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DPT 730: MSK > Cervicothoracic Spine pt. 3: Test 2 > Flashcards

Cervicothoracic Spine pt. 3: Test 2 Flashcards

1
Q

pathomechanics of thoracic outlet syndrome (TOS)

A

compression of subclavian artery and possible brachial plexus (peripheral nerve)

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2
Q

etiology of TOS (specifically how repetitive strain/overuse affects)

A

FHP creates upper thoracic hypomobility into ext

increased tension of subclavian fascia on axillary artery (especially with UE elevation; lack of clavicle rotation)

also scalenes can compress if pt is a chest breather with respiratory dysfunction/excessive use of accessory muscles

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3
Q

why might TOS also be known as T4 syndrome

A

due to most involved segment

upper limb supply from SNS is T1-T9 (PNS is C5-T1)

thoracic sympathetic ganglia are near thoracic joints (flight to fight; vasoconstriction may occur with jt. dysfunction

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4
Q

other general etiology for TOS

A

trauma (like WAD involving scalenes; makes muscles guard and possibly creates adhesions/scarring if torn)

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5
Q

differential diagnosis for thoracic outlet syndrome (other things that may be mistaken for TOS?)

A

cervical rib
pan cost tumor compressing medial cord of brachial plexus
carpal tunnel
spinal nerve impingement
neuromuscular disease (i.e. diabetes or aneurysm)

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6
Q

symptoms of TOS

A

UE glove/sleeve like paraesthesias
-non segmental
-intermittent/short
-fast progression to well defined area
-possible weakness

Clod/swelling with vascular compromise

increased by raising arms, sleeping, or poor posture sitting

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7
Q

observable scan findings of TOS

A

FHP
possible UE discoloration die to artery involvement

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8
Q

scan findings for TOS

A

A/PROM give possible indications of upper thoracic restriction

resisted/MMT possibly decreased with strength/endurance in posterior shoulder and scapular muscles with FHP

derms, DTRs, and myotomes WNL

non segmental hypoactivity (peripheral nerve desensation, possible associated weakness)

positive ULTT dural mobility

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9
Q

dural tension restrictions S&S for TOS

A

paraesthestias increased from both ends

due to decreased elasticity/inflammation

may localize level and structure with palpation (anterior to TP is root, inferior to TP is trunk)

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10
Q

PT Rx for TOS

A

acute = paresthesias at rest
-POLICED
-motion without resistance of symptoms
-STM over segmental level

persistent = paresthesias at resistance
-motion with resistance
-neural mobilizations with resistance at end range once acuity settles

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11
Q

Dural GLIDING restriction S&S/cause

A

paresthesias increased from one end but relieved from the other

due to adhesions

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12
Q

PT Rx for dural gliding restriction

A

acute = same as neural tension

persistaent = same as neural tension but neural mobilizations at MID range

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13
Q

describe when to use neural mobilizations/their effectiveness q

A

moderate to large effect on pain, disability, and mechanosensitivity BUT with limited quality evidence

predictors for good outcome
-absence of neuropathy
-older age
-smaller ROM deficits with median N

Rx is only 10-20 mvmts a day; not a lot

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14
Q

accessory motion testing signs that would be present in a BM exam for TOS

A

more often a U upper thoracic hypo mobility

limits anterior clavicular rotation with UE elevation

increases tension of med cord of brachial plexus

less often sign is limited 1st rib inferior glide (guarded/shorten scales, usually resulting from sublux with violent contraction fair WAD that pulls 1st rib superiorly)

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15
Q

special tests for TOS

A

all individual tests are minimally or not supported

use Gillards cluster (can’t use just one test)

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16
Q

PT Rx for TOS

A

posture/ergonomic (edu, scap taping, etc)

diaphragmatic breathing to minimize accessory respiratory muscles

MT/MET in cervicothoracic regions to improve mobility

MET to increase strength/endurance in posterior shoulder and scalp muscles

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17
Q

describe sitting FHP and musculoskeletal issues

A

can cause up to 300 mmHg of presser within the muscle thus limiting blood supply

30% max voluntary contraction of the muscle will reduce circulation

70% MVC of the muscle will nearly eliminate circulation

proper posture and regular change of positions is helpful

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18
Q

describe the significance of thorax flexion, compression, and depression with FHP

A

diaphragm actively/insufficient and overworked

thorax extensors and accessory muscles overwork to help with respiration

thoracic stiffness develops and may lead to instability at lower cervical

dowagers hump may develop

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19
Q

how does a dowagers hump develop

A

fat pad over the upper C/T junction that develops with atrophy and shearing

wedging of vertebrae due to osteoporosis

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20
Q

decrease of anti gravity reflex of muscles with FHP leads to

A

local muscle inhibition

mouth opening

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21
Q

common thoracic restrictions with FHP

A

MOST common = B loss of upper thoracic ext contributes to neck dysfunction and likely lower cervical instability

U loss of upper thoracic Ext contributes to U TOS as mentioned as well as some shoulder conditions

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22
Q

general Rx for sitting FHP

A

MT/MET with local muscle emphasis to foster more upright position

postural edu to sit and be supported

ergonomic improvements, often with keyboard set up

breathing training for diaphragmatic breathing

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23
Q

describe Internal disc derangement in the acute phase

A

due to trauma like:

annular and end plate tear

acute hernias (least common)

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24
Q

describe IDD at a chronic or persistent Level

A

disc changes due to numerous variables allow hernias to gradually develop over time

slow herniation

MOST PREVALENT IDD

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25
Q

describe the annulus

A

outer = type I collagen

type II increases going inward (blends/forms gradient with nucleus)

fibrocartilage connective tissue

hyper to hypo neural out to in (nociceptive, proprioceptive)

stabilizes like a ligament and leads to multifidi contraction

avascular (slow healing)

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26
Q

what creates tension on an annulus

A

both pulling and pushing creates tension (like a water balloon)

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27
Q

describe the nucleus

A

resist compression (primarily type II collagen; high GAGS)

dense connective tissue

avasculr, depends on diffusion for nutrients, aneural

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28
Q

describe the movement of the annulus and nucleus

A

move as a unit normally

deformation but not migration of nucleus with motion

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29
Q

describe the vertebral end plate

A

highly innervated/vascularized

assists with nutrient diffusion

covers nucleus and MOST of annulus with specialized connective tissue (articular cartilage toward vertebral body, fibrocartilage toward disc)

weak link of intervertebral joint (especially at annular connection)

can calcify and limit diffusion

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30
Q

describe the vertebral body (bone)

A

type I collagen

6 times stiffer and 3 times thicker than a disc

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31
Q

IDD prevalence

A

persistent > acute

rare in thoracic region (also greater consequences in this area due to narrowest canal; less than 1% of all cases)

rare in C2-6 region due to additional stability from UV joints

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32
Q

most common IDD injury

A

posterolateral portion of the disc is most common area

it is weaker, thinner, with more vertical and less oblique annular fibers

transition of the annulus into the endplates is a weak spot (highly connected area)

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33
Q

Structures involved with acute IDD

A

more commonly annular tear and end plate evulsion

less commonly the nucleus pulposus herniation

disc structures are immunoreactive once damaged (body sees as a non self; large inflammatory phase)

large autoimmune inflammatory response occurs

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34
Q

describe why there is a large auto immune inflammatory response with acute IDD

A

excessive osmotic pressure creates disc and spinal nerve swelling

spinal nerve sensitized to pressure/tension

radiculopathy/radicular S&S

poor drainage due to lack of lymphatic vessels

extended inflammatory phase

35
Q

typical posterolateral IDD symptoms

A

dull/achy spinal pain (annulus is highly innervated = lots of pain; less swelling than lumbar disc due to lower number of GAGs)

radiculopathy (possible segmental paresthesias w/I 24 hours to distal extremity; worse if cold indicating circulatory compromise)

referred pain

36
Q

what might increase or decrease pain with acute cervical posterolateral IDD

A

decreased pain when unloaded/supine

increased pain/paraesthesias when looking down

any movement down and away from the issue will cause pain

increased pain in mornings and influenced as above while worsening throughout the day

lots of early symptoms due to pressure from swelling

37
Q

ROM signs for posterolateral IDD

A

all may increase pain

flex and contralateral SB and RT from injured area likely limited and increase extremity/spinal pain die to pressure from pushing swelling towards SC and tension on annulus/endplate tear

ext and RT/SB towards affected area may be less limited (may increase spinal pain due to increased hydrostatic pressure on disc)

38
Q

what is centralization of symptoms

A

inconsistent for discogenic pain but it may be present

abolition of distal and or spinal pain in a distal to proximal direction in response to repetitive motion or sustained positions

39
Q

typical postlat IDD signs

A

resistance and MMT = variable

possible + stress tests with compressions, distractions, and PA pressures (b/c endplate is like cartilage and annulus is like a ligament so all movements have potential)

neuro possibly + depending on timing/severity (myotomal fatigue, hypo reflexive DTR, diminished derm, and + dural mobility)

+ stability tests

40
Q

signs of rare central IDD

A

unique S&S = cord

PT implications = immobilization and emergency referral

41
Q

what is the McKenzie method

A

developed by Robert McKenzie

based on belief that most pain comes from injuries to the disc which is not supported in research

classification of symptoms based on location and positions that decrease symptoms

42
Q

what is directional preference

A

position, motion, and or factor that alleviates symptoms irrespective of location

cervical = may be associated with centralization with the addition of decreasing severity and improving function

43
Q

how well does the McKenzie method work with cervical issues

A

weak evidence for effectiveness

no more beneficial vs general exercise and a control group out to 12 months

44
Q

PT Rx for acute IDD with cervical radiculopathy

A

with cervical radiculopathy and IDD aggressive nonsurgical treatment is successful 24/26

parts of treatment include:
-intermittent traction
-specific therapeutic exercise
-oral anti-inflammatory meds
-pt edu

45
Q

PT Rx for acute IDD

A

POLICED
intermittent traction
neural mobilizations (mvmd without symptom reproduction)
MET ultimately for tissue proliferation and stabilization of muscles

46
Q

why is MET mainly used for tissue proliferation and stabilization for acute IDD

A

improving stabilization offsets the laxity from the tear

add resistance and the right loads/reps to change/heal the tissue

47
Q

persistent IDD is aka

A

degenerative disc disease

age related sic changes (not always due to age alone)

48
Q

incidence/prevalence of persistent IDD

A

lumbar > cervical

when you do have cervical…
-most common at C5,6 and C6,7
-C6 spinal nerve is most involved nerve and largest diameter in lower cervical spine die to numerous innervations from lateral and posterior cord from brachial plexus

48
Q

incidence/prevalence of persistent IDD

A

lumbar > cervical

when you do have cervical…
-most common at C5,6 and C6,7
-C6 spinal nerve is most involved nerve and largest diameter in lower cervical spine die to numerous innervations from lateral and posterior cord from brachial plexus

49
Q

etiology of persistent IDD

A

acute IDD can lead to persistent

sedentary lifestyle

genetics

50
Q

pathogenesis of persistent IDD

A

annular/end plate changes lead to earlier disc changes

in growth of nociceptive pain fivers from acute IDD healing can lead to persistent inflammation/nociplastic pain

persistent inflammation brings excessive and destructive proteins and a low grade infection is likely to enter disc (which can drive inflammation that causes pain)

51
Q

other factors that are included in the pathogenesis of persistent IDD

A

less GAGs so more fibrotic and dehydrated nucleus

more acidic disc that kills disc cells and limited proliferation (loss of water = no dilution = more acidic)

annular disorganization

thinning/loss of cartilage at end plates

increased inflammation and fatty deposits in vertebra

then persistent herniations gradually develop per the miller classifications once changes occur with the discs

52
Q

categories of herniation per miller

A

protrusion (bulge) = nucleus migrates but remains in annulus; MOST common

extrusion = nucleus migrates thru the outer annulus

free sequestration = nucleus breaks away from the annulus

**schmorls nodes likely develop where the nucleus migrates into the vertebral body as well

53
Q

describe the narrowing effect of persistent IDD

A

disc instability may develop

increased load bearing on facets which means age related joint changes may develop

narrowing of the foramen = stenosis may develop

54
Q

S&S of persistent IDD

A

slow change; tissues adapt

gradual onset

may be like acute S&S

also need to consider other conditions that may develop and their respective S&S

may even be a “mixed bag” fo symptoms

55
Q

PT Rx for persistent IDD

A

possibly acute IDD rx

need to consider primary driver of symptoms from the development of other conditions
-IDD
-instabilty
-age related joint changes
-stenosis
-combination of symptoms

56
Q

prognosis of persistent IDD

A

refer to ligament and cartilage notes on healing and extend the timelines due to likely prolonged inflammatory phase of healing

mostly good

57
Q

what is peripheralization with acute IDD and what is significantly associated with it

A

negative outcome predictor

opposite of centralization

significant association with:
-mental distress/depression
-non-organic signs i.e. tumor
-pain behaviors
-somatisation = conversion of anxiety into bodily symptoms
-fear of work

58
Q

MD Rx for acute and persistent IDD

A

-infection benefits from antibiotic treatment
-laminectomy (remove part of lamina to make space)
-partial discectomy (shave off part of disc)
-cervical fusion
-total disc replacement

59
Q

what happens with a cervical fusion

A

increased adj segment motion at the levels above and below

after a 2-level compared with a 1-level anterior cervical disc fusion

60
Q

what happens with a total disc replacement

A

unloads facets superior to TDR and increased loading at level of TDR

are and effective treatmetn more than 5 years postoperatively

restores height, pretenses structure, and allows movement

reverses BM problems to some degree

doesn’t necessarily take all pain away bit greatly helps

61
Q

axis of joint motion is typically maintained by

A

inert structures like ligaments/capsules/discs

contractile structures like local muscles

patterning of CNS/PNS for motor control

62
Q

definition of functional or mechanical instability

A

abnormal movement if spinal segment under loaded conditions resulting in pain and disability that changes the instantaneous axis of motion

63
Q

difference between functional/mechanical instability

A

functional = instability that can be stabilized with muscle activity

mechanical = can’t be completely stabilized with mm activity or positioning

64
Q

risk factors/etiology/prevalence for instability

A

women more than men

traumatic ir reccurent sprains
age related disc changes
repetitive ext activities
creep
adj joint hypo mobility (especially with fusion)
connective tissue disorder

most common at C5-7

65
Q

what are the factors for the beighton scale

A

1 point for each of the following:

stand and palms touch floor
each knee that hyperextends
each elbow that hyperextends
each thumb that touches forearm
each little finger with 90 degrees MCP hyperextension

66
Q

major criteria for instability

A

beighton scale greater than or equal to 4/9 = + test

arthralgia > 3 months in > 4 joints

67
Q

minor criteria for instability

A

beighton scale of 3 or less out of 9

arthralgia > 3 months in 1-3 joints or LBP > 3 months (i.e. spongy condition)

soft tissue injury in more than 3 locations

tall/slim body

abnormal skin

droopy eyes

varicose veins, hernias

68
Q

when is a pt + for BJHS

A

2 major criteria present

1 major and 2 minor criteria present

4 minor criteria present

69
Q

structures that are involved in functional and mechanical instability

A

passive restraints (ligaments, capsules, and disc)
active stabilizers or local muscles inhibited
neurological function

70
Q

symptoms for functional instability

A

predictable pain
recurrent spine and referred pain (possibly paraesthestias)
decreased P! with positional changes/support
increased P! with prolonged positions, looking up, sudden/strenuous ADLs like lifting

catching symptom

easy self manipulation

71
Q

ROM signs for functional instability (primarily limited with, what is better/why, combined, WB)

A

if acute, limited with aberrant motion

primarily limited and painful with ext b/c of lincreased anterior vertebral shearing followed by SB

flx will tend to be better bc of large posterior ligamentous/fascia tightening to help with stabilization

inconsistent WB/NWB findings

often WNL except for ext with creasing

combined motion = inconsistent block

72
Q

signs of functional instability

A

resisted/MMT may be P! if acute; most often string/painless bc global muscles aren’t affected

  • neuro tests except possible hyperesthesia with pinwheel during sensation testing

+ PA stress and linear stability tests that cam be stabilized bye muscle activation or positioning that should tighten the ligament s

hypermobile accessory motion with possible adj hypo mobility

inhibited local muscles

73
Q

symptoms of mechanical instability

A

same as functional except worse and with unpredictable pattern, worsening symptoms, more frequent episodes, and increased pain with even trivial and lesser ADLs

74
Q

signs of mechanical instability

A

same as functional except worse with positive stress tests that won’t stabilize fully

75
Q

PT Rx for functional/mechanical instability

A

Rx like ligament sprain
POLICED
posture edu of sitting tall/activating deep neck flexors
JM- increased adj joint hypo mobility typically at C2 and t-spine
bracing/taping pen

MET with emphasis on stabilization particularly of local muscles; hyperextension is contraindicated

76
Q

MD Rx for mechanical instability

A

in rare cases of shearing/slipping

prolotherapy for stabilization along with PT

fusion surgery (only option for some pts)

77
Q

what is spondylosis

A

age related joint changes at multiple levels

78
Q

when is age related joint changes detected/where are they most common/how do they progress

A

detected as early as 15 years old

most common in C5-7 and L4-S1

progresses along with age related disc changes (bc they take on earlier/more stress if there is a present disc issue)

79
Q

prevalence of age related joint changes

A

most common cause of disability in US

80% of people > 55 yrs

most common at hip/knee followed by spine

similar presence in athletic/non-athletic populations

PA is protective so long as there is no trauma

80
Q

location of articular cartilage

A

covers ends of long bones and facets 2-4 mm thick

near ligaments/tendons

81
Q

main cell of articular cartilage

A

chondrocytes

82
Q

characteristics of articular cartilage

A

frictionless/resistent to wear

aneural/alymphatic/avascular = not capable fo producing inflammatory response

if P!/inflammation = more likely bone

DPT 730: MSK (14 decks)

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