Abnormal Psychology (PSBOMJ3001, III Semester 2024)
Unit I: Abnormality, Earlier Conceptions and Research Methods
Definition and Nature of Abnormal Psychology
Abnormal psychology is the scientific study of unusual patterns of behavior,
emotion and thought, especially as these patterns relate to mental disorders . It
aims to describe, predict, explain and change maladaptive behavior. In general,
abnormal psychology focuses on individuals who are unable to adapt and function
effectively in their environment . By studying psychopathology and its causes,
clinicians and researchers seek to communicate using shared diagnostic criteria
(e.g. those in the DSM-5) and to guide effective treatment.
Criteria of Abnormal Behavior
No single standard defines “abnormal,” but clinicians typically consider several
“disturbance” criteria. A classic formulation lists four Ds – Deviance, Distress,
Dysfunction, and Danger – as markers of abnormality . Deviance means behavior is
unusual or violates social norms. Distress refers to causing significant personal
suffering (e.g. anxiety or depression). Dysfunction means impairment in daily
living (work, relationships, self-care). Danger indicates potential harm to self
or others. (All criteria must be considered in cultural context: what is deviant
or distressing in one culture may not be in another .) In practice, clinicians
judge abnormality by patterns of symptoms (e.g. the DSM-5’s symptom lists) and
their impacts on functioning, rather than any single rule.
Historical Overview (Ancient to Modern)
Ancient and Medieval Views: Early civilizations often attributed abnormal behavior
to supernatural forces. Prehistoric peoples practiced trephination (drilling holes
in the skull) to release evil spirits . Many cultures used exorcism, prayer or
ritual to cast out demons. In contrast, Hippocrates (Greece, 460–377 BCE) was
among the first to reject demonology: he argued mental disorders have natural
(biological) causes, such as brain pathology, head trauma or heredity . He
described disorders like melancholia and mania and proposed the humoral theory
(imbalances of bodily “humors”) as a cause. Greek philosophers (e.g. Plato) and
Roman physicians (e.g. Galen) further promoted the idea that the mentally ill were
not morally culpable and deserved rational, humane care .
During the Middle Ages (ca. 500–1500 AD), supernatural explanations regained
dominance. With the Church’s rise, mental illness was again seen as “possession,”
and treatments included exorcism, confinement, and harsh punishments . Mass
delusions (e.g. “lycanthropy,” dancing manias) occurred in this climate of fear and
plague. The Renaissance (14th–16th c.) saw the slow decline of witch hunts: e.g.
Johann Weyer (16th c.) argued that accused “witches” were mentally ill, not demon-
possessed. However, asylums (like London’s Bethlem, opened 1547) often merely
imprisoned patients under cruel conditions .
Reform and Modern Era: Beginning in the late 18th century, reformers (Pinel in
France, Tuke in England, Dix in the U.S.) launched the “moral treatment” movement.
They emphasized humane care: Pinel famously ordered the chains removed from asylum
inmates and instituted kind treatment (exercise, social support) . These efforts
improved conditions and established asylums as treatment centers. By the early
20th century, however, overcrowding and lack of new treatments led to a return of
custodial care. Through the 20th century to today, understanding shifted toward
scientific models (biological and psychosocial), culminating in modern views that
integrate genetics, neurobiology, and environment (see Unit II below).
Research Methods in Abnormal Psychology
Researchers use several methods to study abnormal behavior, each with strengths and
weaknesses. Key methods include:
• Case Studies: In-depth examinations of a single individual (or small
group) using interviews, observations, and records. Case studies provide rich,
detailed data on rare conditions or new hypotheses . For example, Freud’s early
theories (Anna O., Rat Man, etc.) emerged from clinical case studies . Case
studies can suggest new ideas, but their findings may not generalize, and they are
subject to researcher bias.
• Experimental Research: Controlled studies in which researchers
manipulate one or more variables to test causal hypotheses. Participants are
randomly assigned to conditions, and the effects of the manipulated variables on
behavior or symptoms are measured . For example, a clinician might randomly assign
anxious patients to either a new therapy or a control group to test treatment
efficacy. Experiments offer strong evidence of cause-effect but often require
artificial conditions and may raise ethical issues (e.g. inducing stress).
• Observational Studies: Researchers record behavior as it naturally
occurs, without intervention. This can include naturalistic observation (watching
people in real-life settings) or participant observation (researcher joins the
environment). For instance, a researcher might unobtrusively observe children on a
playground to see how social anxiety manifests . Naturalistic observation yields
high ecological validity (behaviors in real context) , but the researcher has
little control over events, and the presence of an observer can sometimes alter
behavior.
• Correlational (Survey) Studies: These involve measuring two or more
variables in many individuals to determine if they change together. For example,
researchers might use surveys to correlate the number of daily stressors with
levels of anxiety symptoms across a large sample. A correlation coefficient (r)
quantifies the strength and direction of the relationship . Correlational studies
can handle large samples and reveal important associations, but cannot prove
causation. A strong positive correlation (near +1) means two variables rise
together, while a negative correlation (near –1) means one falls as the other rises
.
In practice, a combination of methods is used: case studies and qualitative methods
for early exploration; correlational surveys to identify patterns in populations;
and controlled experiments to test specific hypotheses . Ethical and practical
limits often determine which methods are feasible in clinical research.
Unit II: Classification and Causal Factors of Mental Disorders
DSM-5 Classification of Mental Disorders
Psychiatry uses standardized manuals to classify disorders. The DSM-5 (Diagnostic
and Statistical Manual of Mental Disorders, 5th ed., 2013) is the current U.S.
standard (with a 2022 text revision) . It organizes mental disorders into broad
categories (e.g. Anxiety Disorders, Depressive Disorders, Schizophrenia Spectrum,
etc.) . Each specific disorder (e.g. Panic Disorder, Bipolar I) is defined by a
detailed description and diagnostic criteria (a list of symptoms and duration, plus
exclusion rules) . The DSM-5’s system ensures clinicians worldwide use a common
language: a consistent diagnosis guides treatment and research. (Example
categories include: Anxiety Disorders, Trauma- and Stressor-Related Disorders, Mood
Disorders, Schizophrenia Spectrum, Neurodevelopmental Disorders, etc. .)
Neurosis vs. Psychosis
Historically, psychiatrists distinguished “neurosis” and “psychosis” to describe
severity. Neuroses (a term now largely outdated and absent from DSM-5) referred to
relatively mild disorders characterized by anxiety, distress, or dysfunctional
coping, but without a break from reality . Examples include phobias, obsessive-
compulsive symptoms or chronic worry. Individuals with neuroses are aware of their
irrational fears or anxieties and remain in contact with reality . In contrast,
psychoses (e.g. schizophrenia, severe mania, psychotic depression) involve a
fundamental loss of reality testing. Psychotic symptoms include hallucinations
(sensory experiences not based in reality) and delusions (fixed false beliefs) . A
person in a psychotic state may be unable to recognize that their unusual
perceptions or beliefs are unreal . In short, psychosis implies severe symptoms
and impaired reality testing, whereas neurosis implies distress and maladaptive
behavior with intact reality (though “neurosis” itself is no longer an official
diagnosis ).
Contemporary Etiology: Biopsychosocial Factors
Modern models explain mental disorders by a biopsychosocial perspective: multiple
interacting factors across biological, psychological, and socio-cultural domains
contribute to each disorder . Biologically, genetic predispositions play a major
role. Many disorders run in families and twin studies show high heritability. For
example, research has found genetic overlaps among disorders (autism, ADHD,
bipolar, depression, schizophrenia share common genetic risk factors) . Brain and
neurotransmitter abnormalities are also implicated: e.g. imbalances in serotonin,
dopamine or glutamate systems, and structural/functional brain differences (as seen
in depression and schizophrenia) . Neuroendocrine factors (e.g. stress hormones
like cortisol) and prenatal influences can also predispose individuals.
Psychological factors include maladaptive cognitions and early learning.
Cognitive-behavioral theories emphasize negative thought patterns (e.g.
catastrophizing or hopelessness in anxiety/depression) and behavioral conditioning
(traumatic or learned associations that produce fear or avoidance). Psychodynamic
or personality factors may influence vulnerability (e.g. personality disorders).
Life experiences such as trauma, abuse, or chronic stress can precipitate or worsen
disorders .
Socio-cultural factors cover the broader context: family environment, cultural
norms, socioeconomic status, life stressors, and support systems. Discrimination,
poverty or social isolation can increase risk. For instance, chronic stressors
like unemployment or discrimination contribute to anxiety and depression . Culture
influences how symptoms are expressed and perceived. In sum, no single factor
suffices; mental illnesses typically emerge from complex interactions among genes,
brain mechanisms, personality, and environment .
Unit III: Clinical Features of Anxiety Disorders, Mood Disorders, and Schizophrenia
Anxiety Disorders (GAD, Panic, Social, Specific Phobias)
Anxiety disorders are characterized by excessive fear or anxiety that disrupts
functioning. Generalized Anxiety Disorder (GAD) involves pervasive, chronic worry
across multiple areas of life. Patients feel in a “relatively continuous state of
tension, apprehension, and dread” . They often report restlessness, fatigue,
concentration problems, muscle tension and sleep disturbance.
Panic Disorder is defined by recurrent, unexpected panic attacks – sudden surges of
intense fear or discomfort with physical symptoms (e.g. palpitations, shaking,
shortness of breath). In panic disorder, individuals are “suddenly overwhelmed by
panic even though there is no apparent reason to be frightened” . Often they
develop fear of future attacks (panic phobia).
Social Anxiety Disorder (social phobia) entails an “extreme fear and avoidance of
social situations” . Individuals fear negative evaluation (embarrassment,
humiliation) and may avoid social interactions or endure them with intense anxiety.
Physical symptoms (blushing, trembling) are common.
Specific Phobias involve a “specific unrealistic fear” of an object or situation
(e.g. animals, heights, flying) . Exposure to the phobic stimulus provokes
immediate anxiety or panic, often leading to avoidance. Unlike generalized
anxiety, these fears are circumscribed and recognized by the person as irrational.
(For context, the DSM-5 lists these and other anxiety disorders under separate
categories – for instance, OCD and PTSD are in their own chapters – but all share
the core of excessive fear/anxiety impairing life .)
Mood Disorders (MDD and Bipolar Affective Disorder)
Major Depressive Disorder (MDD) is marked by persistently depressed mood or loss of
interest/pleasure, along with cognitive and somatic symptoms. Clinically, it
involves intense and sustained sadness, melancholia, or despair for at least two
weeks . Patients often experience feelings of worthlessness or guilt, changes in
appetite/sleep, psychomotor slowing or agitation, fatigue, impaired concentration,
and recurrent thoughts of death or suicide. A single episode causes marked
distress or functional impairment.
The DSM-5 also recognizes Persistent Depressive Disorder (dysthymia), a chronic but
milder form of depression.
Bipolar Affective Disorder (BPAD) involves cycling between mood extremes. Bipolar
I requires at least one manic episode: a distinct period of abnormally elevated,
expansive or irritable mood with increased energy or activity lasting ≥1 week (or
any duration if hospitalization is required). Manic symptoms include grandiosity,
decreased need for sleep, rapid speech, racing thoughts, distractibility, and risky
behaviors. Bipolar II involves at least one hypomanic episode (less severe, ≥4
days) and one major depressive episode. In BPAD, mood swings between euphoria and
depression are prominent. As noted, bipolar disorder “is characterized by mood
states that vacillate between sadness and euphoria; a diagnosis of bipolar disorder
requires experiencing at least one manic episode, defined as extreme euphoria,
irritability, and increased activity” . Both depression and bipolar carry high
risk for suicide and often require lifelong management. (Genetic factors are
strong in mood disorders: bipolar has especially high heritability .)
Schizophrenia (Positive, Negative, and Disorganized Symptoms)
Schizophrenia Spectrum Disorders feature persistent psychosis (loss of reality) and
functional decline. Key symptoms fall into positive, negative, and disorganized
domains:
• Positive Symptoms: These are excesses or distortions of normal
function. They include delusions (fixed false beliefs, e.g. persecution or
grandiosity) and hallucinations (perceiving things not present, most commonly
auditory) . Disorganized speech (loose associations, “word salad”) and bizarre,
uncoordinated or agitated behavior are also positive symptoms . (In practice, a
patient may speak incoherently and act inappropriately for the context.)
• Negative Symptoms: These are deficits or losses of normal functions.
Common negative symptoms are blunted or flat affect (reduced emotional expression),
alogia (poverty of speech), avolition (lack of motivation), anhedonia (inability to
experience pleasure), and social withdrawal . Patients may neglect self-care,
avoid social interactions, and show diminished eye contact or emotional response .
Cognitive impairments (poor memory, attention, executive function) often accompany
negative symptoms.
• Disorganized Symptoms: Often grouped with positive symptoms,
disorganized behavior overlaps these categories. It includes disorganized
(incoherent) speech and erratic motor behavior noted above. Thought disorder
(loose connections among ideas) and catatonic behaviors (e.g. unusual motor
rigidity or stereotypy) are examples. Overall, schizophrenia’s clinical picture is
of profound disruption: during active phases, patients may appear completely
unmoored from reality, while in chronic phases, negative symptoms and cognitive
deficits can be the most disabling .
(According to Mayo Clinic, schizophrenia “may result in a mix of hallucinations,
delusions, and disorganized thinking and behavior,” causing loss of contact with
reality .) Treatment typically requires antipsychotic medication for positive
symptoms, with psychosocial interventions addressing negative symptoms and
functional rehabilitation.
Unit IV: Etiology of Anxiety, Mood Disorder, and Schizophrenia
Etiology of Anxiety Disorders
Anxiety disorders arise from multifactorial causes. Biologically, there is a
genetic predisposition: family and twin studies show modest heritability. For
example, a functional variant of the serotonin transporter gene (5-HTTLPR) is
linked to higher anxiety traits . Neural circuitry also matters: hyperactivity of
the amygdala (the brain’s fear center) and dysregulated stress responses
(hypothalamic-pituitary-adrenal axis) can predispose individuals to anxiety. Panic
disorder in particular has been linked to overactivity of the locus coeruleus (a
norepinephrine center) .
Psychological factors include dysfunctional thinking patterns and learning.
Cognitive theories point to maladaptive assumptions (e.g. catastrophizing neutral
events, as seen in GAD ). People with anxiety tend to interpret ambiguous
situations as threatening, fueling worry. Behavioral learning is important too:
classic conditioning can create specific fears (e.g. Little Albert’s white-rat
phobia ), and modeling can transmit fear vicariously (a child learning a dog phobia
by watching a parent’s fear) . Overgeneralization (stimulus generalization) may
expand a specific fear into broader anxiety.
Socio-cultural influences also shape anxiety. Chronic stressors (poverty, daily
hassles, trauma exposure) raise risk . Epidemiologically, women are diagnosed with
anxiety disorders more often than men. Social pressures and gender roles may
contribute: women experience higher rates of certain traumas and may rely more on
emotion-focused coping, which can heighten anxiety . Discrimination and social
defeat (e.g. for minorities) also increase chronic stress and anxiety . In
summary, anxiety disorders reflect a complex interplay of genetics, brain
vulnerability (biological), learning and cognition (psychological), and life
stressors or cultural pressures (social) .
Etiology of Mood Disorders (MDD and BPAD)
Biological Factors: Mood disorders have strong genetic components. First-degree
relatives of major depression patients have roughly double the risk of MDD, while
relatives of bipolar patients have >9× the population risk . Twin studies show
concordance rates around 50% for identical twins with MDD, and ~67% for bipolar,
confirming higher heritability in bipolar disorder . Neurobiologically, mood
disorders involve neurotransmitter imbalances: MDD and BPAD are associated with low
activity of serotonin and norepinephrine systems . Brain imaging finds hyperactive
amygdala responses to negative stimuli and reduced prefrontal cortex regulation in
depression . Dysregulation of stress hormones is also implicated: chronically high
cortisol (from an overactive HPA axis) is common in depressed patients, especially
those with early trauma , and may damage hippocampal neurons over time.
Psychological and Social Factors: Cognitive theories (Beck’s model) emphasize
negative thinking patterns – e.g. a pessimistic view of self, world and future –
that make individuals vulnerable to depression. Learned helplessness (belief that
one’s actions are futile against stress) is another model. Importantly, life
stress is a key trigger: a diathesis-stress model is well-supported. Serious life
events – loss of a loved one, trauma, abuse, chronic stressors – often precede
depressive episodes . Caspi et al. (2003) showed that individuals with a short-
allele variant of 5-HTTLPR were more likely to become depressed after multiple life
stressors, highlighting gene–environment interaction. For bipolar disorder,
stressful events can also precipitate episodes, though extreme mood swings suggest
a particularly strong biological drive (e.g. circadian rhythm disruptions).
Sociocultural Influences: Cultural and interpersonal contexts affect mood
disorders. Chronic socioeconomic disadvantage, lack of social support, and
societal pressures (e.g. on body image, success) can contribute to depression. For
women, gender-based stressors and hormonal factors may partly explain higher
depression rates. Conversely, strong social support and coping resources can be
protective.
In sum, MDD and BPAD arise from multiple factors: inherited vulnerability (genes,
brain chemistry), stressful experiences (trauma, loss), and cognitive styles.
Genetic factors are especially prominent in bipolar disorder , while environmental
stressors often trigger episodes of both depression and mania.
Etiology of Schizophrenia
Schizophrenia’s causes are highly complex and multifactorial. Genetics are a major
risk factor: many susceptibility genes contribute (though no single gene causes the
illness) . Family, twin and adoption studies confirm heritability around 80%.
Neurobiology: Schizophrenia is classically linked to dopamine dysregulation
(“dopamine hypothesis”): excessive dopamine activity in certain brain pathways
likely underlies positive symptoms like hallucinations and delusions. Other
neurotransmitters are also implicated (e.g. glutamate/NMDA hypofunction may explain
cognitive and negative symptoms). Brain imaging shows structural/functional
changes: enlarged ventricles, reduced gray matter, and abnormal activity in
cortical and limbic regions (supporting deficits in emotion and cognition).
Neurodevelopmental insults (prenatal hypoxia, infections, malnutrition) may disrupt
brain maturation and raise risk.
Environmental and Social Factors: Prenatal complications (e.g. maternal influenza,
malnutrition), complications at birth, and early neurological insults are
established risk factors. Psychosocial stressors can precipitate onset in
vulnerable individuals – for example, high-stress life events or social adversity
often precede first episodes. Cannabis use (especially in adolescence) is
associated with increased schizophrenia risk in genetically susceptible youth.
Urbanicity, immigration stress, and social isolation have also been correlated with
higher rates of schizophrenia.
Integrated View: Schizophrenia likely reflects a gene–environment interplay. As
StatPearls notes, “causes include genetic, environmental, and neurobiological
factors… No single gene is responsible; there is an interplay of multiple genetic
factors. Environmental influences include prenatal and obstetrical risks,
psychosocial stressors, and cannabis use” . Thus, an individual inherits a certain
vulnerability (genetic load and early brain insults); later experiences (e.g.
trauma, drug exposure) and neurochemical imbalances then trigger the full-blown
disorder.
References: Authoritative sources on abnormal psychology (e.g., Butcher et al.,
Kring et al., DSM-5, Sarason & Sarason) emphasize that abnormal behavior must be
understood historically and dimensionally. The above summary integrates standard
textbook and review materials , along with up-to-date overviews. The aim is
to provide clear definitions, clinical descriptions, and etiological models for
each topic, suitable for undergraduate psychology students.