Psychopathology PDF

Defining Psychopathology 1.​ Deviation from Social Norms: ○​ Definition: Behavior that deviates from cultural and social norms. ○​ Examples: Public nudity, hearing voices in cultures where it’s not accepted. ○​ Expanded Examples: In Western societies, behaviors like ext...

Defining Psychopathology 1.​ Deviation from Social Norms: ○​ Definition: Behavior that deviates from cultural and social norms. ○​ Examples: Public nudity, hearing voices in cultures where it’s not accepted. ○​ Expanded Examples: In Western societies, behaviors like extreme introversion may raise concerns, while in some Asian cultures, this might be valued. Examples from history include witch hunts, where deviations were pathologized unjustly. ○​ Critiques: ​ Culturally relative: "Normal" differs across societies. ​ Not all deviations imply pathology, e.g., artists and innovators often defy norms. ​ Risks stigmatizing non-conformity (e.g., neurodiversity). ​ Trauma and culture-bound symptoms can influence norms. 2.​ Deviation from Statistical Norms: ○​ Definition: Abnormality defined by rarity in population (e.g., extreme IQ levels). ○​ Expanded Examples: High IQ, rare physical attributes like extreme height, or uncommon behaviors like savant skills in autism. Includes behaviors outside a typical range of functioning that might still be adaptive. ○​ Critiques: ​ Arbitrary thresholds for defining abnormality. ​ Not all rare traits are pathological (e.g., genius). ​ Positive deviations may not need intervention. 3.​ Maladaptive Behavior and Dysfunction: ○​ Focus: Impairment in daily functioning or harm. ○​ Examples: Failing to maintain a job or relationships due to obsessive behaviors. ○​ Context: Used in DSM-5 and clinical practice. ○​ Considerations: ​ Continuum of symptoms (mild to severe). ​ Some behaviors may have adaptive functions, e.g., hyper-vigilance in anxiety can protect in dangerous settings. 4.​ Distress and Disability: ○​ Key Criteria: Personal suffering and functional impairment. ○​ Examples: Silent sufferers of depression vs. those outwardly expressing symptoms. ○​ Recognition: Considers subjective experience while incorporating observable impairments in functioning. Stigma ​ Types: ○​ Social Stigma: Negative societal perceptions about mental illness. ○​ Self-Stigma: Internalized societal stereotypes by individuals. ​ Origins: ○​ Historical fear and misunderstanding of mental illness. ○​ Negative media portrayals (e.g., linking mental health with violence). ○​ Misrepresentation of mental health in education systems and public discourse. ​ Expanded Impact: ○​ Examples of successful anti-stigma campaigns like Time to Change (UK) and Beyond Blue (Australia). ○​ Impacts across cultures: Some cultures view seeking mental health support as dishonorable, often leading to delayed treatment. Historical Models of Psychopathology 1.​ Ancient Greeks (Hippocrates): ○​ Humorism: Imbalance of bodily fluids (e.g., excess black bile linked to melancholia). ○​ Treatments: Bloodletting, dietary adjustments, rest, and exercise. 2.​ Demonology: ○​ Belief: Mental illness as possession by demons (pre-18th century). ○​ Expanded Examples: Cultural variations, such as "spirit possession" rituals in Africa vs. Christian exorcisms. ○​ Treatments: Exorcisms, purging, scarification, and isolation. 3.​ Asylums (1700s-1900s): ○​ Patients treated as inmates, often inhumane conditions. ○​ Interventions: Physical methods like ice baths aimed at "balancing spirits" and moral therapy emphasizing order and discipline. 4.​ Deinstitutionalization (1950s-1970s): ○​ Shift to community-based care. ○​ Introduction of milieu therapy and psychotropic medications. ○​ Examples: Deinstitutionalization led to community programs like "Clubhouse Model" for schizophrenia care and halfway houses. 5.​ Recovery Model: ○​ Focus: Holistic, person-centered care. ○​ Emphasizes personal growth, empowerment, and resilience over "cure." Biological Models 1.​ Genetics: ○​ Mental disorders influenced by multiple genes. ○​ Expanded Example: Twin studies showing 50% concordance rates for schizophrenia in identical twins. ○​ Diathesis-Stress Model: Genetic vulnerability + environmental stress = disorder. Examples include interactions between prenatal factors and later-life stressors. 2.​ Neuroscience: ○​ Focus: Brain abnormalities (structural/functional). ○​ Examples: Dopamine hyperactivity in schizophrenia; serotonin deficits in depression. Neuroimaging studies reveal differences in brain areas like the prefrontal cortex in ADHD. 3.​ Limitations: ○​ Overemphasis on biology can ignore psychosocial influences and cultural contexts. ○​ Ethical Concerns: Risk of over-medicalizing mental health and focusing excessively on pharmacological interventions. Psychological Approaches 1.​ Psychodynamic: ○​ Focus: Unconscious conflicts stemming from early experiences. ○​ Expanded Example: A patient with trust issues traced to early caregiver neglect, manifesting in later difficulties forming relationships. ○​ Techniques: Free association, dream analysis, transference-focused therapy. 2.​ Behaviorism: ○​ Principle: Abnormal behavior results from faulty learning. ○​ Techniques: ​ Classical Conditioning: Systematic desensitization, exposure therapy. ​ Operant Conditioning: Token economies, reinforcement. ○​ Limitations: ​ Focuses on behavior, not root causes. ​ Example: Phobias treated behaviorally may resurface without addressing underlying beliefs or emotional underpinnings. 3.​ Cognitive: ○​ Focus: Changing irrational thoughts and cognitive distortions. ○​ Expanded Example: A patient learns to challenge automatic thoughts like "I'm a failure," supported by evidence-based techniques like cognitive restructuring. 4.​ Humanist-Existential: ○​ Principles: Emphasis on personal meaning, self-actualization, and freedom. ○​ Expanded Example: Grief counseling emphasizing acceptance and growth, facilitating a sense of purpose and self-discovery. Diagnosis and Classification 1.​ DSM-5 vs. ICD: ○​ Comparison Example: Autism classification—DSM-5 uses a single spectrum approach, which provides a unified framework but may oversimplify diversity within the condition. Conversely, ICD categorizes autism into separate categories based on severity and symptoms, offering more granular differentiation but potentially complicating diagnosis and international comparisons. ○​ Advantages of DSM-5: Detailed, structured criteria improve diagnostic precision and are widely used in clinical and research settings in the U.S. ○​ Advantages of ICD: Global acceptance and accessibility make it suitable for international healthcare systems, ensuring broader applicability. ○​ Critiques of DSM-5: Risk of overpathologizing normal variations in behavior and subjectivity in certain criteria. ○​ Critiques of ICD: Less detailed symptom descriptions may lead to variability in interpretations and implementations. 2.​ Advantages of Diagnosis: ○​ Facilitates communication among professionals. ○​ Guides treatment plans and research. ○​ Offers a framework for understanding complex presentations. 3.​ Critiques: ○​ Symptoms may be subjective. ○​ Cultural bias in symptom expression and interpretation. ○​ Homogeneity challenges within diagnoses, with significant overlap between disorders. Assessment Methods 1.​ Clinical Interviews: ○​ Unstructured interviews provide flexibility but can be biased. ○​ Gather detailed symptom, history, and context information. 2.​ Structured Interviews: ○​ Systematic approach enhances reliability but limits flexibility. ○​ Example: Structured Clinical Interview for DSM Disorders (SCID). 3.​ Tests: ○​ Psychological (e.g., MMPI-2), intelligence (WAIS), and neuropsychological tests. ○​ Projective Tests: Rorschach inkblot test, TAT. Useful for uncovering unconscious content but criticized for reliability and validity. 4.​ Clinical Observation: ○​ Direct monitoring of behavior in naturalistic or clinical settings. ○​ Example: Observing a child with ADHD in classroom settings to assess in vivo functioning. Formulation-Based Approaches 1.​ Process: ○​ Gather data about problems and context. ○​ Hypothesize underlying mechanisms (theory-based). ○​ Explore causes and contributing factors. ○​ Develop individualized treatment plans. ○​ Example: 4P model—Predisposing (family history), Precipitating (recent trauma), Perpetuating (avoidance behaviors), Protective (strong support network). Integrating biopsychosocial influences for comprehensive care. Core Clinical Competencies 1.​ Assessment: Gathering comprehensive client information through interviews, tests, and observation. 2.​ Formulation: Creating hypotheses linking theory to practice and tailoring to individual needs. 3.​ Intervention: Tailored treatment strategies addressing biopsychosocial factors. 4.​ Evaluation: Assessing intervention effectiveness using measurable outcomes. 5.​ Research: Incorporating evidence-based practice to ensure high-quality care. Professional Standards 1.​ HCPC Standards: ○​ Prioritize public protection and ethical practice. ○​ Commit to continuing professional development. ○​ Promote service user involvement in care decisions. 2.​ BPS Code of Conduct: ○​ Core values: Respect, competence, responsibility, integrity. ○​ Promote equality, diversity, and inclusion. ○​ Example: Resolving ethical dilemmas by consulting guidelines and involving supervisors or colleagues when necessary. Key Models for Practice 1.​ Reflective Practitioner:  ○​ Continuous self-awareness and improvement. ○​ Ethical, client-centered approaches. ○​ Example: Using feedback from clients to refine therapeutic techniques and enhance rapport. 2.​ Scientist-Practitioner: ○​ Combines research and clinical expertise. ○​ Emphasizes data-driven decisions in therapy while remaining flexible to individual needs. Anxiety Disorders (DSM-5) Types of Anxiety Disorders 1.​ Specific Phobias ○​ Intense fear of specific objects or situations, disproportionate to any real danger. 2.​ Social Anxiety Disorder ○​ Fear of unfamiliar people or social scrutiny, leading to avoidance of social situations. 3.​ Panic Disorder ○​ Recurrent panic attacks and persistent anxiety about these attacks. 4.​ Agoraphobia ○​ Fear of being in places where escape would be difficult or help unavailable during anxiety symptoms. 5.​ Generalized Anxiety Disorder (GAD) ○​ Excessive and uncontrollable worry about various domains (family, health, work/school). Prevalence of Anxiety Disorders ​ 28% of people report experiencing anxiety symptoms. ​ Anxiety disorders were the 10th leading cause of disability worldwide in 2015. Fear vs. Anxiety ​ Fear: A response to an immediate, well-defined threat. Triggers the fight-or-flight response. ​ Anxiety: Apprehension about future threats, conceptualized as a future-focused emotion. Varies widely among individuals and situations. Can increase preparedness. Both are adaptive emotional responses to threat but can become maladaptive, leading to anxiety disorders when excessive in intensity, frequency, or duration. Generalized Anxiety Disorder (GAD) DSM-5 Criteria for GAD ​ Excessive worry about at least two domains (e.g., family, health, finances) for more than 3 months. ​ Worry is associated with at least one of the following symptoms: ○​ Restlessness ○​ Muscle tension ○​ Difficulty concentrating ​ Disturbance leads to significant impairment in daily functioning (social, occupational, etc.). ​ Not attributable to substance use or other medical conditions. Prevalence ​ 0.5% in the UK, 5.7% in the US. ​ More common in women, with peak onset between ages 35-59. Etiology of GAD 1.​ Genetics: Anxiety has a heritable component. Twin studies suggest 30% inheritance risk. 2.​ Brain Regions: Dysfunction in the amygdala and prefrontal regions may contribute to emotional regulation abnormalities. 3.​ Neurotransmitter Imbalance: Imbalances in serotonin, norepinephrine, and GABA are implicated. 4.​ Environmental Factors: Stressful events and parenting style (e.g., attachment style) increase the risk of GAD. Psychological Theories ​ Pathological Worrying: Worry serves as a distraction from distressing emotions. ​ Dispositional Characteristics: People intolerant of uncertainty are more prone to GAD. ​ Cognitive Mechanisms: ○​ Attention to threatening stimuli ○​ Difficulty disengaging from threats ○​ Cognitive biases (e.g., catastrophic thinking) Treatment of GAD ​ Pharmacological: Medications include anxiolytics and antidepressants. ​ Cognitive Behavioral Therapy (CBT): ○​ Exposure: Identifying and confronting worry triggers. ○​ Cognitive Restructuring: Challenging negative thoughts. ○​ Relaxation Training: Progressive muscle relaxation techniques. Panic Disorder and Agoraphobia Panic Disorder ​ Characterized by recurrent, unexpected panic attacks. ​ Symptoms of panic attacks: ○​ Rapid heart rate, sweating, dizziness, trembling. ○​ Feelings of derealization or depersonalization. ○​ Fear of losing control or dying. ​ At least one attack is followed by: ○​ Persistent concern about future attacks. ○​ Maladaptive behavior changes to avoid attacks. Agoraphobia ​ Intense fear of at least two of the following situations: ○​ Public transportation, open spaces, crowds, or being outside the home alone. ​ Fear arises from concerns that escape would be difficult or help unavailable during a panic attack. ​ Leads to avoidance of feared situations, which can cause significant distress or impairment. Prevalence ​ Panic Disorder: 1.5-3% (12-month prevalence). ​ Agoraphobia: 0.4-3% (12-month prevalence). ​ Panic Disorder often co-occurs with agoraphobia. Biological Theories of Panic Disorder 1.​ Hyperventilation: Rapid breathing causes CO2 imbalance, leading to symptoms that mimic panic attacks. 2.​ Noradrenergic Overactivity: Imbalances in noradrenaline contribute to panic attacks. 3.​ GABA Deficiency: Panic disorder sufferers often have low GABA levels, contributing to anxiety. Treatment of Panic Disorder ​ Medication: SSRIs, tricyclic antidepressants (TCAs), and benzodiazepines (short-term). ​ Cognitive Behavioral Therapy (CBT): ○​ Relaxation Training: To manage symptoms of panic. ○​ Interoceptive Exposure: Exposure to bodily sensations that trigger panic, helping to reduce fear.  ○​ Cognitive Restructuring: Challenging catastrophic interpretations of bodily sensations. Eating Disorders Types of Eating Disorders 1.​ Unspecified Feeding and Eating Disorder (UFED): Eating disorder symptoms causing significant distress or impairment but do not meet full criteria for another disorder. 2.​ Anorexia Nervosa (AN): ○​ Restriction of energy intake leading to significantly low body weight. ○​ Intense fear of gaining weight, distorted body image, and refusal to recognize the seriousness of low body weight. 3.​ Bulimia Nervosa (BN): ○​ Recurrent binge-eating episodes followed by compensatory behaviors (e.g., vomiting, excessive exercise). ○​ The cycle occurs at least once a week for 3 months. ○​ Affected individuals experience a lack of control during binge episodes. 4.​ Binge Eating Disorder (BED): ○​ Recurrent binge-eating episodes, but no compensatory behaviors. ○​ Associated with feelings of guilt, disgust, and distress. 5.​ Avoidant/Restrictive Food Intake Disorder: ○​ Lack of interest in eating or food, based on sensory characteristics or fear of negative consequences from eating. 6.​ Pica: Eating non-food items. 7.​ Rumination Disorder: Repeated regurgitation of food. Biological Aspects of Anorexia Nervosa ​ Brain Shrinkage: Starvation reduces brain plasticity and affects cognitive and emotional processing. Co-morbidity ​ Anorexia Nervosa: Often co-occurs with depression (66%), anxiety (25-34%), OCD (21%). ​ Bulimia Nervosa: Common comorbidities include depression (36-63%), bipolar disorder, and substance use disorders. ​ Binge Eating Disorder: Linked with depression (23%), anxiety (18%), and substance use disorders. Biological Risk Factors in Eating Disorders  1.​ Genetic: High heritability (40-60%). First-degree relatives of those with AN have 10x higher risk of developing AN. 2.​ Neural Mechanisms: Imbalances in serotonin and dopamine are implicated in reward processing and appetite regulation. 3.​ Cultural Factors: Exposure to Western ideals has led to increased eating disorder rates in ethnic minorities (e.g., Hispanic American and Asian females). Cultural Influence on Body Image ​ Social Media: Heightened internalization of the "thin ideal" can contribute to body dissatisfaction and eating disorders. Gender Differences in Eating Disorders ​ Male Eating Disorders: Increasing prevalence in males, though likely underreported. Men tend to focus more on muscle mass than thinness. ​ Females: 10x more likely to develop eating disorders than males, with body shape and size being a significant concern. Treatment of Eating Disorders ​ Psychological Interventions: ○​ Cognitive Behavioral Therapy (CBT) is the most effective treatment for anorexia and bulimia. ○​ Focuses on cognitive restructuring, exposure to feared foods, and behavioral strategies to manage eating behaviors. ​ Pharmacological Interventions: ○​ Antidepressants (SSRIs) are commonly prescribed to treat associated depression and anxiety. Mood Disorders Overview Mood disorders are mental health conditions marked by significant disturbances in emotional states, which impair social, occupational, and daily functioning. 1. Unipolar Disorders Primarily Depression: ​ Major Depressive Disorder (MDD): Severe depressive episodes lasting at least two weeks. ​ Persistent Depressive Disorder (PDD): Chronic depression (2+ years), often less severe than MDD. ​ Premenstrual Depressive Disorder: Depressive symptoms tied to menstrual cycles.  ​ Disruptive Mood Dysregulation Disorder: Seen in children, marked by severe irritability and temper outbursts. 2. Bipolar Disorders Mood Swings: Alternates between depressive and manic/hypomanic episodes. ​ Bipolar I: Full manic episodes (lasting 7+ days) with or without depressive episodes. ​ Bipolar II: Hypomanic episodes (lasting 4+ days) paired with major depressive episodes. ​ Cyclothymia: Chronic shifts between mild hypomania and mild depression, not meeting criteria for Bipolar I or II. Major Depressive Disorder (MDD) Symptoms (DSM-5 Criteria) For a diagnosis of MDD, five or more of the following symptoms must persist during a two-week period: 1.​ Depressed mood most of the day. 2.​ Diminished interest or pleasure in activities. 3.​ Significant weight loss or gain. 4.​ Insomnia or hypersomnia. 5.​ Psychomotor agitation or retardation. 6.​ Fatigue or loss of energy. 7.​ Feelings of worthlessness or excessive guilt. 8.​ Difficulty concentrating or making decisions. 9.​ Recurrent thoughts of death or suicide. Symptoms must cause significant distress and impairment in daily functioning and not be attributable to substances, medical conditions, or other mental disorders (e.g., schizoaffective disorder). Course of MDD ​ Relapse and Recurrence Rates: ○​ First episode: 50% chance of recurrence. ○​ After the second episode: 70%. ○​ After the third episode: 90%. ​ Chronic Cases: Up to 27% of cases remain chronic. ​ Triggers: 60%-90% of depressive episodes are linked to life events, such as bereavement or job loss. Biological Theories of MDD 1. Genetic Factors: ​ Heritability: ~40%, higher in women than men. ​ Twin studies show: ○​ Monozygotic concordance: 31%-42%. ○​ Dizygotic concordance: ~20%. ​ First-degree relatives have a 2%-3% increased risk. 2. Neurochemical Factors: ​ Low levels of serotonin, dopamine, and norepinephrine in the limbic system contribute to depressive symptoms. ​ Antidepressants (SSRIs, TCAs) increase neurotransmitter availability. 3. Brain Abnormalities: ​ Hypoactivity in PFC & ACC: Impairs emotional regulation and reward anticipation. ​ Reduced Hippocampal Volume: Linked to poor affective contextualization and higher relapse rates. ​ Hyperactive Amygdala: Heightens sensitivity to perceived threats. Psychological Theories of MDD 1. Behavioral Theories: ​ Depression arises due to reduced environmental rewards and positive reinforcement. ​ Avoidance coping: Depressed individuals avoid situations that could be rewarding, perpetuating depressive cycles. 2. Cognitive Theories (Beck’s Model): ​ Negative Schemas: Dysfunctional beliefs about self, the world, and the future. ​ Cognitive Biases: Errors in thinking include: ○​ Arbitrary inference: Jumping to conclusions without evidence. ○​ Overgeneralization: Applying a single failure across all aspects of life. ○​ All-or-nothing thinking: Viewing situations in black-and-white terms. ​ Negative Automatic Thoughts: Habitual, automatic thoughts that reinforce depressive symptoms. 3. Learned Helplessness (Seligman): ​ Unavoidable negative life events lead to feelings of helplessness and lethargy. Bipolar Disorders Key Features of Bipolar I and II: ​ Bipolar I: Full manic episodes lasting at least seven days. Often accompanied by depressive episodes. ​ Bipolar II: Hypomanic episodes lasting four or more days and depressive episodes. Manic Episode (DSM-5): ​ Elevated mood and three or more of the following symptoms: ○​ Increased goal-directed activity. ○​ Reduced need for sleep. ○​ Racing thoughts or flight of ideas. ○​ Recklessness or impulsivity. ​ Symptoms last at least one week or require hospitalization. Suicide Risk: ​ Up to 15% of individuals with bipolar disorder die by suicide. ​ Suicide attempts are more common during depressive episodes but more severe during manic states. Aetiology of Bipolar Disorder (BD) 1. Genetic Factors: ​ Heritability: ~85%. ​ 40%-70% concordance in monozygotic twins. ​ Strong genetic overlap with schizophrenia spectrum disorders. 2. Neurobiology: ​ Dopamine dysregulation leads to mood shifts: ○​ High levels in mania. ○​ Low levels in depression. ​ Frontal cortex hypoactivity during cognitive processing; limbic system hyperactivity during emotional responses. 3. Immune Dysfunction: ​ High levels of pro-inflammatory cytokines suggest chronic low-grade inflammation. Treatments for Mood Disorders 1. Pharmacotherapy: ​ MDD: SSRIs, SNRIs, and TCAs enhance serotonin and norepinephrine transmission.  ​ BD: Lithium is the gold standard but has a high dropout rate due to side effects (e.g., weight gain, nausea, tremors). 2. Emerging Treatments: ​ Ketamine: Rapid symptom relief in depression (within hours). ​ Psychedelics (e.g., LSD): Experimental but showing promise in meta-analyses. 3. Behavioral Activation: ​ Focuses on increasing exposure to rewarding activities while reducing avoidance. ​ Includes time management, goal-setting, and social skills training. 4. Cognitive Behavioral Therapy (CBT): ​ Identifies and restructures negative automatic thoughts. ​ Combines behavioral activation with cognitive restructuring to address thinking errors. 5. Brain Stimulation Therapies: ​ Electroconvulsive Therapy (ECT): Effective for severe cases of MDD and BD. ​ Transcranial Magnetic Stimulation (TMS): Non-invasive option targeting mood-related brain areas. 6. Guided Self-Help for Bipolar Disorder: ​ For depressive states: Maintain routine, log moods, and avoid biological rhythm disruptions. ​ For mania: Recognize early warning signs, limit impulsive behaviors, and adopt rules (e.g., two-person feedback rule Post-Traumatic Stress Disorder (PTSD) PTSD is a trauma-related disorder triggered by experiencing or witnessing a traumatic event. It affects emotional, cognitive, and behavioral functioning, often impairing social and occupational life. Outline ​ History: Shell Shock (historical term used to describe PTSD symptoms in war veterans). ​ Trauma and Stress-Related Disorders: ○​ Reactive Attachment Disorder (children). ○​ Disinhibited Social Engagement Disorder (children). ○​ PTSD. ○​ Acute Stress Disorder. ○​ Adjustment Disorders. PTSD Diagnostic Criteria (DSM-5) A. Exposure to Trauma One or more of the following: 1.​ Direct exposure to actual or threatened death, serious injury, or sexual violence. 2.​ Witnessing traumatic events. 3.​ Learning that a close friend or relative experienced trauma. 4.​ Repeated or extreme exposure to trauma details (e.g., first responders). B. Intrusive Symptoms At least one of the following: ​ Unwanted, distressing memories. ​ Nightmares related to the trauma. ​ Flashbacks or dissociative reactions. ​ Emotional distress or physiological reactions to trauma-related cues. C. Persistent Avoidance At least one of the following: ​ Avoidance of trauma-related thoughts, memories, or feelings. ​ Avoidance of external reminders (e.g., places, objects) associated with trauma. D. Negative Cognitions and Mood At least two of the following: ​ Inability to recall key aspects of the trauma. ​ Persistent negative beliefs about oneself or the world. ​ Blaming oneself or others for the trauma. ​ Negative emotional state (e.g., fear, guilt). ​ Loss of interest in activities. ​ Feeling detached or estranged from others. ​ Inability to experience positive emotions. E. Arousal and Reactivity At least two of the following: ​ Hypervigilance. ​ Exaggerated startle response. ​ Irritability or aggression. ​ Recklessness or self-destructive behavior. ​ Difficulty concentrating.  ​ Sleep disturbances. Duration: Symptoms last for at least one month and cause significant distress or impairment. Complex PTSD (ICD-11) In addition to standard PTSD symptoms, individuals experience: ​ Emotional Dysregulation: Anger, numbness. ​ Negative Self-Cognition: Shame, feelings of worthlessness. ​ Relational Difficulties: Problems maintaining relationships.​ Linked to prolonged, repeated trauma (e.g., abuse during childhood). Epidemiology ​ Lifetime Trauma Exposure: ~70.4% of individuals experience trauma (Kessler et al., 2017). ​ Lifetime PTSD Prevalence: 2.2%-8.8% (Atwoli et al., 2015). ​ Veterans: ~30% prevalence. ​ Gender Ratio: Women are ~2.4 times more likely to develop PTSD than men (Breslau, 1997). Course of PTSD ​ Symptoms usually begin within days of the trauma. ​ 50% of cases remit within 36-64 months without treatment. ​ Factors Influencing Course: Trauma type (e.g., natural disasters often lead to better outcomes), symptom severity, and access to treatment. Pathophysiology of PTSD Neurobiological Changes: ​ Hyperactive Amygdala: Amplifies fear and threat perception. ​ Hippocampal Volume Reduction: Impaired contextual memory processing. ​ Hypocortisolism: Low cortisol levels may predispose individuals to PTSD. Aetiology Biological Risk Factors: 1.​ Amygdala Hyperactivity: Increased response to negative stimuli, even before trauma. 2.​ Genetics: Family history of trauma-related disorders may increase risk. 3.​ Previous Trauma Exposure: E.g., Vietnam veterans with childhood abuse had higher PTSD rates. Environmental Risk Factors: ​ Pre-Trauma: ○​ Mental health problems. ○​ Previous trauma (if it led to PTSD). ○​ Gender: Women are more likely to develop PTSD, potentially due to higher trait anxiety. ​ Peri-Trauma: ○​ Type, frequency, and duration of trauma. ○​ Perceived threat to life and dissociation during trauma. ​ Post-Trauma: ○​ Lack of social support. ○​ Comorbidities (e.g., depression). Psychological Models of PTSD Cognitive Model (Ehlers & Clark, 2000): ​ Dysfunctional appraisals of trauma maintain PTSD. ​ Example: Believing "I’ll never feel safe again." Conditioning Theory: ​ Classical Conditioning: Neutral cues (e.g., a loud noise) become associated with trauma. ​ Operant Conditioning: Avoidance behaviors are reinforced by reducing fear. Fear Network Theory (Foa et al., 1989): ​ Trauma memory becomes overly generalized, leading to hyperactive fear responses. Dual Representation Theory (Brewin, 2001): ​ Verbally Accessible Memory (VAM): Conscious memory of the trauma. ​ Situationally Accessible Memory (SAM): Unconscious, sensory-driven memories. ​ PTSD treatment focuses on integrating SAM into VAM. Treatments for PTSD 1. Trauma-Focused CBT (TF-CBT): ​ Restructures negative trauma appraisals. ​ Techniques include: ○​ Cognitive restructuring (e.g., addressing guilt or blame). ○​ Imaginal exposure to process trauma memories. 2. Eye Movement Desensitization and Reprocessing (EMDR): ​ Combines exposure with bilateral stimulation (e.g., eye movements) to process trauma memories. 3. Exposure Therapy: ​ Gradual (systematic desensitization) or intense (flooding) exposure to trauma-related stimuli. ​ Types: ○​ In Vivo Exposure: Confronting real-life trauma triggers. ○​ Imaginal Exposure: Reliving the trauma in a safe environment. 4. Pharmacotherapy: ​ SSRIs/SNRIs: Sometimes prescribed but not first-line treatment per NICE guidelines. ​ Hydrocortisone: May prevent PTSD by modulating norepinephrine. Barriers to Treatment ​ Help-Seeking Behavior: ○​ 65.3% seek help in their lifetime; only 7.1% seek treatment within one year of onset. ○​ Median delay: 12 years Substance Use Disorders (SUD) Substance Use Disorders are chronic and relapsing conditions characterized by physical, psychological, social, and environmental factors that impair daily functioning. Key Concepts and Questions 1.​ Is addiction a choice, habit, or brain disease? 2.​ Can behavioral and environmental factors outweigh biological predispositions? 3.​ What role do substances like alcohol, nicotine, and drugs play compared to non-substance-related addictions (e.g., gambling, social media)? 4.​ A complex interaction of factors underpins addiction, including biological dependency, environmental stressors, and psychological vulnerabilities. Defining Substance Use Disorders (DSM-5) A diagnosis requires clinically significant impairment or distress and at least two or more of the following criteriawithin 12 months: ​ Larger amounts or longer use than intended. ​ Persistent desire or unsuccessful attempts to cut down/control use. ​ Excessive time spent obtaining, using, or recovering. ​ Craving or strong urges to use. ​ Recurrent use causing failure in fulfilling major roles (work, school, home). ​ Social or interpersonal problems worsened by substance use. ​ Giving up important activities. ​ Using in hazardous situations. ​ Continued use despite physical or psychological harm. ​ Tolerance: Need for increased amounts to achieve the same effect. ​ Withdrawal: Symptoms upon reducing or stopping use. Prevalence and Epidemiology ​ Alcohol Use: ~60% prevalence, with ~17% considered hazardous users. Only 4%-7% seek treatment. ​ General Trend: Substance use rates are decreasing among younger individuals. ​ Comorbidity: High overlap with mental health conditions like depression, anxiety, PTSD, and ADHD. Characteristics of Substances Substances are classified based on their psychoactive effects: ​ Psycholeptic (calming): Alcohol, sedatives, anxiolytics. ​ Psychoanaleptic (stimulating): Caffeine, nicotine, cocaine, amphetamines. ​ Psychodysleptic (perception-altering): LSD, ketamine, MDMA. Substances also affect neurotransmitter systems, particularly monoamines like dopamine, serotonin, and norepinephrine, which influence reward, mood, and decision-making. Clinical Features ​ Craving and Compulsion: Strong, uncontrollable urges to use despite adverse consequences. ​ Life Impact: Neglect of responsibilities, family problems, and legal issues.  ​ Withdrawal and Relapse: Physical and psychological distress when stopping use; relapse rates are high without intervention. ​ Stigma and Shame: Social consequences and personal guilt worsen psychological outcomes. Aetiology of Substance Use Disorders 1. Biological Factors ​ Genetics: ○​ Polygenic influences, including dopamine (DA), serotonin (5-HT), and norepinephrine (NE) pathways. ○​ Enzymes like alcohol dehydrogenase influence substance metabolism. ​ Neurobiology: ○​ Addiction hijacks the brain's reward systems, transitioning from voluntary use to compulsive seeking due to changes in neural circuits. 2. Early Adversity (Adverse Childhood Experiences - ACEs): ​ Increased risk of SUD linked to physical, emotional, and sexual abuse, neglect, and household substance use. ​ 5+ ACEs increase the likelihood of illicit drug use 7-10 times. 3. Psychological Factors: ​ Self-Medication Hypothesis: Use substances to cope with negative emotions (e.g., anxiety, depression). ​ Behavioral Theories: ○​ Positive reinforcement: Substance use feels rewarding. ○​ Negative reinforcement: Relieves withdrawal or distress. ○​ Conditioning: Cues (e.g., environments) elicit cravings. 4. Sociocultural Factors: ​ Social Influences: Peer pressure, cultural norms, advertising, and availability. ​ Socioeconomic Status (SES): Usage rates vary across SES groups, but outcomes are often worse for lower SES individuals. ​ Traditional Values: Religion and societal norms can act as protective factors. Models of Addiction 1. Opponent Process Model: ​ Initial use is driven by pleasure, but chronic use becomes about avoiding withdrawal or distress. 2. Gateway Hypothesis: ​ Suggests progression from mild substances (e.g., cannabis) to harder drugs, though evidence is mixed. 3. Power Threat Meaning Framework (Johnstone & Boyle, 2018): ​ Emphasizes personal narratives and context: ○​ "What happened to you?" (trauma, adversity). ○​ "What did you do to survive?" (coping mechanisms). ○​ "What are your strengths?" (resilience and resources). Treatment Approaches 1. Holistic Treatment Addresses biological, psychological, social, and environmental factors. 2. Pharmacotherapy: ​ Alcohol Use Disorder: Disulfiram (aversion), Acamprosate (GABA regulation), Naltrexone (reduces cravings). ​ Opioid Use Disorder: Methadone, Buprenorphine. ​ Nicotine Dependence: Nicotine replacement therapy (patches, gums). 3. Psychological Interventions: ​ Cognitive Behavioral Therapy (CBT): ○​ Goal-setting, problem-solving, relapse prevention. ○​ Addresses dysfunctional beliefs and coping strategies. ​ Contingency Management (CM): ○​ Provides tangible rewards for abstinence. 4. Social Interventions: ​ Family therapy, peer support groups (e.g., 12-step programs like AA). ​ Aftercare support (e.g., housing, childcare, financial assistance). Course and Prognosis ​ Remission Rates: 20%-80% recover without treatment. ​ Relapse: 60%-80% relapse within the first year post-treatment, with the highest risk in the first three months. ​ Predictors of Relapse: Stress, cravings, low social stability, trauma history, and comorbid mental health conditions. Compassion-Focused Therapy (CFT) ​ Integrates neurobiology and attachment theory to build self-soothing skills. ​ Promotes emotional regulation by addressing stigma, shame, and isolation Personality Disorders (PDs) Overview ​ Definition: Enduring patterns of inner experience and behavior that markedly deviate from cultural expectations. These patterns are: ○​ Inflexible and pervasive across different situations. ○​ Cause distress or impair social, occupational, or other important functioning. ○​ Differ from temporary mental states, representing enduring personality traits. Personality Traits vs. Disorders ​ Egodystonic vs. Egosyntonic: ○​ Egodystonic: Thoughts, impulses, and behaviors are in conflict with the individual's ideal self-image. ○​ Egosyntonic: Behaviors and thoughts align with the individual’s self-perception (e.g., many PDs). ​ Traits vs. States: ○​ Mental states are temporary emotional or cognitive conditions. ○​ Personality traits are stable over time and context; extreme traits become disorders. DSM-5 Criteria for Personality Disorders 1.​ Deviations in Behavior (Manifest in 2+ areas): ○​ Cognition: Distorted ways of perceiving/interpreting events, self, or others. ○​ Affectivity: Emotional responses that are intense, labile, or inappropriate. ○​ Interpersonal Functioning: Difficulty in relationships and social interactions. ○​ Impulse Control: Poor regulation of impulses or emotions. 2.​ Pervasive/Inflexible: Across personal and social contexts. 3.​ Distress or Impairment: Clinically significant disruptions in important areas of functioning. Clusters of PDs  1.​ Cluster A (Odd/Eccentric): ○​ Traits: Social withdrawal, cognitive distortions, and eccentric behavior. ○​ Disorders: ​ Paranoid: Pervasive distrust/suspicion. ​ Schizoid: Emotional coldness, lack of social engagement. ​ Schizotypal: Eccentricity, discomfort in close relationships, perceptual distortions. 2.​ Cluster B (Dramatic/Emotional): ○​ Traits: Emotional instability, impulsivity, disregard for rules. ○​ Disorders: ​ Antisocial: Disregard for others’ rights; deceitfulness. ​ Borderline: Instability in relationships, self-image, and emotions. ​ Narcissistic: Grandiosity, lack of empathy, need for admiration. ​ Histrionic: Attention-seeking and excessive emotionality. 3.​ Cluster C (Anxious/Fearful): ○​ Traits: High levels of anxiety, fear of rejection, and dependency. ○​ Disorders: ​ Avoidant: Hypersensitivity to rejection, social inhibition. ​ Dependent: Neediness, fear of abandonment. ​ Obsessive-Compulsive: Perfectionism, preoccupation with control. Detailed Disorder Profiles (Davidson, 2002) ​ Paranoid PD: Distrust and suspicion of others; interpreting benign actions as malevolent. ​ Schizoid PD: Detached relationships, minimal emotional expression. ​ Schizotypal PD: Discomfort in relationships, perceptual distortions, eccentric behavior. ​ Antisocial PD (APD): Persistent disregard for others' rights, impulsivity, aggression, and lack of remorse. ​ Borderline PD (BPD): ○​ Instability in personal relationships, self-image, emotions, and impulsivity. ○​ Prone to suicidal gestures, chronic feelings of emptiness, and intense anger. ​ Narcissistic PD: Grandiosity, preoccupation with fantasies of success/power, and lack of empathy. ​ Histrionic PD: Excessive attention-seeking and dramatic behavior. ​ Avoidant PD: Fear of criticism or rejection, leading to social withdrawal. ​ Dependent PD: Submissive, clingy behavior driven by fear of abandonment. ​ Obsessive-Compulsive PD: Over-concern with order, perfectionism, and control. Differentiating Disorders ​ Borderline vs. Bipolar Disorder:  ○​ Borderline: Chronic interpersonal and emotional instability, not limited to mood episodes. ○​ Bipolar: Episodic mood changes, alternating between depression and mania/hypomania. Aetiology of PDs Biological Factors: 1.​ Heritability: ○​ 40-60% for Borderline PD (BPD). ○​ 40-69% for Antisocial PD (APD). 2.​ Brain Function and Structure: ○​ Amygdala: Emotion regulation and fear processing. ○​ Hippocampus: Memory and emotional context. ○​ Frontal Cortex: Impulse control and decision-making. ○​ Neurotransmitters: ​ Serotonin: Impulsivity and aggression. ​ Dopamine: Paranoia and distrust. 3.​ Stress Response: Altered hypothalamic-pituitary-adrenal (HPA) axis in some PDs. Environmental Factors: 1.​ Childhood Adversity: ○​ Physical/emotional/sexual abuse. ○​ Neglect and invalidating environments. 2.​ Parental Issues: ○​ Parental PDs, inconsistent parenting, and lack of warmth. 3.​ Social Modeling: ○​ Bandura’s theory: Behaviors learned from observing others. 4.​ Early Attachment: ○​ Disrupted attachments impair mentalizing and coping mechanisms. Treatment Approaches General Principles: ​ PD treatment is challenging due to the enduring nature of traits. ​ Therapy focuses on reducing maladaptive behaviors, improving functioning, and managing symptoms. Treatment for BPD: 1.​ Dialectical Behavior Therapy (DBT): ○​ Topics: Mindfulness, emotion regulation, distress tolerance, social skills.  ○​ Proven to reduce suicidality and anger; dropout rates lower than other therapies. 2.​ Schema-Focused Therapy: ○​ Identifies maladaptive schemas (e.g., defectiveness, enmeshment). ○​ Focus on early life experiences and attachment. Treatment for APD: ​ Cognitive-behavioral techniques: ○​ Problem-solving, mentalization, and social skills training. ○​ Focus on altering criminal thought patterns and improving interpersonal interactions. Pharmacological Approaches: ​ No specific medications for PDs, but symptoms may be managed with: ○​ Antidepressants: For mood dysregulation and anger. ○​ Mood Stabilizers: To control mood swings and impulsivity. ○​ Antipsychotics: For psychotic symptoms or severe emotional distress. ○​ Anxiolytics: To reduce anxiety and agitation. Challenges in Treatment 1.​ Insight Issues: Many PD behaviors are egosyntonic, reducing motivation for change. 2.​ Comorbidity: High rates with anxiety, depression, PTSD, substance use, etc. 3.​ Therapeutic Relationship: Boundary and trust issues often play out in therapy. 4.​ Risk: ○​ Suicide: ~10% die by suicide; 50% attempt at least once. ○​ Violence and impulsivity complicate treatment further. Assessment Tools ​ NICE Recommendations: ○​ Structured Clinical Interview for DSM Personality Disorders (SCID). ○​ Personality Assessment Schedule (PAS). ○​ Standardized Assessment of Personality (SAP). Attention-Deficit/Hyperactivity Disorder (ADHD) Overview ​ ADHD is a neurodevelopmental disorder characterized by patterns of inattention, hyperactivity, and impulsivity that interfere with functioning. ​ Historical Context:  ○​ First described as "Minimal Brain Dysfunction." ○​ Later termed "Hyperkinetic Disorder of Childhood." ○​ Now categorized as ADHD, with three subtypes: ​ Predominantly Inattentive. ​ Predominantly Hyperactive-Impulsive. ​ Combined Type. Core Symptom Clusters 1.​ Inattention: ○​ Difficulty focusing on tasks or details. ○​ Easily distracted and forgetful. ○​ Fails to complete tasks or follow instructions. ○​ Poor organizational skills and frequent loss of necessary items. 2.​ Hyperactivity: ○​ Constant movement (e.g., fidgeting, running, climbing in inappropriate settings). ○​ Difficulty engaging in quiet activities. ○​ Talks excessively and appears "always on the go." 3.​ Impulsivity: ○​ Blurting out answers prematurely. ○​ Interrupting others during conversations or activities. ○​ Difficulty waiting for their turn. DSM-5 Diagnostic Criteria ​ Symptoms: At least 6+ symptoms in the respective cluster for children or 5+ for adolescents/adults. ​ Duration: Symptoms persist for 6+ months. ​ Onset: Some symptoms must appear before age 12. ​ Settings: Present in 2+ settings (e.g., home, school). ​ Impairment: Significant negative impact on social, academic, or occupational functioning. Prevalence and Demographics ​ Global Prevalence: ~5% of children, lower in adults due to developmental trajectory. ​ Gender Differences: ○​ Boys: Higher diagnosis rates (5:1 in clinical settings, 2-3:1 in epidemiological samples). ○​ Girls: Often exhibit inattentive symptoms, leading to underdiagnosis or delayed recognition.  ​ Cultural Perspectives: ○​ ADHD diagnosis is more prevalent in Western countries, raising questions about societal and cultural influences on recognition and diagnosis. Comorbidities ​ ADHD frequently overlaps with: ○​ Oppositional Defiant Disorder (ODD): Defiance, irritability, and vindictiveness. ○​ Conduct Disorder (CD): Aggressive and rule-breaking behavior. ○​ Anxiety and Depression. ○​ Substance Use Disorders: Increased risk in adolescence and adulthood. ○​ Autism Spectrum Disorder (ASD): Shared neurodevelopmental features. Developmental Impact of ADHD 1.​ Preschool: ○​ Behavioral challenges, difficulty following rules, and early signs of hyperactivity. 2.​ School-Age: ○​ Poor academic achievement due to inattentiveness. ○​ Social impairments: Struggles to maintain friendships. ○​ Emotional challenges: Frustration, low self-esteem. 3.​ Adolescence: ○​ Risk-taking behaviors (e.g., substance use, reckless driving). ○​ Continued academic and social difficulties. 4.​ Adulthood: ○​ Occupational challenges, unstable relationships, and self-esteem issues. ○​ Increased rates of substance abuse, accidents, and health risks. Aetiology Genetic Contributions: ​ Heritability: ~76% (one of the most heritable psychiatric conditions). ​ Risk Factors: ○​ First-degree relatives have a 9x higher risk. ○​ Overlap with genes influencing externalizing disorders (e.g., ASD, anxiety, depression). ​ Polygenic Effects: ○​ Variants in dopamine, norepinephrine, and serotonin systems linked to ADHD. Neurobiological Factors:  ​ Brain Structure and Function: ○​ Reduced prefrontal cortex volume, affecting executive functions. ○​ Abnormalities in the fronto-striatal circuitry, responsible for motor control and reward processing. ○​ Delayed brain maturation (3-year lag in cortical development). ​ Neurotransmitter Dysregulation: ○​ Deficits in dopamine and norepinephrine systems impact attention and impulse control. ​ Executive Functioning: ○​ Impairments in inhibition, working memory, planning, and sustained attention. Environmental and Psychosocial Factors: 1.​ Prenatal Risks: ○​ Maternal smoking and alcohol consumption during pregnancy. ○​ Pregnancy complications (e.g., low birth weight). 2.​ Toxins: ○​ Exposure to lead and food additives may increase risk. 3.​ Parenting: ○​ ADHD in parents can lead to inconsistent discipline and chaotic home environments. ○​ Parental mental health (e.g., depression) can exacerbate family stress. Impact on Functioning For the Child: ​ Academics: Difficulty focusing leads to underachievement. ​ Social: Poor peer relationships due to impulsivity and hyperactivity. ​ Emotional: Frustration, mood swings, and low self-esteem. For the Family: ​ Elevated stress levels and increased risk of parental mental health issues. ​ Marital discord and financial strain due to treatment and support needs. For Society: ​ Increased healthcare and educational system costs. ​ Higher rates of unemployment and legal problems in adults with ADHD. Assessment 1.​ Clinical Evaluation:  ○​ Comprehensive history, including developmental milestones, family dynamics, and trauma exposure. ○​ Coexisting symptoms (e.g., mood disorders, anxiety, sensory issues). 2.​ Observation in Multiple Settings: ○​ Collaboration with teachers to assess school behavior. ○​ Structured clinical observation in office settings. 3.​ Rating Scales: ○​ Conners’ Rating Scale: Parent and teacher versions. ○​ Strengths and Difficulties Questionnaire (SDQ): Measures emotional and behavioral challenges. Treatment Approaches Environmental Modifications: ​ Reducing distractions at home and school (e.g., designated workspaces, quiet environments). ​ Structured routines to improve predictability and focus. ​ Avoiding punitive measures like detentions; promoting positive reinforcement. Behavioral Interventions: ​ Parent Training Programs: ○​ ADHD-specific strategies to improve behavior management. ○​ Teaching consistent reward systems and consequences. ​ School-Based Strategies: ○​ Adjusting seating arrangements and providing additional breaks. ○​ Support systems for completing tasks (e.g., planners, checklists). Psychological Interventions: ​ CBT: ○​ Focuses on managing coexisting problems like anxiety and anger. ○​ Helps improve self-awareness and emotional regulation. ​ Social Skills Training: ○​ Targets difficulties in peer interactions through role-playing and group exercises. Pharmacological Treatments: ​ Stimulants: ○​ Methylphenidate and amphetamines improve focus and impulse control. ○​ First-line treatment; 70% response rate. ​ Non-Stimulants: ○​ Atomoxetine used for those unresponsive to stimulants or with side effects. ​ Considerations: ○​ Medication typically follows behavioral/environmental interventions.  ○​ Regular monitoring for side effects (e.g., appetite suppression, sleep issues). Critical Issues in ADHD 1.​ Diagnosis Challenges: ○​ Cultural and gender biases can lead to underdiagnosis or overdiagnosis. ○​ Overlap with other disorders complicates clear identification. 2.​ Intersectionality: ○​ Recognition of how socio-economic and gender factors affect presentation and treatment access. 3.​ Changing Perspectives: ○​ ADHD increasingly recognized as a neurodiverse condition rather than purely pathological. ○​ Shifts in societal attitudes emphasize strengths (e.g., creativity, hyperfocus