Post on 01-Oct-2020
The Perception of Pain
Touqeer Ahmed PhDAtta-ur-Rahman School of Applied BiosciencesNational University of Sciences and Technology
24th November, 2016
Perception is a product of the brain's abstraction and elaboration of sensory input
Pain
• THE SENSATIONS WE CALL PAIN—pricking, burning, aching, stinging, and soreness—are the most distinctive of all the sensory modalities.
• Pain is a submodality of somatic sensation like touch, pressure, and position sense and serves an important protective function.
• Advantages and consequences: – It warns of injury that should be avoided or treated. When
children with congenital insensitivity to pain injure themselves severely, the injury may go unnoticed and result in permanent damage.
– Pain has an urgent and primitive quality, a quality responsible for the affective and emotional aspect of pain perception.
– The intensity with which pain is felt is affected by surrounding conditions, and the same stimulus can produce different responses in different individuals under similar conditions.
PainPain is a percept; it is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Although pain is mediated by the nervous system, a distinction between pain and the neural mechanisms of nociception (the response to perceived or actual tissue damage) is important both clinically and experimentally.
Certain tissues have specialized sensory receptors, called nociceptors, that are activated by noxious insults to peripheral tissues. Nociception, however, does not necessarily lead to the experience of pain.
(Nociceptors: The relatively unspecialized nerve cell endings that initiate the sensation of pain are called nociceptors (noci is derived from the Latin nocere, “to hurt”).
The highly individual and subjective nature of pain is one of the factors that makes it difficult to define and to treat clinically. There are no “painful stimuli” (stimuli that invariably elicit the perception of pain in all individuals). For example, many wounded soldiers do not feel pain until they are safely removed from battle. Similarly, athletes often do not detect their injuries until their game is over.
What is the Difference Between Nociception and Pain?
• Nociception refers to the peripheral and central nervous system (CNS) processing of information about the internal or external environment, as generated by the activation of nociceptors. The information from activated nociceptors continues to the brainstem and ultimately the cerebral cortex, where the perception of pain is generated.
• Pain is a product of higher brain center processing, whereas nociception can occur in the absence of pain. For example, the spinal cord of an individual who suffered a complete spinal cord transection can still process information transmitted by nociceptors. However, the information cannot be transmitted beyond the transection stimulus-evoked pain is unlikely.
Types of Nerve Fibers in the PNS
CHARACTERISTICS OF PERIPHERAL NERVE FIBER TYPES
Class Stimuli/function Perception Velocity: m/secDiameter:
micronMyelination
A-alpha fibersMotor contraction
Efferent transmissionNone 30-85 12-22 + + +
A-beta fibersVibration and pressure Afferent transmission
Vibration and pressure
30-70 5-12 + + +
A-delta fibers
Cold sensation and pain
Fast pain and localized touch
Afferent transmission
Cold sensation and pain
localized touch5-25 1-4 + +
C fibers
Hot sensation and pain Slow pain and
generalized touch Afferent transmission
Hot sensation and pain
generalized touch0.7-2.0 0.3-1.3 -
Thickness
Noxious Insults Activate Nociceptors
• Harmful stimuli to the skin or subcutaneous tissue, such as joints or muscle, activate several classes of nociceptor terminals which then send signals to the brain. We consider here three major classes of nociceptors. 4th one is silent nociceptors
1. Thermal. (Thermal nociceptors are activated by extreme temperatures (>45°C or < 5°C). They have small-diameter, thinly myelinated Aδ fibers that conduct signals at about 5-30 m/s.)
2. Mechanical. (Mechanical nociceptors are activated by intensive pressure applied to the skin. They also have thinly myelinated Aδ fibers conducting at 5-30 m/s.)
3. Polymodal. (Polymodal nociceptors are activated by high-intensity mechanical, chemical, or thermal (both hot and cold) stimuli. These nociceptors have small-diameter, nonmyelinated C fibers that conduct slowly, generally at velocities of less than 1.0 m/s.)
4. Silent nociceptors.
Nociceptors
• Unlike the specialized receptors, most nociceptors are freenerve endings. The mechanism by which noxious stimulidepolarize free sensory endings and generate actionpotentials is not known.
• The membrane of the nociceptor is thought to containproteins that convert the thermal, mechanical, or chemicalenergy of noxious stimuli into a depolarizing electricalpotential. One such protein is the receptor for capsaicin, theactive ingredient in hot peppers. The capsaicin, or vanilloid,receptor is found exclusively in primary afferent nociceptorsand mediates the pain-producing actions of capsaicin.
• Importantly, these receptors also responds to noxious heatstimuli, which suggests that it also is a transducer of painfulheat stimuli.
Capsaicin Receptor
(A) Some peppers that contain capsaicin. (B) The chemical structure of capsaicin(C) The capsaicin molecule. (D) Schematic diagram of the Vanilloid receptor (VR-1/capsaicinreceptor or TRPV1 channel). This channel can be activated by capsaicin intracellularly, or by moderate heat (nearly 45°C) or protons (H+) at the cell surface.
Vanilloid receptor is found in C and Aδ fibers.
Pain States
• In pathological situations activation of nociceptors can lead totwo types of abnormal pain states: Allodynia and hyperalgesia.
• Allodynia: pain results from stimuli that normally areinnocuous: a light stroking of sunburned skin. Patients withallodynia do not feel constant pain; in the absence of astimulus there is no pain.
• Hyperalgesia: Patients when exposed to an excessive responseto noxious stimuli would result in tissue damage. Hyperalgesiais the state of excessive responsiveness to the noxious stimulusand sometime results in constant pain.
Propagation of action potentials in sensory fibers and pain
Propagation of action potentials in sensory fibers results in the perception of pain. (Modified from Fields 1987.)
A. This electrical recording from a whole nerve shows a compound (summated) action potential of all axons. Even though the nerve contains mostly nonmyelinated axons, the major voltage deflections are produced by the relatively small number of myelinated axons. This is because action potentials in the population of more slowly conducting axons are dispersed in time.
B. First and second pain are carried by two different primary afferent axons. First pain is abolished by selective blockade of Aδ myelinated axons (middle) and second pain by blocking C fibers (bottom).
These three classes of nociceptors (explained above) are widely distributed in skin and deep tissues and often work together. For example, when you hit your thumb with a hammer, a sharp “first” pain is felt immediately (transmitted by Aδ fibers that carry information from thermal and mechanical nociceptors), followed later by a more prolonged aching, sometimes burning “second” pain (slow dull pain is transmitted by C fibers that are activated by polymodal nociceptors).
Nociceptive Fibers Terminate on Neurons in the Dorsal Horn of the Spinal Cord
Nociceptive afferent fibers terminate predominantly in the dorsalhorn of the spinal cord. The dorsal horn can be subdivided into sixdistinct layers (laminae) on the basis of the cytological features of itsresident neurons.
Layer V
Nociceptive Processing
Nociceptive Processing
Referred Pain
• Lamina V contains primarily wide-dynamic-range neurons that project to the brain stem and to regions of the thalamus. These neurons receive monosynaptic input from Aβ and Aδ fibers (Figure). They also receive input from C fibers, either directly on their dendrites, or indirectly via excitatory interneurons that themselves receive input directly from C fibers. Many neurons in lamina V also receive nociceptive input from visceral structures.
• The convergence of somatic and visceral nociceptive input to lamina V neurons may explain “referred pain,” a condition in which pain from injury to a visceral structure is predictably displaced to other areas of the body surface.
• Surprisingly, there are few, if any, neurons in the dorsal horn of the spinal cord that are specialized solely for the transmission of visceral pain.
• Myocardial infarction and angina can be experienced as deep referred pain in the chest and left arm. (From Teodori and Galletti 1962.)
Referred Pain (Underlying Mechanism)
Heart pain
• Other important examples are gallbladder pain referred to the scapular region.
• Esophogeal pain referred to the chest wall
• Ureteral pain (e.g., from passing a kidney stone) referred to the lower abdominal wall
Understanding referred pain can lead to an accurate diagnosis that might otherwise be missed.
Referred Pain (examples)