The Somatosensory System: Pain and Thermal Sensation Flashcards
(24 cards)
What are nociceptors, and what types of stimuli do they respond to?
Learning Objective: Describe the physiological mechanisms underlying pain perception.
Nociceptors are specialized sensory receptors that detect noxious stimuli. They respond to:
Mechanical stimuli (e.g., sharp objects)
Thermal stimuli (extreme heat or cold)
Chemical stimuli (inflammatory mediators such as bradykinin, prostaglandins)
What are the different types of nociceptors?
Learning Objective: Describe the physiological mechanisms underlying pain perception.
Aδ fibers: Respond to sharp, well-localized pain (mechanical and thermal)
C fibers: Respond to dull, aching, burning pain (polymodal, responding to mechanical, thermal, and chemical stimuli)
What is the difference between first and second pain?
Learning Objective: Describe the physiological mechanisms underlying pain perception.
First pain: Sharp, localized pain mediated by Aδ fibers.
Second pain: Dull, aching pain mediated by C fibers.
Describe the ascending pain pathway.
Learning Objective: Explain the neural pathways involved in pain transmission.
1) Nociceptor activation in periphery
2) Transmission to the dorsal horn of the spinal cord
3) Synapse at substantia gelatinosa (lamina I and II)
4) Decussation to contralateral side
5) Ascend via spinothalamic tract to the thalamus
6) Relay to somatosensory cortex for pain perception
What are the two components of the spinothalamic tract?
Learning Objective: Explain the neural pathways involved in pain transmission.
Lateral spinothalamic tract: Carries pain and temperature information
Anterior spinothalamic tract: Carries crude touch and pressure information
How do acute and chronic pain differ?
Learning Objective: Differentiate between acute and chronic pain.
Acute pain: Short duration, protective function, caused by tissue injury.
Chronic pain: Persists beyond normal healing, often maladaptive, involves central sensitization and plasticity.
What are the neural mechanisms contributing to chronic pain?
Learning Objective: Differentiate between acute and chronic pain.
Peripheral sensitization: Increased responsiveness of nociceptors
Central sensitization: Enhanced excitability of dorsal horn neurons
Disinhibition: Reduced inhibitory control in the spinal cord
What is central sensitization?
Learning Objective: Define central sensitization and its role in chronic pain.
Central sensitization is an increase in the excitability of neurons in the central nervous system, leading to:
Enhanced pain sensitivity (hyperalgesia)
Pain perception from non-noxious stimuli (allodynia)
What molecular changes occur in central sensitization?
Learning Objective: Define central sensitization and its role in chronic pain.
Increased NMDA receptor activity
Reduced GABA and glycine inhibition
Increased expression of inflammatory mediators
What brain regions are involved in pain perception?
Learning Objective: Identify the roles of key brain regions in pain processing.
Somatosensory cortex: Localizes and discriminates pain
Anterior cingulate cortex: Emotional aspect of pain
Insula: Autonomic and affective response
Periaqueductal gray (PAG): Modulation of pain through descending inhibition
How does the PAG modulate pain?
Learning Objective: Identify the roles of key brain regions in pain processing.
Activates descending inhibitory pathways
Releases endogenous opioids
Inhibits nociceptive transmission at the spinal cord
What is the gate control theory of pain?
Learning Objective: Explain the gate control theory of pain.
Proposes that non-nociceptive input (e.g., touch, vibration) can inhibit pain signals
Input from Aβ fibers activates inhibitory interneurons in the dorsal horn, “closing the gate” to pain
What is the clinical relevance of the gate control theory?
Learning Objective: Explain the gate control theory of pain.
Basis for techniques like TENS (transcutaneous electrical nerve stimulation)
Explains pain modulation through touch and massage
What are the key mechanisms of endogenous pain modulation?
Learning Objective: Discuss the mechanisms of endogenous pain modulation.
Descending inhibition: From PAG, raphe nuclei, and locus coeruleus
Endogenous opioids: Release of endorphins, enkephalins, and dynorphins
Inhibitory neurotransmitters: GABA and glycine reduce excitability of nociceptive neurons
How do opioids modulate pain?
Learning Objective: Discuss the mechanisms of endogenous pain modulation.
Bind to opioid receptors (mu, delta, kappa)
Inhibit neurotransmitter release
Hyperpolarize nociceptive neurons
What are the clinical conditions associated with altered pain processing?
Learning Objective: Describe the clinical implications of altered pain processing.
Hyperalgesia: Increased pain response to a noxious stimulus
Allodynia: Pain perception from normally non-painful stimuli
Neuropathic pain: Pain resulting from damage to the nervous system
How is neuropathic pain managed?
Learning Objective: Describe the clinical implications of altered pain processing.
Antidepressants (e.g., amitriptyline)
Anticonvulsants (e.g., gabapentin)
Topical agents (e.g., capsaicin)
What receptors are involved in thermal sensation?
Learning Objective: Explain the physiological basis of thermal sensation.
TRPV1: Activated by heat and capsaicin
TRPM8: Activated by cool temperatures and menthol
TRPA1: Activated by extreme cold and pungent substances
How are thermal signals transmitted to the brain?
Learning Objective: Explain the physiological basis of thermal sensation.
Transmitted via Aδ and C fibers
Relayed through the spinothalamic tract to the thalamus and somatosensory cortex
What are the consequences of impaired thermal sensation?
Learning Objective: Describe the clinical consequences of thermal sensation impairment.
Burn injuries: Due to failure to perceive heat
Frostbite: Due to failure to perceive cold
Neuropathy-related temperature insensitivity: Increased risk of injury
How is impaired thermal sensation assessed clinically?
Learning Objective: Describe the clinical consequences of thermal sensation impairment.
Thermal threshold testing
Quantitative sensory testing (QST)
Neurotransmission in the dorsal horn of the spinal cord
1) Action potential
2) Opening of voltage gated Ca2+ channels
3) Ca2+ influx
4) Glutamate release
5) Activation of glutamate receptors
6) Membrane depolarization (EPSP)
7) Opening of voltage gated Na+ channels
8) Action potential
Primary transmitter is glutamate producing a fast EPSP (—-) and neuron
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