Download - Geriatric Case Conferenc e
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Geriatric Case
ConferenceBow&Tum22/6/55
Presentation…
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Patient profileO ผปวยหญงไทยโสด อาย 60 ปO อาชพ รบราชการคร ปจจบนเกษยณแลว
( สอนสงคมศาสตร ม. ตน รร.ปทมคงคา)O การศกษา ปรญญาตรO ภมลำาเนา จ.นนทบรO ศาสนา พทธO สทธการรกษา ขาราชการ
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Chief complaint หลงลม 5 ป
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Present illness5 ปกอน เรมมอาการหลงลม
เรองทเพงทำาไป อารมณฉนเฉยว โกรธงาย หวาดระแวง มปญหาในการ
ทำางานทโรงเรยน อาศยอยคอนโดคน เดยว
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Present illness ป 2550 ผปกครองมาแจงทางโรงเรยนวา
อ. อมใหการบานนกเรยนวาดแผนททกวนซำ5าๆ เรมม ปญหาเรองการสอนทโรงเรยน จดแผนการสอนผด
เขยนใบเสรจไมถกตอง ทางโรงเรยนจงพจารณายายจากอาจารยสอนวชาสงคมมาเปนอาจารยฝาย
แนะแนว เรมมพฤตกรรมกาวราว ดาวาเพอนครใน
โรงเรยน เพอนครจงแนะนำาใหเกษยณกอนกำาหนด และแจงใหญาตทราบ เนองจากผปวยอาศยอยคน
เดยวทคอนโดมาตลอด ญาตไปพบทคอนโดวาปลอย ใหรกรงรง เดนแกผาในหอง ร5อเส5อผา ลมรบประทาน
อาหาร
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ญาตพาผปวยเขารบการรกษาทรพ. พระมงกฎฯ ไดรบยาและตดตามอาการ แตยงมอาการสบสน
เหนภาพหลอน เชน พดคนเดยวกบกระจก พด ไมเปนคำา เรยงประโยคผด อารมณเสยงาย
ชอบดาวาญาตและพดเหตการณเกาๆ ญาตเปน กงวลมากและคดวาผปวยแกลง และคดวาผ
ปวยเปนโรคทางจต ตอมาอาการสบสนเพมมาก ข5น ญาตจงพามารกษาทรพ.รามาธบด
Present illness
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GenogramCA Colon 72 ป
1st 2nd ADDx 40+ yrs
คณหลาน62 ป
คณเป ยก
คณธารณ60 ป
คณดารรตน58 ป
คณโดง CA liver56 ป
คณตง CA liver47 ป
ต41 ป
ตรอง21 ป
ตก20 ป
โอม25 ป
ไอซ21 ป
ดว23 ป
แอน20 ป
แตม17 ป
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Timeline• บรรจราชการครทสงขลา2517-
2519• ยายกลบมาสอนทกรงเทพฯ2520• สามคณหลานไปมภรรยาใหม2517-
2531• สามคณหลานกลบมาคนด• ทะเลาะกบสามคณหลานจนตองยาย
ไปอยคอนโด2531
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Timeline• ผอ.รร. เรยกญาตพบ อ.อมไมปรกต
ประมาณ 1 ป ไมสามารถสอน หนงสอได ทางรร.ใหยายจากกลม
สาระไปกลมกจการแทน
กพ.2551
• Early retirement• เรมเขยนหนงสอไมถก2551• ทำาของหายบอยๆ เชนเอกสาร เงน• กนยาไมถก• เรมใชคำารนแรงดาพนอง
จนตนาการความคดเอง
2552
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Timeline• ใสเส5อผาไมถก เชนกลบตะเขบ ใสซอน
หลายตว• คยกบทว กระจก หแวว คดวาคนอนดา
หวเราะเยาะ• นอยใจวาตวเองถกทอดท5ง อจฉาพนอง
2553
• ยายไปอย Nursing Home, ญาตพาไปรกษาทรพ. พระมงกฎฯ คดวาเปนโรคจต
• ยายมารกษาทรพ.รามาธบด• เยยมบานคร5งท 1
2554
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Problems list
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Differential diagnosis
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O Interfere with work or usual activities
O Decline from prior level of functioning
New Dementia Criteria
Loss cognitive or neuropsychiatric
symptom
O Not explained by delirium or other psychiatric disorder
เสย ADLs R/O other cause
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Loss cognitive or neuropsychiatric
symptom
Visuo-spatial
Executive
function
Language
Memory
Behavior
Impairment ≥ 2
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Physical ExaminationGA : หญงไทยแตงตวด สะอาด ไมคอยแสดงสหนาBP 120/80 mmHg PR 70/minHEENT : not pale, anicteric sclera, normal tooth
& gum, no oral lesionLN : no cervical LN enlargementHeart : regular, normal s1,s2, no murmurLung : clear, equal both, no adventitious soundAbd: soft, no mass, not tender ,no
hepatosplenomegaly
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Physicial ExaminationExt : No edema, no cogwheel rigidity, no
spastic, no resting tremorN/S : pupil 3 mm. RTLBE, full EOM, motor
power gr. V all, BBK – plantar flextion bothGait : normalSpeech : normal
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Test/Date28/6/54 24/1/55 28/2/55
ครงท 1 ครงท 2 ครงท 3Orientation for time 0 0 0Orientation for place 1 2 3Registration 3 2 2Attention/Calculation 0 0 0Recall 0 0 0Naming 2 2 2Repetition 0 0 1Verbal command 1 1 0Writing command 0 1 1Wristing 0 0 0Visuo-contruction 0 0 0
คะแนนรวม 7 8 9
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Test/Date28/6/54 24/4/55
คร5งท 1 คร5งท 2CDT 2/10 1/10
Test/Date28/6/54 24/4/55
คร5งท 1 คร5งท 2Cube incorrect Incorrect
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Dementia?Severity?
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Investigation
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InvestigationCBC
WBC 5200 N 60 L 31 M 6 E 2 B 1Hb 12.7 Hct 40.9 MCV 89 MCH 27.2RBC morpho normochromia
Cr 0.77TSH 1.646 (0.35-4.94)Vitamin B12 338.5 (243.0-894.0)VDRL NR
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MRI brainO Mild volume loss of hippocampi and parahippocampal gyri with
thining of entorhinal cortex, bilaterally which may be represent Alzheimer disease.
O The bilateral pars compacta of the substantia nigra of the midbrain are well identified.
O 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.
ImpressionO Mild volume loss of hippocampi and parahippocampal gyri with
thining of entorhinal cortex, bilaterally which may be represent Alzheimer disease.
O Generalized mild cerebral volume loss.
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FDG PETO The 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.
ImpressionO Severe hypometabolism of bilateral parietotemporal
cortices with less involvement of frontal cortices favor Alzheimer’s disease, less likely Pick’s disease.
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Diagnosis
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Clinical Features Distinguishing AD and Other Dementias
O AD: O Memory, language, visual-spatial disturbances,
indifference, delusions, agitationO Frontotemporal dementia:
O Relative preservation of memory and visual-spatial, skills, personality change, executive dysfunction, excessive eating and drinking
O Lewy body dementia: O visual hallucinations, delusions, extrapyramidal,
symptoms,fuctuating mental status, sensitivity to antipsychotic medications
O Vascular dementia: O abrupt onset, stepwise deterioration, executive
dysfunction, gait changes
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Cognitive domain
AD DLB bvFTD VaD Depres-sion
Free recall +++ ++ +/- + +
Recognition +++ - - - -
Prompting X √ √ √ √
Intrusions +++ +++ +++ + +
Semantic memory (naming)
++ + + + +/-
Procedural memory
- + - + +
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Cognitive domain
AD DLB bvFTD VaD Depression
Working memory
++ +++ +++ ++ +/-
Insight +++ + +++ - -
Attention ++ +++ ++ ++ +++
Executive functions
++ typical AD+++ frontal
variant
+++ +++ +++ ++
Visuospatial skills
++ typical AD+++ PCA
+++ - + +
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Memory impairment in AD
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Memory impairment in AD
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Memory impairment in AD
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Memory impairment in AD
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Memory impairment in AD
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Alzheimer’s dementiacriteria
OProbable ADOPossible ADOProbable or possible AD with
evidence of the AD pathophysiological processO Biomarkers of brain amyloid-beta (Ab)
protein depositionO Biomarkers of downstream neuronal
degeneration or injury
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Atypical ADO Logopenic progressive aphasia
O LanguageO Frontal variant AD
O Behavior, ExecutiveO Posterior cortical atrophy
O Visuospatial
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Frontotemporal dementia
FTD
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FTDO Dementia in persons younger than
65 years
O A neurodegenerative disease of unknown etiology
O Behavioral and language
O Relatively preserved memory
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O Neuroimaging (MRI) usually demonstrates frontotemporal atrophy
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Types of FTDO Behavioral variant frontotemporal
dementia
O Semantic dementia
O Progressive nonfluent aphasia
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Treatment
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MedicationO Rivastigmine patch(10) 1 patch แปะ q
24 hrO Memantine (10) 1 x 1 oral pcO Sertraline(50) 1 x 1 oral pcO Na valproate chrono(500) 1 x 1 oral
pcO Quetiapine (25) 1 x 1 oral hsO Amlodipine (5) 1 x 1 oral pcO Folic (5) 1 x 1 oral pcO Vitamin B1612 1 x 2 oral pc
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Therapeutic strategies
O Symptomatic treatmentO Disease-modifying therapy O Lifestyle
O DietO Physical ExerciseO Mental Exercise
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Cholinesterase Inhibitors
O Donepezil, Rivastigmine, Galantamine
O Mild to moderate dementia
O Benefit in severe dementia not as clear
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MemantineO Mechanism of action: partial NMDA-
receptor antagonistO May block glutamate excitotoxicityO May provide symptomatic benefit via
effects on hippocampal neuronsO Moderate to severeAlzheimer’s
dementiaO Safe in combination with ChEI
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Pharmacologic Treatment of Agitation
Symptoms MedicationAgitation in context of nonacute psychosis
Olanzapine 2.5–10 mg/dQuetiapine 12.5–100 mg/dRisperidone 0.25–3 mg/d
Agitation in context of depression
SSRI, eg, citalopram 10–30 mg/d
Anxiety, mild to moderate irritability
Trazodone 50–100 mg/d
Agitation or aggression unresponsive to first-line treatment
Carbamazepine 300–600 mg/dOlanzapine (intramuscular) 2.5–5 mg IM
Sexual aggression, impulse-control symptoms in men
Second-generation antipsychotic If no response, conjugated equine estrogens 0.625–1.25 mg/d
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DietO Mediterranean diet (Scarmeas N.
JAMA. 2009)O High in vegetables, legumes, fruits,
nuts, cereal, fish, olive oilO Low in saturated fatsO Up to 40% reduction in risk for
developing dementia
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Non pharmacological treatment in dementia
O Cognitive focus interventionO Cognitive stimulation O Cognitive training O Cognitive rehabilitation
O OtherO Music therapy O Aromatherapy O Massage and touchO Exercise
Cognitive stimulation is engagement in a range of activities anddiscussions (usually in a group) aimed at general enhancement ofcognitive and social functioning.
Cognitive 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.
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 impairments
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Cognitive stimulation
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O Control group : usual activityO Doing nothingO Game : bingo, singing, art and crafts
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O Intervention : programmeO 14-session programme , twice a
week, 45min per session over 7 weeks
O Reality orientation and cognitive stimulation
O Topic : using money, word games, the present day and famous faces
O Reality orientation board
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Cognition
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Follow up
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O Communication and social interaction
• QoL
• GDS
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O ADL, Behavior, caregiver non significant
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Cognitive training and cognitive rehabilitation
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O Cognitive training : 9 studies O Cognitive rehabilitation : none
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Change in MMSE
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CHANGE in…O Immediate verbal memory scoresO Delayed verbal memory scoresO Verbal letter fluency scoresO Verbal category fluency scoresO Executive function scoresO Self-report of memory functioningO Participant self-report of mood (depression)O Informant report of participant memory
functioning
Non significant
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CHANGE in…O Informant report of participant mood (depression)O Informant report of participant functional ability
(ADLs)O Informant report of informant reaction to
participant memory and behaviour problemsO (Follow up) immediate verbal memory scoresO (Follow up) executive function (sequencing) scoresO (Follow up) informant report of participant
memory functioningO (Follow up) informant report of participant
functional ability (activities of daily living)
Non significant
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Music therapy
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O Type of music therapyO Receptive music therapyO Active music therapy
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Total minute spent not wandering during all sessions of main therapy
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Mean change in MMSE
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Number of agitated behavior2 week
4 week
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Massage and touch
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O The use of hand massage for an immediate and short-term reduction of agitated behaviour
O The addition of touch to verbal encouragement to eat for the normalization of nutritional intake
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Mean agitate score
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Aroma therapy
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O Only 2 RCT, other not good study design
O Statistical significant in decreased agitated
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Evaluation of Response to Any Cognitive Enhancer
O Elicit caregiver observations of patient’s cognitive function and behavior (alertness, initiative) and follow functional status (ADLs and instrumental ADLs).
O Follow cognitive status (eg, improved or stabilized) by caregiver’s report or serial ratings of cognition (eg, Mini-Cog, MMSE)
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Test/Date28/6/54 24/1/55 28/2/55
ครงท 1 ครงท 2 ครงท 3Orientation for time 0 0 0Orientation for place 1 2 3Registration 3 2 2Attention/Calculation 0 0 0Recall 0 0 0Naming 2 2 2Repetition 0 0 1Verbal command 1 1 0Writing command 0 1 1Wristing 0 0 0Visuo-contruction 0 0 0
คะแนนรวม 7 8 9
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Test/Date28/6/54 24/4/55
คร5งท 1 คร5งท 2CDT 2/10 1/10
Test/Date28/6/54 24/4/55
คร5งท 1 คร5งท 2Cube incorrect Incorrect
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Follow up
O Typical AD MMSE drop ≥ 3/yr
O MMSE drop ≤ 2/yr work
O Advance directive !!!
Follow up
Cognition
Caregiver
BPSD
Function
Sleep
Safety
ANS
Neuro
MMSE
•Hallu/Delu•Apathy•Depression•Agitation•Manic-like/attention
ADLs/
iADLs
•REM•Insomnia•Increase day sleepDriving,
falling, financial
GI, GU, cardio,tem
p, dysphagia
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THANK YOU