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Mark Sullivan, MD, PhD
University ofWashington
American Academy of Psychoanalysis and Dynamic Psychiatry
2018
 Consulting
 Aetna, ChronoTherapeutics, State ofWA
 Research grants
 Pfizer and Purdue and NIDA
“O just, subtle, and all-conquering opium!”
-- Thomas De Quincey,
Confessions of an English Opium Eater, 1821
 38 yr old married RN with 2 children, 8yr, 5yr
 MVA 3 years ago when she was rear-ended
 Initially she had whiplash, chronic neck pain
which gradually spread down her spine and
then her limbs and whole body
 Unable to work since her accident
 Spine MRI reveals only degen. disc disease
 She reports 10/10 pain despite oxycodone SR
80mg BID (240mg MED), asks for more
 IASP definition of pain:
 Pain is an unpleasant sensory and emotional
experience associated with actual or potential
tissue damage or described in terms of such
damage
 IASP chronic pain types
 nociceptive, neuropathic, visceral, central, noci-
plastic
 nociplastic = centralized pain, functional pain,
central sensitization, pain hypersensitivity
 Widespread pain but no abnormalities in
painful muscles
 Hypersensitivity to pressure, heat, cold,
electricity, sound
 Adverse childhood experiences common,
esp. physical and sexual abuse
 Classic example of functional pain syndrome,
somatization, somatoform d/o
 “We can’t find anything wrong with you”
 Similar syndromes:
 Chronic fatigue, irritable bowel, interstitial cystitis
 Often include other dysfunction with:
 Sleep, mood, memory, concentration
 Effective treatments
 Antidepressants, anticonvulsants, CBT, exercise
 Ineffective treatments
 NSAIDs, surgery, local injections, opioids
 Altered CNS nociceptive processing
 Increased activation on fMRI: posterior insula,
secondary somatosensory cortex…
 Increased connectivity between insula and
default mode network, proportional to pain
 Elevated substance P and glutamate in CSF
 Reduced conditioned pain modulation
 Endogenous opioid tone increased
 As part of her initial work-up at pain clinic,
she scored 5/5 on PC-PTSD5 screener
 She re-experiences her MVA in nightmares
 She avoids driving in that part of town
 She is easily startled, angered, w insomnia
 She has withdrawn from colleagues, friends
 She cannot stop blaming herself for the MVA
 She appears to have PTSD
 Dualistic: psychological and biological explanations
compete and exclude each other
 Psychogenic pain opposed to: real pain,
somatogenic pain, purely physical pain
 Cartesian mechanical model (1664)
 “my c-fibers are firing” (1970)
 Wager’s NEJM “neurological signature for
physical pain” (2014??)
 Ideal of a fully objectified and de-psychologized
pain that is the opposite of psychogenic pain
 DSM-III: Psychogenic Pain Disorder
 Severe pain inconsistent with anatomy or grossly
in excess of expected based on physical exam
 DSM-IIIR: Somatoform Pain Disorder
 Drops evidence for psychological cause, adds
preoccupation with pain, now a dx of exclusion
 DSM-IV: Pain Disorder
 Medical and psychological factors, but remains
diagnosis of exclusion w unclear notions causation
 Replaces: somatization disorder, pain
disorder, undifferentiated somatoform d/o
 Not “psychologically caused” or “medically
unexplained”, but “excessive concern”
 Critics: too inclusive, may label medical
illness as mental disorder
 Based on idea that medical and psychological
explanations exclude each other
 Cognitive-behavioral therapy (CBT)
 Focused on appraisal and coping with pain rather
than causation of pain
 In practice, treats pain as given by physiology,
contrasted to suffering and disability which also
arise from psychological and behavioral processes
 CBT focused on helping patients live well with
pain rather than reducing amount of pain
experienced
 Does not challenge somatogenic pain causation
 Acceptance and CommitmentTherapy (ACT)
 does not challenge cognitions like CBT, but urges
mindful commitment to value-based action and
acceptance of pain
 ACT not focused on pain reduction, can be
effective even when pain is severe
 ACT is agnostic about whether pain is
psychogenic or somatogenic
 Prevalence of PTSD in US is 7.8%
 Chronic pain reported in 35-50% of PTSD pts.
 Among patients presenting for care of
chronic pain, 7-50% meet PTSD criteria.
 Common chronic pain: pelvic pain, low back
pain, facial pain, bladder pain, fibromyalgia
 PTSD: more intense pain, affective distress,
disability
 PTSD: opioid therapy more likely, higher
doses, multiple opioids, concurrent benzos,
early refills, adverse events (Seal, 2012)
 PTSD: significant linear association with wide
range of pain outcomes: pain intensity,
activity interference, sleep, disability, global
health, opioid risk (Langford, 2018)
 As you work with Ms. B to address PTSD sxs.
(prazosin), depression (duloxetine) and
disability (PT, OT) she reveals that she was
beaten by her first husband (age 20-23)
 She eventually left this husband, but had
nightmares of beatings for years
 These had resolved about a decade before
her MVA
 Prospective fMRI study of patients w LBP
(Hashimi, 2013)
 LBP progresses- acute subacute chronic
patterns of brain activation shift from
sensory/nociceptiveemotion-related
regions
 But as LBP shifts from somatogenic to
psychogenic, it feels the same to the patient
 This LBP thus does not have a single cause or
“neurological signature” (Wager)
 Most prefer broken leg over broken heart, but
medicine treats broken legs as more real
 Social rejection, exclusion, loss can be the most
“painful” experiences of human life
 Physical injury and social rejection produce
activation of same brain structures on fMRI:
anterior cingulate, anterior insula
 Eisenberger: “social attachment system may
have piggybacked onto opioid substrates of
physical pain system to maintain proximity with
others…”
 Sensitivity to physical and social pain linked
 Same people
 Experiments show persons more sensitive to
physical noxious stimuli also more sensitive to
social rejection
 Same treatments
 Physical and social pain respond to same meds
▪ opioids relieve separation distress (Panksepp, 1978)
▪ Acetaminophen reduces social and physical pain (Dewall,
2010)
 Invertebrates have no EOS
 Amphibians, reptiles, fishes have an EOS that
modulates only physical injury pain
 Suppresses pain if injured while fleeing predator
 Rats forced to swim in ice water
 Injured patients who do not feel pain until at ED
 Mammalian EOS also modulates the pain of
physical injury, but…
 In mammals, opioids also serve to promote
social bonds essential for survival.
 In non-primate mammals, most crucial bonds
are with mates and offspring
 Known to be supported by oxytocin system
 But EOS supports these most basic bonds too
 Rat pups w deficient EOS do not bond to mothers
 EOS necessary for development of social play
 In humans, social play supports social
bonding and social, cognitive, emotional
development
 Adult social relationships  pain tolerance
 fMRI: partner caress EOS  pain tolerance
 Primate EOS allows complex social networks
 As social networks grow from rodents to primates
benefits and conflicts increase
 Endorphin release during primate grooming helps
defuse these stresses and assure relationships
available, but limited to group size of about 20
 Human social bonds more complex, extensive
so need support beyond grooming (Dunbar):
 Laughter “primitive chorusing vocalization”
 Singing, dancing, drama, religious ceremonies
 Adult attachment style related to EOS
 PET: avoidant attachment related to lower mu
receptor availability in amygdala, ACC, insula, PFC
 BPD, ASP show EOS dysregulation (Bandelow)
 Recent neuroimaging studies show many brain
areas active during both pain and depression
(ACC, insula, amygdala, and DLPFC ) are laden
with opioid receptors.
 Baliki and Apkarian have proposed that pain,
anxiety and depression form a continuum of
aversive behavioral learning, which enhances
survival by protecting against threats.
 The transformation of nociception into behavior
to promote survival is extended to incorporate
negative moods.
Mu Opioid Receptor-Mediated
Neurotransmission
AMY
CAU/
NAC/
VP
THA
CING
4
3
2
1
BP
Distributed in pain
regions but also
“affective / motivational
circuits” - neuronal
nuclei involved in the
assessment of stimulus
salience and cognitive-
emotional integration.
Descending
CNS Inhibitory Controls
From Zubieta JK
 FM patients have higher rates of depression,
psychol trauma and PTSD than RA OA pts.
 FM- reduced mu opioid binding potential
associated w increased pain affect and
evoked activity in DLPFC, rACC
 EOS dysregulation leads to hyperalgesia and
allodynia typical of FM, and to nonresponse
to opioid therapy
 During a session on pain coping with MSW,
Ms. B speaks of nightmares of molestation
 She says her grandfather used to visit her
room at night when stayed with them
 This occurred age 7-13 until he died
 She tried to tell her mother, but she said that
“Grandpa wouldn’t do such a thing.”
 Ms. B also reports she drank heavily and took
“pain pills” until she left her first husband
 Ms. B’s trauma history now includes the
essential elements of helplessness and
loneliness (Bergman)
 Survival requires dissociation from the self
that has been overwhelmed and destroyed
 Repeat trauma breaks through dissociation
once again making Ms. B helpless and alone
 So she turns to opioids
 Targeted rejection events (e.g., fired, broken up)
 assoc. with 22x increase in depression
 With rejection, MDE patients show MOR deactivation
but controls show MOR activation in amygdala
 These social rejections are a threat to physical survival
for intensely social primates
 SNP in OPRM1 increases sensitivity to both
physical pain and social rejection
 G allele carriers need more opioids after surgery, tend
to fearful adult attachment
 CRF coordinates autonomic, behavioral, and
cognitive response to stress w endocrine syst.
 In acute stress, CRF acts on LC to increase
arousal, attention, behavioral flexibility
 EOS has opposite effect on LC, helps neurons
and organism recover after stressor is gone
 With chronic stress (PTSD), opioid tolerance
and dependence may develop w/o meds
 Neuroscience suggests that human pain is a
survival-oriented behavioral drive rather than an
injury-caused aversive sensation
 EOS continuously modulates the transmission of
nociception to promote survival
 Brain encodes pain salience, not pain intensity
determined by survival-relevant context
 Pain system is a danger-detection system rather
than a damage-detection system (Moseley)
From Cahill et al, 2014
 DA: in reward-driven actions-- “wanting”
Opioids: in hedonic tone– “liking”
 These systems are integrated to modulate
the valence (positive/negative) and
salience (strong/weak) of pain
 DA encodes motivational salience of pain
 whether pain should be endured for rewards
 when pain has positive valence or low salience
 Chronic pain disrupts hedonic homeostasis,
increasing relevance and reward of pain relief
(Elman and Borsook)
 As persistent stress, chronic pain increases
endogenous opioid tone, but decreases phasic
changes in endogenous opioids in response to
transient stressors.
 Similarly, exogenous opioid therapy initially
induces pain relief, but then induces tolerance
(to pain relief and mood elevation) and
dependence (a need for opioids to avoid pain
and distress).
 Oxycodone provided relief of pain, insomnia,
anxiety, agitation and anger
 But Ms. B kept needing more oxycodone,
developing tolerance and dependence
 Opioids reduce hyperarousal, re-experiencing
but deepen numbing and avoidance
 This leads to PTSD perpetuations
 Human physical and social pain systems are
linked because human physical survival is
dependent on social survival
 Humans thrive in social cooperation, but
must continually modulate disruptive
stresses
 Endogenous opioids are crucial to this, and
are disrupted by continuous exposure to
exogenous opioid medications
 As substance use deepens, relationships
deteriorate
 Does not require development full addiction,
dependence may be enough
 Opioids: “like being hugged by God”
 If substances are to be reduced, relationships
must be recovered
 Reach for the phone rather than pill bottle
 But complicated restoration process in those with
early, multiple or severe trauma
 Opioid taper support trial subjects were
 Surprised that their pain did not increase
 Surprised they no longer felt like “zombies”
 Zombie= social/emotional dysfunction
Spouses confirmed return to old personalities
 Other research: opioid maintenance assoc w
impaired emotion perception and ability to
make inferences about social situations
 Inability to discern sarcasm
 We can now understand that this standard
framing of opioid policy is too simple and
ignores what we have reviewed about EOS
 Many neuroadaptations and harms assoc. w
continuous opioid therapy arise with the
state of dependence, do not require addiction
 Mass exposure only w ER/LA opioids since 1990’s
 High-dose patients may not be able to DC
 DSM-V Opioid Use Disorder is based on the
idea that “opioid physiological dependence”
and opioid addiction are completely distinct
 But social and emotional harms of opioids,
like opioid-induced hyperalgesia,
hypogonadism arise with dependence
 This dependence can arise with clinical use or
non-clinical abuse, requires only sustained
exposure
 Ms. B attempted opioid taper, but became
too anxious, angry and overwhelmed
 Opioids simulated safety too well
 She transitioned onto SL buprenorphine with
improvement in her pain and anxiety
 Currently engaged in Cognitive Processing
Therapy to address her PTSD and trauma
 Hopes to taper off opioids in the future
 Human pain exists to promote both physical
and psychological survival.
 Mammalian social pain system piggybacked
onto physical pain system of non-mammals.
 EOS (+steroid, +dopamine) modulates the
pain of both broken arms and broken hearts
to promote species survival

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Between suffering and survival: understanding the dynamic links among physical pain, social pain and addiction

  • 1. Mark Sullivan, MD, PhD University ofWashington American Academy of Psychoanalysis and Dynamic Psychiatry 2018
  • 2.  Consulting  Aetna, ChronoTherapeutics, State ofWA  Research grants  Pfizer and Purdue and NIDA
  • 3. “O just, subtle, and all-conquering opium!” -- Thomas De Quincey, Confessions of an English Opium Eater, 1821
  • 4.
  • 5.  38 yr old married RN with 2 children, 8yr, 5yr  MVA 3 years ago when she was rear-ended  Initially she had whiplash, chronic neck pain which gradually spread down her spine and then her limbs and whole body  Unable to work since her accident  Spine MRI reveals only degen. disc disease  She reports 10/10 pain despite oxycodone SR 80mg BID (240mg MED), asks for more
  • 6.  IASP definition of pain:  Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage  IASP chronic pain types  nociceptive, neuropathic, visceral, central, noci- plastic  nociplastic = centralized pain, functional pain, central sensitization, pain hypersensitivity
  • 7.  Widespread pain but no abnormalities in painful muscles  Hypersensitivity to pressure, heat, cold, electricity, sound  Adverse childhood experiences common, esp. physical and sexual abuse  Classic example of functional pain syndrome, somatization, somatoform d/o  “We can’t find anything wrong with you”
  • 8.  Similar syndromes:  Chronic fatigue, irritable bowel, interstitial cystitis  Often include other dysfunction with:  Sleep, mood, memory, concentration  Effective treatments  Antidepressants, anticonvulsants, CBT, exercise  Ineffective treatments  NSAIDs, surgery, local injections, opioids
  • 9.  Altered CNS nociceptive processing  Increased activation on fMRI: posterior insula, secondary somatosensory cortex…  Increased connectivity between insula and default mode network, proportional to pain  Elevated substance P and glutamate in CSF  Reduced conditioned pain modulation  Endogenous opioid tone increased
  • 10.  As part of her initial work-up at pain clinic, she scored 5/5 on PC-PTSD5 screener  She re-experiences her MVA in nightmares  She avoids driving in that part of town  She is easily startled, angered, w insomnia  She has withdrawn from colleagues, friends  She cannot stop blaming herself for the MVA  She appears to have PTSD
  • 11.  Dualistic: psychological and biological explanations compete and exclude each other  Psychogenic pain opposed to: real pain, somatogenic pain, purely physical pain
  • 12.  Cartesian mechanical model (1664)  “my c-fibers are firing” (1970)  Wager’s NEJM “neurological signature for physical pain” (2014??)  Ideal of a fully objectified and de-psychologized pain that is the opposite of psychogenic pain
  • 13.  DSM-III: Psychogenic Pain Disorder  Severe pain inconsistent with anatomy or grossly in excess of expected based on physical exam  DSM-IIIR: Somatoform Pain Disorder  Drops evidence for psychological cause, adds preoccupation with pain, now a dx of exclusion  DSM-IV: Pain Disorder  Medical and psychological factors, but remains diagnosis of exclusion w unclear notions causation
  • 14.  Replaces: somatization disorder, pain disorder, undifferentiated somatoform d/o  Not “psychologically caused” or “medically unexplained”, but “excessive concern”  Critics: too inclusive, may label medical illness as mental disorder  Based on idea that medical and psychological explanations exclude each other
  • 15.  Cognitive-behavioral therapy (CBT)  Focused on appraisal and coping with pain rather than causation of pain  In practice, treats pain as given by physiology, contrasted to suffering and disability which also arise from psychological and behavioral processes  CBT focused on helping patients live well with pain rather than reducing amount of pain experienced  Does not challenge somatogenic pain causation
  • 16.  Acceptance and CommitmentTherapy (ACT)  does not challenge cognitions like CBT, but urges mindful commitment to value-based action and acceptance of pain  ACT not focused on pain reduction, can be effective even when pain is severe  ACT is agnostic about whether pain is psychogenic or somatogenic
  • 17.  Prevalence of PTSD in US is 7.8%  Chronic pain reported in 35-50% of PTSD pts.  Among patients presenting for care of chronic pain, 7-50% meet PTSD criteria.  Common chronic pain: pelvic pain, low back pain, facial pain, bladder pain, fibromyalgia
  • 18.  PTSD: more intense pain, affective distress, disability  PTSD: opioid therapy more likely, higher doses, multiple opioids, concurrent benzos, early refills, adverse events (Seal, 2012)  PTSD: significant linear association with wide range of pain outcomes: pain intensity, activity interference, sleep, disability, global health, opioid risk (Langford, 2018)
  • 19.  As you work with Ms. B to address PTSD sxs. (prazosin), depression (duloxetine) and disability (PT, OT) she reveals that she was beaten by her first husband (age 20-23)  She eventually left this husband, but had nightmares of beatings for years  These had resolved about a decade before her MVA
  • 20.  Prospective fMRI study of patients w LBP (Hashimi, 2013)  LBP progresses- acute subacute chronic patterns of brain activation shift from sensory/nociceptiveemotion-related regions  But as LBP shifts from somatogenic to psychogenic, it feels the same to the patient  This LBP thus does not have a single cause or “neurological signature” (Wager)
  • 21.  Most prefer broken leg over broken heart, but medicine treats broken legs as more real  Social rejection, exclusion, loss can be the most “painful” experiences of human life  Physical injury and social rejection produce activation of same brain structures on fMRI: anterior cingulate, anterior insula  Eisenberger: “social attachment system may have piggybacked onto opioid substrates of physical pain system to maintain proximity with others…”
  • 22.  Sensitivity to physical and social pain linked  Same people  Experiments show persons more sensitive to physical noxious stimuli also more sensitive to social rejection  Same treatments  Physical and social pain respond to same meds ▪ opioids relieve separation distress (Panksepp, 1978) ▪ Acetaminophen reduces social and physical pain (Dewall, 2010)
  • 23.  Invertebrates have no EOS  Amphibians, reptiles, fishes have an EOS that modulates only physical injury pain  Suppresses pain if injured while fleeing predator  Rats forced to swim in ice water  Injured patients who do not feel pain until at ED  Mammalian EOS also modulates the pain of physical injury, but…
  • 24.  In mammals, opioids also serve to promote social bonds essential for survival.  In non-primate mammals, most crucial bonds are with mates and offspring  Known to be supported by oxytocin system  But EOS supports these most basic bonds too  Rat pups w deficient EOS do not bond to mothers  EOS necessary for development of social play
  • 25.  In humans, social play supports social bonding and social, cognitive, emotional development  Adult social relationships  pain tolerance  fMRI: partner caress EOS  pain tolerance
  • 26.  Primate EOS allows complex social networks  As social networks grow from rodents to primates benefits and conflicts increase  Endorphin release during primate grooming helps defuse these stresses and assure relationships available, but limited to group size of about 20
  • 27.  Human social bonds more complex, extensive so need support beyond grooming (Dunbar):  Laughter “primitive chorusing vocalization”  Singing, dancing, drama, religious ceremonies  Adult attachment style related to EOS  PET: avoidant attachment related to lower mu receptor availability in amygdala, ACC, insula, PFC  BPD, ASP show EOS dysregulation (Bandelow)
  • 28.  Recent neuroimaging studies show many brain areas active during both pain and depression (ACC, insula, amygdala, and DLPFC ) are laden with opioid receptors.  Baliki and Apkarian have proposed that pain, anxiety and depression form a continuum of aversive behavioral learning, which enhances survival by protecting against threats.  The transformation of nociception into behavior to promote survival is extended to incorporate negative moods.
  • 29. Mu Opioid Receptor-Mediated Neurotransmission AMY CAU/ NAC/ VP THA CING 4 3 2 1 BP Distributed in pain regions but also “affective / motivational circuits” - neuronal nuclei involved in the assessment of stimulus salience and cognitive- emotional integration. Descending CNS Inhibitory Controls From Zubieta JK
  • 30.  FM patients have higher rates of depression, psychol trauma and PTSD than RA OA pts.  FM- reduced mu opioid binding potential associated w increased pain affect and evoked activity in DLPFC, rACC  EOS dysregulation leads to hyperalgesia and allodynia typical of FM, and to nonresponse to opioid therapy
  • 31.  During a session on pain coping with MSW, Ms. B speaks of nightmares of molestation  She says her grandfather used to visit her room at night when stayed with them  This occurred age 7-13 until he died  She tried to tell her mother, but she said that “Grandpa wouldn’t do such a thing.”  Ms. B also reports she drank heavily and took “pain pills” until she left her first husband
  • 32.  Ms. B’s trauma history now includes the essential elements of helplessness and loneliness (Bergman)  Survival requires dissociation from the self that has been overwhelmed and destroyed  Repeat trauma breaks through dissociation once again making Ms. B helpless and alone  So she turns to opioids
  • 33.  Targeted rejection events (e.g., fired, broken up)  assoc. with 22x increase in depression  With rejection, MDE patients show MOR deactivation but controls show MOR activation in amygdala  These social rejections are a threat to physical survival for intensely social primates  SNP in OPRM1 increases sensitivity to both physical pain and social rejection  G allele carriers need more opioids after surgery, tend to fearful adult attachment
  • 34.  CRF coordinates autonomic, behavioral, and cognitive response to stress w endocrine syst.  In acute stress, CRF acts on LC to increase arousal, attention, behavioral flexibility  EOS has opposite effect on LC, helps neurons and organism recover after stressor is gone  With chronic stress (PTSD), opioid tolerance and dependence may develop w/o meds
  • 35.  Neuroscience suggests that human pain is a survival-oriented behavioral drive rather than an injury-caused aversive sensation  EOS continuously modulates the transmission of nociception to promote survival  Brain encodes pain salience, not pain intensity determined by survival-relevant context  Pain system is a danger-detection system rather than a damage-detection system (Moseley)
  • 36. From Cahill et al, 2014
  • 37.  DA: in reward-driven actions-- “wanting” Opioids: in hedonic tone– “liking”  These systems are integrated to modulate the valence (positive/negative) and salience (strong/weak) of pain  DA encodes motivational salience of pain  whether pain should be endured for rewards  when pain has positive valence or low salience
  • 38.  Chronic pain disrupts hedonic homeostasis, increasing relevance and reward of pain relief (Elman and Borsook)  As persistent stress, chronic pain increases endogenous opioid tone, but decreases phasic changes in endogenous opioids in response to transient stressors.  Similarly, exogenous opioid therapy initially induces pain relief, but then induces tolerance (to pain relief and mood elevation) and dependence (a need for opioids to avoid pain and distress).
  • 39.  Oxycodone provided relief of pain, insomnia, anxiety, agitation and anger  But Ms. B kept needing more oxycodone, developing tolerance and dependence  Opioids reduce hyperarousal, re-experiencing but deepen numbing and avoidance  This leads to PTSD perpetuations
  • 40.  Human physical and social pain systems are linked because human physical survival is dependent on social survival  Humans thrive in social cooperation, but must continually modulate disruptive stresses  Endogenous opioids are crucial to this, and are disrupted by continuous exposure to exogenous opioid medications
  • 41.  As substance use deepens, relationships deteriorate  Does not require development full addiction, dependence may be enough  Opioids: “like being hugged by God”  If substances are to be reduced, relationships must be recovered  Reach for the phone rather than pill bottle  But complicated restoration process in those with early, multiple or severe trauma
  • 42.  Opioid taper support trial subjects were  Surprised that their pain did not increase  Surprised they no longer felt like “zombies”  Zombie= social/emotional dysfunction Spouses confirmed return to old personalities  Other research: opioid maintenance assoc w impaired emotion perception and ability to make inferences about social situations  Inability to discern sarcasm
  • 43.  We can now understand that this standard framing of opioid policy is too simple and ignores what we have reviewed about EOS  Many neuroadaptations and harms assoc. w continuous opioid therapy arise with the state of dependence, do not require addiction  Mass exposure only w ER/LA opioids since 1990’s  High-dose patients may not be able to DC
  • 44.  DSM-V Opioid Use Disorder is based on the idea that “opioid physiological dependence” and opioid addiction are completely distinct  But social and emotional harms of opioids, like opioid-induced hyperalgesia, hypogonadism arise with dependence  This dependence can arise with clinical use or non-clinical abuse, requires only sustained exposure
  • 45.  Ms. B attempted opioid taper, but became too anxious, angry and overwhelmed  Opioids simulated safety too well  She transitioned onto SL buprenorphine with improvement in her pain and anxiety  Currently engaged in Cognitive Processing Therapy to address her PTSD and trauma  Hopes to taper off opioids in the future
  • 46.  Human pain exists to promote both physical and psychological survival.  Mammalian social pain system piggybacked onto physical pain system of non-mammals.  EOS (+steroid, +dopamine) modulates the pain of both broken arms and broken hearts to promote species survival