SMT 3 Manual: Part 2

Question 1

Holm

Answer 1

(2002): When supraspinal ligament is loaded 5-10 Newtons there was increased EMG activity of LM at same level and one above and below. Stimulation of annulus or facet induced responses in multifidus on multiple levels and on contralateral side. Concluded facet has a regulatory function in controlling neuromuscular balance of lumbar motion segment.

Question 2

Santilli

Answer 2

(2006) : 64 men and 38 women with acute LBP <10 days, moderate to severe radiating to one leg, and MRI evidence of disc protrusion with intact annulus were randomized to lumbar HVLAT or simulated.
1. Treated 5 days/week with lateral recumbent HVLAT up to 20 sessions.
2. At 6 month follow up:
a. 28% (HVLAT) vs 6% (mob) were pain-free in their back
b. 55% (HVLAT) vs 20% (mob) were pain-free from radiating leg pain
3. HVLAT group had less total number of days with pain and less total number of days with moderate/severe pain
4. At 15 days follow up, HVLAT group had lower mean VAS than mob. group
5. No adverse events
6. MRI findings not changed from baseline
7. Didn’t include CLBP, or those with extrusion/sequestration with rupture of annulus

Question 3

O’Laughlin and Kokosinki

Answer 3

(2008): Pregnant woman with LBP reported bilateral LE weakness preventing ambulation and numbness/tingling with inability to feel herself urinate. Bilateral Achilles reflexes absent. Had emergency MRI and had surgery for L4/L5 central disc extrusion causing cauda equina syndrome. Delivered bay without complication 6 weeks later.

Question 4

Pregnancy and LBP

Answer 4

Fast (1990): All non-pregnant women could perform sit up, 16.6% of pregnant women could not perform single sit up. There was no correlation between sit up/strength of abdominals and LBP.

Question 5

Arendt-Nielsen

Answer 5

(1996): Experimentally induced muscle pain with hypertonic saline solution into longissimus caused 8.5% increase in EMG of paraspinals. Motor output with CLBP and experimentally induced LBP was changed with gait. Excitation during swing phase (when normally silent) and relaxation in double stance (where normally active). First human study to show MSK pain can change motor performance of paraspinals in both CLBP and experimentally induced pain (supports Lund’s pain-adaptation model).

Question 6

Coupled motion of L-spine

Answer 6

Legaspi and Edmond (2007): Reviewed 24 articles and were unable to find evidence of consistent SB and rotation in lumbar spine across studies.

1. No evidence to support use of coupled motion principles for evaluation or treatment (lumbar)
2. Coupled motion reported to be 2.5 degrees or less and highly unlikely this motion can be detected with palpation

Question 7

Richardson

Answer 7

(1999) : 1. Review of muscles of local stabilizing system of spine has determined that of the lumbar muscles, the multifidus is most closely linked to spinal segmental support
2. For the abdominal wall, the TrA is key muscle and it is possible the IO works with the TrA in its supporting function
3. An important factor to consider is the possibility for LM to contribute to tensioning posterior layer of thoracolumbar fascia since it is contained within the sheath formed by the fascia, thus, the TrA and LM have shared function in spinal stability via tensioning of thoracolumbar fascia
4. Reflex inhibition may cause motor control changes and decrease alpha motor neuron pool activity
a. 25 cc fluid in knee causes RI of VMO, 55 cc for entire quad
b. RI linked to joint effusion, pain, ligament stretch, and capsular compression

Question 8

Hides (1996)

Answer 8

39 subjects with acute 1st episode LBP with unilateral segmental inhibition of LM. 34 demonstrated LM atrophy of 25% at L5 level. The L5 level showed greatest differences side to side, minimal atrophy at other levels. Allocated to control (non-active treatment) or treatment group performing specific LM exercises.

1. After 4 weeks, LBP subsided in virtually all subjects and no difference in disability scores between groups. All at normal function at 4 weeks.
2. In control group, multifidus recovery wasn’t spontaneous when symptoms subsided and function returned and difference still present at 10 weeks.
3. Exercise group resulted in complete restoration of LM CSA at 4 week treatment period.
4. 1 year later: only 30% of subjects from LM exercise group suffered reoccurences vs. 80% of control group.

Question 9

Hodges and Richardson

Answer 9

(1996) : In patients with >18 months h/o LBP EMG taken for trunk muscles, Did shoulder movements and most obvious delay for those with LBP was 50-450 ms in onset of TrA. In every trial the TrA was absent in pre-movement period in all 3 shoulder movements, unlike normals with 30 ms feed forward. Since the task only lasted 200 ms, in many trials the contraction occurred after movement finished.
(1998) : Same study but with hip movements. All movements associated with delayed TrA contraction (unlike asymptomatics, where activation of TrA preceded RF by mean of 110 ms). In LBP patients the onset of TrA followed that of prime mover by several hundred milliseconds.

Question 10

Cause of decreased LM size in acute LBP patients

Answer 10

1. Most likely cause is reflex inhibition and not pain inhibition, as decreased muscle size seen after resolution of pain in control group (Hides 1996)
2. Richardson (1999): It is suggested that sensory input from joint is processed in the spinal cord to produce an effect in specific muscles that act on the joint in question
3. Deepest fibers of LM attach to capsules of ZJ’s and cover joints on all be ventral sides (Macintosh 1986)

Question 11

Dan and Saccasan

Answer 11

(1983): Described 7 cases of serious complications after lumbar spine HVLAT, including massive cauda equina compression and vertebral pedicle fracture.

Question 12

Immediate hypoalgesia from joint manipulation

Answer 12

1. Skyba (2003): Pain relief from joint mobilization is from descending inhibitory mechanisms that use serotonin or noradrenaline
2. Paungmali (2004): Suggests a non-opiod mechanism of action for immediate hypoalgesia associated with MWM
3. Wright (1995): Initial pain relieving effects of manual therapy may involve descending pain inhibitory systems projecting from dPAG to spinal cord.

Question 13

Costa

Answer 13

(2009) : Systematic review of 21 studies for reliability of US for thickness, thickness changes, and difference in thickness changes over time for abdominal muscles.
1. Static measures of muscle thickness had ICC ranging from 0.80 to 1.00 (very good)
2. Changes had ICC ranged from 0.26 to 0.85. ICC values in 5 studies that used low back pain were lower than 16 that recruited only asymptomatics.
3. No studies looked at reliability over time.

Question 14

Lee and Elliot

Answer 14

(2008): 46 y.o. man referred to PT for treatment of LBP. UE and LE hyper-reflexia bilaterally, positive Lhermitte’s, Rhomberg, and Hoffman’s. PT contacted MD and expedited cervical MRI performed. MRI revealed C3/C4 and C5/C6 central canal stenosis. It is recommended that PT’s utilize screening questions in regards to changes in sensation, strength, gait, and B/B. Positive response to any of these should prompt thorough neuro exam.

Question 15

Kjaer

Answer 15

(2007) : Took 850 randomly selected 40 and 13 y.o. Danish participants. Using MRI they graded fat infilltration of LM (normal 0-10%, slight 10-50%, severe >50%). Several variables may influence presence of fat in multifidus. 1. BMI 2. Weekly hours of exercise 3. Physical workload 4. Leisure time. Fat infilltration found in 81% of adults and 14% of adolescents (adults: slight in 71% and severe in 10%, adolescents: slight in 14% and severe in 0%).
1. Fat infilltration found most commonly at L5 with no difference between right and left
2. Adults more active had statistically less severe fat infilltrations
3. Positive correlation between fat infilltration in LM and LBP for adults (more infilltration <> more LBP), fat infilltration uncommon for adolescents and no association found
4. Association not affected by BMI, type of work, and level of physical activity during leisure activity
5. The fact that fat infilltration is more common in adults does suggest that it is the LBP that causes muscle degeneration and in adolescents the LBP has not yet lasted long enough to produce such changes.

Question 16

Silfies

Answer 16

(2007) : Impaired proprioception in lumbar spine has been reported with LBP but no studies exist to argue this cause and effect relationship. This was a prospective cohort study with 2-3 year follow up (292 athletes).
1. No significant difference in repositioning errors (JPS) or kinesthesia between athletes with and without history of LB injury
2. No difference in JPS and kinesthesia between those athletes who did and did not get injured during 2-3 year follow up
3. Poor trunk proprioception (JPS and K) does no predispose athletes to low back injury and not a risk factor for sustaining low back injury.

Question 17

Obesity and LBP

Answer 17

Leboeuf-yde (2000): weight gains and obesity are only weakly associated with LBP.

Question 18

Assendelft

Answer 18

(1996) : Literature review of case reports, surveys, and review articles. Most frequent complications reported were VBA stroke after cervical HVLAT or cuada equine syndrome after lumbar HVLAT.
1. Concluded referral for SMT should not be made to practitioners applying cervical rotary HVLAT
2. This statement is not supported by their methods, as they did not track type of HVLAT and this isn’t supported in the literature (Kerry 2008).

Question 19

Mayer

Answer 19

(2005) : Used functional MRI to look at activity levels of lumbar extensor muscles during Roman chair exercise. Contrast shifts in T2 represent muscle activity. looked at 11 healthy participants doing 3 different MVC’s for 4 seconds with Roman Chair (40, 50, 70%). Looked at multifidus, QL, IL, LT. Each repetition started at 75 degrees trunk flexion and then extended to 15 degrees trunk extension. Each repetition completed in 4 seconds (2 sec. conc. and 2 sec. ecc.). Did 3 sets of 10 with 1 min. breaks. MRI done immediately after 3rd set. Repeated again for 50 and 70% MVC. Did 10 transaxial slices with L3/L4 interspace as midpoint. Average T2 value for 10 transaxial slices used. Results: Multifidus displayed largest T2 increase at each of 3 intensities, followed by ES and then QL. Maximum T2 increase occured at 50% for all 4 muscles.
1. 40% MVC was best for multifidus training because QL is minimal at this intensity.
2. 40% MVC for multifidus in the upper body alone in most subjects, dogmatically only need to add 3.5 kg of weight to get there.
3. It is possible the gluteals and hamstrings contributed at >50% once lumbar extensors reached their max T2 levels. To achieve max recruitment of lumbar extensors, max intensities are not needed.

Question 20

Koumantakis

Answer 20

(2005): 55 patients with subacute of CLBP assigned to one of 2 groups.
Group 1: Specific trunk stabilization exercise techniques.
Week 1 and 2: Drawing in to activate TrA and LM at 30% MVC in multiple positions (quadruped, supine, sit, stand, and arm elevation)
Week 3-5: Integration of spinal and/or limb movements with light functional tasks during activation
Week 6-8: Integration into heavier functional tasks
Group 2: General exercise for extensors and flexors at 60-70% MVC.
Both groups received interventions 2x/week for 8 weeks and given back education book. Subjects also asked to do exercises 3x/week at home. Outcomes taken at baseline, 8 weeks after intervention, and 3 months after intervention. There was no difference between the 2 groups for any outcomes at 3 months. Roland Morris improved more in the general exercise group at 8 weeks though. Specific stabilization exercises do not appear to provide additional benefit to patients with subacute or CLBP and have no clinical signs suggesting presence of spinal instability. The general exercise group spent 1/2 time/duration in treatment sessions.

Question 21

Clinical predictors of lumbar facet pain

Answer 21

Laslett (2006): Only controlled intra-articular ZJ inactions or medial branch blocks can diagnose ZJ-mediated LBP. Looked at 120 patients with CLBP, with or without LE pain. Screened before intra-articular ZJ injections or medial branch block. 36% of all CLBP patients responded to ZJ blocks.

1. Negative extension/rotation test, dominance of spinal midline pain, and/or presence of centralization phenomenon effectively rules out ZJ pain
2. Ext/rot has no diagnostic value for ZJ pain but high sensitivity (100%). Will rule out ZJ pain if left and right ext/rot tests are negative (Schwarzer 1994).
3. Dominance of spinal midline pain was not associated with positive response to ZJ blocks
4. Agrees with Young (2003) that found patients experiencing centralization didn’t respond to ZJ blocks

Question 22

TrA and Lumbar Fascia

Answer 22

Hodges (2003) assumed that TrA, by means of its connection to lumbar fascia, is dominant in controlling lumbar stability and any weakness/lack of control would spell trouble for back. Lederman (2007) said this was a dramatic leap of faith and feed-forward activation delay of TrA seen in CLBP likely explained a “reflexive pain evasion action that is unrelated to stability.”

Question 23

Richardson and Jull

Answer 23

(1995): Stated the exercise approach focuses on retraining a precise co-contraction pattern of the deep trunk muscles at submaximal levels (~30%)

Question 24

MacDonald

Answer 24

(2007) : 1. No evidence TrA and DM co-contract or co-contraction helps spinal stability
2. TrA and DM do not contract tonically in function
3. DM, SM, and ES all have predominance of type 1 (slow twitch) fibers, no just DM
4. EMG studies refute belief that DM is tonically active during static postures, gait, or trunk movements
5. Activity or training of DM does not require co-contraction of antagonists
6. Co-contraction of TrA and DM is not necessary for stability and may not need to be trained in LBP patients
7. SM and ES are not just extensors and rotators of the spine, they, like DM, might equally contribute to lumbar stability and help control spinal buckling.

Question 25

Multifidus atrophy in LBP

Answer 25

Kader (2000): Multifidus atrophy was present in 80% of patients with LBP in MRI study. Retrospective study of 78 patients with LBP with or without leg pain.

1. Majority of cases atrophy was bilateral and demonstrated mainly at L4/L5 and L5/S1 levels together but L5/S1 most frequent
2. 85% of patients had degenerated discs, most common at L4/L5 followed by L5/S1
3. Pearson’s correlation between LM atrophy and leg pain was found to be significant (more leg pain associated with more LM atrophy)
4. No statistically significant relationship between LM atrophy and radicular symptoms, nerve root compression, HNP, or number of degenerated discs
5. Correlation between intensity of pain and severity of muscle atrophy was no significant but trending that way
6. 18/38 patients with root pain and 25/57 patients with leg pain (radicular or non-radicular) only had LM atrophy without any other MRI abnormalities (Bogduk 1989 - Lumbar dorsal ramus syndrome caused by irritation to structures innervated by medial branch of posterior primary ramus). LM atrophy may explain referred leg pain in absence of other MRI abnormalities. I

Question 26

Hodges and Moseley

Answer 26

(2003) : Not certain whether pain causes changes in motor control, vice versa, or both. Studies indicate that experimentally induced muscle pain produces identical motor control disorders seen in people with LBP. This supports notion that pain may be the cause of changes in motor control in LBP (pain adaptation model).
1. Delayed activation and tonic activity of TrA seen in patients with LBP and has been replicated when pain induced by intramuscular injection of hypertonic saline into longissimus at L4 (Hodges 2001)
2. Acute experimental pain shown to cause changes in spinal motor neuron activity (Matre 1998).
3. Reflex inhibition of motor neuron excitability has been shown to occur in association with swelling and injury to joint structures
4. When pain-free subjects rapidly move an arm, but are subjected to moderately painful electrical shocks to the back that are unpredictable, the activation of TrA and deep LM are delayed, similar to those with CLBP (Moseley 2001) – Both fear and pain may be responsible for these changes, fear of pain can disrupt normal timing.

Question 27

Morton

Answer 27

(1999): RCT of patients with acute LBP stabilization training for multifidus was found less effective on its own than when combined with a course of manipulation. This is in line with current systematic reviews supporting use of manipulation at acute stage of symptoms (Van Tulder 2000).

Question 28

Macedo

Answer 28

(2009) : Systematic Review. Concluded motor control exercise is superior to minimal intervention and provides benefit when added to another therapy for pain at all time points and for disability at long term follow up. Motor control exercise is not more effective than manual therapy, other forms of exercise, or surgery.
1. MCE was superior to nothing/GP but long term follow up showed 1.43 decrease in NPRS, which is not greater than 2 point MCID
2. Treatment effects favored MCE versus MT at short term follow up and MT at long term follow up.
3. MCE was only better than other forms of exercise for disability at short term follow up. For long term disability, general exercise was better than MCE
4. MCE was as effective at reducing pain and increasing quality of life as less-complex exercise (retraining of specific muscles that is time consuming to PT’s and pt.’s)
5. MCE reduces pain but unknown whether these changes are accompanied by improvements in motor contro, motor control not measured in studies (Hall 2007 found no change in motor control of TrA after training trunk muscles and arm movements)

Question 29

TrA Timing Issues

Answer 29

FFA delay of 20-50 ms noted by Hodges and Richardson (96, 98) were no strength, but timing. Such timings are well beyond conscious control (<250 ms). How does teaching everyone to continuously contract core alter FFA delay? No study to date has demonstrated spinal stability exercises will correct TrA onset timing delay in CLBP (Lederman 2007). But TrA FFA delay has been shown to improve 28% immediately following SIJ HVLAT manipulation (Marshall and Murphy 2006).

Question 30

Matre

Answer 30

(1998) : Muscle pain produced from 5% hypertonic saline in soleus and tibialis anterior muscles. Reflexes were elicited in relaxed and active soleus before, during, and after muscle pain.
1. With pain soleus the mechanical stretch reflex response increased significantly
2. With pain in anterior tibialis the mechanical and EMG responses increased significantly
3. Suggests an increased sensitivity of muscle spindles during muscle pain caused by increased firing rate in gamma motor neurons but this may not be supported since alpha motor neuron pool was unchanged

Question 31

Van Tulder

Answer 31

(2000): Systematic review. Showed spinal stabilization or core strengthening is no more effective than general exercise in the management of LBP. These studies strongly suggest that improvements are due to the positive effects of physical exercise and not improvements in spinal stability, which, to date, actually has not been measured directly post spinal stability exercise intervention program.

Question 32

Evidence supporting stabilization for LBP

Answer 32

-Conducted in very specific groups.
1. Hides 1996, 2001: Acute 1st episode LBP only
2. O’Sullivan 1997: Spondylolisthesis and spondylolysis only
In both of these authors’ studies the effect of specific trunk stabilizing exercises was not compared to general back or abdominal exercises. Daneels (2001) found more increase in LM CSA in chronic LBP for general exercise vs. specific stabilization though.

Question 33

Alteration of paravertebral tone post manipulation

Answer 33

1. Bolton and Budgell (2006): Spinal manipulation preferentially influences a sensory bed that is different from sensory bed influenced by mobilization. Hypothesize that manipulation stimulates receptors within deep intervertebral muscles while mobilization techniques affect more superficial axial muscles (short intervertebral versus multi-segmental muscles)
2. Katavich (1998): Sensory input produced by SMT my stimulate neurophysiological pathways to inhibit pain and muscle responses
3. Colloca (2004): Spinal manipulation increases afferent discharge of mechanoreceptors from disc, ligaments, muscles, and facets.

Question 34

Best way to retrain multifidus

Answer 34

Daneels (2001): CLBP randomly assigned to 1 of 3 groups, 3x/week for 10 weeks
1. 10 wk stabilization training
2. 10 wk stabilization training combined with dynamic conc/ecc resistance training of LM
3. Same as number 2…plus, 5 sec static isometric hold
All groups go diathermy and massage as well. Stabilization training was co-contract LM and TrA in supine, sitting, standing, and during functional activities with ~30% MVC. Group 2 and 3 got quadruped hip ext, trunk lift from prone, and bilateral leg lift in prone. Performed 3 sets of each exercise at 70% of 1 RM which allowed 15-18 reps (weight added if more than 18 reps performed). Multifidus viewed before and after 10 wk of training using CT scan. CSA of LM at all 3 levels (L3-L5) significantly increased for group 3 only, had no effect on groups 1 and 2. Stabilization training plus isometric hold seems to be most appropriate to restore size of LM. Supports notion that multifidus muscle atrophy can be reversed in CLBP patients.

Question 35

Indicators of lumbar ZJ Pain

Answer 35

Wilde (2007): Delphi study of 20 Australian and New Zealand experts in field of LBP. 94% of panel agreed that “localized unilateral LBP” was an indicator of LZJ pain. Diagnosis of LZJ pain should not be based on one indicator alone.

1. Positive response to intra-articular facet injections
2. Localized unilateral LBP
3. Replication/aggravation with unilateral pressure over TP/facet

Question 36

Pain-adaptation model

Answer 36

(Lund 1991): Suggests in event of pain, the alteration of motor control serves to limit movement (velocity, force, and range)
1. May also be general stiffening by co-contraction, if stiffness is increased the CNS may perceive the demand for fine-tuning to be diminished, leading to reduced activity of deep intrinsic spinal muscles.

Question 37

Capra and Ro

Answer 37

(2000): Intramuscular injection of analgesic substance that induced muscle pain reduced proprioceptive signals from jaw of cats.

Question 38

Lumbar multifidus wasting

Answer 38

Hides (1994): CSA measured with real time US in 26 patients with 1st episode acute unilateral LBP. Measures CSA of LM on both sides at all vertebral levels from L2 to S1. LM atrophy found at the symptomatic segment and on the side ipsilateral to the symptoms, confined predominately to that one vertebral level. Magnitude of between-side difference was 31% at level of symptoms in LBP patients (3% difference at L4 level for asymptomatics). One subject displayed asymmetry within 24 hours of injury. Likely explanation is reflex inhibition.

Question 39

Myths of core stability

Answer 39

1. Stevens (2006a): Need 70% MVC to promote strength trunk gains
2. Stevens (2006b): Unlikely abdominals reach 70% MVC during “stability training”
3. Brown and McGill (2006): Conscious attempts to co-contract specific muscles could be dangerous and decrease spine stability
4. Vera-Garcia (2006): Abdominal hollowing was most ineffective and didn’t increase stability, bracing increased spinal compression, natural strategy was superior to both and didn’t increase spinal compression excessively
5. Cholewicki (2002): Can’t control TrA alone
6. Georgopolous (2000): Muscle by muscle activation does not exist
7. Stanton (2004): Subjects who did swill ball training for core stability got very good at using muscles on SB but it had no effect on their running performance
8. Helewa (1999): Strengthening abs did no prevent LBP
9. Nadler (2002): Core strengthening didn’t decrease occurence of LBP in athletes with hip muscle imbalance and LBP
10. Cairnes (2006): No difference in pain and disability between specific stabilization exercise vs. conventional PT