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All lectures Clinical Neuropsychology (including models and images)

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It is quite an extensive document, but it includes all relevant information from the lectures and I think it is easier to read and understand than bulletpoint summaries that I came across. Models and some extra images are added to make it easier to understand. Videos are not included, unless they are relevant to the study material. I looked up the meaning of difficult words that were used (but not explained) in the lectures.

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1




Lecture 1 – Introduction to clinical neuropsychology
The role and value of clinical neuropsychologists
A clinical neuropsychologist is primarily working with the psychological consequences of a neurological
brain condition.

The most important role is to assess mental functions and generate numbers to be able to compare people.
Other roles that were mentioned in the lecture:
• Diagnostic work: identifying neuropsychological abnormalities that make cerebral disorders
plausible.
• Analysis of (neuro)psychological function: inventory of behavioral disorders and their effect on the
person’s daily life.
• (Neuro)psychological treatment and support for patients and their relatives.
• Fundamental scientific research into brain-behavior relations and pathophysiological mechanisms.
• Research of own clinical and research instruments (the validation, reliability, applicability and
standardization).
• Quantitative evaluation of behavioral consequences of medical and non-medical interventions.
• Selection and fenotyping of populations.

Basic anatomy of the brain
The brain consists of four lobes, each has its its own function
• The frontal lobe: modulation of behavior (keeping everything in balance).
• The occipital lobe: vision
• The parietal lobe: language (left hemisphere), body scheme
• The temporal lobe: memory, emotion, hearing

White matter areas have the function to connect. There is cortical gray (higher functions) and subcortical
gray matter (more vital functions). The brain has many specialized areas. The size of a lesion can have
different consequences, dependent on the location. In the more vital areas, a small tumor can have large
effects for instance. In the prefrontal lobe, a tumor might not even be noticed until it is the size of a tennis
ball.

Different kinds of brain damage
Meningeoma (brain tumor)

The tumor originates from the meninge (the outer layers/membranes covering the
brain).

The tumor in this case is in the frontal lobe. This tumor might result in too much
behavior (no inhibition) or too little behavior (apathy).

The left in the picture is actually the right hemisphere.
In brain scans left is right and right is left.



Oligodendroglioma (brain tumor)


This patient lacks a lot of matter in the left side of her brain. The patient had a brain
tumor that was surgically removed.

The patient had problems with word finding, concentrating and a slight memory
problem.

, 2


Cerebral thrombosis
A blood clot in the left hemisphere of the brain




Cerebral hemorrhage

A bleeding that occurs within the brain tissue or
ventricles.




‘Katwijkse disease’

An hereditary disease resulting in micro bleeds. All the dots are spots where
micro bleeds occurred. The black holes are liquor (brain fluid). The micro
bleeds will accumulate and will lead to deficits.




Huntington’s disease (HD)
HD is a neurodegenerative
disease: the neurons in the brain
are affected.

HD is a motor disorder, but
it also is associated with
neuropsychiatric symptoms,
cognitive deficits and dementia.




HD starts with damage to the basal ganglia. Later on, the damage spreads to other parts of the brain.

In 1983 it was discovered that there was an error of a gene on chromosome 4. In 1993 researchers found
the exact gene and found out that there was a mistake in the CAG-repeats (cytosine, adenine, guanine).

The prevalence is 3-7 per 100.000. The disease onset is 40 on average. 10% of patients develop Huntington’s
disease before reaching the age of 20.

, 3


Symptoms:
• Chorea: arrhythmic, involuntary and unpredictable body movements
• Hypokinetic-rigid syndrome: akinesia (loss of voluntary body movement), hypokinesia
(decreased body movement), and/or bradykinesia (slow movement and an impaired ability to
move the body swiftly on command)

Patients that have a chance of developing HD symptoms often become depressive, because they know they
carry the gene, but they don’t know when the disease will start showing. Other neuropsychiatric problems
in people with HD: agitation, anxiety, apathy, OCD, impulsiveness, aggression and worry.

HD cannot be cured, but can be treated by neuroleptics (dopamine antagonists, benzodiazepines).

Parkinson’s disease (PD)
Discovered by James Parkinson in 1817. PD is the degeneration of dopaminergic cells (substantia nigra)
and a disbalance in the cholinergic-domapinergic system. A patient gets the diagnosis if he/she has 2
out of 3 of the following symptoms:
• Bradykinesia (slow movement and an impaired ability to move the body swiftly on command)
• Rigidity
• (Rest)tremor
Other symptoms: postural instability, masked faces, hypophonia (soft speech), dysphagia (difficulty
swallowing), autonomic failure, micrographia (small, cramped handwriting), gait freezing (akinesia),
shuffling gait, neuropsychiatry (depression, hallucinations, REM sleep disorders, cognitive impairment,
dementia)

PD has a subtle onset. Motor features are mostly unilateral. At the time of diagnosis, already 60% of
dopamine in the basal ganglia and possibly 80% of substantia nigra cells will have been lost.

The prevalence is 3% of the population. The average age of onset is 62 years. The mean disease duration is
8 years (ranging from 1-30).

There is no cure. There is treatment in the form of medication that ‘resolves’ the lack of dopamine. The
lack of dopamine is what makes that people with PD cannot control their movements.

Diagnostics
The DSM-5 has a new section dedicated to neurological disorders. There are six broad neurocognitive
domains described:




One of the tasks of a clinical neuropsychologist in practice is to do a mental examination: are there any
abnormalities in one of the six domains? Another task is to look at potential behavioral disorders. A third
important task is to say something about the cause of abnormalities: are there medical or psychological
causes?

, 4


Dementia is now called ‘major neurocognitive disorder’ in the DSM.

3 diagnostic tools:
1. Observation;
2. History taking/anamnesis;
3. Neuropsychological testing (tests alone are not sufficient).

In order to call something an impairment, there have to be disabilities or handicaps in daily life.




An example:
------> Brain tumor ----------> aphasia -----------> social isolation

Dementia
There are three ‘types’ of dementia:




The mental status examination
Diagnostics
The aim of a mental status examination is to determine the extent to which the behavior is caused by
psychological vs medical factors. Methods are observation, anamnesis and (neuro)psychological tests.

Treatment
For example: education, function training, strategy training, cognitive behavioral therapy (CBT), system
therapy (involve the social environment), life style adjustment

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31 maart 2019
Aantal pagina's
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Geschreven in
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