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7/21/2019 Dementia Uwks(Rev) 1/86 DEMENTIA: Alzheimer’s Disease and Vascular Dementia Christian Kamallan Neurologist

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  • DEMENTIA: Alzheimers Disease and Vascular DementiaChristian KamallanNeurologist

  • SKDI

  • I am living with dementia, not dying with dementia.


  • Hippocampus: where short-term memories are converted to long-term memoriesThalamus: receives sensory and limbic information and sends to cerebral cortexHypothalamus: monitors certain activities and controls bodys internal clockLimbic system: controls emotions and instinctive behavior (includes the hippocampus and parts of the cortex)Inside the Human Brain

    Other Crucial PartsSlide 12

  • The Brain in Action Hearing Words Speaking Words Seeing Words Thinking about WordsDifferent mental activities take place in different parts of the brain. Positron emission tomography (PET) scans can measure this activity. Chemicals tagged with a tracer light up activated regions shown in red and yellow. Inside the Human BrainSlide 13

  • NeuronsThe brain has billions of neurons, each with an axon and many dendrites.To stay healthy, neurons must communicate with each other, carry out metabolism, and repair themselves.AD disrupts all three of these essential jobs.Inside the Human BrainSlide 14

  • Plaques and Tangles: The Hallmarks of ADThe brains of people with AD have an abundance of two abnormal structures:An actual AD plaqueAn actual AD tanglebeta-amyloid plaques, which are dense deposits of protein and cellular material that accumulate outside and around nerve cellsneurofibrillary tangles, which are twisted fibers that build up inside the nerve cellAD and the BrainSlide 16

  • Cognitive Continuum

  • Man fools himself. He prays for a long life, yet he fears an old age. Chinese Proverb

  • Dementia cases double every 20 years

  • FunctionAge

  • Mild cognitiveimpairmentAmnesticMild cognitiveimpairmentMultiple domainsslightly impairedMild cognitiveimpairmentSingle non-memory domain

  • Mild Cognitive Impairment(MCI)Criteria:Memory complaintNormal general cognitive functionNormal activities of daily livingMemory impaired for ageNot dementedVIDEO

  • Definition DementiaA decline of intellectual function in comparison with patients previous level of function. Severe enough to cause impairment of social and professional activities Reflected on decline on ADL and IADL Usually associates with behavior changes.

  • Area involves in dementia

  • 1) To be earlier: potential benefitsObtain appropriate treatment earlierHelp the family to understand and acceptFinancial and legal plans while competentEnable the patient and family to make lifestyle choicesInduce better adherence and management of other medical conditionsTake appropriate steps to prevent injury (driving, weapons)Get greater access to help within the healthcare system and within communities

    from Cummings, 2011


    Type of dementia can be defined enough certainty through: Clinical patterns of dementing illness Doing appropriate dementia work-up

  • Steps in Dementia Work-up History taking (Collateral source & patient) Physical examination Mental status examination Relevant laboratory and follow up

  • Collateral Source Usually the spouse or an adult child. ...Observations by the collateral source correlate better with dementia than self-reported complaints which correlate more with depression. Absence of collateral source seriously compromises dementia diagnosis

  • History Taking Consists of Neurobehavioral history General medical history General neurological history Psychiatric history Toxic, nutritional /drug history Familial history

    dementia or not? Possible underlying etiology or other condition associates with dementia

  • Neurobehavioral History Taking Ask the collateral source

    Specifically ask about changes : (ABC)Cognitive function: memory problems, orientation, language, executive function, personality/apathy Change of behavior Degree of interference with ADL and IADL Enquire about:first symptoms time of onset nature of illness

  • Impairment in Memory Symptoms: Repetitive questions or conversations, Misplacing personal belongings, Forgetting events or appointments, Getting lost on a familiar route

  • Impairment in Language Involve speaking, reading, writing Difficulty thinking of common words while speaking, hesitations; speech, spelling and writing errors

  • Impairment Visual spatial & abilities Symptoms: Inability to recognize faces or common objects or to find objects in direct view despite good acuity Inability to operate simple implements or orient clothing to the body.

  • Dysexecutive function Impaired reasoning and handling of complex tasks, poor judgment symptoms poor understanding of safety risks inability to manage finances poor decision-making ability inability to plan complex or sequential activities

  • Changes in personality / character Impaired motivation, initiative Symptoms: increasing apathy & loss of drive social withdrawal decreased interest in previous activities

  • Behavioral and psychological symptoms of dementia (BPSD) Behavioural (observation) Physical aggression, screaming, restlessness, agitation, wandering, culturally inappropriate or sexual abberants behaviours

    Psychosocial (interview) Disinhibition, hoarding, cursing and shadowing Anxiety, depression, hallucination and delusions.

  • Physical Examination General physical examination Neurological Examination:Increased ICP Focal Neurological deficit: Gait, motor & sensory deficit Abnormal muscle tone & movement and primitive reflexes

  • Cognitive Screening Test Considering of practicality A brief screening test for cognitive impairment that can be performed in 10 minutes or less is easier incorporated into daily practice than a comprehensive but time consuming

  • Brief & Objective Screening TestsPatient examination

    Clock Drawing Test (CDT)..............................5 Short Blessed Test (SBT)................................5-10Abbreviated Mental Test .. 5-10 Mini Mental State Examination (MMSE).......10-15 Montreal Cognitive Assessment (MoCA)...... 20-25

  • Psychometric TestingAre not by themselves diagnostic. Help in diagnosis by providing qualitative assessment of mental function and the pattern of involvement. Help in longitudinal assessment of deterioration or improvement with treatment

  • Laboratory Diagnostic Work-up Basic: CBC FBS, liver and renal function tests Thyroid stimulating hormone (TSH) Serum B12

    Ancillary: EEG CSF analysis Serology for syphilis HIV testing Heavy metal screen

  • NEUROIMAGINGStructural MRIHippocampusEntorhinal cortex

    Functional ImagingMRSfMRIPET/SPECT

  • Diagnosis of AD DSM-IV; APA, 1994:Gradual onset & progressive decline in: Memory + at least one of the: 3 A (Aphasia, Apraxia, Agnosia ) Dysexecutive functioning Impairment in social and professional activities, cant be explained by any other neurological, psychiatric, systemic or substance-induced or only occur in delirium.

  • Triggers of Non-AD Diagnosis Onset < 60 y.o; sudden onset, cognition fluctuation, rapid progression Neurologic abnormalities early in course e.g. involuntary movement, focal deficits, gait disturbance, ataxia, seizures BPSD early in course: visual hallucination, disinhibition, marked apathy, social conduct Neuropsychological profile early in course: prominent aphasia, marked deficit in attention, executive function, visual agnosia

  • Common Differential Diagnosis DLB (Dementia Lewy Body)PDD (Parkinson Disease Dementia)FTLD (Fronto-Temporal Lobe Dementia)VaD (Vascular Dementia) Others

  • DLB Clinical Diagnosis(Revised criteria III 2005)Dementia with prominent deficits in attention, executive function, and visuospatial ability.Core features (two core features: probable DLB; one for possible DLB):Fluctuating cognition with pronounced variations in attention and alertness Recurrent of well formed and detailed visual hallucinations Spontaneous features of parkinsonism

  • Clinical Diagnosis(Revised criteria III 2005)Suggestive features REM sleep behavior disorder Severe neuroleptic sensitivity Low dopamine transporter uptake in basal ganglia demonstrated by SPECT or PET imaging

    Probable DLB: 1 or more core features +1 or more suggestive features Possible : if 1 or more suggestive features

  • Fronto-temporal dementia Core diagnostic features A. Insidious onset and gradual progression B. Early decline in social interpersonal conduct C. Early impairment in regulation of personal conduct D. Early emotional blunting E. Early loss of insight

  • Fronto-temporal dementia Supportive diagnostic features A. Behavioral disorder 1. Decline in personal hygiene and grooming 2. Mental rigidity and inflexibility 3. Distractibility and impersistence 4. Hyperorality and dietary changes 5. Perseverative and stereotyped behavior 6. Utilization behavior

  • Fronto-temporal dementia B. Speech and language 1. Altered speech output a. A spontaneity and economy of speech b. Press of speech

    2. Stereotypy of speech 3. Echolalia 4. Perseveration 5. Mutism

  • C. Physical signs 1. Primitive reflexes 2. Incontinence 3. Akinesia, rigidity, and tremor 4. Low and labile blood pressure

    Fronto-temporal dementia

  • Dementia with: Behavioral disturbances & affective symptoms Speech disorders Physical signs of primitive reflexes Incontinence Akinesia and rigidity

    Fronto-temporal dementia

  • Vascular dementia Dementia with: Evident of cerebrovascular disease A clear temporal relationship between dementia and cerebrovascular disease

  • VaDHachinski Ischaemic ScoreA brief clinical tool helpful in the bedside differentiation of the commonest dementia types, Dementia of Alzheimers Type (AD) and Vascular Dementia (VaD)A cut-off score 4 for AD and 7 for VaD has a sensitivity of 89% and a specificity of 89% (Moroney 1997)*

  • *Hachinski Ischaemic Score

    Item No.DescriptionValue1Abrupt onset22Stepwise deterioration13Fluctuating course24Nocturnal confusion15Preservation of personality16Depression 17Somatic complaints18Emotional incontinence19History of hypertension110History of stroke211Associated atherosclerosis112Focal neurological symptoms213Focal neurological signs2

  • AD Vs VaDA good teacher is a perpetual learner

    AD VaDNeuro transmitter defect Hemodynamic defectFemale predominance Male predominanceGradual onset Abrupt onset Steady deterioration Stepwise deterioration, fluctuating course BP normal Hypertension No history of stroke History of stroke Global decline in cognitive function Focal neurological symptoms and signs Unlikely to respond to treatment May respond to a drug which modifies microcirculation and enhance cerebral tissue perfusion

  • Potentially Reversible Dementia 1. Hypothyroidism 2. Pernicious anemia 3. Chronic Subdural Hematoma 4. CNS infections: TB, Cryptococcal, viral, HIV, syphilis 5. Tumors 6. Normal pressure hydrocephalus 7. Drug intoxication 8. Heavy metal poisoning

  • Features suggesting reversibilityShorter duration of illnessSubcortical type of dementiaModerately severe disturbanceYounger age of onsetProminent gait disturbanceUrinary dysfunctionFocal neurological signs

  • Akin To Dementia DeliriumAcute onset Fluctuating courseAutonomic disturbances Precipitating factors like infection, metabolic and drugs

  • MMSE Screening test to provide brief, objective measure of cognitive functionAdministered in 10-15 minutes, scores range from 0 to 30

    Useful in quantitatively estimating the severity of cognitive impairment

    Useful in serially documenting cognitive change in serial

  • Different cognitive domains tested In seven categories: Orientation to time 5 points Orientation to place 5 points Registration of three words 3 points Attention and calculation 5 points Recall of three words 3 points Language 8 points Visual construction 1 point

    Total 30 points

  • MMSE Cut-off Score

    24-30 no cognitive impairment 18-23 mild cognitive impairment 0-17 severe cognitive impairment

  • MMSE Good points of the MMSE Most widely accepted screening test Good internal consistency Good test-retest reliability High validity: good sensitivity and good specificity Correlates well with other screening tests e.g. clock drawing test and Short Blessed test

  • MMSE Limitation

    Confounded by age, education and culture

  • Clock Drawing Test (CDT) A sensitive measure of: Visuo-spatial function and constructional praxis. Higher ordered cognitive abilities like the concept of time Can help differentiate between a constructional vs. conceptual problem

  • 4-Point Scoring Method (Nolan KA, Mohs RC, 1994)

    Draws closed circle 1 point Places numbers in correct positions 1 point Includes all 12 correct numbers 1 point Places hands in correct position 1 point

  • CDT: ExamplesPatients were instructed to draw in the hands at twenty minutes after eight

    Figure A: by a normal elderly control Figure B-E: patients with dementia

  • Interpretation: Clinical judgmentA low score ( 3) indicates the need for further evaluation to source out other evidences of impairment or correlation with other tests

  • The role of medications in the management of dementia1.Cure disease2.Prevent disease or delay onset3.Slow progression of disease4.Treat primary symptoms eg memory5.Treat secondary symptoms eg depression, hallucinations

  • Medications to treat primary symptomscholinesterase inhibitors:donepezilrivastigminegalantaminememantine

  • Cholinesterase inhibitorsthese drugs stop the breakdown of acetylcholine which is an important neurotransmitter in memory and cognitionall show modest improvement in cognition and function, and behavioural symptomsresponse: 1/3 improve, 1/3 stabilise, 1/3 have no responsedo not prevent progression of underlying disease

  • Cholinesterase inhibitorsdonepezil (Aricept)given once daily, dosage of 5mg to 10mgrivastigmine (Exelon)given twice daily, dosages of 3mg to 12mggalantamine (Reminyl)given once daily, dosages of 8mg to 24mg (can also be given twice daily)

  • Use of cholinesterase inhibitorsneed specialist diagnosis of Alzheimers Disease, and a MMSE score of 10 to 24.need to show an improvement on MMSE of 2 points to continue medication on PBSside effects - nausea, vomiting, diarrhoea, dizziness, headache, muscle cramps use carefully if gastric ulcer, heart disease, chronic lung disease present

  • Use of cholinesterase inhibitorswarn against unrealistic expectationswatch for return of insight leading to depression or anxietystopping of medication:unacceptable side effectslack of response to medicationlate stages of the disease

  • Memantine (Ebixa)glutamate is a transmitter in the brain that is affected by Alzheimers Diseasememantine blocks the pathological effects of abnormal glutamate release, and allows better function of the impaired brainindicated for moderate to severe ADtrials show slowing in cognitive and functional decline and decrease in agitation in treated group compared to placebo

  • Memantinecan use with other AD medicationsside effects - headaches, dizzinessdo not use in kidney disease or seizure disordersdosage: start with 5mg daily and increase to10mg twice daily private script - not on the PBS costs approx $160/month

  • Medications to treat secondary symptomsmany people with dementia develop symptoms such as agitation, aggression, depression, delusions, hallucinations, sleep disturbance and wandering

    antidepressants:specific serotonin reuptake inhibitors (citalopram, sertraline)VIDEO

  • antipsychotics:typical antipsychotics (haloperidol) atypical antipsychotics (risperidone)modest effect on symptomswatch for side-effects mood stabilisers:anticonvulsants (carbemazepine)Medications to treat secondary symptoms

  • Several competing hypotheses:

    Cholinergic hypothesis-Caused by reduced synthesis of acetylcholine-Destruction of these neurons causes disruptions in distant neuronal networks (perception, memory, judgment)Amyloid hypothesis-Abnormal breakdown; buildup of amyloid beta deposits -Damaged amyloid proteins build to toxic levels, causing call damage and deathTau hypothesis-Caused by tau protein abnormalities-Formation of neurofibrillary tangles

  • ObesityHigh blood pressureHead traumaHigh cholesterolBeing American!Higher rates in Japanese-Americans than JapaneseAfrican-Americans than AfricansDepressionLower rates in highly educatedBeneficial consequences of learning and memory

  • EducationThe ability of the brain to change suggests to some that staying mentally active as you age may help to maintain healthy brain synapses. A 2002 study reported an association between frequent participation in cognitively stimulating activities (such as reading, doing crossword puzzles, visiting museums) and a reduced risk for Alzheimer's.ExerciseLowers risk of high blood pressure and other risk factors associated with AlzheimersAlcohol ConsumptionMen who consume one to three drinks of alcohol per day cut their risk of developing the disease by nearly half. Among women, however, the risk was reduced by only 4%. The type of alcohol had no effect on the results. But further study is needed. In the meantime, experts do not recommend drinking alcohol to fend off Alzheimer's disease.

  • Between 70 to 90% of people with AD eventually develop behavioral symptoms, including sleeplessness, wandering and pacing, aggression, agitation, anger, depression, and hallucinations and delusions. Experts suggest these general coping strategies for managing difficult behaviors:AD Research: Managing Symptoms

    Stay calm and be understanding.Be patient and flexible. Dont argue or try to convince.Acknowledge requests and respond to them.Try not to take behaviors personally. Remember: its the disease talking, not your loved one.Experts encourage caregivers to try non-medical coping strategies first. However, medical treatment is often available if the behavior has become too difficult to handle. Researchers continue to look at both non-medical and medical ways to help caregivers.

  • Management of Alzheimers Disease

  • Pharmacologic Options for ADCognitive enhancers2 classesCholinesterase inhibitors (ChEIs)NMDA-receptor antagonistDo not cure the disease or reverse cognitive impairmentCan improve cognition and functional abilityReduce the rate of decline 9-12 months (ChEIs)Delay in nursing home placement was 17-21 months (ChEIs)

  • Behavioral and Psychological Symptoms of Dementia (BPSD)Apathy Depressive symptomsAnxietyAgitation/irritability/ aggressionPsychotic symptomsDelusionsHallucinationsDisinhibitionEuphoriaLoss of appetiteSleep disturbancesStereotyped behaviors (eg, pacing, wandering, rummaging, pickingTampi et al. Clinical Geriatrics. 2011;19:41-46.

  • Managing BPSD

    Identify triggersObserve symptom timing and frequencyLook for environmental triggers, eg noise, lightingInvestigate potentially treatable causes, eg painMake adjustmentsAddress medical causesAdapt environmentAdapt caregivingModify as needed

  • Managing BPSDNonpharmacological InterventionsUse the 3 Rsrepeat, reassure, redirectSimplify the environment, task, routineAnticipate unmet needsAllow adequate rest between stimulating eventsUse cuesEncourage physical activityOther interventions



  • ConclusionEarly diagnosis enables prompt and effective management, yields better quality of life for patients and caregiver Neuroimaging especially MRI scan is widely used in clinical setting now. Biomarker especially CSF study has been included in research diagnostic criteria, but not yet recommended for general clinical use, further validation is eagerly awaited

  • The core of all assessment in dementia care is careful enquiry and attentive listening, and There is no substitute for a clinical interview by a trained clinician By doing appropriate work-up and recognizing the clinical pattern, most of the cause of dementia especially Alzheimers disease dementia can be determined on enough certainty


    These images represent a cross-section of the brain as seen from the front. The cross-section on the left represents a normal brain and the one on the right represents a brain with Alzheimer's disease.In Alzheimer's disease, there is an overall shrinkage of brain tissue. The grooves or furrows in the brain, called sulci (plural of sulcus), are noticeably widened and there is shrinkage of the gyri (plural of gyrus), the well-developed folds of the brain's outer layer. In addition, the ventricles, or chambers within the brain that contain cerebrospinal fluid, are noticeably enlarged. In the early stages of Alzheimer's disease, short-term memory begins to fade (see box labeled memory') when the cells in the hippocampus, which is part of the limbic system, degenerate. The ability to perform routine tasks also declines. As Alzheimer's disease spreads through the cerebral cortex (the outer layer of the brain), judgment declines, emotional outbursts may occur and language is impaired. As the disease progresses, more nerve cells die, leading to changes in behavior, such as wandering and agitation. In the final stages of the disease, people may lose the ability to recognize faces and communicate; they normally cannot control bodily functions and require constant care. On average, the disease lasts for 8 to 10 years, but individuals with Alzheimers can live for up to 20 years.

    *Although there is no current cure for Alzheimers disease, both nonpharmacological and pharmacological interventions are needed to optimally treat the cognitive, behavioral and psychological symptoms in patients with the disease. When coordinated with support services, outcomes for the patient, family and caregiver can be improved.*Rate of decline. [Farlow et al. Eur Neurol. 2000;44:236-241. Doody et al. Arch Neurol. 2001;58:427-433. Raskind et al. Neurology. 2000;54:2261-2268. Winblad et al. Neurology. 2001;57:489-495.]NH placement . [Geldmacher et al. JAGS. 2003;51:937-944. Lopez et al. Neurol Neurosurg Psychiatry. 2002;72:310-314. Knopman et al. Neurology. 1996;47:166-177.]

    Cholinesterase inhibitors delay the breakdown of acetylcholine released into synaptic clefts and so enhance cholinergic neurotransmissionMemantine may prevent excitatory neurotoxicity by binding to the NMDA receptor and normalizing the influx of magnesium and calcium into the synapse???

    *Many people with Alzheimers and their families find behavioral symptoms to be the most challenging effects of the disease. BPSD contributes to caregiver burden, cognitive impairment, functional decline and costs of care.Agitation, aggression, depression and psychosis are the leading causes for assisted living or nursing facility placement. [Yaffe et al.JAMA.2002;287:2090. Gauthier et al. IntJGeriatrPsychiatry. 2008;23:537. 60%-90% of patients will have BPSD at some point (higher in institutional settings). [Lyketsos et al. JAMA. 2002;288:1475-1483. Mega et al. Neurology. 1996;46:130-135. Steinberg et al. Int J Geriatr Psychiatry. 2008;23:170-177. Zuidema et al. J Geriatr Psychiatry Neurol. 2007;20:41-49. Haupt M, Kurz A, Janner M. A 2-year follow-up of behavioural and psychological symptoms in Alzheimers disease. Dement Geriatr Cogn Disord. 2000; 11:147-152.]The presence of one or more APOE e4 alleles is a significant predictor of the incidence of delusions. [Scarmeas et al. Neurology. 2002;58:1182-1188.]Leaving patients behavioral and pyschological symptoms of dementia untreated has been associated with caregiver burnout, nursing home placement, poor management of comorbid conditions, and excess health care costs. [Steele C, Rovner B, Chase GA, Folstein M. Psychiatric symptoms and nursing home placement of patients with Alzheimers disease.AmJ Psychiatry. 1990; 147:1049-1051. Cohen-Mansfield J. Assessment of disruptive behavior/agitation in the elderly: function, methods, and difficulties. J Geriatr Psychiatry Neurol. 1995;8:52-60. Ballard C, Neill D, OBrien J, McKeith IG, Ince P, Perry R. Anxiety, depression and psychosis in vascular dementia: prevalence and associations. J Affect Disord. 2000;59:97-106.]

    *Early recognition and treatment of BPSD helps to decrease morbidity, reduce the costs and burden of caring for these patients, and improve patient and carepartner quality of life.The first step to reduce or stabilize BPSD is to identify the trigger. Determining when the behavior occurs and how often is often helpful.Behaviors are a form of communication, especially if the person with dementia cannot communicate in other ways. They may be a response to a symptom of illness, a stressful environment or an unmet need.Common causes include the following;Environmental triggers, such as excessive stimulation, dim lighting, or changing caregiversMedical causes, such as bowel impaction, infection, or untreated pain.Medication side effectsInability to communicate (understand or be understood)Correctly identifying what triggered the behavior can help in selecting the best intervention. *A key principle of intervention is redirecting the persons attention, rather than arguing or being confrontational. Additional strategies include: Simplifying the environment, tasks and routineAnticipating unmet needs, such as hunger, thirst, full bladderAllowing adequate rest between stimulating events Using cues or remindersEncouraging physical activityOther interventions with limited evidence of efficacy include: music therapy, bright light treatment, aromatherapy, sleep hygiene.