PS375 Unit 2 Neurobiology of Addiction Paper Example

Three Stages and a Pill From a Friend: A PS375 Unit 2 Neurobiology Paper

[Student Name]

Purdue University Global

PS375: Psychology of Addiction

Unit 2 Neurobiology Paper

[Instructor Name]

[Date]

The writer, the program, the client and every detail are composite and illustrative; the articles cited are real.

Kayla's Path

Kayla came to our Tulsa outpatient program in October, referred by the emergency department after a nonfatal overdose. She is twenty-six and has a four-year-old son. Three years ago, after a car accident broke her pelvis, her surgeon sent her home with oxycodone. Once the refills ran out, her pain had improved but she felt anxious and sick without the pills. A friend sold her some, and later sold her counterfeit pills that, she learned after the overdose, contained fentanyl. She told me during intake, "I don't even like how they make me feel anymore. I just can't not take them."

Her last sentence describes something the brain research helps explain. As her intake coordinator, I am not a clinician, but understanding the neurobiology helps me explain to clients and families why addiction is so hard to stop, without excusing or blaming.

The Three-Stage Model

In the account by Koob and Volkow (2016), addiction cycles through three stages, and each stage draws on its own set of brain circuits.

The first is binge and intoxication. Drugs of abuse increase dopamine signaling in the basal ganglia, part of the brain's reward system. With repeated use, cues linked to the drug, such as a place, a person or a feeling, come to trigger dopamine release themselves, giving them strong motivational pull. Kayla's early use, when the pills relieved pain and brought calm, fits this stage.

The second is withdrawal and negative affect. With repeated use, the extended amygdala, a region involved in stress, becomes more active when the drug wears off, while reward circuits become less responsive to ordinary pleasures. The result is anxiety, irritability and low mood during withdrawal. The reason for using moves from chasing a good feeling to getting away from a bad one. Kayla's description of feeling sick and anxious without the pills, and of no longer enjoying them, matches this stage.

The third is preoccupation and anticipation. The prefrontal cortex, which supports planning, decision making and inhibiting impulses, functions less well, making it harder to resist cravings and stick to decisions. Kayla's "I just can't not take them" describes a weakened capacity to act on her own intentions.

She had stopped taking the pills for pleasure; she was taking them to stop feeling sick.

Cues in an Ordinary Day

The first stage also explains something Kayla described that puzzled her. She said cravings hit hardest when she drove past the gas station where she used to meet her friend, and on Friday afternoons, when she had usually bought pills for the weekend. Neither the gas station nor Friday has anything to do with opioids, yet both now trigger strong urges. In Koob and Volkow's account, repeated pairing of such cues with the drug gives them motivational power of their own, so that they can start craving before a person has consciously decided anything. Knowing this helped Kayla plan a different route to her son's daycare and arrange to spend Friday afternoons at her mother's house during the first weeks of treatment.

Fear of Withdrawal

The second stage helps explain why Kayla had delayed treatment for a year. She was afraid of withdrawal, which she had experienced once when her supply ran out: two days of sweating, aching, diarrhea and an anxiety she called "like the floor was gone." The negative state that the extended amygdala produces during withdrawal is not only unpleasant; it teaches the person that using makes it stop, which strengthens use. Her fear was reasonable, and it mattered that the program could offer medication that prevents most of that suffering. For many clients, the promise of a tolerable first week is what makes a first appointment possible at all.

What the Model Means and Does Not Mean

Volkow et al. (2016) argue that these changes help explain continued use in the face of serious consequences, and the frequency of relapse even after months or years without using. They also emphasize that brain function can recover, at least partly, with sustained abstinence and treatment, though recovery may take months or longer. They note that adolescents are especially vulnerable, because the prefrontal cortex is still developing.

The model does not mean that Kayla has no choice or responsibility. It means that the choices are harder than they look from outside, and that treatment needs to address the brain changes as well as behavior. For opioid use disorder, that often means medication, which the program discusses with clients like Kayla at the first appointment.

Explaining It to Kayla and Her Mother

Kayla's mother came to the second appointment and asked, "Why can't she just stop for her son?" I used McLellan et al. (2000), who compared drug dependence with chronic illnesses such as diabetes, hypertension and asthma. They found that rates of relapse and of adherence to treatment were similar across these conditions, and argued that addiction should be treated as a chronic illness requiring ongoing care rather than a single episode of treatment. Kayla's mother said that framing helped her see relapse as a reason to keep treating, not a reason to give up.

Limits of the Neurobiological View

The three-stage model is a powerful explanation, but it is not the whole story. It does not explain why Kayla's friend was selling pills, why her prescription ended without a plan for tapering or pain, or why fentanyl had entered her community's drug supply. Those are social and policy factors, which a biopsychosocial view keeps in sight. Neurobiology also cannot predict which person will develop addiction after the same exposure; genetics, stress and environment all play roles.

What It Changed at Intake

Understanding the stages changed three things about how I work. I now ask clients whether they use mainly to feel good or to stop feeling bad, which often reveals the withdrawal stage. I explain cravings as a brain process that weakens with time and treatment, which some clients find hopeful. And I make sure clients with opioid use disorder hear about medication on day one.

Conclusion

Kayla's path from a prescription to counterfeit pills follows the three stages Koob and Volkow describe: binge and intoxication through the basal ganglia, withdrawal and negative affect through the extended amygdala, and preoccupation through a weakened prefrontal cortex. Volkow and colleagues show that recovery of brain function is possible, and McLellan and colleagues' comparison with chronic illness helped Kayla's family see relapse as part of a long-term condition.

References

Koob, G. F., & Volkow, N. D. (2016). Neurobiology of addiction: A neurocircuitry analysis. The Lancet Psychiatry, 3(8), 760-773. https://doi.org/10.1016/S2215-0366(16)00104-8

McLellan, A. T., Lewis, D. C., O'Brien, C. P., & Kleber, H. D. (2000). Drug dependence, a chronic medical illness: Implications for treatment, insurance, and outcomes evaluation. JAMA, 284(13), 1689-1695. https://doi.org/10.1001/jama.284.13.1689

Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). Neurobiologic advances from the brain disease model of addiction. New England Journal of Medicine, 374(4), 363-371. https://doi.org/10.1056/NEJMra1511480