OCD & Mood Disorders Flashcards
What are obsessions?
ego-dystonic and recurring thoughts, images, and impulses that can be accompanied with compulsive behaviors; necessary in OCD
Ego-dystonic
meaning intrusive, unwanted, foreign, and inconsistent with one’s values and beliefs
Common themes in obsessions
contamination, aggression, violence, religion, sexuality, order
What are compulsions?
a repetitive behavior or mental act that the person feels driven to perform to neutralize the obsessions, prevent some dreaded event or situation, and provide relief
How are compulsions related to obsessions?
functionally but not necessarily logically
What are the 5 associated features of compulsions?
mental rituals, fluctuating insight, family involvement, avoidance of objects that prompt obsessions, continuous reassurance-seeking
Fluctuating insight
recognizing that one’s behavior doesn’t make sense from time to time; doesn’t apply to kids
Lifetime prevalence of OCD
3% for everyone (no sex/ethnic differences)
Onset and course of OCD
onset is typically during early adolescence or adulthood but can be earlier; often chronic with only ~40% seeking treatment and most having multiple obsessions
What disorders are comorbid with OCD?
anxiety, mood disorders, depression (in 80% of cases)
Biological factors of OCD
moderately heritable, associated with a lack of serotonin or 5-HT, structural and functional brain abnormalities
How do SSRIs affect OCD?
they increase serotonin, which reduces the emotional force (i.e. intensity or urgency) of obsessions and decreases anxiety
Brain abnormalities causing OCD
slight structural abnormalities in the basal ganglia (responsible for motor control, learning, and reward processes); higher metabolic levels or more activity in other parts of the brain (e.g. thalamus for cleaning and checking)
Psychological factors of OCD
higher attention to disturbing material relevant to the obsessions, thought-action fusion, self-blame, attempts to suppress thoughts increase them, conditioning (behavioral theory)
Thought-action fusion
believing that the mere thought of a bad action or event will influence them happening
How does the behavioral theory explain OCD?
(1) the initial fear or obsession is classically conditioned; (2) compulsions negatively reinforce obsessions through operant conditioning; (3) the stimulus or feared object is generalized into a broader category
Social factors of OCD
social reinforcement or accomodation of obsessions (e.g. telling the person with OCD to avoid the feared object or removing it from their surroundings)
Orbitofrontal cortex
responsible for the role of emotion in reward/punishment anticipation
How do people with OCD experience over-importance of thoughts?
believing it’s possible and necessary to control their thoughts; cognitive distortions (e.g. catastrophic thinking) that are neutralized by doing compulsions; thought-action fusion
Biological symptoms of OCD
increased activity in the basal ganglia (associated with severity of OCD) and orbitofrontal cortex (OFC)
Psychological presentation of OCD
over-importance of thoughts, overestimation of threat (an inflated sense of personal responsibility), perfectionism (doing compulsions perfectly), intolerance of uncertainty
4 kinds of cognitive distortions
black and white thinking, catastrophizing, threat overestimation, mind-reading
Social presentation of OCD
the content of obsessions and whether or not OCD is deemed a problem that needs to be treated depends on one’s culture
Basal ganglia
responsible for the control of motor behavior, learning and reward
Biological treatment of OCD
antidepressants like SSRIs or cingulotomy or surgical correction for extreme cases
Defining feature of mood disorders
extremes of emotion
Cingulum
responsible for limbic system communication; emotional force is decreased when it’s removed through cingulotomy
Psychological treatment of OCD
behaviorally through exposure and response prevention or ERP (reduces compulsions); cognitively by challenging maladaptive thinking patterns
Social treatment of OCD
behavioral change in family/support system by stopping accomodation and gradual/low-intensity exposure to feared object
3 kinds of unipolar depressive disorders
major depressive disorder (MDD), chronic/persistent depressive disorder (PDD), double depression
Extreme emotions experienced in depression and mania
profound sadness and dejection in depression; intense and unfounded elation in mania
2 types of mood disorders
unipolar (only depressive episodes) and bipolar (depressive and manic episodes)
2 main features of major depressive disorder
sad/depressed mood (low 5-HT)and loss of interest/pleasure (low dopamine); need at least 1
Accompanying features of MDD
sleep difficulties, lethargy or agitation, psychomotor retardation (low NE), appetite problems and weight fluctuations, loss of sexual desire, extreme fatigue, unfounded feelings of worthlessness and guilt (low 5-HT), difficulty concentrating, recurrent thoughts of death or suicide (low 5-HT)
Prevalence of MDD
~11% lifetime prevalence and ~4.5% 1-year prevalence with a sex ratio of 2:1 (women:men)
How many depressive episodes do people with MDD experience and for how long?
~80% experience more than 1 episode with an average number of 4 episodes and an average duration of 3-5 months (12% of episodes last more than 2 years)
Kindling hypothesis
each episode makes you more likely to have another one
Persistent depressive disorder (PDD)
chronic low-grade depression lasting for at least 2 years (average duration of 4-5 years) with intermittent normal moods
Double depression
when major depressive episodes are superimposed on PDD
Biological factors of MDD
~35% heritability with 3x higher risk of development when 1st degree relatives have MDD and as a reaction to high levels of stress; dysfunctional serotonin
Heritability
estimate of the likelihood of a disorder happening based on genes; not causal
How is dysfunctional serotonin associated with MDD?
linked to one’s temperament (neuroticism); makes a person hyperresponsive to aversive stimuli and stress, increasing vulnerability for anxiety (as a diathesis or risk factor) and depression
Permissive theory
serotonin regulates other neurotransmitters (e.g. NE and DA) so when it’s dysfunctional, NE and DA become dysfunctional too
Norepinephrine and dopamine levels during mania vs during depression
high NE and DA in mania; low NE and DA in depression
Biological mystery on effect of SSRIs on MDD
giving someone SSRIs increases serotonin (a biological shift) and neurotransmitters eventually return to homeostasis BUT before symptoms (e.g. mood) improve
In what cases of MDD are low metabolite or serotonin levels found?
more often found in those who have suicidal ideation and behavior, not in those with severe depression
Effect of alleles of the 5-HTT (serotonin reuptake) gene on depression
short or “s” allele lowers 5-HT function and is more likely to lead to depression; long or “l” gene is less likely to lead to depression
Effect of stress on the relapse of depression
high cortisol levels result in a high risk of relapse and eventually, after 4-5 episodes, a depressive episode occurs even without the experience of a stressful event
Changes in brain activity during depression
decreased activity in left PFC and anterior cingulate cortex (ACC), increased activity in right PFC and amygdala
Left PFC
responsible for approach behavior, emotion regulation, and turning off the amygdala alarm
Right PFC
responsible for the avoid behavior, inhibition, and negative thinking
Psychological factors of MDD
beck’s cognitive theory, negative cognitive triad, helplessness and hopelessness theory
Beck’s cognitive theory
recurring cycle between negative interpretations of situations/events and feelings of depression
Evidence of beck’s cognitive theory
people with depression are primed to think negatively, lack a positivity bias, and have greater accessibility of negative content
Negative cognitive triad
having negative views about oneself, the world, and one’s future
Helplessness theory
experiencing an uncontrollable event leads to attributions, which leads to learned helplessness, then emerging depression
Depressive/pessimistic attributional style in learned helplessness
making internal (blaming oneself), stable (long-lasting effect), and global (wide-ranging effect) attributions to negative outcomes
Hopelessness theory
experiencing an uncontrollable event leads to attributions or other cognitive factors, a sense of hopelessness, then emerging depression
How does the hopelessness theory explain the comorbidity between anxiety and depression?
while helplessness leads to anxiety, persistent helplessness and hopelessness leads to depression
Difference between helplessness and hopelessness theories
helplessness theory only has 1 diathesis (a pessimistic attributional style) but hopelessness theory has 2 diatheses (a pessimistic attributional style and a state of hopelessness)
Psychoanalytical theory (Freud)
depression is anger turned inward
Why do more women experience depression (2:1 ratio)?
higher cortisol levels, tendency for rumination, greater emotional importance of interpersonal relationship, exposure to traumatic events/chronic negative events (e.g. sexual harassment)
Rumination
unproductive, repetitive, and passive focus on distress and its possible causes/consequences
Social factors of depression
people who are depressed have a negative effect on others (e.g. become irritable) and alienate themselves from their social support network
Evidence for interpersonal theories of depression
people who are depressed tend to have limited social networks and fewer positive social behaviors, initially elicit sympathy and care then hostility and rejection, be insecure in relationships
Biological treatments for depression
pharmacotherapy (e.g. MAOIs, tricyclics, SSRIs, SNRIs) and light therapy
How long does pharmacotherapy take to work?
3-5 weeks
Light therapy
exposure to a certain amount of full spectrum light at certain times of day; typically used for seasonal depression
Biological treatments for treatment-resistant depression
ECT, TMS, ketamine through IV
Potential benefit and risk of ECT on depression
works quickly when it works but may cause brain fog (confusion and memory loss)
Potential benefit and risk of TMS on depression
non-invasive and less intense than ECT but still relatively new in use
Potential benefit and risk of ketamine on depression
works quickly (blocks NMDA receptors and reduces inflammation) but mechanisms and long-term effects are unclear
ECT vs TMS
electric current induces a seizure; magnetic stimulation in parts of the brain
Psychological treatment of depression
psychodynamic therapy focused on the importance of early loss and one’s attachment to their mother/parent, CBT
Primary vs secondary control in CBT
taking action to change a situation if you have control over it; changing the way you perceive a situation if you have no control over it
What is the gold standard treatment for depression?
behavioral treatment or behavioral activation
Behavioral activation
doing activities that are worth exerting your energy in (e.g. those that give you pleasure and increase your sense of mastery)
Social treatment for depression
interpersonal therapy, family and marital therapy
