2.3.2 The role of racial-ethnic disparities
Barnett and colleagues used 2016-2019 Medicare claims data to identify
racial-ethnic differences in the prescription and rates of use of
medications to treat OUD (buprenorphine, intramuscular extended-release
naltrexone) and prevent opioid overdose deaths (naloxone), as well as
high-risk prescription medications (e.g., opioid analgesics and
benzodiazepines)69. They found that Black persons are
less likely to access buprenorphine and naloxone than non-Hispanic White
(NHW) populations. This is particularly concerning, in that Black
persons have experienced greater increases in opioid-involved overdose
deaths than any other racial group, growing by a factor of 7.7 between
2010 and 202070.
Noted disparities in OUD treatment are mirrored by disparities in
chronic pain treatment in minoritized patients living with OUD. Black
and, to a degree, Hispanic adults have been shown to experience greater
clinical pain severity and pain-related disability than NHW
adults71-73. In laboratory models of pain, Black
persons have been found to exhibit lower pain thresholds and lower
tolerance of pain74-80. Growing evidence highlights
that these racial differences in pain perception may result from the
harmful effects of health-care disparities and societal racism in
general.
At the mechanistic level, racism-related stress, or pervasive emotional
distress caused by racial discrimination, may negatively affect pain
perception through sleep disturbance and corticolimbic disfunction, as
demonstrated by Letzen and colleagues81. The authors
assessed the effects of race-related stress on the corticolimbic system,
using positron emission tomography (PET) to evaluate the binding
potential of ยต-opioid receptors; actigraphy sleep variables were also
measured81. An association was demonstrated between
levels of exposure to racism and pain sensitivity through mechanisms of:
(1) race-related stress, (2) sleep disturbances associated with
race-related vigilance, and (3) corticolimbic opioid-receptor modulation
changes. These findings emphasize the role of multi-disciplinary
trauma-informed approach to pain treatment in racialized populations, as
the experience of racism may worsen the experience of pain and be
evident beyond physical domains82.
In summary, biological, psychological, and social factors converge to
impact the experience of chronic pain, challenging holistic pain
assessments. For persons with OUD, this assessment is further
complicated by opioid-related disruptions of pain pathways. For optimal
clinical outcomes, it is imperative to undertake a comprehensive,
multidisciplinary pain evaluation that can account for this complexity
(Figure 1 ).
SPECIAL CONSIDERATIONS
Tolerance and hyperalgesia
Pain assessment in individuals with OUD can be complicated by the
phenomena of tolerance and hyperalgesia, which are opioid-induced
changes to pain systems that can result in increased analgesic demand by
persons with pain26. Tolerance is characterized by a
decreased response to an opioid over repeated administration,
necessitating dose increases to achieve the previous magnitude of
analgesic effects26. Opioid-induced hyperalgesia (OIH)
is a paradoxical state of heightened pain sensitivity that is distinct
from and superimposed on the painful condition26, 83.
As people with chronic pain continue to deteriorate, increasing need for
opioids at higher doses can indicate several diagnostic hypotheses.
First, it may reflect untreated or inadequately treated pain that could
indeed benefit from higher dose adjustments84, 85;
second, it may signal the development of tolerance to the analgesic
effects of the current opioid regimen86, 87; or third
and alternatively, the dose escalation itself may be triggering OIH, in
which case higher doses might, in fact, be
detrimental26, 83.
Multiple mechanisms likely underlie the development of tolerance and
OIH. In some ways similar to mechanisms for pain chronification, these
include NMDA-receptor activation, neuroadaptations in descending pain
modulatory pathways, increased excitatory neuropeptides, and glial cell
activation85, 87, 88. However, the precise etiology
remains incompletely understood. Clinically, distinguishing between
under-treated pain, tolerance to analgesic effects of opioids, and
hyperalgesia is crucial yet challenging in persons with OUD. A
comprehensive phenotyping of the pain experience exploring
characteristics, timing, triggers, and radiation can determine if pain
represents disease progression or an opioid-related effect. A trial of
opioid dose reduction may also clarify if OIH is
present87. Carefully weighing these pain-related
factors helps clinicians to identify the source(s) of pain and optimize
pain management in this complex clinical population.