Mood Disorders PDF

Dr. Nicole Kostiuk, R. Psych. What is Mood? — Long-lasting affective state — Less intense than emotions — Inherent variability — Can be regulated — System allows for flexible response to changing conditions — If system is unable to engage proper responses, mood disorders can occur Occur on a Continu...

Dr. Nicole Kostiuk, R. Psych. What is Mood? — Long-lasting affective state — Less intense than emotions — Inherent variability — Can be regulated — System allows for flexible response to changing conditions — If system is unable to engage proper responses, mood disorders can occur Occur on a Continuum Major Depressive Disorder (MDD) Diagnostic Criteria — DSM-5 Criteria — 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 depressed mood or loss of interest/pleasure — — 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). 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 (anhedonia) MDD — — — — — — — 3. Significant weight loss when not dieting or weight gain (e.g., change of 5% or more in one month) or decrease or increase in appetite nearly every day* 4. Insomnia or hypersomnia nearly every day* 5. Psychomotor agitation or retardation nearly every day (observable by others) 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 selfreproach or guilt about being sick) 8. Diminished ability to think or concentrate or indecisiveness, nearly every day* 9. Recurrent thoughts of death, recurrent suicidal ideation, plan may or may not be present, or suicide attempt MDD — — — — — — E. There has NEVER been a manic or hypomanic episode Can range from full to partial remission Can have seasonal pattern Can be peri- or post-partum Severity can range from mild to severe Can include psychotic features (differential schizoaffective) — Delusion and/or hallucinations — — Mood congruent psychotic features: content of all delusions and hallucinations is consistent with the typical depressive themes of personal inadequacy, guilt, disease, death, nihilism, or deserved punishment Mood incongruent psychotic features: content of delusions or hallucinations does not involve typical depressive themes (see above) Persistent Depressive Disorder (AKA Dysthymia) — DSM-5 Criteria — A. Depressed mood for most of the day, for more days than not, for at least two years — B. Presence, while depressed, of two or more: — — — — — — 1. Poor appetite or overeating 2. Insomnia or hypersomnia 3. Low energy or fatigue 4. Low self-esteem 5. Poor concentration 6. Feelings of hopelessness — C. During the 2 year period, the individual has never been without the symptoms in A and B for more than 2 months at a time — D. Never had a manic or hypomanic episode — Phenomenon of “Double Depression” What Causes Depression? — Neurochemistry — Neuroanatomy — Psychology Neurochemical Factors — Mood disorders linked to deficits/abnormalities in monoamine transmitters — Serotonin — Dopamine — Norepinephrine — Glutamate research underway — Major excitatory transmitter in brain — GABA — Major inhibitory transmitter in brain Neuroanatomy of Depression — Anomalies in emotional processing associated with structural and functional brain anomalies in multiple areas — Amygdala — Overactive — Slow return to baseline — Associated with atrophy in select areas — Hippocampus — — Associated with length of illness Site of neurogenesis in adults — ? Contribution to maintenance of depression Subcortical Pathways o Subcortical reward pathways are underactive o Ventral striatum less active o ? Contribution to apathy/lack of motivation o ? Role of basal ganglia o Psychomotor changes Psychological Explanation — Thinking!? — Our solution to everything and the root of all problems — Depression — Anxiety Functional Connectivity of Brain Regions o Default mode network o Generates internal thoughts about the self o ? Role in depression? o Attentional Bias and Executive Dysfunction o Pay more attention to sad stimuli o Inability to control (top-down deficiency) o Negative feedback loop o Attentional bias interferes even more with executive control Presentation and Course — May have single episode, but typically recurrent — One of the most common disorders — Lifetime prevalence of 16.5% — Higher in females (8.5%) compared to males (4.8%) — Can present differently — Highest among those aged 18-25 (10.9%) — Occurs in children and adolescence — Not part of typical aging — Often overlooked — Report more physical manifestations — Medical conditions that cause symptoms — Mistaken for dementia: “pseudodementia” Pseudodementia — Depression is frequently accompanied by cognitive problems — Cognitive difficulties can be so severe that dementia is diagnosed — Especially true in the elderly — Late-onset depression, particularly in a patient with no previous psychiatric history, could be related to underlying neurodegenerative condition — Symptoms would actually improve with proper treatment of mood disorder — Rate of dementia in these patients is 20% per year, even after full recovery from depression — Risk factor for dementia Pseudodementia — Overlap of symptoms makes it hard to distinguish: — Depressed mood/agitation — History of psychiatric disturbance — Psychomotor retardation — Impaired immediate memory and learning — Disturbance in attention, concentration — Impaired orientation — Listlessness and loss of interest — Limitations in self-care MDD Neuropsychological Assessment Results — Most consistent findings include deficits in attention, working memory, executive functions, and retrieval-based memory, with spared recognition memory — Residual cognitive deficits are found in a subset of recovered depressed patients — Intelligence: intact minus effects of attention, w.m., speed — Attention/Concentration: particularly in acute phase sustained attention — working memory — processing efficiency — speed of performance. — — Processing Speed: decreased rxn time — Motivation/lack of urgency — Language: intact — Lack initiation to interact — Visuospatial Abilities: intact — Memory: stereotypic pattern of deficits especially on list- learning Encoding down — Retrieval deficits — Recognition intact — Story recall intact — Treatment Options — Medications — Can take up to 4-5 weeks before fully effective — — Polytherapy is not uncommon Use of augmenting agents like antipsychotics — Neuroimaging suggests — Amygdala responses decreases — Prefrontal responses increase — Neuropsychological deficits mostly resolve — Antidepressants and cognitive therapy working together on different neural levels? — Negative-emotion attentional bias may persist during remission — Is this a change in neural functioning or a long-standing trait that was a predisposing risk factor — Attentional and executive deficits may persist during remission and increase with further episodes — A “kindling” effect Medications — MAOI’s (e.g., Nardil) — Severe interactions with some foods (e.g., alcohol, cheeses) — Not usually prescribed as first-line — Very effective for atypical cases — Tricyclics (e.g., imipramine, amitriptyline) — Inhibit reuptake/reabsorption of serotonin, norepinephrine, and dopamine — Overdose risk Medications — SSRI’s (preferred) (e.g., prozac, paxil, zoloft) — Fewer side-effects — Atypical — Norepinephrine-dopamine reuptake inhibitors — — — — SNRI’s — — — Mild psychostimulant effects Can increase risk of seizures e.g., Welbutrin Selective Norepinephrine Reuptake Inhibitors e.g., cymbalta, effexor Ketamine — — IV infusions and intranasal administration Potential for treatment-resistant depression and acute suicidal ideation Electroconvulsive Shock Therapy — Unilateral or bilateral — 12 treatments — Maintenance Alternative Treatments — 50% may not improve with traditional treatments — Alternative treatments Noninvasive Stimulation — rTMS Invasive Stimulation Treatments Deep brain stimulation Vagus nerve stimulation Therapy — CBT is often “treatment of choice” — What is CBT? — — CBT Triangle Changeways Program common manualized group treatment — — 5 “modules” — 1. Behavioural Activation — 2. The Nature of Stress, Depression and Lifestyle — 3. Thinking about Thinking — 4. Role of Social Life — 5. Relapse Prevention Statistically significant decreases in depression and hopelessness scores from the moderate to mild range at GNCH — Treatment comparison — Both CT and antidepressants equally effective for severe depression (if CT is provided by experienced cognitive therapists) — — — — — — Relapse and recurrence less with CT when medications are discontinued CT has enduring effect Some evidence that combination leads to significantly better outcomes with severely depressed — Other research suggests that combined treatments produce only a nonsignificant effect, relative to CBT alone Driessen, E. & Hollon, S. D. (2010). Cognitive Behavioural therapy for mood disorders: Efficacy, moderators, and mediators. Psychiatry Clinics North America, 33 (3), 537-555 Butler, A. C., Chapman, J. E., Forman, E. M., & Beck, A. T. (2006). The empirical status of cognitive-behavioural therapy: a Review of metaanalyses. Clinical Psychology Review, 26, 17-31. DeRubeis, R. J., Siegle, G. J., Hollong, S. D., (2008). Cognitive therapy vs medications for depression: Treatment outcomes and neural mechanisms. Natural Review Neuroscience, 9(10), 788-796. Bipolar I and II Disorder — DSM-5 Criteria — Bipolar I : — — Bipolar II: — — — A. Criteria have been met for at least one manic episode — * note: does NOT require a depressive episode A. Criteria have been met for at least one hypomanic episode and one major depressive episode B. There has NEVER been a manic episode For both: — The occurrence of the manic /hypomanic 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 Manic Episode — 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 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: Manic Episode — — — — — — — 1. Inflated self-esteem or grandiosity 2. Decreased need for sleep (e.g., feels rested after 3 hours) 3. More talkative than usual or pressure to keep talking 4. Flight of ideas or subjective experience that thoughts are racing 5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli) 6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation 7. 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) Hypomanic Episode — A. Same as for mania, but lasting at least 4 days — — — — consecutively B. Same as for mania C. Episode is associated with an unequivocal change in functioning that is uncharacteristic of the individual when not symptomatic D. Disturbance in mood and the change in functioning are observable by others E. Episode is NOT severe enough to causes marked impairment in social or occupation functioning, or to necessitate hospitalization*** Diagnostic Problems — Bipolar II < Bipolar I — Not supported — Confounds all the research though — Mixed samples — ”Soft” Bipolar — Presence of psychotic symptoms — More severe illness? — Meta-analysis results Neuropsychological Models of Bipolar Disorder — No unifying theory but mix of findings — Too much activity in limbic structures — Attenuated activity in and reductions in size of frontal/prefrontal areas — Reduced connectivity between these areas — Medial-temporal structures — Volume of amygdala and hippocampus was decreaesed — Causes verbal memory problems? — Enlarged lateral and third ventricles in those with psychosis — Similar to schizophrenia Neuroimaging Findings — Increased white matter hyperintensities — Decrease in density of white matter — Could be due to demyelination, atrophy of neutropil, or ischemic-related microangiopathy — Are non-specific — Could mediate neuropsych findings in Bipolar Disorder Genetic Contributions — Temperamental dysregulation “cyclothymic disposition” is core feature of bipolar disorder — Genetic underpinnings — Psychotic disorders aggregate within some families — Abnormalities on chromosomes 13q31 and 22q12 — In bipolar families with significant psychotic symptoms — Mild cognitive dysfunction found in unaffected first- degree relatives and offspring — More pronounced in relatives of Bipolar I compared to Bipolar II Neuropsychological Assessment Results — Occurs across all stages — deficits may precede onset of clinical symptoms — Particularly — Attention — Verbal learning and memory — Executive functions — More severe illness, greater number of episodes, earlier onset of disease = greater neurocognitive decline — Intelligence: intact crystallized — Language: — Variable — Dependent on cognitive task and stage of the disease (e.g., worse in depression) — Visual-spatial — Less severe than other domains — Attention: — Distractibility is primary during mania — Moderate to severe impairments in sustained attention. — Error rates improve in euthymic periods — Due to increased spare processing capacity/resources? — Processing Speed — Moderate to severe impairments — even during euthymic phase Control reaction time cognitive differences between bipolar and healthy controls is reduced — Psychomotor slowing as compensation? — — — Index of available processing capacity; may mediate other cognitive processes Indicates reduction in efficiency of white matter networks that subserve attention — DTI demonstrates tracts within frontal lobes are disarrayed — Memory: verbal learning and recall deficits commonly and consistently identified, regardless of state. Deficits worsen in acute states. — Nonverbal memory deficits also found — — Executive functions: impaired on multiple aspects — Absence of affective symptoms does not equate to full cognitive recovery — In particular verbal memory and executive functions are reliably found in euthymic states — Note: above findings apply to Bipolar I patients — Less is known about bipolar II — Research is equivocal — Also unclear is effects of psychosis Association of Mood and Cognitive Impairment — By definition, during manic episodes patients experience clinically significant cognitive dysfunction — May persist in euthymic periods as well — Changes in cognition in different mood suggests that the cognitive and emotional systems are not completely independent — Interdependent — ? Antagonistic — Cognition declines when brain regions are “deactivated” as attentional resources allocated to process heightened emotion Treatment of Bipolar Disorder — Requires ongoing monitoring and medication adjustment to maintain mood stability — Mood-stabilizing medications — Lithium — — Negative side-effects result in reduced compliance — Toxicity — Weight gain — Cognitive impairments (particularly slowing) Anticonvulsants — — — — Valproic acid Lamotrigine Topamax Tegretol — Atypical Antipsychotics — Especially during acute, severe manic episodes but also for chronic symptom management — Zyprexa and Abilify — Antidepressants — Used to treat depressive symptoms in combination with other mood stabilizers — Used alone can increase risk of mania/hypomania — ECT, VNS, and rTIMS also used to manage symptoms Lithium Pro’s — Volume increases — Hippocampus — Anterior Cingulate — Ventral Prefrontal Cortex — Amygdala, etc. — Increased activity — Prefrontal cortex — Hippocampus/medial temporal lobe — Results in improved executive functions and memory Lithium Con’s — Common complaints/findings: — Slowed processing speed — Psychomotor slowing — Attention/Concentration problems — Short-term memory problems — Verbal fluency decreased — Miss the “high” Bipolar or Medication Side-Effects — Cognitive impairment unlikely to be primary effect of medication — Medication-naïve patients had worse performance — Euthymic, non-compliant patients had worse performance than highly adherent patients — Known cognitive side-effects of some anticonvlusants — Valproic acid — One study found increased risk of 72-95% of dementia — No available treatments for cognitive deficits associated with Bipolar Treatment Compliance — 20-60% are poorly complaint or completely non- adherent — Regardless of phase of illness — Reduced compliance associated with: — More relapses — Increased risk of suicide — Male gender — Residual depressive symptoms — Higher medication side-effects — Substance use disorder Prognosis — Poor — One of leading causes of world-wide disability — Previously believed to have complete/substantial recovery during remission — High rates of relapse — — — — 30-60% report impairments in cognitive, work, or household functioning — — 37% have manic or depressive episode within one year — Even on medication 2/3 will experience multiple relapses Activity changes precede mood changes 7-9 days Sleep changes preceded mood changes 4-5 days ½ experience persistent unemployment Growing evidence of impairment in social cognition — ? Deficits in theory of mind Assessment of Mood Disorders — Assessment — History — Collateral — Observation — Beck Depression Inventory — MMPI-2 — Scales 2 and 9 — PAI — DEP and MAN