Irish Journal of Medical Science 2020 (May); 189 (2): 543–550 ~ FULL TEXT
Daryoush Didehdar, Fahimeh Kamali, Amin Kordi Yoosefinejad, Mehrzad Lotfi
Department of Physical Therapy,
School of Rehabilitation Sciences,
Shiraz University of Medical Sciences,
BACKGROUND: In patients with chronic nonspecific low back pain (NCLBP), brain function changes due to the neuroplastic changes in different regions.
AIM: The current study aimed to evaluate the brain metabolite changes after spinal manipulation, using proton magnetic resonance spectroscopy (1H-MRS).
METHODS: In the current study, 25 patients with NCLBP aged 20-50 years were enrolled. Patients were randomly assigned to lumbopelvic manipulation or sham. Patients were evaluated before and 5 weeks after treatment by the Numerical Rating Scale (NRS), the Oswestry Disability Index (ODI), and 1H-MRS.
RESULTS: After treatment, severity of pain and functional disability were significantly reduced in the treatment group vs. sham group (p < 0.05). After treatment, N-acetyl aspartate (NAA) in thalamus, insula, dorsolateral prefrontal cortex (DLPFC) regions, as well as choline (Cho) in the thalamus, insula, and somatosensory cortex (SSC) regions, had increased significantly in the treatment group compared with the sham group (p < 0.05). A significant increase was further observed in NAA in thalamus, anterior cingulate cortex (ACC), and SCC regions along with Cho metabolite in thalamus and SCC regions after treatment in the treatment group compared with the baseline measures (p < 0.05). Also, a significant increase was observed in Glx (glutamate and glutamine) levels of thalamus (p = 0.03). There was no significant difference in terms of brain metabolites at baseline and after treatment in the sham group.
CONCLUSION: In the patient with low back pain, spinal manipulation affects the central nervous system and changes the brain metabolites. Consequently, pain and functional disability are reduced.
1H-MRS; Low back pain; Spinal manipulation
From the Full-Text Article:
Nonspecific chronic low back pain (NCLBP) is common disease
in the lumbar area without any neurologic signs and
specific reasons.  NCLBP accounts for 90% of the chronic
low back pain (CLBP) cases. [2, 3] This disorder, which is
associated with pain and disability, negatively affects the patient’s
quality of life, productivity, and occupation. [2, 4] In
chronic pains, after recovering from the early damage, pain is
still perceived, demonstrating the role of changes in the function
of the central nervous system(CNS).  According to the
Tracey theory, pain is transformed from acute to chronic due
to hypersensitivity of pain-processing network in CNS. 
Hardy (1950) stated that chronic pain and hyperalgesia occurred
following the initial damage due to increased CNS
activity and its sensitization.  Therefore, chronic pain and
prolonged sensory impairment following an injury is owing to
the increased CNS excitability involving pain or sensitization. [5, 7] In addition, studies have shown that CLBP causes central
sensitization [8, 9], and patients with CLBP are hypersensitive
to painful stimuli due to neuroplastic changes. 
However, in patients with NCLBP, following a physical
activity, the blood flow increases in regions associated with
pain matrix (SSC, insula, and frontal cortex) Moreover, in
NCLBP patients compared with healthy individuals, neurochemical
metabolites decrease in the DLPFC, thalamus, and
orbitofrontal cortex. [2, 11–15]
To treat and resolve issues associated with NCLBP, medical
treatments and physiotherapy are recommended. Their
purpose is to reduce pain and disability caused by NCLBP. [10, 16, 17] Spinal manipulation is a successful, cost-effective,
and non-invasive treatment for NCLBP. [16, 18]
Researches have confirmed the effect of manipulation on
function improvement and pain reduction in patients with
NCLBP. [19, 20] The neurophysiological mechanism of manipulation
refers to the ability of the central nervous system to
modulate sensory information. 
To evaluate the effect of spinal manipulation on patients’
brain with NCLBP, modern imaging techniques, such as functional
magnetic resonance imaging (fMRI), transcranial magnetic
stimulation (TMS), and 1H-MRS, are used.  1H-MRS
is a non-invasive technique that measures the level of
metabolites such as glutamate, glutamine, N-acetyl aspartate
(NAA), creatine (Cr), myo-inositol, and choline (Cho) in the
living human brain.  The NAA metabolite is synthesized
in neurons and reflects the density of the neurons, and its
reduction indicates the loss of the neuronal function. 
Cho metabolite represents the health of neuron membranes,
and its changes reflect upon the nervous system impairment.  Glutamate and glutamine (Glx) is the main excitatory
neurotransmitter of the brain, binding to both ionotropic and
metabotropic receptors that play an important role in pain. 
Studies have indicated neurometabolite changes in different
regions of the brain (related to pain matrix area) in
patients with chronic low back pain. [13, 15, 22, 25, 26]
Certain studies suggest that neurobiological changes play important
roles in the manifestation of chronic pain and its treatment. [13, 15, 22, 25–27]
There is limited knowledge about the neurobiological
changes in pain-processing regions associated with chronic
pain following manipulation therapy; accordingly, the aim of
this study was to determine the effect of spinal manipulation
therapy on the neurometabolites of the brain and neurochemical
changes in neuronal surfaces using the 1H-MRS technique
as a precise, reliable , and preferred method in patients
with NCLBP. We hypothesized that the brain metabolite
change after treatment by the spinal manipulation.
Materials and methods
The current randomized, double-blind, clinical trial study
(IRCT20150923024149N15) was conducted on patients
randomly divided into treatment and sham groups (Figure 1) (Consort follow chart).
Written informed consent was obtained from all the
After public advertisement, 85 patients with low back pain,
referring to clinics affiliated or non-affiliated to Shiraz
University of Medical Sciences, were selected by simple sampling
method. Out of 85 patients, 60 were excluded since they
did not meet the inclusion criteria. Twenty-five patients were
randomly assigned to either treatment (n = 10, six males and
four females) or sham (n = 15, eight males and seven females)
based on block randomization method (each block was 5)
(Fig. 1). Patients and the examiner were blind to the group
Following the approval of the study protocol by the local
Ethics Committee of Shiraz University of Medical Sciences
(IR.SUMS.REC.1396.139), patients with NCLBP aged 20–
50 years were enrolled based on the following inclusion
criteria: pain intensity ranging from 3 to 7 units based on the
Numerical Rating Scale (NRS), and those who were not treated
within the last 3 months. [29, 30] Exclusion criteria were
patients diagnosed with neurologic, rheumatoid, or diabetic
disorders; the ones with fractures of the ribs, vertebras, and
pelvis, abdominal aortic aneurysm, neoplasm, peripheral neuropathy
and radiculopathy, osteoporosis, fibromyalgia, pain in
other areas of the body, three or more positive results of clinical
tests on the sacroiliac joint (distraction, compression,
thigh thrust, Gaenslen’s sign, FABER, and sacral thrust tests),
and surgical history in lumbopelvic region; and those who
The sample size was set to eight subjects in each group
based on previous studies as well as NAA and Glx metabolite
level in the brain, considering d = 0.06, α = 0.05, and β = 0.2. [22, 26] Given the possibility of withdrawal and 20% rejection
rate, 10 subjects were enrolled in the treatment group,
while with 45%possibility of rejection rate in the sham group,
15 subjects were recruited.
Patients in the treatment group received three sessions (every
other day) of spinal lumbar and sacroiliac joint manipulation
while those in the shamgroup underwent three sessions (every
other day) of positioning similar to that of the manipulation
therapy on lumbar and sacroiliac joint without applying the
Sacroiliac joint manipulation:
Patient is placed in a supine
position on a treatment table, while the therapist is on the
opposite side of the joint to be manipulated. While the patient
interlocks their fingers behind their head, the therapist turns
the patient’s upper trunk toward himself. He further puts another
hand on the anterior superior iliac spine (ASIS) of the
patient, which is far away from him and applies a highvelocity
low-amplitude thrust, while the maximal rotation of
the upper trunk is obtained (Figure 2b).
Manipulation of the lumbar spine:
Patient is placed in a
lateral position on the treatment table, while the therapist
stands in front. The therapist bends the patient upper
leg and places the patient’s ankle on the popliteal
region of the lower leg. Then, the therapist takes the
lower arm and shoulder of the patient and pulls it forward
to make the upper side of the trunk rotate and
bend. Next, the therapist puts one hand on the upper
and anterior part of the patient’s chest while his other
hand is on the patient pelvis to maintain patient’s position.
In this situation, the therapist applies a highvelocity
low-amplitude thrust to the patient’s pelvis in
an anterior direction (Fig. 2a).
Demographic information including age, gender, weight,
and height of the patients was recorded. Before starting
the treatment course, both groups were asked not to use
any medication and treatment during the study. To draw a
comparison, the level of NAA metabolites in the brain
(primary outcome measure), functional disability, and pain
intensity (secondary outcome measure) was measured at
baseline and 5 weeks post-treatment, since brain changes
require more than 5 weeks. 
The NRS with a scoring scale of 0 to 10 was used to determine
pain intensity, with 10 and 0 representing maximum and no
pain, respectively. A 2-unit reduction in pain based on the
NRS was considered as minimally clinical important difference (MCID). 
The Persian version of the Oswestry Low Back Pain
Disability Questionnaire (ODI) was used to examine the patients’
functional disability.  This questionnaire has 10
items scoring from 0 to 5; the maximum disability score is
50, and the values are expressed as percentage. This questionnaire
is reliable for the evaluation of post-treatment clinical
changes in patients with CLBP; a 10% reduction in the reported
score is considered as MCID. 
Measure of brain metabolites
To recordMRS, we employed a single-voxel 1.5-T MRI scanner
(Magnetron Avanto TIM, version B19, Siemens,
Germany), using a point-resolved spectroscopy (PRESS)
technique with pulse sequence (TE, 30 ms; TR, 1500 ms).
Magnetic field homogeneity was optimized for the selected
spectroscopy volume by manual shimming. The resulting
peak width of water at half-maximum was 9 Hz for all voxels.
The voxel 10 × 22 × 14 mm was used to define the anterior
cingulate cortex (ACC) (Figure 3a), the voxel 21 × 17 × 18 mm
to define the left DLPFC (Fig. 3b), the voxel 10 × 22 × 14 mm
to define the left-insular cortex (Fig. 3c), the voxel 10 × 15 ×
14 mm to define the left primary somatosensory cortex
(Fig. 3d), and the voxel 10 × 20 × 13 mm to define the left
thalamus (Fig. 3f). Accordingly, the levels of NAA, Cho, Cr
metabolites, and Glx (glutamate and glutamine) were measured
and compared with the level of Cr as the internal standard
(Fig. 3g). 
Data are analyzed via the SPSS version 23 software, using
non-parametric Mann-Whitney tests to compare the mean difference
between the two groups and the Wilcoxon test to
compare the mean before and after the treatment in each
group. Data are expressed as mean and standard deviation
(SD). p values of < 0.05 were considered statistically
Twenty-five patients were randomly assigned to treatment and
sham groups. During the study, two patients in the sham group
were excluded due to usage of analgesics. At baseline (before
intervention) and 5 weeks following treatment, data related to
pain, functional disability, and brain neurometabolite were
recorded and analyzed (Fig. 1). There was no significant
difference between the groups at baseline regarding demographic
characteristics (Table 1).
Pain and functional disability
According to Table 2, there was no significant difference in
NRS and ODI between the groups at baseline; 5 weeks after
the treatment, the difference became significant and more than
MCID. Moreover, 5 weeks after the treatment, the NRS and
ODI of the treatment group were reduced by 3.6 and 16 units,
respectively (which is more than MCID), while there was no
MCID difference in the sham group (Table 2).
At baseline, the NAA level in the ACC region of the treatment
group (1.36 ± 0.23) was significantly lower than that of the
sham group (1.56 ± 0.23), but no significant difference was
observed among other regions of the brain in terms of metabolites
(Figure 4a). Five weeks after the treatment, the NAA metabolite
increased in the ACC region of the treatment group
(1.54 ± 0.27), with significant mean difference between the
two groups (p = 0.04) (Figure 4b). In addition, 5 weeks after
the treatment, the NAA metabolite in the thalamus, insula,
and DLPFC, and Cho metabolite in thalamus, insula, and
SSC were significantly higher in the treatment group than in
the sham group (Fig. 4b).
In the treatment group, NAA metabolite significantly increased
in the thalamus, ACC, and SSC and Chometabolite in
thalamus and SSC regions 5 weeks after the treatment compared
with the baseline measures (Fig. 4c). Furthermore, in the
treatment group, Glx metabolite in thalamus significantly increased
following the treatment compared with the baseline
measures (Fig. 4c). The metabolites of the brain in the sham
group did not undergo a significant change before and 5 weeks
after the treatment (Fig. 4d).
The results of this study demonstrated that in patients with
NCLBP, 5 weeks after lumbopelvic manipulation, pain and
functional disability were reduced significantly and clinically.
Moreover, a significant increase of metabolite concentrations
was observed (1) 5 weeks after the treatment for the case
group and (2) between groups, mostly after the intervention.
In chronic pain, neurophysiologic and brain metabolite
changes are an indication of neuroplasticity in CNS [5, 7, 34–36]. Additionally, chronic pain is the result of increased
irritability of CNS involved in pain or sensitization. [5, 7]
Furthermore, in patients with NCLBP, blood flow increases
during physical activity in regions associated with pain matrix
(somatosensory cortex, insula, and frontal lobe of the cortex).  Studies have further demonstrated that the level of neurochemical
metabolites (NAA, Glx, and Cho) was decreased
in DLPFC, thalamus, and orbitofrontal cortex in patients with
NCLBP compared with healthy people. [2, 11–15]
The neurophysiologic mechanism of the manipulation is
the result of the CNS’s ability to modulate sensory information
[21, 37]. Sensory afferents from the receptors of the tissue
surrounding the vertebrae are activated by spinal manipulation,
affecting the transmission of painful signals and motor
function from the spinal cord to the cerebral cortex. [21, 37]
Studies have evaluated the effect of spinalmanipulation on the
brain pain matrix regions of patients with low back pain by
fMRI, showing that functional activity in these regions increased
following the spinal manipulation. [38, 39] Murphy
and Hawick Taylor (2007) reported that cortical processing
after manipulation improved function and reduced pain. 
Gussew et al. (2011) examined areas associated with pain
matrix (i.e., thalamus, insula, and ACC) in patients with low
back pain and reported that reduced levels of Glx indicated
impaired glutamatergic neurotransmission due to prolonged
pain perception, while decreased NAA and Cho levels
reflected the impaired function of glial cells and neurons. 
The results of this study showed that following spinal
manipulation in the treatment group, NAA was significantly
elevated in thalamus, ACC, and SSC, as well as Cho in thalamus
and SSC compared with the baseline measures. In addition,
in the treatment group, Glx significantly increased in
thalamus following spinal manipulation treatment compared
with the baseline level, which was associated with decreased
pain and disability. In general, spinal column dysfunction affects
CNS and changes the afferents put into CNS, causing
CNS plasticity following injury and pain.  Furthermore,
spinal manipulation can alter CNS processing and sensorymotor
integration; therefore, neuroplastic changes reflect a
mechanism to reduce pain and improve functional ability after
spinal manipulation. 
Studies have shown that spinal manipulation in patients
with CLBP reduces pain and improves functional ability during
a 3-to-6-month follow-up. [42–44] Additionally, in patients
with NCLBP, lumbopelvic manipulation decreased pain
and improved function with 1 to 6 months of follow-up, similar
to the results obtained from other therapeutic methods,
such as exercise therapy and physiotherapy. [10, 16, 17] The
current study results are in line with the aforementioned studies,
stating that in the treatment group, pain was reduced and
functional disability was ameliorated 5 weeks after
lumbopelvic manipulation compared with the baseline measures.
Pain relief and improved functional disability are associated
with improvement in the neurometabolites of the brain,
demonstrating the impact of spinal manipulation on the brain,
and accordingly, pain relief and disability reduction.
The current study was the first to investigate the metabolites
of the brain following lumbopelvic manipulation in patients
with Nonspecific chronic low back pain (NCLBP). The limitations of the current study were
its high cost, being time-consuming, and 1.5-T magnetic field
strength MRI. It is suggested that 3-T MRI be employed in
future studies to measure glutamine and glutamate levels separately.
Furthermore, another limitation is that we did not record
psychosocial information to evaluate its relationship to
changes of metabolites and pain. It is further recommended
that the effect of other treatments (thermal therapy, physical
therapy, exercise therapy, acupuncture) with spinal manipulation
be evaluated on CNS by the 1H-MRS technique in patients
with nonspecific chronic low back pain (NCLBP).
Spinal manipulation with effect on CNS leads to change and
increase metabolite concentrations in specific brain regions,
thereby, relieving pain and disability following chronic low
This article was extracted from the Physiotherapy Ph.D. thesis (1396-01-06-14881) from Shiraz University of Medical Sciences. The authors wish to thank Mr. H. Argasi at the Research Consultation Center (RCC) of Shiraz University of Medical Sciences for his invaluable assistance in editing this manuscript.
All authors designed the study. Daryoush Didehdar collected and analyzed the data. All authors discussed the results and commented on the manuscript. All authors have carefully read and reviewed the manuscript.
Kamper SJ, Apeldoorn A, Chiarotto A, Smeets R, Ostelo R, Guzman J, Van Tulder M (2015)
Multidisciplinary biopsychosocial rehabilitation for chronic low back pain: Cochrane systematic review and meta-analysis.
Zhao X, Xu M, Jorgenson K, Kong J (2017)
Neurochemical changes in patients with chronic low back pain detected by proton magnetic resonance spectroscopy: a systematic review.
NeuroImage: Clin 13:33–38
Koes B, Van Tulder M, Thomas S (2006)
Diagnosis and Treatment of Low Back Pain
British Medical Journal 2006 (Jun 17); 332 (7555): 1430–1434
Manchikanti L, Singh V, Datta S, Cohen SP, Hirsch JA (2009)
Comprehensive review of epidemiology, scope, and impact of spinal pain.
Pain physician 12(4):E35–E70
Coderre TJ, Katz J, Vaccarino AL, Melzack R (1993)
Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence.
Tracey I, Bushnell MC (2009)
How neuroimaging studies have challenged us to rethink: is chronic pain a disease?
J pain 10 (11):1113-1120
Hardy JD, Wolff HG, Goodell H (1950)
Experimental evidence on the nature of cutaneous hyperalgesia.
J Clin Invest 29(1):115–140
O’Neill S, Manniche C, Graven-Nielsen T, Arendt-Nielsen L (2007)
Generalized deep-tissue hyperalgesia in patients with chronic low-back pain.
Eur J Pain 11(4):415–420.
Giesecke T, Gracely RH, Grant MAB, Nachemson A, Petzke F, Williams DA, Clauw DJ (2004)
Evidence of augmented central pain processing in idiopathic chronic low back pain.
Arthritis Rheum 50 (2):613-623. Doi:doi:
Castro-Sánchez AM, Lara-Palomo IC, Matarán-Peñarrocha GA, Fernández-de-las-Peñas C (2016)
Short-term effectiveness of spinal manipulative therapy versus functional technique in patients with chronic nonspecific low back pain: a pragmatic randomized controlled trial.
Spine J 16(3):302–312
Kregel J, Meeus M, Malfliet A, Dolphens M, Danneels L, Nijs J, Cagnie B (2015)
Structural and functional brain abnormalities in chronic low back pain: a systematic review.
Semin Arthritis Rheum 45(2):229–237
Grachev I, Fredrickson B, Apkarian A (2002)
Brain chemistry reflects dual states of pain and anxiety in chronic low back pain.
J Neural Transm 109(10):1309–1334
Grachev I, Ramachandran T, Thomas P, Szeverenyi N, Fredrickson B (2003)
Association between dorsolateral prefrontal N-acetyl aspartate and depression in chronic back pain: an in vivo proton magnetic resonance spectroscopy study.
J Neural Transm 110(3):287–312
Grachev ID, Fredrickson BE, Apkarian AV (2000)
Abnormal brain chemistry in chronic back pain: an in vivo proton magnetic resonance spectroscopy study.
Siddall PJ, Stanwell P, Woodhouse A, Somorjai RL, Dolenko B, Nikulin A, Bourne R (2006)
Magnetic resonance spectroscopy detects biochemical changes in the brain associated with chronic low back pain: a preliminary report.
Anesth Analg 102(4):1164–1168
Rubinstein SM, van Middelkoop M, Assendelft WJ, de Boer MR, van Tulder MW (2011)
Spinal manipulative therapy for chronic low-back pain.
Cochrane Database Syst Rev (2):Cd008112.
Chown M, Whittamore L, Rush M, Allan S, Stott D, Archer M (2008)
A prospective study of patients with chronic back pain randomised to group exercise, physiotherapy or osteopathy.
Globe, G, Farabaugh, RJ, Hawk, C et al.
Clinical Practice Guideline: Chiropractic Care for Low Back Pain
J Manipulative Physiol Ther. 2016 (Jan); 39 (1): 1–22
Hidalgo, B, Detrembleur, C, Hall, T, Mahaudens, P, and Nielens, H.
The Efficacy of Manual Therapy and Exercise for Different Stages of Non-specific Low Back Pain:
An Update of Systematic Reviews
J Man Manip Ther. 2014 (May); 22 (2): 59–74
Orrock PJ, Myers SP (2013)
Osteopathic intervention in chronic non-specific low back pain: a systematic review.
BMC Musculoskelet Disord 14(1):129
Haavik H, Murphy B (2012)
The Role of Spinal Manipulation in Addressing Disordered Sensorimotor Integration
and Altered Motor Control
J Electromyogr Kinesiol. 2012 (Oct); 22 (5): 768–776
Gussew A, Rzanny R, Güllmar D, Scholle H-C, Reichenbach JR (2011)
1H-MR spectroscopic detection of metabolic changes in pain processing brain regions in the presence of non-specific chronic low back pain.
Harris RE, Clauw DJ (2012)
Imaging central neurochemical alterations in chronic pain with proton magnetic resonance spectroscopy.
Neurosci Lett 520(2):192–196.
Schmidt-Wilcke T (2015)
Neuroimaging of chronic pain.
Best Pract Res Clin Rheumatol 29(1):29–41
Sharma NK, Brooks WM, Popescu AE, VanDillen L, George SZ, McCarson KE (2012)
Neurochemical analysis of primary motor cortex in chronic low back pain.
Brain sci 2(3):319–331
Yabuki S, S-i K, S-i K (2013)
Assessment of pain due to lumbar spine diseases using MR spectroscopy: a preliminary report.
J Orthop Sci 18(3):363–368
Lin A, Ramadan S, Stanwell P, Luu T, Celestin J, Bajwa Z, Mountford C (2010)
In vivo L-COSY MR distinguishes glutamate from glutamine and shows neuropathic pain to cause a build up of glutamine in the brain.
Proc Int Soc Magn Reson Med 18:381
Plitman E, Chavez S, Nakajima S, Iwata Y, Chung JK, Caravaggio F, Kim J, Alshehri Y (2018)
Striatal neurometabolite levels in patients with schizophrenia undergoing long-term antipsychotic treatment: a proton magnetic resonance spectroscopy and reliability study.
Psychiatry Res Neuroimaging 273:16–24
Kamali F, Shokri E (2012)
The effect of two manipulative therapy techniques and their outcome in patients with sacroiliac joint syndrome.
J Bodyw Mov Ther 16(1):29–35
Kent P, Keating JL (2005)
Classification in nonspecific low back pain: what methods do primary care clinicians currently use?
Farrar JT, Young JP Jr, LaMoreaux L, Werth JL, Poole RM (2001)
Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale.
Mousavi SJ, Parnianpour M, Mehdian H, Montazeri A, Mobini B (2006)
The Oswestry disability index, the Roland-Morris disability questionnaire, and the Quebec back pain disability scale: translation and validation studies of the Iranian versions.
Davidson M, Keating JL (2002)
A comparison of five low back disability questionnaires: reliability and responsiveness.
Phys Ther 82(1):8–24
May A (2008)
Chronic pain may change the structure of the brain.
Wand BM, Parkitny L, O’Connell NE, Luomajoki H.
Cortical Changes in Chronic Low Back Pain: Current State of the Art and Implications for Clinical Practice
Man Ther. 2011 (Feb); 16 (1): 15-20
Alleva J, Hudgins T, Belous J, Origenes AK (2016)
Chronic low back pain.
Pickar JG, Bolton PS.
Spinal Manipulative Therapy and Somatosensory Activation
J Electromyogr Kinesiol. 2012 (Oct); 22 (5): 785–794
Neurophysiological Effects of Spinal Manipulation
Spine J (N American Spine Society) 2002 (Sep); 2 (5): 357–371
Yuan W, Shen Z, Xue L, Tan W, Cheng Y, Zhan S, Zhan H (2015)
Effect of spinal manipulation on brain functional activity in patients with lumbar disc herniation.
J Zhejiang Univ Med Sci 44(2):124–130
Kanovský P, Bareš M, Rektor I (2003)
The selective gating of the N30 cortical component of the somatosensory evoked potentials of median nerve is different in the mesial and dorsolateral frontal cortex: evidence from intracerebral recordings.
Clin Neurophysiol 114(6):981–991
Taylor H. H., Murphy B.
Altered Central Integration of Dual Somatosensory Input After Cervical Spine Manipulation
J Manipulative Physiol Ther. 2010 (Mar); 33 (3): 178–188
Gedin F, Dansk V, Egmar A-C, Sundberg T, Burström K (2018)
Patient-reported Improvements of Pain, Disability, and Health-related Quality of Life
Following Chiropractic Care for Back Pain - A National Observational Study in Sweden
J Bodyw Mov Ther. 2019 (Apr); 23 (2): 241–246
Coulter ID, Crawford C, Hurwitz EL, Vernon H, Khorsan R, Suttorp Booth M, Herman PM.
Manipulation and Mobilization for Treating Chronic Low Back Pain:
A Systematic Review and Meta-analysis
Spine J. 2018 (May); 18 (5): 866–879
Licciardone JC, Gatchel RJ, Aryal S (2016)
Recovery from chronic low back pain after osteopathic manipulative treatment: a randomized controlled trial.
J Am Osteopath Assoc 116(3):144–155
Return to LOW BACK PAIN
Return to CHIROPRACTIC SUBLUXATION