Theories of Development: Piaget, Vygotsky & More
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This document provides an overview of key theories of development, including Piaget's constructivist theory and Vygotsky's sociocultural theory. It covers core concepts, stages of development, and mechanisms of development. The document also discusses factors hindering cognitive development, biological links to development, prenatal brain development, and influences on brain development. Additionally, there is coverage of memory development, problem-solving, language development, ADHD, Autism Spectrum Disorder, Substance Use Disorders and more.
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THEORIES OF DEVELOPMENT Thema 1: THEORIES OF DEVELOPMENT Piaget’s Constructivist Theory – Core Concepts Children are mentally active from birth. They construct knowledge through interaction with the environment. Learning is self-driven; rewards are not necessary. "Child as...
THEORIES OF DEVELOPMENT Thema 1: THEORIES OF DEVELOPMENT Piaget’s Constructivist Theory – Core Concepts Children are mentally active from birth. They construct knowledge through interaction with the environment. Learning is self-driven; rewards are not necessary. "Child as a scientist" metaphor – exploration, experimentation, and discovery. Piaget’s Theory – Central Properties Qualitative change: Thinking changes in kind, not just amount, across stages. Broad applicability: Each stage affects multiple domains (e.g., logic, morality, perception). Brief transitions: Transitional periods between stages with fluctuating thinking styles. Invariant sequence: All children progress through the same order of stages, no skipping. Piaget – Key Mechanisms of Development Organization: Schemes (mental structures) organize knowledge and experiences. Adaptation: Cognitive structures change in response to the environment. ○ Assimilation: Integrating new info into existing schemes. ○ Accommodation: Modifying schemes to fit new experiences. Equilibration: Balancing assimilation and accommodation to restore cognitive stability. ○ Equilibrium → Disequilibrium → Re-equilibration Piaget – Stages of Cognitive Development Sensorimotor Stage (0–2 years) Learning through sensory and motor interaction. Develops: ○ Object permanence ○ Deferred imitation Preoperational Stage (2–7 years) Symbolic thinking, increased language use. Limitations: ○ Egocentrism ○ Animism ○ Centration → leads to failure in conservation tasks. Concrete Operational Stage (7–12 years) Logical reasoning about concrete situations. Cannot yet handle abstract or hypothetical ideas. Formal Operational Stage (12+ years) Abstract, hypothetical, and deductive reasoning develops. Not universal; some individuals may not reach this stage. Vygotsky’s Sociocultural Theory – Core Concepts Development is socially mediated and culturally shaped. Learning leads development. Knowledge is co-constructed through interaction with more knowledgeable others (MKOs). No fixed stages – development is more continuous and context-dependent. Vygotsky – Key Concepts Zone of Proximal Development (ZPD) The gap between what a learner can do alone and with help. Optimal zone for teaching and learning. Guided Participation Engagement in culturally relevant tasks with support from others. Learning embedded in real-world, meaningful contexts. Social Scaffolding Temporary support tailored to the learner's needs: ○ Choosing appropriate tasks ○ Explaining steps ○ Demonstrating strategies ○ Gradually withdrawing support Vygotsky – Language and Cognitive Development Language is a key cultural tool that shapes thought. Developmental stages: 1. External regulation: others guide behavior. 2. Private speech: children speak to themselves to regulate actions (4–6 years). 3. Inner speech: private speech becomes internalized. Influenced by cultural norms (e.g., learning not to talk aloud in school). Applications of Piaget & Vygotsky in Education Piaget-inspired: Montessori education: self-exploration and discovery. Emphasis on hands-on experiences. Vygotsky-inspired: Jigsaw approach: group members become topic “experts” and teach others. Reciprocal teaching: teacher models strategies, then students practice and teach each other. Factors Hindering Cognitive Development Hospitalism: emotional/social deprivation in institutions. Neglect & abuse: impacts brain regions like PFC (linked to empathy, reasoning). Low socioeconomic status: less access to education, nutrition, stimulation. Social deprivation: "feral children" or isolation cases show severe delays. Neuroplasticity: allows some recovery, especially with early intervention. Biological Links to Development (connects to Core 1B) Brain development parallels Piaget’s cognitive stages. Sensitive periods for acquiring abilities (e.g., language, logic). Genetic potential unfolds depending on environmental stimulation (nature × nurture interaction). Brain development Prenatal Brain Development (Embryonic Stage) Key Processes: Fertilization of egg by sperm → zygote Mitosis: rapid cell division Around day 16: embryonic cells organize into three germ layers: ○ Endoderm → internal organs ○ Mesoderm → muscles, bones ○ Ectoderm → skin, nervous system Neural Tube Development: Cells in the ectoderm form the neural groove Neural folds rise and fuse → neural tube ○ Becomes brain and spinal cord Neural crest: separates from ectoderm → forms parts of the peripheral nervous system Vesicle Formation Timeline: Week 3: Neural tube forms three primary vesicles: ○ Forebrain (prosencephalon) ○ Midbrain (mesencephalon) ○ Hindbrain (rhombencephalon) Week 5: Differentiation into five secondary vesicles: ○ Telencephalon → cortex, basal ganglia ○ Diencephalon → thalamus, hypothalamus ○ Mesencephalon → midbrain structures ○ Metencephalon → pons, cerebellum Stages of Neural Development Neurogenesis (Neural Proliferation) Begins ~week 6 of gestation Rapid production of neural stem cells Peak: embryonic & fetal period Continues postnatally only in specific regions (e.g., hippocampus) Neuronal Migration Neurons move to their final location in the brain Two types: ○ Radial migration (cortex): neurons move along radial glial cells ○ Tangential migration: neurons move across brain surface Mechanisms: Somal translocation: neuron extends a process and pulls itself forward Glial-guided migration: neuron climbs along glial cells Migrating neurons are immature (no axons/dendrites yet) Aggregation Neurons that reached their target connect to form circuits Use: ○ Cell Adhesion Molecules (CAMs) for binding ○ Gap junctions: direct ion/glucose exchange between neurons Neuron Death & Synaptic Refinement Types of Neuron Death Apoptosis (programmed cell death): planned, healthy Necrosis (accidental death): caused by toxins or lack of oxygen, more damaging Synaptic Plasticity Brain continuously adjusts its synapses through: ○ LTP (Long-Term Potentiation): strengthens frequently used synapses ○ LTD (Long-Term Depression): weakens less-used connections ○ Purpose: strengthens useful pathways, prunes unnecessary ones "Cells that fire together wire together." Sensitive and Critical Periods Sensitive Periods Time windows when the brain is especially responsive to input Skills learned during this time are acquired faster and more deeply Not irreversible if missed, but harder later Example: second language acquisition before age 7 Critical Periods Narrow timeframes where certain input is essential for normal development Missing them causes permanent changes Mostly related to sensory systems Example: if visual input is blocked during early life → permanent blindness Neuroplasticity Changes Over Time Sensory systems: peak plasticity in infancy Executive functions: develop slowly, peak during adolescence Balance: ○ High plasticity = adaptable but less efficient ○ High efficiency = stable but less adaptable Influences on Brain Development Prenatal Influences Genetics: impact sensitivity to environmental risks (e.g., teratogens) Teratogens: substances that cause harm to embryo/fetus (e.g., alcohol, drugs) Maternal nutrition: folic acid (neural tube), omega-3 (brain growth) Hormones & stress: cortisol affects fetal development Infections: e.g., rubella, Zika virus Wilson’s 6 Principles of Teratology 1. Susceptibility depends on genotype 2. Damage depends on timing of exposure (critical periods) 3. Teratogens act through specific mechanisms 4. Higher dose = greater risk (dose-response) 5. Manifestations: death, malformation, growth retardation, functional issues 6. Longer exposure = more severe effects Postnatal Influences Socioeconomic status: affects nutrition, stimulation, education Nutrition: breastfeeding linked to improved brain development Early attachment: secure bonds build emotional regulation and trust Sensory stimulation: shapes synaptic development (e.g., touch, sound) Sleep: essential for brain growth, memory consolidation Peers: become more relevant during adolescence Dual-System Models of Adolescent Brain Development Dual-System Model Explains adolescent impulsivity by imbalance between: 1. Cognitive Control System (prefrontal cortex) Responsible for reasoning, inhibition Matures slowly into the 20s 2. Socioemotional System (amygdala, limbic system) Highly sensitive to peer influence and rewards Develops earlier → risk-taking behavior Maturation-Imbalance Model Limbic system (emotion) develops faster than prefrontal cortex (control) Explains increased impulsivity and emotional reactivity Driven-Dual-Systems Model Builds on previous models Emphasizes dynamic interaction of systems Some impulsivity may have adaptive functions (e.g., self-discovery, motivation) Research Designs in Developmental Psychology Cross-Sectional Design Compares different age groups at one time Pros: fast, economical Cons: no individual development info; cohort effects Longitudinal Design Follows the same individuals over time Pros: tracks real developmental change Cons: time-intensive, drop-out risk Sequential Design Combines cross-sectional and longitudinal methods Pros: separates age and cohort effects Cons: complex, requires large sample Microgenetic Design Observes individuals intensively during short developmental periods Pros: detailed insights into learning processes Cons: resource-heavy, small sample size Manipulating information Core Concept of Information Processing Theory Compares the mind to a computer system: input → processing → storage → output. Emphasizes how children actively process information, rather than passively receive it. Cognitive development is seen as a continuous, gradual process (not stage-based like Piaget). Children are seen as limited-capacity processors: ○ Limited attention span ○ Limited working memory ○ Limited strategy use (early on) These limitations decrease with age as the brain matures, especially the prefrontal cortex (PFC) Working Memory Models Atkinson & Shiffrin's Modal Model (1968) Divides memory into three parts: 1. Sensory Register: brief storage of raw sensory input (e.g., visual or auditory signals) 2. Short-Term Memory (STM): holds about 7 ± 2 items for 15–30 seconds 3. Long-Term Memory (LTM): stores information permanently if well encoded Process flow: Sensory input → STM → LTM ↔ Retrieval Baddeley & Hitch’s Working Memory Model (1974) Focuses on the active nature of short-term memory. Replaces STM with a multi-component working memory system: ○ Central Executive: controls attention and coordinates subsystems. ○ Phonological Loop: processes verbal and auditory information. ○ Visuospatial Sketchpad: processes visual and spatial information. ○ Episodic Buffer (added later): integrates working memory with long-term memory. Attention Development Closely linked to executive functioning and PFC maturation. Improves with age, becoming more selective and sustained. Types of Attention: Selective Attention: focusing on relevant stimuli, ignoring distractions (develops between 3–8 years). Sustained Attention: ability to maintain focus over time (notable growth between 3½–4 years). Executive Attention: resisting impulses, shifting attention, task-switching (6–12 years). Divided Attention: managing multiple tasks at once (develops more slowly). Young children: Scan broadly, inefficiently Are more distractible Older children: Focus more narrowly Sustain and shift attention more effectively Processing Speed and Brain Maturation Processing speed increases with age due to: ○ Myelination: faster signal transmission between neurons. ○ Synaptic pruning: elimination of unused connections, strengthening useful ones. Brain areas develop at different times: Prefrontal Cortex (PFC): supports executive function → matures late. Hippocampus: matures earlier → allows more stable long-term memory. Language and sensory areas mature at different rates to avoid overwhelming the child. Memory Development and Strategy Use Preschool (2–5 years): Strong recognition, weak recall. Rarely use strategies like rehearsal. Working memory can hold ~2–5 items. Early School Age (5–7 years): Begin to use rehearsal (repeating info aloud). Limited metacognition. Start encoding intentionally. Later Childhood (8–12 years): Use organization, chunking, and mnemonics. Memory becomes more efficient and strategic. Begin elaboration: adding meaningful details to remember information. Teenagers and beyond: Use a variety of strategies. Develop metacognitive awareness (know what works for them). Can plan and monitor their learning. Types of Memory Strategies: Rehearsal: repeating information. Organization: grouping related items. Elaboration: connecting new info to prior knowledge or personal experience. Selective attention: focusing only on important details. Production deficiency: knowing a strategy but not using it spontaneously (common in young children). Scripts and Autobiographical Memory Scripts: mental frameworks for repeated events (e.g., brushing teeth, bedtime routines). ○ Become more detailed with age. ○ Developed through social interaction and pretend play. Autobiographical memory: ○ Shaped by early social interaction and emotional context. ○ Elaborative style (open-ended, varied questions) → improves memory. ○ Repetitive style (closed, minimal questions) → less effective. ○ Cultural influences: Western cultures emphasize personal experiences; Eastern cultures emphasize roles and relationships. ○ Young children are susceptible to false memories when guided by adults. Executive Function (EF) Core cognitive control system supported by the prefrontal cortex. Develops throughout childhood, especially during preschool and early school years. Predicts long-term outcomes (e.g., academic success, self-regulation). Three core components: 1. Inhibition: ability to suppress impulses and distractions. 2. Working memory: holding and manipulating information in mind. 3. Cognitive flexibility: switching between tasks or strategies. Overlapping Waves Theory (Siegler) Children use multiple strategies simultaneously. Gradually favor the most efficient one based on experience. Development is continuous and individualized, not stage-based. Emphasizes: ○ Strategy testing ○ Gradual refinement ○ Trial and error Early learners often overestimate their abilities, becoming more accurate over time. Problem-Solving Development Early Childhood (3–5 years): Use guessing, trial-and-error. May break or forget rules. Often struggle with planning. Middle Childhood (5–9 years): Begin using concrete strategies (e.g., counting on fingers, the “min” strategy in math). Start combining rules and logic. Later Childhood (9+ years): Use mental planning, rule inhibition, and structured logic. Better at understanding multiple-step problems. Important concepts: Task analysis: breaking goals into sub-goals; improves with age. Representation: forming internal models of a problem. Transfer: applying strategies from one context to another. Deductive and Analogical Reasoning Deductive reasoning: ○ Moves from general rules to specific conclusions. ○ Slow to develop—requires abstract thinking. ○ Example: All mammals breathe → a whale breathes. Analogical reasoning: ○ Solving problems by recognizing similarities to previously solved problems. ○ Starts around 13 months (simple analogies), becomes more advanced with age and instruction. ○ Needs scaffolding early on (“This is like the puzzle we did yesterday”). Emotions, temperament, and personality Emotion Development Primary Emotions Definition: Innate, universal emotions that emerge early in life and are biologically programmed. Examples: Joy, sadness, anger, fear, disgust, surprise Development: From birth: Reflexive crying, general distress 2–3 months: Joy (social smiles) 4–6 months: Sadness, anger, surprise 6–9 months: Fear (e.g., stranger anxiety) Key Points: Do not require self-awareness Expressed through facial expressions and body language Present across all cultures Secondary (Self-Conscious) Emotions Definition: Complex emotions that involve self-awareness and an understanding of social rules. Examples: Embarrassment, guilt, pride, shame, envy, jealousy Development: Emerge around 18–24 months Require self-recognition and Theory of Mind Key Points: Influenced by social context Harder to observe; often studied through self-reports or behavioral cues Linked to moral and social developmen Emotion Expression vs. Recognition Expression: Showing one’s own feelings (e.g., crying, smiling) Recognition: Understanding others’ emotions via cues (e.g., facial expressions, voice) Timeline: Expression starts at birth Recognition starts ~3 months From 2 years: Children understand emotional display rules By 6 years: Know that facial expressions might not reflect true emotions Emotion Reasoning Definition: Using contextual cues and background knowledge to infer others’ emotions, beyond just facial expressions. Why it matters: "Emotion reasoning" is more accurate than "emotion recognition" since emotions are often masked or context-dependent. Emotion Research Methods Looking-time paradigms: Measure infants’ attention to emotional stimuli Event-related potentials (ERP): Brain response to emotion cues Facial coding systems: FACS, MAX Naturalistic observation: Real-life emotional reactions Violation of expectation tasks Verbal paradigms: Asking children to explain emotional situations Emotion Regulation Emotion Regulation – Development Definition: The ability to manage and adjust emotional reactions to achieve goals or meet social expectations. Developmental Path: Infancy: Self-soothing (e.g., thumb sucking) Toddlerhood: External regulation by caregivers Preschool age: Begin self-regulating using distraction, reappraisal By 8–10: Control display rules based on social norms Influences: Attachment style Parental modeling Cognitive control (prefrontal cortex) Cultural norms (e.g., “boys don’t cry”) Primary vs. Secondary Control Primary control: Changing the environment to meet goals Secondary control: Adjusting one's internal response to the environment (e.g., coping) Facial Expressions & Emotions Facial Expressions: Are They Reliable? Key Idea: Facial expressions are not always reliable indicators of a person's internal emotional state. Why? From age 3: Children start masking emotions By age 6: Understand that expressions can differ from true feelings Adults often conceal emotions based on context or social norms Microexpressions (brief, involuntary) may reveal true emotions Conclusion: Interpretation requires understanding context, body language, and culture Emotional State vs. Emotional Experience Emotional state: Immediate, physiological response (e.g., nervousness, frustration) Emotional experience: Personal, internal feeling shaped by thoughts and context Temperament and Personality Temperament Definition: Biologically based individual differences in emotional reactivity and self-regulation Types (Chess & Thomas, 1987): Easy: Regular routines, positive mood Difficult: Intense reactions, irregular routines Slow-to-warm-up: Low activity, cautious in new situations Stability: Relatively stable over time Serves as a precursor to personality Goodness-of-Fit Model Idea: Child outcomes depend on how well the temperament fits the environment, especially parenting. Example: A sensitive child may thrive with calm, structured caregiving, but struggle with inconsistency. Nature & Nurture in Personality Genetic influence: Temperament, basic tendencies (twin studies) Environmental influence: Parenting style, attachment, culture Dynamic interaction: Child influences environment and vice versa (e.g., outgoing child → more social opportunities) Personality Development Over Time Early years: Family is most influential Later: Peers, school, and social environments shape traits Access to education and gender norms also influence development (e.g., girls encouraged to express emotions more) Adjustment Problems in Childhood Definition: Challenges in adapting to emotional, social, or academic environments Examples: Language delays Behavioral issues Difficulty coping with change Consequences: Poor peer interaction, low academic performance, emotional difficulties Language development 1. General Rules of Language Development (Main Stages + Characteristics) Prenatal to 12 Months (Speech Perception and Early Sounds) Prenatal: Fetuses show preference for mother’s voice and the rhythm (prosody) of native language (DeCasper & Fifer, 1980). 0–6 Months: ○ Categorical perception of phonemes from all languages. ○ Begin recognizing common word patterns and prosody. 6–12 Months: ○ Perceptual narrowing: Lose sensitivity to non-native phonemes (Werker & Tees, 1984). ○ Babbling becomes native-language specific. ○ Word segmentation using stress cues and statistical learning (Jusczyk & Aslin, 1995). 12–24 Months (First Words & Vocabulary Spurt) First words (10–15 months): Refers to familiar people/objects (e.g., “mama”). Overextensions (e.g., calling all four-legged animals “dog”) and underextensions are common. Vocabulary spurt (18–24 months): Children may learn 10–20 new words per week. Fast mapping emerges (Carey & Bartlett, 1978). 24+ Months (Sentence Development) Begin combining two or more words ("want juice", "mommy go work"). Show understanding of syntax, morphology, and start applying grammatical rules. 2. How Grammatical Rules Form & Sensitive Periods Grammar Development Children infer rules through exposure (Pinker, 1994). Overregularization (e.g., “goed” instead of “went”) reflects rule learning. Development follows predictable stages (e.g., Brown’s Morphemes). Sensitive Periods Critical period for native-like acquisition likely ends around puberty (Johnson & Newport, 1989). Brain plasticity is higher in young children (Lenneberg, 1967). Late learners show different brain activation for grammar (Kim et al., 1997). 3. Development of Speech Perception & Word Learning Strategies Speech Perception At birth: Universal phoneme perception. By 12 months: Tuned to native phonemes only. By 6 months: Recognize own name (Mandel et al., 1995). By 14 months: Use object cues for meaning. Word Learning Strategies Statistical learning: Track syllable patterns (Saffran et al., 1996). Mutual exclusivity: Assume new word refers to unknown object. Social cues: Gaze, emotion, context guide word meaning. Syntactic bootstrapping: Use sentence structure to infer meaning. 4. Perspectives on Language Development Chomsky (Nativist Theory) Language is innate, guided by the Language Acquisition Device (LAD). Universal grammar: Basic rules shared by all languages (Chomsky, 1965). Skinner (Behaviorist Theory) Language is learned via reinforcement and imitation (Skinner, 1957). Vygotsky (Sociocultural Theory) Language arises from social interaction. Learning is scaffolded within the Zone of Proximal Development (ZPD). 5. Nature vs. Nurture Nature: Brain specialization, sensitive periods, genetic predispositions. Nurture: Quality and quantity of input, interaction, culture, education. Both are essential; nature provides capacity, nurture activates it. 6. Factors That Help or Hinder Language Development Helping Factors Infant-Directed Speech (IDS): Enhances attention and processing. Joint attention and naming games support word learning. Bilingualism: Enhances cognitive flexibility and executive function (Bialystok, 2009). Parental responsiveness: Rich, frequent input boosts development. Hindering Factors Low SES: Associated with less language input (Hart & Risley, 1995). Language disorders: ○ DLD/SLI: Difficulty with grammar or vocabulary, despite normal IQ. ○ Dysarthria: Motor speech issues. ○ Apraxia: Difficulty with speech planning. ○ Speech sound & fluency disorders (e.g., stuttering). Fragments of Focus ADHD DSM-5 Diagnostic Criteria Symptoms must be present before the age of 12. Symptoms must occur in at least two settings (e.g., school and home). Symptoms must cause clear functional impairment. Subtypes: ○ Inattentive type ○ Hyperactive-impulsive type ○ Combined type Gender Differences More frequently diagnosed in boys. Boys tend to show more hyperactivity and impulsivity. Girls are more likely to show inattentive symptoms (e.g., daydreaming, disorganization). Neurobiology Differences in brain structure and function, especially in the prefrontal cortex. Dual-pathway model: ○ Executive function deficits (e.g., attention control, working memory). ○ Delay aversion (preference for immediate rewards). Treatment Options Medication: ○ Stimulants (e.g., methylphenidate). Behavioral therapy: ○ Parent training ○ Classroom management strategies Multimodal approaches are often most effective. Assessment Tools Clinical interviews and questionnaires (e.g., Conners Rating Scales). Observations in different settings. Reports from parents and teachers. Influences Genetic: High heritability; ADHD often runs in families. Environmental: Prenatal exposure to alcohol or nicotine, low birth weight. Social: Parenting style, school environment. Cultural Perspectives Cultural expectations about behavior influence diagnosis. Underdiagnosis or overdiagnosis depending on societal norms. Access to diagnostic tools and treatment varies by region. Autism Spectrum Disorder (ASD) DSM-5 Diagnostic Criteria Persistent deficits in social communication and interaction: ○ Difficulty with back-and-forth conversation ○ Reduced sharing of interests/emotions ○ Problems with nonverbal communication (e.g., eye contact) ○ Difficulty in forming and maintaining relationships Restricted, repetitive patterns of behavior, interests, or activities: ○ Stereotyped movements or speech ○ Inflexibility to routines ○ Intense, fixated interests ○ Hypo- or hyperreactivity to sensory input Gender Differences Diagnosed more often in boys. Girls may show fewer repetitive behaviors. Girls often develop better masking and compensatory strategies. This may lead to late or missed diagnoses in females. Neurobiology Altered brain connectivity: ○ Increased local connectivity ○ Decreased long-range connectivity Differences in brain regions such as: ○ Amygdala (emotion processing) ○ Fusiform face area (facial recognition) Atypical sensory processing and reward sensitivity. Treatment Options Behavioral interventions: ○ Applied Behavior Analysis (ABA) ○ Social skills training Speech and occupational therapy Educational support tailored to individual needs Medication for comorbid symptoms (e.g., anxiety, aggression) Assessment Tools ADOS-2 (Autism Diagnostic Observation Schedule) ADI-R (Autism Diagnostic Interview-Revised) Developmental history and structured observations Influences Genetic: Strong hereditary component. Environmental: Advanced parental age, prenatal complications. Social: Early social environment affects development. Cultural Perspectives Cultural norms affect how symptoms are recognized and interpreted. Some cultures may delay diagnosis due to stigma. Access to services and awareness varies across regions. I want it, but I hate it Substance Use Disorders (SUD) Definition: Chronic relapsing pattern of problematic substance use. Involves compulsive use despite negative consequences (e.g., work, relationships, health). Diagnosed by meeting 2+ out of 11 DSM-5 criteria in a 12-month period: ○ Mild: 2–3 ○ Moderate: 4–5 ○ Severe: 6+ Main Diagnostic Categories: 1. Impaired Control: excessive use, unsuccessful attempts to cut down, craving. 2. Social Impairment: neglected obligations, social conflicts, reduced activities. 3. Risky Use: hazardous situations, continued use despite harm. 4. Pharmacological: tolerance & withdrawal (substance-specific). Substance-Specific Considerations Withdrawal syndromes: Present for alcohol, opioids, nicotine, cannabis. Tolerance: Develops at different rates for different substances. Hallucinogens: Often lack significant withdrawal effects. Brain Disease Model Addiction is linked to physical changes in the brain: ○ Disruption of the mesolimbic dopamine system (reward pathway). ○ Reduced dopamine receptor availability. ○ Decreased prefrontal cortex function (impaired inhibition). Criticisms: ○ Many people recover without treatment. ○ Emphasizes genetics & brain changes but ignores social/psychological factors. Choice/Moral Model Core Ideas: People dynamically weigh options based on short- vs. long-term outcomes. Addiction = pattern of choosing immediate reward (drug) over long-term gain. Key Concepts: Local vs. Global decision-making: momentary vs. long-term benefit. Delay Discounting: preference for immediate reward. Drug reinforcement: more intense and immediate than natural rewards. Context matters: environment influences perceived value of using. Rational Addiction Theory Individuals logically weigh pros and cons of drug use. Criticisms: ○ Overlooks impulsivity, poor decisions, emotional struggles. ○ Unrealistic assumptions about planning and rationality. Operant Addiction Theory Drug use is a learned behavior: ○ Positive reinforcement: pleasure/euphoria. ○ Negative reinforcement: relief from withdrawal/stress. Paradox: Despite increasing punishment and decreasing reward, use continues. Incentive-Sensitization Theory Addiction driven by "wanting" not "liking": ○ Wanting: Craving, driven by sensitized dopamine system. ○ Liking: Actual pleasure, which may fade over time (tolerance). Drug cues become motivational triggers (incentive salience). Key brain areas: ○ VTA → Nucleus Accumbens → Prefrontal Cortex, Amygdala, Hippocampus. Negative Reinforcement & Dissociation Model Dissociation: Coping by disconnecting from painful emotions. Substance use helps numb distress → reinforces behavior. Linked to trauma, impaired decision-making, compulsivity. Predisposing Factors Genetics Early exposure, method of administration ADHD Socioeconomic status Stress sensitivity Social environment (friends, family, school) Physical Effects of Addiction Vomiting blood, liver damage (alcohol) Lung problems, cancer (tobacco) Neuronal damage (inhalants) Increased HIV risk Skin infections Weight loss Increased heart rate Treatment Approaches 1. Extinction Training: Repeated exposure to drug cues without reinforcement. Aims to reduce conditioned craving. Limitations: Autonomic responses persist, relapse can occur in new contexts. 2. Pharmacotherapy: Withdrawal management. Drug substitution (e.g., methadone). Criticized for not addressing incentive-sensitization. Ideal medications would: ○ Normalize dopamine hypersensitivity. ○ Reduce cue-driven craving. ○ Restore prefrontal control. 3. Psychological Therapy: Teaches coping strategies, self-control, understanding triggers. People with addiction can exert volitional control with support. 4. Contingency Management: Tangible rewards (e.g., money, vouchers) for drug-free behavior. Effective for stimulants like cocaine & methamphetamine. 5. 12-Step Facilitation: Based on AA/NA principles: acceptance, higher power, peer support. Encourages long-term sobriety and accountability. 6. Psychedelic-Assisted Therapy: Psilocybin, LSD, ayahuasca under clinical supervision. Alters brain connectivity, increases openness. Aims for emotional insight and motivation. Must be paired with therapy; research is ongoing. Cue-Triggered Relapse 1. Cue Learning: Stimuli associated with drug use via conditioning. 2. Sensitization: “Wanting” increases even without withdrawal. 3. Craving: Leads to compulsive seeking. 4. Priming: Cues reawaken the incentive system. 5. Persistence: Craving can persist long after withdrawal fades. 6. Implicit: Craving often operates unconsciously, beyond awareness. When the World Turns Gray Depressive Disorders Overview Categories include: ○ Disruptive mood dysregulation disorder ○ Major depressive disorder (MDD) ○ Persistent depressive disorder (dysthymia) ○ Premenstrual dysphoric disorder (PMDD) ○ Substance/medication-induced depressive disorder ○ Depressive disorder due to another medical condition ○ Specified and unspecified depressive disorders Common Features: Sad/empty/irritable mood, cognitive and somatic changes. Differences: Duration, timing, and cause. Major Depressive Disorder (MDD) Diagnostic Criteria Must have 5+ symptoms during same 2-week period, one must be: ○ Depressed mood ○ Loss of interest/pleasure Other symptoms: ○ Weight/appetite changes ○ Insomnia/hypersomnia ○ Psychomotor agitation/retardation ○ Fatigue/loss of energy ○ Worthlessness/guilt ○ Diminished concentration ○ Suicidal ideation/attempt Additional: ○ Distress or functional impairment ○ Not due to substance or medical condition ○ No history of mania/hypomania Risk Factors for Depression Temperamental: ○ Neuroticism, negative affectivity, low self-esteem, poor coping Environmental: ○ Childhood abuse/neglect, loss, violence ○ Chronic stress (poverty, caregiving, conflict) ○ Life events (divorce, job loss, illness) Biological/Genetic: ○ Family history (2–4x higher risk) ○ Heritability (~40%) ○ Monoamine dysregulation (serotonin, dopamine, norepinephrine) ○ HPA axis overactivation (↑ cortisol) ○ Changes in amygdala, hippocampus, PFC Medical/Substance Related: ○ Conditions: Parkinson’s, stroke, MS, hypothyroidism, pain, CVD ○ Substances: Alcohol, sedatives, corticosteroids, beta-blockers Gender/Hormonal: ○ Depression 2× more common in females post-puberty ○ Sensitivity to hormonal fluctuations (e.g., PMDD, postpartum) Developmental: ○ Adolescents: ↑ risk with puberty (esp. girls) ○ Older adults: illness, bereavement, cognitive decline Depression Theories & Models Monoamine Hypothesis: ○ Imbalance of serotonin/dopamine/norepinephrine ○ Antidepressants restore neurotransmitter levels ○ Criticized: oversimplified, outdated Neurocircuitry Models: ○ DMN (rumination), Salience Network (emotional stimuli), CEN (cognitive control) ○ Depression = dysregulated network communication Monoamine Receptor Hypothesis: ○ Focuses on receptor changes post-medication HPA Axis & Stress Model: ○ Chronic stress → HPA overactivity → mood/cognitive issues Neuroinflammation: ○ Cytokines disrupt neurotransmission, plasticity, neurogenesis Cognitive/Psychological Theories: ○ Beck: negative thoughts, learned helplessness, maladaptive beliefs Biopsychosocial Approach: ○ Interplay of genes, trauma, stress, socioeconomic status Neuroplasticity Hypothesis: ○ Depression = impaired synaptic plasticity, reduced BDNF ○ Key regions: PFC, hippocampus ○ SSRIs/ketamine increase BDNF Glutamate Hypothesis: ○ Disruption in glutamate signaling (NMDA, AMPA) ○ Ketamine’s efficacy supports this Antidepressant Treatments Traditional Antidepressants: ○ SSRIs (e.g., fluoxetine): ↑ serotonin ○ SNRIs: ↑ serotonin & norepinephrine ○ MAOIs: prevent monoamine breakdown ○ Effects: mood improvement, BDNF ↑, connectivity ↑ ○ Limitations: delay, side effects, suicidal risk (1 month Distress/impairment must be present Not due to substances or other conditions Specifiers: Dissociative (depersonalization/derealization), Delayed onset (6+ months after trauma) PTSD Brain Changes Key regions: ○ Amygdala: hyperactive (threat detection) ○ Hippocampus: smaller (memory/context) ○ Prefrontal Cortex: hypoactive (regulation/inhibition) Triple Network Dysfunction: ○ Salience Network: threat filtering → overactive ○ Default Mode Network (DMN): rumination → disrupted ○ Central Executive Network (CEN): attention/memory → impaired Cortisol: Often lower in PTSD → blunted stress recovery Biotypes/subtypes: Research aims to personalize treatment based on brain activity patterns PTSD Measurement Tools Biomarkers: cortisol, inflammatory proteins Heart rate, physiological reactivity fMRI/PET: amygdala hyperactivation Clinical interviews, self-report scales PTSD Treatment: Psychological Trauma-Focused CBT: ○ Re-experiencing trauma in a safe setting ○ Memory restructuring, hierarchy exposure ○ Habituation & emotion regulation Prolonged Exposure Therapy: Gradual trauma cue exposure EMDR: ○ Bilateral stimulation while recalling trauma ○ Helps reprocess trauma adaptively Psychodynamic Therapy: ○ Unconscious conflict exploration ○ Transference and repressed emotion work Other options: ○ Yoga, mindfulness, group support PTSD Treatment: Pharmacological SSRIs (e.g., sertraline, paroxetine): mood/sleep/anxiety SNRIs (e.g., venlafaxine): mood & arousal regulation Prazosin: reduces nightmares, improves sleep Ketamine: fast-acting relief in resistant cases Psychedelics (e.g., MDMA, psilocybin): under clinical trial, promising as adjuncts to therapy PTSD – Special Notes Dissociation: can impair memory, increase episode intensity Hormones: testosterone, estrogen fluctuations may influence episodes Comorbidity with depression complicates diagnosis Females: 2–3x higher risk, partly due to violence exposure and stigma Treatment barriers: cost, dropout rates, access (especially for marginalized groups) Summary: PTSD Key Takeaways Defined by trauma exposure and persistent re-experiencing, avoidance, and arousal Symptoms tied to altered brain networks (PFC, amygdala, hippocampus) Measurable by physiological, psychological, and imaging tools Best treated with combination of therapy and medication Individual factors and context strongly affect onset, severity, and recovery Control and distortion OCD Overview & Symptoms OCD = Obsessive-Compulsive Disorder ○ Characterized by obsessions (intrusive, distressing thoughts) and compulsions (repetitive behaviors to reduce distress). Common Obsessions: ○ Contamination, harm, symmetry, taboo thoughts Common Compulsions: ○ Washing, checking, counting, praying Symptoms must be time-consuming (1+ hr/day) or cause impairment OCD Subtypes & Development Pure-O (purely obsessional OCD): ○ No visible compulsions; mental rituals dominate Onset: ○ Childhood to early adulthood (mean ~19.5 years) ○ Males often show earlier onset (before age 10) Often chronic if untreated; ~40% childhood-onset may remit OCD Causes & Risk Factors Biological: ○ ↓ Serotonin (key role), possible dopamine and glutamate involvement Genetic: ○ Family history, genes like SLC1A1 Environmental: ○ PANDAS (post-infectious OCD), trauma, criticism, rituals Cognitive Patterns: ○ Thought-action fusion, over-responsibility, intolerance of uncertainty OCD Treatment Options First-Line: ○ CBT with Exposure & Response Prevention (ERP) Medications: ○ SSRIs (e.g., fluoxetine, sertraline), high doses required ○ Clomipramine (TCA), SNRIs Other: ○ ACT, atypical antipsychotics, TMS, Deep Brain Stimulation (DBS) Eating Disorders Overview Anorexia Nervosa (AN): ○ Restriction → significantly low weight (BMI