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Biopsychology > Lecture 10 > Flashcards

Lecture 10 Flashcards

1
Q

What are the myths surrounding mental illness ?

A
  • People with mental illness are violent and dangerous
  • People with metal illness are poor or less intelligent
  • Mental illness is caused by a personal weakeness
  • Mental illnes is a single, rare disorder
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2
Q

How is mental illness complicated ?

A
  • Comorbidities are common
  • Many people who fit a diagnosis for one mental disorder may partially fit the diagnosis for another as well
  • People may not completely match any specific diagnosis
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3
Q

What is schizophrenia ?

A

a split between the emotional and intellectual aspects of experience

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4
Q

What was schizophrenia previously called ?

A

Dementia Praecoz (“premature dementia”)

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5
Q

What are the positive symptoms of schizophrenia ?

A
  • Disorganized speech
  • Disorganized behaviour
  • Hallucination
  • Delusions
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6
Q

What are the negative symptoms of schizophrenia ?

A
  • Flattened affect and or anhedonia
  • Speech minimized
  • Lack of motivation
  • Social withdrawl
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7
Q

What are the cognitive symptoms of schizophrenia ?

A
  • Poor sustained attention
  • Low psychomotor speed/catatonia
  • Poor learning and memory
  • Poor abstract thinking/problem solving
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8
Q

What symptoms fall under complex syndrome ?

A
  • Psychosis
  • Emotional/Affective symptoms
  • Motivtional impairment
  • Cognitive impairment
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8
Q

What are the types of schizophrenia ?

A
  • Paranoid
  • Catatonic
  • Disorganized
  • Residual
  • Undifferientiated
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9
Q

What is paranoid schizophrenia ?

A

Frequent visual and auditory hallucinations/delusions, disprganized speech, trouble concentrating, and significant behavioural impairment

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10
Q

What is catatonic schizophrenia ?

A

Excessive movement (catatonic excitement), or decreased movement (catatonic stupor)
* inability to speak (mutism). mimicking owrds (echolalia) and mimicking actions (echopraxia)
* Rarest

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11
Q

What is disorganized schizophrenia ?

A

Disorganized behaviours and nonsencial speeach in the absence of delusions and hallucinations
* Most common

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12
Q

What is residual schizophrenia?

A

Previously diagnosed - no longer experiencing prominent symptoms
* still exhibited symtoms including a flattened affect, psychomotor difficulties, and disturbed speech

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13
Q

What is undifferentiated schizpphrenia ?

A

Symptoms fit into more than one subtype of schizophrenia

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14
Q

What is the prevalence of schizophrenia ?

A
  • Prevelance higher in men than women (7:5 ratio)
  • More prevenlent in prosperous countries than 3rd world
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15
Q

How is genetics tied to schizophrenia ?

A
  • People with closer genetic relationships have higher concordance for schizophrenia
  • Adopted children studies suggest a genetic role (Prenatal environment of the biological mother cannot be discontinued)
  • Environmental influence, such as family environment, shown to have a role
  • No common genetic variant produces more than small increase in the probability of schizophrenia
  • A few rare genes are known to greatly increase the risk of schizophrenia, mostly by disrupting the development of glutamate synapses or by interfering with the immune system
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15
Q

What does DISC1 control ?

A

Disrupted in schizophernia 1 controls differentiation and migration of neurons in brain development

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16
Q

What is the DISC1 protein important for ?

A

The DSC1 protein is important for neurodevelopment

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17
Q

What has human studies shown regarding gene mutations ?

A
  • High prevalence of “broken copy” in Large Scottish family over 5 generations - development of schizophrenia, bipolar & other mood disorders
  • Meta-analysis confirmed overall association and found strongest estimate in Chinese population
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18
Q

What has animal studies shown on gene mutations ?

A

Mutant mice with no DISC1 in brain stem stem cells show behaviours that mimic schizophrenia

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19
Q

What is NRG1 important for ?

A

Neuregulin 1 protein is important for neurodevelopment

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20
Q

What do association studies show regarding gene mutations ?

A
  • Iceland population - NRG1 risk allele doubles the risk of schizophrenia
  • Extended to Scottish, Swedish and Chinese populations
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21
Q

What is NRG1 associated with ?

A

Associated with bipolar disorder and creativity, independent of schizotypal traits

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22
Q

What is the recent popular hypothesis ?

A

Not just one gene, but new mutations in any one of hundreds of genes

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23
Q

What was found regarding microdeletions and microduplications ?

A
  • 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 nognitive function
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24
Q

What is the neurodevelopmental hypothesis ?

A

Suggests abnormailities in the neonatal development of the nervous system leads to mild abnormalities of brain anatomy and major abnormalities in behaviour
* abnormalities could result from genetics or other influences
* Environmental influences later in life aggravate the symptoms

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25
Q

What is the season-of-birth-effect ?

A

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

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26
Q

What are some viral infections that a mother can get ?

A
  • Increase cytokines in the mother that impair brain development of fetus
  • Cause fever that damages the fetal brain
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27
Q

What is the research evidence found on viral infections and schizphrenia ?

A
  • 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 epidemics
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28
Q

What are the risk factors falling under the neurodevelopmental hypothesis ?

A
  • Poor nutrition of the mother during pregnancy
  • Premature birth
  • Low birth weight
  • Complications during delivery
  • Extreme stress of mother during pregnancy
  • Immunological rejection
  • Other infections during pregnancy
  • Postnatal stressors
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29
Q

What is the two-hit hypothesis ?

A

Schizophrenia is the result of a combination of a genetic predisposition and impacts from the environement in prenatal/neonatal development, later in life, or both

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30
Q

What are the brain abnormalities tied to schizophrenia ?

A
  • Enlarged lateral ventricle and prominent sulci
  • Decreased tissue cerebral gray matter
  • Smaller PFC and hippocampus
  • Less gray matter and white matter
  • Reduced cortical connectivity and activity
  • Glial reductions (glial theory): oligodentrocytes and mylein integrity (DISC1); altererd microglia in temporal and frontal lobes; astrocyte glutamate transporters in PFC
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31
Q

What is the dopamine hypothesis ?

A

Positive symptoms are caused by over-activity of synapses between DA neurons of then VTA and nucleus accumbems and aymygdala (Mesolimbic)

32
Q

What do antipsychotic drugs (chlorpromazine) do ?

A

Antipsychotic drugs block DA receptors
* Block D2 receptors, preventing receptor activation (antagonist)

33
Q

What resembles shizophrenia ?

A

Amephetamine psychosis resembles schizophrenia
* amphetamines (and cocaine) block DA reuptake thus increase DA levels (agonist)
* Amphetamines exacerbate symptoms

34
Q

What is the glutamate hypothesis ?

A

Schizpohrenia due to excessive glutamate

35
Q

Whay occurs regarding the glutamate hypothesis ?

A
  • Mesolimbic pathway overactivated
  • Glutamate neurons fail excite GABA neurons (GABA=Inhibitory)
  • Glutamate neurons fail to excite DA neurons (negative symptoms)
36
Q

What blocks NMDA receptors ?

A

PCP (angel dust) and ketamine (date rape drug) block N-methyl-D-asparate receptors
* they create all symptoms
* this effect is not observed in preadolesence

37
Q

How were schizophrenic patients treated before the mid 1950’s ?

A

Most people with schizophrenia were idenfinitely confined to mental hospitals

38
Q

How are schizophreniz patients treated today ?

A

Effective drugs and outpatient treatment

39
Q

What does Glycine or D-serine do ?

A

Stimulate NMDA receptors and reduce schizophrenic symptoms
* effective in reducing negative symptoms

40
Q

What does Clozapine do ?

A

Atypical antipsychotic -Clozapine- increases release of DA in PFC and decreases DA in nucleus accumbens - addresses all symptoms

41
Q

What is a partial agonist ?

A

Serves as an agonist in regions of low concentration of the normal ligand and as an antagonist in regions of high concentrations

42
Q

What disorders are included in Major Affective Disorders ?

A

Includes Major Depressive Disorder (MDD) and Bipolar Disorder

43
Q

What is MDD ?

A
  • Unipolar
  • Unremetting depression
44
Q

What is Bipolar Disorder ?

A

Cyclical periods of mania and depression
* BP1: full-blown mania
* BP2: hypomania
* Cyclothymic

45
Q

What are the symptoms of MDD ?

A
  • Hopelessness and helplessness
  • Worthlessness. self-hate, guilt
  • Agitation/irritability
  • Weight loss
  • Concentration
  • Fatigue/lack of energy
  • Isolation/withdrawl
  • Anhedonia
  • Sleep
  • Suicidal thoughts
46
Q

What is the concordance b/w MZ and DZ twins regarding MDD ?

A

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

47
Q

What is the monoamine hypothesis ?

A

Depression is caused by low level of activity of one or more monoaminergic synapses
* Dpamine (DA) - anhedonia
* Nonrepinephrine (NE) - (psychomotor symptoms)
* Serotonin (5HT) - (rumination, impulsive thoughts)

48
Q

What is the evidence for the monoamine hypothesis ?

A

Introduction of monoamine oxidase (mao) inhibitors
* Block degradation of monoamines

48
Q

What is the neurology of MDD ?

A

Decreased activity in left and increased activity in right PFC
Amygdala
* 50-70% increased blood flow and metabolism in amygdala
* activity correlated with severity of symptoms
* faulty amygdala - PFC coupling

49
Q

What is ACC ?

A

Attentional processes that regulate cognition and emotion

50
Q

What is the role of neurogenesis in MDD ?

A
  • Hypothesis: Stress exposure decreases neurogenesis in the dentate gyrus of the hippocampus which causes depression
  • Evidence: Treatment with anti0depressant meds alleviate symtpoms 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 deprresive symptoms
51
Q

What do antidepressant drugs do ?

A
  • SSRI and NRIs - enhance 5-HT and NE (respectively) by inhibiting reuptake of the neurotransmitter
  • Tricyclics (TCAS) - Block tranporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after release
  • MAOIs - enhance monoamines by inhibiting MAO
52
Q

What is Trancranial Magnetic Stimulation ?

A

Pulses of magnetic energy focused over a particular surface along the scalp to deactivate neurons

53
Q

What is Electroconvulsive Therapy (ECT) ?

A

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

54
Q

What are the simplest and least expensive treatments for MDD ?

A
  • Moderate-intensity exercise
  • Alter the sleep scheduele

Periodic sleep deprevation sometimes helpful
* Seasonal affective disorder (SAD)

55
Q

What are the symptoms of bipolar disorder ?

A

Depressive symptoms
Manic episodes
* Elevated moof: hyperactive, increased energy, high self-esteem (false), grandoise/delusions
* Racing thoughts
* loud-rapid speech
* Reckless behaviour: binging, poor judgement, promiscuity, spending sprees
* Agitated or irritated

56
Q

What is the concordance among MZ twins for Bipolar Disorder ?

A

Concordance in MZ twins is 80%

57
Q

What is used to treat Bipolar Disorder ?

A

Lithium
* Stabilizes mood and prevents relaspe in mania or depression
* Exact mechanism is unknown, but shows neurotropic effects
* Works by decreasing glutamate activity and inflammation in the brain

58
Q

What is anxiety ?

A

Unfoundded, unrealistic, chronic fear

59
Q

What are the common types of anxiety disorders ?

A
  • Generalized anxiety disorder
  • panic disorder
  • specific phobias
  • OCD
  • PTSD
60
Q

What is GAD ?

A

Excessive uncontrollable anxiety and worry
* Common co-morbity with depression
* Women > Men

61
Q

What are the symptoms of GAD ?

A
  • Fatigue
  • muscle tension
  • restlessness
  • irritability
  • sleep distrubances
  • concentration problems
62
Q

What is Panic Disorder ?

A

Characterized by repeated and unpexcted panic attacks along with worry about future attacks

63
Q

What are the symptoms of a panic attack ?

A
  • chest pains
  • rapid heartbeat
  • shortness of breath
64
Q

What is a phobia ?

A

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

65
Q

What are the three categories of phobia’s ?

A
  • Agoraphobia
  • Social phobia
  • Specific phobias
66
Q

What is agoraphobia ?

A

Fearful of a public place or being outside of the home to the extent that panic attack or extreme embarassment is possible

67
Q

What is social phobia ?

A

A fear of social activity, especially of being scruntinized and embarassed

68
Q

What are specfic phobias “?

A

Exaggerated fear of specific object/situations not covered by the other two

69
Q

What are the risk factors of anxiety ?

A

Genetics
* heratibility of 31.6%
* 2x more likely to develop GAD if parents has a diagnosis
* Candidate geens that code for the monoaminergic system

Personality trait neuroticism, high stress sensitivity
Childhood maltreatment
Chronic or Traumatic Stress

70
Q

How does anxiety look like in the brain ?

A
  • Increased activation of amygdala and decreased activation of PFC while looking at angry faces
  • In helathy 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
71
Q

What are obsessions ?

A

Thoughts, images, or impulses that are intrusice enough to cause marked rise in anxiety

72
Q

What are compulsions ?

A

Ritualistic behaviours or mental acts that are designed to lower anxiety

73
Q

When do obsessions and compulsions begin ?

A

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

74
Q

How does OCD look like in the brain ?

A

Hyperactivity in
* Caudate nucleus (Basal Gnaglia): compulsivity and impulsivity
* Orbitofrontal cortex (OFC): obsessive thoughts
* Anterios cingulate cortex (ACC): emotion regulation

Dysregulation of cortico-basal ganglia-thalamo-cortical (CBGTC) loop
* System of neural circuits

Dysfuntion in 5HT and DA systems

75
Q

What is PTSD ?

A

Occurs in some people after terrifying expeinces

76
Q

What are some symptoms of PTSD ?

A
  • Frequent distressing recollections
  • Nightmares
  • Avoidance of reminders of the event
  • Exaggerated arousal in response to noises and other stimulu
77
Q

How does PTSD look like in the brain ?

A
  • The amygdala is esstential 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
78
Q

How is mental health tied to intelligence ?

A

Higher rates of mental illness in individuals with
* High IQ
* Artists
* Scientists
* “Geniuses”

Biopsychology (7 decks)

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