PsychoPathology/DSM Diagnoses Study Notes
PsychoPathology/DSM Diagnoses Study Notes
I. Overview of Neurodevelopmental Disorders
Definition: Early-onset developmental deficits affecting:
Personal functioning
Social functioning
Academic functioning
Occupational functioning
Symptom Onset: Symptoms begin early in development (often before school age) and are typically lifelong.
II. Intellectual Developmental Disorder (Intellectual Disability)
A. Diagnostic Criteria (Must include ALL three)
Deficits in Intellectual Functioning:
Confirmed by clinical assessment + standardized testing
IQ ≈ two standard deviations (SD) below the mean (~70 or below)
Deficits in Adaptive Functioning:
Affects conceptual, social, and practical domains
Must limit personal independence and social responsibility
Onset: During developmental period
Severity Specifiers
Severity: Based on adaptive functioning, NOT IQ:
Mild
Moderate
Severe
Profound
B. Etiology
Cause identified in 25–50% of cases. Of known causes:
80–85% prenatal (e.g., genetic/chromosomal, teratogens, maternal illness)
5–10% perinatal (e.g., birth asphyxia)
5–10% postnatal (e.g., TBI, infection, toxins)
Genetic Causes:
Down Syndrome: Most common chromosomal cause (NOT inherited; caused by trisomy 21)
Fragile X Syndrome: Most common inherited cause (mutated gene on X chromosome)
III. Autism Spectrum Disorder (ASD)
A. Diagnostic Criteria (Requires BOTH)
Deficits in Social Communication/Interaction:
Social-emotional reciprocity
Nonverbal communication
Understanding/maintaining relationships
Restricted, Repetitive Behaviors:
Repetitive movements/speech
Insistence on sameness, routines
Highly fixated interests
Hyper- or hypo-reactivity to sensory input
Onset: Symptoms must begin in early development.
B. Associated Features
Intellectual impairment
Language impairment
Self-injury (e.g., head banging, biting)
Motor abnormalities (e.g., clumsiness, toe-walking)
Deficits in face and emotion recognition
C. Prognosis (EPPP MUST KNOW)
Best Outcomes Associated With:
IQ > 70
Functional language by age 5
Fewer comorbid psychiatric conditions
D. Epidemiology
Global prevalence: 1%
U.S. prevalence: 3.2% of 8-year-olds
More common in males (3–4:1)
E. Etiology
Combination of Genetic + Environmental Factors.
Heredity:
Twin studies:
Heritability ≈ 62%
Monozygotic (MZ): 59–84%
Dizygotic (DZ): 3–29%
Environmental Factors:
Very preterm birth (<26 weeks)
Prenatal valproic acid exposure
Advanced parental age
NO evidence linking vaccines → ASD
F. Neurobiology
Accelerated Brain Growth: Between 6 months and preschool
Abnormalities:
Cerebellum
Corpus callosum
Amygdala
Serotonin Irregularities:
Low brain serotonin
High blood serotonin
Also involves dopamine, GABA, glutamate, acetylcholine.
G. Treatment
Nonpharmacological:
Early Intensive Behavioral Intervention (EIBI)
Applied Behavior Analysis (ABA)
Most impact on IQ & language development
Fewer consistent effects on social/adaptive functioning
Medication:
NOT effective for core ASD symptoms
Used for comorbidity:
Stimulants → ADHD symptoms
SSRIs → anxiety/depression
Atypical antipsychotics (e.g., risperidone, aripiprazole) → irritability/aggression
IV. Attention-Deficit/Hyperactivity Disorder (ADHD)
A. Diagnostic Criteria
Symptoms for ≥ 6 months:
Onset before age 12
Present in 2 or more settings
Cause impairment:
Ages ≤16: 6 symptoms required
Ages ≥17: 5 symptoms required
Presentations
Predominantly inattentive
Predominantly hyperactive/impulsive
Combined
B. Common Symptoms
Inattention:
Forgetful
Easily distracted
Careless mistakes
Difficulty sustaining attention
Hyperactivity-Impulsivity:
Excessive talking
Fidgeting
Running/climbing
Interrupts others
C. Epidemiology
Most prevalent diagnosed disorder in youth (U.S.)
2:1 male:female ratio in childhood
1.6:1 ratio in adulthood
D. Course into Adulthood
Hyperactivity → restlessness
Impulsivity → risky decisions
Inattention → chronic disorganization, missed deadlines
Most continue to experience some symptoms as adults.
E. Neurobiology
Structural + functional abnormalities in:
Prefrontal cortex
Striatum
Thalamus
Cerebellum
Amygdala
Neurotransmitter involvement:
Low dopamine and norepinephrine contribute to symptoms.
F. Etiology
Twin studies: show high heritability (~74%)
Environmental Contributors:
Low birth weight
Time in NICU
Developmental delays
G. Treatment
Children:
Preschool: behavioral parent training (PTBM, PCIT)
School age: medication + behavioral interventions
Adolescents: medication + school supports + motivational interviewing (MI), mindfulness
Adults:
First-line: medication
CBT has strongest psychosocial evidence
Stimulant treatment does not increase or decrease later substance use risk.
V. Tic Disorders
Definition: Tic = sudden, rapid, recurrent, non-rhythmic movement or sound.
Types:
Motor Tics: (e.g., eye blink, shrug, grimace)
Vocal Tics: (e.g., throat clearing, barking, echolalia)
A. Disorders
Tourette’s Disorder:
Multiple motor tics + at least one vocal tic
Present for >1 year
Onset before age 18
Persistent (Chronic) Motor or Vocal Tic Disorder:
Motor OR vocal tics (not both)
Present >1 year
Provisional Tic Disorder:
Motor and/or vocal tics
<1 year duration
Peak Severity: Ages 10–12
Common Comorbidity: ADHD
B. Etiology
Biological Factors:
Dopamine overactivity
Smaller caudate nucleus
Genetic factors
C. Treatment
Medications:
Antipsychotics (e.g., haloperidol)
Meds for comorbid ADHD or OCD
CBIT (Comprehensive Behavioral Intervention for Tics):
Habit reversal
Competing response
Relaxation training
VI. Communication Disorders
Childhood-Onset Fluency Disorder (Stuttering)
Key Symptoms:
Sound/syllable repetitions
Prolongations
Blocking
Circumlocutions
Excessive tension
Monosyllabic word repetitions
Onset: Ages 2–7
Recovery Rate: 65–85% recover naturally
Best Treatment: Habit reversal training (regulated breathing)
VII. Specific Learning Disorder (SLD)
A. Diagnostic Criteria
Difficulties in academic skills for ≥ 6 months despite interventions.
Must impair academic, occupational, or daily functioning.
B. Subtypes
Reading (dyslexia)
Written expression
Math (dyscalculia)
80% of SLD cases = reading problems.
Dysphonic dyslexia: Most common type (phonological)
C. Associated Features
Average or above-average IQ
Common Comorbidity: ADHD
Prevalence: 5–15% of school-aged children
VIII. EPPP Quick Reference Summary
IDD: IQ < 70 + adaptive deficits + early onset
ASD: Social communication deficits + repetitive behaviors
ADHD: 6 symptoms/5 symptoms; before 12; 2+ settings
Tourette’s: Motor + vocal tics 1+ year
SLD: Academic difficulties 6+ months despite intervention
ASD Best Prognosis: IQ > 70, language by age 5
ADHD Most Common Comorbidity: Oppositional Defiant Disorder (ODD)
Tourette’s Most Common Comorbidity: ADHD
IX. Schizophrenia Spectrum & Other Psychotic Disorders Study Sheet
1. Core Psychotic Symptoms
Delusions: Fixed false beliefs not culturally shared (e.g., persecutory, grandiose, somatic, referential, erotomanic, nihilistic).
Hallucinations: Sensory experiences without external stimulus (most common: auditory, usually voices).
Disorganized Thinking/Speech: Derailment, tangentiality, incoherence (“word salad”).
Grossly Disorganized or Catatonic Behavior: Bizarre behavior, agitation, rigid postures, mutism, negativism.
Negative Symptoms: Affective flattening, alogia (poverty of speech), avolition (lack of motivation), anhedonia (loss of pleasure), asociality (social withdrawal).
2. Main Diagnoses & Duration Differences (EPPP GOLD)
Think: “1 day → 1 month → 6 months → 6+ months”
- Brief Psychotic Disorder
Duration: ≥ 1 day but < 1 month
At least 1+ psychotic symptom, and one must be:
Delusions
Hallucinations
Disorganized speech
Eventual full return to premorbid functioning.
Often linked to a stressor (with marked stressor subtype).
- Schizophreniform Disorder
Duration: ≥ 1 month but < 6 months
Same core symptom set as schizophrenia (2+ key symptoms).
If symptoms last 6+ months → diagnosis becomes schizophrenia.
- Schizophrenia
Duration: ≥ 6 months total disturbance, with:
At least 1 month of active-phase symptoms.
Active-phase Symptoms (2+ must be significant):
Delusions
Hallucinations
Disorganized speech
Grossly disorganized or catatonic behavior
Negative symptoms
Must cause marked impairment in functioning (work, relationships, self-care).
Not better explained by mood disorder or by a substance/medical condition.
- Schizoaffective Disorder
An uninterrupted period of illness with a major mood episode (depressive or manic) concurrent with active-phase schizophrenia symptoms.
Plus:
At least 2 weeks of delusions or hallucinations without mood symptoms at some point.
Mood episodes (depression or mania) are present for most of the total duration.
Subtypes:
Bipolar type (includes manic ± depressive episodes)
Depressive type (only major depressive episodes)
Key EPPP rule:
If psychotic symptoms only occur during mood episodes → likely mood disorder with psychotic features (NOT schizoaffective).
3. Course & Prognosis in Schizophrenia
Typical Onset:
Late teens to mid-20s in males
Late 20s to early 30s in females
Prodromal phase: Social withdrawal, odd behavior, functioning decline.
Course: Can be chronic with exacerbations & remissions.
Symptoms often lessen with age (especially positive symptoms).
- Better Prognosis Associated With:
Later age of onset
Female gender
Acute onset vs. insidious
Good premorbid functioning
Presence of mood symptoms
Few negative symptoms
Strong social support
- Worse Prognosis Associated With:
Early onset
Male gender
Gradual onset
Strong negative symptoms
Family history of schizophrenia
High expressed emotion in family
4. Etiology of Schizophrenia
Genetics: Highly heritable; polygenic.
Twin/Family Studies:
General population risk: ~1%
First-degree relatives: ~10%
MZ twins: up to ~40–50% concordance
DZ twins: ~10–15%
Risk Increases with Degree of Genetic Relatedness:
Concordance Rate
Parent: 6%
Biological sibling: 9%
Child of one parent with schizophrenia: 13%
Child of two parents with schizophrenia: 46%
Dizygotic (fraternal) twin: 17%
Monozygotic (identical) twin: 48%
Neurotransmitters (Dopamine + more):
Classic Dopamine Hypothesis:
Schizophrenia due to overactivity of dopamine in certain brain areas.
Positive Symptoms: Linked to ↑ dopamine in mesolimbic pathway.
Negative/Cognitive Symptoms: Linked to ↓ dopamine in mesocortical pathway.
Revised Dopamine Hypothesis:
Positive symptoms = dopamine TOO HIGH in subcortical/striatal regions.
Negative symptoms = dopamine TOO LOW in prefrontal cortex.
Environmental & Developmental Factors:
Obstetric complications (e.g., hypoxia)
Prenatal viral infections
Malnutrition
Early CNS insult
Cannabis use (especially high-potency in adolescence) ↑ risk in vulnerable individuals
Stress/trauma and high expressed emotion can trigger relapse in vulnerable individuals.
5. Treatment of Schizophrenia
Antipsychotic Medications:
First-Generation (Typical) Antipsychotics:
Mechanism: Strong D2 receptor blockade.
Best for positive symptoms.
Side Effects:
Extrapyramidal symptoms (EPS):
Acute dystonia (muscle spasms)
Parkinsonism (rigidity, tremor, bradykinesia)
Akathisia (inner restlessness)
Tardive dyskinesia (TD):
Involuntary movements (face, tongue, limbs), often after long-term use
May be irreversible
Neuroleptic malignant syndrome (rare but life-threatening):
Muscle rigidity, high fever, autonomic instability, confusion.
Second-Generation (Atypical) Antipsychotics:
Examples: Clozapine, risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole.
Mechanism: Dopamine + serotonin receptor effects.
Effective for positive symptoms, often some benefit for negative symptoms.
Lower EPS risk (overall) but more:
Metabolic side effects:
Weight gain
Hyperlipidemia
Insulin resistance / diabetes
Clozapine (Special Case):
Very effective for treatment-resistant schizophrenia.
Serious risk: Agranulocytosis (dangerous drop in WBCs) → requires regular blood monitoring.
Also risk of seizures, myocarditis, significant weight gain/sedation.
Psychosocial Interventions:
Best outcomes = meds + psychosocial.
Psychoeducation: Patient & family understanding of illness.
Family interventions: Reduce expressed emotion → lower relapse rates.
Social skills training: Improve communication, functioning.
CBT for psychosis: Target delusional beliefs, coping with voices.
Supported employment: Helps maintain work roles, structure, and recovery.
6. Cultural, Gender, and Age Considerations
Similar Lifetime Prevalence Across Cultures: (~1%)
Content of delusions/hallucinations can be culturally shaped.
Men:
Earlier onset
More negative symptoms
Generally poorer prognosis
Women:
Later onset
More mood symptoms
Better premorbid functioning
Slightly better prognosis
7. Suicide Risk in Schizophrenia
High suicide risk; estimates often around 5–10% die by suicide.
Risk Factors:
Young, male, higher functioning / more insight
Depressive symptoms
Hopelessness
Recent hospital discharge
History of suicide attempts
Many attempts occur during early course or after acute episodes.
8. EPPP-Style Distinctions (Quick Reference)
Duration / Diagnosis:
1 day–<1 month → Brief psychotic disorder
1–<6 months → Schizophreniform disorder
≥6 months → Schizophrenia
Psychosis + mood most of the time + 2+ weeks psychosis alone → Schizoaffective
1+ month delusions only, relatively intact functioning → Delusional disorder
Family Patterns:
Higher risk with closer genetic relationship, history of schizophrenia in first-degree relatives;
MZ twin studies: much higher concordance than DZ.
Treatment:
First-line: Antipsychotics (SGAs often preferred)
Clozapine: For treatment-resistant or high suicide risk
ECT: Sometimes used for catatonia or severe psychosis when meds fail
Psychosocial: family work, CBTp, social skills, supported employment
9. Bipolar & Depressive Disorders Study Sheet
1. Core Mood Episodes
Manic Episode:
Mood: Abnormally elevated, expansive, or irritable
Energy: ↑ Activity/Energy
Duration: ≥ 1 week (or any duration if hospitalization is needed)
Symptoms: 3+ (4+ if mood only irritable), e.g.:
Grandiosity/inflated self-esteem
Decreased need for sleep
Pressured speech
Flight of ideas/racing thoughts
Distractibility
↑ goal-directed activity or psychomotor agitation
Risky behaviors (spending, sex, etc.)
Severity:
Marked impairment in functioning OR
Hospitalization to prevent harm OR
Psychotic features
Hypomanic Episode:
Mood: Elevated, expansive, or irritable
Energy: ↑ Activity/Energy
Duration: ≥ 4 consecutive days
Symptoms: Same list as mania (3+ or 4+ if irritable only)
Severity:
Change in functioning noticeable to others
NO marked impairment
NO hospitalization
NO psychotic features
Major Depressive Episode (MDE):
Duration: ≥ 2 weeks
Symptoms: 5+, with at least one being:
Depressed mood
Loss of interest/pleasure (anhedonia)
Other Possible Symptoms:
Appetite/weight change
Sleep disturbance (insomnia or hypersomnia)
Psychomotor agitation or retardation
Fatigue or loss of energy
Feelings of worthlessness or excessive guilt
Poor concentration/indecisiveness
Recurrent thoughts of death or suicide
Must cause clinically significant distress or impairment.
2. Bipolar Disorders
Bipolar I Disorder:
Requires at least one manic episode.
May also have hypomanic and/or major depressive episodes, but they’re not required.
If mania has EVER occurred → diagnosis is Bipolar I (for life).
Bipolar II Disorder:
Requires:
≥ 1 hypomanic episode
≥ 1 major depressive episode
Never had a manic episode.
If psychosis shows up in a mood episode → it’s mania → Bipolar I, not II.
Cyclothymic Disorder:
Numerous periods of:
Hypomanic symptoms that do not meet full hypomanic criteria
Depressive symptoms that do not meet full MDE criteria
Duration:
Adults: ≥ 2 years
Kids/teens: ≥ 1 year
Symptoms present at least half the time, with no symptom-free period > 2 months.
3. Etiology of Bipolar Disorder (High-Yield Points)
Highly heritable:
Heritability ≈ 60–90%
Twin concordance (approx ranges):
Monozygotic: 40–80%
Dizygotic: 5–30%
Some evidence heritability is greater for Bipolar I than II.
Environmental Risk Factors:
Early parental loss
Childhood maltreatment (esp. emotional abuse)
Medical comorbidities (IBS, asthma, migraine)
Substance use (e.g., cannabis, cocaine)
Highly stressful life events
4. Differential Diagnosis: Bipolar vs ADHD
Shared Symptoms:
Distractibility, irritability, accelerated speech.
Mania in Youth (7–16):
Most specific symptoms: Elation, Grandiosity, Flight of ideas/racing thoughts, Decreased need for sleep, Hypersexuality/developmentally inappropriate sexual behavior.
Adults:
Mania: Mood: Euphoric, elevated, or irritable; Self-esteem: ↑ self-esteem/grandiosity; Distractibility: Due to thought acceleration; Sleep: ↓ need for sleep without fatigue; Sexuality: Often ↑ sexual activity.
Adult ADHD: Mood: Labile, often dysphoric; Self-esteem: Reduced self-esteem; Distractibility: Wandering thoughts, not accelerated; Sleep: Fatigue and discomfort after loss of sleep; Sexuality: Not necessarily ↑ activity, but ↑ risk for sexual disorders and risky sexual behavior.
5. Treatment of Bipolar Disorder
Psychosocial Interventions:
Often combined with meds.
Psychoeducation, Interpersonal and Social Rhythm Therapy, CBT, and Family-focused therapy (targets high expressed emotion to reduce relapse).
Pharmacotherapy:
“Classic” bipolar disorder (best for lithium):
Low likelihood of mixed states or rapid cycling.
Long periods of recovery between episodes.
Onset ~15–19 years → Lithium usually most effective.
“Atypical” bipolar disorder (best for anticonvulsants/SGAs):
Mixed mood states.
Rapid cycling.
Lack of full recovery between episodes.
Earlier onset (~10–15 years) → Anticonvulsants (e.g., carbamazepine, valproic acid).
Second-generation antipsychotics (Note: “classic vs atypical” here is not a DSM-5-TR formal specifier.)
6. Depressive Disorders
Major Depressive Disorder (MDD):
5+ MDE symptoms for ≥ 2 weeks.
At least one is depressed mood or anhedonia.
Persistent Depressive Disorder (PDD/Dysthymia):
Depressed mood plus 2+ symptoms (e.g., low appetite or overeating, insomnia/hypersomnia, low energy, low self-esteem, poor concentration, hopelessness).
Duration:
Adults: ≥ 2 years.
Kids/teens: ≥ 1 year.
If criteria for MDD are ALSO met → diagnose both MDD and PDD and add a PDD course specifier:
With persistent major depressive episode
With intermittent major depressive episode, with current episode
With intermittent major depressive episode, without current episode.
7. Disruptive Mood Dysregulation Disorder (DMDD)
Duration: ≥ 12 months.
Criteria:
Severe, recurrent temper outbursts (verbal and/or behavioral):
Out of proportion to situation
Occur ≥ 3 times per week.
Between outbursts: Persistently irritable or angry mood, visible to others most of the day, nearly every day.
8. MDD Specifiers: Peripartum Onset & Seasonal Pattern
With Peripartum Onset:
Onset: During pregnancy or within 4 weeks postpartum.
“Baby Blues”:
Up to 80% of women experience mild symptoms (sadness, irritability, anxiety).
Smaller % meet full MDD criteria.
About half of those with MDD had symptom onset before delivery.
Evidence-based treatments:
CBT
Interpersonal therapy (IPT)
Antidepressants (esp. sertraline) – must weigh:
Potential risks to fetus/breastfeeding infant
Risks of untreated maternal depression.
Exercise can help, especially when combined with other interventions.
With Seasonal Pattern (Seasonal Affective Disorder – SAD):
Temporal Pattern: Usually winter onset.
Typical Symptoms:
Hypersomnia
Overeating
Weight gain
Carb craving
Biology:
Low serotonin
High melatonin.
9. Gender, Age, and Depression
In Childhood: Depression rates similar for boys and girls.
In Adolescence:
Rate increases sharply for females.
Male rate stays relatively stable.
Female:male ratio ≈ 1.5 to 3:1 and persists into adulthood.
Older Adults:
Less likely to emphasize affective symptoms.
More likely to report somatic complaints, cognitive changes, loss of interest in activities.
10. Etiology of Major Depressive Disorder
Genetic Factors:
Heritability ≈ 30–50%.
Twin Concordance (approx):
MZ: ~46%
DZ: ~20%.
Genetic influence often higher in females.
Personality Trait Neuroticism: Accounts for a large part of genetic risk.
Neurotransmitters & Biology:
Depression associated with low serotonin, norepinephrine, dopamine.
HPA Axis Abnormalities:
Chronic stress → hyperactive HPA axis → ↑ cortisol → Increased risk for depression, especially with early life stress.
Brain Abnormalities:
Prefrontal cortex, cingulate cortex, hippocampus, basal ganglia, amygdala, thalamus, etc.
Pattern:
Ventromedial PFC (vmPFC) = overactive in depression
Dorsolateral PFC (dlPFC) = underactive in depression
Remission linked to ↓ vmPFC activity and ↑ dlPFC activity (after therapy or meds).
11. Behavioral & Cognitive Theories of Depression
Lewinsohn – Social Reinforcement Theory:
Low rate of response-contingent reinforcement for social behaviors → due to lack of environmental reinforcement and/or poor social skills → leads to social isolation, low self-esteem, pessimism, and further ↓ reinforcement → depression cycle.
Seligman – Learned Helplessness/Hopelessness Theory:
Original Model: Repeated exposure to uncontrollable negative events → helplessness → depression.
Reformulated: Negative events interpreted with stable, internal, global attributions → hopelessness is the immediate, sufficient cause of depression stemming from negative events + negative attributional style.
Beck – Cognitive Theory:
Negative cognitive triad: Negative view of self, world, future + cognitive distortions and automatic negative thoughts.
12. Age & Cultural Factors in MDD
Younger Adults:
Risk linked to genetics, stressful life events, limited problem-solving/coping skills.
Older Adults:
Chronic medical illness & reduced physical functioning = major risk factors.
Social isolation plays a large role.
Cultural Differences:
Some Latino, Mediterranean, Middle Eastern, Asian, and other non-Western groups: More likely to report somatic symptoms (sleep, appetite, pain, palpitations).
Western/Euro-Canadian patients: More likely to emphasize psychological symptoms (sadness, hopelessness, loneliness).
13. Comorbidity of MDD
Common Comorbidities:
Substance use disorders (esp. alcohol) – most common
Anxiety disorders
Personality disorders
Sleep Abnormalities:
Prolonged sleep latency.
Reduced REM latency.
Reduced slow-wave sleep.
Increased REM density.
Medical Comorbidities:
Coronary heart disease, stroke, diabetes, Parkinson’s disease, etc.
Often bidirectional: Depression ↑ risk for myocardial infarction; Depression and anxiety are common after MI, with depression more frequent.
14. Treatment of Major Depressive Disorder
General Findings:
Psychotherapy alone vs medications alone → similar effectiveness.
Combined therapy + medications → best for response & remission.
For MDD + SUD:
Concurrent treatment recommended (behavioral/CBT + pharmacotherapy) addressing both at once.
APA Guideline – by Age
Children:
Insufficient evidence to recommend any specific treatment as clearly superior.
Adolescents:
CBT or IPT-A recommended.
Fluoxetine = first-line medication.
Not enough evidence to say therapy vs fluoxetine is better.
Adults:
Offer either:
Psychotherapy (CBT, MBCT, IPT, behavioral, psychodynamic, supportive)
Second-generation antidepressant (SSRI/SNRI)
No clear “winner” among psychotherapies or between medications vs therapy.
Combined CBT/IPT + antidepressant especially for chronic or treatment-resistant depression.
Older Adults:
Group CBT or IPT + second-generation antidepressant.
Limited support for self-guided bibliotherapy or life review therapy.
15. Other Treatments
St. John’s Wort:
Similar efficacy to SSRIs for mild–moderate depression.
Fewer side effects, lower dropout.
Not effective for severe depression.
Significant drug interactions (with SSRIs or other serotonin-increasing medications → risk of serotonin syndrome).
Ketamine/Esketamine:
Fast-acting for treatment-resistant depression and suicidal ideation.
Mechanism: ↑ glutamate.
Esketamine: Nasal spray used with an oral antidepressant.
Electroconvulsive Therapy (ECT):
Very effective for severe or treatment-resistant depression.
Especially when rapid response is needed (e.g., high suicide risk).
Response/Remission Rates:
Response ≈ 80%.
Remission ≈ 70%.
Faster remission than meds or therapy:
ECT: 1–3 weeks.
IPT/CBT: 6–10 weeks.
Antidepressants: 4–12 weeks.
ECT and Memory:
Causes anterograde and retrograde amnesia.
Anterograde amnesia: Difficulty forming new memories after ECT; usually resolved within weeks.
Retrograde amnesia: Loss of memory from before ECT; more severe with bilateral electrode placement; some recent memories may not fully return.
Repetitive Transcranial Magnetic Stimulation (rTMS):
Noninvasive stimulation of left dorsolateral prefrontal cortex.
Used for treatment-resistant depression.
Advantages: No sedation, no memory loss.
Disadvantage: Lower response and remission rates than ECT.
Telepsychology vs. In-Person Therapy:
Outcomes are similar: Symptom reduction, Quality of life, Client satisfaction, Therapeutic alliance.
Physical Activity/Exercise:
Physical activity reduces depressive symptoms even at lower-than-recommended levels.
Evidence suggests: Exercise, therapy, and antidepressants can have comparable effects in mild–moderate depression; Adding exercise → improved outcomes.
16. Suicide in the United States – Key Patterns
Gender & Age:
Men: Suicide rate ≈ 4x women
Highest male rate: 75+ years
Highest female rate: 45–64 years
Race/Ethnicity:
Highest rates: Non-Hispanic American Indian/Alaska Native individuals.
Veterans:
Higher suicide rate than non-veterans; e.g., rates roughly double the general adult rate.
Incarceration:
Higher rates among currently incarcerated and previously incarcerated.
Transgender vs. Cisgender Individuals:
Much higher rates of suicidal ideation and suicide attempts among transgender adults and youth.
XVII. PsychoPathology – Anxiety Disorders & OCD Study Notes
OVERVIEW – Anxiety Disorders
Common Features: Excessive fear + anxiety + behavioral avoidance.
Risk Factors:
Stressful life events
Behavioral inhibition temperament
Having an anxious parent (x2 risk)
Heritability: 30–50%.
MZ twins > DZ twins.
1. Separation Anxiety Disorder
Key Features:
Excessive, developmentally inappropriate fear of separation.
Need 3+ symptoms (crying at separation, physical complaints, avoidance of leaving home, etc.)
Duration: 4 weeks (kids) / 6 months (adults)
School Refusal Clue: Wants to stay home with caregiver, not avoid school itself.
Treatment:
CBT (psychoeducation, exposure, relaxation, restructuring)
Add parent training = improves outcomes.
For school refusal → priority = get child back into school quickly.
2. Specific Phobia
Definition: Fear of a specific object/situation + avoidance or enduring with intense distress; persistent 6+ months.
Types:
Animal
Natural environment
Blood-injection-injury
Situational
Other
Etiology:
30–50% heritability.
Amygdala hyperactivity (fear generation).
vPFC/vACC underactivity (poor fear regulation).
Mowrer’s Two-Factor Theory:
Step 1: Classical Conditioning → creates fear.
Step 2: Operant Conditioning → maintains fear.
3. Social Anxiety Disorder
Key Symptoms:
Fear of scrutiny.
Fear of showing symptoms → negative evaluation.
Avoidance OR endure with intense fear.
Duration: Persistent = 6+ months.
Treatment:
CBT (cognitive restructuring + exposure)
SSRIs/SNRIs
Internet-delivered CBT = as effective as face-to-face.
School-based CBT effective for youth.
4. Panic Disorder
Diagnosis:
recurrent unexpected panic attacks.
At least one attack followed by 1+ month of:
Worry about additional attacks.
Maladaptive behavior change.
Rule Out: Hyperthyroidism, cardiac issues, etc.
Symptoms (need 4+):
Palpitations
Sweating
Trembling
Derealization
Fear of dying
Nausea
Chest pain
Dizziness
Treatment:
Panic Control Treatment (PCT) – Interoceptive exposure (spin, run, breathe through straw) – relaxation + cognitive skills.
Antidepressants (imipramine) or benzos = help but high relapse from use alone.
5. Agoraphobia
Fear in 2+ of 5 Situations:
Public transport
Open spaces
Enclosed spaces
Crowds/lines
Being outside home alone.
Treatment:
In vivo exposure (graded or intense).
Evidence combining in vivo exposure with applied relaxation, breathing retraining, or cognitive techniques does not significantly improve outcomes.
Key mechanism = learning to tolerate high levels of fear and anxiety.
6. Generalized Anxiety Disorder (GAD)
Key Features:
Excessive, uncontrollable worry about multiple areas.
Occurs most days for 6+ months.
Requires 3+ Symptoms (1+ for kids):
Restlessness
Fatigue
Difficulty concentrating
Irritability
Muscle tension
Sleep problems.
Most Common Comorbid Disorder: Major Depression.
Theories of Worry (Know these!)
Cognitive Avoidance Theory (Borkovec):
Worry is verbal to avoid strong emotions; verbalizes instead of picturing scary things; emotional avoidance strategy.
Contrast Avoidance Model (Newman & Llera):
People with GAD remain in a steady low-grade negative mood to avoid sudden drops to negative; emotional bracing.
Intolerance of Uncertainty Model (Dugas):
Allergic to uncertainty + doubt in coping + belief that worry is necessary + avoid mental imagery.
Neurobiology GAD:
Abnormalities in:
Amygdala (hyperreactive)
Prefrontal cortex + ACC → reduced connectivity → weak top-down regulation.
Risk Factors: Anxiety family history, Trauma, chronic stress, Temperament: behavioral inhibition, harm avoidance, neuroticism.
Treatment:
CBT = best (alone or with meds) better than meds alone.
SSRIs & SNRIs = first line.
Buspirone (Buspar) used as adjunct (when antidepressant is only partially effective).
Obsessive-Compulsive and Related Disorders
1. Obsessive-Compulsive Disorder (OCD)
Obsessions::
Intrusive, unwanted thoughts → cause distress.
Compulsions:
Repetitive behaviors/mental rituals → reduce anxiety or prevent harm.
Time Requirement: > 1 hour/day or significant impairment.
Insight Specifier: Good/fair, poor, absent/delusional beliefs.
Etiology:
Heritability:
Adults 27–57%
Children 45–65%
CSTC pathway hyperactivity: Orbitofrontal → basal ganglia → thalamus → back to cortex
Amygdala involvement (fear/anxiety).
Treatment:
ERP (Exposure + Ritual Prevention) = gold standard.
SSRIs.
Combined ERP + SSRI = best for:
Severe symptoms
ERP/SSRI nonresponse
Comorbidities treated with antidepressants.
Motivational interviewing pretreatment boosts outcomes.
ERP delivered in-person or telehealth = equally effective for children & teens.
2. Body Dysmorphic Disorder (BDD)
Key Features:
Preoccupation with imagined/minor defect in appearance.
Repetitive behaviors (mirror checking, grooming, skin picking).
Distress or impairment.
May include ideas/delusions of reference.
Often seeks cosmetic procedures.
Summary for Exam Recall
Separation Anxiety: Child clings, physical complaints → CBT + parent training.
Specific Phobia: Exposure (in vivo); blood-injection → applied tension.
Social Anxiety: CBT + SSRIs/SNRIs; internet CBT works.
Panic Disorder: Panic Control Treatment (interoceptive exposure).
Agoraphobia: Exposure only, nothing fancy.
GAD: Worry theories, CBT, SSRIs/SNRIs, intolerance of uncertainty.
OCD: ERP, SSRIs, combined for severe cases.
BDD: Preoccupation + repetitive behaviors.
Next Steps
Continue with trauma/disassociation/somatic disorders.