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Clinical Neuro psychology > Week 2 H4,13,19 > Flashcards

Week 2 H4,13,19 Flashcards

1
Q

First Imaging Technique in Neuropsychology

A

Computed Tomography (CT)

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2
Q

Types of Neuroimaging

A

Structural: Investigates the anatomy of the brain.
Functional: Depicts underlying processes like water movement or blood flow.

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3
Q

Examples of Structural Neuroimaging

A

CT (Computed Tomography) and MRI (Magnetic Resonance Imaging).

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4
Q

Examples of Functional Neuroimaging

A

PET (Positron Emission Tomography), SPECT (Single Photon Emission Computed Tomography), EEG (Electroencephalogram), MEG (Magnetoencephalography).

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5
Q

How does a CT scan produce a brain image?

A
  1. A motorized X-ray source rotates in a spiral around the patient’s head.
  2. Beams of X-rays are sent through the head from various angles, capturing thin slices of the brain.
  3. Digital X-ray detectors measure the strength of radiation after it passes through the head.
  4. The computer uses this information to calculate areas of stronger or weaker absorption using algorithms.
  5. A two-dimensional image is constructed.
  6. Multiple cross-sectional images are combined to create a three-dimensional image.
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6
Q

which three things do CT images allow a neuroradiologist to observe and deduce about the inside of the head?

A

Atrophy (tissue loss)
Swelling post brain trauma
Congenital abnormalities

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7
Q

How does CT imaging depict changes in brain tissue due to most diseases, and when is CT commonly used in a clinical setting?

A

Most diseases increase the brain tissue’s water content, which appears darker (hypodense) on CT compared to normal tissue. Blood and calcium appear white (hyperdense). CT is frequently used in acute settings for quick patient diagnosis.

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8
Q

How does the presence of radiological contrast agents in the brain indicate potential pathology?

A

When there’s a pathology, the blood-brain barrier is compromised. This allows the contrast fluid to enter the brain, enhancing the CT image, indicating potential cerebral diseases.

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9
Q

What is CT perfusion (CTP) and how does it utilize contrast agents?

A

herhaalde CT-scans worden gemaakt om veranderingen in de bloedstroom en doorbloeding in een specifiek orgaan of weefsel in realtime te meten en in kaart te brengen.

intraveneuze contrastmiddelen geïnjecteerd, en vervolgens worden meerdere opeenvolgende CT-scans gemaakt om de distributie van het contrastmiddel in de weefsels te volgen.

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10
Q

What are two disadvantages of using CT scans?

A

Cannot differentiate between various brain tissue types.
Exposure to radiation poses a risk of DNA damage and potential cancer risk.

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11
Q

How does MRI technology work to visualize the brain?

A
  1. Hydrogen atoms in the body have protons that rotate, creating a magnetic field.
  2. MRI’s strong magnetic field alters the rotation of these protons to align with its axis.
  3. A horizontal radio frequency pulse from the MRI disrupts this alignment (excitation).
  4. When the pulse stops, protons return to their original state, releasing energy (relaxation).
  5. Radio frequency coils capture this energy release.
  6. Computer processes these signals to visualize the brain structure slice by slice.
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12
Q

In MRI scans, how are bright and dark areas described?

A

Bright areas: Hyperintense
Dark areas: Hypointense

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13
Q

How are water-rich structures and fat depicted in T1-weighted MRI images?

A

Water-rich structures: Dark (low signal intensity)
Fat: Light grey to white (short T2 relaxation time)

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14
Q

Why are T1-weighted scans used when viewing the anatomy of the brain?

A

They show good contrast between CSF, grey matter, and white matter.

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15
Q

What is the primary use of T2-weighted images in brain imaging?

A

T2-weighted images are mainly used to detect brain abnormalities, especially those accompanied by an increase in water content in the brain tissue.

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16
Q

What is the FLAIR sequence in MRI?

A

FLAIR (Fluid-Attenuated Inversion Recovery) is an MRI sequence similar to T2-weighted images but with dark CSF.

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17
Q

Why is the FLAIR sequence useful?

A

It detects subtle changes near the CSF (cerebrospinal fluid), especially in the hemispheres and the periventricular area.

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18
Q

In which conditions is FLAIR particularly beneficial?

A

lacunar stroke and multiple sclerosis to reveal ‘white spots’ or scars from inflammations.

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19
Q

What are T2and SWIin MRI, and what techniques are they associated with?

A

T2 and Susceptibility Weighted Imaging (SWI) are gradient echo techniques in MRI.

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20
Q

What do T2* and SWI sequences help visualize?

A

They image deoxygenated blood, hemosiderin residues (blood products), iron, and calcium.

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21
Q

What does MRI with diffusion-weighted imaging (DW) measure? where is it used for?

A
  • DW measures the microscopic movement of water molecules (diffusion) in the brain.
  • It is highly sensitive to acute stroke, assess brain tumors, abscesses, and other brain pathologies.
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22
Q

Describe isotropic vs. anisotropic diffusion in DWI.

A

Isotropic diffusion is the normal, random movement of water molecules.

Anisotropic diffusion indicates restricted water movement due to pathologies like tumors or swollen cells.

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23
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A
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24
Q

What is the difference between DWI and diffusion tensor imaging (DTI) in MRI?

A

DWI primarily measures the magnitude and direction of water diffusion within tissues –> information about the overall diffusion properties of water in tissues –> rapid identification of acute stroke, brain tumors, and areas of inflammation or cellular proliferation in various tissues.

DTI beyond DWI by measuring the diffusion of water in multiple directions within each voxel –> information about the anisotropic diffusion of water –>traumatic brain injury, multiple sclerosis, and neurodegenerative diseases.

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25
Q

What does DTI inform us about white matter pathways?

A

DTI allows us to understand how white matter pathways run in the brain using tractography.

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26
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A
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27
Q

What is perfusion in the context of the brain?

A

refers to the delivery of oxygen and nutrients to the brain through the bloodstream.

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28
Q

List the three types of perfusion techniques and briefly describe each.

A
  1. Dynamic susceptibility contrast (DSC) perfusion: Uses gadolinium and results in T2- or T2*-weighted images.
  2. Dynamic contract-enhanced (DCE) perfusion: Uses gadolinium and results in a T1-weighted image.
  3. Arterial spin labelling (ASL): No contrast agent; uses naturally occurring water in arterial blood as contrast. Mainly for research.
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29
Q

How does MRS differ from MRI in analyzing the brain, and in which patient groups is MRS commonly used?

A
  • mriprovides detailed anatomical images of the brain and its structures.
    MRSgoes beyond anatomical imaging to provide information about the chemical composition of brain tissues.
  • MRS is used in children for metabolic disorder detection, stroke patients, and epilepsy patients.
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30
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A
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31
Q

What is the significance of the BOLD signal in fMRI?

A

The BOLD (Blood Oxygenation Level Dependent) signal reflects the ratio of oxygenated (diamagnetic) to deoxygenated (paramagnetic) blood in brain areas, helping to identify active regions.

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32
Q

How does fMRI help map brain areas involved in specific tasks?

A

fMRI compares resting state images with active state images to identify brain areas involved in certain tasks.

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33
Q

What is the Default Mode Network (DMN) and its main components?

A
  • The DMN represents intrinsic brain activity during rest.
  • Its main components are
    1. the posterior cingulate gyrus,
    2. medial and lateral parietal areas,
    3. the medial prefrontal cortex.
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34
Q

What is the Frontal-Parietal Network (FPN) and its main components?

A
  • active both at rest and during motor and cognitive tasks (spatial attention, mental rotation, working memory tasks).
  • concists of:
    1. the posterior parietal cortex,
    2. premotor,
    3. prefrontal cortex (including the frontal eye field).
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35
Q

What is the Salience Network and its primary regions?

A
  • involved in complex brain functions including communication, social behavior, and self-awareness.
  • Its key regions are:
    1. the anterior insula
    2. dorsal anterior cingulate cortex.
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36
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A
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37
Q

What is nuclear imaging

A

Nuclear imaging involves functional techniques using radioactive substances (bijv PET en SPECT).

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38
Q

How do PET scans work?

A
  1. A radioisotope ‘tracer’ is injected into the patient.
  2. The tracer travels to the brain and disintegrates, emitting a positron.
  3. The positron collides with an electron, releasing gamma rays.
  4. Detectors capture these rays, and a computer generates a 3D image showing the tracer’s distribution.
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39
Q

Disadvantages of PET scan?

A
  1. High cost.
  2. Lower resolution compared to CT and MRI.
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40
Q

Advantages of PET scan?

A
  1. Can detect brain diseases before anatomical changes are visible.
  2. Radiation load on the patient is relatively low.
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41
Q

Difference between SPECT and PET?

A

terwijl SPECT gammastralen detecteert uitgezonden door radioactieve isotopen en 2D-beelden levert, gebruikt PET positron-emitterende isotopen om 3D-beelden te creëren, en biedt over het algemeen een hogere ruimtelijke resolutie en kwantitatieve capaciteiten

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41
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A
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42
Q

two advantages and Disadvantages of EEG?

A
  1. Low cost
  2. extremly High temporal resolution
  3. Low spatial resolution (hard to pinpoint exact activity location)
  4. only captures cortical activity, missing deeper brain areas.
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43
Q

What does MEG do?

A

MEG detecteert de zwakke magnetische velden die worden geproduceerd door de elektrische activiteit van neuronen in de hersenen.

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44
Q

What does vascular cognitive impairment refer to?

A

Vascular cognitive impairment covers the entire spectrum of cognitive consequences resulting from vascular disease, ranging from mild impairment to full-blown dementia.

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45
Q

What causes cerebral infarcts?

A

A blood clot (embolism) blocks an artery in the brain, reducing the oxygen supply to the closed-off parts, which can cause damage.

46
Q
A
47
Q

What is Transient Ischemic Attack (TIA)?

A

TIA is a temporary reduction in blood flow to a small part of the brain, leading to neurological symptoms that resolve within 24 hours. However, some cognitive complaints may persist. It increases the risk of a subsequent stroke.

47
Q

What is a lacunar infarct?

A

It’s an infarct in the small arteries supplying the deeper structures of the brain. This leads to the formation of a small cavity called ‘lacuna’.

48
Q

What are the potential clinical manifestations of a lacunar infarct?

A

While often there are no clinical manifestations, if it occurs in areas like the thalamus or pons, it can lead to temporary motor or sensory impairments.

49
Q

What is cerebral haemorrhage?

A

It is a condition where a blood vessel in the brain ruptures, leading to bleeding in or around the brain.

50
Q

What are common symptoms of cerebral haemorrhage?

A

Reduced consciousness, confusion, and disorientation.

51
Q

What is a subarachnoid haemorrhage (SAH)?

A

SAH is a bleeding that occurs not within the brain itself but between the meninges that surround the brain.

52
Q
A
53
Q

What is the probable link between vascular risk factors and cognitive decline?

A

The association is possibly (at least partly) due to the pathology of the smallest blood vessels in the brain, known as cerebral small vessel disease (CSVD).

54
Q

How is CSVD typically visible in the brain?

A

Through damage to white matter tracts, termed as leukoaraiosis.

55
Q

Which cognitive domains are most frequently impacted post-infarction?

A

Attention, memory, information processing speed, and executive functions.

56
Q

What is the typical cognitive outcome after a TIA?

A

Mild cognitive impairment in most patients, with severe cognitive impairment in a smaller subset.

57
Q

Name the three major arteries supplying blood to the brain.

A
  1. Anterior cerebral artery (ACA),
  2. middle cerebral artery (MCA),
  3. posterior cerebral artery (PCA).
58
Q

What percentage of major stroke patients typically experience cognitive impairment?

A

About two-thirds (2/3) of patients.

59
Q

Which cerebral artery is the largest and most commonly affected by strokes?

A

Middle cerebral artery (MCA).

60
Q

What is anterograde amnesia?

A

The inability or disrupted ability to encode new information post-event or trauma.

61
Q

What is apraxia?

A

The inability to carry out purposeful movements despite having the physical ability to do so.

62
Q

What is neglect and when is it most commonly seen after an MCA stroke?

A

failure to pay attention to stimuli contralateral to the lesion. It’s most commonly seen in the acute phase after an MCA stroke.

63
Q

Differentiate between neglect and extinction.

A

Neglect is the failure to pay attention to stimuli on the opposite side of a lesion. Extinction is the failure to perceive stimuli contralateral to the lesion when two stimuli are presented simultaneously.

64
Q

Which areas of the brain does the MCA supply blood to?

A

Frontal, temporal, and parietal areas, as well as deep brain structures like the thalamus.

65
Q

Which areas of the brain does the PCA (posterior cerebral artery) supply blood to?

A

The occipital and temporal lobes.

66
Q

The posterior cerebral artery (PCA) supplies blood to the occipital and temporal lobes. Some common consequences of damage: hemianopsia?

A

A visual field defect on the contralateral side, leading to blindness in half the field of vision.

67
Q

Define visual agnosia.

A

The impaired ability to recognize objects even though there is no defect in vision.

68
Q

What is prosopagnosia?

A

The inability to recognize familiar faces, even though the ability to recognize objects may remain intact.

69
Q

Describe Anton’s syndrome.

A

Also known as cortical blindness, patients with Anton’s syndrome are blind but deny their blindness and may even claim they are seeing objects or scenes.

70
Q

Which parts of the brain does the ACA (anterior cerebral artery) supply blood to?

A

The dorsal and medial parts of the frontal and parietal lobes.

71
Q

What are the language-related consequences of damage to the ACA?

A

Word-finding problems, disturbed connections between Broca’s and Wernicke’s area, and mutism (complete inability to communicate verbally).

72
Q

How does an ACA stroke impact executive function and social cognition?

A

There can be impairments in executive function, social cognition (like emotion recognition), cognitive flexibility, and behavioral inhibition.

73
Q

Describe the cognitive and emotional consequences of an infarct in the cerebellum.

A

Motor problems, executive function impairments, behavior changes, and potentially cerebellar cognitive affective disorder, which is characterized by cognitive impairment and emotional changes.

73
Q

What cognitive deficits might arise from an infarct in the basal ganglia?

A

Impairments in memory, attention, executive functions, and visuospatial functions.

74
Q

How do infarcts in the thalamus and brainstem affect cognition?

A

They lead to disorders in basic attention processes.

75
Q

What are the diagnostic criteria for VaD?

A

Cognitive impairment in at least one domain. 2. Significant interference with daily activities (not explained by another condition).

76
Q

What sensory change do many patients report after a stroke?

A

Back: Sensory hypersensitivity, feeling like input is no longer filtered.

77
Q

How is dementia referred to in DSM-5?

A

Major Neurocognitive Disorder.

78
Q

What is Mild Cognitive Impairment (MCI)?

A

MCI is a stage where there’s noticeable cognitive decline, but the ability to function independently in daily life is relatively intact. It can be a precursor to Alzheimer’s dementia.

79
Q

What is needed to establish a diagnosis of MCI?

A

A modest cognitive decline verified by an objective cognitive assessment and confirmed by the individual or a reliable informant.

80
Q

What is the average survival duration after a dementia diagnosis?

A

On average, 7-10 years.

81
Q

What characterizes the neuropathology of Alzheimer’s disease?

A

Abnormal accumulation of extracellular plaques of amyloid-beta protein (senile plaques) and intracellular tangles of the tau protein neurofibrillarytangles. which lead to degeneration of nerve cells and ultimately brain atrophy (neurodegeneration)

82
Q

What is the Amyloid Cascade Hypothesis of Alzheimer’s?

A

The idea that an abnormal accumulation of the amyloid-beta protein is the primary driver of Alzheimer’s disease.

83
Q

alzheimers

Describe the sequence in the Amyloid Cascade Hypothesis.

A

Accumulation of amyloid-beta plaques → propagation of tau pathology → synapse loss → neuronal death → cognitive decline → dementia.

84
Q

Is the presence of amyloid-beta plaques definitive for Alzheimer’s disease?

A

No, some healthy individuals also have amyloid-beta plaques and don’t develop dementia.

85
Q

What is the Vascular Hypothesis in relation to Alzheimer’s disease?

A

The idea that vascular risk factors can lead to reduced blood flow and oxygen deficiency in the brain, contributing to the overproduction of amyloid-beta protein and subsequent neurodegeneration.

86
Q

How does reduced blood flow and oxygen deficiency contribute to Alzheimer’s according to the hypothesis?

A

It leads to stiffening of arterial walls and a metabolic reaction that causes overproduction of the amyloid-beta protein, resulting in neurodegeneration.

87
Q

Describe the sequence in the Amyloid Cascade Hypothesis + vascular.Why is the combined hypothesis gaining traction?

A

Evidence is growing that both amyloid-related and vascular factors play roles in the disease process, potentially complementing each other.

88
Q

What do we mean by “Genetic predisposition” for Alzheimer’s?

A

While Alzheimer’s disease is not always inheritable, in rare cases, there’s an autosomal dominant inherited form caused by a mutation in the APP, presenilin-1 (ps-1) or presenilin-2 (Ps-2) gene, known as familial Alzheimer’s disease.

89
Q

What are the initial symptoms most Alzheimer’s patients present with?

A

Difficulties with remembering recent events, forgetting appointments, and having word-finding problems.

90
Q

How is the clinical course of Alzheimer’s disease categorized in terms of stages?

A
  1. Mild cognitive impairment (MCI)
  2. Mild dementia
  3. Moderate dementia
  4. Severe dementia
91
Q

Describe the cognitive profile trajectory in Alzheimer’s disease.

A

Starts with prominent episodic memory deficits → decline in semantic memory, language, working memory, and executive functions → visuoconstructive and praxis deficits in the later stages.

92
Q

What are the characteristics of the Amnestic MCI as the predementia stage (cDR 0.5) in Alzheimer’s disease?

A
  • Episodic memory deficits (anterograde amnesia) due to hippocampal neuronal loss.
  • Word-finding problems.
  • No major functional impairment; complex activities might be challenging.
93
Q

How is Mild dementia (cDR 1) manifested in Alzheimer’s patients?

A
  • Problems with language production, orientation in unfamiliar settings.
  • Category fluency more affected than letter fluency.
  • Episodic memory is affected.
    • Challenges with activities requiring higher-order cognitive processes; may not be able to perform them independently.
94
Q

What cognitive and functional changes are seen in Moderate dementia (cDR 2) in Alzheimer’s?

A
  • Extensive cognitive impairments.
  • Memory deficits extend to more distant past.
  • Orientation in time and place deteriorates.
  • Word-finding, visuoconstruction issues, and apraxia.
  • Difficulties in basic activities like brushing teeth.
95
Q

Describe the state of a patient with Severe dementia (cDR 3) due to Alzheimer’s.

A
  • Severe cognitive loss; complete dependency.
  • Difficulty in communication; loss of speech.
  • Impaired orientation to time, place, and person.
  • Disturbed behavior, basic motor function issues (e.g., swallowing).
  • Incontinence.
  • Often leads to complications like not eating/drinking or infections.
96
Q

What is the significance of the hippocampus in Alzheimer’s diagnosis and how is it assessed?
Back:

A
  • It’s the first structure inspected when Alzheimer’s is suspected.
  • Assessed using the Scheltens scale (MTA scale) based on atrophy in hippocampal areas.
  • MTA score considers width of choroid fissure, width of the temporal horn, and height of the hippocampus.
97
Q

How is EEG (Electroencephalogram) used in the context of Alzheimer’s diagnosis?

A
  • It shows overall slowing of the dominant rhythm (alpha activity).
  • Supports the diagnosis, but a normal EEG doesn’t rule out Alzheimer’s.
    *A normal EEG strongly argues against other forms of dementia.
98
Q

What are the pros and cons of using lumbar puncture for Alzheimer’s diagnosis?

A

Pros:
Cheaper.
Quicker.
Easier.

Cons:
Doesn’t provide information about the localization of pathology.

99
Q

Describe Logopenic variant primary progressive aphasia (lvPPA) and its initial symptoms.

A
  • Also known as the language variant of Alzheimer’s disease.
  • Starts with predominant language and communication deficits: word-finding issues and impaired sentence repeating.
  • Later stages: Impairment in language comprehension, executive functions, and verbal memory.
  • Early atrophy distribution is asymmetrical, most pronounced in the left temporal lobe.
100
Q

Describe the behavioral/dysexecutive variant and its initial symptoms.

A
  • Presents with behavioral changes and impairments in executive function and social cognition.
  • Types of changes range from disinhibition to apathy.
  • Cortical atrophy is initially most pronounced in the frontal lobe regions.
  • Clinical presentation is similar to the behavioral variant of frontotemporal dementia, but PET and CSF biomarkers indicate underlying Alzheimer’s pathophysiology.
    *
101
Q

Describe Posterior Cortical Atrophy (PCA) and its initial symptoms.

A
  • Also known as the visual variant of AD.
  • Characterized by prominent deficits in visuospatial functions.
  • Initial symptoms: Visual agnosia (impaired visuoconstruction and visuoperception) while memory remains intact.
  • Neurodegeneration starts in the parietal and occipital lobe, later spreading to the occipitotemporal lobe.
102
Q

What is early-onset Alzheimer’s disease?

A

It refers to Alzheimer’s disease that begins before the age of 65. This can include both the typical form of Alzheimer’s and the atypical variants.

103
Q

How does brain atrophy in early-onset Alzheimer’s differ from typical Alzheimer’s?

A

Temporo-parietal atrophy differentiates early-onset Alzheimer’s better from normal ageing. The MTA Score might not be as indicative since the hippocampi are relatively spared, similar to healthy adults.

104
Q

What benefits can cholinesterase inhibitors provide?

A

They can help stabilize memory decline and improve attention and alertness in some patients with Alzheimer’s disease.

105
Q

What is Memantine and when is it used?

A

Memantine increases the release of glutamate in the brain and is an option for severe cases of Alzheimer’s disease. It has limited therapeutic effects but can impact daily functioning with fewer side effects compared to other drugs.

106
Q

What is the difference between t1 en t2 weighted MRI images? beschrijf:
Functie
toepassing ziektebeelden

A

t1
* T1-beeldvorming levert anatomische beelden met een goede weergave van de structuur van weefsels in het lichaam
* T1-beeldvorming geeft beelden met een hoge signaalintensiteit voor vetweefsel en een lagere signaalintensiteit voor waterrijk weefsel.
* identificeren van tumoren, het in kaart brengen van bloedvaten

t2
* T2-beeldvorming onthult de weefseleigenschappen
* hoge signaalintensiteit voor waterrijke weefsels en een lagere signaalintensiteit voor vetweefsel en andere structuren.
* ontstekingen te identificeren, de hersenvochtstroming

107
Q

Wat is het verschil tussen temporele en spatiele resolutie?

A

spatiele: structurele details binnen het brein te onderscheiden.

temporeel veranderingen in de hersenactiviteit over tijd te meten.

108
Q

Benoem de mate van temporele en spatiele resolutie.

A
109
Q

benoem de klinische applicatie

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110
Q
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Clinical Neuro psychology (17 decks)

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