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Dementia: role of MRI

updated version
Frederik Barkhof, Marieke Hazewinkel, Maja Binnewijzend and Robin Smithuis
Alzheimer Centre and Image Analysis Centre, Vrije Universiteit Medical Center, Amsterdam and the Rijnland
Hospital, Leiderdorp, The Netherlands


MR protocol

CT protocol
Assessment of MR in Dementia

GCA-scale for Global Cortical Atrophy

MTA-scale for Medial Temporal lobe Atrophy

Fazekas scale for WM lesions

Normal ageing

Strategic infarctions

Koedam score for Parietal Atrophy


Specific Diseases

Alzheimers Disease

Presenile AD

Mild Cognitive Impairment (MCI)

Vascular Dementia (VaD)

Strategic infarcts and small vessel disease

Cerebral Amyloid Angiopathy (CAA)

Frontotemporal Lobar Degeneration (FTLD )

Dementia with Lewy bodies

Progressive supranuclear palsy (PSP)

Multi System Atrophy (MSA)

Creutzfeldt-Jakob disease (CJD)

Corticobasal Degeneration (CBD)

Huntington Disease


Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and

Leukoencehalopathy (CADASIL)
Traumatic Brain Injury (TBI)
Publicationdate January 9, 2012
This review is based on a presentation given by Frederik Barkhof at the Neuroradiology
teaching course for the Dutch Radiology Society and was adapted for the Radiology
Assistant by Robin Smithuis.
First publication: 1-3-2007.
Updated version: 9-1-2012.
This presentation will focus on the role of MRI in the diagnosis of dementia and related
We will discuss the following subjects:

assessment of
MR in

MR protocol
for dementia

findings in the
most common
o Alzhei
e (AD)
o Vascul

o Fronto
al lobe

Short overview of neurodegenerative disorders which may be associated with


Coronal image of the hippocampus.

The role of neuroimaging in dementia nowadays extends beyond its traditional role of
excluding neurosurgical lesions.
Radiological findings may support the diagnosis of specific neurodegenerative disorders and
sometimes radiological findings are necessary to confirm the diagnosis.
It is a challenge for neuroimaging to contribute to the early diagnosis of neurodegenerative
diseases such as Alzheimer's disease.
Early diagnosis includes recognition of pre-dementia conditions, such as mild cognitive
impairment (MCI).
In addition, early diagnosis allows early treatment using currently available therapies or new
therapies in the future.
Neuroimaging may also be used to assess disease progression and is adopted in current trials
investigating MCI and AD.

The coronal image shows the hippocampus, the main structure involved in many forms of

MR protocol
Protocol that is used in the Alzheimer Centre in Amsterdam

Coronal-oblique T1-weighted images are used for the assessment of medial temporal lobe
and hippocampal atrophy.
They are obtained in a plane orthogonal to the long axis of the hippocampus; this plane is
orientated parallel to the brainstem.
These should be thin-section images and are ideally obtained by reformatting a sagittal 3D T1
sequence through the entire brain.
Additional sagittal reconstructions will enable the assessment of midline structures as well as
parietal atrophy, which may be involved in certain neurodegenerative disorders.

FLAIR images are used to assess global cortical atrophy (GCA), vascular white matter
hyperintensities and infarctions.

T2-weighted images are used to assess infarctions, in particular lacunar infarctions in the
thalamus and basal ganglia, which can be missed on FLAIR images.
T2*-weighted images are necessary to detect microbleeds in amyloid angiopathy. These
images can also depict calcifications and iron deposition.
DWI should be considered as a supplemental sequence in young patients or in rapidly
progressive neurodegenerative disorders (DD - vasculitis, CJD).
CT with negative scan angle for optimal vizualisation of the hippocampus in the transverse plane

CT protocol

CT can be useful when contraindications prevent MRI or when the only reason for imaging is
to rule out surgically treatable causes of cognitive decline.
In the transverse plane the scan angle should be parallel to the long axis of the temporal lobe.
Use of multi-detector CT will enable coronally reformatted images to be reconstructed
perpendicular to the long axis of the temporal lobe for optimal vizualisation of the
Spiral CT of the brain with coronal reconstructions.

Use of multi-detector CT will enable coronally reformatted images to be reconstructed

perpendicular to the long axis of the temporal lobe for optimal vizualisation of the

Assessment of MR in Dementia
* Lewi = Dementia with Lewi bodies

An MR-study of a patient suspected of having dementia must be assessed in a standardized

First of all, treatable diseases like subdural hematomas, tumors and hydrocephalus need to be
Next we should look for signs of specific dementias such as:

disease (AD):
temporal lobe
(MTA) and

Frontotemporal Lobar Degeneration (FTLD): (asymmetric) frontal lobe atrophy and

atrophy of the temporal pole.

Vascular Dementia (VaD): global atrophy, diffuse white matter lesions, lacunes and
'strategic infarcts' (infarcts in regions that are involved in cognitive function).

Dementia with Lewy bodies (DLB): in contrast to other forms of dementia usually no
specific abnormalities.

So when we study the MR images we should score in a systematic way for global atrophy,
focal atrophy and for vascular disease (i.e. infarcts, white matter lesions, lacunes).
When we study the MR images we must systematically score for global atrophy, focal
atrophy and for vascular disease (i.e. infarcts, white matter lesions, lacunes).
This standardized assessment of the MR findings in a patient suspected of having a cognitive
disorder includes:
1. GCA-scale
for Global
2. MTA-scale
for Medial
Temporal lobe

3. Koedam score
for parietal
4. Fazekas scale
for WM
5. Looking for strategic infarcts
The central sulcus is more posteriorly on more cranial images.

GCA-scale for Global Cortical Atrophy

GCA scale is the mean score for cortical atrophy throughout the complete cerebrum:

0: no cortical

1: mild
opening of

2: moderate
volume loss
of gyri

3: severe (end-stage) atrophy: 'knife blade' atrophy.

Cortical atrophy is best scored on FLAIR images.

In some neurodegenerative disorders the atrophy is asymmetric and occurs in specific
A radiological report should mention any regional atrophy or asymmetry.
When assessing atrophy in different regions keep in mind that cranially, the central sulcus lies
more posteriorly than you would expect (figure).
MTA-scale for Medial Temporal lobe Atrophy

The MTA-score should be rated on coronal T1-weighted images at a consistent slice

Select a slice through the corpus of the hippocampus, at the level of the anterior pons.
> 75 years : MTA-score 3 or more is abnormal (i.e. 2 can still be normal at this age)

Data from a study with 222 controls and patients with various forms of dementia in which
this visual rating scale was used to assess temporal lobe atrophy suggest that sensitivities and
specificities of 85% can be obtained for patients with AD.
The score is based on a visual rating of the width of the choroid fissure, the width of the
temporal horn, and the height of the hippocampal formation.

score 3: moderate loss of hippocampal volume (decrease in height)

score 0: no

score 1: only
widening of

score 2: also
widening of
temporal horn
of lateral

score 4:
severe volume
loss of

score 0: no

score 1: only
widening of

score 2: also
widening of
temporal horn
of lateral

< 75 years: score 2 or more is abnormal.

> 75 years: score 3 or more is abnormal.
Use scrollbar

Here you can scroll through the images for examples of MTA score 0-4.

score 3: moderate loss of hippocampal volume (decrease in height)

score 4: severe volume loss of hippocampus

< 75 years: score 2 or more is abnormal.

> 75 years: score 3 or more is abnormal.
Medial temporal lobe atrophy in Alzheimer's disease, vascular dementia, dementia with Lewy bodies (DLB) and in controls.

A high MTA-score is very sensitive for the diagnosis of Alzheimer disease and is present in
the vast majority of patients with AD, while in controls a positive score is almost always
absent (table on the left).
Therefore it is a good test to discern controls from patients with AD.
This test is not completely specific for AD however, as MTA can also be found in other forms
of dementias (7).
On the other hand if a patient with mild cognitive impairment (MCI) a possible 'prodromal
state of AD' has a negative MTA-score, it is very unlikely that this patient will develop AD
(high sensitivity yields high negative predictive value), except in very young subjects, in
whom a more posterior pattern of atrophy can be observed in AD.
Coronal T1WI of the hippocampus demonstrating progressive atrophy in familial AD (images kindly provided by Nick Fox).

If there is a strong suspicion of Alzheimer's disease, it can be useful to repeat the examination
to see if there is any progress of the (medial temporal lobe) atrophy.
The images show a follow-up examination at 18 and 36 months in a patient who was at risk
for familial AD, demonstrating progression of the disease.
An alternative approach would be to perform a SPECT- or PET-scan to look for changes in
perfusion/metabolism of the temporo-parietal cortex, as these changes precede the
development of atrophy.
Fazekas scale for WM lesions

On MR, white matter hyperintensities (WMH) and lacunes - both of which are frequently
observed in the elderly - are generally viewed as evidence of small vessel disease.
The Fazekas-scale provides an overall impression of the presence of WMH in the entire
It is best scored on transverse FLAIR or T2-weighted images.

Fazekas 0: None or a single punctate WMH lesion

Fazekas 1: Multiple punctate lesions

Fazekas 2: Beginning confluency of lesions (bridging)

Fazekas 3:

The Fazekas scale for WM lesions predicts future disability in elderly.

Fazekas 1 is considered normal in the elderly.

Fazekas 2 and 3 are pathologic, but may be seen in normally functioning individuals.
They are however, at high risk for disability.
In 600 normally functioning elderly people the Fazekas score predicted disability within one
year (table). In the Fazekas 3 group 25% was disabled within one year (10).
Three year follow-up shows that severe white matter changes independently and strongly
predict rapid global functional decline (17).

Caps and bands

Normal ageing

The findings in a normally aging brain can overlap with findings in dementia.
As implicated earlier, there may be some degree of atrophy, though mainly of the white

matter with increasing prominence of the perivascular (Virchow-Robin) spaces and nonspecific fronto-parietal sulcal widening.
There may also be some degree of medial temporal lobe atrophy.
A MTA-score of 2 for individuals older than 75 years of age may be normal.
As the brain ages, there is an increasing deposition of iron in specific areas of the brain:
mainly the basal ganglia, nucleus ruber and pars reticluaris of the substantia nigra.
There also may develop a rim of high signal intensity on T2W and FLAIR images around the
ventricles, known as caps and bands (figure).
A limited amount of white matter hyperintensities may also occur in the normally ageing
brain (Fazekas grade 1).
Lacunes are always pathological.
Strategic infarctions

Strategic infarctions are infarctions in areas that are crucial for normal cognitive functioning
of the brain.
These areas are summarized in the table.
Strategic infarctions are best seen on transverse FAIR and T2W sequences.
The images show bilateral thalamic infarctions - lesions often associated with cognitive

Transverse FLAIR images in two different patients.

Study the images of two different patients.

Then continue reading.

The image on the far left shows an infarct in the vascular territory of the Posterior Cerebral
Artery (PCA), with involvement of the inferior medial temporal lobe which includes the
This is a strategic infarction, since it is in the dominant hemisphere, it will result in cognitive
The image next to it is a transverse FLAIR image showing another infarct in the PCAterritory, with involvement of the temporo-occipital association area.
This is another example of a strategic infarction that can result in cognitive dysfunction.
Koedam score for Parietal Atrophy

In addition to medial temporal lobe atrophy, parietal atrophy also has a positive predictive
value in the diagnosis of AD.
Atrophy of the precuneus is particularly characteristic of AD (15).
This is particularly the case in young patients with AD (presenile AD), who may have normal
The Koedam scale rates parietal atrophy - assessed in sagittal, coronal and axial planes.

In these planes, widening of the posterior cingulate and parieto-occipital sulci as well as
parietal atrophy (including the precuneus) is rated (Table).
Koedam scale grade 0-1

Koedam scale grade 0-1

Sagittal T1-, axial FLAIR- and coronal T1-weighted images illustrating the Koedam scale of
posterior atrophy.
When different scores are obtained in different orientations, the highest score must be
considered (16).
Koedam scale grade 2-3

Koedam scale grade 2-3

Sagittal T1-, axial FLAIR- and coronal T1-weighted images illustrating the Koedam scale of
posterior atrophy.
The yellow arrows point to extreme widening of the posterior cingulate en parieto-occipital
sulci in a patient with grade 3 posterior atrophy.

In addition to clinical findings, CSF and MRI, PET-imaging is useful in diagnosing AD.
In AD FDG-PET can show hypometabolism in the temporoparietal regions and/or the
posterior cingulum.
This may help differentiate AD from FTD, which shows frontal hypometabolism on FDGPET.
The images show FDG-PET and axial FLAIR images of a normal subject and of patients with
AD and FTD.
FDG-PET (top row) and axial FLAIR images of a normal subject and of AD and FTD
In AD there is a decreased metabolism of the parietal lobes (yellow arrows), whereas in FTD,
there is frontal hypometablism (red arrows).

Specific Diseases

The prevalence of specific forms of dementia is age-dependent.

In patients In patients > 65 years there are more cases of senile AD and vascular dementia.
In many older patients with manifest AD there is co-existing vascular disease, which
contributes to the demented state.
Specimen in end stage AD demonstrating severe global atrophy. Courtesy Webpath (11).

Alzheimers Disease

AD accounts for 50%-70% of all cases of dementia in the elderly population.

Age is a strong risk factor, with the disease affecting approximately 8% of individuals over
the age of 65 and 30% over the age of 85 years.

The progression of AD is gradual and the average patient lives 10 years after the onset of
With the increasing percentage of elderly in the population, the prevalence of AD is expected
to triple over the next 50 years.
In end-stage AD there is widespread atrophy, which is no different from other end-stage
In imaging we therefore have to try to identify AD in an earlier stage and we have to
concentrate on the hippocampus and the medial temporal lobe, because that is where AD
The role of MRI in the diagnostic process of AD is twofold:

Rule out other

causes of

Identify early
onset AD for
therapy and

Study the image, then continue reading.

The findings are consistent with the diagnosis of end stage AD, because there is:

Extreme hippocampal and medial temporal lobe atrophy (MTA score: 4)

Severe global atrophy (GCA scale: 3)

It is not specific for AD however, since severe GCA occurs in other end-stage disorders as
Presenile AD with normal hippocampus and severe parietal atrophy.

Presenile AD

Presenile AD ( Although there usually is some mild hippocampal atrophy, the most striking
finding is parietal atrophy with atrophy of the posterior cingulum and the precuneus; the
hippocampus can be normal.
Mild Cognitive Impairment (MCI)

Mild cognitive impairment is a relatively recent term used to describe people who have some
problems with their memory, but do not actually have dementia, since dementia is defined as

having problems in two or more cognitive domains.

Some of these patients will be in the early stages of Alzheimer's disease or another dementia,
so it is important to identify them.
Finding MTA is a strong risk-factor for progression to dementia.
PCA infarction involving the medial temporal lobe.

Vascular Dementia (VaD)

Vascular dementia (VaD) is thought to be the second most common cause of dementia after
Alzheimer's disease.
It can sometimes be distinguished from AD by a more sudden onset and association with
vascular risk factors.
VaD can be characterized by its stepwise deterioration with periods of stability followed by
sudden decline in cognitive function.
Most patients, however, have small vessel disease, which is typified by a more gradual and
subtle pattern of deterioration.
Control of vascular risk factors is the treatment of choice, but cholinesterase inhibitors (drugs
that are being used in AD) are also increasingly being used to treat vascular dementia.
The images show a patient with a strategic PCA infarction involving the hippocampus.
This type of infarct can result in sudden dementia if located in the dominant hemisphere.
It will usually not result in dementia if it occurs in the non-dominant hemisphere.
Vascular dementia, no medial temporal lobe atrophy.

In most patients with VaD there is diffuse white matter disease with large confluent lesions
(Fazekas 3).
In some of these patients the ventricles may be dilated due to global atrophy and some will
also have medial temporal lobe atrophy.
The images are of a patient who had VaD, but the medial temporal lobe was normal.

Strategic infarcts and small vessel disease

Cognitive dysfunction in VaD can be the result of (2):

Large vessel
o Bilater
al in

o Parietotemporal- and temporo-occipital association areas of the dominant
hemisphere (angular gyrus included)
o o Posterior cerebral artery territory infarction of the paramedian thalamic
region and inferior medial temporal lobe of the dominant hemisphere

Watershed infarctions in the dominant hemisphere (superior frontal and parietal)

Small vessel disease:


Multiple lacunar infactions in frontal white matter(>2) and basal ganglia (>2)

WMLs (at least more than 25% of WM)

Bilateral thalamic lesions

MTA in a patient with VaD

There is an increasing awareness for the importance of small vessel disease as a predictor of
cognitive decline and dementia.
Moreover, it seems to amplify the effects of pathologic changes of Alzheimer's disease.
On the left we see a patient who was diagnosed as having VaD.
White matter disease is seen as severe WMH (hypointense on T1) in the periventricular
In addition to these vascular changes, there is also MTA.
Presumably this patient has both VaD and AD, a finding seen in many elderly patients.
These findings should be described separately as it may have therapeutic consequences.
The problem however is, that white matter hyperintensities and lacunes are also frequently
observed in non-demented elderly and at some level can be regarded as normal findings in
To overcome this problem the NINDS-AIREN International Work Group has formulated
criteria for the history and physical, radiological, (see above) and pathological examination to
classify patients as having possible, probable and definite VaD.
However considerable interobserver variability exists for the assessment of the radiological
part of these NINDS-AIREN criteria and some level of training is mandatory (2).
Bilateral medial strategic thalamus infarctions

The medial nuclei of the thalamus play an important role in memory and learning.
A large unilateral infarction or bilateral infarctions in this region can cause dementia.
You have to pay special attention to these areas to find these small infarctions.
FLAIR misses thalamus infarctions

On FLAIR images you will easily miss these infarctions, because they can be isointense to
the surrounding structures (8).
A high resolution T2WI is needed to detect these thalamic infarcts.
FLAIR in the infratentorial region and in the spinal cord is of limited value as it suppresses
not only the signal of water, but also pathology with a long T1-relaxation time.
This phenomenon can also be seen in the detection of Multiple Sclerosis, where FLAIR is of
limited value in the infratentorial region and of no use in the spinal cord.
Cerebral Amyloid Angiopathy

Cerebral Amyloid Angiopathy (CAA)

Dementia may be the clinical presentation in CAA, a condition in which ?-amyloid is

deposited in the vessel walls of the brain.
The result is hemorrhage, usually microhemorrhages, but also subarachnoid hemorrhage or
lobar hematomas may occur.
On MR, the T2* sequence will show multiple microhemorrhages, typically in a peripheral
location (as opposed to hypertensive microhemorrhages, which are usually more centrally
located, e.g. in the basal ganglia and thalami).
In addition, FLAIR will reveal moderate to sever white matter hyperintensities (Fazekas
grade 2 or 3)

T2* images in a patient with CAA show multiple peripherally located microbleeds.
Cerebral Amyloid Angiopathy

FLAIR images of the same patient show Fazekas 2 white matter hyprintensities.
Cerebral Amyloid Angiopathy

T2* images in a patient with CAA microbleeds.

Cerebral Amyloid Angiopathy

T2* images demonstrate multiple lobar microbleeds in a patient with CAA.

End stage(11).
FTLD with striking atrophy of frontal and temporal lobes. No artophy of parietal and occipital lobes. Courtesy

Frontotemporal Lobar Degeneration (FTLD )

FTLD, formerly called Pick's disease, is a progressive dementia, that accounts for 5-10% of
cases of dementia., and occurs relatively more frequently in presenile subjects
FTLD is clinically characterized by behavioral and language disturbances that may precede
or overshadow memory deficits.
There is currently no treatment for this condition.
Imaging plays an important role in the diagnosis as the findings are easy to recognize.
Radiological findings are pronounced atrophy of frontal and / or temporal lobes.
In some forms of FTLD the atrophy might be strikingly asymmetric, e.g. in Semantic

Dementia, a disease subtype with progressive aphasia and left-sided temporal lobe
FTLD: T2WI and FLAIR with 'knife blade' atrophy of left temporal lobe with normal right temporal lobe

The images are of a patient with progressive aphasia.

The most prominent finding is the striking asymmetric atrophy of the temporal lobe on the
left side with not only atrophy of the hippocampus, but also the temporal poles.
The atrophy has resulted in gyri that appear as sharp as knives ('knife blade atrophy').
There is also some increased signal intensity seen on the FLAIR image, probably due to
These findings are pathognomonic for the diagnosis of FTLD.

Patients with left-sided temporal atrophy are usually clinically obvious.

Right-sided atrophy is usually not as easily recognized as these patients only present with
subtle disturbances in recognizing faces.
Lewi body dementia: normal hippocampus

Dementia with Lewy bodies

Dementia with Lewy bodies is responsible for approximately 25% of dementias and belongs
to the atypical Parkinson syndromes together with progressive supranuclear palsy (PSP) and
multi-system atrophy (MSA).
The clinical manifestations can be similar to that of AD or dementia associated with
Parkinson's disease.
Patients typically present with one of three symptom complexes: detailed visual
hallucinations, Parkinson-like symptoms and fluctuations in alertness and attention.
Pathologically, the disease is characterized by the presence of Lewy bodies in various regions
of the hippocampal complex, subcortical nuclei and neocortex with a variable number of
diffuse amyloid plaques.
Cholinesterase inhibitors are currently the treatment of choice for this condition.
The role of imaging is limited in Lewy body dementia.
Usually the MR of the brain is normal, including the hippocampus.
This finding is important as it enables us to differentiate this disease from Alzheimer';s
disease, the main differential diagnosis.
Nuclear imaging can be used to demonstrate an abnormal dopaminergic system (so-called
PSP with midbrain atrophy

Progressive supranuclear palsy (PSP)

PSP is also one of the atypical parkinsonian syndromes.

In PSP there is pronounced atrophy of the midbrain (mesencephalon), which accounts for the
typical upward gaze paralysis.

PSP: 'humming bird sign' due to midbrain atrophy

Normally the upper border of the midbrain is convex.

The atrophy of the midbrain in PSP results in a concave upper border of the midbrain with the
typical 'humming bird sign' (figure).
'Hot cross bun sign' in MSA

Multi System Atrophy (MSA)

MSA is also one of the atypical parkinsonian syndromes.

MSA is a rare neurological disorder characterized by a combination of parkinsonism,
cerebellar and pyramidal signs, and autonomic dysfunction.
MSA can be classified as MSA-C, MSA-P or MSA-A.
In MSA-C (formerly known as sporadic olivopontocerebellar atrophy or sOPCA) the
cerebellar symptoms predominate, whereas in MSA-P the parkinsonian symptoms dominate
(MSA-P was formerly known as striatonigral degeneration).
MSA-A is the form in which autonomic dysfunction predominates and is the new term for
what was formerly known as Shy-Drager syndrome.
Usually there is pronounced cerebellar atrophy and severe atrophy of the pons.
In MSA-P: low T2 SI dorsolateral putamen and slit-like increased SI lateral to putamen on
In contrast to PSP, we don't see the humming bird sign, because the midbrain has a normal
convex upper border.
The so-called 'hot cross bun sign', which is a result of pontine hyperintensity, is typical for
Changes in the neocortex as seen on FLAIR (left) and DWI (right)

Creutzfeldt-Jakob disease (CJD)

CJD is a very rare and incurable neurodegenerative disease, caused by a unique type of
infectious agent called a prion.
The first symptom of CJD is rapidly progressive dementia, leading to memory loss,
personality changes and hallucinations.
The disease is characterized by spongiform changes in the cortical and subcortical gray
matter, with loss of neurons and replacement by gliosis.

The abnormalities can sometimes be detected on FLAIR, but are most conspicuous on DWI
sequences, affecting either the striatum, the neo-cortex, or a combination of both.
Pulvinar hyperintensity in new variant of CJD. Courtesy Dr. Collie (12)

New variant CJD

New variant of CJD is also known as the 'mad cow disease' (12).
It is a disease fortunately hardly encountered anymore.
In this variant the changes are seen in the posterior part of the thalamus, called the pulvinar.
Corticobasal degeneration

Corticobasal Degeneration (CBD)

CBD is a rare entity which may present with cognitive dysfunction, usually in combination
with Parkinson-like symptoms.
The so-called 'Alien-hand' syndrome is a typical manifestation.
MRI shows asymmetric parietal cortical atrophy, sometimes with associated hyperintensity of
the white matter on T2W images.
Axial FLAIR image shows striking asymmetric cortical parietal atrophy in a patient with
Huntington Disease

Huntington disease is a hereditary neurodegenerative disease (autosomal dominant trait, but

often de novo mutations), and can present with early onset dementia as well as
choreoathetosis and psychosis.
Imaging shows characteristic atrophy of the caudate nucleus and subsequent enlargement of
the frontal horns of the lateral ventricles.
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and
Leukoencehalopathy (CADASIL)

CADASIL is another hereditary disease which may present with a progressive cognitive
Other presenting symptoms include migraines, stroke-like episodes and behavioral
disturbances. It affects the small vessels of the brain.
Confluent white matter hyperintesities in the frontal and especially anterior temporal lobes in
combination with (lacunar) infarcts and microbleeds are seen on imaging.
The FLAIR images show classic findings in CADASIL - confluent white matter
hyperintensities with lacunar infarcts and involvement of the anterior temporal lobes.
Traumatic brain injury

Traumatic Brain Injury (TBI)

Long term sequelae of traumatic brain injury such as cerebral contusions and diffuse axonal
injury (DAI) may include cognitive impairment.
Frontobasal/temporal parenchymal loss or T2* black dots typical for DAI in a patient with a
history of trauma must therefore be taken into consideration when assessing MR images for
The FLAIR images show classic post-traumatic tissue loss with gliosis in both frontal lobes,
the left occipital lobe and right temporal lobe.

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