PSYC 301: Psychiatric Disorders

Psychiatric Dysfunction

what are motivating factors for classifying psychiatric illnesses?

1) guide treatment choices

2) allow clinicians to communicate

3) serve parties who require diagnosis (insurance, CFA, legal)

4) permit research (causes, treatment, prognosis)

what are the three components that a condition must have to be included

in the DSM?

• atheoretical

• operationalist

• categorical

what are criticisms of the DSM criteria?

heterogeneity of criteria

• level of detail

• overlap

• authority

• comparator (compare to self, norm, or none)

what are normative assumptions?

• evaluation of right or wrong

• ex: ought, should

what is deinstitutionalization?

movement to replace long-stay psychiatric facilities w/ community mental health services

what are historical examples & trends of normative assumptions?

homosexuality was classified as a disorder in DSM-I & -II & removed for DSM-III following gay activist protests at APA annual meetings & pressure from the gay PA

what are historical examples & trends of deinstitutionalization?

• movement started in 1950s & 60s

• w/out support, people w/ mental illness are at higher risk of incarceration (unhoused)

what is the relationship between mental illness and violence?

• in absence of substance use disorder, people w/ mental illness are not more violent than other from their same neighbourhoods

  • controlling for poverty

Psychiatric Dysfunction: Schizophrenia

what is the main criteria that goes into a diagnosis of schizophrenia?

• 2+ of the following, present for a significant amount of time during a 1 month period

• 1 must be (1), (2), or (3):

1) delusions

2) hallucinations

3) disorganized speech (frequent derailment or incoherence)

4) grossly disorganized or catatonic behaviour

5) negative symptoms (diminished emotional expression or avolition)

what must the disturbance affect to qualify for the DSM-5 criteria?

• level of functioning

  • ex: work, interpersonal relations, or selfcare

what must the disturbance show to qualify for the DSM-5 criteria?

continuous signs, persisting for at least 6 months

what must be ruled out to qualify for the DSM-5 criteria?

• schizoaffective disorders

• disturbance is not attributable to physiological effects of a substance or another medical condition

what are positive & negative symptoms of schizophrenia?

• positive: hallucinations &/or delusions

• negative: blunted emotional responses, impoverished content of thought & speech, reduced social motivation

what are hallucinations?

• perceptions w/out sensory cause

  • often auditory - voices, noises, music

  • command hallucinations => high risk of harm (suicide)

what are delusions?

• beliefs that are not realistic or culturally appropriate

  • variable

  • the world is full of hidden signs for me; i am being watched

what are symptoms of cognitive abnormalities?

• impaired working memory & executive function

• impaired source monitoring: tendency to misattribute own actions & thoughts to external causes

what are risk factors for schizophrenia?

• genetics

• urban environment

• 1st or 2nd trimester maternal infection or malnutrition

• perinatal complications

• cannabis or stimulant use

• paternal age > 35 y/o

what are common structural brain changes in schizophrenia?

• widespread decreased grey matter in frontal & temporal cortices

• pronounced thinning of dlPFC (working memory)

what does this volume loss result in?

enlarged ventricles

what is the mechanism of volume loss?

reduction in cell processes (axons & dendrites)

what are structural changes in the prefrontal cortex?

• loss of dendritic spine density

• fewer GABAergic interneurons

what are structural changes in the hippocampus?

• atypical layering structure

• atypical neuron shape

what are functional brain changes in schizophrenia?

abnormal (often hypoactive) frontal & temporal lobes including hippocampus

what is the efficacy of nonpharmacological treatments for schizophrenia?

CBT shown promise for managing positive & negative symptoms when combined w/ medication

what is the efficacy for pharmacological treatments for schizophrenia?

• antipsychotic drugs (positive symptoms)

• less luck in treating negative symptoms

what is the dopamine theory of schizophrenia?

maybe it’s caused by too much activity at dopamine receptors

what are the 3 findings that the dopamine theory is based on?

1) brains w/ parkinson’s have marked dopamine depletion; & antipsychotics produce symptoms that are similar to parkinson’s

2) drugs known to increase dopamine levels (amphetamine, cocaine) produce symptoms of schizophrenia

3) efficacy of antipsychotics are correlated w/ the degree to which it blocks activity at dopamine D2 receptors

what are 3 major problems w/ the dopamine theory?

1) newer “atypical” antipsychotic drugs produce a wide variety of changes in the brain & were just as good as traditional antipsychotics

2) takes 2-3 weeks for antipsychotics to work, yet their effects on dopamine receptor activity are immediate

3) most patients show no significant improvement to the 1st antipsychotic they are given

what is the finding of glutamate hypofunction theory of schizophrenia?

PCP & ketamine can induce negative symptoms & psychosis & act antagonistically upon NDMA receptors

what happens if glutamate signaling becomes abnormal?

can lead to:

1) less GABAergic transmission

2) widespread pattern of too much activity

Bipolar Disorder

what is a depressive state?

new or worsened, daily, for 2 weeks in a row & 5+ of:

• depressed mood

• loss of interest or pleasure in almost all activities

• weight or appetite changes

• sleep changes

• psychomotor changes (agitated or slowed)

• tiredness, fatigue, low energy

• sense of worthlessness or guilt

• impaired ability to think

• recurrent thoughts of death, suicidal ideation, or suicide attempts

what is a hypomanic state?

abnormal, persistent elevated, expansive, or irritable mood & increased goal-directed activity or energy, most of the time for at least 4 days

• increased activity

• persistent mild elevation of mood

• marked feelings of well-being & both physical & mental efficiency

• increased sociability & talkativeness (or increased irritability)

• increased sexual energy

• decreased need for sleep

to what degree does a hypomanic state affect ones functioning?

no severe disruptions of work or result in social rejection & no + symptoms (psychosis)

what is a manic state?

• abnormal, persistent elevated or expansive mood & increased goal-directed activity or energy, most of the time, for at least 1 week

• 3 or more of:

  • inflated self-esteem or grandiosity

  • decreased need for sleep

  • more talkative than usual or pressure to keep talking

  • flight of ideas or subjective experience that thoughts are racing

  • distractibility

  • increase in goal-directed activity or psychomotor agitation

  • excessive involvement in activities that have a high potential for painful consequences

how do mood disturbances affect those in a manic state?

mood disturbance causes marked impairment in social or work life, needs hospitalization, or includes psychosis

what is bipolar I?

• at least 1 major depressive episode

• at 1 event of manic episode

what is bipolar II?

• at least 1 major depressive episode

• at least 1 hypomanic episode

what is the prevalence of BD?

• .6% bipolar I & .4% bipolar II vs. 12.5% MDD

• commonly begins in young adulthood

• potential high impact

what is the life course of BD?

• depressive episode is commonly the 1st mood event

• pre-drome: smaller mood events outside of norm but not yet meet criteria

• after both negative mood & mania has occurred then it’s possible to receive a diagnosis

what is the reward hypersensitivity model of BD?

according to this model, hypersensitive to reward is the trait that predisposes someone to developing BD

what does hypersensitive to rewards mean?

reward system responds very strongly when goals are attained or experiences a reward

according to the hypersensitivity model of BD, what can goal attainment can lead to?

loop: goal attainment => excessive reward state => behaviour or cognitive changes => ultimately (hypo)mania episodes

what happens if goal is not attained?

excessive deactivation of reward pathway => producing depressive state

what is the evidence of the reward hypersensitivity model of BD?

• euthymic individuals w/ BD

• prodromal features for hypomania, mania & depressive episodes

• teens who score high on reward sensitivity are more likely to develop BD in a prospective study
  

what is the evidence for euthymic individuals?

• excessive activity in frontal-striatal reward-related areas in responses to reward-related cues

• make more risky choices than controls (gambling)

what is the evidence for prodromal features of hypomania & mania episodes?

excessive goal setting & increased success expectancies

what is the evidence for prodromal features of depressive episodes?

decreased motivation & goal setting & low self-confidence

what is a structural brain change associated w/ BD?

reductions in gray matter

what is this structural change driven by?

time spent in manic episodes, which are associated w/ neuroinflammation, stress hormones

what are functional brain changes associated w/ BD?

• increased responsiveness in limbic & para-limbic areas

• decreased responsiveness in areas associated w/ cognitive control

what are areas in the limbic & para-limbic system?

• amygdala

• ventrolateral prefrontal cortex (VLPFC)

• ventral anterior cingulate cortex (ACC)

what are areas associated w/ cognitive control?

• dorsal anterior cingulate cortex (ACC)

• dorsomedial prefrontal cortex (DMPFC)

• dorsolateral prefrontal cortex (DLPFC)

what are treatment options for BD?

• mood stabilizers

• atypical antipsychotics

• psychotherapy

what psychotherapy have some evidence for treating BD?

• CBT

• health education

• family-focused

Psychiatric Dysfunction: Executive (Dys)functions

what is the tripartite model of executive function?

• cognitive control of behaviour

• involving prefrontal cortex and/or associated projections

what tests are used to measure executive function?

• judgment tests

• verbal fluency

• luria’s 3 step test

• trail-making or drawing patterns

• clock drawing “10 past 11”

what are the 3 components of the tripartite model of executive function?

1) working memory: holding & mental working w/ info in mind

2) inhibitory control: resisting temptations, not acting impulsively or prematurely, overriding automatic behaviour

3) cognitive flexibility: fluidly changing perspectives or approaches to solving a problem, adjusting to new demands switching between priorities or tasks

what test is used for working memory?

• digit or pointing span

• how many can you rememeber?

what are 2 tests used for inhibitory control?

• stroop: blue, yellow, red, black, purple (words written in different colours)

• flanker task: arrows are either congruent, incongruent or neutral (point in same, different direction or 1 arrow)

what are 2 tests used for cognitive flexibility?

• wisconsin card sort (must adapt to changing rules)

• trail-making w/ alternation (A, 1, B, 2, C, 3)

what are higher order “executive functions”?

3 core components depend on:

• planning

• organizing

• multi-tasking

• self-awareness

• regulating emotions

• inhibiting inappropriate behaviour

• motivation

• concentrating

what is neuropsychiatric syndrome of frontal lobe damage?

abulia

what is abulia?

• lack of motivation

• return to primitive reflexes

• ultilization behaviour

  • ex: seeing glasses in front & putting them on even though they already have glasses on

what are 3 frontal-subcortical loops marking subcortical differences between the dorsolateral, orbitofrontal, & medial cortex?

• executive dysfunction

• apathy

• disinihibition

which is area is linked w/ executive dysfunction?

dorsolateral prefrontal cortex

what sub-cortical regions are involved in executive dysfunction?

• dorsolateral prefrontal cortex

  • caudate nucleus

    • globus pallidus

      • thalamus

which area is linked w/ apathy?

medial frontal cortex

what sub-cortical regions are involved in apathy?

• medial frontal cortex

  • nucleus accumbens

    • globus pallidus

      • thalamus

which area is linked w/ disinhibition?

orbitofrontal cortex

what sub-cortical regions are involved in disinhibition?

• orbitofrontal cortex

  • caudate nucleus

    • globus pallidus

      • thalamus

what does dysfunction in the orbitofrontal circuit lead to?

• impulsivity

• socially inappropriate

• poor safety judgment ex: walking out into traffic w/out looking

• difficulty evaluating anticipated rewards & punishments

• don’t “learn from mistakes” due to diminished guilt & regret

what does dysfunction in the dorsolateral circuit lead to?

• distractible

• disorganized

• perseverative: completing action using old rule even when it no longer applies

• difficulty multitasking

• poor time management & prioritization

what does dysfunction in the medial frontal circuit lead to?

• emotion dysregulation: loss of empathy & blunted affect

• apathy (loss of “get up & go”)

• rigidity in thoughts & actions, poor ability to learn from mistakes

• problems thinking ahead, sequencing steps for a task

what are major symptoms of ADHD?

• extreme inattention

• hyperactivity

• impulsivity

how was ADHD previously characterized & how has it changed since then?

• initially characterized as a problem of “moral control” => pathologizing not conformity

• diagnosis intersects w/ societal norms (not just bio) => mismatch between environment & personality

  • shaped by culture & how society thinks we “should” behave, learn, perform

what are trends influencing ADHD diagnoses?

• younger children in a classroom => more likely to get diagnosed (environmental mismatch)

• rapid rise in adult diagnoses => changing social norms & diagnostics

• symptom presentation vary w/ gender => girls underdiagnosed

  • externalizing behaviours (aggression) more likely to receive diagnosis => typically more common in boys

  • dysfunction is more severe in girls bc the point where they receive a diagnosis is when they are really struggling

what is the neurobiology of ADHD?

reduced activity & volume of PFC

what is the evidence supporting reduced activity of PFC?

those w/ ADHD don’t show orbitofrontal activity when withholding a response

• planning & withholding task

what is the evidence supporting reduce volume of PFC?

slower maturation of PFC

• normal cortical thinning is slower between ages 8-17

• but in ADHD PFC is already thinner which is correlated w/ hyperactivity / impulsivity

what is the dual-pathway model of ADHD?

• executive circuit (dysfunction: inattention)

  • dlPFC & caudate

• reward circuit (dysfunction: lack of motivation)

  • OFC, ACC, & nucleus accumbens

    • explains differences in symptoms presentation bc people can have either 1 or 2 or both

what are treatments for ADHD?

• evidence that those w/ ADHD have a hypoactive dopamine system

  • medication that act upon dopamine & norepinephrine systems in PFC & subcortical structures to inhibit reuptake