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NEURO 277 > The Corticohippocampal circuit: Disorder > Flashcards

The Corticohippocampal circuit: Disorder Flashcards

1
Q

(disorder of HF)
STUDY: israeli soldiers

A

remember study, consider how adverse PTSD affects were a result of hippocampal disorder

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2
Q

what happened to HM?

A

he suffered from an accident as a kid and developed epilepsy. Pennfield conducted a ground-breaking procedure (lobotomy, removed temporal lobe and hippocampi)

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3
Q

what was the impact of the lobotomy on HM?

A
  • full anterograde amnesia: couldn’t form new memories in the future
  • retrograde amnesia: couldn’t remember past events, but not complete temporally graded, the further back the memories go the more likely he was to remember them
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4
Q

why would HM experience full anterograde amnesia?

A

may occur because of distributed damage in sensory-associated areas but little in the HF

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5
Q

why would HM experience retrograde amnesia?

A

may occur because localized damage to specific pathways in HF (could also be because prolonged oxygen deprivation)

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6
Q

what did they find in the MRI of HM?

A

removed medial and temporal lobe bue some of HF intact in one hemisphere

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7
Q

what does recent tech about HF give insight into about HF?

A

can unfold HF to see what creates what, possible that targeted certain areas

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8
Q

STUDY: mirror-drawing task

A

tests motor functions for HM
RESULTS: didn’t recognize tasks but performed it progressively better
- learning occurs in the basal ganglia

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9
Q

who experiences loss of hippocampal tissue?

A

technically everyone, could be from aging of conditions, but natural slow loss

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10
Q

what is Alzheimer’s disease?

A

loss of exective control and memory loss
- fMIR finds atrophy in HF
- usually starts out as mild-cognitive-impairment (MCI)

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11
Q

what does the progression from healthy –> AD look like

A

healthy
MCI (greater HF activation, compensatory response
AD (hardly any hippocampal tissue left)

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12
Q

what is dementia?

A

deterioration of cognitive and emotional functioning

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13
Q

what is the greatest risk factor for AD?

A

family history
- sporadic Alzheimer’s disease associated with genetic marker (apoE) (E4 allele) – risk factor
- early onset family disease (known genetic mutations) – guaranteed

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14
Q

what is delusional misidentification syndrome?

A

*super obscure, think invasion of the body snatchers
- capgras syndrome = someone in family you believe to be a stranger
- pygdi syndrome = someone unknown you misidentify as someone known

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15
Q

why does delusional misidentification syndrome occur?

A
  1. false theory: that trauma to brain disconnected amygdala from other parts of brain
  2. correct theory: disorders of memory and damage to HF, failure to assign and remember prior emotional experiences (sometimes because oxygen deprivation)
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16
Q

disorders of dlPFC

A

disorders of executive functioning

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17
Q

(disorder of dlPFC)
STUDY: *recall, MDD to negative facial expressions

A

found hypoactivity of dlPFC
- dlPFC controls emotions, explicit control

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18
Q

what occurs in disorder of cognitive reappraisal?

A

(ex. “the shop is closed but at least I got to get out of the house in this beautiful weather”)
- greater activity in the dlPFC when reappraise (concurrent with amygdala activity)
- capacity to regulate and decrease amgydala response associated with greater dlPFC reaction and lower MDD

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19
Q

how is reappraisal in GAD?

A

when people with MDD can downregulate amygdala activity, they report lower and less severe symptoms
- dlPFC activity increases with lower symptom severity in GAD and PD

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20
Q

is dlPFC just associated with regulating negative emotion?

A

No. also impaired with dysfunction in making good things happen

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21
Q

STUDY: cognitive reappraisal and making good things happen

A

(look at positive scenes and try to increase your positive experience)
- dlPFC connectivity allows greater exertion of control

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22
Q

STUDY: relative threat response in Duke students

A

(did executive control impact better response to threat/ reward)?
- used threat response for amygdala, money for VS activation and memory test for dlPFC
RESULTS:
- high amygdala + low VS = high anxiety
- low dlPFC + high amygdala = high anxiety

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23
Q

what is the impact of CBT?

A

increases dlPFC activity
(task, put numbers in order)

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24
Q

TMS targeting of dlPFC

A

standard protocol, 30% remission, symptom improvement

25
Q

addiction and substance disorders

A
  1. focus on long-term consequences, ties to a goal
26
Q

STUDY: (addiction) asked to think about benefits now vs consequences later

A

dlPFC: activity increased when considered (-) consequences
VS: activity decreased as dlPFC activity increased
craving decreased as VS activity increased

27
Q

is the dlPFC always good?

A

not necessarily, can train executive control to influence bad decisions
* think of body perception study, how greater functional connectivity caused people to eat less the next day

28
Q

STUDY: (using TMS to disrupt left dlPFC)

A

(in order to decrease craving)
- when dlPFC disrupted, lower vmPFC and lower VS
- maintaining DA helps executive control

29
Q

what is ADHD?

A

inattentive DA: focus on task-related information
- decrease frontal parietal cortex, PFC, basal ganglia (motor output, deficient response)
- frontal parietal network, connection between pareital cortex and dlPFC

30
Q

what are thought disorders?

A

deficits in following or generating logical sequences of thoughts, difficulty focusing, inability adapt behavioral response.

31
Q

what is OCD?

A

persistent, uncontrollable, intrusive thoughts/ impulses (obsessions), patterns of uncontrollable and ritualized behavior (compulsions)

32
Q

OCD and WCST (executive control)

A

dysfunction in dlPFC, vmPFC, dACC, DS (hypoactivity)

33
Q

OCD and stroop task

A

heightened sensitivity to error, no trouble with choosing correct color, but take much longerw

34
Q

why people with OCD take longer on stroop task?

A

dysfunction of dlPFC
- greater dACC in incongrunt trials
- greater functional connectivity between dACC and dlPFC
WHY? stuck in a pattern of error recognition, can’t shift attention from intrusive thoughts

35
Q

maladaptive response to compulsions?

A

hyperactivity of dlPFC in anticipation of compulsions can drive physiological arousal and amygdala engagement

36
Q

what treatment is most effective for OCD

A

exposure therapy
- not allowed to engage in compulsions, reduces stress and amygdala response
- strengthens executive control

37
Q

what is bipolar disorder?

A

reoccurring cycles between manic episodes, euthymia, major depressive episodes

38
Q

manic episodes

A

persistent feelings of euphoria

39
Q

euthymia

A

normal mood and affect

40
Q

bipolar disorder in amygdala

A

changes through each state

41
Q

bipolar disorder in vlPFC

A

interestingly, always hypoactive in bipolar disorder

42
Q

MIDT task and bipolar disorder

A

(during euthymia)
greater activity when win money in bipolar disorder

43
Q

working memory task and bipolar disorder

A

less dlPFC activity in bipolar srates than healthy

44
Q

what is schizophrenia?

A

near complete disintegration of the ability to integrate mental processes (cognition, emotion, motivation) in the service of generating adaptive behavioral responses; “split mind.”

45
Q

what is a risk factor for schizophrenia?

A

deficits in executive control

46
Q

positive symptoms (in schizophrenia)

A

delusions, hallucinations, possible violent behiavor

47
Q

negative symptoms (in schizophrenia)

A

loss of emotional responsiveness and motivation, possibly to extreme of catatoniap

48
Q

psychotic break

A

first, often sudden and unexpected episode of positive symptoms, in someone w schizophrenia (usually requires hospitalization)

49
Q

catatonia

A

near-complete lack of movement and interaction with response to others and environment

50
Q

how to treat schizophrenia?

A

hardest to treat, can’t do any of the tasks

51
Q

n-back task and schizophrenia

A
  • less efficient dlFPC
  • hypofrontality (can do fewer iterations), can’t really maintain working memory
  • greater dlPFC activity for lower memory location and lower dlPFC activity in healthy people
52
Q

what was the problem with earlier studies of schizophrenia?

A

incorrectly showed hypoactivity because didn’t consider performance

53
Q

when does psychotic break occur?

A

usually after period of intense stress or mental exertion

54
Q

dlPFC and symtom severity

A

lower symptom severity = higher dlPFC activity

55
Q

schizophrenia and development of cortex

A
  • during thinning, exaggerated and reaches dlPFC (loss of gray matter) (lower spine density)
56
Q

schizophrenia compared to siblings without

A

greater strength of dACC and dlPFC in siblings w schizophrenia, but still high in siblings without
- could be a risk pattern

57
Q

genome study of schizophrenia

A

could be associated with presynaptic pyramidal neurons and postsynaptic pyramidal neurons proteins

58
Q

STUDY: longitudinal study of risk for schizophrenia

A

NO IDEA

59
Q

STUDY: Thinning of cortex

A

greater rate of thinning = greater likelihood of developing schizophrenia

NEURO 277 (9 decks)

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