1998 Third Web Reports
Pain is possibly the most unpleasant sensations our senses can detect. Even though we typically fail to remember what pain feels like when we are not experiencing it, we certainly do not wish to experience pain. Despite pain's unpleasantness, it has to be appreciated for what it is. Namely, a mechanism that allows us to avoid dangerous situations, to prevent further damage, and to promote the healing process. Pain allows us to remove ourselves form dangerous situations, as we attempt to move away from noxious stimuli that cause pain. As we attempt to escape stimuli that cause pain after an initial insult on our body, pain can prevent further damage form occurring. Finally, pain promotes the healing process as we take great care to protect an injured body part form further damage as to minimize the experience of more pain. How is this unpleasant, yet helpful sensation detected?
Nociception is the term commonly used to refer to the perception of pain. The receptors involved in pain detection are aptly enough referred to as nociceptors - receptors for noxious stimuli. (1) These nociceptors are free nerve endings that terminate just below the skin as to detect cutaneous pain. Nociceptors are also located in tendons and joints, for detection of somatic pain and in body organs to detect visceral pain. Pain receptors are very numerous in then skin, hence pain detection here is well defined and the source of pain can be easily localized. In tendons, joints, and body organs the pain receptors are fewer. The source of pain therefore is not readily localized. Apparently, the number of nociceptors also influences the duration of the pain felt. Cutaneous pain typically is of short duration, but may be reactivated upon new impacts, while somatic and visceral pain is of longer duration. (2) It is important to note that almost all body tissue is equipped with nociceptors. (1, 2) As explained above, this is an important fact, as pain has primary warning functions. If we did not feel pain and if pain did not impinge on our well-being, we would not seek help when our body aches. Hence, it makes evolutionary sense for the body to be so well equipped with nociceptors in almost all locations. The most notable exception to this logic is the brain. The brain itself has no nociceptors and therefore is pain insensitive. Why is this all-important structure not equipped with and therefore indirectly protected by nociceptors? Presumably, the brain is not equipped with nociceptors as an impact that is strong enough to 'hurt' the brain would almost certainly be fatal. As evolution is ecological, the brain therefore probably came to have no nociceptors. The meninges, the membranes enveloping the brain are equipped with pain receptors, however. How is the input the nociceptors receive transmitted to the brain? As stated, nociceptors are free nerve endings. These free nerve endings evidently must be part of a neuron. The nociceptors indeed are the nerve endings of neurons that have their cell bodies outside the spinal column in the dorsal root ganglion. Theses neurons may be either of three types. They may be Aa-fibers, Ad-fibers or C-fibers. Aa-fibers are about 3 - 20 mm thick and are covered with relatively thick myelin sheaths. They conduct impulses at the rate of 100 m/sec. Technically, the Aa-fibers are not pure nociception neurons, as they do not distinguish between painful and not painful stimuli, but transmit either. The true nociception neurons are the Ad-fibers and C-fibers. For further discussion of the pain pathway Aa-fibers will be ignored and the discussion will solely refer to the Ad-fibers and C-fibers. (1, 2)
Ad-fibers are about 1 - 3 mm thick and are covered with thin myelin sheaths. Transmission of impulses is slower than for Aa-fibers and lies at about 20 m/sec. C-fibers are up to 1 mm thick and not myelinated. Since the fibers are so thin and because they lack the myelin that speeds transmission immensely, conduction speed is slow; information travels at about 1 m/sec. The Ad-fibers and C-fibers not only differ in terms of their respective structure and transmission speeds, but they are also laid out to detect different stimuli. Ad-fibers transmit sharp, pricking pain. C-fibers, on the other hand, transmit burning, throbbing pain. (1,2) Despite these differences, both fiber types share a common pathway when transmitting detected information. The route the fibers' impulses travel is commonly referred to as the pain pathway. By virtue of the structures the pathway is embedded in and involves, the pain pathway is also called the spinothalamic tract. (1)
As with most of the nomenclature in the natural sciences, the name of the pain pathway spells out the main structures involved in nociception - the spinal chord and the thalamus. The spinal chord is the structure of origin of nociception and the thalamus is the site in the brain where pain is essentially detected. The role of each and the intermediate steps of transmission will be elucidated in the following. The impulses detected by the nociceptors are transmitted via the Ad-fibers and C-fibers. These fibers transmit the information they receive from the nociceptors to the spinal chord by entering the spinal chord via the dorsal horn. Once inside the spinal chord, the fibers ascend or descend spinal chord segments as to enter the substantia gelatinosa (gray matter) of the spinal chord. The substantia gelatinosa contains several laminas. The Ad-fibers and C-fibers may synapse in any lamina, but typically do so in the superficial laminas I and II. (2)At the synapse in the lamina, the neurons release substance P. (2) This excitatory neurotransmitter activates second order neurons. (3) These second order neurons decussate to the anterior commisure and ascend in the spinal column. The neurons ascending neurons are, as the nociceptive neurons, Ad-fibers and C-fibers. Once the Ad-fibers and C-fibers leave the spinal column, the brain structures they target are quite different. (2) The fast fibers, Ad-fibers, synapse in the thalamus with third order neurons. These neurons relay the information to the somatosensory cortex that is located in the postcentral gyrus. (2) One is a able to detect pain as soon as it reaches the thalamus. Physical awareness of the location and extend of the painful stimulus only becomes possible when the somatosensory cortex is activated. This localization is possible, as the body parts are mapped out on the somatosensory cortex. This representation of the body on the somatosensory cortex is referred to as the homunculus. (4) The homunculus receives activation form the body parts it represents. So, when one cuts one's finger, the nociceptors relay information via the spinal chord and the thalamus to the part of the somatosensory cortex where the homunculus' finger is. Notably interesting is that the homunculus is laid out in such a form that it does not represent body parts in proportion to the actual size, but in proportion to the touch receptors that can be found in the particular body part. (4) Generally then, the Ad-fibers are responsible for the perception of intensity and location of the pain experienced.
The C-fibers synapse in the reticular formation and the intralaminar nuclei of the thalamus. As the Ad-fibers, they synapse with third order neurons. However, C-fiber impulses are not relayed to the somatosensory cortex but to the association cortex instead. (2) As cortex consists of motor cortex, somatosensory cortex and association cortex only, C-fiber impulses really are relayed to the whole brain. Their impulses thus are responsible for the affect that accompanies pain. Intuitively it seems as though the Ad-fibers contribute more importantly to the perception of pain than the C-fibers. They transmit faster and they allow one to determine where the insult on the body has taken place. The C-fibers, on the other hand, conduct their inputs very slowly and give one the ability to appraise the painful sensation. Despite this apparent difference in importance of the two sets of fibers, each has its particular virtues and significance.
Lacking Ad-fibers would make pain perception entirely impossible. One would be very prone to injury, as harmful situations could not be classified as such on the basis of experienced pain. Also, internal problems could not be felt. Considering the implications an unnoticed appendix attack or cardiac infarction may have, the importance of Ad-fibers becomes clear. However, C-fibers also carry important implications. If one fails to appraise pain, all detection of it by Ad-fibers is in vain. In reality then, the experience of pain really is nothing else but the interpretation of nociceptive inputs. Were C-fiber relaying of nociceptive inputs not relayed to the association cortex, one may well imaging that pain is not understood as what it is - a warning. A proper appraisal of pain is necessary as to understand that the experience of in the somatosensory cortex has implications for one's health and well being. The appraisal of pain is most likely closely linked to one's pain tolerance - the point at which one cannot take more pain than experienced. If a dissociation between nociception and pain appraisal occurs, the experience of pain would not bear on behavior, as the affect is missing. This affect really makes pain what it is for every individual. It can account for the variability of pain tolerance among individuals. Without C-fibers then, the experience of pain would be similarly impossible as without Ad-fibers. Neither is superior to the other. Actually, the two make up an entity that would be quite incomplete without the other. The neuronal mechanism of nociception and pain perception have been treated. It has been established that the ability to perceive pain is of vital importance in every day life. However, pain is mostly not praised but condemned. An attitude that is readily understood. Especially when considering those unfortunate people who suffer form a pain condition, such a chronic pain, phantom limb, or hyperesthasia. In these instances the experience of pain is in no way beneficial and there also is little help available. Generally, however, pain, as bothersome as it is, really is more friend than foe.
Comments made prior to 2007
am aware that massive stimulation of nociceptors can kill due to its
affects on the autonomic nervous system [causing shock and depriving
the vital organs of blood supply]. The autonomic nervous system is
still fully-active during unconsciousness. Nociceptors can still be
stimulated during total unconsciousness. Nociceptors can still
communicate with the autonomic nervous system during unconsciousess.
The connections between the nociceptors and the autonomic nervous
system are fully-intact during unconsciousness.
So how it it that an unconscious individual can survive extreme stimulation of nociceptors that would kill a conscious individual? ... Green, 23 February 2006