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NSCI 302 > FINAL > Flashcards

FINAL Flashcards

1
Q

What are the two domains of compromised development that provides the basis of the DSM diagnosis for autsim spectrum disorder

A
  1. Social and communication deficits
  2. Repetitive sensory-motor behaviours and fixated interests

Symptoms emerge in early childhood

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2
Q

What is the prevalence of autism spectrum disorder?

A

1 in 88
3-4 times as many boys as girls (could be from missed diagnoses based on outward symptoms)

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3
Q

Define social cognition

A

Learning that occurs through a social context

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4
Q

How do social stimuli affect children?

A
  • Social stimuli are generally more salient for children (caregivers are salient for children)
  • Saliency drives attention, attention drives learning at an early age.
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5
Q

Define theory of mind

A

The ability to attribute mental states to others
- This is a key milestone in development that develops at around 5 years old

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6
Q

Define joint attention

A

The capacity to coordinate one’s visual attention with the attention of another person

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7
Q

What are fixated interests in ASD?

A
  • Preoccupation with one or more stereotyped and restricted pattern of interest that is abnormal in intesity or focus
  • Can lead to Savant Talents
  • Prefer routines, become distressed with change
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8
Q

How are genetics related to ASD? (5)

A
  • ASD has a strong genetic contribution
  • High heredity and family clustering
  • Hundreds of genes identified
  • Mix of risk variants and de novo mutations, with mutations more frequent with older parents
  • ASD is highly comorbid with other disorders
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9
Q

What is the SCN2A gene?

A

A gene that encodes the voltage-gated sodium channel Na(v)1.2, which plays an important role in the initiation and conduction of action potentials

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10
Q

What is the growth dysregulation hypothesis of ASD?

A

Normally well-controlled processes of brain growth and organization go awry, leading to the symptoms of ASD
- growth w/o guidance
- frontal/temporal regions (amygdala)
- 2-4 year old with ASD larger MRI based brain volume

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11
Q

What is the over-pruning hypothesis of ASD?

A

Too many neurons are pruned in the motor and/or sensory regions
- 8-16 year old with ASD smaller MRI based volume

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12
Q

How are mirror neurons affected in ASD?

A
  • Activity in the anterior component of the MNS was found to be reliably greater in typically developing children
  • There is a negative correlation between scores on social subscales and MNS activity
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13
Q

What is the empathizing-systemizing theory in ASD?

A
  • Systemizing is the drive to analyze or construct systems (orderly/patterns)
  • There seems to be an inverse correlation between having: below-average empathizing, above-average systemizing
  • Males tend to be more systemizers than females
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14
Q

What are some current pharmacological interventions of ASD?

A

Oxytocin has been used to reduce social impairment in ASD. Oxytocin reduced the tendency for participants with ASD to fixate on the most systemized stimuli.
- Oxytocin is elevated following childbirth and facilitates bonding and empathy
- Mixed results: Some studies show benefits while others do not (which could be related to dosing, timing, heterogeneity of ASD)

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15
Q

Who is the first person to claim that the left hemisphere was asymmetrically dominant for speech?

A

Marc Dax

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16
Q

How did Broca discover the left hemisphere’s dominance in language?

A

Paul Broca reported the results of postmortem exams of two aphasic patients that they had diffuse left hemisphere damage, centering in an area of the inferior left prefrontal lobe, just in front of the primary motor face area.

  • “LeBrougne” was one of his patients that was only able to say “tan”.
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17
Q

What are the three core symptoms that defines Broca’s aphasia?

A
  • Agrammatism: severe issues using grammar
  • Anomia: inability to produce the right words
  • Articulation problems
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18
Q

What did Carl Werincke report on?

A

A new type of language disorder: Wernicke’s aphasia (inability to comprehend language, but can speak fluently)

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19
Q

What was Liepmann’s work with the left hemisphere?

A

Liepmann showed that apraxia was almost always associated with left hemisphere damage.

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20
Q

What is apraxia?

A

Difficulty performing movements with either side of the body when asked to do so, but not when performing them spontaneously

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21
Q

What is the Wada Test (aka Sodium Amytal test)?

A
  • Sodium amytal is injected into one carotid artery; this anesthetiezes the ipisilateral hemisphere and allows the abilitites of the contralateral hemisphere to be assessed.
  • Administered to patients prior to neurosurgery to determine side of speech lateralization.
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22
Q

What is the dichotic listening task?

A
  • Two different syllables played to different ears.
  • The ear that hears one sound the most means that the contralateral hemisphere is dominant for language
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23
Q

What has fMRI data shown for lateralization?

A
  • During word generation task, (where participants are shown a probe letter and have to think of as many words starting with that letter as possible within 30s) increased fMRI activation found in the dominant hemisphere
  • During passive listening there is increased activation in the dominant hemisphere
  • There is still some activation in the non-dominant hemisphere though!
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24
Q

What did the study by Hausmann find in regards to lateralization?

A

When participants spoke, a majority opened the right half their mouth slighty more than the left

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25
Q

What are the statistics for laterality and handedness?

A
  • Left hemisphere dominance: 88% of right-handers, 78% of left-handers
  • Ambilateralization: 12% of right-handers, 15% of left-handers
  • Right hemisphere dominance: 0% of right-handers, 7% of left-handers
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26
Q

What are the sex differences in laterality?

A
  • Early research seemed to suggest that the brains of males are more lateralized than those of females
  • However, more recent evidence has failed to confirm this
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27
Q

What ability displays the greatest degree of laterality?

A

Language

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28
Q

What is the Wernicke-Geschwind model of language for responding to a heard question?

A
  • Auditory language information is heard by the primary auditory cortex, which then travels to Wernicke’s area where comprehension occurs, and the thought of the response is generated.
  • Then to Broca’s area, where the program of articulation is gneerated and passed to the primary motor cortex
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29
Q

What is the Wernicke-Geschwind Model of reading aloud?

A
  • Words read aloud “read” by primary visual cortex
  • Information travels to the angular gyrus, where it is translated into an auditory form
  • Information then travels to Wernicke’s area for comprehension and response-thought generation
  • Then to Broca’s area and the primary motor cortex, for output
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30
Q

What is the current status of the Wernicke-Geschwind Model of language? (4)

A
  • Broca’s and Wernicke’s area are important in language
  • Expressive aphasia generally results from anterior damage
  • Receptive (fluent) aphasia generally results from posterior damage
  • Little support for other aspects of the model
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31
Q

What are 5 problems with the Wernicke-Geschwind model of language (not including stimulations)?

A
  • No aphasic patients have damage restricted only to Broca’s area or Wernicke’s area
  • Aphasic patients almost always have significant damage to subcortical white matter
  • Damage associated with aphasia is usually not related to damage to Wernicke-Geschwind areas
  • Large anterior lesions are more likely to produce epxressive symtoms, while large posterior lesions are more likely to produce receptive symptoms
  • Fails to consider roles of subcortical structures, like the cerebellum
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32
Q

What are other problems with the Wernicke-Geschwind model of language (in terms of stimulation experiments)?

A

Stimulations of brain regions are more diffuse than the regions outlined by the model

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33
Q

What are the 3 premises of the cognitive neuroscience approach to language?

A
  1. Constituent cognitive processes
  2. Language areas are not exclusive
  3. Areas are small and widely distributed
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34
Q

What is the dual stream model of language?

A
  • Dorsal stream for sensorimotor integration (mostly dominant)
  • Ventral stream for speech comprehension (bilateral)
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35
Q

What is aphasia?

A
  • Aphasia is a disorder that results from dysfunction of the brain’s language systems
  • The disorder can impair the expression and/or understanding of language, as well as reading + writing
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36
Q

Describe the progession of aphasia

A

Usually occurs suddenly, often following a stroke or head injury, but it may also develop slowly, as the result of a brain tumor or neurodegenerative disease

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36
Q

What is another condition that can co-occur with aphasia?

A

May co-occur with other speech disorders, such as apraxia of speech

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37
Q

What is global aphasia?

A
  • Speech is not fluent
  • Lack of language comprehension
  • Cannot repeat words or phrases
  • Damage to extensive portions of the language networks
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38
Q

What is Broca’s aphasia?

A
  • Speech is not fluent
  • Has language comprehension
  • Unable to repeat words/phrases
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39
Q

What is Wernicke’s aphasia?

A
  • Fluent speech
  • Lack of language comprehension
  • Cannot repeat words/phrases
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40
Q

What is anomic aphasia?

A
  • Speech is fluent
  • Has language comprehension
  • Can repeat words/phrases
  • Word retrieval failures and cannot express the words they want to say (particularly nouns + verbs)
  • Lesions associated are the least well-defined, spanning a wide range of areas in the left hemisphere
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41
Q

What is primary progressive aphasia?

A
  • A syndrome wherein language capabilities become slowly and progressively impaired
  • Unlike other forms of aphasia, it is usually cuased by neurodegenerative diseases (e.g. Alzheimer’s Disease), where there is progressive damage to language related areas
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42
Q

What are 4 factors that influence recovery from aphasia?

A
  • Cause of injury
  • Area and extent of damage
  • Age
  • General health
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43
Q

How can therapy with speech-language pathologists support patients in regaining their ability to communicate?

A
  • Therapy aims to improve communicate by:
    1. Activating remaining language abilities
    2. Restoring language abilities as much as possible
    3. Learning other communication skills
  • Language and communication abilities can continue improving for many years
44
Q

What are 5 properties of a neuropsychological test?

A
  • Standardized
  • Reliability
  • Norm-referenced
  • Criterion validity
  • Ecological validity
45
Q

What are 4 examples of neuropsychological tests of working memory?

A
  1. Digits backwards
  2. Tally updating
  3. List sorting
  4. Self-ordered pointing
46
Q

What is the interpretive procedure for neuropsychological tests?

A

Test validity -> Estimated premorbid functioning -> Impaired (+ normal) test scores -> Impaired (+ preserved) abilities -> Etiology/Prognosis + Functional Consequences + Treatment/Management

47
Q

What is an example of how is performance validity assessed?

A

By comparing a “good effort” performance curve looks like to what the tested performance curve looks like.

48
Q

How is premorbid function estimated?

A

Predicted based on age, education level, etc…
- can use “Hold” tests (testing for premorbid intelligence, by measuring abilities that are largely resistant to cognitive decline)

49
Q

What are some limitations to neuropsychological tests? (5)

A
  • Poor access in public health care
  • Most tests measure more than one cognitive ability (interpreting reason for low score can be difficult)
  • Few validated tests for important abilities (e.g. “hot” decision-making, social cognition)
  • Quiet and distraction-free, to get examinee’s “best performance” (may limit ecological validity)
  • Cultural bias in tests and norms
50
Q

What are 8 situations that may need a neuropsychological assessment?

A
  • Differential diagnosis
  • Monitor disease progression
  • Clarify impact of injury/disease
  • Determine rehabilitation needs
  • Capacity for IADLs, work, study
  • Surgical candidacy
  • Legal competency
  • Medicolegal
51
Q

What is the criteria for atypicality? (4)

A

1.Statistical atypicality

2.Violation of socially-accepted standards
- Maladaptivity (counter-productive behaviour)

3.Subjective atypicality and/or discomfort (e.g., Harmful Dysfunction)
- To the “abnormal” individual
- To others

4.Biological injury or atypicality

52
Q

What is the oldest psychiatric hospital in the world?

A

Bedlam

53
Q

What are the 4 purposes of the DSM-5?

A
  1. Guide treatment choices
  2. Allow clinicians to communicate
  3. Please insurance companies who require a concrete diagnosis
  4. Permit research (via categorization)
54
Q

What is the diagnosis criteria for MDD? (9)

A

5+ of the following symptoms present during the same 2-week period; at least 1 of the symptoms is either: (1) depressed mood or (2) loss of interest or pleasure (anhedonia)
1. Depressed mood
2. Anhedonia
3. Significant weight loss/gain, or increase/decrease in appetite
4. Insomnia/Hypersomnia
5. Observable psychomotor agitation/retardation
6. Fatigue/loss of energy
7. Feelings of worthlessness or excessive/inapproporiate guilt
8. Diminished ability to think/concentrate, or indecisiveness
9. Recurrent thoughts of death; recurrent suicidal ideation w/o specific plan; a specific suicide plan; or a suicide attempt

55
Q

What is hypomania in BD? (7)

A

Characterized by some of the following (doesn’t lead to severe disruption of work/result in social rejection; no hallucinations/delusions)
- persistent mild elevation of mood
- increased energy + activity
- marked feelings of well-being and both physical and mental efficiency
- increased sociability + talkativeness (or increased irritability in some)
- increased sexual energy
- decreased need for sleep
- no hallucinations/delusions (i.e., no psychosis)

56
Q

What is the criteria for BD II?

A
  1. Criteria have been met for at least one hypomanic episode and at least one MDD episode
  2. There has never been a manic episode
57
Q

What is the criteria for a manic episode? (7)

A

A. Distinct period of abnormally and persistently elevated/expansive mood and abnormally + persistently increased goal-directed activity/energy, lasting at least 1 week and present most of the day, nearly every day

B. 3+ of the following are present to a significant degree:
- Inflated self-esteem/grandiosity
- Decreased need for sleep
- More talkative than usual/pressure to keep talking
- Flight of ideas/subjective epxerience that thoughts are racing
- Distractibility
- Increase in goal-directed activity or psychomotor agitation
- Excessive involvement in activities that have a high potential for painful consequences

58
Q

What is the most dangerous period in BD?

A

Mixed (most likely to commit suicide)

59
Q

What is the criteria for BD I?

A

Same as BD II, but includes manic episodes

60
Q

What is the prevalence of BD?

A

~ 1% of global population
~ 0.6% BD I
~ 0.4% BD II

61
Q

What is rapid cycling in BD?

A

4 or more mood cycles a year

62
Q

What is euthymia?

A

“Stable” mood state, neither depressive or manic

63
Q

What are 5 major risks with BD?

A
  1. High rate of reccurence
  2. High risk for suicide attempts: 1/3 - 1/2 of persons with a BD
  3. Highest risk for completed suicide among any psychiatric disorder ~20 times higher than rate among general population
  4. 6th leading cause of disability for people aged 15-44 years
  5. All of the above are exacerbated by the fact that individuals with BD often don’t adhere to treatments
64
Q

What are 4 psychiatric comorbidities with BD?

A
  1. Anxiety disorders
  2. Substance use disorders
  3. Attention-deficit/hyperactivity disorder
  4. Personality disroders
65
Q

What are 3 nonpsychiatric comorbidities?

A
  1. Migraine
  2. Cardiovascular disorders
  3. Endocrine disorders
66
Q

What are 3 structural brain changes that occur with BD?

A

1.Reductions in gray matter

2.Several structures smaller in patients with BD:
- Medial PFC + other prefrontal regions
- Left anterior cingulate cortex
- Left superior temporal gyrus
- Hippocampus

3.Increased striatal volume

67
Q

What are cognitive changes that occur with BD? (3)

A
  • Impairments in executive function (particularly inhibition) in individuals with BD who are in remission and in unaffected family members (to a lesser degree)
  • Cognitive impairments more pronounced on tasks using emotional stimuli vs. tasks with neutral stimuli
  • Executve function deficits can be potentially used to predict the onset of a BD in those at risk
68
Q

What are the findings of Kyaga et al. that looked at creativity and psychiatric disorders? (4)

A
  • There is no evidence that depression is associated with creative professions
  • There is no evidence that schizophrenia is associated with creative professions
  • There is evidence that bipolar disorder is associated with creative professions
  • Close relatives of individuals with schizophrenia and bipolar disorders are more likely to hold a creative profession
69
Q

What is a mood stabilizer?

A

A drug that has antimanic and/or antidepressant effects and also prevents cycling

70
Q

What are pharmacological treatments for BD? (3)

A
  • Antidepressants for the depression
  • Antipsychotics (and other drugs) for the mania or hypomania
  • Mood stabilizers
71
Q

What is the Kindling/Sensitization model of BD?

A

Mood episode changes occur from stressors, and overtime, episodes become independent of stressors (spontaneous episodes)
- Conditioned compensatory response is a source of hypomania

72
Q

What are 3 sorts of mood stabilizers?

A
  1. lithium
  2. anticonvulsants (lamotrigine)
  3. atypical antipsychotics (aripiprazole)
73
Q

What is a mood stabilizer with more antidepressant predominance on the polarity index?

A

Lamotrigine

74
Q

How does lithium work? (5)

A
  • Treats current mood episodes and protects against further mood episodes
  • Neuroprotective and preferentially accumulates in brain regions that produce new neurons
  • Chronic administration increases BDNF expression in rat brains
  • Relatively fast-acting anti-suicidal agent
  • Inhibits pro-inflammatory cytokines
74
Q

What is a mood stabilizer with more antimanic predominance on the polarity index?

A

Aripiprazole

75
Q

What is the fastest anti-suicidal agent?

A

Ketamine

76
Q

What are 2 examples of anticonvulsants that are considered to be effective mood stabilizers?

A
  1. Valproate semisodium
  2. Lamotrigine
77
Q

What are 3 examples of atypical antipsychotics that are considered to be effective mood stabilizers?

A
  1. Quetiapine
  2. Olanzapine + SSRI
  3. Aripiprazole
78
Q

What is the reward hypersensitivity model of BD?

A

Vulnerability to BD is the result of a hypersensitive reward system: Overreactive to goal- and reward-cues
- Goal/reward attainment is hypothesized to lead to excessive goal/reward activation which then leads to a cluster of hypomanic/manic symptoms
- Goal/reward nonattainment is hypothesized to lead to excessive goal/reward deactivation which then leads to a cluster of depressive symptoms

79
Q

What are prodromal features of hypomania and mania? (2)

A
  • excessive goal setting
  • increased success expectancies
80
Q

What are prodromal features of depressive episodes? (3)

A
  • decreased motivation
  • decreased goal setting
  • low self-confidence
81
Q

Euthymic individuals with BD tend to make more of what kind of choices/decisions, compared to controls?

A

Riskier choices

82
Q

What do imaging studies show for individuals with BD, that support the reward hypersensitivity model? (3)

A
  • structural imaging studies report abnormalities in PFC volume, and increased striatal volume
  • PET studies show increased metabolism in the striatum of both manic and depressed individuals with BD
  • fMRI studies report excessive increases in frontal-striatal reward-related activities in response to reward-related cues in euthymic states in individuals with BD
83
Q

What did Alloy et al. (2012) find in their study that supports the reward hypersensitivity model?

A
  • Used a prospective design where they selected individuals 14-19 years of age who either scored high on multiple self-report measures of reward sensitivity or who scored average on the same measures
  • Those who scored high were more likely to develop a BD (12% vs. 4%) and had a shorter latency to the onset of a BD (after controlling for family history of BD)
84
Q

Who was the first to synthesize LSD?

A

Dr. Albert Hoffman

85
Q

What receptors are important for binding with LSD?

A
  • 5-HT2A receptor (Serotonin Type 2a receptor)
  • Dopamine Type 1 and Type 2 receptors (metabotropic): associated w/ thought disorder and paranoia
  • Serotonin Type 1a receptor (metabotropic): may be responsible for some of the visual effects associated w/ LSD, psilocybin, and DMT
86
Q

What are the 2 phases of the acute effects of LSD?

A

Early phase = psychedelic (serotonergic)
Late phase = paranoia (not always; dopaminergic)

87
Q

What is the serotonin hypothesis of schizophrenia? (3)

A
  1. The psychological effects of LSD and psilocybin/psilocin are mediated by the 5-HT2A receptor
  2. 5-HT2A receptor abnormalities are evident in the brains of schizophrenia patients and at-risk patients
  3. 5-HT2A receptor antagonism is known to contribute to the effects of atypical antipsychotics (e.g. clozapine, risperidone)
88
Q

What is diagnosis for schizophrenia according to the DSM-5?

A

Two or more of the following, each present for a significant portion of time during a 1-month period. At least one of these must be (1), (2), or (3):
1. Delusions
2. Hallucinations
3. Disorganized speech
4. Grossly disorganized or catatonic behaviour
5. Negative symptoms

Impaired functioning in one or more major areas, such as work, interpersonal relations, or self-care.
Continuous signs of the disturbance persist for at least 6 months.

89
Q

What is the etiology of schizophrenia?

A

A combination of genetic and enviromnetal factors

90
Q

What is the threshold dose for LSD?

A

25 micrograms

91
Q

What is the genetic etiology of schizophrenia?

A

Common variants: SNPs
Rare variants: Deletions/duplications

92
Q

What is the neurodevelopment hypothesis of schizophrenia?

A

Suggests that schizophrenia results from abnormal brain development

93
Q

What are 4 pieces of evidence for the neurodevelopment hypothesis of schizophrenia?

A
  • Pre/post-natal risk factors
  • Altered child development
  • Gross pathology (smaller brain volume, larger ventricles)
  • Microscopic pathology (neuronal migration altered)
94
Q

What is the dopamine hypothesis of schizophrenia?

A

Suggests that schizophrenia results from increased dopamine levels

95
Q

What are 2 pieces of evidence that support the dopamine hypothesis of schizophrenia?

A
  • Drugs decreasing DA transmission alleviate psychosis (antipsychotics act at D2 receptors)
  • Drugs increasing DA transmission can cause psychosis (PCP, ketamine)
96
Q

What are 4 DA pathways?

A
  1. Nigrostriatal pathway (substantia nigra-striatum): Control of voluntary mvmt
  2. Mesolimbic pathway (VTA-Nacc): Reward, salience
  3. Mesocortical pathway (VTA-prefrontal cortex): Cognition, executive function
  4. Tuberoinfundibular pathway (hypothalamus-pituitary): Prolactin secretion
97
Q

What is a risk gene for schizophrenia that is a part of the complement system?

A
  • C4 gene, which produces a protein that attaches to synapses so that microglia phagocytose it
98
Q

What are 2 general approaches to functional imaging?

A
  1. Task based
  2. Resting state
99
Q

What happens to the brain networks of adolescents after a concussion?

A

Becomes more fractured/diffuse throughout the brain

100
Q

What happens to brain states of concussed adolescents?

A

Healthy adolescents switch between brain states
Concussed adolescents are “stuck” in brain state 2

101
Q

What are global metrics with respect to neural networks?

A

Measurement of the structural property regarding to the whole graph

102
Q

What are local metrics with respect to neural networks?

A

Measurement of the structural properties of each single node

103
Q

What is the current view of rest for concussion?

A

Rest is no longer the best medicine for post-acute concussion!
- Aerobic activity is used as a mode of intervention

104
Q

What is the clinical triad of Huntington disease?

A
  • Movement disorder: involuntary (chorea), and voluntary (incoordination)
  • Cognitive deficits: impaired frontal executive function
  • Behavioural changes: psychiatric disorders (depression, anxiety)
105
Q

What brain region is most affected in early cortical loss in Huntington disease?

A

Sensorimotor region is most affected in early cortical loss

106
Q

What are 2 sensory symptoms in patients with HD?

A
  • Reduced awareness of body in space
  • Altered auditory processing
107
Q

Define mesoscale

A

In between, at the network level (imaging or electrode arrays)

NSCI 302 (3 decks)

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