Somatosensory Neurotransmission: Deep and Visceral Pain

This flashcard set covers the neurophysiology of deep and visceral pain, including the mechanisms of referred pain, autonomic pathways, and the modulation of pain signals in the dorsal horn.

Deep Pain

A form of pain that is diffuse, poorly localized, and often accompanied by nausea, sweating, and blood pressure changes due to a deficiency of $A\delta$ fibers.

$A\delta$ fibers

Rapid-conducting nerve fibers responsible for sharp pain which are notably absent in deep structures, resulting in predominately dull, aching sensations.

Hypertonic Saline Model

An experimental tool where injection into periosteum or ligaments reproduces deep, aching visceral-like pain and triggers reflex muscle contractions.

The Vicious Cycle

A self-perpetuating feedback loop where reflex muscle spasm leads to ischaemia, which stimulates pain receptors, causing further muscle spasm.

Visceral Afferents

Sensory fibers that reach the Central Nervous System via sympathetic and parasympathetic nerves, including the facial, glossopharyngeal, and vagus nerves.

Intestinal Colic

Cramping pain produced as the intestine contracts and relaxes, caused by the high sensitivity of visceral wall receptors to distention.

Inflammatory Hyperalgesia

A condition in which the pain threshold of an inflamed visceral organ is dramatically lowered, causing minor stimuli to produce severe pain.

Referred Pain

Pain felt in a somatic structure distant from the actual site of visceral organ irritation, based on shared embryonic segmental origins.

Convergence-Projection Theory

The neurological basis for referred pain where visceral and somatic pain fibers converge on the same second-order neurons in the dorsal horn.

Testicle and Ureter Referral

A specific pattern of referred pain based on the shared embryonic origin of these structures in the primitive urogenital fold.

Facilitation

The mechanism by which prolonged visceral stimulus allows somatic inputs to activate second-order neurons that normally do not respond to them.

Gate Control Theory (Rubbing Effect)

The reduction of pain signals in the dorsal horn caused by the simultaneous activation of cutaneous mechanoreceptors.

Enkephalin and Dynorphin

Endogenous opioid peptides contained in dorsal horn interneurons that act on both presynaptic and postsynaptic sites to reduce nociceptive transmission.

Presynaptic Opioid Mechanism

Activation of opioid receptors that decreases the release of glutamate and substance P by reducing $Ca^{2+}$ influx into the terminal.

Postsynaptic Opioid Mechanism

Activation of opioid receptors that leads to hyperpolarization of the interneuron by increasing $K^+$ efflux.

Glutamate

The primary excitatory neurotransmitter in nociceptive afferents that activates AMPA and NMDA receptors to propagate pain signals.

Substance P

A neuropeptide co-released with glutamate from nociceptive afferents that amplifies and prolongs pain signaling.

Tolerance

The clinical phenomenon where the analgesic effect of a drug diminishes with repeated exposure, requiring escalating doses.