Pain Perception and Types of Pain

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.