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A Intro to Neuro > Mental Illness > Flashcards

Mental Illness Flashcards

1
Q

Neurological vs. psychiatric disorders

A
  • Neurological have organic lesion, single brain area damaged, single cause (e.g. infection)
  • Psychiatric have no organic lesion, CBT can treat to varying degrees
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1
Q

Anxiety disorders

A
  • Encompasses generalized anxiety disorders, OCD, phobias, and more
  • Most common psychiatric disorder
  • Sympathetic activation
  • HPA axis activation
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2
Q

HPA axis

A
  • Involved in release of cortisol (stress hormone)
  • Hypothalamic release of CRH → pituitary release of ACTH → adrenal release of cortisol
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3
Q

How is cortisol measurable?

A

In saliva (when stress increases, cortisol levels increase)

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4
Q

Cortisol relation to glucose

A
  • Cortisol is a glucocorticoid → increases glucose levels in blood, released from adrenal cortex of kidney
  • Binds to glucocorticoid receptors (GCRs) in the body and brain
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5
Q

HPA axis and amygdala

A

The amygdala is involved in emotional response (esp stressful situations), helps combine stimuli to decide if stress response should happen
- Outputs of system activate HPA axis and sympathetic nervous system
- Damage to amygdala decreases stress response
- Inappropriate activation of amygdala has been associated with anxiety disorders

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6
Q

Dysregulation of HPA axis

A

Chronic activation of HPA axis results in chronically elevated cortisol levels → can result in maladaptive changes in HPA axis

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7
Q

Role of hippocampus in HPA axis

A
  • Cortisol interacts with G-protein-coupled receptors on hippocampal cells
  • Hippocampus inhibits activation of HPA axis → can get loss of negative feedback over HPA axis
  • Thus, hippocampal atrophy (decrease in volume) is associated with anxiety disorders
  • High levels of cortisol have been associated with down-regulating birth of new cells (hippocampus is one of few sites of neuronal synthesis) or speeding up death of old cells
  • Electrical activity in PFC (affects amygdala and hippocampus) also associated with anxiety disorders
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8
Q

What happens to the hippocampus during chronic activation of the HPA axis?

a) Increased neurogenesis
b) Atrophy and reduced feedback on the HPA axis
c) Increased activity to counter stress response
d) Overactivation leading to heightened anxiety

A

b) Atrophy and reduced feedback on the HPA axis

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9
Q

Categories of drug treatments for anxiety disorder

A
  • Benzodiazepines
  • Imidazopyridines
  • SSRIs
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10
Q

Response rate to anxiolytic drugs (benzos, etc)

A

High response rate (80%)

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11
Q

Benzodiazepines

A
  • E.g. valium
  • Give immediate response
  • Activate GABA channels (inhibitory), which causes a greater influx of Cl-
  • Ethanol can also bind to these channels → explains why people can sometimes self-medicate with alcohol
  • Labelling with radioactive benzodiazepines demonstrates that brain of person with anxiety disorder (right brain) has lower concentration of GABA receptors (may correlate with intensity of anxiety disorder)
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12
Q

What NT do benzos activate?

A

GABA

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13
Q

Brains of people with anxiety disorders have a ___ concentration of GABA receptors

A

Lower

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14
Q

Imidazopyridines

A
  • Z-drugs
  • Give immediate response
  • Binds to the same site as benzodiazepines and increased Cl- influx but with fewer side effects
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15
Q

Which has more side effects: benzodiazepines or imidazopyridines?

A

benzodiazepines

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16
Q

SSRIs

A
  • E.g. Prozac and tricyclic antidepressants including monoamine oxidase
    inhibitors i.e. MAOIs
  • Give delayed response (6-8 weeks)
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17
Q

CBT for anxiety

A
  • Delayed response
  • Experience dependent plasticity (target particular behavior or deal with specific set of stimuli) → altering learned responses
  • Gold standard therapy
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18
Q

Diagram of GABA-gated CL- channel mechanism

A

Also used to treat insomnia and epilepsy

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19
Q

Which of the following statements about anxiety disorder treatments is TRUE?

A. Benzodiazepines activate GABA channels, leading to an immediate response but carry a risk of addiction.
B. Ethanol binds to the same site as benzodiazepines, which may explain why some people self-medicate with alcohol.
C. Imidazopyridines bind to the same site as benzodiazepines and decrease chloride influx, resulting in fewer side effects.
D. SSRIs, such as Prozac, provide relief for anxiety symptoms but have a delayed response of 6-8 weeks.
E. More than one of the above.
F. All of the above.

A

E. More than one of the above.

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20
Q

Medication and CBT may work complementarily

A

Medications opens
up person’s mind to CBT vs. CBT opens up person to taking medication more regularly

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21
Q

Affective Disorders

A
  • Encompass Major Depressive Disorder (MDD) and Bipolar Disorder
  • High recurrence: Recurs in 50% of cases and 90% after 3 or more episode
  • MDD lifetime prevalence: 6-20% (16.5% according to the NIMH)
  • MDD 12-month prevalence: 6.7% (30.4% of these cases are severe)
  • MDD usually doesn’t last longer than 2 years but chronic course can happen in 17% of cases
  • Somewhat more common in women than men
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22
Q

Phenotype of affective disorders

A
  • No longer responds to surrounding but persists in a state of low mood or inability to feel joy (“anhedonia”)
  • Mood
  • Sleep (too much or too little)
  • Weight/appetite (might eat too much or not enough, lose or gain weight)
  • Self-esteem (sense of worthlessness, guilt)
  • Depressive episodes can come and go but major depression only diagnosed when symptoms have been present for 2 weeks
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23
Q

Monoamine hypothesis of mood disorders

A
  • Disruption in monoamine systems (serotonin and NE)
  • Disfunction can happen a multiple possible levels: synthesis, release, reuptake, breakdown, receptors, 2nd messenger systems
  • Accidentally discovered when blood pressure medication (for people with high blood pressure) targeting norepinephrine (which constricts blood vessels) caused depression
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24
Q

Treatment for mood disorders according to monoamine hypothesis

A
  • Drugs that potnetiate monoamine systems (MAOIs, tricyclics, SSRIs)
  • But immediate rise in transmission takes several weeks to have effects (and drugs that raise NE transmission (e.g. cocaine) are not effective as antidepressants
  • Mood disorder therapies probably promote long-term adaptive changes in the brain, involving alterations in gene expression
25
Q

HPA axis as cause of mood disorders

A
  • Activation affects glands, hormones, receptors, brain areas associated w/stress response
  • May explain comorbidity with anxiety (greater % of people with anxiety have depression compared to general population) b/c HPA axis affects both
26
Q

Monoamine systems and depression - treatments

A
  • Therapies must rectify decreased transmission of monoamines
  • MAO inhibitor: Inhibits monoamine oxidase (enzyme that breaks 5-HT and NE)
  • Tricyclic antidepressants: Inhibit reuptake of 5-HT and NE from cleft
  • Fluoxetine (Prozac): more precise b/c affects reuptake of 5-HT preferentially
27
Q

Why might SSRIs take several weeks to alleviate symptoms of depression?

A. They require that monoamine receptors downregulate first.
B. Their effects are mediated through long-term changes in gene expression and brain plasticity.
C. They initially reduce monoamine levels before stabilizing them.
D. They are not effective until cortisol levels decrease.
Answer: B

A

Answer: B

28
Q

Glutamate hypothesis

A
  • Theory: overstimulation of NMDA receptors leads to MDD and bipolar disorder pathology
  • Monoamine release may affect glutamate signaling in the brain
  • Potential solution: Ketamine works as an NMDA channel blocker
  • So far has been highly successful in patients who have not responded to other treatments
29
Q

Stress-depression connection

A
  • Depression increases cortisol release and adrenal gland size (both can decrease with treatment)
  • Effects of cortisol on brain include changing transcription factors, growth factors, glucocorticoid receptors in hippocampus (this can cause hippocampal cell death)
  • Just like anxiety, leads to hippocampal cell death
  • Stress in early life (even before you are born but also including childhood abuse or neglect) can increase incidence of these disorders
30
Q

Diathesis-stress hypothesis of affective disorders

A
  • “HPA axis is the main site where genetic and environmental influences converge to cause mood disorders”
  • Inserting CRH into animals can cause depression-like symptoms
31
Q

Genes, monoamines, and early childhood experience regulate number of
___ on ___:

A

Glucocorticoid receptors on hippocampus

32
Q

Evidence that genes, monoamines, and early childhood experience regulate number of
glucocorticoid receptors on hippocampus

A

Maternal care increases # of glucocorticoid receptors in rat pups → better negative feedback on HPA axis (so better control over stressors) BUT childhood abuse and neglect can do the opposite i.e. increase risk for depression

33
Q

Which of the following statements accurately reflects the stress-depression connection?

A. Depression increases cortisol release, which can lead to hippocampal cell death and reduced regulation of the HPA axis.
B. Early life stress, such as neglect, decreases glucocorticoid receptor expression in the hippocampus, reducing the brain’s ability to manage stress.
C. Maternal care enhances glucocorticoid receptor expression in the hippocampus, improving stress regulation in offspring.
D. The diathesis-stress hypothesis emphasizes that genetic and environmental factors converge at the HPA axis to influence mood disorders.
E. All of the above

A

E. All of the above

34
Q

Gonadal hormones and stress

A
  • Increase in diagnosis of depression in women between puberty and menopause (levels of estrogen generally higher during this time b/c maturation of follicles → estrogen levels dropping after menopause are correlated with decreased severity and frequency of depressive events)
  • Hormonal supplements and oral contraception can affect mood
  • Link also demonstrated by premenstrual mood effects and postpartum
    depression (after childbirth)
35
Q

ECT (electroconvulsive therapy)

A
  • Only for severe cases not responding to therapy:
  • Reserved for second line of treatment for those with high suicide risk BUT has side effects like disrupting memory
  • Most effective: Have immediate effects
36
Q

Side effects of ECT

A

Memory disruption

37
Q

Side effect of ketamine

A

Psychotic episodes

38
Q

Deep brain stimulation

A
  • More precise way of delivering electrical stimulation (deliver small current in small area of
    brain instead of ECT which puts surface electrodes on scalp) BUT highly invasive
  • Electrical stimulation can actually decrease activity in brain circuits that are chronically
    overactive
  • Related intervention is Vagus nerve stimulation (stimulate inputs/outputs to brainstem)
  • TMS can be directed over brain to search for areas effective in treating people
39
Q

Bipolar disorder

A
  • Characterized by unusual shifts in mood, energy, activity levels, and ability to carry out day-to-day tasks: People can cycle between feeling “normal,” depression, hypomanic, and manic
    ○ Depression state: Similar to unipolar depression/MDD
    ○ Hypomania (“just below manic”): Able to focus on tasks but very high energy
    ○ Manic state: Feeling very “up,” high energy, talking fast, flight of ideas,
    distractibility, increased goal-directed activity doing many things especially participating in risky behaviors (gambling, excessive shopping, risky sexual behavior)
40
Q

Lithium for bipolar disorder

A

Lithium can act as a mood-stabilizing drug
● Effect discovered accidentally: Injecting lithium salts into guinea pigs (during experiment on urine of manic patients) had calming effects
● Lithium depression stops cycling between mania and depression

41
Q

Type I vs. II bipolar disorder

A
  • Type I: manic with/without depression
  • Type II: hypomania always found with depression
42
Q

Schizophrenia

A
  • Name means “split mind” but it is NOT “split personality disorder” (which is called Dissociative Identity Disorder)
    ● May have very strong genetic link: 17% comorbidity in fraternal twins and 50% comorbidity in identical twins (compared to affecting 1% of world population)
    ● Important Definitions: Positive symptoms are abnormal psychotic behaviors not generally seen in healthy people vs. negative symptoms are associated with disruptions to normal emotions and behaviors
    ○ Positive symptoms: Psychosis (hallucinations, delusions), disorganization (being perplexed or overwhelmed, includes disorganized speech), catatonic behavior
    ○ Negative symptoms: Lack of engagement, lack of interest, lack of pleasure, lack of speech, lack of goal-directed behavior, lack of expression of emotion, memory impairment → mood instability from these negative symptoms can sometimes lead to false diagnosis of depression
    ● Cognition is essence of this disorder: Poor performance on Wisconsin Card Sorting (tests prefrontal function, we covered this earlier as a working memory task)
43
Q

Time course of schizophrenia

A
  • Time course suggest that schizophrenia may be a neurodevelopmental disease (has something resembling critical periods)
  • Typically diagnosed in late-teens and early 20’s (positive symptoms are most apparent at this time) but you can go back after diagnosis to realize some pre-psychotic symptoms (ex. misdiagnosis of depression) and premorbid symptoms from further in past
44
Q

Neurobiology of schizophrenia

A
  • Dilated (expanded) lateral ventricles: Accelerated loss of gray matter and loss of white matter around ventricles
  • Hypoactive dorsolateral prefrontal cortex: Less focal activation at left PFC so worse at “prefrontal tasks” (can see by comparing groups), deafferented animals show analogous symptoms
  • Decreased density of synapses in cortex
45
Q

Dopamine hypothesis of schizophrenia

A
  • Due to overactive dopamine system
  • First found because medication that blocked dopamine receptors was helpful
  • Treatment using neuroleptic drugs may take a while (unlike immediate effect seen in anxiety disorders)
  • Certain neuroleptics can cause tardive diskenesia (motor disorders, involuntary movmeents of lips and jaw) → can be avoided by using atypical neuroleptics
    that do not act directly on DA receptors
46
Q

How to avoid tardive diskenesia as an effect of neuroleptics?

A

Using atypical neuroleptics
that do not act directly on DA receptors

47
Q

What is the most important change from blocking dopamine receptors (schizophrenia)?

A

Probably happens in prefrontal cortex (which is involved in schizophrenia)

48
Q

Glutamate hypothesis of schizophrenia

A
  • Due to underactive glutamate hypothesis
  • NMDA receptors in particular
  • Drugs like PCP and ketamine that block NMDA channels produce behaviors similar to schizophrenia
49
Q

According to the glutamate hypothesis, people in schizophrenia have an ___ glutamate system

A

Underactive (NMDA receptors in particular)

50
Q

Other notes on schizophrenia

A
  • Possible protective role of estrogen: Less prevalent in women, less severe in women, later age of onset in women
  • Genes that increase susceptibility are broadly related to neuronal transmission, myelination, metabolic pathways, but not a clear relationship between risk genes and function
51
Q

Development of schizophrenia

A
  • Starts in parietal region → progresses toward frontal region
  • Patients who are medicated have a decreased rate of loss of gray
    matter (as well as severity of symptoms)
52
Q

DMN in schizophrenia

A

Involved in self-referential processing, play hypothesized role in introspection and consciousness, also affected by gray matter loss, include PFC, parietal cortex, cingulate cortex

53
Q

Plasticity in schizophrenia

A
  • In schizophrenic patients, recent study showed dynamic cortical reorganization:
    temporo-limbic and fronto-parietal regions showed decreased thickness
  • Occipital region showed increased thickness
54
Q

What evidence supports the glutamate hypothesis of schizophrenia?

A. Dopamine receptor blockers effectively reduce symptoms.
B. Reduced serotonin levels correlate with symptom severity.
C. Drugs like PCP and ketamine, which block NMDA receptors, mimic schizophrenic behavior.
D. Increased amygdala activity is seen during psychotic episodes.

A

C. Drugs like PCP and ketamine, which block NMDA receptors, mimic schizophrenic behavior.

55
Q

Which of the following will cause an increase in norepinephrine and serotonin in synapses?

a) MAOIs
b) SSRIs
c) Tricyclic antidepressants
d) More than one of the above
e) All of the above

A

d) More than one (SSRIs only affect serotonin)

56
Q

One mechanism thought to play a role in anxiety disorders includes a low density of GABA receptors leading to ___excitable circuits in the cortex

A

Hyperexcitable

57
Q

What mental illness is associated with loss of cortical grey matter?

A

Schizophrenia

58
Q

Deep brain stimulation and transcranial magnetic stimulation of the __________ has been
demonstrated to relieve symptoms of major depression

a) left inferior temporal (IT) cortex
b) left dorsolateral prefrontal cortex
c) right posterior parietal cortex
d) right amygdala

A

b) left dorsolateral prefrontal cortex (DLPFC)

59
Q

Of the following disorders, which affects the highest number of people in a given year?

a) schizophrenia
b) major depression
c) anxiety disorder
d) bipolar disorder (I and II)

A

c) anxiety disorder

60
Q

Tricyclic antidepressants function by ___

A

preventing the reuptake of norepinephrine and serotonin

61
Q

Which mental illness has the strongest genetic cause?

a) depression
b) anxiety
c) bipolar disorder
d) schizophrenia

A

d) schizophrenia

A Intro to Neuro (22 decks)

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