Lesson 28: Mood, Schizophrenia & Other Disorders

(a) Hook

Two people both tell you, "I haven't felt like myself for weeks."

The first has been sleeping twelve hours and still dragging, has lost interest in everything that used to light them up, and quietly believes they're worthless and always will be. That's been true, more or less, every day for a month.

The second felt exactly that way last month — but this week they've barely slept, are talking a mile a minute, have started three businesses, and feel invincible, like sleep is for people who lack vision.

Same opening sentence. Completely different conditions. The first is describing major depressive disorder. The second is describing bipolar disorder — and the manic week is the tell that changes everything, including the treatment.

This lesson is where AP Psych gets precise about suffering. The exam will not let you call something "depression" when the scenario quietly hands you a manic episode. Your job is to learn the diagnostic categories cleanly — because these are conditions people have, not labels they are, and naming them correctly is the first act of taking them seriously.

(b) Core Concepts

A quick orientation: AP Psych frames all of this through the DSM (the Diagnostic and Statistical Manual), the standard classification system, and through a recurring causal idea you met in Lesson 27 — the diathesis-stress model, which says a disorder emerges when a diathesis (an underlying predisposition — genetic, biological, or psychological) meets a stressor (a triggering life event). Hold onto that; it explains why two people with similar genes can have very different outcomes.

Depressive disorders

Major depressive disorder (MDD) is diagnosed when a person experiences at least five symptoms — including either depressed mood or anhedonia (loss of interest or pleasure) — most of the day, nearly every day, for at least two weeks, with real impairment. The other symptoms cluster around sleep and appetite changes, fatigue, worthlessness or guilt, trouble concentrating, and sometimes thoughts of death. The key word is episode: MDD tends to come in discrete episodes that can lift and recur.

Persistent depressive disorder (formerly dysthymia) is the lower-intensity, longer-haul version: a depressed mood more days than not for at least two years. It's less severe at any given moment but grinding in its duration — the difference between a storm (MDD) and a chronic overcast (persistent depressive disorder).

Why does depression happen? AP wants both halves of the biopsychosocial story.

Biological factors. Depression is associated with reduced activity of the neurotransmitters serotonin and norepinephrine. This is the rationale behind antidepressants like SSRIs (which you'll meet fully in Lesson 29), which increase available serotonin. Twin and family studies also show a heritable component — a genetic diathesis.

Cognitive factors. This is where named theory matters. Aaron Beck argued that depression is sustained by a negative cognitive triad: persistently negative views of the self ("I'm worthless"), the world ("everything is against me"), and the future ("it will never get better"). Beck saw depression as driven by automatic, distorted thoughts that the person treats as facts.

Two more cognitive concepts: learned helplessness — Martin Seligman's finding that organisms repeatedly exposed to uncontrollable aversive events stop trying to escape even when escape becomes possible, generalizing "nothing I do matters" — and a negative explanatory style, the habit of explaining bad events as internal ("it's me"), stable ("it's permanent"), and global ("it ruins everything"). Layer on rumination — repetitively dwelling on one's distress and its causes without moving toward solutions — and you have a cognitive engine that keeps depression running.

Try This. Take an everyday setback — bombing a quiz. Write the negative explanatory style version (internal/stable/global: "I'm just dumb, I always will be, my whole future is sunk") and then the adaptive version (external/unstable/specific: "I didn't sleep, it was one quiz, I can study differently"). Feeling the difference is the point — same event, opposite explanatory habits.

Bipolar disorders

The single most tested distinction in this lesson: depression alone is unipolar; bipolar disorders involve mania.

A manic episode is a distinct period of abnormally elevated, expansive, or irritable mood with high energy, lasting at least a week. Its features read like the photo-negative of depression: decreased need for sleep (feeling rested after three hours), grandiosity (inflated self-esteem), racing thoughts and pressured rapid speech, distractibility, and impulsive, risky behavior (spending sprees, reckless decisions). Bipolar I disorder requires at least one full manic episode (depressive episodes usually occur but aren't required for the diagnosis). Bipolar II involves hypomania — a milder, shorter elevation — plus major depressive episodes.

The clinical stakes are real: treating bipolar depression as if it were plain MDD can backfire, which is exactly why the exam drills the distinction.

Schizophrenia spectrum

Schizophrenia is a disorder marked by disturbances in thought, perception, emotion, and behavior — a "split from reality," not a "split personality" (that confusion is a trap, addressed below). Its symptoms divide into two families, and getting this right is worth points every year.

Positive symptoms are additions to normal experience — things present that shouldn't be:

• Delusions — false beliefs held despite contrary evidence (e.g., delusions of persecution, "agents are tracking me," or grandeur).
• Hallucinations — false sensory perceptions, most commonly auditory (hearing voices).
• Disorganized speech — incoherent, derailed language ("word salad").

Negative symptoms are subtractions — normal functions that are diminished or absent:

• Flat affect — reduced emotional expression.
• Avolition — loss of motivation and goal-directed behavior.
• Catatonia and social withdrawal also fall here.

Mnemonic: positive = added, negative = removed. It's not "good vs. bad symptoms" — it's plus vs. minus. Misreading "positive" as "the good kind" is the single most common error on this topic.

What causes it? Several converging lines:

• Dopamine hypothesis — schizophrenia, especially its positive symptoms, is associated with overactivity of dopamine systems. (Evidence: drugs that block dopamine reduce positive symptoms; drugs that raise dopamine can induce psychotic-like symptoms.)
• Brain factors — enlarged fluid-filled ventricles and reduced activity in some regions.
• Genetic factors — strong heritability: an identical twin of someone with schizophrenia has a far higher concordance rate than a fraternal twin (you'll interpret these numbers in section (f)).
• Onset — symptoms typically emerge in late adolescence to early adulthood, often earlier in men, and frequently after a stressor — a clean illustration of the diathesis-stress model: genetic predisposition plus environmental trigger.

Somatic & dissociative disorders

Somatic symptom disorder involves distressing physical symptoms (pain, fatigue) accompanied by excessive thoughts and anxiety about them — the symptoms are real and the distress is disproportionate; this is not "faking."

Dissociative disorders involve a disruption in consciousness, memory, or identity:

• Dissociative amnesia — an inability to recall important personal information, usually after trauma, that's too extensive to be ordinary forgetting (sometimes with fugue, traveling away and confused about identity).
• Dissociative identity disorder (DID) — the presence of two or more distinct identity states with gaps in memory between them. DID is genuinely controversial: some clinicians see it as a real trauma response; skeptics argue it may be partly shaped by therapist suggestion or media portrayals, and diagnoses spiked after high-profile cases. AP wants you to know both the definition and that the controversy exists.

Feeding and eating disorders (brief)

Anorexia nervosa — restriction of food intake leading to significantly low body weight, intense fear of weight gain, and a distorted body image. Bulimia nervosa — cycles of binge eating followed by compensatory behavior (vomiting, excessive exercise), typically at a more normal body weight. These are serious, biologically dangerous conditions, not lifestyle choices.

Neurodevelopmental (brief)

Attention-deficit/hyperactivity disorder (ADHD) — a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning, with onset in childhood. It is a neurodevelopmental condition, not a failure of willpower.

Personality disorders

Personality disorders are enduring, inflexible patterns of inner experience and behavior that deviate from cultural expectations, are stable over time, and impair functioning. The DSM groups them into three clusters: A (odd/eccentric — e.g., paranoid, schizotypal), B (dramatic/erratic — e.g., antisocial, borderline, narcissistic), and C (anxious/fearful — e.g., avoidant, dependent). Two Cluster B exemplars to know:

• Antisocial personality disorder — a persistent disregard for and violation of others' rights, often with deceit, impulsivity, and a lack of remorse.
• Borderline personality disorder — pervasive instability in relationships, self-image, and emotions, with impulsivity and intense fear of abandonment.

(c) Classic Studies Spotlight

The dopamine connection — antipsychotics and the dopamine hypothesis (1950s–1970s).

Who & when: A line of research beginning in the 1950s, when the drug chlorpromazine was found to calm psychotic symptoms, and developed through the 1960s–70s as pharmacologists worked out why.

What they did: Researchers compared a range of antipsychotic drugs and measured, in the lab, how strongly each one blocked dopamine receptors (specifically D2 receptors). They then lined that up against how clinically effective each drug was at reducing the positive symptoms of schizophrenia.

What they found: A striking correlation — the more powerfully a drug blocked dopamine receptors, the more effective it tended to be at reducing delusions and hallucinations. Separately, amphetamines (which increase dopamine activity) could induce psychotic-like symptoms in otherwise healthy people.

Why it matters: These two findings — blocking dopamine relieves positive symptoms, boosting dopamine induces them — became the empirical backbone of the dopamine hypothesis: that the positive symptoms of schizophrenia involve excess dopamine activity. For the AP exam, this is your go-to evidence linking a neurotransmitter to a disorder, and a clean example of how studying a treatment can reveal a cause. (The modern picture is more nuanced — negative symptoms involve other systems — but the dopamine link to positive symptoms remains foundational.)

(d) Application Practice

Scenario 1. For the past three weeks, Marcus has slept poorly, lost interest in soccer and friends, can't concentrate in class, and keeps thinking he's a failure who will never amount to anything. There's no history of unusually elevated, high-energy periods.

Which disorder, and what rules out the alternative? This is major depressive disorder — the cluster of low mood, anhedonia, sleep and concentration problems, and worthlessness over a two-plus-week period. Critically, the absence of any manic episode rules out bipolar disorder; without mania, the depression is unipolar. His belief that he's a failure who'll never improve also illustrates Beck's cognitive triad (negative views of self and future).

Scenario 2. A clinician notes that a client hears voices commenting on her actions and believes her neighbors are broadcasting her thoughts (positive symptoms), but also shows little facial expression and has stopped initiating any goal-directed activity.

Classify each symptom. The voices (hallucinations) and the false belief about broadcasting (delusion) are positive symptoms — added experiences. The reduced expression (flat affect) and loss of motivation (avolition) are negative symptoms — diminished functions. Recognizing that one person can show both is exactly the nuance the exam rewards.

Scenario 3. After a severe car accident, Dana cannot recall anything about the day of the crash or the week surrounding it, far beyond ordinary forgetting, though her memory is otherwise intact and she knows who she is.

Which disorder — and which closely related one does it resemble but isn't? This is dissociative amnesia: trauma-linked memory loss for personal information, too extensive to be normal forgetting. It is not dissociative identity disorder — Dana shows no separate identity states, only a memory gap. The distinction (memory loss alone vs. distinct identities) is a classic trap.

(e) Traps & Confusions

Positive vs. negative symptoms of schizophrenia. The deadliest trap in the unit. "Positive" does not mean "good." Positive = added experiences (hallucinations, delusions, disorganized speech). Negative = removed functions (flat affect, avolition). Think + (added) vs. − (subtracted). If something is present that shouldn't be, it's positive; if something normal is missing, it's negative.

MDD vs. bipolar disorder (unipolar vs. bipolar). Both feature depressive lows, so students default to "depression." The diagnostic switch is mania: a single full manic episode makes it bipolar I, not MDD. Scan every depression scenario for any past period of euphoria, racing thoughts, or no need for sleep — if it's there, it's bipolar.

Dissociative amnesia vs. DID. Amnesia = a memory gap (can't recall personal info), with one identity intact. DID = two or more distinct identity states with memory gaps between them. Amnesia is about lost memory; DID is about multiple identities. And neither is "split from reality" — that's schizophrenia.

Schizophrenia is NOT "split personality." The "split" in schizophrenia is a split from reality (psychosis), not a split into multiple personalities (that's DID). This swap is one of the most common public misconceptions, and the exam tests whether you avoid it.

(f) Practice Problems

Four-choice MCQs in current AP format. Answers and explanations in section (h).

(g) FRQ Practice — Article Analysis Question (AAQ)

Respond to all six parts (A–F) in complete sentences using appropriate psychological terminology.

Stimulus — summarized study

Introduction. Researchers examined whether a structured cognitive-training program targeting negative explanatory style would reduce depressive symptoms relative to a control activity, drawing on Beck's account of the cognitive factors in depression.

Participants. 120 adults (ages 25–60; M = 41.3, SD = 8.7) who had been screened and scored in the mild-to-moderate range on a standardized depression inventory volunteered through a community health clinic. The sample was 64% women and 36% men; self-reported race/ethnicity was 50% White, 22% Hispanic/Latino, 16% Black, 9% Asian, and 3% Other. Before participating, each person was told the purpose, risks, and benefits of the study and signed a form indicating they agreed to take part; they were informed they could withdraw at any point.

Method. Participants were randomly assigned to one of two conditions for eight weeks. The cognitive-training group completed weekly guided exercises in which they identified negative automatic thoughts and reframed them in more accurate, balanced terms. The control group completed weekly journaling about daily activities with no reframing instruction. At the end of eight weeks, all participants completed the same standardized depression inventory, scored from 0 (no symptoms) to 63 (severe symptoms).

Results. Mean post-program depression-inventory scores were 14.2 for the cognitive-training group and 21.8 for the control group. The difference between the two groups was reported as statistically significant (p < .05).

A. Identify the research method used in this study.

B. State the operational definition of the dependent variable as used in this study.

C. Describe what the difference in mean depression-inventory scores indicates about the two groups. (Cite the numbers.)

D. Identify one ethical guideline the researchers applied, and describe how they applied it.

E. Explain the extent to which the findings are or are not generalizable, using specific evidence from the study.

F. Explain how the findings support or refute the claim that cognitive factors play a role in depression. In your explanation, apply a relevant psychological concept from the study of depressive disorders.

Model answer (earns 7/7)

A. The research method was an experiment, because participants were randomly assigned to conditions and the researchers manipulated an independent variable (cognitive training vs. control journaling). (1 pt — names the method)

B. The dependent variable was operationally defined as each participant's score on the standardized depression inventory, ranging from 0 to 63, measured at the end of the eight-week program. (1 pt)

C. The means indicate that the cognitive-training group reported lower depressive symptoms than the control group at the end of the program — 14.2 versus 21.8, a difference of 7.6 points — and because the difference was statistically significant (p < .05), it is unlikely to be due to chance, suggesting the training was associated with reduced symptoms. (1 pt — cites the numbers)

D. The researchers applied informed consent: each participant was told the study's purpose, risks, and benefits and signed a form agreeing to take part before participating. (Naming right to withdraw — participants were told they could withdraw at any point — would also earn the point.) (1 pt)

E. The findings have limited generalizability because all participants were adults aged 25–60 recruited from a single community health clinic who already scored in the mild-to-moderate depression range, so the results may not extend to adolescents, to people with severe depression, or to populations outside that clinic; the sample's inclusion of a range of racial/ethnic backgrounds does support somewhat broader applicability within that adult, mild-to-moderate group. (1 pt — commits to one direction with study evidence)

F. The findings support the claim that cognitive factors play a role in depression: the group trained to identify and reframe negative automatic thoughts showed lower depression scores than the control group, which is consistent with Beck's theory that depression is maintained by a negative cognitive triad of distorted views of the self, world, and future. By teaching participants to replace internal, stable, global interpretations (a negative explanatory style) with more balanced ones, the program targeted the cognitive engine Beck identified — and the symptom reduction suggests that altering those cognitions can reduce depression, supporting a cognitive contribution. (2 pts — states support AND applies a genuine psychological concept)

Where students commonly lose points

• Part A: writing "random assignment" or "correlational study" instead of naming the method (experiment). Random assignment is a feature of the experiment, not the method itself.
• Part C: stating the direction of the difference but omitting the actual numbers (14.2 vs. 21.8) — an automatic miss, even though the prompt explicitly asks for them.
• Part D: naming an ethical guideline (e.g., "informed consent") but failing to describe how it was applied using a detail from the study.
• Part E: hedging in both directions ("it's generalizable but also not") instead of committing to one, or asserting (non)generalizability without citing evidence from the participant description.
• Part F: asserting "it supports the claim" without applying a real psychological concept (Beck's cognitive triad, negative explanatory style, rumination). Vague references to "thinking patterns" without naming the concept won't earn the second point.