Outline The Processes Of Nociception

The perception of pain and the emotions that control intensity differ in individuals. Since feeling pain is somewhat adaptive, when one experiences it, he or she becomes aware of an injury and tries to remove oneself from the source that caused the injury. For this reason, pain is considered neuropathic or inflammatory in nature. Thus, when pain is the outcome from the damage caused to the neurons of the peripheral and central nervous system, then that pain is neuropathic. However, if the pain signals any kind of tissue damage, then the pain is inflammatory in nature. Due to various types of pain, the interpretation of pain by neurons and the source of that pain

As well as these there are also the axon of the cell which is covered in myelin sheaths which carried information away from the cell body and hands the action potentials, these are small short bursts of change in the electrical charge of the axon membrane through openings of ion channels, off to the following neurons dendrites through terminal buttons at the end of the axons. Whenever an action potential is passed through these terminal buttons it releases a chemicals that pass on the action potential on to the next neuron through the terminal button and dendrite connection. The chemicals that are

Pain effects the body through the nerves. The phenomena of pain is conveyed from a peripheral part of the person, through afferent nerves to a part of the brain, similar to sight, touch, and hearing. These signals are then interpreted by the brain as pain (Murphy, 1981). The nerve cells used to relay pain messages to the brain are specific nerve cells called nociceptors. These nerves do not send messages until "the stimulus reaches noxious levels," (McClesky, 1992).

Pain is not just a symptom, but a specific problem that needs to be treated. Pain is a neurologic response to unpleasant stimuli. What is the gate control theory of pain? What are the classifications of pain? What are some ways to manage pain?

Once a presynaptic neuron is passive, an electrical current is spread along the length of the axon (Schiff, 2012). This is known as action potential (Pinel, 2011). Action potential happens once an abundant amount of depolarisation reaches the limit through the entry of sodium, by means of voltage gated sodium channels

C ) (1) neurotransmitter released (2) diffused across the synaptic cleft to a receptor amino acid (3) binding of the transmitter opens pores in the ion channels and positive ions move in.

As an action potential travels down the axon of the presynaptic neuron, the action potential reaches the axon terminal synaptic vesicles which migrate toward the synapse. They then release neurotransmitters into the synaptic cleft. The neurotransmitters travel through the synaptic cleft and bind to ligand-gated ion channels on the postsynaptic neuron membrane. The channels open and allow chemicals to enter the cell (i.e. sodium). Then positively charged sodium enters the cell and causes the cell to depolarize. The depolarization spreads down the axon and an action potential is generated. The process then starts over at the axon terminals.

Acute pain is a sudden onset of an unpleasant sensation and is usually sharp in quality. It serves to alert the body that something is wrong. There are many factors that could cause acute pain such as surgery, broken bones, dental work, burns, cuts, labor, or childbirth to name a few (Acute, 2014). Pain is the response triggered by the nervous system in response to tissue damage or damage to the body. Microscopic pain receptors, called nociceptor, within the skin register this occurrence and become active and begin sending electrical signals through, depending on the type of pain, either A-delta or C nerve fibres . This signal is passed from neuron to neuron through the spinal cord across junctions called synapses. Eventually this signal reaches

Pain receptors in the skin sense pain and send signals through the spinal cord. Once the signals arrive at the brain, several parts of the brain begin to process it instead of just one part.

An action potential travels down the axon of the presynaptic neuron; once the action potential reaches the axon terminal synaptic vesicles migrate toward the synapse. They then release neurotransmitters into the synaptic cleft. The

Impulses will travel along the neuron pathways as the electrical charges move across each neural membrane. Ions that are moving across the membrane can cause the impulse to move along the nerve cells.

As the message arrives at the end of the nerves, the message is transmitted to the muscles. Before the message is transmitted to the muscles it has to pass the space between the end of the nerve and the muscle, and that space is called neuromuscular junction. The message is transmitted from the brain to the end of the nerve and from the nerve to the neuromuscular junction, and when the message arrives the chemical called neurotransmitters are released.

The International Association for the Study of Pain defined pain as “an unpleasant sensory and emotional experience with actual or potential tissue damage, or described in terms of such damage” (Unk, 2007). Pain being described such as this allows us to see that pain is a perception, not unlike seeing or hearing. Pain is the most common reason that people seek medical attention but pain is very hard to define because it is subjective. Pain perception is the process by which a painful stimulus is relayed from the site of stimulation to the central nervous system (Freudenrich, 2008). In order to determine if pain is a perception of the mind or if it is biological we must first understand how the process of pain works.

The electrical event that projects the signal along these distances is known as an action potential. The action potential runs from the axon hillock to the end of the axon where more synaptic contacts are made. Target cells of neurons include nerve cells in your brain, spinal cord, cells of your muscles and various glands.

The compound action potential adds up all the action potentials that each individual neuron experiences in the sciatic nerve. Different stimulus amplitudes cause different neurons to fire an action potential; this is due to the fact that each neuron has a different threshold potential, or the minimum voltage the neuron needs to fire an action potential. The individual neuron action potential is an ‘all-or-nothing’ event, but the CAP, as a summation of different individual neurons, is not. The CAP amplitude will increase with larger stimulus potentials because more neurons with higher individual thresholds will be recruited. For this frog sciatic nerve, there are three fiber types, A, B, and C. A fibers are further divided, in the order of decreasing diameter, into α, β, γ, and δ fibers. There is an inverse relationship between the diameter of the nerve fiber and the threshold potential: the larger the diameter, the lower the threshold. Thus, as the largest fibers, the Aα neurons will be the first to be stimulated at a low stimulus potential, and the Aδ neuron fibers will be the last to be recruited. Because the sciatic nerve is mostly composed of A fibers, the recruitment of A-subtype nerve fibers are more readily distinguishable from the data. The minimum potential required to stimulate the Aα fibers was between 75 mV and 80 mV. Once the stimulus potential reached 90 mV, Aβ neurons were recruited and contributed to the increase in amplitude of the CAP. At a stimulus