Clinical Bioethics: Chronic Pain and Substance Abuse
by James Giordano, PhD and Rachel Wurzman, MS
 Chronic pain is frequently accompanied by a
constellation of psychological characteristics, that may co-present as frank
psychopathology. Several studies have shown the high co-morbidity of chronic pain,
depression, anxiety, and/or somatization disorder.1-8 Given that: (1) chronic
pain and psychological factors are co-morbid and reciprocally-interactive, and (2)
unrecognized and/or untreated psychopathology may increase the experience of, and
reactivity to (chronic) pain, then it becomes clear that the co-morbidity and putative
relationship of these disorders must be considered in any meaningful paradigm for chronic
pain management.
Substance Abuse as Bio-psychological Co-morbidity
While considerable research has focused upon particular psychological disorders (e.g.,
depression, anxiety) that are co-morbid to chronic pain, it is equally important to
consider the evident problem of substance abuse (and addiction) in this light, given the
noted prevalence of pain, psychologic and substance abuse disorders, and the growing body
of evidence to support the putative relationship of these disorders. The abuse of
controlled substances among chronic pain patients is common, and is a significant
epidemiological problem that exacerbates the impact of chronic pain and psychological
conditions, and thus imposes further burdens, if not impediments, upon practical pain
management.9-11
By definition, chronic pain is both a physiologic and psychological event, and we have
posited that chronic pain and particular Axis I psychological disorders (e.g., depression,
anxiety, somatization and substance abuse) have common underlying substrates.12 But such
substrates are not invariably expressed; we believe that this correlation of chronic pain,
emotional reactivity, and substance abuse demonstrate the interplay of genetic,
phenotypic, and environmental-situational factors occurring as a spectrum disorder.12-15
On the biological level, several genetic (e.g., serotonin transporter gene) molecular
(e.g., variants of the serotonin transporter, 5-HTT(LPR)); neuropharmacologic (e.g.,
serotonin, norepinephrine, dopamine, glutamate, opiate); and neuroanatomical systems
(e.g., orbital cortex, cingulate, and central and medial divisions of the amygdala) are
common to these disorders.16-18 We have raised the possibility that in pain
spectrum disorders, the neural and/or glial function, and/or (micro/macro) anatomy of
brain networks mediating noxious sensation and perception(s)—as well as those
involved in cognitive and emotive dimensions of reinforcement and/or reward—in some
way become disrupted or dysfunctional. Genetic variation(s) could predispose the
expression of phenotypes for neural and/or glial function to alter the network properties
and activity pattern(s) within brain systems to elicit the differential presentation of
various features along a pathologic continuum (i.e.- a spectrum of chronic pain,
depression, somatization and/or substance abuse).19 The affective components of
chronic pain are similar (if not identical) to those of mood disorder with somatic
features.20 We have posited that “…particular individuals have a
pre-disposition to…neural sensitization within these pathways, as a consequence of
over-reactivity to insult and trauma, inflammation, or aberrant response to environmental
input(s)… [this] might induce pathologic patterns of sensory (hyper)reactivity,
altered cognitive processing and emotional responses, and loss of impulse control. In this
way, persistent pain, psychopathology, and substance abuse may be correlated and reflect
related mechanistic processes…”.21 In this way, psychopathology
(including substance abuse) can be seen as an aberrant responsiveness of the peripheral
and central nervous system. Koob and LeMoal claim that this could establish
“…addiction [as] a type of chronic pain syndrome characterized by emotional
pain, dyshporia…and interpersonal difficulties… [for which certain] …drugs
can be…self-medication.”22
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— June 2008
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