Pain: Encyclopedia II - Pain - Physiology

Pain - Physiology

Pain - Pain receptors

All pain receptors are free nerve endings. There are mechanical, thermal and chemical pain receptors. 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 is experienced.

Pain receptors do not adapt to stimulus. In some conditions, excitation of pain fibres becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia.

Nociceptors are the free nerve endings of neurons 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 like the branches of small bushes.

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 metres 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 fibres that send signals at rates of between 0.5 to 2 metres per second, is an aching, throbbing, burning pain. Chemical pain is an example of slow pain.

Pain - Transmission of pain signals in the central nervous system

The perception of pain occurs when the nociceptors are stimulated and 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. The signals are sent to the thalamus, in which pain perception occurs. From the thalamus, the signal travels to the somatosensory cortex in the cerebrum, at which point the individual becomes fully aware of the pain.

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

• Fast pain travels via type Aδ fibres to terminate on lamina I (lamina marginalis) of the dorsal horn. Second order neurons of the neospinothalamic tract then take off and give rise to long fibres which cross the midline through the anterior commisure and pass upwards in the contralateral anterolateral columns. These fibres then terminate on the 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 dorsa 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 fibres from the fast pathway, crossing to the opposite side via the anterior commisure, and travelling 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 mesencephalon. Slow pain is poorly localized.

Pain - Analgesia

The gate control theory of pain, proposed by Patrick Wall and Ron Melzack, postulates that pain is "gated" by non-painful 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 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 pain inhibitory neurons within the dorsal horns of the spinal cord, which act to inhibit 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 endogenous 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.

Adapted from the Wikipedia article "Physiology", under the G.N U Free Docmentation License. Please also see http://en.wikipedia.org/wiki