The Corticohippocampal circuit: Disorder Flashcards
(disorder of HF)
STUDY: israeli soldiers
remember study, consider how adverse PTSD affects were a result of hippocampal disorder
what happened to HM?
he suffered from an accident as a kid and developed epilepsy. Pennfield conducted a ground-breaking procedure (lobotomy, removed temporal lobe and hippocampi)
what was the impact of the lobotomy on HM?
- 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
why would HM experience full anterograde amnesia?
may occur because of distributed damage in sensory-associated areas but little in the HF
why would HM experience retrograde amnesia?
may occur because localized damage to specific pathways in HF (could also be because prolonged oxygen deprivation)
what did they find in the MRI of HM?
removed medial and temporal lobe bue some of HF intact in one hemisphere
what does recent tech about HF give insight into about HF?
can unfold HF to see what creates what, possible that targeted certain areas
STUDY: mirror-drawing task
tests motor functions for HM
RESULTS: didn’t recognize tasks but performed it progressively better
- learning occurs in the basal ganglia
who experiences loss of hippocampal tissue?
technically everyone, could be from aging of conditions, but natural slow loss
what is Alzheimer’s disease?
loss of exective control and memory loss
- fMIR finds atrophy in HF
- usually starts out as mild-cognitive-impairment (MCI)
what does the progression from healthy –> AD look like
healthy
MCI (greater HF activation, compensatory response
AD (hardly any hippocampal tissue left)
what is dementia?
deterioration of cognitive and emotional functioning
what is the greatest risk factor for AD?
family history
- sporadic Alzheimer’s disease associated with genetic marker (apoE) (E4 allele) – risk factor
- early onset family disease (known genetic mutations) – guaranteed
what is delusional misidentification syndrome?
*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
why does delusional misidentification syndrome occur?
- false theory: that trauma to brain disconnected amygdala from other parts of brain
- correct theory: disorders of memory and damage to HF, failure to assign and remember prior emotional experiences (sometimes because oxygen deprivation)
disorders of dlPFC
disorders of executive functioning
(disorder of dlPFC)
STUDY: *recall, MDD to negative facial expressions
found hypoactivity of dlPFC
- dlPFC controls emotions, explicit control
what occurs in disorder of cognitive reappraisal?
(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
how is reappraisal in GAD?
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
is dlPFC just associated with regulating negative emotion?
No. also impaired with dysfunction in making good things happen
STUDY: cognitive reappraisal and making good things happen
(look at positive scenes and try to increase your positive experience)
- dlPFC connectivity allows greater exertion of control
STUDY: relative threat response in Duke students
(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
what is the impact of CBT?
increases dlPFC activity
(task, put numbers in order)
TMS targeting of dlPFC
standard protocol, 30% remission, symptom improvement
addiction and substance disorders
- focus on long-term consequences, ties to a goal
STUDY: (addiction) asked to think about benefits now vs consequences later
dlPFC: activity increased when considered (-) consequences
VS: activity decreased as dlPFC activity increased
craving decreased as VS activity increased
is the dlPFC always good?
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
STUDY: (using TMS to disrupt left dlPFC)
(in order to decrease craving)
- when dlPFC disrupted, lower vmPFC and lower VS
- maintaining DA helps executive control
what is ADHD?
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
what are thought disorders?
deficits in following or generating logical sequences of thoughts, difficulty focusing, inability adapt behavioral response.
what is OCD?
persistent, uncontrollable, intrusive thoughts/ impulses (obsessions), patterns of uncontrollable and ritualized behavior (compulsions)
OCD and WCST (executive control)
dysfunction in dlPFC, vmPFC, dACC, DS (hypoactivity)
OCD and stroop task
heightened sensitivity to error, no trouble with choosing correct color, but take much longerw
why people with OCD take longer on stroop task?
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
maladaptive response to compulsions?
hyperactivity of dlPFC in anticipation of compulsions can drive physiological arousal and amygdala engagement
what treatment is most effective for OCD
exposure therapy
- not allowed to engage in compulsions, reduces stress and amygdala response
- strengthens executive control
what is bipolar disorder?
reoccurring cycles between manic episodes, euthymia, major depressive episodes
manic episodes
persistent feelings of euphoria
euthymia
normal mood and affect
bipolar disorder in amygdala
changes through each state
bipolar disorder in vlPFC
interestingly, always hypoactive in bipolar disorder
MIDT task and bipolar disorder
(during euthymia)
greater activity when win money in bipolar disorder
working memory task and bipolar disorder
less dlPFC activity in bipolar srates than healthy
what is schizophrenia?
near complete disintegration of the ability to integrate mental processes (cognition, emotion, motivation) in the service of generating adaptive behavioral responses; “split mind.”
what is a risk factor for schizophrenia?
deficits in executive control
positive symptoms (in schizophrenia)
delusions, hallucinations, possible violent behiavor
negative symptoms (in schizophrenia)
loss of emotional responsiveness and motivation, possibly to extreme of catatoniap
psychotic break
first, often sudden and unexpected episode of positive symptoms, in someone w schizophrenia (usually requires hospitalization)
catatonia
near-complete lack of movement and interaction with response to others and environment
how to treat schizophrenia?
hardest to treat, can’t do any of the tasks
n-back task and schizophrenia
- 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
what was the problem with earlier studies of schizophrenia?
incorrectly showed hypoactivity because didn’t consider performance
when does psychotic break occur?
usually after period of intense stress or mental exertion
dlPFC and symtom severity
lower symptom severity = higher dlPFC activity
schizophrenia and development of cortex
- during thinning, exaggerated and reaches dlPFC (loss of gray matter) (lower spine density)
schizophrenia compared to siblings without
greater strength of dACC and dlPFC in siblings w schizophrenia, but still high in siblings without
- could be a risk pattern
genome study of schizophrenia
could be associated with presynaptic pyramidal neurons and postsynaptic pyramidal neurons proteins
STUDY: longitudinal study of risk for schizophrenia
NO IDEA
STUDY: Thinning of cortex
greater rate of thinning = greater likelihood of developing schizophrenia
