OCD / MOOD DISORDER Flashcards
Recurrent and persistent thoughts, urges or images as intrusive and inappropriate
and generally cause marked anxiety or distress
▪ Attempt to ignore or suppress the thought, image, urge by engaging in
compulsions
Obsessions
DSM5 Criterion A for Obsessive Compulsive
Disorder
A. Presence of obsessions, compulsions or both
Repetitive behaviours (e.g., handwashing, praying..) that are rigid and rule‐bound, that people feel compelled to perform in response to an obsession
▪ The behaviours are done to prevent or reduce distress, or to prevent a dreaded act
or event (even though they are not connected and are clearly excessive
Compulsions
OCD Criteria B‐D
B. The obsessions or compulsions are:
▪ Time‐consuming (more than an hour a day)
▪ Distressing
▪ Or cause impairment
C. Not attributable to a substance or a medical condition
D. Not better explained by another mental disorder (e.g., excessive
worry in GAD; worry about appearance in Body Dysmorphic Disorder;
hoarding in Hoarding Disorder)
Types of Compulsions / Obsessions
“Symptom Subtypes”
- Symmtery / Exactness
- Forbidden thoughts or actions
- Cleaning / Contamination
- Hoarding
(Specific obessions and compulsions associated vary, see diagram)
Barlows model of OCD (memorize from text)
g
OCD Treatments
▪ Exposure and response prevention (ERP; e.g., Abramowitz, Taylor &
McKay, 2012)
SSRIs help, but less effective than ERP ‐ relapse (e.g., Dougherty,
Rauch, & Jenike, 2012)
▪ No advantage to pairing SSRIs and ERP (Romanelli et al., 2014)
▪ Surgery (lesion of the cingulate bundle) is a desperate last resort.
– Only about a third benefit ‐ side effects of this approach
A desperate last resort of OCD treatment is ____, and only _______ benefit.
Surgery (lesion of the cingulate bundle) is a desperate last resort.
– Only about a third benefit ‐ side effects of this approach
OCD related Disorders
Trichotillomania
Excoriation Disorder
Hoarding Disorder
repetitive hair
pulling/plucking
compulsion leading to
physical damage
Trichotillomania
repetitive skin picking
compulsion leading to
physical damage
Excoriation Disorder
extreme difficulty
discarding objects/
animals; ignoring living
in extreme clutter/
disorganization and
sometimes
contaminants
Hoarding Disorder
An OCD / related somatic disorder that is hard to classsify
Body Dysmorphic Disorder
Obsessive preoccupation with one’s appearance;
imagined/exaggerated defects (repeated mirror
checking)
- ___,___ , and ____ are the top three fixations
(Phillips et al., 2005)
Body Dysmorphic Disorder
Skin, hair and nose
45% of people at the dermatologists; 8‐25% at
plastic surgeons (Barnard, 2000; Crerand et al.,
2004)
* Dissatisfied after plastic surgery – nosejobs
most common
Body Dysmorphic Disorder
Treatment for Body Dysmorphic Disorder is the same as
OCD
Major Depressive Disorder Criteria A
&
1-9
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.
- Depressed mood most of the day, nearly every day
- Markedly diminished interest or pleasure in all, or almost all, activities most of
the day, nearly every day - Significant weight loss when not dieting or weight gain, or decrease or increase
in appetite nearly every day. - Insomnia or hypersomnia nearly every day.
- Psychomotor agitation or retardation nearly every day.
- Fatigue or loss of energy nearly every day.
- Feelings of worthlessness or excessive or inappropriate guilt
- Cognitive issues
- Suicidal ideation
Major Depressive Disorder Criteria B-E
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.
D. The occurrence of the major depressive episode is not better
explained by schizoaffective disorder, schizophrenia,
schizophreniform disorder, delusional disorder, or other specified
or unspecified schizophrenia spectrum and other psychotic
disorders.
E. There has never been a manic episode or a hypomanic episode
Major Depressive Disorder Epidemiology
▪ Canadian lifetime prevalence (Patten et al., 2015): 9.9%
– Past year prevalence: 3.9% (male: 2.8%, female:4.9%)
▪ Mean age of onset is 25 years of age in community samples (Burke, Burke,
Regier, & Rae, 1990).
– Prevalence increases in adolescents, especially in females (Georgiades et al., 2006)
▪ Occurrence of one lifetime depressive episode is rare (Angst, 2009)
– 85% experience a second episode
– In first year likelihood of recurrence is 20%, second year 40% (Boland & Keller, 2009)
– Median lifetime number of episodes 4‐7; 6+ for 25% of individuals
Major Depressive Disorder
Larger role of major life stress in first episode than subsequent
– After the first episode, less and less stress is required to trigger onset of future episodes
This is known as the _______
Kindling Hypothesis
Table 6.2 | obsessions and intrusive thoughts
reported by nonclinical Samples*
see text
involuntary movement (sudden jerking of limbs, for example) is generally known as a
Tic Disorder
OCD and tic disorder seem to be ______
Comorbid
In some cases, these movements are not tics but may
be compulsions,
- Approximately 10 to 40 percent of children and adolescents with
OCD also have had tic disorder at some point (Leckman et al.,
2010).
The obsessions in tic-related OCD are almost always
related to symmetry
The obsessions in tic-related OCD are almost always
related to
symmetry
More complex tic disorders with involuntary
vocalizations are referred to as ______
Tourette’s disorder
The DSM5 lists five basic somatic symptom and related disorders:
- somatic symptom disorder
- illness anxiety disorder
- psychological factors affecting medical condition
- conversion disorder,
- Factitious disorder (stand alone branch of conversion disorder)
symptom disorder, illness anxiety disorder, and psycho
logical factors affecting medical condition—_________
overlap considerably
a person has a significant focus on physical symptoms, such as pain, weakness or shortness of breath, to a level that results in major distress and/or problems functioning.
- excessive thoughts, feelings and behaviors relating to the physical symptoms.
- symptoms may or may not be associated with a diagnosed medical condition, but they truly believe it and are not faking
somatic symptom disorder
Illness anxiety disorder was formerly known as
hypochondriasis
This somatic symptom disorder includes
- physical symptoms are either not experienced at the present time or are very mild, but severe anxiety is focused on the possibility of having or developing a serious disease.
Illness Anxiety Disorder
The essential feature of this disorder
is the presence of a diagnosed medical condition clearly caused by a known medical condition (ie cancer) that is adversely affected (increased in frequency or severity) by one or more psychological or behavioural factors.
pSychological FactorS aFFecting
meDical conDition
generally have to do with physical malfunctioning, such as paralysis, blindness, sense of touch, or difficulty speaking (aphonia), without any physical or organic pathology to account for the malfunction
Conversion disorders
Closely Related Disorders to Conversion Disorders / Types of conversion disorders that stand out
malingering
factitious disorders,
faking illness
malingering
symptoms are under voluntary control, as with
malingering, but the person has no obvious reason for voluntarily
producing the symptoms except, possibly, to assume the sick role
and receive increased attention.
may extend to producing symptoms in other members of the family.
factitious disorders
example of a factitious disorder (Conversion disorder)
factitious disorder imposed on another /
Munchausen syndrome by proxy
Persistent Depressive Disorder Criteria (dysthymia) A-H (holy shit)
A. Depressed mood for most of the day, for more days that not, as
indicated by either subjective account or observation by others, for
at least 2 years.
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‐year period of the disturbance, the person has never
been without the symptoms in criteria A and B for more than 2
months at a time.
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
G. The symptoms are not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical
condition (e.g., hypothyroidism)
H. The symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
Etiology Hypotheses of Depressive Disorders
Monoamine Hypothesis (Heninger, Delgado, & Charney, 1996)
– Depleted Serotonin/Norepinephrine
▪ Learned helplessness theory (Seligman, 1975)
– Inescapable shock experiments (dog only escapes when knowing it can, when it think it cant, wont)
▪ Cognitive Theory (Beck, 1967)
– Cognitive Triad – negative thoughts about self, world, and future
Genetics of Depressive Disorders
Moderate heritability h2 = .37 in meta‐analysis (e.g., Sullivan et al., 2000)
▪ Relatives of those with depression have a 2‐3 x higher risk than others
▪ Higher severity, recurrence and earlier onset assoc with highest rates of
depression in relatives (Kendall et al., 2021)
▪ In a large study of 2000 female twins, the genetic risk for depression, shared with panic and anxiety too (Kendler et al., 1995)
▪ Polygenetic – no one gene implicated
▪ General disposition (e.g., neuroticism) and the form and type of disorder depends on other biopsychosocial factors?
Neurostructural perspectives of Depressive Disorders
Functional neuorimaging confirm volume and metabolic
changes in these areas: prefrontal cortex, orbitofrontal
cortex, anterior cingulate cortex, amygdala, and
hippocampus (e.g., see Pizzagalli, 2011)
– Frontocingulate dysfunction
▪ Postmortem cell‐counting confirm lower density of glial
cells and neurons (in both MDD and bipolar disorder) (e.g.,
Rajkowska, 2003)
Neurochemical perspectives of Depressive Disorders
Chemicals are out of balance – early roots in humors
▪ Low levels of serotonin relative to the other monoamines “permits” them to go awry permissive hypothesis
▪ Clinical trials show that ADMs work; their main mechanism is via monamine restoration, thus, the it must be an imbalance, right?
▪ Appealing as it takes away stigma?
– Not supported.
– In a study of those with depression, half were told they took a chemical imbalance test that indicates they have a chemical imbalance and the other half were told their neurotransmitters were normal. The Chemical imbalance group had increased helplessness
and hopelessness and believed medication would be more effective than CBT; there was no difference with respect to stigma (Kemp et al., (2014)
Is there any support for the chemical
imbalance theory of Depressive Disorders?
▪ Not theory driven, accidentally discovered (3 studies) rats on reserpine (a monoamine depleter) became sluggish and nonresponsive— ergo, depression caused by low/later imbalance monoamines.
– But, DA
– But: Only 6% of those given reserpine developed depression; marked reductions in NE, 5HT or DA did not produce depression (Mendels & Frazer, 1972); increasing chemicals (e.g., cocaine) does not produce symptom improvement (for review, see Valenstein, 1998)
– Some early antidepressants did not operate on 5HT or NE (Kuhn, 1990)
▪ Moncrieff (2003) inert placebos produce larger antidepressant effects than active ones
– Inert placebos unmask (no longer blind)
The problem with the data in depressive disorders
Kirsch & Sapirstein (2008) reanalyzed ALL AD
trials data submitted to the FDA and found
that antidepressants fare better than placebos
ONLY for most severe depressions (effect no
bigger for ADMs, just the placebo effect is
smaller)
– correlation between placebo effect and drug effect
.90 (drug ES relates to placebo characteristic of the
study)
– 25% of drug response is an active placebo effect
▪ Moncrieff (2003) inert placebos produce larger
antidepressant effects than active ones
– Inert placebos unmask (no longer blind)
Treatments for Depression
– Psychotherapy
▪ Cognitive behavioural therapy
▪ Interpersonal psychotherapy
– Psychopharmacology
▪ Antidepressant medications
– Brain stimulation
▪ Electroconvulsive therapy
▪ Transcranial magnetic stimulation
Bipolar that has
– Presence of at least 1 manic episode
– Major Depressive episode not
required but can occur
– Hypomanic episode not required
but can occur
Bipolar I
Bipolar that has
Hypomanic episode
* Major Depressive episode
* No lifetime history of manic
episode
Bipolar II
A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal‐directed activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration if hospitalization is necessary)
Manic Episode
Difference between a manic and hypomanic episode
Less severe
– Does not cause marked impairment in important areas of functioning
– Does not necessitate hospitalization
– Duration of 4 days instead of 1 week
– No psychotic features
Manic Episode Criteria A-D and symptoms 1-7
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal‐directed activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration if hospitalization is necessary)
B. During the period of mood disturbance and increased 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 (e.g., feels rested after only 3 hours of
sleep) - More talkative than usual or pressure to keep talking.
- Flight of ideas or subjective experience that thoughts are racing.
- Distractibility (i.e. attention too easily drawn to unimportant or irrelevant
external stimuli), as reported or observed. - Increase in goal‐directed activity (either socially, at work or school, or sexually) or psychomotor agitation (e.g., purposeless non‐goal directed activity).
- Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments)
C. The mood disturbance is sufficiently severe to cause marked
impairment in social or occupational functioning or to necessitate
hospitalization to prevent harm to self or others, or there are
psychotic features.
D. The episode is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication, other treatment) or
to another general medical condition.
Bipolar Disorders Epidemiology
▪ Canadian life prevalence (Macdonald et al., 2015)
– BP I: 0.87%
– BP II: 0.57%
▪ Mean age of onset (Merikangas et al., 2007)
– BP I: 18.2
– BP II: 20.3
▪ Gender Differences
– Equally distributed prevalence and similar mean age of onset
– Higher frequency of depressive and mixed episodes in females (Schneck et al.,
2004)
– 60‐90% of rapid‐cycling patients are female
– 60‐90% of rapid‐cycling patients are ___
female
Rapid Cycling Specifier
Criteria: At least 4 manic or depressive episodes within a year
▪ 20‐50% of patients
▪ Poorer response to treatment
▪ More severe depressive episodes and higher rate of suicide (Coryell et al., 2003)
▪ Rapid cycling may increase in frequency over time (rapid switching)
– Ultra‐rapid cycling length of days/weeks
– Ultra‐ultra rapid cycling less than 24 hours
Can be precipitated by antidepressant use (Schneck et al., 2008)
– Anticonvulsants or mood stabilizers recommended
▪ Not permanent
– 80% non‐rapid‐cycling within 2‐year period (Coryell et al., 2003)
– 3‐5% continue cycling across 5‐year period (Coryell et al., 1992)
Etiology of Bipolar Disorders
Neurochemistry
– Dopamine related to mood cycling and increased during manic episodes (Salvadore et al., 2010)
▪ Neurocircuitry
– Mesolimbic pathway related to reward seeking (Johnson, Joorman, Lemoult, & Young, 2009)
▪ Biopsychosocial model
– Behavioural Approach System, Reward Hypersensitivity, and Social Rhythms (Boland et al., 2016)
Treatment of Bipolar Disorders
Pharmacotherapy
– Lithium Carbonate
▪ Treatment of choice
▪ Mood stabilizer
▪ Mechanism of action unknown
– Antidepressants, anticonvulsants, antipsychotics (Vazques et al., 2015)
▪ Interpersonal and Social Rhythm Therapy (Frank, Swartz, Kupfer,
2000)
– Stabilize dysregulated biological and social rhythms
