Neurology 4: Temperature And Nociception Flashcards
List the main nociceptors present in the skin and indicate the stimuli to which these respond
Temperature receptors in skin slide 6
Nociceptors in skin slide 9 ,10 and 11
Describe how cool, cold and warm temperatures are detected by the skin
Slide 6, 7
Briefly describe the main pathways involved in somatic and visceral Nociception
Lateral Spinothalmic tract - Nociception and pain
Anterior Spinothalmic tract- non discriminative touch and pressure
Describe how Nociception can become sensitised by co-existing inflammation
J
Briefly explain the mechanism involved in “wind up” of the pain response
Slide 33
Explain the difference between inflammatory and neuropathic pain
Inflammatory pain:
- active inflammation present
- spontaneous and stimulus dependant
- sensory amplification
- evoked by low- and high- intensity stimuli
- long term, but reversible
- protects by producing pain hypersensitivity during healing
Meh slide 30, 31 and 32
And neuropathic pain 37
-nervous system lesion or disease present
-spontaneous and stimulus dependant pain
-sensory amplification
-evoked by low- and high-intensity stimuli
-long lasting; maladaptove and persistant- serves no useful purpose
-maintained independent of nervous system lesion or disease
Briefly explain the 2 major mechanism whereby nociceptive signals can be modified by the body.
J
Contrast all the neurological deficits (sensory and motor) that may be evident in a patient with complete transaction of the spinal cord at the level of the:
- cranial cervical region
- cervicothoracic (brachial) plexus
- thoracolumbar region
- lumbosacral plexus
-Loss of pain sensation 1-2 levels below lesion die to 1st order afferents fibres descending in zone of lissauers
-lesion at cervical level
-complete loss of pain (
Slide 18
Discuss the thalamic convergence of the Spinothalmic and trigeminothalmic pathways
Slide 20
Reffered pain- discuss it
Slide 25
What is nociceptive pain?
Normal response
No nervous system lesion or inflammation
Stimulus-dependant
Evoked by high-intensity noxious stimuli
Protects by signalling potential tissue damage
27
What are the fibres that enter the dorsal horn?
Slide 28
Inflammatory pain
Inflammatory pain:
- active inflammation present
- spontaneous and stimulus dependant
- sensory amplification
- evoked by low- and high- intensity stimuli
- long term, but reversible
- protects by producing pain hypersensitivity during healing
Peripheral sensitisation of nociceptors
-Inflammatory mediators activate and augment response of nociceptive fibres
-neuropeptides substance P and CGRap cause:
-plasma extravasation
-histamine release from mast cells
-vasodilation
Histamine decreases threshold for nociceptor activation
Assosiated with hyperalgesia
Central sensitisation
- enhancement, potentiation or facilitation of synaptic activity on dorsal horn
- typically assosiated with severe and persistence tissue damage/inflammation
- activity level in nociceptive afferents that were previously sub threshold now sufficient to generate AP’s in 2nd order dorsal horn neurons
- have enlargement of nociceptive neuron fields beyond initial site of tissue damage/ inflammation (secondary hyperalgesia)
- spontaneous activity present, and nociceptive signals may be generated by innocuous mechanical stimuli via AB afferents
