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Block 3.6. Neuropsychology (Clinical Specialization): Problem 4 Degenerative Disorders, english summary $7.21
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Block 3.6. Neuropsychology (Clinical Specialization): Problem 4 Degenerative Disorders, english summary

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  • Course
  • 3.6 Neuropsychology
  • Institution
  • Erasmus Universiteit Rotterdam (EUR)

Summary document of course 3.6. Neuropsychology. The grade obtained for the course was 8.6, It includes summary of articles and Chapters that we had to read every week.

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Document information

  • March 22, 2021
  • 10
  • 2019/2020
  • Summary

Subjects

  • psychology
  • clinical specialization
  • problem 4
  • block 36
  • neurodegenerative disorders

Written for

  • Erasmus Universiteit Rotterdam (EUR)
  • International Bachelor In Psychology
  • 3.6 Neuropsychology
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Really good summary notes, well written, clear and concise. Formatted well, good use of diagrams and tables, etc. Thank you!

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PROBLEM 4. NEUROGENERATIVE DISORDER 1

Chapter 27: Disorders
Motor disorders
A. Hyperkinetic (dystonic syndrome)

Huntington’s Tourette’s syndrome
 Intellectual problems, personality changes 1. Multiple tics (twitches of face,
& “choreas” limbs or whole-body)
 Progression: abnormal/involuntary 2. Inarticulate cries + multiple tics
movements are rare and not intense in the 3. Echolalia + Coprolalia (shit-talk) +
beginning but strong and frequent later cries + tics
 Behavioral symptoms:  Intelligent, productive NOT neurotic
Symptoms o Impairment of recent memory or psychotic
o Disability to manipulate acquired  Prevalence: 1/360
knowledge
o Slowed information processing Tics of eye, head, face, upper limbs, lower
 Emotional: Anxiety, depression, mania, limbs > complex movements (hitting,
schizophrenia-like psychoses, suicide (is touching, jumping) > Coprolalia (develops
possible) in 60%, but disappears in 1/3 of them)
Age of onset Usually 30-50, white Europeans 2-15 (M = 7), by 11 97% symptomatic
Autosomal dominant genetic disorder, CAG -
Genetics
repetition chromosome 4
Mechanisms Basal ganglia (atrophied & neuronal loss) Abnormalities in dorsal stream
Shrinkage and thinner cortex Basal ganglia dopamine system,
 Explanation: imbalance among various NT excessive cell number (lower symptoms
systems in basal ganglia with anti-dopaminergic drugs)
 Glutamate projection from cortex to bg
 Dopamine projection from substantia nigra  Cognitive abnormalities: mainly of
to basal ganglia the right hemisphere e.g. drawing,
 DIE - GABA projection from basal ganglia remembering complex figures,
to substantia nigra (initiation of movement) remembering locations in daily life.
 DIE - ACh neurons in basal ganglia
 Dead GABA & Ach  decreased
inhibition of dopamine cell by GABA 
increased dopamine release in basal ganglia
 “choreas”



B. Hypokinetic
 Parkinson’s: 0.1 to 1% of world population, w/ rise in the old age

Positive symptoms: acquire normally inhibited beh Negative symptoms: loss of normal behaviors
1. Tremor at rest: stops during voluntary 1. Postural disorders
movement or sleep, pill-rolling hand tremors o Disorder of fixation: inability/difficulty to hold normal
2. Muscular rigidity: movement resisted but w/ position of certain body parts
force they can still do short distance again o Disorder of equilibrium: problems with standing or
resistance, cogwheel rigidity (passive flexion or maintaining standing position w/o support
extension of a joint in series of steps) 2. Righting disorders: difficulty standing from lying
3. Involuntary movements: to relieve stiffness, position, in advanced cases rolling problems
tremor or for no reason 3. Locomotive disorders: problem w/ initiating stepping,
o Akathisia (cruel restlessness): co-occur w/ if they walk short steps & support
inactivity o Festination: increasing fast steps  running
o Oculogyric crisis: posture distortion, involuntary 4. Speech disturbance: absence of tone (prosody)
head and eye turns for minutes or hours 5. Akinesia: slow, poor movement (even in face or blinks,
walk, speech or fidgeting), poor repetitive movements,

, PROBLEM 4. NEUROGENERATIVE DISORDER 2
in extreme form still for hours


Genetics Not inherited - relativity component (25 % of pts have a relative), more gen. variants greater risk
Gradual start of pos and neg symptoms w/ tremor in one hand and stiffness in distal parts,
movements slow, eye-blinking and poverty of expression, motionless, speech slows, difficulty
Progression w/ swallowing
o Rare fast progression, usually 10-20 years
o On-off quality: remission in activating situations (emergency)
o Idiopathic: unknown
o Post-encephalitic: encephalitic lethargica
Causes
o Drug-induced: tranquilizers (usually reversible), heroin
o Neurotransmitter: Dopamine and norepinephrine low degeneration of basal ganglia cells
o Counselling on symptoms
o Physical therapy e.g. massage and heat
Treatment: o Drug therapy: i) increase dopamine activity, ii) suppress other structures heightened
symptoms and activity (L-dopa, MAOI, TCAs)
support no o Transplant of dopaminergic cells
treatment o DBS + drugs  most effective
 Psychological aspect: decrease of cognitive function, low mood, lack of motivation
 Similar to frontal lobe basal ganglia symptoms (parallels Alzheimer’s)


Dementias
Acquired and persistent syndrome of intellectual impairment (> 65
years)
 The most prevalent is Alzheimer’s (65% of dementias)
1. Major Neurocognitive disorder (NCD)
 Substantial cognitive decline from the previous level of
performance, decline in test performance
 Marked impairment in daily life
2. Mild Neurocognitive disorder (mild NCD)
 Similar definition w/o the marked impairment in functioning

Brain correlates of Alzheimer’s

1. Neuritic (amyloid) plaques: increase of plaques (tau protein)
2. Paired Helical Filaments/ neurofibrillary tangles: in cortex and hippocampus (mainly posterior)  tau-related &
present in other disorders (e.g. other dementias, Parkinson’s and Down Syndrome)
3. Neocortical changes: mainly posterior parietal, inferior temporal and limbic cortices
 1/3 of the volume is lost after progression of AD
4. Paralimbic cortex changes: entorhinal cortex most severely and earliest impaired region  assoc. w/ memory 
explains early memory loss
5. Cell changes: loss/atrophy of large neurons, hippocampus neuronal damage of AD = healthy person > 80 years old
6. NT changes: Ach, noradrenaline, dopamine, serotonin, and glutamate receptors (AD: reduction in 2 or more)
Cause

 Genes: increased risk w/ relative AD mainly if sibling or even higher AD parent  3 genes
1. B-APP (on chromosome 21)  amyloid plaques & neurofibrillary tangles
2. Tau protein
3. Prensenilin proteins
 Trace metals: x10-30 more Alu
 Immune reactions: anti-brain antibodies  degeneration
 Blood flow: poor blood circulation and glucose metabolism (causal or secondary??)

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