Visceral Pain

Vagal afferents convey predominantly physiological information, while spinal afferents convey noxious stimuli.

There are likely to be three types of nociceptive sensory receptors: High threshold noxious, Low threshold innocuous to noxious, while some are silent and recruited by tissue injury and inflammation.

All can be sensitized, and drive central sensitisation that can persist even after the initial insult has resolved. Damage and inflammation also affects normal motility and secretion, producing changes to the nociceptor environment. While ascending pathways include the spinothalamic tract, the dorsal column is more important in nociceptive transmission. Ascending tracts synapse at the thalamus, limbic centres, and the somatosensory cortex. There is no somatotropic representation in the cortex. Pain is represented in the secondary somatosensory cortex. Visceral pain elicits nausea and hypotension, the opposite to somatic pain.

Peripheral sensitisation can occur, but the mechanisms differ from cutaneous sensitisation. Functional visceral disturbance can persist even after the initial insult has resolved. While with central sensitisation, NMDA receptors are likely to play significant role.

Visceral pain is initially described as vague, central sensation felt anterior or posterior, accompanied by various neurovegetative symptoms such as malaise, nausea, sweating, palour , anxiety, and sense of impending doom (‘true visceral pain’). Eventually this subsides, and is followed by a variety of symptoms and signs perceived in somatic areas receiving the same innervation. Skin, subcutis and muscle are all involved. Initially, the symptoms of pain rather than pain itself is felt. As time progresses, signs start to develop. The muscle layer is earliest and most commonly involved layer. However, the skin and subcutaneous layers are also commonly involved with hyperalgesia, and sudomotor signs. These symptoms and signs can persist even when the visceral insult has resolved. These symptoms and signs may also, in turn, influence visceral symptoms.

Clinical Characteristics

From Cervero et al 1999

Symptoms & Signs	Neurobiology
Not evoked from all viscera	Not all viscera are innervated by sensory receptors.
Not linked to injury	Functional properties of visceral sensory afferents
Referred to body wall	Viscerosomatic convergence in central pain pathways
Diffuse and poorly localised	Few sensory visceral afferents. Extensive divergence in central nervous system
Intense motor and autonomic reactions	Mainly a warning system, with substantial capacity for amplification

Pain is not evoked from all viscera.

It is generally evoked from the liver, kidney, lung parenchyma, and most solid viscera. These features are due to the functional properties of the peripheral receptors of the nerves that innervate certain visceral organs and to the fact that many viscera are innervated by receptors that do not evoke conscious perception and, thus, are not sensory receptors in the strict sense

Pain is not linked to injury.

Cutting the intestine causes no pain. But stretching it does (without injury). Pain can be produced by ischaemia, inflammation of the lining of the hollow viscus, stimulation (chemical or mechanical) of inflamed mucous membranes, traction compression or twisting of the mesentery, organ ligaments or blood vessels, or necrosis of the viscera such as the pancreas or myocardium.

Visceral pain is referred to the body wall

Viscero-somatic convergance and referred pain, muscle spasm, and hyperalgesia. All viscera are innervated by thoracolumbar outflow of sympathetic nervous system T1 - L2 via cardiac and splanchnic nerves, with cell bodies in the dorsal root ganglion. During development, viscera change position, drawing their innervation with them. This leads to a mismatching of intra abdominal position and segmental innervation, and enables understanding of pain referral patterns. Visceral sensations are mediated through convergent signals via somatosensory pathways.

Visceral afferents and cutaneous nociceptors converge on similar neurons at some point in the sensory pathways probably at a spinal level, but could occur at thalamic and cortical levels. The resulting impulses may be then misinterpreted at a spinal level as originating in the skin or other somatic structure. Most second order neurons receiving visceral input in laminae I and V, some in ventral horn. Fewest in the superficial dorsal horn. Most in the deep dorsal and ventral horn. Here they have diffuse and bilateral visceral and somatic input, are subject to descending excitatory and inhibitory control. Visceral afferents comprise fewer than 10% of all spinal afferent input. Therefore, visceral sensations can be mediated only through convergent signals via somatosensory pathways.