.
3
Results
• Greater tension on
one side increasing
proprioceptor firing.
Afferent input will
increase tension,
increase reflexive
activity, increase
sensitivity to the
gamma motor neuron
and increased alpha
motor neuron output.
Clinical Presentation
• Hyperesthesia of the muscles and
vertebrae
• Hyperirritability with altered muscular
activity
• Changes in tissue texture and local
circulation
• Altered visceral function.
OL / FS: Example
• Far greater spread to a lesioned segment
than from one.
– Ex.: A patient with a T-4 lesion, has a low
threshold to pressure at T-4. T-10 had a high
threshold to pressure, due to a lack of lesion;
however, produced contraction at the T4 level
even following local anesthetic.
Myofascial Pain Syndrome
Primary
Muscle
Clinical Findings: OL
• Denslow: Clinical evidence: hyperalgesia,
abnormal skin texture, anatomic
assymetry, and disturbance in range and
ease of joint motion.
• Digital palpation: painful, thickened soft
tissue, muscular rigidity.
• Hyperalgesia due to visceral, emotional,
and other disturbances.
Treatment
Manipulation:
• Induces muscle
relaxation
• Removing excitation
• Easing tension on
proprioceptors
• Lowering the
bombardment of impulses
from that segment to the
spinal cord
• Relieves hyperalgesia
• Normalize tissue texture
and joint restrictions
• Allows the body to
combat the original
infection
• Breaks up the reflexes
between the soma and
viscera
• Increases blood flow to all
areas
• Facilitates venous and
lymphatic drainage
4
Maigne / CTPM
Syndrome
Maigne:
Cellulotenoperiosteomyalgia
CTPM
• Segmental dysfunction altering the
sensitivity and texture of soft tissues:
detected by careful palpation of the
cutaneous (cellulalgia), muscular
(myalgia), and tenoperiosteal tissues.
• These will effect the same tissues for a
given segment.
Maigne: Findings
• Subcutaneous swelling and induration in
all or part of the dermatome: cellulalgic
• Indurated myalgic cords (trigger points)
localized in some muscles of the myotome
• Hypersensitivity of the tenoperiosteal
insertions of the scleratome on palpation.
Increased afferent
Barrage to DH
Manifestations
Source of
Nociception
Maigne
• A focusing factor, the irritation of the
corresponding spinal nerve. Near constant
bombardment of the spinal cord can bring
about a state of facilitation of a neuron
whose cellular body is localized to the
same spinal cord segment and provoke
motor and autonomic responses.
Neurodynamics
5
Neurodynamics: Background
Neurodynamics and Neuropathy
• Walsh2005 and Shacklock 2005
• “Mechanical and physiologic properties of the
peripheral nervous system that are dynamically
interdependent, and correlates the effects of
tension and excursion on the peripheral nervous
system.”
• “Alterations in neurodynamics will manifest as
adverse neural tension. Changes in neural
physiology and mobility may result in the
development of the patient’s symptoms.”
• Treatment to restore normal neural physiology
• Adverse neural tension presents with
neuropathic pain as a primary feature.
• Neuropathic pain: “pain initiated or caused
by a primary lesion or dysfunction in the
peripheral nervous system”
AIGS
Neuropathic pain
• If a nerve is damaged by trauma or
disease, it may become demyelinated
resulting in an abnormal impulse
generating site.
• Central sensitization – causative factor,
may need to be treated to break cycle.
Neural tension testing:
Findings
• Active and passive motion dysfunction
• Palpable neural hyperalgesia
Hyperalgesia
• Local tender points in tissues innervated
by the hypothesized segment.
Myalgia and cellulalgia
• Presence of local dysfunction.
Segmental dysfunction
• May be linked to stress via the
sympathetic nervous system and antalgic
posturing to relieve mechanical tension on
the offending neural tissues.
Central
Sensitization
6
Central Sensitization
• Woolf 1993: (Melzak and Wall) CS is a response
of the dorsal horn neurons to normal afferent
input which is augmented or facilitated. This is
the result of modification of the receptive field
properties of dorsal horn neurons including:
• Reduction in threshold
• Increase in responsiveness
• Recruitment of novel inputs : A-beta
• Increase in size of the receptive field.
• Spread of pain to uninjured sites.
– Ji and Woolf
• Cellular change from repeated input due to
functional plasticity of the CNS.
• Local anesthesia to the site of injury has
no effect.
• Recruitment of receptive fields outside of
this region means a change within the
CNS and not an increased sensitivity of
the peripheral terminals of sensory fibers
innervating the injured tissue – peripheral
sensitization.
• CS vs PS: PS is a source, not needed to
maintain.
Neuroimm
Proinflam. Cytokines.
Activate glial cells.
Inhibits the inhibitory interneuron
Inf Mediators
Trauma
Synthesize cytokines, proteases,
NO, glutamate, Stimulates
NMDAR
Ion channels: cyclic and self
sustaining.
Sensitization
Noci:C&Ad
Peripheral sensitization:
Cyclic and self sustaining.
• Early on after injury: neuroimmune
activation induces central sensitization
either directly or indirectly by inhibiting the
inhibitory interneuron activity at the dorsal
horn.
DRG
Dorsal Horn. Central processing.
Up to thalamus to become
Conscious.
Decreased Threshold!
• May become sensitized by: an emotional
event or residual somatic symptoms of
depression or anxiety rather than from a
peripheral painful input.
– (Stress may sensitize emotional centers in the
amygdale and limbic cortex, to precipitate
anxiety and affective disorders that are
amplified and endure long after the stress has
abated).
• Rationale for chronic pain clinics.
• Guarding against the possibility of pain
and anticipation of its occurrence activates
cells in the rostroventral medulla that
function to amplify incoming pain signals
at the level of the Dorsal Horn.
• The simple act of anticipating a pain and
expecting it to be important are sufficient
to trigger these “on cells”. In essence
activating the amplifiers before the pain
stimulus has begun!
7
Cytokines
DRG
Peripheral
DH
1. Facilitates continual input into
the dorsal horn
Neuroimmune
Releases glutamate
and inflammatory
mediators.
Peripheral Sens
Sprouting of sympathetic
Axons in DRG
3 directions:
cortex, motor,
sympathetic
DRG
2. Resulting in spontaneous
N, C/A Fibres
firing C,
of C-fibers
Inc. NMDARs, React to inflam
Inc depol by open ion channels
NO
Neighboring neurons
Increase ion
3. Increasing dorsal horn
Sympathetic
sensitization
Sprouting of sympathetic neurons.
Normally innocuous stimuli
become painful!
Neighboring neuron
Substance P removes Mg
block to NMDARs. Inc
stim through Ion
channels depolarization
by glutamate.
Sympathetic efferent stimulation of
afferent neurons
NO St neighboring
neurons referred
pain. Further
releases substance P.
And Stimulates the
DH directly.
Central Sensitization
Sympathetic
Vascular and
Dermis
DH
Visceral
Relocation of Ab
fibers to lamina I
and II - allodynia
Sympathetic Involvement
Descending pathways
• Constant firing of A-beta fibers can lead to
the reorganization of A-beta terminals in
the dorsal horn of the spinal cord.
• From deeper to more superficial laminae,
normally areas of C-fiber termination.
•
Stem from cortico-reticular system, locus ceruleus, hypothalamus,
brain stem, and local spinal cord interneurons.
• Ascending and descending pathways are
interactive and function bidirectionally; both
pathways have the properties of both
facilitating and inhibiting pain, depending on
the site of action.
•
(Negative affect activates the right cerebral hemisphere that
potentiates further adverse stimuli, including pain, integrating the
depression and pain in these patients.)
Referred Pain
•
1.
2.
3.
4.
•
Theores:
Impulses from deep tissue injury producing
sensitization of the referred area by axon reflex
Misinterpretation of inputs whose axons also branch to
the referred areas
Convergence projection theory: axons from the injured
and referred areas converge on the same cells in the
spinal cord with a misinterpretation
Facilitation of cells in the cord along with axons from
the referred area.
modulation of somatosensory sensitivity at referred
sites is mediated by central mechanisms.
Facilitated
Segment
Osteopathic
Lesion
Maigne
Syndrome
Central Sens.
Neurodynamics
Process
Hyperactive,
Somatic and
sympathetic
over-activity.
Sustained
barrage of
impulses to
DH
Augments and
maintains
an
alteration
through
nervous
system
including
ANS reflex
activity.
Constant
bombardmen
t of spinal
nerve.
Facilitation
of the
neuron.
Provokes
motor and
ANS
responses.
Facilitated dorsal
horn input
with
reduction in
threshold
and increase
in receptive
field
Abnormal impulse
generating site
resulting in
changes in the
DRG and CNS
Findings:
Muscle and
subcutaneou
sDecreased
jt mobility.
Fibrositis
ANS
changes
Tissue texture
changes.
Altered
ANS,
Hyperirritability
Tissue texture
changes &
sensitivity.
Muscle
changes.
Hypersensitiv
ity
Hypersensitivity.
Changesin
A-beta
fibers. ANS
changes
Motion restrictions.
Hyperalgesia,
myalgia and
cellulalgia,
segmental
dysfunctions.
Treatment
Break the cycle
Break the cycle
Break the cycle
Break the Cycle
8
Visceral
Visceral
• Korr: referred pain of the
viscera to the soma in
areas morphologically
separate from the
disease process though
related segmentally in the
nervous system.
THE “HIDDEN
PATHWAYS”
WE INFLUENCE
IN MANUAL
THERAPY
Visceral
THE SOMATOVISCERAL
REFLEX
• Input from irritation in
the viscera renders
the nerves to the
same segment,
hyperirritable, the
“irritable focus”.
• Cutaneous, muscular
(rigidity and sustained
contraction), and spinous
process tenderness to the
level of the viscus.
Visceral
• Secondary tissues of irritation may
become a source of irritation : vicious
cycle.
• Then there is no further dependence on
afferent impulses due to sustained
facilitation.
• Treatment: interruption of cycle
9
HEART (pericarditis)
C4 - Phrenic Nerve
•
•
Sympathetic
segment
T1-4 (T5)
Symptoms
Parasympathetic
Dorsal motor
nucleus of CN X
and nucleus
ambiguus
•Pressure on chest,
squeezing, heaviness,
burning indigestion,
stabbing shortness of
breath, anxiety
• Dyspnea- shortness of
breath
• Pain sometimes down
both arms.
Electrical Skin Resistance
Sympathetic segment
T1-4 (T5)
• Characteristic electric skin
resistance patterns 3 weeks
prior to coronary occlusion
(Korr 1949).
Segmental Dysfunction
•
Comparing segmental somatic dysfunction with significant accuracy
for 50 patients with:
•
1. Cardiovascular disease
•
2. Pulmonary disease
•
Symptoms
•
3. Gastrointestinal disease
•
Pressure on chest, squeezing, heaviness,
burning indigestion, stabbing shortness of
breath, anxiety
•
4. Disorders in the musculoskeletal system
•
Dyspnea- shortness of breath
•
Pain sometimes down both arms.
Korr, I.M.: “Skin Resistance Patterns Associated with Visceral Disease.” Proc. 8: 87-8, 1949.
Sympathetic Distribution
T4 Syndrome:
• Paresthesias, numbness, or upper
extremity pains associated with or without
headaches and upper back stiffness.
• Normal neurological.
• Upper Ts joint dysfunction, especially at T4.
• A nontraumatic onset is common and the
peculiar glove-like distribution of hand or
Beal MC, Dvorak J. Palpatory Exam of the Spine. Manual Medicine 1:25-32,
1984.
T4 and Coronary Disease
• A double blind study documenting
palpatory T4 findings with coronary artery
disease defined by cardiac
catheterization.
forearm pain.
DeFranca GG, Levine LJ. The T4 syndrome. J
Manipulative Physiol Ther. 1995 Jan;18(1):34-7.
Cox, I.M., et al.: “Palpable Musculoskeletal Findings in
Coronary Artery Disease.” JAOA 82: 832-6, 1983.
10
Manipulation for Visceral
Symptoms
LUNGS (pleuropulmonary)
Sympathetic: T2-5
Parasympathetic: Dorsal
motor nucleus of CN X
100 cases of functional heart disease
and 50 cases of organic heart disease.
A controlled study of chronic, obstructive lung disease
randomly assigned to:
A. Medical care
B. Medical care + Manipulations.
Significant improvements of somatic dysfunction
in both groups. Group B had decreased objective
evidence of somatic dysfunction and subjective
improvements in the ability to do physical work.
Symptoms
Somatic dysfunction at T2-T6
all patients showed symptomatic
relief with manipulation.
Koch RS. A Somatic Component in Heart
Disease. JAOA 60:735-40, 1961.
•
Sharp ache, stabbing in and over involved lung
fields
•
Wheezing
•
Dyspnea
•
Hyperventilation
•
Shoulder pain relieved by lying on involved side
Miller WD. Treatment of Visceral Disorders by Manipulative Therapy.
Dept. of Health, Education and Welfare, Bethesda, Maryland 1975.
KIDNEY
•
•
Sympathetic
segment
T9-L2
Physician blind study of vertebral and
costal motion dysfunction of T7-T12
in patients with renal disease
(Johnston et al 1984).
SYMPTOMS
Usually unilateral pain, dull ache, boring, intense abdominal
spasms, nausea, vomiting, testicular pain, unrelieved by
chance of position.
Urgent desire to evacuate bowel/bladder with little passage
of urine or feces.
Illlustrated:
Bilateral Pain Pattern
Johnston WL, et al. A Clinical Research Study Of Somatic
Manifestations in Renal Disease. JAOA 84:73, 1984.
Radiology
• Over-reliance on imaging findings derives,
in part, from the persistence of obsolete
concepts concerning nociceptive pain.
• A situation can be worsened by health
care providers who attribute the pain to
incidental findings on imaging that may
bear only a modest relationship to the
pain!
Pain from Noxious Stimuli
(Physiologic Pain)
Noxious stimulus
processed through
the nocioceptive
system.
Example of pain pattern
in local shoulder
pathology.
11
Pain from Segmental Facilitation
(Pathophysiologic Pain - Neuropathic Pain)
Prolonged peripheral
noxious stimulus leading
to a centrally enhanced
pain state.
Chronic Pain
(Complex Regional Pain Syndrome)
Neuropathic Pain—
pain initiated or
caused by a primary
lesion or dysfunction
in the nervous sytem
IADP/Merskey 1994).
Example of pain
pattern with
segmental facilitation
(C6).
The pain pattern is
disproportionate to the
stimulus and not limited
to a single somatic
structure’s distribution
pattern.
Palpation/Mobility Testing
Testing for Facilitated Segment
Compression of tissue texture changes and resistance to
segmental motion showed T1-T5 associated with cardiac
disease, and T5-T12 associated with gastrointestinal
disease.
A blind study comparing the two categories showed an
accuracy of 76% .
Beal MC, Kleiber GE. Somatic Dysfunction as a Predictor of
Coronary Cardiovascular Disease. JAOA 82:822-31, 1983.
Signs and Symptoms of FS
•
Motor
• Sensory
• Subjective numbness
• Hyperactive immune system
• Visceral
• Psychological
Clinical Testing for FS
•Basic neurological evaluation
•Excessive sudomotor activity (sweating) (Sugenoya et al.
1990, Allen et al. 2004)
•Scratch test: histamine/sympathetic reaction (turns white)
•Scratch test: hyper-reactivity (central and peripheral)
•Pinch / Roll (central and peripheral)
•Interspinous Ligament Palpation
•Trigger points and somatic points in distribution
•Piloerection (hair folicles), altered color or temperature
(Allen et al. 2004).
•Electrical skin conductance (segmental)
•Cold sensitivity / not heat (segmental)
12
Nerve Root Pathology
Scratch Test: Histamine
• Symmetrical scratch along
Sens. Motor Reflex Pain
Nerve Root
Irritation
Mixed
Stage
Nerve Root
Compression
+
+
+
+/- +/- +/- +/-
-
-
Scratch Test: Hyper-reactive
-
Pinch-Roll Test
• Centrally: scratch
anterolateral cervical
spine from C1-C7 levels
• Test for segmental thickening and hypersensitivity of the skin
C4
• Peripherally: scratch
around limb, crossing
dermatome levels
C5
T2
T1
C6
C8
• Positive is hyperalgesia
in region
+
posterior spine
• Initial redness (histamine
response of vasodilation)
• Sympathetic system
causes vasoconstriction
(turns white)
• Level of lesion has
asymmetrical loss of
redness
and subcutaneous tissues (Maigne 1980).
• Skin taken between the thumb and fore finger of the
examining hand and rolled.
• The area of painful, thickened skin found on the involved side
differs from the contralateral region where the skin is normal in
texture and sensitivity.
• Central anterolateral neck or lateral to spinous process.
• Peripheral around extremity, crossing dermatomes.
C7
Remember:
Suggested Treatment for
Segmental Facilitation
The most recent evidence shows
that pain is a creation of the
nervous system and not just a
gauge of nociceptor activation!
13
Soft Tissue Techniques:
Indications
• Pain
• Muscle guarding
• Decreased
extensibility
• Decreased circulation
• Lymphatic congestion
• Scar tissue adhesions
• Decreased fluid
dynamics
• Joint stiffness
• Decreased muscle
recruitment
• Decreased
coordination
• Increased tension
Medical Exercise Therapy
(1965)
• “Through a systematic
approach and with
active participation by
the patient, Medical
Exercise Therapy aims
to improve one or
several functional
properties by
utilization of
objectively graded
activity.”
Goals
• Decrease / inhibit
pain
• Decrease / inhibit
muscle guarding
• Increase extensibility
• Improve circulation
• Improve lymphatic
drainage
• Remodeling of scar
tissue
• Improve fluid
dynamics
• Improve joint
lubrication
• Improve muscle
recruitment
• Improve
proprioception
• Promote relaxation
• Decrease stress
Exercise Principles are
the Same
in Athletes as in Patients,
the Difference is in
Dosage and Specificity
Oddvar Holten 1965
Manipulation Approaches
Tissue Training Effects :
•
Muscular Influence: Strength - Volume
•
Vascular Influence: Endurance
•
Articular Influence: R.O.M. - Shock
Absorbance
•
•Robert Maigne:
•Rotate away from
pain (neurophys
model)
Collagenous Influence: Mobility - Stability Elasticity
•
Neuro-Muscular Influence: Coordination
14
Manipulation Above and Below the
Level of Lesion
Cervical Manipulation for Segmental
Tone Inhibition
• Cervical patients with inhibition in their biceps,
• Results suggest that a C7-T1
cervical ROM restricted laterally and increased
manipulation induced changes in
pressure pain sensitivity.
pressure pain thresholds in both right
• Manipulation at C5/6/7.
and left C5-C6 zygapophyseal joints in
• Significant reduction in biceps inhibition, increase
healthy subjects.
in biceps force.
•Cs ROM and pressure pain thresholds increased.
Suter E, McMorland G. Decrease in elbow flexor inhibition after cervical spine manipulation in
patients with chronic neck pain. Clin Biomech (Bristol, Avon). 2002 Aug;17(7):541-4.
Fernández-de-Las-Peñas C, et al. Changes in pressure pain thresholds over C5-C6 zygapophyseal joint after a cervicothoracic
junction manipulation in healthy subjects. J Manipulative Physiol Ther. 2008 Jun;31(5):332-7.
Cervical Manipulation for
Segmental Tone Facilitation
•
Reduce Water in Glass
• Treat the cause not the symptoms
High-velocity low-amplitude thrust, right rotation
C5/6, increases resting EMG activity of the biceps
bilaterally, irrespective of whether or not cavitation
occurs (Dunning J, et al. 2008)
• Tissue repair training
• Biomechanical issues
• Training deficits
•
Cs manipulation of dysfunctional cervical joints may
alter specific central facilitatory and inhibitory
neural processing and cortical motor control of 2
upper limb muscles (Taylor HH, et al. 2008).
• Posture / ergonomics
• Psychological
• Diet / nutritional / immune system
References not already sited
•
•
•
•
•
•
•
•
Alexander CC. The role of the osteopathic lesion in functional and organic
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Cole WV. The osteopathic lesion syndrome. VII. the effects of the experimental
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15
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•
•
•
•
•
•
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•
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Old School
Segmental Facilitation
•Segmental innervation of blood vessels described (Di Palma and Foster 1942)
•Segmental circulatory: skin temperature, erythema and photoelectric measurement of
the vascular coloration of the skin (Wright et al. 1960)
•Segmental pattern for cutaneous tenderness and muscle rigidity (Korr et al. 1962)
•Segmental reduction in electrical skin resistance in FS (Thomas and Korr 1957, Korr et
al. 1958).
•Segmental increase in sweating (Thomas and Korr 1951)
•Segmental spasm of erector spinae (Denslow et al. 1947).
•Inhibition tissue regeneration with hyperactivity of the sympathetic system (Cruickshank
1957).
•Influential impacts of segmental facilitation include neurogenic pulmonary edema, peptic
ulcer, pancreatitis, arteriopathy, cardiovascular-renal syndromes, heart disease,
hypertension, post-traumatic pain syndromes, hepatotoxicity and shock (Korr 1978).
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