Fig. 4.1
First, we have a population of individuals none of whom have been exposed to opioid use. Within that population are those who do not have addictive disease involving opioids; these individuals will not demonstrate signs and symptoms of addiction whether exposed to opioids or not. A smaller group within the population, shown in red and blue, has addictive disease. Those shown in blue do not know they have addictive disease simply because they have never been exposed to opioids. Phenotypically, then, they do not have addiction despite the underlying physiology. The group of individuals depicted in red, however, will show signs of addiction, resulting from medical or nonmedical use of opioids
The two populations can be subdivided differently. Users of any substance, for medical or nonmedical reasons, do so with a range of frequency and quantity (addicted people have a further non-correlated range of disease severity). People with addictive disease might actually use less of the substance less frequently than those without addictive disease, particularly when those without addiction use the substance because they have been prescribed it. It is equally critical to realize that patients with addictive disease and with pain might use opioids precisely as prescribed with close monitoring and that in such cases the signs and symptoms of addiction may be absent despite the development of physiologic dependence.
Clinical evaluation and treatment are complicated when pain and addiction coexist. When addiction is present without the added component of pain, the focus is not on dissecting what a patient means by terms such as “occasional” or “experimental” use but on why the patient has used at all. When pain is added to the equation, that signal is valueless, because the patient has been prescribed the substance and is expected to use it. Furthermore, because denial is inherent to addictive illness, one always questions subjectively provided information when a patient is being treated for addiction but not pain. When pain is added, detective work is needed to determine whether the patient has taken the amount prescribed; whether he has doctor shopped to gain access to additional medication; whether he is taking the opioid only to avoid withdrawal; whether objective data exist to support the subjective report of pain; and many other factors.
Background
A subset of patients who are prescribed opioids for pain will eventually use their medication in ways not intended by their prescribing clinicians. Addiction is one reason why. Addiction prevalence among opioid-treated pain patients has been reported between 2 and 5 % [1, 2]; however, the prevalence of problematic opioid use is far higher. A prospective cohort study showed that 62 of 196 (32 %) patients enrolled in a chronic pain disease management program had at least one episode of opioid misuse after 1 year [3].
Patients who engage in multiple, repeated, or egregious aberrant drug-related behaviors are in danger of self-harm and are nearly certain to realize poor outcomes from pain therapy. Many problematic drug-related behaviors can be handled by screening opioid candidates, stratifying patients by risk category, monitoring them closely, and treating them for comorbid depression, anxiety, and other mental conditions. Patients with strong risk factors for problematic opioid use, such as a family history of addiction or a personal history of addictive disease, present a special challenge because the potential for triggering or reactivating a substance-use disorder is real. Another reality is the frequent overlap of pain and addiction. In a study of patients receiving methadone for chemical dependency, 37 % experienced chronic, severe pain [4]. In a separate study, an association between chronic pain and self-reported prescription drug abuse was confirmed in veterans referred for a behavioral health evaluation [5]. Given the subjective nature of pain, these studies suggest the possibility that those with addictive disease are either more aware of painful stimuli or more susceptible to a subjective experience of pain than those without addictive illness when exposed to identical stimuli. This is consistent with Hennecke’s findings with respect to stimulus augmentation in children of alcoholic fathers [6].
Failure to treat pain is poor medical practice as is failure to treat addiction, including opioid use disorders. Physicians, however, often receive little medical training on addiction or clinical pain treatment [7]. The treatment plan for chronic nonmalignant pain may include opioids, even for patients with substance-abuse histories or strong risk factors, if accompanied by careful screening, medication selection, and monitoring. However, some patients cannot be managed with opioid therapy, because their nonadherence or lack of analgesic response renders opioid therapy more harmful than helpful. In such cases, compassionate discontinuation of opioids can improve outcomes. The key is to personalize the treatment plan and to adjust when needed.
Scientific Foundation of Addiction
Definitions
The field of addictive disease suffers from a plethora of terminology, much of which has been defined and redefined over the years by different groups of specialists. Use, abuse, misuse, heavy use, dependence, and addiction: these terms are all in general use. Dependence carries a specific meaning to the pain physician as it refers to a physiologic neuroadaptation of the central nervous system to the effects of a given substance, in which an individual will experience objective physiologic symptoms of withdrawal should the substance use be terminated without tapering. Dependence has a different meaning to the reader of DSM-IV-TR where it refers to the medical disorder in which an individual repetitively uses an addictive substance despite that person’s best interest. This latter definition is more widely applied to the class of disease known as addiction, with the acknowledgment that consensus among experts regarding terminology is not complete. Table 4.1 contains suggested definitions to clarify opioid use and misuse [8, 9].
Misuse | Use of a medication for a medical purpose other than as directed or as indicated, whether willful or unintentional and whether harm results or not |
Abuse | Any use of an illegal drug; the intentional self-administration of a medication for a nonmedical purpose such as altering one’s state of consciousness (e.g., getting high) |
Addiction | A primary, chronic neurobiologic disease influenced by genetic, psychosocial, and environmental factors. It is characterized by impaired control over drug use, compulsive use, continued use despite harm, and craving |
Tolerance | A physiologic state resulting from the regular use of an opioid where increased doses are needed to maintain the same effects. In analgesic tolerance, increased opioid doses are needed to maintain pain relief |
Physical dependence | A physiologic state characterized by abstinence syndrome (withdrawal) if an opioid is stopped or decreased abruptly or if an opioid antagonist is administered. It is an expected result of opioid therapy and does not, by itself, equal addiction |
The critical point is that, whatever terminology you choose, addictive disease is an illness or class of illnesses of the brain in which one marker is that of repetitive substance use; this approach simplifies the concept of pre-addiction, in which an individual is predisposed to the development of observable symptoms but has not yet developed them as a result of not having been exposed to the drug.
Neurobiology of Addiction
As addiction develops, changes occur within neuroanatomic structures, communication pathways, and neurochemical processes of the nervous system. Drugs of abuse impact the mesolimbic dopaminergic system, the region of the brain linked to basic emotions, by activating the ventral tegmental area and releasing dopamine into the nucleus accumbens, amygdala, prefrontal cortex, and ventral palladium [10]. Dopamine has been called the master molecule of addiction, but glutamate and gamma-amino butyric acid (GABA) also play key roles [10]. Opioids and other drugs decrease GABA activity in the ventral tegmental area, causing an increase in glutamate release in the nucleus accumbens which increases dopamine release. The release of dopamine in the nucleus accumbens appears to reinforce memories of pleasant drug experiences, boosting craving.
The amygdala mediates anxiety and other strong emotions. Not only does it help to regulate craving and relapse in addicted people, but amygdala stimulation may partially explain why certain chronic pain patients overuse opioids or anxiolytics, looking for relief from the stress and fear associated with chronic pain.
The activation of the reward pathway from the ventral tegmental area to the nucleus accumbens is crucial to the formation of addiction but is not in itself sufficient to cause addiction. Changes, which are both structural and functional, create in the vulnerable individual a behavioral compulsion to use drugs. With repeated use, the brain experiences neuroadaptive changes that can include tolerance, necessitating larger quantities of the substance to achieve the desired effects, and sensitization or heightened reward. Chronic drug abuse results in neuroplastic learning and altered brain systems with results that are observable in behavior. The brain becomes unable to distinguish between stimuli to engage in behaviors related to survival, such as eating, and the reward incentive delivered by addictive drugs. The result is a compromised reward system, and the changes are long term.
Observing the addicted brain is easier than understanding how it got that way, and the reason why some people become addicted while others do not must remain the subject of ongoing inquiry. Genetic and environmental vulnerabilities exist for the individual, who, in order to trigger the underlying neurobiologic mechanisms that lead to addiction, must be exposed to a drug of abuse. According to the National Institute on Drug Abuse, changes in frontal activity that accompany loss of control and compulsive drug intake are observable in addicted people during brain imaging studies [11]. What is still unclear is whether the changes preceded or followed drug use. Young people, whose central nervous systems are still developing, appear to be at particular risk for sustaining changes to the prefrontal cortex that could lead to compulsive drug behaviors when drug use is initiated early [12]. A study conducted by researchers at Rockefeller University in New York City found that adolescent mice allowed to self-administer oxycodone took less of the drug than adult mice did; however, when reexposed as adults, they exhibited increased striatal dopamine levels at the lowest dose [13]. Neither effect was found in the adult mice studied, and investigators concluded that both effects suggest greater sensitivity to oxycodone’s effects in younger mice [13].
Disorders such as posttraumatic stress disorder, depression, and anxiety disorders also frequently coincide with substance abuse [12]. Whether psychiatric disorders confer vulnerability to addiction or vice versa – or whether both proceed from a common genetic vulnerability – is a question still to be answered.
Clinical Practice
Screening Opioid-Treated Patients for Risk of Abuse or Addiction
The universal precautions of opioid prescribing include initial screening and ongoing assessment for the presence of substance-use disorders [14]. High-risk patients, those likely to fit in the right-hand circle of Fig. 4.1, generally display risk factors such as personal or family history of substance abuse [2, 5], younger age [2, 5], history of preadolescent sexual abuse [2], mental disease [2, 5], social patterns of drug use [15], psychological stress [15], lack of a 12-step program [16], polysubstance abuse [16], poor social support [16], cigarette dependency [5, 17], and repeated drug or alcohol rehabilitations [17]. Conversely, low-risk patients, those likely to fit in the left-hand circle of Fig. 4.1, are those with fewer risk factors. Perhaps, they have completed a regimen of opioids in the past without difficulty or evidence of addiction.
Several tools are available to screen for the risk of opioid abuse. Opioid guidelines jointly released by the American Pain Society (APS) and the American Academy of Pain Medicine (AAPM) [18] endorse the Opioid Risk Tool (ORT) [2], the Screener and Opioid Assessment for Patients with Pain (SOAPP) [19], and the Diagnosis, Intractability, Risk, Efficacy (DIRE) [20]. Unlike the ORT and the SOAPP, which guide risk stratification, the DIRE purports to identify who would not be a suitable candidate. Other opioid-specific tools include the Screening Instrument for Substance Abuse Potential (SISAP) [21] and the Pain Medication Questionnaire (PMQ) [22].
A comparison study of the SOAPP, the ORT, and the DIRE found the SOAPP to be the most sensitive, followed by the ORT and then the DIRE [23]. Little data exist to differentiate the validity of self-administered vs. clinician-administered tools, although face-to-face interviews may give the clinician opportunity to gauge the patient’s reactions and facial cues. However, self-administered tools are more practical for most clinical environments, and the choice is likely to be influenced by the time available.
The possibility of deception always exists when a patient is asked to share sensitive information. It is important to build trust and rapport during the assessment process to encourage honesty. The validity of the information provided is enhanced when [10]:
Confidentiality is observed.
Patients fear no negative consequences from disclosing information.
The information disclosed has a likelihood of subsequent verification.
The clinician is nonjudgmental and matter of fact.
The clinician treats substance-use questions as an important, routine component of the medical history, no different than data on diet, exercise, and smoking.
Management of High-Risk, Opioid-Treated Patients
Screening can help clinicians to stratify and monitor patients by risk level – usually high, moderate, or low risk. There is a triage associated with chronic pain treatment [14]. The highest-risk patients who also experience moderate-to-severe chronic pain should be treated only by physicians trained to care for this complex population. In moderate-to-high-risk patients, care may be coordinated with appropriate specialists in addiction, pain, and mental health. Low-risk patients typically may be treated by primary care physicians.
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