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FALL 2023 > Bio Psych Exam #3 > Flashcards

Bio Psych Exam #3 Flashcards

1
Q

Psychopharmacology

A

the study of drugs that affect the nervous system and behavior

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2
Q

What is a drug?

A

An exogenous (made outside of the body) chemical not necessary for normal cellular functioning that significantly alters the functions of certain cells of the body when taken in relatively low doses

(exogenous, low doses, not necessary

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3
Q

Drugs and behavior

A

The changes a drug produces in an animal’s physiological processes and behavior
- Ex: morphine/heroine and other opioids are pain relievers

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4
Q

Drugs have sites of action

A

each drug has a unique effect and a site of action
**Ex: there are specialized receptors for opioids; when molecules of heroin activate these opioid receptors the activity of the neuron changes

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5
Q

Pharmacokinetics

A

what the body does with the drug

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6
Q

Absorption types

A

1) Intravenous (IV) injection - into a vein
2) Intraperitoneal (IP) injection - into space surrounding stomach, liver → usually in animals
3) Intramuscular injection (IM_: vaccines
4) Subcutaneous injection (SC) = into the space beneath the skin
5) Orally = swallow pill
Sublingual - under the 6)tongue
7) Inhalation - smoked
8) Intranasal - snort
9) Topical - into skin

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7
Q

Cocaine absorption

A

1) IV: strong high immediately
2) smoking: similar to IV, less higher
3) snorting: takes a bit to kick in, less high but lasts longer
4) oral: takes an hour to kick in, less high but lasts very long

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8
Q

Oral dose vs. Sublingual

A

1) Oral: Has to go through many steps to get to the brain
2) Sublingual: under the tongue
- Dissolve and can get into the blood system immediately: travel through the capillaries in your mouth
Goes to the brain almost immediately

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9
Q

Distribution of drugs within the body

A

After absorption, the drug distributes to interstitial and intracellular fluids → depends on some physiological factors and physicochemical properties

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10
Q

Body parts with high drug distribution

A

The liver, kidneys, brain, and other well-irrigated (have the most blood supply) organs receive most of the drug

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11
Q

Body parts with low drug distribution

A

Release to muscles, most viscera, and adipose tissue (fat) is slower

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12
Q

What prevents drugs from getting to the brain?

A
  • Blood-brain barrier: a barrier that restricts the indiscriminate access of certain substances in the bloodstream to the CNS
  • A layer of astrocytes that prevents substances in the circulating blood from freely entering the extracellular fluid of the brain
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13
Q

lack of blood brain barrier in:

A

1) Pituitary gland
2) Pineal gland (day/night cycle) → drugs can easily impact sleep
3) Area postrema (vomit toxic substances): in the brain stem

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14
Q

Metabolism

A

Set of reactions and transformations that drugs undergo in the body

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15
Q

Excretion

A

Elimination by the body of residues of drug metabolism

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16
Q

Kidney and excretion

A

Take blood and filter out waste products

**most important excretory organ

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17
Q

Excretion pathways

A

1) Renal (kidneys)
2) Biliary (bile) and fecal (poop)
3) Pulmonary (lungs)
4) Sweat, saliva, and tears
5) Breast milk

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18
Q

Dose response curve

A

Systematically titrate the dose of the drug: see what the effect of the drug is at each dose

Left: The dose is too low to have any therapeutic benefit
Right: point where the dose plateaus → If you give the patient a larger dose, the therapeutic benefit does not increase

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19
Q

The margin of safety on a dose response curve

A

1) The effective dose (orange)
2) Where it becomes lethal (purple) → opioids will stop respiration

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20
Q

Tolerance

A

A decrease in the effectiveness of a drug administered repeatedly
- Once someone has developed tolerance, they will likely show withdrawal symptoms
- Decrease in effectiveness of binding, **receptors become less sensitive or receptors decrease in overall numbers

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21
Q

Sensitization

A

An increase in the effectiveness of a drug that is administered repeatedly
Less common than tolerance
Can get both tolerance and sensitization

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22
Q

Example of sensitization and tolerance

A

Example: movement effects of cocaine show sensitization → repeated use leads to movement disorders./convulsions whereas euphoric effects don’t show sensitization, maybe even tolerance
Can develop tolerance to the euphoria
Can develop sensitization for movement disorders

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23
Q

Agonists

A

A drug that mimics or facilitates the effects of a neurotransmitter on the postsynaptic cell
- a drug that helps the system

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24
Q

Birth of agonists

A

some neurotransmitters need raw/precursor materials

*If we administer more of the precursor, we get more neurotransmitters → our effects are enhanced

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25
Q

Antagonists

A

A drug that opposes or inhibits the neurotransmitter on the postsynaptic cell – harms the system

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26
Q

Antagonist birth

A

Birth: some of the synthesizing steps are controlled by enzymes

*if we neutralize the enzymes with a drug, it prevents the neurotransmitter from being produced (effects blocked)

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27
Q

Competitive binding

A

only one spot (for drug or neurotransmitter)
- Direct agonis or Direct antagonist

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28
Q

Noncompetitive binding

A

It is possible for NT to bind to one part and the drug to bind to another part
- Indirect agonist or Inverse agonist

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29
Q

Psychotropic

A

drugs that impact behavior

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30
Q
A
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31
Q

1) Antidepressants:

A

used to lift mood out of a depressive episode

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32
Q

Antidepressants treat

A

Depression (mainly)
Anxiety disorders
OCD
Panic disorders
Phobias
Bulimia
PTSD

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33
Q

Neurotransmitters involved in mood disorders

A

Dopamine
Noradrenaline
Serotonin

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34
Q

Mood disorders

A

symptomatic issues in people’s affect

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35
Q

Symptoms of mood disorders

A

1) Reduction in positive affect: loss of happiness, loss of interest less and/or energy (nor and dop affected)
2) Increase in negative affect: more depressed mood, more guilt, more anxiety, etc. (nor and serotonin affected)

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36
Q

Types of antidepressants

A

1) Selective serotonin reuptake inhibitors (SSRIs)
2) Serotonin-norepinephrine reuptake inhibitors (SNRIs)
3) Norepinephrine and dopamine reuptake inhibitors (NDRIs)
4) Tricyclics: not used anymore due to side effects / MAOs

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37
Q

mood stabilizers:

A

regulate mood so it doesn’t get too low (depression) or too high (mania)

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38
Q

Types of mood stablizers

A

Lithium:
Mechanism of action not known
Effective for manic episodes and maintaining remission
Helpful for suicide prevention

Anticonvulsants (anti-epileptic):
Uncertain mechanisms of action (might act on GABA)
Effective for acute manic phases of bipolar disorders
Inconclusive for bipolar depression
Many side effects (exhaustion)

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39
Q

anti-anxiety medications

A

high overlap with depression
SSRI and SNRI
Anticonvulsants
Benzodiazepines

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40
Q

Benzodiazepines

A

Depressants and sedatives → feelings of calm drowsiness, GABA agonists
Inhibits the arousal system
People tolerate well but risk of dependence, abuse, and withdrawal reactions
Examples: Xanax, Valium, Ativan
** do not combine with alcohol

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41
Q

Benzodiazepines and alchol

A

Chloride channel: when GABA binds, it opens the channel; why it is inhibitory (lets more negative in)
Alcohol increases GABA binding → chloride channel open for longer
Noncompetitive binding: Benzodiazepines can bind and open the channel even more
Effects summate (level up)

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42
Q

stimulants

A

Usually used to treat ADHD and some sleep disorders

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43
Q

Types of stimulants

A

Amphetamines
Adderall: blocks the reuptake of norepinephrine and dopamine
Ritalin: non-competitively blocks the reuptake of dopamine and noradrenaline
Major potential for abuse
**do not combine with alcohol

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44
Q

typical antipsychotics

A

First generation → 1950s
Generally, they are blocking dopamine at D2 receptors → tight binding
Useful but prescribed out of desperation → high risk of side effects

Ex: Haldol and Thorazine

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45
Q

Psychosis

A

a condition where people lose touch with reality
- Hard to tell what is real and what is not
Delusions and hallucinations

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46
Q

Atypical antipsychotics:

A

Second generation (1990s)
Also blocking dopamine at D2 receptors → use loose binding (not as stuck into the receptor)
Very useful
Side effects are not as bad as typical antipsychotics
Ex: Risperdal, Olanzapine

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47
Q

Order of operations: what should be treated first?

A

1)alcohol/stimulant/substance abuse
2) mood disorders
3) anxiety disorders
4) ADHD
5) nicotine dependence

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48
Q

Substance abuse disorder

A

The compulsion to seek out and take the drug
Impaired control in limiting intake (can not stick to having “just one”)
Persistent despite very clear evidence of overtly harmful consequences
Progressive neglect of alternative pleasures or interests
Relapse → not required for substance use disorder but common

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49
Q

Positive reinforcement

A

something good is added
A positive consequence will increase behavior
Ex: rapid euphoria after taking a drug will increase drug-taking behavior

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50
Q

Neural mechanism of positive reinforcement

A

Synaptic strengthening in the ventral tegmental area (green pathway is strengthened)
VTA: sits next to SN → also dopaminergic
Mesolimbic pathway (from VTA to the ventral striatum (aka nucleus accumbens))

**Ventral striatum (nucleus accumbens) → inital stages of addiction behaviors
Dorsal striatum (caudate + putamen): habit-formation; cue induced

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51
Q

Negative reinforcement

A

A response/behavior is strengthened when you remove/avoid the aversive thing
Ex: feeling of alleviated pain after drug taking will increase drug-taking behavior

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52
Q

Incentive-sensitization theory of substance abuse

A

Wanting and liking are different and mediated by different brain circuitry
- wanting: based on cues from the environment, becomes hyperactive over time (compulsive)
- liking: actual pleasurable impact of the reward consumption

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53
Q

Neural pathways of wanting and liking

A

Striatum (midbrain) to nucleus accumbens
White: liking pathway
Gray: wanting pathway

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54
Q

Risk factors of addiction

A

Age: older adults more likely to abuse certain styles of drugs
Genetics
Environment:
- Adverse childhood experiences (ACEs)

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55
Q

Neurological disorders definition

A

diseases of the central and peripheral nervous system

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56
Q

Mental disorder

A

generally characterized by a combination of abnormal thoughts, perceptions, emotions, behavior, and relationships with others

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57
Q

Psychiatrist

A

able to conduct psychotherapy and prescribe medications and other medical treatments

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58
Q

Psychologist

A

often has extensive training in research or clinical practice
Psychologists treat mental disorders with psychotherapy and some specialize in psychological testing and evaluation
Research PhD

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59
Q

DSM

A

Lists symptom checklists for many disorders → have to see where your symptoms cluster as there is no physiological test for a disorder

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60
Q

What you need for a mental health disorder diagnosis

A

Impairment of functioning that impacts quality of life
Duration → needs to be persistent

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61
Q

Pros of the symptom checklist approach

A

Measures the invisible
Standardization
Can help rule things out

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62
Q

Cons of the symptom checklist approach

A

Wrong way of measuring?
Different clinical presentation earns the same diagnosis → depression can be different for everyone
Is it helpful for understanding?

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63
Q

History of depression

A

-not a diagnosis until the early 1900s
-1930s: benzine was marketed as a treatment for fatigue and mild depression-like symptoms (not depression)
-1940s: ECT to treat depression, don’t know why it works but it is effective
1950s: drugs for anxiety came out but they didn’t really help with depression
Late 1950s: first drugs that do seem to treat depression (meant to treat tuberculosis)

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64
Q

Serotonin hypothesis of depression

A

If we block the reuptake of MAO and people get happier, there must be low levels of these neurotransmitters in people with depression

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65
Q

Is the serotonin hypothesis of depression correct?

A

**NO evidence to suggest that low levels of neurotransmitters cause depression → These drugs do help but this is not the root cause

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66
Q

Neurotrophic

A

related to the growth/survival of neurons

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67
Q

Neurotrophic hypothesis

A

**depression is caused by low lebels of neurotrophins (BDNF) which leads to neuronal loss

increased 5-HT (serotonin) and NE activity at certain synapses → leads to important downstream actions that may underlie the observed antidepressant effects

**metabatropic receptors: downregulation of post synaptic receptor

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68
Q

Downregulation

A

decreased response and/or decreased number of or sensitivity of receptors

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69
Q

BDNF

A

BDNF: brain-derived neurotrophic factor → involved in plasticity for learning and memory
**When stress hormones increase, BDNF decreases - antidepressants may work to reverse this

70
Q

Transcription

A

the process by which a cell makes an RNA copy of a piece of DNA → this RNA copy (messenger RNA, mRNA) carries the genetic information needed to make protein in a cell

71
Q

Why is it hard to treat depression?

A

Other symptoms
Underlying mechanisms
Max efficacy

72
Q

Prescription of drugs

A

SSRIs are usually tried first because they are generally well-tolerated
Choose a low dose (often not even therapeutic) and slowly ramp up
Adequate trial is at least 6 weeks at a therapeutic dose

73
Q

Biorhythm

A

natural rhythm in behavior or a bodily process

74
Q

Circannual biorhtyhms

A

yearly
ex: migration of birds

75
Q

Infradian

A

more than a day
- ex: human menstrual cycle

76
Q

Circadian

A

daily
- ex: human-sleep wake cycle

77
Q

Ultradian

A

less than a day
- human eating cycles

78
Q

diurnal

A

the opposite of nocturnal (active during the day)

79
Q

Circadian rhythms are not just sleep but…

A

pulse, blood pressure, body temperature, alertness, feeding behavior and more

80
Q

Are biorhythms endogenous (internal) or exogenous (external)

A

Biorhythms are endogenous (internal) - we have a biological clock in the neural system that times behavior by producing biorhythms

81
Q

Bunker sleep study

A

Over time: sleep times shift but are not chaotic → stays constant but shifts a bit (a slow progressive shift that is not linked to external cues)
Over time: getting up when the night was → the rhythm did not go away but it was not synced to the world

82
Q

Biological clock

A

Synchronized behavior to the passage of a real day and make predictions about tomorrow
Anticipate events, and prepare for them physiologically and cognitively
Regulates feeding times, sleeping times, etc

83
Q

What impacts circadian rhythms

A

Light pollution (phones)
Jet lag (going west to east is more challenging than going east to west)

84
Q

Master clock neurology

A

Superchiasmic nucleus of the hypothalamus (SCN)
** above the optic chiasm

85
Q

Retinohypothalamic pathway

A

We get visual information which hits photoreceptors (tells us light or dark
Activates RGCs → produce melanopsin (hormone) → talks directly to the suprachiasmatic nucleus

86
Q

If dark is signaled to the SCN

A

signal goes to the Ventrolaterial preoptic area

87
Q

If light is signaled to the SCN

A

signaled to Orexin neurons (lateral hypothalamus)

88
Q

SCN sends information to …

A

Hypothalamus
Thalamus
Pituitary
Autonomic neurons in the spinal cord

89
Q

Master Clock Summary

A

1) special photopigment in ganglion cells
2) relevant information travels to SCN (retinohypothalamic pathway)
3) SCN is the master clock: daily rhythms observed in firing rate of cells
4) SCN exerts control by: direct synaptic connections with other regions, secreting neuromodulators (melatonin)

90
Q

Sleep stages

A

1) awake
2) non REM (N1, N2, N3)
3) REM

91
Q

awake EEG

A

alpha activity + beta activity
- Alpha: higher amplitude → resting/relaxing
- Beta: smaller amplitude → alert, attentive, thinking

92
Q

N1 EEG

A

theta activity
Alpha activity decreases, slow rolling eye movements, motor activity slightly reduced, partial awareness of surrounding

93
Q

N2 EEG

A

sleep spindle → k complex
Eye movements are rare, not much motor movement, some bursts of waves, sleeping soundly

94
Q

N3 EEG

A

delta activity:
Aka SWS (slow-wave sleep): high voltage waves, eye movements rare, not much motor movement
**deepest sleep

95
Q

REM (rapid eye movement) sleep

A

theta activity → beta activity
EEG reverts to a mix of beta and theta, bursts of eye movements, muscle paralysis
EEG output is very similar to when you are awake

96
Q

Full night sleep cycle

A

90 minutes → go through 5-6 of these cycles per night
REM happens around the end of the 90-minute period
Adults who sleep 8 hours spend about 2 hours in REM sleep

97
Q

Changes in sleep over the lifespan

A

As we get older:
We get less sleep overall
Less REM sleep

98
Q

What happens in N sleep

A

Dreaming occurs in N-sleep but is not as vivid
Sleepwalking
Sleep-talking
Night terrors (40% of children): the only type of vivid dream in N sleep
Talking or grinding teeth
Flailing, banging an arm, kicking a foot
Maintaining muscle posture

99
Q

Maintaining muscle posture

A

Sleep may occur in a variety of positions → standing up, sitting, or several reclining positions – in N sleep

100
Q

REM sleep: (R-sleep)

A

Atonia: no muscle tone; conditions of complete muscle inactivity produced as sleep regions of the brainstem inhibit motor neurons
Mechanisms that regulate body temperature stop working → body temp moves towards room temp (gets higher)
Dreaming

101
Q

Dreaming

A

Vivid dreams in REM
Everyone dreams a number of times each night
Dreams appear to take place in real-time; dream sessions get longer throughout a sleep session

102
Q

Histamine

A

keeps you awake

103
Q

Orexin

A

How we control staying awake (motivation)

104
Q

What area controls sleep patterns?

A

Ventrolateral preoptic area (VLPOA)

105
Q

Ventrolateral preoptic area (VLPOA)

A

GABAergic neurons (inhibitory)
Inhibits the around brain systems (flip-flop circuit)
**see images here

106
Q

Why do we sleep?

A

Energy conservation
Restoration
Learning and memory

107
Q

Sleep for energy conservation

A

Reduces a person’s energy demand during part of the day/night when it’s least efficient to hunt for food
Support: body has decreased metabolism when sleeping

108
Q

Sleep for restoration

A

Sleep lets the body repair and replete cellular components necessary for biological functions that become depleted throughout an awake day
Clears out waste products of neural activity

109
Q

Sleep for learning and memory

A

Patterns that you experience during the day reactive when sleeping (almost reliving) → keeping important memories and reliving to better remember them (neurons that fire together wire together)

110
Q

Sleep disorders

A

Narcolepsy
REM sleep behavior disorder

111
Q

Narcolepsy

A

Slow-wave sleep disorder in which a person uncontrollably falls asleep at inappropriate times

112
Q

Symptoms of narcolepsy

A

1) Cataplexy: sudden loss of muscle tone → slurred speech, weakness → often triggered by a strong emotion
2) Sleep paralysis: temporary inability to move or speak while falling asleep or upon waking → can remember these events
3) Hypnagogic hallucinations: particularly vivid and frightening because you may not be fully asleep when you begin dreaming and you experience your dreams as reality

113
Q

Neural Features of narcolepsy

A

Low levels of orexin/hypocretin
Genetic: 20-40x more likely to get it if you have a family member with narcolepsy

114
Q

REM sleep behavior disorder

A

Physically act our vivid, often unpleasant dreams
- Sleep talking, shouting, screaming, hitting, punching, etc. → can be dangerous
- no atonia of muscles
- Seems to be linked to Parkinson’s and other neurodegenerative disorders but it is unclear why

115
Q

Manipulations technique definition

A

Manipulation technique: the structure or function of the brain is altered and the resulting effects on behavior are observed
*hard

116
Q

Measurement technique definition

A

brain activity is measured during a task to identify brain areas that might be involved in the performance of that task

117
Q

Manipulations

A

1) lesions
2) Brain stimulation (DBS, TMS, optogenetics)

118
Q

Lesions

A

Assumption: The function of a brain area can be inferred from the behavior that can no longer be performed after the area is damaged

119
Q

Cons of lesions

A

Control: something bad has to happen
non-specific/diffuse damage
Cortical reorganization
Was the behavior localized to begin with?

120
Q

Deep brain stimulation (DBS)

A

Place an electrode into the brain → invasive for research only
Used to treat:
Parkinson’s disease
OCD

121
Q

Cons of DBS

A

Usual surgery risks (risks increase with age): can outweigh the benefits
What if the placement isn’t exactly perfect

122
Q

Transcranial magnetic stimulation (TMS)

A

Place a coil over a particular area
Current passes through, causing cortical cells to depolarize (in a semi-local way → not perfect but ok)

123
Q

Pros of TMS

A

Noninvasive
Clinically used for depression
Used in research

124
Q

Cons of TMS

A

How localized is it really?
Makes interpretation quite difficult
Reproducibility issues
Safety if doing it at home

125
Q

Optogenetics

A

Genetically engineered mice → to express membrane channels that are light-sensitive
Light triggered: depolarization of hyperpolarization of cells
Can insert these proteins into particular areas and then apply light

**understanding neural circutry in living organisms

126
Q

Cons of Optogenetics

A

Cells are responding to light, nut not how they would normally respond (validity)?
Trying to get more precision for the subtypes of neurons → What kind of membrane channels can you engineer
Not at the human level → no genetic engineering

127
Q

Measurement examples

A

1) electrical activity (single/multi cell recordings, EEG, ECog, MEG)
2) functional brain imaging (PET, MRI, fMRI)
3) structural methods (CT/CAT, MRI)

128
Q

Intracellular recording

A

tiny electrode inserted directly inside a neuron to record its electrical sensitivity

129
Q

Extracellular recording

A

tiny electrodes inserted into the fluid surrounding neurons to record electrical currents generated by the neuron in the electrode’s vicinity

130
Q

Electroencephalography (EEG)

A

Put electrodes on the scalp to record “brain waves”
Measuring the summed graded potentials from thousands of neurons
Done while someone does something/something is happening (like a seizure)

  • When ions flow in and out, they cause distortions in the electrical field
131
Q

Pros of EEG

A

Really great temporal resolution (order of milliseconds)

132
Q

Event-related potentials (ERP)

A

EEG that is synchronized with a task

133
Q

cons of EEG

A

Poor spatial resolution → can be hard to figure out where exactly electrical signals came from
The skull distorts signals → since measuring from outside, bone distorts electrical activity

134
Q

Electrocorticography (ECoG)

A

Intracranial EEG → remove the skull and directly place electrodes on the brain
See the prosopagnosia video from vision 2 lecture
For research purposes → often paired with some form of stimulation (manipulation)
Both manipulation and measurement
Usually people who are undergoing brain surgery anyway (often for epilepsy)

135
Q

Magnetoencephalography (MEG)

A

Very similar to EEG, but magnetic waves are not distorted by the skull
Used MEG is overlaid on top of high-resolution MRI
Better spatial resolution

136
Q

Cons of MEG

A

Need to should out any other magnetic fields → including Earth’s magnetic field
Have to create a room that blocks all magnetic fields
Have to keep the room cold: requires liquid helium to cool some of the sensors
~100 machines in the whole world → $2 billion each (2007 data)
Mobile MEGs are in the works

137
Q

Positron emission tomography (PET)

A

Different radioactive agents can be used with biomarkers of disorders and pathologies
Radioactive things decay over time: can attach the radioactive agents to some construct of interest and follow it over time

138
Q

Types of tracers in PET

A

FDG: analog of glucose
Oxygen-15: blood flow
Can also label chemicals such as neurotransmitters (e.g. dopamine)

139
Q

Pros of PET

A

good for studying…
Task-related activations
Brain metabolism and neurochemistry

140
Q

Cons of PET

A

ack of structure → can overlay this with a structural image
Lower spatial resolution (mm-cm)
Slower temporal resolution (tracer needs to watch out between experimental conditions)
Doesn’t image brain structure
Dealing with radioactive isotopes → hard to get past IRB and have a nurse on-site to inject and monitor the patient

141
Q

MRI

A

Relies on magnets (~60,000x stronger than Earth’s magnetic field) → generally 3T sometimes 7T/11T
VERY strong

142
Q

Pros of MRI

A

Non-invasive: subjection only exposed to magnetic field and radio waves
High spatial (~1mm voxels) → very clear and crisp

143
Q

What does an MRI show?

A

White/gray matter
Bone shown, but CT is better for this
Cortical thickness (distance between gray matter and white matter)

144
Q

fMRI

A

Most often measures the blood oxygen level-dependent (BOLD) signal
Indirect measure of neural activity

145
Q

BOLD signal

A

When neurons fire, they require additional oxygen → BOLD relies on the different magnetic properties of oxygenated and deoxygenated blood

BOLD: ratio of oxygenated to deoxygenated blood
Decrease in BOLD: the area just used oxygen and now replenishing

146
Q

Deoxy-hemoglobin

A

Paramagnetic iron → attracted to the magnet
Low BOLD signal

147
Q

Oxy-hemoglobin

A

Diamagnetic iron → repelled by the magnet
Normal BOLD signal

148
Q

Hemodynamic response function (HRF)

A

Time 0: when the stimulus is shown → immediately uses up a bit of oxygen
Time 4: overcompensation (increase in BOLD signal) → peaks about 5 seconds after activity happened
Comes back down
Undershoots

**see graph in notes

149
Q

voxel

A

a 3D pixel: usually 1-3mm cubes and contain 100,000+ neurons
About 1,000,000 voxels in a brain scan

150
Q

Cons of MRI AND fMRI

A

Movement matters → in order to get a clear image, the person has to be very still
- Who are we scanning → if you can’t move, you have to scan people who can lie still (not good for people with Parkinson’s or kids) + claustrophobia
Expensive
Statistical woes

151
Q

Computerized tomography (CT/CAT)

A

Rotates an X-ray around the patient’s head

152
Q

Pros of CT/CAT

A

Feaster and cheaper than MRI, but lower resolution
Can be used in situations where magnets cannot (implanted metal devices in the body)
Can detect major structural problems (tumor, bleeding, TBI)

153
Q

Mind as a blank slate

A

nothing is given to us and everything is determined by our sensory experiences

154
Q

Mind as a black box

A

stimuli comes in (sensations) and something happens that we can not see (mental processes) and then we get a product (behavoir)

155
Q

Consilience

A

conceptual integration - hierarchy and similarities of information

156
Q

Mind as a sponge

A

Given a tool to soak up information but not built in

157
Q

Proximate vs. ultimate explanations

A

Proximate explanation: mechanisms and developmental history
- Immediate cause

Ultimate explanation: adaptive functions and phylogenetic history
Evolutionary cause (functional advantage)
- The “why

158
Q

Mild depression and evolution

A

“survival value” as a social-emotional hibernation that allows humans to:
- Conserve energy
- Avoid conflicts and other risks
- Let go of unattainable goals
- Take time to contemplate (rumination)
- Signal to others the need for assistance

159
Q

Actigraphy

A

Actigraphy looks at:
Sleep activity
Sleep variability
Sleep timing
Sleep duration
Sleep onset latency: how long it takes to fall asleep
- collected on watches

160
Q

Pros of actigraphy

A

measures biological sleep data

161
Q

Cons of actigraphy

A

can not measure the subjective “goodness” of sleep

162
Q

Social disadvantage and brain structure of infants

A

Greater irregularity in mothers’ sleep schedule = smaller cortical brain matter volume, white matter volume, smaller cortex ** sleep may be a mediator
Increased Chronodisruption = smaller brain volumes
Increase chronotype = smaller brain volumes

163
Q

Social disadvantage and chronodisruptions

A

sleep less/more varied due to stress, jobs, unpredictability of where you will sleep etc.

164
Q

Chronodisruption

A

irregularity in the sleep period as indexed by variability in daily sleep duration

165
Q

Sleep and depression

A

90% of adults and 73% of youth diagnosed with major depressive disorder report sleep disturbances
- May predict and precede depression symptoms and depression episodes
*depression does NOT cause sleep disturbances

166
Q

Childhood depression

A

Depression onset at ages 3-5
- difficult for caregivers to detect

167
Q

Subjective vs. objective measures of sleep

A

More sleep problems = more likely to show depression symptoms (concurrent association)
Caveat: not on subjective interviews (parents)
- you need to have both to get the full picture on sleep

168
Q

Sleep disturbances and early childhood depression

A
  • Sleep disturbances in infancy and toddlerhood precut the emergence of early childhood depression (at age 3)
  • More sleep problems = more likely to show depression symptoms (concurrent association)
    **early sleep disturbances and later depressive symptomology
169
Q

Pharmacodynamics

A

What the drug does to the body

170
Q

3 categories of symptoms for clinical disorders

A

1) emotional
2) neurovegatative
3) neurocognitive

171
Q
A

FALL 2023 (5 decks)

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