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BA EXAM > Clinical Neuroscience > Flashcards

Clinical Neuroscience Flashcards

1
Q

The ToM (mentalizing) mechanisms helps us infer mental states of other people. The False Belief test is typically passed at what age?

A

4 years old

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2
Q

What are the substrates of social cognition?

A

TPJ, medial PFC, and mirror neurons system

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3
Q

What is TPJ responsible for?

A

Reasoning about mental states of others, redirecting attention in both social and nonsocial situations (lesions=> impaired ToM task)

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4
Q

What is the medial PFC responsible for?

A

Reasoning about other people as entitites, social tasks (lesions=> do not impair ToM tasks)

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5
Q

What is the mirror neurons system made up of?

A

Premotor cortex, parts of superior temporal sulcus, intraparietal cortex

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6
Q

Say a similarity and a difference between ToM and mirror neurons systems.

A

Similarity: they both engage TPJ areas.
Difference: Mirror Neurons system engages lateral motor cortex (for actions) and ToM engages medial PFC (for perceiving mental states)

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7
Q

Autism Spectrum Disorders are developmental disorders with deficits in:

A

Social communication/interaction and restricted, repetitive behaviors

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8
Q

What are the 3 types of social deficits in ASD?

A

-Social-emotional reciprocity
-Non-verbal communicative behaviors in social interactions (poor eye contact)
-Developing, mantaining and understanding relationships deficits (control, sociality, motivation)

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9
Q

What are the 4 types of restricted, repetitive patterns of behaviors, interests or activities in ASD?

A

-Stereotyped or repetitive behavior
-Insistence on sameness
-Highly restricted, fixated interests
-Hyper- or hypo-activity

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10
Q

How can ASD be assessed psychologically?

A

-Verbal+Non-verbal Skills assessment (comunication)
-Social-Adaptive and Social Emotional Behaviors
-Autism Diagnostic Interview-Revised (ADI-R): interview of caregivers
-Autism Diganostic Observation Schedule (ADOS): patients are observed

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11
Q

What is the most connected structure in the brain?

A

MTL

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12
Q

Amygdala is involved in:

A

-Fear-related processing (psychic blindness, no fear cause by damage to amygdala in monkeys and in patient S.M.)
-Arousal/salience/vigilance: stimuli are made salient, it activates arousal, it reacts to both positive and negative stimuli

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13
Q

What does LeDoux’s theory say?

A

There is a low-road made up of subcortical structures (thalamus-amygdala; quick and shallow processing for fight-or-flight), and a high-road made up of cortex (thalamus-sensory cortices-amygdala; slow or sophisticated processing).

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14
Q

What are the antecedent-focused ER?

A

Situation selection, situation modification, attentional deployment, reappraisal

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15
Q

What is the response-focused ER?

A

Supression

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16
Q

What regions are involved in emotion-down regulation?

A

Prefrontal and parietal control regions (healthy subject VMPFC can decrease amygdala activity during regulation, in depressed subjects the opposite effect occurs)

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17
Q

In order to diagnose someone with depression, the following have to be present:

A

-a major depression episode
-depressed mood/interest for at least 2 weeks
-significant distress, disengagement, anhedonia

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18
Q

What are the brain changes in depression?

A

-In chemistry: serotonin, norepinephrine, cortisol
-Structural: reduced gray matter volume in hippocampus, thalamus, frontal cortex, prefrontal cortex, enlarged amygdala (acutely) vs reduce (chronically)
-Functional: networks of brain areas are under- or over-activated

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19
Q

What disorders are anxiety disorders?

A

Panic disorders, generalized anxiety disorder,obsessive compulsive disorder (OCD), phobias (specific vs social)

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20
Q

What are the two types of traumatic brain injuries (TBIs)?

A

-Open head/pentrating head injury
-Closed-head/blunt head injury (rapid acceleration followed by deceleration; coup vs countercoup injury)

21
Q

What can happen after a traumatic brain injury?

A

-Diffuse axonal injury (shearing and tearing)
-Edemas (swelling of the brain or icnreased intracranial pressure) => main cause of death
-Herniation (downward displacement of the brain caused by edema or hematoma/pool of blood) [if brain stem => coma, respiratory failure, death]

22
Q

What does Glasglow coma scale measure?

A

Depth and duration of coma on 3 types of responses: motor, verbal, eye-opening. Lower score= worse functioning

23
Q

What are the 3 types of TBIs by severity?

A

-Mild (Glasgow Coma Scale: 13-15; Consciousness Loss: <30 min; Post-Traumatic Amnesia: <24h)
-Moderate (Glasgow Coma Scale: 9-12; Consciousness Loss: 30 min-24h; Post-Traumatic Amnesia: 1-7days)
-Severe (Glasgow Coma Scale: 3-8; Consciousness Loss: >24h; Post-Traumatic Amnesia: >7 days)

24
Q

What neuropsychological assessments are used for identifying deficits after TBIs in intelligence, attention/concetration, memory, and executive functions?

A

Intelligence: WAIS-R (age-corrected)
Attention/concentration: Digit span, mental control, WMS, Trails A and B
Memory: Verbal and Non-verbal (WMS, Rey-Osterrieth)
Executive functions: Stroop, Wisconsin Card Sorting Test, WISC-R Mazes, Design, Fluency

25
Q

What neuropsychological assessments are used for identifying deficits after TBIs in perception, sensations and motor areas, and emotional areas?

A

Perception: Rey-Osterrieth Complex Figure Copy, Hooper Visual Organization Test
Sensation and motor: Grip strength, Finger tapping
Emotional status: Beck Depression Inventory

26
Q

What is the anatomy of memory?

A

-Medial temporal lobe: hippocampus and interconnected structures (entorhinal, perihinal, parahippocampal cortex), amygdala
-PFC: WM, LTM, working with memory

27
Q

What brain regions are responsible for recollection and familiarity?

A

Recollection: hippocampus
Familiarity: perirhinal cortex

28
Q

Retrograde amensia is a deficit in:

A

recollecting past memories

29
Q

Anterograde amensia is a deficit in:

A

forming new memories

30
Q

Patient H.M. lead to which discovery?

A

His hippocampus and MTL cortices were removed, which lead to gloval anterograde amnesia, temporarily limited retrograde amnesia (intact remote memories) with intact STM => STM (procedural/implict memory) is distinct from LTM (explicit memory)

31
Q

Hyperthymestic syndrome is a autobiographical memory syndrome in which a person spends an abnormally large amount of time thinking about their personal past and have an extraordinary capacity to recall specific past personal event. True or false?

A

True

32
Q

What is malingering?

A

Intentional production of false/grossly exaggerated physical or psychological problems

33
Q

What are the neural substrated of speech perception?

A

-Left perisylvean language network
-STG (lesion => pure word deafness)
-Primary Auditory cortex

34
Q

What is Broca’s aphasia?

A

Expressive aphasia/problem related to production and understanding syntax cause by lesions in left inferior frontal gyrus (Broca’s area) typically also involving surrounding white matter and subcortical structures.

35
Q

What are symptoms of Broca’s aphasia?

A

Telegraphic speech, agrammatism

36
Q

What is Wernicke’s aphasia?

A

Receptive aphasia/disturbance in comprehension cause by lesion in posterior third of left superior temporal gyrus (Wernicke’s area)

37
Q

What are symptoms of Wernicke’s aphasia?

A

Word salad, neologisms, semantic paraphasias

38
Q

What is conduction aphasia?

A

Problem with moving linguistic info rapidly from input to output (damage to articulate fasciculus=bundle of neurons which connect Broca’s and Wernicke’s areas) [can understand words and own errors]

39
Q

What is global aphasia?

A

The inability to comprehend or produce speech (extensive lesions in the left perisylvean area)

40
Q

What is dyslexia?

A

Difficulty in reading, not due to sensory or intellectual impairment, which can be at surfface (appearance of language) or deep (sound structure) level. (less activity in Wernicke’s area, compensatory activity in the left anterior language areas and the right hemisphere)

41
Q

What is the anatomy of cognitive control?

A

-lateral PFC: selective attention, STM, planning, action selection, response inhibition
-vmPFC/orbitofrontal cortex: emotion and reward processing, decision making
-medial frontal cortex/ACC: error detection, resolving conflict, rational cognitive functions

42
Q

What are the processes involved in goal-oriented behavior?

A

Planning, sequencing, goal maintanance, switching, selection of relevant information/inhibition of irrelevant information, goal monitoring

43
Q

Damage to dorsolateral PFC can lead to impaired:

A

Planning (psychological ineritia, patient W.R. who “lost his ego”) and sequencing (tested by Tower of London task)

44
Q

Goal maintenance can be tested with the wander off task. Damage to PFC lead to impairment in this task. True or false?

A

True

45
Q

How can switching be tested?

A

Trail-making task, Wisconsin card sorting task (frontal lobe patients show perseveration)

46
Q

Dorsolateral PFC is involved in _____, while ventrolateral PFC is involved in _____.

A

creatining and mantaining attentional set; inhibition (Stroop test, Go/No-Go task)

47
Q

In the food version of Go/No-Go task, succesful weight losers have greated dlPFC activation when viewing high-energy food, while unsuccessful/overweight participants have higher activation in:

A

Ventral striatum & anterior cingulate cortex.

48
Q

Error detection hypothesis states that:

A

ACC is involved in detecting errors to increase cogntive control (error-related potential reduced in frontal lobe patients and increased in OCD)

49
Q

Response conflict hypothesis states that:

A

ACC evaluates response conflict (evidence from Stroop task: ACC higher in incongruent trials even when no mistakes are made) => ACC is modulated by monitoring demands

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