Lecture 13 Flashcards
What is the anterolateral system: spinothalamic tract?
Primarily concerned with pain and temperature
Principal target of the spinothalamic pathway is the primary and secondary somatosensory cortex
Primary somatosensory is where perception of pain starts
Slide 1
How do the neuron signal travel through CNS differ for afferent neurons from pain or temperature versus receptors for body movement, limb positions, etc?
Afferent neuron from pain or temp receptor: anterolateral system: primary afferent axons terminate in dorsal horn -> secondary axons cross the midline -> ascend contralateral anterolateral column time thalamus
Receptors for body movement, limb positions, etc: mechanosensory: primary afferent axons enter spinal cord -> ascend ipsilateral dorsal columns -> synapse in medulla -> secondary axons cross the midline -> ascend to contralateral thalamus
Slide 2
What is brown-séquard syndrome?
Incomplete spinal cord lesion characterized by clinical presentation reflecting hemisection of the spinal cord (spinal cord tumor, trauma, ischemia, infections)
Very important clinically- shows difference between 2 systems- pain crosses right away, mechanosensory doesn’t cross right away
Different symptoms for different sensory losses
A lesion restricted to left half of spinal cord results in dissociated sensory loss and mechanosensory deficits on the left half of the body, with pain and temp deficits are seen on the right
Slide 3
What are the 2 components of pain perception?
Sensory- discrimination aspects of pain (location, intensity, quality of stim)
Primary and secondary somatosensory cortex
Affective- motivational aspects of brain (unpleasant feeling, fear and anxiety, autonomic activation)
Anterior cingulate and insular cortex
Slide 4
What is the placebo affect?
Physiological response following administration of a pharmacologically inert “remedy”
Shows power of mind over body
Improve pain through expectations
75% patients suffering from postoperative wound pain reported stims factory relief after an injection of sterile saline
Slides 5-6
What is the dopamine placebo in Parkinson’s?
Placebo given decreases striatal radioactivity which reflects an increase in the synaptic level of dopamine, which inhibits RAC from binding ti dopamine receptors sites
Slide 7
What is the physiological basis of pain modulation (the descending nerve travelling)
Periaqueductal gray neurons project to serotonergic (raphe nucleus) and noradrenergic (locus ceruleus) descending pathways to inhibit nociceptive projection neurons in the superficial layers of the dorsal horn
Activation of descending pain modulating pathways that project to the dorsal horn of spinal cord produce analgesia
Slide 8
What do descending monoaminergic pathways regulate?
Descending monoaminergic pathways regulate nociceptive relay neurons in the spinal cord
Descending projections exert effects by acting in synaptic terminals of nociceptive afferents, excitatory and inhibitory interneurons, and synaptic terminals of other descending paths
Slide 9
What is opiate induced analgesia?
Opium derivates (morphine) are powerful analgesics
Many brain regions susceptible to the action of opiate drugs (especially periaqueductal gray and other descending projections)
Opiate drugs act at these sites to produce their dramatic pain relieving effects
Endogenous opiate receptors must exist, several different categories of endogenous opioids are found in the same regions that are involved in modulation of nociceptive afferents (enkephalins, endorphins, dynorphins)
Slide 10
Study the differences of nociceptive signals with and without opiates/opioids slide 11
Action potential is narrowed (smaller action potential, less release of neurotransmitter) with opiates
No sensory input + opiates leads to hyperolarization
Slide 11
What does activation of a nociceptor lead to?
What are opiates affect on it?
Activation of a nociceptor leads to release of glutamate and neuropeptides from primary sensory neuron, producing an excitatory postsynaptic potential in the projection neuron
Opiates decrease the duration of the postsynaptic potential, probably by reducing Ca influx and thus decreasing the release of transmitter from the primary sensory terminals
Opiates also hyperpolarize the dorsal horn neurons by activating K+ conductance and thus decrease the amplitude of the postsynaptic potential in dorsal horn neuron
Slide 12-13
How do we restrict opioids to areas that we want?
Want to target peripheral brain areas without central effects
Designed a drug that only acts on that receptor when it is an acidic condition (there isn’t a central reduction in pH)
Slide 14-15
A new opioid can target disease specific confirmations of receptors and ligands by selectively activating opioid receptors where acidic conditions prevail, as in tissues affected by inflammation or injury
Opioids bring pain relief to site of inflammation without affecting healthy tissues
Slide 16
What is physical pain and social pain?
Physical- defined as unpleasant experience that is associated with actual or potential tissue damage
Social- the unpleasant experience that is associated with actual or potential damage to ones sense of social connection or social value
Experiences of social rejection can be some of the most painful experiences that we endure
Slide 17
Can social pain be processed by the same neural circuitry that processed physical pain?
Rejection really hurts: social distress can cause physical pain
Factors associated with greater sensitivity to social exclusion (low self esteem, anxious attachment, socially disconnected) have been shown to be associated with increased neural activity in the anterior cingulate and insular cortex in response to social exclusion
Factors associated with reduced sensitivity to social exclusion (social support) have be shown to be associated with reduced activity in the anterior cingulate and insular cortex
