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Exam 4 Flashcards

1
Q

Biorhythm

A

Cyclical changes in behavior or bodily functions

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2
Q

Zeitgeber

A

a clock-setting cue

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3
Q

Entrainment

A

when a biorhythm is reset by a zeitgeber

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4
Q

Free-running rhythm

A

cycle that has a period of the body’s own devising

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5
Q

Jet lag

A

disruption of the body’s circadian phase

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6
Q

Circannual

A

yearly biorhythm (ex: migratory cycle of birds)

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7
Q

Circadian

A

daily biorhythm (ex: human sleep-wake cycle)

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8
Q

Ultradian

A

less than a day biorhythm (ex: human eating cycles)

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9
Q

Infradian

A

more than a day biorhythm (ex: human menstrual cycle)

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10
Q

Suprachiasmatic nucleus

A

master biological clock, mostly responsible for maintaining Circadian rhythms

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11
Q

Where is Suprachiasmatic nucleus located and what larger structure is it a part of?

A

It is located in the Hypothalmus and is part of the retinohypothalmic pathway

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12
Q

How do light signals (melanopsin photopigment signals) get from the retina to the SCN of the hypothalmus?

A

Light activates a special group of photoreceptors in the retina that send melanospin photopigment signals, via the retinal hypothalmic pathway (respond more slowly to light)

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13
Q

The pineal gland is an endocrine gland that produces the neurohormone melatonin at night.
In what situation mght taking a melatonin supplement be helpful?

A

Taking melatonin can help with insomnia. Taking it in the afternoon can phase-advance the biological clock, which can help relieve some jet lag.

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14
Q

What is the difference between advanced sleep phase disorder and delayed sleep phase disorder?

A

Advanced sleep phase disorder is when your rhythm makes you go to bed earlier while Delayed sleep phase disorder is when your rhythm you go to bed later

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15
Q

List interruptions of consciousness

A

Coma, vegetative state, minimally conscious state, and brain death

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16
Q

Coma

A

extended period of unsciousness caused by head trauma, stroke, or disease characterized by low brain activity that remains fairly steady

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17
Q

Vegetative state

A

person alternates between periods of sleep and moderate arousal but no awareness of surrounding

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18
Q

Minimally conscious state

A

one stage higher than a vegetative state marked by occassional brief periods of purposeful action and limited speech comprehension

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19
Q

Brain death

A

no sign of brain activity and no response to stimulus

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20
Q

Why do we sleep?

A

Conservation of energy, repair & restoration (release growth hormone to repair tissue), and learning & memory consolidation

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21
Q

Who sleeps more predator or prey?

A

Predatory animals sleep more than prey

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22
Q

When is human body temperature lowest during a 24-hour cycle?

A

Human termperature is lowest at 4:30 Am

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23
Q

What are growth hormones good for (besides growth) and when are they released during the 24-hour cycle?

A

Growth hormones are also good for regeneration of tissue, secreted during sleep

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24
Q

What tools do we use to measure that activity of the brain and body during sleep?

A

Polysomnograph
Electroencephalogram (EEG)
Electromyogram (EMG)
Electroculogram (EOG)

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25
Q

Polysomnograph

A

measure activity of brain & body

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26
Q

Electroencephalogram (EEG)

A

record brain wave activity

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27
Q

Electromyogram (EMG)

A

record muscle actvity

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28
Q

Electroculogram (EOG)

A

record eye movement

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29
Q

Stage 1 of sleep

A

Overall brain activity is high, but declining
Alpha rhythm: relaxation; brain waves of 8-12 Hz

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30
Q

Stage 2 of sleep

A

Sleep spindles & K-complexes

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31
Q

Sleep spindles

A

memory consolidation and declarative memories

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32
Q

K-complexes

A

sharp, high amp negative wave followed by slower positive wave; protect person from waking due to stimuli; lows of make up

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33
Q

Stage 3 & 4 of sleep

A

Slow wave sleep
Heart rate, breathing, brain activity slow with each stage
Percent of slow, high amp waves increases

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34
Q

What in particular occurs in stage 4 of sleep

A

thalmus stops relaying sensory info to cortex (unless extreme or relevant)

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35
Q

REM sleep stage

A

Paradoxical sleep
Considerable brain activity, HR, BP and breathing are more variable; more facial twitches
Postural muscles of bofy are most relaxed
REM seems to intensify dreams, but REM x=x dreaming

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36
Q

Which is stage of sleep is paradoxical sleep and why?

A

Rapid Eye Movement (REM) sleep is also known as paradoxical sleep because it is the lightest sleep, weirdest dreams, and paralyzed body.

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37
Q

Which neurotransmitters begin and end REM sleep?

A

Acetylcholine begins REM sleep
Seratonin ends REM sleep

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38
Q

Atonia

A

a lack of muscle tone

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39
Q

How does age affect sleep patterns?

A

Duration of REM sleep varies with age and changes dramatically over the life span. It is high in infancy, increased during growth spurts, in conjunction with physical exertion, and during pregnancy.
Developing brain needs lots of sleep.
As we age neurons in certain reticular nuclei tend to degenerate.
Normal rhythm of sleep becomes dysregulated (less orderly sleep patterns and less deep slow wave sleep from stage 3 & 4)
Insomnia is very common in older people

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40
Q

Insomnia

A

sleep disorder associated with inadequate sleep
Occurs in NREM
Caused by: noise, stress, pain medication, disorders like epilepsy or Parkinson’s disease, depression, anxiety, other psychatric conditions, dependence on sleeping pills, shifts in circadian rhythms

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41
Q

Sleep apnea

A

sleep disorder known for inability to breathe while sleeping for a prolonged period of time
Occurs during both REM and NREM?
Symptoms: sleepiness during day, impaired attention, depression, sometimes heart problems

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42
Q

Narcolepsy

A

sleep disorder characterized by frequent periods of sleepness
Occurs during NREM?
Symptoms: gradual or sudden sleepiness, occasional cataplexy, sleep paralysis, hypnagogic hallucinations

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43
Q

Cataplexy

A

muscle weakness triggered by strong emotions

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44
Q

Hypnagogic hallucinations

A

dreamlike experiences the persona has dfficulty distinguishing from reality

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45
Q

REM behavior disorder

A

vigorous movement during REM sleep
Acting out dreams (damage to pons)

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46
Q

Night terrors

A

experiences of intense anxiety from which a person awakens
During NREM

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47
Q

Sleep talking

A

occurs during both REM and NREM sleep

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48
Q

Sleep walking

A

runs in families, mostly in young children, and occurs mostly stage 3 & 4 of sleep (NREM)

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49
Q

Contrast sleep paralysis and sleep walking

A

Sleep paralysis is wakefulness while your motor system is still inhibited while Sleep walking is movement while your awareness is still inhibited

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50
Q

What are the effects of sleep deprivation (general, not specific peripheral effects)?

A

Cognitive deficits, poor reaction time, memory loss, mood imbalance, and hallucinations
Lack of sleep is secondarily deadily to humans (negative outcomes are deadily)

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51
Q

When do we dream?

A

Dream in both REM (real time, vivid dreams) and NREM (brief nightmares)

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52
Q

Learning

A

a change in an organism’s behavior as a result to experience

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53
Q

Memory

A

the ability to recall or recognize previous experience

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54
Q

Neuroplasticity

A

the nervous system’s potential for physical or chemical change, which engances its adaptibility

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55
Q

Associative learning

A

linkage of two or more unrelated stimuli to elicit a behavioral response

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56
Q

Classical conditioning

A

Pairing of 2 stimuli (conditioned stimuli + unconditioned stimuli = unconditioned response that turns conditioned)

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57
Q

Operant conditioning

A

instrumental conditioning, responses followed by reinforcement or punishment to either strengthen or weaker behavior

58
Q

Latent learning

A

knowledge that only becomes clear when an organization has an incentive to display it (learning without obvious rewards or punishments)

59
Q

Observational (social) learning

A

learning occurs by watching other’s behavior and observing the resulting consequences

60
Q

Insight learning

A

the abrupt realization of a problem’s solution (firgure it out all on your own)

61
Q

Who pioneered Classical conditioning (2 stimuli)

A

Ivan Pavlov

62
Q

Who pioneered Operant conditioning (1 stimuli & 1 behavior)?

A

B.F. Skinner and Edward Thorndike

63
Q

Albert Bandura believed that…

A

Observational (or social) learning because we see what behaviors by others are punished or rewarded

64
Q

Long term memory (LTM)

A

memory of events from times further back

65
Q

Working memory

A

emphasis on temporary storage of information to actively attend to it and work on it for a period of time

66
Q

Consolidation

A

permanently storing short term memory into long term

67
Q

What are the two types of long-term memory

A

Explicit/Declarative and Implicit/Non-Declarative

68
Q

Explicit/Declarative memory

A

memories you can explain like events & facts

69
Q

Implicit/Non-Declarative memory

A

memories you can show (skill memories)

70
Q

What are the two types of Declarative/Explicit memory?

A

Episodic and Semantic memory

71
Q

Episodic memory

A

memories for specific autobiographical events (ex: first kiss)

72
Q

Semantic memory

A

memories for facts and general knowledge (ex: teacher’s name)

73
Q

Anterograde vs. Retrograde amnesia

A

Anterograde amnesia is not being able to make memories moving forward while Retrograde amnesia is a loss of past memories

74
Q

Who is patient H.M.?

A

Henry Molaison had a doctor perform a bilateral medial temporal lobe resection

75
Q

What was learned from patient H.M.’s surgery?

A

Different brain circuits for different memories.
Can’t make episodic memories, but can make procedural (implicit).

76
Q

What is working memory good for?

A

Gathering temporary memory that can be consolidated into long term memory

77
Q

What part of the brain is important for consolidation?

A

Hippocampus (memory & mood)

78
Q

What brain regions are implicated in emotional memories?

A

Amygdala (main), Hypothalmus and PAG, Basal ganglia, Medial temporal cortext, (Frontal, Parietal, Temporal, Occipital, Cingulate cortices)

79
Q

Alzheimer’s disease

A

associated with gradually progressive loss of memory often occuring in old age
Affects people 50% over 85

80
Q

Difference between early-onset vs. late-onset AD

A

Early onset seems to be influenced by genes, but 97-99% of cases are late onset

81
Q

What are plaques?

A

Amyloid beta protein which produces widespread atrophy of the cerebral cortex, hippocampus, and other areas
Accumulation of sticky protein bits and pieces

82
Q

What are tangles?

A

An abnormal form of the tau protein, part of intracellular support system neurons
Structures formed from degenerating structures within a neuronal body

83
Q

What are some treatment options for AD?

A

Most treatments aimed for improving cognition work short term. Most immunizing strategies haven’t worked in trials.
The key is to prevent instead of treat (melatoning & good sleep)

84
Q

Korsakoff syndrome

A

Permanent loss of ability to learn new information and to retrieve old information

85
Q

What causes Korsakoff syndrome

A

Diecephalic damage from chronic alcoholism or malnutrition that produces a vitamin in B1deficiency

86
Q

What are the symptoms of Korsakoff Syndrome?

A

apathy, confusion, forgetting, and confabulation

87
Q

Confabulation

A

taking guesses to fill in gaps in memory

88
Q

Hebbian synapse

A

a synapse that increases in effectiveness because of simultaneous activity in pre- and post-synaptic neurons

89
Q

What is the role of enriched environments or experiences on plasticity in the brain?

A

When an axon successfully stimulates a cell it will be even more successful in the future. Cells that fire together, wire together (more connections between axon to axon terminal)

90
Q

Is stress good for memory

A

Yes and no… it depends.
Small to moderate amounts of adrenaline and cortisol activate amygdala & hippocampus where enhance storage & consolidation
Prolonged stress leads to prolonged cortisol, that impairs memory and hippocampus loses volume

91
Q

Do we get new neurons?

A

Yes, in the Hippocampus to plump it back up when it shrinks due to stress/traumatic events

92
Q

Diagnosis

A

involves distinguishing one illness from another

93
Q

Etiology

A

apparent causation & developmental history of illness

94
Q

Prognosis

A

a forecast about probable course of an illness

95
Q

Clinical neuroscience

A

speciality in neuroscience that focuses on the diagnosis and treatment of diseases & disorders affecting the brain & CNS

96
Q

How is clinical neuroscience different from neurology?

A

Neurology focuses on disorders that are part of the general nervous system while clinical neuroscience focuses on disorders of the brain & CNS

97
Q

What is the main document utilized in the US to diagnose disorderded behavior?

A

American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-V)

98
Q

What is the estimate from the NIMH for US citizens with a diagnosable behavioral disorder?

A

1:5 people

99
Q

Are checklists for behavior all we have to help with diagnoses?

A

No, we also have genetic analysis and neuroimaging

100
Q

What types of causes are relatively straightforward for organic-neurological disorders?

A

Abnormality of brain anatomy and behavior

101
Q

Positive (Add) symptoms of Schizophrenia

A

delusions, hallucinations, disorganized speech, disorganized behavior or excessive agitation, catatonic behavior

102
Q

Negative (Subtract) symptoms of Schizophrenia

A

blunted emotions or loss of interest and drive; the absence of some normal response

103
Q

Delusions

A

beliefs that disotrt reality

104
Q

Hallucinations

A

distorted perceptions

105
Q

Disorganized speech

A

incoherent statements

106
Q

What are some brain abnormalities in schizophrenia?

A

Lack of activity in the prefrontal cortex
Disorganized pyramidal neurons
Large ventricles and thinner cortex (medial temporal & frontal regions)
Composition of neurons and fibers (temporal & frontal lobes) changes
Abnormal dendritic fields in cells of the dorsal prefrontal regions, hippocampus, and entorhinal cortex

107
Q

What is the evidence for a role of genetics in schizophrenia?

A

Diaphisis Stress Model

108
Q

Neurodevelopmental Hypothesis of Schizophrenia

A

Suggests abnormalities in the prenatal or neonatal development of the nervous system

109
Q

Dopamine hypothesis of Schizophreniz

A

suggests that schizophrenia results from abnormal activity at dopamine synapses in certain areas of the brain

110
Q

Glutamate hypothesis of Schizophrenia

A

suggests the problem relates partially to deficient activity at glutamate receptors, especially in prefrontal cortex

111
Q

Signs of Major depressive disorder signs

A

prolonged feelings of worthlessness and guilt; disruption of normal eating habits; sleep disturbances; generaly slowing of behavior; frequent thoughts of suicide

112
Q

Signs of Mania

A

characterized by excessive euphoria (subject perceives as typical); affected person often formulates grandioseplans and is uncontrollably hyperactive

113
Q

Signs of Biopolar I

A

full manic episodes

114
Q

Signs of Biopolar II

A

mil (hypo-) manic episodes that consist mostly of agitation or anxiety

115
Q

Cognitive Behavioral therapy (CBT)

A

problem-focused, action-oriented, structured treatment for eliminating dysfunctional thoughts & maladaptive behavior

116
Q

What type of disorder responds well to CBT?

A

Depression

117
Q

What are the 4 categories of antidepressants?

A
  1. Tricyclics
  2. Selective serotonin/norepinephrine reuptake inhibitors (SSRIs or SNRIs)
  3. MAOI’s
  4. Atypical antidepressants
118
Q

Tricyclics

A

Lots of different chemicals, was originally prescribed to treat depression but a lot of side affects

119
Q

Selective serotonin/norepinephrine reuptake inhibitors (SSRIs or SNRIs)

A

If mess with one side of brain, less side effects
It stopes reuptake channels and encourages inhibtion
by postsynaptic cell so it thinks it has more than it does

120
Q

MAOI’s

A

monoamine oxoamine enzyme (inhibits enzyme)

121
Q

Emotional part of Manic vs Depressive episode

A

elated, euphoric, very sociable, impatient at hinderence

gloomy, hopeless, socially withdrawn, irritable

122
Q

Cognitive part of Manic vs. Depressive Episode

A

characterized by racing thoughts, flight of ideas, desire for action, and impulsive behavior; talkative, self-confident, experiencing delusions of graneur

characterized by slowness of thought processes, obsessive worrying, inability to make decisions, negative self-image, self-blame, and delusions of guilt & disease

123
Q

Motor part of Manic vs. Depressive Episode

A

Hyperactive, tireless, requiring less sleep than usual, showing increased sex drive and fluctuating appetite

less active, tired, difficulty sleeping, decreased sex drive & decreased appetite

124
Q

Difference between Bipolar I and Bipolar II?

A

Bipolar I is full manic while Bipolar II is mild (hypo-) manic

125
Q

Treatment option for Bipolar disorder I?

A

Lithium
a salt that stabilizes mood and prevents relapse in mania or depression
Mood stabilizer
But toxic after long period of time

126
Q

Treatment option for Bipolar II?

A

Anticonvulsants
includes valproate (Depakote) and carbamazepine
Previously prescribed for seizures
Minimize activity

127
Q

4 main treatment types for disorders

A

Neurosurgical, Electrophysiological, Pharmacological, and Behavioral

128
Q

Neurosurgical treatment

A

skull is opened and some intervention is performed on the brain (ex: Deep brain stimulation; electrical stimulation)

129
Q

Electrophysiological treatment

A

brain function is modified by stimulation through the skull (ex: Electroconvulsive Therapy)

130
Q

Pharmocological treatment

A

a chemical that affects the brain is either ingested or injected (ex: drugs)

131
Q

Behavioral treatment

A

treatment manipulates the body or expereince, which in turn influence the brain (ex: therapy)

132
Q

Can things like exercise, music, and virtual reality help?

A

Yes
Music affects arousal and activates the motor and premotor cortical
Physical activity, including playing sports, combined with other therapies (counteracts effects of depression)

133
Q

In general, what are some of the research challenges related to investigation and diagnosis of disorded behavior?

A

Organizational Complexity
Systematic Complexity
Neuronal Plasticity
Compensatory Plasticity
Technical Resolution
Modeling Simplicity
Modeling Limitations

134
Q

Organizational Complexity

A

brain is the most complex organ

135
Q

Systematic Complexity

A

Multiple receptor types for neurotransmitters, and effect is different at different types

136
Q

Neuronal Plasticity

A

Everyone’s brain is different due to experience and genetics

137
Q

Compensatory Plasticity

A

If there is a problem, there seems to be several “backups” in place

138
Q

Technical Resolution

A

Is our technology good enough to see what might be there?

139
Q

Modeling Simplicity

A

Drug help isn’t always directly at receptors for that drug

140
Q

Modeling Limitations

A

Non-human animal model x=x human

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