In the past decade of pain research, a network of pain transmitting areas within the CNS has been established, based on both animal studies (Wall and Melzack 2006) and findings from functional imaging studies in humans (Peyron et al. 2000). Consequently, the neurobiology of pain is increasingly understood as an integration of activity in distinct neuronal structures. Evidence of altered local brain chemistry (Grachev et al. 2000) and functional reorganization in chronic back pain (CBP) patients (Flor et al. 1997) supports the idea that chronic pain could be understood not only as an altered...
In the past decade of pain research, a network of pain transmitting areas within the CNS has been established, based on both animal studies (Wall and Melzack 2006) and findings from functional imaging studies in humans (Peyron et al. 2000). Consequently, the neurobiology of pain is increasingly understood as an integration of activity in distinct neuronal structures. Evidence of altered local brain chemistry (Grachev et al. 2000) and functional reorganization in chronic back pain (CBP) patients (Flor et al. 1997) supports the idea that chronic pain could be understood not only as an altered functional state, but also as a consequence of central plasticity (Flor 2003).
Recent neurobiological findings suggest cortical reorganization on a functional level (Grusser et al. 2004). For example, amputation of a limb is very often accompanied by phantom pain. In these patients, the deafferentation leads to cortical reorganization where the representational fields of adjacent areas move into the into the representation zone of the deafferented limb (Pons et al. 1991; Flor et al 2006). This ‘functional reorganization’ was not only detected in patients suffering from phantom limb pain (Flor et al. 1995), but also in CBP patients (Flor et al. 1997). Regarding CBP, increased cortical activity and a shift of the cortical representation of the back, which was interpreted as an expansion of the back's representation into the neighbouring foot and leg area (Flor et al. 1997), was found. In patients with chronic regional pain syndrome (CRPS Type I), a shrinkage of the representational field of the affected arm was found and the extent of shrinkage correlated highly with the intensity of pain and the magnitude of mechanical hyperalgesia (Maihofner et al. 2003; Pleger et al. 2004). It is noteworthy, that the functional changes in CRPS (Maihofnere et al. 2004) and in phantom pain (Flor et al. 2001) were dynamic, (i.e. cortical reorganization reversed coincident with clinical improvement).
Currently, chronic pain states are attributed to abnormal nociceptive/antinociceptive function on different levels of the neuroaxis (Wall and Melzack 2006) with a normal brain structure. However, any significant challenge that requires a specific function, including learning a specific task, has the potential to alter brain structure (May et al. 2007). Given that the initiation of chronification of pain involves nociceptive input, one would expect that neuroplasticity would probably occur in modulatory areas of nociception—namely, the antinociceptive system.
An alternative view of the cumulative human brain imaging studies regarding pain is that we have firmly established that various brain regions are activated in a reproducible pattern for acute and experimental pain conditions. Yet, brain activity for chronic pain is distinct from acute pain (Apkarian et al. 2005). Moreover, the ‘pain matrix’ assumed to underlie pain in general in fact corresponds to spinothalamic inputs to the cortex and as such identifies brain areas involved in acute nociception. Even for acute pain, the involvement of primary somatosensory cortex (S1) remains unresolved. Multiple evoked potential studies assert its role while functional brain imaging, primarily functional magnetic resonance imaging (fMRI), studies often fail to find activity in appropriate parts of S1, however, with some exception (Bingel 2004). Animal studies have shown that the S1 body map is dynamic and reorganizes with body part use or neglect, as well as with peripheral nerve injuries. Recently, this was also shown for humans (Flor et al. 1995, 2002). Thus, changes in somatotopy in S1, which have been described in various chronic pain conditions and which were determined mainly for non-painful tactile stimuli, may be a consequence of behavioural modifications of body use due to coping strategies necessary for living with chronic pain.
There is now accumulating evidence that brain activity for acute and chronic pain (especially for fluctuations of spontaneous pain) are distinct from each other, and that brain activity for various clinical chronic pain conditions are also distinct from each other (Apkarian et al. 2009). For example, in CBP patients, activity in the medial prefrontal cortex (mPFC) identifies the intensity of patients’ pain with a predictive power larger than 80% (Baliki et al. 2006). When in the same patients brain activity for acute thermal pain is examined, applied on the back at a location closest to the back pain, the mPFC activity show no related activity, and instead parts of the insula code the perceived intensity at a comparable predictive level as the mPFC for spontaneous pain. Moreover, the brain activations for acute thermal pain in CBP engages the same brain regions as seen in healthy subjects, and contrasting these activations between the two groups shows no brain region to be more active or less active in either group, thus demonstrating that acute thermal pain brain activity does not differ between CBP and normals, and spontaneous pain of CBP activates distinct pattern.
Chapter. 5942 words.
Subjects: Neuroscience ; Pain Medicine
Full text: subscription required