As professionals working with individuals who misuse addictive substances, we sometimes are asked to evaluate someone who suffers from both a potential substance misuse problem and a chronic pain disorder. We hope that our treatment intervention works—that the person improves, thanks us profusely, and goes on to live a healthy, happy life. Yet in the real world, this outcome is rare.
We usually prepare the client and the family for treatment trials, partially successful outcomes, and even outright treatment failure. Part of the lack of treatment success may stem from not understanding the distinction between substance misuse and expected pharmacologic response to opiate pain relievers. This article describes some of the component parts of each of these possibilities when applied to an individual with chronic pain, guiding the reader in determining if use of pain relievers is bringing about a substance abuse problem.
Making the distinction
We know that the attraction of a medication that produces analgesia and intense pleasurable feelings is self-reinforcing (i.e., the drugs produce an effect that the user wants to experience repeatedly). Clinical confusion occurs with long-term administration of opiates for pain relief when development of tolerance, withdrawal, and hyperalgesia occurs. The development of these hallmarks of substance use problems in fact mimics substance misuse syndromes but does not contain the critical symptom: loss of control.1,2 If we start from the premise that use of opiates for any significant period will result in tolerance, which is an inevitable consequence of narcotic use otherwise known as pharmacologic or physiologic dependence, then we also must accept that these responses are not always problematic. To differentiate problematic use from expected pharmacologic response, or normal tolerance, we first must understand the processes involved in the brain's neurologic reward initiation and propagation systems.
Pain modulation and opiate binding sites share the same neural structures and pathways. This shared structure system offers us the first hint of overlap between reward and pain modulation in the brain. Without digressing into a complex neuroanatomy review, it's sufficient to know that these systems stimulate or modulate (slow down) pathways that produce both euphoria and pain modulation.
In an individual with persistent pain conditions, there is an increased responsiveness of spinal cord neurons and excitation of the central nervous system (CNS), resulting in a hypersensitized state of pain perception and hyperexcitability in the spinal cord.1 In other words, if I touch your shoulder you experience it as a touch, but in someone with hypersensitive touch it may actually hurt.
Persistent irritation at the site of neuroreceptors stimulates the release of two neurotransmitters: glutamate and nitric oxide. Researchers have hypothesized that glutamate and nitric oxide contribute to long-term structural and functional CNS changes in pain transmission.3,4 Glutamate is not only an excitatory neurotransmitter, it is also very irritating and can be damaging to neurons. Hyperexcitability (along with neuronal injury due to chronic glutamate induction) results in dramatic and permanent changes in the CNS's reaction to sensory inputs. In short, this generates pain that is highly exaggerated in quality and quantity, as well as resistant to usual treatment methods,5,6 meaning that it is much harder to treat and needs more medication to quiet it down.
In moving on to the reward part of brain functioning, we need to look at the mu-opioid receptors, where opiates produce their pharmacologic effects. These receptors are located primarily in the brain's reward system.6,7 Opiates increase neuron cell firing and stimulate production of the neurotransmitter dopamine, the chemical primarily responsible for feelings of pleasure as it is released in the nucleus accumbuns.6 Dopamine, along with the neurochemical gamma-aminobutyric acid (GABA), results in that “rush of well-being which is highly rewarding, and reinforcing.”6
The brain's limbic structures, where most of this activity is occurring, are highly responsive to opiates. If we activate these pain receptors for a long period, the limbic structures system will override the analgesic effect, creating decreased tolerance to pain.8 This decreased tolerance to pain is a neuroadaptive response to the opiate. In other words, it is an adaptive response, not a maladaptive response. It looks like the individual is “hooked” on the narcotic pain reliever, when in fact he/she is not in the sense that we as addiction professionals would define as “hooked.” The individual has developed an adaptive brain override resulting from a change in the brain's actual physical ability to process pain perception and pain relievers.