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
describe the annulus
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)
26
what creates tension on an annulus
both pulling and pushing creates tension (like a water balloon)
27
describe the nucleus
resist compression (primarily type II collagen; high GAGS) dense connective tissue avasculr, depends on diffusion for nutrients, aneural
28
describe the movement of the annulus and nucleus
move as a unit normally deformation but not migration of nucleus with motion
29
describe the vertebral end plate
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
30
describe the vertebral body (bone)
type I collagen 6 times stiffer and 3 times thicker than a disc
31
IDD prevalence
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
32
most common IDD injury
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)
33
Structures involved with acute IDD
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
34
describe why there is a large auto immune inflammatory response with acute IDD
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
typical posterolateral IDD symptoms
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
what might increase or decrease pain with acute cervical posterolateral IDD
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
ROM signs for posterolateral IDD
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
what is centralization of symptoms
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
typical postlat IDD signs
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
signs of rare central IDD
unique S&S = cord PT implications = immobilization and emergency referral
41
what is the McKenzie method
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
what is directional preference
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
how well does the McKenzie method work with cervical issues
weak evidence for effectiveness no more beneficial vs general exercise and a control group out to 12 months
44
PT Rx for acute IDD with cervical radiculopathy
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
PT Rx for acute IDD
POLICED intermittent traction neural mobilizations (mvmd without symptom reproduction) MET ultimately for tissue proliferation and stabilization of muscles
46
why is MET mainly used for tissue proliferation and stabilization for acute IDD
improving stabilization offsets the laxity from the tear add resistance and the right loads/reps to change/heal the tissue
47
persistent IDD is aka
degenerative disc disease age related sic changes (not always due to age alone)
48
incidence/prevalence of persistent IDD
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
incidence/prevalence of persistent IDD
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
etiology of persistent IDD
acute IDD can lead to persistent sedentary lifestyle genetics
50
pathogenesis of persistent IDD
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
other factors that are included in the pathogenesis of persistent IDD
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
categories of herniation per miller
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
describe the narrowing effect of persistent IDD
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
S&S of persistent IDD
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
PT Rx for persistent IDD
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
prognosis of persistent IDD
refer to ligament and cartilage notes on healing and extend the timelines due to likely prolonged inflammatory phase of healing mostly good
57
what is peripheralization with acute IDD and what is significantly associated with it
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
MD Rx for acute and persistent IDD
-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
what happens with a cervical fusion
increased adj segment motion at the levels above and below after a 2-level compared with a 1-level anterior cervical disc fusion
60
what happens with a total disc replacement
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
axis of joint motion is typically maintained by
inert structures like ligaments/capsules/discs contractile structures like local muscles patterning of CNS/PNS for motor control
62
definition of functional or mechanical instability
abnormal movement if spinal segment under loaded conditions resulting in pain and disability that changes the instantaneous axis of motion
63
difference between functional/mechanical instability
functional = instability that can be stabilized with muscle activity mechanical = can't be completely stabilized with mm activity or positioning
64
risk factors/etiology/prevalence for instability
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
what are the factors for the beighton scale
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
major criteria for instability
beighton scale greater than or equal to 4/9 = + test arthralgia > 3 months in > 4 joints
67
minor criteria for instability
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
when is a pt + for BJHS
2 major criteria present 1 major and 2 minor criteria present 4 minor criteria present
69
structures that are involved in functional and mechanical instability
passive restraints (ligaments, capsules, and disc) active stabilizers or local muscles inhibited neurological function
70
symptoms for functional instability
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
ROM signs for functional instability (primarily limited with, what is better/why, combined, WB)
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
signs of functional instability
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
symptoms of mechanical instability
same as functional except worse and with unpredictable pattern, worsening symptoms, more frequent episodes, and increased pain with even trivial and lesser ADLs
74
signs of mechanical instability
same as functional except worse with positive stress tests that won't stabilize fully
75
PT Rx for functional/mechanical instability
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
MD Rx for mechanical instability
in rare cases of shearing/slipping prolotherapy for stabilization along with PT fusion surgery (only option for some pts)
77
what is spondylosis
age related joint changes at multiple levels
78
when is age related joint changes detected/where are they most common/how do they progress
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
prevalence of age related joint changes
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
location of articular cartilage
covers ends of long bones and facets 2-4 mm thick near ligaments/tendons
81
main cell of articular cartilage
chondrocytes
82
characteristics of articular cartilage
frictionless/resistent to wear aneural/alymphatic/avascular = not capable fo producing inflammatory response if P!/inflammation = more likely bone