Lecture on Pain

Definition of Pain

• Unpleasant sensory and emotional experience linked to tissue damage or potential tissue damage.
• Definition by the International Association for the Study of Pain.
• Different from other sensory stimuli like touch, sight, sound, or taste due to the emotional component.

Triggers for Pain

• Mechanical stimuli (pressure, physical force)
• Thermal stimuli (temperature)
• Chemical stimuli (chemicals released due to damage)

Pain Receptors

• Free nerve endings, unmyelinated.
• Two main types of fibers:
  • A-delta fibers: Thin, poorly myelinated, fast signal (~15 m/s), sharp/stabbing pain.
  • C fibers: Thinner, unmyelinated, slow signal (~0.5-1 m/s), dull/aching pain.

Types of Receptors

• High-threshold mechanical receptors (mechanical stimuli)
• Mechano-thermal receptors (mechanical and temperature)
• Polymodal receptors (mechanical, thermal, and chemical)

Pathways of Pain

Ascending Pathway

• Spinothalamic Tract:
  • Contains both A-delta and C fibers.
  • Neo spinothalamic pathway for A-delta (localized, sharp pain).
  • Paleo spinothalamic pathway for C fibers (diffuse, aching pain).
  • A-delta fibers synapse early and cross over in spinal cord, then ascend.
  • C fibers branch and interact with other brain areas like reticular system (arousal) and limbic system (emotion).
  • All pain pathways ultimately synapse in the thalamus and proceed to the cortex.

Pain Modulation

• Peripheral Chemicals: Glutamate, Substance P, Potassium, Bradykinin, Prostaglandins - reduce the threshold for pain signal transmission.
• Pain Gate Theory: Rubbing an injured area stimulates touch receptors which inhibit pain signals via interneurons.
• Descending Inhibitory Pathway: Involving serotonin and noradrenaline, promotes the release of endogenous opioids like endorphins, enkephalins, and dynorphins which reduce pain by inhibiting neurotransmitter release or binding.

Clinical Implications

• Brown-Sicard Syndrome: Damage to one side of the spinal cord affects touch and pain differently on each side of the body below the lesion.

Pain Types

• Acute Pain (less than 3 months) vs. Chronic Pain (more than 3 months)
• Nociceptive Pain vs. Neuropathic Pain
  • Nociceptive: Linked to tissue damage or potential damage, often leads to chronic pain if untreated.
  • Neuropathic: Result of neuron changes or damage, often chronic, without clear underlying cause.

Pain Management

Medications

• NSAIDs: Aspirin, Ibuprofen, Celecoxib - block Cox enzymes, reducing prostaglandin production and inflammation.
• Opioids: Morphine, Fentanyl - mimic endogenous opioids but have addictive properties and other side effects like respiratory depression.
• Antidepressants: SSRIs, SNRIs, and Tricyclics - block reuptake of serotonin and noradrenaline, also block sodium and calcium channels.
• Anticonvulsants: Gabapentin - block calcium channels to inhibit neurotransmitter release.

Important Concepts

• Endogenous Opioid System: Descending pathways inhibit pain using endorphins, enkephalins, and dynorphins.
• Central Sensitization: Decreased threshold and increased receptor density in central neurons leading to chronic pain.
• Terms:
  • Analgesia: Absence of pain.
  • Allodynia: Pain from stimuli that usually don’t provoke pain.
  • Hyperalgesia: Increased pain response.
  • Hypoalgesia: Decreased pain response.

Key Takeaways

• Pain is complex, involving sensory and emotional components, and is modulated at various levels in the nervous system.
• Different fibers (A-delta, C fibers) and receptors handle different types of pain stimuli.
• Pathways of pain and touch are distinct, leading to different clinical manifestations when spinal cord is injured.
• Pain management involves a combination of medications that target different pathways and mechanisms of pain.