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Dr Srikanta Biswas
Junior resident
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-
75%
• Vascular dementia  5 – 20
%
NEURO-
DEGENERATIVE
Alzheimer's Ds; Dementia with Lewy Bodies; Fronto-
temporal dementia; Parkinson’s Ds
VASCULAR Infarction; Hemodynamic insufficiency
NEUROLOGICAL Multiple Sclerosis; Normal Pressure Hydrocephalus
ENDOCRINE Hypothyroidism
NUTRITIONAL Def. of Vit. B12, Thiamine, Niacin
INFECTIOUS HIV; Prion Ds; Neurosyphilis; Cryptococcus
METABOLIC Hepatic/ Renal Insufficiency; Wilson’s Ds
TRAUMATIC Subdural Haematoma; Dementia pugilistica
TOXIC AGENTS Alcohol; Heavy Metals; Anticholinergic Med; CO
 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
imaging.
 Structural Imaging :
1. CT scan and
2. MRI.
 Functional Imaging :
1. Functional MRI,
2. PET and
3. SPECT.
CT SCAN
Limitation : in soft tissue characterisation
particularly in the temporal lobes and
posterior fossa due to beam hardening
artefacts.
 Radiation hazards
 For preliminary assessment particularly
disorder with haemorrhage.
MRI
 Modality of choice for investigation of
dementia.
 Multiplaner capability
 Excellent soft tissue characterisation.
 Lack of radiation related hazards.
1. fMRI
2. PET
3. NICOTINE PET
4. SPECT
 Used in selected groups , having familial risk
factors of developing dementia related
disorder and also for research purpose.
 Traditional T1, T2 weighted sequence
 FLAIR
 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
biasness.
 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'
atrophy.
 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
is abnormal.
score Width of
choroid
fissure
Width of
tempora
l horn
Height of
hippocam
pal
formation
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
atrophy
Mild widening of
posterior cingulate
and parieto occipital
sulci
Grade 2 Substantial parietal
atrophy
Substantial widening
of the sulci
Grade 3 End–stage ‘ knife-
blade’ atrophy
Extreme widening of
the posterior cingulate
and parieto-occipital
sulci
 The Fazekas-scale provides
an overall impression of the
presence of WMH in the
entire brain.
It is best scored on axial
FLAIR or T2-weighted
images.
Score:
 Fazekas 0: None or a single
punctate WMH lesion
 Fazekas 1: Multiple punctate
lesions
 Fazekas 2: Beginning
confluency of lesions
(bridging)
 Fazekas 3: Large confluent
lesions
 Clinical issues
 Most common dementia(50-60% of all cases)
 Prevalence increases 15-25% per decade after 65 years
 Etiopathology
 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.
 Imaging
 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
Method.
Volumetric assessment of hippocampal
atrophy contributing medial temporal lobe
atrophy has emerged as a surrogate bio
marker of AD
 Clinical issues
 Second most common dementia
 Commonly mixed with other dementias
 Multiple strokes episodic step-like deterioration
 Etiopathology
 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
factors stratification
 Imaging
CT :
shows generalised volume loss with multiple cortical &
subcortical and basal ganglia infarcts. patchy or confluent
hypodensities in the subcortical and deep peri-ventricular
WM.
MRI :
 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
identified .
 T2WI scan show multifocal ,diffuse & confluent
hyperintensities in BG & WM.
 T2 ‘blooming black dots’ (amyloid or hypertension
associated)
 FTLD, formerly called Pick's disease, is a progressive
dementia, that accounts for 5-10% of cases of
dementia.,
 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.
 IMAGING :
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
imaging.
 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
AD.
The role of imaging
is limited in Lewy
body dementia.
Usually the MR of
the brain is normal,
including the
hippocampus
 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-
hypertensive hge.)
 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
matters.
 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.
Classification :
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
pontocerebellar tracts
◦ pons: hot cross bun sign (MSA-C)-due to selective loss of melinated
transeverse pontocerebellar fibre & neurons of median raphe.
◦ middle cerebellar peduncles
◦ cerebellum
 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
 MSA-C
◦ 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
“Hot cross burn sign Putaminal rim sign
 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.
 IMAGING :
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-
like symptom
 Typically affect 50-70yrs
 MRI shows asymmetric
fronto-parietal cortical
atrophy. The prefrontal and
perironaldic cortex, striatum
& midbrain tegmentum more
severely affected.
 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
 IMAGING :
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
Oppenheimer varient
 Newer sub type of CJD known as mad cow disease
 Slective pulvinur degeneretion is hall mark of ‘MAD COW
DISEASE’
Pulvinar degeneration
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
encephalopathy.
CT
Imaging findings include:
 diffuse and symmetric cerebral atrophy, out of proportion in
keeping with age of patient
 symmetric periventricular and deep white matter
hypoattenuation
MRI
 symmetric periventricular and deep white matter T2
hyperintensity
 confluent or patchy
 no mass effect
 no enhancement
 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
hereditary neurodegenerative
disease (autosomal dominant
trait), and can present with early
onset dementia as well as
choreoathetosis and psychosis.
IMAGING :
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
common
 Traid dementia ,gait ataxia , urinary
incontinence
 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.
 Normal hippocampus
 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* (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
dementia.
 The FLAIR images show classic
post-traumatic tissue loss with
gliosis in both frontal lobes,
the left occipital lobe and right
temporal lobe.
 Structural neuro imaging particularly MRI has a great
role in establishing diagnosis, classification of
different type of dementia and assessment of
prognosis.
 This is very helpful in treatment planning including
triage of our limited resources and motivation in old
age care.
 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
functional imaging.
Radiological evaluation of Dementia

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Radiological evaluation of Dementia

  • 1. Dr Srikanta Biswas Junior resident Department of Radio diagnosis Burdwan medical college & Hospital
  • 2.  DEMENTIA- the disease with acquired deterioration in cognitive/ intellectual abilities without impairment of consciousness  Cognitive deficit represent a decline from previous level of functioning
  • 3.  ~ 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- 75% • Vascular dementia  5 – 20 %
  • 4. NEURO- DEGENERATIVE Alzheimer's Ds; Dementia with Lewy Bodies; Fronto- temporal dementia; Parkinson’s Ds VASCULAR Infarction; Hemodynamic insufficiency NEUROLOGICAL Multiple Sclerosis; Normal Pressure Hydrocephalus ENDOCRINE Hypothyroidism NUTRITIONAL Def. of Vit. B12, Thiamine, Niacin INFECTIOUS HIV; Prion Ds; Neurosyphilis; Cryptococcus METABOLIC Hepatic/ Renal Insufficiency; Wilson’s Ds TRAUMATIC Subdural Haematoma; Dementia pugilistica TOXIC AGENTS Alcohol; Heavy Metals; Anticholinergic Med; CO
  • 5.  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 imaging.
  • 6.  Structural Imaging : 1. CT scan and 2. MRI.  Functional Imaging : 1. Functional MRI, 2. PET and 3. SPECT.
  • 7. CT SCAN Limitation : in soft tissue characterisation particularly in the temporal lobes and posterior fossa due to beam hardening artefacts.  Radiation hazards  For preliminary assessment particularly disorder with haemorrhage.
  • 8. MRI  Modality of choice for investigation of dementia.  Multiplaner capability  Excellent soft tissue characterisation.  Lack of radiation related hazards.
  • 9. 1. fMRI 2. PET 3. NICOTINE PET 4. SPECT  Used in selected groups , having familial risk factors of developing dementia related disorder and also for research purpose.
  • 10.  Traditional T1, T2 weighted sequence  FLAIR  Diffusion and Perfusion weighted sequences  SPGR,FEISTA for evaluation of temporal lobe
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  • 13. Radiological assessment scales are utilised for establishing the diagnosis and evaluation of disease progression without subjective biasness.  GCA scale (Global cortical atrophy),  MTA scale (Medial temporal lobe atrophy )  Koedam Score for parietal lobe atrophy,  Fazekas scale for white matter lesion.
  • 14. 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' atrophy.  Cortical atrophy is best scored on FLAIR images.
  • 15.  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 is abnormal.
  • 16. score Width of choroid fissure Width of tempora l horn Height of hippocam pal formation 0 N N N 1 ↑ N N 2 ↑↑ ↑↑ ↓ 3 ↑↑↑ ↑↑↑ ↓↓ 4 ↑↑↑ ↑↑↑ ↓↓↓
  • 17. Koedam score for parietal lobe atrophy Grade 0 No cortical atrophy Closed sulci of parietal lobes and cuneus Grade 1 Mild parietal cortic atrophy Mild widening of posterior cingulate and parieto occipital sulci Grade 2 Substantial parietal atrophy Substantial widening of the sulci Grade 3 End–stage ‘ knife- blade’ atrophy Extreme widening of the posterior cingulate and parieto-occipital sulci
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  • 19.  The Fazekas-scale provides an overall impression of the presence of WMH in the entire brain. It is best scored on axial FLAIR or T2-weighted images. Score:  Fazekas 0: None or a single punctate WMH lesion  Fazekas 1: Multiple punctate lesions  Fazekas 2: Beginning confluency of lesions (bridging)  Fazekas 3: Large confluent lesions
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  • 21.  Clinical issues  Most common dementia(50-60% of all cases)  Prevalence increases 15-25% per decade after 65 years  Etiopathology  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.
  • 22.  Imaging  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
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  • 24.  Visual assessment– MTA Score  Volumetric assessment – Stereological Method. Volumetric assessment of hippocampal atrophy contributing medial temporal lobe atrophy has emerged as a surrogate bio marker of AD
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  • 26.  Clinical issues  Second most common dementia  Commonly mixed with other dementias  Multiple strokes episodic step-like deterioration  Etiopathology  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 factors stratification
  • 27.  Imaging CT : shows generalised volume loss with multiple cortical & subcortical and basal ganglia infarcts. patchy or confluent hypodensities in the subcortical and deep peri-ventricular WM. MRI :  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 identified .  T2WI scan show multifocal ,diffuse & confluent hyperintensities in BG & WM.  T2 ‘blooming black dots’ (amyloid or hypertension associated)
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  • 29.  FTLD, formerly called Pick's disease, is a progressive dementia, that accounts for 5-10% of cases of dementia.,  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.  IMAGING : 1.Frontotemporal volume loss(frontal v temporal) 2.Asymetric/ symetrical atrophy 3. RT vs Lt predomance. 4. FDG-PET- hypometabolism at frontotemporal .
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  • 31.  Typically the diagnosis of exclusion in structural imaging.  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 AD.
  • 32. The role of imaging is limited in Lewy body dementia. Usually the MR of the brain is normal, including the hippocampus
  • 33.  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- hypertensive hge.)  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 matters.
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  • 35.  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. Classification : 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.
  • 36. MRI – modality of choice.  T2/ FLAIR hyperintensities typically present in the pontocerebellar tracts ◦ pons: hot cross bun sign (MSA-C)-due to selective loss of melinated transeverse pontocerebellar fibre & neurons of median raphe. ◦ middle cerebellar peduncles ◦ cerebellum  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  MSA-C ◦ 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
  • 37. “Hot cross burn sign Putaminal rim sign
  • 38.  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.  IMAGING : 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
  • 39. ‘’ Penguine beak or humming bird sign” at midbrain
  • 40.  CBD is a rare entity which may present with cognitive dysfunction, usually in combination with Parkinson- like symptom  Typically affect 50-70yrs  MRI shows asymmetric fronto-parietal cortical atrophy. The prefrontal and perironaldic cortex, striatum & midbrain tegmentum more severely affected.  sometimes with associated hyperintensity of the white matter on T2/FLAIR images.
  • 41.  Creutz feldt Jakob disease  Mad Cow Disease  AIDS Dementia Complex
  • 42.  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  IMAGING : 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 Oppenheimer varient  Newer sub type of CJD known as mad cow disease  Slective pulvinur degeneretion is hall mark of ‘MAD COW DISEASE’
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  • 45. 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 encephalopathy. CT Imaging findings include:  diffuse and symmetric cerebral atrophy, out of proportion in keeping with age of patient  symmetric periventricular and deep white matter hypoattenuation MRI  symmetric periventricular and deep white matter T2 hyperintensity  confluent or patchy  no mass effect  no enhancement
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  • 47.  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.
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  • 49. Huntington disease is a hereditary neurodegenerative disease (autosomal dominant trait), and can present with early onset dementia as well as choreoathetosis and psychosis. IMAGING : 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 common
  • 50.  Traid dementia ,gait ataxia , urinary incontinence  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.  Normal hippocampus
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  • 52.  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* (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 dementia.  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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  • 54.  Structural neuro imaging particularly MRI has a great role in establishing diagnosis, classification of different type of dementia and assessment of prognosis.  This is very helpful in treatment planning including triage of our limited resources and motivation in old age care.  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 functional imaging.