Degenerative disorders of the spine are the most common cause of chronic low back pain (cLBP); in Western Europe alone, billions of euros are spent each year on both conservative and surgical treatments for cLBP. And though only 5% of all patients with low back pain suffer from lumbar disc herniation (LDH), more than 30% of the overall annual cost of treating cLBP goes to this one agonizing and disabling pain disorder. Previous findings have shown that intervertebral disc herniation can occur in people who are asymptomatic (Jensen et al., 1994). However, much effort has been expended to identify prognostic variables based on the classification of the magnetic resonance imaging (MRI) of the spine. Unfortunately, no factor has yet been revealed that reliably distinguishes between patients who should be treated conservatively and those who would instead benefit from surgery. In fact, only a weak correlation has been observed between the size of the prolapsed disc and the presence of clinical symptoms (Benson et al., 2010). Since it is the brain that ultimately interprets pain, the neuroscientific community has in recent years increased its focus on studying pain-induced cerebral alterations. And indeed, the adult human brain has an astonishing capacity for the morphological alterations that follow the learning and adaptation processes necessary to a changed environment (Draganski et al., 2004). Until recently, chronic pain was thought to be associated with abnormal nociceptive function but an unchanged brain structure. Now, however, a large body of new evidence supports the idea that chronic pain not only signals an altered functional state but is also a consequence of central plasticity (May, 2011). While acute pain is associated with structural changes appearing mainly in the somatosensory system, predominantly the thalamus, chronic pain is believed to be more complex. Since the pioneering work of Apkarian and colleagues (2004), who were the first to observe cortical alterations in chronic pain, more than 50 studies investigating patients suffering from headache, migraine, phantom pain, fibromyalgia, and trigeminal and low back pain documented structural brain alterations that had occurred in the different chronic pain states. A striking characteristic of these observed structural alterations is that the changes are not distributed randomly (Smallwood et al., 2013). Thus, structural alterations of the brain were found frequently in the dorsolateral prefrontal cortices, basal ganglia and hippocampus. However, the precise locations of the regions that are affected by structural reorganization do slightly differ among the various studies. This lack of consistency is difficult to explain, but may be due to the different neuropathological mechanisms of the processes that ultimately lead to pain chronification. But it is still not at all clear why some people develop chronic pain syndromes and why others do not. It has been hypothesized that patients with long lasting pain have lost the ability to habituate themselves to pain due to increased cortical activity and/or a shift of the cortical representation, which is interpreted as either an expansion or a shrinkage of the representational field of the affected part of the body (May, 2011). The ensuing heightened sensitivity for pain is a result of central plasticity in the nociceptive pathways of the brain. This central sensitization, a form of (maladaptive) central synaptic plasticity, is a main pathophysiological cause for the development of chronic pain. Once chronic pain is generated, the increased sensitivity typically persists for a long time, even though the underlying cause of the pain is disappeared. Therefore, chronic pain is maladaptive in the sense that the pain neither protects nor support healing and repair. The underlying central malfunctions have been considered as a disease on its own right (Costigan et al., 2009).
Read full abstract