Emotional influences on pain Flashcards
what is the gate-control theory?
provided the first mechanism by which emotions could influence pain - suggested that inhibitory neurons in the spinal cord could regulate incoming nociceptive signals
these neurons could be influenced by central controls, thus causing hypoalgesia (reduced pain) or even analgesia (elimination of pain)
appetitive vs defensive systems
appetitive system: activated by survival-promoting stimuli (e.g., sex, food) - results in appetitive behaviors (e.g., sustenance, procreation) and positive emotions
defensive system: activated by harmful or potentially harmful stimuli (e.g., predator, somatic threat) - results in defensive behaviors (e.g., withdrawal, attack) and negative emotions
* pain is a part of the defensive system and helps organisms detect and avoid somatic dangers
* pain system activation results in negative affect → promotes avoidance and learning so that danger can be circumvented in the present and future
valence vs arousal
valence = the pleasantness/unpleasantness of emotional experience - provides information about the motivation system activated (appetitive or defensive, respectively)
arousal = the intensity of the emotional experience - serves as an indirect readout of the degree of motivation system activation
what is the motivational priming theory?
explains the relationship between emotions and outputs/responses from appetitive and defensive systems
* argues that activation of a motivational system primes it = facilitates responses from the same system and inhibiting responses from the opposite system
* e.g. priming the defensive system with aversive stimuli leads to facilitation of startle (defensive reflex) - but priming appetitive system would inhibit startle
* the degree of motivation system activation plays a role - e.g. greater appetitive/defensive activation results in greater inhibition/facilitation
observations:
positive emotions generally inhibit pain, whereas negative emotions generally enhance pain
emotional modulation of pain (Rhudy, 2016)
emotions evoked by painful stimuli (pain-related emotions) direct attention toward pain & emotions evoked by non-painful stimuli (pain-unrelated emotions) direct attention away from pain
pain-related emotion studies:
* pain intensity and unpleasantness were increased by neg emotions and decreased by pos
* some stimuli produce fear conditioning (negative affect) and hyperalgesia more readily
* pain and nociceptive flexion reflex (NFR) were enhanced when participants anticipated a strong electric shock
pain-unrelated emotion studies:
* reading sad statements enhanced pain relative to neutral statements
* pain and NFR were enhanced during unpleasant pictures and reduced during pleasant pictures - indicates that positive and negative emotions engage brain-to-spinal cord circuits to modulate spinal nociception
observations
degree of motivation system activation affects the degree of pain inhibition/facilitation
emotional modulation of pain (Rhudy, 2016)
valence reflects which motivational system is activated, arousal provides the degree of the motivation system
NFR are facilitated by unpleasant pictures and inhibited by pleasant pictures
degree of arousal associated with degree of facilitation/inhibition
* most arousing unpleasant pictures (mutilation) led to the greatest facilitation
* most arousing pleasant pictures (erotica) led to the greatest inhibition
low intensity emotions produce little inhibition/facilitation
observations
emotional stimuli that elicit simultaneous (and equal) defensive and appetitive activation have no net effect on pain
emotional modulation of pain (Rhudy, 2016)
MPT implies that stimuli that elicit a mix of appetitive and defensive activation will have a zero effect on pain, because simultaneous inhibition and facilitation cancel each other out
a few observations support it - e.g. cold pressor pain following the presentation of erotic pictures:
* women reacted with sexual arousal (appetitive) and disgust (defensive), resulting in no modulation of their pain response; men reacted with only appetitive activation and pain was inhibited
observations
emotions modulate all pain related (defensive) outcomes in parallel
emotional modulation of pain (Rhudy, 2016)
if pain and pain-related responses originate from defensive activation, all should be inhibited by appetitive activation and facilitated by defensive activation
emotional modulation of the NFR and pain-evoked ERPs parallel the modulation of pain
revision on motivational priming theory
to include findings that neg emotions can inhibit pain
revision of MPT: argues that MPT characterizes the effects of emotions on pain only when motivational systems are low-to-moderately activated - explains why studies find negative emotion induced hyperalgesia (increased sensitivity to pain)
* the emotion-induction procedures used should not produce active defense and intense, highly arousing, neg emotions in nonclinical samples
* BUT, when neg emotion induction involved a somatic threat cue paired with severe somatic threat, phobic stimuli, or life-threatening events → evoked highly arousing negative emotions and hypoalgesia
relationship between negative emotions and pain is nonmonotonic:
* low-to-moderately arousing negative emotions result in hyperalgesia
* highly arousing negative emotions result in hypoalgesia
relationship between positive emotions and pain is monotonic:
* positive emotions always inhibit pain (hypoalgesia)
emotional modulation of pain in clinical populations
- disorders of emotion (e.g. depression) and pain are often comorbid - affective disturbance might serve as a risk factor for chronic pain
- chronic pain patients may have a reduced capacity to engage in pain-inhibitory mechanisms
- pos emotions and intense negative emotions may not be able to elicit hypoalgesia as they do in healthy individuals
- study: controls had normal emotional modulation of pain intensity, but emotional modulation of pain was disrupted in fibromyalgia patients (pain higher during pleasant and unpleasant)
emotional contagion and pain
Cognitive and emotional control of pain and its disruption in chronic pain (Bushnell, 2013)
found that when subjects were positively empathizing with the individual in pain, their own pain experience was enhanced = emotional contagion
a noxious insult to the body is not necessary for the experience of pain or for the activation of pain pathways
* simply observing another person in pain activates some pain-related regions + activation is stronger when observing a loved one
* activation of these regions in the absence of a pain stimulus could induce a state of ‘priming’ in the brain → enhanced pain experience
how do attention and emotion influence pain differently?
Cognitive and emotional control of pain and its disruption in chronic pain (Bushnell, 2013)
both attentional and emotional factors are known to modulate pain perception - but the nature & mechanisms of this modulation differ
* focusing on pain → increases the perceived intensity of the sensation
* when focusing on pain: pain-evoked activity in S1, insula and ACC is stronger than when distracted
* negative emotional state → increases the perceived unpleasantness of the pain without altering the intensity
study: emotional valence influenced pain ratings and a spinal nociceptive reflex in the same direction but distraction reduced pain while increasing the reflex
= appears that different systems may be involved in the modulation of pain by attention and emotions
modulatory systems involved in the attentional & emotional control of pain
Cognitive and emotional control of pain and its disruption in chronic pain (Bushnell, 2013)
separate modulatory systems may underlie attentional and emotional influences on pain
* outputs from forebrain regions (ACC, PFC and amygdala) reach the PAG - suggests that these descending systems could be activated by psychological factors
when emotion and arousal are dissociated from attention:
* increased negative emotion associated with activation of the ACC–fronto–PAG circuitry
* yhis activation correlated with negative mood-related increases in pain-evoked activity in the ACC
when subjects intentionally direct their attention to or away from a painful stimulus:
* attention-related alterations in pain-evoked activity in the insula correlated with activity in the superior parietal cortex
* SPC: part of the ‘top-down orienting of attention’ system - descending pathways from the insula to the amygdala provide a possible descending component to the attentional modulation of pain
how does anticipation of pain relief activate descending pathways?
Cognitive and emotional control of pain and its disruption in chronic pain (Bushnell, 2013)
anticipation of the relief of pain is a primary contributor to placebo analgesia → causes activation in the ACC-fronto-PAG pathway and activates similar regions that are activated when a positive emotional state reduces pain
descending modulatory pathways involved in placebo analgesia may overlap with those involved in the emotional modulation of pain
* conversely, circuitry involved in the attentional modulation of pain does not appear to be activated during expectation-related placebo analgesia
* but placebo analgesia does not depend on the active redirection of attention
Cerebral and spinal modulation of pain by emotions (Roy, 2009)
aim & method
aim: identify the brain generators of cerebrospinal modulatory effects + investigate additional brain mechanisms underlying the modulation of pain by emotions
* modulation of spinal activity is expected to affect the transmission of nociceptive signals and the response of their target brain regions through the multiple ascending pathways
method:
* combination of spinal nociceptive reflex recordings (RIII) and cerebral (fMRI) measures
* pain and emotion related activation: electric shocks while seeing blocks of pleasant, unpleasant or neutral pictures
* connectivity analyses to reveal networks of brain regions associated with the effects of emotions on pain-related brain activation
