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Block 3.6. Neuropsychology (Clinical Specialization): Problem 4 Degenerative Disorders, english summary €6,49   In winkelwagen

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

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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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  • 22 maart 2021
  • 10
  • 2019/2020
  • Samenvatting
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Door: esbilyalin • 7 maanden geleden

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Door: akiestudholme • 1 jaar geleden

Really good summary notes, well written, clear and concise. Formatted well, good use of diagrams and tables, etc. Thank you!

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foteinisav
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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