Advances in the neuroscience of pain processing have provided support for the role of higher brain centers, i.e., those responsible for emotion and cognition, in influencing pain transmission from the periphery (Melzack 1999), lending support for the biopsychosocial approach. Abandoning the archaic Cartesian viewpoint of the brain as a passive recipient of pain information from the periphery, the neuromatrix model acknowledges that the brain is dynamically involved in the processing (inhibition, modulation, or excitation) of pain. This is thought to involve the sensory, thalamic, limbic, hypothalamic-pituitary axis (HPA), and cortical pathways (Melzack 1999, Rome and Rome 2000) (Fig. 12.1).
Normally, physical and/or psychological stress triggers mechanisms to attempt to restore homeostasis. When stress persists (e.g., in the form of ongoing pain, psychological distress, inadequate coping with environmental stressors, and persisting depression), multiple processes are set in motion that exceed the delicately balanced regulatory homeostatic mechanisms initially intended to effectively manage stress, and instead generate destructive processes perpetuating pain. Several lines of research have pointed to plausible mechanisms underlying the reciprocal relationships between pain, affective distress, and stress:
Increased Glucocorticoid Activity
Increased Glucocorticoid Activity
• The amygdala, a limbic structure, acts as the interface between pain and emotional states; chronic negative affective states can influence the amygdala to enhance the response to pain (Neugebauer et al. 2004).
• Stress, depression, and pain can produce dysregulation of the HPA, increasing systemic sympathetic tone in the body as a whole. This, in turn, has multiple influences including activation of macrophages and heightened cortisol secretion.
• Activation of macrophages results in the release of pro-inflammatory cytokines (leading to the lowering of pain thresholds and reductions of monoamine release)
• Systemically, glucocorticoids can produce diffuse effects, including bone demineral-ization, muscle atrophy, and immune dysregulation all of which have the propensity to enhance pain and injury and thereby increasing the potential for pain. Centrally, the actions of glucocorticoid excess can interfere with serotonin and norepinephrine monoamine neurotransmission, neurotransmitters implicated in the modulation of pain information emanating from the periphery. The net effect is to disinhibit potential pro-algesic pain information relayed from the periphery.
• Stress and pain can alter the mechanisms by which the brain functions in its own maintenance (Duman and Monteggia 2006, Duric and McCarson 2005). Presumably through heightened glucocorticoid activity, stress and pain can alter the expression of neurotrophic factors, e.g., brain-derived neurotrophic factor (BDNF), reducing dendritic branching within hippocampal structures and predisposing one toward depression. Down-regulation of BDNF is preventable with antidepressant medication and, in the course of depression treatment, antidepressants can restore normal serum BDNF levels (Gonul et al. 2005).
In the composite, such evidence, and related emerging research, lends support for theoretical conceptualizations such as that of the biopsychosocial approach. Together, these lines of evidence begin to delineate the complex interactions of CNS mechanisms involved in pain and emotional processing, stress regulation, and cognitive processing.
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