Understanding Pain and Its Types

Pain Overview

• Pain is an unpleasant sensory and emotional experience.
• Nociception is the neural response to potentially tissue-damaging stimuli.
• Pain is a symptom, protective, and modified by factors like development, behavior, personality, and culture.
• Associated signs of pain include crying, sweating, increased heart rate and blood pressure, and behavioral changes.

Types of Pain

• Fast pain (e.g., sharp, pricking, acute): felt within 0.1 seconds of stimulus, well-localized, not felt in deeper tissues.
• Slow pain (e.g., burning, aching, throbbing, chronic): felt after 1 second or more, increases slowly, poorly localized, usually associated with tissue damage, can cause prolonged and almost unbearable suffering.

Pain Receptors

• Pain receptors are free nerve endings.
• Widespread in superficial skin layers and internal tissues (excluding brain and lung parenchyma).
• Examples include periosteum, arterial walls, and joint surfaces.
• Types of stimuli include mechanical, thermal, and chemical.
• Fast pain is elicited by mechanical and thermal stimuli.
• Slow pain is elicited by all three types of stimuli.
• Chemicals like bradykinin, serotonin, potassium ions, histamine, hydrogen ions (H+), lactic acids, acetylcholine (ACh), proteolytic enzymes, leukotrienes, and cytokines contribute to pain.
• Prostaglandins and substance P increase nociceptor sensitivity to other stimuli.

Pain Receptors and Stimulation

• Pain receptors do not immediately adapt.
• As pain stimulus continues, the excitation of pain fibers increases and pain receptor sensitivity increases (hyperalgesia).
• The rate of tissue damage correlates with the intensity and rate of pain.

Cause of Pain

• Tissue damage: Bradykinin is believed to be the main contributor, with pain intensity correlating with increased potassium ion concentration and proteolytic enzymes.
• Ischemia: Blocked blood flow results in tissue pain, with pain occurring more quickly with increased metabolism and lactic acid buildup.
• Muscle spasm: This contributes to pain by directly stimulating mechanosensitive receptors and indirectly by compressing blood vessels, causing ischemia.

Dual Pain Pathways

• Neospinothalamic tract: transmits fast, acute pain (Aδ fibers)
  • First-order neurons terminate in lamina I, then excite second-order neurons.
  • Glutamate is the neurotransmitter.
  • Second-order neurons decussate to the opposite side through the anterior commissure and travel up the lateral spinothalamic tract.
  • Most fibers terminate in the thalamus, some in the brainstem reticular formation and somatosensory cortex.
  • Fast pain is localized more exactly.
• Paleospinothalamic tract: transmits slow, chronic pain (C fibers)
  • First-order neurons synapse in laminae II and III, neurotransmitter is substance P.
  • Second-order neurons cross to the opposite side and travel up the lateral spinothalamic tracts.
  • Fibers terminate in the thalamus and reticular nuclei, tectal area, and periaqueductal gray, then to somatosensory cortex.

Pain Perception

• Thalamus is an important center.
• Lesions produce "thalamic pain".
• Sensory cortex is crucial for localization and intensity.
• Other areas include reticular formation, limbic areas, and hypothalamus.

Process of Pain Physiology

• Transduction: noxious stimuli converted to electrical energy (transduction).
• Transmission: impulses conveyed by Aδ or C fibers through the spinothalamic tract.
• Perception: nociceptive input reaches cortex (complex interaction in neurons)
• Modulation: CNS ability to control pain transmission (inhibition using endogenous opioids).

Pain Modulation/Modification

• Pain modulation refers to variability in pain perception.
• Endogenous and exogenous mechanisms influence pain thresholds, increasing/decreasing.
• Enhancement/inhibition occurs at all levels of the nervous system (peripheral nerve, spinal cord, brain).

Pain Modulation (Pain Suppression)

• Analgesia system blocks pain signals.
• Includes periaqueductal gray, periventricular areas of mesencephalon and pons, raphe magnus nucleus, nucleus reticularis.
• Transmitters like enkephalin and serotonin cause pre- and post-synaptic inhibition of incoming pain fibers and release enkephalin.
• Brain's opioid system (endorphins, enkephalins, dynorphins) plays a role.

Opioid Actions

• Endogenous opioids (endorphins, enkephalins, dynorphins) and exogenous opioids (morphine, codeine, fentanyl, pethidine, opium, heroin) act presynaptically or postsynaptically.
• They block calcium channels, inhibit calcium influx preventing the release of pain neurotransmitters.
• They open potassium channels, which leads to membrane hyperpolarization and inhibits pain neurotransmitter activity.
• They activate the descending inhibitory pathway.
• They inhibit GABA-mediated inhibition.

Pain Modulation (Gate Control Theory)

• Non-painful input closes gates to painful input.
• Substantia gelatinosa (SG) in the dorsal horn acts as a gate, only allowing specific impulses to pass.
• SG activation is triggered (Aβ neurons stimulated). This closes the gate to Ad and C fibers.
• Ad and C fiber stimulation blocks the gate allowing Aβ fibers to be triggered.
• Methods employing this theory for pain relief include massage, applying irritants, transcutaneous electrical nerve stimulation, and acupuncture.

Varieties of Pain

• Phantom pain: felt without stimulus due to injured nerve ending abnormal action potential (e.g., amputated limb).
• Psychogenic pain: felt, but cause is emotional, not physical
• Neuropathic pain: caused by lesion or disease somatic sensory nervous system, (e.g., diabetes neuropathy).

Pain in Dentistry

• A-delta fibers are stimulated by air, cold, heat, and drilling, resulting in fast, sharp, well- localized pain.
• C-fibers are stimulated by inflammatory mediators, mechanical deformation, heat, resulting from slower, dull, lingering, poorly localized pain.

Orofacial Pain Pathway

• Somatic input from the face and oral structures uses the trigeminal nerve (CN V) to reach the spinal cord. This nerve and its pathway differs from nerves for other areas.

Dental Pain of Pulp Origin

• Visceral in character, threshold-based, responds to noxious stimuli, but not usually to masticatory function.
• Not localized at first.
• Becomes chronic or spreads to periodontal ligament structures.

Dental Pain of PDL Origin

• Deep somatic pain, localized.
• Related to biomechanical function(masticatory).
• Receptors are capable of precise localization.
• Characterized by biting discomfort under occlusal pressure.