Pain Physiology & Pathophysiology Challenge base video-1

1. The Purpose and Trigger of Pain
Pain is a protective mechanism that signals tissue damage. It is unique because pain receptors (nociceptors) are non-adapting—they don’t "get used" to the stimulus. Instead, they can become more sensitive (hyperalgesia), ensuring you remain aware of the damage as long as it persists.
2. Fast Pain vs. Slow Pain
When you are injured, you often feel a "double" pain sensation because the signals travel at different speeds through two different "highways":
The Fast-Sharp Pathway (Neospinothalamic)
Stimulus: Mechanical (cuts) or acute thermal (burns).
Fibers: Aδ (A-delta) fibers. These are thin but myelinated, allowing speeds of 6–30 m/sec.
Neurotransmitter: Glutamate (acts in milliseconds).
Destination: Terminates in Lamina I of the spinal cord, then travels to the thalamus and somatosensory cortex.
Function: Tells you exactly where the pain is so you can react instantly.
The Slow-Chronic Pathway (Paleospinothalamic)
Stimulus: Mostly chemical (bradykinin, lactic acid, potassium).
Fibers: C fibers. These are very small and unmyelinated, crawling at 0.5–2 m/sec.
Neurotransmitter: Substance P (released slowly, builds up over time).
Destination: Terminates in Laminae II and III (substantia gelatinosa), then projects mostly to the brain stem (reticular formation).
Function: Provides the "suffering" quality of pain (aching, throbbing). It is poorly localized and causes arousal, making it hard to sleep when in pain.
3. Causes of Clinical Pain
Beyond direct cuts or burns, pain is frequently caused by:
Ischemia: Lack of blood flow leads to the buildup of lactic acid and bradykinin, which chemically excite nerve endings.
Muscle Spasm: This triggers pain in two ways—by physically squeezing mechanoreceptors and by compressing blood vessels to cause ischemia.