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Descending modulatory pain pathways
Descending pathways contribute to the modulation of pain transmission in the spinal cord via
presynaptic actions on primary afferent fibres, postsynaptic actions on projection neurons, or
via effects on intrinsic interneurons within the dorsal horn. Sources include direct corticofugal
and indirect (via modulatory structures such as the PAG) pathways from the cortex, and the
hypothalamus, which is important for coordinating autonomic and sensory information. The
RVM receives afferent input from brainstem regions (PAG, parabrachial nucleus and nucleus
tractus solitarius) as well as direct ascending afferent input from the superficial dorsal horn,
and is an important site for integration of descending input to the spinal cord (Millan, 2002).
The relative balance between descending inhibition and facilitation varies with the type and
intensity of the stimulus and also with time following injury (Vanegas & Schaible, 2004; Heinricher
et al, 2009; Tracey & Mantyh, 2007). Serotonergic and noradrenergic pathways in the dorsolateral
CHAPTER 1 funiculus (DLF) contribute to descending inhibitory effects (Millan, 2002) and serotonergic
pathways have been implicated in facilitatory effects (Suzuki et al, 2004).
Neuropathic pain
1.1.3
Neuropathic pain has been defined as ‘pain initiated or caused by a primary lesion or
dysfunction in the nervous system’ (Merskey & Bogduk, 1994; Loeser & Treede, 2008). Although
commonly a cause of chronic symptoms, neuropathic pain can also present acutely following
trauma and surgery. The incidence has been conservatively estimated as 3% of acute pain
service patients and often it produces persistent symptoms (Hayes et al, 2002). Similarly, acute
medical conditions may present with neuropathic pain (Gray, 2008) as discussed further in
Section 9.
Nerve injury and associated alterations in afferent input can induce structural and functional
changes at multiple points in nociceptive pathways. Damage to peripheral axons results in loss
of target‐derived growth factors and marked transcriptional changes in DRG of injured
neurons (including downregulation of TRP and sodium channels) and a differing pattern in
non‐injured neighbouring neurons that contributes to spontaneous pain (Woolf & Ma, 2007). In
the spinal cord, activation of the same signal transduction pathways as seen following
inflammation can result in central sensitisation, with additional effects due to loss of inhibition
(Sandkuhler, 2009). Central neurons in the RVM were sensitised after peripheral nerve injury
(Carlson et al, 2007) and structural reorganisation in the cortex after spinal cord injury (Wrigley et
al, 2009), and changes in cerebral activation have been noted in imaging studies of patients
with neuropathic pain (Tracey & Mantyh, 2007).
1.2 PSYCHOLOGICAL ASPECTS OF ACUTE PAIN
Pain is an individual, multifactorial experience influenced, among other things, by culture,
previous pain experience, belief, mood and ability to cope. Pain may be an indicator of tissue
damage but may also be experienced in the absence of an identifiable cause. The degree of
disability experienced in relation to the experience of pain varies; similarly there is individual
variation in response to methods to alleviate pain (Eccleston, 2001).
The IASP’s definition of pain (Merskey & Bogduk, 1994) emphasises that pain is not a directly
observable or measurable phenomenon, but rather a subjective experience that bears a
variable relationship with tissue damage. The task of researchers and clinicians is to identify
any factors that might contribute to the individual’s pain experience. These could include
somatic (physical) and psychological factors, as well as contextual factors, such as situational
6 Acute Pain Management: Scientific Evidence
