clinical

diagnostic issues: severity and duration distinguish mood fluctuations and mood disorders.

MDD: recurrent, episoded between 6-9 months, avg. Last for years sometimes. Most suffer from another comorbid disorder, such as anxiety.

Persistent depressive disorder: chronic low mood, lasting at least 2 years. Less likely to respond to standard depression treatment than episodic.

Bipolar mood disorders: mania is a distinct period of elevated, expansive, or irritable mood, lasting at least 1 week with at least 3 symptoms. Hypomania is a severe form of mania but only 4 days of symptoms.

Bipolar 1: person has a history of 1 or more manic episodes with or without depressive symptoms

bipolar 2: history of 1 or more hypomanic episodes (shorter) with 1 or more depressive symptoms. Can be harder to diagnose than bipolar 1

cyclothymia: chronic but less severe form of bipolar disorder. history of at least 2 years of alternating hypomanic episodes and depression that do not fulfil criteria for major depression.

rapid cycling specifier: 4 or more manic/depressive symptoms/episodes in 12 months. episodes separated by 2 or more months by remission or switch to opposite mood state. Higher rates of disability and lower response to treatment. Need mood stabilizer with antidepressants.

Mood disorder with seasonal pattern/seasonal affective disorder (SAD): characterized by recurrent episodes tied to changing seasons. “phase delayed circadian rythym” means when days are shorter/darker = more drowsy.

Mood disorder with peri or postpartum onset: up to 2 weeks after childbirth, women experience mood swings and feelings of depression, can even lead to psychosis and hallucinations.

peripartum = last month of gestation or first few months after delivery and/or in the postpartum period, which = any time after that.

risk factors for ppo: family history of depression, history of depression, poor marriage, low social support, stressful life events concurrent with, or following childbirth.

premenstrual dysphoric disorder (PMDD): marked affective lability, irritability, depressed mood, anxiety, plus presence of symptoms of loss of interest in activities, concentration difficulties, low energy, changes in appetite and/or sleep, feelings of loss of control, and/or physical symptoms. Five of the symptoms must be present and significantly interfere with woman’s functioning and present for most menstrual cycles in year.

treatment for PMDD: SSRIs and birth control suppressing ovarian cyclicity/contain progestins.

psychodynamic personality theories: dependency and self-criticism are 2 personality patterns that provide a risk for depression.

dependence: rely on relationships for sense of identity, needy, fear abandonment, and feel helpless.

self-critical: fears of failure, self-blame, inferiority and guilt. Develops because of maladaptive parenting and/or traumas early in development. Renders people vulnerable to depression when they face a stressful life event that triggers the personality theme.

cognitive distortions: all-or-nothing thinking, overgeneralization, magnification, jumping to conclusions.

schemas: hypothetical structures in mind containing beliefs about the self, world, and future. Cognitive triad.

Beck’s cognitive model: diathesis-stress model- proposed negative cognitive schemas of depression-prone person remain inactive in mind, and serve as silent vulnerability factors (diatheses) that don’t express until activated/primed by a stressful event. depressogenic schema structure is rigid and tightly interrelated.

interpersonal models: depression leads to deficient social skills, less frequent eye contact, less facial animation, less modulation in tone of voice.

Swann’s theory: negative feedback seeking is tendency to seek out criticism and other negative interpersonal feedback.

excessive reassurance seeking: tendency to repeatedly seek assurance about one’s worth and lovability from others, regardless of whether such assurances have been provided already.

Life stress perspective: stressful life event can trigger a downward spiral into depression. personality and cognitive vulnerability characteristics/diatheses makes some more likely than others to develop depressive or manic episodes.

Genetics: chromosome 17 has the serotonin transporter gene (HTT). alleles of this gene can be short/long. L allele results in greater activity of the gene and in higher function of serotonin in the brain. People with (ss) or (sl) gene show higher rates of MDD in response to stressful life events than those homozygous for long allele (ll).

neurotransmitters: chemical substances manufactured at neuron and released at synapse. they can have excitatory or inhibitory effects, increasing/decreasing firing action potentials.

neurotransmitters in depression: there is a dysfunction in catecholamine norepinephrine (NE) and indoleamine serotonin (5-HT) neurotransmitters. Both are responsible for disturbed sleep, appetite, energy, and activity level. Low NE activity appears to be a key feature of both bipolar disorder and severe unipolar depression.

fewer 5-ht receptors are present in depressed people: means that 5-ht released at a synapse has fewer places to bind on the post-synaptic cell, leading to less action potentials and lower 5-ht neurotransmission.

low levels of serotonin = lower dopamine levels

stress and the hypothalamic-pituitary-adrenal axis: when stressed, brain releases corticotropin-releasing hormone (CRH). Leads to the release of adrenocorticotropic hormone (ACTH) from pituitary gland and release of cortisol from the adrenal gland. chronic stressors result in sustained release of cortisol and a breakdown of negative feedback inhibition of the HPA axis. Prolongued periods of cortisol hyper secretion have been found to kill brain cells and cause permanent damage to the hippocampus.

Pro-inflammatory cytokines in high levels lead to: depression

PET: bipolar and unipolar depression are associated with decreased bloodflow and reduced glucose metabolism in frontal regions of cerebral cortex, particularly on left side. Reverse effect when shift from depression to mania. increased glucose metabolism in depression.

MRI: neural circuits involved in cognitive-emotional deficits of depressed individuals. elevated amygdala activity when rating negative words. Showed possible inability to disengage from negative information. Mood disorder have strong neurobiological bases.

Suicidal ideation: thoughts and plans of death/suicide

suicidal gestures: behaviours that look like a suicide attempt but non life-threatening

suicide attempt: carrying out of a suicide plan, which is unsuccessful but clear intent

risk factors for suicide: being male, Indigenous, untreated mental disorder, low serotonin.

psychological factors for suicide: interpersonal model (high levels of perceived burdensomeness and thwarted belongingness, feeling alone = suicidal ideation)

motivational volitional model of suicide: cognitions of defeat, humiliation, and entrapment in response to stressful life events are motivation for it when motivational moderators are high.

treatment for suicide: CBT and antidepressants, ketamine (hospitalized), therapy

bipolar disorder (CASE): patient has depression diagnosis, followed by temper, tearfulness and lack of sleep. inflated self-esteem, grandiosity, sleep less, excessive involvement in activities that have a high potential for painful consequences, pressured speech, increased psychomotor agitation, distractibility. not attributable to effects of a substance and causing impairment.

heritability of bipolar disorder: very strong genetic contribution to bipolar disorder. 1st degree relatives are 7-15 times more likely to have it. Adoption studies confirm it is genetic, rather than environmental.

anxiety: extreme worry about future events that cause marked impairment in daily functioning

fear: emotion in response to a real/perceived current threat. elicits fight or flight.

panic: extreme fear even though there is nothing to be afraid of (false alarm).

until 1980, anxiety disorders were classified with somatoform and dissociative disorders, called neurosis

Freud: claimed there was a difference between objective fears and neurotic anxiety. Said neurotic anxiety is signal from anxiety to ego that an unacceptable drive is pressing for conscious representation.

Etiology of anxiety: genetics and neuroanatomy

neuroanatomy in anxiety: neural fear circuits begin with registry of sensory information at the thalamus, then sent to amygdala then hypothalamus, then midbrain and finally thr brain stem and spinal cord.

brain stem and spinal cord connect with autonomic and behavioural outputs expressing fear. higher cortical areas aren’t involved, as they extinguish conditioned fear. Instead the subcortical network is aroused and interacts.

the most pervasive neurotransmitter in the brain is GABA, and it is distributed along the neural fear circuit.

benzodiazepines are an anti-anxiety med that operate on GABA.

behavioural causes for anxiety: classical conditioning, two-factor theory, also vicarious learning/modelling of fears, or hearing fear-related info.

cognitive factors of anxiety: Beck and Biases claimed people are afraid because of perceptions they have about the world, future, and themselves.

interpersonal factors of anxiety: anxious parents foster helplessness and uncontrollability in kids, also early ‘anxious ambivalent’ attachment relationship or fear of abandonment.

Barlow’s triple vulnerability claims anxiety is caused by interplay between bio, psyc and interpersonal factors.

Barlow’s ‘alarm theory’: ‘false alarm’ triggered through neural cues from classical conditioning and person may fear internal/external stimuli.

panic disorder: recurrent and unexpected panic attacks, both psychological and physiological symptoms. comorbid with disorders such as depression, substance abuse, and is a common feature of other anxiety disorders.

agoraphobia: anxiety about being in places or situations where it may be difficult to escape or in which they wouldn’t have the help readily available. diagnosed when panic attacks lead to apprehension/worry over having more panic attacks.

Diagnosing agoraphobia: clinical interview, behavioural measurement, psychophysiological tests and self-report indices.

symptom induction test: bring on symptoms of panic to assess severity and find strategy for exposure treatment

psychophysiological tests: heart rate, breathing, blood pressure, and galvanic skin response during panic attack.

etiology of panic attacks: biological (rooted in families) and psychological (misrepresentations of bodily sensations).

specific phobia: fears that cause marked stress and significant disruption to daily life. diagnosis requires anxiety reaction to exposure that is excessive and uncontrollable.

specifiers of phobias: animal type, natural environment type, blood injection-injury type, situational, and other. More likely to have more than one in same category.

nonassociative model of phobias: proposes the process of evolution endowed humans to respond fearfully to a select group of stimuli (Menzies and Poulton 2002).

Biological preparedness model of phobia: people are more likely to fear certain stimuli that represented threats to our species over the course of evolution (Seligman 1971)

disgust sensitivity: degree to which people are susceptible to being disgusted by stimulie

social anxiety disorder: marked and persistent fear of social or performance-related situations. provokes anxiety and panic attacks.

performance only social phobia: fear specific social situations/activities. includes casual speaking, eating or writing in public, or giving formal speeches. diagnosed by interview and self-reporting.

etiology for SAD: genetic predisposition, neuro structures involved in fear recognition play a role, disregulation of neurotransmitters, and negative cognition/judgements about self and others, abnormal processing of social info.

Psychosocial factors in SAD: majority of people were bullied in childhood, exposed to more parental criticism, overprotection and control. Develop lack of confidence and negative self.