ABNORMAL PSYCHOLOGY

UNIT 2: NEURODEVELOPMENTAL DISORDERS

Name Symptoms Biological Causes Brain stuff Other Causes

ADH Inattention, - More likely to have the disorder - slightly smaller volume of the Have a relatively smaller role
D hyperactivity/ if someone in the family has it too brain (3-4%) -Psychosocial distress
impulsivity (the family, in general shows an -Afflicted areas: those involved in -Alcohol use
increase in psychopathology)- self-organisation -Parental marital instability
- slow to toilet Shared genetic deficits -ADHD is associated with weaker and discord
train, -Specific genotype function and structure of -Negative responses from
oppositional, -Dopamine transporter (DAT1) prefrontal cortex (PFC) circuits, others around
active, -D1, D4, and D5 receptor gene especially in the right - Maternal stress
mischievous -Serotonin transporter hemisphere. The prefrontal - Hostile home environments
-Moderate heritability association cortex is crucial in - Affects prognosis (negative
-Highly influenced by genetics regulating attention, behaviour, responses, constant
mutations that either create extra and emotion, with the right reminders to behave- fear of
copies of a gene on one hemisphere specialised for rejection, poor/negative self-
chromosome or result in the behavioural inhibition. image, low self-esteem)
deletion of genes (called copy - Slower brain waves seen in the
number variants— CNVs) EEG
-Dopamine, serotonin, - Delay in posterior to anterior - Boys>Girls (anxiety turned
norepinephrine, GABA cortical maturation inwards)
-specific areas of interest for - Identified around 3-4 years
ADHD are the brain’s attention of age
system, working memory
functions, and impulsivity.
-Poor inhibitory control
-Maternal smoking ( when
there’s mutation in DAT1)
-Low birth weight
-Specific gene defect: adrenergic
alpha-2A receptor gene
(ADRA2A)
-Toxins (allergens, pesticides and
food additives)

- ADHD and learning disabilities

have common biological base

ASD -Impairment in - moderate heritability: Families - Amygdala: fewer neurons - prenatal exposure to toxins
social that have one child with ASD have - young children with ASD: - unusual speech patterns
communication about a 20% chance of having larger Amygdala (causes (avoid first-person)
 -Restricted another child with the disorder. excessive anxiety and fear– social - Self-concept may be
repetitive This rate is more than 100 times withdrawal; continuous release lacking when people with
behaviours, the risk in the general population of cortisol damages the ASD also have cognitive
interests, and amygdala, causing relative disabilities or delays, not
activities - numerous genes on several absence in adulthood) because of the disorder
- social chromosomes are implicated - neuropeptide oxytocin- bonding itself.-- lack of awareness of
reciprocity, non- - oxytocin: relationships and + increasing trust + reducing fear→ their own existence
verbal social memory reduced level of oxytocin in the - social deficiencies- imp.
communication, - paternal age ( age —> risk) blood (it is a neurochemical)
initiating and - de novo mutations: mutations in - Males>Females
maintaining social the sperm or the mother’s eggs - 31% have ID- Degree of
relationships intellectual disability defines
- joint attention prognosis
- lacking facial - Language abilities also
expressions and affect prognosis
prosody
- Echolalia
- Lacks
perspective
taking and fails to
show interest in
others interests
-uninterested in
social situations
diagnosis:
- degree of
impairment that
distinguishes
individuals
previously
diagnosed with
other disorders

ID below average - genetic Cranial: - prenatal

intellectual and Phenylketonuria (diet related; - Macrocephaly (rare) FAS, Smoking, radiation,
adaptive inability to breakdown - Microcephaly disease, malnutrition
functioning which phenylalanine; recessive gene), - Hydrocephaly (CSF - perinatal
causes deficits in Tuberous sclerosis (seizures and accumulation, enlarged head) Hypoxia, anoxia
social,concptual characteristic bumps on the skin - postnatal
and practical that looks like acne; Dominant head injury, infections like
domains gene disorder), meningitis
Lesch-Nyhan (gene on X - environmental
areas such as chromosome of males; cerebral general: abuse, neglect,
communication, palsy and self-injurious deprivation, malnutrition
self-care, home behaviour; recessive X) toxins: pesticides, mercury,
living, social and lead, arsenic
interpersonal
 skills, use of - chromosomal
community Down syndrome or trisomy 21(
resources, self- have certain characteristic
direction, features; maternal age and
functional hormonal disbalances are key
academic skills, contributors)
work, leisure, Fragile X syndrome (x
health, and safety. chromosome linked— males are
mainly afflicted with moderate to
Four levels of ID: severe ID, hyperactivity, short
mild, which is attention span, gaze avoidance,
identified by an IQ repetitive speech; larger ears,
score between 50– testicles and head circumference;
55 and 70; females have mild to severe SLD)
moderate, with a
range of 35–40 to Mitochondrial disorders (defects
50–55; severe, in mitochondria, which are
ranging from 20– compartments found in most
25 to 35–40; and human cells that generate the
profound, which majority of energy needed by the
includes people cells to function)
with IQ scores
below 20–25. De Novo mutations

AAIDD definition Mutations in genetic material can

of ID is its occur at various points in
description of development
different levels of
this disorder, Maternal age: 35-45
which are based
on the level of
support or
assistance peo-
ple need:
intermittent,
limited, extensive,
or pervasive

SLD difficulty in learning Genetic - Left Hemisphere Environmental

and using academic - Runs in families; similar - SES
skills in any ⅙ areas : genes for all learning Dyslexia - parental child
- inaccurate or difficulties Broca’s area: word analysis and interactions
slow and effort articulation - Support in school
full reading
 - Not Chromosomal Left parietotemporal area: Word - Cultural expectations
understanding the - 1,2,3,6,11,12,15,18— analysis - Child management
meaning of what chromosomes related to Left occipitotemporal area: practices
is being read difficulties in word Recognising word form - Home reading habits
(comprehension) recognition or dyslexia - reduces the genetic
- Difficulty with Dyscalculia impact of at risk
spelling Left intraparietal sulcus: children
- Difficulty with Discrepancy of more than 2 Number sense
written standard deviations between Cultural
expression achievement and IQ No particular area for written - Prevalent among
- Difficulty in expression English and French
mastering number speakers — PET
sense scans shows reduced
- Difficulty in activation in the
mathematical temporal lobe which
reasoning is attributed to the
characteristics of the
SPECIFIERS languages.
Impairment with:
readings, Economic differences in
expression, diagnosis
mathematics

Treatments
- FOR ADHD
-Ritalin targets DAT1 (inhibits)+ increases dopamine levels
-Psychosocial treatments- focus on improving academic performance, decreasing disruptive behaviour, and improving social skills
-Biological treatment- reduce impulsivity and hyperactivity to improve attentional skills
-Ritalin+Adderall-stimulants
-Atomoxetine (Strattera)- SNRI
-Clonidine + Imipramine- dopamine and serotonin pathways
-Methylphenidate- adrenergic alpha-2A receptor gene (ADRA2A)

- FOR ASD
- focused on teaching social skills, enhancing their communication and daily living skills and on reducing problem behaviors,
such as tantrums and self-injury
- behavioural approaches- skill building and treatment of problem behaviours
- teaching how to communicate (more details on page 539, Barlow).
- Rewards and reinforcements
- naturalistic teaching strategies
- incidental teaching, pivotal response training, Milieu teaching: increase a variety of social communication skills (e.g., making
requests, interactions with peers, joint-attention skills, play skills) among those with more severe forms
- early intervention for toddlers with ASD include programs specifically targeting joint attention and play skills
- a variety of pharmacological treatments are used to decrease agitation- major tranquillizers and SSRIs are most helpful

- FOR ID
-mild ID— SLD treatments: specific deficits are identified and the child gets help, additional support to live in the community
1. Behavioural/task analysis: breaking down various tasks into smaller components that are taught in succession until mastered.
2. Communication
Mild ID: goals range from increasing articulation to organising a conversation
Severe and profound ID:
Augmentative communication— using more visual and auditory-based cues to teach them how to communicate easily.
3. Community
Helping them find and participate in jobs satisfactorily
- National Head Start Porgram: it combines educational, medical, and social supports for these children and their families
- Prenatal Gene Therapy
- Benefits of treatment:
- Increases independence and satisfaction
- Helps in communicating needs
- Refusing aggressive and self injurious behaviour
- Reducing frustration

- FOR SLD
- Comorbid with ADHD: stimulant medications
- Educational interventions : specific skill instruction and strategy instruction
- A combination of Direct instruction, teaching for mastery and constant assessment to track progress
- Evidence for educational and behavioural interventions: fMRI study between those with and without reading disorders

GENERAL NOTE: biological risk factors for several developmental disorders include malnutrition and
exposure to toxins such as lead and alcohol. Although medical researchers can identify the role of these
biological events in cognitive development, psychologists will need to support these efforts. Behavioural
intervention for safety training (for example, involving lead-based paints in older homes), substance-
use treatment and prevention, and behavioural medicine (for example, “wellness” efforts) are examples
of crucial roles played by psychologists in helping to prevent certain forms of developmental disorders.

UNIT 3: ANXIETY & ANXIETY RELATED

DISORDERS
Name Symptoms Biological Causes Psychological Cause
Panic - recurrent unexpected - Moderate heritability - Onset: 23-34 years
Disorder panic attacks. 4/13 - Genetic vulnerability (neuroticism) - Chroic, but waxes and wanes over time
symptoms are present - Locus coerulus (brain stem)- - Women>Men– Sociocultural differences
(palpitations/ Stimulation of the central nucleus - Comorbidity: generalized anxiety disorder, social
Pounding of the amygdala is known to phobia, specific phobia, PTSD, depression, and
heart/accelerated heart stimulate the locus coeruleus as substance-use disorders, avoidant PD.
rate; sweating; well as the other autonomic, - Although panic attacks themselves appear to come
trembling/shaking; neuroendocrine, and behavioural “out of the blue,” the first one occurs following
feelings of choking; chest responses that occur during panic feelings of distress or some highly stressful life
pain or discomfort; attacks circumstance.
nausea/abnormal - Norepinephrine
distress; feeling - Increased activity in the - Learning theory of PD (interoceptive and
dizzy/unsteady/light- Amygdala exteroceptive conditioning)- anticipatory anxiety
headed/faint; chills /heat + fear network (connections and agoraphobic fear
sensations; paresthesias; between the lower areas in the - Impaired discriminative conditioning
derealisation/ brain (locus coerulus) and the - People with certain genetic, temperamental/
depersonalisation; fear of higher areas of the brain (PFC)) —> personality, cognitive-behavioural vulnerabilities-
losing control/going panic attacks show stronger conditioning (both anxiety and panic)
crazy; fear of dying) -Periaqueductal gray (midbrain)- - Personality variable serves as a risk- neuroticism
- An attack was followed implicated - Cognitive theory of PD: individuals with panic
by 1 month of either - Abnormally sensitive fear disorder are hypersensitive to their bodily
persistent worry about networks may have a partially sensations and are very prone to giving them the
having another attack or heritable basis but may also direst possible interpretation- to catastrophise
avoidant behaviours develop as a result of repeated about the meaning of their bodily sensations. These
- not attributable to stressful life experiences, frightening thoughts may cause many more
drugs or another medical particularly early in life physical symptoms of anxiety, which further fuel
condition - Hippocampus: learned emotions the catastrophic thoughts, leading to a vicious circle
- not better explained by (avoidance as seen in agoraphobia) culminating in a panic attack.
another mental disorder - Higher cortical centres: - People with panic disorder already start at a higher
threatening bodily sensations level of arousal than others and are very familiar
- Greater activation in the brain in with these early warning cues.
response to threat words
- Stress on the neurobiological -Appraisal: the learning theory model is better able
system is heightened to explain the occurrence of the panic attacks that
- Two neurotransmitter systems often occur without any preceding negative
implicated: noradrenergic automatic thoughts, as well as the occurrence of
(stimulate cardiovascular nocturnal panic attacks that occur during sleep; the
symptoms associated with panic occurrence of both of these kinds of attacks is
attacks ) & serotonergic systems difficult for the cognitive model to explain
- Serotonergic system decreases - Anxiety sensitivity is a trait-like belief that certain
noradrenergic symptoms bodily symptoms may have harmful consequences.
Such a person would endorse statements such as,
 - Inhibitory GABA: anticipatory “When I notice that my heart is beating rapidly, I
anxiety (low in certain parts of the worry that I might have a heart attack.
cortex of the brain + related to how - Perceived Control
they cannot unlearn learned fears) - People with panic disorder are biased in
processing threatening information. Such people
Treatments: interoceptive not only interpret ambiguous bodily sensations as
exposure, cognitive restructuring, threatening, but they also interpret other ambiguous
CBT, panic control treatment (more situations as more threatening.
in Butcher). Changing their - Safety behaviours + safety person– maintenance of
cognitions about their bodily faulty cognitions
symptoms should reduce or - Infusions of sodium lactate, inhaling air with
prevent panic. Evidence that altered amt. of CO2, ingesting large amounts of
cognitive therapy for panic works is caffeine— panic provocation procedures
consistent with this prediction.
Generalised - excessive anxiety and - Modest heritability Role impairment and reduced quality of life- as seen
Anxiety worry occurring for - Neuroticism in depression
Disorder/ more days than not for 6 - Deficiency in GABA, Serotonin, Chronic
Free- months Norepinephrine Disappears after 50 years of age, but may be replaced
Floating - difficulty in controlling - Suppressing stress hormone by another somatic symptom disorder (with physical
anxiety worry cortisol: anxiety producing symptoms)
- anxiety or worry is hormone called the CRH— effects Women>Men
associated with 3/6 on the bed nucleus of the stria Comorbidity: other anxiety and mood disorders
symptoms (only 1 terminalis (an extension of the such as panic disorder, social phobia, specific
required in children): amygdala)- important brain area phobia, PTSD, and major depressive disorder
easily fatigued, difficulty mediating generalized anxiety
concentrating or mind - HPA axis - Psychoanalytic viewpoint: A person’s defence
going blank, muscle - Smaller hippocampal region- due mechanisms have broken down or never developed;
tension, irritable, sleep to cell atrophy or cell death unconscious conflict between id and ego;
disturbance, suppression of sexual and aggressive impulses;
restless/feeling keyed overwhelmed defence mechanisms; blocked id
up/on edge impulses.
- impairment in - Uncontrollability and unpredictability
important areas of - Lack of safety signals- constantly tense and
functioning vigilant
- not attributable to - Process threatening information in a biased way,
substance or medical perhaps because they have prominent danger
conditions schemas
- another mental - Far less tolerance for uncertainty
disorder does not better - Over-controlling parenting styles may promote
explain condition anxious behaviours; think of world as an unsafe
 place in which they need protections and have little
control
- Constant vigilance
- Excessive worry- for a subset of people with GAD,
these positive beliefs (superstitious avoidance of
catastrophe, avoidance of deeper emotional topics,
coping and preparation) about worry play a key role
in maintaining high levels of anxiety and worry,
especially in early phases (worry is self-sustaining)
- Attempts to control thoughts and worry may
paradoxically lead to increased experience of
intrusive thoughts and enhanced perception of
being unable to control them

Agoraphobi - Marked fear or anxiety about two (or more) of the following five situations: (Using public transportation, being in open
a spaces, being in enclosed places, standing in line or being in a crowd, being outside of the home alone.)
- The individual fears or avoids these situations because of thoughts that escape might be difficult or help might not
be available in the event of developing panic-like symptoms or other incapacitating or embarrassing symptoms - The
agoraphobic situations almost always provoke fear or anxiety
- The agoraphobic situations are actively avoided, require the presence of a companion, or are endured with intense
fear or anxiety.
- The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic situations and to the
sociocultural context.
- 6 months or more
- The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
- If another medical condition (e.g., inflammatory bowel disease, Parkinson’s disease) is present, the fear, anxiety, or
avoidance is excessive
- The symptoms of another mental disorder do not better explain the fear, anxiety, or avoidance (social anxiety
disorder, OCD, body dysmorphic disorder, PTSD, or separation anxiety disorder).
Note: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an individual’s presentation meets
the criteria for panic disorder and agoraphobia, both diagnoses should be assigned.

- Causes are same as ones listed under Panic Disorder

Specific Fear or anxiety about a - A person’s genetic makeup - Overcome with fear or anxiety, which may vary
Phobia specific object or (temperament or personality) from mild feelings of apprehension and distress to
situation influences the likelihood of full-fledged activation of the fight-or-flight
Subtypes: - Phobic object/situation acquisition of fears and phobias response.
Blood- always provokes - Carriers of the s allele (serotonin- - Phobic behaviour reinforcement- reduction of
Injection- fear/anxiety transporter gene linked with high anxiety every time a phobia-inducing situation is
avoided.
injury - Actively avoided or neuroticism): superior fear - Secondary benefits: Increased attention, sympathy,
phobia endured with intense conditioning and some control over the behaviour of others-
(highly fear/anxiety - Carriers of the COMT met/met reinforce a phobia.
heritable)- - fear or anxiety is out of genotype: enhanced resistance to - Women>Men
read more proportion to the actual extinction - Age of onset varies widely (childhood: animal,
from the danger posed by the specific - Behavioural inhibition: higher blood-injection, dental; adolescence: claustrophobia
textbook object or situation and to risk of developing multiple phobias and driving).
the sociocultural context.
(butcher pg at a very early age - Psychoanalytic View
- 6 months or more
168) - Modest genetic contribution Phobias represent a defence against anxiety that
- Clinically significant
- Amygdala stems from repressed impulses from the id. Because
distress and impairment
it is too dangerous to “know” the repressed id
in important areas of
impulse, the anxiety is displaced onto some external
functioning
object or situation that has some symbolic
- Not better explained by
relationship to the real object of the anxiety
the symptoms of another
- Learned Behaviours
mental disorder
- Wolpe and Rachman
(agoraphobia, OCD,
- Classical Conditioning: The fear response can
PTSD, separation
readily be conditioned to previously neutral stimuli
anxiety, social anxiety)
when these stimuli are paired with traumatic or
painful events. The fears are then generalised to
In Children: expressed
other similar stimuli.
by crying, tantrums,
- Vicarious Conditioning
clinging, and freezing.
- Observational learning
- Watching a non-fearful person undergo a
Specify type:
frightening experience can also lead to vicarious
1. Animal
conditioning.
2. Natural environment
- Importance of mass media
(e.g., heights, storms, and
- Individual Differences
water)
- Differences in life experiences influence whether
3. Blood injection injury
conditioned fears or phobias develop.
4. Situational (e.g.,
- Certain experiences serve as risk factors, while
planes, elevators, or
others serve as protective factors
enclosed places)
- Importance of familiarity with an object - if a child
5. Other (e.g., phobic
has extensive exposure to a non-fearful parent
avoidance of situations
behaving bravely with the phobic object or situation
that may lead to
of the other, phobic parent, this may serve as a
choking, vomiting, or
protective factor and immunise the child against the
contracting an illness; or
effects of later seeing the phobic parent behaving
in children, avoidance of
fearfully with the phobic object.
loud sounds or costumed
- Events that occur during a conditioning experience
characters)
and before it is also important in determining the
level of fear that is conditioned.
- Experiences after a conditioning experience
- Inflation Effect: later exposure to uncontrollable
stress; verbal info that later alters the way
information is interpreted; experiences before and
after the event (Butcher 170)
- Cognitive View
- Development and maintenance of phobia
- Constant vigilance for phobic stimulus
- Cognitive bias: overestimating the probability that the
feared objects have been/will be followed by frightening
events→ strengthening of fear over time
- Evolutionary Preparedness
- evolutionary history has affected which
stimuli we are most likely to come to fear-
Primates and humans seem to be evolutionarily
prepared to associate certain objects with
frightening or unpleasant events rapidly.
- This prepared learning occurs because,
throughout evolution, those primates and humans
who rapidly acquired fears of certain objects or
situations that posed real threats to our early
ancestors may have enjoyed a selective advantage.
- “Prepared” fears are not inborn or innate but are
easily acquired or especially resistant to extinction.
- Fear is conditioned more effectively to fear-
relevant stimuli than fear-irrelevant stimuli.
-Once a conditioned response is formed, the fear
response can be elicited even when the stimuli are
presented subliminally.
- Fear may arise from cognitive structures that are
not under conscious control
- Selective association of fear-relevant stimuli with
threat or danger
Social - Marked fear/anxiety in - Amygdala: central structure in - Comorbidity with Avoidant PD, Anxiety disorders,
Anxiety one or more social fear learning (people with social depressive disorders, alcohol abuse
Disorder situations in which the phobia show greater activation of - Women>men
individual is exposed to the amygdala and other brain areas - Onset: early/middle adolescence or early
scrutiny by others involved in emotion processing in adulthood
- fears that they will act response to negative facial - Lower employment rates and lower SES.
in a way or show anxiety expressions- this activity is
symptoms that will be heightened by criticism). - Vicarious Classical Conditioning
negatively evaluated - Neuroticism and Introversion- - They showed fear conditioning when the
- social situations almost Modest genetic contribution (30% unconditioned stimulus was socially relevant (critical
always provoke fear or variance liability) facial expressions and verbal insults) as opposed to
anxiety. - Behavioural inhibition: Those more nonspecifically negative stimuli (such as
- avoided or endured who had been assessed as being unpleasant odours and painful pressure)
with intense fear or high on behavioural inhibition - People with generalised social phobia also may be
anxiety. between 2 and 6 years of age were especially likely to have grown up with parents who
- fear or anxiety is nearly three times more likely to be were emotionally cold, socially isolated, and
disproportionate to the diagnosed with social phobia even avoidant.- devalue sociability and discourage
actual threat posed by in middle childhood. attendance for social events + development of a
the social situation and diminished sense of personal control
the sociocultural context. - Criticism from others for experiencing anxiety
- 6 months or more, symptoms and feeling self-conscious and
- impairment in uncomfortable in public as a consequence of past
important areas of criticism
functioning - Problems with peers- “not fitting in”
- not attributable to - Social phobias and fears occur due to dominance
substance or medical hierarchies common in social arrangements-
conditions aggressive encounters between members where the
- another mental defeated individual acts fearfully and submissively,
disorder does not better but does not try to escape the situation
explain the condition - Humans have the predisposition to acquire fears
- If another medical for social stimuli that signal dominance and
condition (e.g., aggression from others (facial expressions,
Parkinson’s disease, contempt, anger)
obesity, disfigurement - Perceptions of uncontrollability and
from burns or injury) is unpredictability- submissive and unassertive
present, the fear, behaviour, especially if it stems from social defeat
anxiety, or avoidance is ( submissive behaviour and fear)
unrelated or is - Diminished sense of personal control
excessive.
- Cognitive Factors
- Sub-types: - Expectations of negative evaluation-> a sense of
vulnerability around those who “pose a threat.”
 Performance (public - Danger schemas: expectations of unacceptable
speaking) and non- behaviours on their part that may lead to rejection
performance and loss of status
- Preoccupation with bodily responses; negative
In children: Occurs in self-image in social situations
peer settings and not just - Intense preoccupation with self-> hindered ability
adult interaction. The to interact in public
anxiety is expressed by - Interpretation of situations and responses as
crying, tantrums, negative (even though they are neutral)
freezing, clinging, - negatively biased interpretations that socially
inability to speak, anxious people- remembered.
shrinking. - These biased cognitive processes combine to
maintain social phobia and possibly even contribute
to its development
Somatic A. One or more somatic Psychosocial
Symptom symptoms that are - these disorders develop in the context of a stressful life event- many disorders (like
Disorder distressing and/or result anxiety disorders).
in significant disruption - people who develop these disorders tend to have had a disproportionate incidence of a
of daily life. disease in their family when they were children.
B. Excessive thoughts, - important social and interpersonal influence may be involved (benefits of being sick -
feelings, and behaviours sick role).
related to the somatic
symptoms or associated Cognitive
health concerns as - Misinterpretations of bodily sensations are currently a defining feature of the
manifested by ⅓: syndrome, but in the cognitive-behavioural view, these misinterpretations also play a
Disproportionate and causal role
persistent thoughts - they perceive their symptoms as more dangerous than they are and judge a particular
about the seriousness of disease to be more likely or dangerous than it is– Catastrophising
symptoms; High level of - Once they have misinterpreted a symptom, they tend to look for confirming evidence
health-related anxiety; and in discounting evidence that they are in good health. (Healthy = Symptom-free)
Excessive time and - the probability of being able to cope with the illness as extremely low; see themselves as
energy devoted to these weak
symptoms or health - Vicious cycle —> symptoms of anxiety [psychological or behavioural factors, particularly
concerns. anxiety and distress, are compounding the severity and impairment associated with the
C. Although any one physical symptoms]
symptom may not be - past experiences with illnesses (in both herself and others, and as observed in the mass
continuously present, the media) lead to the development of a set of dysfunctional assumptions about symptoms
state of being and disease
symptomatic is - interpret ambiguous stimuli as threatening
persistent (> 6 months).
Biological
Specifiers:
 With pain (previously - enhanced perceptual sensitivity to illness cues.
pain disorder) - runs in families - modest genetic distribution (stress response)
Severity:
Mild - 1 symptom from B
Moderate - 2+ symptoms
from B
Severe - All of B plus
multiple somatic
complaints
Functional A. One or more “Functional” refers to a symptom without an organic cause.
Neurological symptoms of altered La Belle Indifference: a paradoxical absence of psychological distress despite having a
Symptom voluntary motor or serious medical illness or symptoms related to a health condition.
Disorder sensory function. Precipitated by marked stress, which takes the form of physical injury.
B. Clinical findings Comorbid with anxiety and mood disorders
provide evidence of Women>Men
incompatibility between
the symptom and Psychodynamic:
recognised neurological - First: the individual experiences a traumatic event— in Freud’s view, an
or medical conditions. unacceptable, unconscious conflict.
C. Another medical or - Second: because the conflict and the resulting anxiety are unacceptable, the
mental disorder does not person represses the conflict, making it unconscious.
better explain the - Third: the anxiety continues to increase and threatens to emerge into
symptom or deficit. consciousness, and the person “converts” it into physical symptoms, thereby
D. The symptom or relieving the pressure of having to deal directly with the conflict. This reduction of
deficit causes clinically anxiety is considered to be the primary gain or reinforcing event that maintains
significant distress or the conversion symptom.
impairment in social, - Fourth: the individual receives greatly increased attention and sympathy from
occupational, or other loved ones and may also be allowed to avoid a difficult situation or task. Freud
important areas of considered such attention or avoidance to be the secondary gain, the secondarily
functioning or warrants reinforcing set of events.
medical evaluation - Conversion symptoms are caused by the conversion of sexual conflicts or other
psychological problems into physical symptoms (no longer accepted)
[(1) sensory - - The primary gain for conversion symptoms is continued escape or avoidance of a
anaesthesias, blindness, stressful situation. Because this is all unconscious (i.e., the person sees no relation
etc. between the symptoms and the stressful situation), the symptoms go away only if the
(2) motor -aphonia, stressful situation has been removed or resolved.
Globus hystericus, etc. - The term secondary gain, which initially referred to advantages that bestow beyond the
(3) seizures (psychogenic “primary gain” of neutralising intrapsychic conflict (reduced anxiety due to escape), has
non-epileptic seizures) also been retained. Generally, it refers to any “external” circumstance, such as attention
(4) a mixed presentation] from loved ones or financial compensation, that would tend to reinforce disability
maintenance.
 Psychosocial
- Sexual abuse, parental divorce or death (parent or close family member), physical abuse,
difficulties in school
- Overprotective or overinvolved mothers
- More prominent in lower educated and lower socioeconomic groups- low knowledge
about disorders and diseases in general
- Prior experience with real physical problems, usually among another family members,
tends to influence the later choice of specific conversion symptoms– more knowledge

Biological
- lower levels of brain-derived neurotrophic factor kinda?
- conversion tremor- lower activity in the right inferior parietal cortex (Functions to
compare internal predictions with actual events. Because we think about making a
movement before we do it, the brain concludes (correctly in most cases) that we caused
the movement to occur. But if this area of the brain is not functioning properly, the brain
might conclude that the movement is involuntary). – Unclear whether this is cause or
effect.
- Individuals may have a marked biological vulnerability to develop conversion disorder
when under stress
- Strong connection between conversion disorders and parts of brain regulating emotions
(Amygdala)
- Factitious Disorders: symptoms are under voluntary control, as with malingering,
but there is no obvious reason for voluntarily producing the symptoms except,
possibly, to assume the sick role and receive increased attention.
- When an individual deliberately makes someone else sick, the condition is called
factitious disorder imposed on another. It was also known previously as
Munchausen syndrome by proxy. It is really an atypical form of child abuse
Illness
Anxiety Notes + PPT (Notion)
Disorder

Note: For Anxiety Disorders, the last criterion is always compared with other anxiety disorders, OCD,
PTSD, and body dysmorphia.
 UNIT 4: MOOD DISORDERS
Criteria

Major Depressive Disorder

Diagnostic Criteria:
A: At least one major depressive episode
B: Occurrence is not better explained by schizoaffective, schizophrenia, etc. schizo spectrum and other psychotic
C: There has never been a manic episode or hypomanic ep (doesnt apply if manic symptoms are substance induced)

Specifiers:
- Single or recurrent
- Mild, moderate, sever
- With anxious distress
- With mixed features
- With melancholic features
- With atypical features
- With mood-congruent psychotic features
- With mood-incongruent psychotic features
- With catatonia
- With peripartum onset
- With seasonal pattern (recurrent only )
- In partial remission/full remission
Stats:
- 35% to 85% of people with single-episode occurrences of major depressive disorder later experience a second episode
- In the first year following an episode, the risk of recurrence is 20%, but it rises as high as 40% in the second year
- Depression is a chronic condition
- Median lifetime number of MDD episodes is 4-7
- Median duration of MDD episodes is 4 to 5 months
Onset and duration:
- U-shaped pattern, such that symptoms of depression were highest in young adults, decreased across middle adulthood,
and then increased again in older age, with older people also experiencing an increase in distress associated with these
symptoms
- Duration untreated is about 4 to 9 months.
- Fully 25% of people 18 to 29 years had already experienced major depression

Major Depressive Episodes

Extremely depressed mood state (absence of manic episodes) that lasts at least 2 weeks and is characterized by cognitive
symptoms and disturbed physical functions to the point that even the slightest activity or movement requires an overwhelming
effort; crucial indicator: anhedonia.

DSM Criteria: Mnemonic - SIGECAPS

A. 5 or more symptoms for 2 week period and represent change; at least one is either (i) depressed mood (ii) anhedonia
1. Depressed moods most of the day, nearly every day (can be irritable mood in children)
 2. S - Sleep loss, insomnia or hypersomnia nearly every day
3. I - Interest - Markedly diminished interest or pleasure in all, or almost all, activities most of the day nearly every day
4. G - Guilt - Feelings of worthlessness or excessive, inappropriate guilt (may be delulu)
5. E - Energy - Fatigue or loss of energy nearly every day
6. C - Concentration - Diminished ability to think or concentrate, or indecisiveness, nearly every day
7. A - Appetite loss/gain –> weight loss/weight gain (in children its the failure to make expected weight gain)
8. P - Psychomotor agitation or retardation nearly every day
9. S - Suicidal thoughts or ideation
B. Symptoms cause clinically significant distress or impairment in areas of functioning
C. Symptoms are not effects of a substance or medical condition

Mania

A. Distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently
increased goal-directed activity or energy; 1 week and present for most of the day nearly daily.
B. During the period of mood disturbance and increased energy or activity, three (or more) of the following symptoms (four
if the mood is only irritable) are present to a significant degree and represent a noticeable change from usual behaviour
(inflated self-esteem or grandiosity, decreased need for sleep, more talkative, flight of ideas or subjective experience that
thoughts are racing, distractibility, increase in goal-directed activity or psychomotor agitation, Excessive involvement in
activities that have high potential for painful consequences
C. Clinically significant impairment in important areas of functioning necessitating hospitalisation to prevent harm to self or
others
D. Not attributable to substance or another medical condition

- Note:
- Full manic episodes emerge during antidepressant treatment but persist at a fully syndromal level beyond the physiological
effect of that treatment is sufficient evidence for a manic episode and, therefore, a bipolar I diagnosis.
- Criteria A–D constitute a manic episode. At least one-lifetime manic episode is required for the diagnosis of bipolar I disorder.

Hypomania: a person experiences abnormally elevated, expansive, or irritable mood for at least four days. The person must have
at least three other symptoms similar to those involved in mania but to a lesser degree (e.g., inflated self-esteem, decreased need
for sleep, flights of ideas, pressured speech, etc.). There is much less impairment in social and occupational functioning in
hypomania, and hospitalisation is not required.

Persistent Depressive Disorder (Dysthymia)

A. Depressed mood for most of the day, for more days than not, as indicated by either subjective account or observation by
others, for at least 2 years. Note: In children and adolescents, mood can be irritable and duration must be at least 1 year.
B. Presence, while depressed, of two (or more) of the following: 1. Poor appetite or overeating
2. Insomnia or hypersomnia
3. Low energy or fatigue
4. Low self-esteem
5. Poor concentration or difficulty making decisions
6. Feelings of hopelessness
C. During the 2 years (1 year for children or adolescents) of the disturbance, the person has never been without the
symptoms in criteria A and B for more than 2 months.
D. Criteria for major depressive disorder may be continuously present for 2 years.
 E. There has never been a manic episode or a hypomanic episode, and criteria have never been met for cyclothymic disorder.
F. The disturbance is not better explained by a persistent schizoaffective disorder, schizophrenia, delusional disorder, or
other specified or unspecified schizophrenia spectrum and other psychotic disorder.
G. The symptoms are not attributable to the physiological effects of a substance or another medical condition.
H. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of
functioning.

Specify if:
● Current severity: Mild, moderate, severe
● With anxious distress
● With mixed features
● With melancholic features
● With atypical features
● With mood-congruent psychotic features
● With mood-incongruent psychotic features
● With peripartum onset
● Early onset: If onset is before age 21 years
● Late onset: If onset is at age 21 years or older
Specify (for most recent 2 years of dysthymic disorder):
● With pure dysthymic syndrome: if full criteria for a major depressive episode have not been met in at least the preceding
2 years
● With persistent major depressive episode: if full criteria for a major depressive episode have been met throughout the
preceding 2-year period
● With intermittent major depressive episodes, with current episode: if full criteria for a major depressive episode are
currently met, but there have been periods of at least 8 weeks in at least the preceding 2 years with symptoms below the
threshold for a full major depressive episode
● With intermittent major depressive episodes, without current episode: if full criteria for a major depressive episode are
not currently met, but there has been one or more major depressive episodes in at least the preceding 2 years
● In full remission
● In partial remission

Cyclothymic Disorder

A. For at least 2 years (at least 1 year in children and adolescents), there have been numerous periods with hypomanic
symptoms that do not meet the criteria for a hypomanic episode and numerous periods with depressive symptoms that do
not meet the criteria for a major depressive episode.
B. During the above 2-year period (1 year in children and adolescents), the hypomanic and depressive periods have been
present for at least half the time and the individual has not been without the symptoms for more than 2 months at a time.
C. Criteria for a major depressive, manic, or hypomanic episode have never been met.
D. The symptoms in Criterion A are not better explained by schizoaffective disorder, schizophrenia, schizophreniform
disorder, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorders.
E. The symptoms are not attributable to the physiological effects of a substance or another medical condition.
F. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of
functioning.
Specify if: With Anxious Distress

Bipolar I and Bipolar II Disorder

Bipolar I Disorder (Mania + Depressive mood, but not severe enough to qualify for a Major Depressive Episode)
A. Criteria have been met for at least one manic episode
B. At least one Manic Episode is not better explained by schizoaffective disorder. It is not superimposed on schizophrenia,
schizophreniform disorder, delusional disorder, or other specified or unspecified schizophrenia spectrum and other
psychotic disorders.

Specify: Mild, Moderate, Severe

Bipolar II Disorder (Hypomania + Major Depression//Sub-threshold: Unipolar MDD with hypomanic symptoms that do not
qualify (duration-wise) for a full-blown hypomanic episode)
A. Criteria have been met for at least one hypomanic episode and at least one major depressive episode. Criteria for a
hypomanic episode are identical to those for a manic episode, with the following distinctions:
a. Minimum duration is four days
b. Although the episode represents a definite change in functioning, it is not severe enough to cause marked social
or occupational impairment or hospitalisation
c. There are no psychotic features.
A. There has never been a manic episode.
B. The occurrence of the hypomanic episode(s) and major
depressive episode(s) is not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder,
delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorders.
C. The symptoms of depression or the unpredictability caused
by frequent alternation between periods of depression and hypomania causes clinically significant distress or impairment
in social, occupational, or other important areas of functioning.

Specify current or most recent episode:

Hypomanic: If currently (or most recently) in a hypomanic episode.
Depressed: If currently (or most recently) in a major depressive episode.

Specify if:
➔ With anxious distress
➔ With mixed features
➔ With rapid cycling
➔ With mood-congruent psychotic features
➔ With mood-incongruent psychotic features
➔ With catatonia
➔ With peripartum onset
➔ With seasonal pattern

Specify course if full criteria for a mood episode are not currently met: In full remission, in partial remission
Specify severity if full criteria for a mood episode are currently met: Mild, moderate, severe

A mixed episode is characterised by symptoms of both full-blown manic and major depressive episodes for at least 1 week,
whether the symptoms are intermixed or alternate rapidly every few days.

Schizophrenia

A. Two (or more) of the following, each present for a significant portion of time during 1 month (or less if successfully
 treated). At least one of these must be (1), (2), or (3):
1. Delusions
2. Hallucinations
3. Disorganized speech (e.g., frequent derailment or incoherence)
4. Grossly disorganized or catatonic behavior
5. Negative symptoms (i.e., diminished emotional expression or avolition)
B. For a significant portion of the time since the onset of the disturbance, level of functioning in one or more major areas,
such as work, interpersonal relations, or self-care, is markedly below the level achieved prior to the onset (or when the
onset is in childhood or adolescence, there is failure to achieve expected level of interpersonal, academic, or occupational
functioning).
C. Continuous signs of the disturbance persist for at least 6 months. This 6-month period must include at least 1 month of
symptoms (or less if success- fully treated) that meet Criterion A (i.e., active-phase symptoms) and may include periods of
prodromal or residual symptoms. During these prodro- mal or residual periods, the signs of the disturbance may be
manifested by only negative symptoms or by two or more symptoms listed in Criterion A present in an attenuated form
(e.g., odd beliefs, unusual perceptual experiences).
D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either 1)
no major depressive or manic episodes have occurred concurrently with the active-phase symptoms; or 2) if mood
episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the
active and residual periods of the illness.
E. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or
another medical condition.
F. If there is a history of autistic spectrum disorder or a communication disorder of childhood onset, the additional
diagnosis of schizophrenia is made only if prominent delusions or hallucinations, in addition to the other required
symptoms of schizophrenia, are also present for at least 1 month (or
less if successfully treated).

Specify if: With catatonia

Causes

Biological Causes Psychological Causes

Unipolar Disorders

● Genetic contribution - 31 to 42% (for unipolar; not as large Women>Men

for bipolar or dysthymia) Onset: 18-22 years
○ serotonin transporter gene (ss allele) - Mediated by underlying biological changes that they initiate.
● Neurochemical - monoamine (norepinephrine and (eg., the influence of stressors on biochemical and hormonal
serotonin) theory of depression - depression was at least balances and biological rhythms)
sometimes due to an absolute or relative depletion of one ● Stressful Life Events
or both of these neurotransmitters at important receptor ○ Depression is more severe for those who have
sites in the brain experienced such events (esp. For the first
● dopamine dysfunction onset).
● Hormone regulatory and immune systems ○ Precipitating factor (especially for women):
 ○ Stress response is associated with elevated activity loss of loved one, threat to close relationships/
of HPA axis and partially controlled by occupation, serious economic or health
monoamines problems. Losses involving humiliation and
○ perception of threat leads to norepinephrine caregiver stress.
activity causing release of CRH from ○ Dependent life events: events generated by
hypothalamus - triggers release of ACTH —> depressed person’s behaviour or personality.
adrenal glands where cortisol is released Stronger role than independent life events.
○ Elevated cortisol activity is highly adaptive in the ○ Minor stress causes recurrent episodes, than
short term because it promotes survival in the initial onset. Chronic stress increases the
response to life-threatening or overwhelming life risk associated with the onset, maintenance,
circumstances. and recurrence of MDD.
○ Blood plasma levels of cortisol are known to be ○ People with genetic vulnerability have an
elevated in some 20 to 40% of outpatients with elevated response to stress.
depression and in about 60 to 80% of hospitalised ● Types of Vulnerabilities
patients with severe depression ○ Personality and Cognitive Diathesis
○ dexamethasone (suppressor of plasma cortisol) - ■ Neuroticism is the main personality
fails to suppress cortisol variable. It predicts the occurrence of
○ Cell death in hippocampus causing memory loss stressful events.
○ disturbances to the HPA axis is also linked to ■ Low Positive Affectivity:
mood disorders (hypothyroidism) unenthusiastic, unenergetic, dull, flat.
○ dysregulation of immune system ■ Negative thinking patterns make
● Brain vulnerable individuals more likely to
○ damage to left anterior prefrontal cortex leads to become depressed when faced with
depression; even if not damages maybe lower stress. Attribution to internal, stable
activity? and global causes.
○ High activity in the right hemisphere of the ○ Early Adversity Diathesis
prefrontal cortex (increase vulnerability to ■ Family turmoil, parental
negative feedback), and low activity in the left psychopathology, physical or sexual
hemisphere of the prefrontal cortex (reduced abuse, intrusive/harsh/coercive
positive affect and distancing from reward) parenting—cause short and long term
○ orbital prefrontal cortex - responsivity to reward vulnerability to depression, and
○ Lower levels of activity in the dorsolateral increase sensitivity to stress in
prefrontal cortex, which are associated with adulthood.
decreased cognitive control. ■ Long-term effects mediated by
○ hippocampus damage ^^^ - hippocampal volume biological (alterations in HPA axis) and
○ anterior cingulate cortex psychological (low self-esteem,
○ amygdala - increased activation (more perceptive insecure attachment, pessimistic
to threat and negative emotions) attribution) variables.
● Sleep ■ Moderate adversity may make the
○ Sleep cycle (4NREM and 1 REM): SCNucleus - individual resilient instead of
Reduced latency to enter REM sleep and the susceptible.
decreased amount of deep sleep ● Psychological Theories of Depression
○ Circadian Rhythm - Body temperature, propensity ○ Psychodynamic
to REM sleep, and secretion of cortisol, thyroid- ■ Depression is anger turned inwards.
stimulating hormone, and growth hormone Regression to oral stage.
○ Size or magnitude of the rhythms is blunted ■ Response to imagined or symbolic
○ Various of these become desynchronised or losses.
 uncoupled (Thase, et al., 2002) ■ Found similarities between mourning
○ Sunlight (SAD): Increased appetite and and depression, and how loss plays a
hypersomnia, all rhythms affected & light therapy crucial role (real or imagined).
○ Hormonal factors: fluctuations in ovarian ○ Behavioural
hormones cause sex differences (differing ■ Depression occurs when their
conclusions, but identification as a vulnerability). responses no longer produce positive
reinforcement or when rate of
negative experiences (stressful events)
increases.
■ However, are they causes? Maybe
pessimism leads to negative
reinforcement.
○ Beck’s Cognitive Theory
■ Cognitive symptoms precede affective
symptoms.
■ Depressogenic schemas: underlying
dysfunctional beliefs that are rigid,
extreme, and counterproductive. They
aren’t sufficient to cause depression,
they need to be activated by stressful
events. They can also be activated by
simply inducing a depressed mood
(sad songs). They develop during
childhood due to early negative
experiences (underlying diathesis).
■ When activated by stressors, these
schemas create a thinking pattern of
negative automatic thoughts—
unpleasant, pessimistic predictions
occurring below the surface of
awareness. Centre around the
negative cognitive triad: (a) self, (b)
one’s experiences and the surrounding
world, (c) one’s future.
■ Triad maintained by cognitive biases:
Dichotomous or all-or-none thinking,
Selective Abstraction, Arbitrary
Inference
○ Hopelessness and Helplessness Theory
■ Martin Seligman’s Learned
Helplessness: when individuals have
no control over aversive events, they
may learn that they are helpless, and
become unmotivated to eventually
respond, instead exhibiting passivity
and depressive symptoms.
■ They are slow to learn that any
 response they make is effective.
■ Attributions made to uncontrollable
negative events: (a) internal/external,
(b) unstable/stable, (c) global/specific.
Pessimistic attributional style acts as a
diathesis, develops partly through
social learning.
■ Hopelessness is more necessary than
an attributional style. Depression-
prone individuals make negative
inferences about other negative
consequences of the event, and about
implications of the event on self-
concept.
■ Individuals with depression have
ruminative responses, whereas others
have action-oriented problem-solving
responses. Self-focused rumination
brings out negative autobiographical
memories. Men engaging in distractive
responses (alcohol consumption).
○ Interpersonal Theory
■ Interpersonal issues can cause
depression, and can also be a result of
depression.
■ People who are lonely, socially
isolated, or lacking social support are
more likely to have depression—
depression may also cause people to
have lower social networks. People
with depression have social-skills
deficits (speech, eye contact).
■ Behaviour of a depressed individual
forces others to provide sympathy,
support, and care—this may not lead
to positive reinforcement, instead, it
elicits negative feelings and rejection.
Social rejection likely if depressed
individual engages in excessive
assurance-seeking.
■ Unsatisfying marriages (high levels of
criticism and hostility) worsen
depression. Criticism serves as a
trigger. Marital distress co-occurs
with depression, as behaviour of
depressed partner causes a negative
affect (excessive preoccupation with
 self).
■ Children and Depressed Parents:
inheriting temperament, low positive
affect, and low emotional regulation.
Negative interactional patterns
between mothers and children
(multiple opportunities for
observational learning of negative
cognitions, depressive behaviour, and
depressed affect).
● Difference between Anxiety and Depression. Both have
high negative affect and common genetic vulnerability
and linkages. Anxiety has a highly positive affect and
anxious hyperarousal—which is the opposite in
depression. They follow a sequential relationship:
agitation and anxiety followed by despair and
depression.

Bipolar Disorders

- Genes Onset: 5 years later than Bipolar I

- Greater genetic contribution: first-degree relatives are at Recurrent episodes (either one after another or in intervals)
elevated risk for unipolar depression (atypical)/bipolar disorder
- Identical twins>Fraternal twins - Stressful Life Events
- 80-90% of the variance in liability to develop bipolar I (higher - Precipitate bipolar depressive episodes and manic episodes
than the heritability for depression/other psychiatric conditions) - Influence timing: acting as an underlying vulnerability
- Stronger influences for early onset than later onset - Worsens prognosis and treatment
- Bipolar and Unipolar may have a similar underlying base - Even minor negative events increase time to recovery
- People with bipolar: genetically susceptible to both depression - As the illness unfolds, the manic and depressive episodes
and mania (independent susceptibilities). become more autonomous and do not usually seem to be
- Several genes implicated- polygenic precipitated by stressful events: stress played a less important
role in precipitating episodes for people who had had more
- Neurochemical Factors episodes
- Monoamine Hypothesis: Increased norepinephrine activity - Critical effects on biological rhythms (promising hypothesis
during mania (inconsistent results for depression). Low Serotonin for manic episodes)
activity in both depression and mania.
- Norepinephrine, Serotonin, and Dopamine are involved in - Other Psychological Factors
regulating mood states - Low social support- depressive recurrence, independent
- Increased dopaminergic activity in several brain areas may be of the effects of stressful life events
related to manic symptoms (hyperactivity, grandiosity, and
euphoria) [drugs that stimulate dopamine activity also produce - Personality and Cognitive Variables
manic-like behaviours] - May interact with stressful life events in determining
- Lithium- reduce dopamine activity likelihood of relapse
- Depression: decrease in Norepinephrine and Dopamine - Neuroticism: associated with symptoms of depression and
mania ( depressive symptoms)
- Hormonal Regulatory Systems - Are related to goal-striving, drive, and incentive motivation
- HPA Axis: Elevated cortisol levels in depression/reverse effect in have been associated with bipolar disorder
mania. - Two personality variables associated with high levels of
- Dexamethasone: suppressed the HPA loop; patients with bipolar achievement striving and increased sensitivity to rewards in
disorder show abnormalities in the Dexamethasone Suppression the environment predicted increases in manic symptoms—
Test (DST); abnormalities persist even during complete remission especially during periods of active goal striving or goal
or asymptomatic periods. attainment
- DST is lower during Mania - Pessimistic attributional styles ( depressive symptoms and
– Abnormalities in Thyroid functions- accompanied by changes in in manic symptoms at other points in time)
mood [Administration of thyroid hormone makes antidepressants
work better]
- Thyroid hormone: precipitate manic episodes

- Neuropsychologic and Neuroanatomic Influences

- PET Scan: variations in the blood glucose metabolic rates in
depressed and manic states (great difficulty in studying manic
patients]
- Blood flow to left PFC: mania (certain other parts of the PFC);
Depression → Shifting patterns of brain activity during mania,
depressed and normal moods.
- Deficits in the activity of the PFC- Deficits in problem-solving,
planning, working memory, attention shifting, and sustained
attention
- Deficits in the Anterior Cingulate Cortex
- Certain subcortical structures, the Basal Ganglia and Amygdala
are enlarged (reduced in depression)
- No changes in Hippocampal volume (reduced in Depression)
- fMRI: Activation in subcortical regions involved in emotional
processing (Thalamus and Amygdala)

- Sleep and Other Biological Rhythms

- Disturbances in biological and circadian rhythms, even after
symptoms have remitted
- Mania: limited sleep (by choice)- most common symptom that
occurs before the onset of a manic episode
- Depression: hypersomnia
- Bipolar disorder also sometimes shows a seasonal pattern in the
same way unipolar disorder does, suggesting disturbances of
seasonal biological rhythms, although these may be the result of
circadian abnormalities in which the onset of the sleep–wake cycle
is set ahead of the onset of other circadian rhythms.
- Patients with bipolar disorder seem especially sensitive to, and
easily disturbed by, any changes in their daily cycles that require a
resetting of their biological clocks.

Schizophrenia

- Genetics: Psychosocial and Cultural Factors

- One may inherit a general predisposition for schizophrenia that ● Role of Families
manifests in the same form or differently from that of your ○ Rejection of Old View:
parents: familial risk for a spectrum of psychotic disorders related ■ Parents attributed for schizophrenia
to schizophrenia in children—hostility, deliberate
- Higher risk for monozygotic twins than dizygotic twins rejection, parental ineptitude. Idea of
- Importance of gene-environment interaction in family, twin, the schizophrenogenic mother: cold
and adoption studies. and aloof behaviour as root cause of
- Genetic vulnerability coupled with environmental dysfunctions: schizophrenia.
varied time of onset, presentation of symptoms, diagnosis and ■ Double Bind Hypothesis: parents
prognosis. present children with ideas, feelings,
- De novo mutations and demands that are mutually
- Unshared environments: even siblings who are close in every incompatible (mother may complain
aspect of their lives can still have considerably different about son’s lack of affection, but may
experiences physically and socially as they grow up, which may freeze up/reprimand him on being
result in vastly different outcomes. approached affectionately—causing
- The disorders in the schizophrenia spectrum overlap defeating situations for the child, and
considerably increasing anxiety). This disorganised
- children of parents with schizophrenia have a much higher behaviour is reflected in own thinking.
chance of having the disorder themselves. At the same time, there ■ Conflict/disturbances caused in the
appears to be a protective factor if these children are brought up family, because of having someone
in healthy supportive homes. with psychosis, and not the other way
- Increased risk for children of parents who have a round. (family communication
fraternal/identical twin with schizophrenia problems- communication deviance)
- chromosomes implicated: 1, 2, 3, 5, 6, 8, 10, 11, 13, 20, and 22 ○ Relapse higher when patients return to
- Secretions from chromosome 8, 6, and 22- increased families after hospitalisation—highly
susceptibility emotional family environments are stressful.
- Ednophenotypes: discrete, stable, and measurable traits that are ○ Expressed Emotion (EE): measure of family
thought to be under genetic control. environment based on how a family member
- basic processes that contribute to the behaviours or symptoms of speaks about the patient during a private
the disorder and then find the gene or genes that cause these interview. Three main elements: criticism,
difficulties—a strategy called endophenotyping. – determining hostility, emotional overinvolvement (EOI).
other genes that are responsible for, or may be implicated in, Living in high EE environment doubles risk of
schizophrenia relapse.
○ Patients extremely susceptible to stress. High
- Neurobiological Influences EE environments are extremely stressful, and
- Dopamine: hallucinations and other positive symptoms (too trigger cortisol release, which impact
active) dopamine and glutamate systems. Negative
- while some dopamine sites may be overactive, others show behaviours by relatives can increase unusual
little/lesser activation thinking in patients.
- D1 and D4 receptors ● Urban Environment
- D1 receptors: less activity in parts of the brain that are used for ○ Living in urban areas increases the risk of
thinking and reasoning schizophrenia.
- D2: results in schizophrenia (partially); these cells control ● Immigration
movement, balance, and walking, and they rely on dopamine ○ Recent immigrants are at a higher risk of
functions schizophrenia compared to natives due to
- Inconclusive/inconsistent support for dopamine activity as a higher stressful events. Second-gen
base for schizophrenia as many patients are not helped even after immigrants at a higher risk than first-gen
use of dopamine antagonistic medication immigrants (due to cultural clash??)
- Glutamate and its specific receptors (NMDA) ○ Cultural misunderstandings increase
diagnosis.
- Brain structures ○ Individuals with genetic predisposition to
- Brain damage or dysfunction may cause or accompany schizophrenia more likely to move.
schizophrenia, although no one site is probably responsible for the ○ Role of discrimination: darker skinned
whole range of symptoms immigrants more likely to develop
- Enlarged ventricles (dilation (enlargement) of the ventricles schizophrenia, as their experiences with
indicates that adjacent parts of the brain either have not developed discrimination lead them to be paranoid and
fully or have atrophied, thus allowing the ventricles to become suspicious. Stress from social disadvantage
larger)--> Men>women; enlarge in proportion to age and duration and social defeat impacts dopamine release.
of the disorder ● Cannabis Usage
- Hypofrontality: range of deficits in the PFC (smaller PFC) ○ Schizophrenia patients are twice as likely to
- deficient activity in a particular area of the frontal lobes, the smoke cannabis.
dorsolateral prefrontal cortex (DLPFC), may be implicated in ○ People with the COMT gene (1 or 2 copies of
schizophrenia- there is less connectivity between this region and the val allele) are more vulnerable to
other brain regions, meaning the DLPFC is “communicating” less developing schizophrenia in adulthood if they
with other brain regions smoke cannabis in adolescence
- lower white matter volume and larger third ventricular volume ○ Cannabis worsens symptoms, as THC in
were associated with the risk for schizophrenia, and these cannabis increases the synthesis of dopamine.
differences appeared to be influenced by genetic factors. ○ Schizophrenia patients who consume cannabis
- Anoxia have a marked decrease in brain volume.
- Implicated areas: PFC, various cortical and subcortical regions ● Diathesis Stress Model of Schizophrenia
(Thalamus and Striatum) ○ interplay between genetic factors, prenatal
- Broca’s area: active during auditory hallucinations→people who are events, brain maturational processes, and
hallucinating are not hearing the voices of others but are listening stress in the development of schizophrenia.
to their own thoughts or their own voices and cannot recognize ○ predisposing genetic factors must have
the difference combined in additive and interactive ways
with multiple environmental risk factors,
some known and some still unknown, that
- Prenatal and Perinatal Influences operate prenatally, perinatally, and also
- Viral infection, pregnancy/delivery complications, prenatal postnatally- abnormal brain development
exposure to influenza, viruses, and infections ○ (Figure 13.11 in Butcher)
- the genes carried by the fetus that make it vulnerable to
schizophrenia may themselves contribute to the birth
complications.
- Maternal stress during pregnancy: Increased risk
- Early nutritional deficiency

- people who use marijuana in high doses have an increased

likelihood of developing schizophrenia for those with CNR1
genotypes.
- people with schizophrenia are more likely to have a cannabis use
disorder than individuals without schizophrenia

- Rhesus incompatibility
- Rh incompatibility between an Rh-negative mother and an Rh-
positive fetus can cause blood disease in newborns- increased risk
of schizophrenia.
- The increased risk of schizophrenia due to Rh incompatibility
could involve oxygen deprivation (hypoxia) during development
elevating the risk of brain abnormalities associated with
schizophrenia

Additional Information

Symptoms in Schizophrenia:
1. Positive: Hallucinations and Delusions
2. Negative: Flat affect (reduced/negligible emotional expression; prosody is a related concept which refers to lack of
intonation while speaking), Alogia (relative absence of speech), Avolition (inability to initiate or persist in goal-directed
behaviours/apathy), Anhedonia (loss of pleasure in previously pleasurable activities), social withdrawal (lack of interest in
social situations and interactions
3. Disorganised Symptoms: erratic behaviour (hoarding, catatonia, waxy flexibility, catalepsy, cataplexy), disorganised speech
(jump from topic to topic/talk illogically-tangentiality, loose association or derailment; cognitive slippage), inappropriate
affect

- Prodromal Symptoms: a 1- to 2-year period before the serious symptoms occur but when less severe yet unusual
behaviours start to show themselves (magical thinking, ideas of reference, illusions, isolation, marked impairment in
functioning, and a lack of initiative, interests, or energy.

- Attenuated Psychosis Syndrome: Some individuals who start to develop psychotic symptoms such as hallucinations or
delusions are often sufficiently distressed to seek help from mental health professionals. They can be at high risk for
developing schizophrenia and may be at an early stage of the disorder (called prodromal). Although they may not meet the
full criteria for schizophrenia, they may be good candidates for early intervention in an effort to prevent symptoms from
worsening.
- Delusional Disorder: Delusions without any of the negative symptoms

For Schizophrenia
Mesolimbic Dopaminergic Pathway

Cognitive Dysfunction in Schizophrenia

For Depression

The Hypothalamo-Pituitary-Adrenal Axis: Stress→ Hypothalamus→ (CRH)->Ant. Pituitary-

>(ACh)->Adrenal Gland->(Cortisol)->deactivation feedback to hypothalamus

*The entorhinal cortex is the major relay through which information from the neocortex gets to the
hippocampus and related structures and is then sent back to the neocortex