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Dr Srikanta Biswas
Department of Radio diagnosis
Burdwan medical college & Hospital
DEMENTIA- the disease with acquired
deterioration in cognitive/ intellectual
abilities without impairment of consciousness
Cognitive deficit represent a decline from
previous level of functioning
~ 5 to 8 % at age 65 to 70
~ 15 to 20 % at age 75 to 80
up to 40 to 50 % over age 85
• Alzheimer's disease is most
common dementia 50-
• Vascular dementia 5 – 20
To exclude space occupying lesions like tumour,
hematoma, abscess etc
To evaluate strategic territorial vascular insult,
responsible for cognitive impairment.
To improve the clinical differential diagnosis.
To evaluate the disease progression and
response to treatment protocols.
For research purpose particularly functional
Structural Imaging :
1. CT scan and
Functional Imaging :
1. Functional MRI,
2. PET and
Limitation : in soft tissue characterisation
particularly in the temporal lobes and
posterior fossa due to beam hardening
For preliminary assessment particularly
disorder with haemorrhage.
Modality of choice for investigation of
Excellent soft tissue characterisation.
Lack of radiation related hazards.
3. NICOTINE PET
Used in selected groups , having familial risk
factors of developing dementia related
disorder and also for research purpose.
Traditional T1, T2 weighted sequence
Diffusion and Perfusion weighted sequences
SPGR,FEISTA for evaluation of temporal lobe
Radiological assessment scales are utilised for
establishing the diagnosis and evaluation of
disease progression without subjective
GCA scale (Global cortical atrophy),
MTA scale (Medial temporal lobe atrophy )
Koedam Score for parietal lobe atrophy,
Fazekas scale for white matter lesion.
GCA scale - mean score for cortical atrophy
throughout the complete cerebrum:
0: no cortical atrophy
1: mild atrophy: opening of sulci
2: moderate atrophy: volume loss of gyri
3: severe (end-stage) atrophy: 'knife blade'
Cortical atrophy is best scored on FLAIR images.
Coronal T1-weighted images
at a consistent slice
position(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)
< 75 years: score 2 or more
score Width of
0 N N N
1 ↑ N N
2 ↑↑ ↑↑ ↓
3 ↑↑↑ ↑↑↑ ↓↓
4 ↑↑↑ ↑↑↑ ↓↓↓
Koedam score for parietal lobe atrophy
Grade 0 No cortical atrophy Closed sulci of parietal
lobes and cuneus
Grade 1 Mild parietal cortic
Mild widening of
and parieto occipital
Grade 2 Substantial parietal
of the sulci
Grade 3 End–stage ‘ knife-
Extreme widening of
the posterior cingulate
The Fazekas-scale provides
an overall impression of the
presence of WMH in the
It is best scored on axial
FLAIR or T2-weighted
Fazekas 0: None or a single
punctate WMH lesion
Fazekas 1: Multiple punctate
Fazekas 2: Beginning
confluency of lesions
Fazekas 3: Large confluent
Most common dementia(50-60% of all cases)
Prevalence increases 15-25% per decade after 65 years
Neurotoxic ‘amyloid cascade’
o Aβ42 accumulation-senile plaques,amyloid angiopathy
Taupathy-neurofibrillary tangles’neuronal death
Atrophy of hippocampus thus contributing temporal lobe
atrophy is the hall mark in senile AD
AD in pre senile group atrophy starts from pareital region,
precuneus and posterior cingulum.
Fronto-parietal dominant lobar atrophy
Medial temporal lobe particularly the Hippocampus,
entorhinal cortex disproportionately affected
Volumetric analysis of hippocampus & parahippocampal
gyri is helpful.
T2 *( GRE, SWI ) sequences are much more sensative in
detecting cortical microhemarrhage T2 ‘blooming black
dots’ suggests Amyloid angiopathy
MRS shows decreased NAA & increased mI
FDG PET shows hypometabolism
Visual assessment– MTA Score
Volumetric assessment – Stereological
Volumetric assessment of hippocampal
atrophy contributing medial temporal lobe
atrophy has emerged as a surrogate bio
marker of AD
Second most common dementia
Commonly mixed with other dementias
Multiple strokes episodic step-like deterioration
Multiple ischaemic episodes
Can be small or large vessel
Atherosclerosis ,arteriosclerosis , amyloidangiopathy
Rarely caused by inherited disorder like CADASIL or
mitrochondrial encephalopathy .
Fazekas scale for white matter (Hyper intensities in T2
and FLAIR) is very helpful for the evaluation of small
vessel disease in combination with appropriate risk
shows generalised volume loss with multiple cortical &
subcortical and basal ganglia infarcts. patchy or confluent
hypodensities in the subcortical and deep peri-ventricular
T1WI shows greater than expected volume loss. Multiple
hypo-intensities in BG & deep WM are typical. Focal cortical &
larger territorial infarct with encephalomalacia can be
T2WI scan show multifocal ,diffuse & confluent
hyperintensities in BG & WM.
T2 ‘blooming black dots’ (amyloid or hypertension
FTLD, formerly called Pick's disease, is a progressive
dementia, that accounts for 5-10% of cases of
occurs relatively more frequently in presenile
subjects (peak 45-65 yrs)
FTLD is clinically characterized by behavioral and
language disturbances that may precede or
overshadow memory deficits.
1.Frontotemporal volume loss(frontal v temporal)
2.Asymetric/ symetrical atrophy
3. RT vs Lt predomance.
4. FDG-PET- hypometabolism at frontotemporal .
Typically the diagnosis of exclusion in structural
Considerable overlapping of clinical spectrum of
this type of dementia with dementia of AD.
Other diseases with lewy bodies includes PD ,PDD
Patients typically present with one of three
symptom complexes: detailed visual
hallucinations, Parkinson-like symptoms and
fluctuations in alertness and attention.
Absence of hippocampal atrophy may exclude
The role of imaging
is limited in Lewy
Usually the MR of
the brain is normal,
Dementia may be the clinical presentation in CAA, a
condition in which ?-amyloid is deposited in the vessel
walls of the brain
Multiple areas of micro hemorrhage in both cerebral
hemispheres particularly at the periphery .( D/D-
Occasionally sub arachonoid hemorrhage and intracerebral
hemorrhage may occurs
T1/T2/T2 Flair and GRE, SWI are helpful in diagnosis
Sometimes coexisting T2/Flair hyperintensities in white
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.
1. MSA-C (formerly known as sporadic olivopontocerebellar
atrophy or sOPCA) the cerebellar symptoms predominate,
2. MSA-P the parkinsonian symptoms dominate
(MSA-P was formerly known as striatonigral degeneration).
3. MSA-A is the form in which autonomic
dysfunction predominates and is the new term for what was
formerly known as Shy-Drager syndrome.
MRI – modality of choice.
T2/ FLAIR hyperintensities typically present in the
◦ pons: hot cross bun sign (MSA-C)-due to selective loss of melinated
transeverse pontocerebellar fibre & neurons of median raphe.
◦ middle cerebellar peduncles
putaminal findings in MSA-P
◦ reduced volume
◦ reduced GRE and T2 signal relative to globus pallidus
◦ abnormally high T2 linear rim at lateral border of the putamen
("putaminal rim sign"), seen in 1.5 T
◦ disproportionate atrophy of the cerebellum and brainstem
(especially olivary nuclei and middle cerebellar peduncle)
ADC values: higher in the pons, cerebellum, and putamen
than in Parkinson disease or controls
PSP is also one of the atypical parkinsonian
syndromes. ( 2nd most common cause of PD )
Insidious onset 6th to 7th decades.
It is characterised by supranuclear gaze paralysis,
postural instability & mild dementia.
1. midbrain volume loss ( sagital midbrain volume
< 70cc , Midbrain : Pons = <0.15)
2. Penguin or 'humming bird sign'
3. superior cerebellar peduncle atrophic and
quadrigeminal plate thinned
4. widened adjacent cisterns
‘’ Penguine beak or humming
bird sign” at midbrain
CBD is a rare entity which
may present with cognitive
dysfunction, usually in
combination with Parkinson-
Typically affect 50-70yrs
MRI shows asymmetric
atrophy. The prefrontal and
perironaldic cortex, striatum
& midbrain tegmentum more
sometimes with associated
hyperintensity of the white
matter on T2/FLAIR images.
Creutz feldt Jakob disease
Mad Cow Disease
AIDS Dementia Complex
CJD is neurodegenarative diseases caused by prion protein,
characterised by rapidly progressive dementia, leading to
memory loss, personality changes and hallucinations.
Progressive spongiform degeneration of cortical and sub
cortical grey matter
1.T2 and FLAIR hyperintensities at BG ,thalami, cortex.
2. Pulvinar sign –posterior thalami
3. Hokey stick sign –posteromedial thalami
4. DW1 sequence detects diffusion restriction in
much early stage.
5. Occipetal cortex in Heidenhain varient
6. cerebellum is primarily affected in Brownell
Newer sub type of CJD known as mad cow disease
Slective pulvinur degeneretion is hall mark of ‘MAD COW
AIDS dementia complex (ADC), corresponds to a neurological
clinical syndrome seen in patients with HIV infection. The
associated imaging appearance is generally referred to as HIV
Imaging findings include:
diffuse and symmetric cerebral atrophy, out of proportion in
keeping with age of patient
symmetric periventricular and deep white matter
symmetric periventricular and deep white matter T2
confluent or patchy
no mass effect
Cerebral Autosomal Dominent Arteriopathy with
Subcortical Infarcts and Leukoencephalopathy.
Young & middle age adult presents with
recurrent ischemic stroke , migraine headache,
psychiatric disturbances ,cognitive impairment
-progresses to dementia.
IMAGING : Multiple lacunar infarction in BG with
bilateral multifocal T2/FLAIR hyperintensitiis in
subcortical ,periventricular & deep WM.
involvment of anterior temporal lobes & external
capsules has high sensitivity and specificity.
Huntington disease is a
disease (autosomal dominant
trait), and can present with early
onset dementia as well as
choreoathetosis and psychosis.
Bilateral Caudate nucleui atrophy
resulting in dilatation of frontal
horns of both lateral ventricles.
Diffuse cerebral volume loss with
T2/FLAIR hyperintensities in
shrunken caudate head .
putaminal hyperinsities is
Traid dementia ,gait ataxia , urinary
Ventricles and sylvian fissures are dilated out
of proportion of sulcul dilatation.
Enlarged lateral ventricles with rounding frontal
horn, 3rd ventricle moderately enlarged while
4th ventricle appears normal.
Flow void at the region of aqueduct is present.
Long term sequelae of
traumatic brain injury such as
cerebral contusions and diffuse
axonal injury (DAI) may include
parenchymal loss or T2* (GRE
,SWI) 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
Structural neuro imaging particularly MRI has a great
role in establishing diagnosis, classification of
different type of dementia and assessment of
This is very helpful in treatment planning including
triage of our limited resources and motivation in old
Functional imaging is still in the process of evolution.
Intervention will be possible long before the actual
structural damage will occur with the help of