Substance and Non Substance Related Addiction Disorders: Diagnosis and Treatment

Addictive disorders are diseases of the brain. Addictions like chronic illness may have remissions and relapses. These are caused by genetic, biological, psychological, social and economic factors. Reward pathways for all substance and non-substance related addictive behavior (gambling, sex and food addiction etc.) are similar and are mediated through nucleus accumbens and associated circuits. Negative preexisting emotional state or due to withdrawal from substance and self-medication to seek relief may perpetuate addictive behavior. Substance or non-substance related addictive behavior-pleasure-reinforcement-reuse paradigm perpetuates addictive behavior. Environmental cues and memories associated with addiction related activities contribute to craving and relapse. Dopamine neurotransmitter plays major role in addictive behaviors. Treatment consideration should factor in all of these biopsychosocial factors.

Urine drug screens can add accountability to a patient’s recovery plan. An upfront discussion of the role of the urine drug screen in treatment is important for a solid provider client therapeutic relationship. Substance use disorders are relapsing and remitting disorders. The goal of treatment is to extend the duration of sobriety until it is life-long, a lifestyle. The role of the urine drug screen in a treatment program should be therapeutic not penalizing. Understanding what a drug screen can and can not do in providing information is important. Using a consistent screen and appropriately certified laboratory is a must. This chapter covers the types of drug screens, the substances identified in a standard urine dug screen and provides guidance on when other substances may need to be requested during screening. Some substances such as “bath salts” are not identified in current urine drug screens. In clinical situations it will be important to confirm any positive results found on a urine drug screen. Common agents and medications that cause false positive or negative results are identified in the chapter. Proper process for obtaining and handling the urine sample including proper chain of custody are presented.

Addictive disorders are complex diseases influenced by both genetic and environmental factors. Heritability of these disorders is moderate to high. Genes that increase the risk of addiction to a substance actually increase the risk of addiction to other substances. This means it is mainly through broad externalizing pathways that genes increase the risk of addiction. The current level of our knowledge in genetics is less than enough to have clinical applications. Probably, in the near future, we will be able to provide our patients with individualized report about their susceptibility to addiction.

Dual diagnosis exists when there is a substance use disorder occurring in conjunction with another non-substance mental health diagnosis. The presence of dual diagnosis is common and poses significant challenges to health care providers, due to both the increased severity and poorer treatment outcomes compared to when there is a single condition. Substance use disorders may develop in response to a mental health condition, although this is not always the case. A key diagnostic task is to conduct a thorough assessment that considers a full range of issues. Treatment should attempt to address both aspects of a dual diagnosis in an integrated and coordinated manner. If this is not possible, treatment for both conditions should at least be concurrent. This is in contrast to past perspectives embracing a sequential approach. Treatments for dual diagnoses are effective and may include a variety of interventions including psychotherapy, pharmacotherapy, and community self-help groups. The current chapter utilizes a case example to illustrate many of the relevant issues.

Management of substance use disorders is challenging, there are no medications that directly treat the use disorders, substitution therapy in opioid use disorders and potential anti-craving medications for alcohol use disorder are the closest available. Successful management of withdrawal syndromes and craving can improve the chances of sobriety. The presence of underlying medical and psychiatric disorders can derail attempts at long term sobriety if not managed. This chapter provides information on medications commonly used in the management of withdrawal symptoms and co-morbid psychiatric disorders, such as depression and anxiety, in the dually diagnosed patient. Tables of medications from the following classes are included: benzodiazepines and other antianxiety agents, antidepressants, mood stabilizers, anticonvulsants and antipsychotic medications. Key points in the patient specific selection, dosing and monitoring of these medications and management of their side effects are identified. Insomnia can derail sobriety and needs to be addressed. Information on sleep hygiene and medications for insomnia are also presented. Information on the individualization of treatment is also discussed. It is important to note that many of the medications presented in this chapter are being used for both US FDA labeled and off-label indications.

Motivational interviewing (MI) is to motivate patients with addictive and non-addictive disorders like noncompliant patients, to help them develop skills to find intrinsic motivation for change through resolution of ambivalence . Ambivalence may lead to arguments against change referred to as sustain talk. Strategies to decrease sustain talk may promote change talk. These strategies include: straight reflection, amplified reflection, double sided reflection, emphasizing autonomy, agreeing with a twist, reframing, running head start, and coming along side. Five principles for creating condition for change are: expressing empathy, avoiding confrontation, supporting selfefficacy, rolling with resistance, and developing discrepancy between the patient’s behavior and his/her own goals and values. Key skills needed for MI include: open ended questioning, reflective listening, affirmations, periodic summarization of the content of the session, and informing and advising with permission of patient. The successful therapeutic process for MI involves: establishing rapport, setting the agenda, assessing readiness for change, sharpening the focus to what the patient truly wants to change, identifying ambivalence, eliciting self-motivating statements, handling resistance, and shifting focus of conversation to get around resistance. The stages of change model is distinct from MI but naturally fit together. MI helps patients move from one stage of change to another e.g. from pre-contemplation, contemplation, preparation, action, to maintenance.

This chapter reviews the epidemiology and pathophysiology of alcohol use disorders. No two patients with alcohol use disorders are the same and recognition of these patients in our practice is the first priority. Diagnostic indicators and the CAGE questions that can be used to assist in the identification of patients with alcohol use disorders are presented. Non-drug therapies are integral and include lifestyle changes, group therapies (alcoholics anonymous), and individual therapies (i.e., cognitive behavioral therapy). These and other non-drug treatment options are discussed in this chapter. Medication options for the management of outpatient alcohol withdrawal are discussed and include benzodiazepines and anticonvulsant agents (off-label use). Medications to assist in maintaining sobriety and reduce craving should be offered to all patients. Medications discussed in this chapter include acamprosate, naltrexone and disulfiram. The information presented includes discussion of patient specific characteristics such as renal and hepatic function and underlying psychiatric issues such as anxiety, depression and insomnia that may affect medication selection and outcome. This chapter includes key learning points and a patient vignette to assist the learner. A patient education sheet on alcohol use disorders and additional patient resources accompanies the chapter.

This chapter discusses epidemiologic, pathophysiology and diagnostic issues associated with long term none medical use of Anabolic Androgenic Steroids (AAS) .These agents are synthetic derivatives of the hormone testosterone with higher bioavailability and activity [1]. These drugs are used by athletes to gain muscle mass thereby gaining advantage. As a result many users often don’t disclose their use to their doctors [2, 3]. Medical complications may include, hypertension, cardiomyopathy and hypogonadism. Psychiatric complications may include mood and psychotic disorders [4]. Withdrawal may lead to dysphoria and irritability. Patients usually do not consider themselves as addicted. They traditionally think that they are more knowledgeable about these drugs than their doctors [2, 3]. In USA, AAS are currently schedule class III drugs requiring prescription, however they can be easily obtained online from other countries.

80% of the World’s population consumes caffeine. Its impact on mental health often goes unrecognized. Caffeine use has comorbidity with other substance use disorders. Caffeine is a methylxanthine and exerts its actions by inhibiting adenosine receptors. Caffeine is a stimulant, mild to moderate use has beneficial effects like improving attention and concentration, but problem use can mimic anxiety, sleep and mood disorders. High dose caffeine can even result in death. In this chapter, we discuss common presentations of caffeine use disorders, their recognition and management. Caffeine withdrawal can present with mood disturbance and headaches, instant alleviation of these symptoms with caffeine perpetuates its use. Caffeine withdrawal with abrupt cessation typically lasts 2-4 days. Calculating baseline consumption and gradually reducing the caffeine intake can address the impact of the withdrawal symptoms.

Cannabis or marijuana also called pot, grass, weed, herb etc. is derived from flowers, leaves, stem or seeds of cannabis sativa plant. It is consumed by smoking or mixing it with foods and beverages. Hashish is a resinous material made from cannabis plant . Cannabis and illicit synthetic THC compounds like “spice” K2” have similar psychoactive effects which are mediated through binding with cannabinoid receptor CB1. Whereas binding with CB2 receptors impacts immunity. Anandamides are the endogenous ligands for these receptors. THC is lipophilic and is deposited in fatty tissue and can be detected in the urine in chronic cannabis users for up to 30 days. THC synthetic compounds, Dronabinol (Marinol) and Nabilone (Cesamet) are approved for medicinal use in oncology, ophthalmology and AIDS. CB1 receptors binding in hippocampus causes short-term memory problems whereas binding in nucleus accumbens causes euphoria. Psychiatric disorders are mood and anxiety disorders. Psychosis is also reported. Genetic factors, as evidenced by twin studies, contribute from 30 to 80% variance to this risk. There are no pharmacological treatments approved for cannabis withdrawal. Short-term symptomatic treatment with nonbenzodiazepine anxiolytics, antidepressants, or hypnotics may be considered. Cognitive-behavioral, motivational enhancement and family therapy, contingency management and self-help groups are valuable psychosocial treatment options.

Ecstasy or 3, 4- methylenedioxymethamphetamine also called a club drug because of its use in “rave” parties has both stimulant and psychedelic effects. Stimulant effect which precedes psychedelic effect causes euphoria. In addition through release of oxytocin prosocial and empathic behavior as well as sense of intimacy is experienced. The psychedelic effect causes distortion of sensory perceptions. This drug is popular with adolescents and young adults and often associated with prolonged weekend “rave” parties. Its use causes depletion of serotonin which may cause depression and suicidal behavior. Depression may also be caused by “crash” from stimulant effect. With intoxication of ecstasy patient often experiences autonomic effects like elevated blood pressure, elevated temperature, cardiac arrhythmia, and panic attacks. In addition patient may experience headaches, vertigo, seizure and loss of consciousness. For intoxication treatment is supportive and symptomatic. There are no specific medications for its treatment. Psychosocial interventions like cognitive behavioral therapy, social and coping skills training and treatment of comorbid psychiatric disorder are very valuable options.

LSD is the most potent hallucinogen. This as well as other hallucinogens have been used for religious rituals by Native Americans for centuries. LSD chemical structure has similarity to serotonin and works through post synaptic 5-HT2A receptor agonistic effects. LSD was first synthesized in late nineteen thirties. LSD intoxication significantly increases central autonomic activity leading to panic states, tachycardia, increased blood pressure and body temperature, pupillary dilatation, piloerection, tremor and hyperreflexia. The panic states, perceptual disturbances and flashbacks are often referred to as “trips”. Patient may experience these “trips” long after cessation of its use. Subjective effects of LSD start with somatic symptoms followed by perceptual disturbances, lability of mood, depersonalization, altered sense of time, visual distortions, mixing of sensations like “seeing” smells and “hearing” colors. This mixing of sensations is called synesthesia. LSD is not addictive but tolerance to behavioral effects and cross tolerance to other hallucinogens drugs are reported. Acute intoxication results in somatic, perceptual and psychic effects. Some patients also relive these experiences through flashbacks even long after cessation of its use. No withdrawal symptoms are reported. Long -Term effects of LSD use may include psychosis, depression, paranoid delusions and flashbacks. The treatment therefore will consist of targeting the specific clinical syndrome like with SSRIs for depression, antipsychotics like chlorpromazine for psychosis and bad “trips”. As with acute effects safety of the user must be assured and may require inpatient admission. Comorbid mental disorder should be treated to improve outcome. Cognitive behavioral therapy, social skills enhancement training can help to improve adaptive functions.

Inhalation of volatile hydrocarbon-based substances produces intoxication and pleasurable effects. Use of inhalants usually starts in adolescence ages 12 to 17 often precedes use of tobacco, alcohol and illicit substances. It decreases gradually after the age of 20 years. These substances are lipophilic, cross the blood-brain barrier rapidly and cause CNS depressant effect mediated through gamma-aminobutyric acid (GABA) agonism or NMDA receptor antagonism. In addition to CNS toxicity these substances also have significant toxicity to other body organs like liver and kidneys. Prolonged use may lead to neurocognitive disorders, anxiety and even psychosis. Use of inhalants can lead to serious medical complications such as cardiac arrhythmias and seizures. Sudden heavy sniffing may lead to death due to asphyxiation. Intoxication syndrome includes euphoria, excitation, disinhibition, slurred speech, memory impairment and delirium and coma with high doses. Sudden discontinuation of inhalants may lead to a withdrawal syndrome similar to alcohol. However benzodiazepines, other CNS depressants and adrenergic drugs should be avoided. Psychosocial interventions are valuable.

This chapter discusses epidemiologic, pathophysiology and diagnostic issues associated with opioid use disorders. Differentiation of the recreational user and the user who was prescribed narcotics for a diagnosed pain issue is an important variable in the approach to management. Absolute sobriety from opiates/opioids is difficult to achieve and a multifaceted approach is a necessity. This chapter also describes nondrug therapies used in the management of opioid use disorders, including narcotics anonymous, cognitive behavioral therapies and others. For many patients, substitution therapy may be necessary for the short or long term to prevent further issues with opioid use and a better outcome. Buprenorphine substitution therapy requires special provider training while methadone must be dispensed by a licensed opiate treatment program. Withdrawal from opioids is not life threatening but is subjectively very distressing. Management of opioid withdrawal can include treatment with buprenorphine or methadone resulting in relief of withdrawal symptoms and then slowly tapering off the medication. Alternatively non-opiate agents such as clonidine and other medications for symptom relief are used to ameliorate withdrawal. The chapter includes key points and a case vignette to assist the learner. A patient education sheet and further resources are included.

PCP is highly lipophilic dissociative anesthetic and a hallucinogen. This has been available since early 1950s. Its recreational use started in 1960’s. It is smoked, snorted or consumed orally. PCP works through NMDA receptor antagonism as well as through direct and indirect dopaminergic effects leading to psychosis. Intoxication with low to moderate dose produce numbness in the extremities, unsteady gait, slurred speech, bloodshot eyes, horizontal, vertical or rotator nystagmus, tachycardia, hypertension, elevation of body temperature, shallow breathing, dry skin, loss of balance, muscle rigidity, agitation, aggression false sense of invulnerability and superior strength leading to daring acts like jumping off of high building. A moderate dose may produce analgesia and anesthesia. High dose may cause drop in blood pressure, heart and respiratory rate, seizures, coma and death. The presence of nystagmus may assist in differentiating PCP psychosis from other causes of psychoses.. Long-term effects of PCP may include “flash-backs”, similar to LSD, persistent speech problems, memory impairment, chronic anxiety, depression or psychosis. There is no specific PCP antagonist medication. Supportive care in an environment of reduced sensory stimulation, urine acidification, and sedation with benzodiazepines is recommended. For patients with psychosis antipsychotic medication may be warranted. Psychosocial interventions add significant value.

Sedative Hypnotic Agents (SHAs) are prescribed across several medical disciplines, however, these carry a risk of addiction in small percentage of patients. SHA use for more than a month can result in tolerance and pharmacological dependence. This often requires dose escalation during the first 10-12 weeks of treatment . This pharmacological dependence should be distinguished from SHA use disorder. In this chapter we discuss the factors associated with risk and risk mitigation for SHA use disorder. Use of lowest possible effective dose for shorter period of time with close monitoring a valuable strategy to prevent addiction. Sudden SHA withdrawal specially from barbiturates may be fatal. We discuss the safe strategy for acute withdrawal by converting the drug of addiction to equivalent dose of a long halflife benzodiazepine or barbiturate. Stabilizing on that drug dose and gradually tapering from that. We also suggest treatment with adjunctive medications for comorbid psychiatric disorders. We conclude this chapter with a brief discussion of psychosocial strategies to promote abstinence and recovery.

Stimulant and cocaine use disorders are major public health problems. The prevalence of these disorders is on the rise around the globe and within in the US. Often more than one stimulant is used concurrently more often in patients with other psychiatric disorders like depression. These drugs are ingested, injected, smoked or snorted. Short-term effects lasts for about 40-60 minutes for cocaine and up to 12 hours for meth amphetamine, is characterized by initial “rush”, increased energy, a general sense of wellbeing, euphoria, increased sex drive, increased self-confidence and decreased appetite, which typically lasts 40-60 minutes for cocaine and 6–12 hours for methamphetamine. Long-term use may result in psychosis and cognitive impairment. The economic, medical and societal impact of these disorders is substantial. The cost increases are due to 24 fold increase in myocardial infarction or infectious diseases like HIV and hepatitis in IV drug users, increased prevalence of psychosis and mood disorders as well as cost incurred by criminal justice system. Cognitive behavioral therapy has been extensively used for stimulant use disorders. Medication management with stimulants and anticonvulsants has shown modest improvement for relapse prevention. Contingency contracting coupled with medication management has resulted in improvement.

Tobacco is one of the most widely used drugs of abuse, and represents the single most preventable cause of death. Physicians should take every opportunity to encourage their patients who smoke to quit. Most smokers are aware of the health hazards of smoking and want to quit. Smokers also need to be made aware of the health and economic benefits of a tobacco free life. Several pharmacological agents are available to help the patient who is committed to quitting. Nicotine replacement (patch, gum, lozenge, inhaler) is the most widely used, is available over the counter, and has a success rate about twice that of placebo. Bupropion (Zyban, Wellbutrin) has a slightly higher success rate, and can be used in conjunction with nicotine replacement. Varenicline (Chantix) probably provides the best success rates. Support and self-help groups are also a very useful resource for many patients.

Historically, since ancient times mankind around the globe has resorted to gambling behavior in one or other form, there is no specific cause for gambling addiction. Like other addictions genetic, biological, psychological and environmental causes play a part. Often competitive workaholics are drawn to gambling. Drugs like levodopa for parkinsonism may increase gambling behavior. Gambling is more common in younger individuals with no difference between sexes. Gambling has similar reward pathways as for other addictions and has impulsive and compulsive quality. These individuals show preoccupation with gambling, seek thrill from it, hide or lie about losses and at times experience remorse or guilt and try unsuccessfully to cut down and often chase their losses with a hope to “hit a big jackpot”. Diagnosis is based on DSM-5 criteria. Certain scales can be used to assess its severity. There are no known proven preventive strategies for gambling. Also there are no approved pharmacological interventions, however research favors therapeutic value of SSRIs, mood stabilizers and opiate antagonists . Like for other addictions gambling and related disorders also benefit from motivational enhancement, individual, group, couple and family therapies as well as self-help groups like Gambling Anonymous (GA).

The effectiveness of psychosocial evidenced-based behavioral interventions for substance and non-substance related disorders are comparable to their effectiveness for other psychiatric disorders . Cognitive behavioral therapy addresses the negative and dysfunctional thoughts and emotions related to these disorders and their reinforcing effects. This also helps develop cognitive skills to deal with cue driven craving leading to reengagement in addictive behaviors. Contingency management uses tangible rewards to support addiction free life style evidenced by negative drug screen participation in individual and group therapy. Behavioral self-control promotes goal setting and self-monitoring for harm reduction. Self-help 12-step programs promote acceptance, surrender to a higher power and self-governance through utilization of support from AA fellowship community. Motivational enhancement therapy is to help individuals to move higher on stages of change and to promote self-efficacy. Solutionbased therapy helps patients find solutions while reinforcing their successes in solving those problems. All these therapies with or without pharmacotherapy have value in achieving addiction free life style.