Neuroanatomy and Neuropsychology of Pain

Abstract

We have reviewed here the neuroanatomical and neuropsychological literature of the human brain and have proposed the various pain mechanisms that we currently know of. Essentially when tissue is damaged, peripheral nociceptors are activated continuously and prostanoids are hence produced. Nonsteroidal anti-inflammatory drugs (NSAIDs) and medications aim to target these prostanoids to treat the inflammatory component of pain. Normal pain tends to have a protective response. It is important for the nervous system to learn and recognize this painful stimulus earlier and quicker with repeated exposure to avoid tissue damage. This neuronal plasticity and gain in sensitivity result in sensitization of the nervous system, both centrally and peripherally and help in earlier detection of the pain sensation. However, persistent pain can become pathologic and will eventually result in the loss of protection pain offers to the body. Pain-related fear has been implicated in the transition from acute to chronic low back pain and the persistence of disabling low back pain, making it a key target for physiotherapy intervention. The current understanding of pain-related fear is that it is a psychopathological problem where people who catastrophise about the meaning of pain become trapped in a vicious cycle of avoidance behaviour, pain and disability, as recognised in the fear-avoidance model. We looked at how pain is perceived, especially in low-back pain patients. It has been hypothesized that individuals with low-back pain (LBP) can change their motor behavior, which is fundamentally an adaptation mechanism aimed at minimizing the real or perceived risk of further pain.

Keywords: motor control; neuroanatomy; neuropsychology; nociception; orbitofrontal cortex; pain; reinforcement learning.

Figure 1. General cross-sectional anatomy of the spinal cord.

Cells and connections in Laminae of Rexed are indicated. Large-diameter, heavily myelinated afferents (1) enter medially through the posterior funiculus, whereas small-diameter afferents (2) enter laterally near the substantia gelatinosa. This corresponds to the way tactile and proprioceptive information is processed, relative to pain and temperature information. These afferents then contact interneurons (3) and, in some cases, motor neurons (4) directly.

Figure 2. Spinothalamic tract.

Pain, temperature, and some touch and pressure afferents end in the posterior horn. Second- or higher-order fibers cross the midline, form the spinothalamic tract, and ascend to the ventral posterolateral (VPL) nucleus of the thalamus (and also to other thalamic nuclei not shown). Thalamic cells then project to the somatosensory cortex of the postcentral gyrus, to the insula, and to other cortical areas (also not shown). Along their course through the brainstem, spinothalamic fibers give off many collaterals to the reticular formation (RF). The inset to the left shows the lamination of fibers in the posterior columns and the spinothalamic tract in a leg-lower trunk-upper trunk-arm sequence. The inset to the right shows the longitudinal formation of the spinothalamic tract. Primary afferents ascend several segments in Lissauerʼs tract before all their branches terminate; fibers crossing to join the spinothalamic tract do so with a rostral inclination. As a result, a cordotomy incision at any given level would spare most of the information entering the contralateral side of the spinal cord at that level, and to be effective, the incision must be made several segments rostral to the highest dermatomal level of pain.

Figure 3. Pain, plasticity and gain.

The three forms of neural plasticity that increase gain in the somatosensory system to produce pain hypersensitivity are illustrated, highlighting changes they produce and their effects on pain transmission.

Figure 4. Target sites for management of pain.

Pharmacologic approaches to management of pain are based on location in the nervous system.