Chronic Pain and the Brain: Difference between revisions

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== Brain Areas in the Neuromatrix and the Changes Due to Chronic Pain. ==


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Studies using functional MRI have identified six common regions activated in acute pain. These regions include the primary somatosensory cortex (S1), secondary somatosensory cortex (S2), anterior cingulated cortex, insular cortex, prefrontal cortex and the thalamus. It is these regions that make up the pain neuromatrix which Melzack<ref>Melzack R (2001) Pain and the neuromatrix in the brain. Journal of Dental Education 65(12): 1378-1382</ref> has identified.<br>
 
In a review conducted by Lithwick et al (2013), the role of these areas in producing pain is explained in depth.<ref>Lithwick A, Lev S, Binshtock  A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45</ref> The primary somatosensory cortex is responsible for sensory discrimination, determining where the pain messaging is coming from. In patients with chronic pain, a more widespread contralateral activation was observed, compared with acute pain where only the ipsilateral side was activated. Another study found that individuals with chronic pain also have a small cortical representation of S1 and implied that “there was dissociation between activation of primary sensory areas and the actual origin of pain.”<ref>Lithwick A, Lev S, Binshtock  A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45</ref>
 
<br>The anterior cingulated cortex (ACC) is associated with emotional and cognitive-evaluative aspects of pain processing along with sensory perceptions due to convergence with the S1. In chronic pain patients, there is bilateral and more widespread ACC activation compared with acute pain.<ref>Maihofner C, Handwerker HO, Birklein F (2006) Functional imaging of allodynia in complex region pain syndrome. Neurology 66(5): 711-717.</ref> The authors concluded that this indicated a heightened sensation of pain in chronic pain patients. Another study found in chronic pain patients “that the ACC and the insula demonstrated a significantly altered correlation to the medial PFC.”<ref>Baliki MN, Baria AT, Apkarian AV. (2011) The cortical rhythms of chronic back pain. Journal of Neuroscience. 31 (39): 13981-13990.</ref> This represents a shift towards a more emotional aspect in chronic pain.
 
<br>The secondary somatosensory cortex (S2) is associated with the discrimination of pain intensity and with a coactivation between the primary somatosensory cortex. In patients with chronic pain, there is “a bilateral activation pattern, as compared to a contralateral activation pattern as seen in acute pain.”<ref>Lithwick A, Lev S, Binshtock  A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45</ref> This indicates that there is less of a representation of the initial pain and may contribute to the widespread, vague pain described by chronic pain patients.
 
<br>The insular cortex (IC) has a role in both sensory and affective perception of pain – the suffering aspect of pain. It is often coactivated with the anterior cingulated cortex. In chronic pain, there is a more widespread activation of the IC compared to acute pain. The IC is also more linked with sensory discrimination in chronic pain, rather than emotional processing. The IC’s role in suffering “ is minimised so as to accommodate the vast increase in activation that is seen in S1 and S2.”<ref>Lithwick A, Lev S, Binshtock  A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45</ref> This change would contribute to allodynia and hyperalgesia as seen in chronic pain.
 
<br>The prefrontal cortex is responsible for the cognitive evaluation of pain. Three areas are associated with pain: the medial prefrontal cortex (mPFC), dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex. m PFC represents the affective aspect of pain, the DLPFC is involved in localising painful stimuli and the orbitofrontal cortex is a link between painful area discrimination, memory and emotion. Lithwick (2013) observed that in individuals with chronic back pain, m PFC was in a significant hyperactive state, which may reduce brain activity in other areas overall, affecting the brain’s ability to perform other tasks.<ref>Lithwick A, Lev S, Binshtock  A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45</ref> Overall, the change in PFC due to chronic pain represents a shift towards increased emotional processing.
 
<br>Not only are different parts of the brain activated when pain becomes chronic, but there can also be smudging of the sensory and motor homunculus. Smudging refers to the changes in the brain areas devoted to detecting the stimulation of body parts and performing functions begin overlapping. This process is why some body parts may become difficult to use or other areas become sensitive compared to the injured area. For more information on this, please see central sensitisation.Flor (2003) hypothesised that this overall widespread activation and expansion of the representational zone may lead to pain perceptions in the absence of peripheral stimulation.<ref>Flor H. (2003) cortical reorganisation and chronic pain: implications for rehabilitation Journal of Rehabilitative Medicine Suppl. 41: 66-72</ref>
 
<br>These changes in brain anatomy are a result of increased nociceptive input from the periphery which results in the systemic and anatomical changes discussed above. Wand et al (2011) conclude that “it is likely that part of the pain experience of CLBP patients is mediated by sensitivity changes within the central nervous system and the demonstrated brain changes are a probable contribution to this."<ref>Wand BM, Parkitny L, O’Connell NE, Luomajoki H, McAuley JH, Thacker M, Moseley L. (2011) Cortical changes in chronic low back pain: current state of the art and implications for clinical practice. Manual Therapy 16: 15-20</ref> Nociceptive information accesses the cortex through multiple pathways in the spinal cord. Modulating of these cortical areas occurs due to a continuous barrage of nociceptive inputs associated with chronic pain.
 
<br>A study conducted by Seminowicz et al in 2011 investigated the effect of chronic pain on brain anatomy and whether effective treatment would reverse these changes. They found that in chronic pain patients, there was a decreased cortical thickness in the DLPFC, anterior insula, anterior cingulate cortex and primary somatosensory cortex.<ref>Seminowicz DA, Wideman TH, Naso L, Hatami-Khoroushahi Z, Fallatah S, Ware MA, Jarzem P, Bushnell C, Shir Y, Ouellet JA (2011) Effective Treatment of Chronic Low Back Pain in Humans Reverses Abnormal Brain Anatomy and Function. The Journal of Neuroscience 31(20): 7540-7550</ref> The loss of cortical thickness corresponds with a loss of neurons and a slower speed of synapses. They then treated the patient’s pain with a nerve root block or spinal surgery to determine if these cortical areas became thicker again with reduced pain. The only statistically significant finding was an increase in the thickness of the DLPFC in patients who reported a decrease in pain intensity and improvements in physical impairments. The authors concluded that more research is needed to determine if interventions targeting psychosocial rather than biomechanical components of chronic pain would result in similar recovery of cortical thickness. <br>


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Revision as of 20:25, 26 November 2014

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Brain Areas in the Neuromatrix and the Changes Due to Chronic Pain.[edit | edit source]

Studies using functional MRI have identified six common regions activated in acute pain. These regions include the primary somatosensory cortex (S1), secondary somatosensory cortex (S2), anterior cingulated cortex, insular cortex, prefrontal cortex and the thalamus. It is these regions that make up the pain neuromatrix which Melzack[1] has identified.

In a review conducted by Lithwick et al (2013), the role of these areas in producing pain is explained in depth.[2] The primary somatosensory cortex is responsible for sensory discrimination, determining where the pain messaging is coming from. In patients with chronic pain, a more widespread contralateral activation was observed, compared with acute pain where only the ipsilateral side was activated. Another study found that individuals with chronic pain also have a small cortical representation of S1 and implied that “there was dissociation between activation of primary sensory areas and the actual origin of pain.”[3]


The anterior cingulated cortex (ACC) is associated with emotional and cognitive-evaluative aspects of pain processing along with sensory perceptions due to convergence with the S1. In chronic pain patients, there is bilateral and more widespread ACC activation compared with acute pain.[4] The authors concluded that this indicated a heightened sensation of pain in chronic pain patients. Another study found in chronic pain patients “that the ACC and the insula demonstrated a significantly altered correlation to the medial PFC.”[5] This represents a shift towards a more emotional aspect in chronic pain.


The secondary somatosensory cortex (S2) is associated with the discrimination of pain intensity and with a coactivation between the primary somatosensory cortex. In patients with chronic pain, there is “a bilateral activation pattern, as compared to a contralateral activation pattern as seen in acute pain.”[6] This indicates that there is less of a representation of the initial pain and may contribute to the widespread, vague pain described by chronic pain patients.


The insular cortex (IC) has a role in both sensory and affective perception of pain – the suffering aspect of pain. It is often coactivated with the anterior cingulated cortex. In chronic pain, there is a more widespread activation of the IC compared to acute pain. The IC is also more linked with sensory discrimination in chronic pain, rather than emotional processing. The IC’s role in suffering “ is minimised so as to accommodate the vast increase in activation that is seen in S1 and S2.”[7] This change would contribute to allodynia and hyperalgesia as seen in chronic pain.


The prefrontal cortex is responsible for the cognitive evaluation of pain. Three areas are associated with pain: the medial prefrontal cortex (mPFC), dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex. m PFC represents the affective aspect of pain, the DLPFC is involved in localising painful stimuli and the orbitofrontal cortex is a link between painful area discrimination, memory and emotion. Lithwick (2013) observed that in individuals with chronic back pain, m PFC was in a significant hyperactive state, which may reduce brain activity in other areas overall, affecting the brain’s ability to perform other tasks.[8] Overall, the change in PFC due to chronic pain represents a shift towards increased emotional processing.


Not only are different parts of the brain activated when pain becomes chronic, but there can also be smudging of the sensory and motor homunculus. Smudging refers to the changes in the brain areas devoted to detecting the stimulation of body parts and performing functions begin overlapping. This process is why some body parts may become difficult to use or other areas become sensitive compared to the injured area. For more information on this, please see central sensitisation.Flor (2003) hypothesised that this overall widespread activation and expansion of the representational zone may lead to pain perceptions in the absence of peripheral stimulation.[9]


These changes in brain anatomy are a result of increased nociceptive input from the periphery which results in the systemic and anatomical changes discussed above. Wand et al (2011) conclude that “it is likely that part of the pain experience of CLBP patients is mediated by sensitivity changes within the central nervous system and the demonstrated brain changes are a probable contribution to this."[10] Nociceptive information accesses the cortex through multiple pathways in the spinal cord. Modulating of these cortical areas occurs due to a continuous barrage of nociceptive inputs associated with chronic pain.


A study conducted by Seminowicz et al in 2011 investigated the effect of chronic pain on brain anatomy and whether effective treatment would reverse these changes. They found that in chronic pain patients, there was a decreased cortical thickness in the DLPFC, anterior insula, anterior cingulate cortex and primary somatosensory cortex.[11] The loss of cortical thickness corresponds with a loss of neurons and a slower speed of synapses. They then treated the patient’s pain with a nerve root block or spinal surgery to determine if these cortical areas became thicker again with reduced pain. The only statistically significant finding was an increase in the thickness of the DLPFC in patients who reported a decrease in pain intensity and improvements in physical impairments. The authors concluded that more research is needed to determine if interventions targeting psychosocial rather than biomechanical components of chronic pain would result in similar recovery of cortical thickness.

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References[edit | edit source]

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  1. ↑ Melzack R (2001) Pain and the neuromatrix in the brain. Journal of Dental Education 65(12): 1378-1382
  2. ↑ Lithwick A, Lev S, Binshtock A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45
  3. ↑ Lithwick A, Lev S, Binshtock A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45
  4. ↑ Maihofner C, Handwerker HO, Birklein F (2006) Functional imaging of allodynia in complex region pain syndrome. Neurology 66(5): 711-717.
  5. ↑ Baliki MN, Baria AT, Apkarian AV. (2011) The cortical rhythms of chronic back pain. Journal of Neuroscience. 31 (39): 13981-13990.
  6. ↑ Lithwick A, Lev S, Binshtock A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45
  7. ↑ Lithwick A, Lev S, Binshtock A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45
  8. ↑ Lithwick A, Lev S, Binshtock A (2013) Chronic pain-related remodelling of cerebral cortex – ‘pain memory’: a possible target for treatment of chronic pain. Pain Management 3(1): 35-45
  9. ↑ Flor H. (2003) cortical reorganisation and chronic pain: implications for rehabilitation Journal of Rehabilitative Medicine Suppl. 41: 66-72
  10. ↑ Wand BM, Parkitny L, O’Connell NE, Luomajoki H, McAuley JH, Thacker M, Moseley L. (2011) Cortical changes in chronic low back pain: current state of the art and implications for clinical practice. Manual Therapy 16: 15-20
  11. ↑ Seminowicz DA, Wideman TH, Naso L, Hatami-Khoroushahi Z, Fallatah S, Ware MA, Jarzem P, Bushnell C, Shir Y, Ouellet JA (2011) Effective Treatment of Chronic Low Back Pain in Humans Reverses Abnormal Brain Anatomy and Function. The Journal of Neuroscience 31(20): 7540-7550

 

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