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PSY 445, Exam 3, Exam 2, similar to NTs, act the same, but different…
PSY 445
Exam 1
History
brain in control
Hippocrates
brain is control center (not heart)
humoral theory: balance 4 humors
Galen
1st clinical neuroscientist
every nerve comes from brain/spinal cord
animal spirits stored in vesicles, animal experiemnts
Descartes
animal spirits in pineal gland
Dualism: mind and brain as separate entities
reflexes
localizing brain functions
Willis
focus on cerebral cortex, link b/n human and animal brains, structure and function
brain stem
clinical insights:
heritability of intelligence
alcohol leads to mental impairment
relationship b/n mania and melancholia
"the virtuosi", experimentation
Gall
localization of SPECIFIC traits
father of phrenology
Broca
left lateralization of language function (localization of language)
Broca's area: speech production
lesion work to support clinical
Cellular investigations
the architects
Golgi
silver stain on neural tissue
neural net theory
Cajal
shared Nobel w/ Golgi
disproved neural net theory, saw individual neurons with modified silver stain
Sherrington
cortical lesions result in SPECIFIC damage
theorized a functional junction: synapse
mechanisms of motor relfexes
the engineers
Loewi
drugs effect brain processes, pharmacologist
frog heart experiemnt
Dale copied him: extracted acetylcholine from horse spleen
theorized use of chemical communications (NTs)
Adrian
electrical communication, recorded electrical signaling b/n neurons
all or none
transduction: convert physical energy into electric
nerulogical approaches to mental illness
Meynert
relationship b/n nervous system and mental illness
Kraeplin
dementia praecox (schizophrenia)
disorders had developmental courses
categorize/classify mental illness
Charcot
started good, but then inspired Freud
Macroanatomy
nervous system
CNS
brain
macroanatony
major divisions
prosencephalon (FOREBRAIN)
telencephalon
8 more items...
diencephalon
6 more items...
mesencephalon
midbrain
3 more items...
rhombencephalon (brainstem)
metencephalon
3 more items...
mylencephalon
1 more item...
protection
meninges
arachnoid mater
dura mater
subarachnoid space (w/ CSF)
CSF produced in VENTRICLES
1 more item...
pia mater
subdural space
skull
spinal cord
anatomy
minor:
sacrum
coccyx
major:
cervical
thoracic
lumbar
communication
afferent
sensory
dorsal
efferent
motor
ventral
PNS
autonomic
parasympathetic
rest and digest; maintains
sympathetic
fight or flight; arousal
somatic
Therapies
psychopharmacology
sedatives, barbiturates
laxatives, opium, morphine, bromine
biological therapies
coma therapy
ECT
inducing fevers through malaria
psycho surgery
lobotomy
the asylum
pinel:tried to fix it, got rid of them mostly yay
behaviorism
Mary cover jones
Pavlov
social learning
bandura
Rotter: external internal locus of control
little Albert
2 approaches:
psychosocial
CBT
group therapy
behavioral therapy
biomedical
drug therapy
medical diagnoses
microanatony and the neurons
cell structure
cytoskeleton
microtubules
transportation of substances w/in cell
KINESIN
anterograde transport: fromsoma to termianl buttons
protein filament
DYESIN
retrograde transport: carries from terminal to soma
cytoplasm
cell membrane
Blood brain barrier
blanketed by astrocytes
crossing
can cross
dissolvable molecules
active transport things
small uncharged molecules
tight junction b/n epithelial walls in blood caps
Nervous sytem cells
neurons
interneurons
sensory (afferent)
motor (efferent)
glia
Schwann cells: Myelin in PNS
astrocytes
nutrients: glycogen
DILATE BLOOD VESSELS
provide support
clean up dead neurons
oligodendrocytes: myelin in CNS
microglia
phagocytosis
action potentials
resting potential
outside of cell: positive
inside cell: -70 mv
b/c sodiumpotaasium pump: pump in 2 NA pump out 3 K
2 gradients:
electrical gradient: neg inside cell
concentration gradient: more K inside cell (wants to leave)
action potential: rapid depolarization, reverses polarity
propagation
saltatory
approaches to mental health
developmental
critical windows
environmental
concentric circles
microsystem, meso, exo, macro
genetic perspective
gene expression in mental functioning
evolutionary
how and why certain behaviors evolve
ultimate causes
neurobiological approach
neuroanatomical
phineas gage
neurochemical
neurophysiological
manipulating
TMS, tDCS
invasive: deep brain stimulation
measuring
fMRI, NIRS
EEG. MEG
cultural
Sites of drug action
affect post-syn receptors
competitive binding (same site)
direct agonist
drug binds w/ and activates receptor, acts like NT
direct antagonist
receptor blocker, binds w/ channel making it inpossible for NT to bind and activate it
noncompetitive binding (alt. binding site)
indirect agonist
attach to alt. binding site on protein and facilitates receptors' job
indirect antagonist
attaches to alt. binding site. INTERFERES w/ receptors job
affect storage and transmission of NTs
agonist
bind w/ proteins and trigger release
antagonist
block transporter molecules that filll vesicles
prevent NT release at terminal
deactivate proteins so vescle can't fuse w/ membrane
affect other receptors
affect pre-synaptic receptors
agonist
block pre-syn receptors
increase production/release of NT b/c auto receptor can not tell how much has already been produced and cant shut down production
antagonist
activate auto receptors
decreases NT release b/c antagonist tells auto receptor there is already enough so the cell stops producing
affect the production of NTs
antagonist
inactivate enzyme that produces the NT
eg. AMPT (a-methyl-p-tyrosine) blocks NE and DA synthesis by inhibiting tyrosine hydroxylase
agonist
be a precursor, induce production of NT
eg. L-DOPA --> DA
affect termination
agonist
drugs bind w/ destructive enzyme so it cant destroy the NT
drugs block reuptake
SSRI/ SNRI
neurotransmitters
excitatory or inhibitory
inhibitory: causes hyper polarization (IPSP)
excitatory: causes depolarization (EPSP)
NT receptors
ionotroipc
metabotropic
G protein
second messenger
G protein activates an enzyme which produces a secind. messenger
termination of synaptic transmission
reuptake
enzymatic deactivation
diffusion
types of neurotransmitters
neuropeptides
endogenous opioids
endogenous opiates: naturally occurring opiates
enkephalins
dynorphins
endorphins (endogenous morphine)
function
analgesic (pain relieving)
euphoric effects
source
been around a long time, derived from poppy
opium, morphine, codeine, heroin
termination
NO reuptake
enzymatic diffusion
passive diffusion
drugs
antagonist
naloxone
treats OD
blocks mu receptor
agonist
codeine, morphine, oxycodone, heroin
cause analgesia, euphoria, respiratory depression
receptor
mu receptor (metab.)
neurohormones
oxytocin
function
binds to target organ receptors
uterus
mammary gland
brain
reproductive organs, social bonding, familial/warm feelings
comes from Hypothalamic neurons
vasopressin (AVP) (ADH)
monogamy? in voles.
function
PNS: water absorption, blood thickness
CNS: learning/avoidance, social mammal behavior
frim posterior pituitary gland (hyp.)
small molecules NTs
catecholamines (share a common catechol nucleus)
function
epinephrine (EPI)
dopamine (DA)
ventral tegmental/substantia nigra --> basal ganglia
reward processing/seeking, movement control
norepinephrine (NE)
brainstem --> that, hypothalamus, limbic,
attention, reward, huger/thirst
synthesis
tyrosine
L-DOPA
DA
NE
EPI
tyrosine hydroxyls
dopa decarboxylase
dopamine B hydrolase
termination
reuptake
DA/NE reuptake transporter
enzymatic deactivation
DA
MAO (monoamine oxidase)
NE
COMT (catecholamethyltransferase)
diffusion
acetylcholine (ACh)
receptors
ionotropic
nicotinic receptor
neuromuscular junction
DA? movement?
autonomic ganglia
some CNS pathways
metabotropic
muscarinic receptor
parasympathetic
heart
smooth muscle
glands
termination
reuptake
choline reuptake transporter
enzymatic deactivation
acetylcholine esterase (AChE)
function
PNS
all muscular movement, parasympathetic NS
CNS
memory, REM, attention, mood
synthesis
acetate
cation from Acetyl Coenzyme A (Acetyl CoA)
ChAT
choline acetyl transferase
choline
drugs
agonist
physostigmine
inactivates AChE
antagonist
botulinum toxin
inhibits ACh release
curare
occupies and blocks pst-sun ACh recptors
serotonin (5-HT)
function
mood, attention, arousal, sleep, dreams, temp, aggression, respiration, hormones, pain
raphe nucleus in BRAINSTEM --> forebrain/hippocampus/thal./hypothal/cerebellum/midbrain (sub nigra, VTA)
pons and medulla to spinal cord
synthesis
tryptophan
5-HTP (5- hydroxy-tryptophan)
5-HT (serotonin)
TPH -1 (tryptophan hydroxylase)
BAS -1 (aromatic amino acid decarboxylase
termination
reuptake
serotonin reuptake transporter (SERT)
enzymtic deactivation
MAO (prod. 5-HIAA)
diffusion
amino acid NTs
INHIBITORY
GABA (gamma aminobutyric acid)
synthesis
glutamate
GAD (glutamic acid decarboxylase
receptors
ionotropic
GABA a
opens Cl channel
metabotropic
GABA b
autoreceptor
neg. feedback loop, pre synaptic neuron
function
cortex --> striatum, thalamus
inhibitory CNS
termination
astrocytes reuptake
drugs
agonist
benzoadepines and barbiturates
lead to relaxation
alcohol
inc. Cl anions, inc. inhibitory. effects
glycine
function
inhibitory brainstem, spinal cord, retina? (GABA of brainstem)
drugs
antagonist
tetanus bacteria
blocks receptors
hyperstimaultion of motor neuron junction
can't relax muscles: lock jaw
EXCITATORY
glutamate
synthesis
byproduct of using glucose
ac=strocytes helpful in production
glutamine: precursor to glutamate
prod. in glia
glutaminase
in terminal converts it to Glu
stored until depolarization
function
learning, brain plasticty, memory
cortical and subcortical function (cognitive stuff)
NOT CROSS BBB
receptors
ionotropic
NMDA
AMPA
KAinate
metabotropic
Metabotrpic-1
metabotropic-2
Exam 3
Substance use disorders
why use
to feel better
to do better
to feel good
curiosity/ socia pressure
consequences
short term
long term
physiological
tremors
blood pressure inc.
heart rate inc.
psychological
anxiety
irraitiablity
depression
DSM
inc. Tolerance and withdrawal
classic psychology
REINFORCEMNET
positive reinforcement
add a good thing
euphoria leads to more drug use
negative reinforcement
take away a bad thing
stopping withdrawal symptoms leads to more drug use
CONDITIONING
conditioned positive reinforcemnt
location/drug stuff
euphoria
conditioned negative reinforcement
associating something with withdrawal moments/ abstinence
reinforce drug use
consists of
diminished control
desire to take
risk factors
environmental
home abuse
family use
social skills
school
peers
biological
teens
any other mental illness
genes
other
easy access
mechanism of administration
reaches brain faster
effects closer to moment: stronger positive reinforcement
early use
BRAIN
negative affect/withdrawal
extended amygdala signals HPA to release CRH
stress/anxiety part of withdrawal
drugs inc. DA
receptors become less sensitive
withdrawal symptoms b/c brain expects same amount of DA
preoccupation/anticiaptinog
OFC
maintaining addictions
like OCD
binge/intoxication
NAcc
neuro stuff
chemistry
endorphins
DA
inc. DA in SUD
dec. DA in Parkinsons
ACh
brakes to DA? Inc. ACh dec. effect of DA
GABA
modulates DA
anatomy
NAcc
reward seeking behavior
receives info from VTA, hippocampus, medial PFC, amygdala
endpoint of MEIDAL forebrain bundle
meditates limbic and striatum
Olds study on mice: activating NAcc leads to incredibly compulsive behavior
pathways
cognition
mesocortical
motor response
nigrostriatal (sub nigra to stratum/basal ganglia)
reward
mesolimbic dopamine
therapies
behavioral treatments
acupuncture
incentive treatments
groups
aa
Drug Addiction therapy
detoxification
can use meds to help
clear system
avoid relapse
immunotherapy
passive
active
stress and coping
stress research
Hans Selye
noted relationship b/n stress and disease
developed Generral Adaptation Syndrome
alarm response
resistance
high levels of cortisol
exhaustion
in response to sever chronic stress
trier social stress test
types of stress reponses
chronic
acute
studying stress
evoking stress criteria
species specific
artificial stimuli may lead to distorted response
ecological relevance (natural)
habituation
measuring stress
physiological
heart rate
skin conductance response
self report
cortisol
effects
inc. catecholamine synthesis (DA, NE, Epi)
sensitive to stimuli (thal)
inhibits inflammation
enhanced memory (hippocampus)
stress effects on
hippocampus
glucocorticoids lead to dendritic restrucing
excessive glutamate stu=imulating NMDA recpetors on extrasynaptic cleft
signal cell death
memory deficits
higher cortisol shrinks hipp
stress: physical, mental or emotional factor that causes bodily tension
external vs. internal stressors
experiemtns
Harlows monkeys
romanian orphans
abnormal HPA axis
not normal cortisol fluctuations
meany's rat pups
loving mother can nurture coldness out of rat
methyl groups silence gene expression
coping
social support
affiliative social contact
mood disorders
brain regions
amygdala
inc. volume and activity
Anterior Cingulate cortex
ventral
emotional signaliing
inc. activity
dorsal
signal sneed for control
reduced activity
reduced signals for control
hippocampus
reduced volume
NAcc
malfunction leads to...
anhedonia
learned helplessness (tendency to give up)
decreased response
reward seeking behavior
PFC
cellular loss
regulation, concentration
neurochemistry
NE
from the locus coreolus, from brainstem
decreased in MDD
NE depletion studies
tyrosine --> L-dopa --> DA --> NE --> epi
AMPT: inhibits tyrosine hydrolase, NE antagonist
possible role in modulating other systems
corticosteroids (replacement for natural cortisol)
ACTH and CRH signal for release of cortisol
increased in depression:
cortisol
ACTH and CRH
cortisol releasing neurons
5-HT
serotonin depletion hypothesis
b/c SSRIs raise serotonin levels, but symptoms improve WEEKS after
tryptophan depletion stuides
tryptophan --> 5-HT
should have made depression worse across the board
only made it worse for people who had been on SSRIs
low tryptophan diet
SSRIs may have made receptor less sensitive b/c AUTO receptors
too little
HPA axis
negative feedback loop malfunction
excess cortisol does not effectively signal HPA to stop producing (Dexamethasone suppression test)
evolutionary (survival)
steer away from threat, submissive
mind becomes analytical
help from others
risks
women more likely
irritable when younger
60% comorbid anxiety
genetic
polygenic
symptoms
cognitive
impaired concentration (PFC)
negative cognitions
impaired memory (hippocampus)
indecisive (PFC)
confusion
somatic
sleep
energy
appetite
motivational
loss of drive
difficulty initiating activity (NA)
anhedonia
emotional
anxiety (amygdala)
irritability
hopelessness
guilt
sadness (ACC)
treatments
physical
ECT
blood flow
dendritic growth in rats
rTMS
cingulate gyrus maybe
DBS
subgenus ACC
therapy
CBT
psychopharmacological
SSRIs
NERIs
MAO (dea tivates DA)
tricyclics
block reuptake of 5-HT and DA
MAOI
inhibits breakdown of DA, inc. DA
CRH blockers
prevents CRH release, slows cortisol
aggression
risk factors
biological
top down brakes
OFC
regulating emotions
ACC
bottom up drive
amygdala
ventromedial hypothalamus
threat response
insula
decisions, motor control
vmPFC
regulation
environemtnal
parenting (real or perceived)
peers
poverty
psychopathy
social deviant and antisocial lifestyle
violate societal norms
sexual promiscuity
criminal behavior
adult versions of CD
interpersonal and affective traits
narcissistic traits
impulsive traits
CU traits
disorders
Conduct disorder
4 areas
3 w/in 12 motnhs, 1 w/in 6
CD
life course persistant
w/o limited prosocial emotions (NO cu)
with limited prosocial (w/ CU)
lack of remorse/guilt
callous/lack of empathy
unconcerned about performance
shallow/ deficient affect
adolescent limited
umbrella term
Antisocial personality disorder
CD, 3 behaiviors after 15 yo
Oppositional defiant disorder
spiteful/vindictive at east 2 times in 6 months
biology
reactive loop
vmPFC: binding together data (dec.)
dmPFC
amygdala: inc. and dec.
striatum
responding (dec.)
types of aggression
proactive
premeditated, more effort
for a goal
reactive
evoked and emotional
less effort
spontaneous
treatment
pharmacological
for cooccurring symptoms
stimulants for ADHD
SSRIs (and and dep)
psychotherapy
family therapy
peer group therapy
CBT
DBT
PCIT
PMT
positive reinforcement
BRAIN and different substances
alcohol (barbiturates)
inhibits GABA
which increases DA release
inc DA activity in NAcc
nictonie
maybe blocks receptors so DA keeps being prodcued
stimulates nicotinic receptor (ACh recpetor)
stimulants
mechanism
amphetamine: inc. release of DA
cocaine: blocks reuptake
ritalin blocks reuktake in a more gradual way
function: increase alertness, mood, motor activity, excitement
examples: amphetamines, cocaine
marijuana (THC)
attaches to cannabinoid receptors
triggers DA release
inhibit GABA
areas
cerebral cortex
hippocampus
basal ganglia
cerebellum
opiates
morphine, heroin
analgesia and euphoria
attach to endorphin receptors
inhibit GABA
PTSD
HPA axis disreulation
in. catecholmanies
decreased cortisol
interferes w/ feedback loop
brain regions
ACC
dec. activity
hipp
reduced volume
medial PFC
dec. activity
disregulated threat response
amygdala
inc. activity/sensitivity
symptoms
avoidance
negative cognition and mood
intrusion
hyperarousal
exposure
1 month
distress/impariemtn
treatment
CBT
exposure theapry
stress inoculation training
target cortisol
early administration soon after traumatic event
block glucocorticoid recpetor
phar
SSRIs
tricyclics
Exam 2
anxiety disorders
anxiety disorders
agoraphobia
6+ months
Panic disorder
1+ panic attack
2 kinds of panic attacks
unexpected
expected
symptoms
dizzy, lightheaded
derealization
nausea/digestive problems
depersonalization
shortness of breath/choking
fear "going crazy"
shaking
paresthesia
sweating
chills/hot flushes
heart palpitations
anxiety about other panic attacks
1 month after attack
behavior changes
selective mutism
social anxiety disorder
6+ months
seperation anxiety
specific phobias
6+ months
generalized anxiety
fear and the brain
present threat
thalamus
relegates
hippocampus
fear associations and memory
amygdala: evaluates emotional significance
essential role in threat response
attention and alertness
imagined threat
also amygdala, thalamus, and hippocampus
Orbitofrontal cortex (OFC)
can maintain a mental image of fear related stimuli
schemas and working memory
amygdala, thalamus, hippocampus
treatments
psychopharmacological
SNRIs
tricyclic antidepressants
SSRIs
benzodiazepines
OCD
CLomipramine
anxiolytics
SSRIs
CBT
4 Rs
reattribute origin of thoughts to disorder
refocus during thoughts and substitute w/ the thoughts
Relabel unwanted thoughts
revalue- unwanted thoughts are worthless and should be ignored
ERP (exposure and response preventions)
excessive fear about a threat that is NOT immediately present
3 kinds of responses
conscious feelings
physiological
behavioral
adaptive to a certain point
3 categories
OCD
obsessions, compulsions, or both
common obsession/comulsion pairs
harm and checking
contamination and cleaning
cycle that reinforces itself
the brain
OFC
cognition, thoughts
cingulate gyrus
emotion/limbic system/activates caudate
caudate
movement, automatic behavior, learning
thalamus
amygdala
nucleus accumbent
reward/reinforcement
facts
late adolescence/earlt adulthood onset
bimodal distribution
genetic
twin studies
2-3% of population
neurtransmitters
modulators
serotonin
GP
dopamine
caudate
GABA (caudate, GP and GP, that)
higher glutamate (OFC thalamus and caudate)
PTSD
anxiety disorders
anxiety decreases w/ age
females more likely than men
evolutionary perspectives of OCD
FAPs (fixed action patterns)
neurodegenerative diseases
Parkinson's
affects VOLUNTARY movements
also: loss of olfaction, depression, ,memory and reasoning defects
characterized by muscle tremors, rigidity, difficulty initiating movements
brain stuff
Suibstantia nigra
DOPAMINE facilitates movement
dopaminergic pathway
Neurons in the substantial nigra become impaired and die
lack of dopamine for dopaminergic pathways
2 dopaminergic pathways
direct
interruption allows for excessive inhibitory signals to thalamus
facilitates movement
indirect
inhibits movement
interruption allows for an imbalance of excitatory to inhibitory sigals
from sub. nigra to thalamus (through putamen and GP)
biomarkers
lewy bodies
folded protiens
early signs: Parkinson's walk, loss smell, masked face, soft voice (vocal motor control)
progresses like TBI
causes
environemntal
head injury
exposure to toxins
aging
cells may be more susceptible to harm w/ time
genetic
specific genes indicate increased risk
treatments
pharmacological
enzymatic deactivation
MAO b inhibitors
COMT inhibitors
anticholinergic drugs
reduce tremors and muscle rigidity
L-dopa (carbidopa-levadopa)
dopmine agonsit
Deep Brain stimulation
probably of Sub. nigra
brain surgery
thalamotomy
pallidotomy (GP)
too much ACh, need more DA
Alzheimer's disease
most common from of dementia
brief mental status exam
awareness of symtpoms
knowldegeof date/time/place
short word list
simple calculation
biomarkers
interfere with action potentials
neuronal death
2 kinds
tau protein tangles (inside cell)
amyloid plaques (outside cell)
decline in ACh
ACh for memory and learning
treatment
pharmacological
cholinesterase inhibitor (ACh agonist)
NMDA antagonist
stem cells
embryonic
pluripotent
virtually immortal
from blastocyst (early, preembryonic tissue)
potential applications for
parkinsons
alzheimers
spinal cord injury
normal aging
no reduction in glial cells
significant changes
axons get shorter
reduced exapanse of dendrites
reduction in neurogenesis
normal loss: only 10% b.n 20-90 yrs old
neurodevelopment
postnatal neurodevelopment
adaptation/learning
esp in # of connections
esp. in cortex
more/new storage
neurogenesis
new neurons developmed by division of cells
in youth- growth in number of axons especially
adolescent brain
gray matter inc. right before adolesence
white matter increases w/ age
limbic: very developed, PFC: underdeveloped
natal stages
proliferation
neuralation
neural tube
neuropores
neural plate
neural crest
12 weeks
tlencephalon
diencephalon
mescencephalom
metencesphelon
mylencephalon
induction
zygote
cleavage
gastrulation
endoderm
internal organs
ectoderm
skin, nerve cells, neuroglia, neural plate
mesoderm
muscles, skin, skeleton, connective tissue
pluripotent
migration
growth cones w/ filopodia
radial glia
roadmap for cell migration (act as scaffold)
neurons attach by growth cone
become astrocytes
2 ways neurons know where to go
long range: chemoattraction/repulsion
neurotrophins
repel and attract filopodia
examples
BDNF (promotes growth)
NGF (growth of presynaptic neuron axon by post-synaptic neuron)
CAM (cell adhesion molecules; guide axons)
contact attraction/repulsion
to form connections; circuits at synapses
aggregation
neurons grouping togther
differentiation
specialization
certain genes turned on/off
synaptogenesis
growth of axons and synapses fro circuits (formation of synapses)
and synaptic competition
neural darwinism
use it or lose it
overproduction in neurogenesis (50-80%)
regulation of connections
access to neurotrophins
interaction w/ target organ/neuron
apoptosis
controlled by genes
removing neutrophils
loss of feedback
synapse rearrangement
loss and establishment of neural synapses
Brain tissue damage
CTE
build tau proteins
modd swings, depression, dementia, impulse control issues, suicidal thoughts
degenerative brain disorder associated w/ repetitive head injury
risk increases each year playing sports
TBI
risk factors
alcohol
violent enviorments
male
sports
age
2 kinds of effects
secondary
PCS
extra glutatmet signals for apoptosis (NMDA)
hyperglycolysis
longer tem damage
primary
examples
axon shearing
lesions
contusions (bruising)
epidural hematoma
subdural hematoma (dura still attached to skull
damages brain's circulatory system
immediate
causes
2 kinds of causes
exogenous
endogenous
most frequent
cars
violence
falls
sports
combat/.blasts
determining severity
Glasgow Coma Scale
higher score = better
regional effects similar to PTSD
irratibiltiy
fatigue
sleep probs
avoidance
depression/anxiety
areas
entorhinal-hippocampal cortex
attention, memory
amygdala
emotion, fear
Ventral brain stem
arousal, modulating nts
temporal polar
memory, sensory limbic
cerebellum
coordination, working mea, mood
orbitofrontal cortex
social
dorsolateral PFC
executive funtioncs
treatment
pharmacological
cognitive issues:
ACh and DA agonsist
just bandaids, treating symptoms
moods
SSRIs
swelling/edema
glucocorticoids
progesterone for swelling and general survivability
surgery
cognitive rehab
constraint induced movement therapy
environmental enrichment
prevention
active
passive
more effective
neurodevelopmental illnesses
ADHD
development
slower developing cortex esp in frontal and temporal
some brain parts are smaller -language, attention, movement
wrong netword=s working qt a time
frequency
1/20
neurocongitive model of ADHD
executive dysfunction
FRonto-striato-thalamic circuitry
thalamus
striatum
basal ganglia
caudate/putamen
PFC
temporal info processing
corticocerebellar
PF cortex
cerebellum
delay aversion
ventral -striatal-orbitofrontal
OFC
straitum
putamen
caudate
VTA
emotional dysregulation
paralimbic
OFC
amygdala
DSM
criteria
2 settings
age of onset under 12
over 6 motnsh
and significant impairment
6 or more
examples
hyperactive
on the go
talks a lot
leaves seta frwquently
hard time waiting turn
fidgets/squirms
blurts out answers
act w/o thinking
inattention
hard time organizing tasks and activities
avoids sustained mental effort
not listen to directions
loses things
careless mistakes
easily distracted
treatment
psychopharmacological
Adderall
targets DA and NE
NE: CNS
DA: attention
affects striatum, ant. ring. cortex, PFC
ADHD brain looks more similar to typical brain after stimulant
behavioral
Parent training
change detrimental parts of enviornemnt
help the child practice opportunities of self regulation
executive function training game-ify
similar to NTs, act the same, but different sources, transportation, and longer effects
.