Sensory System II - Pain Mechanisms

Sensory System II

• Pain Sensation: Pain is an unpleasant sensation for body protection, occurring with tissue damage.
• Damaged tissue releases chemicals (bradykinin, prostaglandins, substance P, K+, and H+) initiating inflammation.
• Pain Receptors (Nociceptors): Free nerve endings, categorized as mechanosensitive (strong mechanical stimuli), thermosensitive (extreme thermal stimuli), and chemosensitive (histamine and strong acids).
• Pain Receptor Distribution: More receptors in skin, periosteum, arteries, joint surfaces, falx & tentorium cerebelli, and cranial sinuses. Fewer in deep tissue (e.g. liver, lung alveoli, brain, which are pain insensitive).
• Pain Receptor Nerve Fibers: A delta and C fibers.
• Pain Receptor Adaptation: Slow or non-adaptive receptors

Types of Pain

• Somatic Pain: Originates from skin and deep tissues.
• Cutaneous Pain: Surface pain (e.g., prickling, fast pain, burning, slow pain). Fast pain is characterized by a quick, sharp sensation, while slow pain is a lingering, aching sensation affecting skin. Includes quick prickling sensations and slower burning sensations.
• Deep Pain: Deep tissue pain from muscles, tendons, ligaments, and periosteum. Characterized by dull aching and poor localization, often associated with nausea and vomiting. It can be referred to the skin. (e.g. musculoskeletal pain)
• Visceral Pain: Originates from internal organs. Poorly localized (few receptors) and often described as dull, aching, burning, or colicky.
  • Referred Pain: Pain originating in a visceral structure that is perceived as being from an area of skin innervated by the same segmental level as the visceral afferent. Examples: Anginal pain (referred to the left shoulder and arm), gastric pain (referred to the epigastrium above the umbilicus), gall bladder pain (referred to the right shoulder), renal pain (referred to the inguinal region and testis), appendicular pain (referred to the umbilicus), and tooth pain (referred to the head). Visceral pain can trigger autonomic or emotional responses (e.g. nausea, vomiting, bradycardia).

Pain Receptors

• Occur in various locations (skin, arteries, meninges), different types of nociceptors react to various stimuli.
• These receptors exist in different parts of the body, allowing for the perception of various sensations and pain.
• Mechanisms
• The mechanisms of transmission and localization of pain signals play a key role in the experience of pain in different parts of the body.

Pain Control

• This involves extensive modification of sensory signals along sensory pathways before reaching the central nervous system.
• Gate Control Theory: In the Posterior Horn of the Spinal Cord, pain signals are reduced or interrupted by gate mechanisms. This occurs via two key mechanisms:
  • Lateral Inhibition: Collaterals originating from ascending sensory neurons produce a reduction of signal strength through collateral modulation.
  • Analgesia System: Descending pathways from higher brain centers suppress pain signals.

Pain-Analgesia System

• The brain's built-in pain control system (analgesia).
• Mechanisms for suppressing pain transmission:
  • Opioid receptors (endorphins, enkephalins, dynorphins)
• Components of the opioid analgesic system:
• Periaqueductal gray matter and periventricular area, raphe magnus nucleus in the lower pons and upper medulla, pain inhibitory complex in the dorsal horn of the spinal cord

Lesions of Sensory System

• Peripheral Nerves: Lesions on one or multiple peripheral nerves cause loss of sensation in the affected areas.
  • Loss of sensation, diffuse lesion (e.g., peripheral neuritis leading to glove and stocking neuropathy), lesion of dorsal root, loss of sensation from dermatomes, hyperalgesia (increased pain sensitivity in inflamed areas).
• Spinal Cord: Different lesions within the spinal cord result in varying sensory deficits.
  • Herpes zoster affecting the dorsal root ganglion, inflammation leading to widening of the central canal (syringomyelia), tabes dorsalis (posterior column degeneration), Brown-Séquard syndrome (hemisection of the spinal cord)
• Thalamus: Damage to specific thalamic structures can result in specific syndromes (e.g., thalamic syndrome).
• Brain stem: Lesions can cause loss of all sensations on opposite side of the lesion.
• Cortical lesions: Damage can affect fine localization, perception of pressure, stereognosis, and body part orientation.

Headaches

• Intracranial headaches:

  • Meningeal irritation (e.g. meningitis, brain tumor).
  • Migraine headaches (vascular phenomenon, vasospasm followed by vasodilation).
  • Hypertension (cerebral vessel expansion).
  • Constipation (toxin absorption leading to meningeal irritation).

• Extracranial headaches:

  • Muscle spasm.
  • Irritation of nasal sinuses
  • Issues from refraction, Otitis media, toothache, systemic disorders (e.g., anemia).