This handwritten (on my ipad) summary contains the lectures 1-6 of the course ‘Brain & Cognition 3: Cognitive Neuroscience’ of Radboud University Nijmegen . The summary contains lots of pictures and graphics that make learning more easier:)
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D
If your behavior Changes , your brain
Changes as well
Why cogn psychology ? Mind vs. Brain
☐ Neuro
.
"
•
Descartes 11633) Inputs are passe d on by the sensor y organs to the pineal
:
"
Gland in the brain 2 from there to immateriell Spirit
G- all In 1800) localisation of function just like in the
' '
phrerology
:
•
→
,
Organs regional speeiaeisation )
I
•
Broca 11864) :
fand evidence for localisation soo
patient Mr Tan
t
precious view :
abnormal Neurology psychiatry
behavior Iobservable brain looking
I normal
abnormalities) )
brain
{ -
see what took iqnothin9.tn
Wrong in the brain → vorgreifen
Current view :
abnormal t
Neurology Psychiatry to understand dis -
behavior twbed behavior ,
Neuro psychiatry Neuropsychologie
, , you had to
Cognitive Neurology understand the brain
D Methods of Cognitive neuropsychologie
conditions are Stronger when
(1) (ogn .
psychology and behavioral research supporter by different
we do not
by perceive the world but
direct approaches to the Jane
•
,
'
ratner interpret in corning information question
'
•
mental processing as an information processing
Problem :
>
information processing deperds on pre existing internat representation -
/ like
beliess concepts des ines per options)
, , ,
> these mental representation hndogo transformations
→
cogn Psychology uses behavioral experiments to find out what thee
representation
.
ae
parallel or social
processing ?
RT increases with number of
items ,
in line with
seially
processing each item in
tun
limitation
information processing form in also in about
transformations
•
vs mental
g. Stroop task e.
•
Limitation :
> cannot probe anything that is not expressed in behavior
> no
insignt in how the processes are implemented in the brain
,b) patient studies
•
study the cogn function of brain regions through brain damage
.
•
functions ollen have Many Components what Component Mads to the disability
:
in the patient ? e. g.
reading
D dissoüation lesion ✗ impairs task B
Single : task A ,
but not
D double dissertation : lesion ✗ impairs task A 2 les ich Y im pairs task
Many forms of brain damage: not
•
tele vs what regions are necessary , but
vascular ' '
tumors how a normal brain works
degenerative diseases (e.g. Parkinson, Limitation :
Compensation Mechanism
Alzheimer)
brain damage following trauma Be beware of causation vs .
correlation
epilepsy
(3) man ipulaling the brain
trans cranial simulation ITMS)
Magnetic
•
•
pharmacology ( Communication beta . new ons is based on neurotransmitter
(4) looking inside the brain
research tools each with
mary
•
,
their and weaknesses
Own
strength
•
Method alter mines which con -
clusions
you can dran !
Methods to complemlrt
Combi
ning
•
verging evidence /
'
each other " con
1-
strengther conceusions
, ☐
anatomy of the eye + retina
light enter
through Cornea t activales receptor alls of the
•
retina located along surface
↳ rods low levels of light
} luminoso diverses
: •
•
distributed throughout retina
↳ (Ones : more inverse
light
.
}
"
blue 1430mm)
"
(Ones Shooter Wave
length
•
" "
Color
green ( Ones Medium Wave length 1560mm
•
1530hm)
" "
longer length
•
red (Ones Wave
dlnsely packend in fovea
•
↳ White
light such as day light activates all three
Raptors bc.it contains all Wave length
•
Output of the receptor des is processed in the middle
lager of the retina &
the axons of the
then
relayed to the Central nervous system via the 0PM neue ,
aus
ganglion
☐ The ventral & dorsal pathways :
knowing what & whee
projektions from V1 to
higher areas in the Cortex be Öuvided into two
can
roughly
•
major parallel pathways :
what ) temporal
'
↳ ventral l
pathwayleading from v1 to the lobe
'
paietal
'
↳ das all )
pathway leadingqrom v1 to the lobe
'
w here
when are the obiects related to
my space
projektion pathways the visual
☐ The
Primar y of system
right
¥ eye
right eye
÷
blindmess
bi temporal
~ blindmess
corticoeblierdfiel§
diblindsignl@S0mlsi9nalsarejgnaegan.u
left visual legion in visual
primary
→
field ( LVF)
Cortex Patient might still
¥
:
hemianopia
respond to Stimuli in the
F-
blind mess I just not visual)
processed
,
.mg k
in superior
in V1
collinen ,
bypassing both paths are
visual Cortex into dorsal Stream blocked
In tat navigation after bilateral los
☐
Striche Cortex
•
example video of blind patient Walking through
:
he is a Corridor & avoiding
all the Obst alles ( can success
fully navi gate himself)
↳ patient lesioning each visual Cortex Clinical blindmess over his Whole
visual gield
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