Summary LITERATURE & LECTURES B&C2: Clinical Neuropsychology (Radboud University Nijmegen)
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Course
B&C 2: Clinical Neuropsychology (PSB2BC10EA)
Institution
Radboud Universiteit Nijmegen (RU)
Book
Klinische neuropsychologie
This document covers all relevant information from both the Clinical Neuropsychology book as well as the lectures for the course B&C2: Clinical Neuropsychology (2019/2020).
The clinical application of the scientific area that studies the relations between brain and behaviour,
related to assessment, treatment and care of individuals with (presumed) cognitive (dys)function as
a result of developmental disorders, brain disease or psychiatric disorders
Clinical neuropsychology is more than localization of functions, but psychosocial factors, somatic etc.
also play a role:
ICF model:
Used to describe the consequences of a disease/disorder. The different levels of description refer to
the different levels of problems patients can have (level of function; level of activity; level of
participation).
- Model helps to identify the moderating factors and identify target for treatment
Assessment
Using tests, questionnaires, observation scales, interview techniques
- Diagnostic cycle used (formulate hypotheses, test them, reject them, reformulate etc.
Goal of neuropsychological assessment:
- Differential diagnosis (does patient have …. Or not?)
- Identifying developmental delay
- Functional analysis (impaired versus intact abilities or consequences)
- Advice on interventions or everyday function
,The neuropsychological method:
Neuropsychological tests
Diagnostic cycle→complaints analysis (patient and informants are interviewed), problem analysis
(problem is analyzed through different tests), diagnosis, indication for treatment (need for further
diagnostics or options for treatment is examined)
- The boundaries between these stages are not clear. (also see past courses); formulate
hypotheses-test them-reject them-reformulate
Referral question→for example “referred for a neuropsychological assessment in relation to his poor
study results, are these due to his stroke”
Interview with the patient→collecting information about current complaints and symptoms and
their progression; initial impression of the patient´s cognitive abilities and their behavior; building a
working relationship with the patient
Interview with informant (partner etc.)→get information that patient is not aware of (behavior
changes etc.); permission needs to be given by the patient
Observation→should be as freely from interpretation as possible; also how was a certain score
achieved? (logical structure or guessing), poor performances not necessarily mean that there is a
cognitive disorder
Tests and questionnaires→predetermined set of tests the same for every patient (batteries flexible
and depending on the referral question they are adjusted to the patient)
- Sensitivity→likelihood that a test will identify a person with a disorder as “disturbed”
- Specificity→likelihood that a test will identify a person without a disorder as “not disturbed”
- Often tests with high sensitivity are chosen, because any cognitive disorder should not be
missed
Interpretation→integration of interview with patient/informant, observations and test results;
- Primary considerations (are test results reliable, valid, truly reflect level of
cognitive/emotional functioning of the patient?)
- Determine cut-off point (know how the normative data were determined meaning which age
groups, gender, educational level etc.)
- Abnormal performances during tests do not always indicate persistent cognitive disorders
and there could still be a disorder, however the tests do not show it
- Errors while interpretation: complaints are equated to disorders; confirmation bias
Reporting→can be done verbally and written
Reliability and validity
Reliability→test-retest reliability extent to which a test yields the same results when it is taken at
different times by same patient; also important that different researchers obtain comparable results
under the same conditions; the degree of correspondence between the results of different
researchers is called the inter-rater reliability (cohen´s kappa)
,Validity→face validity (extent to which a test initially seems to measure what it is supposed to
measure); content validity (is a test representative of the topic that is to be measured); construct
validity (is the result of the test actually reflecting the construct that is being assessed?); criterion
validity (can a test predict the performance of a patient with regard to an external criterion);
ecological validity (extent to which a test predicts how a patient functions in their own environment
Confounding factors→need to be taken into consideration when interpreting test results
Underperformance→(patient extremely nervous etc. will perform worse; might lead to wrong
diagnosis); patient may also simulate or exaggerate symptoms, so that their performance is wrongly
ascribed to for example brain damage
- Symptom validity tests can identify underperformance (they are quite easy, but seem to be
difficult
Intentional underperformance→ for example to get milder prison sentence; TOMM (test of memory
malingering) test→patients need to know the correct answer in order to systematically choose the
incorrect response
The professional field
Hospitals→main work of neuropsychologist is to carry out diagnostics (identify the cause of a
complaint or to assess the effects of a recognized brain injury); they also assess the effectiveness of a
treatment or intervention
Rehabilitation centers→focus is more on treatment than on diagnostics, but assessment is
important to assess whether certain types of behavior are a result of brain injury or a personality
trait
Mental-health care→neuropsychologists play essential role in drawing up treatment plan
Residential homes/nursing homes→mostly elderly patients; main task of neuropsychologist is
evaluating cognitive skills, exploring cause and expected course of complaints, giving advice
Forensic institutions→”could the disorder of response inhibition explain the impulsive behavior?”
,Parkinson spectrum (Parkinson´s disease) (21)
- Parkinson spectrum is a group of progressive neurodegenerative disorders involving motor
symptoms called parkinsonism or hypokinetic-rigid syndrome.
- Parkinson´s disease is the most common. It is not predictable and not curable. How fast the
disease progresses differs for each individual.
- Core features of Parkinson: tremor, slowness, stiffness
There are various forms of atypical Parkinson, which look like PD but they have other clinical
features. In general, PD is more treatable than these forms and many of them have a shorter and
more disabling course.
Idiopathic Parkinson´s disease→typically symptoms starts on one side (unilateral), but eventually go
to the other side. Each person experiences Parkinson´s symptoms differently.
- Shaking of hand etc. when resting
- Problems with moving one leg
- Voice changes; less facial movement; writing style changes
Primary motor symptoms:
1. Lack of movement/slowness (bradykinesia)
- Akinesia→movement cannot be started immediately after the command has been given
(walking etc.)
- Hypokinesia→decreased bodily movement with limited facial expression, saliva flow, loss of
automatic movement
- Bradykinesia→making slow movements; leads to difficulties in everyday life (brushing teeth,
cutting food etc.); difficulties with repetitive actions
- Rapid fatigue and freezing (stiffening of a movement) are other symptoms.
2. Rigidity
- Tight and sore muscles. Movements are stiff and jerky (cogwheel phenomenon). Muscles do
not relax. Hard for people to move (people with PD usually do not swing their arms.
- Hypohonia→limited vocal volume
3. Resting tremor
- Only present if the part of the body involved does not move. The trembling can hardly be
suppressed. Appears generally at rest. Most noticeable outward sign and about 70% develop
it.
4. Postural instability
- Forward-bent posture, which can result in falls. Usually occurs later in the course of the
disease. If a disease starts with this symptom, an atypical parkinsonian syndrome should be
considered (see graphic above).Pull test→examiner pulls patient backwards and PD patients
will fall and won´t be able to gain balance
,Secondary motor symptoms:
- Freezing→person hesitates before stepping forward (feeling of feet glued to the floor);
interestingly it hardly ever happens when walking upstairs
- Micrographia→shrinking in hand writing (can be explained by bradykinesia)
- Mask-like expression→people show less facial expressions
- Unwanted accelerations→affecting the gait & the speech (uncontrollable)
More symptoms: tendency to lean forward, dystonia (involuntary muscle contractions), akathisia
(inner restlessness), speech problems, difficulty swallowing, sexual dysfunction, cramping, drooling
- The secondary symptoms do not have to be present in every Parkinson patient
Non-motor symptoms:
Early symptoms:
- Fatigue, hyposmia (disturbed sense of smell), sleep disorders, apathy, cognitive impairments,
psychoses, affective disorders, mood disorders, low blood pressure.
These non-motor symptoms precede the motor symptoms by years (premotor phase). However,
these are not that specific, so you cannot predict Parkinson by that, but still they are “markers”.
- Non-motor symptoms occur often in atypical primary parkinsonian syndromes.
- People with REM sleep behavior disorder move and cry out while sleeping because the
normal motor suppression that occurs during REM sleep is lacking.
Diagnosis:
- Parkinson´s disease is diagnosed if there is bradykinesia combined with rigidity, rest tremor
or postural instability. A diagnosis of PD is less likely if the motor symptoms do not improve
after treatment with the appropriate medication.
- If patient experiences visual hallucinations and dementia syndrome, clearly before motor
symptoms, Dementia with Lewy Bodies would be considered.
- Diagnosis is based on the history of the person´s illness and the clinical examination. There is
no blood or radiologic test in common usage.
- Initial complaints commonly very non-specific. In initial stage, it is often impossible to
distinguish between PD and atypical parkinsonian syndromes.
- MRI/CT scan is only meaningful in the advanced stages of the disease, but it is used to
exclude the presence of other diseases like any of the atypical parkinsonian diseases. SPECT
and PET scans do that as well. Not for diagnosis to clearly say that a person has PD.
- Transcranial ultrasound is used to see alterations in the substantia nigra, but about 10% of
people also show these alterations without having PD. So, there is no single marker to clearly
show that a person has PD.
Multiple System Atrophy→decreased balance of torso with rapid progression, severe speech
disorders and cold blue feet (dependent on wheelchair)
Progressive Supranuclear Paralysis→straight posture, impairments in eye movement, disinhibition
and emotional instability
Corticobasal degeneration→results in aphasia, apraxia and strong asymmetrical parkinsonism
- Subtypes of PD are important, because they are treated differently. Tremor-
dominant→fewer non-motor symptoms.
Patients with first symptoms on left side (right hemisphere affected) experience more cognitive
problems than those with symptoms on right side.
- A diagnosis before the age of 50 is a young-onset of Parkinson
,Hoehn and Yahr scale:
Advantage of the scale is that its simple and easily applied, however it is not so comprehensive. It
captures typical patterns of progressive motor impairment. The progression of patient in the scale
has been found to correlate with motor decline, deterioration in quality of life and dopaminergic
loss.
Unified Parkinson´s Disease Rating Scale (UPDRS):
Used to follow the longitudinal course of PD. It comprises different sections that assess different
areas of everyday life. Also comprises the Hohn & Yahr scale.
Epidemiology and severity of Parkinson´s disease:
- PD is the second most common age-related neurodegenerative disorder after Alzheimer´s
disease. 7-10 million people suffer from it.
- Prevalence→ranges from 41 people per 100.000 in the fourth decade of life to more than
1.900 people per 100.000 among those who are 80 or older.
- Incidence→(rate of newly diagnosed cases), generally increases with age, although it can
stabilize in people who are older than 80. Just about 4% of people with PD are diagnosed
before 50. Average age of onset of PD is about 59.
Prognosis:
- PD itself is not fatal (you die with it, not from it; worse symptoms can lead to incidents which
might results in death)
Aetiology & Pathology:
- Unknown aetiology. But there are some ideas (in nicotine users PD is less common, MPTP
drug damaging Substantia Nigra, genetic factors).
- Caused by the degeneration of dopamine-producing neurons in the part of the substantia
nigra (part of Basal Ganglia) referred to as the compact part.
→Decrease in dopamine disrupts the balance between the cortico-basal ganglia-
thalamocortical circuit in which the subthalamic nucleus becomes hyperactive. This causes
decreased activation of the motor cortex via the thalamus. The motor pathways (indirect
and direct pathways) are out of balance in PD. Indirect inhibits movement and direct
facilitates movement.
, - If approximately 50% of the dopaminergic neurons in SN break down (or 80% of the
dopamine itself is lost), patient experiences parkinsonian symptoms. Until that point, the
brain can somehow compensate the loss. A major stressful event can trigger the symptoms
and knock the system out. Substantia Nigra in patients much lighter than in normal people.
- Also changes in noradrenergic, serotoninergic and cholinergic system.
- Lewy bodies may be present as well. This lewy body is a clumb of brain protein inside the
neuron. There is parkinsonism with and without alpha-synuclein pathology (most important
protein in Lewy Bodies).
Cognitive symptoms:
- 40-50% of patients show cognitive deficits. These deficits resemble those that patients with a
frontal lobe damage have (executive functions like planning, inhibition, problem solving,
anticipation).
- Wisconsin Card Sorting Test is used to measure executive function→rule of sorting cards is
changed and time is measured how long it takes for the patient to understand the new rule
and so on.
- Stroop test→patient is asked to say the color of the word (red).
- Tower test→patient has to plan ahead how he can move the tower step by step, by just
moving one piece at a time.
- Slowed thinking and attention difficulties are symptoms that PD patients experience.
- Problems with learning and remembering information: prospective memory, verbal and
nonverbal recall, recognition. Deficiencies in active retrieval (episodic memory)→coming up
with words due to slowed thinking.
- They also have problems with imagery and spatial processes (for example neglect in patients
with right hemisphere dysfunction).
Dementia with lewy bodies→severe cognitive impairment early on in PD along with hallucinations.
PD dementia→severe cognitive impairment develops late in the course of PD
!The risk of developing dementia is 4 to 6 times higher in people with PD!
Affective symptoms:
Dopamine deficiency might correlate with a loss in motivation. In patients with PD it is hard to
distinguish depression and apathy (lack of interest, motivation, emotion).
- Difficulties with emotion recognition and theory of mind.
- Impulsivity
- Depression, anxiety, and apathy is often characterized by a depressed mood and are related
to off-periods (in which people are not in medication)
- Psychotic symptoms→hallucinations, delusions etc. later in the course of the disease; the
psychotic symptoms usually start as not threatening and start to deteriorate later on.
The anti-Parkinson´s drugs and DBS may lead to increased impulsiveness (pathological gambling;
hypersexuality; compulsive eating). Patients with L-dopa addiction use more drugs than they require
and not just to prevent the off stages.
Treatment:
- Parkinson´s disease cannot be cured or slowed down. Treatment focuses on suppressing the
symptoms. When a patient starts having functional disabilities, you usually start with
medication.
, - Levodopa→crosses from blood to brain and is there converted to dopamine; restores
dopamine in the substantia nigra and striatum. Combined with carbidopa (this makes sure
that the levodopa is not already converted do dopamine in the intestines but in the brain).
- COMT inhibitors→block the COMT enzyme and helps more levodopa to reach the brain
- Dopamine agonists→mimic action of dopamine at the dopamine receptor; given to patients
that show end-of-dose failure (wearing-off) which often happens when patients take the
levodopa for years and it start to not work anymore.
- Monamine oxidase inhibitors→enhance and prolong the effect of dopamine; first drug for
treatment of early PD or for patients experiencing end-of-dose failure using only levodopa
The drugs may cause narcolepsy, confusion, hallucinations, psychosis, delusions. Dopamine agonists
and levodopa are associated with impairments in impulse control.
- Wearing off: motor fluctuations develop→”off” times (medication suddenly no longer
works): state of decrease mobility (bradykinesia) and stiffening. About 40% of PD patients
will experience motor fluctuations within 4-6 years of onset.
- In the long term, the use of levodopa results in hyperkinetic movements or dyskinesias
which are abnormal involuntary movements (especially when levodopa concentration is at
peak level).
- Freezing→inability to move or getting stuck, which usually happens in the off-periods and
more often when people multitask (feet glued to the floor)
If medication no longer works properly, brain surgery is used:
- Ablative surgery→also known as brain lesioning; certain parts of the brain are being
destroyed (globus pallidus, STN); prone to more side effects
- DBS→planting electrode which gives electric impulses to STN and globus pallidus;
- Restorative therapies→try to regrow cells into the brain (only done experimental and in
research)
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