When does acute pain become chronic? | Br. J. Anaesth. (2010)
The transition from acute to chronic pain appears to occur in discrete pathophysiological and histopathological steps.
Chemical, mechanical, and thermal receptors, along with leucocytes and macrophages, determine the intensity, location, and duration of noxious events.
Noxious stimuli are transduced to the dorsal horn of the spinal cord, where amino acid and peptide transmitters activate second-order neurones. Spinal neurones then transmit signals to the brain.
Throughout these processes, prostaglandins, endocannabinoids, ion-specific channels, and scavenger cells all play a key role in the transformation of acute to chronic pain.
A better understanding of the interplay among these substances will assist in the development of agents designed to ameliorate or reverse chronic pain.
Current theories propose that a prolonged experience of acute pain in which long-standing changes are seen within and external to the central nervous system (CNS) creates chronic pain with a histological and pathological basis.
Furthermore, chronic pain development after surgery likely occurs as a result of complex biochemical and pathophysiological mechanisms that differ in type among different surgical procedures.
This article focuses on how postoperative, traumatic, and neuropathic nociception are generated and inter-related, with the goal of providing a deeper understanding of how long-term pain develops so that we can prevent and treat it more effectively, in the hope of stimulating more research and inquiry.
Mechanism for acute pain generation: peripheral effects and spinal and central effects
A long and detailed, highly technical explanation of “how pain happens” follows in the article: Mechanism for acute pain generation: peripheral effects and spinal and central effects
Neuroplasticity, or the physical remodelling of neuronal cytoarchitecture, occurs shortly after the onset of persistent acute pain and leads to the transition from acute pain into a chronic pain state.
As a result of a peripheral lesion that persistently generates pain impulses to the spinal cord, inhibitory interneurones responsible for modulating painful nerve transmission impulses eventually die.
Furthermore, glial cells remodel neuronal synapses to intensify nociceptive transmission. These pain-transmitting neurones become more sensitive, react more intensely to stimuli, and grow more connections to second-order neurones within the CNS.
In short, this process of neuroplasticity leads to central sensitization in which activity dependent phenotypic changes are seen in the dorsal horn neurones and other CNS structures, including higher centres
The mechanisms of post-procedural pain and chronic post-surgical pain are complex and poorly understood. Many of the syndromes are, at least in part, neuropathic that result from neuroplastic changes after injury.
After surgical intervention, patients experience ongoing pain or are sensitive to incidental, normally non-painful stimulation. This period of time varies, and with uncomplicated wound healing this pain progressively attenuates and disappears.
The patient population with persistent post-surgical pain experience deep pain or referred pain that lasts months or years.
From the perspective of patient’s overall assessments of their health, even low levels of residual pain significantly affect social and physical function.
Surgery causes the release of inflammatory and other mediators. Initially, these mediators activate nociceptors, however during persistent pain nociceptors become sensitized.
If this persistent pain resolves in the process of normal wound healing, this process of sensitization and facilitation of synaptic transmission to the CNS reverts to normal intrinsic nociceptor activity.
For many surgery-related reasons, such as prolonged inflammatory states with the insertion of mesh materials or chronic nerve stretching in bunionectomy, this process of sensitization and facilitation can cause phenotypic and pathophysiological changes in nociceptors.
- changes in gene expression,
- receptor translocation to the cell membrane,
- sustained activation of inflammatory and glial cells, and
- spinal inhibition and facilitation.
Once these structural changes occur, chronic pain pathophysiology becomes established.
Nerve injury causes both neural and immune changes that give rise to neuropathic pain.
There is a large body of evidence that shows the pathophysiology of different pain types such as inflammatory, neuropathic, or cancer-related pain is distinct from one another
Many patients with post-procedural pain report both sensory abnormalities and localized stimulus-evoked pain, suggesting that both abnormal sensory nerve function and ongoing nociception play a role.
The question of whether acute pain causes chronic pain has not been completely resolved, but some type of stimulus or continuous nociceptive process provides the impetus for chronic pain to develop. The mechanisms are multifactorial and complex.
They encompass inflammatory and neuropathic processes, and multiple ligand- and voltage-gated ion channels that activate intracellular cascades, necessitating multimodal treatment.
Pain is also tissue-specific, influenced by underlying genetics and mental state. The duration and intensity of the initial insult leads to both peripheral and central sensitization that synergistically exacerbate pain perception.
Many details remain unclear, such as the time interval required for pain progression and a deeper understanding of the overlap between the myriad pain mechanisms and comorbidities.
The increased use of comprehensive standardized pain evaluation and treatment protocols, coupled with the use of multimodal analgesic techniques aimed at both peripheral and central mechanisms, are likely to become the mainstay of complete perioperative analgesia in the prevention of chronic pain.
Navigate This Article
- Mechanism for acute pain generation: peripheral effects and spinal and central effects
- Post-procedural pain
- Neuropathic pain
- Epidemiology of chronic pain
- Development of chronic pain
- Preventing neuroplastic changes
- Psychosocial factors
- Surgical factors
- Anaesthetic factors
- Predicting postoperative pain
- Clinical evidence of multimodal treatment strategies
- Conflict of interest