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Questions and Answers
What is pain a symptom of?
What is pain a symptom of?
According to the IASP, what is pain defined as?
According to the IASP, what is pain defined as?
What is nociception?
What is nociception?
Which of the following is NOT a factor that can modify pain?
Which of the following is NOT a factor that can modify pain?
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What is the primary purpose of pain?
What is the primary purpose of pain?
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What is the role of serotonin in pain modulation?
What is the role of serotonin in pain modulation?
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Which component is NOT part of the pain inhibitory complex in the dorsal horns of the spinal cord?
Which component is NOT part of the pain inhibitory complex in the dorsal horns of the spinal cord?
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How do endogenous opioid peptides primarily function in pain modulation?
How do endogenous opioid peptides primarily function in pain modulation?
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Which theory suggests that non-painful input can close the gates to painful input?
Which theory suggests that non-painful input can close the gates to painful input?
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Which of the following effects does the activation of K+ channels have in pain modulation?
Which of the following effects does the activation of K+ channels have in pain modulation?
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What type of pain is characterized by being felt within 0.1 seconds after the stimulus is applied?
What type of pain is characterized by being felt within 0.1 seconds after the stimulus is applied?
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Which type of pain is poorly localised and usually associated with tissue destruction?
Which type of pain is poorly localised and usually associated with tissue destruction?
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What type of nerve fibre is associated with fast pain?
What type of nerve fibre is associated with fast pain?
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Which types of stimuli can elicit slow pain?
Which types of stimuli can elicit slow pain?
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Which chemical is NOT known to directly stimulate nociceptors?
Which chemical is NOT known to directly stimulate nociceptors?
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What is the primary characteristic of the non-adapting nature of pain receptors?
What is the primary characteristic of the non-adapting nature of pain receptors?
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Which of the following is a characteristic of fast pain?
Which of the following is a characteristic of fast pain?
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In which tissues are pain receptors NOT widely found?
In which tissues are pain receptors NOT widely found?
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What type of pain is caused by a lesion or disease of the somatosensory nervous system?
What type of pain is caused by a lesion or disease of the somatosensory nervous system?
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Which nerve carries sensory input from the face and mouth to the brain?
Which nerve carries sensory input from the face and mouth to the brain?
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What phenomenon is characterized by the sufferer feeling pain for emotional rather than physical reasons?
What phenomenon is characterized by the sufferer feeling pain for emotional rather than physical reasons?
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In orthodontic pain pathways, where do first-order trigeminal neurons synapse?
In orthodontic pain pathways, where do first-order trigeminal neurons synapse?
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What happens to the second-order neurons in the orthodontal pain pathway after they receive impulses?
What happens to the second-order neurons in the orthodontal pain pathway after they receive impulses?
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What condition could lead to continuous pain due to damage to small blood vessels supplying nerves?
What condition could lead to continuous pain due to damage to small blood vessels supplying nerves?
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Which structure integrates and converges the pain signals from the orthodontic pathway before they reach consciousness?
Which structure integrates and converges the pain signals from the orthodontic pathway before they reach consciousness?
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What is the outcome of repeated activation of peripheral nerves during neuropathic pain?
What is the outcome of repeated activation of peripheral nerves during neuropathic pain?
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What is the role of the thalamus in pain perception?
What is the role of the thalamus in pain perception?
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Which process involves the conversion of noxious stimuli to electrical energy?
Which process involves the conversion of noxious stimuli to electrical energy?
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What types of fibers carry the pain impulse along the spinothalamic tract?
What types of fibers carry the pain impulse along the spinothalamic tract?
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Which brain areas are involved in pain perception aside from the sensory cortex?
Which brain areas are involved in pain perception aside from the sensory cortex?
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Pain modulation influences the pain perception variability through what mechanisms?
Pain modulation influences the pain perception variability through what mechanisms?
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What occurs during the perception phase of pain physiology?
What occurs during the perception phase of pain physiology?
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Which option best describes pain modulation?
Which option best describes pain modulation?
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Which aspect of pain is primarily handled by the sensory cortex?
Which aspect of pain is primarily handled by the sensory cortex?
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What is hyperalgesia in relation to pain receptors?
What is hyperalgesia in relation to pain receptors?
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Which type of tissue damage is primarily linked to the intensity of pain felt?
Which type of tissue damage is primarily linked to the intensity of pain felt?
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Which agent is thought to be most responsible for causing pain following tissue damage?
Which agent is thought to be most responsible for causing pain following tissue damage?
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What physiological effect can muscle spasms have on pain perception?
What physiological effect can muscle spasms have on pain perception?
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What type of pain does the neospinothalamic pathway primarily transmit?
What type of pain does the neospinothalamic pathway primarily transmit?
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What is the primary neurotransmitter used by Aδ fibers in the neospinothalamic tract?
What is the primary neurotransmitter used by Aδ fibers in the neospinothalamic tract?
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In which part of the nervous system do first-order neurons in the neospinothalamic tract terminate?
In which part of the nervous system do first-order neurons in the neospinothalamic tract terminate?
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What factor contributes to the acute pain experienced during tissue ischemia?
What factor contributes to the acute pain experienced during tissue ischemia?
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Which of the following statements about pain transmission is true?
Which of the following statements about pain transmission is true?
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Which condition is likely to increase pain due to muscle spasm?
Which condition is likely to increase pain due to muscle spasm?
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Study Notes
Pain Perception
- Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage (International Association for the Study of Pain).
- Nociception is the neural response to potentially tissue-damaging stimuli.
- Pain occurs when tissues are damaged, causing the individual to react to remove the stimulus.
- Pain is a symptom, subjective, protective, and modified by developmental, behavioral, personality, and cultural factors.
Types of Pain
-
Fast pain: Also called sharp, pricking, acute, or electric pain.
- Felt within 0.1 seconds after the stimulus.
- Well-localized.
- Not felt in deeper tissues.
- Caused by thin myelinated nerves (A delta fibers).
-
Slow pain: Also called slow burning, aching, throbbing, nauseous, or chronic pain.
- Felt after 1 second or more, increasing slowly over seconds or minutes.
- Poorly localized.
- Usually associated with tissue destruction.
- Can lead to prolonged, almost unbearable suffering.
- Caused by unmyelinated nerve fibers (C fibers).
Classification of Nerve Fibers
- Nerve fibers are classified by their diameter and speed.
- Larger diameter fibers conduct impulses faster.
- Different types of fibers carry different sensory information, including touch, pressure, pain, and temperature.
- A-alpha (Aa) and A-beta (Ab) fibers carry information about touch, pressure, and proprioception.
- A-delta (Aδ) fibers transmit fast pain.
- C fibers transmit slow pain.
Pain Receptors and Stimulation
- Pain receptors are free nerve endings widespread in superficial skin layers, somatic tissues, and some internal tissues (excluding brain and lung).
- Stimuli can be mechanical, thermal, and chemical.
- Fast pain is elicited by mechanical and thermal stimuli.
- Slow pain is elicited by all three types (mechanical, thermal, chemical).
- Chemicals like bradykinin, serotonin, potassium ions, histamine, H+, lactic acids, ACH, proteolytic enzymes, and leukotrienes are involved in pain.
Neurotransmitters of Pain
- Substances like histamine, prostaglandins, bradykinin, and 5-HT (serotonin) bathe nociceptors, activating and sensitizing them.
- Prostaglandins and bradykinin sensitize nociceptors to low-intensity stimuli.
- Histamine and 5-HT cause pain when directly applied to nerve endings.
- Hydrogen ions and 5-HT directly affect ion channels on the cell membrane, while others bind to receptors, activating second-messenger systems via G proteins.
Pain Receptors and Their Stimulation
- Pain receptors do not adapt, sometimes not at all, responding to maintained stimuli.
- Prolonged stimulation leads to a greater pain response.
- The rate of tissue damage correlates strongly with pain intensity.
Cause of Pain
- Tissue damage is the primary cause of pain, with bradykinin thought to be important in initiating pain sensations.
- Intensity of pain correlates with increases in potassium ions and proteolytic enzymes, locally.
- Reduced blood flow (ischemia) leads to increased pain, with lactic acid accumulation being significant during anaerobic metabolism.
- Muscle spasm contributes to pain both directly and indirectly through compressing blood vessels, leading to ischemia and the production of pain-inducing substances.
Dual Pain Pathways
- Neospinothalamic Tract (Fast-Acute): Transmits sharp, well-localized pain (Aδ fiber).
- Paleospinothalamic Tract (Slow-Chronic): Transmits dull, poorly localized pain (C fiber).
Referred Pain
- Pain that originates in one location but is perceived in another.
- Sensations from multiple areas converge on a single sensory neuron in the spinal cord.
- This phenomenon is explained by convergence theory.
- Individual experiences a simultaneous response to somatic and visceral inputs through a shared pathway.
- Examples include cardiac pain in the left arm, pain from the maxillary sinus to a nearby tooth, etc.
Pain Perception - Aware of Pain
- Pain is perceived at different levels, including the thalamus (crucial for pain perception), with lesions causing thalamic pain.
- Sensory cortex is essential for localizing and determining pain intensity.
- Other brain areas, such as the reticular formation, limbic areas, and hypothalamus, also play a role.
Process of Pain Physiology
- Transduction: noxious stimuli convert to electrical energy.
- Transmission: pain impulse travels along peripheral nerve fibers (Aδ or C) to the spinothalamic tract.
- Perception: input from nociceptors reaches the brain's cortex allowing conscious perception.
- Modulation: the brain's ability to control pain signals, through inhibitory neurotransmitters (like endogenous opioids) that hinder pain transmission.
Pain Modulation/Pain Modification
- Pain perception variability is influenced by endogenous and exogenous factors that can increase or decrease pain threshold.
- Modulation occurs through all levels of the nervous system.
Pain Modulation (Pain Suppression)
- Pain suppression occurs through analgesia systems.
- Three components: periaqueductal gray, raphe magnus nucleus, and pain inhibitory complex in dorsal horns of spinal cord.
- Transmitters like enkephalins and serotonin inhibity pain signals.
- Endorphins and enkephalins (opioid peptides) are released to inhibit pain transmission in brain and spinal cord.
Opioid Actions
- Endogenous opioid peptides like endorphins, enkephalins, and dynorphins, and exogenous opioids like morphine, codeine, and others act presynaptically or postsynaptically.
- They block calcium channels, preventing release of pain neurotransmitters like glutamate and substance P.
- They may open potassium channels leading to membrane hyperpolarization.
- They activate descending pain modulatory pathways and prevent GABA-mediated inhibition affecting pain pathways.
Gate Control Theory
- Non-painful input closes the gate to painful input.
Varieties of Pain
- Phantom pain: pain felt in a missing limb or body part.
- Psychogenic pain: emotionally-induced pain.
- Neuropathic pain: pain caused by a sensory nerve problem.
Pain in Dentistry
- Pulp origin: visceral pain, threshold type, responds to all noxious stimuli, but may become chronic.
- PDL origin: deep somatic musculoskeletal pain, more localized than pulpal pain, intimaeted to biomechanical function.
Orofacial Pain Pathway
- Primarily through CN V (trigeminal nerve) which handles all sensory inputs in the face, including the teeth, jaw, etc.
Orthodontic Pain Pathway
The pathway for orthodontic pain involves several steps: (1) trigeminal neurons in the trigeminal ganglia detect the nociceptive stimuli and send signals to the trigeminal nucleus caudalis; (2) the second-order neurons cross over on the opposite side and ascend to the ventroposterior nucleus of the thalamus; (3) and finally third-order neurons in the thalamus relay the impulse to the somatosensory cortex.
Dental Pain of Pulpal Origin
- Visceral in nature, threshold type, responding to noxious stimuli like ordinary masticatory function.
- Non-localized.
- Generally resolves, but sometimes becomes chronic or progresses to periodontal ligament (PDL) structures.
Dental Pain of PDL Origin
- Deep somatic pain, more localized than pulp pain, closely related to biomechanical function, precisely localized with discomfort during biting, and under occlusal pressure pain.
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Description
Explore the nuances of pain perception, including its definition, types, and the underlying mechanisms. This quiz covers fast and slow pain, their characteristics, and how various factors influence the experience of pain.