DEMENTIA 9/29/16. Introduction. Introduction. Signs and Symptom. Epidemiology. Dementia. Dr. Yotin Chinvarun M.D. Ph.D.

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1 Introduction DEMENTIA Dr. Yotin Chinvarun M.D. Ph.D. Neurology, Pramongkutklao hospital In 1901 Auguste Deter, a woman in her early 50s, became 1 st person diagnosed with Alzheimer's disease, a form of dementia. The disease is named after the doctor who first described it, Alois Alzheimer The disease is characterized by Odd behavior Memory problems Paranoia Disorientation, agitation, and hallucinations Introduction Signs and Symptom Dementia refers to a group of symptoms caused by several different brain disorders Dementia is characterized by impaired intellectual functioning that interferes with daily activities or personal relationships. This impairment can include memory loss, language difficulty, decreased perception, and impaired reasoning Most common affected areas include memory, Visual-spatial Language Attention Executive function (problem solving) Most types of dementia are slow and progressive Additional psychological and behavioral problems include: Balance problems Tremor Speech and language difficulty Trouble eating or sw allow ing Memory distortions Wandering or restlessness Behavioral and psychological symptoms of dementia(bpsd) almost always occur in all types of dementia. BPSDs may manifest as Agitation, Depression, Anxiety, Abnormal motor behavior, Elated mood, Irritability, Apathy, Disinhibition and impulsivity, Delusions or hallucinations Changes in sleep or appetite Epidemiology Dementia In individuals who ultimately develop AD, presumes A gradual progression of the pathologic process which begins with normal aging and evolves to clinically probable AD and ultimately to neuropathologically proven AD Per 100,000 As longevity increases, diseases of aging become more prominent It is likely these individuals pass through a transitional stage between normal aging and clinically probable AD In 2000, approximately 4.5 million individuals with AD in United States and will be increase up to 14 million by 2050 The prevalence of AD also doubles every five years, a greater prevalence of AD in women than in men reflects the greater longevity of women 1

2 Mild cognitive impairment Mild cognitive impairment In recent years, mild cognitive impairment has been documented in individuals who typically have Memory impairment But are only mildly functionally impaired. These persons do not meet criteria for clinically probable AD yet are worthy of identification and monitoring In the first stages of dementia, signs and symptoms subtle The earliest stage of dementia called mild cognitive impairment (MCI) 70% of MCI progress to dementia at some point Person with MCI scores on the Mini-Mental State Examination (MMSE), which is a normal score They may have some memory trouble and trouble finding words But they solve everyday problems and handle own life affairs well Dementia The most common form of is Alzheimer s type (or AD), accounts 65% of dementias in late life Prevalence of AD increases with age, afflicting approximately 13% of age 65 years old and older and up to 50% of those over 85 years Dementia Dementia Other common forms of dementia e.g. Vascular dementia (VAD), estimated 15 20% of dementias in U.S.A and Europe; and up to 50% of dementias in Japan Dementia with Lewy bodies (DLB) 30% of dementias Frontotemporal dementia (FTD), particularly affects persons under 65 yrs, accounts 5% of dementias, although some estimates are higher Other common forms of dementia e.g. Less frequent dementia syndromes include Creutzfeldt-Jakob disease, HIV-associated dementia, neurosyphilis, Parkinson s dementia PDD, Normal pressure hydrocephalus, Dementias resulting from exposure to toxic substances (e.g., alcohol, heavy metals, illicit substances), metabolic abnormalities, and psychiatric disorders 2

3 Dementia Importance of making a specific diagnosis Clinical features and diagnostic criteria for Alzheimer's disease Frontotemporal dementia Diffuse Lewy Body disease Preclinical dementia syndromes, characterized by milder forms of memory loss and no functional impairment, are prevalent in general population Identification is important because early pharmacologic interventions in dementia may delay onset and slow progression of AD AD, DLB or FTD Does it Make a Difference? Drug treatment differs In FTD no evidence of a cholinergic deficiency In FTD behavior less likely to respond to usual drug treatments and appear to be more spontaneous rather than responsive to environment Understanding behavior can help caregivers In DLB hallucinations may respond to ChEls In FTD and DLB impaired initiative is easily confused with depression In FTD and DLB amyloid strategies are inappropriate Prognosis and genetics differ Alzheimer's Disease NINCDS/ADRDA Insidious onset of gradual progressive dementia, account 60% of all dementia Memory loss usually initial and most prominent symptom, eventually affects language, visuospatial ability and behavior No focal weakness or sensory loss Gait normal and continent until late illness Criteria for Diagnosis of Probable AD: a. Dementia established by clinical examination, and documented by a standard test of cognitive function,and confirmed by neuropsychological tests. b. Significant deficiencies in two or more areas of cognition, for example, word comprehension and task completion ability. c. Progressive deterioration of memory and other cognitive functions. d. No loss of consciousness. e. Onset from age 40 to 90, typically after 65. f. No other diseases or disorders that could account for the loss of memory and cognition. NINCDS-ADRDA criteria validated The Continuum of AD Sperling RA

4 Current approach to Clinical assessment of Early AD Current diagnosis is based on a multimensional clinical picture: cognition,, function, behavior, QoL Hx, caregiver reports, symptom pattern, duration PE, brief neurological exam Mental status tests Ideally need to accurately identification AD even earlier and monitor progression and Rx response Clinical evaluation of AD Currently AD is a clinical diagnosis based on Hx and neurological and cognitive exams Neuropsychological testing may help distinguish AD from age-related decline Depression (may be comorbid) Imaging may be helpful in ruling out other CNS causes of cognitive decline Tumor, stroke 4

5 Diagnosis: AD New criteria for early diagnosis of AD New criteria for early diagnosis Why early diagnosis is important MRI in AD AD Dx and DDX F18-FDG-PET Dopamine transporter imaging (DaT) Amyloid and Tau imaging 2 Set of criteria have evolved IWG/Dubois criteria National institute on Aging/Alzheimer s Association criteria These have many similarities New criteria Identify biology of AD before any symptom appear Identify a prodromal or MCI form of AD when symptoms are present, but criteria for dementia are not met New criteria for early diagnosis of AD Biomakers in new criteria identify pre-dementia forms of AD Neurodegeneration in MRI atrophy Reduced metabolism in FDG-PET Fibrillar amyloid deposition in amyloid PET AD CSF signature of high tau and low amyloid (AB42) 5

6 DDx of Dementia AD Mixed dementia (AD plus vascular dementia) Diffuse Lewy disease Fronto-temporal dementia Pure vascular dementia Other Parkinson-plus syndrome Reversible causes Metabolic, infectious, toxic, alcohol etc. Neuroimaging in AD: Previously Dx of exclusion CT: reveals changes characteristic of AD in later stages Diffuse cortical atrophy Enlarge cortical sulci Ventricle enlargement Drawbacks Ionizing radiation Atrophy may be present in healthy individuals Some patient have dementia, but no atrophy Normal variations in skull size Serial scans not clinically useful Specificity not well established Neuroimaging in AD: Volumetric MRI Rationale for Early diagnosis MRI Measures hippocampal atrophy and cortical thinning Tissue contrast Absence of ionizing radiation Drawbacks Expense Claustrophobia Presence of metal implants or devices Lack of standardized acquisition parameters or quantitative analytic protocols 10 Phase 3 trial failure at the stage of AD ove rthe past decade Intervention before dementia (stage of irreversible brain cell loss) may have better chance of changing clinical course of the disease Delaying dementia by 5 years, reduce projected medicare cost by nearly 50% Appropiate use of imaging modalities has clinical utility 6

7 Alzheimer disease Alzheimer disease Estimate the mean age of onset (typically in the 40s) 20 years before dementia onset, beta-amyloid levels in cerebrospinal fluid began to drop 15 years before dementia onset, beta-amyloid deposits can be detected by amyloid imaging scans, Tau levels begin rising in cerebrospinal fluid, Atrophy of the brain begins to become detectable by MRI 10 years before dementia onset, brain metabolic changes are present on FDG-PET and the first hints of episodic memory deficits begin 5 years before dementia onset, patients develop mild cognitive impairment. Importance of Early diagnosis Identify people at risk for progression to AD Begin therapy as early as indicated Life planning Relationship preservation Clinical trial participation Brain imaging can assist in Early Dx and DDX MRI atrophy FDG-PET in AD FDG-PET in DDx of AD and FTD I-123 PET in AD and DLB Amyloid PET Tau PET 7

8 Fluid biomakers and Genetics in AD diagnosis CSF Amyloid b-1-42 Total Tau; phosphorylated tau Combination/ratios Plasma measures are not yet useful Genetic APOE e4 Autosomal dominant mutation (rare) Beta-amyloid PET F18 agents Flobetapir Flutemetamol Flobetaben C-11 PIB compound 8

9 9

10 Diffuse Lewy Body Disease lnsidious onset of gradual progressive dementia Memory loss usually initial and most prominent symptom Hallucinations/misperceptions Often Gait and motor symptoms 'within 1 year of onset of dementia Attention and sleep abnormalities 10

11 Diffuse Lewy Body Disease Revised consensus criteria Unlike AD, most DLB patients more likely to be men, and the illness has a shorter course (<10 years) than AD Most cases of DLB occur > 65 yrs Characterized by frontal-subcortical cognitive deficit pattern (early and prominent impairment in attention and executive dysfunction, compared with less prominent and later memory impairment), fluctuating level of cognition and alertness, parkinsonism, and visual hallucinations DLB may be difficult to distinguish from Parkinson s disease, Parkinsonism in DLB differs from Parkinson s disease by being more often symmetric, with less pronounced tremor Hallucinations more prominent in Parkinson s disease than in DLB Central Features: Progressive cognitive decline that interferes with normal function. Prominent deficits on testing in one or more areas of attention, executive function, and visuo-spatial ability. Memory impairment which may occur later in the disease. Core Features: Pronounced variations in attention, alertness, and cognition. Visual hallucinations which are typically well-formed Parkinsonism Suggestive features REM sleep behavior disorder Severe neuroleplic sensitivity Low dopamine transporter uptake in basal ganglia demonstrated by SPECT or PET imaging Fronto-temporal Dementia (FTD) FTD: Three Clinical profiles lnsidious onset of progressive dementia Disturbing behavior and speech problems most prominent, less evident memory loss Perseveration, decreased verbal fluency Typical behavioral changes including apathy unrestrained and inappropriate social conduct Memory loss often not prominent; AD screening tests may be insensitive May be associated with motor neuron disease Frontotemporal dementia behavioral variant (FTDbv): Personality change, disordered social conduct. lnstrumental functions relatively well preserved. Progressive nonfluent aphasia (PA): Expressive language deficit is the dominant feature initially and throughout the illness. Otherwise cognition relatively well preserved. Semantic aphasia and associative agnosia dementia (Semantic dementia, SD): impaired understanding of word meaning and/or object identity. Diagnostic features of frontotemporal dementia behavioral variant Core diagnostic features of FTD lnsidious onset and gradual progression Early decline in social interpersonal conduct Early impairment of personal conduct Early emotional blunting Early loss of insight Supportive diagnostic features of FTD Behavioral disorder Speech and language Physical signs Diagnostic features of Progressive non-fluent aphasia Core diagnostic features of PA lnsidious onset and gradual progression Nonfluent spontaneous speech with: agrammatism, phonemic paraphasias, anomia Supportive diagnostic features of PA Speech and language. 1. Stuttering or oral apraxia 2. Impaired repetition 3. Alexia, agraphia 4. Early preservation of word meaning, 5. Late mutism Behavior. 1. Early preservation of social skills 2. Late behavioral changes similar to FTD Physical signs: late contralateral primitive reflexes, akinesia. rigidity. and tremor 11

12 Diagnostic features of Semantic aphasia and Associative agnosia Core diagnostic features of SD lnsidious onset and gradual progression Language Disorder and/or Perceptual disorder Preserved perceptual matching and drawing reproduction Preserved single-word repetition Preserved ability to read aloud and write to dictation orthographically regular words Supportive diagnostic features of semantic dementia Speech and language Behavior Physical signs FTD May Mimic AD Criteria are subjective and must be interpretated AD more prevalent than FTD, especially age >65 Behavior disturbance also common in AD AD is sometimes asymmetric causing prominent aphasia Most patients with FTD eventually develop a significant memory disturbance Most patients with FTD also meet NINCDS-ADRDA criteria for AD (Varmaet al. JNNP 1999;66: ) Clinicians depend upon relative severity of symptoms; none are pathognomonic NACC Accuracy study 88 (16.7%) of NACC person with clinical diagnosis AD did not met neuropath of AD Median report sensitivity for clinical diagnosis of AD 87%, but median specificity 58% Primary finding in 8 cases NeuropathoAD (below criteria) 17 Tangle predominance AD 15 Fronto-temporal dementia 15 Cerebrovascular disease 10 Lewybody disease 10 Hippocampal sclerosis (with or without AD) 9 N Preclinical dementia Two common preclinical syndromes include A. Age-associated memory impairment (AAMI) B. Mild cognitive impairment (MCI) A. Age-associated memory impairment (AAMI) Mildest form of age-related memory loss Occurs in persons > 50 years Characterized by self-reported memory complaints, decreased memory performances compared with younger adults (1 SD below young adults on memory tests), but normal memory compared with age peers. Prevalence 40% in people 65 years of age or older Approximately 1% develop dementia each year. Beach TG et.al., 2012 Preclinical dementia B. Mild cognitive impairment (MCI) Typically involves a more severe loss of memory that is still not associated with functional decline Reductions in memory or other cognitive domains compared with age peers Many persons with MCI show similar cerebral pathology to persons with AD Approximately 15% of persons with MCI develop dementia annually and most often AD. Obstacles to Accurate Diagnosis of Dementia Previous studies indicate that false-negative diagnoses occur 50 90% of cases, mistakenly attribute early cognitive decline to normal aging Evaluation and treatment may be delayed until disease severity and neuronal damage progressed Overreliance on and over interpretation of CT and MRI results Similarly, overreliance on typical cutoff scores on mental status or cognitive screening tests, or using such tests for sole purpose of diagnosis Highly educated individuals who suffered cognitive decline may show normal function on cognitive screening tests such as Mini Mental State Exam (MMSE) Whereas persons w ith low education may appear to have cognitive impairment or dementia when they actually have not declined 12

13 Why PET lmaging? Recognition of dementia is often delayed and diagnoses are often nonspecific Physicians lack diagnostic confidence Clinical MRI and CT don't provide information about biochemical and physiological changes that are characteristic of the most common dementing disorders Current clinical diagnostic criteria are imperfect e.g., patients with FTD often meets criteria for AD PET lmaging is Not A Panacea for Memory Evaluations lmaging (radiologists) will never be able to determine whether someone has dementia -symptoms determine that Imaging will adds another piece of information that has to be interpreted (clinical correlation recommended) and incorporated into decision-making Benefit should be to increase accuracy and diagnostic confidence in dementia and patient with memory impairment 1 8-F Flurodeoxyglucose Positron Emission Tomography (FDG-PET) FDG-PET provides unique information, complementary to structural imaging Short-lived positron-labeled form of sugar that follows the early steps of glucose, but gets trapped in the cell Fluorine -18: 120 min PET scanner uses physical properties of positrons to localize relevant radioactive emissions and discards others (improving resolution compared to SPECT) What Glucose Metabolism Measures Under normal conditions the brain uses glucose as its sole source of energy Glucose metabolism primarily reflects synaptic activity Hypometabolism may not correspond to areas with greatest changes in routine neuropathology Routine neuropathology is better at detecting loss of neuronal cell bodies than synapses It is not directly affected by intracellular or extracellular inclusions FDG-PET lnterpretation Usefulness of FDG-PET in dementia Evaluate the PATTERN of regional glucose hypometabolism, not just individual region, hot or cold spot, or global changes in metabolism Evaluate whether there are structural abnormalities that might affect metabolism Cases discussed tonight had no focal structural brain abnormalities on CT or MRI Consider the clinical context What is the clinical question? Medications, delirium, behavior during FDG uptake can all effect scan results Adding PET to a clinical dementia evaluation can enhance diagnostic sensitivity The sensitivity for detecting histopathologically confirmed AD using PET falls in the range of 91.5% ± 3.5%, compared with 66% ± 17% to identifying probable AD in clinical evaluations performed without PET In cases with possible or probably dementia, specificity without PET then falls to a range (55.5% ± 5.5%) that is substantially lower than that achieved when using PET (70% ± 3%). 13

14 Usefulness of FDG-PET in dementia Usefulness of FDG-PET in dementia Autopsy confirmed AD or FTD 31 AD patients 14 FTD patients Six dementia specialists decide on diagnosis with degree of confidence twice: After review of clinical history Then after FDG-PET 98% specificity for FTD in autopsy-confirmed cases In patients already diagnosed with dementia PET scan can clarify the diagnosis, which is relevant to appropriate treatment, for example Differentiating AD from FTD, because unlike AD, FTD does not respond well to acetylcholinesterase inhibitor treatment Also, might be useful to DDX from others type of dementia Lewis body dementia Cortical basal degeneration (CBD) Parkinson s disease dementia (PDD) Usefulness of FDG-PET in dementia Usefulness of FDG-PET in dementia A major clinical challenge is early identification of patients who will develop AD or other dementias, which is relevant to earlier treatment intervention and planning for a patient s future needs Several studies showed PET sensitive to AD-like hypometabolic brain changes in non-demented persons with the apolipoprotein epsilon 4 (APOE-4) genetic risk for AD PET predicts cognitive decline in persons with APOE-4, in normal elderly persons, in persons with mild memory complaints, in persons with questionable dementia. Some patients with a normal initial evaluation request a PET study because they are concerned about their personal risk for dementia, such as Prior head trauma Family history of dementia. A negative PET may reassure these worried well If, however, the scan results are consistent with a progressive neurodegenerative dementia, then patients can consider early treatment intervention strategies to slow progression of cognitive impairment, although considered an off-label use of medication Recent studies also support use of PET to predict Conversion of MCI to dementia for differentiating stable from progressive amnestic MCI, particularly in combination with memory test performance scores Case FDG-PET diagnosis F 65 yrs old Complained with poor short-term memory for 6 months Usually forgetful things, poor concentration Not disturbed normal function, able to work, have to take care husband who have stroke for a year PE: normal general and neurological examination MRI brain shows mild generalized cortical atrophy Have been treated with AChEI Alzheimer's disease Temporoparietal cortex hypometabolism > frontal cortex Posterior cingulate cortex hypometabolic Frontotemporaldementia Frontal cortex hypometabolism > temporoparietal cortex Anterior temporal and anterior cingulate cortex hypometabolic When several areas affected, are AD or FTD regions most hypometabolic 14

15 PET Tau Tracers PET Tau Tracers Tau p ro tei n s result from single microtubule-associated protein tau gene in humans, discovered in 1975 Healthy neurons contain microtubules, support structure and guide nutritional supplies Chemical changes (namely hyperphosphorylation) occur in tau protein in AD Causing disintegration of microtubules, collapse of neuron s transport system, formation of extremely insoluble aggregates, disrupt neuronal communication and lead to cell death Development of PET ligands for tau (detect neurofibrillary tangles) Seven tau pathology PET tracers have been developed and used in clinical studies: C-11 PBB3, F-18 THK-523, F-18 THK- 5105, F-18 THK-5117, F-18 T808, F-18 FDDNP, and F-18 T807 18F-AV-1451 selectively bound to Phosphorylated helical filaments (PHFs), and has very weak or no affinity to the β- amyloid accumulation Case M 69 yrs old Progressive memory loss for two years, poor short term memory, Language is normal but unable to speak full sentence, deterioration of self care, unable to dress himself and buttoning, Normal gait, impaired calculation, recall, clock drawing Unable to travel by himself, mood is stable PE general examination is normal, neurological examination revealed well dress man, oriented, poor recall 0/3, calculation impaired, naming preserved MRI brain shows moderate generalized cortical atrophy Case: AD M 87 yrs old Hx of progressive cognitive impairment for > 5 yrs Hx of HT, memory decline with poor short term memory, repetitive speaking and doing the same thing repetitively, poor recall, good mood, normal perception PE: oriented, language able to speck in a long sentence, usually repetitive word while having a conversation, also doing the repetitive task General examination was unremarkable Case Diagnosis: Alzheimer's dementia M 62 yrs old Frontotemporal dementia Progressive cognitive impairment for 6 months, rapidly decline in the last 4 months Behavioral change with aggressive behavior, usually spitting saliva all over, walking is normal, unable to naming, less talking and recently mute, poor sleep-wake cycle disturbance, hyperphagia, agitation, urgency incontinence Also, had several episodes of blank staring lasting for several minutes with confusion afterward, frequency 3-4 per month 15

16 Frontotemporal dementia Case PE: well dressed gentleman, agitated, response to verbal command, able to tell name, objects, echolalia General examination was normal Neurological examination CN: WNL, motor all gr V, cerebellar system was normal, normal gait Current med LVT, VPA, Exelon patch, Ebixa M 76 yrs old Hx of chronic insomnia and having a bad dream frequently, on Clonazepam and zopidem for a long time period, progressive memory decline with poor short term memory, poor concentration PH of HT and CAD, still driving a sport care, sometime driving up with high speed, sometime up to 200 km/hr, now able to drive everyday PE Sleepy, general and neurological examination was unremarkable Regidity +ve, instability Diagnosis possibly dementia with early Parkinson s disease REM Behavior Disorder Lewis body dementia Older males Injurious or disruptive behaviour during sleep Easily aroused; Dream recall prominent Two-thirds of patients develop Parkinsons mean latency of 13 years; associated with synucleinopathies (PD, Lewis body dementia, MSA) Polysomnography diagnostically helpful There are very few neuropathologically-confirmed imaging studies of LBD. More occipital atrophy in LBD than in AD has been reported by a group with a good diagnostic record In agreement is the finding of decreased metabolism in occipital association cortex Highly responsive to Clonazepam Case Non-amyloid dementias F 78 yrs Hx of progressive cognitive impairment with impairment of speech for a year, hallucination PE: aphasia, bed ridden, apraxia, regidity +ve CT brain mild to moderate generalized cortical atrophy 16

17 Case M 55 yrs Hx of pulmonary edema with pneumonia after cardiac arrest, ARDS, ATN with CRF and dialysis dependent, large umblilical hernia and epilepsy Case Dx: Dementia with probably cortical basal degeneration Patient has ataxic gait, parkinsonism features, mostly apathy, speechless Mild Cognitive Impairment Mild Cognitive Impairment Transitional state between healthy aging and dementia, during able to perform usual activities of daily living but suffer isolated memory difficulties exceeding those expected on the basis of normal aging, might be risk for developing future AD However, not all MCI patients develop AD MCI patients usually present on PET with mild global and regional hypometabolism FDG PET examinations revealed MCI patients show a pattern of brain hypometabolism that is topographically consistent with that observed in clinical AD As the clinical diagnosis per se is often uncertain, PET evaluations are increasingly used to support the clinical diagnosis early stages of AD. However, some studies did not observe the same distribution of cortical metabolic deficits in MCI, particularly in the case of very mildly affected subjects Mild Cognitive Impairment Mild Cognitive Impairment Mesial temporal lobe hypometabolism in MCI can be identified Studies that used quantitative measures have shown significant absolute reductions of glucose metabolic rates in MCI patients relative to controls. These reductions are milder than in AD and affect the MTL (7% 17%), lateral temporal (8%), and posterior cingulate cortices (23%). A growing body of longitudinal FDG PET studies has been carried out to examine the predictive value of cerebral metabolic measures in the decline from MCI to AD Demonstrating metabolic changes share the same topography of the characteristic AD PET pattern, i.e., reduced parietotemporal and posterior cingulate cortex metabolism, and are detectable several years before clinical diagnosis Metabolic reductions in the declining MCI patients are progressive, indicating PET measures are both predictors and correlates of decline to AD 17

18 Case M 77 yrs old, a retired top army officer Presenting with poor short term memory for a year, often forgetful things, found it very difficult to recall the name of the familial people case Patient was diagnosed as MCI with probably an early development of AD Playing golf every week and able to do normal daily activities, still travel aboard occasionally Language function is normal, recently reported by patient s wife as having labile mood, sometime agitated PE: normal general and neurological examination MRI brain shows mild general cortical atrophy 18

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