dementialec[1] (1)
TRANSCRIPT
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DEMENTI
EUFEMIO E. SOBREVEGA, MDFELLOW, PHIL. NEUROLOGICAL ASSOCIATION
FELLOW, PHIL. PSYCHIATRIC ASSOCIATION
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PPRO CH TO P TIENTS COMPL INING OF
“FORGETFULLNESS”
Primary Care Visit
Diagnosis
Evaluation
Treatment
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PRIMARY CARE VISIT
• Patient complains of
worsening of cognitive functioning
or caregiver/clinician noticescognitive impairment in the patient.
• suggestive of DEMENTIA?
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PPRO CH TO P TIENTS COMPL INING OF
“FORGETFULLNESS”
Primary Care Visit
Diagnosis
Evaluation
Treatment
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DIAGNOSIS
• CONFIRM DEMENTIA:
•CLINICAL ASSESSMENT
• INTERVIEW WITH CAREGIVER/PATIENT
•NEUROPSYCHOLOGICAL EXAMS
•ANCILLARY PROCEDURES
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DIAGNOSIS – Diagnostic Tests
• Exclude treatable causes which may be contributing to thedementia:
- BLOOD CHEMISTRIES
- CT SCAN
- MRI
- CSF EXAM
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DIAGNOSIS - Exclusion
• Potentially treatable causes of dementia
A. Infections
- MENINGITIS
- HIV encephalitis
- Neurosyphilis
- Creutzfeldt-Jakob Disease
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DIAGNOSIS - Exclusion
B. Metabolic and Toxic
- Alcoholism
- Hypothyroidism
- Hepatic or renal failure- Psychoactive medications
- Vitamin B12 or folate deficiency
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DIAGNOSIS - Exclusion
C. Neoplastic
- Brain tumors
- Carcinomatosis
Others:- Subdural Hematoma
- Normal pressure hydrocephalus
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DIAGNOSISGeneral Cognitive Screening Tests
1. Mini-Mental State Examination
2. Clock drawing test
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MINI – MENTAL STATE
EXAMINATION
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MINI – MENTAL STATE EXAMINATION
• ORIENTATION• TIME 5PTS
• PLACE 5PTS
• REGISTRATION 3PTS
• ATTENTION AND CALCULATION 5PTS
• RECALL 3PTS• LANGUAGE
• NAMING 2PTS
• REPETITION 1PT
• 3 STAGE COMMAND 3PTS
• READING 1PT
• WRITING 1PT
• COPYING 1PT
• TOTAL = 30PTS
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A.1. Orientation
• What is the Points Score
Year? 1 1
Season? 1 1
Date? 1 1Day? 1 1
Month? 1 1
TOTAL = 5PTS
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A.2. Orientation
• Where are we? Points Score
Province? 1 1
Country? 1 1
Town or City? 1 1Hospital? 1 1
Floor? 1 1
TOTAL=5PTS
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B. Registration (Total points = 3)
• Name three (3) objects, taking one second to say each (e.g.apple, table, coin). Then ask the patient all three (3) after
you have said them.
• Repeat the answers until the patient learns three(3), up to 6trials
• Give one point for each correct answer
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C. Attention and Calculation(Total points = 5)
• Serial sevens. Instruct patient to subtract 7 from 100 in increments.Stop after 5 answers. Alternate: Spell WORLD backwards (e.g.DLROW = 5, DLRW = 4, DLW = 3, OW = 2, DRLWO = 1 )
•
Give one(1) point for each correct answer or number of letter.
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D. Recall (Total points =3)
• Ask for names of three (3) objects learned in section B( e.g. apple, table, coin).
• Give 1 point for each correct answer.
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E. 1. Language – Naming
(Total points = 2)
• Point to a pencil and a watch.
Have the patient name the objectas you point.
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E. 2. Language – Repetition
(Total point = 1)
• Ask the patient to repeat the phrase,
“No ifs, ands or buts” after you.
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E.3. Language – 3 Stage Command
(Total points = 3)
• Have the patient follow a 3-stage command:
1. Take the paper in your right hand
2. Fold the paper in half 3. Put the paper on the floor
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E.4. Language – Reading(Total point = 1)
• Have the patient read and obey the following: (1 point)
“CLOSE YOUR EYES”
(Write it in LARGE LETTERS)
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E. 5. Language – Writing
(Total point = 1)
• Have the patient write a sentence of his or her own choice. (1point)
• (The sentence should contain a subject and a verb and shouldmake sense. Ignore spelling errors when scoring)
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E.6. Language - Copying
(total point = 1)
• Have the patient copy the figure below. (Give one (1)point if all sidesand angles are preserved and if the intersecting sides form aquadrangle)
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SCORES
•Maximum Total Score is 30•Total Score ____
•Suggested guidelines for determining the severityof cognitive impairment
Mild: MMSE > 21
Moderate:MMSE 10 -- 20
Severe: MMSE < 9
Expected decline in MMSE scores in untreatedmild to moderate Alzheimer’s patient is 2 to 4points per year.
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PPRO CH TO P TIENTS COMPL INING OF
“FORGETFULLNESS”
Primary Care Visit
Diagnosis
Evaluation
Treatment
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COMMON CAUSES OF DEMENTIA
56.8% AD
19.3% Others
13.3%
Multi-inflarct
dementia
1.5%
Medications
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ALZHEIMER’S DISEASE
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EVALUATION
ALZHEIMER,S DISEASE
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Alzheimer’s disease
• Alzheimer’s disease (AD) is the most frequent cause ofdementia – it represents more than half of all dementiacases.
• AD is most likely to occur in people aged over 65 –70 years of age (late-onset), although it can occur earlier (early- onset).
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Alzheimer’s disease
• Alzheimer’s disease (AD) develops slowly over a period of years.
• progression of early-onset AD is more rapid.
•AD is associated with general impairment of higher cortical functions.
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EVALUATION
•Alzheimer’s disease (AD)
-diagnosis should only be made after other causes ofdementia have been excluded by lab test, physical and
neurological exams and patient history.
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DSM- IV DEFINITION OF DEMENTIA OFALZHEIMER’S TYPE
•MEMORY LOSS
• IMPAIRMENT IN AT LEAST 1 OTHER COGNITIVEDOMAIN
•GRADUAL ONSET AND SLOWLY PROGRESSIVE
•NOT DELIRIOUS
•DISABLING
•NO ALTERNATE EXPLANATION
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DSM-IV DEFINITION OF DEMENTIA OFALZHEIMER’S TYPE
• MEMORY LOSS:
* INABILITY TO LEARN NEW MATERIAL ;POOR REMOTE RECALL
• IMPAIRMENT IN AT LEAST 1 OTHER COGNITIVEDOMAIN:
* APHASIA (LANGUAGE) *APRAXIA (MOTOR ACTS, VISUOSPATIAL) * AGNOSIA
(VISUAL RECOGNITION) * DISTURBEDEXECUTIVE FUNCTION (PLANNING, ETC.)
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MEMORY and the FORGOTTEN SELF
•SYSTEMATIC RETROGRADE AMNESIA: *
CANNOT LEARN NEW INFORMATION. * CANNOTRECALL MOST RECENT LEARNEDINFORMATION.
•PROGRESSIVE RETROGRADE AMNESIA: * ERASING
THE “LINE OF LIFE” FROM NEAREST TO OLDEST.* LOSS OF SEMANTIC (FACTUAL) AND
EPISODIC (PERSONAL) MEMORY.
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CRITERIA FOR DIAGNOSIS OF ALZHEIMER’SDISEASE
• PROBABLE ALZHEIMER’S DISEASE:
* DEMENTIA BY DSM-IV AND MMSE
* PROGRESSIVE MEMORY IMPAIRMENT* NO DISTURBANCE IN
CONCIOUSNESS
* BETWEEN 40 AND 90 AGE OF ONSET* ABSENCE OF SYSTEMICBRAIN DISEASE; SUPPORTED BY FAMILYHISTORY; CEREBRAL ATROPHY BY CT SCAN.
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CRITERIA FOR THE DIAGNOSIS OFALZHEIMER’S DISEASE
• DEFINITE ALZHEIMER’S DISEASE:
* CLINICAL CRITERIA FORPROBABLE ALZHEIMER’S D.
*HISTOPATHOLOGIC EVIDENCE(AUTOPSY OR BIOPSY)
NINCDS-ADRDA
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Neuropathological changescharacteristic of AD
Normal AD
AP NFT
AP = amyloid plaques
NFT = neurofibrillary tangles
Courtesy of George Grossberg, St Louis University, USA
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Amygdala
Hippocampus
Entorhinal region and
the nucleus basalis of
Meynert
Hippocampus
DISEASE PROGRESION
Near regions
of cortexfrontal
Lobe
Parietal
Lobe
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Paired helical
filaments
accumulate in
neuron
2
These develop into NTFs, w/c
build up in the neuron, disrupting
function
3
Abnormal tau protein
and paired helical
filaments also promote
development of
neuritic plaques
4
Neuron
NTFs
Phosphateaccumulation on
tau protein leads to
development of
paired helical
filaments
1
Abnormal Tau protein
Microtubules
Neuritic
plaque
Paired
helicalfilament
The neuron
eventually dies
5
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Structural Changes in Alzheimer’s D. Brain
Neuron Loss
• Large Cortical Neurons
• Amygdala
• Hippocampus• Entorhinal cortex
• Basal forebrain cholinergic
nuclie
• Locus ceruleus
• Dorsal raphe neurons
Structural Alterations
• Neuritic plaques
• Neurofibrillary tangles
• Amyloid deposition• Inflammation
• Neuropil threads
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Two Important Histological Markers
• Neuritic Plaques
• Amyloid PrecursorProtein(APP) A β 1-42
• Extracellular deposit
6-10nm fibrils
• Neurofibrillary Tangles• Derived from Tau protein
• Microtubule associated protein(MAP)
• Collection of paired helicalfilaments (intracellular)
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Neuritic
Plaques
Neurofibrillary
Tangles
Neuronal
Dysfunction and
Synapse Loss
Acetylcholine andOther
Neurotransmitter
Deficiencies
Clinical
Symptoms
Peter Whitehouse, MD 1997
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Amyloid cascade
Histologic changes
Biochemical deficits
Dementia syndrome
Jeffrey L. Cummings, MD
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Amyloid
Cascade
Regional
CholinergicDeficiency
Regional
Cell Loss
OrbitofrontalFrontal
andTemporal
Reticulofrontal
AgitationPsychosisDelirium Disinhibition
Medial
Frontal
Apathy
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OTHER DEGENERATIVE DEMENTIAS
• PICK DISEASE• RARE TYPE OF DEMENTIA CHARACTERIZED BY SELECTIVE ATROPHY OF THE FRONTAL
AND TEMPORAL LOBES OF THE BRAIN
•
DEMENTIA WITH LEWY BODIES• DEMENTIA IN THE ELDERLY
• Presence of Lewy bodies in the neurons of the brainstem and cerebral cortex
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OTHER DEGENERATIVE DEMENTIAS
• HUNTINGTON’S DISEASE (CHOREA)• HEREDITARY DEGENERATIVE DISEASE (AUTOSOMAL DOMINANT) CHARACTERIZED BY:
• COGNITIVE DISTURBANCES,
• SLOWLY PROGRESSIVE DEMENTIA,
• EXTRAPYRAMIDAL MOTOR SYPTOMS OF CHOREA,RIGIDITY, BRADYKINESIA
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PPRO CH TO P TIENTS COMPL INING OF
“FORGETFULLNESS”
Primary Care Visit
Diagnosis
Evaluation
Treatment
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TREATMENT
•
Non-pharmacological•Pharmacotherapy
•Non-cognitive symptoms
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TREATMENT
•Non-pharmacological
- Patient, caregiver and healthcare workers
education
-Caregiver support
- Patient psychosocial treatment
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Pharmacological Treatment of AD
Practice Recommendations:(AAN 2001)
• Cholinesterase inhibitors should be considered
in mild to moderate AD patients(standard).
• Vitamin E (1000 IU po bid) should be considered
in an attempt to slow progression of AD(guideline).
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Treatment - Pharmacotherapy
A. Mild to moderate AD
- Cholinesterase inhibitors
(e.g. Rivastigmine, Donepezil and Galantamine)
B. Moderate to severe AD
- NMDA receptors
( e.g. Memantine)
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Treatment: Pharmacotherapy
• Cognitive Symptoms
A. Cholinesterase Inhibitors
- considered for mild to moderate AD
Mechanism of Action:
*all inhibit cholinesterase in the synaptic cleft thereby
enhancing central cholinergic function.
(e.g. Rivastigmine, Donezepil, Galantamine)
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Treatment: Pharmacotherapy
A. Cholinesterase Inhibitors1. Rivastigmine (exelon):
- inhibits both acetylcholinesterase andbutyrylcholinesterase.
- initial dose: 1.5 mg PO BID; may increase to3 mg PO BID after > if tolerated.
- may increase dose by 1.5 mg/dose every 2
weeks as tolerated.- maximum dose: 12 mg/day
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Treatment: Pharmacotherapy
A. Cholinesterase Inhibitors
2. Donepezil (aricept):- inhibits acetylcholinesterase but not
butyrylcholinesterase which may be acomponent of neuritic plaques andtangles.
- initial dose: 5mg PO once daily at HS;
may increase to 10 mg PO OD at HS after4-6 weeks, if tolerated.
- maximum dose: 10mg/day
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Treatment: Pharmacotherapy
A. Cholinesterase Inhibitors
2. Galantamine (reminyl):
- inhibits acetylcholinesterase and providesallosteric modulation of nicotinic
receptors which may have a disease-modifying benefit.
- initial dose: 4mg PO BID X 4 weeks; iftolerated, increase to 8 mg PO BID X > or
equal to 4 weeks; if still tolerated,increase to 12 mg PO BID.
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Treatment: Pharmacotherapy
B. NMDA – receptor antagonist
1. Memantine (abixa):
- considered in patients with moderate-
severe AD.ACTIONS:
- low to moderate affinity, uncompetitiveN-methyl-D-aspartate receptor
antagonist that block the pathological butnot physiological activation of NMDA receptor.
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Memantine
DOSAGE:-
* 1st week > 5 mg PO OD
* 2nd week > 5 mg PO BID
* 3rd week > 10 mg PO am and 5 mg
PO in the evening* 4th week & thereafter > 10 mg PO BID
Treatment: Pharmacotherapy
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Treatment: Pharmacotherapy
Memantine
EFFECTS:
- to decrease the decline cognition and daily
functioning in patients with moderate to severeAD.
- combination with cholinesterase inhibitors hasbeen shown to be safe and effective with
cholinesterase inhibitor alone.
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Treatment: Pharmacotherapy
Vitamin E- considered in AD patients to slow diseaseprogression.
ACTION:- antioxidant; it slows nerve cell damage.
EFFECT:
- decrease the rate of functional decline of ADpatients.
- few drug interactions or side effects.
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TREATMENTNon-cognitive symptoms
-Antipsychotics
-Benzodiazepines-Antidepressants
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TreatmentNon-cognitive symptoms
Rationale:
To minimize psychotic symptoms
(paranoia, hallucinations )orindependent symptoms (e.g.screaming, violence).
To help to increase comfort andsafety of patients and families.
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Treatment :Non-cognitive symptoms
for psychosis and agitation
Principles in Tx:
-Intervention used should be directed
by the level of anguish experienced bythe patient and risk to caregivers andpatient.
-Violent behavior needs to be treatedwith pharmacotherapy.
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Treatment :Non-cognitive symptoms
For psychosis and agitation
Principles in Tx:
Agitation needs to be investigatedfurther to reveal underlying causes.
If agitation continues repeatedly,psychosocial measure should be the1st line therapy.
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Treatment :Non-cognitive symptoms
For psychosis and agitation
Principles in Tx:
If psychosocial measures areunsuccessful or if agitation is thought
to be dangerous to patient/caregiverthen pharmacotherapy is warranted.
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Treatment :Non-cognitive symptoms
For psychosis and agitation
1. ANTIPSYCHOTICS
- 2nd line therapy to control psychosis oragitation in demented patients.
- ATYPICAL agents are BETTER tolerated than typicalantipsychotics.
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Treatment :Non-cognitive symptoms
For psychosis and agitation
1. Antipsychotics
- choice of agent is based on the
side effect profile that is mostsuited to the patient.
- administered in the evening to help
sleep and treat sundowningeffect.
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Treatment :Non-cognitive symptoms For
psychosis and agitation
1. Antipsychotics
- oral route is preferred
- start with low doses; increase dosecarefully and cautiously.
* elderly are more sensitive to the side effects ofantipsychotic.
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Treatment :Non-cognitive symptoms For
psychosis and agitation
•Atypical or Novel Anti-psychotics
*Olanzapine (Zyprexa)
*Quetiapine (Seroquel)
*Clozapine (Leponex)
*Risperidone (Risperdal)
*Aripiprazole (Abilify)
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Treatment :Non-cognitive symptoms For
anxiety and agitation
2. Benzodiazepines
- for agitation, where anxiety is a prominent feature.
- useful as start doses for occasional agitation or whesedation is needed.
- risk of disinhibition, over sedation falls or delirium.
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Treatment :Non-cognitive symptoms For
anxiety and agitation
2. Benzodiazepines
- start with low doses; increase dose carefully andcautiously.
- short acting agents that do not require metabolism for
activation are preferred.- elderly are more sensitive to the side effects ofbenzodiazepines.
T N i i
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Treatment :Non-cognitive symptomsfor depression and apathy
3. Tricyclic antidepressants (TCA), MAOIs and SSRI
- may be used to treat depression
- SSRI are preferred agents
- occasionally cognitive deficits, may recover partially or
fully ( in pseudo- dementia) with treatment ofdepression.
T N i i
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Treatment :Non-cognitive symptomsfor depression and apathy
1. Tricyclic antidepressants (TCA), MAOIs and SSRI
- choice of agents depends on drug interactions, side effects and desiredaction:
a. TCAs have significant CVS side effects and anticholinergicproperties.
b. SSRI have better side effect profile
c. Dietary restrictions (high tyramine food), drug interactions andside effects tend to limit the usefulness of MAOIs.
T t t N iti t
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Treatment :Non-cognitive symptomsfor depression and apathy
1.Tricyclic antidepressants (TCA), MAOIs andSSRI
- Start with low doses; increase dose
carefully and cautiously.- elderly are more sensitive to the
side effects of antidepressants.
T t t N iti t
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Treatment :Non-cognitive symptomsfor depression and apathy
•Selective Serotonin Re-uptake Inhibitors
*Fluoxetine (Prozac)
*Sertralline (Zoloft)*Citalopram (Lupram)
*Paroxetine (Seroxat)
T t t N iti t
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Treatment :Non-cognitive symptomsfor depression and apathy
•Selective Norepinephrine – SerotoninReuptake Inhibitor
* Duloxetine (Cymbalta)
* Venlafaxine (Efexor)
T t t N iti t
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Treatment :Non-cognitive symptomsfor depression and apathy
•Tricyclics
*Imipramine (Tofranil)
*Maprotilline (Ludiomil)*Dothiapine (Prothiadine)
T t t N iti t
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http://slidepdf.com/reader/full/dementialec1-1 81/83
Treatment :Non-cognitive symptomsfor depression and apathy
•Reversible MAO-Inhibitor A
*Meclobemide (Aurorix)
•Other Antidepressants
*Tianeptine (Amineptine)
*Mirtazapine (Remeron)
*Trazodone (Depresil)
8/20/2019 dementiaLEC[1] (1)
http://slidepdf.com/reader/full/dementialec1-1 82/83
Long Term Goals Of lzheimer’s
Disease Management
•Monitor treatment of cognitive symptoms.
•Detect and treat non-cognitive symptoms.
•Balance supervision with meaningful activity.
•Educate and advise regarding prognosis and transitions.