Atormac
Neurology India
Open access journal indexed with Index Medicus
  Users online: 326  
 Home | Login 
  About Current Issue Archive Ahead of print Search Instructions Online Submission Subscribe Etcetera Contact  
  Navigate Here 
 Search
 
  
 Resource Links
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Article in PDF (398 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this Article
   References

 Article Access Statistics
    Viewed518    
    Printed1    
    Emailed0    
    PDF Downloaded11    
    Comments [Add]    

Recommend this journal

 


 
Table of Contents    
NI FEATURE: THE EDITORIAL DEBATE I-- PROS AND CONS
Year : 2017  |  Volume : 65  |  Issue : 2  |  Page : 255-256

Role of functional MRI in identifying network changes in chronic pain syndromes


Department of Radiology, Aster D. M. Healthcare, Bangalore, Karnataka, India

Date of Web Publication10-Mar-2017

Correspondence Address:
Uday D Patil
Department of Radiology, Aster D. M. Healthcare, Bangalore, Karnataka
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.201853

Rights and Permissions



How to cite this article:
Patil UD. Role of functional MRI in identifying network changes in chronic pain syndromes. Neurol India 2017;65:255-6

How to cite this URL:
Patil UD. Role of functional MRI in identifying network changes in chronic pain syndromes. Neurol India [serial online] 2017 [cited 2017 Aug 24];65:255-6. Available from: http://www.neurologyindia.com/text.asp?2017/65/2/255/201853


Chronic pain is a debilitating problem in the world, leading to loss of productivity as well as resulting in disability, lifestyle limitations and impaired independence. The complexity of the neuronal mechanism of chronic pain is poorly understood. Acute and chronic pain differ in the neuronal mechanisms, and in chronicity, changes occur in the entire central nervous system. Chronic pain has physical as well as psychological elements. Hence neuroimaging, especially functional magnetic resonance imaging (fMRI) has increasingly been used to study how chronic pain is perceived and processed by the brain and the changes that occur as a consequence.

fMRI allows for an indirect measurement of brain activity by tracking changes in blood oxygenation level dependent signals (BOLD). BOLD fMRI experiments are performed using two methods. The older method is 'Activation fMRI,' where changes in the regional BOLD signals (changes in blood oxygen level) are mapped in response to stimuli, both physical or event related, as compared to the BOLD signals in the absence of these signals by a block design of periodic stimuli, and a block design without stimuli. The difference in the signals, if it is consistent and repeated over the blocks, is considered as activation, and is mapped to the anatomical location. A more recent introduction is 'Resting State fMRI (RS-fMRI),' which maps the spontaneous fluctuations in BOLD signal without any stimuli or activity. RS-fMRI is used to explore the functional organization and regional as well as global connectivity in the healthy subjects; as well as its alteration in patients with neurological or psychiatric diseases and in different stages of consciousness and across species. These represent patterns of synchronous activity of the brain. While the activation fMRI is dominantly qualitative, assessing activation versus no activation; RS-fMRI can be quantitative, measuring the activation as well as connectivity.

The utility of fMRI lies in being able to identify the brain structure and activity in chronic pain states; and, in attempting to localise the specific brain regions which can be targeted for chronic pain therapy. Chronic pain and its comorbid symptoms cause neurological changes across several brain regions - primary somatosensory cortex and posterior insular cortex in individuals with chronic low back pain (cLBP); the secondary somatosensory cortex (SII) has shown both structural and functional alterations.[1] The primary motor cortex, premotor cortex and supplementary motor areas also play a role in regulation of chronic pain.

RS-fMRI experiments have demonstrated that the networks affected during chronic pain are primarily the default-mode networks (DMN), salience and executive control networks and sensory motor networks.[2] Decreased DMN connectivity, specifically within the medial posterior frontal cortex, posterior cingulate cortex (PCC) and amygdala, has been observed in cLBP.[3]

It would be expected that sedation and anesthesia would alter the functional connectivity networks; and are expected to depend on the dose and mechanism of action of the drugs used. This process involves the DMN, components of the reticular activating system, the thalamus, and parts of the cortex.[4] In this issue of Neurology India, Sriganesh et al., in the paper “Effect of propofol anesthesia on resting state brain functional connectivity in Indian population with chronic back pain,”[5] demonstrate that there is increase in function connectivity in the PCC and thalamus with a generalized decrease in the integration within large scale brain networks after propofol sedation, and there is no diffferecne in the functional connectivity in the subjects with cLBP and in healthy volunteers on RS-fMRI. Martuzzi R, et al.,[6] have shown similar results and have also found little change between sedated/anesthetized and awake states using sevoflurane.

Such studies will contribute towards understanding the mechanism of action of the drugs used for sedation and anesthesia, and may lead to optimization of the doses required to obtain the required levels of analgesia and consciousness in different levels of pain as well as in psychological and diseased states.

The technical advances in imaging have repeatedly introduced new technology, and the discovery of its utility and limitations has always followed the introduction of the technology. fMRI inherently is based on the detection of very low signal strength, and the magnetic resonance data and its reconstruction varies across the different manufacturers. The post-processing of the data is based on statistical and mathematical models, which differ across the software used for fMRI analysis; and, the brain differs across individuals. Given this complex environment, reproducibility of the results tends to get limited, and is often not comparable across the different studies. Hence, the technical factors must be kept under consideration when evaluating the results from such studies.

Declaration: The author is a research consultant at Global Research, an initiative of General Electric (GE) at John F Welch Technology Center, Bangalore.

 
  References Top

1.
Rodriguez-Raecke R, Ihle K, Ritter C, Muhtz C, Otte C, May A. Neuronal differences between chronic low back pain and depression regarding long-term habituation to pain. Eur J Pain 2013;18:701-11.  Back to cited text no. 1
    
2.
Greicius MD, Krasnow B, Reiss AL, Menon V. Functional connectivity in the resting brain: A network analysis of the default mode hypothesis. Proc. Natl Acad. Sci USA 2003;100:253-8.  Back to cited text no. 2
    
3.
Baliki MN, Geha PY, Apkarian AV, Chialvo DR. Beyond feeling: Chronic pain hurts the brain, disrupting the default-mode network dynamics. J Neurosci 2008;28:1398-1403.  Back to cited text no. 3
    
4.
Stamatakis EA, Adapa RM, Absalom AR, David K, changes in resting neural connectivity during propofol sedation. PLOS: http://dx.doi.org/10.1371/journal.pone. 0014224. Published: December 2, 2010 [Last accessed on 2017 Jan 18].  Back to cited text no. 4
    
5.
Sriganesh K, Balachandar R, Bagepally B, Saini J, Umamaheswara Rao GS. Effect of propofol anesthesia on resting state brain functional connectivity in indian population with chronic back pain. Neurol India 2017;65:286-292.  Back to cited text no. 5
  [Full text]  
6.
Martuzzi R, Ramani R, Qiu M, Rajeevan N, Constable RT. In Functional connectivity and alterations in baseline brain state in humans. NeuroImage. 2010;49:823-34.  Back to cited text no. 6
    




 

Top
Print this article  Email this article
   
Online since 20th March '04
Published by Wolters Kluwer - Medknow