Summary Cognitive Psychology II (PPT + extra notes)

Cognitive psychology II




Chapters
GUEST LECTURE: Parkinson’s disease .......................................................................................................................................... 1

GUEST LECTURE: Mindfulness and Cognition ....................................................................................................................... 36

GUEST LECTURE: Eating Disorders ............................................................................................................................................. 56

GUEST LECTURE: Social Cognition and ASD .......................................................................................................................... 73

GUEST LECTURE: Unilateral neglect following brain damage ......................................................................................... 85

GUEST LECTURE: Sleep Disorders and Cognition .............................................................................................................. 106




Algemene competenties
1. The student will acquire advanced knowledge about human cognition.
2. The student will obtain a deeper understanding of the interaction between theory and
research in cognitive (neuro)psychology.
3. The student can independently engage in scientific reasoning, and critically evaluate new
scientific findings.




 Gastcolleges (6)
 English Multiple Choice Exam

,GUEST LECTURE: PARKINSON’S DISEASE
Theoretical background

Parkinson’s disease (PD)
Chronic Progressive Degenerative Brain Disorder
 ‘chronic’ ⇛ persistent disease, can’t be cured as of yet
 ‘progressive’ ⇛ symptoms worsen over time
 ‘degenerative’ ⇛ disease is result of a continuous process based on degenerative cell changes,
which will increasingly deteriorate over time




↬ Fastest growing neurological disorder
 # People with PD ⇛ doubled with 6 million over last 3 decades
⇛ will double again with over 12 million by 2040
↬ Second-most common neurodegenerative disorder
 2-3% of population ≥65 years of age
↬ Cause: degeneration of dopamine-producing cells in the
substantia nigra of the basal ganglia
 Dopamine = neurotransmitter ⇛ loss of dopamine in people with PD causes cascade of
activity changes in brain, which manifest in the following effects:
↬ Effect:
 Typical motor symptoms: resting tremor, general slowness of movements, rigidity & postural
instability
 Non-motor features: cognitive deficits
 Neurobehavioral abnormalities:

Epidemiology
↬ Estimated global incidence: 5 to 230 new cases per 100,000 individuals yearly. Rare before age 50
↬ Incidence 5 to 10-fold from ages 60-90
↬ Global prevalence estimated 0.3%
 Increases to >3% in >80 years
↬ Usually: onset between ages 60-70
↬ Genetic variant: Young Onset PD (occurs in younger adults)
 5-20% of persons w/ PD




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,↬ Generally speaking, mortality is not increased in first 10 years after disease onset, but it does
increase afterwards, sometimes eventually even doubling compared to general population

Male: Female distribution ± 1.5:1




↬ Almost twice as common in ♂ than in ♀ in most populations
↬ Females sex hormones, genetic mechanisms, or sex specific differences in exposure to
environmental risk factors may explain why ♂ are most likely to get PD

Etiology
↬ Most cases: idiopathic (no known cause)
↬ Most likely a combination of factors:
 Age
⤷ largest risk factor for developing PD; not very clear how it works
 Environmental (toxins, pesiticides, insecticides: rotenone, paraquat, MPTP)
ex. MPTP = toxin: organic compound which induces toxic effects on substantia nigra
(regulation of motor skills) ⇾ MPTP toxin gives Parkinson’s like symptoms: kind of mimics
pathophysiological mechanism which causes PD
 Dietary (pollutants)
 Genetic predisposition (mutations in ⍺-synuclein, LRRK2, GBA) e.g. Ashkenazi Jews (Israel), Inuit (Alaska)
⤷ genetics cause 10-15% of PD
⤷ in some families changes in mutations in certain genes are inherited from generation to
generation
⤷ some ethnical groups more commonly carry genes linked to PD (see e.g. above) ex. LRRK2
 Brain trauma, stroke, viral inflammation
⤷ even years after injury
 Both environmental & genetic factors contribute to onset of illness (age remains main factor)
Oxidative stress destroys mitochondria ⇛ apoptosis (cell death) of dopaminergic cells.
⤷ cigarette smoking & caffeine may decrease risk ⇛ mostly due to protective factor of nicotine &
caffeine

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, Pathophysiology
Characteristic features:
1. Loss of dopaminergic neurons in the pars compacta of the substantia nigra
 NO general macroscopic atrophy (shrinking) of the brain, but degeneration in certain types of
neurons within particular brain regions.
E.g. early-stage PD: loss of dopaminergic neurons restricted to VL substantia nigra
⤷ suggest that degeneration in this region starts before onset of motor symptoms
end-stage PD: more widespread loss
 Resulting in a reduction of the neurotransmitter dopamine in the basal ganglia




 Panels A and B represent the human postmortem bilateral midbrain of normal and
Parkinsonian subjects, respectively.
 Much less pronounced dark area with dopaminergic cells in substantia nigra in B than in A
2. Widespread protein (⍺-synuclein) accumulation (“Lewy Bodies”) in neurons




 Proteins accumulate in substantia nigra & form clusters = “Lewy Bodies”

The Basal Ganglia: Aantomy
5 interconnected sub-cortical nuclei:




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