Diagnosing Dementia: Signs & symptoms, differential diagnosis of common dementias, and non-degenerative memory loss
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1 Diagnosing Dementia: Signs & symptoms, differential diagnosis of common dementias, and non-degenerative memory loss
2 Incidence of Common Neurological Diseases Incidence New Cases Disease (per 100,000) (per year) Dementia ,000 Alzheimer s disease ,000 Stroke ,000 Seizures ,000 Parkinson s disease 16 40,000 Primary neoplasm 15 37,500 Amyotrophic lateral sclerosis 6 15,000 Primary brain tumor 6 15,000 Multiple sclerosis 2 5,000 Gullain Barre 1 2,500 Huntington s disease
3 Diagnostic Classifications
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5 Mild Cognitive Impairment Cognitive Mild Cognitive Impairment MCI (memory) 10% - 15% conversion to AD per year 50% Conversion after 5 yrs >90% conversion by 10 years Criteria Memory difficulties corroborated by informant that interfere with adaptive functioning Selective deficit as measured by neuropsychological tests; other functions normal or near normal Intact IADLs Not demented Petersen 98 Neurology; Fisk 03 Neurology, Morris 01, Neurology
6 Diagnostic Criteria of MCI Clinical and cognitive criteria Cognitive concern reflecting a change in cognition reported by patient or informant or clinician (historical or observed evidence of decline) Objective evidence of impairment in one or more cognitive domains, typically including memory (formal or bedside testing) Preservation of independence in functional abilities Not demented Examine etiology of MCI consistent with AD pathophysiology Rule out vascular, traumatic, medical causes of cognitive decline Provide evidence of longitudinal decline in cognition Report history consistent with AD genetic factors Albert et al, Alzheimer s and Dementia 2011
7 Clinical Criteria for MCI of AD Type Subjective memory complaint reported by subject or informant Global cognition intact (MMSE >25) Memory impairment confirmed objectively ADL impairment is insufficient for diagnosis of dementia; IADL may be effected (GDS = 3 or CDR = 0.5) No medical / other etiology for memory deficit.
8 MCI: Definitions and Categories MCI Amnestic Forms Non Amnestic Forms Single Domain Multiple Domains Single Domain Multiple Domains
9 Albert 2011, Alzforum.org
10 Diagnosis of MCI Not established by consensus criteria Clinically apply Petersen criteria Neuropsychological assessment Apo E genotyping Screening eval (imaging, standard labs) low yield
11 Prediction of Conversion from MCI to AD MCI conversions to AD can be predicted by Worse memory scores Smaller hippocampi Low CSF Ab and high tau (ADNI reports that 33/37 subject converting to AD within one year had the CSF profile) ApoE4 positivity PIB uptake
12 Follow-Up of PIB-Positive ADNI MCI s N = 65, 12 mo. follow-up PiB(+)= 47 Converters to AD=14 PiB(-)=18 Converters to AD=3
13 PiB-Positivity in Predicting Clinical Conversion in MCI Melbourne Cohort N=28, 21 mo. follow-up PiB(-)=13 Converters to AD=1 PiB(+)=15 Converters to AD=12 Pittsburgh Cohort N=23, 24 mo. follow-up PiB(-)=10 Converters to AD =0 PiB(+)=13 Converters to AD =5
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16 Diagnostic Criteria of Dementia A. Dementia Interferes with ability to function at work or at usual activities A decline from a previous level of functioning Not delirium or psychiatric disorder Diagnosed by history, examination Involves at least 2 cognitive domains: Memory Reasoning and judgment Visuospatial Language Personality, behavior, comportment McKhann et al, Alzheimer s and Dementia 2011
17 Diagnostic Criteria of AD A. Probable AD [based on clinical criteria] Dementia Insidious onset Worsening of cognition over time Amnestic vs. non-amnestic presentation Not due to another dementia diagnosis B. Probable AD with evidence of AD pathophysiology Ab (CSF or amyloid PET) Neuronal injury (CSF tau, FDG-PET, structural MRI) McKhann et al, Alzheimer s and Dementia 2011
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19 2018 ATN Criteria
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21 Differential Diagnosis of Dementia Alzheimer s Disease (AD) Dementia with Lewy Bodies (DLB) AD & Vascular Dementia (mixed) Vascular Dementia Frontotemporal Dementia (FTD) Parkinson s Disease Huntington s Disease Other Degenerative Diseases (PSP, OPCA, ALS with dementia) Dementias Secondary to Alcohol Depression/Pseudodementia Normal Pressure Hydrocephalus (NPH) Structural Lesions Metabolic Disorders (Hypothyroidism) Infections (e.g. neurosyphillis, AIDS, CJD) Drug Intoxication
22 Dementia with Lewy Bodies Parkinsonism coexisting with cognitive decline Visual hallucinations Clinical fluctuations Neuroleptic sensitivity Newest criteria: REM behavioral disturbance Cognitive pattern may be subcortical or mixed cortical/subcortical with prominent visuospatial abnormalities Prone to other neuropsychiatric features May possibly progress faster Pathologically characterized by worse cholinergic loss, fewer plaques and tangles, neocortical Lewy bodies, lower Braak stages. Treatment could include cholinesterase inhibitors and L-dopa
23 Vascular Dementia May start abruptly immediately after a cerebrovascular accident Multi-focal distribution of cognitive decline Focal neurologic exam Gait disturbance, incontinence, and fluctuating changes are common (aka Binswanger s [290.12] Vascular changes on imaging obligatory NINDS-AIREN criteria applicable Most vascular dementia mixed with AD Hachinski Score 7 Treatment involves management of stroke risk factors and ChEIs
24 Frontotemporal Dementias Also known as Pick s disease Now many linked to Chromosome 17 ( the tau-opathies ) Usually earlier age of onset compared to AD (average years old) Early prominent language changes including anomia, aphasia, echolalia, and perseverative speech Social skills lost early Inappropriate behavior and judgement, disinhibition, and lack of insight Personality changes and withdrawal prominent
25 Progressive Aphasias Early prominent language changes including anomia, aphasia, echolalia, and perseverative speech Three subtypes now recognized (logopenic progressive aphasia-frontal variant, semantic dementia, progressive non fluent aphasia Progressive non fluent aphasia Involves effortful speech with agrammatism and frequent apraxia of speech Post-hoc comparisons with HC showed bilateral GM atrophy in the caudate, putamen and thalamus, in bvftd; a left-confined GM reduction in the amygdala in SD; and bilateral GM atrophy in the caudate and thalamus, and left-sided GM reduction in the putamen and amygdala in PNFA. Left insula and adjacent inferior frontal gyrus Pathologically associated with CBD or FTLD pathology with tau inclusions or PSP Semantic dementia Characterized by loss of word and object meaning and understanding Abnormalities in the left rostral temporal lobes Ubiquitin positive TDP proteinopathy pathology have both been associated with it Logopenic Progressive Aphasia speech rate was slow, with long word-finding pauses. Grammar and articulation were preserved, although phonological paraphasias could be present. Moderate anomia Repetition and comprehension were impaired for sentences but preserved for single words, and naming was moderately affected. Atrophy or decreased blood flow was consistently found in the posterior portion of the left superior and middle and posterior temporal gyri and inferior parietal lobule. Recent studies suggest that Alzheimer disease may be the most common pathology underlying the LPA clinical syndrome.
26 Degenerative Dementias AD DLB FTD Mixed Dementias Prion Diseases Parkinson s Disease Huntington s Disease Progressive Supranuclear Palsy Guamanian ALS-PD-AD
27 Dementias Possibly Amenable to Treatment Hypothyroidism Neurosyphillis/ Infectious Etiologies Normal Pressure Hydrocephalus Vascular Dementia Vitamin B12 Deficiency Structural Lesions Metabolic Disorders Drug Intoxication Depression/Pseudodementia Wilson s Disease Alcohol Related Dementias
28 Dementias Associated with Other Neurological Signs and Symptoms AIDS (neuropathy, myopathy) Normal Pressure Hydrocephalus (gait disturbance, incontinence) Tumors/Mass Lesions (stroke-like symptoms that are subacute and evolving) Subdural Hematoma (stroke-like symptoms that are acute or subacute and evolving)
29 Normal Pressuer Hydrocephalus
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32 Dementias Associated with Other Neurological Signs and Symptoms Huntington s Disease (chorea, depression, psychosis, parkinsonism) Creutzfeldt Jakob Disease (myoclonus, rapid dementia, EEG changes) Parkinson s Disease (rigidity, bradykinesia, gait disturbance, tremor) B12 Deficiency (Often associated with subacute combined degeneration: proprioceptive loss, parethesias, hyperreflexia)
33 Ten Warning Signs of AD Memory loss that affects job skills Difficulty performing familiar tasks Problems with language Disorientation to time and place Poor or decreased judgement Problems with abstract thinking Misplacing things Changes in mood or behavior Changes in personality Loss of initiative
34 Risk Factors for cognitive decline
35 Risk Factors for Cognitive Decline age genetic influences ApoE status female gender medical comorbidities
36 Risk Factors for Cognitive Decline: Medical Comorbidities Hypertension Heart disease Diabetes Elevated low-density lipoprotein cholesterol High homocysteine levels Transitory ischemic attacks (TIAs) Head trauma Environmental exposure to toxins (particularly lead)
37 Approach to diagnosis
38 Why is an accurate diagnosis important in AD? Accurate diagnosis reduces uncertainty and anxiety Accurate diagnosis allows increased confidence in distinguishing AD from other dementias Accurate diagnosis allows realistic prognostication Accurate diagnosis allows increase treatment precision Accurate diagnosis allows open discussion of expectations
39 Evaluation of Patients with Dementia Routine History Mental Status Exam Neurological Exam Chemistry Panel Complete Blood Count Vitamin B12 level Thyroid function studies CT/MRI Optional Syphilis serology Sedimentation Rate Chest X-Ray Electrocardiogram Urinalysis Drug Levels HIV testing Lyme Serology EEG PET/SPECT Apo E genotyping CSF (Ab42/tau or for CJD)
40 Case Vignette 72 y.o. female with 16 years of education presents with 2 years of progressive cognitive decline manifested by repeating questions and statements. She has disorientation to time and date, functional decline manifested by inability to complete household tasks and word finding difficulty. Neuro Exam is normal and MMSE is 25/30. Before ordering any tests, what is the diagnosis and how accurate are you?
41 Probable or Possible AD 70%
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44 New Concept: Diagnosis of AD RPR no longer required; now considered optional; appropriate if risk factors are present Structural imaging is now considered a standard Apo E genotyping is an option CSF studies is an option for detection of AD and CJD Functional imaging approved with caveats
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46 The Apolipoprotein E Genotype Advantages Highly predictive of AD; an E4 carrier that is symptomatic has a 94-97% of having AD pathology 50% of MCI subjects that are E4 homozygotes convert to AD in 3 years versus 20% of non-e4 carriers MCI subjects (amnestic subtype) that are E4 carriers convert to AD >99% of the time when they convert It is a simple blood test Can assist in assessing risk of offspring May predict effect of medication Disadvantages May or may not be covered by Medicare or secondary insurance $>350 cost non E4 carrier does not equal no AD. Apo E estimates risk and is not a sine qua non for AD.
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49 What about CSF testing for AD? CSF testing is desirable because it directly measures changes occurring in the CNS CSF testing can measure Ab, tau, p-tau AD subjects have reduced Ab42, increased tau and increased p-tau CSF testing for NTP has not been accurate or reliable and may reflect leakage from blood (FDA denied approval)
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51 CSF Testing for AD Advantages Allows precise measurement of AD specific changes Ab42 combined with tau has a sensitivity of 89% and a specificity of 90.2% compared to controls p-tau increases specificity to 85% from other dementias and 92% from controls New data from ADNI suggest that CSF predicts conversion from MCI to AD before symptoms fully manifes Disadvantages Requires LP Usually not covered by Medicare >$1000
52 Proportion free of very mild AD Proportion free of AD Abnormal CSF Tau/Aβ 42 and Prediction of Clinical Decline CSF amyloidβ level (pg/ml) Normal Consistent with AD pathology From normal to very mild AD CSF tau level (pg/ml) From MCI to AD 27% vs 1% annual conversion rate CSF tau/ab 42 < Time (years) Normal Pathological CSF CSF Time (months) Shaw LM et al. Ann Neurol. 2009;65: Fagan AM et al. Arch Neurol. 2007;64: Li G et al. Neurology. 2007;69: Hansson O et al. Lancet Neurol. 2006;5:
53 Structural Neuroimaging for AD Diagnosis Advantages MRI and CT have high sensitivity in detecting structural abnormalities and large pathological events (e.g. tumors, hydrocephalus, stroke) Cost is $ and is covered by insurance Disadvantages Clinical MRI and CT have low sensitivity to detect AD Clinical MRI and CT have very low specificity to distinguish one type of dementia from another New structural imaging technology requires serial imaging for accuracy
54 MRI: Hippocampal Atrophy in AD Normal AD
55 PET Scan for AD Advantages Sensitivity >90% even at fairly early stage Positive predictive value >90% Relatively non-invasive Disadvantages Costs between $ Significant radiation exposure Interpretation highly variable according to radiologist training Specificity 75% Requires Medicare prior authorization which is complicated and time consuming
56 FDG-PET in Normal Aging, MCI, AD, and FTD NL MCI pad ftd NL = normal; pad = probable Alzheimer s disease; ftd = frontotemporal dementia. Reiman EM et al. N Engl J Med. 1996;334: Reiman EM et al. Proc Natl Acad Sci U S A. 2001;98: Reiman EM et al. Proc Natl Acad Sci U S A. 2004;101: Reiman EM et al. Proc Natl Acad Sci U S A. 2005;102:
57 F18 Amyloid Imaging Tracers Flutemetamol 1 Florbetapir 2 AD Interpreting amyloid PET scans Negative Positive NL A A Florbetaben 3 Navidea NAV C D C D AD B B NL 1. Vandenberghe R et al. Ann Neurol. 2010;68: Wong DF et al. J Nucl Med. 2010;51: Barthel H et al. Lancet Neurol. 2011;10: Chen K et al. Alzheimers Dement. 2012;8(4 suppl):p14(abstract IC-P-011).
58 Specific binding (fmol/mg) Bound/Fr ee Amyloid imaging with florbetapir F 18 5,00 0 4,00 0 3,00 0 2,00 0 1, Kd = 3.51 nm Bmax = 7,215 fmol/mg) ,0002,0003,0004,0005,0006,0007,000 Florbetapir (pm) Florbetapir F 18 2,50 5,000 7,500 0Bound Clark CM 1,2, Schneider JA 3, Bedell BJ 4,5, Beach TG 6, Mintun MA 1,7, Pontecorvo MJ 1, Hefti F 1, Carpenter A 1, Flitter M 1, Krautkramer M 1, Kung HF 2, Coleman RE 8, Fleischer A 9,10, Sabbagh M, Sadowsky C, Doraiswamy PM 8, Reiman EM 9, Skovronsky DM 1, and the AV45-A07 study group. Validation of Florbetapir-PET for Imaging Alzheimer s Disease Amyloid Pathology. JAMA 2011; 305(3): A. B. C. D. E. F.
59 Amyloid positivity (%) Amyloid Positivity, by Cognition and Age Prevalence estimates of amyloid positivity according to cognitive status and age Normal cognition (n = 2914) SCI (n = 697) MCI (n = 3971) Age (years) SCI = subjective cognitive impairment The prevalence estimates were generated from generalized estimating equations. Shading indicates 95% CI. Jansen WJ et al. JAMA. 2015;313:
60 Conclusions The identification of MCI can be made with more confidence The prediction of conversion from MCI to AD can be made with greater accuracy AD is no longer a diagnosis of exclusion Technology is becoming available that greatly improves the diagnostic accuracy of AD
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