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Fall 2022 > OMM Week 1+2+3+4 > Flashcards

OMM Week 1+2+3+4 Flashcards

1
Q

Thrusting techniques risks

A

Most severe iatrogenic complications. Example is cervical HVLA, may lead to occipital infarction, vertigo, etc.
Dekleyn test:testing patients tolerance by extending and rotating head for 30 seconds while watching for nausea, dizziness, etc. May actually create incident and frequently reveals no accurate results.

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2
Q

Muscle energy treatments risks

A

Safe. Some stiffness and soreness may occur. Complications may include aggravation of herniated disk syndrome and increased pain

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3
Q

Counterstrain technique risks

A

Safe, purely positional, no force necessary. May feel sore after treatment. Major problem is patients inability to assume certain positions because of preexisting positions

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4
Q

Facilitated positional release techniques risks

A

FRP plus compressive force shouldn’t be used in radiculopathy of cervical spine

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5
Q

Myofascial release, balanced ligamentous tension, and ligamentous articular strain techniques risk

A

Gentlest, aggravation of disc symptoms and muscle spasms. Headaches, increased pain, costochondral

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6
Q

Cranial treatment risks

A

Gentle, farthest reaching side effects when improperly done. Fatigue, lethargy, nausea, dizziness, loss of appetite. Hypopituitarism, emotional release

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7
Q

Inhibition techniques risk

A

Initially painful, little to no side effects after. Most common is bruising

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8
Q

Anatomical barrier

A

Movement beyond may disrupt tissues. Active range of motion plus passive range of motion

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9
Q

Physiological barrier

A

Active range of motion ends

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10
Q

Elastic barrier

A

Motion between physiologic and anatomic barriers

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11
Q

Restrictive barrier

A

Can be eliminated with the use of osteopathic treatment

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12
Q

Symptoms of acute somatic dysfunction

A

Increased temp, boggy texture, moist, rigid/board like tension, greatest tenderness, edema, venous congestion, persistent erythema

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13
Q

Symptoms of chronic somatic dysfunction

A

Slightly increased or decreased (coolness) temp, thin/smooth texture, dry, slightly increased/ropy/stringy tension, less tenderness but may still be present, edema not likely, neovascularization, redness fades quickly or blanching occurs

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14
Q

Goals of OMT

A

Relief of pain and reduction of other symptoms, improvement of function, increased functional movement, improved blood supply and nutrition to the affected areas, sufficient return of flow of fluid via the lymphatic and venous systems, removal of impediments to normal nerve transmission

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15
Q

Direct manipulation

A

Restricted joint or tissue is initially taken in direction of the restriction to motion, then joint or tissue is moved beyond restrictive barrier

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16
Q

Indirect manipulation

A

Initially position the joint or tissue away from a barrier to motion and toward the relative ease of freedom of motion

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17
Q

Combination manipulation

A

Indirect, then direct is most common

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18
Q

Passive manipulation techniques

A

Performed by physician without any active participation by patient

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19
Q

Active manipulation techniques

A

Require significant participation by the patient, guided by the physician

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20
Q

Isotonic contraction

A

Muscle shortens

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21
Q

Isometric contraction

A

Muscle maintains same length

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22
Q

Isolytic contraction

A

Muscle contracts while being lengthened

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23
Q

Isokinetic contraction

A

Muscle contracts as the same speed

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24
Q

Concentric contraction

A

Muscle shortens, using property of contractility

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25
Q

Eccentric contraction

A

Muscle lengthens, using extensibility

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26
Q

Static contraction

A

Muscle is in partial or complete contraction without changing its length, no rotary joint motion

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27
Q

Vertebral motion segments

A

Superior and inferior adjacent vertebrae and intervening disk and ligamentous structures.

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28
Q

Overturning movement

A

Rotation around an axis

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29
Q

Translatory movement

A

Translation along an axis

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30
Q

Forward bending

A

Superior vertebra rotates anteriorly around the x axis and translated forward along the z axis. Anterior longitudinal ligament becomes lax, pressure is placed on intervertebral disk, posterior ligament becomes more tense.

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31
Q

Backward bending

A

Vertebra rotates backward around the x axis and move posteriorly along the z axis. Anterior longitudinal segments becomes more tense, less tension on posterior ligament

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32
Q

Side bending

A

Rotation around anteroposterior z axis, translation along horizontal x axis, and rotation around vertical y axis. z and x axis directions are dependent on direction of side bending, y axis direction (rotation) can vary and is dependent on the vertebral segment involved.

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33
Q

Soft tissue technique: traction

A

Linear force acting to draw structures apart, origin and insertion of the myofascial structures being treated are longitudinally separated. Great for herniated disks

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34
Q

Soft tissue treatment: linear stretching

A

Kneading motion, direction of force is applied parallel to the long axis of the structure

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35
Q

Soft tissue treatment: lateral stretching

A

Kneading motion, origin and insertion are held stationary, the central portion of the structure is stretched perpendicular to the long axis of the structures (bowstringing)

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36
Q

Soft tissue treatment: deep pressure

A

Sustained inhibitory pressure over a hypertonic myofascial structure

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37
Q

Soft tissue indications

A

Reduce muscle hypertonicity, muscle tension, fascia tension, muscle spasms
Stretch and increase elasticity
improve circulation to specific region
Increase venous and lymphatic drainage to decrease local and or distal edema
Stimulate the stretch reflex in hypotonic muscles

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38
Q

Soft tissue contraindications

A

Acute sprain or strain
Fracture or dislocation
Neurological or vascular compromise
Osteoporosis and osteopenia
Malignancy
Infection
Irfanomegaly
Undiagnosed pathology / pain

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39
Q

Spine of scapula level

A

T3

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40
Q

Iliac crest level

A

L4

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41
Q

Posterior superior iliac spine level

A

S2

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42
Q

Inferior angle of scapula level

A

T7 spinous and T8 transverse process

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43
Q

Vertebra prominent level

A

C7 spinous process

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44
Q

Autonomic innervation level: Head and neck

A

Sympathetic: T1-T4
Parasympathetic: CN III, VII, IX, X

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45
Q

Autonomic innervation level: Heart

A

Sympathetic: T1-T5
Parasympathetic: CN X

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46
Q

Autonomic innervation level: Lungs

A

Sympathetic: T1-T6
Parasympathetic: CN X

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47
Q

Autonomic innervation level: Esophagous

A

Sympathetic: T2-T8
Parasympathetic: CN X

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48
Q

Autonomic innervation level: Upper Gi tract (stomach, liver, gallbladder, spell, partial pancreas, duodenum

A

Sympathetic: T5-T9
Parasympathetic: CN X

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49
Q

Autonomic innervation level: Middle GI tract (partial pancreas, duodenum, jejunum, ilium, ascending and proximal (right) 2/3 of transverse colon)

A

Sympathetic: T10-T11
Parasympathetic: CN X

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50
Q

Autonomic innervation level: Distal (left) 1/3 transverse colon, descending and sigmoid colon, rectum

A

Sympathetic: T12-L2
Parasympathetic: S2-S4

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51
Q

Autonomic innervation level: Appendix

A

Sympathetic: T12 on right
Parasympathetic: CN X

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52
Q

Autonomic innervation level: Kidney

A

Sympathetic: T10-T11
Parasympathetic: CN X

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53
Q

Autonomic innervation level: Adrenals

A

Sympathetic: T10-T11
Parasympathetic:—

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54
Q

Autonomic innervation level: Gonads

A

Sympathetic: T10-T11
Parasympathetic:—

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55
Q

Autonomic innervation level: upper ureter

A

Sympathetic: T10-T11
Parasympathetic:CN X

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56
Q

Autonomic innervation level: erectile tissue (penis and clitoris)

A

Sympathetic: T11-L2
Parasympathetic: S2-S4

57
Q

Autonomic innervation level: lower ureter

A

Sympathetic: T12-L1
Parasympathetic: S2-S4

58
Q

Autonomic innervation level: bladder

A

Sympathetic: T12-L2
Parasympathetic: S2-S4

59
Q

Autonomic innervation level: prostate

A

Sympathetic: T12-L2
Parasympathetic: S2-S4

60
Q

Autonomic innervation level: uterus and cervix

A

Sympathetic: T10-L2
Parasympathetic: S2-S4

61
Q

Autonomic innervation level: arms

A

Sympathetic: T2-T8
Parasympathetic:none

62
Q

Autonomic innervation level: legs

A

Sympathetic: T11-L2
Parasympathetic: none

63
Q

Preganglionic neuron

A

Cell body in brain or spinal cord, axon synapses on postganglionic neuron located in peripheral autonomic ganglion. Long for parasympathetic, short fiber for sympathetic

64
Q

Postganglionic neuron

A

Cell body in autonomic ganglion or within the wall of the organ that it innervation. Axon terminates in a visceral effector (smooth muscle, cardiac muscle, glands)

65
Q

Sympathetic efferent neurons

A

Communicate with target organs using norepinephrine (accelerates body functions). Preganglions located in lateral horn of spinal cord levels T-L3. Exit spinal cord in ventral root to postganglion in peripheral sympathetic ganglion. Postganglions travel within spinal nerve to supply innervation to target tissues

66
Q

Parasympathetic efferent neurons

A

Communicate with targets using acetylcholine. Preganglions located in brain stem and sacral spinal cord. Axons exit CNS in CN III, VII, IX, and X and S2-S4 (pelvic splanchnic nerves). Exit spinal cord in ventral roots, synapse on postganglions in the walls of the target organs

67
Q

General visceral afferent neurons

A

Sensory innervation to visceral organs. Sends signals to brain that modulates sympathetic and parasympathetic output. Neurotransmitters include calcitonin, substance P, and neurokinins A and B.
Data from thorax return to brain via vagus nerve (CN X). Visceral pain transmitted to spinal cord alongside sympathetic fibers. Lower pelvic pain alongside parasympathetic fibers. Afferent signals enter spinal cord and ascend to control centers of brain for interpretation

68
Q

First synapse (sympathetic and parasympathetic)

A
  1. Preganglionic axon synapses on postganglionic neuron
  2. ACh released from axon terminal of presynaptic neuron, crosses synaptic cleft
  3. ACh binds to postsynaptic nicotine’s receptors (transmembrane ion channels)
  4. Channel opens and allows Na+ to diffuse into postganglionic neuron
  5. Influx of Na+ depolarizes cell and results in generation of action potential
69
Q

Second synapse: Sympathetic neurons

A
  1. Signal travels along postganglion sympathetic fiber to reach destination. Releases neurotransmitter (usually norepinephrine). Dopamine released by neurons supplying blood vessels of kidney, ACh released by neurons supplying eccrine sweat glands
  2. Neurotransmitter binds to receptors knows as adrenergic receptors on target organ (G protein-coupled receptor, classified as alpha or beta with subtypes of each)
  3. Activated intracellular signaling cascade that produces physiological response in organ/tissue

DIFFERENT FOR ADRENAL GLAND
Presynaptic nerve fiber travels directly (no postganglion neuron in adrenal gland), cells release epinephrine (adrenaline) or norepinephrine into systemic circulation. Produce fight or flight response

70
Q

Second synapse: Parasympathetic neurons

A

After Preganglions neuron release ACh, which binds to nicotine receptors on postganglion, postganglionic neuron then synapses on target organ again releasing ACh. This time it binds to cholinergic receptor MUSCARINIC RECEPTOR (G protein-coupled receptor)

71
Q

Solitary nucleus

A

Synthesizes information from the vagus nerve CN X and other sensory inputs. Located in the medulla oblongata of the brain stem. Neurons project to hypothalamus, reticular formation, brain stem parasympathetic neurons, and spinal cord sympathetic neurons

72
Q

Effects of ANS on target organs

A

Sympathetic: increase HR and force of heart contraction, constrict blood vessels, increase BP, relax bronchi to allow more air into lungs, promotes conversion of glycogen to glucose to provide energy
Parasympathetic: slow HR, increase glandular secretions such as salivary and gastric

73
Q

Cervical-thoracic junction

A

T1-T3
Backward bending/LORDOTIC

74
Q

True thoracics

A

T4-T9
Forward bending/ KYPHOTIC

75
Q

Thoraco-lumbar junction

A

T10-T12
Backward bending/ LORDOTIC

Apex is T5-T6

76
Q

Rule of Threes (for thoracic spine only)

A

T1, T2, T3- spinous process is at same level as transverse process
T4, T5, T6- spinous process halfway between transverse process and the one below it
T7, T8, T9- spinous process is at level of the transverse process below. T8 transverse process are posterior and directly lateral to the spinous process of T7. T8 transverse processes are posterior and superior to T8 by one full vertebral level
T10 is like to T7-T9
T11 is like T4-T6
T12 is like T1-T3

77
Q

Term for joint

A

Zygapophyseal

78
Q

Flexion at the vertebrae pair

A

Superior (upper) segments inferior (lower) facets move superiorly and anteriorly to the period facets of the lower segment. Opposite for extension; facets “close”

79
Q

Intervertebral discs contain

A

Nucleus pulposis - elastic
Annulus fibrosis- fibrocartilage
(Weight bearing)

80
Q

Thoracic facet orientation for thoracic spine

A

Backwards Upwards Lateral (BUL)

81
Q

Fryettes principles: first

A

Side bending is introduced into a neutral spine, bodies of vertebra rotate to the side of the convexity. Side bending and rotation occur in opposite direction, not affected by flexion or extension
Group curves (3+ vertebral bodies) or neutral curves
Type 1 somatic dysfunctions follow this

82
Q

Fryettes principles: second

A

Side bending is introduced into a non-neutral spine (flexed OR extended), bodies of vertebra rotate to side of concavity. The coupled motions of side bending and rotation occur in same direction.
Applies to single vertebral unit (two vertebrae)
Type II somatic dysfunctions follow this

83
Q

Fryettes principles: third

A

Initiating motion of a vertebral segment in any plane of motion will modify movement of that segment in other planes of motion

84
Q

Neutral dysfunction

A

Group dysfunction (3+)
May be adaptation
No exaggeration of the deformity in either extreme of flexion or extension
eg: T5-T9 N S right R left
Neutral, Side bent Right, Rotated Left

85
Q

Type I somatic dysfunction

A

formed gradually usually as compensation.
Maintained by long paraspinal restrict or muscles-erector spinae

86
Q

Type II somatic dysfunction

A

occur as result of trauma/abnormal twisting
Maintained by short restrictions- (rotatores breves and intertransversari muscles)
Should be treated before type 1 lesions
Found at apex or extremes of type 1 curves

87
Q

Extended dysfunction (type II somatic dysfunction)

A

(ERS) “disappear” in extension and are accentuated in flexion. In extreme flexion when both posterior facets should open, one remains closed and the vertebra rotates and side bends to that side

88
Q

Flexed dysfunction (type II dysfunction)

A

(FRS) “disappear” in flexion and are accentuated in extension. In extreme extension when both posterior acts should close, one remains open and the vertebra rotates and side bends to the opposite side

89
Q

Nomenclature for somatic dysfunctions

A

For type II, rotation and side bending (C5 F RSL). If R is written before S, rotation and side bending are understood to be the same side
For type I, side bending and then rotation (S is written before R) opposite sides

90
Q

Layer palpating exercise

A

Gently put hand on top of skin, sense of warmth, tenderness, etc. displace hand inferiorly and superiorly. Use more pressure to get to subcutaneous tissue. Look at ease of moving hand medially, laterally, proximal, distally. Third layer is deep fascia which surrounds muscle bundles. Pressing deeper, muscles, move hand to all sides. Evaluate muscle and move carefully inferiorly, apply pressure again.

91
Q

Skin drag test

A

Pt sitting up or standing. Pads of two fingers index and middle, palpate where spine is, begin in upper thoracic layer lateral to spine. Test for drag you encounter moving down skin gently. Move inferiorly
Observe for change in tempo moving downward
Shows biofilm of moisture in area

92
Q

Red reflex test (arethyma test)

A

Pt sitting upright, checks for acute or chronic changes in thoracic and lumbar spine
Two fingers index and middle, find midline first, go lateral to midline with both fingers. Firm stroke at upper thoracic area. Continue moving down to lumbar, look for change in skin coloration (right or left or upper or lower) and how long it lasts. Redness long is acute. Blanching is chronic

93
Q

Observation

A

Look for trauma, infection, abnormalities (like hair growth), asymmetry, tattoos, acne, discolorations, scratching.

94
Q

Temperature change test

A

Keep palm and other side of hand hovering over body part to feel for heat radiation. Palpate for temp change, should get colder closer to lumbar spine

95
Q

Fascial palpatiln

A

Slight downward pressures, both palms down. Flexion move hands upwards, then pick hands up and place in original position. Repeat moving downwards for inflexion, right and left. Sidebending by rotating hands in original position and moves towards fingertips, repeat for other side.

96
Q

Turgur test

A

Take fingers and pinch skin, see how long it takes for skin to go back to normal

97
Q

Bilateral thumb pressure

A

Soft tissue technique. Pt Lay on back, start from upper back region in front of pt, find T1, put thumbs laterally to spinous process. Push down move up and lateral release thumbs when moving back around to medial, continue and move onto next segment

98
Q

Unilateral prone pressure (thoracic region)

A

Identify spinous processes, don’t slide on skin. L shape with both hands one on top of another, push down and move anteriorly. Move down body .

99
Q

Bilateral prone pressure/counter pressure

A

Soft tissue technique , find spinous processes, one hand pointed towards head and one towards feet on lateral sides of spine. Push down and move toward directions of fingers . Don’t slide on skin

100
Q

Bilateral trapezius pressure/direct inhibitory method

A

Rest arms, sit at head of table. Contact trapezius, use thumbs anteriorly and fingers posteriorly, apply pressure and pinch fingers towards each other. Hold as muscle relaxes and add pressure

101
Q

Upper thoracic with shoulder block: lateral recumbent

A

Pt laying on side. Use one hand on top of scapula and shoulder, using other hand, identify medial border or scapula, medial of that. Add force laterally rhythmic movement to musculature. Hold for hypertonic areas. Can rest patients arm to rest on the arm of the hand holding shoulder

102
Q

Head forward carriage

A

Head pushed forward, knees constantly extended, pelvic pushed posteriorly

103
Q

Military posture

A

Shoulder thrown back, minimizes normal kyphosis of spine.

104
Q

Sway back/hyperlodosis posture

A

Belly forward, stress on back in upper thoracic region. significant headaches

105
Q

Slouch posture

A

Shoulder brought forward . Exaggerate thoracic kyphosis, tightens thorax. Extra work on body

106
Q

Muscle tones

A

Hypertonic-increase in normal tone
Hypotonic- decrease in normal tone
Atonic- no tone, limp, flaccid muscle

107
Q

Contraction

A

Normal tension build up in muscle as it shortens

108
Q

Contracture

A

Abnormal fixing of muscle in shortened position with fibrous changes in tissue

109
Q

Spasm

A

Abnormal contraction maintained beyond physiological need

110
Q

Bogginess

A

Increased fluid in hypertonic muscle; feels like wet sponge

111
Q

Ropiness

A

Cordlike or rope like feeling to a muscle that’s been chronically contracted

112
Q

Stringiness

A

Finer version of ropiness, muscle feels like it were made a tense string

113
Q

Thoracic spinal motions least to greatest motion

A

Extension, flexion, lateral flexion, rotation

114
Q

TART - restriction of motion for thoracolumbar spine

A

Flexion 0-80 degrees
Extension 0-30 degrees
Side bending 0-35 degrees
Rotation 0-45 degrees

115
Q

Muscle energy technique

A

Direct, patient activates muscle against physicians counterforce. Patients dysfunction is positioned toward the restrictive barrier

116
Q

Post isometric relaxation

A

Mechanism of MET, direct and active form of muscle energy technique using isometric contraction of golgi tendon apparatus

117
Q

Treatment with MET

A

position body part to be treated
Instruct patient to try to push back against your resistance in specific direction
Provide isometric resistance for 3-5 seconds
Ask patient to relax, then wait 1-2 seconds
Reposition patient into new barrier
Repeat steps 2-5 above 3-5 times, final repositioning into the new barrier is a passive stretch
Reassess somatic dysfunction

118
Q

Counterstrain technique

A

Indirect and passive, counterstrain point is treated by positioning patient to shorten the involved muscle of ligament. Position is held until tissue releases

Fold and hold

119
Q

Counterstrain point diagnosis

A

Lateral points are transverse processes, midline points are spinous processes. PT1 lateral, PT2 midline, etc.

120
Q

Counterstrain point treatment

A

Find Counterstrain point (tender)
Set the pain scale (this pain is 10/10)
Set up patient into position one ease
Use pain scale to determine if adjustment necessary
Adjust positioning if needed (pain should be 3/10 or less)
Hold for 90 seconds (keep finger on point )
Slowly return patient to neutral position
Re-evaluate tender point using pain scale

121
Q

Muscle depolarization

A

After action potential travels down axon of motor neuron and reaches presynaptic neuron terminal, current stimulates calcium to enter the terminal. Calcium influx leads to release of neurotransmitter acetylcholine from presynaptic terminal.
ACh depolarizes muscle cell. Diffuses across synaptic cleft and binds to receptors on folded section of sarcolema (muscle cell membrane) (receptors are nicotinic) After binding, influx of sodium occurs into muscle cell, causes depolarization, leading to muscle contraction

122
Q

Skeletal muscle tissue

A

Contain myofibrils, collection of tiny structures called sarcomeres (individual contractile units of the muscle cell). Made up of actin (thin) and myosin (thick). Slide against each other to shorten (contract the muscle)
Actin filaments anchored at the ends of sarcomere and contains proteins of the troponin complex (Tn, troponin C, I, and T) and G (globular) actin, attached to double helix alpha - tropomyosin

123
Q

Troponin complex

A

TnC binds Calcium, TnI binds actin and Inhibits actin -myosin interaction, TnT binds to Tropomyosin double helix
Each globular actin molecule along the myofilament has active site that can bind with adjacent myosin filaments. Under the right conditions, fixed actin filaments can bind the moveable myosin filaments and causes them to move.

124
Q

Steps for skeletal muscle contraction

A

Calcium released from sarcoplasmic reticulum, binds to TnC, allows tropomyosin to move and reveal myosin binding sites on G actin. Myosin head cocked, in high energy state.
Myosin head binds to G actin binding sites making cross bridge. Pi leaves
Cross bridge generates force, and actin slides over myosin. Actin displaces reaction products (ADP and Pi). Sarcomere, myofibril and cell contract.
Actin myosin bride very rapidly dissociates due to ATP binding to myosin

Cycle occurs very rapidly. Can get multiple cross bridge cycles from single pulse of calcium

125
Q

Intrafusal muscle fibers

A

Specialized muscle fibers that act as sensory receptors within muscles. When bundled together, called muscle spindle. Sense current length and motion velocity of muscle and report to afferent nerves that run to brain. Conscious proprioception, posture, coordinate motion

126
Q

Google tendon organs

A

Located within tendons at the origins and insertions of muscle into bone, sense load or force being applied to muscle using stretch sensitive ion channels that open in response to tension generated by contracting muscle. Work with intrafusal muscles to adjust muscle contractions

127
Q

Cardiac muscle contraction

A

Depolarizes using current that enters cell from adjoining cardiac myocyte via gap junctions. Current depolarizes cell which stimulates entry of calcium from outside the cell through voltage gated calcium channels. Causes release from sarcoplasmic reticulum inside myocyte, increasing intracellular calcium concentration more. Starts the contraction process

128
Q

Smooth muscle contraction

A

Same initiation as cardiac muscle, with voltage gates calcium channels and gap junctions
Smooth muscle calcium causes phosphorylation of myosin chains. Causes them to bind to actin chains and induces shortening and contracting. Calcium enters cell through calcium channels and binds to calmodulin, complex then activated myosin light- chain kinase which phosphorylates myosin

129
Q

Smooth muscle relaxation

A

Activation of myosin light -chain phosphastase removes phosphate groups from myosin, causing actin myosin myofilament to lengthen and relax the muscle. Can be caused by nitric oxide released in nearby cells

130
Q

High velocity low amplitude

A

Rapid, therapeutic force of brief duration that travels short distance within the anatomic range of motion of a joint
Engaged restrictive barrier to elicit release of restriction
Frequently associated with audible and palpable release in form of a pop

Passive- patient relaxed- physical does all work
Direct- into barrier

Increases joint mobility, reduce muscle spasms, increased range of motion, decreased pain, improved muscle strength, improved autonomic balance

131
Q

Articulately technique (ART)

A

Passive, direct treatment method employing low velocity/ moderate to high amplitude force applied to dysfunctional joint against restrictive barrier

132
Q

“Pop” with HVLA

A

Pressure change results in phase change from liquid synovial fluid to gas
Elastic recoil of synovial capsule as it snaps back from capsule-synovial fluid interface

133
Q

Tribonucleation theory

A

Opposing surfaces resist separation until a critical point where they separate rapidly, creating a phase change from liquid to gaseous cavities

134
Q

When to use HVLA

A

Somatic dysfunction is judged to be an actual joint motion restriction
Joint fixation
To disrupt connective tissue adhesions
Treat chronic dysfunction resistant to other treatment modalities
Modify reflexes

135
Q

Absolute contradictions of HVLA

A

rheumatoid arthritis, Down syndrome, achondroplasia dwarfism, fracture/ dislocation spinal or joint instability, joint infection, bony malignancy, surgical fusion, inflammatory joint disease, etc

136
Q

AA instability

A

Atlantoatlis junction , transverse ligament is more laxed, increased risk of injury (mostly with Down syndrome and rheumatoid arthritis)

137
Q

Relative contradictions of HVLA

A

acute herniated nucleus pulposus, acute whiplash, severe muscle spasms/ strain, osteopenia/osteoporosis, metabolic bone disease, hyper mobility syndromes, acute radiculopathy

138
Q

possible Side effects of HVLA

A

Transient: local pain or discomfort, headaches tiredness/fatigue dizziness, nausea, stiffness, hot skin, fainting
Substantial reversible impatient: intervertebral discs herniating, nerve root compression, fractures, disc prolapse

139
Q

HVLA approach

A

Ask patient permission
Proper diagnosis of joint somatic dysfunction
Initial positioning
Engagement and stacking of barriers (opposite of diagnosis)
Accumulation of forces to engage restrictive barriers
Final corrective thrust

Positioning into barriers and thrust into freedom

Fall 2022 (15 decks)

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