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Lecture summary Diagnostics in Clinical Neuropschology (6464CN10H)
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Summary of lecture 1-6 of Diagnostics course
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Lectures DiagnosticsLecture 1: Introduction & principles
Definition: Art of distinguishing a disease/ the recognition of a disease from its symptoms
3 fundamental aspects
1) Symptom is not equal to disease: Need knowledge of symptoms and syndromes.
2) Recognition: Observation is key
3) Making hypotheses and testing them is key
a) Reason for diagnostic research and research question
Knowledge/ awareness: What are the problems?
Explanation/diagnosis: Why are certain problems noticeable?
Prediction: How will problems develop?
Indication: How can we help patient with the problem?
Evaluation: Did intervention help sufficiently, did symptoms change over
time?
b) Formation of hypotheses.
c) More sources of information -> Greater reliability. Anamnesis, hetero-anamnesis,
tests, questionnaires etc.
Anamnesis: Background information, medical history, spontaneous
complaints and question for treatment, functioning, other factors, effect of
problems on daily life.
Hetero-anamnesis: Additional value when patient is unable to communicate
adequately, it’s a check if the picture presented by patient is adequate, is
patient aware of problems and what information is missing? Beware: Can be
very subjective.
d) Differential diagnosis: Try to find out whether there is a certain cluster of symptoms
that points to a syndrome. Beware of the ‘halo-effect’ (= When you already believe
something in your head that guides the way you are questioning, keep an open
mind). Formulate different hypotheses which you then are subsequently going to
test.
e) Choosing a test. One test often only measures one function so we need more tests.
We need to take the possibilities of the patient in consideration (e.g. visual
impairment or paresis of dominant hand). Quality is paramount in choosing a test:
Validity, reliability and norms.
Validity: Does the test measure what it’s supposed to measure?
Reliability: Do the scores represent actual functioning or is the measure error
too big? Especially important when testing multiple times.
Norms (age, sex, level of education)
f) Repeated testing: In theory, if a score the second time of testing is outside of the
confidence interval of the fist -> significant difference between the scores. Beware of
test-retest bias -> practice effects.
g) Building the test-battery. Length: Short (1,5 hrs) or long (2x4 hrs) test battery? As
short as possible. Also, fixed battery or flexible (individualized) battery? Pro’s fixed
, battery: Standardization means that the whole battery together has been validated
and is easy to compare to other patients. You know what the effects of the one test
on the other are. Con’s: Can you test all your hypotheses, and not do too much?
Beware of:
Interference effects
Some tests use the same pictures
Practice effects
Fatigue
Motivation and anxiety
h) Importance of standardization
Instructions
Environment
i) Observations during testing
When standardization gives too little information: Try to figure out why patient cannot
perform tests. See what a patient is able to do without time pressure. See whether they are
able to handle time pressure, have slow information processing etc.
,Lecture 2: TBI and stroke
Part 1: TBI
Traumatic brain injury is most common cause of … in patients under 30 years old.
Traumatic brain injury: Damage to living brain tissue caused by an external mechanical force
or motion. Characterized by period of altered consciousness that can be very brief or very
long. TBI can be a closed or an open brain injury.
Risk:
- Men > women
- Young > old
- Urban > rural
- Low SES > high SES
Open/penetrative vs closed brain injury.
- Closed TBI more prevalent
- Open TBI more often results in death
- Open TBI tend to damage localized areas of the brain whereas closed TBI typically
cause diffuse tissue damage
- Open TBI results in more discrete and predictable disabilities whereas closed TBI
results often in disabilities which are generalized and highly variable.
Lecture will be about closed TBI.
- Primary injury: Damage that occurs at the time of the impact
o Bruising of brain parenchyma
o Laceration of nerve fibers
o Disruptions of blood vessels
- Secondary injury: Damage caused by the effects of the physiological processes set in
motion by the primary injury.
o
Impact loading:
- Acceleration: Moving object against fixed head. Most common.
- Deceleration: Moving head against stationary object.
- Coup: Disruption of tissue at the point of the impact
- Contre-coup: (Indirect) disruption of tissue located opposite to the site of impact.
How is brain impacted?
Velocity, duration, acceleration-deceleration rate and direction of head movement affect
severity of damage.
Upper part of the brain moves faster than lower part of the brain.
- Law of inertia (Wet van traagheid): Once an object is in motion, it remains in motion
at a constant velocity until acted upon by a force in opposite direction.
, o When the skull stops, the brain within the skull moves bach and forth a
couple of times and collides with inside of the skull (front and back).
Front of skull: Hyperextension (Head backwards).
Back of skull: Hyperflexion (Head forward).
o Inside of skull is not smooth (Especcially medially) -> Causes damage (Think
prominences and ridges). Even if the violent impact is in front of the skull,
there can be bruising at the base of the brain and the back of the skull.
- Linear or rotating forces on nerve fibers (white matter): Rotating forces cause diffuse
axonal injury (DAI/TAI).
When the brain moves, the nerve fibers also move (density/ distance to brain stem).
When the head suddenly stops, layers furthest from the brain stem move the fastest.
o Twisted action
o Sheared action
o Stretched action
o Compressed action
- Disruption of blood vessels: Rupture may lead to heavy bleeding. Is primary injury,
also leading to secondary injuries such as swelling and intracranial pressure.
o Intracerebral hematoma:
o Epidural hematoma: Formed between skull and dura
o Subdural: Between dura mater and underlying membranes covering the brain.
Epidural and subdural bleeding: Risk of shift of brain matter. This is live
threatening. = TSAH (Traumatic subarachnoid heamorrhage). Presence
is associated with poorer outcome.
Secondary brain damage: Treatment must focus on limiting secondary processes. Is caused
by physiological processes set in motion by primary injury. Occurs gradually.
- Intracerebral
o Delayed axotomy: Axonal injury (primal) causes release of many
neurotransmitters. Cause chemical damage to brain tissue. Brain releases
glutamate which causes access of calcium which irreversibly damages the
brain tissue.
o Intracranial pressure
Massive edema (abnormal extracellular accumulation of fluid)
Cerebral hemorrhage
Cause pressure in brain -> Brain tissue shifts -> Damage
o Disturbed blood flow: Disruption of blood vessels can cause disturbed blood
flow (secondary). Can cause local swelling of brain. Hinders supply of oxygen
and nutrients to cell (hyproxia).
o Coagulopathy
o Pyrexia
- Extracerebral
o Hypoxia (cerebral anoxia) in the brain due to:
Massive loss of blood in other parts of the body
Diminished lung capacity (lungcontusion/ pneumothorax)
Course of TBI: Patients suffering from TBI pass through predictive phases:
- Impairment of consciousness (brief clouding – coma)
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