Pain Transmission Report Examples
Pain Transmission Report Examples
Pain is an essential part of the body’s defense system which is perceived as an unpleasant feeling. Pain produces a quick warning to the central nervous system to start motor response as a minimization of harm. Lack of pain perception is dangerous can cause grave problems such as Auto-amputation, corneal scarring or self-mutilation. Researchers in the medical profession have distinguished between pain and what is known as nociception. Nociception occurs when signals get to the central nervous system as a result of the activation of nociceptors (Svokos & Goldstein, 2009). Nociceptors are special sensory receptors which relay information regarding tissue damage. Pain may be explained as the unpleasant feeling resulting from nociception. This paper provides material on the subject of pain, while focusing on nociception, endogenous opioids, pathophysiology of neuropathic pain, how it is experienced by individuals and the cultural perceptions of pain.
According to Svokos & Goldstein (2009), nociception is the process through which tissue damage is detected by specialized receptors known as nociceptors. Nociception is a term that is used by many to refer to pain. However, there is a difference. Nociception is only the transmission of tissue damage information to the brain with no reference to the development of emotional or other responses to the noxious stimulus. There are two types of nociceptive pain. The pain that emanates from the skin and inner tissues (muscles and joints) is known as somatic pain while pain that comes from internal organs is known as visceral pain. Somatic pain is localized and easy tom point out while visceral pain is not. Stimuli that may cause damage such as chemical, thermal or mechanical stimuli cause cutaneous pain by affecting primary afferent nociceptors. Nociceptors are found distributed in skin, connective tissue, muscles, viscera and blood vessels. They are pseudonipolar neurons found with the cell body which is located inside the dorsal root ganglion (DRG). Nociceptors have a cell body which contains a peripheral terminal (ending) and axon that elicit a response to stimuli and have a central branch which transmits information into the Central Nervous System (CNS). There are two main types of nociceptors which respond to various modalities from noxious stimuli. The largest of the nociceptors is known as C-fibers and is connected to unmyelinated axons. C-fibers conduct information at a slow pace and respond to noxious stimuli such as thermal, chemical or mechanical stimuli. Natural thermal, chemical or mechanical are transduced into electrical signals by proteins found in the membrane of nociceptors. These electrical impulses are transmitted along the central and peripheral nociceptor axon into the CNS. Analysis reveals that the transducer molecules activated by noxious stimuli include TRPV1 and TRPM8. TRPV1 responds to heat, reduction in pH as happens in the chemical capsaicin and inflammation. TRPM8 responds to noxious cold. These molecules are usually targeted in therapeutic interventions for clinical pain conditions.
The second type of nociceptor population comprises of thinly myelinated axons known as A-delta fibers. These nociceptors are responsible for faster transmission than unmyelinated C-fibers. They convey sharp and momentary pain rather than the slow and distributed pain which is associated with the C-fibers. Another category of nociceptors that has unique properties is known as the “silent” or “sleeping” nociceptors. This category is not responsive to noxious intensities of mechanical stimulus except when the intensity is extreme. It is hard to activate silent nociceptors within the normal noxious stimulus intensity range after tissues are injured; these nociceptors “wake up” due to the effect of endogenous chemical mediators that are associated with injury to tissues. This type of nociceptors is usually related to increased responsiveness to noxious and innocuous intensities.
The Central Nervous System
The nociceptor’s central branch ends inside the spinal cord dorsal horn. It has synaptic linkages with an intricate array of neurons which play different roles as nociceptive processors. Some interneurons are connected to motor neurons which generate withdrawal reflexes. The spinal cord output neurons transmit nociceptive messages to the thalamus and brainstem reticular formation.
Opioid compounds as well as their receptors are found in the peripheral nervous system and CNS as well as in tissues (Koneru, Satyanarayana & Rizwan, 2009). Opioid systems take part in a variety of homeostatic functions and control of movement as well as in the processing of noxious impulses. Opioid analgesics have different effects which may be understood by reviewing the various types of opioid peptides.
Endogenous Opioid Peptides
There are different endogenous opioid Peptides which are produced in the body. These include endorphins, dynorphins, enkephalins and endomorphines. Each of these families of opioid peptides comes from a particular type of precursor protein and has a unique anatomical distribution. Endorphins are opioid polypeptide compounds which are produced in the pituitary gland and hypothalamus in vertebrates in the course of strenuous exercise, pain, excitement and orgasm. They have opiate-like characteristics because they can create analgesia and a feeling of well-being. They are “natural pain relievers” and can be found in more than 20 different points in the body such as in the nervous system, brain and the pituitary gland. The name “endorphin” implies a pharmacological process rather than a particular chemical formation. “Endorphin” is used for many proteins with opioid-like attributes. There are four types of endorphins namely alpha (α), beta (β), sigma (σ) and gamma (ɤ) (Koneru, Satyanarayana & Rizwan, 2009). The differences between the four endorphins are in the number and type of amino acids in their molecules. Each has between 16 and 31 in each molecule. During stress or pain, endorphins are released in the pituitary gland (Koneru, Satyanarayana & Rizwan, 2009).
According to Koneru, Satyanarayana & Rizwan (2009), enkephalins are pentapeptides which are involved in the regulation of nociception in the body. Two types of enkephalins exist. One is leu-enkephalins and the other is met-enkephalins. Met-enkephalins are a variety of naturally-occurring endogenous opioid peptide neurotransmitters which are found in the brains of humans and many animals. Leu enkephalins create pharmacological effects at the µ and δ opioid receptors. They select δ receptors more than µ receptors and have minimal effect to κ opioid receptors if any.
Dynorphins emerge from the prodynorphin precursor protein. Dynorphins are created in different regions of the brain like the hypothalamus, midbrain, hippocampus, pons, spinal cord and the medulla. Dynorphins have many physiological functions which are dependent on the site at which they are produced in the body. For example, those created in the magnocellular oxytocin neurons result in negative feedback inhibition of the secretion of oxytocin. Those created in the lateral hypothalamus’ arcuate nucleus result in appetite control. Dynorphins show their effects through the κ opioid receptors while acting as pain response modulators. They maintain homeostasis by controlling the appetite. There are two types of endomorphins. These are endomorphin-1 and endomorphin-2. Endomorphins have a very high specificity and affinity for µ opioid receptors. Endomorphin-1 is densely and widely distributed in the upper brainstem and the brain. It may regulate arousal or sedative behavior. On the other hand, endomorphin-2 is mostly found in the lower brainstem and the spinal cord. It plays a significant role in pain perception as well as in responses related to stress, reward, vigilance and arousal.
Opioid receptors fall into the categories κ, µ and δ. They are characterized by seven trans-membrane domains. They are found in high densities in CNS areas which are associated with the integration of information regarding pain. These areas of the CNS include medial thalamus, spinal cord, limbic system, hypothalamus and the brainstem. µ receptors have high morphine affinity. These are the main receptors that mediate the action of morphine and its congeners (Koneru, Satyanarayana & Rizwan, 2009). The endogenous ligands for the µ receptors are Endomorphins-1 and 2 which are located in the mammalian brain. There are two subtypes of receptors that exist: µ1 and µ2. µ1 has a greater morphine affinity. It mediates supraspinal analgesia and is blocked selectively by naloxone. µ2 has a lesser morphine affinity and mediates spinal analgesia, constipation and respiratory depression action. The κ receptor has a great affinity for Dynorphin A and ketocyclazocine. The δ receptor has a high leu/met Enkephalins affinity.
How normal pain is transmitted
Normal pain circuitry comprises of nociceptor activation response after a stimulus of pain is received. A depolarization wave is transmitted to the first order neurons. Sodium rushes in through sodium channels while potassium rushes out. The first-order neurons stop at the trigeminal nucleus of the brainstem or in the spinal cord dorsal horn. This is where the electrochemical signal causes the voltage-gated calcium channels to open in the pre-synaptic terminal. Calcium is the allowed in. In turn, calcium allows the excitatory neurotransmitter glutamate to be freed into the synapse. Glutamate then binds itself to NMDA receptors located on the second-order neurons. This causes depolarization. The neurons then cross into the spinal cord and travel up the hypothalamus (Svokos & Goldstein, 2009). Once in the hypothalamus, the neurons synapse with the third-order neurons. These then connect to the cerebral cortex and the limbic system. An inhibitory pathway prevents pain from being transmitted in the dorsal horn. The anti-nociceptive neurons move from the brain stem to the spinal cord where they Synapse at the dorsal-horn with short inter-neurons through the release of norepinephrine and serotonin. The synapse between the first- and the second-order neurons is modulated by the inter-neurons through the release of gamma amino-butyric acid (GABA), which is an inhibitory neurotransmitter. When pain ceases, it is as a result of the inhibition of the synapses between first-order and second-order neurons. On the other hand, enhancement of pain results when inhibitory synaptic connections are suppressed.
Pathophysiology of neuropathic pain
Neuropathic pain may be defined as the pain which is initiated by a dysfunction or primary lesion of the nervous system. Neuropathic pain comprises of “negative” symptoms (numbness and loss of senses) and “positive” symptoms (spontaneous pain, heightened sensation of pain and paresthesias) (Svokos & Goldstein, 2009).
Neuropathic pain is caused when the nervous system is damaged, injured or rendered dysfunctional. Neuropathic pain, unlike is the case for physiologic pain (nociceptive pain), is not self-limited. In addition, it is not treated easily. It is common in medical practice and is often a challenge to clinicians and patients alike. Neuropathic pain results in damage of either peripheral or CNS. The nerve fibers, once damaged, send the wrong signals to pain centers. Nerve fiber injury may result in a change in the function of nerves at the site where the injury has occurred or areas around the site of injury. Manifestations of neuropathic pain may include spontaneous pain, hyperalgesia and parasthesias. Neuropathic pain is associated with conditions which may be categorized in two main groups; pain as a result of CNS damage and pain as a result of peripheral nervous system damage (Svokos & Goldstein, 2009). Damage to the CNS is manifested in clinical conditions such as cortical strokes, syringe-myelia, neoplastic lesions, and trigeminal neuralgias. Peripheral nervous system damage is manifested through clinical conditions such as nerve compression, ischemic neuropathy, plexopathies and nerve root compression.
Pathophysiological processes involved in neuropathic pain
The mechanisms associated with neuropathic pain area not well understood. Animal studies have indicated that various mechanisms may be part of this process. However, it is important to understand that what may apply for animals does not necessarily have to apply for humans. First-order neurons can increase their firing if partially damaged, increasing the sodium channels. Enhanced depolarization on some sites along the fiber may cause ectopic discharges which in turn cause spontaneous pain as well as movement-related pain. Impairment of the inhibitory circuits may be done at the brainstem, dorsal horn or both. This allows impulses of pain to travel unimpeded (Svokos & Goldstein, 2009). Second-order and third-order neurons may create a memory of pain and be sensitized. One of the main challenges in the study of neuropathic pain is in being able to assess it. This challenge may be broken down into two components: (1) assessing the intensity, improvement and quality; and (2) diagnosing neuropathic pain with accuracy. Clinicians may use some diagnostic tools in the course of evaluating neuropathic pain. Nerve condition studies can be used to identify and quantify the degree of damage to the sensory (not nociceptive) pathways through monitoring of neurophysiological responses to stimuli of an electrical nature. Quantitative sensory measures the perception in response to stimuli of different intensities by the application of stimuli to the skin.
Inter-individual differences in pain sensitivity
The way people perceive pain differs from one person to the other. Individual pain perception differences have been the subject of inquiry in clinical practice for a long time. One individual may have an experience of pain that it totally different from another person experiencing the same pain stimulus (Coghill, 2012). Functional brain imaging techniques (fMRI) have been employed in analyzing the level of brain activity. This approach is used with the view to contributing to the creation of psychological/ psychophysical models that may be used to take pain treatment to an optimum. Understanding the differences in pain perception may be attributed to several factors such as environmental, genetic, ethnicity and gender, psychological, and cognitive variables (Coghill, 2012).
Genetic variables may be responsible for the differences in the level of pain perception between individuals. This is because the mechanisms that cause the differences in pain perceptions are dependent on a substrate which is partially determined by genetic factors. The study of twins gives insight into this matter. For example, 26-32% of the differences in heat pain between individuals are accounted for by genetics in twins. 21% in chemical pain and 60% of variability in cold noxious pain is genetically determined (Coghill, 2012). Interactions between sociological and genetic factors may also contribute to these differences in pain perception between individuals.
Ethnicity and gender have a genetic component and may cause these differences. Studies indicate that females are a bit more sensitive to thermal pain than males (approximately 8% difference). Females also withdraw their hand from cold noxious stimulus about 40% earlier than males. Ethnic differences also carry a substantial component of genetics which is manifested in differences in heat perception. For example, there are differences in which Southern Europeans, Northern Europeans, African Americans and Jews perceive pain. Asian-Americans have been proven to be more sensitive to pain than Hispanics or African Americans. Ethnic differences may also be experienced in a qualitative and not quantitative sense. Hispanic subjects tend to feel more of an itch upon the application of capsaicin to their skin while Asians and European Americans feel pain (Coghill, 2012). African Americans experience warmth with minimal pain.
Psychological factors can also contribute to how pain is experienced. There is diversity in internally maintained affective and cognitive information that can contribute to how pain is perceived. Such information may substantially alter how nociceptive information is interpreted.
Cultural influences on how pain is perceived
How people perceive pain and how they behave while in pain is greatly influenced by their sociocultural contexts (Calliste, 2003). Pain perception is made up of interactive, emotional and sensory components. The definition of pain can only be offered by the individual experiencing it. Patterns and meaning of pain across cultures has been a subject of constant inquiry. Studies show that there are differences in how people cope with pin across cultures. When American, African and Caucasian students were evaluated for coping styles for thermal pain, Africans gave the highest rating for unpleasantness (Calliste, 2003). Cutaneous pain perceptions were compared in African Americans and Caucasians where African Americans registered a higher rating for unpleasantness and gave lower tolerances (Calliste, 2003). Childbirth pain is also a major area for pain studies. In Kartchner & Callister (2003), mastering and overcoming childbirth pain was regarded as self-actualization. Women who were more religious seemed to have accepted that pain was inevitable and important in life. They depended on a higher power to enable them overcome childbirth pain. Hispanics and African Americans were noted to have the lowest tolerance for pain while people from Eastern countries have very high tolerances for pain (Calliste, 2003). Pain behavior is also different across cultures. In some cultures, people believe that pain is a personal experience and so they bear it privately. Some cultures verbalize pain more and this has been explained as the belief that pain is something bad which should be eliminated with speed.
Pain is an essential part of the body’s defense system which is perceived as an unpleasant feeling. Pain provides warning to the CNS to initiate motor responses in an effort to avoid further damage to tissue. Nociception is the process through which tissue damage is detected by specialized receptors known as nociceptors. There are different types of nociceptors which serve different purposes in pain perception. While the mechanisms for pain transmission and perception are similar for all people, people in different cultures perceive pain differently and behave differently in response to it (Calliste, 2003). There are also stark differences in how individuals experience pain, which may be explained in terms of genetics, ethnicity and psychological factors.
Calliste, L. C. (2003). Cultural Influences on Pain Perceptions and Behaviors. Home Health Care Management & Practice, 15(3), 207-211.
Coghill, R. C. (2012). Individual differences in the subjective experience of pain: New insights into mechanisms and models. Headache: The Journal of Head and Face Pain, 50(9), 1531-1535. Retrieved April 1, 2013, from http://dx.doi.org/10.1111/j.1526-4610.2010.01763.x
Kartchner, R., & Callister, L. C. (2003). Giving birth: The voices of Chinese women. Journal of Holistic Nursing.12(2), 12-45.
Koneru, A., Satyanarayana, S., & Rizwan, S. (2009). Endogenous Opioids: Their Physiological Role and Receptors. Global Journal of Pharmacology, 3(3),
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