The sensation of pain ranges from mild discomfort to excruciating agony and is experienced when sensory nerve fibers are stimulated by mechanical thermal, or chemical stimuli. These stimuli may be associated with tissue injury or inflammation. The pain threshold, which is the degree of stimulus required to cause the perception of pain, is variable among individuals.
Pain is a complex phenomenon composed of the physiological mechanisms associated with sensory stimuli and transmission and the individual's interpretation of those stimuli and transmission and the individual's interpretation of those signals molded by emotions, memory and expectations.
There are three physiologic components that affect pain perception afferent pathways the central nervous system (CNC), and efferent pathways. The sensation of pain begins with stimulation of peripheral free nerve endings (nociceptors) located in the skin, blood vessels, subcutaneous tissues, viscera joints and other structures throughout the body.
Among the substances that can stimulate nociceptors are prostaglandins, leukotrientes, and bradykinin. Prostaglandins, particularly prostaglandin, sensitize nerve endings so that they are more responsive to the actions of other stimuli, such as bradykinin.
Activation of nociceptors results in the transmission of an impulse along the afferent nerve fibers to the spinal column, and then onto the brain. There are two subtypes of afferent nerves: C fibers and A fibers. C fibers are unmyelinated nerves that transmit impulses slowly. They detect burning, aching and diffuse pain. Conversely, A fibers are covered with a myelin sheath, which allows for fast transmission of impulses, and are responsible for our ability to feel sharp localized sensations of pain.
The second area of pain perception is the CNS, consisting of the spinal column and the brain. The CNS is responsible for our ability to interpret the pain signal. For example our ability to differentiate between an aching or a sharp pain and our ability to localize the pain source. The efferent pathways travel from the brain towards the peripheral nerve endings and provide our ability to modify pain sensation.
Prostaglandins, leukotrienes, bradykinin, substance P and other substances released by mast cells, such as histamine and serotonin, appear to act synergistically to enhance the transmission of pain signals and augment the inflammatory response. The number of cells and chemical mediators involved in the production and maintenance of pain illustrate the complexity of this biological response.
We will explore the role of prostaglandins as mediators of pain and inflammation in greater details in subsequent section of this program.
Pain is a complex phenomenon composed of the physiological mechanisms associated with sensory stimuli and transmission and the individual's interpretation of those stimuli and transmission and the individual's interpretation of those signals molded by emotions, memory and expectations.
There are three physiologic components that affect pain perception afferent pathways the central nervous system (CNC), and efferent pathways. The sensation of pain begins with stimulation of peripheral free nerve endings (nociceptors) located in the skin, blood vessels, subcutaneous tissues, viscera joints and other structures throughout the body.
Among the substances that can stimulate nociceptors are prostaglandins, leukotrientes, and bradykinin. Prostaglandins, particularly prostaglandin, sensitize nerve endings so that they are more responsive to the actions of other stimuli, such as bradykinin.
Activation of nociceptors results in the transmission of an impulse along the afferent nerve fibers to the spinal column, and then onto the brain. There are two subtypes of afferent nerves: C fibers and A fibers. C fibers are unmyelinated nerves that transmit impulses slowly. They detect burning, aching and diffuse pain. Conversely, A fibers are covered with a myelin sheath, which allows for fast transmission of impulses, and are responsible for our ability to feel sharp localized sensations of pain.
The second area of pain perception is the CNS, consisting of the spinal column and the brain. The CNS is responsible for our ability to interpret the pain signal. For example our ability to differentiate between an aching or a sharp pain and our ability to localize the pain source. The efferent pathways travel from the brain towards the peripheral nerve endings and provide our ability to modify pain sensation.
Prostaglandins, leukotrienes, bradykinin, substance P and other substances released by mast cells, such as histamine and serotonin, appear to act synergistically to enhance the transmission of pain signals and augment the inflammatory response. The number of cells and chemical mediators involved in the production and maintenance of pain illustrate the complexity of this biological response.
We will explore the role of prostaglandins as mediators of pain and inflammation in greater details in subsequent section of this program.
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