Embed Size (px)
Citation preview
-Findings by imaging.
*Parietal and medial temporal cortical atrophy.
-Role of diagnostic imaging
*Exclude treatable dementias.
*Identify early onset for possible innovative therapy
-Instrumentations and discipline of imaging *NECT, Corresponding clinical findings
*MRI, MRS, F.MRI
*RN SCAN (PET and SPECT)
X-Ray CTThis is just a morphological assessment (not diagnostic)
to show degree and place of brain atrophy in medial temporal and parietal lobes, perihippocampal fissures due to atrophy of hippocampus and parahippocampal gyrus, preferential volume loss in temporal and parietal lobes and large temporal horns (compensatory local hydrocephaly) ,medial temporal lobe atrophy.
Another point is to see DDX.
Multi-infarct dementia in 63M
Bilateral SDHs
Multi-Infarct dementia
MRIConventional, Functional, Volumetric analysis and MRS
A) Conventional MRI: shows the same changes as in X-ray CT and findings also are non-specific
B) Functional MRI: low activation in various brain regions following memory tasks
C) Volumetric analysis: small hippocamp, parahippocamp, hippocamp gyrus (Risk for preceding AD )
D) Perfusion MRI: dynamic MRI with contrast, low GBV in temporal and perietal regions (with correlation with low rCBF on PET and SPECT)
T1 FlairAtrophy in inf. Temporal lobes and enlargement of sylvian fiss.
Decrease N-acetyl aspartate (neuronal loss) and high myoinositol level (gliosis)
T2
Bilateral hippocampal atrophy in A.D.
RN SCAN, PET and SPECT
A) High specificity/ sensitivity of FDG PET limited. (can`t distinguish AD from PD dementia)
B) Regional hypometabolic areas(low glucose, O2
utilization in temporal and parietal lobes, correlate with severity of cognitive impairment)
C) Perfusion deficits: low rCBF on PET using O15H2O or SPECT in hippocamp and temporal regions
Hypometabolism by FDG PET
Both parietal lobes Both pos. temporal lobes
How to request image?
A) First and the best: coronal MRI in T1, T2, Flair, SPGR for detect atrophy and to exclude other causes of dementia, wide cisternal spaces and wide temporal horns.
B) Second, also the best: PET helps to DDX, AD from vascular or frontotemporal dementia when clinical diagnosis of AD uncertain.
C) Third and complimentary: Axial T2 MRI to see specific region of atrophy.
D) Forth volumetric MRI of hippocampus, entrohinal cortex
E) Fifth: MR brain activation studies for diagnosis and following therapy.
F) Sixth: Molecular imaging
DDX by Imaging
A) Creutzfeldt- jakob: dementia + myoclonus + abnormal EEG T2 = Hyper. In BG, Thalamus, Cortex
B) Reversible dementia: Alcohol as third most comon cause of dementia, endocrinopathy, hypothyroidism, B12 deficiency, depression as pseudodementia, NPH hydrocephaly, head trauma, chronic sub dural hematoma large sub frontal meningioma, infection e.g.neurosyphilis and HIV.
C) Vascular dementia: second most common e.g. chronic infarct with focal atrophy
D) Diffuse lewy body disease: hypometabolism of entire brain ,visual cortex and cerebellum
E) Frontotemporal dementia (pick disease) asymmetric frontal and anterior temporal atrophy (volumetric studies differentiate from AD)
F) Corticobasal degeneration: severe frontoparietal atrophyG) Other neurodegenerative disorders: Hontington disease, Parkinson disease
DDXDDX B12 Def.
Menin
gio
ma
Sdhs
CJD
Image interpretations pearls
A) Every brain atrophy is not AD
B) If no brain atrophy patient unlikely to have AD
C) For AD diagnosis atrophy is necessary
D) FDG PET has prognostic value
AD
Multi-infarct dementia
NPH
Pick disease
AIDS
Parkinson
Thank youThank you
Thank you
Thank you
Thank you
Thank you
Thank you
Thank you
Thank you
