BioMed Central (BMC) Musculoskeletal Disorders2012 13:162 Pierre Balthazard, Pierre de Goumoens, Gilles Rivier, Philippe Demeulenaere,Pierluigi Ballabeni, Olivier Dériaz KEY POINTS FROM THIS ARTICLE: The aim of this study was to assess whether manual therapy (MT) has animmediate analgesic effect, and to compare the lasting effect on functional disabilityof MT plus AE to sham therapy (ST) plus AE. This is the first controlled study toassess the efficacy of spinal manipulation/mobilization followed by specific activeexercises. 1) Recent clinical recommendations still propose active exercises (AE) for chronicnon-specific low back pain (CNSLBP). 2) Current evidences suggest that manual therapy (MT) induces an immediateanalgesic effect through neurophysiologic mechanisms at peripheral, spinal andcortical levels. [Key Point] 3) Randomization: Patients in this study selection were aged 20 to 65 years with non-specific low backpain with or without leg symptoms, for a period between 12 and 26 weeks. Theyhad no radiologic abnormalities other than degenerative disease.22 patients were assigned to manual therapy plus active exercise.20 patients were assigned to sham therapy (dysfunctional ultrasound) plus activeexercise. Active exercise was started in the clinical setting and was eventually performed at home.Eight therapeutic sessions were delivered over 4 to 8 weeks.Patients were evaluated at each session, before and after treatment, at week 8 andagain at 3 and 6 months using standard measurement outcomes, which included: * Visual Analogue Scale (VAS) for pain intensity * Oswestry Disability Index (ODI) for disability 4) MT intervention induced a better immediate analgesic effect. 5) MT + AE induced lower disability (-7.1, ODI) and lower pain (-1.2, VAS). 6) This study confirmed the immediate analgesic effect of MT over ST. Followedby specific active exercises, it reduces significantly functional disability and tends toinduce a larger decrease in pain intensity, compared to a control group. 7) These results confirm the clinical relevance of MT as an appropriatetreatment for CNSLBP. 8) These authors propose that CNSLBP and its clinical presentations andmanifestations may be linked to alterations in neuro-cortical function. Theneurophysiologic mechanisms at cortical level should be investigated morethoroughly for MT. [Key Point] 9) Randomized controlled trials reported that manual therapy is more effectiveon physical function, mental health, physical disability and/or pain than nointervention, sham manipulation, light exercises or general active exercises. 10) Manual therapy may interfere with the neuromuscular, autonomic andendocrine responses, produce a placebo effect and/or alter the patientspsychological state. [Key Point] 11) The manual therapy consisted of: A)) Passive intervertebral movements with postero-anterior pressure applied onpainful or stiffed vertebral segment(s) with the patient lying prone. AND/OR B)) A muscle-energy technique using a hold-relaxed technique on an iliumdysfunction with the patient side lying. AND/OR C)) High velocity, low amplitude rotational-lateral flexion dynamic thrust(manipulation) performed on a stiffed vertebral segment(s) with the patient sidelying. 12) The active exercise consisted of: A)) Educational information on low back anatomy and biomechanics and ways toprotect the spine during activities of daily. B)) 2 home mobility exercises (supine pelvic tilt and low back lateral flexion), tobe performed twice a day, 2 sets of 10 repetitions. C)) After the 3rd or 4th session, the recommendation of home exercises changesto stretching and motor control exercises. D)) Mobility exercises during the 8 therapeutic sessions to improve patientsspinal range of motion. E)) Passive stretching exercises for the spine, hamstring, iliopsoas, rectusfemoris, and piriformis. F)) Strengthening exercises for weak superficial trunk muscles. 13) For MT/ST intervention, the immediate effect of intervention was in favor ofmanual therapy over detuned ultrasound, with a greater decrease in pain level. 14) The main original result of this study is that manual therapy, immediatelyfollowed by active exercise, accelerates reduced disability in CNSLBP patients. 15) The analgesic effect of MT combined with exercises can be efficient todecrease pain for CNSLBP. The analgesic effect of manual therapy (i.e., theimmediate effect) may allow the patient to perform better/more accurate activeexercises. 16) The present study confirms the immediate analgesic effect of manual therapyfor CNSLBP. Followed by specific active exercises, it significantly reduces functionaldisability and tends to induce a larger decrease in pain intensity, compared to acontrol group. 17) CNSLBP is largely characterized by structural, functional and neurochemicalcortical modifications. [Key Point] 18) Improving the knowledge of the precise neurophysiologic mechanisms ofmanual therapy at cortical level seems essential in order to validate the choice ofthis therapy for CNSLBP. 19) For CNSLBP, the use of spinal manipulation/mobilization is favorablyrecommended. COMMENTS FROM DAN MURPHY Since both manual therapy and sham therapy (dysfunctional ultrasound) were bothfollowed with active exercise, the clear conclusion for CNSLBP treatment is: 1) Manual therapy is a lot better than sham therapy. 2) Manual therapy is a lot better than exercise (since the same exercises wereperformed by the sham dysfunctional ultrasound group). Importantly, these authors contend that CNSLBP involves alterations in neurocorticalfunction, and that manual therapy can improve this neuro-cortical function. Importantly, these authors acknowledge that manual therapy affects autonomicand endocrine responses, a key point for chiropractors.

Peter Schmidt, MD; Thomas E. Mayer, MD; Robert Drescher, MD, MAFrom the Department of Neuroradiology, Institute of Radiology, University HospitalJena, Jena, Germany The purpose of this study was to evaluate the normal anatomical variability of thealar ligaments in asymptomatic individuals with 3-T magnetic resonance imaging(MRI) and to compare the findings with standard 1.5-T examinations. Thirty-sixparticipants underwent 3-T and 1.5-T MRIs. Alar ligament MRI findings wereanalyzed with regard to the features detectability, signal intensity compared with muscle tissue, homogeneity, shape, spatial orientation, and symmetry.Evaluated images were coronal T2-weighted MRI with a slice thickness, 0.8 mm. KEY POINTS FROM THIS STUDY: 1) Rupture of the alar and transverse ligaments due to whiplash injury can leadto upper cervical spine instability and subsequent neurological deterioration. 2) Delineation of the alar ligaments was significantly better on 3-T images. 3) This study demonstrates that high-field 3-T MRI provides better visualizationof the alar ligaments compared with 1.5-T MRI. The higher signal-to-noise ratioallows detection of small signal changes. 4) Approximately 25% of whiplash-injured patients experience prolongedmorbidity, with little prospect of complete resolution of pain and other symptoms. 5) 24-70% of whiplash-injured patients suffer from long-term symptoms. 6) Up to 16% [of whiplash-injured patients] remain severely impaired manyyears after the accident, which interferes with their activities of daily living. 7) The alar ligaments are considered an important ligamentous craniocervicalstructure for the integrity and stability of the craniocervical junction. Due to the lackof a disk and the horizontal nature of the facet joints, the stability of theatlantoaxial joint depends mainly on ligaments and muscles. 8) The most important function of the alar ligaments is the limitation of axialrotation, and they are most vulnerable when the head is rotated and flexed. 9) Magnetic resonance imaging (MRI) is the modality of choice to visualizeanatomy and pathology of the alar ligaments because of its high tissue contrast andmultiplanar imaging capability. 10) 9.7% of the alar ligaments were difficult to detect on 3-T MRI compared with55.6% on 1.5-T MRI. 11) This study demonstrates that reliable assessment of alar ligaments by meansof MRI can be achieved and that high-field 3-T MRI provides better visualization ofthe alar ligaments compared with 1.5-T MRI. 12) A 2009 study reported that high signal changes of the alar and transverseligaments are common in whiplash-associated disorders and unlikely to representage-dependent degeneration. 13) These authors note that the studies that claim there is no significance to alarligament signal abnormality and chronic whiplash symptoms were performed on a1.5-T MRI. They suggest that the findings and conclusion would most likely bedifferent had the authors used a 3.0-T MRI unit. 14) Alar ligament imaging is difficult because of their subtle structures andvariable orientation. T2 contrast is helpful to differentiate the ligamentousstructures of the spine from surrounding fatty tissue and muscles, as well as fromcerebrospinal fluid. 15) The higher signal-to-noise ratio of 3-T MRI compared with 1.5-T MRI allowsfor the detection of small signal changes of a ligament, which at 1.5 T will likely notovercome the noise threshold. [Key Point] 16) High-field 3-T MRI is a valuable diagnostic tool for imaging of the alarligaments because of its excellent delineation of these ligaments compared withstandard 1.5-T MRI. 17) High-field 3-T MRI increases the reliability and accuracy of alar ligamentlesion classification. COMMENTS FROM DAN MURPHY: Alar ligament integrity is of critical importance to both upper cervical chiropractorsand to chiropractors managing whiplash injuries. A number of studies we havereviewed indicate that: 1) Alar ligaments are specifically injured in motor vehicle collisions. 2) Injured alar ligaments are primarily responsible for chronic whiplashsymptoms, especially post-traumatic headaches. This study clearly points out that 3.0-T MRI has more diagnostic accuracy than dothe standard 1.5-T MRI units.

Paul D. Giles, DO, MS, Kendi L. Hensel, DO, PhD, Christina F. Pacchia, PhD, MichaelL. Smith, PhD: From the Department of Integrative Physiology, University of NorthTexas Health Science Center. BACKGROUND FROM DAN MURPHY: Heart rate variability (HRV) is the variation in the time interval between heartbeats.It is largely under the control of the autonomic nervous system.The parasympathetic influence lengthens HRV via the release of acetylcholine bythe vagus nerve (slowing the heart rate).The sympathetic influence shortens HRV via the release of epinephrine andnorepinephrine (accelerating the heart rate). Vagal and sympathetic nerve activity constantly interact; under resting conditions,vagal tone prevails. KEY POINTS FROM THIS STUDY: 1) Osteopathic manipulative treatment (OMT) focusing on the upper cervicalspine is theorized to affect the function of the vagus nerve and thereby influencethe parasympathetic branch of the autonomic nervous system. 2) This study was designed to determine the acute effect of upper cervical spinemanipulation on cardiac autonomic control as measured by heart rate variability. Itused 19 healthy, young adult subjects underwent cervical osteopathic manipulationand sham manipulation. Six minutes of electrocardiographic data were collectedbefore and after each intervention, and heart rate variability was assessed. 3) Study exclusion factors included:hypertension, caffeine consumption within 4 hours, tobacco use within 48 hours,history of cardiovascular disease, neuropathic disorders, unexplained episodes ofsyncope, and any musculoskeletal signs/symptoms. 4) The anatomical relationship of the efferent vagus nerve to the musculoskeletal structures at the occiput lends credence to the hypothesis thatosteopathic manipulative treatment at this location, such as suboccipitaldecompression, could affect vagal functions. 5) Previous studies have shown that manual therapies can affect vagal function. 6) Cervical manipulation may have direct effects on the parasympatheticnervous system. 7) Decompression of the occipito-atlantal junction, a technique that focuses ontreating an articular compression between the occiput and the atlas, may improveconditions relating to the path of the vagus as it exits the skull. 8) Because of the proximity of the vagus to the musculoskeletal structures inthe suboccipital region, it is plausible that local inflammation, edema, musclehypertonicity or spasm, or other somatic dysfunctions could cause either a chemicalor compressive effect on the vagus, thereby affecting its optimum function. 9) Since the vagus plays a significant role in the autonomic control of heartrate, it is therefore also plausible that if optimum performance of the vagus isimpeded by dysfunction in the surrounding structures, its ability to contributeeffectively to the autonomic control of heart rate might also be affected. 10) The manipulation protocol involved the treatment of the subjects posteriorcervical musculature by using kneading and stretching. The kneading force wasapplied perpendicular to the long axis of the muscle. The stretching was aseparation of the origin and insertion of a muscle. This soft tissue treatment wasperformed for about 5 minutes. Then occipital-atlas decompression was applied for 2 – 3 minutes by using the index fingers to contact the occiput as near to theoccipital condyles. The sham treatment placed the fingers near the occipitalcondyles, but no tension was applied in any direction, for about 8 minutes. 11) Heart rate variability is used to assess changes in autonomic control of heartrate under a variety of conditions including with manual therapies. Heart ratevariability was measured as an index of autonomic control. 12) The changes in the frequency domain indices of heart rate variability wereconsistent with an enhanced parasympathetic control associated with the OMTtreatment. 13) These data demonstrate that suboccipital decompression, a soft tissuemanipulative technique, can affect indices of heart rate variability. 14) Many forms of manipulative medicine have been theorized to affect theautonomic nervous system, and it has been espoused that this can include bothstimulatory and inhibitory effects on the respective branches of the autonomicnervous system. 15) The data in our study consistently point to an effect of suboccipitaldecompression to moderately enhance parasympathetic control of heart rate and/orshift the sympatho-vagal balance to a more predominant vagal control. These 3effects were associated with a slowing of heart rate accompanying suboccipital decompression. 16) This study shows changes in the heart rate variability indices relating to areduced sympathetic and enhanced parasympathetic control. [Key Point] 17) The suboccipital decompression used in this study caused significant changesconsistent with an enhanced parasympathetic control of heart rate. 18) This study demonstrates that suboccipital manipulative decompression canaffect heart rate variability. This effect is consistent with potential changes in thecontrol of heart by the parasympathetic nervous system. These data support the hypothesis that upper cervical spine manipulation can acutely affect measures ofheart rate variability in healthy individuals. COMMENTS FROM DAN MURPHY The bottom-line conclusion of this study is that upper cervical spine mechanicalfunction is influenced by upper cervical spine manipulation, which in turn influencesthe vagus parasympathetic control of the heart.These authors suggest that the mechanism whereby upper cervical spinalmanipulation influences the vagus nerve and therefore the balance ofparasympathetic and sympathetic control of the heart is mechanical.We have reviewed 2 other articles with the same conclusions (upper cervical spinemechanical function is influenced by upper cervical spine manipulation, which inturn influences the vagus parasympathetic control of the heart), but with a differentmechanism. Their mechanism is that upper cervical spine mechanoreceptorsneurologically fire to the medullary Nucleus Intermedius which then fires to theNucleus Tractus Solitarius (a sensory nucleus of the vagus nerve in the medulla),which in turn influences cardiorespiratory function. Interestingly, both studies favorably mention chiropractic upper cervical adjusting to influence blood pressure: Article Review #13-08 The Neurochemically Diverse Intermedius Nucleus of the Medulla as a Source ofExcitatory and Inhibitory Synaptic Input to the Nucleus Tractus SolitariiThe Journal of Neuroscience; August 1, 2007; 27(31); pp. 8324-8333.Ian J. Edwards, Mark L. Dallas, Sarah L. Poole, Carol J. Milligan, Yuchio Yanagawa,Gabor Szabo, Ferenc Erdelyi, Susan A. Deuchars, and Jim Deuchars Article Review #3-11: The intermedius nucleus of the medulla: A potential site for the integration ofcervical information and the generation of autonomic responses.Journal of Chemical Neuroanatomy; November 2009, 38, pp. 166 – 175.Ian J. Edwards, Susan A. Deuchars, Jim Deuchars

Journal of Neurotrauma January 30, 2013 [ebub] Hasadsri L MD; Wang BH, MD;, PhD; Wang BH MD; Lee JV PhD; Erdman JW PhD;Llano DA MD, PhD; Wszalek T PhD; Sharrock MF BSc First author is from the Department of Neurosurgery, University of Illinois College ofMedicine. This article has 190 references KEY POINTS FROM THIS ARTICLE: 1) Traumatic Brain Injury (TBI) is a global public health epidemic. 2) In the US more than 3 million people sustain a TBI annually. 3) TBI may cause motor and sensory deficits and lead to severe cognitive,emotional, and psychosocial impairment, crippling vital areas of higher functioning. 4) TBI is the signature injury in wounded soldiers in Iraq and Afghanistan. 5) TBI may have a devastating impact on athletes playing contact sports. 6) There has been little progress in developing effective TBI interventions. 7) Nutritional intervention may provide a unique opportunity to enhance theneuronal repair process after TBI. 8) The two omega-3 fatty acids that are most promising for their neurorestorativecapacities in TBI are docosahexaenoic acid (DHA) and eicosapentaenoicacid (EPA). 9) Chronic repetitive sub-concussive head impacts may also result incumulative long-term deleterious effects. 10) Long-term health disorders associated with TBI include: A)) Post-traumatic stress disorder (PTSD) B)) Neurodegenerative diseases (Alzheimer’s disease or Parkinsonism) C)) Neurocognitive deficits D)) Psychosocial health problems (e.g., binge drinking, major depression,impairment of social functioning and ability to work, suicide) E)) Epilepsy F)) Pain G)) Other alterations in personality or behavior 11) Nutritional intervention, such as supplementation with n-3 (also known asomega-3) fatty acids, may be of therapeutic benefit in acute injury to the brain. 12) Omega-3 fatty acids have long been known to play a restorative role inseveral pathways implicated in traumatic insult to the brain. 13) Case studies show great benefit on the use of omega-3s in the acute phase ofsevere head injury. 14) N-3 polyunsaturated fatty acids (PUFAs) are uniquely protective againstdegeneration induced by TBI, and they improve behavioral and cognitive outcomesin patients with TBI. 15) The most important n-3 fatty acids for human health and nutrition aredocosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and alpha-linolenic acid(ALA). 16) Humans can convert a limited amount of ALA into EPA and DHA, butsynthesis of EPA and especially DHA from ALA is insufficient to supplant dietaryintake. [Important, especially for strict vegetarians] 17) DHA comprises more than 50% of brain neuronal membrane phospholipids. 18) Omega-3 fatty acids, especially DHA, are essential for maintaining membranefluidity. DHA is tremendously flexible allowing it to under go rapid interconversionsbetween multiple torsional states, and to readily undergo complex yet minimal energy-requiring conformational changes. [Fluidity] 19) During neuronal stress, both EPA and DHA are released from membranephospholipids and converted into compounds called resolvins, which resolveinflammatory processes, protect against oxidative stress, and maintain synapticintegrity. [Resolvins] 20) In the brain, omega-3s, especially DHA: A)) Increased the size of neurons B)) Increases the complexity of dendritic arboritizations C)) Increased the number of neurons D)) Increases serotonin and acetylcholine receptors E)) Improved attention, task performance, learning, and memory F)) Improves dopamine neurotransmission increases dopamine receptors, whichimproves motivational behavior and emotional functions 21) DHA is neuroprotective, and supplementation significantly amelioratessecondary mechanisms of injury and reduces the number of damaged axons. 22) Supplementation with n-3 fatty acids significantly decrease the productionof reactive oxygen species (ROS) and improve cognitive function. 23) DHA has an essential role in nervous system development and are requiredfor proper synaptogenesis, neural membrane synthesis, and the building offunctionally critical circuits within the brain. 24) DHA deficiency is associated with aging and neurodegenerative conditionssuch as Alzheimers disease, while DHA consumption has been shown to improveperformance on visuospatial learning and memory tasks in patients with age-relatedcognitive decline. 25) Dietary supplementation with omega-3 fatty acids improves functionalrecovery in subarachnoid hemorrhage and stroke. 26) Omega-3 fatty acids in the brain appear be neuroprotective in TBI becausethey protect against inflammation, apoptosis, and oxidative stress mechanisms. 27) TBI causes diffuse axonal destruction, demyelination, and neuronal cell death.This is followed by a secondary wave of disruption in the subsequent hours anddays due to inflammatory responses, excitotoxicity, and oxidative stress. 28) Omega-3 fatty acids mitigate the consequences of several key pathologicalpathways in TBI, such as mitochondrial malfunction, apoptotic cell death,glutamate-triggered excitotoxicity, and injury-induced oxidative stress andinflammation. 29) Omega-3 fatty acids may play a critical role in the restoration of cellularenergetics and repair of neuronal damage after TBI. 30) The production of pro-inflammatory prostaglandins is stimulated by andderived from the release of arachidonic acid (AA) secondary to disruption ofneuronal cell membranes. Arachidonic acid is rapidly converted into potentinflammatory mediators such as prostaglandins and leukotrienes. 31) DHA functions in a neuroprotective capacity, antagonizing the pro-deathsignaling pathways initially triggered by AA. 32) The release of the excitotoxic neurotransmitter glutamate is a destructiveevent following acute traumatic injury in the brain. Excess glutamate causesoveractivation of N-methyl d-aspartate (NMDA) and calcium-permeable AMPAreceptors, leading to a massive influx of Ca++ and the induction of bothprogrammed and necrotic cell death via calcium-dependent proteases. DHA: A)) Reduces glutamate excitotoxicity B)) Downregulates the expression of AMPA receptor subunits C)) Decreases Ca++ influx into the neuron 33) The most detrimental consequence of excess intracellular Ca++ is increasedoxidative stress, a key contributor to the pathophysiologic changes that occur afterTBI. 34) The influx of excess Ca++ into mitochondria increases ROS formation,damaging DNA and proteins, inducing programmed cell death. 35) ROS causes lipid peroxidation on a catastrophic scale, further disruptingneuronal membrane integrity and function. 36) The antioxidant defense mechanisms are relatively scarce in the human brain. 37) Traumatic disruptions in cerebral blood flow causes ATP energy depletion andcollapse of energy-dependent ion transport and active pumps, allowing intracellularCa++ overload. 38) Brain oxidative stress causes inflammation and additional microvasculardamage, secondary ischemia, and neuronal cell death. 39) The sex steroid progesterone reduces cerebral edema and has neuroprotective effects. 40) Multiple clinical trials have shown that high-dose fish oil consumption is safeeven in patients receiving other agents that may increase the risk of bleeding, suchas aspirin and warfarin. 41) DHA at doses up to 6g/d does not have deleterious effects on plateletaggregation or other clotting parameters in normal individuals, and fish oil does notaugment aspirin-induced inhibition of blood clotting. 42) It may be prudent to discontinue high-dose omega-3 supplementation in thesetting of an acute bleeding illness or in patients at high risk for hemorrhagicstroke. 43) PUFAs have high susceptibility to lipid peroxidation which may have apotential carcinogenic role.[This is why I advocate taking antioxidant co-factors] 44) High intake of fish may increase the risk of exposure to environmental toxinsand contaminants such as mercury and polychlorinated biphenyls; purified fish oilsare much safer. 45) Omega-3 fatty acids restore cellular energetics, reduce oxidative stress andinflammation, repair cellular damage, and mitigate the activation of apoptoticprocesses after TBI.