Acute vs Chronic Pain: A Neurophysiological Perspective for Med Students

Not all pain is created equal – and understanding the neurophysiology behind acute and chronic pain is foundational for clinical practice.

🔹 Acute Pain: Fast, Protective, Predictable

Triggered by actual or potential tissue damage.

Nociceptors (Aδ fibres for sharp pain, C fibres for dull, burning pain) respond to mechanical, thermal, or chemical stimuli.

Signals synapse in the dorsal horn of the spinal cord, ascend via the spinothalamic tract, and are processed in the thalamus and somatosensory cortex.

Usually resolves with healing – the nervous system returns to baseline.

🔑 Key points:

Inflammatory mediators like bradykinin, prostaglandins, and substance P lower the activation threshold of nociceptors.

Descending inhibitory pathways (e.g., from the periaqueductal grey, locus coeruleus, and raphe nuclei) modulate the pain experience via serotonin, noradrenaline, and endogenous opioids.

🩺 Clinical example:

A 21-year-old presents with sharp right lower quadrant pain and rebound tenderness – typical of acute appendicitis. Inflammatory activation of nociceptors leads to a protective pain response.

💊 Treatment implications:

Typically responsive to NSAIDs (targeting prostaglandins) or opioids (acting on central and peripheral opioid receptors).

🔹 Chronic Pain: When the System Malfunctions

Defined as pain lasting >3 months or beyond expected tissue healing time.

It’s more than just persistent nociception – it involves maladaptive neuroplasticity:

Peripheral Sensitisation

Ongoing inflammation increases expression of ion channels (e.g., TRPV1, Nav1.7) on nociceptors.

Reduced threshold → innocuous stimuli can now trigger pain (allodynia).

Central Sensitisation

Repeated nociceptive input leads to increased excitability of dorsal horn neurons.

“Wind-up” phenomenon via NMDA receptor activation (glutamate-mediated).

Loss of inhibitory interneurons (e.g., GABAergic) worsens transmission.

Cortical Reorganisation

Functional and structural changes in the anterior cingulate cortex, insula, and prefrontal cortex.

Pain perception becomes more about processing abnormalities than direct nociception.

Descending Modulation Dysfunction

Impaired endogenous analgesia (e.g., reduced opioid and monoaminergic activity).

Glial cell activation releases proinflammatory cytokines that maintain pain signalling.

🩺 Clinical example:

A 53-year-old woman reports burning, electric pain months after shingles – consistent with post-herpetic neuralgia. The pain reflects central and peripheral sensitisation, despite resolution of the initial tissue damage.

💊 Treatment implications:

May require neuromodulators (e.g., amitriptyline, pregabalin), CBT, and interdisciplinary care. Opioids often ineffective and potentially harmful long-term.

🧠 Chronic pain becomes a disease state in its own right – not just a symptom – with biological, psychological, and social contributors. Understanding this is key to applying the biopsychosocial model in real-world practice.

💬 Your turn:

What clinical examples have you seen that highlight the difference between acute and chronic pain? Or which mechanisms are still tripping you up? Drop a comment below – let’s learn together! 👇 

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