Premed · Premed · Introductory Psychology
Lecture 24: Psychological Disorders: Schizophrenia and Personality Disorders
Introductory Psychology
Learning Objectives
By the end of this lecture, students will be able to:
- Describe the positive, negative, and cognitive symptoms of schizophrenia
- Explain the biological and environmental risk factors for schizophrenia, including the dopamine hypothesis and neurodevelopmental models
- Distinguish among the three clusters of personality disorders and their defining features
- Describe the key characteristics and etiology of antisocial personality disorder and borderline personality disorder
- Discuss the dissociative disorders and the controversy surrounding dissociative identity disorder
Lecture Content
I. Schizophrenia Spectrum Disorders: Overview
Schizophrenia is a severe psychological disorder characterized by profound disturbances in thought, perception, emotion, and behavior. The term refers to a "splitting" of mental functions, not to a split personality. It is among the most debilitating of all mental disorders, affecting approximately 1% of the population worldwide with equal prevalence in men and women. Onset typically occurs in late adolescence to the mid-20s and tends to appear earlier in men. The course is highly variable — some individuals recover substantially, but many experience a chronic relapsing pattern. Schizophrenia is associated with a reduced life expectancy of approximately 15-20 years, attributable to comorbid conditions, suicide, and lifestyle factors.
II. Symptoms of Schizophrenia
Symptoms are organized into three categories. Positive symptoms represent the presence of abnormal experiences — things "added" to normal functioning. Delusions are false beliefs held with conviction despite contradictory evidence. The most common are persecutory delusions (belief that others are plotting harm), but grandiose delusions (extraordinary powers or identity), referential delusions (random events are directed at oneself), and delusions of control (thought insertion, withdrawal, or broadcasting) also occur. Hallucinations are sensory experiences without external stimulation; auditory hallucinations — typically voices commenting on behavior, arguing, or giving commands — occur in 60-80% of cases and are the most common form. Disorganized speech, or formal thought disorder, manifests as loose associations (rapid shifting between unrelated topics), tangentiality, word salad, neologisms (invented words), and clanging (speech driven by word sounds). Disorganized or catatonic behavior ranges from unpredictable agitation and bizarre posturing to catatonia — marked motor disturbances including immobility with waxy flexibility, excessive purposeless activity, or mutism.
Negative symptoms represent the absence or diminishment of normal functions. Flat or blunted affect involves reduced emotional expression in face, voice, and gesture. Alogia is poverty of speech. Avolition is a lack of motivation to initiate goal-directed activities. Anhedonia is the inability to experience pleasure. Asociality is reduced social drive. Negative symptoms are often more debilitating than positive ones and are more resistant to treatment.
Cognitive symptoms include impairments in working memory, attention, executive function, abstract thinking, and processing speed. These symptoms are present before onset, persist between psychotic episodes, and are strong predictors of functional outcome.
<image>A multi-panel figure illustrating schizophrenia symptoms. Panel A: A categorized table dividing symptoms into three columns — "Positive Symptoms" (delusions listed by type with brief examples, hallucinations by sensory modality with prevalence percentages, disorganized speech subtypes), "Negative Symptoms" (flat affect, alogia, avolition, anhedonia, asociality, each with a one-line description), and "Cognitive Symptoms" (working memory impairment, attentional deficits, executive dysfunction). Panel B: A brain diagram highlighting structural abnormalities associated with schizophrenia — enlarged lateral ventricles, reduced prefrontal cortex gray matter, reduced temporal lobe (especially superior temporal gyrus) volume, and thalamic abnormalities, with arrows pointing to each region and brief annotations explaining the functional consequence. Panel C: A timeline showing the typical course of schizophrenia — premorbid phase (subtle social and cognitive deficits), prodromal phase (attenuated symptoms, declining function), active phase (full psychotic symptoms), and residual phase (negative and cognitive symptoms predominate), with annotations indicating where positive and negative symptoms are most prominent.</image>
III. Etiology of Schizophrenia
Schizophrenia has a heritability of approximately 80%. Concordance rates are about 48% for identical twins and 17% for fraternal twins, and risk increases with genetic relatedness to an affected individual. No single gene is responsible; hundreds of genetic variants each contribute small effects. Key implicated genes include DISC1, neuregulin 1, COMT, and genes in the major histocompatibility complex (MHC) region.
The original dopamine hypothesis proposed that excess dopamine activity causes schizophrenia. Supporting evidence includes the fact that dopamine-increasing drugs (amphetamines, cocaine) can produce psychotic symptoms, and that antipsychotic medications work by blocking dopamine D2 receptors. The revised dopamine hypothesis recognizes greater complexity: overactivity in the mesolimbic pathway produces positive symptoms, while underactivity in the mesocortical pathway contributes to negative and cognitive symptoms. Other neurotransmitter systems are also implicated. NMDA receptor hypofunction in the glutamate system may contribute, as evidenced by the schizophrenia-like symptoms produced by PCP and ketamine. Serotonin is involved as well — atypical antipsychotics act on serotonin receptors, and serotonin-dopamine interactions play a role.
Structural brain abnormalities include enlarged lateral ventricles (indicating loss of brain tissue), reduced gray matter in the prefrontal cortex, temporal lobes, and hippocampus, reduced prefrontal activity during cognitive tasks (hypofrontality), and abnormal connectivity between brain regions. The neurodevelopmental model proposes that schizophrenia originates from disruptions in brain development during the prenatal and early postnatal period. Prenatal risk factors include maternal infection (especially influenza during the second trimester), nutritional deficiency, obstetric complications, and maternal stress. Abnormal synaptic pruning during adolescence may unmask the disorder.
Environmental risk factors include growing up in an urban environment, migration and minority status (involving social adversity and discrimination), cannabis use during adolescence in genetically vulnerable individuals, and childhood adversity. Expressed emotion — a family environment characterized by criticism, hostility, and emotional overinvolvement — predicts higher relapse rates, though it is considered a maintaining factor rather than a cause.
IV. Personality Disorders: Overview
A personality disorder is an enduring pattern of inner experience and behavior that deviates markedly from cultural expectations, is pervasive and inflexible, begins in adolescence or early adulthood, remains stable over time, and leads to distress or impairment. The DSM-5 organizes personality disorders into three clusters.
Cluster A (Odd/Eccentric) includes paranoid personality disorder (pervasive distrust and suspiciousness), schizoid personality disorder (detachment from social relationships with restricted emotional expression), and schizotypal personality disorder (social and interpersonal deficits with cognitive and perceptual distortions and eccentric behavior). Schizotypal personality disorder is considered part of the schizophrenia spectrum and may share genetic liability.
Cluster B (Dramatic/Emotional/Erratic) includes antisocial personality disorder (disregard for others' rights), borderline personality disorder (instability in relationships, self-image, and emotions with marked impulsivity), histrionic personality disorder (excessive emotionality and attention-seeking), and narcissistic personality disorder (grandiosity, need for admiration, and lack of empathy).
Cluster C (Anxious/Fearful) includes avoidant personality disorder (social inhibition and hypersensitivity to negative evaluation), dependent personality disorder (excessive need to be cared for), and obsessive-compulsive personality disorder (preoccupation with orderliness and control, distinct from OCD). Overall, approximately 9-15% of the population meets criteria for at least one personality disorder, and comorbidity both among personality disorders and with other mental disorders is high.
V. Antisocial Personality Disorder and Psychopathy
Antisocial personality disorder (ASPD) involves a pervasive pattern of disregard for and violation of others' rights beginning before age 15 (evidenced by conduct disorder) and formally diagnosed at age 18 or older. Key features include deceitfulness, impulsivity, irritability, aggressiveness, reckless disregard for safety, consistent irresponsibility, and lack of remorse. ASPD affects approximately 3% of men and 1% of women and is heavily represented in criminal justice populations.
Psychopathy, as assessed by Hare's Psychopathy Checklist-Revised (PCL-R), overlaps with but is not identical to ASPD. The PCL-R assesses two factors: an interpersonal/affective dimension (superficial charm, grandiosity, pathological lying, shallow affect, callousness, lack of empathy) and a lifestyle/antisocial dimension (impulsivity, irresponsibility, criminal versatility). Many individuals with ASPD are not psychopaths; psychopathy is a narrower, more specific construct.
The etiology of ASPD and psychopathy involves moderate heritability (approximately 50%), with callous-unemotional traits in childhood being especially heritable. Brain abnormalities include reduced amygdala volume and reactivity (impairing fear conditioning and empathy) and reduced prefrontal cortex function (compromising impulse control). Reduced autonomic arousal, including low resting heart rate and low skin conductance, suggests a fearless temperament. Environmental risk factors include childhood abuse, neglect, inconsistent parenting, and poverty. Gene-environment interactions are significant: Caspi and colleagues (2002) found that a variant of the MAO-A gene interacts with childhood maltreatment to predict antisocial behavior.
VI. Borderline Personality Disorder
Borderline personality disorder (BPD) is characterized by a pervasive pattern of instability in interpersonal relationships, self-image, and emotions, along with marked impulsivity. Key features include frantic efforts to avoid real or imagined abandonment; unstable and intense relationships that alternate between idealization and devaluation ("splitting"); identity disturbance; impulsive self-damaging behaviors (spending, substance abuse, reckless driving, binge eating); recurrent suicidal behavior or self-mutilation (approximately 10% die by suicide); intense and rapidly shifting emotions; chronic feelings of emptiness; inappropriate intense anger; and transient, stress-related paranoia or dissociative symptoms.
BPD affects approximately 1.5-2% of the population and is more commonly diagnosed in women, though this may reflect diagnostic bias. It frequently co-occurs with depression, anxiety disorders, substance use disorders, and eating disorders.
Marsha Linehan's biosocial theory proposes that BPD arises from the interaction of biological emotional vulnerability — innate high emotional reactivity coupled with a slow return to baseline — and an invalidating environment during childhood, in which emotional expressions were dismissed, punished, or trivialized. Genetic heritability is moderate (40-50%), and approximately 70% of individuals with BPD report a history of physical, sexual, or emotional abuse. Neurobiologically, BPD involves amygdala hyperreactivity and reduced prefrontal cortex regulatory control.
<image>A multi-panel figure on personality disorders. Panel A: A visual summary of the three DSM-5 personality disorder clusters — Cluster A (Odd/Eccentric) shown in blue with paranoid, schizoid, and schizotypal listed beneath, Cluster B (Dramatic/Erratic) shown in red with antisocial, borderline, histrionic, and narcissistic listed beneath, and Cluster C (Anxious/Fearful) shown in green with avoidant, dependent, and OCPD listed beneath, each cluster accompanied by a one-line descriptor of the core theme. Panel B: Antisocial personality disorder and psychopathy — a Venn diagram showing the overlap between ASPD (broader, behaviorally defined) and psychopathy (narrower, emphasizing interpersonal/affective traits), with distinguishing features listed in non-overlapping regions and shared features in the overlap. Panel C: Linehan's biosocial model of BPD — a diagram showing two arrows converging: "Biological vulnerability" (high emotional sensitivity, intense reactions, slow return to baseline) and "Invalidating environment" (dismissal, punishment, oversimplification of emotions), merging to produce "Emotion dysregulation" at the center, with downstream consequences radiating outward (unstable relationships, identity disturbance, impulsive behavior, self-harm).</image>
VII. Dissociative Disorders
Dissociation refers to a disruption in the normally integrated functions of consciousness, memory, identity, or perception. Dissociative amnesia involves the inability to recall important autobiographical information, usually of a traumatic nature, that is too extensive to be explained by ordinary forgetting. A subtype, dissociative fugue, involves sudden, unexpected travel with inability to recall one's past and possible identity confusion. Depersonalization/derealization disorder involves persistent experiences of feeling detached from one's own mind or body (depersonalization) or that surroundings are unreal (derealization), with reality testing remaining intact.
Dissociative identity disorder (DID), formerly called multiple personality disorder, involves the presence of two or more distinct personality states that recurrently take control of behavior, accompanied by extensive gaps in recall. It is associated with severe childhood trauma in virtually all documented cases. DID is highly controversial. The posttraumatic model views it as a genuine condition caused by severe childhood abuse, with dissociation functioning as a defense mechanism. The sociocognitive model, advocated by Spanos and Lilienfeld, argues that DID is created through therapist suggestion, social reinforcement, media portrayals, and cultural expectations. Supporting this view, DID is rare outside North America, diagnoses increased dramatically after the media portrayal of "Sybil" in 1973, and many cases emerge only during therapy. Neuroimaging studies show some brain differences between alter states, but their interpretation remains debated.
VIII. Other Disorders of Note
Somatic symptom and related disorders include somatic symptom disorder (distressing physical symptoms accompanied by excessive health-related thoughts and behaviors), illness anxiety disorder (preoccupation with having a serious illness despite minimal symptoms), and conversion disorder (neurological symptoms such as paralysis or blindness without identifiable neurological cause, often related to stress or trauma).
Eating disorders include anorexia nervosa (severe restriction leading to significantly low body weight, with intense fear of gaining weight and disturbed body image — the mental disorder with the highest mortality rate), bulimia nervosa (binge eating followed by compensatory behaviors), and binge-eating disorder (recurrent binges without compensatory behaviors).
