Pain (Suss) Flashcards
Define the temporal components of pain.
Local anesthetics involvement in these temporal components.
First pain - A (gamma) fiber
Second pain - C fiber
LA block sodium channels to prevent conduction of impulses along C fibers.
Draw and describe the anterolateral pathways that mediates the affective-motivational aspects of pain (spinoreticular and spinomesencephalic)
Spinothalamic: discriminative aspects of pain and T (tells you that you’ve stepped on something sharp -> facts)
Spinoreticular: emotional and arousal aspects of pain (tells you to start sweating, cry)
- Projects to amygdala, hypothalamus, reticular formation
Spinomesencephalic: central modulation of pain (tells you to feel better, that pain is reducing)
- Projects to periaqueductal gray, superior colliculus (in midbrain)
Describe the basic clinical consequences of lesions and know some of the neuropathies associated with the spinothalamic and trigeminal pain pathways.
Lesion of parietal lobe or primary sensory cortex:
Contralateral numb tingling or pain
Lesion of thalamus:
Contralateral burning pain = Dejerine-Roussy (Thalamic/Central) Syndrome
Lesion of DCMLS:
Tingling, numb sensation
Tight band-like sensation around the trunk or limbs
Feeling of having gauze on fingers
Electricity sensation down back and extremities upon neck flexion = Lhermitte’s sign
Lesions of STT pathways:
Sharp, burning or searing pain
Lesion of nerve roots:
Radicular pain with numbness and tingling in dermatomal distribution = radiculopathy
What happens w repeated application of noxious stimuli?
What is the point of sensitization?
Following repeated application of noxious stimuli, neighboring nociceptors that were not responsive now become responsive.
Hyperalgesia = the phenomenon of stimuli that are normally perceived as slightly painful as significantly more painful
Allodynia = induction of pain by what is normally an innocuous stimulus (ex: sore throat… swallowing shouldn’t hurt)
Point of sensitization = projects injured area, promotes healing and prevents infection
Nociception and temperature
Non-nociceptive thermoreceptors continue to respond at same rate even at higher T.
Nociceptors respond at high T ONLY.
Describe the mechanism for local modulation of pain sensation (Gate Theory).
Gate Theory of Pain: Local Modulation of Nociceptive Information
Pain results from balance of activity in nociceptive and non-nociceptive afferents
A(beta) fibers help to limit amount of pain perception
- Firm synapses with interneurons in dorsal horn - these interneurons are inhibitory to the C fibers
- Interneuron to inhibit pain transmission (close the gate) so there is reduced C fiber activation
Describe the pathways for visceral and referred pain.
Visceral Pain: Dorsal Column
- does NOT decussate and form anterior lateral tract
- goes to the dorsal columns ipsilaterally and then decussates in medulla before making its way to VPL -> INSULAR CORTEX
Referred Pain: also conveyed centrally by neurons that carry cutaneous pain
- won’t be able to distinguish where pain originated b/c they converge on the same second order projection neuron
What is central sensitization?
Mechanisms?
An immediate, activity dependent increase in the excitability of neurons in the dorsal horn of the spinal cord following high levels of activity in the nociceptive afferents to increase pain sensitivity
Mechanisms:
- Transcription independent (windup) lasts only during stimulation = acute
- if you give same stimulus repeatedly, it becomes more and more painful - Transcription dependent (allodynia) outlast stimulus for hours and can be mediated by COX = chronic
- neighboring area will be activated in addition to immediate area
