Describe the pathways responsible for modulation of painful stimuli in the central nervous system
Introduction
Pain is caused by threatened or actual tissue damage that stimulates nociceptive (pain sensitive) neural receptors. Pain may also be caused by damage to the transmission system itself. However, thee stark statements do not actually help us understand and actual person’s pain experience. It is like describing a sunset in terms of the physical stimulation of the retina! We do need to know about the pain receptors and their pathways to the brain.
Pain Receptors
The train of events that leads to pain begins when pain receptors are stimulated by mechanical, chemical or thermal sources. Nerve receptors for pain (nociceptors) differ from the complex receptors for vision and other senses. Nociceptors are simply free nerve endings occurring in almost all type of tissue. Nociceptors react only to changes very close to them and they require a relatively high level of stimulation to be activated. However, once their threshold is exceeded they continue to actively communicate the presence of the painful stimulus (slow adaptation). Nociceptors can also become sensitized so that continues to discharge long after the stimulus is removed. Most is known about pain coming from receptors in the skin. It is assumed that pain receptors in deeper tissue are similar, but they may operate differently.
Pain Experience
Once nociceptors are stimulated, the impulse they discharge travels as electrical activity to the spinal cord and on to the brain. This electrical activity becomes the experience of pain when it reaches the brain. There are no “pain impulses” as such. However, if the neural pathway for these impulses is blocked, pain is also blocked since the impulses do not reach the brain. Pain pathways can be blocked by (a) surgically cutting the, (b) drugs that inhibit the activity of the pathway’s fibers, and (c) natural (endogenous) methods of blocking portions of the pain pathway.
Nerve Pathways
Nerve Fibers that carry somatosensory information from the body periphery to the spinal cord include A-beta, A-delta, and C fibers. A-type fibers have a myelin sheath that speeds up information transmission. A-delta fibers transmit pain. A-beta fibers are larger and carry other sensory information. C fibers transmit pain more slowly because they have no myelin sheath.
Pain sensation following stimulation of A-delta fibers differs from that following C-fiber stimulation. A-delta activity is experienced as sharp, easily localized pain. C-fiber activity is felt more slowly after painful stimulation. It is persistent, dull, and aching and is difficult to localize. Recall when you received an injection or stubbed your toe. A sharp, well-localizes sensation occurred first (a-delta activation) followed by a persistent, dull, aching sensation (C-fiber activation).
Spinal Cord Pathways
Different transmissions pathways in the spinal cord contribute to the experience of various qualities of pain. The major spinal tract carrying painful information to the brain is the spinothalamic tract. Some fibers of this tract go directly to the thalamus. From there they pass to the somasensory cortex, which involved in discriminating the quality and localization of pain. Other fibers branch diffusely out to the many areas of the brain associated with emotion and motivation. The direct path of pain from spinal cord thalamus to somasensory cortex is sometimes called the neospinothalamic tract (neo means new). This appears to be of more recent evolutionary development. The diffuse path of pain goes to more diverse brain centers. It is called the paleosinothalamic tract, since it seems to be an earlier evolutionary development. The receptors for pain and various areas of the brain activated by pain dictate a complex response to painful stimuli. Painful stimulation provides (A) information (about the character, intensity, and location of the insult, (B) motivation to behave.
Gate-Control Model of Pain
The physiology of pain transmissions and perception is less well understood than the underlying physical structure (anatomy). There are various theoretical models attempting to explain how neural units interact during the experience of pain.
In 1965, and presented the first version of the gate control theory. They suggested the existence of a “gate” that could either facilitate or inhibit the transmissions of pain signals. The gate is controlled by the dynamic function of certain cells in the spinal cord’s dorsal horn. The fibers bringing information about pain from tissue synapse for the first time in laminae of the dorsal horn. Laminae II is known as the substantia gelatinosa. The SG is visually distinct from other laminae when the spinal cord is inspected in cross section. and proposed that the SG is the anatomic location of the gate. Both small fibers and large fibers converge in SG. The theory suggests that the excitatory and inhibitory links from the SG to the transmission cells as well as descending inhibitory control from brain-stems. The action may be presynaptic, postsynaptic, or both. All connections are excitatory, except the inhibitory link from SG to T cell.
Pain Therapy – Non-analgesic Medication
Much pain therapy is conducted by administering medications that act specifically on the particular end organ that is the source of pain. Such medications act directly on the pain-producing organ itself. Rather than on the higher centers responsible for pain perception. For example, medications such as nitroglycerin relieve the pain of angina pectoris by affecting the heart – the painful end organ; atropine may relieve pain caused by smooth muscle spasm by relieving the muscle spasm; ergotamine constricts overdistended arteries in the brain, thereby relieving the pain of some migrane headaches. Such medications are not analgesics, analgesics act peripherally or centrally to modify pain perception or reaction.
Placebos
Placebos, or pharmacologically inactive substances, e.g. sodium bicarbonate, vitamins and lactose. Currently they are used extensively as a control in experiments examining the effects of medication.
Recorded history allows us to see that pain has been an integral component of the human experience. When a person is in pain, the person will try to find every measure that can lessen that pain and give him or herself comfort. What could be considered as comfort could not be considered comfort to another person. This mirrors that both pain and comfort are subjective. Traditionally, pain has been viewed simply as a symptom of an illness or condition. However, at present, pain itself is considered to be a separate disease and merits special consideration. Knowing that pain affects every aspect of a client’s life, pain management and the provision of comfort from that pain is one of the most researched concepts in nursing ( & , 2004).
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