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Imaging in Dementia: Options for Clinical Practice PowerPoint Presentation

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Description : Check out this medical presentation on amyloidosis, which is titled "Imaging in Dementia: Options for Clinical Practice", to know about early imaging in dementia, indications for imaging in dementia, imaging techniques (MRI and PET), imaging of Alzheimer’s disease, and future directions.

Tags : amyloidosis, Imaging, Dementia, imaging techniques, MRI, PET, Alzheimer’s disease

Published on : May 06, 2021 | Views : 1103 | Downloads : 1

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Slide 1-

Imaging in Dementia:Options for Clinical Practice John A. Bertelson, MD Clinical Chief of Neurology, Seton Brain and Spine Institute Assistant Professor of Medicine, Dell Medical School, UT Austin Clinical Assistant Professor of Psychology, UT Austin
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Disclosures None
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Outline Early Imaging Indications for Imaging in Dementia Imaging Techniques MRI PET Imaging of Alzheimer’s Disease Future Directions
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Early Imaging Modality What am I? Initially described in 1918 1 Low resolution High morbidity, including: Meningeal irritation, 6 hrs: Headache Nausea Emesis Elevation in BP Became obsolete in 1971 1: AJNR 2012
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Early Dementia Imaging What am I? Initially described in 1918 1 Low resolution High morbidity, including: Meningeal irritation, 6 hrs: Headache Nausea Emesis Elevation in BP Became obsolete in 1971 1: AJNR 2012 2: http://www.isradiology.org/tropical_deseases/tmcr/chapter45/imaging.htm 2
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Early Dementia Imaging What am I? Initially described in 1918 1 Low resolution High morbidity, including: Meningeal irritation, 6 hrs: Headache Nausea Emesis Elevation in BP Became obsolete in 1971 Pneumoencephalography 1: AJNR 2012 2: http://www.isradiology.org/tropical_deseases/tmcr/chapter45/imaging.htm 2
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Pneumoencephalogram: “dementia paralytica” Hydrocephalus “ex vacuo” pattern with diffuse widening of the cortical sulci Ciudad Sanitaria Provincial, Madrid Spain JNNP 1979
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Modern Imaging
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Traditional Role for Neuroimaging in Dementia Indication: Rule out reversible process Quality Standards Subcommittee of the AAN, 1994: “Neuroimaging should be considered in every patient with dementia” “… potentially treatable disorders that can otherwise be missed, such as tumors, subdural hematomas, hydrocephalus, and strokes.” “… there is no consensus on the need for such studies in the evaluation of patients with the insidious onset of dementia after age 60 without focal signs or symptoms, seizures, or gait disturbances.” Alter M, 1994
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Evolution of Indications for Neuroimaging in Dementia From: Bertelson and Ajtai, 2014 Key: AAN: American Academy of Neurology CCD: Canadian Consensus Conference on Dementia EFNS: European Federation of Neurological Subspecialties
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Reversible Causes of DementiaCopenhagen Memory Clinic Potentially reversible etiologies for cognitive symptoms In 1000 memory clinic patients Hejl A 2002 4-5%
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Neuroimaging in Dementia
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Imaging Modalities Magnetic Resonance Imaging Positron Emission Tomography
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Magnetic Resonance Imaging (MRI)
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Minimum MRI Sequences for Dementia Evaluation Multiplanar Imaging Axial, coronal, sagittal Multiple Modalities T1W, T2W, FLAIR, DWI Screening for Abnormal Blood Products GRE or SWI Contrast-Enhanced (select situations)
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Other MR Modalities Volumetric MRI CSF flow studies MR spectroscopy fMRI Diffusion tensor (DTI) MR perfusion
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Other MR Modalities Volumetric MRI CSF flow studies MR spectroscopy fMRI Diffusion tensor (DTI) MR perfusion Semi-routinely utilized for clinical assessment of dementia
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Rapidly progressive dementia “Hockey stick” sign DWI hyperintensity in the bilateral medial thalami and pulvinar Variant Creutzfeldt-Jakob Disease (vCJD) From: Bertelson and Ajtai, 2014
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Positron Emission Tomography (PET)
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FDG PET Medicare CoverageDementia and Neurodegenerative Diseases Effective 9/15/2004, “An FDG PET scan is considered reasonable and necessary in patients with: a recent diagnosis of dementia, documented cognitive decline of at least 6 months, meet diagnostic criteria for both AD and FTD.” http://www.cms.gov/Regulations-and-Guidance/Guidance/Manuals/downloads/ncd103c1_Part4.pdf
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FDG PET Medicare CoverageDementia and Neurodegenerative Diseases Additional prerequisites include: Comprehensive evaluation already completed, including brain CT or MRI Evaluation by “a physician experienced in the diagnosis and assessment of dementia” Evaluation is indeterminate and FDG PET is reasonably expected to clarify the diagnosis between FTD and AD SPECT or PET have not already been obtained in the past 12 months AND significant clinical changes have occurred
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FDG PET AD FTD PPA
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From: Bertelson and Ajtai, 2014 Parkinson-plus syndrome Atrophic midbrain Normal midbrain Reduced AP midbrain diameter
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From: Bertelson and Ajtai, 2014 Parkinson-plus syndrome Atrophic midbrain Normal midbrain Reduced AP midbrain diameter Progressive Supranuclear Palsy
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Alzheimer’s Disease (AD)
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Alzheimer’s Disease The most common cause of dementia Affects over 5 million Americans 6th leading cause of death for people in the US Affects 1 in 9 age 65 and older, 1 in 3 over age 85 About 10% of people have early onset which affects people under age 65
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Histopathologic Hallmarks of AD Major histopathologic hallmarks include Amyloid- plaques Neurofibrillary tangles Neuronal and synaptic loss AP = amyloid plaques.NFT = neurofibrillary tangles. Courtesy of Albert Enz, PhD, Novartis Pharmaceuticals Corporation. AP NFT
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Model of the Dynamic Biomarkers of Alzheimer’s Disease Sperling RA, 2011
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NIA-AA Diagnostic Criteria for Dementia due to Alzheimer’s Disease Probable AD dementia Possible AD dementia Pathophysiologically proved AD dementia Dementia unlikely to be due to AD McKhann GM, 2011
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NIA-AA Diagnostic Criteria for Dementia due to Alzheimer’s Disease Probable AD dementia w/ evidence of the AD pathophysiological process Possible AD dementia w/ evidence of the AD pathophysiological process Pathophysiologically proved AD dementia Dementia unlikely to be due to AD “To improve the certainty that the basis of the clinical dementia syndrome is the AD pathophysiological process” McKhann GM, 2011
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AD Biomarkers NIA-AA Criteria (2011) Brain Aß amyloidosis PIB/florbetapir-PET ↓ CSF Aß-42 Neuronal injury FDG-PET ↑ CSF-tau MRI atrophy Medial temporal lobes Paralimbic Temporoparietal cortex
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Imaging Findings in AD MRI Early: “Normal” or medial temporal atrophy Late: Generalized atrophy FDG PET Early: Hypometabolism in the temporal/parietal regions Late: Generalized hypometabolism (with sparing of primary sensorimotor cortex) Amyloid PET All stages: Generalized cortical amyloid deposition Amyloid binding may also occur with normal aging
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MRI and AD
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MRI and AD: Atrophy Coronal MRI can demonstrate progressive medial temporal and generalized atrophy in patients with AD
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Automated volumetric MRI analysis Hippocampal Volume Eval. NeuroQuant®, CorTechs Labs Commercially available Reported: Volumes of hippocampi (HV) and inferior lateral ventricle (ILV) Volumes as % of intracranial volume Normative %, based on age and gender
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Volumetric MRI Analysis- NeuroQuant® http://www.cortechs.net/products/neuroquant.php
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Volumetric MRI Analysis- NeuroQuant® http://www.cortechs.net/products/neuroquant.php
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Progressive Cognitive Decline T=0 years T=3 years T=8 years
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Progressive Cognitive Decline T=0 years T=3 years T=8 years P R I M A R Y P R O G R E S S I V E A P H A S I A
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“PET” and Dementia FDG PET Amyloid PET
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FDG PET in AD Profoundly diminished [18F]FDG uptake in the temporoparietal and parietal regions bilaterally (arrows), seen on (A) axial and (B) parasagittal images From: Bertelson and Ajtai, 2014
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Pittsburgh Compound-B (PIB) Radiolabeled thioflavin derivative [N-methyl-(11)C]2-(4’-methylaminophenyl)-6-hydroxybenzothiazole Selectively binds to amyloid plaque and cerebrovascular amyloid Significant retention seen in: 90+% AD patients 60% patients with MCI 30% “normal” elderly Very short half life: 20 minutes Amyloid Imaging:Pittsburgh Compound-B PET Mathis J Med Chem 2003;46(13) Applied Neurology, Nov. 2005 (suppl) Mosconi J Alzheimer’s Dis 2010 T1W-MRI PIB- PET Control AD
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Commercially Available Amyloid-binding Radionucleotides Florbetapir (Amyvid) 1 Marketed in US by Eli Lilly Approved by FDA, not covered by CMS for routine use 2 Half life 110 minutes Additional FDA-approved radionucleotides 3 Florbetaben (Neuraceq, Piramal Imaging) Flutemetamol (Vizamyl, GE Healthcare) 1: Florbetapir, package insert 2: CMS Memo (CAG-00431N) 3: Alzforum, downloaded 8.5.14
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But… Aẞ burden as assessed by positron emission tomography(PET) does not strongly correlate with cognitive impairment in AD patients
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Tau Imaging Human postmortem studies have shown that it is the density of NFTs and not of Aẞ insoluble plaques that strongly correlates with neurodegeneration and cognitive deficits. Villemagne 2014
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Tau Imaging Phosphoprotein 6 isoforms Stabilizes microtubules Cytoskeletal support Intracellular transport (organelles, neurotransmitters, etc) Associated with AD, PSP, CBGD, CTE, and several variants of FTD.
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Neurofibrillary Tangles . AD and the Brain NIA/ADEAR
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Progression of tau deposition in AD Braack and Braak (I-VI), and Delacourte staging (S1-10) Villemagne 2015
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Tau Tracers Villemagne 2014
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AD hemibrain sectionsTau and Amyloid imagingTau Immunohistochemistry Villemagne 2014
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MRI and tau/aẞ PET Villemagne 2015
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Other Degenerative Dementias Frontotemporal dementia (FTD) Vascular dementia (VAD) Chronic traumatic encephalopathy (CTE) Lewy Body dementia (LBD) Parkinson’s disease dementia (PDD) Etc
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What’s next?? Wider utilization of biomarkers to: Clarify the diagnosis Monitor response to disease modifying agents Greater implementation of multimodal imaging Limitations Cost Access to advanced imaging Inadequacy of response to disease modifying agents
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Clinical, genetic, and pathological spectrum of misfolded proteins in neurodegenerative disease Villemagne 2015
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Multimodal Imaging- tau and Aẞ Tau -/Aẞ - Tau +/Aẞ + Tau -/Aẞ + Tau +/Aẞ - Normal aging, depression, meds Alzheimer’s disease, AD/LBD Premorbid AD, normal aging CTE, FTD, MSA > AD
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What should I do today??? I want to work up a patient with cognitive symptoms. What imaging modality should I order? “I'm sorry, my responses are limited. You must ask the right question.” Hologram of Dr. Lanning (James Cromwell) to Det. Spooner (Will Smith): From: I, Robot Film released by 20th Century Fox in 2004 Based on a series of short stories by Isaac Asimov
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I want to work up a patient with cognitive symptoms. What imaging modality should I order? What is the clinical suspicion(s)? What is the local access to advanced imaging techniques? Do patient comorbidities suggest a wider DDx? Are there any patient-specific limitations to imaging (foreign body, tolerance of prolonged scan times, body habitus, etc)?
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“That, detective, is the right question” Dr. Lanning to Det. Spooner From: I, Robot Thank You
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References Villemagne, VL et al. Tau imaging: early progress and future directions. Lancet Neurology 14 :1(2015) 114-24. Villemagne VL and Okamura N. In vivo tau imaging: Obstacles and progress. Alzheimer’s and Dementia 10(2014) S254-64.
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References Alter, M et al (Quality Standards Subcommittee of the AAN). Practice parameter for diagnosis and evaluation of dementia. Neurology 1994; 44:2203-6. Knopman DS et al. Practice Parameter: diagnosis of dementia (an evidence-based review). Neurology 2001; 56:1143-53. Kalkonde YV et al. Difference between clinical subspecialties in the outpatient evaluation and treatment of dementia in an academic medical center. Dement Geriatr Cogn Disord 2010; 29:38-36. Hejl A et al. Potentially reversible conditions in 1000 consecutive memory clinic patients. J Neuro Neurosurg Psychiatry 2002; 73(4): 390-4. Jack CR Jr, Albert M, Knopman D, McKhann G, Sperling R, Carrillo M, et al. Introduction to the revised criteria for the diagnosis of Alzheimer’s disease: National Institute on Aging and the Alzheimer’s Association workgroup. Alzheimers Dement 2011;7:257-62. McKhann GM, Knopman DS, Chertkow H, Hyman BT, Jack CR Jr, Kawas CH, et al. The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging and the Alzheimer’s Association workgroup. Alzheimers Dement 2011;7:263-69. Sperling RA, Aisen PS, Beckett LA, Bennett DA, Craft S, Fagan AM, et al. Towards deﬁning the preclinical stages of Alzheimer’s disease: recommendations from the National Institute on Aging and the Alzheimer’s Association workgroup. Alzheimers Dement 2011;7:280-92. Albert M, DeKosky ST, Dickson D, Dubois B, Feldman H, Fox NC, et al. The diagnosis of mild cognitive impairment due to Alzheimer’s disease: report of the National Institute on Aging and the Alzheimer’s Association workgroup. Alzheimers Dement 2011;7:270-9.
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References Borghesani PR et al. Neuroimaging in the clinical diagnosis of dementia: observations from a memory disorders clinic. Journal of the American Geriatrics Society 2010; 58(8): 1453-8. Heister D et al. Predicting MCI outcome with clinically available MRI and CSF biomarkers. Neurology 2011; 77:1619-28. Dickerson BC et al. Alzheimer-signature MRI biomarker predicts AD dementia in cognitively normal adults. Neurology 2011; 76: 1395-402. Dickerson BC et al. MRI cortical thickness biomarker predicts AD-like CSF and cognitive decline in normal adults. Neurology 2012; 78: 84-90. Petersen RC. New clinical criteria for the Alzheimer’s Disease Spectrum. Minnesota Medicine 2012. Price DL et al. “Investigation of acoustic noise on 15 MRI scanners from 0.2T to 3T.” J Magn Reson Imaging 2001; 13(2):288-93.
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References Rabinovici GD, Rosen HJ, etal. Amyloid vs. FDG-PET in the differential diagnosis of AD and FTLD. Neurology 2011; 77:2034-42. Suárez J et al. Characterizing radiology reports in patients with frontotemporal dementia. Neurology 2009; 73(13): 1073-4. Kerholz K et al. “Positron emission tomography imaging in dementia.” British Journal of Radiology 2007; 80:S160-7. Mosconi L et al. “Pre-clinical detection of Alzheimer’s disease using FDG-PET with or without amyloid imaging.” J Alzheimers Dis. 2010; 20(3): 843-54. Laino C Two radioactive tracers detect amyloid, may aid in AD diagnosis. Neurology Today 2012; 12(10): 16-7. Li TQ and Wahlund LO. The search for neuroimaging biomarkers of Alzheimer's disease with advanced MRI techniques. Acta Radiologica. 2011; Vol. 52 (2): 211-22. Gorno-Tempini ML et al. “Classification of primary progressive aphasia and its variants.” Neurology 2011; 76:1006-14. Snowden JS et al. Distinct behavioural profiles in frontotemporal dementia and semantic dementia. J Neurol Neurosurg Psychiatry 2001; 70: 323-32.