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Visceral pain

Updated: Mar 7, 2022

Introduction | Types of nociceptors | Visceral nociceptive pathways | Convergence | Biochemistry of afferents | Central visceral pain pathways |



Visceral pain is disorders of the internal organs such as the stomach, kidney, gallbladder, urinary bladder, intestines, and others.

These disorders include distension

from impaction or tumours, ischaemia, inflammation, and traction on the mesentery

that can cause associated symptoms such as nausea, fever, malaise, and pain.

Solid organs are less sensitive than those with a hollow viscus

Severity of pain does not correlate with the seriousness of disease. For example, very severe cancer may cause minimal pain compared to the distension caused by wind within the gut.

Strangely, actual tissue damage to visceral structures, such as directly cutting bowel, can cause very little pain.

Visceral pain is often diffuse and is often referred. It can often be associated with significant autonomic changes also.


Types of nociceptors

High-threshold - These are generally mechanoreceptors and occur in organs where non-noxious stimuli rarely comes from e.g. kidney.

Low-threshold - These mechanoreceptors are commonly found in hollow organs (such as gut, bladder), and have a low threshold to 'normal' triggering factors such as stretch and tension.

Silent-nociceptors - These are nociceptors that become active in the setting of inflammation and tissue injury. It is likely these become sensitised and contribute to pain sensation for 'normal' actions of visceral tissues such as stretch of the bladder.

Central sensitisation in visceral pain is likely from both high-threshold, and silent nociceptors becoming increasingly active.


Visceral Nociceptive Pathways

Visceral afferents project to the CNS through both the sympathetic and parasympathetic pathways.

Sympathetic nerve fibres travel along the hypogastric, splanchnic, and lumbar colonic nerves via prevertebral and post vertebral ganglia.

Parasympathetic nerves travel via the vagal nerve and pelvic nerves.


The vagal afferents have their cell bodies within the nodose ganglion and come from the nucleus of the solitary tract of the brain stem and provide innervation to the gut from oesophagus to transverse colon

Sympathetic innervation:

These fibres divide profusely in the dorsal horn including going rostrally and caudally for up to 5 segments and also terminating in laminae 1, 2, 5, and 10. It is this profuse innervation that increases the risk of 'cross-talk' between spinal afferents that contributes to the diffuse nature of pain sensation and referred pain.

Somatic neurone on the L, Visceral innervation on the R.



Viscero-somatic convergence may explain why visceral pain can trigger somatic pain sensations and vice-versa. Viscero-visceral convergence can also occur.

In all, only 7% of afferent input to the spinal column comes from visceral tissues. This is somewhat surprising given the amount of neurones involved within certain areas such as the gut.


Biochemistry of afferents

Most visceral primary afferents are peptidergic and release substance P, somatostatin, and CRGP. These generally innervate the dorsal column in laminae 1,2 and 5. Non-peptidergic neurones generally innervate in laminae 2.


Central visceral pain pathways

Spinal afferents from visceral tissues synapse with second order neurones and ascend to the somatosensory cortex through several spinal pathways including the spinothalamic, spinohypothalamic, spinoreticular tract etc. And also in the dorsal columns.

Spinothalamic tracts project to the somatosensory cortex through the lateral nociceptive thalamus and the limbic system via the medial nociceptive thalamus. The insular cortex integrates sensory inputs from visceral structures with emotional components (e.g. contraction of smooth muscle in response to noxious stimuli)

(Remember: Somatosensory cortex is responsible for intensity and localisation of the stimulus whereas the limbic regions through the angulate Cingular gyrus are responsible for the affect-motivational components of pain experience)

(Remember: The limbic system is a set of structures in the brain that deal with emotions and memory)

As an example, in IBS FMRI has shown reduced function of the periacqueductal grey (PAG - area involved in descending inhibition) and abnormal activation of the anterior cingulate cortex (ACC).


Descending control pathways

Remember - Descending pathways can act as facilitators or inhibitors of neural transmission. ACC --> PAG is the main way the brain controls descending inhibition of spinal cord sensitisation and activation.

Facilitators/activators - Signals from the PAG are sent to the Rostral ventral medulla and the nucleus raphe Magnus (NRM) and increase the response to pain particularly in types of heightened arousal and emotional distress.

Inhibitors - Signals from the periacqueductal grey and rostral ventral medulla can inhibit pain signalling from the spinal cord. This was shown in studies where they electrically stimulated these areas while providing a noxious stimuli to the gut and it led to reduction in pain.

Reflexes - The PAG is also involved in reflex arcs for visceral organs. For example, a nociceptive input can cause a reflex bradycardia and hypotension response through the PAG. It is likely opioids have action here in leading to a reduced response to external stimuli in people under the influence of opioids.


USyd Masters Document - 2021

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