Patricia Kooyman, D.O.OMM Department

August 16, 2011

Viscerosomatic Reflexes

�Inflammation is a powerful stimulator of local nociceptors.

�The convergence of visceral nociceptorswith the nociceptorsfrom all somatic tissues produces several clinical effects:�Referred pain�Segmental facilitation at

the spinal cord level

Primary Afferent

Nociceptors (PANs) Can be activated by stretch or

by chemicals in the

surrounding media

Factors activating

PANs:Bradykinins

Histamines

Prostaglandins

Serotonin

H+ and K+

Cytokines

ATP

Neuropeptides

Primary Afferent

Nociceptors (PANs) Can be activated by stretch or

by chemicals in the

surrounding media

Factors activating

PANs:Bradykinins

Histamines

Prostaglandins

Serotonin

H+ and K+

Cytokines

ATP

Neuropeptides

Neurosecretoy Function of: Primary Afferent

Nociceptors(PANs)They release these (dilatory)

peptides:Substance P

Calcitonin Gene-Related Polypeptide

Somatostatin�Normally, a basal release of

these peptides; they are targeting the resistance arterioles, to act as a counterbalance to the SNS (since

NO PNS to the extremities)� However, can have a NeurogenicInflammatory Response, if a lot of

these are released vs. the basal release.

Primary Afferent

Nociceptors (PANs) Can be activated by stretch or

by chemicals in the

surrounding media

Factors activating

PANs:Bradykinins

Histamines

Prostaglandins

Serotonin

H+ and K+

Cytokines

ATP

Neuropeptides

Neurosecretoy Function of: Primary Afferent

Nociceptors(PANs)They release these (dilatory)

peptides:Substance P

Calcitonin Gene-Related Polypeptide

Somatostatin�Normally, a basal release of

these peptides; they are targeting the resistance arterioles, to act as a counterbalance to the SNS (since

NO PNS to the extremities)� However, can have a NeurogenicInflammatory Response, if a lot of

these are released vs. the basal release.

Results of PAN activation:Lowering

thresholdsClinically, the

development of hyperalgesia

Primary Afferent

Nociceptors (PANs) Can be activated by stretch or

by chemicals in the

surrounding media

Factors activating

PANs:Bradykinins

Histamines

Prostaglandins

Serotonin

H+ and K+

Cytokines

ATP

Neuropeptides

Neurosecretoy Function of: Primary Afferent

Nociceptors(PANs)They release these (dilatory)

peptides:Substance P

Calcitonin Gene-Related Polypeptide

Somatostatin�Normally, a basal release of

these peptides; they are targeting the resistance arterioles, to act as a counterbalance to the SNS (since

NO PNS to the extremities)� However, can have a NeurogenicInflammatory Response, if a lot of

these are released vs. the basal release.

Results of PAN activation:Lowering

thresholdsClinically, the

development of hyperalgesia

To spinal cord:

increased afferent

drive, due to this

sensitization of the

primary afferent

fibers

Descriptive model from

Frank Willard, PhD

Then �TART findings occur: muscle spasm, sensitivity to

touch

Spinal cord facilitation/

Segmental facilitation�Reduced threshold for firing of the interneurons receiving

nociceptive input� interneurons = a neuron between a primary sensory neuron and a final

motorneuron, or any neuron whose processes are entirely confined within a specific area

� internuncial neurons = transmitting impulses between two different parts.

�Then - a change occurs at the level of the genes – of those interneurons/internuncial neurons.

�Exaggerated segmental autonomic and alpha-motor response occurs; produces boggy spasm, increased temperature, increased sweat.

�Exaggerated ascending tract input to higher centers, produces hyperasthesia, and referred pain

�Alters autonomic outflow to viscera

From Frank Willard, PhD

discussion of: Research by and

Mary F. Anderson and Barbara

J. Winterson of UNECOM -

Brain Research 678:140-150,

1995. After making a cut at the

area of the green pointer, 85% of

the facilitation remained.

Therefore, the muscle spindle

alone isn’t sustaining the

somatic dysfunction. The small-

caliber system is necessary for

the initiation of this spinal

facilitation, but then once

initiated, this afferent drive is

not needed to sustain the spinal

/segmental facilitation.

Visceral Sympathetics �Thyroid T1-4

�Mammary T1-6

�Esophagus T1-6

�Lung T1-6

�Heart T1-6

�Stomach T5-9 Left

�Liver T5-9

�Gallbladder T5 Right

�Pancreas T7 Right

�Spleen T7 Left

�Small intestine to right colon T10-11

�Left colon to rectum to pelvic organs T12-L2

�Appendix T10 (T9-T12)

�Ovary/Testes T10-11

�Kidney T10-11

�Uterus T12-L2

�Bladder T12-L2

Levels cited from Kuchera, Osteopathic Considerations in Systemic Dysfunction

Osteopathic treatment

considerations - Diagnosis�First and foremost is to treat the underlying

pathology responsible for the reflex.�Somatic dysfunction resulting from a visceral

pathology generally has an acute, boggy, rubbery end feel.

�Reflexes can be palpated and distinguished through tissue texture changes. (+ red reflex secondary to inc. erythema, + skin drag secondary to inc. moisture )

�Beal’s compression test – gently lift up in the paravertebral area bilaterally to detect changes to tissue texture

Osteopathic treatment considerations�Prolonged hyperactivity of the autonomic

nervous system can lead to facilitation of the spinal cord and lower thresholds for autonomic firing.

�Treatment is directed towards breaking the facilitation, and restoring balance between the sympathetic and parasympathetic systems.

�Understanding the anatomy of the SNS and PSNS will assist in treatment.

�Reflexes are acute changes. Treatments are generally more effective and better tolerated utilizing gentle, indirect and passive techniques.

Treatment techniques - SNS�Addresses T1-L2 along

sympathetic chain ganglion corresponding to the level of the reflex

- Inhibitory pressure

- Soft tissue myofascial release

- Rib raising

Rib Raising�“initially stimulates regional sympathetic

efferent activity to organs related to that level of sympathetic innervation, but in the long run, rib raising results in a prolonged reduction in sympathetic nervous system outflow from the area treated.”

�p. 53 Nelson

Treatment techniques - PSNS�Vagus – CN X – Address the occipital and upper

cervical region as reflex can lead to dysfunctions of the OM suture, OA, C1-3.

Treatment techniques - PSNS�Parasympathetic fibers arise

from roots S2,3,4 and are distributed as the pelvic splanchnic nerves to the pelvic viscera.

�Treatment to address PSNS of the lower GI and GU systems target the sacrum and pelvis.

Treatment techniques - PSNS�For Vagus – OA decompression, sub-occipital

release techniques, balanced ligamentous tension (BLT), FPR, myofascial releases, inhibition

�For Pelvic splanchnics (S2-4) – lumbosacral myofascial, sacral rock, BLT, inhibition

�The above list is just a sample of techniques; as long as the treatment is gentle, indirect, and passive it would be better tolerated.

Chapman’s Reflexes�Chapman’s reflexes are a system of reflex points

originally used by Frank Chapman, D.O.

�These reflexes present as predictable anterior and posterior fascial tissue texture abnormalities.

�Gangliform contraction that blocks lymphatic drainage.

�Sympathetic nervous system dysfunction and lymphatic pathology following viscerosomatic reflexes.

Chapman’s Reflexes

�On palpation, Chapman reflexes are located deep to the skin, most often lying on the deep fascia or periosteum.

�Usually found paired on both the dorsal and ventral parts of the body.

�Small, smooth, firm nodules approximately 2-3mm in diameter and exquisitely tender to palpation but non-radiating.

Key Chapman’s Points�Tip of the 12th rib for appendix reflex.

�Colon reflex reflected onto the iliotibial fascial tract.

�Upper respiratory system (pharynx/nasal sinuses) points around the clavicle and 1st intercostal space.

�Myocardium point in 2nd intercostal space.

�GI and GU points to help differentiate causes or source of visceral pain.

Chapman’s Reflexes Treatment�Primarily a diagnostic tool.

�Find the dysfunction anteriorly but treat posterior points since they are generally less tender.

�Treat somatic dysfunctions of the pelvis first.

�Apply firm pressure with finger pad of one finger in a circular fashion, and attempt to flatten the mass. Treatment usually requires 10 to 30 seconds.

�Treatment ends when the mass disappears.

Application of OMM

Diagnostic

AdjunctiveTherapeutic

Treatment�Hospital based – any disease state will have an

effect on the sympathetic tone and respiratory excursion of the patient. Gentle manipulation can help facilitate the body towards recovery.

�Ambulatory care – osteopathic physicians have a unique qualification to utilize osteopathic manipulation as a therapeutic or adjunctive treatment for many disease states.

Effects of Osteopathic Treatment�Develop a unique relationship with the patient by taking

the time to talk, listen, and touch them.�Provide pain relief and increased range of motion for

musculoskeletal dysfunctions.�Break viscerosomatic cycles to facilitate healing. �Reduce the need for medication and potential side

effects.�Improve circulation to enhance healing by removing

tissue restrictions and allowing proper circulatory and lymphatic flow.

�Treating dysfunctions of the body to promote optimal functioning, and permit the body’s inherent ability to heal itself.

Questions???"To find health should be the object of the doctor. Anyone can find disease."- Dr. A.T. Still