Brain Response to Non-Painful Mechanical Stimulus to Lumbar Spine

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Abstract

Pressure application to the lumbar spine is an important assessment and treatment method of low back pain. However, few studies have characterized brain activation patterns in response to mechanical pressure. The objective of this study was to map brain activation associated with various levels of mechanical pressure to the lumbar spine in healthy subjects. Fifteen healthy subjects underwent functional magnetic resonance imaging (fMRI) scanning while mechanical pressure was applied to their lumbar spine with a custom-made magnetic resonance imaging (MRI)-compatible pressure device. Each subject received three levels of pressure (low/medium/high) based on subjective ratings determined prior to the scan using a block design (pressure/rest). Pressure rating was assessed with an 11-point scale (0 = no touch; 10 = max pain-free pressure). Brain activation differences between pressure levels and rest were analyzed. Subjective pressure ratings were significantly different across pressure levels ( p < 0.05). The overall brain activation pattern was not different across pressure levels (all p > 0.05). However, the overall effect of pressure versus rest showed significant decreases in brain activation in response to the mechanical stimulus in regions associated with somatosensory processing including the precentral gyri, left hippocampus, left precuneus, left medial frontal gyrus, and left posterior cingulate. There was increase in brain activation in the right inferior parietal lobule and left cerebellum. This study offers insight into the neural mechanisms that may relate to manual mobilization intervention used for managing low back pain.

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Most cited references 26

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Evidence of augmented central pain processing in idiopathic chronic low back pain.

Thorsten Giesecke, Richard Gracely, Masilo A B Grant … (2004)

For many individuals with chronic low back pain (CLBP), there is no identifiable cause. In other idiopathic chronic pain conditions, sensory testing and functional magnetic resonance imaging (fMRI) have identified the occurrence of generalized increased pain sensitivity, hyperalgesia, and altered brain processing, suggesting central augmentation of pain processing in such conditions. We compared the results of both of these methods as applied to patients with idiopathic CLBP (n = 11), patients with widespread pain (fibromyalgia; n = 16), and healthy control subjects (n = 11). Patients with CLBP had low back pain persisting for at least 12 months that was unexplained by MRI/radiographic changes. Experimental pain testing was performed at a neutral site (thumbnail) to assess the pressure-pain threshold in all subjects. For fMRI studies, stimuli of equal pressure (2 kg) and of equal subjective pain intensity (slightly intense pain) were applied to this same site. Despite low numbers of tender points in the CLBP group, experimental pain testing revealed hyperalgesia in this group as well as in the fibromyalgia group; the pressure required to produce slightly intense pain was significantly higher in the controls (5.6 kg) than in the patients with CLBP (3.9 kg) (P = 0.03) or the patients with fibromyalgia (3.5 kg) (P = 0.006). When equal amounts of pressure were applied to the 3 groups, fMRI detected 5 common regions of neuronal activation in pain-related cortical areas in the CLBP and fibromyalgia groups (in the contralateral primary and secondary [S2] somatosensory cortices, inferior parietal lobule, cerebellum, and ipsilateral S2). This same stimulus resulted in only a single activation in controls (in the contralateral S2 somatosensory cortex). When subjects in the 3 groups received stimuli that evoked subjectively equal pain, fMRI revealed common neuronal activations in all 3 groups. At equal levels of pressure, patients with CLBP or fibromyalgia experienced significantly more pain and showed more extensive, common patterns of neuronal activation in pain-related cortical areas. When stimuli that elicited equally painful responses were applied (requiring significantly lower pressure in both patient groups as compared with the control group), neuronal activations were similar among the 3 groups. These findings are consistent with the occurrence of augmented central pain processing in patients with idiopathic CLBP.

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Abnormalities in hippocampal functioning with persistent pain.

Ghazal Banisadr, Daniel Radzicki, Lejian Huang … (2012)

Chronic pain patients exhibit increased anxiety, depression, and deficits in learning and memory. Yet how persistent pain affects the key brain area regulating these behaviors, the hippocampus, has remained minimally explored. In this study we investigated the impact of spared nerve injury (SNI) neuropathic pain in mice on hippocampal-dependent behavior and underlying cellular and molecular changes. In parallel, we measured the hippocampal volume of three groups of chronic pain patients. We found that SNI animals were unable to extinguish contextual fear and showed increased anxiety-like behavior. Additionally, SNI mice compared with Sham animals exhibited hippocampal (1) reduced extracellular signal-regulated kinase expression and phosphorylation, (2) decreased neurogenesis, and (3) altered short-term synaptic plasticity. To relate the observed hippocampal abnormalities with human chronic pain, we measured the volume of human hippocampus in chronic back pain (CBP), complex regional pain syndrome (CRPS), and osteoarthritis patients (OA). Compared with controls, CBP and CRPS, but not OA, had significantly less bilateral hippocampal volume. These results indicate that hippocampus-mediated behavior, synaptic plasticity, and neurogenesis are abnormal in neuropathic rodents. The changes may be related to the reduction in hippocampal volume we see in chronic pain patients, and these abnormalities may underlie learning and emotional deficits commonly observed in such patients.

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Evidence of dysfunctional pain inhibition in Fibromyalgia reflected in rACC during provoked pain.

Serena Carville, Peter Fransson, Yves Mainguy … (2009)

Over the years, many have viewed Fibromyalgia syndrome (FMS) as a so-called "functional disorder" and patients have experienced a concomitant lack of interest and legitimacy from the medical profession. The symptoms have not been explained by peripheral mechanisms alone nor by specific central nervous system mechanisms. In this study, we objectively evaluated the cerebral response to individually calibrated pain provocations of a pain-free body region (thumbnail). The study comprised 16 female FMS patients and 16 individually age-matched controls. Brain activity was measured using functional magnetic resonance imaging (fMRI) during individually calibrated painful pressures representing 50 mm on a visual analogue scale (VAS) ranging from 0 to 100 mm. Patients exhibited higher sensitivity to pain provocation than controls as they required less pressure to evoke equal pain magnitudes (U(A)=48, p<.002). Despite lower pressures applied in patients at VAS 50 mm, the fMRI-analysis revealed no difference in activity in brain regions relating to attention and affect or regions with sensory projections from the stimulated body area. However, in the primary link in the descending pain regulating system (the rostral anterior cingulate cortex) the patients failed to respond to pain provocation. The attenuated response to pain in this brain region is the first demonstration of a specific brain region where the impairment of pain inhibition in FMS patients is expressed. These results validate previous reports of dysfunctional endogenous pain inhibition in FMS and advance the understanding of the central pathophysiologic mechanisms, providing a new direction for the development of successful treatments in FMS.

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Journal

Journal ID (nlm-ta): Brain Sci

Journal ID (iso-abbrev): Brain Sci

Journal ID (publisher-id): brainsci

Title: Brain Sciences

Publisher: MDPI

ISSN (Electronic): 2076-3425

Publication date (Electronic): 01 March 2018

Publication date Collection: March 2018

Volume: 8

Issue: 3

Electronic Location Identifier: 41

Affiliations

[1 ]Department of Physical and Occupational Therapy, Hashemite University, Zarqa 13115, Jordan; zaid.modhi@ 123456hu.edu.jo

[2 ]Hoglund Brain Imaging Center, University of Kansas Medical Center, Kansas City, KS 66160, USA; lmartin2@ 123456kumc.edu (L.E.M.); rlepping@ 123456kumc.edu (R.J.L.); wbrooks@ 123456kumc.edu (W.M.B.)

[3 ]Department of Preventive Medicine and Public Health, University of Kansas Medical Center, Kansas City, KS 66160, USA

[4 ]Department of Rehabilitation Sciences, Jordan University of Science and Technology, Irbid 22110, Jordan; sfkanaan@ 123456just.edu.jo

[5 ]Laureate Institute for Brain Research, 6655 South Yale Ave, Tulsa, OK 74136, USA; hyeh@ 123456laureateinstitute.org

[6 ]Department of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, Kansas City, KS 66160, USA

Author notes

[* ]Correspondence: nsharma@ 123456kumc.edu ; Tel.: +1-913-588-4566

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Rebecca J. Lepping https://orcid.org/0000-0001-9269-051X

Article

Publisher ID: brainsci-08-00041

DOI: 10.3390/brainsci8030041

PMC ID: 5870359

PubMed ID: 29494490

SO-VID: 79314b3f-b231-4e85-bb8b-864a171b1bb0

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Brain Response to Non-Painful Mechanical Stimulus to Lumbar Spine

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Most cited references 26

Evidence of augmented central pain processing in idiopathic chronic low back pain.

Abnormalities in hippocampal functioning with persistent pain.

Evidence of dysfunctional pain inhibition in Fibromyalgia reflected in rACC during provoked pain.

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