SMT 1 - Outcomes with HVLAT Flashcards
Dosage for neck manipulation?
Bale and Newell (2005) did pilot study of 21 and divided patients into acute pain less than 7 weeks and chronic with pain over 7 weeks. Acute pain required 4 HVLAT treatments over 3 weeks. Chronic required 10 weeks with 31% needing 4 times, 62% needing 5-10, and 7% needing more than 10 treatments.
PPT changes after cervical HVLAT?
Fernandez-de-las-Penas (2007) did C5/C6 HVLAT, sham HVLAT, or control intervention on 3 separate days for those without symptoms and looked at PPT over lateral epicondyles. No significant change after sham or control but 35.5% increase in PPT for ipsilateral elbow and 24.8 for contralateral elbow for single C5/C6 HVLAT.
Systematic review of systematic reviews for SMT?
Ernst and Carter (2006) evaluated the evidence from 16 systematic reviews from 2000-2005 for spinal pain and non-MSK conditiosn (asthma, allergies, etc.). Concluded the effectiveness of SMT is not supported. Of 4 reviews for LBP, only 1 supported its use. 2 out of 3 reviews for headache did not find conclusive evidence in favor of SMT. The reviews for non-spinal/MSK pain were uniformly negative. All 3 of the overtly positive recommendations for LBP, neck pain, and HA came from the same chiropractor (Brontfort 2001 and 2004).
Bialosky (2009) Neurophys. - Spinal Mechanisms?
Suggested to act as counter-irritant to modulate pain (Boal and Gilette 2004). Joint based MT speculated to “bombard CNS with sensory input (Pickar and Kang 2006).” Only indirect evidence of spinal cord mediated mechanism post-MT. MT associated with hypoalgesia, afferent discharge, reduction in motor neuron pool activity, changes in muscle activity, all which indirectly implicate spinal cord mediated effect.
Boal and Gillette (2004) - Long Term Potentiation?
SMT may reverse LTP. SMT may activate small diameter, A-delta fibers, providing input to the spinal cord neurons causing spinal long term depression. These changes may occur at central/supraspinal synaptic targets, causing central supression. In vivo A-delta fiber stimulation was shown to reverse LTP previously established by c-fiber activation of the same dorsal horn neurons in rats. Acupuncture activates A-delta fibers as well and is suspected to trigger LTD. LTD is possible mechanism for anti-nociceptive effects of manual therapies. SMT serves as counter-irritant to peripheral nociceptive input received by dorsal horn cells.
Mansilla-Ferragut (2009) conclusions?
- The new position of the OA junction may have modified jaw position and hence, ROM.
- The OA manipulation may have increased cervical ROM, facilitating increase in mouth opening
* ***3. Reduction of reflex inhibition, allowing the masseter to relax and increase mouth ROM.
* Has been hypothesized that nociceptive inputs from the the upper cx segments may cause refelx contraction of masticatory muscles.
Bialosky (2009) Neurophys. - Supraspinal Mechanisms?
ACC, amygdala, PAG, RVmM are instrumental in pain experience. Groups as supraspinal descending inhibition. Direct support for supraspinal mechanism comes from Malisza (2003), who applied joint based MT to LE of rats following capsaicin injections; functional MRI of supraspinal region quantified response of hind paw to light touch after injection.
Ernst and Carter (2006) individual systematic review findings?
Assendelft (2004) most authoritative systematic review on LBP showed HVLAT/mob were superior to sham and ineffective/detrimental treatments but not other interventions. Gross (2004) most authoritative on neck pain showed HVLAT/mob only effective when combined with exercise. Bronfort (2004) both HVLAT and mob effective for neck and LBP, Bronfort (2001) HVLAT better than massage and comparable to prophylactic drugs for HA. Reid and Rivett (2005) only limited evidence from methodologically poor trials for cervicogenic dizziness.
Changes in trunk muscle thickness after lumbar HVLAT?
Koppenhaver (2011) looked at 81 students with LBP. They looked at TrA, IO, and LM muscle thickness at L4/L5 and L5/S1 with ultrasound at rest and during contralateral arm lift on day 1, 3 or 4, and 1 week. ODI used to examine relationship between change in thickness and pain/disability. Contracted TrA and IO muscle thickness decreased immediately after HVLAT but no different after day 3-4 and 1 week. LM significantly increased at days 3-4 immediately after session 2 of HVLAT but no diff. immediately after session 1 and at 1 week. TrA/IO changes were transient and unrelated to improved disability. Only statistically sig. interaction occured from baseline to day 3-4 immediately after HVLAT for LM at L5/S1 (not at L4/L5). So changes weren’t there after 1st session, only occured at L5/S1, didn’t last to 1 week, and were only present a few seconds. This change in contracted LM thickness at one-week only explained 7% of variance in ODI scores.
George 2006?
Looked at immediate hypoalgesic effects of lumbar HVLAT on thermal sensitivity before and 5 min. after in asymptomatic subjects. Subjects rated their 1st pain intensity (A-delta fiber input) with 3 second heat stimuli from 35-50 degrees Celsius. Subjects then rated their delayed second pain intensity (c-fiber) after 1st, 3rd, and 5th heat pulses less than 1 second. Subjects did either bike x5 min, 3x15 lumbar extension, or Chicago HVLAT. Press ups and SMT reduced temporal summation, suggesting SMT may reduce dorsal horn wind up and may act as counter-irritant specific to c-fiber pain perception. Inhibition of this wind-up may mean subject less likely to develop chronic LBP.
Boal and Gillette (2004) - Neuronal Plasticity?
Neuronal plasticity refers to behavior changes in dorsal horn neurons influence by previous events contributing to persistent pain states. It provides mechanisms that contribute to amplification of synaptic transmission in nociceptive circuits, leading to central neuronal elements overreacting to normal input.
Wind Up
Wind up results from constant peripheral c-fiber input and is an example of central sensitization in dorsal horn cells. This tonic activation induces central hyperalgesia at spinal cord level such that subsequent pain stimuli of standard amplitude are incorrectly relayed as increased in intensity.
Boal and Gillette (2004) - Effects on CNS?
SMT may alter afferent input to the CNS, as a result, altering reflex mechanisms and ascending/descending pain modulation. Speculated that SMT causes coactivation of large diameter A-beta, small diameter A-delta, and c-fiber mechanosensitive afferents which provides a counter-irritant.
Bialosky (2008)?
60 healthy subjects without LBP were divided into 1 of 3 groups before lumbar HVLAT: positive, negative, and neutral expectation. C-fiber pain was assessed on plantar foot using 10 heat pulses every 3 seconds and rating delayed pain from 0-100. Done to LBP too and rated 0-100 as well. Pain perception in low back was dependent on expectation (positive expectation DECREASED 7.7/100 and significant INCREASE of 6.98 in negative expectation group). C-fiber hypoalgesia occurred regardless of expectation.
Bishop (2011)?
Tested whether regional pain modulation occurs in cervical and lumbar innervated areas after thoracic HVLAT. Looked at 1st pain on volar forearm and upper calf, and second pain heat pulses on thenar eminence and medial arch. Patients randomly assigned to upper thoracic HVLAT, DNF training, or control supine position. No significant changes for PPT or 1st thermal pain in any group. For second pain the thoracic HVLAT had significant reduction, and significantly greater than any other group. Primary finding was that changes in TSS occured immediately after thoracic HVLAT in both UE and LE, subjects didn’t have neck or back pain though.
