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
How are the pain signals modulated?
Sensory signals can be modulated as they travel along sensory pathways
-facilitation of into ton of signals can change how the info is finally percieved
-within spinal cord, somatic signals from non-painful sources can inhibit pain signals
-in humans, this is why rubbing a painful area helps relieve the
pain
-referred to as the gate-control theory of pain modulation
Slide 40,41 and 42
