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In order to understand pain and the management of pain, it is helpful to have a basic understanding of the neurophysiology associated with the transmission of painful impulses. Pain can be caused by mechanical stimulation such as overstretching of a body cavity. Pain can also be caused by chemical irritation such as occurs when the appendix ruptures and spills its contents into the abdominal cavity. Excessive heat or cold can cause pain. Other causes include hypoxia, inflammation and tissue injury. While each of these etiologies appears to be quite different, the neurophysiology remains the same. Pain has several component parts: neurons must receive the impulse, the impulse must be transmitted to the brain so that the pain can be perceived, and the body must respond to the pain.1
In the event of tissue damage due to an injury, the body needs to be able to identify the problem and take steps to protect itself from further damage. Without this protective ability we would succumb to all sorts of minor injuries. For example, when you cut your hand, free nerve endings in the skin identify this as noxious stimuli (nociceptive) and begin the process of transmitting this information to the brain. Free nerve endings located throughout the body that respond to noxious stimulation are called nociceptors. Some nociceptors are specialized and only recognize very specific types of pain, others are more general and respond to multiple types of noxious stimulation. There are two types of nociceptors, A-delta fibers and C fibers. A-delta fibers are myelinated and transmit impulses quickly. They are responsible for sharp, stabbing and well-localized pain sensations. The C fibers are slower and transmit dull, aching and poorly localized sensations. There are more A-delta fibers located on the skin than there are inside the body. This helps to explain why it is easier for us to localize pain due to injury of the skin than pain due to an internal injury. Injury or damage to tissues results in the release of several substances at the cellular level which irritate these free nerve endings. These neurotransmitters facilitate the transmission of the stimuli.2
In order for an impulse to be transmitted from one neuron to another, chemical substances called neurotransmitters are needed. The neurotransmitters that are responsible for the transmission of these impulses include acetylcholine, serotonin, dopamine, histamine and Substance P. An impulse travels from the free nerve endings to the dorsal horn of the spinal cord. From the dorsal horn, with the aid of the neurotransmitter, Substance P, the impulse is transmitted to the spinothalamic tract.3
Spinal cord transmission of noxious stimuli has two major pathways. The first pathway is a protective mechanism for the body. Noxious stimuli from the periphery is transmitted to the spinal cord via afferent fibers. In the spinal cord they meet with efferent motor neurons. This causes the mechanism referred to as a reflex arc. This shortcut allows the body to respond to an injury quickly without waiting until the brain interprets the information. Touching a hot stove will cause the muscles to contract and allow you to quickly pull your hand away from the stove. This process occurs without the aid of higher brain functions.2
The other mechanism of transmission occurs in the spinal cord. Here the impulse travels from the afferent fibers to the dorsal horn. From the dorsal horn they cross over to the opposite side of the spinal cord and travel upward to the thalamus via the spinothalamic tracts. The impulse pauses at the thalamus, which acts as a relay station.4
The thalamus is responsible for interpreting the data from the nociceptors. It is here that the stimuli are recognized as pain. The thalamus then sends the impulse along to higher levels of the brain, such as the limbic system, the reticular system and the cerebral cortex.4
The limbic system is the part of the brain that controls our emotions. The interpretation of the pain impulses by the limbic system account for our emotional reaction to pain and our ability to cope with pain. This system is associated with pleasure as well as pain.5 The limbic system controls our involuntary behaviors associated with survival.
Once the impulses are transmitted from the thalamus to the cerebral cortex the body is able to localize the problem. It is here that the pain sensation is interpreted, based on our memory of past experiences with pain.4 This helps to explain why individuals respond to pain in different ways.
The reticular formation is responsible for arousal and alertness. It interacts with the limbic system to perceive pain. Factors that increase or decrease consciousness will effect pain perception. If we decrease arousal by using analgesics, we can decrease the perception of pain. If arousal is increased due to stressors such as lack of sleep, fear or anxiety, then pain perception is increased.6 This is especially important to remember when caring for hospitalized patients.
Over the years scientists studying pain have attempted to develop adequate theories to describe pain transmission. There are three major pain theories: the specificity theory, the pattern theory, and the gate-control theory. None of these theories are able to provide all of the answers to questions related to pain transmission.7
Specificity Theory. In the 17th Century, Descartes proposed the specificity theory of pain transmission. This theory proposes that there are specific pain receptors in body tissues, and these are the ones that create and transmit pain to the central nervous system. In this theory the receptors recognize the stimulus as pain immediately.8
Pattern Theory. In this theory it is proposed that a pattern or coded sequence of stimuli are interpreted by the central nervous system as pain.8 This theory, as well as the specificity theory, do not adequately explain individual differences in response to pain.
Gate-Control Theory. This theory was first proposed in 1965 by Melzack and Wall.9 This theory proposes three interactive systems. The first system is the substantia gelatinosa, located in the dorsal horn of the spinal cord. This is the site of impulse regulation of the primary stimuli. The central control system, which is located in the thalamus and cortex regulates the transmission of the impulse from the cord to the brain. The last system is the neural system which is charged with the perception of pain. Pain impulses travel from their origin to the dorsal horn of the spinal cord and are able to pass through an open gate in the substantia gelatinosa. From here the impulse travels to the spinothalamic tract and to the thalamus and cortex. It is here that the perception of pain occurs. Melzack and Wall theorize that this gate can be closed by competing impulses in the skin, the reticular formation, brain stem or thalamus. This may explain why emotions and past experience play such a large role in an individual's reaction to pain.10
The body produces pain-mediating substances. These, in effect, close the pain gates and decrease the perception of pain by preventing the transmission of noxious stimuli to the brain. The naturally occurring pain mediators are enkephalins and endorphins. They attach themselves to the opiate receptor site and block the transmission of pain. They produce analgesia by closing the pain gate. There are three types of receptor sites that are involved in analgesia: mu, kappa and sigma. Drugs that attach to mu receptors produce analgesia, sedation and respiratory depression. Drugs that attach at kappa receptor sites are less likely to produce respiratory depression. Drugs that attach at sigma receptor sites are most likely to cause confusion and hallucinations.11
Endorphins are thought to be released in response to extreme stress. Studies demonstrate low endorphin levels in patients with chronic pain. It is possible that the depletion of endorphins from prolonged pain actually increases the perception of pain by permitting the pain gates to remain open.12
Many of the physiological responses we have come to expect from pain are really just the reaction of the body to stress. To understand this better, we need to look at the neurophysiology of stress. In 1976 Selye proposed the general adaptation syndrome (GAS). This process has three stages: the alarm stage, the reaction stage and the exhaustion stage. This theory proposes that regardless of the stressor, our bodies respond in a predictable manner. The interaction between the nervous and endocrine systems account for the signs and symptoms we see.13
Alarm Stage. In this stage the body mobilizes its resources to protect itself. Increased hormone production prepares the body to act. The mind becomes sharper, the person more alert. The heart rate and blood pressure increase to provide more energy to tissues. The respiratory rate increases to provide more oxygen. Pupils dilate to improve vision. The posterior pituitary produces more antidiuretic hormone (ADH). This decreases urine output and increases cardiac output. The anterior pituitary increases production of adrenocorticotropic hormone (ACTH). This stimulates the adrenal cortex and results in increased levels of cortisol and aldosterone. Increased cortisol prepares the body to metabolize fat and protein for extra energy. The increased aldosterone prevents water loss by increasing sodium and water reabsorption in the kidneys. This increases the blood volume and results in increased preload. The end result of increased preload is increased cardiac output and increased blood pressure.14
The sympathetic nervous system produces epinephrine and norepinephrine. These increase the blood sugar, heart rate and blood pressure. Blood flow is increased to vital areas such as the skeletal muscles and decreased to areas that are considered less essential for survival, such as the skin and the GI tract.14
Many of the signs and symptoms we look for in patients who report pain are those that are related to the body's response to stress. The fast heart rate, high blood pressure, cold clammy skin and nausea are indicators of stress. However, not all people will respond to stress the same. How the stressor is perceived, our previous experience with pain, and available coping mechanisms will affect our reactions to stress.15
Reaction Stage. In this stage the body is attempting to adapt to the stressor. The hormone levels return to normal, and the vital signs return to their previous level. If the stress is relieved, this episode is filed away for future use by the brain. If the stressor remains, and coping mechanisms fail, the person enters the exhaustion phase.12
Exhaustion Stage. This occurs when the body can no longer tolerate the stressor. All of its resources are used up. If the stressor continues, exhaustion and death will occur.13
Pain is a major stressor. The symptoms we commonly associate with pain are the symptoms seen in the alarm stage of the GAS. While these may occur with episodes of acute pain, the lack of such symptoms may be due to the body's inability to respond to high metabolic demands over a prolonged period of time. Persons with chronic pain will rarely exhibit symptoms such as tachycardia and hypertension. An understanding of these concepts demonstrates why the dependence on physical symptoms for the assessment of pain can result in underestimation of pain.
Answer the following questions related to neurophysiology.
Answers:
1. e
2. b
3. c
4. a
5. b
6. b
7. b
8. c
9. d
10.d
11.b
12. d