Table of Contents
Depression................................................................................................................................................2
Bipolar disorder......................................................................................................................................13
OCD........................................................................................................................................................21
GAD........................................................................................................................................................27
Additional - Anxiety disorders.................................................................................................................32
Additional - Schizoaffective.....................................................................................................................35
Psychotic disorder – General and schizophrenia......................................................................................35
Borderline Personality Disorder – Emotionally unstable PD.....................................................................46
Anorexia Nervosa...................................................................................................................................52
Bulimia Nervosa.....................................................................................................................................61
Binge Eating Disorder.............................................................................................................................66
Alcohol Use Disorder...............................................................................................................................68
Formulation – Psychiatric assessment & MSE structure/content.............................................................75
BASIC MENTAL HEALTH – FORMULATION/MH DISORDERS
KCL
PATRYCJA_KUSACZUK@ICLOUD.COM
1
,Depression
Signs/symptoms – clinical features
Depressed mood
Negative thinking
Lack of enjoyment (anhedonia)
Reduced energy
Slowness
ALL LEAD TO DECREASED SOCIAL AND OCCTUPATIONAL FUNCTIONING
Appearance Dress and grooming neglected
Facial features – turning downward of the corners of the mouth, vertical furrowing of the centre of
the brow
Reduced blinking rate
Shoulder bent and the head inclined forward so the direction of gaze in downward
Gestures and movements are reduced
Mood Mood is one of misery
Mood does not improve substantially in circumstances where ordinary feelings of sadness would be
alleviated
Low mood is pervasive
Mood experiences is often experienced as different from ordinary sadness
Mood is often worse in the morning, improving as the day wears on – diurnal variation of mood
Depressive Worthlessness – failing in what they do, and that other people see them as a failure, no longer feel
cognitions confident, discount ay success as a chance happening for which they can take no credit
Pessimism – concern future prospects, patients expect the worst, they foresee failure in work, the
ruin of finances, misfortune for family, and an inevitable deterioration in health
Guilt – unreasonable self-blame about minor matters, blame themselves for their misery and
incapacity and attribute it to personal failing and moral weakness
Hopelessness – often accompanied by the thought that life is no longer worth living and that death
would come as welcome release
Goal-directed Lack of interest and enjoyment (anhedonia) is frequent
behaviour No enthusiasm for activities and hobbies
No zest for living and no pleasure in everyday thing
Withdraw from social encounters
Reduced energy – lethargic, find everything an effort, leave tasks unfinished
ANHEDONIA – important symptoms because it can distinguish between moderate severity and
milder disorders
Psychomotor Walks and acts slowly
changes Slowing of thought is reflect in speech – significant delay in answering, pauses in conversation
Agitation – inability to relax, such as movements in their legs
Anxiety – frequent
Irritability – responds with undue annoyance to minor demands and frustrations
Biological Sleep disturbance – early morning waking but delay in falling asleep (2-3 hours before usual wake
symptoms up), lies feeling unrefreshed, restless and agitated
Diurnal variation in mood
Loss of appetite – decrease but can be increased
Loss of weight – due to lack of appetite, but can gain weight if they eat more than usual, eating
typically brings temporary relief of distressing feelings
Constipation, fatigue, aching discomfort
Loss of libido
Women (amenorrhoea)
Other Depersonalisation
features Obsessional symptoms
Panic attacks
Dissociative symptoms – e.g., loss of function of a limb
Poor memory
2
,Symptoms needed to meet the criteria for ‘depressive episode’ – ICD-10
A Depressed mood Mild depressive disorder
Loss of interest and enjoyment At least 2 of A
Reduced energy and decreased activity At least 2 of B
B Reduced concentration Moderate depressive disorder
Reduced self-esteem and confidence At least 2 of A
Ideas of guilt and unworthiness At least 3 of B
Pessimistic thoughts
Ideas of self-harm Severe depressive disorder
Disturbed sleep All 3 of A
Diminished episode At least 4 of B
Core Symptoms Severity Mild
Hypothmia (Low mood) Moderate
Anhedonia (Loss of interest in Severe
previously pleasurable activities) Special features With melancholic symptoms
Anergia (Low energy) With atypical symptoms
With prominent anxiety
Associated Symptoms With psychotic symptoms
reduced concentration and attention With agitation
reduced self-esteem and self- With retardation or stupor
confidence The course Single or recurrent episodes
ideas of guilt and unworthiness Aetiological factors Organic
bleak and pessimistic views of the Family history of mood disorder
future Personal history of mood disorder
ideas or acts of self-harm or suicide; Childhood experiences
disturbed sleep Personality
diminished appetite Social support
Life events
A. Five (or more) of the following symptoms have been present during the same 2-week period and represent a change
from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or
pleasure.
Note: Do not include symptoms that are clearly attributable to another medical condition.
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad,
empty, hopeless) or observation made by others (e.g., appears tearful). (Note: In children and adolescents, can
be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as
indicated by either subjective account or observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a
month) or decrease or increase in appetite nearly every day. (Note: In children, consider failure to make
expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of
restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not
merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or
as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a
suicide attempt or a specific plan for committing suicide.
B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of
functioning.
C. The episode is not attributable to the physiological effects of a substance or to another medical condition.
3
, Note: Criteria A–C represent a major depressive episode.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural disaster, a serious medical
illness or disability) may include the feelings of intense sadness, rumination about the loss, insomnia, poor appetite,
and weight loss noted in Criterion A, which may resemble a depressive episode. Although such symptoms may be
understand- able or considered appropriate to the loss, the presence of a major depressive episode in addition to the
normal response to a significant loss should also be carefully considered. This decision inevitably requires the exercise
of clinical judgment based on the individual’s history and the cultural norms for the expression of distress in the context
of loss
D. The occurrence of the major depressive episode is not better explained by schizoaffective disorder, schizophrenia,
schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other
psychotic disorders.
E. There has never been a manic episode or a hypomanic episode.
Note: This exclusion does not apply if all of the manic-like or hypomanic-like episodes are substance-induced or are
attributable to the physiological effects of another medical condition.
Definitions
Linking word by sound rather than meaning - Clang Association
Continuous, rapid speech that changes focus from moment to moment based on association, distractions, or plays on
words - Flight of ideas
Attention is drawn to irrelevant stimuli - Distractibility
Perception in the absence of a stimulus – Hallucination
A belief, out of keeping with the individual's cultural origins, that is held with strong conviction despite superior
evidence to the contrary - Delusion
Excessive or incongruous displays of emotion - Labile affect
Abnormally increased arousal, responsiveness to stimuli, and screening of the environment for threats – hypervigilance
unintentional and purposeless motions that stem from mental tension and anxiety of an individual – psychomotor
agitation
Habitual sleeplessness; inability to sleep - Insomnia
Lack of enjoyment taken from things previously enjoyed - Anhedonia
Loss of appetite for food - Anorexia
Lack of restraint manifested in disregard for social conventions, impulsivity, and poor risk assessment – Disinhibition
Abnormal lack of energy - Anergia
A psychological state that is normal, neither elated nor depressed - Euthymic
A state of depression - Hypothymia
A mild form of mania marked by elation and hyperactivity – Hypomanic
Affect is dulled in tone and reduced in intensity. The person is observed to be unengaged and emotionally-unreactive –
Blunted affect
Delusion that things, including self, do not exist; a sense that everything is unreal - nihilistic delusion
Classification
Depressive disorders in DSM-5
No general agreement about the best method of classifying depressive disorders.
A number of approaches have been tried based on the following: presumed aetiology, symptomatic picture, course
Assessment
Clinical screening for bipolar depression
Have you ever had a period of time when you were feeling so good, ‘high’, excited, or hyper that other people thought
you were not your normal self, or you were so hyper that you got into trouble?
If yes, was this most of the day and nearly every day and for at least four days?
YES + YES Investigate for bipolar disorder
NO or NO bipolar disorder unlikely
- Hamilton Depression Rating Scale (HDRS)25
- Montgomery-Asberg Depression Rating Scale (MADRS)
- The main difference between these two scales is that MADRS is more sensitive to change and does not emphasise
somatic symptoms as much as does HDRS.
Aetiology – prevalence, onset, course, co-morbidity, impairment
Genetic
o Family and twin studies
4
, Depression tends to run in families and the risk in first-degree relatives is high
Heritability of major depression has been estimated at 37% (Bienvenu et al., 2011)
Twin studies also suggested that susceptibility to major depression and GAS involves similar genes but
different environmental risk factors (Hettema et al., 2005)
o Mode of inheritance
Female preponderance of depression is well established – possible that genetic factors play a
somewhat greater aetiological role in woman
Seems likely that genetic liability to depression results from the combined action of multiple genes of
modest, or small effect in a context od gene-environment interaction
o Molecular genetics
Monoamine theory of depression suggests that allelic variation in gene coding for monoamine
synthesis or metabolism or specific receptors may contribute to the risk of mood disorders
Personality
o What is recognised as a personality characteristic may in fact represent a milder form of an illness
o Some personality features might influence the way in which people respond to adverse circumstances and
thus make depressive disorder more likely – e.g., a cognitive style characterised by a strong need for approval
is associated with increased risk of depression after adverse life events (Mazure and Maciejewski, 2003)
o Certain kinds of personality development and depressive disorder may share common genes – e.g.,
neuroticism predisposes to major depression, but twin studies suggest that neuroticism and major depression
have genes in common (Fanous and Kendler, 2004)
Early environment
o Parental deprivation
Childhood deprivation of maternal affection through separation or loss predisposes to depressive
disorder in adult life
Family discord and lack of adequate car predispose to depression even in families where separation
does not occur (Brown, 2009)
o Relationship with parents
Non-caring and overprotective parenting styles are associated with non-melancholic depression in
adulthood (Parker and Hadzi-Pavlvic, 1992)
Mothers with post-natal depression may manifest a rearing style that is characterised b neglect and
emotional indifference – this could lead to longer term deleterious effects on self-esteem and
attachment style in the child thus increasing the risk of depression in the subsequent generation
(Ramchandani et al.., 2009)
Precipitating factors
o Recent life events
Sixfold excess of adverse life events in the months before the onset of depressive disorder
An excess of similar events also precedes suicide attempts, and the onset of anxiety disorders and
schizophrenia
In general, ‘loss’ events are associated with depression and ‘threat’ events are associated with anxiety
Life events are important antecedents of all forms of depression, but appear to be relatively less
important in established melancholic-type disorders and where there is a strong family history of
depression
o Vulnerability factors and life difficulties
Events immediately preceding a depressive disorder act as the ‘last straw’ for a person who has been
subjected to a long period of adverse circumstances
Good evidence for poor social support, measured as a lack of intimacy or social integration, is
associated with an increased risk of depression (Brown, 2009)
o The effects of physical illness
Medical illnesses and their treatment can act as non-specific stressors which can lead to mood
disorders in predisposed individuals
Sometimes they can play a more direct role in causing the mood disorder – e.g., brain disease, certain
infections, including HIV and endocrine disorders
The resulting mood disorders are known as organic mood disorders
Psychological approaches
o Cognitive theories
Depressed patients characteristically have recurrent and intrusive negative thoughts
Beck (1967) proposed that these depressive cognitions reveal negative views of the self, the world
and the future and persist because of illogical ways of thinking called cognitive distortions
Arbitrary inference – drawing a conclusion when there is no evidence for it and even some evidence
against it
5
, Selective abstraction – focusing on a detail and ignoring more important features of a situation
Overgeneralisation – drawing a general conclusion on the basis of a single incident
Personalisation – relating external events to oneself in an unwanted way
These cognitions are dysfunctional beliefs or schemas
Early experience formation of dysfunctional assumptions critical incidents assumptions
activated negative automatic thoughts symptoms of depression negative automatic
thoughts
Neurobiological approaches
o Monoamine hypothesis
Suggests depressive disorder is due to an abnormality in a monoamine neurotransmitter system at
one or more sites in the brain
Three monoamine transmitters have been implicated – serotonin (5-HT), noradrenaline, and
dopamine
5-HT function – decreased plasma tryptophan contributes to impairments of brain 5-HT function in
depressed patients, blunted neuroendocrine response, low brain 5-HT function is not sufficient to
cause depression because tryptophan depletion fails to alter mood in those who are not vulnerable to
mood disorder, low brain 5-HT functions appear to interact with other vulnerability factors to cause
depressive symptoms
Noradrenaline function – evidence that brain or CSF concentrations of noradrenaline are altered in
depressed patients (Anand and Charney, 2000), increasing noradrenaline functions increases ACTH,
cortisol and growth hormones
Dopamine function – dopamine neurons play a key role in incentive behaviour and reward; these
processes are disrupted in depression due to melancholic states
Role of monoamines in depression – unmedicated depressed patients have abnormalities in various
aspects of monoamine function, some abnormalities may persist into clinical recovery suggesting that
they are related to vulnerability to illness rather than the acute depressive state
o Amino acid neurotransmitters
Decreased levels of glutamate in the anterior brain regions in depressed patients (Arnone et al., 2015)
Brian levels of GABA are also lowered in depression
o Endocrine abnormalities
Endocrine pathology and depression
About 50% of patient with Cushing’s syndrome suffer from major depression which usually
remits when the cortisol hypersecretion is corrected
Depression also occurs in Addison’s disease, hypothyroidism and hyperparathyroidism
Endocrine changes may account for depressive disorder that occur premenstrually, during
the menopause and after childbirth
HPA axis
Increase in cortisol secretion is associated with enlargement of the adrenal gland and
increased cortisol response to ACTH
About 50% of depressed inpatients do not show the normal suppression of cortisol secretion
induced by administering 1mg of the synthetic corticosteroid dexamethasone
CRH may play a direct role in the aetiology of depression – CRH levels may be increased in
the CSF of depressed patients, therefore it is possible that hypersecretion of CRH could be
involved in the pathophysiology of the depressed state
Thyroid function
Circulating plasma levels of free thyroxine appear to be normal in depressed patients but
levels of free triiodothyronine may be decreased
25% of depressed patients have a blunted thyrotropin=stimulating hormone (TSH) response
to intravenous TRH – also found in alcoholism and panic disorder
Abnormalities in thyroid function that are found in depressed patients may eb associated
with changes in central TRH regulation (Bunevicius and Prange, 2010)
o Depression and the immune system
Immune activation with increases in the release of certain pro-inflammatory cytokines – known to
provoke the HPA axis activity and therefore changes in immune regulation may play a role in HPA axis
dysfunction in depression
o Sleep changes in depression
Impaired sleep continuity and duration
Decreased deep sleep
Decreased latency to the onset of rapid eye movement (REM) sleep
An increase in the proportion of REM sleep in the early part of the night
6
, o Brain imaging in mood disorder
Structural brain imaging
Changes in brain volume – enlarged lateral ventricles, decreased hippocampal volume,
decreased volume of basal ganglia structure, decreased grey matter in the anterior brain
areas, including frontal cortex, orbitofrontal cortex, and cingulate cortex
White matter hyperintensities – in depression increased deep white matter hyperintensities
are associated with late onset of depressive disorder, greater illness severity and poorer
treatment response, apathy, psychomotor slowness and retardation, the presence of
vascular risk factors
Cerebral blood flow and metabolism
Growing consensus that the abnormalities in functional brain imagine in depression support
a circuitry model in which mood disorders are associated with abnormal interaction between
several brain regions rather than major abnormality in a single structure
Neuropsychological changes in mood disorder
o Impairment in attention, learning, memory, and executive function
Biological and psychological mechanisms in mood disorders
- MONOAMINE HYPOTHESIS
Depression is caused by reduced levels of serotonin, noradrenalin and dopamine in the limbic system
Evidence for theory
o Most commonly prescribed antidepressants are selective serotonin reuptake inhibitors (SSRI’s) and
noradrenaline reuptake inhibitors (NRI’s)
o Drugs work by increasing activity in serotonin and noradrenalin systems, and both are effective at
alleviating the symptoms of major depression
o Neuroimaging and post-mortem studies of depressed patients’ brain scans show that they have fewer
serotonin receptors, and their receptors tend to be less sensitive compared to healthy controls
Evidence against the theory
o SSRI’s alter serotonin function immediately, but people need to take them for several weeks before
they see an improvement in symptoms
o Observed deficits in serotonin function might reflect changes in the brain that occur as a consequence
of chronic depression, rather than being a cause of it
o We know that neurotransmitters do not function in isolation, and we have to consider the
interactions between different neurotransmitters (glutamate, GABA, acetylcholine) in order to
understand mood disorders properly
o Current biological theories of mood disorders on abnormal function in different regions of the brain,
rather than the activity levels of different neurotransmitters
Abnormal brain function in depression
- Network of brain structures was implicated in major depression
- These regions are included within the medical prefrontal cortex (MPFC) and the limbic system, and the connections
between the two
- In mood disordered patients we can see reduced grey matter volume (a structural deficit) and glucose metabolism (a
marker of brain activity) in specific regions of the MPFC, particularly the left anterior cingulate cortex (ACC)
Important because the MPFC normally inhibits activity in the limbic system, so one indirect consequence of
reduced activity in the MPFC would be increased activity in the limbic system
This is exactly what we see in mood disorders – activity in the limbic systems increased in major depression
patients when they are in the middle of a major depressive episode, and the level of increased activity in these
regions is associated with the magnitude of emotional processing biases in depressed patients
- Antidepressants normalise activity in these regions
- CBT may work in a different way, by increasing activity in the MPFC and therefore indirectly increasing inhibition of the
limbic system
- Antidepressants and CBT can normalise an overactive limbic system, but their mechanism of action is very different
Top-Down action for CBT – the MPFC changes first and then influences activity in the limbic system
Bottom-Up action for antidepressants – the limbic system changes first, and then activity in the MPFC changes
afterwards
Environmental factors
- A number of environmental factors have been posited which may have more or less relevance at different points in
development
Parenting
7
, o The more negative the parenting, the worse the depression
o But we cannot conclude that parenting causes depression
Standard of living / social economic status
Childhood abuse
Bullying
Life events
o Life events have been consistently associated with depression
Multiple stressful events lead to Kindling
o A major life stressor is needed to trigger the initial depressive episode
o Once the person has recovered from this episode, their threshold for experiencing a subsequent
episode is lowered
o This continues until at some point a very minor stressor is sufficient to cause a major depressive
episode
o After that, an environmental trigger may not be needed, and it can occur spontaneously
o There is a declining relationship between life stress and major depressive episodes over time: the first
episode is almost always linked to a major stressor, but recurrences can occur independent of life
stress
Gene-Environment interactions
- Individuals with a heritable risk for mood disorder are more likely to report symptoms of depression, but only after a
stressful life event
- In the absence of a stressful life event, there is no relationship between heritable risk for depression and experiencing
the symptoms of depression
- Gene and environment cannot be disentangled as easily as we would like, because people at increased heritable risk for
depression also tend to have more stressful environments
Explanation using the biopsychosocial model
Biological Psychological Social
Female Childhood Abuse/Trauma Young children (>3 under
Unclear about genetic Insecure attachment as a child age 15)
loading Personality traits - Anxiety or Eating disorder Financial worries
HPA axis abnormalities PTSD Work changes
Need to rule out physical Depression in childhood Separation from partner
causes, medication use and High levels stress and anxiety Single parent
illicit drug use. Ongoing stress Financial worries
Non concordance with Co-morbidity (including substance abuse and Good structure in daily
treatment personality disorder) routine
Older age at onset Insidious onset Employment
Chronic physical illness Chronic residual symptoms Good social support –
Concordance with Insight sister/partner/friends
treatment Seeking support
Exercise Engagement in psychological therapy – CBT /
Acute onset Psychotherapy
First degree relative with Emotional, Social, physical, sexual traumas
depression increases risk 3- Financial worries
fold Health problems
Unemployment
BIOLOGICAL: An important genetic contribution to mood disorders is made by multiple gens of small individual effect. This
genetic contribution may be expressed directly through modification of relevant cortical circuitry, or indirectly through effects
on personality and psychological coping mechanisms.
SOCIAL: Adverse early life experiences also shape personality and limit subsequent attachment behaviour and ability to access
social support. In addition, adverse early life experience may affect development of the HPA axis and neurobiological responses
to stress in adulthood.
SOCIAL: Depressive disorders are often triggered by current life events, particularly in people who lack social support. The
impact of life events is modified by early life experience, personality, and genetic inheritance. The interaction of these factors
determines the resilience or vulnerability of an individual to a life event, and the subsequent risk of clinical mood disturbance.
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