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Systems Neuroscience > Mental Illness > Flashcards

Mental Illness Flashcards

1
Q

Who proposed the separation of body and mind?

A

Descartes

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2
Q

What are the two major assumptions of Freud?

A
  1. That much of mental life is unconscious
  2. That past experiences, particularly in childhood shape how a person feels and responds throughout life

Mental illness comes about when the conscious comes into conflict with the unconscious

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3
Q

What is the most common psychiatric disorder?

A

Anxiety disorder

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4
Q

What is a panic disorder?

A

Where sudden feelings of intense terror that occur without warning (panic attacks) repeatedly occur.

Women twice as likely as men to suffer

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5
Q

What is sever anxiety about being in situations where escape might be difficult or embarrassing called?

A

Agoraphobia. Eg. being afraid alone in an open market.

Women twice as likely as men to suffer.

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6
Q

What is obsessive compulsive disorder (OCD)?

A

People that have obsessions (eg. with ideas of being infected) and compulsion (eg. hand washing to address infection).

Usually appears in young adult life and the symptoms fluctuate

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7
Q

What are four hallmarks of the stress response?

A
  • Avoidance behaviour
  • Increases vigilance and arousal
  • Activation of the sympathetic division of the ANS
  • Release of cortisol from the adrenal glands
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8
Q

What mediates the humoral response to stress in the brain?

A

The hypothalamic-pituitary-adrenal (HPA) axis.

This axis is activated by corticotropin releasing hormone containing neurons in the hypothalamus, resulting in the release of cortisol from the adrenal cortex.

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9
Q

How is the HPA (hypothalamic-pituitary-adrenal axis) activated?

A

The amygdala and hippocampus activate it

  • The amygdala becomes active when sensory information related to fear enters the central nucleus of the amygdala, a stress response follows activation. Downstream from the amygdala, the bed nucleus of the stria terminalis activates the HPA axis and the stress response.
  • Hippocampal activation inhibits CRH release from the HPA axis.
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10
Q

How does the hippocampus suppress CRH (corticotropin releasing hormone) release?

A

Numerous glucocorticoid receptors of the hippocampus respond to the HPA system and inhibit CRH release by feedback inhibition. This prevents cortisol levels from getting too high. Chronic stress can cause hippocampal neurons to whither and die in experimental animals, setting off a vicious cycle where stress response becomes more pronounced. This is perhaps how post traumatic stress disorder (PTSD) becomes so insidious.

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11
Q

How can psychotherapy be used to treat anxiety disorders?

A

Through the learning component of fear. Where a patient is exposed to adverse stimuli, to diminish fear response by proving that it’s harmless.

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12
Q

What are medications that reduce anxiety called? How do they act?

A

Anxiolytic drugs, act by altering chemical synaptic transmissions in the brain

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13
Q

Where are two major classes of anxiolytic drugs?

A
  • Benzodiazepines

- Serotonin-selective reuptake inhibitors (SSRIs)

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14
Q

How do benzodiazepines work to reduce anxiety? What are some examples?

A

Benzodiazepines bind to GABA receptors and make them more effective in opening the channel and producing inhibition of the brain, particularly in brain circuits used in stress response. Ethanol (drinking alcohol) and Valium are well known examples of benzodiazepines.

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15
Q

What is Prozac and how does it work?

A

A Serotonin-Selective reuptake inhibitor (SSRI). Can treat mood disorders and anxiety disorders (notably OCD). Serotonin originating from Raphe nuclei (and other places) is secreted all over the brain and modulated by G-protein receptors. The action of serotonin is terminated by uptake, SSRIs act to inhibit reuptake

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16
Q

Which work faster for treating anxiety? Benzodiazepines or SSRIs?

A

Benzodiazepines work almost immediately, SSRIs take weeks.

This implies that immediately having more serotonin activation isn’t immediately benefitting. The nervous system probably adapts to having elevated serotonin action in a way that is anxiolytic. One adaptive response to SSRIs is an increase in glucocorticcoid receptors in the hippocampus, perhaps enhancing feedback inhibition of the HPA axis

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17
Q

What are the 6 symptoms of major depression which must be present everyday for two wakes to make a positive diagnosis?

A
  • Loss of appetite
  • Insomnia
  • Fatigue
  • Feelings of worthlessness or guilt
  • A diminished ability to concentrate
  • Recurrent thoughts of death
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18
Q

What is dysthymia?

A

A milder but longer lasting form of depression. Seldom disappears spontaneously like depression does (in about 4-12 months)

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19
Q

What are the 6 symptoms of manic episodes in people who have bipolar disorder (alternating depression and mania)?

A
  • Inflated self esteem or grandiosity
  • A decreased need for sleep
  • Increased talkativeness or feelings of pressure to keep talking
  • Flight of ideas
  • Distractibility
  • Increases goal-directed activity

Also impaired judgement

20
Q

What is type I bipolar disorder?

A

Manic episodes with or without the depression

21
Q

What is type II bipolar disorder?

A

Characterized by hypomania, where the manic episodes are milder and actually productive. Depression is always associated.

22
Q

What do Monoamine oxidase (MAO) drugs cause?

A

Destroys catecholamines and serotonin, leading to elevation in mood (what?)

23
Q

What is the monoamine hypothesis of mood disorders? How did it come about?

A

Depression is caused by a deficit in one of these diffuse modulatory systems (norepinephrine or serotonin)
- Discovered through monoamine oxidase (MAO) drugs for treating tuberculosis and reserpine (blood pressure drug, caused depression).

24
Q

What are two problems with the monoamine hypothesis of mood disorders?

A
  • Antidepressant action of these drugs takes several weeks to develop, even though they have immediate effects on diffuse modulatory system transmission
  • Drugs that raise NE levels in synaptic clefts, such as cocaine, are not effective as antidepressants.
25
Q

What is the diathesis hypothesis of mood disorders?

A

The HPA axis is the main site where genetic and environmental influence converges to cause mood disorders.

  • Gene disposition
  • Environmental influence (eg. trauma)
26
Q

During depression is it true that the HPA is commonly activated to hyperactivity? What does this cause?

A

True, hyperactivity of the HPA axis from greater amount of CRH secretion cause depression like effects in animals.

27
Q

What are factors in regulating glucocorticoid receptor numbers?

A
  • Genes
  • Monoamines
  • Early childhood experience

This lead researchers to believe that these three things are highly influential in causing mood disorders. (diathesis-stress hypothesis of mood disorders)

28
Q

What does a greater number of glucocorticoud receptors in the hippocampus cause? How are these increased?

A

Causes a greater tolerance for stress later in life. Can only increase number of glucocorticoid receptors early in life, most effectively by providing tactile stimulation from mom.

29
Q

How does electroconvulsive therapy treat affective disorders?

A

Probably by effecting the hippocampus, as memories are usually effected. Relief is normally immediate, so this is a good treatment for suicidal patients. Anaesthesia and muscle relaxants are given to prevent violent behaviours from the induced seizure activity in the brain

30
Q

What are 4 common treatments for affective mood disorders?

A
  • Electroconvulsive therapy
  • Psychotherapy
  • Antidepressants
  • Lithium
31
Q

How to antidepressants work (in a broad sense)?

A

They elevate monoamine neurotransmitters in the brain, the therapeutic effects take weeks to develop though.

32
Q

What are the three types of antidepressants?

A
  • Tricyclides (block reuptake by transporters)
  • Fluoxetine (prozac, inhibits reuptake)
  • MAO inhibitor (inhibits MAO enzyme degradation of NE and serotonin)
33
Q

What does lithium do as a psychiatric treatment?

A

Stabilizes the mood of bipolar patients, both with mania and depression. Lithium prevents the turnover of PIP2, which are generated in response to G protein receptors. Also interferes with adenylyl cyclase and glycogen synthase kinase.

Lithium therefore appears to cause an adaptive change in the nervous system through long term use

34
Q

What are four positive symptoms of schizophrenia?

A
  • Delusions
  • Hallucinations
  • Disorganized speech
  • Grossly disorganized or catatonic behaviour

Positive symptoms reflect the presence of abnormal thoughts

35
Q

What are four negative symptoms of schizophrenia?

A
  • Reduced expression of emotion
  • Poverty of speech
  • Difficulty in initiating goal orientated behaviour
  • Memory impairment

Negative symptoms are those that reflect a loss in normal cognitions

36
Q

What are the types of schizophrenia?

A
  • Paranoid schizophrenia (best outlook)
  • Disorganized schizophrenia (no remmissions)
  • Catatonic schizophrenia (bizarre movements and vocalization)
37
Q

How do shared genes contribute to the risk of developing schizophrenia?

A

As amount of shared genes increases the risk for developing schizophrenia increases. It maxes out at 50% chance for identical twins. This indicates a fairly large genetic factor in developing schizophrenia.

38
Q

What are some biological bases changes that take place in the brains of schizophrenic patients?

A

Loss of brain tissue around the lateral ventricles, making them appear enlarged. Also defects in myelin sheath.

39
Q

What can an overdose from amphetamines cause?

A

Symptoms almost exactly like those of schizophrenics. Suggesting that psychosis might be related to to too much catecholamine (eg. dopamine) in the brain

40
Q

How do neuroleptic drugs treat schizophrenia? What symptoms do they treat?

A

Block dopamine receptors. Treat positive symptoms of schizophrenia.

Can also be used to treat cocaine and amphetamine psychosis

41
Q

What is the dopamine hypothesis of schizophrenia?

A

Psychotic episodes in schizophrenia are triggered specifically by the activation of dopamine receptors

42
Q

What are atypical neuroleptics?

A

Schizophrenia treatments that don’t block dopamine receptors.

43
Q

What is PCP (phencyclidine)?

A

A treatment for schizophrenia by inhibiting NMDA receptors for glutamate (glutamate hypothesis of schizophrenia). Called angel dust on the street

44
Q

What is the glutamate hypothesis of schizophrenia?

A

The disorder reflects diminished activation of NMDA receptors in the brain

45
Q

What side effects do conventional neuroleptics cause? How?

A

They cause Parkinson’s disease like symptoms by effecting the dopaminergic inputs from the substantia nigra to the striatum.

Can also result in tardive dyskinesia, the involuntary movements of the lips and jaw.

Systems Neuroscience (15 decks)

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