Exam 4 Flashcards

1
Q

Prevalence of Schizophrenia

A

12% of population
1 in 5 in USA
more women than men

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2
Q

Positive symptoms of schizophrenia

A

Psychosis
Hallucinations
Delusions
Disorganized thought and speech

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3
Q

Negative symptoms of schizophrenia

A

Lack of emotional expression
Reduced facial expression
Anhedonia
Alogia
Social withdrawal

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4
Q

Anhedonia

A

no pleasure in things that are normally enjoyable

Symptom of schizophrenia

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5
Q

Alogia

A

Lack of spontaneous speech

Symptom of schizophrenia

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6
Q

Cognitive symptoms of schizophrenia

A

Memory impairment
Poor attention span
Difficulty making plans
Reduced decision-making
Poor social cognition

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7
Q

Twins and schizophrenia

A

Concordance rate in identical twins is 50%, down to 17% in fraternal

Shows that there is some genetic factor, but environment is also involved

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8
Q

Features of twin with schizophrenia

A

Lower birth weight, more physiological distress, more sensitive behavior, subtle neurological signs

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9
Q

Schizophrenia and eye movement

A

People with schizophrenia display difficulty with smooth movement of the eyes

Smooth pursuit
Free-viewing
Saccade
Fixation stability

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10
Q

Integrative model of schizophrenia

A

More than 100 genes influence it, including DISC1

Paternal age is an epigenetic factor

INTERACTION BETWEEN GENETIC FACTORS AND STRESS

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11
Q

Stressors that may lead to schizophrenia

A

Transition from childhood to adulthood
Prenatal stress
Maternal illnesses
City Living

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12
Q

Influence of cities on schizophrenia

A

Population influences risk of developing it

Also what age you move there and how long you stay there

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13
Q

Schizophrenia vulnerability and development

A

Onset in males 2-3 years earlier
Some women get it during menopause
Increase in symptoms during synaptic rearrangement

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14
Q

Brain abnormalities in patients with schizophrenia

A

Enlarged lateral ventricles
Structure/function of corpus callosum
Accelerated cortical thinning
Reduced subcortical volume

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15
Q

DISC1 mutation and lateral ventricles

A

Mice with a mutated DISC1 gene developed enlarged lateral ventricles, just like schizophrenia patients

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16
Q

Schizophrenia and frontal lobes

A

reduced metabolic activity in frontal lobes

Decreased blood flow to frontal lobes

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17
Q

Hypofrontality hypothesis

A

frontal lobes are underactive in people with schizophrenia

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18
Q

Historical treatment for schizophrenia

A

lobotomy

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19
Q

First effective medication for schizophrenia

A

Chlorpromazine - antipsychotic
Reduced positive symptoms
Targets dopamine receptors

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20
Q

Dopamine hypothsis

A

Schizophrenia is caused by an excess of either dopamine release or dopamine receptor

More likely related to dopamine SYNTHESIS, not receptors

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21
Q

Problems with the dopamine hypothesis

A

Drugs block D2 receptors faster than symptoms are reduced

Some effective atypical neuroleptics actually increase dopamine levels

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22
Q

Side effects of antipsychotics

A

Dyskinesia
Tardive Dyskinesia
Supersensitivity psychosis

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23
Q

Dyskinesia

A

Side effect of antipsychotics

initial, maladaptive motor symptoms, disappear when dose is reduced (dose dependent)

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24
Q

Tardive Dyskinesia

A

Side effect of antipsychotics

late onset, repetitive, involuntary movements, irreversible, may be due to dopamine receptor supersensitivity

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25
Supersensitivity psychosis
marked increase in positive symptoms of schizophrenia upon discontinuation of antipsychotic drugs
26
Second-Generation antipsychotics
atypical antipsychotics have lower affinity for D2 receptors, their highest affinity is for serotonin receptors Clozapine
27
Glutamate hypothesis of schizophrenia
Schizophrenia is caused by an under activation of glutamate receptors Prompted by effects of PCP and ketamine
28
PCP and schizophrenia
PCP is an NDMA receptor antagonist Prevents glutamate from acting normally Noncompetitive antagonist Produces schizophrenia like symptoms
29
Depression is characterized by:
Unhappy mood Loss of interest/reduced energy Changes in appetite Disrupted sleep patterns Difficulty in concentration Restless agitation or torpor Pessimism and thoughts of death
30
Prevalence of mental illness among college students
32% of college students report having mental illness (female>male)
31
Presence of mental illness greater in women
Patterns of seeking help Gender differences in endocrine physiology, related to the reproductive cycle Postpartum and postmenopausal depression
32
Brain changes associated with depression
Increased activation in: -prefrontal cortex during cognitively demanding tasks -Amygdala during emotional processing Decreased activity on: -Hippocampus -Anterior cingulate cortex
33
Habenula and depression
Habenula is dysfunctional in people with depression Mediates low mood and loss of pleasure Stimulation reduces depressive behavior
34
Pharmacological treatment for depression
Monoamine oxidase inhibitors Tricyclics SSRIs
35
Monoamine Oxidase (MAO) Inhibitors
MAO is an enzyme that inactivates the monoamines Inhibit MAO = increase monoamines at the synapse Pharmacological treatment for depression
36
Monoamine hypothesis of depression
Depression is due to reduced monoamine activity
37
Tricyclics
Pharmacological treatment for depression Second generation of antidepressants Inhibits reuptake of monoamines
38
SSRIs
Pharmacological treatment for depression Bock reuptake of serotonin
39
Problems with SSRIs
SSRI benefits are often not much different than placebo Not everyone responds to SSRIs Long lag time between treatment and reduction of symptoms Anti-depressant discontinuation syndrome
40
Non-traditional pharmacological treatments of depression
Ketamine Psychedelic drugs that target 5-HT
41
Ketamine as a treatment for depression
Non-traditional NMDA receptor antagonist Can be administered via inhaler at ER Rapid reduction in suicide ideation
42
Psychedelic drugs as a treatment for depression
Non-traditional Targets 5-HT Psilocybin LSD
43
Non-pharmacological treatments for depression
Electroconvulsive shock therapy (ECT) Repetitive transcranial magnetic stimulation (rTMS) - alters cortical electrical activity Deep brain stimulation (DBS) - surgically implanted electrode Cognitive behavioral therapy Exercise
44
Bipolar disorder
Characterized by alternating periods of mania and depression Men and women equally affected Type I and Type II
45
Mania symptoms
Expansive mood Excessive talkativeness Grandiosity Increased energy/reduced sleep
46
Rapid cycling in bipolar disorder
Four or more cycles / pear (some people have several per day)
47
Treatment of bipolar disorder
Lithium Affects serotonin and dopamine activity Increases gray matter Must be carefully monitored for toxic side effects
48
Brain changes in bipolar disorder
Brain changes akin to those in schizophrenia Enlarged ventricles and reduced gray matter
49
Side effects of lithium
Tremors Weight gain Flattened mood Cognitive impairment
50
Type I Bipolar Disorder
More mania Less depression
51
Type II Bipolar Disorder
Less mania More depression
52
Anxiety
psychological, physiological, and behavioral state induced in humans and other animals by a threat to well-being or survival, either actual or potential
53
Anxiety disorders
Phobic disorders Panic Disorder GAD PTSD
54
Phobic disorders
intense irrational fears centered on an object, activity, or situation that a person avoids
55
Panic disorder
recurrent transient attacks of intense fearfulness
56
Generalized anxiety disorder
persistent, excessive anxiety and worry
57
PTSD
Memories of a horrible episode persist (uncontrollable intruding)
58
PTSD symptoms
Memoria changes (amnesia) Flashbacks Deficits in short-term memory
59
Prevalence of PTSD
~10% of people who experience a traumatic event
60
Hippocampus and PTSD
People with PTSD have a smaller hippocampus Not sure if cause or outcome
61
Neurophysiological model of PTSD
Acute neurochemical responses and Amygdala go back and forth Sensitization from subsequent stressors can bring it up again Causes a traumatic response
62
Anxiolytic drugs
Benzodiazepines Serotonin agonists Serotonin reuptake inhibtors (Buspirone)
63
Benzodiazepines
Anxiolytic drug Bind to GABAa receptors and enhance GABA's inhibitory actions
64
GABAa receptors and anxiety
Receptors are widely distributed, especially in the cortex, hippocampus, and amygdala
65
Buspirone
Anxiolytic drug Targers 5-HT(a) receptors
66
Non-traditional treatment for PTSD
MDMA
67
OCD
Anxiety disorder Recurrent unwanted thoughts (obsessions) Repetitive behaviors without reason or ability to stop (compulsions)
68
Integrative model of genetics, environment, and neurobiology of OCD
Environmental Factors (Stress, trauma) Genetic Factors Affect neural substrates (cortex, striatum, thalamus) Leading to dimensions of OCD
69
Neurotransmitters involved in OCD
Glutamate Serotonin Dopamine
70
Areas of the brain involved in OCD
Cortex, striatum, thalamus (Cycle)
71
Treatment options for OCD
CBT SSRIs Cingulotomy DBS
72
What often occurs with OCD?
Depression
73
Cingulotomy
Treatment for OCD lesions made in the cingulate cortex to disrupt connections
74
DBS for OCD
Electrodes implanted in basal ganglia and nucleus accumbens
75
Tourette's Syndrome
Heightened sensitivity to tactile, auditory, and visual stimuli May fling arms, kick, or make violent shoulder movements
76
Tourette's comorbidities
OCD or ADHD Both involve abnormalities of the basal ganglia
77
Tourette's age of diagnosis
Early, 6-7 yrs
78
Tourette's cause
Affected patients have more dopamine D2 receptors in the caudate nucleus of the basal ganglia
79
Treatment of Tourette's syndrome
Haloperidol (D2 receptor antagonist) Atypical antipsychotics Behavior modification DBS
80
Genome-Wide Association Studies (GWAS)
Schizophrenia and Bipolar disorder share have of their predictive genetic variants
81
Animal models of anxiety
Open field Elevated plus maze
82
Thigmotaxis
Mouse in a box will stick to the edges due to anxiety (anti-predator behavior)
83
H.M.
Had surgery for epilepsy Developed anterograde amnesia
84
Retrograde amnesia
loss of memories formed before onset of amnesia
85
Anterograde amnesia
Inability to form memories after onset of a disorder
86
H.M. Brain
Removed.. -Amygdala -Most of hippocampus -Cortex from both temporal lobes
87
Medial temporal lobe memory system
Parahippocampal gyrus -Hippocampus -Perirhinal cortex -Entorhinal cortex
88
Medial temporal lobe and delayed matching-to-sample task
Showed that hippocampus is involved in memory, but memory is most impaired with damage to... -Parahippocampal gyrus -Extended to the anterior entorhinal and perirhinal cortices (shows that more than just the hippocampus is involved)
89
H.M. and mirror tracing task
H.M. had this ability, which shows that he didn't lose his procedural (nondeclarative) memory
90
Two types of long-term memory
Declarative Non-declarative (procedural)
91
Declarative memory
Things you know that you can tell others H.M. did not have
92
Nondeclarative (procedural) memory
Things you know that you can show by doing H.M. did have
93
Patient N.A.
Stabbed himself with sword Damage to... -dorsomedial thalamus -mammillary bodies Developed anterograde amnesia
94
Importance of similarity of symptoms between N.A. and H.M. despite different lesions
Suggests a larger memory network
95
Mammillary bodies purpose
May serve as a processing system connecting the medial temporal lobes to thalamus and other cortical tissues
96
Damage to the medial diencephalon can cause...
amnesia
97
Korsakoff's syndrome
Degenerative disease Lack of thiamine Patients do not recognize impairment May confabulate
98
Treatment for korsakoff's syndrome
thiamine
99
confabulate
Found in Korsakoff's syndrome fill a gap in memory with a falsification, often without even realizing it
100
Patient K.C.
Motorcycle accident Damage to... -left frontoparietal cortex -right parieto-occipital cerebral cortex -shrinkage of the hippocampus Impaired episodic memory
101
Two types of declarative memory
Semantic Memory Episodic Memory
102
Semantic Memory
Type of declarative memory generalized declarative memory
103
Episodic memory
Type of declarative memory Detailed autobiographical memory
104
Current model of declarative memory formation
Sensory processing in cortex Parahippocampal gyrus Hippocampus Medial diencephalon (mammillary bodies) Declarative memory storage in cortex
105
Skill Learning
Non-Declarative Memory Learning to perform a challenging task through repetition Sensorimotor, perceptual, and cognitive
106
Skill learning is impaired by damage to..
Basal ganglia
107
Priming
Nondeclarative memory A change in stimulus processing due to prior exposure to the stimulus Perceptual priming (visual) Conceptual priming (meaning)
108
Associative learning
Nondeclarative memory The association between two stimuli, or between a stimulus and response (Pavlov)
109
Conditioned eye blink reflex
Person with damage to cerebellum will still blink to air puff, but cannot develop a conditioned response Due to the bell and air puff both activating the cerebellum and leading to the same outcome
110
Nonassociative learning
Nondeclarative memory Habituation to a certain stimulus over time Snail siphon example
111
Operant conditioning
nondeclarative memory An association is made between a behavior (instrumental response) and the consequences of the behavior (reward)
112
Neurons in the "reward circuit) encode reward type
Nucleus accumbens neurons become active when the rate presses the lever Neurons respond to presses for one type of reward but not the other
113
Spatial learning
Nondeclarative memory Allocentric and Egocentric
114
Allocentric spatial learning
nondeclarative memory Path according to external cues
115
Egocentric spatial learning
nondeclarative memory Path according to one's own position or sequential events
116
Cells involved in representation of space in the brain
Place cells Grid cells Boundary cells Head direction cells
117
Place cells
Representation of space in the brain Encode 2D and 3D space Hippocampus
118
Grid cells
Representation of space in the brain Still encode location in space, but different than place cells in that it creates patterns of larger areas, not just activating when in a certain place Medial entorhinal cortex
119
Boundary/border cells
active when on specific borders Can be remapped when new boundaries are placed Medial entorhinal cortex
120
Head direction cells
Where you are in space and what direction or trajectory you are looking in or going Presubiculum
121
Human place cells
Found in epilepsy patients 317 neurons in the Hippocampus, parahippocampal region, amygdala, and frontal lobes
122
Development of navigation cells
Develop early and change with age
123
Age differences in spatial memory
Younger participants took less time and less total distance to solve the virtual spatial maze
124
Types of nondeclarative memory
Skill learning (procedural) Priming Classical conditioning Nonassociative learning Spatial memory
125
Short-Term memory
Working memory ~30 seconds Sensory buffer Can last more with rehearsal
126
Stages of memory
Incoming information Sensory buffers Encoding Short-term memory Consolidation Long-term memory
127
Retrieval
Going from long-term memory to short-term memory
128
Sensory buffer
Before short-term memory The briefest recollection of sensory impressions
129
Long-term memory
Weeks, months, or years Very large capacity Influenced by emotion
130
LTM capacity
Log scale shows that there seems to be no upper limit on memory
131
Long-term memory is susceptible to...
Forgetting Alteration during retrieval
132
Changes during LTM that result in a more effective synapse
More NT release Post-synaptic membrane larger or more sensitive Enlargement both pre- and post-synaptically
133
3 modalities of neuroplasticity and learning (what happens to the neurons themselves)
Interneurons causes the release of more NT from the pre-synaptic neuron The pre-synaptic neuron "sprouts" collaterals More frequently used pathway takes over other synapses
134
Complex environment and brain changes
animals in the enriched condition developed... -Heavier, thicker cortex -Larger cortical synapses -More dendritic branches and spines on cortical neurons
135
Long-term potentiation
a stable and enduring increase in the effectiveness of synapses
136
3 circuits in the hippocampus known to display LTP
Perforant pathway Mossy fibers Schaffer collaterals
137
Things that induce/cause LTP
Tetanus - brief, high-frequency burst of electrical stimuli
138
Tetanus effect of synapses
Pre-synaptic neurons produce a high rate of action potentials Post-synaptic neurons produce larger EPSPs
139
Neurochemical induction of LTP
More glutamate released due to repeated use of synapse Stronger stimulation of AMPA receptors depolarizes membrane Mg gets released from NMDA receptors NMDA receptors can now respond to glutamate, allowing Ca to enter Ca activates intracellular enzymes, causing changes in AMPA receptors
140
Does NMDA normally respond?
No, it is blocked by Mg it only responds when AMPA is activated enough to free the Mg, causing LTP
141
Postsynaptic changes in LTP
Enzymes activated by NMDA receptors cause inactive AMPA receptors to be added increase conductance of ions More receptors are produced
142
Presynaptic changes in LTP
Retrograde transmitter that travels back across synapse ensures that more glutamate will be released and further strengthens the synapse
143
Hebbian synapses
Fire synchronously Strengthens the synapses that successfully drive the postsynaptic cell
144
Research support for LTP as a mechanism of memory
Time course of LTP is similar to memory formation Pharmacological treatments that block LTP also impair learning Mice that overexpress NMDA receptors have enhanced LTP and better long-term memory
145
Theory of LTM storage in cortex
Axons from the amygdala and the hippocampus to the first layer of the cortex induce plasticity Fearful stimulation intensifies plasticity of the pyramidal neurons that have apical dendrites in layer 1
146
Plasticity and memory
Makes memory last longer
147
Fear and memory
Makes memory more vivid
148
Attention (selective attention)
process of selecting or focusing on one or more stimuli
149
Cocktail party effect
Selective attention filters out stimuli not being attended to
150
Attention focuses...
Cognitive processing resources on a particular target
151
Overt attention
Obviously listening (i.e. eye contact)
152
Covert attention
Attention is centered outside the focus or fixation point
153
Dichotic presentation
Stimulus delivery of different stimuli to left and right ears Subjects can report little about the stimuli heard in the nonattended ear Limitation of attention
154
Attentional bottleneck
Works as a filter to select only the most important stimuli for processing
155
Two cognitive models of attention bottlenecks
Early-selection Late-selection
156
Early-selection model of attention
Filtering occurs at the sensory level and non-attended information never reaches higher-order cognitive processes Some unattended stimuli are processed and may still capture attention Cocktail party effect
157
Late-selection model of attention
the bottleneck occurs later, after substantial unconscious processing has occurred (after meaning has been placed on the information)
158
Perceptual load
the immediate processing demands presented by a stimulus determines how much of our perceptual resources are left available by a task
159
Sustained attention task
a single stimulus must be held in the spotlight for an extended length of time
160
Voluntary attention
Endogenous Directed towards aspects of the environment according to our interests and goals
161
Symbolic cuing task
Measures reaction time for noticing the appearance of a specific target preceded by a symbolic cue Measures voluntary (endogenous) attention Arrow
162
Peripheral spatial cuing
Same as symbolic cuing task but illuminated box instead Measures reflexive (exogenous) attention
163
Reflexive attention
Exogenous Involuntary reorienting of attention toward a sudden or important event
164
Gender differences in visual selective attention
Females show a higher validity effect Males have a quicker reaction time in general
165
Reflexive attention onset
Rapid orientation but quickly fades
166
Voluntary attention onset
slower to rise but can be maintained longer
167
Feature search
a search in which the target pops out right away due to a unique attribute
168
Conjunction search
a search based on two or more features that together distinguish the target
169
Reaction times for different types of searches
Conjunction search with target absent takes the longest Conjunction search with target present next Feature search the fastest, regardless of the number of objects In general, more objects = longer reaction time
170
Choice Reaction-Time (RT) Tests
RT = 300-350 ms
171
Measuring attention with EEG
When many neurons work together on a task, the EEG appears synchronized Averaging EEGs during several repeated trials gives the event-related potential (smoothed out potentials)
172
Event-related potential (ERP) from auditory attention
Initial positive wave (P1) Immediately followed by a larger negative wave (N1)
173
Event-related potential (ERP) from visual attention
Similar P1, then N1 P1 effect is enhanced compared to auditory ERP when the stimulus is a valid cue Not enhanced with an invalid cue
174
Visual attention P1 wave is specific to...
Visual tasks using spatial attention No other features (color or other properties) cause the P1 wave
175
Delay between sensory cue and target Affect on P1 wave
As the delay between the sensory cue and target lengthens, P1 enhancement is reduced and eventually becomes inverted
176
Subcortical structures involved in attention
Superior colliculus Pulvinar
177
Superior Colliculus
Attention Guides movement of eyes toward objects of attention Attending to the stimulus activates this area more
178
Pulvinar
Attention Involved in visual processing, orienting and shifting attention, and filtering of stimuli Tasks with more distractors activate it more
179
Dorsal frontoparietal network
Top-down control of attention Voluntary Intraparietal sulcus (IPS) Frontal eye field
180
Temporoparietal network
Bottom-up control of attention Reflexive Right side Temporoparietal junction (TPJ) Ventral frontal cortex (VFC)
181
Frontal eye field
Part of dorsal frontoparietal network (top-down control of attention) directs gaze according to cognitive goals
182
Temporoparietal junction (TPJ)
Part of temporoparietal network (Bottom-up control of attention) directing attention to novel unexpected stimuli (alerting mechanism) Right TPJ activity increased no matter if stimulus is right or left
183
TPJ connections
Receives input directly from visual cortex Strong connections with VFC (other part of temporoparietal network) involved in working memory
184
Hemispatial neglect
Attention deficit due to right hemisphere lesions (overlapping with attentional networks) No attention paid to one side of the body or things presented to that side simultaneous extinction
185
Simultaneous extinction
Found in patients with hemispatial neglect Inability to identify the identical objects in the left and right visual fields only report the right visual field (unaffected left side) Less likely to show extinction if the objects differ
186
Split brain patients and attention
Perform conjunction search 2x faster than normal since each hemisphere has its own attentional scanning mechanism