Pain physiology

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"Nociception is the term introduced almost 100 years ago by the great physiologist Sherrington (1906) to make clear the distinction between detection of a noxious event or a potentially harmful event and the psychological and other responses to it.^[1]"

Nociception is also known as nociperception and physiological pain.

Pain often has a physical cause, an injury to the body outside of the nervous system. In these cases, pain is initiated by mechanical, thermal or chemical changes in non-nervous tissues; this causes activation of specific nerves which relay to spinal centres concerned with the detection of injury, and thence to the thalamus and cortex, as well as to the reticular system. This hard-wired injury detection mode for pain is called "nociception", meaning detection of harm, while the nerves which detect the damage are called nociceptor nerves ("nociceptors" for short).

Common causes of nociceptive pain include traumatic injury (fractures, torn tissue and burns), degenerative conditions such as osteoarthritis, infections and inflammatory conditions such as abscesses or sunburn, and cancers causing tissue breakdown.

Nociceptors (Pain receptors)[edit]

All nociceptors are free nerve endings that have their cell bodies outside the spinal column in the dorsal root ganglion and are named based upon their appearance at their sensory ends. These sensory endings look microscopically like the branches of small bushes. There are mechanical, thermal, and chemical nociceptors. They are found in skin and on internal surfaces such as periosteum and joint surfaces. Deep internal surfaces are only weakly supplied with pain receptors and will propagate sensations of chronic, aching pain if tissue damage in these areas occurs.

Two main types of nociceptor, Aδ and C fibres, mediate fast and slow pain respectively. Thinly myelinated type Aδ fibres, which transmit signals at rates of between 6 to 30 meters per second mediate fast pain. This type of pain is felt within a tenth of a second of application of the pain stimulus. It can be described as sharp, acute, pricking pain and includes mechanical and thermal pain. Slow pain, mediated by slower, unmyelinated ("bare") type C pain fibers that send signals at rates between 0.5 and 2 meters per second, is an aching, throbbing, burning pain. Chemical pain is an example of slow pain. Nociceptors do not adapt to stimulus. In some conditions, excitation of pain fibers becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia.

Transmission of nociception (pain) signals in the central nervous system[edit]

There are 2 pathways for transmission of nociception in the central nervous system. These are the neospinothalamic tract (for fast pain) and the paleospinothalamic tract (for slow pain).

• Fast pain travels via type Aδ fibers to terminate on lamina I (lamina marginalis) of the dorsal horn of the spinal cord. Second order neurons of the neospinothalamic tract then take off and give rise to long fibres which cross the midline through the grey commissure and pass upwards in the contralateral anterolateral columns. These fibres then terminate on the reticular formation,Ventrobasal Complex (VBC) of the thalamus. From here, third order neurons communicate with the somatosensory cortex. Fast pain can be localised easily if Aδ fibres are stimulated together with tactile receptors.

• Slow pain is transmitted via slower type C fibres to laminae II and III of the dorsal horns, together known as the substantia gelatinosa. Second order neurons take off and terminate in lamina V, also in the dorsal horn. Third order neurons then join fibers from the fast pathway, crossing to the opposite side via the grey commisure, and traveling upwards through the anterolateral pathway. These neurons terminate widely in the brain stem, with one tenth of fibres stopping in the thalamus, and the rest stopping in the medulla, pons and tectum of midbrain mesencephalon, periaqueductal grey. Slow pain is poorly localized.

Consequences of nociception[edit]

When the nociceptors are stimulated they transmit signals through sensory neurons in the spinal cord. These neurons release glutamate, a major exicitory neurotransmitter that relays signals from one neuron to another.

If the signals are sent to the reticular formation of brain stem, thalamus, then pain enters consciousness, but in a dull poorly localised manner. From the thalamus, the signal can travel to the somatosensory cortex in the cerebrum, when the pain is experienced as localised and having more specific qualities.

Feinstein and colleagues found that nociception could also, "activate generalized autonomic responses independently of the relay of pain to conscious levels" causing "pallor, sweating, bradycardia, a drop in blood pressure, subjective "faintness," nausea and syncope" ^[2].

Analgesia[edit]

The gate control theory of pain, proposed by Patrick Wall and Ron Melzack, postulates that nociception (pain) is "gated" by non-nociception stimuli such as vibration. Thus, rubbing a bumped knee seems to relieve pain by preventing its transmission to the brain. Pain is also "gated" by signals that descend from the brain to the spinal cord to suppress (and in other cases enhance) incoming nociception (pain) information.

The analgesia system is mediated by 3 major components : the periaquaductal grey matter (in the midbrain), the nucleus raphe magnus (in the medulla), and the nociception (pain) inhibitory neurons within the dorsal horns of the spinal cord, which act to inhibit nociception(pain)-transmitting neurons also located in the spinal dorsal horn.

The body has several different types of opioid receptors that are activated in response to the binding of the body's endorphins. These receptors, which exist in a variety of areas in the body, inhibit firing of neurons that would otherwise be stimulated to do so by nociceptors.

References[edit]