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Flashcards in ANS and Homeostatic Clinical Examples Deck (57)
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Define the ANS

Two-neuron chain connecting preganglionic neurons through ganglia to visceral target tissues


Components of sympathetic ANS

Cervical ganglia (superior, middle, stellate)

Paravertebral ganglia (thoracolumbar)

Prevertebral ganglia (celiac, superior mesenteric, inferior mesenteric)


Components of parasympathetic ANS

CN3 — eye

CN7 — lacrimal, palatine, and submandibular

CN9 — parotid

CN10 — cardiopulm, GI

Sacral (S2, S3, S4) — colon, rectum, GU


What are paraganglia?

Extrasuprarenal aggregations of chromaffin tissue — abdominal, adrenal, and paraspinal

Synthesize and store catecholamines

[pheochromocytoma sxs = HA, sweating, and tachycardia]


Distribution of sympathetic vs. parasympathetic in terms of vascular and visceral supplies

Sympathetic: vascular includes fascia, smooth muscle and sweat glands + trunk and extremities; visceral includes smooth muscle, cardiac, nodal and glandular tissue in thoracoabdominopelvic cavity

Parasympathetic: no extremities! Visceral — same as sympathetic but also in viscera of head and neck


What is meant by “allostatic load”?

Frequent activation of allostatic systems — continuation of feedback pathways meant to reestablish normal homeostasis

Longterm exposure may cause atrophy of hippocampus affecting feedback, memory, and autonomic function

[allostasis = adaptation in the face of potentially stressful challenges involves activation of neural, neuroendocrine and neuroendocrine-immune mechanisms]


A facilitated segment is also known as somatic dysfunction — what are 2 hallmarks of a facilitated segment?

Lowered neuronal threshold

Hypersensitivity of receptive fields


Goals of OMT in reestablishing homeostasis

Reduce allostatic load by balancing ANS

Reduce postural strain

Improve biomechanics of gait

Remove obstructions to fluid flow and drainage, augment fluid flow

Improve biomechanics of respiration

Optimize tissue healing and homeostatic reserve


Limbic system —> hypothalamus —> sympathetic nervous system —> ???

SNS —> lateral horn of the thoracolumbar spinal cord —> paravertebral and prevertebral ganglia —> end organ


Limbic system —> hypothalamus —> parasympathetic nervous system —> ???

PNS —> brainstem nuclei and lateral horn of sacral SC —> organ ganglia —> end organ


Thoacolumbar (T1-L2) system arising from the intermediolateral cell column of the lateral horn of the SC acting through chain ganglia and collateral ganglia



Craniosacral system arising from brainstem nuclei associated with CNs III, VII, IX, and X and from the intermediate gray in the S2-S4 SC



Sympathetic innervation of head/neck, heart/lungs, and upper GI

Head/Neck = T1-4
Heart lungs = T1-6
Upper GI = T5-9


Sympathetic innervation of small intestine+right colon, appendix, and left colon+pelvis

Small intestine+right colon = T10-11

Appendix = T12

L colon/pelvis = T12-L2


Sympathetic innervation of adrenals, GU tract, and upper/lower ureter

Adrenals = T10-T11

GU tract = T10-L2

Upper/lower ureter = T10-11/T12-L2


Sympathetic innervation of bladder and upper/lower extremities

Bladder = T12-L2

Extremities upper/lower = T2-8, T11-L2


Parasympathetic innervation of vagus n. (CN X) involves what structures?

Heart, lungs, thyroid, carotids

Upper/middle GI, liver

Kidney, upper ureter



S2-4 Pelvic splanchnic nn. of parasympathetic nervous system innervate what structures?

Lower GI, uterus/cervix, penis/clitoris

Lower ureter, bladder


Assessment of sympathetics

Appropriate spinal levels

Paraspinal muscle spasms

Rib restrictions

Distant ganglia — cervical, celiac, mesenteric


Parasympathetic assessment

Vagus — look for condylar compression, OM suture restrictions, OA/AA SDs

Sacrum (S2-4) — sacral somatic dysfunction


Define somatic dysfunction

Impaired or altered function of related components of the somatic (body framework) system: skeletal, arthrodial, myofascial structures, and their related vascular, lymphatic, and neural elements

Important people = J.S. Denslow, DO, and Irvin Korr, PhD


Define spinal facilitation

The maintenance of a pool of neurons in a state of partial or subthreshold excitation; in this state, less afferent stim is required to trigger discharge of impulses

Facilitation may be d/t sustained increase in afferent input, aberrant patterns of afferent input, or changes within affected neurons themselves or their chemical environment — once established, facilitation can be sustained by normal CNS activity


General technique for balancing the ANS



Regional techniques for balancing the ANS

Rib raising
Paraspinal muscle inhibition
Abdominal collateral ganglia techniques
Target type II SDs if present
Suboccipital inhibition
Sphenopalatine ganglia release
Sacral inhibition and rocking
SI joint gapping


OMT used to decrease sympathetic activity

Rib raising
Paraspinal muscle inhibition
Cervical ganglia inhibition
Abdominal collateral ganglia technique
Target non-neutral (type II) SD if present


OMT to normalize parasympathetic tone

Suboccipital inhibition
Sphenopalatine ganglion release
Sacral inhibition and rocking
SI joint gapping
Gentle muscle energy


Who performed the prospective controlled study with rabbits in which SD was induced weekly at atlas, C6, and T3 with subsequent measurement of pulse, response to exercise, EKG, and tissue sample?

Louisa Burns, DO


What were the results of Dr. Burns’ research in terms of functional changes as a result of T3 SD?

Immediate: rapid, weak, and somewhat irregular pulse

10 minutes later: slightly stronger, slower an dmore regular, but did not return to normal as long as SD persisted

2 months later: gradually weaker with staccato quality similar to that found in elderly [this was not present in rabbits without T3 SD]


What were the results of Dr. Burns’ research in terms of functional changes as a result of atlas SD?

Immediate: stronger and irregular pulse

10 minutes later: closer to normal as long as SD persisted

2 months later: developed arrhythmias [theorized to be d/t vagal n. facilitation]


Cardiac cross section findings in rabbits after atlas and T3 induced SD

Abnormalities in muscle patterns — abnormal color, cross striations, abundant fibrils, variable nuclear relations


Hemorrhagic areas

Overgrowth of CT

[neurotrophic findings]