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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
  11. 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.
  12. 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.
  13.  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.
  14. 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 ↑↑↑ ↑↑↑ ↓↓↓
  15. 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
  16.  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
  17.  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.
  18.  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
  19.  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
  20.  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
  21.  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)
  22.  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 .
  23.  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.
  24. The role of imaging is limited in Lewy body dementia. Usually the MR of the brain is normal, including the hippocampus
  25.  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.
  26.  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.
  27. 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
  28. “Hot cross burn sign Putaminal rim sign
  29.  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
  30. ‘’ Penguine beak or humming bird sign” at midbrain
  31.  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.
  32.  Creutz feldt Jakob disease  Mad Cow Disease  AIDS Dementia Complex
  33.  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’
  34. Pulvinar degeneration
  35. 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
  36.  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.
  37. 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
  38.  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
  39.  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.
  40.  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.