Stimulant-Related Disorders

Learning Objectives

  • Identify stimulants and describe how they affect the brain and body
  • Describe the diagnostic features and development of stimulant use disorder, stimulant intoxication, and stimulant withdrawal

Stimulants are drugs that tend to increase overall levels of neural activity. Many of these drugs act as agonists of the dopamine neurotransmitter system. Dopamine activity is often associated with reward and craving; therefore, drugs that affect dopamine neurotransmission often have abuse liability. Drugs in this category include cocaine, amphetamines (including methamphetamine), cathinones (i.e., bath salts), MDMA (ecstasy), nicotine, and caffeine.

The use of stimulants in humans causes rapid weight loss; cardiovascular effects such as an increase in heart rate, respirations, and blood pressure; emotional or mental side effects such as paranoia, anxiety, and aggression; and a change in the survival pathway known as the reward/reinforcement pathway in our brain. An increase in energy, a reduced appetite, increased alertness and a boost in confidence are all additional side effects of stimulant use when introduced to the body.

Cocaine can be taken in multiple ways. While many users snort cocaine, intravenous injection and ingestion are also common. The freebase version of cocaine, known as crack, is a potent, smokable version of the drug. Like many other stimulants, cocaine agonizes the dopamine neurotransmitter system by blocking the reuptake of dopamine in the neuronal synapse. Cocaine’s most dangerous side effects include the following:
  • increased body temperature (high fever)
  • irregular heart rate or rapid heart rate
  • high Blood Pressure
  • increased risk of heart attack
  • strokes
  • sudden death from cardiac arrest
  • sudden aggression
  • sudden extreme paranoia
  • feeling, seeing, or hearing things that are not really there (hallucinations), including feeling like there are insects under the skin (this is called formication or coke bugs)

Dig Deeper: Crack Cocaine

Crack (Figure 1) is often considered to be more addictive than cocaine itself because it is smokable and reaches the brain very quickly. Crack is often less expensive than other forms of cocaine; therefore, it tends to be a more accessible drug for individuals from impoverished segments of society. During the 1980s, many drug laws were rewritten to punish crack users more severely than cocaine users. This led to discriminatory sentencing with low-income, inner-city populations receiving the harshest punishments. The wisdom of these laws has recently been called into question, especially given research that suggests crack may not be more addictive than other forms of cocaine, as previously thought (Haasen & Krausz, 2001; Reinerman, 2007).

A photograph shows crack rocks. A ruler indicates that each crack rock is approximately 1–2 inches wide.

Figure 1. Crack rocks like these are smoked to achieve a high. Compared with other routes of administration, smoking a drug allows it to enter the brain more rapidly, which can often enhance the user’s experience. (credit: modification of work by U.S. Department of Justice)

Amphetamines have a mechanism of action quite similar to cocaine in that they block the reuptake of dopamine in addition to stimulating its release (Figure 2). While amphetamines are often abused, they are also commonly prescribed to children diagnosed with attention deficit hyperactivity disorder (ADHD). It may seem counterintuitive that stimulant medications are prescribed to treat a disorder that involves hyperactivity, but the therapeutic effect comes from increases in neurotransmitter activity within certain areas of the brain associated with impulse control.

An illustration of a presynaptic cell and a postsynaptic cell shows these cells’ interactions with cocaine and dopamine molecules. The presynaptic cell contains two cylinder-shaped channels, one on each side near where it faces the postsynaptic cell. The postsynaptic cell contains several receptors, side-by-side across the area that faces the presynaptic cell. In the space between the two cells, there are both cocaine and dopamine molecules. One of the cocaine molecules attaches to one of the presynaptic cell’s channels. This cocaine molecule is labeled “bound cocaine.” An X-shape is shown over the top of the bound cocaine and the channel to indicate that the cocaine does not enter the presynaptic cell. A dopamine molecule is shown inside of the presynaptic cell’s other channel. Arrows connect this dopamine molecule to several others inside of the presynaptic cell. More arrows connect to more dopamine molecules, tracing their paths from the channel into the presynaptic cell, and out into the space between the presynaptic cell and the postsynaptic cell. Arrows extend from two of the dopamine molecules in this in-between space to the postsynaptic cell’s receptors. Only the dopamine molecules are shown binding to the postsynaptic cell’s receptors.

Figure 2. As one of their mechanisms of action, cocaine and amphetamines block the reuptake of dopamine from the synapse into the presynaptic cell.

In recent years, methamphetamine (meth) use has become increasingly widespread. Methamphetamine is a type of amphetamine that can be made from ingredients that are readily available (e.g., medications containing pseudoephedrine, a compound found in many over-the-counter cold and flu remedies). Despite recent changes in laws designed to make obtaining pseudoephedrine more difficult, methamphetamine continues to be an easily accessible and relatively inexpensive drug option (Shukla, Crump, & Chrisco, 2012).

The cocaine, amphetamine, cathinones, and MDMA users seek a euphoric high, feelings of intense elation and pleasure, especially in those users who take the drug via intravenous injection or smoking. Repeated use of these stimulants can have significant adverse consequences. Users can experience physical symptoms that include nausea, elevated blood pressure, and increased heart rate. In addition, these drugs can cause feelings of anxiety, hallucinations, and paranoia (Fiorentini et al., 2011). Normal brain functioning is altered after repeated use of these drugs. For example, repeated use can lead to overall depletion among the monoamine neurotransmitters (dopamine, norepinephrine, and serotonin). People may engage in compulsive use of these stimulant substances in part to try to re-establish normal levels of these neurotransmitters (Jayanthi & Ramamoorthy, 2005; Rothman, Blough, & Baumann, 2007).

Caffeine is another stimulant drug. While it is probably the most commonly used drug in the world, the potency of this particular drug pales in comparison to the other stimulant drugs described in this section. Generally, people use caffeine to maintain increased levels of alertness and arousal. Caffeine is found in many common medicines (such as weight loss drugs), beverages, foods, and even cosmetics (Herman & Herman, 2013). While caffeine may have some indirect effects on dopamine neurotransmission, its primary mechanism of action involves antagonizing adenosine activity (Porkka-Heiskanen, 2011).

While caffeine is generally considered a relatively safe drug, high blood levels of caffeine can result in insomnia, agitation, muscle twitching, nausea, irregular heartbeat, and even death (Reissig, Strain, & Griffiths, 2009; Wolt, Ganetsky, & Babu, 2012). In 2012, Kromann and Nielson reported on a case study of a 40-year-old woman who suffered significant ill effects from her use of caffeine. The woman used caffeine in the past to boost her mood and to provide energy, but over the course of several years, she increased her caffeine consumption to the point that she was consuming three liters of soda each day. Although she had been taking a prescription antidepressant, her symptoms of depression continued to worsen and she began to suffer physically, displaying significant warning signs of cardiovascular disease and diabetes. Upon admission to an outpatient clinic for treatment of mood disorders, she met all the diagnostic criteria for substance dependence and was advised to dramatically limit her caffeine intake. Once she was able to limit her use to less than 12 ounces of soda a day, both her mental and physical health gradually improved. Despite the prevalence of caffeine use and the large number of people who confess to suffering from caffeine addiction, this was the first published description of soda dependence appearing in scientific literature.

Nicotine is highly addictive, and the use of tobacco products is associated with increased risks of heart disease, stroke, and a variety of cancers. Nicotine exerts its effects through its interaction with acetylcholine receptors. Acetylcholine functions as a neurotransmitter in motor neurons. In the central nervous system, it plays a role in arousal and reward mechanisms. Nicotine is most commonly used in the form of tobacco products like cigarettes or chewing tobacco; therefore, there is a tremendous interest in developing effective smoking cessation techniques. To date, people have used a variety of nicotine replacement therapies in addition to various psychotherapeutic options in an attempt to discontinue their use of tobacco products. In general, smoking cessation programs may be effective in the short term, but it is unclear whether these effects persist (Cropley, Theadom, Pravettoni, & Webb, 2008; Levitt, Shaw, Wong, & Kaczorowski, 2007; Smedslund, Fisher, Boles, & Lichtenstein, 2004).

Link to Learning

To learn more about some of the most commonly abused prescription and street drugs, check out the Commonly Abused Drugs Chart from the National Institute on Drug Abuse and the Commonly Abused Prescription Drugs Chart .

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Stimulant-Related Disorders

Stimulant use disorder is a type of substance use disorder that involves the abuse of stimulants. Stimulants are the most widely used drugs in the world today; approximately 200 million Americans have used some type of stimulant in the past year alone. Caffeine and nicotine are the most popular stimulants used today, with roughly 400 million cups of coffee consumed daily and 36.5 million current cigarette smokers, according to a 2015 study conducted by the Centers for Disease Control and Prevention.

Stimulant disorders described in the DSM-5 include cocaine use disorder, amphetamine-use disorder, and tobacco-use disorder. While not listed as its own disorder, certain isolated conditions related to caffeine are recognized in the DSM-5’s “substance-related” section: caffeine intoxication, caffeine withdrawal, and other caffeine-induced disorders.

Diagnostic Criteria

A stimulant use disorder is diagnosed as a pattern of amphetamine-type substance, cocaine, or other stimulant use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

  1. The stimulant is often taken in larger amounts or over a longer period than was intended.
  2. There is a persistent desire or unsuccessful efforts to cut down or control stimulant use.
  3. A great deal of time is spent in activities necessary to obtain the stimulant, use the stimulant, or recover from its effects.
  4. The craving, or a strong desire or urge to use the stimulant is present.
  5. Recurrent stimulant use results in a failure to fulfill major role obligations at work, school, or home.
  6. Stimulant use is continued despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the stimulant.
  7. Important social, occupational, or recreational activities are given up or reduced because of stimulant use.
  8. Stimulant use is recurrent in situations in which it is physically hazardous.
  9. Stimulant use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the stimulant.
  10. Tolerance is present, as defined by either of the following:
    • a. a need for markedly increased amounts of the stimulant to achieve intoxication or desired effect
    • b. a markedly diminished effect with continued use of the same amount of the stimulant
    • Note: This criterion is not considered to be met for those taking stimulant medications solely under appropriate medical supervision, such as medications for attention-deficit/hyperactivity disorder or narcolepsy.
  11. Withdrawal is manifested by either of the following:
    • a. the characteristic withdrawal syndrome for the stimulant
    • b. stimulant (or a closely related substance) used to relieve or avoid withdrawal symptoms
    • Note: This criterion is not considered to be met for those taking stimulant medications solely under appropriate medical supervision, such as medications for attention-deficit/hyperactivity disorder or narcolepsy.

If a substance is used over a long period of time and the user becomes dependent upon it, a substance abuse issue begins to appear. Substance abuse may lead to substance dependence and with time, addiction. Both mental and physiological dependence requires the development of tolerance leading to withdrawal symptoms.

Stimulant intoxication is marked by clinically significant problematic behavioral or psychological changes (e.g., euphoria or affective blunting; changes in sociability; hypervigilance; interpersonal sensitivity; anxiety, tension, or anger; stereotyped behaviors; or impaired judgement) that developed during, or shortly after, use of a stimulant. Cocaine intoxication refers to the deleterious effects of cocaine on the body. These effects can develop over time with regular use or can be the result of acute intoxication due to a single intake of the substance.

Stimulant withdrawal is marked by the following diagnostic criteria:

A. The cessation of (or reduction in) prolonged amphetamine-type substance, cocaine, or other stimulant use occurs.
B. Dysphoric mood and two (or more) of the following physiological changes develop within a few hours to several days after Criterion A:

  • Fatigue.
  • Vivid, unpleasant dreams.
  • Insomnia or hypersomnia.
  • Increased appetite.
  • Psychomotor retardation or agitation.

C. The signs or symptoms in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication or withdrawal from another substance.

Note: Amphetamine, cocaine, or other stimulant withdrawal can only occur in the presence of a moderate or severe amphetamine, cocaine, or other stimulant use disorder. For example, cocaine withdrawal happens when a person who uses a lot of cocaine stops using cocaine. It can also happen when a person who uses a lot of cocaine starts using less cocaine than they did before. When a person who is used to using cocaine stops right away, they will go through what is called a “crash” along with many of other cocaine withdrawal symptoms, like

  • paranoia
  • depression
  • exhaustion (feeling very tired)
  • anxiety
  • itching
  • mood swings (quick changes in emotions
  • irritability (feeling easily annoyed)
  • fatigue (feeling tired), sleeping many hours
  • insomnia (trouble sleeping)
  • a very strong craving for more cocaine
  • nausea and vomiting

Withdrawal symptoms can last for days, weeks, months, and on rare occasions, years, depending on the frequency and dosages used by the individual. Unless intensive medical and psychological treatment is sought after, there is a very high likelihood of relapse among the user.

Tobacco-Related Disorders

A carton of cigarettes.

Figure 3. First-time nicotine users develop a dependence about 32% of the time.

Tobacco use disorder, as described in the DSM-5, is a problematic pattern of tobacco use leading to clinically significant impairment or distress, as manifested by at least two of the 11 symptoms listed in the diagnostic criteria above.

Nicotine dependence is a state of dependence upon nicotine. Nicotine dependence is a chronic, relapsing disease defined as a compulsive craving to use the drug, despite harmful social consequences. Tolerance is another component of drug dependence. Nicotine dependence develops over time as a person continues to use nicotine. Nicotine dependence is a serious public health concern due to it being one of the leading causes of avoidable deaths worldwide.

First-time nicotine users develop a dependence about 32% of the time. There are approximately 976 million smokers in the world. There is an increased frequency of nicotine dependence in people with anxiety disorders. Nicotine is a parasympathomimetic stimulant that attaches to nicotinic acetylcholine receptors in the brain. Neuroplasticity within the brain’s reward system occurs as a result of long-term nicotine use, leading to nicotine dependence. There are genetic risk factors for developing dependence. For instance, genetic markers for a specific type of nicotinic receptor (the α5-α3-β4 nicotine receptors) have been linked to increased risk for dependence. Evidence-based medicine can double or triple a smoker’s chances of quitting successfully.

Caffeine-Related Disorders

Consumption of one to one-and-a-half grams (1,000–1,500 mg) per day is associated with a condition known as caffeinism. Caffeinism usually combines caffeine dependency with a wide range of unpleasant symptoms including nervousness, irritability, restlessness, insomnia, headaches, and palpitations after caffeine use.

Caffeine overdose can result in a state of central nervous system over-stimulation known as caffeine intoxication, a clinically significant temporary condition that develops during, or shortly after, the consumption of caffeine. This syndrome typically occurs only after ingestion of large amounts of caffeine, well over the amounts found in typical caffeinated beverages and caffeine tablets (e.g., more than 400–500 mg at a time).

Caffeine intoxication may be diagnosed if five (or more) of the following symptoms develop after recent consumption of caffeine: restlessness, nervousness, excitement, insomnia, flushed face, diuresis (increased production of urine), gastrointestinal disturbance, muscle twitching, rambling flow of thought and speech, tachycardia (increased heart rate) or cardiac arrhythmia, periods of inexhaustibility, and psychomotor agitation.

Treatment for Stimulant Use Disorders

Treatments for stimulant use disorders first involve addressing any emergency issues, such as treating cocaine-associated high body temperature with a benzodiazepine and physical cooling.

Twelve-step programs like Cocaine Anonymous (modeled on Alcoholics Anonymous and Narcotics Anonymous) have been widely used to help people addicted to cocaine, though some other psychotherapies have proven more helpful. Common therapies include motivational interviewing, contingency management, a community reinforcement approach, and cognitive behavioral therapy. Medications that have been studied to treat cocaine withdrawal include acetylcysteine, baclofen, bupropian, vanoxerine, and vigabatrin. Since there is no antidote nor reversal agent for caffeine intoxication, treatment of mild caffeine intoxication is directed toward symptom relief; severe intoxication may require peritoneal dialysis, hemodialysis, or hemofiltration.

Motivational interviewing (MI) is a treatment approach that helps individuals overcome ambivalent feelings and insecurities. In the process, individuals become motivated to change their behavior and reduce or stop their stimulant use. Five underlying principles guide how providers should interact with clients while using this practice:

  • Express empathy through reflective listening.
  • Identify discrepancies between a client’s goals or values and their current behavior.
  • Avoid arguments and direct confrontations with a client.
  • Adjust to a client’s resistance rather than opposing it directly.
  • Support self-efficacy and optimism.

Studies indicate that use of MI for people with stimulant use disorders was associated with reductions in the number of days of stimulant use and the amount of stimulant used per day.

Contingency management (CM) is a type of behavioral therapy grounded in the principles of operant conditioning. Operant conditioning is a method of learning in which desired behaviors are reinforced with prizes, privileges, or cash. For treatment of stimulant use disorders, incentivized behaviors might include attendance at treatment sessions, adherence to prescribed medications for other health conditions, or provision of stimulant-negative urine specimens.

In a clinical setting, reinforcement is often provided in the form of vouchers that can be exchanged for retail goods and services. It may also include access to certain privileges, the opportunity to win a prize, or even direct cash payments. While contingency management (CM) may be structured in several different ways, two widely used approaches include

  • the Fishbowl Method (popularized by Dr. Nancy Petry) where clients who have earned an incentive draw a token from a “fishbowl” for a chance to win a prize of varying value.
  • voucher-based reinforcement therapy (popularized by Dr. Stephen Higgins) where clients earn vouchers for completion of desired behaviors with the level of vouchers increasing according to an escalating schedule of reinforcement.

Studies included in this evidence review demonstrated that the use of contingency management (CM) for people with stimulant use disorders was associated with reductions in the number of days of stimulant use, stimulant cravings, new stimulant use, and HIV-risk behaviors.

One behavioral therapy approach that is commonly used in combination with CM is the community reinforcement approach (CRA). This treatment was originally developed by Nathan Azrin and his colleagues for alcohol use disorder, and was later adapted for stimulant use disorder, particularly cocaine use. The goal of community reinforcement approach (CRA) is to identify behaviors reinforcing stimulant use and make a substance-free lifestyle more rewarding than one that includes drugs and alcohol. Community reinforcement approach (CRA) includes multiple elements such as analyzing clients’ substance use, relationship counseling, vocational guidance, and job skills training. CRA therapy also focuses on building social and drug refusal skills. Ultimately, clients are encouraged to make substantial behavioral changes, engage in new recreational activities, and develop new social networks. When used in combination with CM, clients who demonstrate positive behaviors such as drug abstinence, are typically provided material incentives to encourage skills development to build a rewarding substance-free life.

Cognitive behavioral therapy (CBT) is a short-term, goal-oriented psychotherapy treatment that enables individuals to understand their current problems, challenges, and experiences in order to change their behaviors and patterns of thinking. CBT helps clients develop accurate assessments of circumstances and their feelings so they can develop realistic strategies. CBT is used also to address depressive cognitions and other cognitive distortions associated with depression, generalized anxiety disorders, and substance use disorders. Through CBT, people with stimulant use disorders are trained to evaluate faulty patterns of thinking, actions, and negative feelings associated with their drug use. CBT is tailored to the needs of the individual, with the goals of each therapy session uniquely based on the client’s experiences with stimulant use and personal circumstances.

Key Takeaways: Stimulant Use Disorder

[1]

[2]

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Glossary

euphoric high: feelings of intense elation and pleasure from drug use

methamphetamine: type of amphetamine that can be made from pseudoephedrine, an over-the-counter drug; widely manufactured and abused

stimulant: drug that tends to increase overall levels of neural activity; includes caffeine, nicotine, amphetamines, and cocaine

stimulant intoxication: clinically significant problematic behavioral or psychological changes that develop during, or shortly after, the use of a stimulant

stimulant withdrawal: marked by significant behavioral and psychological changes following the cessation of (or reduction in) prolonged amphetamine-type substance, cocaine, or other stimulant use

stimulant use disorder: a type of substance use disorder that involves the abuse of stimulants

  1. Compton, W. M., Han, B., Blanco, C., Johnson, K., & Jones, C. M. (2018). Prevalence and Correlates of Prescription Stimulant Use, Misuse, Use Disorders, and Motivations for Misuse Among Adults in the United States. The American journal of psychiatry, 175(8), 741–755. https://doi.org/10.1176/appi.ajp.2018.17091048 ↵
  2. Center for Substance Abuse Treatment. Treatment for Stimulant Use Disorders. Rockville (MD): Substance Abuse and Mental Health Services Administration (US); 1999. (Treatment Improvement Protocol (TIP) Series, No. 33.) Chapter 5—Medical Aspects of Stimulant Use Disorders. Available from: https://www.ncbi.nlm.nih.gov/books/NBK64323/ ↵