week 13 Flashcards

1
Q

What are some myths around mental illnesses? And what is true?

A

People with mental illness are violent and dangerous
More likely to be a victim
People with mental illness are poor or less intelligent
Most ppl with mental illness tend to be about avg, in intelligence
Mental illness is caused by a personal weakness
Not ture
Mental illness is a single, rare disorder
Not a single disease, many subcategories

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2
Q

How does Walter Cannon understand Fight or Flight?

A

Fight or flight response is a physiological response to an acute threat

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3
Q

How does Hans Selye explain “stress”? And what is General Adaptation Syndrome?

A

“Stress” is a non-specific physiological response to demand made on the organism
General Adaptation Syndrome; provides an outline of the htee difference stages in which an organism may go through when exposed to prolong periods of stress, 3 phases; alarm, resistance and exhaustion

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4
Q

Describe the 3 phases of genera l adaptation Syndrome.

A

alarm; heart rate and blood pressure rise, manage what the threat is
resistance ; maintain high level heart rate and blood pressure, survive
exhaustion; all resources are depleted

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5
Q

How does Richard Lazarus understand stress? And what is Transactional Model of Stress?

A

Stress is experienced when one perceives that demands outweigh resources
Transactional Model of Stress: three process; primary appraisal (appraise environment, is it a pos. or neg. situation? A threat?), secondary appraisal (how am i gonna cope with this situation?) third appraisal (is this working?)

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6
Q

How did Bure McEwen explain the biological parameters of managing a changing environment?

A

Allostatic Load is the wear and tear of the organism due to repeated allostasis
Allostatic Load Index: Neuroendocrine, cardiovascular, metabolic, immune

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7
Q

What is the difference between acute and chronic stress? And Absolute and relative Stress?

A

Acute (good stress, to ensure survival, able to habituate to stressful situations) vs. Chronic Stress (unable to habituate)
Absolute(we would respond similarly e.g., car crash) vs. Relative Stress (singulalry responsing, e.g., neg. Self talk)

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8
Q

What is Chronic Stress associated with?

A
Cardiovascular disease
Metabolic disorder
Poor Sleep
Depression
Anxiety
Cognitive impairment
Accelerated biological aging
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9
Q

What was Schizophrenia originally called? and what was it orgnailly thought to be?

A

Originally called Dementia Praecox (Emile Kraepein, 1883).
Was Seen as cognitive deterioration
We know its not dementia now

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10
Q

Who coined the term Schizophrenia? and how did he explain it?

A

Schizophrenia “Split mind”, a split between the emotional and intellectual aspects of experience (Eugen Bleuler

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11
Q

Are the symptoms of Schizophrenia the same across all types of Schizophrenia? Are the symptoms immediate? Is the prevalence higher in men or women? And is it easy to diagnose?

A

Symptoms vary, depending on type of schizophrenia you have.
Symptom onset is gradual and insidious.
Prevalence higher in men than women (7: 5 ratio)
Difficult to diagnose – need for differential diagnosis

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12
Q

What are Positive Symptoms(should be absent) of Schizophrenia?

A

Disorganized speech
Disorganized behavior
Hallucinations
Delusions

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13
Q

What are Negative Symptoms: (expect to see but not shown) of Schizophrenia?

A

Flattened affect and /or anhedonia
Speech minimized
Lack of motivation
Social withdrawal

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14
Q

What are Cognitive Symptoms of Schizophrenia?

A

Poor sustained attention
Low psychomotor speed /catatonia
Poor learning and memory
Poor abstract thinking and problem solving

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15
Q

What is Complex Syndrome in respect to Schizophrenia?

A

Psychosis
Emotional/Affective Symptoms
Motivational impairment
Cognitive impairment

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16
Q

Who is Louis Wain?

A

Around his 50s his paintings started to take this delirious turn when we started to show signs of Schizophrenia, paintings started to look less and less like cats

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16
Q

What are some Etiological Theories of Schizophrenia?

A

Genetic Theories
Twin studies
Adoption studies
Gene mutation

Neurodevelopment Hypotheses
Seasonal effects
Neurology of Schizophrenia

Dopamine & Glutamate Hypothesis
looking at chemical imbalance in brain

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17
Q

What does utero environment tell us about Schizophrenia?

A

Assuming that Schizophrenia plays a part in the utero environment b/c twins have the highest risk of developing Schizophrenia
Monozygotic twin with the same placenta(monochronic) vs. two different placentas (diachronic) has a higher association of risk of developing Schizophrenia

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18
Q

What happens in the Study (Tienari et al 2004)?

A

Finnish National Sample: Investigated adopted offspring of mothers with and without schizophrenia
Study Design: 21-year follow-up
Measured family environmental factors
Question: What is the contribution of family predisposition (genetic risk) vs. environment (adoptive rearing) on development of schizophrenia?
Study Results: Decreased risk of diagnosis in predisposed kids living on healthy environment vice versa for unhealthy environment

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19
Q

What is DISC1 protein important for?

A

DISC1 protein is important for neurodevelopment

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20
Q

What Animal studies show the mutations of DISC1 protein in people with Schizophrenia?

A

Animal studies:
Mutant mice with no DICS1 in brain stem cells show behaviors that mimic schizophrenia
Down regulation of DISC1 in dentate gyrus leads to schizo-typo behaviors
Transgenic mice expressing DISC1 mutation display enlarged lateral ventricles

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21
Q

What is Neuregulin 1 (NRG1 ) important for?

A

Neuregulin 1 protein important for neurodevelopment

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22
Q

What is the association study between Neuregulin 1 (NRG1 ) and Schizophrenia?

A

Association studies:
Icelandic population - gene doubles the risk of schizophrenia (Steffanson et al., 2002)
Extended to Scottish, Swedish and Chinese populations (Li, Collier He, 2006)
NRG1 also associated with creativity, independent of schizotypal traits (Kéri, 2019) Yayoi Kusama

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23
Q

What is a Recent popular hypothesis about Schizophrenia regarding genes?

A

Recent popular hypothesis: not just one gene, but new mutations in any one of hundreds of genes

Microdeletions and microduplications
Found in 15% schizophrenia patients; 20% if onset before 18 years. Compared to 5% in control group.
Not random, but selective for genes that are important for production of proteins involved in neurodevelopment and cognitive function

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24
Q

What is the Neurodevelopmental Hypothesis?

A

The neurodevelopmental hypothesis suggests abnormalities in the neonatal development of the nervous system leads to mild abnormalities of brain anatomy and major abnormalities in behavior
Abnormalities could result from genetics or other influences (e.g., intrauterine environment)
Environmental influences later in life aggravate the symptoms ?( eg.,high school or uni)
E.g., onset after stress
Risk of schizophrenia by population density (e.g., big vs small city)
more prevalent in high-density cities

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25
Q

What is Season-of-birth-effect onto schizophrenia?

A

Babies born in late winter and early spring months are at higher risk of “positive” schizophrenia

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26
Q

What infects in the mother can lead to a development of schizophrenia?

A

Increase cytokines in the mother that impair brain development of fetus
Cause fever that damages the fetal brain

Research evidence:
Babies born from mother who contracted flu in 1st trimester 7x more likely to develop schizophrenia
Increased schizophrenia rates among people born 2-3 months after major influenza epidemic

27
Q

What are Risk factors that increase the likely hood of developing schizophrenia?

A

Poor nutrition of the mother during pregnancy
Premature birth
Low birth weight
Complications during delivery
Extreme stress of mother during pregnancy
Immunological rejection e.g., Rhesus factor(Rh) incompatible
Other infections during pregnancy (Toxoplasma gondii)
Postnatal stressors

28
Q

how is brain of people with schizophrenia different from a healthy brain?

A

Enlarged lateral ventricle and prominent sulci
Decreased tissue - cerebral gray matter
Smaller cell bodies in PFC and hippocampus
Reduced cortical connectivity and activity
Glial reductions (glial theory) : oligodendrocytes and myelin integrity (DISC1); altered microglia in temporal and frontal lobes; astrocyte glutamate transporters in PFC
Brain “insults” may not be apparent until later
- clear effect of injury is not prevalent till later

29
Q

What is the Dopamine Hypothesis?

A

Dopamine Hypothesis: comes from drug studies that showed that antipsychotic effects of certain drugs has an effect of patients with schizophrenia, decrease positive symptoms
positive symptoms are caused by over-activity of synapses between DA neurons of the ventral tegmental area and nucleus accumbens and amygdala (Mesolimbic)

30
Q

How do Antipsychotic drugs effect the brains of people with Schizophrenia?

A

Antipsychotic drugs (chlorpromazine) block DA receptors
Block D2 receptors, preventing receptor activation (antagonist)
amphetamine psychosis resembles schizophrenia
Amphetamines (and cocaine) block DA reuptake thus increase DA levels (agonist).
Amphetamines exacerbate symptoms

31
Q

What effect does positive symptoms have on DA?

A

Hyperactivity of DA projections to nucleus accumbens from VT.
Amphetamines exacerbate symptoms.

32
Q

What effect does Negative & Cognitive symptoms have on DA?

A

Hypofrontality of DA activity of the (dorsolateral) PFC

Perform poorly on neurocognitive tests that are sensitive to frontal lobe damage.

33
Q

How are Positive and Negative/Cognitive Symptoms linked in Schizophrenia?

A

Evidence indicates these symptoms are linked—prefrontal hypoactivity causes hyperactivity of mesolimbic dopaminergic neurons
Glutamate hypothesis: Schizophrenia due to under-stimulation of glutamate receptors.
PCP (angel dust) and ketamine (date rape drug) create all symptoms
This effect is not observed in preadolescence

34
Q

What are treatments of Schizophrenia?

A

Glycine or D-serine stimulate NMDA receptors and reduce schizophrenic symptoms – namely, effective in reducing negative symptoms
Atypical antipsychotic - Clozapine- increases release of DA in PFC and decreases DA in nucleus accumbens - rids of all symptoms
Partial agonist: drug has very high affinity for a particular receptor but activates that receptor less than the normal ligand does; serves as an agonist in regions of low concentration of the normal ligand and as an antagonist in regions of high concentrations

35
Q

What are some Major Affective Disorders?

A

Includes Major Depressive Disorder (MDD) and Bipolar Disorder

MDD (unipolar): unremitting depression
Bipolar: cyclical periods of mania and depression

BPI: full-blown mania
BPII: hypomania

36
Q

What are sympotoms of MDD?

A
Hopelessness and helplessness
Worthlessness, self-hate, guilt
Agitation/ irritability
Weight loss
Concentration
Fatigue/lack of energy
Isolation/withdrawal
Anhedonia
Sleep
Suicidal thoughts
Females> Males
37
Q

What are Etiological Theories of MDD?

A

Genetics
Chemical Imbalance
Neurogenesis, neurology
Neurology of MDD

38
Q

What do twin studies and gene mutations show about MDD?

A

Concordance in MZ twin is ~ 65% vs 13% in DZ twins

Serotonin transporter gene (s/l allele)
2 copies of s allele higher chance of developing MDD

Gene-Environment Interaction
Being in a stressful environment increases MDD along with the short allele)
Increase in developing MDD when you have both an allele and a lot of stressful events

39
Q

What is the Monoamine Hypothesis?

A

depression is caused by low level of activity of one or more monoaminergic synapses
Dopamine, NE, 5HT

40
Q

What is Depletion Studies? tryptophan or tyrosine

A

Deplete levels of a certain neurotransmitter by depleting the precursor.
Tryptophan depletion precursor to serotonin
Tyrosine depletion precursory to catecholamine

Study: Delgado et al 1999
3 groups: SRI responders; NRI responders; healthy controls
Depleted of tryptophan or tyrosine

SSRI group:
depletion of Tryptophan lead to increase of depression symptoms
Depletion of Tyrosine lead to no return of depression symptoms

NRI group:
Depletion of Tryptophan no impact on symptoms
Depletion of Tyrosine lead to return of depression symptoms

Depression has underlying mechanisms

41
Q

What is the role of Neurogenesis to MDD? And what is Glucocorticoid cascade hypothesis?

A

Hypothesis: Stress exposure decreases neurogenesis in the dentate gyrus of the hippocampus which causes depression. (Glococorticoid cascade hypothesis)
Glucocorticoid cascade hypothesis: through chronic exposure distress, this has a neurotoxic effect on cells of the hippocampus can lead to depression or cognitive impairment

Evidence: Treatment with anti-depressant meds alleviate symptoms at the same time that they facilitate neurogenesis in the rodent HC

Evidence: Exercise enhances neurogenesis in the HC of both animals and humans and alleviates depressive symptoms

42
Q

What are the brain abnormality prevalent in people with MDD? Amygdala.

A

Decreased activity in left and increased activity in right PFC (recall Emotions chapter)
Amygdala (applies to bipolar too)
50-70% increased blood flow & metabolism in amygdala
Amygdala activity correlated with severity symptoms
Faulty amygdala-PFC coupling

43
Q

What are the brain abnormality prevalent in people with MDD? Subgenual Anterior Cingulate Cortex.

A

Subgenual Anterior Cingulate Cortex important for emotion
Smaller volume in MDD and Bipolar
In healthy adults: 5HT s allele carriers had 25% reduction in sgACC volume
Gotlib et al 2005 - increased activity in depressed patients
Coincides with deep brain stimulation studies

44
Q

What are drug treatments for MDD?

A

Antidepressant drugs
MAOIs - enhance monoamines by inhibiting MAO. Interaction effects with food containing tyrosine
TCAs - enhance monoamines by blocking reuptake of 5-HT and NE
SSRIs and NRIs - enhance 5-HT and NE (respectively) by inhibiting reuptake of the neurotransmitter.
Atypical AD - inhibit reuptake of DA

45
Q

What are some forms of treatment that is a 2nd option for a person isn’t responding to other therapy?

A

Transcranial Magnetic Stimulation
Pulses of magnetic energy focused over a particular surface along the scalp to inactivate neurons.

Electroconvulsive therapy (ECT)
An electrically induced seizure used for the treatment of severe depression.
For Non-responders or suicidal patients
Applied every other day for a period of two weeks
Side effects include memory loss
Memory loss can be minimized if shock is localized to the right hemisphere

Light therapy
May be more effective than certain medications (Lam et al 2016 JAMA)

Sleep Deprivation - mimics SSRIs
Sleep patterns in depression
Typically fall asleep but awaken early; unable to get back to sleep
Enter REM sleep earlier and have an increased average number of eye movements during REM sleep
Reduced time in slow wave sleep
A night of total sleep deprivation is the quickest method of relieving depression
Benefit is brief, and increases sensitivity to pain
As soon as they get a good nights sleeps symptoms will return

46
Q

How does treatment effect the faulty amygdala and PFC connection?

A

Taking SSRIs can calm down the amygdala,
cognitive therapy, strengthening PFC

combination of both therapy’s heavily surpasses symptoms of MDD

47
Q

Treatment in the brain in non-responsive MDD patients

A

Deep brain stimulation for non-responsive depressives
Deep brain stimulation damping the activity of a part of the brain
Mild electrical stimulation through an implanted electrode
Premise: increased activity of subgenual ACC in depressed patients

more effective than medication

48
Q

What are symptoms of Bipolar

A

Depressive symptoms (can last 3 times longer than mania)
Manic episodes
Elevated mood: hyperactive, increased energy, high self-esteem (false), grandiose/delusions
Racing thoughts
loud-rapid speech
Reckless behavior: binging, poor judgment, promiscuity, spending sprees
Agitated or irritated
Females = males; earlier onset than unipolar

49
Q

What are Etiological Theories of bipolar?

A

Genetics
Concordance in MZ twins is 80%

Neurology of Bipolar
Overactive Amygdala (see MDD)
Overactive subgenual ACC (see MDD)
Enlarged lateral ventricles (remember DISC1?

50
Q

What is a first line of treatment for bipolar? and how does it work?

A

Lithium
Stabilizes mood and prevents relapse in mania or depression
Exact mechanism is unknown, but shows neurotrophic effects

Drug shown to works by:
Decreasing glutamate activity
Decreases inflammation in the brain
inflammation is involved in depression

51
Q

What is Anxiety and what are some common types?

A

Anxiety = unfounded, unrealistic, chronic fear

Common types:
Generalized anxiety disorder
Panic disorder
Specific phobias
Obsessive compulsive disorder
Post-traumatic stress disorder
52
Q

What part of the brain is important for imagined fear?

A

Amygdala activates in response to threat in the environment, imitate threat

Bed nucleus of the stria terminalis (BNST): regulates long-term, generalized emotional arousal, fear of something that might happen
BNST activated to impending threat
Sexual dimorphic
Receptors for 5HT and GABA

53
Q

What is a symptom of GAD? What is it common with? How is it more prevalent in and when does it often begin?

A

Excessive uncontrollable anxiety and worry
Symptoms: fatigue, muscle tension, restlessness, irritability, sleep disturbances concentration problems
Common co-morbidity of depression
Women > Men; Onset often begins in childhood or adolescence
Symptoms exacerbated by stress and can wax and wane throughout a person’ life

54
Q

What is Panic Disorder?

A

Characterized by repeated and unexpected panic attacks along with worry about future attacks
Symptoms of panic attack are similar to those of heart attack and include chest pains, rapid heartbeat, shortness of breath, dizziness, etc.
Anxiety sensitivity

55
Q

What is a Phobia?

A

An unreasonable or excessive fear of an object, situation, or activity

Three broad categories:
Agoraphobia: fearful of a public place or being outside of the home to the extent that a panic attack or extreme embarrassment is possible
Social phobia: a fear of social activity, especially of being scrutinized and embarrassed
Specific phobias: exaggerated fear of specific objects/situations not covered by the other two

56
Q

What are risk factors of anxiety disorders?

A

Genetics
Meta-analysis: heritability of 31.6%;
2x more likely to develop GAD if parent has diagnosis
Candidate genes that code for the monoaminergic system
Personality trait neuroticism, high stress sensitivity
Childhood maltreatment
Chronic or Traumatic Stress

57
Q

What parts of the brain have increased activation in people with anxiety disorders?

A

Increased activation of amygdala and decreased activation of prefrontal cortex (PFC) while looking at angry faces
In healthy controls, vmPFC decreases activation of amygdala, but not in persons with anxiety
High levels of anxiety correlates with increased activation of amygdala, insular cortex and anterior cingulate cortex
In anticipation of phobia-related stimuli, patients with specific phobia display enhance activation of the BNST(anticipation of something harming you), ACC(emotion regulation), and insula compared with non-phobia controls (Straube et al. 2007)

58
Q

What is OCD?

A

Obsessions: thoughts, images, or impulses that are intrusive enough to cause marked rise in anxiety

Compulsions: ritualistic behaviours or mental acts that are designed to lower anxiety

Usually begins at ages 6-15 for females and 20-29 for males

59
Q

What parts of the brain are connected to people with OCD?

A
Orbitofrontal cortex
Anterior Cingulate Cortex (ACC)
Caudate Nucleus (Basal Ganglia)
Important for how the brain learns
Cortico-basal ganglia-thalamo-cortical (BGTC) loop
Similar to other movement disorders, PD and HD
Learned behaviour that is motor 
Dysfunction in 5HT and DA system
60
Q

What is PTSD?

A

Post-traumatic stress disorder (PTSD) occurs in some people after terrifying experiences and includes the following symptoms:
Frequent distressing recollections
Nightmares
Avoidance of reminders of the event
Exaggerated arousal in response to noises and other stimuli

61
Q

What is a treatment used for OCD?

A

SSRIs

drugs that increase dopamine, minimized symptoms of OCD

62
Q

What parts of the brain are effected in those with PTSD?

A

The amygdala is essential for the extreme emotional impact that produces PTSD
Dysregulation of HPA-axis: Lower than normal cortisol levels and blunted cortisol response to acute stressor
Smaller than average hippocampus

63
Q

What happened in the Gilbertson et al. 2002: Chicken or Egg, veteran twin study.

A

Is it that PTSD leads to shrinking of the hippocampus or did they begin with smaller hippocampus’
Looks at veteran twins, one twin went ot war the other twin did not. Some vets reports PTSD. MZ twins, brain would be similar.
Results: going to war with a small hippocampus increases the risk of developing PTSD

64
Q

Briefly state the connection between stress and the brain.

A

Predisposition to increase stress reactivity
- genetics/heredity (e.g., 5HT transporter gene)
- personality traits (e.g., neuroticism, very stress reactive)
- neurodevelopment (e.g., HCV)
Environmental challenges
Chronic activation of the stress response
Allostatic Load (wear and tear of our interconnected biological systems, fight or flight)
Wiring the brain/building circuitry

factors that make up our entire and how is that supporting to damaging your wellness

65
Q

What Human studies show the mutations of DISC1 protein in people with Schizophrenia?

A

High prevalence of “broken copy” in large Scottish family over 5 generations - development of schizophrenia, bipolar & other mood disorders (St. Clair et al, 1990)
Meta-analysis confirmed overall association and found strongest estimate in Chinese population (Wang et al., 2018)