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SMT > SMT Books 1-3 > Flashcards

SMT Books 1-3 Flashcards

1
Q

Who mentioned that upper cervical and thoracic HVLAT is more effective than mobilizations?

A

Dunning

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2
Q

Who mentioned that HVLAT is a bilateral event?

A

Dunning

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3
Q

Do you need a cavitation at C5/6 to elicit increased EMG activity in the biceps, and who discovered this?

A

No, Dunning

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4
Q

Who discovered that a HVLAT produces hypoalgesic effects through increased pressure pain thresholds?

A

Cassidy et al.
A CAST will sure as fk increase the pain threshold.

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5
Q

Neurophysiologically, Is HVLAT excitatory or inhibitory?

A

There’s conflicting evidence - Peterson et al.
Could never tell if Jordan Peterson is excitatory or inhibited.

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6
Q

Who discovered that HVLAT causes a segmental reflexive contraction?

A

Herzog and Simons
- Hazaaah! (Will make you reflexively contract).

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7
Q

Who discovered that HVLAT causes an immediate increase in strength?

A

Colloca and Keller
- cool killers have to be strong.

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8
Q

CGH - manipulate what?

A

Cervical and Thoracic - Dunning

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9
Q

T or F: The intra-articular bubble collapse is all that occurs with a HVLAT?

A

F. Several phenomenon are likely occuring - Dunning.

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10
Q

Who discovered that we’re not sure which segments the pops are coming from?

A

Dunning

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11
Q

What is Craniopharyngioma?

A

A benign neoplasm and is that to be caused by brain maldevelopment that can occur in children and adults in the seller and/or suprasellar regions - Firas Mourad

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12
Q

What did the American College of Physicians say about acute, subacute, and chronic LBP?

A

Acute and subacute: pt’s should select non-pharmacological tx with superficial heat, massage, and acupuncture. No improvement, then add manipulation.

Chronic: a bunch of interventions as well as acupuncture and spinal manipulation.

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13
Q

Does the Ontario CPG recommend spinal manipulation for acute and chronic LBP?

A

Yes.

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14
Q

What does the European CPG recommend for early management of LBP?

A

Manipulation and acupuncture.

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15
Q

Who determined that the 25 CPR’s for PT’s management of LBP are not ready for clinical use?

A

Haskins et al.
- Haskin is askin’ for something better. How bout you do something tho. Shithead.

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16
Q

Why are most of the CPRs shit? May and Rosedale 2009

A

None of the studies were of high quality -

  • Mayday, we’re going down.
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17
Q

What did Stanton et al. In 2010 say about the CPR’s?

A

The reason they’re so shit is because most studies cannot differentiate between predictors or response to treatment and general predictors.
- with stanton he can’t predict what response is gonna happen when he swings

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18
Q

Why can’t CPRs be recommended?

A

They are still in their initial development.
- Haskins et al.
Haskin is still askin’

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19
Q

Which study, which was published twice, is the only study that shows the “cracking” noise is not necessary?

A

The flynn et al. Study
- Not Necessaey (NN)

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20
Q

What did the Hancock et al. Study in 2008 demonstrate regarding the CPR for manipulation?

A

That the SMT CPR could NOT predict who was a good candidate for SMT.
- Hancock. HANCANNOT HAH

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21
Q

What did the Reggars study in 1996 discover?

A

On average there’s 2.5 cavitations per thrust.
- Reggars (regular maniper, nothing special)

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22
Q

What did Bolton et al. discover with cervical thrusts?

A

With rotational thrusts the cavitation is more likely to occur on the contralateral side.
SB thrusts = on either side.

  • BoltON THIS SIDE
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23
Q

Dunning in 2013 demonstrated how many pops on average? Is it a bilateral cavitation?

A

6.95 and that it was a bilaterral event. It is no more likely to occur on one side vs. the other.

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24
Q

How do Bolton and Dunning’s research differ?

A

Bolton said it was on one side.
Dunning said it was bilateral.

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25
Q

How do Dunning and Reggars research differ?

A

Dunning said 6.95 pops on average
Reggars said 2.5

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26
Q

What did Ross et al. Say about the pops?

A

The more pops, the more likely it came from the targetted joint.

  • Ross from friends eventually targetted the right girl.
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27
Q

What did Ernst and Canter say about SMT in 2006?

A

SMT might offer some relief for back pain, but there’s a lack of evidence. They advised caution with cervical manipulations

  • Ernst ain’t liking the evidence and Canter cautions cervical.
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28
Q

What did the the Cochrane Review in 2010 say about neck pain?

A

Mod-low quality of evidence that SMT is effective.

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29
Q

Dunning et al. Discovered that HVLAT improves RR by ___ and LR by ___. This led to a ____ in motor performance of the deep cervical flexors.

A

RR: 4.9 degrees
LR: 3.4 degrees

Increase in motor performance.

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30
Q

Usworth in 1971 thought the pop orginated from where?

A

CO2 gas release and said
There’s 15-30 minute refractory period.

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31
Q

What did Cascioli et al. in 2003 say the pop was from?

A

There’s no evidence of a gas release or joint space increase. Instead, it’s the collagen fibers of the articular capsule being stretched.
- A cast involving Coil needs to stretch

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32
Q

What did Smith and Bolton in 2013 say regarding WAD?

A

With non-serious, idiopathic, or WAD (grade II), the use of manipulation for neck pain is at best “empirical.”

Empirical menas based on experience, there’s no evidence to support these claims.

“Smith and western is empirical.”

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33
Q

What did Wand et al in 2012 say regarding manipulation of the C spine?

A

Abondon it. It’s not safe.

Wand waved his wand no.

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34
Q

What 3 things did Cassidy in 2012 say regarding manipulation of the C spine?

A
  1. Don’t abandon it. It has significant Short term improvements on disability.
  2. It’s better than Medication.
  3. There’s no evidence that mobilization is safer or more effecTive than HVLAT.

CAST-SMT
- short term
- medication
- effective

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35
Q

What did Michaleff et al. In 2012 say about SMT?

A

It’s cost effective.

  • MichalEFFECTIVE
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36
Q

How does SMT relieve pain?

A

A 1. Manipulation induced Analgesia.
N 2. Non-opiod mechanisms
SN 3. Serotinergic and Nonadrenergic pathways
P 4. Stimulates dPAG-descending inhibition

AN-SNP (Andddd Snap)

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37
Q

How does SMT increase circulation?

A
  1. Sympathetic and parasympathetic effects on vasculature.
  2. Sympathoexcitatory: decreases skin temperature and increases skin conductance.
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38
Q

What is the vascular risk when manipulation the C-spine?

A

It can vary from 1/50,000 to 1/5.8 million and it may not be cause and effect

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39
Q

What did Haldeman and Rubenstein in 1992 estimate the risk of manipulating the c-spine was?

A
  1. Less than 1/10million for VBA/ICA dissection.
  2. 3/10M for sudden death
  3. There’s no accurate way to assess it.
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40
Q

What did Cassidy et al. In 2008 say about VBA?

A

There’s a stronger correlation PCP visits than chiropractor visits when it comes to VBA dissection. Especially of PCP visits and those < 45 y.o.

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41
Q

What did Murphy in 2010 say about screening CAD and VBI Tests?

A

There’s a lack of reliability of tests and there’s no benefit in screening someone who is at “risk.”

Additionally, VAD is NOT a complication of Cervical Manipulation.

  • Murphy, there’s no benefit, no complication
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42
Q

What 6 Tests do Kerry and Taylor recommend doing for the assessment of CAD in pt’s presenting with neck pain and a headache?

A
  1. CN and eye exam
  2. BP testing
  3. Signs of ICA and VA Dissection (non-ischemic and ischemic.
  4. PMH atherosclerosis
  5. Hand-held doppler Ultrasound
  6. Functional CAD positional test (rotation for VA, and extension for ICA).
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43
Q

How much strain did Symons et al. Find on the CONTRALATERAL side of the C-Spine during SMT? (Idk which segment they popped)

A

6.2% at C0-1 loop
2.1% at C6

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44
Q

How much strain is required in the VAs before mechanical failure according to Symons et al.?

A

139-162%

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45
Q

What FRACTIONAL force is required for a C-spine manipulation compared to the mechanical failure rate?

A

1/9th the force

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46
Q

What was the conclusion from Symons et al. In 2002 regarding cervical manipulation and VAD?

A

SMT is very unlikely to mechanically disrupt the VAs

Symon says it won’t cause VAD

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47
Q

Austin et al. In 2002 exposed rats to 1000 strain cycle and observed how much microdamage with 6% and 30% force?

A

6% = no microdamage
30% = significant microdamage, ~50% damage.

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48
Q

According to Austin et al. In 2002, What was the average peak forces and speed to the neck during SMT?

A

Peak force: 100-150N
Speed: 80-150ms

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49
Q

Wuest et al. 2010, what was the mean peak force of a neck HVLAT and regular HVLAT?

A

Neck: 72N
Lumbar: 200N

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50
Q

What was the peak VA strain for a c2-3 and c4-5 manipulation in compared to VBI and PROM?

A

C2-3: 2.2%
C4-5: 3.1%

VBI Testing: 8.5%
PROM: 13%

Thus the VA strain is 1/5th during manipulation compared to neck AROM.

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51
Q

Herzog et al. 2012, do trained clinicians strain the VA’s with SMT?

A

No. The VA is not a factor in VB injuries.

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52
Q

Buzzati et al. Can a HVLAT at c1-2 endanger the SC or VA?

A

No

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53
Q

Symons et al. 2012, what was the biomechanical force and speed of a c-spine manipulation in cadavers vs. living subjects?

A

Cadaver: 284N and 120ms
Living: 190N and 175ms

Conclusion: a thrust on a cadaver is faster and requires more force to cavitate.

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54
Q

Thomas et al. Observed how much INFLOW into the brain and how much CHANGE in blood flow when using MRI with cervical rotation, rotation and distraction, C1-2 rotation, and distraction?

A
  • The average inflow into the brain is 6.98 mL/s.
  • Blood flow was compensated by a decrease in one vessel resulted in an increase in others.
  • Overall, most positions increased overall blood flow.
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55
Q

What did Quesnele et al. in 2024 discover with blood blow changes in positions if neutral, 45 deg. rotation, or full rotation?

A

No significant change in blood flow.

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56
Q

What was Hutting et al. findings in 2013 from the VBI literature review?
- quality?
- sensitivty?
- specificity?

A
  1. All questionable quality
  2. 0-57% sensitivity (a lot of false-negatives and missed too many patients.
  3. 67-100% specificity
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57
Q

What did Puentedura et al. in 2012 say regarding the VBI testing?

A

Regardless of the evidence, or lack thereof, it is the responsibility of the clinician to perform screening examinations and clearly document their use to reduce legal risk.

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58
Q

What was Kerry and Taylor’s 6 screening for CAD in pt’s with neck and headache symptoms?

A

CE BS PUP

  1. CN and eye exam
  2. BP testing
  3. Signs of ICA and VA dissection (non-ischemic and ischemic)
  4. PMH of factors related to atherosclerosis
  5. Hand-held doppler US
  6. Functional CAD positional tests (rotation for VA and extension for ICA)
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59
Q

What was Kerry and Taylor’s 3 S&S of Vertebral/CAD?

A

Cranial and headaches

  1. “Head and neck pain that feels like no other.”
  2. Fronto-temporal headache, upper cervical, antero-lateral, or postero-lateral neck pain, facial pain, or facial sensitivity
  3. CN palsies (9-12)
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60
Q

What symptom was found in 82% of ICA dissections?

A

Horner’s Syndrome

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61
Q

What are the 6 symptoms of Horner’s Syndrome?

A
  1. Head, neck, and facial pain
  2. Ptosis (drooping eyelid)
  3. Enopthalmos (sunken eye)
  4. Miosis (small, restricted pupil)
  5. Facial dryness
  6. Retinal and Cerebral Signs (ICA supplies the retina via the opthalmic artery)
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62
Q

3 S&S of VBA Dissection; what is the most prominent sign?

A
  1. 85% - Occipital Headache
  2. 67% - Balance or Ataxia problems
  3. 25% - Dizziness

Vbad bod

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63
Q

4 S&S of ICA Dissection; what is the most common?

A

When the ICA goes out you lose your HP and feel weak

  1. 75% - Retro-orbital or temporal headache
  2. 60% - Ptosis
  3. 60% - Facial Palsy
  4. Limb Weakness (65% upper, 50% lower)
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64
Q

What was an unexpected finding from HVLAT regarding facet displacement?

A

There’s less displacement of facets with HVLAT than mobilizations

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65
Q

What was the complication rate of HVLAT from Cassidy et al.?

A

1/50,000 - 1/4,000,000 and may not be cause and effect.

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66
Q

From Purntedura et al 2012, what were the most common adverse events of HVLAT?

A
  1. Arterial Dissection - 37.3%
  2. Disc Herniation - 18.7%
  3. CVA - 13.4%
  4. Dislocation or fracture - 6.7%
  5. Death - 5.2%

DDCDD

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67
Q

From Purntedura et al 2012, chiropractors cause what percentage of problems?

A

70%

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68
Q

From Purntedura et al 2012, how many deaths from HVLAT were caused by PT’s?

A

None.

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69
Q

What percentage of adverse events were preventable; and what percentage of them had vascular pathologies?

A

45% - preventable due fo bony or vascular pathologies (severe spondy, osteoporosis, RA, ankylosing soondylitis, cervical stenosis).
20% - inapproprite to manipulate

Thus, 65% of the cases should NOT HAVE BEEN MANIPULATED.

13% vascular pathologies

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70
Q

What percentage of adverse events were unpreventable?

A

10.4%

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71
Q

What are Maitland’s Grades of Manipulations?

A

Grade I: SMALL amplitude at the BEGINNING of the range

Grade II: LARGE amplitude within the MIDRANGE if movement

Grade III: LARGE amplitude at the END range

Grade IV: LARGE amplitude at the END range when tissue is limiting motion (NOT PAIN)

Grade V: SMALL amplitude, quick THRUST manipulation at end range

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72
Q

Klein et al., what was the largest and smallest ranges of HVLAT?

A

Rotation: 12-46 degrees

Lateral flexion: 31-62 degrees

Flexion: 0-23 degrees

  • HVLAT should NOT exceed physiological AROM.
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73
Q

Who determined that the lateral glide test was valid?

The hypomobile side moved ___ mm less than the contralteral dysfunctional side

A

Fednandez de las Penas et al. 2005

3.44 mm

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74
Q

According to Jull et al. 1994, what percentage of agreement is there between an experienced therapiest and the dysfunctional segment?

A

94-98%

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75
Q

According to Jull et al. in 1997, what was the 3 most dysfunctional segments?

A
  1. C1/2 - 95%
  2. C2/3 - 45%
  3. C0/1 - 30%
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76
Q

Who determined the mean pre-thrust ROM, and what was it?

A

Klein et al. 2003

Rotational: 30 degrees
Lateral bending: 46 degrees
Flexion: 2 degrees
De-rotation: 5 degrees (come off the barrier)
Mean thrust displacement: 12 degrees

Klein on this line

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77
Q

Herzog et al 1993, lateral break technique speed for

Speed to beat?

cervical?

thoracic/SIJ?

A

135 ms (need for be faster than the biomechancial protective muscular response).

Cervical: 80-100 ms
Thoracic and SIJ: 120-200 ms

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78
Q

Who determined that less force and faster speeds are more effective?

A

Kawchuk et al. 1992

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79
Q

Herzog and Simons 2001, mean preload and peak forces?

A

Preload: 24N
Peak: 238N

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80
Q

T or F: A stiff joint requires more preload and thrusting force?

A

True

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81
Q

What is the mean duration of manipulation from contact time to thrust?

A

7 seconds - Klein et al 2003

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82
Q

Is SMT delivered to the target joint?

A

No - herzog and simons 2001.

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83
Q

What is the appropriate amount of skin lock?

A

33-38 mm - Bereznick et al. 2002

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84
Q

What percentage of lumbar manipulations resulted in a single pop vs. multiple pops?

A

36.5% - single pop
63.5% - 2-6 pops

Ross et al.

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85
Q

The SIJ thrust and L5/S1 thrusts cavitated which segment the most often?

A

SIJ - L5/S1 upside facet

L5/S1 - L3/4 upside facet

  • Beffa and Matthews 2004
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86
Q

What is the purpose of HVLAT according to Herzog et al. 1993?

A
  1. Restore joint integrity
  2. Restore joint ROM
  3. Pain reduction via relaxation if hypersensitive muscles
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87
Q

Which two studies support putting the SIJ back in place?

A

CIbulka et al 1998 - found changes in the Innominate post-chicago HVLAT SIJ (pelvic tilting)

Childs et al. 2004b: restoration of bony symmetry 4 days post-chicago HVLAT (iliac Crest Heights)

Triple C’s - chicago, cibulka, childs

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88
Q

Which study shows HVLAT does NOT change the SIJ position?

A

Tullberg et al. 1998

  • NOTullberg
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89
Q

What did Hungerford et al. 2004 notice in patients with pelvic pain?

A

The WBing leg does not posteriorly rotate on the symptomatic side.

The pelvis is hung anteriorly

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90
Q

What did Timgren and Soinila in 2006 find with leg length discrepancies and iliac crest heights and OA?

A

ALL patients also had asymmetry of the OA joint via x-ray.

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91
Q

Timgren and Soinila 2006, found narrowing between the TP and C1 on the contralateral elevated iliac crest in patients with a _-type scoliosis.

A

C-type scoliosis on the Contralteral side.

S-type scoliosis on the ipSilateral side.

  • just try this. It makes sense.
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92
Q

Timgren and Soinilla did a _____ to restore pelvic symmetry in patients with scoliosis?

What percent of imorovement at 6 months f/u?

Was their a correlation between length of case history and the outcome?

A

HVLAT or MET to the SIJ

88%

No correlation between length of case and outcome.

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93
Q

What did Hartman 2006 say regarding the SIJ positioning?

A

Forget the position, just manipulate it.

-Hartman, determining the position is too hard-man.

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94
Q

Mansilla-Ferragut et al. 2009 observed an increase of ____ mm mouth opening following a single L and R OA.

What are the 3 hypothesis that caused this increase?

A

3.5 mm

  1. New OA position MODIFIED JAW POSITION
  2. New OA position may FACILITATE mouth opening
  3. Reflex inhibitin to the MASSETER muscle (trigeminocervical nucleus inputs causes a reflexive contraction in the masseter restricting motion)
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95
Q

What did Ernst and Canter in 2006 say regarding manipulation?

A

“Absense of evidence is not the same as evidence of absense of an effect. None of the systematic reviews demonstrate that SMT is ineffective.”

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96
Q

Bronfort et al. 2004, compared SMT and mobilization for acute and long term LBP and what was the conclusion?

A

SMT was better. Moderate evidence for SMT, strengthening exercises, prescription of NSAIDs, and exercise.

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97
Q

Cochrane review in 2010 reported what for neck pain?

A

Low quality evidence for SMT/Mobilizations

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98
Q

Lehman et al. 2001, what does HVLAT stimulate?

A

Gamma motor neurons, which reflexively stimulates alpha motor neurons via muscle spindles (hypertonicity).

Lehmanna (gamma gain).

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99
Q

Lund et al 2010, how can muscle spindles cause pain?

A

Muscle spindles contain pain receptors which can further stimulate gamma gain

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100
Q

Travell et al 1942, what increases the sensitivity of muscle spindles?

A

The accumulation of muscle metabolites excites GMN’s and reflexively increases sensitivity of muscle spindles, which then cause alpha motor neuron activitation and hypertonicity.

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101
Q

What did Shah et al. in 2008 notice about active MTrP’s?

A

They were significantly more acidic than latent, and latent were more acidic than normal muscle.

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102
Q

According to Indahl et al. 1997, what does a stretch of the facet capsule do?

A

It stimulates inhibitory interneurons, which decreases activity in the paraspinals

Indahl = inhibitory

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103
Q

Describe the Energy Crisis Hypothesis

A

Ach - compression - sensitizing substances.

  1. Excessive release of Ach causes a sustained depolarization of muscle fibers.
  2. The sustained contractions of muscle compresses local blood supply resulting in an energy crisis in the local region.
  3. This crisis produces sensitizing substances which interact with nociceptive nerves which localizes pain within the muscle/NMJ.
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104
Q

What did Boal and Gillette demonstrate with rats?

A

Hyperalgesia is established by C-fiber activation of dorsal horns.

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105
Q

Bolton and Budgell 2006, noticed that manipulation and mobilizations stimulate which kind of muscles?

A

Manipulation - stimulates receptors within short and deep intervertebral muscles.

Mobilization - stimulates more superficial axial (multi-segmental muscles).

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106
Q

Beattie et al. 2013, observed that spinal manipulation does what to the disc?

A

Causes intervertebral disc diffusion.

(Beattie - beat old age with disc healing)

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107
Q

Colloca et al 2004 showed that spinal manipulation increases afferant discharge from the ___ ___ ___ ___ and quiets _____.

A

Increases: afferent discharge of mechanoreceptors from the disc, ligaments, muscles, and facets.

Quiets: the alpha motor neuron pool.

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108
Q

What did Indahl et al. in 1997 notice when he injected 1 mL of saline into the lumbar facets and e-stim to the annulus?

A

That there’s a connection between the lumbar facets, multifidus, and IVD.

It caused an immediate (<5 min) reduction in multifidus and longissimus EMG activity. Also, e-stim of the annulus of the disc elicits a reflex in these two muscles.

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109
Q

Summary: What are the reasons for applying a thrust?

A
  1. To facilitate movement
  2. Relieve pain
  3. Increase circulation
  4. Immediate neuro physiological reflex response
  5. Immediate increase in strength
  6. To release entrapment
  7. Powerful psychological effect
  8. Quicker than mobilizing
  9. Correction of positional faults
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110
Q

What are the 4 ways that manipulation decrease pain?

A

ANSNP
1. Manipulation induced analgesia (MIA)
2. Non-opiod mechanisms
3. Serotonergic and nonadrenergic pathways
4. Stimulates dPAG - decreasing inhibition

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111
Q

How does manipulation increase circulation?

A
  1. Sympathetic and parasympathetic effects on vasculature
  2. Sympathoexcitatory response: decreases skin temperature and increases skin conductance
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112
Q

How does manipulation immediately cause muscle relaxation?

A

It immediatelty resets the muscle spindles.

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113
Q

What is the odds of worsening a LDH (lumbar disc herniation) with manipulation?

A

1/3.7M

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114
Q

What are the 3 absolute VASCULAR contraindications to HVLAT?

A

CAH

CAD, aortic aneurysm > 5cm, severe hemophilla

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115
Q

What are the BONE absolute contraindications to HVLAT?

A

Tumor, TB infection, metabolic (osteomalacia, congenital dysplasias, fracture, iatrogenic (long-term corticosteroid use), inflammatory (chronic RA), ankylosing spondylitis, upper cervical instability

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116
Q

What are the 3 NEUROLOGICAL absolute contraindications to HVLAT?

A

Cauda equina, cervical myelopathy, radiculopathy (but neurogenic pain is NOT an absolute contradiction).

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117
Q

What are the OTHER 3 absolute contraindications to HVLAT?

A

Excessive/Extreme pain
A lack of a clinical diagnosis
Lack of pt consent

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118
Q

What are the relative contraindications to HVLAT?

A

PPP

  1. Disc herniation/prolapse (1:3.7M)
  2. Pregnancy (No at 3-4 months), this is BSO guidelines, there’s no research showing a miscarriage
  3. Osteoporosis, RA, Spondy (avoid extension), and advanced DJD
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119
Q

What 5 things do Ross and Cheeks recommend doing for testing upper cervical stability, ligament integrity, and fractures?

A

Sharp 40 CNX

  1. Intermittent sharp pain just below the base of the skull, most noticeable with ROT
  2. ROT < 40
  3. C-spine rules
  4. Neurological exam (sensation, strength, gait, bowel/bladder, UMN/LMN, DTR’s
  5. Standard 3 view series of cervical A-P, lateral, and open-mouth views
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120
Q

What are the 3 x-ray images for upper cervical stability?

A
  1. Cervical A-P
  2. Lateral
  3. Open-mouth views
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121
Q

What % of cervical fractures involve the odontoid in people > 65 y.o?

A

20%

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122
Q

What are the 3 types of odontoid fractures?

A
  1. Oblique fx in the upper odontoid
  2. Fracture at the base as it attaches to C2
  3. Fracture line extends through the body of the axis
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123
Q

What is the sensitivity and specificity if the canadian c-spine rules? What are the rules?

A

Sensitivity: 100%
Specificity: 43%

  1. > 65 y.o OR
  2. Paresthesias in the extremities OR
  3. Dangerous MOI (fall > 3 feet/5 stairs, MVA > 62 mph, axial load (diving injury), etc.
  4. < 45 degrees of neck rotation in both directions without pain

Any present? = imaging.

  • sixty five, drive fast, sense deprive
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124
Q

Is the transverse ligament test good?

A

It has not been validated

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125
Q

Is sharp purser test good? Sensitivity/specificity?

A

Yes.

Sensitivity: 69%
Specificity: 96%

Stabilize C2 and push the head back.

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126
Q

What is the tectorial membrane test?

Sensitivity?

A

Supine.
Pincer grasp C2
Distract cranium

> 2mm of movement is positive

Sensitivity: 70%

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127
Q

What are the 6 symptoms of craniOvertebral instability?

A
  1. Occipital numbness
  2. Neck-tongue syndrome
  3. Headache with sustained neck flexion
  4. Lump in throat with neck flexion
  5. CN Testing
  6. Cord Signs (Lhermitte’s or Rhomberg’s sign)
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128
Q

What is Lhermitte’s sign?

What does it indicate?

A

An electrical sensation down the back and into the limbs produced by neck flexion or ext. It indicates a lesion of the DCML, caudal medulla, MS, or SC compression

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129
Q

What is Rhomberg’s sign?

A

A neurological test to assess the DCML (which is essential for joint positional sense (JPS), proprioception, and vibration.

Eyes closed with arms out and pt loses balance.

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130
Q

Out of the DCML System, which tracts are the pyramidal and extrapyramidal tracts?

A

Pyramidal: Lateral and Anterior corticospinal tracts

Extrapyramidal: Instead of CCTV, it’s RRTV
1. Rubrospinal tract
2. Reticulospinal tract
3. Tectospinal tract
4. Vestibulospinal tract

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131
Q

Out of the sensory and ascending (afferent) pathways, which are apart of the:
DCML:
Spinocerebellar:
Anterolateral system:

A

DCML: Gracile and Cuneate fasciculus

Spinocerebellar: Ant. and Post. Spinocerebellar

Anterolateral: Anterior and Lateral Spinothalamic tracts

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132
Q

Which tract does Hoffman’s sign assess?

A

The corticospinal tract (flick the 3rd or 4th finger

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133
Q

What are the 3 main features to look for with an open mouth x-ray?

A

Is the C2 SP in midline? Indicates an alar ligament rupture

Are the peri-odontoid spaces equal?

Are the articular margins of C1-2 lined up?

  • MOA
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134
Q

What % of chiropractors believe that diseases are caused by misalignments?

A

68%

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135
Q

What % of chiropractors believe in the vertebral subluxation complex without any research supporting this claim?

A

88%

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136
Q

Do chiropractors claim to treat all 10 organ systems?

A

yes

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137
Q

Do chiropractors sign death and birth certificates?

A

yes

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138
Q

Do chiropractors deliver babies or perform minor surgeries?

A

yes

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139
Q

What are some weird conditions that chiropractors claim to treat with SMT?

A

ADHD, ear infections, allergies, colic, and autism

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140
Q

Do chiropractors require even a bachelor’s degree?

A

no

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141
Q

Do chiropractors believe the vertebral subluxation complex causes disease in organs?

A

yes

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142
Q

What is the most accurate way to diagnose and manage SIJ Dysfunction according to Laslett?

A

Fluoroscopy guided injection, followed by an anesthetic block - 80% pain relief.

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143
Q

What are the six Laslett Cluster tests?

How many tests needs to be positive?

What is the sensitivity and specificity?

A
  1. posterior thigh thrust
    2+3. Gaenslen’s test on R L
  2. ASIS Distraction
  3. ASIS Compression
  4. Sacral compression

3/6 positive

Sensitivity: 91%
Specificity: 87%

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144
Q

Van der Wurff et al. in 2006 created his own pain provocation tests (PPT), what is the difference between his tests and laslett’s?

A

Wurff replaced the sacral compression with Patrick’s sign (FABER’s)

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145
Q

What is the inter-rater reliability of Van der Wurff’s PPT’s?

A

100%

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146
Q

Does Laslett and Van der Wurff claim that you need to rule out a disc first?

A

Laslett says you do.
Wurff says you don’t.

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147
Q

What did Gutke et al. in 2009 discover when doing Laslett’s cluster tests on patients?

A

That the PPT’s were still negative in patients with a lumbar disc herniation. Thus, you do not need to rule out the disc.

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148
Q

Why did Berthelot et al. in 2006 say that SIJ blocks are unreliable for diagnosing SIJ pain?

A

unidentical, diffuses, ligaments

  1. The effects of 2 consecutive SIJ blocks are identical in only 60% of cases.
  2. The anesthetic diffuses out of the SIJ in 61% of cases and contacts the adjacent nerve trunks and cords, they are <10 mm away.
  3. The pain patterns believe to come from the SIJ can be related to extra-articular surfaces, most notably the ligaments surround the SIJ.
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149
Q

Why are SIJ motion tests not reliable?

A
  1. Poor inter-test reliability
  2. Less than 50% sensitivity and specificity
  3. <2 mm and <2 degrees of rotation
  4. SIJ is 5-7 mm deep to the skin
  5. There are 7 anatomical layers overlying the superior and middle aspects of the SIJ
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150
Q

What did Robinson et al. in 2007 say about SIJ palpation tests and joint play?

A

they have poor inter-examiner reliability

Robin is robbing the palpation tests

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151
Q

Which SI tests did Riddle and Freburger in 2002 determine had poor reliability for clinical use?

A

Standing flexion, prone knee flexion, supine to sit, and sitting PSIS tests

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152
Q

What did Hartman 2006 say about the SIJ

A

Forget the tests, just manipulate it.

  • manipulating is an art
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153
Q

According to Van der Wurff et al. in 2006, what were the pain referral patterns of the SIJ

A
  1. Pain in the buttock, posterior thigh, medial and lateral lower leg, and dorsimedial and dorsilateral sides of the foot
  2. 100% felt pain in Fortin’s area
  3. 100% felt pain just inferolateral to Fortin’s area, ischial tuberosity, and lateral thigh
  4. The thigh, lower leg, and foot
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154
Q

How can the SIJ refer pain to the thigh, lower leg, and foot?

A

It is supplied ventrally by L3-S2 and dorsally by S1-S4

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155
Q

What did Mens et al. say regarding a pelvic belt?

A

Performing an ASLR with a pelvic belt improved in 20/21 pt’s.

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156
Q

How many mm’s of a step was observed in the pubic margins during an ASLR?

A

5 mm

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157
Q

If the R pubic bone is smaller than the L, which way is the nominate rotated?

A

The R is anteriorly rotated

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158
Q

What is the sensitivity and specificity of an ASLR while palpating the pubic bones?

A

87% sensitivity
94% specificity

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159
Q

What are the 4 best clinical diagnosis tests for SIJ?

A
  1. Laslett’s cluster 3/6
  2. Fortin’s Area
  3. ASLR
  4. Trigger points (piriformis BL-54 and QL BL-23
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160
Q

What did Mens et al. in 2000 say regarding the lumbopelvic stabilization?

A

25% of the experimental group (force closure group) had to cease exercises due to increases in pain.

Men can deal with pain (not really)

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161
Q

What did Nilsson-Wikmar et al. and Dumas in 1998/1995 say regarding exercises for the SIJ?

A

It’s not effective.

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162
Q

Hungerford et. al in 2003 found a delay in which 3 lumbopelvic muscles when there’s pain?

A

Internal Oblique
Lumbar Multifidus
Glute max

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163
Q

What did Almeida et al. in 2010 find regarding HVLAT to the SIJ?

A

HVLAT can alter the tone of the pelvic floor (perineal muscles) and improve stress urinary incontinence, pelvic pain, etc.

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164
Q

Did Stuge et al. in 2006 recommend manipulating the SIJ before or after exercise?

A

before

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165
Q

What are the 5 goals of HVLAT to the SIJ?

A
  1. Decrease pain
  2. Increase ROM
  3. Increase muscle strength (force closure)
  4. Improve feed forward activation times
  5. Put it back in place (maybe, Cibulka found changes in the innominate, and Child found iliac crests even, but Tullberg found no change in the SIJ)
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166
Q

According to Childs et al. in 2007 is exercise beneficial for the SIJ?

How much better or worse was the ex group?

A

No. The exercise group was 8x worse.

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167
Q

Why do we get an immediate hypoalgesia response from manipulating the SIJ?

A
  1. Descending inhibitory mechanisms (dPAG)
  2. Non-opioid mechanisms
  3. Possibly from immediate form-closure improvement - Stuge et. al
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168
Q

To date, are there any “empirical” evidence that supports the use of specific or global “stabilization” exercises for SIJ pain?

A

No.

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169
Q

To date, is there evidence that supports the use of mobilization or manipulation in pt’s diagnosed with SIJ?

A

1 cohort study exists - Shearar et al. 2005

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170
Q

To date, is there any evidence that treating a specific positional fault of the sacrum gives better outcomes than simply just manipulating it?

A

No.

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171
Q

What did Moset et. al observe when he tested HVLAT’s effects on the hemodynamics of the VA?

Maximal neck rotation:
Maximal neck rotation+HVLAT:
Changes in cerebral hemodynamics:
Functional connectivity in the posterior cerebrum and cerebellum (MRI):

A

Maximal neck rotation: changes in blood flow

Maximal neck rotation+HVLAT: also changes in blood flow

Changes in cerebral hemodynamics: No changes.

Functional connectivity in the posterior cerebrum and cerebellum (MRI): significant increases with both tests.

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172
Q

What did Kranenburg et al. find with head and neck positions on the VA, ICA’s, and Intracranial Arteries?

A

“It may not alter blood flow as much as previously expected.

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172
Q

What did Ian et al. observe from one sessions of manipulating the t-spine in patients with C-RAD?

A
  1. Improvements in pain, disability, and ROM
  2. Improved deep neck flexor endurance

These effects lasted for 48-72 hours

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172
Q

What did Raymond Butts et al. observe from a literature review for TMD

A
  1. Limited support for strengthening exercises and soft tissue targeting the muscles of mastication.
  2. Limited evidence for splinting and electrophysical modalities (laser, ultrasound, TENS, and iontophoresis)
  3. Manipulation to the TMJ or upper-cervical were generally supported.
  4. DN/Acupuncture to the lateral pterygoid and posterior periarticular connective tissue led to significant improvements in pain and disability
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173
Q

Raymond Butts concluded from a literature review that the best areas to impact for TMD are:

A
  1. Joint capsule
  2. Articular disc and muscles of mastication (mostly the superior and inferior head of the lateral pterygoid)
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174
Q

Dunning et al. found that manipulation was superior to mobilization in patients with CH based on what criteria?

A

Significantly greater reductions in headache intensity, disability, frequency, and shorter duration at 3 months.

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175
Q

Dunning et al. found manipulation superior to mobilization in patients with mechanical neck pain in the short- or long-term?

A

short-term

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176
Q

What did Keating et al. say regarding the chiropractor subluxation theory in 2005?

A

It stands pretty much where it did in the 20th century, an interesting notion without validation.

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177
Q

Mirtz et al. in 2009 did a literature review of the subluxation theory and found what?

A

There’s no evidence of anything.

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178
Q

T or F: DeBoer and Hansen 1993, and Henderson et al. in 2007 both failed to isolate the subluxation as a quantifiable lesion.

A

True

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179
Q

What % of Canadian chiropractors still believe most diseases are caused by spinal misalignments (2002)?

A

68%

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180
Q

According to McDonald et al. in 2004, what percent of chiropractors still retain the term vertebral subluxation?

What percent still believe the subluxation is a significant contributor to 50% or more visceral disorders?

A

88%

75%

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181
Q

How many different types of headaches are there recognized by the IHS?

A

14 types, CGH is one of them

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182
Q

According to the IHS, what are the 5 symptoms of CGH?

A

Neck movements, posture, unilateral

  1. Pain localized to the neck and occipital region.
  2. Pain is aggravated by neck movements.
  3. Sustained posture
  4. Side dominant (may refer to the forehead)
  5. Orbital, temples, ears
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183
Q

What are the 4 diagnostic criteria recognized by the IHS for CGH?

A

They must have at least one of the following: ROM, tone, radiological, tender (1RR-TT)
1. Resistance/limited neck PROM
2. Changes in neck muscle contour, texture, and tone.
3. Abnormal neck tenderness
4. Radiological exam reveals at least one of the following (movement abnormality with flexion/ext, abnormal posture, or fracture, congenital abnormalities, bone tumors, etc.)

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184
Q

Sjaastad et al. in 1998 mentioned these 4 symptoms as CGH?

A
  1. Unilateral head pain
  2. Without side shift
  3. Neck pain (with movement and palpation)
  4. Limited cervical ROM

US-PC gives you a headache

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185
Q

What is the cervicogenic prevalence rate?

A

4.1%

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186
Q

T or F: Cervicogenic headache is 1 of the 3 most common recurrent headaches?

A

True

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187
Q

What are the most common CGH Symptoms, and by how much?

A

100%: Unilateral, mechanical precipitation, diffuse arm discomfort.

97%: Posterior onset

93%: Restricted ROM

Other symptoms:
1. increased sedentary lifestyle
2. No affect from migraine meds
3. Nausea, phono/photophobia, dizziness, blurred vision, difficulty swallowing, and periocular edema

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188
Q

What are the 2 main vascular issues causing CGH?

A
  1. Greater Occipital and Lesser Nerves
  2. The Greater Auricular Branch of the Facial and Vagus Nerves
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189
Q

What are the four parts of the Trigeminocervical Nucleus?

A

TriegmmmMMSA

  1. Mesencephalic nucleus
  2. Main sensory nucleus
  3. Spinal nucleus (contains branches to the maxillary and mandibular branches)
  4. Additional afferents from Facial, Vagus, and Glossopharyngeal (ear and throat)
190
Q

What does the Mesencephalic nucleus sense?

A

proprioception

Mesence-proprioception

191
Q

What does the main sensory nucleus sense?

A

Sense the TPs

touch and pressure

192
Q

What does the spinal nucleus sense?

A

pain and temperature (contains branches to the maxillary and mandibular branches)

Spinal - PT

193
Q

T or F: Migraine is the 19th leading cause of years lived with disability

A

True

194
Q

What % of people have migraines?

A

12%

195
Q

What age group mostly has migraines?

A

Ages 12-40

196
Q

IHS classification for Migraine Headaches WITHOUT AURA

A

UP? Na. uni, pulsating, nausea, avoid physical activity

At least 5 attacks fulfilling the below criteria:
1. Attacks lasting 4-72 hours
2. Headaches has at least two of the following:

  • unilateral location
  • PULSATING quality
  • moderate-severe pain intensity
  • aggravation or avoiding physical activity
  • during headache at least one of the following (nausea/vomiting, photo- and phonophobia, not attributed to any other cause)
197
Q

IHS classification for Migraine Headaches WITH AURA

A

At least one of the following: speech, visual, sensory

  1. Fully reversible visual symptoms including positive features (flickering lights, spots or lines, and/or negative features of loss of vision
  2. Fully reversible sensory symptoms including pins and needles and/or numbness
  3. Fully reversible dysphasic speech disturbance
198
Q

Describe the process of the trigeminocervical nucleus causing the CGH:

A
  1. The migraine begins with cortical spreading hyperactivity followed by a depression
  2. The hyperexcitability, then depression causes an increase then decrease in blood flow and subsequent release of NO and glutamate (hyperexcitability is connected with the aura)
  3. NO and glutamate trigger a pain response in the trigeminocervical nucleus via calcitonin gene related peptide
199
Q

IHS classification of Tension Type Headaches (TTH):

How many days?
Symptoms?

A

Tension - Twelve BPNN, bilateral, pulsating, not aggravated by PT, nausea

More than 10 episodes occurring less than 1 day per month, or on average, less than 12 days/yr and fulfilling the criteria of:

  1. Headache lasting 30 mins to 7 days.
  2. Headache has at least 2 of the following:
    - BILATERAL location (frontal-occipital
    - pressing/tightening (NON-PULSATING)
    - mild or moderate intensity
    - NOT aggravated by routine physical activity
    - both of the following: No nausea/vomiting, or no more than 1 episode of photophobia or phonophobia
    - not attributed to any other disorder
200
Q

What is the most common type of recurring headache?

A

TTH

201
Q

What population is TTH the most common in:

Men vs. Women?
Older or Younger than 50 y.o?

A

4:1 women
Young adults < 50 y.o

202
Q

What manual tests are specifically accurate for diagnosing CGH?

A

Lateral glide testing - Fernandez de las Penas claims it’s as good as a radiological examination for C3-7

Flexion Rotation Test - the greater restriction, the more severe the headache

203
Q

What is the inter-rater agreement of the lateral glide test for C0-C3?

A

70% Jul et al. 1997

204
Q

What is the sensitivity and specificity of the Flexion/ROT test for CGH?

Positive likelihood ratio?
Negative likelihood ratio?

A

91% Sensitivity
91% Specificity
10.65 positive likelihood ratio
0.095 negative likelihood ratio

205
Q

According to Hall et al., what is a positive Flexion-Rotation Test, and which headache does it indiciate?

A
  1. > 10 degree restriction indicates a positive test
  2. < 30 degrees of rotation

CGH

206
Q

What is the diagnostic accuracy of flexion-rotation test?

A

85% for CGH

207
Q

According to Toby et al., Can the Flexion Rotation Test (FRT), be used to diagnose lower c-spine facet pain vs. CGH?

Specificity?

A

Yes, 92% specificity and 9.4 positive likelihood ratio.

They should have a lot of ROM with reproduction of pain.

208
Q

According to Jul et al. in 1999, what is the normal criteria for the craniocervical flexion test?

mmHg?
duration?
repetitions?

A

26-28 mmHg
10 second holds
10 repetitions

209
Q

According to Olson et al. in 2006 what is the normal height and duration for the Neck Flexion Endurance Test?

A

2 cm (2 fingers off the table)
Males: 25 seconds
Females: 20 seconds

210
Q

According to Deborah Falla et al., does training the cervical muscles with prescribed motor tasks change the muscle activation during a functional activity?

A

No.
Low-intensity flexor endurance, or high-intensity did not change it.

211
Q

According to Gemma et al., What is the best practice for reducing pain and improving cervical motion in pt’s with TTH?

A

MT + HVLAT

212
Q

Is manipulation or MT better for CGH?

A

Manipulation - Bronfort 2001

213
Q

The Cochrane Review of 2005 recommended what treatment for CGH and migraines?

A

SMT + low-intensity endurance training for CGH

SMT has a similar affect as amitriptyline for migraines

214
Q

According to Jull et al. in 2002, what % of patients diagnosed with CGH will respond to SMT and/or exercise?

A

76%

215
Q

What four criteria should we look for if we could improve a patient’s headache according to Niere in 1998?

A

Frequency, affective, uni, diet
FrAUD

  1. Low frequency headaches
  2. Affective and autonomic pain descriptors
  3. Unilateral headaches
  4. Dietary aggravators suggestive of poor outcomes
216
Q

With headaches, what 3 criteria were NOT suggestive of poor outcomes from PT?

A

Age intensitt chronic
AIC

Age
High Intensity
Chronicity

217
Q

Niere 1997: Is headache frequency, intensity, or duration the best indicator of treatment effect?

A

Headache FREQUENCY is the most valuable rather than intensity or duration

218
Q

According to Dunning et al., How much better was the cervical and upper thoracic group vs. non-thrust in pt’s with CGH headache?

A

4.6x more likely to achieve 50% or more improvement in headache intensity at 3 months.

Cervical-Upper Thoracic (CUT 46WC)

219
Q

According to Dunning et al., How much reduction in disability did the manipulation vs. mobilization CGH groups improve?

A

65.7% vs. 30.1%

Thus, 9.6x more likely to obtain 50% reduction in disability at 3 months

220
Q

Dunning: At 3 months, the HVLAT group was taking how much less medication vs. mobilizations in pt’s with CGH?

A

56.9% vs. 25%

4x more likely to completely stop taking medicine

221
Q

What % of patients with CGH had a successful outcome with manipulation?

A

89.7%

222
Q

T or F: Dunning: Pt’s receiving HVLAT were 5x more likely than non-thrust mobilization and exercise to experience no headaches or less than 5 hours of headaches per week at 3 months follow-up

A

True

223
Q

What did Boyle et al. in 1999 conclude about shoulder impingement or a RTC tear?

A

It’s likely a 2nd rib sprain, strain, or subluxation

224
Q

What did Boyle et al. in 1999 say needs to be included in the assessment of acute/chronic shoulder pain?

A

palpation of the 2nd rib

225
Q

According to Boyle et al., in 1999, what may indicate 2nd rib dysfunction?

A

increased tone of the posterior scalene

226
Q

What are the common clinical manifestations of rib dysfunction?

A
  • Shoulder pain (A-P and central)
  • Referred pain to the anterior upper arm
  • Limited ROM
  • Shoulder ABD limited by pain
  • (+) Hawkin’s Kennedy
  • Levator scapulae and scalene muscles in spasm
  • 2 cortisone injections giving short term relief
  • C6/7 hypomobile and tender
  • P/A motion of 2nd rib is extremely painful and hypomobile
  • RTC muscles are weak and painful likely from pain inhibition
227
Q

What are the 2 possibly MOI’s to 2nd rib dysfunction?

A
  1. Direct violence to the rib or acute spasm of the POSTERIOR SCALENE
  2. Insidious onset from habitual over-activity of the POSTERIOR SCALENE resulting in chronic superior and anterior subluxation of the 2nd rib at the vertebral articulation
228
Q

Beattie et al. in 2013 observed that HVLAT increased what?

A

IVD diffusion

229
Q

Who invented the myth of core stability?

A

Eyal Lederman 2008

Aye-yall this ain’t true

230
Q

Has any study to date demonstrated that LBP is due to spinal instability?

A

No.

231
Q

What is the real reason for chronic LBP?

A

There’s a delay in motor activation control (motor control impairment syndrome)

232
Q

Who started lumbar spine instability (LSI)?

A

Richardson 1990s

Rich thought he’d get rich off this idea.

233
Q

Why was Richardson’s research for LSI so bad?

A

He tried to sense deep musculature with surface level EMG

234
Q

When you stand is the TrA active?

A

No. You need to PPT to activate the TrA, when you stand you’re in APT.

235
Q

Has any study to date shown a positive effect on muscle activation in the low back?

A

No.

236
Q

McGill 2010: Why is there a delay in muscle activation in the low back?

A

Pain-inhibition response from your spine delays muscle activation

237
Q

Why does the CNS cause a delay in muscle activation in the low back?

A

Reflex inhibition due to joint effusion (similar concept of quadriceps swelling)

238
Q

Why is there no effect from TrA training?

A

It’s not high enough intensity

239
Q

What did Hong 2006 say regarding reducing LBP efficiently?

A

Treating the facet is more effective than treating the periphery

  • Hong, hong treat the facet
240
Q

What is the recurrence rate of LBP in pt’s who performed lumbar multifidus strengthening vs. not?

A

30% vs. 80%

241
Q

Does a T3-4 change the pupil diameter? Sillevis et al 2010

A

No

242
Q

Cross et al., Is there strong or weak evidence supporting the use of T-Spine HVLAT for short-term benefits in pt’s with acute or subacute mechanical neck pain?

A

It’s weak evidence because of a limited number of RCTs

243
Q

Dunning: how much less disability and pain in the manipulation group vs. mobilization for cervical?

A

50.5% less disability
58.5% less pain

244
Q

Dunning: how much more cervical RROT was improved vs. LROT?

A

RROT: 8.4 degrees
LROT: 5.9 degrees

245
Q

Dunning: How much did the deep neck flexor strength improve?

A

3.4 mmHg

246
Q

Was their a change in LM thickness following SMT? Koppenhaver et al. 2011

A

Immediately no, but after 3-4 days yes, but it did not last more than a week

247
Q

According to Hancock et al. 2007, what was the prevalence of each of structure as being the source of LBP:
Disc:
Facet Joint:
SIJ:

A

Disc: 39% (range of 20-79%)
Facet: 15% (range of 12-61%)
SIJ: 13% (range of 28-61%)

248
Q

Is there currently a universal gold standard for the diagnosis of LBP?

A

No

249
Q

What 3 features on an MRI are informative (+LR >2) as indicating the disc as the source of their LBP?

A

HDEee

  1. High intensity zone
  2. End-plate changes
  3. Disc Degeneration
250
Q

What was the only clinical feature that increases the likelihood as the disc being the source of their LBP? (+LR 2.8)

A

Centralization

251
Q

What was the only test to reduce the likelihood as the disc being the source of their pain radiologically? 5x more likely to not have the disc as the pain generator

A

Absence of disc degeneration on an MRI

252
Q

What is Revel’s Criteria?

A

Need 5/7 clinical characteristics for facet joint pain:

  1. > 65 y.o
  2. Pain relieved by recumbent posture
    3,4,5. No pain exacerbation with coughing, forward flexion, or with rising from sitting (RCF)
  3. Pain with hyperextension
  4. Pain with extension and rotation

REvels
Recumbent
RCF - Rising, Coughing, Flexion
Extension + ROT
Hyperextension

253
Q

What is the sensitivity and specificity of Revel’s Criteria?

A

85% sensitivity
89% specificity

254
Q

What is the positive and negative LR of multiple SIJ tests?

A

+3.2
-0.29

255
Q

Hancock et al. 2007: Conclusion #1:

Are their clinical tests to both increase AND decrease the likelihood of the disc as the source of LBP?

A

No.

256
Q

Hancock et al. 2007: Conclusion #1:

Does the MRI high intensity zone, disc degeneration, end-plate changes, and centralization have informative +LR’s?

A

Yes

257
Q

Hancock et al. 2007: Conclusion #1:

Are their good diagnostic tests for the facet joint that appears informative?

A

No. However, their are great tests to predict the disc and SIJ

258
Q

Hancock et al. 2007: Conclusion #2:

For the studies investigating the facet joint as the source of the patient’s symptoms, have good validity?

A

No, the tests have limited or no diagnostic validity

259
Q

Hancock et al. 2007: Conclusion #3:

Is there research indicating the knowledge of the source of LBP leads to improved outcomes?

A

Currently their is not easily available methods to identify the source of LBP.

260
Q

What did Lim et al. 2011 find regarding reducing LBP?

A

Pilates is more effective than other exercises

261
Q

Child et al., Did the LBP CPR perform well at identifying patients with acute, non-specific LBP who were most likely to respond to SMT?

A

No, it’s no better than chance

262
Q

What is the CPR for LBP?

A

16, 19, hip, knee, back

<16 days duration of current episode

No sx distal to the knee

FABQ < 19

At least 1 hypomobile lumbar segment on PA testing

> 35 degrees of hip IR

263
Q

Are there any reliable tests to diagnose LSI? O’Sullivan 2006

A

No

264
Q

According to Hayes et al. in 1989, ______% of asymptomatic patients had at least 1 lumbar segment exceeding the instability threshold on flexion/extension radiographs of the lumbar spine. Thus, there’s a high false-positive

A

42%

265
Q

What does Delitto et al. 1995 BELIEVE as the confirmatory data for LSI?

A

DeLOST-FB

  1. Lateral shift deformity
  2. Use of Oral contraceptives
  3. Short-term relief from manipulation
  4. Hx of trauma
  5. Frequent recurrences of LBP
  6. Improved symptoms with the use of a Brace
266
Q

Which two famous therapist’s mentioned the “step-off” between the SP’s?

A

Paris 1985 and Maitland 1986

267
Q

What 3 characteristics did O’Sullivan in 2000 describe as the signs as LSI?

A
  1. Giving way, slipping out, or locking
  2. Instability catch
  3. Aberrant motions (However, studies have shown aberrant movements to be normal in some imaging studies)

O’GIA

268
Q

Is the prone instability test valid?

A

No.

  • add compression while they raise legs to see if it reduces LBP
269
Q

3 Other Findings for LSI form the LSI Convention:

A
  1. Pain immediately upon sitting, and relieved in standing - Paris and Maigne
  2. Painful arc through the ROM and uses hands to stand up - Kirkaldy-Willis and Farfan 1982, O’Sullivan 2000
  3. Increased global muscular tone - Panjabi 1992, Cook et al. 2006

Met SAM at the convention
Sitting
Arc
Muscle tone

270
Q

Is the posterior shear test valid? Delitto et al. 1995

A

No

  • Produce a posterior force through the pt’s abdomen and anterior force with opposite hand through pelvis (in standing). Test repeated at all lumbar levels
271
Q

Objective indicators for LSI according to Paris 1985, 2003:

A
  1. Instability catch
  2. Hypertrophied band horizontally, raised muscle tone in standing
  3. Step-off on standing that disappears in lying
  4. Shaking/Juddering on FB
  5. Imbalance on single leg standing
  6. Grade 5 or 6 PIVM
  • instability, hypertrophied, step-off, juddering, imbalance, grade 5

IHSJIG

272
Q

Spine instability is best classified into which two categories?

A
  1. Radiological appreciable instability - marked disruption of passive Osseo-ligamentous constraints.
  2. Clinical instability - more subtle and challenging to diagnose. It involves the NM system with inconsistent findings during traditional radiographic analysis
273
Q

When is a lumbar fusion used? Sonntag and Marciano

A
  1. > 4 mm of translation or 10 degrees of rotation
  2. AND they have failed conservative treatment
274
Q

Delphi Study: What are the 3 subjective indicators of LSI

A

GF’s

  1. Giving way
  2. Self-manipulator
  3. Frequent episodes of symptoms
275
Q

Delphi Study: What are the 3 objective indicators of LSI

A
  1. Poor lumbopelvic control
  2. poor coordination/NM control including juddering/shaking
  3. Decreased strength and endurance of local muscles at the level of segmental instability
276
Q

Cook and Hegedus 2011:

T or F: The lateral glide test for C2-3 was found as an effective diagnostic test

A

True

277
Q

Cook and Hegedus 2011:

T or F: The PA’s and Spurling’s tests were effective only as screening tools, but NOT FOR DIAGNOSIS

A

TRUE

278
Q

Cook and Hegedus 2011:

Which 3 lumbar tests are useful for diagnosis?

A
  • Centralization, PAIVMS, Percussion, Supine

Laslett 2005: centralization for discogenic pain.

Fritz et al 2005: Lumbar PAIVMs and PPIVMs diagnostic for radiological instability

Percussion and supine sign diagnostic for compression fracture

279
Q

What test was good for SCREENING ZJ pain?

A

ER test

280
Q

What test was good for SCREENING nerve root compression?

A

SLR test

281
Q

Conclusions for LBP

A
  1. Most clinicians do not make clinical decisions based on a single test finding
  2. Clusters provide more promising findings and assist clinical decision making
  3. Stand alone tests only provide marginal value
282
Q

Alqami et al. 2011: Determined that the passive lumbar extension test may be useful for diagnosing a structural LSI based on what sensitivity, specificity, and +LR?

A

84% sensitivity
90% specificity
8.8 +LR

283
Q

Hicks et al 2005: Is it possible to accurately diagnose LSI?

A

No, there’s no true reference standard so Flynn et al. made a CPR for stabilization exercises

284
Q

What is Flynn et al CPR for manipulation (only the Chicago SI Technique)?

3/5 positive = x%?

A

Duration of sx < 16 days
FABQ < 19
Lumbar hypomobility on spring test
At least one hip > 35 degrees IR
No symptoms distal to the knee

4/5: 49-95% probable success with manipulation
3/5: 68%

285
Q

What % of patients had a successful lumbar manipulation without any attempt at prediction?

A

45%

286
Q

What was the single best predictor of success with manipulation?

A

duration of sx < 16 because it’s basically an acute pt

287
Q

What % of success did Cleland et al in 2006 have with the lateral recumbent lumbar roll HVLAT using 4/5 Flynn’s criteria?

A

92%

288
Q

Are manual therapy techniques specific?

A

Not really.

Lee et al. 2005: PA to C3 moved everything from occiput to T3. PA at L3 moved T10-sacrum

289
Q

Beffa and Matthews 2004: Manipulations targeted at the L5 vertebrae cavitated which segment?

A

Cavitated L3/4 more than 50% of the time

290
Q

Ross et al 2004: What % of manipulation techniques in the lumbar spine were found to accurately produce clicks at the targeted vertebrae?

A

46%

291
Q

What was Cleland et al.’s conclusion in 2006 regarding if manual therapy is specific or not?

A

Manipulation are not as specific as we think, thus the choice of one technique over the other may be less important than previously thought

292
Q

According to Chiradejnant and Haas on NS-LBP, are specific or random mobilizations better?

A

There’s no difference in specific vs. not specific (of course, you did a non specific LBP)

293
Q

Bjorkman 1999: With NSAIDs, Adverse events occur in _% of patients and significant complications occur in _% of patients

A

Adverse: 25%
Significant complications: 1-4%

294
Q

Graumlich 2001: GI complications due to NSAIDs cause more than ______ hospitalizations and an estimated _____ deaths each year

A

100,000 complications

16,500 deaths

295
Q

Henriques et al. 2001 and Kardaun et al. 1990: What is the chances of cauda equina syndrome (CES) following lumbar surgery?

Any complication rate?

Mortality rate?

A

CES: 0.2-1% of patients

Complication rate: 3.7%

Mortality rate: 1.5%

296
Q

Have NSAIDs or surgery been proven to be more effective in the tx of LDH than spinal manipulation?

A

No - Oliphant 2004

297
Q

Fritz et al. 2005: What was the chance of a successful outcome with manipulation on hypomobile and hypermobile patients?

A

Hypomobile: 74% successful outcome
Hypermobile: 17% successful. 22% for stabilization

298
Q

What was Bronfort’s 4 main conclusions regarding acute LBP and HVLAT?

A
  1. HVLAT > mobilizations and detuned diathermy for short-term
  2. HVLAT+Exercise > NSAIDs for short- and long-term relief
  3. SMT/MOB > HEP
  4. SMT/MOB > general practice and PT
299
Q

What were the 3 main findings from the UK Beam Trial?

A

SMT over a 12 week period produced benefits relative to best care in general medical practice at both 3 and 12 months

SMT is cost-effective

Manipulation ALONE is > Manipulation and exercise

300
Q

What did Giles and Mutler in 2003 find for chronic spinal pain?

A

short-term HVLAT > acupuncture or medication

GM
Grade V > Medication

301
Q

Herzog et al. 1991: Was there a difference between SMT, back education, and exercise in pain and disability?

A

There’s no significant difference in the short-term.

302
Q

Rubenstein et al 2011 Cochrane Review: T or F: SMT is effective as other physiotherapy techniques

A

True

303
Q

What was the problem with Richardson’s studies in 1990, 1992, 1999, and 2000?

A

They never measured the TrA or LM, and thus, never measured spinal stability

The authors conclusions did not support the study results

304
Q

What did MacDonald in 2007 find regarding the TrA and deep multifidus?

A

There’s no evidence that the TrA and deep multifidus co-contract for spinal stability

The SM and ES may equally contribute to lumbar stability

305
Q

What did Hodges and Richardson find in 1996 regarding TrA muscle activation?

A

There was a significant DELAY between 50-450 MS in the onset of contraction of TrA

In asymptomatic patients the TrA preceded by a mean of 110ms

306
Q

How does reflex inhibition (RI) cause a muscular delay?

A

RI produces a decreased activation level of the alpha motor neuron at the ventral horn. RI is linked to joint effusion, pain, ligament stretch, and capsular compression. Thus, the alpha motor neuron is pool is less excitable.

307
Q

What did Costa et al. in 2009 say regarding the use of ultrasound measurements?

A

There’s multiple sources of error. Thus, no studies evaluated the reproducibility of the difference in thickness change over time.

308
Q

Stevens et al. 2006: You need a _% MVC to promote strength trunk gains (likely not being achieved with breathing, tilting, or drawing in manuevers.

A

70%

309
Q

Brown and McGill et al 2006: Found that co-contracting specific muscles could be ___ and ___ spine stability

A

Dangerous and decrease

310
Q

Vera-garcia 2006: Found that abdominal hollowing and bracing were of the ___ stabilization maneuvers

A

worst

311
Q

Cholewicki et al. 2002: T or F: You cannot contract the TrA alone

A

True

312
Q

Helewa et al 1999: Did strengthening of the abdominals prevent LBP?

A

No.

Hallaluah, someone is saying it’s not the core

313
Q

Nadler 2002: Did strengthening the core decrease the occurrence of LBP?

A

No

314
Q

Cairnes et al. 2006: Was there a difference in specific exercise vs. general exercise for LBP?

A

No difference

Cairnes doesn’t care what exercise you do.

315
Q

Core stability assumptions:

A

Basically that a strong core reduces back pain

316
Q

Fast et al 1990: Is there a correlation between sit-up performance and LBP?

A

No correlation

317
Q

Leboeuf-Yde 2000: Is weight gain and obesity associated with LBP?

A

There’s a very weak association

318
Q

Lederman 2007: Can you correct TrA onset timing with exercise?

A

There’s no study to date that demonstrates exercise can alter TrA timing

319
Q

Marshall and Murphy 2006: There’s a _% improvement in onset timing immediately following SIJ HVLAT?

A

28%

320
Q

What is the one study that shows that strengthening the abdominals can reduce LBP and in which population?

A
  • SS

O’Sullivan et al in 1997 in Spondylolysis/listhesis patients only.

321
Q

Silfies et al. 2007: Do impairments in trunk position sense predispose athletes to future LBP injuries?

A

No

322
Q

What’s the summary on exercise for LBP?

A

Neither general or specific exercises are more effective in the management of LBP. However, there’s research for training the multifidus in ACUTE and SUBACUTE only.

323
Q

What did Hides et al. in 1994 find in patients with LBP vs. asymptomatic patients?

A

Marked side-to-side asymmetry of the CSA (cross-sectional area) of the LM. The atrophy was ipsilaterally on the symptomatic side

  • Hides was hiding fat
324
Q

Which lumbar segment had the greatest atrophy at the LM CSA?

A

L5

Multi-fidus
5-5

325
Q

How long of an exercise program did it take to see a change in the LM CSA?

A

After 4-weeks the LM CSA improved by 0.7%

326
Q

What % of subjects from the LM group suffered recurrences of LBP?

A

30%, while the control group reinjured at a much higher rate of 80%

327
Q

Kader et al. looked at the LM and graded the amount of atrophy, what % of patients with LBP and LM atrophy?

A

80%

328
Q

Which lumbar disc segment most commonly had degeneration?

A

L4/5, followed by L5/S1

329
Q

What is the Lumbar Dorsal Ramus Syndrome?

A

LBP with referred leg pain induced by irritation to structures innervated by the dorsal ramus nerve triggers a self-sustained vicious cycle of myofascial pain, spasm, and ischemia that promotes LM muscle atrophy

330
Q

What does the Dorsal Ramus Nerve Innervate (Medial Branch of Posterior Primary Ramus)?

A
  1. Facet Joints
  2. LM Muscle
  3. Interspinous ligament

M1ZIMP

331
Q

What is the best way to train the multifidus? Danneels et al. 2001:

A

Static isometric holding for 5 seconds between the concentric and eccentric phase was found to be critical in inducing muscle hypertrophy during the 10 weeks of training.

70% MVC REQUIRED

332
Q

What exercise displayed the largest T2 increase in multifidus, followed by the ES (LT and IL), and finally the QL.

A

Dynamic Roman Chair trunk extension with 50-70% intensities (there was no difference between the 50-70% intensities).

333
Q

Did Danneels et al. find a more increase in LM CSA in general exercise vs. stabilization exercises?

A

general exercise. The stabilization breathing sht doesn’t work

334
Q

What did Skyba hypothesize as giving pain relief from joint mobilization?

A

A descending inhibitory mechanism that utilizes serotonin and noradrenaline

-sky is all about the descent

335
Q

What did Paungali et al 2004 suggest as the immediate hypoalgesia associated with MWM?

A

A non-opioid mechanism

336
Q

What did Wright 1995 suggest gives the initial pain relief of MT?

A

Involves descending pain inhibitory systems projections from the dPAG to SC

  • wright was right about descending pain
337
Q

Bolton and Budgell believe there’s a different impact on receptors from manipulation and mobilization, what’s the difference?

A

Manipulation stimulates receptors within deep intervertebral muscles, while mobilization affects more superficial axial muscles

338
Q

What did Katavich 1998 say SMT stimulates?

A

SMT stimulates neurophysiological pathways to inhibit pain and muscle responses

Indahl katavichh

339
Q

What did Colloca et al 2004: SMT ___ afferent discharge of mechanoreceptors from disc, ligaments, muscles, and facets.

A

Increases

340
Q

Hodges and Moseley 2003: Experimentally induced muscle pain studies strongly support the notion that pain may be the cause of the changes in ___ ___ in LBP

A

motor control

  • moseley - motor control
341
Q

Matre et al 1998: Observed that acute experimental pain caused changes in?

A

Spinal motoneuron activity

MAtre - Motorneuron Activity

342
Q

What may be responsible for the changes in the TrA and LM delayed activation?

A

Fear and pain

343
Q

Holm et al 2002, caused swelling by injecting lidocaine into the facet capsule and what was the result?

A

It decreased MUAPs of multifidus within 30s, but on average within 5 minutes after.

344
Q

Capra and Ro in 2000 did an intramuscular injection with an algesic substance (causing muscle pain) and noticed a ____ in proprioceptive signals from the jaw muscles

A

decrease

345
Q

Matre et al 1998: suggested a ___ sensitivity of the muscle spindles during muscle pain.

A

Increased

346
Q

What did Arendnt-Nielsen et al 1995 observe regarding motor performance?

A

This was the first study to show that MSK pain can change the motor performance of the paraspinals during gait. It represents a direct interaction between NOCICEPTIVE AFFERENTS and motor neuron pool excitability, that could be mediated by a spinal reflex pathway.

347
Q

Laslett et al 2006: did intra-articular injections into the ZJ, or medial branch blocks to diagnose ZJ mediated LBP. What % of patients responded to the ZJ blocks?

A

36% of all CLBP pt’s responded to the ZJ blocks

348
Q

What did Laslett say is an indicator for ZJ mediated pain?

A

spinal midline pain and/or the centralization phenomenon effectively rules out the ZJ

349
Q

Young et al. 2003: T or F: Said that patients experiencing centralization did NOT respond to ZJ blocks.

A

True

350
Q

Laslett in 2005: Has centralization been found to be highly specific or sensitive for pain provocation during discography?

A

Specific

351
Q

Wilde et al 2007: Is there a valid and reliable way to diagnose lumbar ZJ’s as the source of LBP?

A

Nope

352
Q

Wilde et al 2007: Is the clinical feature of extension, lateral flexion, and rotation validated to diagnose Lumbar ZJ pain?

A

Nope

353
Q

What are the highest indicators of Lumbar ZJ pain?

A
  1. 94% - Localized unilateral LBP
  2. 89% - Worse with unilateral pressure
  3. 89% - Lack of radicular features
  4. 78% - Pain eased by flexion
  5. 72% - If there’s referred pain, it does not pass the knee
354
Q

According to Legaspi and Edmond in 2007, is coupled motion of the lumbar spine evidenced-based?

A

No.

355
Q

Lee and Elliot 2008: What are the findings for Myelopathy?

A
  1. UE and LE hyperreflexia bilaterally.
  2. Sometimes, Lhermitte’s sign aka the Barber Chair Phenomenon
  3. Rhomberg’s sign
  4. Hoffman’s sign
356
Q

According to Dan and Saccasan in 1983, is a lumbar HVLAT without potential risk?

A

No. There’s 7 serious complications

357
Q

Santilli et al. SMT for acute LBP with disc protrusion resulted in ___% of pt’s being pain-free, and a relief of radiating pain into the legs for ___% of pt’s.

A

28% pain-free
55% no radicular sx

358
Q

According to Laslett in 2003 and 2005, what is the gold-standard for pain-relief? It led to an 80% pain relief.

A

Fluoroscopy guided injection with anesthetic block

359
Q

According to Laslett, if all 6 SIJ provocation tests do not provoke the familiar pain…

A

The SIJ is not the source of the back pain

360
Q

Berthelot et al. 2006: ___% of anesthetic diffuses out of the SIJ and often hits the adjacent nerve root

A

61%

361
Q

Van der Wurff’s Sensitivity and Specificity?
x/5 tests positive?

A

3/5 positive

85% sensitivity
79% specificity

Replace sacral compression with FABERs

362
Q

Riddle and Freburger 2002: Is it possible the determine which position the sacrum is stuck in?

A

No.

363
Q

Peace and Fryer 2004: Is there a correlation between bony asymmetry and LBP?

A

No

364
Q

Mens et al. do SIJ stabilization or diagonal trunk training (IO, EO, LM, GMax, Lats) exercises help?

A

no

365
Q

Nilsson-Wikmar et al. is there a difference between in-clinic or at home PT (SIJ)?

A

No

366
Q

Dumas et al. 1995: Did exercise have an effect on the prevention or treatment of pelvic pain during or after childbirth?

A

no

367
Q

O’Sullivan 1997: Does specific training focusing on the TrA or LM help individuals with spondy?

A

Yes

368
Q

Hides et al 1996, 2001: is lumbar multifidus training supported in the acute 1st STAGE ONLY

A

Yes

369
Q

Pool-Goudzwaard et al 2004, observed that pelvic floor muscles ___ the pelvic ring

A

stiffen

370
Q

Cervical Radiculopathy Test

A
  1. Spurling’s test- median N.
  2. Cervical distraction, rotation - symptomatic side < 60 degrees
  3. NDI > 10/50
  4. 18-65 yo

Spurs scored 60 and the nets scored 10, 18-65 yo

371
Q

Does Laslett find manipulation to be effective in treating SIJ pain?

Instead, what does Laslett find to be effective in the management of SIJ pain?

A

No

Corticosteroid injections, phenol injections, and radiofrequency neurotomy. Also surgical debridement and fusion have a moderate chance of pain reduction

372
Q

To date, is there evidence that supports the use of specific or global stabilization exercises in those patients diagnosed with SIJD

A

No

373
Q

Are SIJ symmery and motion tests reliable?

A

no

374
Q

What is the best-practice for SIJ diagnosis?

A

Multi-test regimen of pain provocation tests and Forton’s area

375
Q

Is there any evidence supporting the use of mobilization or HVLAT for SIJD?

A

No

376
Q

Is there any evidence directly addressing whether manipulation should precede or follow stabilization in SIJ?

A

No

377
Q

Should you address form-closure or force-closure first?

A

Form-closure first, then force-closure

378
Q

When an SIJ dysfunction diagnosis has been made, is there any evidence to support the notion that specific positional fault diagnosis of the sacrum or the innominate gives better outcomes than just sacral or innominate HVLA thrust irrespective of mal-alignment dysfunction

A

No

379
Q

According to Childs et al in 2007, patients who completed the exercise intervention without manipulation were _x more likely to experiencing a worsening disability

A

8x

380
Q

Kavcic et. al 2004: lumbar stability depends on __ trunk muscles

A

all

381
Q

Stuge et al. 2004, 2006: effective tx of PPPP was best achieve when the ___ spinal musculature was included

A

Entire

382
Q

Almeida et al. 2010: Intravaginal pressure increased from __ mmHg to __ mmHg immediately following a sacral HVLAT

A

56.01 - 64.65
+8.64

383
Q

Osterbauer et al. 1993 and Cibulka et al. 1998: T or F: HVLAT to the SIJ statistically improved pain and disability

A

True

384
Q

Clements et al. 2001, T or F: AA ROT asymmetry was restored regardless if the HVLAT was applied unilateral towards the restriction, or away from it.

A

True

385
Q

What are the goals of HVLAT to the SIJ?

A

Decrease pain

Increase ROM

Reduce Disability

Increase muscle strength “force closure”

Improve feed forward activation times

Maybe put it back in place

386
Q

Is there any substantatial evidence that supports or refutes the hypothesis that a reversal of a positional fault is the predominant mechanisms of action for MWM, although improvements in ROM have been shown?

A

No

386
Q

Timgren and Soinilla 2006: Following an ankle HVLAT or SIJ MET all patients had an immediate…?

At 6 months?

A

Reestablishment of pelvic symmetry

6 months: 88% improvement

387
Q

Hungerford et al. In patients with posterior pelvic pain, the WB innominate rotated _____ with single leg stance?

In subjects without pain…?

A

It anteriorly rotated and translated inferiorly

Without pain: the WB innominate posteriorly rotated and translated superiorly

388
Q

Stuge et al 2004, 2006: T or F: HVLAT to the SIJ improved immediate form closure

A

True

389
Q

Lewitt 1985: Are manipulation and mobilization used synonymous?

A

Yes

390
Q

Mennell 1960: Manipulation is a manual procedure used to treat ___ dyfunction

A

JOINT dysfunction

391
Q

Cyriax: Passive movement of a joint with therapeutic intent, using the ____

A

hands

392
Q

Maitland 1986: There’s two definitions of manual therapy

Loosely and restricted?

A

Loosely refers to any kind of passive movement

Restricted is a small amplitude, rapid movement (not necessarily at end range), that the pt cannot prevent

393
Q

HVLAT American Heritage Dictionary:

A

to operate or control by skilled use of the hands

394
Q

Paris 1979 HVLAT:

A

Skilled passive movement of a joint

395
Q

APTA 1999 and APTA 2000 definitions of HVLAT

A

1999: Manipulation is a small amplitude high velocity, Mobilization is variable amplitude and speeds

2000: Manip = mob

396
Q

Grade V vs. HVLAT

A

Grade V is more of a school definition involving oscillations or an audible pop

HVLAT is more for the neurophysiological effects:
1. Immediate reduction in paravertebral mm tone
2. Immediate increases in cervical flexor strength (Metcalfe 2006)
3. Immediate improvement in LM TrA contraction (Gill and Brenner 2007)

397
Q

VA Chiropractor’s Association of Spinal Manip vs. Mob

A

Manip: Cavitation/pop
Mob: No caviation or pop

398
Q

What is the problem with CS HVLAT research?

A

Few, Small, Poor, Inconclusive

  1. There’s only a few RCTs
  2. Most have small sample size and poor methodology
  3. SRs are inconclusive

Bronfort, Gross, Haneline, and Vernon

399
Q

CS HVLAT: Chronic neck pain

is HVLAT or MOB superior?

A

Neither is superior. Both are effective

400
Q

CS HVLAT: WAD:

Who found HVLAT is effective in acute WAD?

A

Fernandez de-las Penas 2004

FernanWAD

401
Q

CS HVLAT: HA/Dizziness:

Which authors looked at:

RCT for CGH using mob/HVLAT?

SR for TTH and HVLAT?

SR for HA and HVLAT?

A

RCT for CGH using mob/HVLAT? Jull 2002 (JG)

SR for TTH and HVLAT? Lenssinck 2004 (Lens-Tension)

SR for HA and HVLAT? Astin Ernst 2002 (H-ASTIN)

402
Q

T or F: There are low quality RCTs for cervicogenic dizziness, but they are finding a positive result from MT

A

True

403
Q

CS HVLAT: Is there sufficient evidence to draw conclusions for radiating arm pain?

A

No - Cagnie 2008

404
Q

What is the mean thrust duration according to Ngan 2005?

A

158 ms

405
Q

According to Triano 1992, what is the physiological reaction time, essentially when the biomechanical effects are completed before any protective muscular response?

What manipulation did he look at?

A

135 ms

C2/3 lateral break

406
Q

According to Herzog 2005, what is the required speed for a cervical and lumbar manipulation?

A

CSP: 80 ms
LSP: 200 ms

407
Q

What is the pre-thrust rotation accoridng to Ngan and Triano Schults?

A

Rotation: 30-54 degrees
Flexion: 2-30 degrees
Lateral bending: 6-46 degrees

408
Q

According to Ngan, what is the mean de-rotation?

A

4.8 degrees

409
Q

What is the mean peak acceleration?

A

2183 deg/s/s

410
Q

Do you need to rotate/flex down to the level?

A

no

411
Q

With Ross et al. how far away was the average cavitation from the targeted joint in the lumbar?

A

3.9 cm

412
Q

Ross et al deemed what % of thrusts affected the targeted jonit?

A

46%

413
Q

Fernandez de las penas: Following a C5-6 HVLAT how much did the pain threshold increase on the ipsilateral vs. contralateral side

A

Ipsilateral: 35.5%
Contralateral: 24.8%

414
Q

Cochrane (Gross) Review 2004: In summary, Manipulation/Mob for neck pain is what level of evidence?

A

Moderate to very low level of evidence

415
Q

What are the measurements for a c-spine manipulation?

A

30 ROT
46 SB
2 degrees flexion above C3, 2 degrees extension below C3

416
Q

What is the required force for a cervical manip?

A

118N

417
Q

What is the required force for a thoracic manip?

A

238N

418
Q

What is the average degree velocity of a manip?

A

72 deg/sec

419
Q

What is the peak DEGREE velocity of a manip?

A

127 deg/sec

420
Q

What is the average time for a cervical manipulation?

A

< 135 ms

421
Q

Summarize the UK Beam Trial outcomes

A

Exercise alone = no benefit at 12 months.

Anything with SMT = small, but significant benefit at 12 months

422
Q

What are the 3 conclusions from the UK Beam Trial

A
  1. SMT at 12 weeks = significant benefit
  2. SMT is cost effective
  3. SMT alone gives better value for money than SMT+exercise
423
Q

How much blood flow comes from the ICA’s vs. the VBA?

A

80% ICA
20% VBA

424
Q

Does Laslett HVLAT the SIJ?

A

No. He stopped doing mob/manip due to poor outcomes. SMT is unsuccessful or aggravates symptoms.

425
Q

What are the major complications of NSAIDs?

Adverse events:
Significant complications:
Hospitalizations:
Deaths:

A

Adverse events: 25%
Significant complications: 1-4%
Hospitalizations: > 100k/yr
Deaths: 16.5k/yr

426
Q

What are the major side effects on NSAIDs?

A
  • GOSH BA

GI ulceration
Bleeding
Hepatorenal dysfunction
Organ failure
Skin reactions
Accelerated cartilage destruction

427
Q

LS HVLA is ___ times safer than NSAIDS for a LS disc herniation

A

37K-148K

428
Q

Cervical: Time to peak force?

A

0.135 sec

429
Q

Cervical: How fast?

A

80-200 ms

430
Q

Cervical: Mean time of SMT:

A

158ms/135ms

431
Q

Cervical: Velocity of SMT

A

127/sec

432
Q

Cervical: Force?

A

118N

433
Q

Cervical: Mean duration of SMT

A

102ms/80-100ms

434
Q

Cervical how many cracks?

A

2.5

435
Q

Cervical: Acute neck pain, number of SMT’s per week?

A

4 SMTs/3 weeks

436
Q

Cervical: Chance of adverse event?

A

1/1.3M

437
Q

Cervical ROM testing compared to VA strain

A

1.2-12.5%

438
Q

Cervical: HVLAT average strain on VA

A

6.2%

439
Q

Cervical: % of mechanical failure of VA

A

139-162%

440
Q

Lumbar Force

A

500N

441
Q

Thoracic Force:

A

238N

442
Q

Thoracic: mean duration of SMT

A

150-200ms/120-200ms

443
Q

Thoracic preload:

A

24N

444
Q

Thoracic avg. rate of force

A

1368 N/s

445
Q

Thoracic movement at peak force

A

9.8 mm (1cm)

446
Q

Thoracic skin lock

A

33-38 mm (3cm)

447
Q

Thoracic, avg number of clicks

A

2-6 cavitations

448
Q

Thoracic: average error from target

A

3.5cm

449
Q

Lumbar: average error from target

A

5.29cm

450
Q

Thoracic: movement of vertebrae (mm)

A

6-12mm anteriorly and 3-6mm laterally

451
Q

Thoracic: movement of vertebrae (deg)

A

0.4-1.2 deg axial
0.5-1.8 deg sagittal

452
Q

Sympathetic efferent to the UE is ____ and to the head it’s ____.

A

UE: T5-9
Head: T1-4

453
Q

How can rib dysfunction cause arm pain via the sympathetic system?

A

The sympathetic chain interface with the white rami communicates up or down 5 levels and out to the upper limbs via the satellite ganglion, which is anterior to the 1st rib

454
Q

What are the scalene’s attachment points?

A

Anterior C3-6 and insert on the posterior tubercles to R1,2

455
Q

How can a rib manipulation decrease arm pain?

A

Mechanoreceptors in the facet joint capsule and ligaments in the paravertebral muscles may be responsible for altered afferent barrage and inhibition of the alpha motor neuron pool excitability levels, thus immediate reduction in segmentally association.

456
Q

Which muscle has been shown in the literature by Lindgren Leino 1998 to repeatedly compress the brachial plexus?

A

The anterior scalene

457
Q

What were the main findings from Boyle 1999 regarding shoulder impingement?

A

Palpate the 2nd rib, posterior scalene’s, and lower CS mobility. Additionally the signs and symptoms may NOT always be reproducible with R2 accessory motion.

458
Q

According to Maigne in 1991, what does the dorsal ramus of the 2nd thoracic do, and where is it located?

A

It provides cutaneous distribution to the posterolateral shoulder

It’s nerve continues just lateral to the acromion. It is often limited caudally by the rib and laterally by the superior costotransverse ligament

459
Q

According to McGuckin in 1986, What is T4 syndrome?

A

Glove like paresthesia
Pain in one or both limbs

Sympathetic changes:
1. Triple response of Lewis
2. Cold hands, discoloration, mottled, clammy
3. Head and neck symptoms, nausea, vomiting, dizziness
4. severe TTP to superior light touch over fixated segment

Tx: manipulate facet (costovertebral)

460
Q

Who was the first to describe 2nd rib syndrome?

A

Grieve 1998

  • He’s grieving cause I ain’t never heard of him.
461
Q

Indahl: How much reduction in MUAP (motor unit action potentials) of the multifidus within 30 seconds of saline injected into the lumbar ZJ?

A

74%

462
Q

Indahl: Summary

A

(Inner-network)

The outer annulus of the disc, capsule of the ZJ, ligaments, and paraspinal muscles have an innervation network that is probably part of the proprioception system that recruits muscles for motion and stabilization of motion segments

463
Q

How can we reduce the muscle spasm of the thoracic spine?

A

E-stim elicits a reflex
HVLAT elicits a stretch reflex and causes inhibition.

464
Q

What % of individuals with WAD had dizziness/vertigo?

A

20-58% - Wrisley 2000
80-90% - Heikkila 2000

465
Q

Who first described CG Dizziness?

A

Ryan and Cope 1955

Ryan cope’d with the dizziness

466
Q

Who found that vertigo could be induced by changes of position of the neck?

A

LuxON 1984 - brought ON the dizziness

467
Q

How can vertigo be caused neck position?

A

It is a malfunction or disturbance in afferent flow of impulses from deep cervical tissues and cervical proprioceptors

468
Q

In CG Dizziness, what is the dizziness proportioned too?

A

The CS pain, stiffness, or numbness

469
Q

Which studies show that HVLAT is effective to manage dizzines?

A

Cote 1991
Cagle 1995
Cronin 1997

The Cervicogenic C squad

470
Q

How does manual therapy restore dizziness?

A

restore normal arthrokinematics of the ZJ and normal afferent input will also be restored to the dorsal roots of C2-3, which synapses with the nucleus abducens in the vestibular nuclei

471
Q

Who first introduced CGH?

A

Sjaastad 1983 - can’t speak

472
Q

What is the cervicogenic neuroanatomy?

A

CN5 (Trigeminal) and the C1-3 segments converge in the brainstem, which is why the pain may refer to the trigeminal nerve distribution.

Additionally, the trigeminocervical nucleus also receives afferents from CN 7, 9, 10 (Facial, Vagus, Hypoglossal)

473
Q

Fernandez de las penas observed that with the lateral glide test the hypomobile side move ____ mm than the contralateral side

A

3.44 mm

SMT (1 decks)

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