Exogenous psychotic disorders

 Epileptic illness.

 Psychical disorders and disorders of behavior as a result of the use of alcohol and alcoholic psychoses.

 

Alcoholism

The word alcohol comes from the Arabic “Al Kohl,” which means “the essence.” According to the American Medical Association, “alcoholism is an illness characterized by significant impairment that is directly associated with persistent and excessive use of alcohol. Impairment may involve physiological, psychological or social dysfunction.” Psychologically speaking, alcoholism has less to do with “how much” someone is drinking, and more to do with what happens when they drink. If you have problems when you drink, it mean that you have a drinking problem.

 The reality is that alcohol is often abused because it initially offers a very pleasant things. During mild intoxication most of the people become more relaxed, carefree, preexisting problems tend to fade into the background. Alcohol can be used to increase a moo. Initially, alcohol allows the drinker to feel quite pleasant, with no emotional costs. As an individual’s drinking progresses, however, it takes more and more alcohol to achieve the same good state. Eventually the good state is hardly present.

The prevalence of alcoholism

According to the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), Alcohol Dependence and Alcohol Abuse are among the most common mental disorders in the general population, with about 8 % of the adult population suffering from alcohol dependence and 5 %from alcohol abuse.

It is widely accepted that there is a genetic predisposition toward alcoholism. According to DSM-IV, the risk for alcohol dependence is three to four times higher in close relative of people with alcohol dependence.

A child born to a woman who drinks during her pregnancy may have a condition called fetal alcohol syndrome, causing a number of birth defects.

Symptoms of Alcohol and Substance Abuse

Abuse of alcohol or a substance (such as cocaine, nicotine, marijuana, etc.) is generally characterized by a maladaptive pattern of alcohol or substance use leading to significant impairment or distress, as manifested by 1 or more of the following, occurring within a one year period:

• Recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences or poor work performance related to substance use; substance-related absences, suspensions, or expulsions from school; neglect of children or household) 
• Recurrent alcohol or substance use in situations in which it is physically dangerous (e.g., driving an automobile or operating a machine when impaired by substance use) 
• Recurrent alcohol or substance-related legal problems (e.g., arrests for alcohol or substance-related disorderly conduct) 
• Continued alcohol or substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol or substance use (e.g., arguments with spouse about consequences of intoxication, physical fights)

The symptoms must also have never met the criteria for alcohol/substance dependence for this class of substance or alcohol.

Alcohol and substance dependence symptoms (alcoholism, addiction)

The dependence from alcohol or other psychoactive substances (marijuana, cocaine, nicotine, caffeine etc.) is characterized by the inadequate use of these substances, leading to clinically significant impairment or distress, as manifested by 3 or more of the following, occurring at any time in the same 12-month period:

1.     Tolerance, as defined by either of the following: 

§  A need for markedly increased amounts of the alcohol or substance to achieve intoxication or desired effect

§  Markedly diminished effect with continued use of the same amount of the alcohol or substance

2.     Withdrawal, as manifested by either of the following:

§  2 or more of the following, developing within several hours to a few days of reduction in heavy or prolonged alcohol or substance use:

o   Sweating or rapid pulse

o   Increased hand tremor

o   Insomnia

o   Nausea or vomiting

o   Physical agitation

o   Anxiety

o   Transient visual, tactile, or auditory hallucinations or illusions

o   Grand mal seizures

§  The same substance (or another substance) or alcohol is taken to relieve or avoid withdrawal symptoms

3.     The substance or alcohol is often taken in larger amounts or over a longer period than was intended 

4.     There is a persistent desire or unsuccessful efforts to cut down or control use of alcohol or the substance 

5.     A great deal of time is spent in activities necessary to obtain alcohol or the substance (e.g., visiting multiple doctors or driving long distances), using alcohol or a substance (e.g., chain-smoking), or recovering from its effects 

6.     Important social, occupational, or recreational activities are given up or reduced because of the continued alcohol or substance use 

7.     The substance or alcohol 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 substance (e.g., current cocaine use despite recognition of cocaine-induced depression, or continued drinking despite recognition that the hypertension was made worse by alcohol consumption)

The stages of the alcoholism

Alcoholism is a progressive disease and follows several phases:

The phase of the social drinking. Social drinkers have few problems with alcohol. A social drinker can basically take or leave it. There is no preoccupation with drinking. A social drinker is able to control the amount of alcohol consumed and rarely drinks to reach the intoxication. For these individuals, drinking is a secondary activity. It is the party, the meal, the wedding that interests the social drinker, but not the opportunity to take alcohol.

The first stage of alcoholism. An individual who is experiencing the early stages of alcoholism will begin to have a lot of problems associated with drinking. In early stage of alcoholism, a person may start to sneak drinks, begin to feel guilty about his or her drinking, and become preoccupied with alcohol. Blackouts, drinking to the point of intoxication, and increased tolerance (need of more alcohol to achieve the same effect) are all signs of early alcoholism.

In this stage of alcoholism an individual will look for the companions who are heavy drinkers and lose interest in activities not associated with drinking. Family and friends may begin to worry about the person’s use of alcohol. Work problems, such as missing work or tardiness, may also be present.

The second stage of alcoholism. If someone has entered the second stage of alcoholism, his or her life has become uncontrolled, although the alcoholic still denies that he or she has any problem. At this point, the alcoholic will often drink more than supposed. He or she will drink in an attempt to erase feelings such as anger, depression and social discomfort. The alcoholics drink in the morning to relieve a bad hangover. The individual may try to stop drinking, but without success. Job loss, medical problems, and serious family conflicts occur during this phase.

The third stage of alcoholism. At this stage, the alcoholic’s life has become completely unmanageable. Medical complications are numerous and include liver diseases such as cirrhosis or hepatitis. High blood pressure, bleeding of the esophageal veins, acute pancreatitiscoulb be the result of long term use. The heart and brain are compromised so that an alcoholic is at a higher risk for a heart attack or stroke. Depression and insomnia and even suicide are more prevalent at this stage. A condition known as Wernicke-Korsakoff Syndrome, which involves memory loss, indicates that the individual has brain damage from drinking.

An alcoholic at this stage has become physically addicted to alcohol and will experience seizures or delirium tremens (DTs) if he or she stops drinking. It is extremely important to seek out medical care at this point in the disease process.

Alcohol Tolerance

Tolerance to alcohol lead to both physical and psychological dependence after continued abuse. It causes dependence in much the same way as any other central nervous system depressant, such as a barbiturate. This dependence is the first sign that the heavy drinker has developed a progressive problem that is now out of control.

Tolerance is a physical sign and symptom that is inherited, not a personality factor such as low self-esteem or inferiority complex or other deep-rooted psychological problem. Those with a low risk for alcoholism do not adapt well to the presence of alcohol in their brains. The reaction to the lack of tolerance is dysphoria, disturbed mood, headache, nausea, vomiting and general ill feeling that only gets worse with alcohol. The person that is not alcoholic actually feels better as the alcohol leaves the body so there appears to be little reinforcement to drink more alcohol. The alcoholic, on the other hand, feels better as the blood-alcohol level rises in the body and brain so that the motivation is to drink more.

Tolerance to alcohol or the lack of it appears to be inherited. Whether someone is likely to develop alcoholism appears to depend on whether he or she has the genes for alcohol. If someone has tolerance for alcohol, he or she may be at risk for developing alcoholism. The opposite may also be true; if someone lacks tolerance to alcohol, he or she probably will not develop alcoholism.

Scientists believe that the brain areas responsible for responding to alcohol with a positive feeling, reward and attention may be determined by genetic makeup.

The tolerance rises up on the first stages of alcoholism and after some period of the disease it decrease.

Addiction and Habituation

You are physically dependent upon alcohol or drugs when:

• you need the substance to reduce your withdrawal cravings;
• you are not able to control when and how you use the substance;
• you require an increasing amount of the substance to become intoxicated; and
• you spend an increasing amount of time seeking out the substance.

Common signs of addiction include hangovers, blackouts, poor health, tremors, mood swings, alienation from family and friends, and involvement with law enforcement. Depending on the level of dependency, some alcoholics and drug addicts require detoxification. Detoxification from alcohol and drugs requires medical supervision!

When the dependence is on an activity or a ritual, it is called a “habituation.” Habituations include: codependency, sexual and relationship “addictions,” spending compulsions, binge eating, gambling, and raging. Though usually not quite as dangerous or physically debilitating as substance dependence, these rituals are integrated into one’s lifestyle and are as difficult to change.

Alcohol intoxication

Alcohol intoxication (also known as drunkenness or inebriation) is a physiological state induced by the consumption of alcohol.

Problems accumulate when alcohol builds up in the bloodstream faster than it can be metabolized by the liver. Some effects of alcohol intoxication are central to alcohol’s desirability as a beverage and its history as the world’s most widespread recreational drug. Common effects are euphoria and lowered social inhibitions. Other effects are unpleasant or dangerous because alcohol affects many different areas of the body at once and may cause progressive, long-term harm when consumed in excess.

Common symptoms of alcohol intoxication include slurred speech, euphoria, impaired balance, loss of muscle coordination (ataxia), flushed face, dehydration, vomiting, reddened eyes,reduced inhibitions, and erratic behavior. Sufficiently high levels of blood-borne alcohol will cause coma and death from the depressive effects of alcohol upon the central nervous system. “Acute alcohol poisoning” is a related medical term used to indicate a dangerously high concentration of alcohol in the blood, high enough to induce coma or respiratory depression. It is considered a medical emergency. The term is mostly used by health care providers. Toxicologists use the term “alcohol intoxication” to discriminate between alcohol and other toxins.

Pathophysiology

Alcohol is metabolized by a normal liver at the rate of about one ounce (one two-ounce shot of spirits, a normal beer, a regular sized glass of wine) every 90 minutes. An “abnormal” liver with conditions such as hepatitis,cirrhosis, gall bladder disease, and cancer will have a slower rate of metabolism.

Ethanol is metabolised to acetaldehyde by alcohol dehydrogenase (ADH), which is found in many tissues, including the gastric mucosa. Acetaldehyde is metabolised to acetate by acetaldehyde dehydrogenase (ALDH), which is predominantly found in liver mitochondria. Acetate is used by the muscle cells to produce acetyl-CoA using the enzyme acetyl-CoA synthetase, and the acetyl-CoA is then used in the citric acid cycle. It takes roughly 90 minutes for a healthy liver to metabolize a single ounce, approximately one hour per standard unit.

Ethanol’s acute effects are largely due to its nature as a central nervous system depressant, and are dependent on blood alcohol concentrations:

As drinking increases, people become sleepy, or fall into a stupor. After a very high level of consumption, the respiratory system becomes depressed and the person will stop breathing. The most important thing for people who witness someone “passing out” from too much alcohol is to get them emergency medical treatment. Comatose patients may aspirate their vomit (resulting in vomitus in the lungs, which may cause “drowning” and later pneumonia if survived). CNS depression and impaired motor co-ordination along with poor judgement increases the likelihood of accidental injury occurring. It is estimated that about one third of alcohol-related deaths are due to accidents (32%), and another 14% are from intentional injury.

In addition to respiratory failure and accidents caused by effects on the central nervous system, alcohol causes significant metabolic derangements. Hypoglycaemia occurs due to ethanol’s inhibition of gluconeogenesis, especially in children, and may cause lactic acidosis, ketoacidosis and acute renal failure. Metabolic acidosis is compounded by respiratory failure. Patients may also present with hypothermia.

Blood alcohol level

Blood alcohol level  (BAL), also called blood alcohol concentration, blood ethanol concentration, or blood alcohol content is most commonly used as a metric of alcohol intoxication for legal or medical purposes.

Blood alcohol level is usually expressed as a percentage of alcohol (generally in the sense of ethanol) in the blood. For instance, a BAL of 0.10 means that 0.10% (one tenth of one percent) of a person’s blood, by volume (usually, but in some countries by mass), is alcohol.

 

Progressive effects of alcohol
BAC (% by vol.)	Behavior	Impairment
0.010–0.029	·         Average individual appears normal	·         Subtle effects that can be detected with special tests
0.030–0.059	·         Mild euphoria ·         Relaxation ·         Joyousness ·         Talkativeness ·         Decreased inhibition	·         Concentration
0.06–0.09	·         Blunted feelings ·         Disinhibition ·         Extroversion	·         Reasoning ·         Depth perception ·         Peripheral vision ·         Glare recovery
0.10–0.19	·         Over-expression ·         Emotional swings ·         Anger or sadness ·         Boisterousness ·         Decreased libido	·         Reflexes ·         Reaction time ·         Gross motor control ·         Staggering ·         Slurred speech ·         Temporary erectile dysfunction ·         Possibility of temporary alcohol poisoning
0.20–0.29	·         Stupor ·         Loss of understanding ·         Impaired sensations ·         Possibility of falling unconscious	·         Severe motor impairment ·         Loss of consciousness ·         Memory blackout
0.30–0.39	·         Severe central nervous system depression ·         Unconsciousness ·         Death is possible	·         Bladder function ·         Breathing ·         Dysequilibrium ·         Heart rate
0.40–0.50	·         General lack of behavior ·         Unconsciousness	·         Breathing ·         Heart rate ·         Positional Alcohol Nystagmus
>0.50	·         High risk of poisoning ·         Possibility of death

 

 Stages of Change

Almost 20 years ago, two well-known alcoholism researchers, Carlo C. DiClemente and J. O. Prochaska, introduced a five-stage model of change to help professionals understand their clients with addiction problems and motivate them to change. Their model is based not on abstract theories but on their personal observations of how people went about modifying problem behaviors such as smoking, overeating and problem drinking.

The six stages of the model are:

• precontemplation
• contemplation
• determination
• action
• maintenance
• termination

Understanding your readiness to change by being familiar with the six-stage model of change can help you choose treatments that are right for you. A treatment professional with the right training will understand where you are in terms of readiness to stop drinking and help you find and maintain the motivation to stop drinking.

Precontemplation
Individuals in the precontemplation stage of change are not even thinking about changing their drinking behavior. They may not see it as a problem, or they think that others who point out the problem are exaggerating.

There are many reasons to be in precontemplation, and Dr. DiClemente has referred to them as “the Four Rs” —reluctance, rebellion, resignation and rationalization:

• Reluctant precontemplators are those who through lack of knowledge or inertia do not want to consider change. The impact of the problem has not become fully conscious.
• Rebellious precontemplators have a heavy investment in drinking and in making their own decisions. They are resistant to being told what to do.
• Resigned precontemplators have given up hope about the possibility of change and seem overwhelmed by the problem. Many have made many attempts to quit or control their drinking.
• Rationalizing precontemplators have all the answers; they have plenty of reasons why drinking is not a problem, or why drinking is a problem for others but not for them.

Contemplation
Individuals in this stage of change are willing to consider the possibility that they have a problem, and the possibility offers hope for change. However, people who are contemplating change are often highly ambivalent. They are on the fence. Contemplation is not a commitment, not a decision to change. People at this stage are often quite interested in learning about alcoholism and treatment. They know that drinking is causing problems, and they often have a mental list of all the reasons that drinking is bad for them. But even with all these negatives, they still cannot make a decision to change.

In the contemplation stage, often with the help of a treatment professional, people make a risk-reward analysis. They consider the pros and cons of their behavior, and the pros and cons of change. They think about the previous attempts they have made to stop drinking, and what has caused failure in the past.

Determination: commitment to action

Deciding to stop drinking is the hallmark of this stage of change. All the weighing of pros and cons, all the risk-reward analysis, finally tips the balance in favor of change. Not all ambivalence has been resolved, but ambivalence no longer represents an insurmountable barrier to change. Most individuals in this stage will make a serious attempt to stop drinking in the near future. Individuals in this stage appear to be ready and committed to action.

This stage represents preparation as much as determination. The next step in this stage is to make a realistic plan. Commitment to change without appropriate skills and activities can create a fragile and incomplete action plan. Often with the help of a treatment professional, individuals will make a realistic assessment of the level of difficulty involved in stopping drinking. They will begin to anticipate problems and pitfalls and come up with concrete solutions that will become part of their ongoing treatment plan.

Action: implementing the plan

Individuals in this stage of change put their plan into action. This stage typically involves making some form of public commitment to stop drinking in order to get external confirmation of the plan. If they have not done so already, individuals in this stage may enter counseling or some form of outpatient treatment, start to attend anonymous alcoholics meetings or tell their family members and friends about their decision—or all of the above.

Making such public commitments not only helps people obtain the supports they need to recover from alcoholism, but it creates external monitors. People often find it very helpful to know that others are watching and cheering them on. What about the others who may secretly, or not so secretly, hope they will fail? For people who get sober and stay sober, one of the many pleasures is to disprove the negative predictions of others.

Nothing succeeds like success. A person who has implemented a good plan begins to see it work and experiences it working over time, making adjustments along the way. The many things that alcohol may have taken from the person begin to be restored, along with hope and self-confidence and continued determinatioot to drink.

Maintenance, relapse and recycling

The action stage normally takes three to six months to complete. Change requires building a new pattern of behavior over time. The real test of change is long-term sustained change over many years. This stage of successful change is called “maintenance.” In this stage, an alcohol-free life is becoming firmly established, and the threat of a return to old patterns becomes less intense and less frequent.

Because alcoholism is a chronic disease, the possibility of relapse is always present. Individuals may experience a strong temptation to drink and fail to cope with it successfully. Sometimes relaxing their guard or “testing” themselves begins a slide back. People at this stage of change are armed with a variety of relapse prevention skills. They know where to get the supports they need.

Alcoholics who relapse learn from the relapse. The experience of relapsing and returning to sobriety often strengthens a person’s determination to stay sober.

Termination
The ultimate goal in the change process is termination. At this stage, the alcoholic no longer finds that alcohol presents a temptation or threat; he has complete confidence that he can cope without fear of relapse.

Stress and drinking

Studies indicate that many people drink as a means of coping with modern life and its accompanying economic stress, job stress and marital discord. Today’s fast-paced society offers little in the way of social support. While a drink after work or with dinner can be pleasurable and safe and is commonplace, people with excessive or chronic stress often drink to excess.

Whether an individual drinks to excess in response to stress appears to depend on early childhood experiences and the individual’s previous drinking behavior. Prolonged stress in infancy may permanently alter the hormonal stress response and subsequent reactions to new stressors, including alcohol consumption. Animal studies have helped to understand the relationship between child-rearing and stress and vulnerability to alcohol abuse. Monkeys who were reared by peers, consume twice as much alcohol as monkeys who are mother-reared. Adult rats handled for the first three weeks of life demonstrate markedly reduced hormonal responses to a variety of stressors compared with rats not handled during this time.

In humans, Cloninger reported an association between certain types of alcoholism and adverse early childhood experiences. High levels of stress may influence drinking frequency and quantity. This relationship between stress and drinking even is stronger when alternative coping mechanisms and social supports are lacking. Finally, when individuals believe that alcohol will help to reduce the stress in their lives, alcohol is most likely to be used in response to stress. Drinking appears to follow stress but some evidence also links excessive drinking to the anticipation of a major stress or even during times of stress.

A clear association between stress, drinking behavior and the development of alcoholism in humans has yet to be established. Stress may be well understood from the point of view of brain events and hormonal response, but it appears that what is stressful to one person is not always stressful to another. Furthermore, stress response among people with a strong family history of alcohol dependence and also those with a personal history of alcohol dependence is not as similar as we might think to those without these risk factors.

Researchers have found that animals which have been bred to prefer alcohol rather than water have a different physiological response to stress than animals that do not prefer alcohol. Alcohol may be more reinforcing and “therapeutic,” making dependence more likely among the most vulnerable. While this is speculation, in the patient with alcohol dependence there often is a clearer connection between stress and alcohol relapse.

If you interview alcoholics who have relapsed, they often will describe chronic life stressors as causing their alcohol relapse. Stress makes relapse more likely when it cannot be controlled by the person because of their coping skills, additional psychiatric and physical problems, and lack of social support. Stress-related relapse is most likely among alcoholics who do not attend meetings or those who do not avoid people, places and things associated with their drinking.

Treatment

Treatment is often seen as having four general phases:

• Getting started (assessment and evaluation of disease symptoms and accompanying life problems, making treatment choices and developing a plan)
• Detoxification (stopping use)
• Active treatment (residential treatment or therapeutic communities, intensive and regular outpatient treatment, medications to help with alcohol craving and discourage alcohol use, medications to treat concurrent psychiatric illnesses, 12-step programs, other self-help and mutual-help groups)
• Maintaining sobriety and relapse prevention (outpatient treatment as needed, 12-step programs, other self-help and mutual-help groups)

Getting started

First, the alcoholic must overcome denial and distorted thinking and develop the willingness to begin treatment—what Alcoholics Anonymous (AA) calls “the desire” to stop drinking. At this stage, it is important to obtain the help of someone knowledgeable about treatment and the options available.

When getting started, some people have lost control over alcohol to such an extent that they will only be able to make immediate decisions and set the most basic goal of quitting drinking. Development of a detailed treatment plan with goals and choices may have to wait until after detoxification.

On the other hand, “getting started” is exactly the place where some people with alcohol problems “get stuck.” In being stuck, denial is always a problem, but complete denial is not universal; people have various levels of awareness of their alcohol use problems, which means they are in different stages of readiness to change their drinking behavior. Professionals have taken advantage of this insight about alcoholism to develop treatment approaches that are matched to a person’s readiness to change.

Detoxification
The second phase of treatment is stopping use, which can be done on either an inpatient or outpatient basis. Medical evaluation and treatment are particularly important at this stage. A large proportion of alcoholics develop dangerous withdrawal symptoms that must be medically managed either in a hospital or on an outpatient basis.

Although detoxification is a critical step for many alcoholics, most treatment professionals are reluctant to call it treatment, and for good reason. Treatment is what helps a person develop a commitment to change, keep the motivation to change, create a realistic plan to change and put the plan in action. Successful treatment means a person begins to experience the rewards of seeing the plan work. Just taking away the alcohol does not automatically produce any of these outcomes.

Active treatment

Relapse to alcohol addiction is most likely to occur in the first three to six months after a person stops drinking, a period characterized by physiological abnormalities, mood changes and complaints of anxiety,depression, insomnia and hormone and sleep problems. Getting active help and support during the early months of sobriety is critical for treatment to succeed.

In the third phase of treatment, a person typically gains the motivatioecessary to maintain a commitment to sobriety, the knowledge and skills necessary to stay sober, and the support systems necessary to cope with the problems of daily life—the problems that everyone has to face—without resorting to the old “solution” of drinking. This is where the help of a treatment professional is important. A professional will help you better understand how alcohol has affected your health and your life, so that you can set goals and develop a plan to stay sober and choose the treatments that are right for you.

Some proven medications are available to help with alcohol craving and discourage alcohol use. A treatment professional will also help you choose medications and treatments for concurrent psychiatric illnesses, like depression or anxiety, if that is appropriate, or for a variety of health problems that often accompany alcoholism.

Research has shown that the longer people stay in treatment—that is, the longer they remain sober and actively committed to sobriety—the more likely it is that they will maintain sobriety. Some treatment professionals think of the phase of active treatment as lasting from six months to a year. During the first critical months of treatment, people ofteeed a variety of supports, especially AA or other self-help groups, to achieve and maintain lasting sobriety.

Maintaining sobriety and relapse prevention

It is often difficult to pinpoint when the active treatment phase ends and a person enters the maintenance phase of recovery. In the active stage of treatment, people learn what they need to do to stay sober and develop the many skills they will use to avoid relapse. A person could be said to enter the maintenance stage when he or she is comfortable with these skills and has had a chance to rely on them to stay sober when life throws them the inevitable curveballs, both in crisis situations and in everyday problem situations.

Many people in recovery attribute their ongoing sobriety to participation in a support group such as AA or Women for Sobriety.

 

 

Drug Abuse & Addiction

Signs, Symptoms, and Help for Drug Problems and Substance Abuse

Some people are able to use recreational or prescription drugs without ever experiencing negative consequences or addiction. For many others, substance use can cause problems at work, home, school, and in relationships, leaving you feeling isolated, helpless, or ashamed.

Learning about the nature of drug abuse and addiction—how it develops, what it looks like, and why it can have such a powerful hold—will give you a better understanding of the problem and how to best deal with it.

People experiment with drugs for many different reasons. Many first try drugs out of curiosity, to have a good time, because friends are doing it, or in an effort to improve athletic performance or ease another problem, such as stress, anxiety, or depression. Use doesn’t automatically lead to abuse, and there is no specific level at which drug use moves from casual to problematic. It varies by individual. Drug abuse and addiction is less about the amount of substance consumed or the frequency, and more to do with the consequences of drug use. No matter how often or how little you’re consuming, if your drug use is causing problems in your life—at work, school, home, or in your relationships—you likely have a drug abuse or addiction problem.

As with many other conditions and diseases, vulnerability to addiction differs from person to person. Your genes, mental health, family and social environment all play a role in addiction. Risk factors that increase your vulnerability include:

§  Family history of addiction

§  Abuse, neglect, or other traumatic experiences in childhood

§  Mental disorders such as depression and anxiety

§  Early use of drugs

§  Method of administration—smoking or injecting a drug may increase its addictive potential

Drug addiction and the brain

Addiction is a complex disorder characterized by compulsive drug use. While each drug produces different physical effects, all abused substances share one thing in common: repeated use can alter the way the brain looks and functions.

§  Taking a recreational drug causes a surge in levels of dopamine in your brain, which trigger feelings of pleasure. Your brain remembers these feelings and wants them repeated.

§  If you become addicted, the substance takes on the same significance as other survival behaviors, such as eating and drinking.

§  Changes in your brain interfere with your ability to think clearly, exercise good judgment, control your behavior, and feel normal without drugs.

§  Whether you’re addicted to inhalants, heroin, Xanax, speed, or Vicodin, the uncontrollable craving to use grows more important than anything else, including family, friends, career, and even your own health and happiness.

§  The urge to use is so strong that your mind finds many ways to deny or rationalize the addiction. You may drastically underestimate the quantity of drugs you’re taking, how much it impacts your life, and the level of control you have over your drug use.

People who experiment with drugs continue to use them because the substance either makes them feel good, or stops them from feeling bad. In many cases, however, there is a fine line between regular use and drug abuse and addiction. Very few addicts are able to recognize when they have crossed that line. While frequency or the amount of drugs consumed don’t in themselves constitute drug abuse or addiction, they can often be indicators of drug-related problems.

§  Problems can sometimes sneak up on you, as your drug use gradually increases over time. Smoking a joint with friends at the weekend, or taking ecstasy at a rave, or cocaine at an occasional party, for example, can change to using drugs a couple of days a week, then every day. Gradually, getting and using the drug becomes more and more important to you.

§  If the drug fulfills a valuable need, you may find yourself increasingly relying on it. For example, you may take drugs to calm you if you feel anxious or stressed, energize you if you feel depressed, or make you more confident in social situations if you normally feel shy. Or you may have started using prescription drugs to cope with panic attacks or relieve chronic pain, for example. Until you find alternative, healthier methods for overcoming these problems, your drug use will likely continue.

§  Similarly, if you use drugs to fill a void in your life, you’re more at risk of crossing the line from casual use to drug abuse and addiction. To maintain healthy balance in your life, you need to have other positive experiences, to feel good in your life aside from any drug use.

§  As drug abuse takes hold, you may miss or frequently be late for work or school, your job performance may progressively deteriorate, and you start to neglect social or family obligations. Your ability to stop using is eventually compromised. What began as a voluntary choice has turned into a physical and psychological need.

The good news is that with the right treatment and support, you can counteract the disruptive effects of drug use and regain control of your life. The first obstacle is to recognize and admit you have a problem, or listen to loved ones who are often better able to see the negative effects drug use is having on your life.

MYTH 1: Overcoming addiction is a simply a matter of willpower. You can stop using drugs if you really want to. Prolonged exposure to drugs alters the brain in ways that result in powerful cravings and a compulsion to use. These brain changes make it extremely difficult to quit by sheer force of will.

MYTH 2: Addiction is a disease; there’s nothing you can do about it. Most experts agree that addiction is a brain disease, but that doesn’t mean you’re a helpless victim. The brain changes associated with addiction can be treated and reversed through therapy, medication, exercise, and other treatments.

MYTH 3: Addicts have to hit rock bottom before they can get better. Recovery can begin at any point in the addiction process—and the earlier, the better. The longer drug abuse continues, the stronger the addiction becomes and the harder it is to treat. Don’t wait to intervene until the addict has lost it all.

MYTH 4: You can’t force someone into treatment; they have to want help. Treatment doesn’t have to be voluntary to be successful. People who are pressured into treatment by their family, employer, or the legal system are just as likely to benefit as those who choose to enter treatment on their own. As they sober up and their thinking clears, many formerly resistant addicts decide they want to change.

MYTH 5: Treatment didn’t work before, so there’s no point trying again. Recovery from drug addiction is a long process that often involves setbacks. Relapse doesn’t mean that treatment has failed or that you’re a lost cause. Rather, it’s a signal to get back on track, either by going back to treatment or adjusting the treatment approach.

Although different drugs have different physical effects, the symptoms of addiction are similar. See if you recognize yourself in the following signs and symptoms of substance abuse and addiction. If so, consider talking to someone about your drug use.

Common signs and symptoms of drug abuse

§  You’re neglecting your responsibilities at school, work, or home (e.g. flunking classes, skipping work, neglecting your children) because of your drug use.

§  You’re using drugs under dangerous conditions or taking risks while high, such as driving while on drugs, using dirty needles, or having unprotected sex.

§  Your drug use is getting you into legal trouble, such as arrests for disorderly conduct, driving under the influence, or stealing to support a drug habit. 

§  Your drug use is causing problems in your relationships, such as fights with your partner or family members, an unhappy boss, or the loss of old friends.

Common signs and symptoms of drug addiction

§  You’ve built up a drug tolerance. You need to use more of the drug to experience the same effects you used to attain with smaller amounts.

§  You take drugs to avoid or relieve withdrawal symptoms. If you go too long without drugs, you experience symptoms such as nausea, restlessness, insomnia, depression, sweating, shaking, and anxiety.

§  You’ve lost control over your drug use. You often do drugs or use more than you planned, even though you told yourself you wouldn’t. You may want to stop using, but you feel powerless.

§  Your life revolves around drug use. You spend a lot of time using and thinking about drugs, figuring out how to get them, and recovering from the drug’s effects.

§  You’ve abandoned activities you used to enjoy, such as hobbies, sports, and socializing, because of your drug use.

§  You continue to use drugs, despite knowing it’s hurting you. It’s causing major problems in your life—blackouts, infections, mood swings, depression, paranoia—but you use anyway.

Drug abusers often try to conceal their symptoms and downplay their problem. If you’re worried that a friend or family member might be abusing drugs, look for the following warning signs:

Physical warning signs of drug abuse

§  Bloodshot eyes, pupils larger or smaller than usual

§  Changes in appetite or sleep patterns. Sudden weight loss or weight gain

§  Deterioration of physical appearance, personal grooming habits

§  Unusual smells on breath, body, or clothing

§  Tremors, slurred speech, or impaired coordination

Behavioral signs of drug abuse

§  Drop in attendance and performance at work or school

§  Unexplained need for money or financial problems. May borrow or steal to get it.

§  Engaging in secretive or suspicious behaviors

§  Sudden change in friends, favorite hangouts, and hobbies

§  Frequently getting into trouble (fights, accidents, illegal activities)

Psychological warning signs of drug abuse

§  Unexplained change in personality or attitude

§  Sudden mood swings, irritability, or angry outbursts

§  Periods of unusual hyperactivity, agitation, or giddiness

§  Lack of motivation; appears lethargic or “spaced out”

§  Appears fearful, anxious, or paranoid, with no reason

Warning Signs of Commonly Abused Drugs

§  Marijuana: Glassy, red eyes; loud talking, inappropriate laughter followed by sleepiness; loss of interest, motivation; weight gain or loss.

§  Depressants (including Xanax, Valium, GHB): Contracted pupils; drunk-like; difficulty concentrating; clumsiness; poor judgment; slurred speech; sleepiness.

§  Stimulants (including amphetamines, cocaine, crystal meth):

 Dilated pupils; hyperactivity; euphoria; irritability; anxiety; excessive talking followed by depression or excessive sleeping at odd times; may go long periods of time without eating or sleeping; weight loss; dry mouth and nose.

§  Inhalants (glues, aerosols, vapors): Watery eyes; impaired vision, memory and thought; secretions from the nose or rashes around the nose and mouth; headaches and nausea; appearance of intoxication; drowsiness; poor muscle control; changes in appetite; anxiety; irritability; lots of cans/aerosols in the trash.

§  Hallucinogens (LSD, PCP): Dilated pupils; bizarre and irrational behavior including paranoia, aggression, hallucinations; mood swings; detachment from people; absorption with self or other objects, slurred speech; confusion.

§  Heroin: Contracted pupils; no response of pupils to light; needle marks; sleeping at unusual times; sweating; vomiting; coughing, sniffling; twitching; loss of appetite.

§ 

Warning signs of teen drug abuse

While experimenting with drugs doesn’t automatically lead to drug abuse, early use is a risk factor for developing more serious drug abuse and addiction. Risk of drug abuse also increases greatly during times of transition, such as changing schools, moving, or divorce. The challenge for parents is to distinguish between the normal, often volatile, ups and downs of the teen years and the red flags of substance abuse. These include:

§  Having bloodshot eyes or dilated pupils; using eye drops to try to mask these signs

§  Skipping class; declining grades; suddenly getting into trouble at school

§  Missing money, valuables, or prescriptions

§  Acting uncharacteristically isolated, withdrawn, angry, or depressed

§  Dropping one group of friends for another; being secretive about the new peer group

§  Loss of interest in old hobbies; lying about new interests and activities

§  Demanding more privacy; locking doors; avoiding eye contact; sneaking around

If you suspect that a friend or family member has a drug problem, here are a few things you can do:

§  Speak up. Talk to the person about your concerns, and offer your help and support, without being judgmental. The earlier addiction is treated, the better. Don’t wait for your loved one to hit bottom! Be prepared for excuses and denial by listing specific examples of your loved one’s behavior that has you worried.

§  Take care of yourself. Don’t get so caught up in someone else’s drug problem that you neglect your own needs. Make sure you have people you can talk to and lean on for support. And stay safe. Don’t put yourself in dangerous situations.

§  Avoid self-blame. You can support a person with a substance abuse problem and encourage treatment, but you can’t force an addict to change. You can’t control your loved one’s decisions. Let the person accept responsibility for his or her actions, an essential step along the way to recovery for drug addiction. 

§  Attempt to punish, threaten, bribe, or preach.

§  Try to be a martyr. Avoid emotional appeals that may only increase feelings of guilt and the compulsion to use drugs.

§  Cover up or make excuses for the drug abuser, or shield them from the negative consequences of their behavior.

§  Take over their responsibilities, leaving them with no sense of importance or dignity.

§  Hide or throw out drugs.

§  Argue with the person when they are high.

§  Take drugs with the drug abuser.

§  Feel guilty or responsible for another’s behavior.

Discovering your child uses drugs can generate fear, confusion, and anger in parents. It’s important to remain calm when confronting your teen, and only do so when everyone is sober. Explain your concerns and make it clear that your concern comes from a place of love. It’s important that your teen feels you are supportive.

Five steps parents can take:

§  Lay down rules and consequences. Your teen should understand that using drugs comes with specific consequences. But don’t make hollow threats or set rules that you cannot enforce. Make sure your spouse agrees with the rules and is prepared to enforce them.

§  Monitor your teen’s activity. Know where your teen goes and who he or she hangs out with. It’s also important to routinely check potential hiding places for drugs—in backpacks, between books on a shelf, in DVD cases or make-up cases, for example. Explain to your teen that this lack of privacy is a consequence of him or her having been caught using drugs.

§  Encourage other interests and social activities. Expose your teen to healthy hobbies and activities, such as team sports and afterschool clubs.

§  Talk to your child about underlying issues. Drug use can be the result of other problems. Is your child having trouble fitting in? Has there been a recent major change, like a move or divorce, which is causing stress?

§  Get Help. Teenagers often rebel against their parents but if they hear the same information from a different authority figure, they may be more inclined to listen. Try a sports coach, family doctor, therapist, or drug counselor.

§  Addiction involves craving for something intensely, loss of control over its use, and continuing involvement with it despite adverse consequences.

§  Addiction changes the brain, first by subverting the way it registers pleasure and then by corrupting other normal drives such as learning and motivation.

§  Although breaking an addiction is tough, it can be done.

The word “addiction” is derived from a Latin term for “enslaved by” or “bound to.” Anyone who has struggled to overcome an addiction—or has tried to help someone else to do so—understands why.

Addiction exerts a long and powerful influence on the brain that manifests in three distinct ways: craving for the object of addiction, loss of control over its use, and continuing involvement with it despite adverse consequences.

For many years, experts believed that only alcohol and powerful drugs could cause addiction. Neuroimaging technologies and more recent research, however, have shown that certain pleasurable activities, such as gambling, shopping, and sex, can also co-opt the brain.

Although a standard U.S. diagnostic manual (the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition or DSM-IV) describes multiple addictions, each tied to a specific substance or activity, consensus is emerging that these may represent multiple expressions of a common underlying brain process.

Nobody starts out intending to develop an addiction, but many people get caught in its snare. Consider the latest government statistics:

§  Nearly 23 million Americans—almost one in 10—are addicted to alcohol or other drugs.

§  More than two-thirds of people with addiction abuse alcohol.

§  The top three drugs causing addiction are marijuana, opioid (narcotic) pain relievers, and cocaine.

In the 1930s, when researchers first began to investigate what caused addictive behavior, they believed that people who developed addictions were somehow morally flawed or lacking in willpower. Overcoming addiction, they thought, involved punishing miscreants or, alternately, encouraging them to muster the will to break a habit.

The scientific consensus has changed since then. Today we recognize addiction as a chronic disease that changes both brain structure and function. Just as cardiovascular disease damages the heart and diabetes impairs the pancreas, addiction hijacks the brain. This happens as the brain goes through a series of changes, beginning with recognition of pleasure and ending with a drive toward compulsive behavior.

Pleasure principle

The brain registers all pleasures in the same way, whether they originate with a psychoactive drug, a monetary reward, a sexual encounter, or a satisfying meal. In the brain, pleasure has a distinct signature: the release of the neurotransmitter dopamine in the nucleus accumbens, a cluster of nerve cells lying underneath the cerebral cortex (see illustration). Dopamine release in the nucleus accumbens is so consistently tied with pleasure that neuroscientists refer to the region as the brain’s pleasure center.

All drugs of abuse, from nicotine to heroin, cause a particularly powerful surge of dopamine in the nucleus accumbens. The likelihood that the use of a drug or participation in a rewarding activity will lead to addiction is directly linked to the speed with which it promotes dopamine release, the intensity of that release, and the reliability of that release.

Even taking the same drug through different methods of administration can influence how likely it is to lead to addiction. Smoking a drug or injecting it intravenously, as opposed to swallowing it as a pill, for example, generally produces a faster, stronger dopamine signal and is more likely to lead to drug misuse.

 

 

 

Brain’s Reward Center

Addictive drugs provide a shortcut to the brain’s reward system by flooding the nucleus accumbens with dopamine. The hippocampus lays down memories of this rapid sense of satisfaction, and the amygdala creates a conditioned response to certain stimuli.

Learning process

Scientists once believed that the experience of pleasure alone was enough to prompt people to continue seeking an addictive substance or activity. But more recent research suggests that the situation is more complicated. Dopamine not only contributes to the experience of pleasure, but also plays a role in learning and memory—two key elements in the transition from liking something to becoming addicted to it.

According to the current theory about addiction, dopamine interacts with another neurotransmitter, glutamate, to take over the brain’s system of reward-related learning. This system has an important role in sustaining life because it links activities needed for human survival (such as eating and sex) with pleasure and reward.

The reward circuit in the brain includes areas involved with motivation and memory as well as with pleasure. Addictive substances and behaviors stimulate the same circuit—and then overload it.

Repeated exposure to an addictive substance or behavior causes nerve cells in the nucleus accumbens and the prefrontal cortex (the area of the brain involved in planning and executing tasks) to communicate in a way that couples liking something with wanting it, in turn driving us to go after it. That is, this process motivates us to take action to seek out the source of pleasure.

Determining whether you have addiction isn’t completely straightforward. And admitting it isn’t easy, largely because of the stigma and shame associated with addiction. But acknowledging the problem is the first step toward recovery.

A “yes” answer to any of the following three questions suggests you might have a problem with addiction and should—at the very least—consult a health care provider for further evaluation and guidance.

§  Do you use more of the substance or engage in the behavior more often than in the past?

§  Do you have withdrawal symptoms when you don’t have the substance or engage in the behavior?

§  Have you ever lied to anyone about your use of the substance or extent of your behavior?

Over time, the brain adapts in a way that actually makes the sought-after substance or activity less pleasurable.

Iature, rewards usually come only with time and effort. Addictive drugs and behaviors provide a shortcut, flooding the brain with dopamine and other neurotransmitters. Our brains do not have an easy way to withstand the onslaught.

Addictive drugs, for example, can release two to 10 times the amount of dopamine that natural rewards do, and they do it more quickly and more reliably. In a person who becomes addicted, brain receptors become overwhelmed. The brain responds by producing less dopamine or eliminating dopamine receptors—an adaptation similar to turning the volume down on a loudspeaker wheoise becomes too loud.

As a result of these adaptations, dopamine has less impact on the brain’s reward center. People who develop an addiction typically find that, in time, the desired substance no longer gives them as much pleasure. They have to take more of it to obtain the same dopamine “high” because their brains have adapted—an effect known as tolerance.

Compulsion takes over

At this point, compulsion takes over. The pleasure associated with an addictive drug or behavior subsides—and yet the memory of the desired effect and the need to recreate it (the wanting) persists. It’s as though the normal machinery of motivation is no longer functioning.

The learning process mentioned earlier also comes into play. The hippocampus and the amygdala store information about environmental cues associated with the desired substance, so that it can be located again. These memories help create a conditioned response—intense craving—whenever the person encounters those environmental cues.

Cravings contribute not only to addiction but to relapse after a hard-won sobriety. A person addicted to heroin may be in danger of relapse when he sees a hypodermic needle, for example, while another person might start to drink again after seeing a bottle of whiskey. Conditioned learning helps explain why people who develop an addiction risk relapse even after years of abstinence.

It is not enough to “just say no”—as the 1980s slogan suggested. Instead, you can protect (and heal) yourself from addiction by saying “yes” to other things. Cultivate diverse interests that provide meaning to your life. Understand that your problems usually are transient, and perhaps most importantly, acknowledge that life is not always supposed to be pleasurable.

 

 

 

Substance dependence, commonly called drug addiction, is a compulsive need to use drugs in order to functioormally. When such substances are unobtainable, the user suffers fromwithdrawal.

The section about substance dependence in the Diagnostic and Statistical Manual of Mental Disorders (more specifically, the 2000 “text revision”, the DSM-IV-TR) does not use the wordaddiction at all. It explains:

When an individual persists in use of alcohol or other drugs despite problems related to use of the substance, substance dependence may be diagnosed. Compulsive and repetitive use may result in tolerance to the effect of the drug and withdrawal symptoms when use is reduced or stopped. This, along with Substance abuse are considered Substance Use Disorders..

Discussions about drug addiction involve much discussion about compulsive behaviors and disorders.

Doug Sellman at the National Addiction Center offers what he calls “The 10 most important things to know about addiction”. He offers the following points, before explaining them in more detail (although even his full paper does not presume to be able to discuss all the important facts about addiction). First, Sellman says that the most important thing to know about addiction may be that addiction is “fundamentally about compulsive behavior“. Second of all, such habits originate outside of consciousness (i.e. from the unconscious mind). The compulsive sequence of behaviors are so practiced that they can be extremely difficult to avoid initiating, and even harder to interrupt. Sellman maintains, thirdly, that addiction is 50% heritable. In other words, family background and genetics play a large role.

The fourth most important thing is that people with addictions often have other psychiatric problems (e.g. psychiatric disorders), which can complicate matters. Next, fifth, Sellman explains that addiction is characterized by frequent relapse, and that one should not expect to overcome addiction on the first try. The sixth point he makes is that the different forms of psychotherapy all produce similar results that may be based on what is common between them (i.e. a strong bond with a trusted friend). Sellman’s seventh most important thing about addiction is that ‘come back when you’re motivated’ is an inappropriate approach to addiction.  Individuals have very specific problems, and so it is important to find ways to engage the addicted individual (Sellman describes how empathy is crucial, for example). His next, eighth point expands on this idea: Sellman says that doctors should apply as broad an approach to the individual as possible. This means combining various rejuvenating approaches, includingprescription drugs, family therapy, social and legal support, providing accommodations, and more. The ninth important thing about addiction is that epiphanies are rare, even though they are the most popular kind of story to spread.

The tenth, and final important thing that Sellman explains is that change takes time (months or years of failing and trying again). He advocates for the importance of patience and persistence in practicing new behaviors over long periods of time. He concludes by appealing to all professionals involved in combating addiction; he asks that they all work together – because the combined knowledge of all fields is what is required.

According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), substance dependence is defined as:

When an individual persists in use of alcohol or other drugs despite problems related to use of the substance, substance dependence may be diagnosed. Compulsive and repetitive use may result in tolerance to the effect of the drug and withdrawal symptoms when use is reduced or stopped. This, along with Substance Abuse are considered Substance Use Disorders….

Substance dependence can be diagnosed with physiological dependence, evidence of tolerance or withdrawal, or without physiological dependence.

By the American Society of Addiction Medicine definition, drug addiction differs from drug dependence and drug tolerance.^[4] It is, both among scientists and other writers, quite usual to allow the concept of drug addiction to include persons who are not drug abusers according to the definition of the American Society of Addiction Medicine. The term drug addiction is then used as a category which may include the same persons who, under the DSM-IV, can be given the diagnosis of substance dependence or substance abuse. (See also DSM-IV Codes)

The terms abuse and addiction have been defined and re-defined over the years. The 1957 World Health Organization (WHO) Expert Committee on Addiction-Producing Drugs defined addiction and habituation as components of drug abuse:

Drug addiction is a state of periodic or chronic intoxication produced by the repeated consumption of a drug (natural or synthetic). Its characteristics include: (i) an overpowering desire or need (compulsion) to continue taking the drug and to obtain it by any means; (ii) a tendency to increase the dose; (iii) a psychic (psychological) and generally a physical dependence on the effects of the drug; and (iv) detrimental effects on the individual and on society.

Drug habituation (habit) is a condition resulting from the repeated consumption of a drug. Its characteristics include (i) a desire (but not a compulsion) to continue taking the drug for the sense of improved well-being which it engenders; (ii) little or no tendency to increase the dose; (iii) some degree of psychic dependence on the effect of the drug, but absence of physical dependence and hence of an abstinence syndrome [withdrawal], and (iv) detrimental effects, if any, primarily on the individual.

In 1964, a new WHO committee found these definitions to be inadequate, and suggested using the blanket term “drug dependence”:

The definition of addiction gained some acceptance, but confusion in the use of the terms addiction and habituation and misuse of the former continued. Further, the list of drugs abused increased iumber and diversity. These difficulties have become increasingly apparent and various attempts have been made to find a term that could be applied to drug abuse generally. The component in common appears to be dependence, whether psychic or physical or both. Hence, use of the term “drug dependence”, with a modifying phase linking it to a particular drug type in order to differentiate one class of drugs from another, had been given most careful consideration. The Expert Committee recommends substitution of the term “drug dependence” for the terms “drug addiction” and “drug habituation”.

The committee did not clearly define dependence, but did go on to clarify that there was a distinction between physical and psychological (“psychic”) dependence. It said that drug abuse was “a state of psychic dependence or physical dependence, or both, on a drug, arising in a person following administration of that drug on a periodic or continued basis.” Psychic dependence was defined as a state in which “there is a feeling of satisfaction and psychic drive that requires periodic or continuous administration of the drug to produce pleasure or to avoid discomfort” and all drugs were said to be capable of producing this state:

There is scarcely any agent which can be taken into the body to which some individuals will not get a reaction satisfactory or pleasurable to them, persuading them to continue its use even to the point of abuse – that is, to excessive or persistent use beyond medical need.

The 1957 and 1964 definitions of addiction, dependence and abuse persist to the present day in medical literature. It should be noted that at this time (2006) the Diagnostic Statistical Manual (DSM-IV-TR) now spells out specific criteria for defining abuse and dependence. (DSM-IV-TR) uses the term substance dependence instead of addiction; a maladaptive pattern of substance abuse, leading to clinically significant impairment or distress, as manifested by three (or more) specified criteria, occurring at any time in the same 12-month period. This definition is also applicable on drugs with smaller or nonexistent physical signs of withdrawal, e.g., cannabis.

In 2001, the American Academy of Pain Medicine, the American Pain Society, and the American Society of Addiction Medicine jointly issued “Definitions Related to the Use of Opioids for the Treatment of Pain”, which defined the following terms:

Addiction is a primary, chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterized by behaviors that include one or more of the following: impaired control over drug use, compulsive use, continued use despite harm, and craving.

Physical dependence is a state of being that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist.

Tolerance is the body’s physical adaptation to a drug: greater amounts of the drug are required over time to achieve the initial effect as the body “gets used to” and adapts to the intake.

Pseudo addiction is a term which has been used to describe patient behaviors that may occur when pain is undertreated. Patients with unrelieved pain may become focused on obtaining medications, may “clock watch,” and may otherwise seem inappropriately “drug seeking.” Even such behaviors as illicit drug use and deception can occur in the patient’s efforts to obtain relief. Pseudoaddiction can be distinguished from true addiction in that the behaviors resolve when pain is effectively treated.

A definition of addiction proposed by professor Nils Bejerot:

An emotional fixation (sentiment) acquired through learning, which intermittently or continually expresses itself in purposeful, stereotyped behavior with the character and force of a natural drive, aiming at a specific pleasure or the avoidance of a specific discomfort.

Drugs known to cause addiction include both legal and illegal drugs as well as prescription or over-the-counter drugs, according to the definition of the American Society of Addiction Medicine.

·         Stimulants (psychical addiction, moderate to severe; withdrawal is purely psychological and psychosomatic):

·         Amphetamine and methamphetamine

·         Cocaine

·         Caffeine

·         Nicotine

·         Sedatives and hypnotics (psychical addiction, mild to severe, and physiological addiction, severe; abrupt withdrawal may be fatal):

·         Alcohol

·         Barbiturates and glutethimide

·         Benzodiazepines, particularly alprazolam, flunitrazepam, triazolam, temazepam, and nimetazepam

·         Z-drugs like zopiclone have a similar effect in the body to benzodiazepines

·         Methaqualone and the related quinazolinone sedative-hypnotics

·         Opiate and opioid analgesics (psychical addiction, mild to severe, physiological addiction, mild to severe; abrupt withdrawal is unlikely to be fatal):

·         Morphine and codeine, the two naturally occurring opiate analgesics

·         Semi-synthetic opiates, such as heroin (diacetylmorphine; morphine diacetate), oxycodone, buprenorphine, and hydromorphone

·         Fully synthetic opioids, such as fentanyl, meperidine/pethidine, and methadone

Addictive drugs also include a large number of substrates that are currently considered to have no medical value and are not available over the counter or by prescription.

Several theories of drug addiction exist, some of the main ones being genetic predisposition, the self-medication theory, and factors involved with social/economic development. There are strong associations between poverty and addiction.^[6] It has long been established that genetic factors along with social and psychological factors are contributors to addiction. A common theory along these lines is the self-medication hypotheses. Epidemiological studies estimate that genetic factors account for 40–60% of the risk factors for alcoholism. Similar rates of heritability for other types of drug addiction have been indicated by other studies. Knestler hypothesized in 1964 that a gene or group of genes might contribute to predisposition to addiction in several ways. For example, altered levels of a normal protein due to environmental factors could then change the structure or functioning of specific brain circuits during development. These altered brain circuits could change the susceptibility of an individual to an initial drug use experience. In support of this hypothesis, animal studies have shown that environmental factors such as stress can affect an animal’s genotype.

Addictive potential

The addictive potential of a drug varies from substance to substance, and from individual to individual. Dose, frequency, pharmacokinetics of a particular substance, route of administration, and time are critical factors for developing a drug addiction.

An article in The Lancet compared the harm and addiction of 20 drugs, using a scale from 0 to 3 for physical addiction, psychological addiction, and pleasure to create a mean score for addiction. A caffeine control was not included in the study. Selected results can be seen in the chart below.

Drug	Mean	Pleasure	Psychological dependence	Physical dependence
Heroin	3.00	3.0	3.0	3.0
Cocaine	2.37	3.0	2.8	1.3
Alcohol	1.93	2.3	1.9	1.6
Barbiturates	2.01	2.0	2.2	1.8
Benzodiazepines	1.83	1.7	2.1	1.8
Amphetamine	1.67	2.0	1.9	1.1
Cannabis	1.51	1.9	1.7	0.8
Ecstasy	1.13	1.5	1.2	0.7
LSD	0.90	1.3	1.1	0.3

Self-medication hypotheses

Espoused by both psychoanalysts and biological researchers, self-medication hypotheses predict that certain individuals abuse drugs in an attempt to self-medicate their unique and seemingly intolerable states of mind. The self-medication theory has a long history. Freud in 1884, first raised this concept ioting the anti-depressing properties of cocaine. Stress has long been recognized as a major contributor for drug cravings and relapse and is therefore supportive of the self-medication theory. In line with this theory, a person’s use of a particular drug of choice is not an accident, but rather it is chosen for its pharmacological effect in relieving stressful symptoms or unwanted feelings. Research has shown that people who survive disasters are prone to stress-related disorders such as posttraumatic stress disorder (PTSD) and depression. People who experience major trauma in their life may self-medicate with alcohol or other drugs to relieve the symptoms of PTSD and depression.

Social development

Social development and adjustment factors also play a role in drug abuse and addiction. An assumption of the developmental perspective, as mentioned by Thornberry 1987, is that the course of one’s life is a process in which life circumstances change, milestones are met or missed and new social roles are created while old ones are abandoned. There are well known and widely accepted norms about when certain developmental events should happen in a person’s life. Studies of the social factors involved in drug use have mostly focused either on adolescence or young adulthood, but surprisingly a significant amount of cocaine users may not initiate use until middle adulthood. The majority of people enter into adult social roles on schedule. However, some people enter these roles earlier or later than their same-age peers. The developmental perspective predicts that this will lead to less than satisfactory adjustment and possibly negative consequences including drug and alcohol dependence.^[11]

Social pathology

Neuroscientist Carl Hart argues that the addictive power of drugs has been exaggerated and that interest in drugs diminishes markedly for both laboratory rats and people when “alternative reinforcers” of an “enriched environment” are offered to the subjects. Rather than addiction, poverty, and crime being inevitable consequences of drugs; drugs are more likely to be a consequence of poverty, and crime.

Researchers have conducted numerous investigations using animal models and functional brain imaging on humans in order to define the mechanisms underlying drug addiction in the brain. Changes to several areas of the brain are thought to be involved.

Acute effects

Acute (or recreational) use of most psychoactive drugs causes the release and prolonged action of dopamine and serotonin within the reward circuit. Different types of drugs produce these effects by different methods. Dopamine (DA) appears to harbor the largest effect and its action is characterized. DA binds to the D1 receptor, triggering a signaling cascade within the cell. cAMP-dependent protein kinase (PKA) phosphorylates cAMP response element binding protein (CREB), a transcription factor, which induces the transcription of certain genes including C-Fos.

Reward circuit

When examining the biological basis of drug addiction, one must first understand the pathways in which drugs act and how drugs can alter those pathways. The reward circuit, also referred to as the mesolimbic system, is characterized by the interaction of several areas of the brain.

·         The ventral tegmental area (VTA) consists of dopaminergic neurons which respond to glutamate. These cells respond when stimuli indicative of a reward are present. The VTA supports learning and sensitization development and releases dopamine (DA) into the forebrain. These neurons also project and release DA into the nucleus accumbens, through the mesolimbic pathway. Virtually all drugs causing drug addiction increase the dopamine release in the mesolimbic pathway,^[17] in addition to their specific effects.

·         The nucleus accumbens (NAcc) consists mainly of medium-spiny projectioeurons (MSNs), which are GABA neurons. The NAcc is associated with acquiring and eliciting conditioned behaviors and involved in the increased sensitivity to drugs as addiction progresses.

·         The prefrontal cortex, more specifically the anterior cingulate and orbitofrontal cortices, is important for the integration of information which contributes to whether a behavior will be elicited. It appears to be the area in which motivation originates and the salience of stimuli are determined.

·         The basolateral amygdala projects into the NAcc and is thought to be important for motivation as well.^[19]

·         More evidence is pointing towards the role of the hippocampus in drug addiction because of its importance in learning and memory. Much of this evidence stems from investigations manipulating cells in the hippocampus alters dopamine levels in NAcc and firing rates of VTA dopaminergic cells.

 

 Role of dopamine

Dopamine is the primary neurotransmitter of the reward circuit in the brain. It regulates movement, emotion, cognition, motivation, and feelings of pleasure. Natural rewards, like eating, as well as recreational drug use cause a release of dopamine, and are associated with the reinforcing nature of these stimuli.  Nearly all addictive drugs, directly or indirectly, act upon the brain’s reward system by flooding the circuit with dopamine. When addictive drugs are abused, dopamine release can be two to ten-fold over what is released under “normal” conditions. Since addictive drugs are perceived by the brain as being very rewarding, this can lead to repetitive behavior.

Individuals vulnerable to addiction (due to genetics, developmental or environmental factors) tend to use long-term. Long-term abuse of drugs results in repeated release of high amounts of dopamine, which in turn affects the reward circuit in multiple ways. Abnormally high levels of dopamine can block subsequent dopamine from binding and leave excess amounts of dopamine in the synapse. In turn, the bombardment of the receptors by dopamine results in a down regulation of the receptors. This is confirmed in PET imaging studies, which have found that drug addicts have reduced levels of dopamine receptors. The down regulation of receptors results in a decrease in the sensitivity to natural reinforcers. This is why individuals who are substance dependent lose interest iormal activities; these activities are no longer perceived as pleasurable. Long-term drug use also results in the individual feeling normal rather than high. In turn, drug abusers have to continuously increase the amount of drug they are using if they want to continue to feel normal or rewarded; this is referred to as tolerance.

Another affect of long-term use is the loss of control, and their ability to make sound decisions. Dopamine is also involved in the prediction of reward and may play a role in triggering cravings even to non-drug-related environmental stimuli.  Overall, continued use leads to dopamine tolerance, which alters the circuitry of the brain and the reward system leading to altered behavior. This can potentially lead to severely compromised long-term health and functioning of the person’s brain.

Inherent differences in the dopamine system between individuals may also increase the vulnerability of some to become and addict. Using PET imaging, it has been determined that individuals who already possess a reduced number of dopamine receptors are more likely to describe drug use as pleasurable than those who have more receptors.  So a high number of dopamine receptors may result in a natural aversion to drug use.

Stress response

In addition to the reward circuit, it is hypothesized that stress mechanisms also play a role in addiction. Koob and Kreek have hypothesized that during drug use, the corticotropin-releasing factor (CRF) activates the hypothalamic-pituitary-adrenal axis (HPA) and other stress systems in the extended amygdala. This activation influences the dysregulated emotional state associated with drug addiction. They have found that as drug use escalates, so does the presence of CRF in human cerebrospinal fluid (CSF). In rat models, the separate use of CRF antagonists and CRF receptor antagonists both decreased self-administration of the drug of study. Other studies in this review showed a dysregulation in other hormones associated with the HPA axis, including enkephalin which is an endogenous opioid peptide that regulates pain. It also appears that the µ-opioid receptor system, which enkephalin acts on, is influential in the reward system and can regulate the expression of stress hormones.

Behavior

Understanding how learning and behavior work in the reward circuit can help understand the action of addictive drugs. Drug addiction is characterized by strong, drug seeking behaviors in which the addict persistently craves and seeks out drugs, despite the knowledge of harmful consequences. Addictive drugs produce a reward, which is the euphoric feeling resulting from sustained dopamine concentrations in the synaptic cleft of neurons in the brain. Operant conditioning is exhibited in drug addicts as well as laboratory mice, rats, and primates; they are able to associate an action or behavior, in this case seeking out the drug, with a reward, which is the effect of the drug.  Evidence shows that this behavior is most likely a result of the synaptic changes which have occurred due to repeated drug exposure. The drug seeking behavior is induced by glutamatergic projections from the prefrontal cortex to the NAc. This idea is supported with data from experiments showing the drug seeking behavior can be prevented following the inhibition of AMPA glutamate receptors and glutamate release in the NAc.

Allostasis

Allostasis is the process of achieving stability through changes in behavior as well as physiological features. As a person progresses into drug addiction, he or she appears to enter a new allostatic state, defined as divergence from normal levels of change which persist in a chronic state. Addiction to drugs can cause damage to a brain and body as an organism enters the pathological state; the cost stemming from damage is known as allostatic load. The dysregulation of allostasis gradually occurs as the reward from the drug decreases and the ability to overcome the depressed state following drug use begins to decrease as well. The resulting allostatic load creates a constant state of depression relative to normal allostatic changes. What pushes this decrease is the propensity of drug users to take the drug before the brain and body have returned to original allostatic levels, producing a constant state of stress. Therefore, the presence of environmental stressors may induce stronger drug seeking behaviors.

Neuroplasticity

Neuroplasticity is the putative mechanism behind learning and memory. It involves physical changes in the synapses between two communicating neurons, characterized by increased gene expression, altered cell signaling, and the formation of new synapses between the communicating neurons. When addictive drugs are present in the system, they appear to hijack this mechanism in the reward system so that motivation is geared towards procuring the drug rather thaatural rewards. Depending on the history of drug use, excitatory synapses in the nucleus accumbens(NAcc) experience two types of neuroplasticity: long-term potentiation (LTP) and long-term depression (LTD). Using mice as a model, Kourrich et al. showed that chronic exposure to cocaine increases the strength of synapses in NAc after a 10–14 day withdrawal period, while strengthened synapses did not appear within a 24 hour withdrawal period after repeated cocaine exposure. A single dose of cocaine did not elicit any attributes of a strengthened synapse. When drug-experienced mice were challenged with one dose of cocaine, synaptic depression occurred. Therefore, it seems the history of cocaine exposure along with withdrawal times affects the direction of glutamatergic plasticity in the NAc.

Once a person has transitioned from drug use to addiction, behavior becomes completely geared towards seeking the drug, even though addicts report the euphoria is not as intense as it once was. Despite the differing actions of drugs during acute use, the final pathway of addiction is the same. Another aspect of drug addiction is a decreased response to normal biological stimuli, such as food, sex, and social interaction. Through functional brain imaging of patients addicted to cocaine, scientists have been able to visualize increased metabolic activity in the anterior cingulate and orbitofrontal cortex (areas of the prefrontal cortex) in the brain of these subjects. The hyperactivity of these areas of the brain in addicted subjects is involved in the more intense motivation to find the drug rather than seeking natural rewards, as well as an addict’s decreased ability to overcome this urge. Brain imaging has also shown cocaine-addicted subjects to have decreased activity, as compared to non-addicts, in their prefrontal cortex when presented with stimuli associated with natural rewards. The transition from recreational drug use to addiction occurs in gradual stages and is produced by the effect of the drug of choice on the neuroplasticity of the neurons found in the reward circuit. During events preceding addiction, cravings are produced by the release of dopamine (DA) in the prefrontal cortex. As a person transitions from drug use to addiction, the release of DA in the NAcc becomes unnecessary to produce cravings; rather, DA transmission decreases while increased metabolic activity in the orbitofrontal cortex contributes to cravings. At this time a person may experience the signs of depression if cocaine is not used. Before a person becomes addicted and exhibits drug-seeking behavior, there is a time period in which the neuroplasticity is reversible. Addiction occurs when drug-seeking behavior is exhibited and the vulnerability to relapse persists, despite prolonged withdrawal; these behavioral attributes are the result of neuroplastic changes which are brought about by repeated exposure to drugs and are relatively permanent.

The exact mechanism behind a drug molecule’s effect on synaptic plasticity is still unclear. However, neuroplasticity in glutamatergic projections seems to be a major result of repeated drug exposure. This type of synaptic plasticity results in LTP, which strengthens connections between two neurons; onset of this occurs quickly and the result is constant. In addition to glutamatergic neurons, dopaminergic neurons present in the VTA respond to glutamate and may be recruited earliest during neural adaptations caused by repeated drug exposure. As shown by Kourrich, et al., history of drug exposure and the time of withdrawal from last exposure appear to play an important role in the direction of plasticity in the neurons of the reward system.^[An aspect of neuron development that may also play a part in drug-induced neuroplasticity is the presence of axon guidance molecules such as semaphorins and ephrins. After repeated cocaine treatment, altered expression (increase or decrease dependent on the type of molecule) of mRNA coding for axon guidance molecules occurred in rats. This may contribute to the alterations in the reward circuit characteristic of drug addiction.

Neurogenesis

Drug addiction also raises the issue of potential harmful effects on the development of new neurons in adults. Eisch and Harburg raise three new concepts they have extrapolated from the numerous recent studies on drug addiction. First, neurogenesis decreases as a result of repeated exposure to addictive drugs. A list of studies show that chronic use of opiates, psychostimulants, nicotine, and alcohol decrease neurogenesis in mice and rats. Second, this apparent decrease in neurogenesis seems to be independent of HPA axis activation. Environmental factors other than drug exposure such as age, stress and exercise, can also have an effect oeurogenesis by regulating the hypothalamic-pituitary-adrenal (HPA) axis. Mounting evidence suggests this for three reasons: small doses of opiates and psychostimulants increase corticosterone concentration in serum but with no effect of neurogenesis; although decreased neurogenesis is similar between self-administered and forced drug intake, activation of HPA axis is greater in self-administration subjects; and even after the inhibition of opiate induced increase of corticosterone, a decrease ieurogenesis occurred. These, of course, need to be investigated further. Last, addictive drugs appear to only affect proliferation in the subgranular zone (SGZ), rather than other areas associated with neurogenesis. The studies of drug use and neurogenesis may have implications on stem cell biology.

 

Psychological drug tolerance

The reward system is partly responsible for the psychological part of drug tolerance.

The CREB protein, a transcription factor activated by cyclic adenosine monophosphate (cAMP) immediately after a high, triggers genes that produce proteins such as dynorphin, which cuts off dopamine release and temporarily inhibits the reward circuit. In chronic drug users, a sustained activation of CREB thus forces a larger dose to be taken to reach the same effect. In addition it leaves the user feeling generally depressed and dissatisfied, and unable to find pleasure in previously enjoyable activities, often leading to a return to the drug for an additional “fix”.

A similar mechanism, interfering also with the dopamine system, but relying on a different transcription factor, CEBPB, has also been proposed. In this case dopamine release onto the nucleus accumbens neurons would trigger the increased synthesis of substance P which, in turn, would increase the dopamine synthesis in the VTA. The effect of this positive feedback is suggested to be dampened by repeated substance abuse.

Sensitization

Sensitization is the increase in sensitivity to a drug after prolonged use. The proteins delta FosB and regulator of G-protein Signaling 9-2 (RGS9-2) are thought to be involved:

A transcription factor, known as delta FosB, is thought to activate genes that, counter to the effects of CREB, actually increase the user’s sensitivity to the effects of the substance. Delta FosB slowly builds up with each exposure to the drug and remains activated for weeks after the last exposure—long after the effects of CREB have faded. The hypersensitivity that it causes is thought to be responsible for the intense cravings associated with drug addiction, and is often extended to even the peripheral cues of drug use, such as related behaviors or the sight of drug paraphernalia. There is some evidence that delta FosB even causes structural changes within the nucleus accumbens, which presumably helps to perpetuate the cravings, and may be responsible for the high incidence of relapses that occur in treated drug addicts.

Regulator of G-protein Signaling 9-2 (RGS9-2) has recently been the subject of several animal knockout studies. Animals lacking RGS9-2 appear to have increased sensitivity to dopamine receptor agonists such as cocaine and amphetamines; over-expression of RGS9-2 causes a lack of responsiveness to these same agonists. RGS9-2 is believed to catalyze inactivation of the G-protein coupled D2 receptor by enhancing the rate of GTP hydrolysis of the G alpha subunit which transmits signals into the interior of the cell.

Individual mechanisms of effect

The basic mechanisms by which different substances activate the reward system are as described above, but vary slightly among drug classes.

Depressants

Depressants such as alcohol, barbiturates, and benzodiazepines work by increasing the affinity of the GABA receptor for its ligand; GABA. Narcotics such as morphine and heroin work by mimicking endorphins—chemicals produced naturally by the body which have effects similar to dopamine—or by disabling the neurons that normally inhibit the release of dopamine in the reward system. These substances (sometimes called “downers”) typically facilitate relaxation and pain relief.

Stimulants

Stimulants such as amphetamines, nicotine, and cocaine increase dopamine signaling in the reward system either by directly stimulating its release, or by blocking its absorption (see “Reuptake“). These substances (sometimes called “uppers”) typically cause heightened alertness and energy. They cause a pleasant feeling in the body and euphoria, known as a high. Once this high wears off, the user may feel depressed. This makes them want another dose of the drug, and can worsen the addiction.

Addiction is a complex but treatable disease. It is characterized by compulsive drug craving, seeking, and use that persists even if the user is aware of severe adverse consequences. For some people, addiction becomes chronic, having periodic relapses even after long periods of abstinence. As a chronic, relapsing disease, addiction may require continued treatments to increase the intervals between relapses and diminish their intensity. While some with substance issues recover and lead fulfilling lives, others require ongoing additional support. The ultimate goal of addiction treatment is to enable an individual to manage their substance misuse; for some this may mean abstinence. Immediate goals are often to reduce substance abuse, improve the patient’s ability to function, and minimize the medical and social complications of substance abuse and their addiction this is called Harm Reduction.

Treatments for addiction vary widely according to the types of drugs involved, amount of drugs used, duration of the drug addiction, medical complications and the social needs of the individual. Determining the best type of recovery program for an addicted person depends on a number of factors, including: personality, drug(s) of choice, concept of spirituality or religion, mental or physical illness, and local availability and affordability of programs.

Many different ideas circulate regarding what is considered a “successful” outcome in the recovery from addiction. Programs that emphasize controlled drinking exist for alcohol addiction. Opiate replacement therapy has been a medical standard of treatment for opioid addiction for many years.

Treatments and attitudes toward addiction vary widely among different countries. In the USA and developing countries, the goal of commissioners of treatment for drug dependence is generally total abstinence from all drugs. Other countries, particularly in Europe, argue the aims of treatment for drug dependence are more complex, with treatment aims including reduction in use to the point that drug use no longer interferes with normal activities such as work and family commitments; shifting the addict away from more dangerous routes of drug administration such as injecting to safer routes such as oral administration; reduction in crime committed by drug addicts; and treatment of other comorbid conditions such as AIDS, hepatitis and mental health disorders. These kinds of outcomes can be achieved without eliminating drug use completely. Drug treatment programs in Europe often report more favourable outcomes than those in the USA because the criteria for measuring success are functional rather than abstinence-based. The supporters of programs with total abstinence from drugs as a goal believe that enabling further drug use just means prolonged drug use and risks an increase in addiction and complications from addiction.

It is occasionally sometimes difficult to convince people with substance dependencies to engage in any form of treatment. Family Interventions have been highly successful in helping these people accept help they need.

 

Residential

Residential drug treatment can be broadly divided into two camps: 12 step programs or Therapeutic Communities. 12 step programs have the advantage of coming with an instant social support network, though some find the spiritual context not to their taste. In the UK drug treatment is generally moving towards a more integrated approach with rehabs offering a variety of approaches. These other programs may use a Cognitive-Behavioral Therapy approach, such asSMART Recovery, that looks at the relationship between thoughts, feelings and behaviors, recognizing that a change in any of these areas can affect the whole. CBT sees addiction as a behavior rather than a disease and subsequently curable, or rather, unlearnable. CBT programs recognize that for some individuals controlled use is a more realistic possibility.

One of many recovery methods is the 12 step recovery program, with prominent examples including Alcoholics Anonymous, Narcotics Anonymous, Drug Addicts Anonymous and Pills Anonymous. They are commonly known and used for a variety of addictions for the individual addicted and the family of the individual. Substance-abuse rehabilitation (or “rehab”) centers offer a residential treatment program for some of more seriously addicted in order to isolate the patient from drugs and interactions with other users and dealers. Outpatient clinics usually offer a combination of individual counseling and group counseling. Frequently a physician or psychiatrist will assist, with prescriptions, the side effects of the addiction. Medications can help immensely with anxiety and insomnia, can treat underlying mental disorders (cf. Self-medication hypothesis, Khantzian 1997) such as (manic-)depression, and can help reduce or eliminate withdrawal symptomology when withdrawing from physiologically addictive drugs. Some examples are using benzodiazepines for alcohol detoxification, which prevents delirium tremens and complications; using a slow taper ofbenzodiazepines or a taper of phenobarbital, sometimes including another antiepileptic agent such as gabapentin, pregabalin, or valproate, for withdrawal from barbiturates or benzodiazepines; using drugs such as baclofen to reduce cravings and propensity for relapse amongst addicts to any drug, especially effective in stimulant users, and alcoholics (in which it is nearly as effective as benzodiazepines in preventing complications); using clonidine, abenzodiazepine, and loperamide for opioid detoxification, for first-time users or those who wish to attempt an abstinence-based recovery (90% of opioid users relapse to active addiction within 8 months and/or are “multiple relapse patients”); or replacing an opioid that is interfering with or destructive to a user’s life, such as illicitly-obtained heroin, Dilaudid, or oxycodone, with an opioid that can be administered legally, reduces or eliminates drug cravings, and does not produce a high, such as methadone or buprenorphine – opioid replacement therapy – which is the gold standard for treatment of opioid dependence in developed countries, reducing the risk and cost to both user and society more effectively than any other treatment modality (for opioid dependence), and shows the best short-term and long-term gains for the user, with the greatest longevity, least risk of fatality, greatest quality of life, and lowest risk of relapse and/or legal issues including arrest and incarceration.

In a survey of treatment providers from three separate institutions (the National Association of Alcoholism and Drug Abuse Counselors, Rational Recovery Systems and the Society of Psychologists in Addictive Behaviors) measuring the treatment provider’s responses on the Spiritual Belief Scale (a scale measuring belief in the four spiritual characteristics AA identified by Ernest Kurtz); the scores were found to explain 41% of the variance in the treatment provider’s responses on the Addiction Belief Scale (a scale measuring adherence to the disease model or the free-will model addiction).

Anti-addictive drugs

Other forms of treatment include replacement drugs such as suboxone/subutex (both containing the active ingredient buprenorphine),and methadone, and all are used as substitutes for illicit opiate drugs. Although these drugs perpetuate physical dependence, the goal of opiate maintenance is to provide a clinically supervised, stable dose of a particular opioid in order to provide a measure of control to both pain and cravings. This provides a chance for the addict to functioormally and to reduce the negative consequences associated with obtaining sufficient quantities of controlled substances illicitly, by both reducing opioid cravings and withdrawal symptomology. Once a prescribed dosage is stabilized, treatment enters maintenance or tapering phases. In the United States, opiate replacement therapy is tightly regulated in methadone clinics and under the DATA 2000 legislation. In some countries, other opioid derivatives such as levomethadyl acetate,  dihydrocodeine, dihydroetorphine and even heroin are used as substitute drugs for illegal street opiates, with different drugs being used depending on the needs of the individual patient. Baclofen has been shown successful in attenuating cravings for most drugs of abuse – stimulants, ethanol, and opioids – and also attenuates the actual withdrawal syndrome of ethanol. Many patients have stated they “became indifferent to alcohol” or “indifferent to cocaine” overnight after starting baclofen therapy. It is possible that one of the best, albeit relatively unexplored, treatment modalities for opioid addiction – notoriously the most difficult addiction to treat (and to recover from), having relapse rates of around 60% at four weeks and 97% at twelve months if not on maintenance therapy with a mu-opioid agonist – would be to combine an opioid maintenance agent, such as methadone or buprenorphine, to block withdrawal symptomology, with baclofen, to attenuate cravings and the desire to use, in people who find that they are still using or still craving drugs while on methadone or buprenorphine maintenance.

Substitute drugs for other forms of drug dependence have historically been less successful than opioid substitute treatment, but some limited success has been seen with drugs such as dextroamphetamine to treat stimulant addiction, and clomethiazole to treat alcohol addiction. 

Bromocriptine and desipramine have been reported to be effective for treatment of cocaine but not amphetamine addiction.

Other pharmacological treatments for alcohol addiction include drugs like naltrexone, disulfiram, acamprosate and topiramate, but rather than substituting for alcohol, these drugs are intended to reduce the desire to drink, either by directly reducing cravings as with acamprosate and topiramate, or by producing unpleasant effects when alcohol is consumed, as with disulfiram. These drugs can be effective if treatment is maintained, but compliance can be an issue as alcoholic patients often forget to take their medication, or discontinue use because of excessive side effects. Additional drugs acting on glutamate neurotransmission such as modafinil, lamotrigine, gabapentin andmemantine have also been proposed for use in treating addiction to alcohol and other drugs.

Opioid antagonists such as naltrexone and nalmefene have also been used successfully in the treatment of alcohol addiction, which is often particularly challenging to treat. Some have also attempted to use these drugs for maintenance treatment of former opiate addicts with little success. They cannot be started until the patient has been abstinent for an extended period – unlikely with opioid addicts who are not on maintenance with a full or partial mu-opioid agonist – or they will trigger acute opioid withdrawal symptoms. No study has found them to be efficacious treatments in preventing relapse. They do nothing to block craving, and block endorphin and enkephalin, two natural neurotransmitters that regulate one’s sense of well-being. An addict must discontinue the drug for just eighteen hours in order to use again.

Treatment of stimulant addiction can often be difficult, with substitute drugs often being ineffective, although newer drugs such as nocaine, vanoxerine and modafinil may have more promise in this area, as well as the GABA_B agonist baclofen. Another strategy that has recently been successfully trialled used a combination of the benzodiazepine antagonist flumazenil with hydroxyzine and gabapentin for the treatment of methamphetamine addiction.

Another area in which drug treatment has been widely used is in the treatment of nicotine addiction. Various drugs have been used for this purpose such as bupropion, mecamylamine and the more recently developed varenicline. The cannaboinoid antagonist rimonabant has also been trialled for treatment of nicotine addiction but has not been widely adopted for this purpose.

Ibogaine is a hallucinogen (psychotomimetic) that some claim interrupts addiction and reduces or eliminates withdrawal syndromes, specifically in regards to opioids. Its mechanism of action is unknown, but likely linked to nAchR α3ß4 antagonism. In one animal trial, it was shown to slightly reduce self-administration of cocaine.  Another uncontrolled trial showed it reduced tremor by a mild to moderate degree during morphine withdrawal in rats. These finding caot be extrapolated to human beings with any certainty. Research is complicated by the fact that ibogaine is illegal in many developed countries, and a Schedule I substance in the US, and as a result no controlled human trials have ever been performed. A semi-synthetic analogue of ibogaine, 18-methoxycoronaridine was developed, in an attempt to reduce the toxic (ibogaine is significantly cardiotoxic, and several deaths have been reported from its use; because of its illegal, underground nature, it is impossible to know how toxic the drug is) and psychotomimetic effects of the drug.

Behavioral programming

Behavioral programming is considered critical to helping those with addictions achieve abstinence. From the applied behavior analysis literature and the behavioral psychology literature several evidenced based intervention programs have emerged (1) behavioral marital therapy; (2) community reinforcement approach; (3) cue exposure therapy; and (4) contingency management strategies. In addition, the same author suggest that Social skills training adjunctive to inpatient treatment of alcohol dependence is probably efficacious. Community reinforcement has both efficacy and effectiveness data.^[89] In addition, behavioral treatment such as community reinforcement and family training (CRAFT) have helped family members to get their loved ones into treatment.

Alternative therapies

Alternative therapies, such as acupuncture, are used by some practitioners to alleviate the symptoms of drug addiction. In 1997, the American Medical Association (AMA) adopted as policy the following statement after a report on a number of alternative therapies including acupuncture:

There is little evidence to confirm the safety or efficacy of most alternative therapies. Much of the information currently known about these therapies makes it clear that many have not been shown to be efficacious. Well-designed, stringently controlled research should be done to evaluate the efficacy of alternative therapies.

Acupuncture has been shown to be no more effective than control treatments in the treatment of opiate dependence. Acupuncture, acupressure, laser therapy and electrostimulation have no demonstrated efficacy for smoking cessation.

Important phases in treating substance dependence include establishing coping mechanisms to deal with the hardships of withdrawal symptoms. Additionally, precautions should be established with the patient to avoid relapse by designing a treatment plan around the patients lifestyle. With the correct approaches, the patient can live a healthier life.

Online websites have been a resource to aid in helping people to overcome addictions. These websites act as ways for struggling addicts, family members of addicts, and people who are in the recovery stage to confide in each other (anonymously if they so choose). They provide an alternative way for these people to seek help, support and information. Sites typically include chat rooms, forums, and blogs for members to interact.

Background on Substance Dependence from an Evolutionary Perspective

Psychoactive drugs activate the reward circuit (see “Reward Circuit” above) in the brain, which simulates an increase in fitness level. Continued drug use puts humans at risk for drug dependence, because their reward circuit has evolved to seek out an increase in fitness level due to subsequent increases in reproduction. Given this predisposition, social context can trigger substance overuse. Drug use can replace typical adaptive behaviors that active the reward system, leading to substance dependence.

An evolutionary link between social relationships and drug abuse has been supported. Drugs hijack the reward circuit in the brain that may originally have been selected for, due to the benefits of pair bonding. There is activity in both cortical and subcortical regions of the brain when a person views a picture of a rejected lover and when a person uses cocaine. The angular gyrus has also been associated with both romantic love and cigarette cravings. Further evidence supports that the reward circuit in the brain evolved to reinforce social relationships that aid in survival. Selection has favored traits that lead to fitness benefits in subordinate individuals because they typically comprise the majority of a group. Social relationships are highly beneficial for subordinate individuals, and abused substances mimic these rewarding relationships in the brain. Evidence shows that those dependent on drugs often personify substances they are abusing, thus supporting this theory.

An evolutionary perspective may enlighten the heritability of alcohol dependence. An association between the dopamine receptor D2 gene and alcoholism supports a genetic predisposition for alcoholism. To date, no adaptive purpose for this has been found. There is an association between low rates of alcoholism in Asian populations and a single gene nucleotide change slowing the rate of alcohol breakdown.  Speculation on this correlation suggests this single gene nucleotide change may be an adaptation against alcoholism.

Addiction as the Result of an Evolutionary Mismatch

Substance dependence is hypothesized to be a result of an evolutionary mismatch between the environment to which human hominin ancestors adapted (typically referred to as the environment of evolutionary adaptedness or EEA) and the current environment. Evidence suggests it was unlikely that prevalence of psychoactive substances was high enough in the EEA to exert selective pressures. Thus, psychoactive substances in the current environment hijack the reward circuit in the brain adapted to reinforce certain behaviors. These behaviors activate pleasure systems in the brain that reinforce their fitness benefits. Through repeated usage, drugs displace other rewards, and the reward circuit cao longer distinguish between the positive and negative effects of rewards.

The mismatch theory has been explored specifically for alcoholism. Alcoholics exhibit traits that are beneficial in some environments but are serious risk factors for alcohol abuse in a modern context. Type 1 alcoholism results from abusing alcohol to relieve anxiety. In another context, anxiety leading to reward-seeking behavior could be adaptive. For instance, anxiety leads primate infants to stay close to their mothers who provide protection and food. Type 2 alcoholism results from antisocial behavior and impulsivity. When food is scarce, solitary behavior can be favored because an individual can forage independently and receive more resources. Impulsivity can be favored because it allows access to food and mates, which other less impulsive individuals will not seek out.  Aggressive behavior often results from impulsivity in type 2 alcoholics. In a physically competitive environment, aggression could be beneficial. These traits are mismatched for our modern environment, however, and function instead as risk factors for alcoholism.

The self-perceived survival ability and reproductive fitness (SPFit) theory is a corollary of the mismatch theory. This theory posits that drugs mimic self-perceived power and sexual attractiveness. Since power and sexual attractiveness are basic qualities that lead to reproductive success, drugs are likely to be abused. The distinction between the SPFit theory and other mismatch theories is that other theories highlight pleasure-seeking in addiction, while the SPFit theory states that pleasure is not a significant enough motivator to outweigh the fitness costs of addiction. Power and sexual attractiveness are qualities directly awarded by reproductive success, making them strong enough motivators to lead to substance dependence.

Addiction as the Result of Coevolution with Psychoactive Substances

Conflicting research posits that hominins evolved with psychoactive substances, and this coevolution has led to the evolution of pleasure responses from these substances. Natural psychoactive drugs induce pleasure responses in humans due to human chemical-ecological adaptations to counteract the effects of plant chemical defense mechanisms. Specific examples of human adaptations to counter plant toxins include liver enzymes, tasting food, olfaction, and vomiting. Humans, chimpanzees, and monkeys have utilized eating earth substances like soil as a method for detoxification. There is also evidence of plant adaptations specifically for human consumption. Some psychoactive drugs target human pathogens. For instance, tobacco leaves and nicotine extract can be used to fight helminth infections in livestock. Plants have also evolved chemicals that mimic humaeurotransmitters. These examples imply that humans coevolved with psychoactive substances.

“Coevolution theories” are compatible with mismatch theories in that psychoactive drugs are able to hijack the reward circuit in the brain, leading to vulnerability for substance dependence.

Reconciliation of Theories

Coevolution and mismatch theories are not mutually exclusive. Humans may have evolved with natural psychoactive substances, but modern psychoactive substances, such as heroin, are far more potent than those likely found in the EEA. Thus, many modern drugs can still be considered the result of an evolutionary mismatch.

“Primate Frugivory Theory,” Overturned

It was proposed that alcoholism originated from a primate frugivore adaption to locate fruit through the smell of ethanol. Additionally, the association of ethanol with nutritional benefits from the fruit would favor ethanol consumption. Subsequent studies found that ethanol is not present in high enough concentrations in ripe fruit to act as a selective pressure for excessive alcohol consumption behavior. Ripe fruit was also preferred by frugivores over rotting fruit, despite a higher ethanol content in rotting fruit. These findings overturned this primate frugivore theory.

Evolutionary Perspectives on Vulnerability to Addiction

Psychoactive drugs hijack systems evolved to reward an increase in fitness. Fitness is crucial to survival and reproduction, so it is unlikely the negative effects of substance dependence will act as a strong enough selective pressure to alter the reward circuit.

An evolutionary perspective can also explain why certain groups in the population are more prone to addiction than others.  Impulsivity and risky behaviors are only rewarded when reproductive prospects seem unlikely. This predicts that young men will be most prone to impulsive behaviors like substance abuse because competition for mates and resources is highest at that time. These rates of substance abuse in males should decrease with age as men generally start families and must invest in their offspring’s success As reproductive competition in human females does not vary significantly, there should be fewer impulsive behaviors, like substance abuse, in females because it is more beneficial for them to invest in long-term reproductive success.

Substance abuse variation can also be predicted by environmental differences. Impulsivity is only favored in dangerous and unpredictable environments, so it follows substance abuse will be more likely to occur in these environments.

Relevance of the Evolutionary Perspective to Treatment and Prevention

The evolutionary perspective can help show reasons for substance dependence. This can help therapists address the roots of substance dependence issues with their patients and develop long-term solutions.  For instance, the SPFit theory proposes psychoactive substances increase self-perceived levels of fitness. Therapists using an evolutionary perspective can evaluate what the abuser is seeking when he or she abuses substances, and work towards fixing underlying problems in their patients’ lives.

An evolutionary perspective supports that stopping drug use is the first step of effective treatment. These drugs must also be replaced by natural rewards, like friendship, evoking positive feelings. Because drug use is so heavily tied to emotion, harboring positive emotions should be considered essential, rather than supplementary, to treatment. Recognizing that substance abuse is tied to the evolution of brain systems that are meant to reward social relationships can also influence new methods of treatment.  Those who abuse substances often personify addictive substances, and treatment that encourages disentangling oneself from a harmful relationship with substance abuse may help. This is already evident in Alcoholics Anonymous as they encourage gaining control over alcohol.

Anticipating that adolescents, particularly adolescent males, are especially prone to drug abuse can be used to provide programs for these adolescents to direct them towards natural stimuli and away from potentially addictive substances. This is especially true for adolescents in marginalized populations, as their environment is more likely to foster impulsive behaviors. Overall awareness of these risks can aid in the design of better preventative measures.

Legislation

Depending on the jurisdiction, addictive drugs may be legal, legal only as part of a government sponsored study, illegal to use for any purpose, illegal to sell, or even illegal to merely possess.

Most countries have legislation which brings various drugs and drug-like substances under the control of licensing systems. Typically this legislation covers any or all of the opiates, amphetamines, cannabinoids, cocaine, barbiturates, benzodiazepines, anesthetics, hallucinogenics, derivatives and a variety of more modern synthetic drugs. Unlicensed production, supply or possession is a criminal offence.

Usually, however, drug classification under such legislation is not related simply to addictiveness. The substances covered often have very different addictive properties. Some are highly prone to cause physical dependency, while others rarely cause any form of compulsive need whatsoever. Also, under legislation specifically about drugs, alcohol, caffeine and nicotine are not usually included.

Although the legislation may be justifiable on moral or public health grounds, it can make addiction or dependency a much more serious issue for the individual: reliable supplies of a drug become difficult to secure, and the individual becomes vulnerable to both criminal abuse and legal punishment.

It is unclear whether laws against illegal drug use do anything to stem usage and dependency. In jurisdictions where addictive drugs are illegal, they are generally supplied by drug dealers, who are often involved with organized crime. Even though the cost of producing most illegal addictive substances is very low, their illegality combined with the addict’s need permits the seller to command a premium price, often hundreds of times the production cost. As a result, addicts sometimes turn to crime to support their habit.

From Wikipedia, the free encyclopedia

Substance abuse
Classification and external resources
Comparison of the perceived harm for various psychoactive drugs from a poll among medical psychiatrists specialized in addiction treatment.
ICD–10	F10.1-F19.1
ICD–9	305
DiseasesDB	3961
MedlinePlus	001945
MeSH	D019966

Substance abuse, also known as drug abuse, is a patterned use of a substance (drug) in which the user consumes the substance in amounts or with methods neither approved nor supervised by medical professionals. Substance abuse/drug abuse is not limited to mood-altering or psycho-active drugs. If an activity is performed using the objects against the rules and policies of the matter (as in steroids for performance enhancement in sports), it is also called substance abuse. Therefore, mood-altering and psychoactive substances are not the only types of drugs abused. Using illicit drugs – narcotics, stimulants, depressants (sedatives), hallucinogens, cannabis, even glues and paints, are also considered to be classified as drug/substance abuse. Substance abuse often includes problems with impulse control and impulsive behaviour.

The term “drug abuse” does not exclude dependency, but is otherwise used in a similar manner ionmedical contexts. The terms have a huge range of definitions related to taking apsychoactive drug or performance enhancing drug for a non-therapeutic or non-medical effect. All of these definitions imply a negative judgment of the drug use in question (compare with the term responsible drug use for alternative views). Some of the drugs most often associated with this term include alcohol, amphetamines, barbiturates, benzodiazepines (particularlyalprazolam, lorazepam, and clonazepam), cocaine, methaqualone, and opioids. Use of these drugs may lead to criminal penalty in addition to possible physical, social, and psychological harm, both strongly depending on local jurisdiction. There are many cases in which criminal or antisocial behavior occur when the person is under the influence of a drug. Long term personality changes in individuals may occur as well. Other definitions of drug abuse fall into four main categories: public health definitions, mass communication and vernacular usage, medical definitions, and political and criminal justice definitions. Substance abuse is prevalent with an estimated 120 million users of hard drugs such as cocaine, heroin, and other synthetic drugs.

Substance abuse is a form of substance-related disorder.

Public health definitions

Source: A Public Health Approach to Drug Control in Canada, Health Officers Council of British Columbia, 2005

Public health practitioners have sometimes defined substance use from a broader perspective than the individual, emphasizing the role of society, culture, and availability. Rather than accepting the loaded terms alcohol or drug “abuse,” many public health professionals have adopted phrases such as “substance and alcohol type problems” or “harmful/problematic use” of drugs.

The Health Officers Council of British Columbia — in their 2005 policy discussion paper, A Public Health Approach to Drug Control in Canada — has adopted a public health model of psychoactive substance use that challenges the simplistic black-and-white construction of the binary (or complementary) antonyms “use” vs. “abuse”. This model explicitly recognizes a spectrum of use, ranging from beneficial use to chronic dependence (see diagram to the right).

 

Medical definitions

In the modern medical profession, the three most used diagnostic tools in the world, the American Psychiatric Association‘s Diagnostic and Statistical Manual of Mental Disorders (DSM),theWorld Health Organization‘s International Statistical Classification of Diseases and ICRIS Medical organization Related Health Problems (ICD), no longer recognize ‘drug abuse’ as a current medical diagnosis. Instead, DSM has adopted substance abuse as a blanket term to include drug abuse and other things. ICD refrains from using either substance abuse or drug abuse, instead using the term “harmful use” to cover physical or psychological harm to the user from use. Physical dependence, abuse of, and withdrawal from drugs and other miscellaneous substances is outlined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) ). Its section Substance dependence begins with:

Substance dependence When an individual persists in use of alcohol or other drugs despite problems related to use of the substance, substance dependence may be diagnosed. Compulsive and repetitive use may result in tolerance to the effect of the drug and withdrawal symptoms when use is reduced or stopped. These, along with Substance Abuse are considered Substance Use Disorders…

However, other definitions differ; they may entail psychological or physical dependence, and may focus on treatment and prevention in terms of the social consequences of substance uses.

 

Drug misuse

Legal drugs are not necessarily safer. A study in 2010 asked drug-harm experts to rank various illegal and legal drugs. Alcohol was found to be the most dangerous by far.

Drug misuse is a term used commonly for prescription medications with clinical efficacy but abuse potential and known adverse effects linked to improper use, such as psychiatric medications with sedative, anxiolytic, analgesic, or stimulant properties. Prescription misuse has been variably and inconsistently defined based on drug prescription status, the uses that occur without a prescription, intentional use to achieve intoxicating effects, route of administration, co-ingestion with alcohol, and the presence or absence of abuse or dependence symptoms. Tolerance relates to the pharmacological property of substances in which chronic use leads to a change in the central nervous system, meaning that more of the substance is needed in order to produce desired effects. Stopping or reducing the use of this substance would cause withdrawal symptoms to occur.

The rate of prescription drug abuse is fast overtaking illegal drug abuse in the United States. According to the National Institute of Drug Abuse, 7 million people were taking prescription drugs for nonmedical use in 2010. Among 12th graders, prescription drug misuse is now second only to cannabis. “Nearly 1 in 12 high school seniors reported nonmedical use of Vicodin; 1 in 20 reported abuse of OxyContin.”

Avenues of obtaining prescription drugs for misuse are varied: sharing between family and friends, illegally buying medications at school or work, and often “doctor shopping” to find multiple physicians to prescribe the same medication, without knowledge of other prescribers.

Increasingly, law enforcement is holding physicians responsible for prescribing controlled substances without fully establishing patient controls, such as a patient “drug contract.” Concerned physicians are educating themselves on how to identify medication-seeking behavior in their patients, and are becoming familiar with “red flags” that would alert them to potential prescription drug abuse.^[9]

 

 

Classification of Neurotic, Stress-Related and Somatoform Disorders (F40-F48)

F40   Phobic anxiety disorders 

F41   Other anxiety disorders       

F42   Obsessive-compulsive disorder 

F43   Reaction to severe stress, and adjustment disorders      

F44   Dissociative [conversion] disorders 

F45   Somatoform disorders         

F48   Other neurotic disorders

 

Normal anxiety is a normal response to an abnormal situation (anxiety at being threatened by a mugger). Pathological anxiety is an abnormal response to a normal situation (anxiety at needing to leave the home).

In agoraphobia, social and specific phobias, anxiety is evoked predominantly by certain well-defined situations or objects, which are external to the individual and are not currently dangerous. As a result, these situations or objects are characteristically avoided or endured with dread.

Phobic anxiety fluctuates from mild uneasy to terror. The individual’s concern may focus on individual symptoms such as palpitations or feeling faint and is often associated with secondary fears of dying, losing control, or going mad. The anxiety is not relieved by the knowledge that other people do not regard the situation in question as dangerous or threatening.

 

Classification of Phobic anxiety disorders.

F40.0          Agoraphobia 

F40.1          Social phobias 

F40.2          Specific (isolated) phobias 

F40.8          Other phobic anxiety disorders 

F40.9          Phobic anxiety disorder, unspecified

 

Agoraphobia

Agoraphobia includes various phobias embracing fears of leaving home: fears of entering shops, crowds, and public places, or of traveling alone in trains, buses, underground or planes. The lack of an immediately available exit is one of the key features of many agoraphobic situations. The avoidance behaviour causes sometimes that the sufferer becomes completely housebound.

Most sufferers are women. Onset – early adult life. The lifetime prevalence – between 5—7%. High co-morbidity with panic disorder; depressive and obsessional symptoms and social phobias may be also present.

Social Phobias

Fear of scrutiny by other people in comparatively small groups leading to avoidance of social situations, restricted to eating in public, to be introduced to other people, to public speaking, or to encounters with the opposite sex, diffuse – social situations outside the family circle. Direct eye-to-eye confrontation may be stressful.

The most common clinical features of social phobias are:

Low self-esteem and fear of criticism.

Symptoms may progress to panic attacks.

Avoidance – almost complete social isolation.

Usually start in childhood or adolescence.

Estimation of lifetime prevalence – between 10-13 %.

It is equally common in both sexes.

Secondary alcoholism.

Specific (Isolated) Phobias

Usually arise in childhood or early adult life and can persist for decades if they remain untreated. Lifetime prevalence – between 10-20%.

There are tree clusters:

1.     Fears of proximity to particular animals:

·        spiders (arachnophobia)

·        insects (entomophobia)

·        snakes (ophidiophobia)

2.     Fears of specific situations such as

·        heights (acrophobia)

·        thunder (keraunophobia)

·        darkness (nyctophobia)

·        closed spaces (claustrophobia)

3.     Fears of diseases, injuries or medical examinations:

·        visiting a dentist

·        the sight of blood (hemophobia) or injury (pain —odynophobia)

·        the fear of exposure to venereal diseases (syphilidophobia) or AIDS-phobia.

Specific phobias

As briefly mentioned above, a specific phobia is a marked and persistent fear of an object or situation which brings about an excessive or unreasonable fear when in the presence of, or anticipating, a specific object; furthermore, the specific phobias may also include concerns with losing control, panicking, and fainting which is the direct result of an encounter with the phobia. The important distinction from social phobias are specific phobias are defined in regards to objects or situations whereas social phobias emphasizes more on social fear and the evaluations that might accompany them.

The DSM breaks specific phobias into five subtypes: Animal, Natural Environment, Blood-Injection-Injury, Situational, and Other. In children, phobias involving Animals, Natural Environment (darkness), and Blood-Injection-Injury usually develop between the ages of 7 and 9, and these are reflective of normal development. Additionally, specific phobias are most prevalent in children between ages 10 and 13.

Diagnosis

The diagnostic criteria for 300.29 Specific Phobias as outlined by the DSM-IV-TR:

1.               Marked and persistent fear that is excessive or unreasonable, cued by the presence or anticipation of a specific object or situation (e.g., flying, heights, animals, receiving an injection, seeing blood).

2.               Exposure to the phobic stimulus almost invariably provokes an immediate anxiety response, which may take the form of a situationally bound or situationally predisposed panic attack. Note: In children, the anxiety may be expressed by crying, tantrums, freezing, or clinging.

3.               The person recognizes that the fear is excessive or unreasonable. Note: In children, this feature may be absent.

4.               The phobic situation(s) is avoided or else is endured with intense anxiety or distress.

5.               The avoidance, anxious anticipation or distress in the feared situation(s) interferes significantly with the person’s normal routine, occupational (or academic) functioning, or social activities or relationships, or there is marked distress about having the phobia.

6.               In individuals under the age of 18, the duration is at least 6 months.

7.               The anxiety, panic attack, or phobic avoidance associated with the specific object or situation are not better accounted for by another mental disorder, such as Obsessive-Compulsive Disorder (e.g., fear of dirt in someone with an obsession about contamination), Posttraumatic Stress Disorder (e.g., avoidance of stimuli associated with a severe stressor), Separation Anxiety Disorder (e.g., avoidance of school), Social Phobia (e.g., avoidance of social situations because of fear of embarrassment), Panic Disorder With Agoraphobia, or Agoraphobia Without History of Panic Disorder.

Social phobia

The key difference between specific phobias and social phobias is social phobias include fear of public situations and scrutiny which leads to embarrassment or humiliation in the diagnostic criteria. In social phobias, there is also a generalized category which is included as a specifier below. Unlike specific phobias which may develop before the age of 10, social phobias are typically not present until pubertal transition. After this transition, the prevalence of social phobia increases with age. Many adolescents who develop a social phobia consequentially become rejected by their peers. As interpersonal dysfunction is a risk factor for depression, there are some negative outcomes for adolescents with social phobia. For example, about 20% of adolescents diagnosed with a social phobia also suffer from depression and use alcohol or other substances.

Diagnosis

The diagnostic criteria for 300.23 Social Phobia as outlined by the DSM-IV-TR:

1.               A marked and persistent fear of one or more social or performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others. The individual fears that he or she will act in a way (or show anxiety symptoms) that will be humiliating or embarrassing. Note: In children there must be evidence of the capacity for age-appropriate social relationships with familiar people and the anxiety must occur in peer settings, not just in interactions with adults.

2.               Exposure to the feared social situation almost invariably provokes anxiety, which may take the form of a situationally bound or situationally predisposed panic attack. Note: In children the anxiety may be expressed by crying, tantrums, freezing, or shrinking from social situations with unfamiliar people.

3.               The person recognized that the fear is excessive or unreasonable. Note: In children this feature may be absent.

4.               The feared social or performance situations are avoided or else are endured with intense anxiety or distress.

5.               The avoidance, anxious anticipation, or distress in the feared social or performance situation(s) interferes significantly with the person’s normal routine, occupational (academic) functioning, or social activities or relationships, or there is marked distress about having the phobia.

6.               In individuals under age 18, the duration is at least 6 months.

7.               The avoidance is not due to the direct physiological effects of a substance (e.g. a drug of abuse, a medication) or a general medical condition and is not better accounted for by another mental disorder (e.g. Panic Disorder With or Without Agoraphobia, Separation Anxiety Disorder, Body Dysmorphic Disorder, a Pervasive Developmental Disorder, Schizoid Personality Disorder).

8.               If a general medical condition or another mental disorder is present, the fear in Criterion A (Exposure to the social or performance situation almost invariably provokes an immediate anxiety response) is unrelated to it, e.g., the fear is not of Stuttering, trembling in Parkinson’s disease, or exhibiting abnormal eating behavior in Anorexia Nervosa or Bulimia Nervosa.

Specify if:

Generalized: if the fears include most social situations (also consider the additional diagnosis of Avoidant Personality Disorder).

Etiology

Environmental

Much of the progress in understanding the acquisition of fear responses in phobias can be attributed to the Pavlovian Model which is synonymous with Classical Conditioning. Myers and Davis (2007) describe the acquisition of fear as when a conditioned stimulus (e.g., a distinctive place) is paired with an aversive unconditioned stimulus (e.g. a electric shock) to an end result in which the subject exhibits a conditioned feared response to the distinctive place (CS+UCS=CR). For how this model works in the context of phobias, one simply has to look at the fear of heights, or acrophobia. In this phobia, the CS is heights such as the top floors of a high rise building or a roller coaster. The UCS can be said to originate from an aversive or traumatizing event in the person’s life such as being trapped on a roller coaster as a child or in an elevator at the top floor of a building. The result of combining these two stimuli leads to a new association called the CR (fear of heights) which is simply the CS (heights) transformed by the aversive UCS (being trapped on a roller coaster or elevator) leading to the feared conditioned response. This model does not suggest that once you have a conditioned feared response to an object or situation you have a phobia. As listed above, to meet the criteria for being diagnosed with a phobia one also has to show symptoms of impairment and avoidance. In the example above, for the CR to be classified as a phobia it would have to exhibit signs of impairment due to avoidance. Impairment, which can be considered along the same lines as a disability from a clinician’s standpoint, is defined as being unable to complete tasks in one’s daily life whether it be occupational, academical, or social. In the recent example, an impairment of occupation could result from not taking on a job solely because its location happens to be at the top floor of a building, or socially not participating in a social event at a theme park. The avoidance aspect is defined as behavior that results in the omission of an aversive event that would otherwise occur with the goal of the preventing anxiety. The above direct conditioning model, though very influential in the theory of fear acquisition, should not suggest the only way to acquire a phobia. Rachman proposed three main pathways to acquire fear conditioning involving direct conditioning, vicarious acquisition and informational/instructional acquisition.

As experimentation with the aforementioned direct conditioning modeling continued, it became increasingly evident that more than just classical conditioning can influence the onset of a phobia. Rachman (1978) proposed that vicarious acquisition was a critical component to the etiology of phobias, so it was decided to include information and instruction from the parent and family members to better understand its onset. Of the research conducted in this area, one of the best examples of how vicarious conditioning, more specifically modeling, effects the acquisition of a phobia can be said to have come from Cook & Mineka’s (1989) work on rhesus monkeys. In this experiment, Cook & Mineka, through the use of video, appraised 22 rhesus monkeys on their fear to evolutionary relevant stimuli (e.g. crocodiles and snakes), and evolutionary irrelevant stimuli (e.g. flowers and artificial rabbits) to see if fear conditioning using the direct conditioning model (Pavlov’s model) leads to fear acquisition (or more specifically the conditioned fear response). The results of the research showed that after 12 sessions the rhesus monkeys acquired a fear to the evolutionary relevant stimuli and not to the evolutionary irrelevant stimuli; furthermore, the experiment also revealed that when they exposed monkeys to other monkeys that interacted with snakes without showing fear, this group did not acquire the fear which supports the theory of vicarious conditioning through modeling. According to Pavlov’s theory of classical conditioning, the experimenters should have been able to condition a feared response within the rhesus monkeys to the evolutionary irrelevant stimuli because the Pavlovian model posits that any UCS can elicit a CR. The result show the necessary augmentation of the Pavlov model with the vicarious acquisition model.

Evolutionary

The circumstance that specific phobias tend to be directed disproportionately against certain objects such as snakes and spiders may have evolutionary explanations. In this view phobias are adaptations that may have been useful in the ancestral environment. On the savanna, unlike dangers such as large predators, snakes and spiders tend to be hidden from view until very close and may be a particular danger to infants and small children, favoring the development of an instinctive fearful response. This view does not necessarily hold that phobias are genetically inevitable. Instead, there may be a genetic predisposition to learn to fear certain things more easily than other things.

Similarly, primary agoraphobia may be due to its once having been evolutionary advantageous to avoid exposed, large open spaces without cover or concealment. Generalized social phobia may be due to its once being usually very dangerous to be confronted by a large group of staring, non-kin, unknown, and not smiling strangers.

Sexual dimorphism, with women having much higher incidence of phobias than men, may be a result of selection during the Mesozoic (mammalian) period reflecting the higher cost to progeny of the loss of nursing females compared to “expendable” males.

Treatments

Various methods are claimed to treat phobias. Their proposed benefits may vary from person to person.

Some therapists use virtual reality or imagery exercise to desensitize patients to the feared entity. These are parts of systematic desensitization therapy.

Cognitive behavioral therapy (CBT) can be beneficial. Cognitive behavioral therapy allows the patient to challenge dysfunctional thoughts or beliefs by being mindful of their own feelings with the aim that the patient will realize their fear is irrational. CBT may be conducted in a group setting. Gradual desensitisation treatment and CBT are often successful, provided the patient is willing to endure some discomfort. In one clinical trial, 90% of patients were observed with no longer having a phobic reaction after successful CBT treatment.

CBT is also an effective treatment for phobias in children and adolescents, and it has been adapted to be appropriate for use with this age. One example of a CBT program targeted towards children is the Coping Cat. This treatment program can be used with children between the ages of 7 and 13 to treat social phobia. This program works to decrease negative thinking, increase problem solving, and to provide a functional coping outlook in the child. Another CBT program was developed by Ann Marie Albano to treat social phobia in adolescents. This program has five stages: Psychoeducation, Skill Building, Problem Solving, Exposure, and Generalization and Maintenance. Psycho education focuses on identifying and understanding symptoms. Skill Building focuses on learning cognitive restructuring, social skills, and problem solving skills. Problem Solving focuses on identifying problems and using a proactive approach to solving them. Exposure involves exposing the adolescent to social situations in a hierarchical approach. Finally, Generalization and Maintenance involves practicing the skills learned.

Eye Movement Desensitization and Reprocessing (EMDR) has been demonstrated in peer-reviewed clinical trials to be effective in treating some phobias. Mainly used to treat Post-traumatic stress disorder, EMDR has been demonstrated as effective in easing phobia symptoms following a specific trauma, such as a fear of dogs following a dog bite.

Hypnotherapy coupled with Neuro-linguistic programming can also be used to help remove the associations that trigger a phobic reaction.^[34] However, lack of research and scientific testing compromises its status as an effective treatment.

Antidepressant medications such SSRIs, MAOIs may be helpful in some cases of phobia. Benzodiazepines may be useful in acute treatment of severe symptoms but the risk benefit ratio is against their long-term use in phobic disorders.

There are also new pharmacological approaches, which target learning and memory processes that occur during psychotherapy. For example, it has been shown that glucocorticoids can enhance extinction-based psychotherapy.

Emotional Freedom Technique, a psychotherapeutic alternative medicine tool, also considered to be pseudoscience by the mainstream medicine, is allegedly useful.

Another method psychologists and psychiatrists use to treat patients with extreme phobias is prolonged exposure. Prolonged exposure is used in psychotherapy when the person with the phobia is exposed to the object of their fear over a long period of time. This technique is only tested when a person has overcome avoidance of or escape from the phobic object or situation. People with slight distress from their phobias usually do not need prolonged exposure to their fear.

For children and adolescents, one of the most effective treatments for specific phobias is participant modeling and reinforced practice. In this treatment method, the therapist models for the child how they should respond to their fears and then encourages the child to practice this behavior and reinforces their efforts.

These treatment options are not mutually exclusive. Often a therapist will suggest multiple treatments.

Hypnosis

Hypnosis is a process to get the individual into a relaxed state of mind, where the brainwaves slow down and the subconscious mind can be engaged. It is a focused state of relaxation. When it comes to treatment, agoraphobic patients tend to be highly resistant, therefore its up to the therapists to make important decision about the treatment programme and how to utilize the actions in order to effect change. The source of phobia tends to lie in the distant past and focuses on one or more traumatic event(s) in childhood. When using hypnoanalysis in hypnosis, the patient is encouraged to re-experience the traumatic events, but this must be done with care at all times. When using hypnosis it is recommended to employ a dissociative technique during the process: this might include, for example, the patient watching a younger version of themselves or watching a film or seeing a reflection. It is essential that the therapist should provide the patient with the opportunity to integrate the present with the past, traumatic experience and that the purpose of the hypnosis should be to help learn from the events and to become stronger as a result.

The psychodynamic psychotherapy at the beginning of each session is used to encourage the recall of stimuli in the hypnoanalysis. In the following weeks, the patient will recall several memories in the past, which would illustrate the roots of the phobia. Over a number of sessions, the patient will be encouraged to express these feelings to their family members. Also, the patients continue to practice the vivo exposure tasks in which they make a significant improvement.

Sometimes these types of sessions can be done in groups instead of a one to one with the therapist. Patients like to be with others that are facing the same situation so they join a support group. One of the steps for the therapist is to focus on reducing the panic attacks without the use of medication. Hypnosis was introduced as an extension to mediation, and patents were gradually able to respond adequately well to the therapist’s suggestions. During hypnosis the patient is given an ego strengthening to provide with the ability to function. For example, those who suffer from agoraphobic the therapist would provide the patient the ability function out of the house, and, using guided imagery, the patient began by sitting in the car, and worked towards on just driving around. This process of systematic desensitization was slow. Whenever the patient became anxious, the patient would raised their finger and were able to reduce their anxiety by taking deep breaths. These particular exercises were taped and were practiced religiously at home. As a result of all the work done in the consulting room, watching the tapes at home, and with continued support patients made a significant recovery.

 

Other Anxiety Disorders

F41.0          Panic disorder (episodic paroxysmal anxiety)

F41.1          Generalized anxiety disorder 

F41.2          Mixed anxiety and depressive disorder 

F41.3          Other mixed anxiety disorders 

F41.8          Other specified anxiety disorders 

F41.9          Anxiety disorder, unspecified

Manifestations of anxiety are also the major symptoms of these disorders, however, it is not restricted to any particular environmental situation.

 

Panic Disorder

The term panic comes from the Greek god, Pan. He was the god of flocks, music, sensuality and sexuality. He was also the god of panic and nightmares, and took pleasure in frightening (panicking) people and animals in the woods.

The essential features are recurrent attacks of severe anxiety (panic attacks) which are not restricted to any particular situation or set of circumstances.

Typical symptoms are palpitations, chest pain, choking sensations, dizziness, and feelings of unreality (depersonalisation or derealization). Individual attacks usually last for minutes only. The frequency of attacks varies substantially. Frequent and predictable panic attacks produce fear of being alone or going into public places. The afflicted persons used to think that they got a serious somatic disease.

The course of panic disorder is long-lasting and is complicated with various comorbidities, in half of the cases with agoraphobia. The estimation of lifetime prevalence moves between 1-3%.

DIFFERENTIAL DIAGNOSIS

Panic attacks may be seen in simple phobia, social phobia, posttraumatic stress disorder, and obsessive-compulsive disorder. In these disorders, however, the panic attacks are precipitated. For example, if the simple phobic has to approach a snake, the social phobic public speaking, the posttraumatic patient a situation reminiscent of the original trauma, or the obsessive-compulsive patient a contaminated object, a severe panic attack may indeed occur. If, however, these patients can avoid the stimuli, there are no panic attacks. In such cases a separate diagnosis of panic disorder is not made.

Occasionally an otherwise normal individual experiences a spontaneous panic attack; to qualify, however, for a diagnosis of panic disorder, the attacks must be either severe enough to cause marked distress or be frequent, occurring generally once a month or more.

Panic attacks are also seen with some frequency in patients suffering from a depressive episode either as part of major depression or bipolar disorder. In some cases the panic attacks may actually predate the onset of the depressive symptoms, and when they are concurrent with depressive symptoms, no relationship between them and the severity of the depressive symptoms is evident. In such cases a separate panic disorder is occurring in addition to the depressive disorder, and consequently, two diagnoses are given.

A number of conditions may produce symptomatic episodes that may very closely resemble panic attacks, thus engendering some diagnostic confusion (see the box on this page). Usually, however, certain differential points allow a correct diagnosis.

Parkinson’s disease is associated with panic attacks when patients are treated with levodopa and have a prominent “on-off” effect. Here, as the preceding dose of levodopa wears off and the parkinsonism worsens, patients may have a panic attack very similar to those seen in panic disorder.

Patients suffering a myocardial infarction or an attack of angina pectoris may complain of chest pain, dyspnea, nausea, diaphoresis, and often a sense of impending doom. Radiation of pain to the neck or arm is not an infallibly reliable diagnostic point, since this may also occur during a panic attack. The general medical setting of the illness is often diagnostically helpful. Clearly, if the patient is elderly, with known cardiac disease or multiple coronary risk factors, one might lean toward a diagnosis of myocardial insufficiency. Conversely, if the patient is young, with no risk factors, one might be inclined toward a diagnosis of panic disorder, especially with a history of numerous prior identical attacks.

At the moment of lodgment of a relatively large pulmonary embolus, patients may have a sudden onset of chest discomfort, dyspnea, nausea, diaphoresis, and significant anxiety, thus presenting a clinical picture quite similar to a panic attack. The dispro­portionate emphasis on dyspnea relative to other symptoms is a helpful diagnostic point for pulmonary embolus. Likewise, hemoptysis or wheezing point immediately to the correct diagnosis; however, these latter two symptoms are ofteot present. As is the case with myocardial ischemia, the setting of the illness may be a helpful point. Prolonged immobilization, thrombophlebitis or cardiac failure would make one’s index of suspicion higher for pulmonary embolus, especially if this were a first episode.

Paroxysmal supraventricular tachycardia (SVT), also known as paroxysmal atrial tachycardia, occasionally may cause diagnostic problems because the patient may become quite anxious during an attack of tachycardia. Two diagnostic points strongly suggest SVT: first, a hyperacute onset (often less than a second) and, second, the ability of the patient to terminate the attack by a Valsalva maneuver. Holter monitoring will help establish the diagnosis; however, it is important to utilize “event monitoring” so that the episode is not missed.

Simple partial seizures may occasionally be characterized by a panic attack. Clues to this diagnosis include not only the occurrence, at other times, of other seizure types (e.g., grand mal or complex partial) but also the exquisitely paroxysmal nature of the ictal panic attack: whereas panic attacks in panic disorder take minutes to crescendo, the ictal anxiety peaks within seconds. An EEG may or may not be helpful in such cases, as it may be normal even while the patient is having the seizure.

A minority of patients with pheochromocytoma have paroxysmal attacks that very closely resemble panic attacks. Typically, though, in contrast to patients with panic attacks, these patients have a prominent headache. Furthermore, hypertension is always present during the attack and is often also present between the attacks. Furthermore, although paroxysms in pheochromocytoma may occur spontaneously, at times they are precipitated by abdominal compression or micturition, factors that clearly distinguish them from panic attacks.

Mastocytosis may present with episodes of light-headedness, palpitations, headaches, dyspnea, chest pain, and nausea. Though these episodes, in these respects, are similar to panic attacks, certain points suggest the correct diagnosis. Patients with mastocytosis almost always experience intense flushing during the episode. Interestingly, though this can be profound, they rarely complain of it and must be questioned directly about the presence or absence of flushing. Furthermore, after the attack most patients experience profound lethargy to the point of prostration, which may last for days or longer. Such post-attack prostration is not seen after a panic attack. Finally, physical examination generally reveals

Conditions that may Produce Symptomatic Episodes that Resemble Panic Attacks

Parkinson’s disease

Myocardial infarction

Angina pectoris Supraventricular tachycardia Pulmonary embolus

Simple partial seizures

Hypoglycemia

Pheochromocytoma

Mastocytosis

Carcinoid syndrome

urticaria pigmentosa, although not all patients with mastocytosis have this.

 

Carcinoid syndrome is often included in the differential diagnosis of panic attacks, but it would appear difficult to confuse the two. The flushing and diarrhea that are hallmarks of the carcinoid syndrome are relatively minor in a panic attack.

Certain other disorders are often included on the differential diagnosis for panic disorder, including hyperthyroidism, certain drug intoxications, and certain drug withdrawals; however, the anxiety seen in these disorders is generally not paroxysmal. The anxiety of hyperthyroidism may wax and wane, but is not episodic. Drugs such as caffeine, cocaine, amphetamines and various over-the-counter sympathomimetics may produce an episode of anxiety, but, unless the durg is injected intravenously or taken by inhalation, the onset is usually gradual. Withdrawal from alcohol, benzodiazepines or other sedative-hypnotics is often accompanied by anxiety which may at times undergo an episodic surge similar to a panic attack. In such cases, these “attacks” subside with abstinence.

TREATMENT

The goal of treatment in panic disorder is twofold: to prevent future attacks and to relieve anticipatory anxiety and enable patients to velcome any avoidance behavior they may have developed. Both cognitive-behavioral treatment and medication have a role; Dedications are discussed first.

When initiating pharmacologic treatment one must impress on he patient the fact that, short of intravenous medication, probably othing is available that reliably aborts an attack once it has begun, and that therefore the thrust of drug treatment is to prevent future attacks.

Once the patient has decided on prophylactic treatment, the step is to select the prophylactic agent best suited for the patient. Two groups of medicines provide effective prophylaxis: benzodiazepines and most of the currently available anti-depressants. Which group to choose has been the subject of intense debate. Buspirone is not effective.

Four benzodiazepines are clearly effective: alprazolam, lorazepam and diazepam. The benzodiazepines offer in advantages. They have a rapid onset of action, generally few. The total daily dose is gradually titrated up until symptoms are controlled: alprazolam may be started at from 0.75 to 1.5 mg, with most patients respond- to doses of from 1.5 to 6 mg; comparable figures for donazepam are 0.5 to 1.5 mg to start, titrating to from 1.0 to 4.0 mg, for lorazepam 1 to 2 mg to start, titrating to from 2 to 6 mg, and for diazepam 4 to 10 mg to start, titrating to from 10 to 60 mg. Alprazolam, if given in the extended-release formulation, may be given once daily; otherwise the total daily dose must be divided into three or more administrations; clonazepam and diazepam are generally given in two divided doses.

Given the risk of neuroadaptation with benzodiazepines, many clinicians prefer to start with an antidepressant, choosing an SSRI, tricyclic or MAOI. The SSRIs are generally better tolerated than the tricyclics, and the MAOIs, though undoubtedly effective, are generally held in reserve given their side-effect profile and dietary requirements. Regardless of which antidepressant is chosen it is generally prudent to start with a low dose: although in most cases a full “antidepressant” dose is required, starting at or near such a dose often precipitates either agitation or a “flurry” of panic attacks, and consequently one should begin with a dose from one-tenth to one-third of the “full” dose, followed by an upward titration, in similar increments, every week or so. Importantly, although most patients do indeed both tolerate and require a titration to a “full dose” there is a small minority of patients who do not tolerate more than a small amount but yet do get a good anti-panic effect from it. Unfortunately, one cannot as yet tell prospectively which patients will have this sort of response. Once an optimum dose has been reached, a response may not be seen for weeks, and a full response may be delayed for up to 3 months. Given this potentially long delayed response, many clinicians will begin treatment with a combination of a benzodiazepine and an SSRI (e.g., clonazepam and sertraline) and then taper off the benzodiazepine once the SSRI has had a chance to become effective.

Among the SSRIs, the following (with their average doses) have been shown to be effective in double-blinded studies: paroxetine (40 mg), fluoxetine (20 mg), fluvoxamine (150 mg), citalopram (20 mg), escitalopram (10 mg) and sertraline. In the case of sertraline, it appears that any dose between 50 and 200 mg is effective.

Of the tricyclics, imipramine, in doses of 150 to 200 mg, although effective, and indeed the “gold standard,” is generally poorly tolerated over the long haul. Nortriptyline, in doses of from 50 to 150 mg, desipramine, in doses of from 150 to 200 mg, and clomipramine, in doses of from 50 to 150 mg, are alternatives.

Of the MAOIs, phenelzine, in doses of 30 to 90 mg, is effective. Two other reversible MAOIs, not yet available in the United States, are also effective, namely brofaromine and moclobemide.

Other medications that may be considered include propranolol and inositol. Propranolol, in total daily doses of roughly 180 mg, may be effective, but the clinical impression is that it is less reliably so than a benzodiazepine or an antidepressant. Inositol is an isomer of glucose which serves as a precursor for inositol, an intracellular “second messenger”: remarkably, in a double-blinded comparison, with doses of roughly 6000 mg bid, it was more effective than fluvoxamine. Clearly, this is very promising, and bears watching for replication.

Response to medical treatment is usually quite good. Many patients become completely free of panic attacks. However, a large percentage continue to have attacks, albeit much less frequently and of much less severity.

Cognitive-behavior therapy, used either independently or in conjunction with medical treatment, should also be considered, especially in light of the fact that in addition to reducing the frequency of panic attacks, it is also an effective treatment for agoraphobia.