Puzzle 07: Neurological Adaptations & Pain Pathophysiology

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Across
  1. 5. Nerve root compression or inflammation as it exits the spinal column, resulting in dermatomal pain and numbness.
  2. 6. Slow-conducting C fibers lacking this sheath, responsible for carrying dull, burning, or aching chronic pain signals.
  3. 9. Specialized free nerve endings in peripheral tissues that detect harmful mechanical, thermal, or chemical stimuli.
  4. 11. A chronic disorder characterized by widespread musculoskeletal pain, fatigue, and centralized pain processing defects.
  5. 14. An unpleasant sensory and emotional experience associated with actual or potential tissue damage.
  6. 15. The microscopic junction between two neurons where pain signals are chemically modulated via neurotransmitters.
  7. 18. The primary metabolic fuel utilized by brain tissue; its delivery is heavily compromised during acute ischemic cascades.
  8. 19. The localized redness secondary to neurogenic inflammation driven by antidromic release of vasoactive neuropeptides.
  9. 22. A severe hyperreflexia syndrome seen in patients with spinal injuries above T6, triggered by noxious stimuli.
  10. 23. The sensation of severe, real pain localized in a limb or body part that has been surgically or traumatically amputated.
  11. 26. The primary ascending sensory pathway in the spinal cord responsible for transmitting pain, temperature, and crude touch signals to the brain.
  12. 29. An increased, exaggerated clinical sensitivity and response to a stimulus that is normally only mildly painful. EXCITOTOXICITY Pathological cell injury or death caused by excessive accumulation of glutamate in the synaptic cleft.
Down
  1. 1. Lipid compounds derived from cell membranes that do not cause pain directly directly but markedly sensitize nociceptors to other mediators.
  2. 2. Fast-conducting A-delta fibers wrapped in this lipid sheath, responsible for transmitting sharp, localized initial pain.
  3. 3. A specific, well-defined area of cutaneous skin supplied by a single spinal nerve root carrying pain fibers.
  4. 4. Prolonged pain lasting beyond the normal tissue healing timeframe, usually defined clinically as greater than three to six months.
  5. 7. Pathology or compression isolated strictly to a single peripheral nerve, such as the median nerve in carpal tunnel.
  6. 8. Exogenous or endogenous compounds (like endorphins) that bind to specific receptors in the CNS to inhibit pain transmission.
  7. 10. The primary excitatory amino acid neurotransmitter in the central nervous system involved in pain amplification.
  8. 12. A potent inflammatory peptide released during tissue injury that directly activates nociceptors and causes local vasodilation.
  9. 13. Inhibitory spinal cord cells that function as the physiological 'gate' in Melzack and Wall's gate control theory.
  10. 16. A major neuropeptide neurotransmitter released in the dorsal horn that co-transmits slow, chronic pain signals.
  11. 17. An descriptors for the unmitigated sympathetic discharge seen in dysreflexia states below the level of spinal injury.
  12. 20. A painful clinical response to a normally non-painful stimulus, such as a light touch on sunburned skin.
  13. 21. A type of sensitization where inflammatory mediators lower the activation threshold of primary nociceptive neurons.
  14. 24. A distributive classification of shock caused by loss of sympathetic vasomotor tone, resulting in bradycardia and profound hypotension.
  15. 25. The clinical triad of bradycardia, bradypnea, and widened pulse pressure signaling decompensated intracranial pressure.
  16. 27. The central relay station of the brain where ascending pain pathways are sorted and projected to the somatosensory cortex.
  17. 28. A sudden, paroxysmal electrical discharge from cortical neurons resulting in transient alterations in brain function.