ChiroACCESS Article

Losing Your Mind From Back Pain

This information is provided to you for use in conjunction with your clinical judgment and the specific needs of the patient.

ChiroACCESS Editorial Staff



Published on

July 6, 2011

Text Size:   (-) Decrease the text size for the main body of this article    (+) Increase the text size for the main body of this article
Share this:  Add to TwitterAdd to DiggAdd to del.icio.usAdd to FacebookAdd to GoogleAdd to LinkedInAdd to MixxAdd to MySpaceAdd to NewsvineAdd to RedditAdd to StumbleUponAdd to Yahoo

It might sound strange, but multiple studies now document the morphologic changes in the brain as a result of chronic pain. The brain gets smaller! The morphological changes involve a decrease in cortical grey matter and white matter volume. Rapid synaptic remodeling also occurs in the somatosensory cortex. Other studies associated with chronic pain patients found decreases in the thalamic size. In a McGill University study of chronic low back pain subjects the brain changes were reversible with treatment. “These data indicate that functional and structural brain abnormalities-specifically in the left DLPFC-are reversible, suggesting that treating chronic pain can restore normal brain function in humans.”

We hope not to see future advertisements for increasing your brain size with chiropractic care!

Note:  These mini-reviews are designed as updates and direct the reader to the full text of current research.  The abstracts presented here are no substitute for reading and critically reviewing the full text of the original research.  Where permitted we will direct the reader to that full text.

Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function.  [Link]

J Neurosci. 2011 May 18;31(20):7540-50.

Seminowicz DA, Wideman TH, Naso L, Hatami-Khoroushahi Z, Fallatah S, Ware MA, Jarzem P, Bushnell MC, Shir Y, Ouellet JA, Stone LS.
Alan Edwards Centre for Research on Pain, McGill Scoliosis and Spine Research Group, Faculty of Dentistry, Departments of Anesthesiology, Pharmacology and Therapeutics, and Neurology and Neurosurgery, Faculty of Medicine, and Department of Psychology, Faculty of Science, McGill University, Montreal, Quebec H3A 1A4, Canada, and Alan Edwards Pain Management Unit and Division of Orthopaedics, McGill University Health Centre, Montreal, Quebec H3G 1A4, Canada.

Chronic pain is associated with reduced brain gray matter and impaired cognitive ability. In this longitudinal study, we assessed whether neuroanatomical and functional abnormalities were reversible and dependent on treatment outcomes. We acquired MRI scans from chronic low back pain (CLBP) patients before (n = 18) and 6 months after (spine surgery or facet joint injections; n = 14) treatment. In addition, we scanned 16 healthy controls, 10 of which returned 6 months after the first visit. We performed cortical thickness analysis on structural MRI scans, and subjects performed a cognitive task during the functional MRI. We compared patients and controls, as well as patients before versus after treatment. After treatment, patients had increased cortical thickness in the left dorsolateral prefrontal cortex (DLPFC), which was thinner before treatment compared with controls. Increased DLPFC thickness correlated with the reduction of both pain and physical disability. Additionally, increased thickness in primary motor cortex was associated specifically with reduced physical disability, and right anterior insula was associated specifically with reduced pain. Left DLPFC activity during an attention-demanding cognitive task was abnormal before treatment, but normalized following treatment. These data indicate that functional and structural brain abnormalities-specifically in the left DLPFC-are reversible, suggesting that treating chronic pain can restore normal brain function in humans.

Brain functional and anatomical changes in chronic prostatitis/chronic pelvic pain syndrome.  [Link]

J Urol. 2011 Jul;186(1):117-24. Epub 2011 May 14.

Farmer MA, Chanda ML, Parks EL, Baliki MN, Apkarian AV, Schaeffer AJ.
Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

PURPOSE: Research into the pathophysiology of chronic prostatitis/chronic pelvic pain syndrome has primarily focused on markers of peripheral dysfunction. We present the first neuroimaging investigation to our knowledge to characterize brain function and anatomy in chronic prostatitis/chronic pelvic pain syndrome.

MATERIALS AND METHODS: We collected data from 19 male patients with chronic prostatitis/chronic pelvic pain syndrome, and 16 healthy age and gender matched controls. Functional magnetic resonance imaging data were obtained from 14 patients with chronic prostatitis/chronic pelvic pain syndrome as they rated spontaneous pain inside the scanner. Group differences (16 patients per group) in gray matter total volume and regional density were evaluated using voxel-based morphometry, and white matter integrity was studied with diffusion tensor imaging to measure fractional anisotropy. Functional and anatomical imaging outcomes were correlated with the clinical characteristics of chronic prostatitis/chronic pelvic pain syndrome.

RESULTS: Spontaneous pelvic pain was uniquely characterized by functional activation within the right anterior insula, which correlated with clinical pain intensity. No group differences were found in regional gray matter volume, yet density of gray matter in pain relevant regions (anterior insula and anterior cingulate cortices) positively correlated with pain intensity and extent of pain chronicity. Moreover the correlation between white matter anisotropy and neocortical gray matter volume was disrupted in chronic prostatitis/chronic pelvic pain syndrome.

CONCLUSIONS: We provide novel evidence that the pain of chronic prostatitis/chronic pelvic pain syndrome is associated with a chronic pelvic pain syndrome specific pattern of functional brain activation and brain anatomical reorganization. These findings necessitate further investigations into the role of central mechanisms in the initiation and maintenance of chronic prostatitis/chronic pelvic pain syndrome.

Changes in regional gray and white matter volume in patients with myofascial-type temporomandibular disorders: a voxel-based morphometry study.  [Link]

J Orofac Pain. 2011 Spring;25(2):99-106.

Gerstner G, Ichesco E, Quintero A, Schmidt-Wilcke T.
Department of Biologic and Materials Sciences, School of Dentistry, University of Michigan, Ann Arbor, MI 48109-1078, USA.

AIMS: To use magnetic resonance imaging (MRI) and voxel-based morphometry (VBM) to search for evidence of altered brain morphology in patients with temporomandibular disorders (TMD).

METHODS: Using VBM, regional gray and white matter volume was investigated in nine TMD patients and nine carefully matched healthy controls.

RESULTS: A decrease in gray matter volume occurred in the left anterior cingulate gyrus, in the right posterior cingulate gyrus, the right anterior insular cortex, left inferior frontal gyrus, as well as the superior temporal gyrus bilaterally in the TMD patients. Also, white matter analyses revealed decreases in regional white matter volume in the medial prefrontal cortex bilaterally in TMD patients.

CONCLUSION: These data support previous findings by showing that TMD, like other chronic pain states, is associated with changes in brain morphology in brain regions known to be part of the central pain system.

Different pain, different brain: thalamic anatomy in neuropathic and non-neuropathic chronic pain syndromes.  [Link]

J Neurosci. 2011 Apr 20;31(16):5956-64.

Gustin SM, Peck CC, Wilcox SL, Nash PG, Murray GM, Henderson LA.
Department of Anatomy and Histology, University of Sydney, Sydney, New South Wales, Australia.

Trigeminal neuropathic pain (TNP) and temporomandibular disorders (TMD) are thought to have fundamentally different etiologies. It has been proposed that TNP arises through damage to, or pressure on, somatosensory afferents in the trigeminal nerve, whereas TMD results primarily from peripheral nociceptor activation. Because some reports suggest that neuropathic pain is associated with changes in brain anatomy, it is possible that TNP is maintained by changes in higher brain structures, whereas TMD is not. The aim of this investigation is to determine whether changes in regional brain anatomy and biochemistry occur in both conditions. Twenty-one TNP subjects, 20 TMD subjects, and 36 healthy controls were recruited. Voxel-based morphometry of T1-weighted anatomical images revealed no significant regional gray matter volume change in TMD patients. In contrast, gray matter volume of TNP patients was reduced in the primary somatosensory cortex, anterior insula, putamen, nucleus accumbens, and the thalamus, whereas gray matter volume was increased in the posterior insula. The thalamic volume decrease was only seen in the TNP patients classified as having trigeminal neuropathy but not those with trigeminal neuralgia. Furthermore, in trigeminal neuropathy patients, magnetic resonance spectroscopy revealed a significant reduction in the N-acetylaspartate/creatine ratio, a biochemical marker of neural viability, in the region of thalamic volume loss. The data suggest that the pathogenesis underlying neuropathic and non-neuropathic pain conditions are fundamentally different and that neuropathic pain conditions that result from peripheral injuries may be generated and/or maintained by structural changes in regions such as the thalamus.

Rapid synaptic remodeling in the adult somatosensory cortex following peripheral nerve injury and its association with neuropathic pain.  [Link]

J Neurosci. 2011 Apr 6;31(14):5477-82.

Kim SK, Nabekura J.
Division of Homeostatic Development, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.

Structural and functional plastic changes in the primary somatosensory cortex (S1) have been observed following peripheral nerve injury that often leads to neuropathic pain, which is characterized by tactile allodynia. However, remodeling of cortical connections following injury has been believed to take months or years; this is not temporally correlated with the rapid development of allodynia and S1 hyperexcitability. Here we first report, by using long-term two-photon imaging of postsynaptic dendritic spines in living adult mice, that synaptic connections in the S1 are rewired within days following sciatic nerve ligation through phase-specific and size-dependent spine survival/growth. Spine turnover in the S1 area corresponding to the injured paw markedly increased during an early phase of neuropathic pain and was restored in a late phase of neuropathic pain, which was prevented by immediate local blockade of the injured nerve throughout the early phase. New spines that generated before nerve injury showed volume decrease after injury, whereas more new spines that formed in the early phase of neuropathic pain became persistent and substantially increased their volume during the late phase. Further, preexisting stable spines survived less following injury than controls, and such lost persistent spines were smaller in size than the surviving ones, which displayed long-term potentiation-like enlargement over weeks. These results suggest that peripheral nerve injury induces rapid and selective remodeling of cortical synapses, which is associated with neuropathic pain development, probably underlying, at least partially, long-lasting sensory changes in neuropathic subjects.

Hypothalamic gray matter volume loss in hypnic headache.  [Link]

Ann Neurol. 2011 Mar;69(3):533-9.

Holle D, Naegel S, Krebs S, Gaul C, Gizewski E, Diener HC, Katsarava Z, Obermann M.
Department of Neurology, University of Duisburg-Essen, Germany.

OBJECTIVE: Hypnic headache (HH) is a rare primary headache disorder characterized by strictly nocturnal headache attacks that mostly occur at the same time at night. The pathophysiology of this disease is poorly understood, but hypothalamic involvement was suspected as the hypothalamus represents the cerebral management center of sleep regulation and pain control.

METHODS: Fourteen patients with HH and 14 age-matched and gender-matched healthy controls were investigated using magnetic resonance imaging-based voxel-based morphometry.

RESULTS: We detected gray matter volume decrease in the posterior hypothalamus of HH patients. Additional gray matter decrease was observed in brain areas known to be associated with cerebral pain processing, including the cingulate cortex, operculum, and frontal lobe, as well as in the temporal lobe.

INTERPRETATION: Our data confirm the hypothesized involvement of the posterior hypothalamus in the pathophysiology of HH and emphasize the importance of this structure for sleep regulation and pain control.
Share this:  Add to TwitterAdd to DiggAdd to del.icio.usAdd to FacebookAdd to GoogleAdd to LinkedInAdd to MixxAdd to MySpaceAdd to NewsvineAdd to RedditAdd to StumbleUponAdd to Yahoo