13Loss cognitive or neuropsychiatric symptom New Dementia CriteriaLoss cognitive or neuropsychiatric symptomInterfere with work or usual activitiesDecline from prior level of functioningNot explained by delirium or other psychiatric disorderเสีย ADLsR/O other cause
14Loss cognitive or neuropsychiatric symptom Visuo-spatialExecutive functionLanguageMemoryBehaviorImpairment ≥ 2
15Physical ExaminationGA : หญิงไทยแต่งตัวดี สะอาด ไม่ค่อยแสดงสีหน้า BP 120/80 mmHg PR 70/min HEENT : not pale, anicteric sclera, normal tooth & gum, no oral lesion LN : no cervical LN enlargement Heart : regular, normal s1,s2, no murmur Lung : clear, equal both, no adventitious sound Abd: soft, no mass, not tender ,no hepatosplenomegaly
16Physicial Examination Ext : No edema, no cogwheel rigidity, no spastic, no resting tremor N/S : pupil 3 mm. RTLBE, full EOM, motor power gr. V all, BBK – plantar flextion both Gait : normal Speech : normal
23Investigation CBC Cr 0.77 TSH 1.646 (0.35-4.94) WBC 5200 N L M 6 E 2 B 1Hb 12.7 Hct MCV 89 MCH 27.2RBC morpho normochromiaCrTSH ( )Vitamin B ( )VDRL NR
24MRI brainMild volume loss of hippocampi and parahippocampal gyri with thining of entorhinal cortex, bilaterally which may be represent Alzheimer disease.The bilateral pars compacta of the substantia nigra of the midbrain are well identified.The rest of brain parenchyma shows normal signal intensity without space occupying lesion. Brainstem and the cerebellum are unremarkable. The calvarium and the skull base have normal marrow signal intensity. No midline shifting, hydrocephalus or extraaxial collection is detected.ImpressionGeneralized mild cerebral volume loss.
25FDG PETThe study reveals severely decreased FDG activity in bilateral parietotemporal cortices which is relative symmetric. There is also mildly to moderately decreased FDG activity in the frontal cortices, right slightly involved more than left. The tracer distribution in the rest of the scanned regions appears within normal limits. Limited low dose, noncontrast CT images show no corresponding abnormality.ImpressionSevere hypometabolism of bilateral parietotemporal cortices with less involvement of frontal cortices favor Alzheimer’s disease, less likely Pick’s disease.
35Alzheimer’s dementia criteria Probable ADPossible ADProbable or possible AD with evidence of the AD pathophysiological processBiomarkers of brain amyloid-beta (Ab) protein depositionBiomarkers of downstream neuronal degeneration or injury
42Diagnostic Behavioral and Language Features of Frontotemporal Dementia Variants Behavioral variant frontotemporal dementiaSemantic dementiaProgressive nonfluent aphasiaCore featuresInsidious onset and gradual progressionEarly decline in social and interpersonal conductLanguage disorder characterized by progressive, fluent, empty, spontaneous speech; loss of word meaning; impaired naming and comprehension; semantic paraphasiaNonfluent, spontaneous speech with at least one of the following: agrammatism, phonemic paraphasia*, anomiaEarly impairment in regulation of personal conductPerceptual disorder characterized by impaired recognition of familiar faces and/or objects—
43Diagnostic Behavioral and Language Features of Frontotemporal Dementia Variants Behavioral variant frontotemporal dementiaSemantic dementiaProgressive nonfluent aphasiaCore featuresEarly emotional bluntingPreserved perceptual matching and drawing reproduction—Early loss of insightPreserved single-word repetition and ability to read aloudSupportive featuresBehavioral disorder, with decline in personal hygiene; distractibility and impersistence; hyperorality; dietary changes; repetitive stereotypic behavior; utilization behaviorBehavioral changes with loss of sympathy and empathy; narrowed preoccupations; parsimonyBehavioral changes with early preservation of social skills; late behavioral changes similar to behavioral variant frontotemporal dementia
44Diagnostic Behavioral and Language Features of Frontotemporal Dementia Variants Behavioral variant frontotemporal dementiaSemantic dementiaProgressive nonfluent aphasiaSupportive featuresSpeech and language changes with altered speech output; echolalia†; perseveration‡; mutismSpeech and language changes with press of speech; idiosyncratic word usage; absence of phonemic paraphasia*; dysgraphia§; preserved calculationSpeech and language changes with stuttering; impaired repetition; alexia∥; dysgraphia§; early preservation of word meaning; late mutism
45AD Criteria, con’t Pathophysiologically proved AD dementia Meets clinical criteria + neuropathological examDementia unlikely to be due to ADDoes NOT meet clinical criteriaORMeets criteria but there is evidence for alternative diagnosis, such as HIV dementia or HD that rarely overlap with ADMeets criteria but both Aβ and neuronal injury biomarkers are negative
46MCI due to AD Criteria Establish clinical and cognitive criteria Cognitive concern reflecting a change in cognitionreported by patient or informant or clinician (i.e., historical or observed evidence of decline over time)Objective evidence of Impairmentin one or more cognitive domains, typically including memory (i.e, formal or bedside testing to establish level of cognitive function in multiple domains)Preservationof independence in functional abilitiesNot dementedExamine etiology of MCI consistent with AD pathophysiological processRule out vascular, traumatic, medical causes of cognitive decline, where possibleProvide evidence of longitudinal decline in cognition, when feasibleReport history consistent with AD genetic factors, where relevant
47New Dementia Criteria Cognitive or neuropsychiatric symptoms: Interfere with work or usual activitiesDecline from prior level of functioningNot explained by delirium or other psychiatric disorderImpairment involves 2 or more of the following:Inability to acquire and remember new informationImpaired reasoning and handling of complex task; poor judgmentImpaired visuospatial abilitiesImpaired languageChange in personality behavior, or comportment
51Cholinesterase Inhibitors Donepezil, Rivastigmine, GalantamineMild to moderate dementiaBenefit in severe dementia not as clear
52Memantine Mechanism of action: partial NMDA-receptor antagonist May block glutamate excitotoxicityMay provide symptomatic benefit via effects on hippocampal neuronsModerate to severeAlzheimer’s dementiaSafe in combination with ChEI
53Pharmacologic Treatment of Agitation SymptomsMedicationAgitation in context of nonacute psychosisOlanzapine 2.5–10 mg/dQuetiapine 12.5–100 mg/dRisperidone 0.25–3 mg/dAgitation in context of depressionSSRI, eg, citalopram 10–30 mg/dAnxiety, mild to moderate irritabilityTrazodone 50–100 mg/dAgitation or aggression unresponsive to first-line treatmentCarbamazepine 300–600 mg/dOlanzapine (intramuscular) 2.5–5 mg IMSexual aggression, impulse-control symptoms in menSecond-generation antipsychoticIf no response, conjugated equine estrogens 0.625–1.25 mg/d
54Diet Mediterranean diet (Scarmeas N. JAMA. 2009) High in vegetables, legumes, fruits, nuts, cereal, fish, olive oilLow in saturated fatsUp to 40% reduction in risk for developing dementia
55Non pharmacological treatment in dementia Cognitive focus interventionCognitive stimulationCognitive trainingCognitive rehabilitationOtherMusic therapyAromatherapyMassage and touchExerciseCognitive stimulation is engagement in a range of activities anddiscussions (usually in a group) aimed at general enhancement ofcognitive and social functioning.Cognitive rehabilitation is an individualised approach where personallyrelevant goals are identified and the therapist works withthe person and his or her family to devise strategies to addressthese. The emphasis is on improving performance in everyday liferather than on cognitive tests, building on the person’s strengthsand developing ways of compensating for impairmentsCognitive training is guided practice on a set of standard tasksdesigned to reflect particular cognitive functions; a range of difficultylevelsmay be available within the standard set of tasks to suitthe individual’s level of ability. It may be offered in individual orgroup sessions, with pencil and paper or computerised exercises.
57Control group : usual activity Doing nothingGame : bingo, singing, art and crafts
58Intervention : programme 14-session programme , twice a week, 45min per session over 7 weeksReality orientation and cognitive stimulationTopic : using money, word games, the present day and famous facesReality orientation board
81Only 2 RCT, other not good study design Statistical significant in decreased agitated
82Evaluation of Response to Any Cognitive Enhancer Elicit caregiver observations of patient’s cognitive function and behavior (alertness, initiative) and follow functional status (ADLs and instrumental ADLs).Follow cognitive status (eg, improved or stabilized) by caregiver’s report or serial ratings of cognition (eg, Mini-Cog, MMSE)