SPRING Frontostriatal Disorders Flashcards

1
Q

define executive function

A

encompasses activities we need to do as humans

regulation and motor control

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2
Q

what is the basal ganglia

A

group of complect grey matter structures beneath the cortex- protected by neocortex
highly connected to frontal cortex with relay system between f.cortex and thallamus
regulates higher order cog function and execution of complex motor strategies - in charge of overall processess but not direct involvement

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3
Q

what makes up the ventral striatum of the basal ganglia

A
caudate nucleas (inside putamen)
nucleas accumbens ('reclining nucleas')
putamen
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4
Q

what makes up the lenticular nuclease of the basal ganglia

A
putamen
globus pallidus (GPe-external, GPi-internal)
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5
Q

what makes up the whole of the BG

A
caudate nuclease
nucleus accumbens
putamen
global pallidus (GPe/GPi)
subthallamic nucleas
substantia nigra (pars reticula(SNr)/Compacta(SNc)
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6
Q

what are the different frontostriatal circuits

A
DLPFC (cognitive)
motor
oculomotor (eye)
orbitofrontal (Affect)
anterior (limbic) cingluate (Affect) 
- all pass through the striatum and are densely linked to the frontal cortex
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7
Q

BG involvement in frontostriatal circuits

A

intermediatary for communication between cortex and thallamus to initiate activity
indirect role in modulating and regulating the motor cortex to the skeletal system
enables the movement/beh to run smoothly and filters out unnecessary/unwanted

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8
Q

how does the BG connect to the frontostriatal circuits

A

BG same function across circuits

topographic organisation of PG mens pathways are segregated and haves specific patterns of neuronal firing per circuit

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9
Q

motor system and BG research in rats

A

motor system has systematic projections that are specific to its function
parallel to other systems
thought to be the same in all other circuits

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10
Q

what is the general flow of info for frontostriatal circuits through the BG

A

input from cortex via excitatory gluatmate

to BG - CN/putamen/VS/NA - output to GPe/GPi - thallamus (relat to VL/VA) & back to cortex

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11
Q

damage to BG

A

interferes with appropriate application of actions - BG finetunes therefore:
slower/move too much, tremors, extra movements etc
qualitatively different behaviours

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12
Q

damage to DL PIFC

A

involved in cognitive circuit/executive function/top down control
affect WM and lead to subcortical dementia
problems responding to external situations and executing internal willpower to perform a behaviour
Absence of external direction - Being able to respond and initiate
Lack of insight- poor self monitoring
Cant complete problem solving acitivities ie coming up with new ways to tackle a logical problem etc – must have to be able to stop previous response set, need executve control to remove irrelevant info and come up with new strategies

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13
Q

deficits in DLPFC

A

dysexecutive syndrome
problems with organisation, maintaining and shifting attention, mental flexibility, WM, reasoning and personality (not respoding to environment in the same way)

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14
Q

symptoms of subcortical dementia

A

Bradyphrenia
Perseveration – stuck in thought, repetitive, loop of thought
Executive function deficits
Language and visuospatial preservation
Mild amnesia
Social functioning often preserved
Neurological symptoms of the primary disorder

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15
Q

what is hypokinesia

A

lack of movement
cant initiate (akinesia), cant execute (bradykinesia) and low muscle tone (hypotonia)
IE PARKINSONS

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16
Q

what is hyperkinesia

A

excess of movement
involuntary movements (dyskinesia), dystonic and dance like movementa (chorea) slow continuous movements (athetosis)
IE HUNTINGTONS

17
Q

motor ciruit deficits

A

hypokinesia: parkinsons

hyperkinesia : huntingtons

18
Q

occulomotor deficits

A

delayed saccade or increased no saccades

19
Q

what is the orbitofrontal circuit involved in

A

personality and mood affect
social restraint, self monitoring and inhibition of external cues
Suppression of irrelevant stimuli & prepotent responses
Recognition of reinforcing stimuli & S-R learning
Coding for change in reinforcement contingencies
Emotionality & personality

20
Q

damage to the orbitofrontal circuit

A
responding differently to stimuli in environment and can be seen as affecting emotions and personality
Obsessions compulsions
Disinhibition of thinking
Improper emotions 
	- outbursts of aggression
	- sociopathy, impulsiveness
	- obsessions & compulsions
	- excessive pleasure seeking & insensitivity to risk
	- inappropriate lewdness
	- sporadic hypomania
	- fatuous euphoria
Failure to respond to social cues
Lack of empathy
Cognitive/Behavioural disinhibition
21
Q

what is the anterior cingulate cortex involved in

A

motivational affect

22
Q

deficit in anterior cingulate cortex circuit

A

Tend to not respond very much to the outside world
Basic urges don’t get much of a response – apathy at a physiological level and simply not engaging
Decreased motivation & drive
Reduced initiative
Indifference to pain, thirst, hunger
Lack of verbalisation and response to commands
Akinetic mutism/abulia

23
Q

parkinsons circuitory deficits

A

underactive motor and occulomotor, DLPFC and OFC-ACC circuits

24
Q

huntontons circuitory defcits

A

overactive motor, DLPFC and OFCACC circuits

25
Q

OCD/ADHD/TOURETTES/AUTISM circuitory deficits

A

overactive ACC path, underactive OFC path

26
Q

Alz circuitory deficits

A

hypofunction of DLPFC

27
Q

schizophrenia circuitory deficits

A
  • Decreased activity in the DLPFC circuit

* Increased activity in the ACC circuit

28
Q

depression circuitory deficits

A

• Decreased activity OFC, ACC, DLPFC circuit