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FAST =
message impulse (endoneural tube = axon)
A fibers (alpha-fastest) and (Beta-fast)
Quick, stabbing and sharp muscle proprioceptors → proprioceptors = fastest of all A fibers
Withdrawal reflex, 10-30 meters/second
LARGE, MYELINATED and fast
Group III nociceptors
Lamina II and IV
pain goes up and down the tract of Lissauer
C-fibers
Fast (not the fastest)
burning and achy, reticular formation
Deep viscera and somite, substance P and inflammation
SMALL, UNMYELINATED, “less fast”
group IV nociceptors, Lamina II
Convergence
input from large fibers will inhibit small pain fibers
Soma =
full of Neurotransmitters → synapses out in soma = lots of NTs to facilitate them
Hillock
area where action potential is reached / not reached
Thick myelinated nerves are mor sensitive to
compression than non-myelinated or thinly myelinated nerves
Slow / AXT = trophic (microtubular network in epineurium) → fast
Antegrade (400mm / day)
proximal to distal
feeding (protein and sugars)
(FAXT) fast axoplasmic transport
bulk
slow
Slow / AXT = trophic (microtubular network in epineurium) → slow
Retrograde (1-3 mm / day)
Terminals to cell body
Recycling (NGF and neurotransmitters)
Neuroplasticity
collateral fibers
slower
ANS balancing system: 3 components
sympathetics
parasympathetics
enteric (intestinal wall of GI tract)
All ANS preganglionic fibers are
cholinergic, only sympathetic portion have adrenergic (post ganglion) fibers
Sympathetic (“domino effect”)
T1-L2/L2 (interomedial cell column or sympathetic chain)
“fight or flight”
eyes DILATE, TACHYCARDIA
Sympathetics have exclusive control over temperature
Vasomotor = shunt to large muscles
Pilomotor = hair on end
Sudomotor = wet palms
Sympathetic → intrasegmental
exit directly to organ
Sympathetic → intersegmental
ascend or descend before exit
Sympathetic: short preganglionic nerve
Acetylcholine
Sympathetic: Long postganglionic nerve
Epinephrine and Norepinephrine
Epinephrine uses
Alpha and beta catecholamines → BRONCHOCHONSTRICTION exclusively in fight or flight
Norepinephrine uses
ALPHA only!
decreased threshold, increased action potential, increased pain
Sympathetic → supra-renal glands have
chromaffin cells that synthesize catecholamines for sympathetic post ganglionic fibers
Alpha catecholamines EXCITE smooth muscle (nor and epi)
Beta catecholamines INHIBIT smooth muscle (epi only)
Parasympathetic (“vegetative component”)
CN 3, 7, 9 and 10 (vagus), S2-S4 (bowel and bladder)
cranio-sacral
Not body walls or limbs
BRADYCARDIA, increased saliva, increased GI Enzymes, Decreased heart, lung and respiration
Stores, conserves and replenishes body energy
Parasympathetic Long preganglionic nerve
Acetylcholine
Parasympathetic short postganglionic nerve
acetylcholine
Enteric system
Not innervated by CNS, can be influenced by a few nerves from sympathetics and parasympathetics but can ‘act’ autonomously
Uses NT VIP (vaso intestinal peptide in gut, DRG, brain)
Includes: myenteric and submucosal plexuses
in times of great stress, sympatheticotonia can override enteric system and decrease GI function
Aganglionic = Hirschsprung’s disease
Selye → developed LAS and GAS (general adaptation syndrome)
he described the bodies reaction to chronic stress in stages
Selye: Alarm
perception of chronic stress
Thymicolymphatic, lymph involution, decreased WBC, increased eosinophils, increased ACTH, increased cortisol
Selye: resistance
depends on heredity, nutrition, sleep, sodium, corticoids
Selye: exhaustion
diseases of adaptation (kidney, RA, thyroid, ulcer, etc)
Perceived chronic stress causes
neuroendocrine response (often pituitary) this suppresses the thymicolymphatic system and reduces the resistance of the body (decreased immunity)
The neurodystrophic theory
uses much of selye’s work. sympathetic nervous system immunity
it is the link: CNS → Sympathetics → immunity
Sympathetic cell column travels close to
anterior aspect of disc, body and costovertebral joints
can be effected structurally by: AS, severe osteoporosis, diaphragm. psoas major
stress effects cortisol examples include: selye, PTSD, fibromyalgia
Acute stress =
increased immunity
Chronic stress
decreased immunity
Sympathetic chain can be directly compressed by
anterior thoracic body osteophytes
Upper cervical subluxation can effect upper cervical ganglion because the ganglion is the
largest near the C2 TP and vertebral artery
Cervicogenic headache
Cervical headache subluxation usually located at C0-C1 (general population C2-C3)
Headache due to convergence projection
signs and symptoms of most headaches: hypomobility, trigger points, and decreased ROM
Cervicogenic dorsalgia
neck problem causes pain between shoulder blades
structural causes usually indicate nociceptive referral from disc and dura
Horner’s syndrome can cause
blurring of vision
vertigo has multiple causes including
neuro, vascular, physical
Brain hibernation (aka ischemic periumbra)
decreased blood flow and decreased function
cells alive, but function ceased, if circulation restored, cells can be reactivated
Can be milk like giddy, nervousness, headache, tantrum, etc. adjustments can help
Adjustment can increase CSF flow
Disc (derangement)
30-50 y/o, reoccurrence frequency, long recovery, surgery rarely helps
contra: cauda equina syndrome
Treatment of disc
adjustment first 2 weeks, increased pain frequency, side posture, flexion-distraction, extension mobilization
corset, traction, ice, massage, electrical therapy
Exercises: flexion decreases pain 37%, extension decreases pain 33%
Autism
theories of brain growth disturbances (amoxicillin)
Alzheimer’s
neurotangles consisting of microtubule protein tau
seizures
decrease in GABA
Myasthenia gravis
auto antibodies attacking ACH receptors
Herpes virus
uses retrograde channels to get the neurosoma and hide (Dormant)
Local anesthetic blocks
action potentials by binding sodium channels
Potassium and sodium are electrolytes, so
edema and dehydration effect neural transmission
Catecholamines
dopamine can make norepinephrine, norepinephrine can make epinephrine
Cholinergic drugs affect
acetylcholine
Noradrenergic drugs affect
NE
Beta blockers affect
EPI Only
Equilibrium triad
Muscle: GTO and muscle spindle
Vestibular (inner ear)
visual system
Golgi tendon organ
TENSION
fatigue and rapid stretch
Muscle spindle
constant control, CNS communication
Anterior vertebral joint is for
weight bearing → body and disc 75% of weight
Posterior vertebral joint is for
movement → facet 25% of weight
Lateral bending stresses
intertransverse ligaments
L5 → can have
corpotransverse ligament (ilio-lumbar ligament) → checks rotation
The nerve roots most vulnerable in
lateral bending are lower cervical nerve roots and brachial plexus
Dura mater forms the
epineurium passes through IVF
transforaminal ligaments (TFL)
ligamentous band crossing IVF
can fill 1/3 of IVF → 1-4 transforaminal ligaments at each level
Biomechanical stress is disturbed most by
unilateral problems (unilateral sacralization)
Nuclear fibers resist
compression
annular fibers resist
torsion (outer 1/3 sensory and vasomotor) (inner 1/3 most sensitive)
Nuclear impression (notochordal remnant)
is from disc and alar plate (cupid’s bow AP xray)
Disc is made up of
nucleus, annulus and end plate (weakest with compression forces)
endplate is 1mm thicker in the medial region
Sinu vertebral (aka recurrent meningeal nerve) → segmental artery follows spinal nerve)
PLL, annular fibrosis, posterior joint flava, dura, veins, fat
Posterior rami
paraspinals, multifidi, fascia, S-I joint, posterior joint, supraspinous ligament
Muscles
create movement
Ligaments
restrict movement
joints
guide movement
Alar ligament
1.) checks rotation and lateral bending (check and dentate ligament)
2.) upper alar ligament restricts contralateral lateral bending (occiput- C2)
3.) lower alar ligament restricts ipsilateral rotation (C1-C2)
Apical ligament
top of dens (suspensory ligament)
Transverse ligament
checks flexion and extension, FLEXION compresses cord (portion of cruciate ligament)
located in groove posterior to the dens, synovium on either side
Flava ligament
most elastin (yellow ligament) most important ligament to absorb flexion forces
Cervical and thoracic: flava ligament
compressive myelopathy
Lumbars: flava ligament
radicular compression, causes radiculopathy
ALL
damaged in hyperextension
PLL
causes most disc damage (discopathy), thinnest at L5
Interspinous and nuchal
damaged in hyperflexion
rectus capitus major attaches to
meninges between C1 and C2
RCP minor attaches to meninges
between occiput and C1
Cervical curve
C2-T2
Thoracic curve
T2-T12 (Apex T7)
Lumbar curve
T12-L5 (Apex L3)
Co-C1
more flexion if chin is retracted
C1-C2
creates V shape ADI In flexion
Mid cervicals
most lateral bending
Lower cervicals
have “stair step” translation, most flexion-extension (C5-C6)
Upper cervical facets
35 degree angle
Lower cervical facets
60 degree angle
Upper throacics
most rotation
lower thoracics
most flexion/extension and lateral bending, most motion at T11-T12 (not true ribs)
L5-S1
most flexion-extension
L1-L2
second most flexion-extension
Rotation is very limited in the lumbars
primary purpose of lumbar facets is to reduce rotation
Hypomobility
restriction of motion (smith, langworthy, paxon)
Hypermobility
excessive motion, not life threatening
Instability
pathological state causing intolerable and dangerous signs and symptoms
non-manipulable (contraindication to adjustment)