Substance-Related Disorders

1. Substance Use Overview

●​ Many people have tried alcohol, tobacco, or other drugs.

●​ Substance use is not always pathological; it becomes disordered when it leads to
impairment or harmful consequences.

2. Definitions

●​ Substance Abuse: Excessive use leading to hazardous behavior or persistent life

problems.
●​ Substance Dependence: More severe, involves tolerance and/or withdrawal.
●​ Tolerance: Needing more of a substance for the same effect.
●​ Withdrawal: Physical/mental symptoms when not using the substance.

3. Psychoactive Substances (affect CNS):

●​ Legal (e.g., alcohol, nicotine), medical (e.g., barbiturates), and illegal (e.g., heroin,
Ecstasy).

4. Alcohol Use Disorder (AUD)

●​ WHO prefers terms like "harmful use of alcohol" over "alcoholism."

●​ Binge drinking = 6+ drinks on one occasion, once/month.
●​ Alcohol use has a long history across cultures.

5. Prevalence & Demographics

●​ 13% of Americans have experienced alcohol abuse; ~5% dependence.

●​ 52.2% of Americans 12+ reported drinking in the past 30 days.
●​ High risk of injury, violence, cognitive and health problems.
●​ Affects all social classes and professions.
●​ Workplace alcohol use is notable.
●​ Men historically more affected, but gender gap is narrowing.
●​ Higher rates in Native Americans; lower in Asian Americans.
●​ 10% of men over 65 are heavy drinkers.

6. Comorbidity:

●​ 37% of alcohol abusers have another mental disorder.

●​ Common with depression, eating disorders, personality disorders, and suicide.
●​
7. Misconceptions (From Table 11.1):

●​ Alcohol is both a stimulant and depressant.

●​ Judgment can be impaired before signs of drunkenness.
●​ Mixing drinks doesn't increase intoxication—blood alcohol level does.
●​ Coffee, cold showers, or exercise don’t sober you up.
●​ Alcohol is addictive like heroin and can cause severe withdrawal.
●​ Not everyone drinks—many are abstainers.

DSM-5 outlines Alcohol Use Disorder (AUD) as a problematic pattern of alcohol use leading to
clinically significant impairment or distress, shown by at least two of the following 11 symptoms
within a 12-month period:

1. Alcohol is taken in larger amounts or over longer periods than intended.

2. Persistent desire or unsuccessful efforts to cut down or control alcohol use.

3. A lot of time is spent obtaining, using, or recovering from alcohol.

4. Craving or a strong urge to drink alcohol.

5. Failure to fulfill major role obligations at work, school, or home due to alcohol use.

6. Continued use despite social or interpersonal problems caused by alcohol.

7. Important activities (social, occupational, recreational) are given up or reduced.

8. Physically hazardous use, like drinking and driving.

9. Continued use despite knowing it causes or worsens a physical or psychological problem.

10. Tolerance, shown by needing more alcohol or getting less effect from the same amount.

11. Withdrawal symptoms or using alcohol (or similar substances) to relieve them.

These symptoms reflect behavioral, psychological, and physiological aspects of alcohol use.
The severity of the disorder is categorized as mild (2–3 symptoms), moderate (4–5 symptoms),
or severe (6 or more symptoms).

Mnemonic: "CUT DOWN THAT SIP"

Each letter stands for one criterion:

C - Cut down attempts fail

U - Use more/longer than intended
T-Time spent using/recovering

D - Desire or craving
O - Obligations not met
W - Withdrawal symptoms or avoidance
N- Neglect activities (social, work, fun)

T - Tolerance developed
H - Hazardous use
A - Awareness of harm, but continued use
S - Social/interpersonal problems continue

Clinical Picture of Alcohol-Related Disorders

Alcohol is a psychoactive substance that affects both the brain and body. People may drink
alcohol occasionally without major problems, but when alcohol use becomes excessive or
frequent, it can lead to serious health, psychological, and social consequences.

1. Effects on the Brain and Behavior

Alcohol primarily acts as a depressant on the central nervous system. When a person
consumes alcohol:

●​ At lower levels, it produces a sense of relaxation and well-being by stimulating the

brain’s "pleasure areas." People may feel more sociable, talkative, and confident.
●​ At higher levels, alcohol slows down brain activity. It inhibits a neurotransmitter called
glutamate, which plays an important role in learning, memory, and brain alertness. This
results in poor coordination, slowed reactions, impaired judgment, and decreased
self-control.
●​ Chronic use of alcohol can lead to long-term brain damage and changes in behavior and
thinking.

2. Physical Effects of Alcohol

●​ Intoxication begins when blood alcohol levels reach around 0.08%. This level can be
reached quickly, especially when drinking on an empty stomach or consuming large
amounts in a short time.
●​ Hangovers often occur the next day and include symptoms like headache, nausea,
dizziness, and sensitivity to light and sound. These result from dehydration, low blood
sugar, and toxic substances produced during alcohol breakdown.
●​ Tolerance develops with regular use, meaning the person needs to drink more to feel the
same effects.
 ●​ Withdrawal symptoms may appear if the person suddenly stops drinking after regular
use. These symptoms include sweating, shaking, anxiety, and in severe cases, seizures.

3. Long-Term Health Effects

Chronic or heavy alcohol use can lead to serious health conditions:

●​ Liver damage: Long-term drinking can cause fatty liver, hepatitis, and eventually
cirrhosis, which is the permanent scarring of liver tissue.
●​ Digestive problems: Alcohol irritates the stomach lining and can lead to ulcers, acid
reflux, and damage to the pancreas.
●​ Malnutrition: Alcohol interferes with the body’s ability to absorb nutrients, leading to
vitamin deficiencies, especially vitamin B1 (thiamine).
●​ Heart problems: Increased risk of high blood pressure, irregular heartbeat, and heart
disease.
●​ Brain damage: Prolonged alcohol use can shrink brain tissue and affect cognitive
functioning, especially in memory and problem-solving.

4. Psychological and Social Consequences

People with alcohol-related disorders often face emotional, mental, and social difficulties:

●​ Fatigue and depression are common, as alcohol disrupts sleep and brain chemistry.
●​ Personality changes such as irritability, aggression, and withdrawal from social life may
occur.
●​ Relationship issues: Frequent alcohol use can lead to conflicts with family and friends,
domestic violence, and neglect of responsibilities.
●​ Occupational problems: Poor performance at work or school, absenteeism, and even job
loss are often reported.

5. Severe Forms of Alcohol-Related Disorders

There are two serious conditions associated with long-term alcohol abuse:

●​ Alcohol Withdrawal Delirium (Delirium Tremens): This occurs in people who stop
drinking suddenly after heavy use. Symptoms include confusion, disorientation, vivid
hallucinations (especially of animals or insects), extreme fear, tremors, sweating, and
high blood pressure. If untreated, this condition can be life-threatening.
●​ Alcohol Amnestic Disorder (Korsakoff’s Syndrome): This condition is caused by a
deficiency of thiamine (vitamin B1) due to poor nutrition and long-term alcohol use. The
person may have severe memory problems, be unable to learn new information, and fill
in memory gaps with made-up stories (confabulation). With early treatment, especially
vitamin B1 supplements, some improvement is possible.
1. Biological Causal Factors:

The biological aspects of alcohol dependence are primarily linked to how alcohol affects the
brain and an individual’s genetic makeup.

a. Neurobiology of Addiction:
●​ Alcohol, like many other substances, has the ability to activate the brain's
mesocorticolimbic dopamine pathway (MCLP). This pathway is often referred to as the
brain's reward system because it is responsible for feelings of pleasure, reinforcement,
and motivation. The pathway involves several key areas of the brain, such as:

○​ Ventral tegmental area (VTA): The origin point of dopamine neurons.

○​ Nucleus accumbens (NAcc): A key structure involved in reward and pleasure.
○​ Prefrontal cortex (PFC): This area of the brain helps with decision-making,
impulse control, and moderating behavior.

●​ When alcohol is consumed, it triggers the release of dopamine in this reward pathway,
leading to feelings of euphoria or pleasure. Over time, repeated alcohol use leads to
neuroplastic changes—the brain's adaptive response to the continued stimulation, which
results in tolerance (requiring more alcohol to achieve the same effect) and dependence
(feeling unable to function without alcohol).

b. Genetic Vulnerability:
●​ Research has shown that genetics plays a crucial role in determining an individual’s risk
for developing alcohol dependence. Studies have suggested that:
○​ Family History: Individuals with parents who struggle with alcohol dependence
are at a higher risk themselves. A study found that nearly one-third of alcoholics
had at least one parent with alcohol problems (Cotton, 1979).
○​ Genetic Predisposition: Certain genes that affect neurotransmitter systems (such
as dopamine and serotonin) can make individuals more susceptible to the
reinforcing effects of alcohol. For example, people who have a genetic
predisposition to lower levels of dopamine may seek out substances like alcohol
to compensate for this lack of pleasure or reward in daily life.
○​ Prealcoholic Personality: Studies have suggested that individuals who are
predisposed to alcoholism often display certain personality traits, such as
impulsivity, risk-taking behavior, and emotional instability. These traits are thought
to be both genetically influenced and learned over time.

c. Genetics and Learning Interaction

●​ While genetic factors provide an initial vulnerability, exposure to alcohol and other
environmental factors can significantly influence whether a person develops an alcohol
use disorder. For example:
 ○​ Environmental Exposure: In societies where alcohol is easily available,
individuals (especially young people) may be more likely to start drinking and,
over time, develop dependence. Peer pressure, family behavior, and the
normalization of drinking in social settings all play key roles.
○​ Conditioned Responses: People who have a genetic vulnerability may
experience stronger conditioned responses to alcohol-related cues (like the smell
of alcohol or certain social situations). These cues can trigger cravings or
drinking behavior, making it difficult to resist further use.

2. Psychosocial Causal Factors

Psychosocial factors are psychological and social influences that shape an individual's
relationship with alcohol.

a. Stress and Coping: For many individuals, alcohol becomes a means of coping with stress,
anxiety, depression, or trauma. This coping mechanism is maladaptive, as it offers temporary
relief while contributing to long-term problems. Some individuals may start drinking in response
to difficult life events (e.g., job loss, death of a loved one) or chronic stress, leading to a pattern
of alcohol use as a means of escape. Over time, these coping mechanisms can escalate into a
dependence on alcohol.

b. Personality Traits: Certain personality traits are strongly linked to an increased risk of
alcohol abuse. For example:

○​ Impulsivity: Impulsive individuals, who are quick to act without thinking of the
consequences, may be more likely to try alcohol at an early age and continue
drinking excessively.
○​ Emotional Instability: People who have trouble managing their emotions or who
experience frequent mood swings may use alcohol to regulate their emotional
state. Alcohol can provide a temporary escape from negative feelings, reinforcing
the behavior.
○​ Sensation-Seeking: Individuals who are inclined toward novelty and thrill-seeking
behaviors may be more likely to experiment with alcohol or engage in binge
drinking.

c. Family Dynamics and Early Environment: Family environment plays a pivotal role in the
development of alcohol use disorders. Children raised in homes where alcohol use is frequent
or where there is alcohol abuse may:

○​ Model drinking behaviors: If parents or caregivers regularly consume alcohol,

children may view drinking as a normal, acceptable behavior.
○​ Experience emotional neglect or trauma: Dysfunctional family environments,
such as those involving abuse, neglect, or high levels of conflict, can increase the
likelihood of using alcohol as a coping mechanism.
3. Sociocultural Causal Factors:

Sociocultural factors include societal and cultural influences on alcohol use and abuse.

a. Social Availability and Cultural Norms: The cultural acceptance of alcohol use is a major
sociocultural factor that influences drinking behavior. In cultures where alcohol is readily
available and socially encouraged (e.g., through celebrations, religious rituals, or socializing),
individuals may be more likely to drink excessively. Furthermore:

○​ Socialization: Young people are often introduced to alcohol by family or peers in

social settings. If drinking is normalized or celebrated in these contexts,
individuals may develop a habit of heavy drinking.
○​ Social Approval: In some cultures, excessive drinking is seen as a sign of
masculinity or social status. This societal endorsement can contribute to binge
drinking and dependence, especially among men.

b. Peer Pressure and Media Influence: Peer pressure, particularly in adolescence, can be a
significant factor in the initiation of alcohol use. Peer groups often act as influencers, and
individuals who seek to fit in may begin drinking to align with the group's behavior. Media
portrayals of alcohol also play a role:

●​ Advertising: Alcohol advertising often depicts drinking as glamorous or fun, leading

individuals, especially young people, to associate alcohol with positive experiences.
●​ Television and Movies: The portrayal of alcohol use in entertainment can normalize
excessive drinking, making it seem like a harmless or even desirable activity.

c. Economic and Legal Factors: The availability of alcohol in a given society is also influenced
by economic and legal factors. For instance, in countries or regions where alcohol is easily
accessible, cheaper, or less regulated, rates of alcohol abuse are typically higher. Conversely,
stricter alcohol laws and higher taxes can sometimes reduce excessive drinking, although
cultural attitudes may still play a role.

Conclusion:

In conclusion, alcohol abuse and dependence result from a complex interaction of biological,
psychosocial, and sociocultural factors. Biological factors, such as neurobiological changes and
genetic predispositions, create vulnerability to addiction. Psychosocial factors, including stress,
personality traits, and family dynamics, influence how individuals cope with life challenges and
may lead to alcohol use as a maladaptive coping strategy. Finally, sociocultural factors, such as
cultural norms, peer pressure, and media portrayal of drinking, shape societal attitudes toward
alcohol and affect individual drinking behaviors. Understanding the interplay of these factors is
crucial in addressing and preventing alcohol abuse and dependence.
The treatment of alcohol-related disorders is multifaceted, aiming at addressing the physical,
psychological, and social aspects of alcohol use. Here's an elaboration of the key components
involved:

Challenges in Treating Alcohol Use Disorders

●​ Denial and Resistance: A significant barrier in treatment is the denial many individuals
exhibit toward their alcohol abuse. This denial often continues until they hit "rock
bottom," and even then, treatment adherence can be problematic. Many individuals
leave treatment before it is completed.
●​ Relapse: Relapse is a common feature of alcohol abuse, and it’s considered a part of the
recovery process that needs to be addressed during therapy.

Key Treatment Objectives

●​ Detoxification: The first step is to rid the body of alcohol and manage withdrawal
symptoms.
●​ Physical Rehabilitation: Addressing the physical effects of alcohol abuse, such as organ
damage, nutritional deficiencies, and overall health.
●​ Behavioral Control: Helping individuals regain control over their drinking habits.
●​ Psychological Adaptation: Assisting the individual in realizing they can cope with life’s
challenges without resorting to alcohol.

Approaches to Treatment

1. Traditional Treatment Methods

●​ Abstinence is often the primary goal, though some programs focus on controlled
drinking. The goal is to reduce alcohol consumption without requiring total abstinence.
●​ Programs like Brief Motivational Interviewing (BMI) aim to provide information about the
consequences of alcohol use, challenging individuals to reflect on their drinking
behaviors and make informed decisions.

2. Biological Treatments

Medications are crucial in addressing both the psychological cravings for alcohol and the
physical symptoms of withdrawal:

●​ Disulfiram (Antabuse): Causes severe nausea and vomiting if alcohol is consumed,

serving as a deterrent. However, it’s not often used alone due to the risk of patients
discontinuing it once treatment ends.
●​ Naltrexone: Blocks the pleasurable effects of alcohol, reducing cravings and helping
individuals resist drinking.
 ●​ Acamprosate: Studies show it is effective in reducing heavy drinking, though more
research is needed.

3. Detoxification and Withdrawal

●​ The process of eliminating alcohol from the body is crucial in managing withdrawal
symptoms. Benzodiazepines (like Valium) help manage withdrawal symptoms, but
there's concern that they may become addictive themselves, transferring one
dependency for another.

Psychological Approaches

Once detoxification is completed, psychological interventions become essential:

1. Group Therapy:

●​ Effective for confronting and addressing the denial and avoidance often seen in
individuals with alcohol use disorders.
●​ Group settings help individuals realize the impact of their behavior and offer new
strategies for coping with their issues.

2. Family Therapy:

●​ Alcohol abuse often strains family relationships. Family therapy helps educate family
members about the consequences of alcohol use and facilitates improved
communication and support systems within the family.

3. Environmental Interventions:

●​ Treatment must address the individual’s social environment. Alcoholics often face social
isolation, unemployment, or a lack of social support. Halfway houses and community
resources play a key role in reintegration into society.

4. Behavioral and Cognitive-Behavioral Therapy (CBT):

●​ Aversive Conditioning: Pairs alcohol consumption with unpleasant stimuli (e.g., electric
shock, nausea) to create an aversion to drinking.
●​ CBT: Focuses on changing cognitive patterns and behaviors associated with alcohol
use. It helps individuals identify triggers, develop coping mechanisms, and manage
stress.

5. Motivational Interviewing:
●​ A therapeutic approach that engages individuals in conversations about their drinking
habits, aiming to resolve ambivalence and motivate change.
 ●​ Abstinence vs. Controlled Drinking

○​ Abstinence is commonly believed to be the only effective long-term solution.

However, some argue that moderate drinking may be achievable for certain
individuals with less severe alcohol problems. Studies show that controlled
drinking can work for a small percentage of individuals, particularly those with
mild alcohol abuse issues.

Alcoholics Anonymous (AA)

●​ AA has become one of the most popular and widespread recovery programs,
emphasizing a spiritual approach to recovery and focusing on mutual support.
●​ AA operates on the principle that alcoholism is a lifelong condition, and individuals are
always in “recovery.”
●​ 12-step programs and support groups like Al-Anon and Alateen provide peer support for
individuals and their families.
●​ While the success of AA is largely anecdotal, some studies show it to be as effective as
other treatment methods, though further research is needed.

Conclusion

Treating alcohol-related disorders requires a comprehensive approach that combines biological,

psychological, and social interventions. While abstinence is often the goal, strategies like
controlled drinking may be effective for some individuals, particularly those with less severe
problems. The integration of medications, psychological therapies, and peer support plays a
crucial role in managing alcohol dependence and promoting long-term recovery.

Outcomes

The treatment of alcohol-related disorders is complex, and the success of treatment depends on
several factors, including patient characteristics, treatment facilities, and methods used.
Research shows varying success rates, with some treatments having a recovery rate as high as
70-90% when modern procedures are used. The effectiveness of treatment is greatest when the
individual recognizes the need for help, has access to proper facilities, and attends treatment
regularly.

In the past, psychoanalytic and psychodynamic therapies, along with aversion therapies, were
common approaches. However, more recent methods like Motivational Interviewing (MI) have
gained attention. MI is a brief, client-centered therapy that emphasizes collaboration rather than
confrontation, helping patients explore the pros and cons of their drinking behavior and decide
on their readiness to change. Research has shown that MI can significantly reduce drinking and
aggression in adolescents, even after a single brief session.
Some studies have suggested that matching patients' characteristics (e.g., severity, personality)
with specific treatments could improve outcomes. However, the "Project MATCH" study found
no significant difference in outcomes between the treatment approaches tested. This indicates
that as long as the program is competently managed, the specific type of treatment may not
matter as much as previously thought.

A major challenge in alcohol treatment is relapse prevention. While many treatment programs
help individuals stop drinking, maintaining long-term abstinence is a significant hurdle. Relapse
can be triggered by small, seemingly insignificant decisions that gradually lead to a return to
maladaptive behaviors. Cognitive-behavioral therapy (CBT) incorporates relapse prevention
techniques, which focus on recognizing early warning signs and high-risk situations that may
lead to relapse. Clients are also taught to handle relapse without losing confidence or feeling
that they've failed completely. This approach has been shown to improve long-term recovery
outcomes.

Relapse prevention strategies can involve teaching clients how to manage triggers, high-risk
situations, and feelings of guilt after setbacks, helping them maintain control over their addiction.

Common Psychoactive Drugs Associated with Abuse and Dependence

1. Alcohol: Widely used, alcohol can reduce tension, facilitate social interaction, and "blot out"
feelings or events. It can lead to dependence and abuse when consumed heavily.

2. Opiates: These include substances like opium, morphine, heroin, and synthetic narcotics like
methadone. They alleviate pain and induce feelings of relaxation and euphoria, which can lead
to dependence.

3. Stimulants: These include drugs like amphetamines (e.g., Benzedrine, Dexedrine,

methamphetamine), cocaine, caffeine, and nicotine. They increase alertness, decrease fatigue,
and can stimulate the sex drive, but can be highly addictive.

4. Sedatives (Barbiturates): These drugs, such as Nembutal and Seconal, reduce tension and
induce a sense of calm. However, they carry a risk of abuse and dependence.

5. Hallucinogens: Drugs like marijuana, hashish, LSD, and mescaline (peyote) alter mood,
thoughts, and behavior, often causing a distortion of reality or "mind expansion."

6. Antianxiety Drugs (Minor Tranquilizers): Medications like Valium, Xanax, and Librium are
used to reduce anxiety and induce relaxation or sleep. These can become addictive with
prolonged use.

7. Pain Medications: OxyContin and similar pain medications are often abused for their euphoric
effects, leading to a risk of addiction.
Statistics on Drug Use

●​ General Use: Approximately 21.6 million Americans (ages 12 and older) use illicit drugs
each year.
●​ Prevalence Among Teens and Young Adults:

○​ 37% of 12th graders use illicit drugs annually.

○​ 35% of college students report drug use.
○​ 34% of individuals aged 19-28 use illicit drugs.

●​ Drug abuse is most common in adolescence and young adulthood.

Employment & Drug Use: A survey found that:

●​ 19% of those aged 18 or younger used illicit drugs in the past month.
●​ 10.3% of 18-25-year-olds used illicit drugs.

Drug use at work is a significant issue, with some workers admitting to using drugs while on the
job.
Drug abusers often have unstable employment, with many working for multiple employers in a
year.

Patterns of Drug Abuse

Drug abuse patterns vary based on:

●​ Type of Drug: Each drug affects the body differently, which influences patterns of abuse.
●​ Amount & Duration: The more frequently or intensely a drug is used, the higher the
likelihood of dependence.
●​ Individual Differences: Personal factors, such as genetic predisposition and mental
health, play a role in susceptibility to abuse.

Commonly Used Opiates and Their Effects

1. Major Opiates and Derivatives

●​ Opium: Contains ~18 alkaloids; used historically as a "cure-all."

●​ Morphine: Most potent alkaloid (10–15% of opium); powerful pain reliever and sedative.
●​ Heroin: Synthesized from morphine; acts faster and is more addictive.
●​ Codeine: Less potent; used in cough medications.

2. Historical Usage
 ●​ Morphine was widely used during the American Civil War → "Soldier’s illness"
(addiction).
●​ Heroin was once seen as a safer alternative to morphine.
●​ The Harrison Act (1914) restricted unauthorized sale, turning addiction into a criminal
issue.

Biological Effects

Methods of Use: Smoking, snorting, eating, skin popping (under the skin), mainlining (into the
bloodstream).

Short-Term Effects:

●​ Immediate rush (euphoria) lasting ~60 seconds

●​ Followed by 4–6 hours of relaxation, reduced bodily needs
●​ Nausea and vomiting may occur

Long-Term Effects:

●​ Tolerance and dependence

●​ Withdrawal symptoms start ~8 hours after last dose:
●​ Sweating, chills, cramps, diarrhea, tremors, insomnia
●​ Withdrawal peaks by Day 3–4, fades by Day 7–8

Social and Health Consequences

●​ Behavioral impact: Stealing, lying, prostitution to fund addiction

●​ Physical risks:

○​ Weakened immune system

○​ Hepatitis, AIDS from needle sharing
○​ Risk of fatal overdose, especially with impure street drugs

●​ Pregnancy risks: Premature birth, neonatal withdrawal

Causes of Opiate Abuse

●​ Common reasons: Pleasure (81%), curiosity, peer pressure

●​ Other factors: Life stress, maladjustment, sensation seeking
●​ Genetic & environmental influences both contribute

Neural Basis of Addiction

●​ Opiates bind to specific brain receptors related to pain, pleasure, and breathing
 ●​ Endorphins: Body’s natural opiates; heroin mimics but acts faster and stronger

Dopamine Theory:

●​ All addictive drugs activate the dopamine reward pathway

●​ Pathway: Ventral tegmental area → Nucleus accumbens → Prefrontal cortex

Reward Deficiency Syndrome:

Some people have underactive reward systems, needing stronger stimuli

"Wanting vs. Liking":

Dopamine: Drives wanting

Opioid system: Responsible for liking

Opioid Addiction & Psychopathology

●​ 70% of opioid abusers have other mental health disorders

●​ 50% have other substance abuse issues
●​ 36% have a history of trauma
●​ Abuse linked to broader medical and psychological problems

Stimulants: Overview

Stimulants are drugs that speed up the central nervous system (CNS), in contrast to opiates,
which slow it down. Common stimulants include:

●​ Cocaine
●​ Amphetamines
●​ Methamphetamine
●​ Caffeine
●​ Nicotine

Amphetamines: Overview

Amphetamines are central nervous system stimulants initially introduced in the 1920s. They
include:

●​ Benzedrine (amphetamine sulfate)

●​ Dexedrine (dextroamphetamine)
●​ Methedrine (methamphetamine or “speed” – the most potent and dangerous)
History & Uses

●​ First marketed in the 1930s as nasal decongestants.

●​ Their stimulating effects were discovered by users who misused the inhalers.
●​ Popular among soldiers (WWII), night workers, truck drivers, students, athletes.

Used for:

●​ Weight loss (appetite suppressant)

●​ Counteracting sedatives (like barbiturates)
●​ Treating narcolepsy
●​ Managing ADHD (paradoxically calming in hyperactive children)
●​ Alleviating mild depression and fatigue

Legal Status

●​ Classified as Schedule II controlled substances (high abuse potential; prescription-only).

●​ Medical use has declined, but illicit use remains common worldwide.
●​ Around 7% of drug-related ER visits involve amphetamines or methamphetamine.

Effects of Amphetamine Abuse

Not a source of extra energy—they push the body to overwork its own resources.

Can cause:

●​ High blood pressure

●​ Dilated pupils
●​ Tremors, sweating, confusion
●​ Sleeplessness, excitability
●​ Loss of appetite
●​ Amphetamine psychosis (resembles paranoid schizophrenia)
●​ Risk of violence, suicide, or death (especially with Methedrine injection)
●​ Highly addictive both psychologically and physically.
●​ Tolerance develops rapidly, leading users to take dangerously high doses.

Withdrawal & Treatment

Research is limited, but withdrawal is typically not life-threatening.

Symptoms of withdrawal:

●​ Depression (peaks in 2–3 days, may last weeks/months)

 ●​ Fatigue, cramping, nausea, diarrhea
●​ In some cases: convulsions

Long-term effects (especially with brain damage):

●​ Poor concentration, memory issues

●​ Personality and social functioning deterioration
Caffeine and Nicotine: Overview

Both are legal, widely used, and addictive substances recognized by the DSM-5 as potentially
problematic. Although not as destructive as other drugs, they pose significant physical and
mental health risks due to:

●​ Early exposure and social acceptance

●​ Strong addictive properties
●​ Difficulty quitting due to habit and withdrawal symptoms
●​ High health risks—especially nicotine (e.g., 1 in 7 deaths in the U.S. is linked to
smoking)

CAFFEINE

●​ Sources: Coffee, tea, cola, chocolate

●​ Addictive potential: Moderate
●​ Problems mostly from intoxication, not withdrawal

DSM-5 Symptoms:

●​ Restlessness
●​ Nervousness, excitement
●​ Insomnia
●​ Muscle twitching
●​ Gastrointestinal issues

Withdrawal: Usually mild (e.g., headache)

NICOTINE

●​ Main ingredient in tobacco (cigarettes, cigars, chewing tobacco)

●​ Also used as an insecticide
●​ Highly addictive, with use often beginning in adolescence
●​ Linked to anxiety disorders and possible activity in the insula (brain region related to
addiction)
●​ Tobacco use disorder is diagnosed using criteria similar to other addictions
Nicotine Withdrawal (DSM-5 Criteria)

After regular use, stopping leads to:

●​ Cravings
●​ Irritability, frustration, anger
●​ Anxiety, restlessness
●​ Difficulty concentrating
●​ Increased appetite, weight gain
●​ Sleep disturbances, tremors, headaches

Symptoms can last days to weeks, sometimes months

Treatment of Nicotine Addiction

●​ Behavioral therapies and cognitive-behavioral therapy

●​ Nicotine Replacement Therapies (NRT): gum, patches, lozenges
●​ Social support groups

Medications:

●​ Bupropion (Zyban): helps prevent relapse (effective while taking it)

●​ Success rate: Generally 20–25%, higher with strong interventions
●​ Highest quit rates seen in hospitalized patients (e.g., cancer, heart, or lung disease)

Cocaine

●​ Origin: Derived from coca plant leaves; used historically in South America.
●​ History: Promoted by Freud and once included in Coca-Cola; later made illegal due to its
harmful effects.
●​ Forms: Can be sniffed, swallowed, injected, or smoked (crack cocaine).
●​ Mechanism: Blocks dopamine reuptake, increasing dopamine in the
synapse—especially in the brain's reward center (nucleus accumbens).
●​ Effects: Euphoria, increased energy, confidence, reduced hunger; lasts 4–6 hours.
●​ Side Effects: Headache, dizziness, psychotic symptoms (hallucinations), cognitive
impairments.
●​ Addiction: High risk of dependence and tolerance.
●​ Social Impact: Leads to legal, occupational, and relationship problems.
●​ Pregnancy Risks: No clear fetal crack syndrome, but higher risks of infant mistreatment
and maternal loss.

Treatment of Cocaine Dependence

●​ Medications: Naltrexone, methadone (help reduce cravings).

 ●​ Psychological Therapies:

○​ CBT (Cognitive Behavioral Therapy): Teaches coping skills to avoid drug use.
○​ CM (Contingency Management): Uses rewards (like money) for drug-free
behavior; slightly more effective than CBT.

●​ Effectiveness: Proven effective for both genders and across populations, including those
in the criminal justice system.

Effects of Sedatives on the Brain (Barbiturates)

●​ Barbiturates are powerful sedatives used for over a century, mainly to induce sleep.
●​ They act as CNS depressants, similar to alcohol, slowing down brain activity.
●​ Effects include:

○​ Relaxation and reduction of tension

○​ Drowsiness and sleep
○​ Impaired decision-making and cognitive performance
○​ Sluggishness, mood swings, slow speech

●​ High doses can cause respiratory paralysis and death.

●​ Tolerance develops with use, but not for fatal doses—increasing overdose risk.

Dependence and Abuse

●​ Leads to both psychological and physiological dependence.

●​ Can result in brain damage and personality deterioration.
●​ Commonly misused by middle-aged or older individuals as sleeping aids.
●​ Referred to as "silent abusers" due to private, non-disruptive use.
●​ Mixing barbiturates with alcohol is dangerous—can be lethal due to drug potentiation.

Treatment and Withdrawal

●​ Barbiturate withdrawal is severe, long-lasting, and dangerous, more so than opioid

withdrawal.
●​ Symptoms include:

●​ Anxiety, tremors, insomnia, nausea, vomiting

●​ Abdominal cramps, weight loss, rapid heart rate, high BP
●​ In severe cases: delirious psychosis

●​ Withdrawal can last up to a month, but usually improves within a week.

●​ Managed through gradual tapering using barbiturates or similar drugs.
 ●​ Extra caution needed if user is also dependent on alcohol or other substances.

types of hallucinogens:

1. LSD (Lysergic Acid Diethylamide)

●​ Overview: LSD is a potent synthetic hallucinogen first synthesized by Swiss chemist

Albert Hofmann in 1938. It is known for its powerful psychological effects, even in very
small doses. LSD is typically sold as blotter paper, soaked with the drug, which is then
ingested by placing it under the tongue.

●​ Effects: After ingestion, LSD alters perception and cognition. Users typically experience
intense visual and auditory hallucinations, where colors and shapes may appear
distorted or exaggerated. Time perception is often altered, and people may feel
detached from their bodies or sense that their environment is unreal.

●​ Negative Effects: While many users experience a euphoric “trip,” LSD can also lead to
dangerous “bad trips.” These can include terrifying hallucinations, extreme paranoia, and
delusions. In severe cases, users may become self-destructive or attempt risky
behaviors due to the altered state of consciousness. Long-term use can lead to
persistent changes in mood, perception, and sometimes even flashbacks of the
experience (known as Hallucinogen Persisting Perception Disorder or HPPD).

2. Mescaline

●​ Overview: Mescaline is a naturally occurring hallucinogen found in certain cacti, most

notably the peyote cactus. It has been used for centuries by indigenous cultures,
particularly in religious and spiritual ceremonies.

●​ Effects: When consumed, mescaline induces vivid visual hallucinations, often

characterized by intense color patterns and geometric shapes. Users also experience
alterations in time perception, sensory enhancement (e.g., heightened taste or sound),
and an altered sense of reality. It can induce feelings of euphoria, spiritual
enlightenment, or profound insights.

●​ Negative Effects: Like other hallucinogens, mescaline can cause confusion, anxiety, and
panic, especially in high doses or in unfamiliar settings. The duration of the effects can
last up to 12 hours, and the psychological impact can be overwhelming, sometimes
leading to bad trips and psychological distress.

3. Psilocybin

●​ Overview: Psilocybin is the active compound in "magic mushrooms," a group of fungi

that has been used for thousands of years for religious, spiritual, and recreational
 purposes. Psilocybin is converted into psilocin in the body, which produces the
hallucinogenic effects.

●​ Effects: Psilocybin causes visual and auditory distortions, feelings of euphoria, and a
distorted sense of time. The experience can lead to intense introspection, where users
may feel like they are gaining new insights into themselves or the universe. Some people
also report feeling a sense of connection to nature or a higher power.

●​ Negative Effects: Although the effects of psilocybin are generally milder than those of
LSD, they can still cause significant distress, including confusion, anxiety, and panic
attacks. In rare cases, it may trigger long-lasting psychiatric conditions such as anxiety
disorders or psychosis in vulnerable individuals. Like other hallucinogens, it is possible to
experience "bad trips" that may lead to psychological trauma.

4. Ecstasy (MDMA)

●​ Overview: MDMA, also known as Ecstasy or Molly, is a synthetic drug that combines the
stimulant properties of amphetamines with mild hallucinogenic effects. MDMA is often
used recreationally in party or rave environments due to its ability to enhance sensory
experiences and promote emotional bonding between users.

●​ Effects: MDMA increases the release of serotonin in the brain, which produces feelings
of euphoria, empathy, and enhanced emotional connection. Users also report
heightened sensory perceptions, such as intensified colors and sounds. It is often used
at social events because of the sense of energy and excitement it provides.

●​ Negative Effects: Despite the positive feelings induced by the drug, MDMA can have
serious side effects. These include nausea, blurred vision, muscle cramping, anxiety,
and agitation. It can also cause dehydration, overheating, and in extreme cases, heart
failure. Long-term use of Ecstasy can lead to memory impairments, mood disorders, and
damage to serotonin-producing neurons in the brain. In addition, MDMA use is often
associated with risky behaviors, including unsafe sexual practices and binge drinking.

Synthetic Cannabinoids and Cathinones

●​ Synthetic Cannabinoids (e.g., "Spice" or "K2"): These are chemically engineered

substances designed to mimic the effects of THC, the active compound in marijuana.
However, synthetic cannabinoids can have more severe and unpredictable effects,
including extreme anxiety, tachycardia, psychosis, and seizures.

●​ Synthetic Cathinones (e.g., "Bath Salts"): These synthetic drugs imitate the stimulant
and hallucinogenic effects of drugs like amphetamines and cocaine. They can cause
 agitation, violent behavior, hallucinations, and severe medical complications like heart
attack and kidney failure.

●​ Hallucinogens, both natural and synthetic, can lead to profound changes in perception
and consciousness, but they come with significant risks, including psychological distress,
addiction, and even life-threatening medical conditions.
Marijuana

Marijuana is a drug made from the Cannabis sativa plant. It’s mostly smoked, but can also be
used in edibles or tea. The main ingredient that causes its effects is THC
(tetrahydrocannabinol).

Short-Term Effects

1. Euphoria & Relaxation: Many people feel happy and relaxed after using marijuana.
2. Heightened Senses: Colors, sounds, and tastes can feel more intense.
3. Time Distortion: Time may feel slower or faster.
4. Memory Issues: It can be hard to remember things or focus.
5. Increased Appetite: People often feel hungrier, which is called "the munchies."

Negative Effects

1. Anxiety & Paranoia: Some people feel anxious or paranoid, especially in high doses.
2. Cognitive Impairment: It can make it harder to think clearly or make decisions.
3. Psychosis: In rare cases, it can trigger mental health issues like psychosis.
4. Impaired Motor Skills: It can affect coordination, making activities like driving dangerous.
5. Respiratory Problems: Smoking marijuana can harm the lungs, causing coughing and
irritation.

Long-Term Effects

1. Addiction: About 9% of users can become addicted, especially those who start young.
2. Memory & Learning Issues: Regular use may affect memory and learning.
3. Mental Health Risks: Long-term use may increase the risk of mental health issues like
depression or anxiety.
4. Lack of Motivation: Some users report feeling less motivated or interested in things.

Medical Uses

Marijuana is used in medicine for:

1. Chronic Pain: It can help with long-term pain, like from arthritis or cancer.
2. Nausea & Vomiting: It helps people who feel sick, especially those on chemotherapy.
3. Appetite Loss: It’s used to help people who struggle to eat due to illness.
4. Mental Health: Some use it for anxiety or PTSD, though it can make these worse for others.

Synthetic Cannabinoids

Some synthetic versions of marijuana, like "Spice" or "K2," are much stronger and more
dangerous, causing serious side effects like seizures or hallucinations.
Mood Disorders

Mood disorders are mental health conditions marked by significant disturbances in emotional
states, typically involving periods of depression, mania, or both. The two primary emotional
extremes central to mood disorders are:

Depression: This mood state is commonly associated with profound sadness, feelings of
hopelessness, and a pervasive sense of dejection.

Mania: This is characterized by an exaggerated sense of excitement, energy, and euphoria that
is often unrealistic. In some cases, mania may also present with intense irritability.

Some individuals with mood disorders experience only depressive episodes, where they feel
persistently low or lose interest in activities they once enjoyed. Others may alternate between
episodes of depression and mania at different times. In many cases, individuals experience
normal moods in between these episodes. Traditionally, depression and mania are seen as
opposite ends of a mood continuum, with a normal mood positioned in between. However, this
model doesn’t fully capture the complexity of mood disorders. Some individuals experience
mixed episodes, where symptoms of depression and mania appear simultaneously or rapidly
alternate within the same period. During such episodes, people may display rapidly shifting
emotions such as sadness, euphoria, and irritability, all within a single phase of illness.

Categories of Mood Disorders

Mood disorders are generally classified into two main categories:

1. Unipolar Depressive Disorders

These disorders involve the experience of only depressive episodes, without any history of
mania or hypomania.

The most common form of unipolar disorder is Major Depressive Disorder (MDD), where the
individual experiences prolonged periods of deep depression or an inability to find pleasure in
previously enjoyable activities.

A depressive episode typically lasts at least two weeks and may include:

●​ Significant changes in sleep and appetite

●​ Persistent fatigue or loss of energy
●​ Feelings of worthlessness or inappropriate guilt
●​ Difficulty concentrating or making decisions
●​ Suicidal thoughts or behaviors
2. Bipolar and Related Disorders

These involve both depressive and manic (or hypomanic) episodes.

A manic episode is a distinct period during which the person experiences abnormally elevated,
expansive, or irritable mood, lasting for at least one week.

During manic episodes, individuals may display:

●​ Inflated self-esteem or grandiosity

●​ Decreased need for sleep
●​ Excessive talkativeness
●​ Racing thoughts or “flight of ideas”
●​ Increased goal-directed behavior or psychomotor agitation
●​ Engaging in risky behaviors, such as reckless spending or unsafe sexual practices

If the symptoms are less intense and persist for at least four days, it is referred to as a
hypomanic episode. Hypomania includes similar symptoms to mania but with milder severity,
and it typically does not cause significant social or occupational dysfunction, nor does it
necessitate hospitalization.

Prevalence of Mood Disorders

Mood disorders are remarkably common and occur much more frequently than other severe
psychiatric conditions like schizophrenia. They are almost as prevalent as all anxiety disorders
combined.

Unipolar Major Depression

Major Depressive Disorder (MDD) is the most common mood disorder, affecting a significant
portion of the population.

Epidemiological data from the National Comorbidity Survey Replication (NCS-R) indicate:

Nearly 17% of people will experience unipolar major depression at some point in their lives.

About 7% experience major depressive episodes within a 12-month period.

The rates of MDD appear to have increased over recent decades.

Cultural and Ethnic Differences

Mood disorders are reported to be less prevalent among African Americans when compared to
European White Americans and Hispanics, whose prevalence rates are roughly similar.
Native Americans, however, show significantly higher rates of mood disorders than European
White Americans.

In contrast, bipolar disorder does not demonstrate significant differences in prevalence across
these cultural and ethnic groups.

Socioeconomic Status (SES) and Mood Disorders

There is an inverse relationship between socioeconomic status and unipolar depression. Higher
rates of unipolar depression are found in lower socioeconomic groups.

This trend is often attributed to the greater levels of adversity and life stress experienced by
individuals from lower SES backgrounds.

Earlier theories proposed that bipolar disorder was more common among people from higher
socioeconomic backgrounds, but more recent, well-controlled studies have not supported this
claim. Bipolar disorder appears to be unrelated to socioeconomic class.

Mood Disorders and Creativity

Research has shown a notable link between mood disorders, particularly bipolar disorder, and
high creativity.

Individuals who have made significant achievements in the arts—such as poets, writers,
composers, and visual artists—are disproportionately affected by mood disorders.

The well-known psychologist Kay Redfield Jamison has studied the connection between
creativity and mood disorders extensively. Her research highlights how the manic and
hypomanic phases of bipolar disorder may boost productivity and motivation, even if they do not
necessarily enhance creativity itself.

Conversely, the emotional pain and introspection brought on by depressive episodes may serve
as a source of inspiration for creative work.

Case Example: Emily Dickinson

Studies suggest that Emily Dickinson, the renowned American poet, experienced both panic
disorder and depression, which provided the emotional depth for some of her most celebrated
poetry.

Her periods of hypomania seemed to increase her motivation and productivity, though they
didn’t necessarily make her poetry more creative.
Unipolar Depressive Disorders

These are mood disorders where a person experiences depressive episodes only, without any
history of mania or hypomania (which are part of bipolar disorders). The most common feeling is
deep sadness, hopelessness, and loss of interest in life.

1. Major Depressive Disorder (MDD):

A serious mood disorder where the person experiences a major depressive episode that lasts
for at least two weeks or longer.

Symptoms

●​ Persistent sadness, hopelessness

●​ Loss of interest or pleasure in activities
●​ Changes in appetite and sleep (either too much or too little)
●​ Fatigue or loss of energy
●​ Feelings of worthlessness or guilt
●​ Difficulty concentrating
●​ Thoughts of death or suicide

Example (Jennifer’s Case):

Jennifer’s life fell apart after her husband left. She couldn’t enjoy things she used to, lost interest
in her kids and work, and even started having suicidal thoughts. This shows how MDD affects
thoughts, emotions, behavior, and physical health.

2. Persistent Depressive Disorder (Dysthymia):

A chronic, long-term form of depression lasting at least 2 years (1 year for children/adolescents).

Symptoms Are Milder But Last Longer:

●​ Low mood most of the day

●​ Poor appetite or overeating
●​ Insomnia or sleeping too much
●​ Low energy or fatigue
●​ Low self-esteem
●​ Poor concentration
●​ Feelings of hopelessness

Note:
Sometimes a person with dysthymia can experience a major depressive episode on top of their
chronic depression. This is called "double depression."
3. Depression Across the Life Span:

Children (School Age):

About 1-3% experience depression. It was once thought children couldn’t be depressed, but
they can be, although the symptoms might look different (irritability rather than sadness).

Adolescents:
15-20% experience major depressive disorder (MDD). It’s a time of emotional upheaval, and
depression often begins here. Girls have higher rates than boys after puberty.

Adults (Late Adolescence to Middle Age):

This is the most common age of onset for depression.

Older Adults (65+):

Depression is less common but still serious. It can be hard to diagnose because its symptoms
overlap with physical illness or dementia.

4. Depression As a Recurrent Disorder:

First Episode vs. Recurrent Episode:

Single Episode: First time a person experiences MDD.

Recurrent Episode: If the person has two or more episodes of depression during their lifetime.

Relapse vs. Recurrence:

Relapse: Return of symptoms shortly after recovery, often because the treatment stopped too
soon.

Recurrence: A completely new episode after recovery.

Chances of Recurrence:
40-50% of people with one episode will have another. The more episodes a person has, the
more likely they are to have more.

5. Specifiers for Major Depressive Episodes (as per DSM-5):

These are additional features or patterns that may accompany depression and help guide
treatment.

a) With Melancholic Features:

Symptoms:

●​ Loss of pleasure in almost everything

●​ Depression worse in the morning
●​ Early morning waking
●​ Weight loss
●​ Excessive guilt

Associated With:
Childhood trauma and genetic risk factors.

b) With Psychotic Features:

Symptoms:

●​ Delusions (false beliefs)

●​ Hallucinations (false sensory experiences)
●​ Usually negative themes like guilt, punishment, or death

More Severe:
Longer episodes, worse cognitive issues. Requires both antidepressants and antipsychotics.

c) With Atypical Features:

Symptoms:

●​ Mood improves with positive events (mood reactivity)

●​ Weight gain or increased appetite
●​ Sleeping too much (hypersomnia)
●​ Feeling heavy in limbs
●​ Sensitive to rejection

More Common In:

Women and people with early-onset depression. May respond better to a specific
antidepressant class (MAOIs).

d) With Catatonic Features:

Symptoms:

●​ Motor immobility or excessive movement

●​ Mutism (not speaking)
●​ Rigidity
More Common In:
Depression and mania, even more than schizophrenia.

e) With Seasonal Pattern (Seasonal Affective Disorder, SAD):

Symptoms:

●​ Depression comes in fall/winter and improves in spring

●​ Must have had two or more seasonal episodes in 2 years

Common In:
People living in northern regions with less sunlight.

Other Forms of Depression

While many depressive episodes are triggered by stressful life events, some life
experiences—especially loss or the birth of a child—can make people particularly vulnerable.
These events can bring about specific forms of depression, or emotional experiences that look
similar to depression but aren’t always diagnosed as a mental disorder.

1. Loss and the Grieving Process

What happens?
When we lose someone close (like a spouse, parent, or friend), we experience grief. Grief is a
natural, emotional reaction to loss.
Think of grief as the mind and heart trying to adjust to a painful reality.

Bowlby’s 4 Phases of Grief (1980):

Psychiatrist John Bowlby observed that most people go through these phases after a major
loss:

1. Numbing and disbelief

(You feel shocked, almost unable to believe the person is gone.)

2. Yearning and searching

(You feel a deep longing and might even imagine you see or hear the person.)

3. Disorganization and despair

(The pain really hits, and you start realizing life will never be the same.)
4. Reorganization
(You slowly adjust, rebuild your life, and find a new normal.)

Men vs. Women in Grief:

Research suggests that grieving might be harder for men than women. Possibly because
women are often more socially supported in expressing emotions.

DSM and Bereavement:

Earlier (DSM-IV-TR): You wouldn’t diagnose major depressive disorder (MDD) right after a
death. There was a 2-month rule—even if someone had all the symptoms of MDD, it was
considered normal grief during that time.

DSM-5 removed this bereavement exclusion. Now, if someone meets MDD criteria, they can be
diagnosed, even shortly after losing someone.
This is controversial! Some argue it pathologizes normal grief; others say it helps people get
help sooner.

Resilience After Loss:

Not everyone who loses someone falls into depression.

About 50% of people show resilience, meaning they adapt and recover without serious, lasting
depression.

This doesn’t mean they didn’t love the person! They just have different coping styles or strong
support systems.

2. Postpartum “Blues” and Depression

Isn’t having a baby supposed to be joyful?

You’d think so! But for many new mothers (and sometimes fathers), it can be emotionally
overwhelming.

Postpartum Blues:
●​ Very common!
●​ About 50-70% of new mothers experience postpartum blues within the first 10 days after
giving birth.
Symptoms:

●​ Mood swings
●​ Crying spells
●​ Sadness
●​ Irritability
●​ Mixed with happy moments

Good news:
●​ It’s temporary. Most women recover on their own without needing treatment.
Postpartum Major Depression (PPD):

●​ More serious and longer-lasting than the blues.

●​ It was once thought to be common, but new research shows PPD isn’t more frequent in
new mothers than depression is in other women of the same age group.

What Increases the Risk of PPD?

If postpartum blues are severe, there’s a higher chance they can develop into major depression.

Biological Factors:

●​ Hormonal changes after birth (drop in estrogen and progesterone).

●​ Changes in neurotransmitters like serotonin and noradrenaline.

Psychological/Social Factors:

●​ Lack of support from family/friends.

●​ Difficulty adjusting to the new role as a parent.
●​ Personal or family history of depression increases risk.

Real-Life Example for Postpartum Blues:

A new mother feels tearful and overwhelmed a few days after coming home with her baby. She
feels exhausted, cries without knowing why, and worries she’s not a good mother. But she also
smiles when holding her baby and starts feeling better after a week or two—this would be
postpartum blues.

If her sadness deepens, she withdraws from her baby, and feels hopeless for weeks, that could
be postpartum depression.

Causal factors of mood disorders

Biological Causal Factors of Major Depressive Disorder (MDD)

Biological causes of depression are multi-faceted, involving genes, neurotransmitters,

hormones, brain structures, immune responses, and biological rhythms. These factors interact
with environmental stressors, shaping an individual's risk for developing depression.

1. Genetic Influences

●​ Family and twin studies show that genetics play a moderate role in causing MDD.
 ●​ People who have close relatives with unipolar depression are two to three times more
likely to develop the disorder.
●​ Twin studies reveal that monozygotic twins (identical) have a 31–42% shared genetic
risk for MDD. This risk can rise to 70–80% for more severe, early-onset, or recurrent
depression.
●​ While genetics contribute, nonshared environmental factors (like unique personal
experiences) have an even bigger impact.
●​ Unlike bipolar disorder, persistent depressive disorder has little evidence of genetic
influence due to limited research.

Candidate Genes

●​ Focus has been on the serotonin-transporter gene (5-HTT), which regulates serotonin
levels.
●​ People with two short alleles (s/s) are more vulnerable to depression, especially when
exposed to stressful life events or childhood maltreatment.
●​ This interaction between genes and life stress supports the diathesis-stress model.

Some studies have supported this interaction, while others (like Risch et al., 2009) have
questioned its validity. However, later meta-analyses reaffirmed the gene-environment
interaction, especially when life stress is carefully measured.

2. Neurochemical Factors

●​ The monoamine hypothesis from the 1960s suggested depression results from a
deficiency in neurotransmitters like norepinephrine and serotonin.
●​ Antidepressants increase levels of these neurotransmitters at synapses, leading
researchers to initially believe that depression was due to their depletion.
●​ However, evidence later revealed mixed findings:

Some people with depression show increased norepinephrine levels.

Low serotonin activity is mainly associated with suicidal thoughts and behaviors, not with
depression in general.

Antidepressants work immediately on neurotransmitter levels but clinical improvements take

weeks, suggesting a more complex mechanism.

Dopamine

Reduced dopamine activity is linked to anhedonia, the inability to experience pleasure, which is
a core symptom of depression.

Current Understanding
Depression likely results from interactions among multiple neurotransmitters and hormonal
systems, rather than a single neurotransmitter deficiency.

3. Hormonal and Immune System Dysregulation

​ HPA Axis and Cortisol

●​ The hypothalamic-pituitary-adrenal (HPA) axis regulates stress responses.

Overactivity results in elevated cortisol levels, common in depression.
●​ About 20–40% of depressed outpatients and 60–80% of hospitalized patients
have high cortisol levels.
●​ Chronic high cortisol leads to health problems, including memory issues and cell
death in the hippocampus (key for memory and stress regulation).
●​ Dexamethasone suppression tests show that many depressed patients can't
suppress cortisol production, indicating HPA axis dysfunction.
​ Thyroid Function

●​ Hypothyroidism can cause depression. Some patients with normal thyroid

hormone levels show axis dysregulation.
●​ Adding thyrotropin-releasing hormone (TRH) can help certain patients
unresponsive to antidepressants.
​ Immune System

●​ Depression is linked to inflammation and increased proinflammatory cytokines

like interleukin and interferon.
●​ These inflammatory markers may directly cause depressive symptoms.

4. Neurophysiological and Neuroanatomical Influences

●​ Damage to the left anterior prefrontal cortex (from strokes) often leads to depression.
Depressed people without brain injury also show less activity in this region.
●​ EEG and PET scans confirm left-right hemisphere asymmetry: low activity on the left
side (linked to reduced positive emotions) and high activity on the right (linked to
increased anxiety).
●​ These patterns can be found even in remission and in at-risk children, suggesting they
may predict future depression.

Brain Regions Involved

●​ Prefrontal Cortex: Reduced volume, especially in areas regulating rewards and

decision-making.
●​ Hippocampus: Decreased volume due to chronic stress; linked to memory problems.
 ●​ Anterior Cingulate Cortex: Lower activity and volume; affects attention, decision-making,
and emotion regulation.
●​ Amygdala: Increased activity; associated with heightened emotional sensitivity,
especially to negative information.

5. Sleep and Biological Rhythms

Depression is often linked to disturbed biological rhythms, especially sleep cycles.

●​ Common sleep issues include insomnia, early morning waking, and reduced deep sleep
(Stage 3 & 4), with increased REM sleep.
●​ Seasonal Affective Disorder (SAD) is linked to light exposure. Symptoms typically
worsen in fall/winter and improve in spring/summer.
●​ Light therapy (even with artificial light) can effectively reset biological rhythms and treat
SAD.

Psychological causal factors in unipolar depression

. 1. Psychological Factors in Depression

Psychological factors are as significant as biological ones.

Stress can trigger biological changes that lead to depression.

2. Stressful Life Events

Severe stressors (loss of a loved one, health problems, job loss) can trigger unipolar
depression.

This effect is particularly strong in young women.

Caregiver stress (e.g., caring for someone with Alzheimer’s) increases depression risk.

3. Dependent vs. Independent Life Events

Independent: Out of the person's control (e.g., natural disasters).

Dependent: Influenced by the person’s behavior (e.g., poor conflict resolution).

Dependent events are more strongly linked to depression onset.

4. The Role of Perception

Depressed individuals may perceive events as more stressful due to their negative cognitive
biases.

Sophisticated interview-based assessments are used to objectively measure life stress,

removing personal bias.

5. Severity and Timing

Severe life events often lead to depression within a month.

70% of first-time depression cases follow a major stressful event.

Chronic stress (e.g., poverty, family issues) increases risk for developing and relapsing into
depression.

6. Vulnerabilities to Stress

People differ in their sensitivity to stress, partly due to genetic factors.

Those at higher genetic risk are more affected by life stress (gene-environment interaction).

7. Psychological Vulnerabilities (Diatheses)

Neuroticism (negative emotionality): Major risk factor.

Introversion/low positive affect: May also contribute but evidence is mixed.

Negative cognitive styles (e.g., pessimism, internal attributions for failure) increase vulnerability.

8. Early Life Adversity

Early trauma or harsh parenting can create long-term vulnerability.

These effects are biological (stress-response system changes) and psychological (low
self-esteem, attachment issues).

Some people become more resilient through moderate adversity (stress inoculation).

9. Interconnected Vulnerabilities

Genetic factors, personality traits (like neuroticism), and early experiences are interconnected.

Early life experiences (e.g., poor parenting) shape cognitive vulnerabilities (negative thinking).
This is a great overview of two major psychological theories explaining depression:
Psychodynamic and Behavioral. Here's a simplified breakdown if you're looking to summarize or
clarify the concepts:

Psychodynamic Theories

Origin: Sigmund Freud’s classic work Mourning and Melancholia (1917).

Main Idea: Depression mirrors grief and mourning after the loss of a loved one.

Key Concepts:

Introjection: The mourner unconsciously incorporates the lost person into their own identity.

Anger Turned Inward: People may harbor unconscious anger towards the lost person (for
abandoning them). This anger is redirected toward themselves, leading to self-reproach and
depression.

Imagined/Symbolic Loss: Depression can also arise from symbolic losses, like failing at
school or in relationships, which can feel like losing parental love or approval.

Contribution: Highlighted the role of loss—real, symbolic, or imagined—as a key trigger for
depression, and drew attention to the similarity between mourning and depressive symptoms.

Later Theorists: Expanded on Freud’s ideas (e.g., Bowlby, Levy & Wasserman), focusing on
attachment and loss.

Behavioral Theories

Origin: Behavioral psychology tradition, developed mainly in the 1970s and 1980s.

Main Idea: Depression results from a decrease in positive reinforcement or an increase in

negative experiences.

Key Points:

●​ People become depressed when their behaviors no longer lead to rewards, or when they
experience too many unpleasant events.
●​ Depressed individuals often get less positive reinforcement from friends and family.
●​ They also experience lower activity levels, fewer pleasurable experiences, and their
mood worsens as negative experiences increase.

Cause vs. Effect Issue: It’s unclear whether fewer rewards cause depression or if depression
(low energy, pessimism) leads to fewer rewarding experiences—likely a feedback loop.
Behavioral Activation Treatment: A modern therapy based on these ideas. Encourages
depressed people to increase engagement in rewarding activities, shown to be effective (e.g.,
Dimidjian et al., 2011; Martell, 2009).

Beck’s Cognitive Theory of Depression (1967)

Founder: Aaron Beck

Main Idea: Depression is primarily caused by negative thinking patterns, not just mood or
emotion problems.

Core Concepts:

1. Cognitive Symptoms Cause Mood Symptoms

Beck believed that thoughts (cognitions) come before feelings.

Example: If you constantly think, “I’m a failure,” it can cause a depressed mood.

2. Depressogenic Schemas (Dysfunctional Beliefs)

Deep-rooted, rigid, and unrealistic beliefs formed in childhood or adolescence due to negative
experiences.
Examples:

“If everyone doesn’t love me, my life is worthless.”

“If I’m not perfect, I’m a nobody.”

These schemas are often dormant until stressful events activate them.

3. Negative Automatic Thoughts

Once schemas are triggered, they produce automatic negative thoughts, which reinforce
depression.

These thoughts often fly under the radar but impact how you feel and act.

Negative Cognitive Triad

Three types of negative thoughts:

1. Self: “I’m worthless.”

2. World: “No one loves me.”

3. Future: “It will always be this way; things won’t get better.”

Cognitive Distortions (Thinking Errors):

These faulty thinking patterns help maintain depression:

1. All-or-None Thinking (Dichotomous Reasoning):

“If it’s not perfect, it’s a failure.”

2. Selective Abstraction:
Focusing on one bad thing while ignoring the positives.
E.g., “Today was terrible,” despite a few good moments.

3. Arbitrary Inference:
Jumping to negative conclusions with little evidence.
E.g., “This therapy won’t work after one bad day.”

Cycle of Depression (Vicious Cycle):

Negative schemas → Automatic negative thoughts → Depressive symptoms (sadness, lack of

motivation) → reinforce schemas and thoughts → cycle repeats.

Evaluation of Beck’s Theory:

Strengths

●​ Well-supported descriptively.
●​ Depressed individuals consistently show more negative thoughts about self, world, and
future.
Led to Cognitive Therapy (CT), one of the most effective treatments for depression.

Causal Evidence:

●​ Mixed results.
●​ Some longitudinal studies support that dysfunctional beliefs + stress lead to depression
(e.g., Lewinsohn et al., 2001).
●​ But not all studies show this diathesis-stress interaction consistently.

New Insights
Depressogenic schemas can be reactivated by sad moods, even without external stressors.
E.g., Listening to sad music can trigger old patterns in vulnerable individuals.

Final Takeaway:
Beck’s theory highlights how thinking patterns influence and maintain depression. While there's
strong support for its descriptive aspects (how depression works), evidence for its causal claims
(what triggers depression) is still being explored.

Sure! Here's a paraphrased and elaborated version of your text with headings and bullet points
for clarity.

Helplessness and Hopelessness Theories of Depression

1. Learned Helplessness Theory of Depression

Developed by Martin Seligman in the 1970s.

Originated from animal studies, specifically with laboratory dogs.

Key Findings

Dogs subjected to uncontrollable electric shocks eventually stopped trying to escape, even
when escape was possible later.

These animals exhibited passivity, lack of motivation, and behaviors that resembled depressive
symptoms.

Main Concept

When humans or animals perceive they have no control over negative events, they may learn to
behave in a helpless manner.

This learned helplessness can result in:

●​ Reduced motivation
●​ Difficulty learning that future actions can change outcomes

Symptoms resembling depression, such as:

●​ Lower aggression
●​ Loss of appetite
●​ Weight loss
●​ Neurochemical changes (affecting monoamine neurotransmitters)
Human Application

●​ Seligman and colleagues later demonstrated similar effects in humans.

●​ People exposed to uncontrollable stressors may develop helplessness, increasing
vulnerability to depression.

2. Reformulated Helplessness Theory

Proposed by Abramson, Seligman, and Teasdale (1978) to address human complexities.

Key Contributions

Humans tend to ask “Why did this happen?” when faced with uncontrollable events.

The explanations (attributions) they make influence whether they become depressed.

Three Attribution Dimensions

1. Internal vs. External

Internal: “It’s my fault.”

External: “It’s someone else’s fault.”

2. Stable vs. Unstable

Stable: “This will always happen.”

Unstable: “This is temporary.”

3. Global vs. Specific

Global: “This affects everything in my life.”

Specific: “This only affects this one situation.”

Pessimistic Attributional Style

Depression is more likely when a person makes internal, stable, and global attributions.

Example: Believing “I’m boring and unlovable” instead of “He was just in a bad mood.”

Development of Cognitive Style

Often learned through:

●​ Observing and imitating parental behaviors.

●​ Experiencing negative parenting (criticism, lack of warmth).

Evidence and Research

●​ Many studies support the connection between pessimistic attributional style and
depression.
The theory explains why some people are more vulnerable to depression when facing stressful
life events.

3. Hopelessness Theory of Depression

An extension of the reformulated helplessness theory, developed by Abramson et al. (1989).

Core Idea

Depression results when a person experiences a sense of hopelessness.

Hopelessness involves:
●​ Belief in no control over outcomes.
●​ Certainty that bad things will happen or good things won’t.

Revised Attribution Focus

Emphasized stable and global attributions rather than internal/external.

People at risk tend to:

●​ Make negative inferences about:

●​ Future consequences (“Bad things will keep happening.”
●​ Self-worth (“I’m a failure.”)

Research Support

Longitudinal studies found:

●​ Individuals with pessimistic attributional styles and dysfunctional beliefs were more likely
to experience major depression.
●​ High-risk individuals were 4 times more likely to have first episodes and 3 times more
likely to have recurrent episodes of depression.

Applications
Helps explain:

Sex differences in depression (women’s increased risk due to societal roles and greater
exposure to uncontrollable stressors).

How neuroticism increases sensitivity to adversity, contributing to higher depression rates,

particularly in women.

4. Ruminative Response Styles Theory of Depression

Developed by Susan Nolen-Hoeksema (1991, 2000, 2012).

Basic Premise

Focuses on how people respond to feelings of sadness and distress.

Two Types of Responses

1. Rumination

Constantly thinking about:

How bad they feel.

Why they feel that way.

Involves passive, repetitive, and negative thinking.

2. Distraction or Problem-Solving

Engaging in other activities to divert attention from negative emotions.

Taking action to solve the problems causing distress.

Consequences of Rumination Leads to

●​ Longer periods of depressive symptoms.

●​ Higher likelihood of developing major depressive disorder.

●​ Triggers negative memories, reinforcing depressive thinking.

Gender Differences
Women are more likely to:

●​ Ruminate, increasing depression risk.

Men often:

●​ Distract themselves or use substances like alcohol.

●​ Distraction is associated with reducing depression.

Prevention Implications

Teaching girls to use distraction strategies instead of ruminating may help prevent depression.

Individuals with negative thinking styles and high rumination are at greater risk for clinical
depression.

Bipolar and Related Disorders

Types of Bipolar Disorders: Distinctions and Features

Bipolar disorders differ from unipolar mood disorders mainly due to the presence of manic or
hypomanic episodes, often interspersed with depressive episodes. A manic episode involves an
excessively elevated, euphoric, or expansive mood, sometimes punctuated by irritability or
aggression—especially if others resist the manic individual’s grand plans. Hypomanic episodes
share the same core symptoms but are generally milder, causing less disruption to daily
functioning and not requiring hospitalization.

1. Cyclothymic Disorder (Cyclothymia)

Definition: Cyclothymic disorder is characterized by chronic, fluctuating mood disturbances,

including periods of hypomanic symptoms and periods of depressive symptoms that don't meet
the criteria for major depressive or full hypomanic episodes.

Duration: Symptoms must persist for at least 2 years in adults (1 year in children and
adolescents).

Severity: Less severe than full-blown bipolar disorder but more intense than typical mood
swings.

Symptoms in Hypomanic Phase:

●​ Increased energy, creativity, and productivity.

●​ Enhanced physical and mental activity.
Symptoms in Depressive Phase:

●​ Low energy and motivation.

●​ Feelings of inadequacy.
●​ Social withdrawal.
●​ Pessimistic outlook and brooding behavior.

Risk: Individuals with cyclothymia are at a higher risk of progressing to Bipolar I or II disorders.

2. Bipolar I Disorder

Definition: Bipolar I involves at least one manic episode, often coupled with depressive
episodes. Even without meeting the full criteria for major depression, a diagnosis of Bipolar I
can be made if mania occurs.

Manic Episode Features:

●​ Grandiosity (e.g., unrealistic plans or beliefs).

●​ Decreased need for sleep.
●​ Excessive involvement in risky activities (e.g., spending sprees, reckless behavior).
●​ Pressured speech and racing thoughts.

Depressive Episode:

●​ May or may not meet full criteria for major depressive disorder.

Mixed Episodes:

●​ Co-occurrence of manic and depressive symptoms.

●​ Associated with a worse long-term prognosis.

Case Example:

Tim, a 25-year-old, experienced periods of severe depression and recently exhibited classic
mania—grandiose ideas, excessive spending, risky behavior, and sleep deprivation.

3. Bipolar II Disorder

Definition: Bipolar II is characterized by at least one hypomanic episode and one or more major
depressive episodes. There are no full manic or mixed episodes.

Features:

●​ Hypomanic episodes are less intense than manic ones.

 ●​ Major depressive episodes are often severe and debilitating.

Progression:

Bipolar II rarely evolves into Bipolar I (5-15% of cases).

Prevalence:

Slightly more common or equally common compared to Bipolar I.

Onset:

Typically occurs about five years later than Bipolar I.

Gender Distribution:

Occurs equally in men and women, though depressive episodes are more common in women.

4. Rapid Cycling Bipolar Disorder

Definition: A specifier used when a person experiences four or more mood episodes (manic,
hypomanic, or depressive) in one year.

Characteristics:

More common in women.

Associated with early onset and frequent mood episodes.

Increases the risk of suicide attempts.

Triggers:

Sometimes induced by certain antidepressant medications.

Prognosis:

In about 50% of cases, rapid cycling subsides within two years.

Key Features Across Bipolar Disorders

Age of Onset:
Bipolar I: Typically between 18-22 years.

Bipolar II: Onset generally five years later than Bipolar I.

Recurrence:

Both Bipolar I and II are recurrent disorders.

Seasonality:

Episodes may follow seasonal patterns, leading to a diagnosis of bipolar disorder with a
seasonal pattern.

Symptom Duration:

Manic/hypomanic episodes are generally shorter than depressive episodes.

Depressive phases can last three times as long.

Severity:

Bipolar depressive episodes are more severe than unipolar depression, with more mood
swings, psychotic symptoms, and psychomotor retardation.

Misdiagnosis Risks:

Misdiagnosing bipolar depression as unipolar depression can lead to inappropriate treatments,

including antidepressants that may trigger manic episodes.

Long-Term Prognosis and Recovery

Challenges:

Bipolar disorders often involve chronic impairment in occupational and interpersonal functioning.

Recovery Rates:

Even with treatment, many patients spend about 20% of their lives experiencing mood
episodes.

High relapse rates: About 77% relapse within four years, and 82% within seven years.

Residual Symptoms:
Many individuals continue to experience subclinical symptoms for nearly half of their lives,
predominantly depressive symptoms.

Causal factors of Bipolar disorder

1. Biological Causal Factors (Primary Focus)

These are the dominant contributors to bipolar disorder.

a. Genetic Influences:

Strong genetic component, more than in unipolar depression.

First-degree relatives of someone with bipolar I disorder have an 8-10% risk, compared to 1% in
the general population.

Twin studies show:

About 60% concordance in monozygotic twins.

About 12% concordance in dizygotic twins.

Genes may account for 80-90% of the risk of developing bipolar I.

Polygenic inheritance: many genes contribute rather than one single gene.

Some genetic factors overlap with schizophrenia and depression.

b. Neurochemical Factors:

Norepinephrine: Increased during manic episodes; lower during depressive episodes.

Serotonin: Low during both mania and depression.

Dopamine: Increased dopamine linked to manic symptoms like euphoria and grandiosity. Drugs
that increase dopamine (like cocaine) can trigger mania.

Lithium: Works by reducing dopamine activity, acting as an anti-manic agent.

c. Hormonal Regulatory Systems:

HPA axis dysfunction:

Elevated cortisol in bipolar depression (similar to unipolar depression).

Less cortisol elevation during mania.

Thyroid function abnormalities:

Can affect mood.

Thyroid hormones can improve antidepressant effects but may trigger mania.

d. Neurophysiological & Neuroanatomical Influences:

PET and MRI scans show:

Decreased activity in the left prefrontal cortex during depression.

Increased activity in other prefrontal areas during mania.

Cognitive deficits: Problems with memory, attention, planning, etc.

Structural differences:

Basal ganglia and amygdala enlarged in bipolar disorder.

Hippocampal volume not decreased (unlike in unipolar depression)

Emotional processing areas like the thalamus and amygdala show increased activity.

e. Sleep and Biological Rhythms:

Disturbances in circadian rhythms are common:

Mania: Decreased need for sleep (often precedes manic episodes).

Depression: Hypersomnia (excessive sleep).

Sleep issues persist even between episodes.

Seasonal patterns suggest circadian involvement.

Bipolar individuals are sensitive to disruptions in their daily routines and biological clocks.
1. Cultural Influence on Expression of Mood Disorders

Cultural factors affect how mood disorders are expressed and how common they are.

Research often combines unipolar and bipolar disorders when looking at sociocultural
influences because many studies don’t separate them clearly.

2. Cross-Cultural Differences in Depressive Symptoms

Depression is universal—found in all cultures studied.

But the symptoms of depression look different across cultures:

Western cultures:

Focus on psychological symptoms (e.g., guilt, feelings of worthlessness, suicidal thoughts).

Non-Western cultures (e.g., China, Japan):

More physical (somatic) symptoms (e.g., sleep problems, appetite loss, weight loss, reduced
sexual interest).

Reasons for differences:

Asian cultures emphasize mind-body unity, meaning emotional distress often shows up as
physical symptoms.

Less emotional expressiveness and stigma around mental illness make people less likely to talk
about feelings like guilt.

Cultural values:

Western cultures focus on individualism → blame themselves for failures.

Many Asian cultures focus on interdependence, which affects how self-blame and guilt are
experienced.

Urbanization and Westernization:

As some countries (e.g., China) adopt Western values, rates of depression have increased.

Example: Hong Kong adolescents had higher levels of depressive symptoms and hopelessness
than American teens.
3. Cross-Cultural Differences in Prevalence of Mood Disorders

Mood disorder rates vary widely between countries.

WHO World Mental Health Survey showed:

0.8% prevalence in Nigeria.

9.6% prevalence in the United States.

Possible reasons:

Differences in stigma and willingness to report mental health issues.

Different psychosocial risk factors (e.g., stress, social support).

Cultural differences in pessimistic thinking and coping styles.

Early research suggests rumination, hopelessness, and pessimistic attribution styles are risk
factors in various cultures (e.g., China).

Here’s a simplified breakdown of the Treatments and Outcomes for mood disorders from the
material you shared:

Treatments and Outcomes for Mood Disorders

General Trends

●​ Many people with mood disorders (especially unipolar depression) don’t seek treatment.
●​ Even without treatment, most people recover within a year, but often the recovery is
temporary.
●​ Since the late 1980s, more people have sought treatment, especially with
antidepressants, although psychotherapy use has declined.
●​ Still, 60% of people with mood disorders don’t get proper treatment.
●​ Severe cases (both unipolar and bipolar) are more likely to get treatment than mild ones.

Pharmacotherapy (Medications)

1. Antidepressants

●​ Monoamine Oxidase Inhibitors (MAOIs)

●​ First generation antidepressants (1950s).
Prevent breakdown of norepinephrine and serotonin.
Effective, but dangerous if certain foods (like cheese, wine) are eaten → rarely used now.
Work well for atypical depression.

Tricyclic Antidepressants (TCAs)

●​ Main drugs from 1960s to early 1990s (e.g., imipramine).

●​ Increase norepinephrine and serotonin levels.
●​ Effective, but Only 50% of patients show strong improvement.
●​ Have unpleasant side effects (dry mouth, weight gain, sexual dysfunction).
●​ Toxic in large doses → risky for suicidal patients.

Selective Serotonin Reuptake Inhibitors (SSRIs)

●​ Commonly prescribed today (e.g., Prozac, Zoloft).

●​ Increase serotonin only.
●​ Fewer side effects than TCAs.
●​ Side effects: sexual problems, insomnia, agitation, upset stomach.
●​ Better tolerated, less dangerous in overdose.
●​ Often used for mild and severe depression, but most helpful in severe cases.

Atypical Antidepressants

Newer drugs like bupropion (Wellbutrin) and venlafaxine (Effexor).

●​ Bupropion: fewer sexual side effects, helps with low energy and weight gain.
●​ Venlafaxine: works well for severe or chronic depression, similar side effects to SSRIs.

Antidepressant Treatment Course

●​ Usually takes 3-5 weeks to feel better.

●​ If no improvement in 6 weeks, doctors may switch drugs.
●​ Stopping medication too early (after 3-4 months) often leads to relapse.
●​ Long-term use is often recommended to prevent recurrence, but 25% relapse even with
ongoing treatment.
●​ Residual symptoms increase relapse risk.

2. Mood-Stabilizing Drugs (For Bipolar Disorder)

Lithium

●​ Classic mood stabilizer for both mania and depression.

●​ Helps prevent mood swings, including cycling between mania and depression.
●​ 3/4 patients improve during manic episodes.
 ●​ Side effects: sluggish thinking, weight gain, poor coordination, kidney issues.
●​ Many patients stop taking it because they miss the highs of mania.
●​ Only about 1/3 stay episode-free over 5 years, but still better than no treatment.

Anticonvulsants

●​ Examples: carbamazepine, divalproex, valproate.

●​ Helpful if lithium doesn’t work or causes side effects.
●​ Higher suicide risk than lithium.
●​ Can be combined with lithium in some cases.

Antipsychotic Medications

●​ Given if patients (with unipolar or bipolar depression) have psychotic symptoms like
hallucinations or delusions.
●​ Often used alongside antidepressants or mood stabilizers.

2.Psychotherapy for Mood Disorders

●​ Since the 1970s, several specialized psychotherapy methods have been developed to
effectively treat unipolar depression.
●​ These treatments show improvement rates comparable to those of medications.
●​ Studies suggest psychotherapy, alone or combined with medication, can significantly
reduce the risk of relapse over a two-year period (Hollon & Dimidjian, 2009).

Cognitive-Behavioral Therapy (CBT)

●​ CBT, developed by Aaron Beck and his colleagues, is one of the most researched and
effective treatments for unipolar depression.
●​ It typically involves 10 to 20 sessions focusing on current problems rather than past
causes.
●​ Patients are taught to identify and challenge their negative thoughts and beliefs.
●​ CBT uses an empirical approach, encouraging patients to test their beliefs through
behavioral experiments.
●​ Studies confirm CBT is as effective as medication when administered by trained
therapists (Hollon et al., 2006).
●​ CBT has an advantage in preventing relapse, comparable to continued medication use
(Hollon & Ponniah, 2010).
●​ Brain imaging shows that CBT and medications affect different brain areas, suggesting
different mechanisms (Clark & Beck, 2010).
Effectiveness of CBT and Medication

●​ Both CBT and medication are equally effective for severe depression (DeRubeis et al.,
1999).
 ●​ In one study, 58% of patients responded to either treatment (DeRubeis et al., 2005).
●​ After a two-year follow-up, relapse rates were lower in patients who had CBT (25%)
compared to those who had medication (50%) (Hollon et al., 2005).

Mindfulness-Based Cognitive Therapy (MBCT)

●​ MBCT was designed for people with recurrent depression (Segal et al., 2002).
●​ Rather than changing negative thoughts, MBCT teaches patients to change their
relationship with their thoughts.
●​ It involves mindfulness meditation, helping patients accept thoughts and feelings without
judgment.
●​ Research shows MBCT reduces relapse risk in individuals with multiple previous
episodes of depression (Piet & Hougaard, 2011).

CBT and Bipolar Disorder

Modified CBT can be effective for bipolar disorder when combined with medication (Lam et al.,
2003).
MBCT may also help bipolar patients between mood episodes (Williams et al., 2008).

Behavioral Activation Therapy

●​ A newer approach focusing on increasing patients' activity levels and engagement with
their environment.
●​ Techniques include scheduling activities, rating enjoyment, and role-playing to develop
new behaviors.
●​ Emphasizes behavior change rather than cognitive restructuring.
●​ Behavioral activation can be as effective as CBT or medication for moderate to severe
depression (Dimidjian et al., 2006).
●​ It's easier to train therapists in this method, making it a promising area for future
treatment expansion.

Interpersonal Therapy (IPT)

●​ IPT focuses on resolving current relationship issues and maladaptive interaction

patterns.
●​ It is as effective as CBT and medication for unipolar depression (Hollon, Thase, &
Markowitz, 2002).
●​ Maintenance IPT, especially when combined with medication, reduces the risk of relapse
(Cuijpers et al., 2011).
●​ Adaptations of IPT for bipolar disorder focus on stabilizing daily routines and social
rhythms (Miklowitz & Craighead, 2007).

Family and Marital Therapy

 ●​ Addressing family stress and criticism can help prevent relapse in both unipolar and
bipolar disorders (Hooley, 2007).
●​ For bipolar patients, family interventions that reduce hostility and improve coping skills
are beneficial (Miklowitz, 2009).
●​ Marital therapy can be as effective as CBT for depressed individuals in conflicted
marriages and often leads to greater relationship satisfaction (Beach & Jones, 2002).

Conclusions on Psychotherapy

●​ Most patients recover from mood episodes within a year, even without treatment.
●​ Modern treatments have improved outcomes, but many individuals still do not receive
adequate care.
●​ Relapse and recurrence are common but can be minimized with continued medication
and therapy.
●​ Depression and bipolar disorder carry higher mortality risks due to suicide, health
neglect, and accidents (Goodwin & Jamison, 2007).
●​ Ongoing research is essential to develop better treatments and preventive strategies.
Clinical Picture of Schizophrenia (DSM-5)

The DSM-5 criteria for schizophrenia are continually evolving as research advances. Although
they closely resemble earlier versions (like DSM-IV-TR) and align with ICD criteria, one notable
change is the removal of the rule that an additional symptom need only be present when
delusions are bizarre or when certain types of auditory hallucinations occur.

Beyond a mere list, the symptoms illustrate the complex, multifaceted nature of schizophrenia.

Positive symptoms

Positive symptoms of schizophrenia are defined as excesses or distortions of normal mental

functions, including hallucinations, delusions, disorganized thinking, and abnormal motor
behavior.

Delusions

●​ Fixed, false beliefs maintained despite clear contradictory evidence.

●​ Derived from the Latin word for “to play,” implying that the mind is being tricked.

Characteristics

●​ Often unique to the individual, not shared by those with similar backgrounds.
●​ Can become complex systems where one belief leads to a network of related delusional
ideas.
●​ Not exclusive to schizophrenia but are present in over 90% of affected individuals.

Hallucinations

●​ Perceptions that appear real but occur without any external stimulus.
●​ Distinguished from illusions (misinterpretations of real stimuli).

Sensory Modalities

●​ Can affect any sense (auditory, visual, olfactory, tactile, gustatory).

●​ Auditory hallucinations (hearing voices) are the most common.

Key Points:

●​ Studies across countries report that about 75% of patients experience auditory
hallucinations.
●​ Visual hallucinations are less frequent (around 39%), and other types (olfactory, tactile,
gustatory) are rare.
 ●​ Even individuals who are deaf may report auditory-like hallucinations.
●​ Hallucinations often carry personal emotional or conceptual meaning and may even
influence behavior.

Disorganized Speech

●​ Reflects a disruption in the form (rather than the content) of thought.

●​ Patients may follow conventional language rules but their speech lacks coherent
meaning.

Manifestations:

●​ “Cognitive slippage” or “derailment” where associations loosen.

●​ Extreme forms may include incoherence or the use of neologisms—new, made-up words
that resemble real words but have no defined meaning.
●​ Such speech disturbances reveal the underlying breakdown in organized thought.

Disorganized Behavior and Catatonia

Disorganized Behavior:

●​ Marked by significant disruption in purposeful, goal-directed activity.

●​ Affects daily routines such as work, social interactions, and self-care.
●​ May manifest as neglect of personal hygiene or engagement in bizarre, seemingly
purposeless actions (for example, dressing inappropriately for the weather).
●​ Often linked to impairments in executive functions, notably those associated with the
prefrontal cortex.

Catatonia:

●​ Represents a severe form of disorganized behavior.

●​ Patients may display extreme motor abnormalities:
●​ Stupor: Near-complete absence of movement or speech.
●​ Maintained Postures: Holding unusual positions for extended periods without discomfort.
●​ Catatonic symptoms can be among the most striking and are sometimes considered for
novel treatment approaches (e.g., using transcranial magnetic stimulation).

Negative Symptoms of Schizophrenia

Negative symptoms in schizophrenia refer to a loss or reduction of normal functions, contrasting

with positive symptoms like delusions and hallucinations, which reflect excesses or distortions of
normal behavior.

Main Domains of Negative Symptoms

(Barch, 2013; Kring et al., 2013)

1. Reduced Expressive Behavior:

Blunted Affect: Decreased intensity of emotional expression.

Flat Affect: Complete lack of emotional expressiveness.
Alogia: Poverty of speech, reflecting diminished thought productivity.

2. Decreased Motivation and Pleasure:

Avolition: Inability to initiate or sustain goal-directed activities (e.g., neglecting work or social
interactions).
Anhedonia: Diminished ability to experience pleasure from normally enjoyable activities.

Clinical Significance

Prognostic Value: The presence of persistent negative symptoms often predicts poorer
outcomes, including long-term functioning and quality of life (Malla & Payne, 2005; Milev et al.,
2005).

Emotional Experience vs. Expression

●​ Although patients may appear emotionally flat, research (e.g., Kring & Neale, 1996)
shows they often experience emotions normally or even intensely.
●​ For instance, when watching emotional film clips, patients showed less facial
expressiveness, but reported similar or greater emotional feelings than healthy controls
and even demonstrated greater physiological arousal.

Research Insights

●​ Emotional unresponsiveness in schizophrenia is often misinterpreted as emotional

numbness.
●​ The disconnection between internal emotional experience and external expression is a
defining feature of negative symptoms.
●​ These findings challenge stereotypes of individuals with schizophrenia as unemotional
or indifferent.

Implications for Treatment

●​ Negative symptoms are less responsive to antipsychotic medications than positive

symptoms.
●​ Effective treatment often includes psychosocial interventions, such as:
 ○​ Cognitive-behavioral therapy (CBT) focused on motivation.
○​ Social skills training to enhance expressive behavior.
○​ Occupational therapy to support goal-directed activity.

Schizophrenia Subtypes (Historical Classification – Pre-DSM-5)

Before the publication of the DSM-5 in 2013, schizophrenia was divided into five subtypes:
paranoid, disorganized (hebephrenic), catatonic, residual, and undifferentiated. These subtypes
were meant to capture variations in symptom patterns and aid in diagnosis and treatment
planning. However, due to overlapping symptoms, inconsistent reliability, and lack of predictive
validity, the DSM-5 eliminated these categories, shifting to a dimensional approach that
assesses symptom severity across domains (positive, negative, disorganized, cognitive, and
motor symptoms).

Despite their removal from current diagnostic manuals, these subtypes still offer clinical insight
into the diverse presentations of schizophrenia.

1. Paranoid Schizophrenia (Former Subtype)

●​ Characterized mainly by delusions and auditory hallucinations.

●​ Most common and best-known subtype before DSM-5.

Key Features:

●​ Prominent persecutory or grandiose delusions.

●​ Auditory hallucinations (voices giving commands or commentary).
●​ Relatively preserved cognitive and emotional function.
●​ Minimal disorganized behavior.
●​ Later onset (late 20s–30s).

Symptoms

●​ Positive: Delusions, hallucinations, paranoia.

●​ Negative: Mild (e.g., social withdrawal).
●​ Cognitive: Generally intact.

Treatment
●​ Typical and atypical antipsychotics, CBT, family therapy, social skills training.

Prognosis
●​ Often more favorable than other subtypes.
2. Disorganized Schizophrenia (Hebephrenic Type)

●​ Defined by severe disorganization in speech, behavior, and affect.

●​ Usually has early onset and chronic progression.

Key Features:

●​ Incoherent speech (e.g., loose associations, word salad).

●​ Inappropriate or flat emotional expression.
●​ Erratic or bizarre behavior.

Symptoms:

●​ Positive: Disorganized speech and behavior.

●​ Negative: Blunted affect, social withdrawal.
●​ Cognitive: Significant impairment.

Onset
●​ Late teens to early 20s.

Treatment
●​ Atypical antipsychotics, CBT, occupational therapy, social training.

Prognosis
●​ Less favorable due to early onset and severe disorganization.

3. Catatonic Schizophrenia

●​ Characterized by extreme motor disturbances, ranging from immobility to hyperactivity.

Key Features:

●​ Motoric immobility (stupor), waxy flexibility.

●​ Mutism, negativism.
●​ Posturing, stereotypy, echolalia, echopraxia.

Symptoms

●​ Positive: Echolalia, echopraxia, agitation.

●​ Negative: Mutism, rigidity, stupor.
●​ Cognitive: Impaired by psychomotor symptoms.

Treatment
●​ First-line: benzodiazepines (e.g., lorazepam); ECT for severe cases; supportive care.
Prognosis:
●​ Good with early intervention; poor if chronic or untreated.

4. Residual Schizophrenia

●​ Represents a chronic phase with persistent negative symptoms after active psychosis
subsides.

Key Features:

●​ Absence of prominent delusions or hallucinations.

●​ Persistent negative symptoms (e.g., flat affect, avolition).
●​ Occasional low-level psychotic features.

Symptoms

●​ Negative: Avolition, anhedonia, flat affect.

●​ Cognitive: Impaired attention, memory.
●​ Positive: Mild or absent.

Treatment
●​ Maintenance antipsychotics, CBT, vocational rehab, social support.

Prognosis
●​ Chronic functional impairments; requires long-term care.

5. Undifferentiated Schizophrenia

●​ A catch-all category for individuals who meet general criteria for schizophrenia but do not
clearly fit into any one subtype.

Key Features

●​ Mixed or overlapping symptoms from other subtypes.

●​ Inconsistent presentation.
●​ Often used when symptom profile is variable or evolving.

Symptoms

●​ Combination of positive, negative, cognitive, and/or disorganized features.

Treatment:
●​ Tailored to individual symptoms; often requires flexible and multidisciplinary intervention.
Prognosis:
●​ Varies widely depending on dominant symptoms and treatment response.

DSM-5 Note

●​ The DSM-5 (2013) discontinued the use of subtypes due to their poor reliability and
limited clinical utility.
●​ Schizophrenia is now diagnosed using a dimensional approach that assesses severity
across multiple symptom domains:

●​ Positive symptoms
●​ Negative symptoms
●​ Disorganized thinking/behavior
●​ Cognitive impairment
●​ Psychomotor (catatonic) features

Schizophrenia – Simplified DSM-5 Criteria

A. Main Symptoms (at least 2, lasting for at least 1 month):

At least one must be from 1, 2, or 3:

1. Delusions – Strong beliefs that aren’t based in reality (e.g., thinking others are out to harm
you).
2. Hallucinations – Seeing or hearing things that aren’t there.
3. Disorganized speech – Talking in a confused way that’s hard to follow.
4. Disorganized or catatonic behavior – Acting strangely, or not moving/responding at all.
5. Negative symptoms – Lack of emotion, motivation, or speech.

B. Life Disruption:
The person has trouble functioning at work, school, in relationships, or taking care of
themselves.

C. Duration:
The illness lasts at least 6 months, including at least 1 month of major symptoms (from A).
Other times may include milder symptoms (like odd thoughts or reduced motivation).

D. Rule Out Mood Disorders:

Other conditions like depression or bipolar disorder with psychotic features have been ruled out
because:
●​ Either no mood episodes happened during the illness,
●​ Or if they did, they were brief compared to the whole illness.

E. Not Caused by Substances or Medical Conditions:

The symptoms are not due to drugs, alcohol, or other medical problems.
F. If Autism or Childhood Language Problems Are Present
A diagnosis of schizophrenia is only made if delusions or hallucinations are clear and last at
least 1 month.

Schizoaffective Disorder

Schizoaffective disorder is a mental health condition that includes symptoms of schizophrenia

(like hallucinations or delusions) and major mood disorder symptoms (like depression or mania).
It’s kind of a mix between schizophrenia and a mood disorder.

There are two subtypes:

●​ Depressive type – if the mood problems are only depression

●​ Bipolar type – if mood includes both depression and mania

People with this disorder experience:

●​ Psychotic symptoms (like hearing voices or having strange beliefs)

●​ Mood changes (feeling extremely sad or very high/energetic)

DSM-5 Criteria for Schizoaffective Disorder (Simplified)

A. Mixed Symptoms:
The person has a time period where:

●​ They show schizophrenia symptoms (like delusions, hallucinations, disorganized

speech),
●​ At the same time as a major mood episode (either depression or mania).
●​ (Note: Depression must include low mood.)

B. Psychotic Symptoms Alone:

There must be at least 2 weeks of delusions or hallucinations without mood symptoms.
(This helps show that the psychosis is not only caused by the mood disorder.)

C. Mood Symptoms Last Longer:

The mood symptoms (depression or mania) must be present for more than half of the total time
the person is unwell.

D. Not Due to Substances or Medical Illness:

The symptoms are not caused by drugs, alcohol, or other medical problems.

Prognosis (What Happens Long-Term?)

Outcome is usually better than schizophrenia

But not as good as people who have just mood disorders
With proper treatment, people often do well over time

Schizophreniform Disorder

●​ Schizophreniform disorder is similar to schizophrenia, but it lasts for a shorter time.

●​ It includes the same kinds of symptoms as schizophrenia.
●​ But it lasts at least 1 month and less than 6 months.
●​ Because it’s shorter, people often recover faster and better than those with full
schizophrenia.

DSM-5 Criteria for Schizophreniform Disorder (Simplified)

A. Core Symptoms (at least 2, lasting at least 1 month)

At least one must be from 1, 2, or 3:

1. Delusions – false beliefs not based on reality.

2. Hallucinations – seeing/hearing things that aren't there.
3. Disorganized speech – talking in a confusing way.
4. Disorganized or catatonic behavior – strange movements or no movement at all.
5. Negative symptoms – reduced emotions, speech, or motivation.

B. Duration:
The episode lasts at least 1 month but less than 6 months.
If the person hasn’t recovered yet, the diagnosis is called “provisional”.

C. Rule Out Mood Disorders

The symptoms are not better explained by:

A mood disorder like depression or bipolar with psychosis,

OR, if mood symptoms are present, they are brief compared to the psychotic symptoms.

D. Not Caused by Drugs or Medical Conditions

The symptoms are not due to drug use or a medical illness.

Prognosis (Outcome)

●​ Better than schizophrenia, especially if treated early

●​ Some people recover completely after one episode

Delusional Disorder

Delusional disorder is when a person has one or more strong false beliefs (delusions) that last
for at least 1 month.
These beliefs may seem strange or untrue to others, but the person otherwise acts quite
normal.

Unlike schizophrenia:

●​ There’s no major disorganized behavior

●​ The person can often work and socialize normally
●​ They don’t lose touch with reality completely

DSM-5 Criteria for Delusional Disorder (Simplified)

A. Delusions Lasting 1 Month or More

●​ The person has one or more fixed false beliefs (e.g., being followed, loved by someone
famous, poisoned).

B. No Schizophrenia Diagnosis

●​ The person has never met full criteria for schizophrenia (e.g., no major hallucinations,
disorganized speech, etc.).

C. Normal Functioning (Besides the Delusion)

●​ Apart from the delusion, the person’s life is usually normal.

●​ Their behavior isn’t obviously strange or bizarre.

D. Mood Episodes Are Brief (If Present):

●​ If there are mood issues like depression or mania, they are short compared to the
delusion period.

E. Not Caused by Drugs or Other Medical Issues:

●​ The symptoms are not due to substance use, medication, or another mental/medical
condition.

Brief Psychotic Disorder

●​ This disorder is a short, sudden episode of psychotic symptoms like:

●​ Delusions (false beliefs),

●​ Hallucinations (seeing/hearing things that aren’t there),
●​ Disorganized speech,
●​ Or very strange behavior (catatonia).
It usually:

○​ Happens suddenly, often after stress,

○​ Lasts for at least 1 day but less than 1 month,
○​ And the person completely recovers and goes back to normal functioning.

DSM-5 Criteria for Brief Psychotic Disorder (Simplified)

A. Main Symptoms (1 or more):

At least one of these must be present:

1. Delusions
2. Hallucinations
3. Disorganized speech
4. Disorganized or catatonic behavior

Note: These symptoms should not be part of a cultural or religious belief system.

B. Duration:
The episode lasts at least 1 day but less than 1 month,
and the person returns to normal afterward.

C. Not Due to Other Conditions

The symptoms are not caused by:

●​ A mood disorder with psychosis (like bipolar or major depression),

●​ Schizophrenia or similar psychotic disorders,
●​ Drugs, medications, or a medical illness.

Extra Note:

●​ Often triggered by intense stress (like trauma or a sudden loss).

●​ People may never have another episode again.

Causal factors for schizophrenia

I. Genetic and Biological Causes

1. Genetic Contributions

●​ Schizophrenia is highly heritable, but it’s not caused by one gene.

●​ It results from multiple common genetic variants, each contributing small risk, or rare
mutations (e.g., microdeletions or duplications of DNA).
●​ Risk increases with genetic closeness:
 ○​ 1st-degree relatives (parents, siblings, children): ~10% risk.
○​ Monozygotic twins: ~48%.
○​ General population: ~1%.

2. Prenatal and Perinatal Risk Factors

These are early life complications that interact with genetic vulnerability:

a) Prenatal Infections

Exposure to viruses like influenza during the first or second trimester increases risk. One study
found a 7-fold increase in offspring schizophrenia after first-trimester flu exposure.

b) Nutritional Deficiency

During the Dutch Hunger Winter (1944–45), children conceived in famine had double the risk of
schizophrenia, linking early malnutrition (especially folate, iron) to faulty brain development.

c) Maternal Stress

Stressful events in early pregnancy (e.g., death of a close relative) are linked to a 67%
increased risk for schizophrenia in the child. Elevated maternal cortisol may affect fetal brain
development.

d) Rh Incompatibility & Oxygen Deprivation

Rh incompatibility and obstetric complications (like prolonged labor or cord issues) may lead to
hypoxia (oxygen loss), increasing schizophrenia risk.

II. Neurodevelopmental Factors

●​ Schizophrenia may begin early in fetal brain development. Environmental events (like
viruses or malnutrition) can affect gene expression, disturbing neuronal migration or
connectivity before birth.
●​ Symptoms usually emerge in late adolescence when the brain undergoes key changes
(e.g., synaptic pruning, white matter expansion), revealing earlier damage.

III. Brain Abnormalities

1. Structural Brain Changes

a) Enlarged Ventricles
Ventricles are fluid-filled brain spaces. Enlarged ventricles suggest brain tissue loss, especially
in frontal, temporal, and limbic areas.
b) Reduced Gray Matter

Patients often show 3% less gray matter, especially in early stages. Progressive gray matter
loss continues with illness progression.

c) White Matter Abnormalities

Patients show disrupted myelination and reduced white matter volume, affecting brain
connectivity. This explains cognitive dysfunction, hallucinations, and fragmented thinking.

2. Functional Abnormalities

a) Frontal Lobe Dysfunction

●​ “Hypofrontality” is observed—reduced activation in tasks involving planning, attention, or

problem-solving.
●​ Explains negative symptoms and poor executive function.

b) Temporal & Limbic Abnormalities

●​ Abnormalities in the hippocampus, amygdala, and thalamus relate to memory, emotion,

and sensory integration.

IV. Neurochemical Theories

1. Dopamine Hypothesis

●​ Schizophrenia involves excess dopamine activity in the mesolimbic pathway (causing

positive symptoms) and dopamine deficiency in the prefrontal cortex (causing negative
symptoms).
●​ This is supported by:

○​ Antipsychotics blocking dopamine receptors.

○​ Drugs increasing dopamine (like amphetamines) worsen symptoms.

2. Glutamate Hypothesis

●​ NMDA glutamate receptor dysfunction may cause cognitive deficits and psychosis.
●​ Drugs like ketamine or PCP (which block glutamate) mimic schizophrenia symptoms.

V. Psychosocial and Environmental Factors

1. Expressed Emotion (EE) in Families

●​ Families high in criticism, hostility, or over-involvement can increase relapse rates in

patients.
●​ EE is not a cause, but it affects the course of the disorder.

2. Urban Living

●​ Higher schizophrenia rates are found in urban areas, possibly due to social stress or
environmental toxins.

3. Migration

●​ Second-generation immigrants face higher risks, likely due to social adversity and
discrimination.

4. Cannabis Use

●​ Heavy adolescent cannabis use increases risk, particularly in genetically vulnerable

individuals.
●​ Cannabis users with schizophrenia show faster gray matter loss over time.

VI. Diathesis–Stress Model

●​ Schizophrenia results from a combination of biological vulnerability (diathesis) and

environmental stressors.
●​ For example, a genetically at-risk individual exposed to early infections or family stress is
more likely to develop the disorder.

Clinical Outcome of Schizophrenia and Treatment

Clinical Outcome

The prognosis for schizophrenia has significantly improved since the 1950s, thanks to the
advent of antipsychotic medications. Clinical outcomes vary, but around 38% of patients show
favorable outcomes with recovery, meaning they can function well with therapy and medication.
However, full recovery to the pre-illness state is rare. For some patients, long-term
institutionalization is necessary, and about a third continue to show significant symptoms,
particularly negative ones. Recovery rates can be even lower (around 14%) when stringent
criteria are applied. Interestingly, individuals in less industrialized countries tend to fare better
than those in more industrialized nations, possibly due to lower levels of expressed emotion
(EE) in families.

Mortality and Health Risks

Schizophrenia is associated with a reduced life expectancy, with individuals dying 14.6 years
earlier (for men) or 17.5 years earlier (for women with schizoaffective disorder) than expected.
Contributing factors include long-term use of antipsychotic medications, obesity, smoking, poor
diet, and physical inactivity. There is also a high suicide risk, with 12% of patients with
schizophrenia taking their lives. However, antipsychotic medications reduce mortality when
compared to untreated patients, likely because they help manage psychotic symptoms that
could pose a risk to self-harm.

1.Pharmacological Approaches

First-Generation Antipsychotics

These medications, such as chlorpromazine (Thorazine) and haloperidol (Haldol), were

revolutionary when introduced in the 1950s. They block dopamine D2 receptors in the brain,
which helps alleviate positive symptoms like delusions and hallucinations. Although they are
effective, they come with significant side effects, such as:

Extrapyramidal Symptoms (EPS): These include muscle spasms, rigidity, and tremors that
resemble Parkinson’s disease.
Tardive Dyskinesia: Long-term use can cause involuntary movements of the mouth, lips, or
tongue.
Neuroleptic Malignant Syndrome: A rare, but potentially fatal reaction causing high fever and
severe muscle rigidity.

Second-Generation Antipsychotics

Introduced in the 1980s, medications like clozapine (Clozaril), risperidone (Risperdal), and
olanzapine (Zyprexa) are considered second-generation or atypical antipsychotics. These
medications are associated with fewer EPS than first-generation drugs but still cause common
side effects like:

●​ Weight gain
●​ Drowsiness
●​ Diabetes: Increased risk, particularly with medications like olanzapine.
●​ Agranulocytosis: A serious drop in white blood cells, particularly with clozapine, requiring
regular blood tests.

Second-generation antipsychotics are often preferred due to their more favorable side effect
profile, but their efficacy does not significantly surpass first-generation drugs, except for
clozapine, which is especially helpful for treatment-resistant cases.
2.Other Approaches

Recent research suggests that estrogen might play a role in improving symptoms of
schizophrenia, especially in women. A study found that women treated with estrogen patches, in
addition to antipsychotics, showed significant symptom improvement, particularly in positive
symptoms like delusions and hallucinations. This offers promising insight into potential
adjunctive treatments, though further research is needed.

2.1 The Patient’s Perspective

This section emphasizes the challenges faced by patients with schizophrenia when it comes to
treatment, particularly the long-term use of antipsychotic medications. While these medications
can help manage symptoms like hallucinations and delusions, many patients experience
significant side effects, such as tiredness, depression, weight gain, and involuntary movements.
These side effects can lead to a lack of adherence to medication regimens.

Key Points:

●​ Side Effects: Even when medications provide relief, the side effects (such as weight gain
or movement issues) can significantly affect a patient's quality of life.
●​ Reluctance to Take Medication: Some patients might resist taking medications because
doing so might confirm for them that they are mentally ill. This sense of stigma or denial
can be a major barrier to treatment adherence.
●​ Need for Better Medications: The article stresses the importance of developing
medications with fewer side effects, or using lower doses to minimize the negative
impact while still providing clinical benefits.
●​ The patient’s experience is central to understanding the complex nature of schizophrenia
treatment. It isn't just about managing the illness but also acknowledging the
psychological burden of having to take medication for the long term, especially if the
individual is struggling with self-stigma.

2.2. Psychosocial Approaches

Medications are essential in the treatment of schizophrenia, but the importance of psychosocial
approaches cannot be overstated. These approaches aim to address the social and functional
challenges that arise from the illness.

Family Therapy

●​ Expressed Emotion (EE): One important concept is "expressed emotion" (EE), which
refers to the negative attitudes and behaviors displayed by family members, such as
criticism, hostility, and emotional over-involvement. High EE is linked to relapse in
schizophrenia patients, making family therapy an important part of treatment.
 ●​ Family Intervention Programs: These programs aim to reduce high EE by educating
families about schizophrenia and helping them develop better coping, communication,
and problem-solving skills. Research shows that when families participate in these
programs, patients experience fewer relapses, and there are generally better clinical
outcomes.
●​ Cultural Sensitivity: The effectiveness of family therapy has also been demonstrated
across different cultures, making it a widely applicable intervention.

Case Management

●​ Role of Case Managers: Case managers help patients navigate the complex mental
health system, ensuring that they get the necessary services, such as housing,
employment, and healthcare. Assertive community treatment programs are a more
intensive form of case management that involve multidisciplinary teams who work
directly with patients to ensure stability and prevent them from getting "lost in the
system."
●​ Cost-Effectiveness: These programs are not only effective but also cost-efficient. They
reduce hospitalizations and help maintain stable living situations for patients, which is
crucial for long-term recovery.

Social-Skills Training

●​ Functional Outcome vs. Clinical Outcome: A major challenge for patients with
schizophrenia is the difficulty they face in social situations, such as making friends,
holding down a job, or living independently. Functional outcomes (real-world abilities) are
often less focused on in traditional treatments, but social-skills training seeks to address
this gap by helping patients develop interpersonal, employment, and daily living skills.
●​ Training Approach: Social-skills training breaks down tasks like conversation into
smaller, manageable components (e.g., making eye contact, speaking at a moderate
volume), allowing patients to learn, practice, and apply these skills in real-life settings.
Research indicates that this type of training improves patients' social functioning and
reduces relapse rates.

Cognitive Remediation

●​ Cognitive Deficits: Schizophrenia often involves cognitive impairments such as issues

with attention, memory, and executive functioning (planning, problem-solving, etc.).
Cognitive remediation seeks to address these deficits through exercises and training,
helping patients improve skills like memory and focus, which can enhance their overall
functioning.
●​ Long-Term Benefits: Cognitive remediation appears to be effective even for patients who
have been ill for many years, making it a promising area of treatment. It can be
 combined with other rehabilitation strategies like employment training to further improve
outcomes.

Cognitive-Behavioral Therapy (CBT)

●​ CBT for Schizophrenia: CBT is a widely used therapy for mood and anxiety disorders,
and it has gained traction as a treatment for schizophrenia. The goal is to help patients
understand and challenge the delusions and hallucinations that they experience by
examining evidence for and against these beliefs.
●​ Effectiveness: Research on CBT for schizophrenia has yielded mixed results. While it
seems to help with positive symptoms (delusions, hallucinations), it does not appear to
be effective for negative symptoms (e.g., lack of motivation, social withdrawal). Recent
meta-analyses suggest that CBT might not be superior to other treatments like
supportive counseling.
●​ Subgroup Effectiveness: However, CBT may still be beneficial for certain subgroups of
patients, suggesting that more targeted approaches may be needed to fully harness its
potential.

Individual Treatment

●​ Early Psychoanalytic Therapy: Prior to the 1960s, psychoanalytic therapy (based on

Freudian principles) was considered a standard treatment for schizophrenia. However,
research in the 1980s showed that such treatments could sometimes worsen patients'
conditions.
●​ Personal Therapy: Today, treatments like personal therapy are more effective. This
non-psychodynamic approach focuses on providing patients with coping strategies and
skills at different stages of their recovery. Personal therapy may include stress
management, relaxation techniques, and social skills training. It aims to improve the
patient’s social adjustment and role performance, making them more capable of living
independently.
●​ Psychoeducation: Educating patients about their illness and treatment options (called
psychoeducation) is also essential for improving outcomes. Studies have shown that
patients who receive psychoeducation are less likely to relapse and are more satisfied
with their treatment.

3. Summary and Conclusion

In conclusion, the treatment of schizophrenia requires a multifaceted approach that balances

pharmacological treatments with psychosocial interventions. Medications alone are often not
enough, as patients need support in various areas of their lives, such as managing social
interactions, improving cognitive function, and coping with the stigma of mental illness.
Pharmacological Treatment: Medication remains the cornerstone for managing the core
symptoms of schizophrenia, but side effects and the stigma of taking medication can present
significant challenges for patients.

Psychosocial Approaches: Family therapy, case management, social-skills training, cognitive

remediation, and CBT all offer complementary benefits, addressing the broader psychosocial
needs of patients.

Support and Respect: Throughout all treatments, it is critical to provide patients and their
families with support, validation, and respectful care. Schizophrenia treatment is not
one-size-fits-all, and ongoing, personalized care is necessary for the best outcomes.

Progressive Muscle Relaxation (PMR) from the article:

What It Is

Progressive Muscle Relaxation (PMR) is a stress-reduction technique developed by Edmund

Jacobson in the 1920s. It involves systematically tensing and then relaxing different muscle
groups in the body to promote deep physical relaxation and increase awareness of physical
tension.

Purpose

The main goal of PMR is to calm the nervous system by reducing the physical symptoms of
stress (like muscle tension) and to train the body to recognize and release that tension.

Steps to Practice PMR

1. Get Comfortable – Sit or lie down in a quiet space.

2. Focus on Breathing – Begin with slow, deep breaths.

3. Tense and Relax Muscles – Starting from the feet and working upwards:

Tense each muscle group (e.g., feet, calves, thighs, abdomen, etc.) for about 5 seconds.
Release for 10–20 seconds and notice the contrast between tension and relaxation.

4. Repeat as Needed – Go through all major muscle groups or focus on areas of tension.

Behind the Science

PMR works by calming the sympathetic nervous system (which controls the fight-or-flight
response) and activating the parasympathetic nervous system, which helps the body relax.
Tensing muscles mimics the physical state of stress, and relaxing them teaches the brain to shift
into a calmer state.
This change lowers heart rate, blood pressure, and breathing rate.

Why It’s Needed

PMR is especially useful in modern life due to high stress levels and sedentary habits that lead
to chronic tension. It’s beneficial for:

Anxiety and depression: Shown to reduce symptoms by nearly 50% in some studies.
Blood pressure control: Helps lower both systolic and diastolic levels.
Headaches: Reduces the frequency and severity of migraines and tension headaches.
Chronic pain: Aids in managing conditions like fibromyalgia and osteoarthritis.

Absolutely! Here's a more elaborated version of the study notes for Mindfulness Exercises from
the Mayo Clinic, perfect for deeper understanding and revision:

---

Mindfulness Exercises – Elaborated Study Notes

---

I. Understanding Mindfulness

Definition:

Mindfulness is the practice of paying full attention to the present moment — without judgment.

It involves becoming fully aware of where we are, what we’re doing, and how we’re feeling,
rather than being reactive or overwhelmed by what's happening around us.

Core Principle:

"Be here now." Mindfulness trains the mind to focus on the present rather than dwelling on the
past or worrying about the future.

Psychological Benefits:

Reduces symptoms of stress, anxiety, and depression.

Enhances self-awareness, emotional regulation, and resilience.

Improves cognitive flexibility and attention span.

---

II. Key Mindfulness Exercises

1. Focused Breathing

How to Practice:

Sit comfortably, close your eyes if you’re comfortable doing so.

Pay attention to your breath as it enters and exits your nose or mouth.

Observe the rhythm, depth, and sensation of breathing.

Purpose & Benefits:

Anchors your mind to the present.

Soothes the nervous system and calms mental chatter.

Reduces physiological symptoms of stress (like heart rate and blood pressure).

Tips:

If your mind wanders (which it will), gently guide it back to the breath.

Practice for 5–10 minutes to start, then increase over time.

---

2. Body Scan Meditation

How to Practice:
Lie down or sit in a comfortable position.

Slowly direct your attention to different parts of your body—starting from your toes and moving
upward.

Notice sensations (warmth, tension, tingling) without trying to change them.

Purpose & Benefits:

Enhances body awareness and helps identify areas of stress or discomfort.

Encourages relaxation and self-connection.

Useful for managing chronic pain and tension.

Tips:

Take deep breaths as you shift focus from one part of the body to another.

Don’t analyze or label sensations—just observe and accept.

---

3. Sitting Meditation

How to Practice:

Sit in a quiet space with your back straight, hands in your lap or on your knees.

Breathe naturally and observe your thoughts, feelings, and bodily sensations as they come and
go.

Purpose & Benefits:

Trains non-judgmental awareness.

Increases tolerance of difficult emotions and thoughts.

Cultivates patience and inner stillness.

Tips:

Set a timer (start with 5–10 minutes).

Use a mantra or word (like "peace" or "now") to anchor your attention if helpful.

---

4. Walking Meditation

How to Practice:

Walk slowly and mindfully in a quiet space (indoors or outdoors).

Focus on the movement of your legs and feet, the contact with the ground, and the rhythm of
your steps.

Tune into the sensations of each step and the environment around you.

Purpose & Benefits:

Combines movement and mindfulness.

Grounds you in the present and improves physical awareness.

Great for those who find sitting still difficult.

Tips:

Walk at a slower pace than usual.

Avoid distractions like phones or conversations.

---
III. Daily Practice Tips

Start small – even 2–5 minutes daily can make a difference.

Be consistent – regular practice builds long-term benefits.

Be kind to yourself – it’s normal for the mind to wander.

Use reminders – set an alarm or use apps to stay consistent.

---

IV. Long-Term Benefits of Mindfulness

1. Emotional Health:

Improved mood and reduced emotional reactivity.

2. Cognitive Benefits:

Better focus, memory, and decision-making.

3. Physical Health:

Lower blood pressure, better sleep, reduced chronic pain.

4. Social Benefits:

Enhanced empathy, communication, and relationships.

---
Would you like a visual summary or flashcards based on these notes? Or want me to turn this
into a printable PDF?

HYPNOTHERAPY STUDY NOTES

1. What is Hypnotherapy?

Definition:
Hypnotherapy, also called hypnosis, is a guided therapeutic technique that uses deep relaxation
and focused attention to access a person's subconscious mind.
In this state, the individual is more receptive to suggestions, which can help them make positive
changes in their thoughts, feelings, or behaviors.

State of Hypnosis:
Hypnosis is a natural state similar to daydreaming or being deeply absorbed in a book or movie.
The person is not asleep but is in a trance-like condition with heightened focus and
concentration.

2. How Does Hypnotherapy Work?

Induction Phase:
The hypnotherapist helps the client relax using techniques like guided imagery, verbal repetition,
and calming tones. This process is called induction.

Therapeutic Phase:
While in this relaxed state, the therapist makes positive and goal-oriented suggestions. These
suggestions can influence the person’s thoughts, emotions, perceptions, or behaviors.

Termination Phase:
The therapist gradually brings the client back to full awareness, and the client usually
remembers everything that occurred during the session.

Important Note:
Despite popular myths, the person under hypnosis is not asleep, and cannot be made to do
something against their will.

3. What Can Hypnotherapy Help With?

A. Mental and Emotional Health:

●​ Anxiety and Stress

 Helps reduce generalized anxiety, test anxiety, and performance anxiety by promoting
calmness and control.
●​ Phobias
Effective in treating irrational fears (e.g., fear of flying, heights, public speaking).
●​ Depression and Low Mood
Can support other therapies by reinforcing positive thoughts and behaviors.
●​ Insomnia and Sleep Disorders
Promotes relaxation and can help establish healthier sleep patterns.
●​ Post-Traumatic Stress Disorder (PTSD)
Used carefully to reduce flashbacks and emotional distress.

B. Physical Health Conditions:

●​ Chronic Pain
Reduces the perception of pain in conditions like arthritis, migraines, and fibromyalgia.
●​ Irritable Bowel Syndrome (IBS)
Research supports its effectiveness in easing IBS symptoms through gut-directed
hypnotherapy.
●​ Nausea and Vomiting (especially in cancer patients)
Helps manage side effects of chemotherapy or other medical treatments.
●​ Skin Conditions
Can improve symptoms of psoriasis, eczema, or even help remove warts through mental
suggestion.
●​ Pain During Medical Procedures
Used during childbirth, dental treatments, and surgeries to reduce pain and anxiety.

C. Behavioral and Habitual Issues:

●​ Smoking Cessation
Helps people quit smoking by reducing cravings and changing thought patterns around
tobacco.
●​ Weight Loss and Eating Habits
Encourages better self-control, healthy eating, and regular exercise.
●​ Addiction Support
Used alongside other treatments to help reduce urges and promote healthy behaviors.
●​ Performance Enhancement
Helps improve concentration, motivation, and confidence for students, athletes, and
performers.

4. Effectiveness of Hypnotherapy

Results Vary
Hypnotherapy is not equally effective for everyone. People who are highly imaginative,
open to suggestions, or motivated tend to benefit more.
Better as a Complementary Therapy
Often most effective when combined with Cognitive Behavioral Therapy (CBT),
medication, or medical treatment.

Evidence-Based Areas
Research shows strong evidence for its use in IBS, chronic pain, anxiety, and behavioral
change.

5. Myths vs. Reality

6. Safety and Ethical Considerations

Safe in Most Cases

●​ When done by a trained and certified professional, hypnotherapy is safe and low-risk.

Caution Needed For:

●​ People with severe mental illnesses (like schizophrenia or psychosis)

●​ Those with dissociative disorders
●​ Individuals who may have false memories triggered

Professional Training Required

●​ Therapists should be licensed and trained in clinical hypnotherapy or medical hypnosis.

7. Conclusion

●​ Hypnotherapy is a powerful, evidence-supported therapeutic tool.

●​ It can address a wide range of mental, emotional, physical, and behavioral issues.
●​ While it may not be suitable for everyone, many people find it helpful as part of a holistic
treatment plan.As always, consult a qualified professional before starting hypnotherapy.
Neuro-Linguistic Programming (NLP): Concepts, Techniques, and Applications

Neuro-Linguistic Programming (NLP) is a psychological approach developed in the 1970s by

Richard Bandler and John Grinder. It explores the connection between neurological processes
(neuro), language (linguistic), and behavioral patterns learned through experience
(programming). The main goal of NLP is to help individuals understand how they think, behave,
and communicate — and to use that understanding to achieve personal and professional goals.

Core Concepts

●​ Modeling Success: NLP involves identifying and replicating the behaviors, beliefs, and
language patterns of successful individuals to produce similar results.
●​ Personal Reality Maps: Everyone experiences reality differently. NLP helps people
become aware of their unique mental maps and how these influence their decisions and
behavior.
●​ Sensory Awareness: Enhancing awareness of visual, auditory, and kinesthetic cues can
lead to improved communication and understanding.
●​ Representational Systems: NLP suggests we process the world using our senses —
visual (seeing), auditory (hearing), and kinesthetic (feeling).

Popular NLP Techniques

As emphasized by Tony Robbins:

1. Modeling Excellence: Study successful individuals to understand and adopt their mindset,
language, and habits.

2. Physiology and State Management: Your body posture and physical state directly affect your
emotional state. Adjusting your body can help shift your mood.

3. Reframing: Change the way you perceive an experience to change how you feel about it.

4. Anchoring: Associate a physical gesture or trigger with a positive emotion so you can
recreate that feeling on demand.

5. Swish Pattern: Replace an unwanted behavior or thought with a desired one through
visualization, “swishing” from negative to positive imagery rapidly.

Applications of NLP

●​ Therapy: Used to treat phobias, anxiety, PTSD, and depression.

●​ Business: Improves leadership, persuasion, sales, and negotiation skills.
●​ Education: Enhances teaching strategies and learning techniques.
 ●​ Sports: Supports mental conditioning and peak performance.

Criticism and Limitations

●​ Despite its popularity, especially in coaching and self-development circles, NLP faces
criticism from the scientific community. There is limited empirical evidence to support its
effectiveness, and it lacks a strong theoretical framework. As a result, many consider it a
pseudoscience, even though individual results can vary.

Final Thoughts

NLP offers a unique toolkit for understanding and improving human behavior, communication,
and mindset. While it may not be universally accepted in clinical settings, many—like Tony
Robbins—have successfully used NLP strategies to empower individuals and create
transformational change.