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SMT > SMT-1 Manual, pgs 72-78 > Flashcards

SMT-1 Manual, pgs 72-78 Flashcards

1
Q

According to Zito et al 2006 were all hypomobile cervical joints painful?

A

No, not all hypomobile cervical joints were painful

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2
Q

According to Zito et al 2006 were all painful cervical joints hypomobile?

A

Yes, all painful joints on PPIVM testing were hypomobile

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3
Q

What group in Zito 2006 had increased muscle tightness?

A

Cervicogenic headache group

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4
Q

What group in Zito 2006 demonstrated poorer performance at 26, 28, and 30 mmHG in the CCFT?

A

Cervicogenic headache group

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5
Q

In Zito 2006 how did the authors discriminate CGH from other headaches? How successful were they?

A

C1-C2 painful and hypomobile on PPIVM was able to discriminate CGH group from migraine and control subjects with 80% sensitivity

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6
Q

According to Boddeck 2005, is the origin of a headache able to be distinguished?

A

No because trigeminal muscles can

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7
Q

Zito 2006 found CGH to have a neural component when U/LE NTPT testing was added. What other author found this to be true?

A

Jull 2001 found 10% of 200 CGH’s to have neural component

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8
Q

According to Hall & Robinson 2004 comparing CGH to asymptomatic patients, which group had decreased flexion rotation on testing?

A

CGH group 24/28 patients, with primary motion segment of C1-C2. 4/28 CGH patients had primary motion segment of C2-C3. No asymptomatic patients had positive flexion-rotation test

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9
Q

In Hall & Robinson 2004 were active ROM in cardinal planes different between CGH and asymptomatic groups?

A

NO - meaning the adjacent levels compensate

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10
Q

What were the average AROM movements in flexion rotation between groups reported in Hall & Robinson 2004?

A

44 degree in asymptomatic patients and 28 degrees in CGH group

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11
Q

What did the Pearson’s correlation test indicate in Hall & Robinson 2004?

A

The greater the restriction in flexion-rotation test then the more severe the headache would be in terms of frequency, duration, and intensity

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12
Q

What cervical segment was most symptomatic in Hall & Robinson 2004?

A

C1-C2 motion segment was the most frequent symptomatic cervical motion segment in CGH

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13
Q

The results regarding primary affected motion segment in CGH stated in Hall & Robinson 2004 are in agreement with reports from what author?

A

Jull et al 1997

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14
Q

The results regarding primary affected motion segment in CGH stated in Hall & Robinson 2004 are in contrast with reports from what author?

A

Bogduk 2005 who implicated C2-3

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15
Q

According to Schwartz 1998 what is the most common type of headache?

A

Tension type headache

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16
Q

According to Rasmussen 1991, what is the lifetime gender prevalence for TTH in the general population?

A

69% of men and 88% of women

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17
Q

According to the IHS, what is the definition of chronic TTH?

A

Headache at least 15 days a month for at least 6 months

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18
Q

According to systematic review by Lenssinck et al 2004 is there sufficient evidence to support or refute SMT for TTH?

A

NO - insufficient evidence to support or refute

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19
Q

Von Piekartz et al 2006 found what neurodynamic component in children with CGH?

A

36 degree of neck flexion during long sitting slump test for CGH patients, versus 85 degree for migraines, and 101 degree for control group

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20
Q

What authors stated that 10% of CGH have a neural component?

A

Michael Shacklock (2005) and Gwendolen Jull (2002)

21
Q

Can you reproduce the headache by sensitizing the neural system?

A

Yes, look for change in symptoms with distal tensioning in the slump test. Or try upper cervical flexion and then UE abduction to 90degree as in NTPT I or III

22
Q

What are the most valid and reliable outcome measures for CGH patients?

A

1) Neck Disability Index ( Vernon & Moir, 1991)
2) Frequency, intensity, and duration records kept daily or weekly by patient
3)Flexion-Rotation Test (Ogince et al 2007 = valid)
20 degree is mean FRT for CGH, 32 degree is cut off for positive FRT in CGH pop. 91% sen and 90% sp
4) Craniocervical flexion test with PBU 20-30mmHG
5) Neck flexion endurance test (reliability established, no validity as of yet)

23
Q

What are the key factors in differential diagnosis for CGH and migraines?

A

CGH, migraine, and TTH symptoms often overlap. Occipital, cervical, facial, shoulder, and periorbital pain can occur in CGH and migraine.
Consider CGH component if migraine medications provide only partial relief.

24
Q

Describe the results of the 4 case reports on CGH performed by Xiaobin 2005?

A

All patients had positive Tinel’s sign over occipital nerve
Occipital neuralgia is likely a subcategory of CGH
After nerve block patients had gradual return of symptoms in 10 days, 2 weeks, 40 days and 2 months

25
Q

What two types of clinicians did Laslett 2003 and 2005 use to diagnosis SI joint dysfunction?

A

Radiologist & Physical Therapist

26
Q

What were the inclusion criteria in the Laslett studies?

A

Buttock pain +/- other pain

27
Q

What were the exclusion criteria in the Laslett studies?

A

midline or symmetrical pain

28
Q

In the Laslett studies, how did the radiologist diagnosis SI joint dysfunction?

A

Positive reference standard (gold), using fluoroscopically guided injection, led to provocation of familiar pain followed by 80% pain relief with anaesthetic block

29
Q

In the Laslett studies, how did the PT diagnosis SI joint dysfunction?

A

Positive physical examination was multi-test regimen of pain provocation tests that produced familiar pain.

30
Q

What was the percentage of positive tests for SI joint dysfunction identified by radiologists in the Laslett studies?

A

33%

31
Q

What was the percentage of positive tests for SI joint dysfunction identified by physical therapists’ in the Laslett studies?

A

31 to 50%

32
Q
  1. According to Bogduk 2005, is the origin of a HA able to be distinguished? (pg. 57 SMT-2)
A
  1. No, because the trigeminal nucleus can be evoked from the upper cervical stimulation as a stimulus from frontal, periorbital, facial, occipital, temporal regions.
33
Q
  1. According to Bronfert et al 2005, what tx was found to be effective for CGH?
A
  1. SMT and low intensity endurance training
34
Q
  1. Bronfort et al 2005, is SMT effective for migraine?
A
  1. May be effective, has a similar effect to amytriptyline, but less effective for TTH’s.
35
Q

Jull et al 2002 (pg. 59 SMT-2):
248. What did Jull et al 2002 study for CGH?

  1. What was used as an outcome measure?
  2. What were the results?
  3. Did combined tx improve outcomes?
  4. What % had decreases in HAs?
  5. What % had 100% resolution?
  6. How did med intake change @ 12 months?
  7. Who performed the best on the CCFT at 6 weeks and 12 months?
A
  1. RCT of 10 week tx with 8-12 tx sessions, no longer than 30 minutes
  2. HA frequency/intensity/duration, pain provocation with MT, CCFT test
  3. Three groups: MT alone, Ex alone, MT+Ex. Found with all groups a significant decrease in HA frequency and intensity, Northwick compared to control at 6 weeks, 3, 6 and 12 months.
  4. No better than individual for duration, but MT+EX was better than Ex for duration.
  5. 76% gained a 50% or better decrease in HA frequency in the 3 tx groups.
  6. 35%
  7. decreased 93-100% in all 3 intervention groups, increase 33% in control (medication only) group.
  8. Any tx that involved EX, p
36
Q
  1. According to Hides et al 1996, did MT improve DNF test despite pain relief?
A
  1. No
37
Q
  1. Does improving the CCFT change pain or disability?
A
  1. No
38
Q
  1. 62 of 91 subjects in Niere and Robinson 1997 had improved HAs by what %?
  2. How many had some improvement?
  3. How many reported a deterioration of HA?
  4. How many reported no change?
  5. p values for Niere and Robinson 1997 following SMT: HA frequency? Duration? Intensity?
  6. What may be the most valuable indicator of tx effect rather than intensity or duration?
A
  1. 50%
  2. 70 out of 91
  3. 15
  4. 6
  5. HA frequency: p=0.000, Duration: p=0.025, Intensity: p=0.000
  6. frequency
39
Q
  1. According the Haas et al 2004, how frequent should you tx CGH? (pg. 61 SMT-2)
A
  1. 9-12 txs over 3 weeks did better than 3 tx’s over 3 weeks.
40
Q
  1. What % in Jull et al 2002 did not improve HA with SMT and/or Ex?
A
  1. 24%
41
Q
  1. Did Jull and Stanton 2005 find age, high intensity and chronicity to be suggestive of poor outcome?
A
  1. No
42
Q
  1. What did Niere et al 1998 find as a predictor of GOOD outcome for SMT and CGH?
A
  1. Frequency of HA
43
Q
  1. According to Zito et al 2006, when comparing CGH, migraine with aura and non-HA controls who had decreased AROM?
A
  1. The CGH group for flexion and extension.
44
Q
  1. What group in Zito et all 2006 had pain provocating with PPIVM’s?
A
  1. CGH C0-C3 p
45
Q
  1. What did Niere et al 1998 find as predictor of BAD outcome for SMT and CGH?
A
  1. Affective and Autonomic pain descriptors
46
Q
  1. Is maxillary/mandibular pain usually involved according to Bogduk 2005?
A
  1. Not as common as frontal and periorbital secondary to weak branch innervation into trigeminal nucleus from opthalmic branch.
47
Q
  1. What other regions can be involved in HAs according to Bogduk 2005?
A
  1. Nasal, oral, teeth, TMJ, paranasal sinuses, dura mater of anterior/poserior cranial fossa.
48
Q
  1. According to Bogduk 2005 what other cranial nerves may be involved in HAs?
A
  1. Facial VII, Glossopharyngeal IX, Vagus X

SMT (11 decks)

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