About These Guidelines
As an initial step in developing this document, the Orange County
Vital Aging (OCVA) team reviewed published guidelines for managing
D i s C l A i m e r
dementia from the American Geriatrics Society, the American Academy of Family Physicians, and the College of Physicians. This provided a solid
These guidelines are intended to be informational only.
basis for guidance with demented patients.
These guidelines are not intended to be, and should
Because managing cognitive health in a primary care setting requires
not be considered, a substitute for medical or other
early intervention against all conditions that impair cognition, these
professional advice and clinical experience. Medical
guidelines cover a broad spectrum of physician behavior and decision-
procedures, treatments, and their outcomes are highly
making. All recommendations herein are founded on published
dependent on individual circumstances, and should
research in the fields of patient education, risk factors that affect
always be considered in the context of appropriate
cognitive health, medical practice management and logistics, cognitive
medical or other professional advice and clinical
assessment tools and methods, diagnosing medical conditions that
impair cognition, and treating medical conditions that impair cognition.
While information provided here is based on various
Best practices were gleaned from the medical literature and reviewed
published scientific studies and existing guidelines
by the OCVA Expert Panel Physicians to finalize the guidelines.
as of the time it was written, research on medical and health issues is constantly evolving, and dose schedules
OCVA expert Panel Physicians
for medications are frequently revised to reflect the most up-to-date knowledge. Readers must therefore
Valerie Acevedo, D.O. (Neurology)
always check product information and procedure instructions with the most up-to-date, published,
Alvin Chang, M.D. (Internal Medicine)
product information and data sheets, provided by the
Bruce Cleeremans, M.D. (Neurology)
manufactures, and the most recent codes of conduct and
John Gregory Duffy, M.D. (Psychiatry)
Sam Elsanandi, M.D. (Psychiatry)
The Orange County Vital Aging Program and its members make no representations or warranties to readers,
David Gehret, M.D. (Neurology)
express or implied, as to the accuracy or completeness
Jorge Rivero, M.D. (Family Medicine/Geriatrics)
of these guidelines, including without limitation that they make no representations or warranties as to the
William R. Shankle, M.D. (Neurology)
accuracy or efficacy of the drug dosages mentioned in
William Tsai, M.D. (Internal Medicine)
thee guidelines. The Orange County Vital Aging Program
James Weiss, M.D. (Internal Medicine/Pulmonary)
and its members do not accept, and expressly disclaim, any responsibility for any liability, loss, or risk that may be
Janice Young, M.D. (Neurology)
claimed or incurred as a consequence of the use and/or
Guidelines on pharmacologic treatment of Alzheimer's disease are
application of any of the contents of this material.
based on FDA approved "Prescribing Information." Certain portions of the prescribing information are appended with clinical expertise from the OCVA Expert Panel Physicians, to describe well-tested dosage and titration strategies.
Finally, the guidelines for treating Alzheimer's disease through psycho-
Table of Contents
social interventions are based on a thorough literature review by a key community partner in the OCVA Program:
Cordula Dick-Muehlke, Ph.D.
section 1 Clinical Path Overview
Executive DirectorAlzheimer's Family Services Center, Huntington Beach, CA
section 2 Educate Your Patients
section 3 Select Appropriate Patients For
section 4 Select Appropriate Cognitive
section 5 Diagnosis
5.1 Differential Diagnostic Workup for
Alzheimer's Disease and Related Disorders
5.2 Other Differential Diagnostic Workup
section 6 Treatment
6.1 Pharmacologic Treatment Strategies
for Alzheimer's Disease
6.2 Background For Pharmacologic
Treatment of Alzheimer's Disease
6.3 Psychosocial Interventions in MCI
and Early Alzheimer's Disease
section 1 OCVA Clinical Path Overview
1. educate Your Patients
Patients who are educated about the causes of memory loss, and
Clinical Path Overview
who are aware of risk factors for cognitive decline, are more likely
to proactively manage their cognitive health. This will help you intervene early when treatment can be most effective.
2. select Appropriate Patients For Assessment
The current medical insurance environment requires physicians to establish "medical necessity" before conducting a reimbursable
cognitive assessment. The criteria are clear and easily met. The
PATIENTS FOR ASSESSMENT
OCVA guidelines will help you offer the highest standards of care
Healthy Brain Checklist
within an economically viable model.
3. select Appropriate Cognitive Assessment method
There are 3 pathways for having your patients assessed for cognitive deficits. You may:
1. Perform an office-based assessment and earn reimbursement.
Objective cognitive assessment (e.g.
MCI Screen) positive?
2. Refer to your usual channels for neuropsychological evaluation, or 3. Refer to the OCVA memory assessment service.
Regardless of the assessment method chosen, your patients will likely remain in your care and need further management following
Diagnosis & Treatment
the assessment. The nature of this clinical management will
Any abnormality found in diagnostic
workups (e.g. history, lab work)?
depend on whether or not any cognitive impairment was objectively identified in the assessment process.
Negative - No Cognitive
Positive – Cognitive
physician has (If Preferred)
Reassure patient, educate
Pursue diagnosis of
them about risk factors they
underlying cause in
Diagnosis & Treatment
should manage, and plan to
accordance with OCVA
Any abnormality found in imaging
re-assess their memory in
Guidelines and monitor
cognition via quarterly memory assessment.
It is important to treat all underlying medical conditions that are causing the cognitive impairment, including Alzheimer's disease. Generally, the earlier the treatment starts, the better the outcome will be.
section 2 educate Your Patients
Patients who are educated about the causes of memory loss, and who
Patients For Assessment
are aware of factors that impact the risk of cognitive decline, are more
As described in more detail below, many patients should have their
likely to raise timely concerns about their cognitive health. Therefore,
cognition assessed while many others need not. Following these basic
well-educated patients are more likely to engage you constructively
guidelines will ensure that you offer your patient population the highest
and to receive a high standard of care from your practice.
justifiable standards of care in an economically prudent manner.
To address this opportunity, the OCVA program offers two free
establishing medical Necessity
educational brochures for your practice. We encourage you to order these OCVA brochures and make them available to your patient
Insurance companies, including Medicare, do not reimburse routine
memory assessment without medical necessity. Any one or more of the following establishes medical necessity:
About memory loss
• a cognitive concern expressed by the patient.
Educate Your Patients
This educational brochure explains
• a cognitive concern expressed by the patient's family member
the many common causes of memory
loss and emphasizes the importance
• a concern or observation by the physician or medical staff.
of early intervention to optimize
treatment efficacy, regardless of the
cause of the memory loss. The purpose
Office Visits for General (Non-Cognitive) Care
of this brochure is to encourage those
Regardless of the purpose of the patient's visit, it makes good sense
patients in your waiting room, who
to be vigilant about signs of memory loss in your "at-risk" or Medicare
have a memory concern, to express that
population, and to assess memory when medical necessity is met.
concern during their visit. You may order
The Healthy Brain Checklist is a short, check-box form that should be
the brochure from the OCVA Program.
provided to patients at registration for each visit to your office. This is an excellent mechanism for proactively identifying early problems and for enabling patients to document medical necessity for further
risk Factors for memory loss
assessment. Patients should have their memory assessed only if they meet
This educational brochure explains the many risk factors for memory
loss and other cognitive impairments. It also describes strategies for managing and reducing those risks. The purpose of this brochure is to
Be Aware of the "High risk" Group
help those patients who are in good cognitive health to manage their
Those patients aged 50 and older, with any one or more of the
risk factors and remain so. Please request materials from the OCVA
following risk profiles, warrant attention. They should have the
opportunity to either complete the Healthy Brain Checklist, or be engaged in a direct discussion about their cognitive health:
• Personal history of stroke or head injuries• Family history of AD or related disorders• Cardiovascular risks, including high cholesterol, hypertension,
obesity, and smoking
All of these patients are at higher risk for cognitive problems, but do
select Appropriate Cognitive
not meet medical necessity for further cognitive assessment based
section 4 Assessment method
solely on their risk profile. These patients should be made aware of their increased risk and have their memory assessed only if they meet
There are three pathways from which you can choose how best to have
medical necessity (as outlined above).
your patients assessed for cognitive deficits. Each pathway is equally effective and physicians should choose the one that best fits within the scope and capabilities of their practice.
medicare routine Physical exams
Beginning in January 2011, CMS will honor two new reimbursement
Three Pathways to Assess Your Patients
codes*, one for a "Welcome to Medicare Visit" that can be used within
1. You may perform an office-based assessment and earn
the first year of Medicare eligibility, and one for an annual "Medicare
Wellness Visit". The guidelines for each of these visits stipulate that
2. You may refer to your usual channels for neuropsychological
the physician assesses the patient for cognitive impairment. All of these
patients should complete the Healthy Brain Checklist.
3. You may refer to the OCVA memory assessment service.
* Centers for Medicare Services established the two following codes
1. Office-Based Assessment
taking effect on January 1, 2011:
Assessing memory in your office involves using a cognitive assessment instrument to objectively measure the patient's
• G0438 – Annual Wellness Visit; includes a personalized prevention
performance on a series of cognitive tasks, and then scoring
plan of service (PPPS), first visit
their performance in accordance with established means for their
• G0439 – Annual Wellness Visit; includes a personalized prevention
demographic peer group. There are many instruments available
plan of service (PPPS), subsequent visit
and several are briefly described below.
Any patient you see for an Annual Wellness Visit, who indicates a
concern on the Healthy Brain Checklist, should be further evaluated.
• mCi screen – This is the tool recommended, but not required, for
Guidelines for such further evaluation are summarized under "Select
Patients For Assessm
participating physicians in the OCVA program. It is a ten-minute,
Appropriate Cognitive Assessment Method"
electronically scored test of short-term memory and has the highest sensitivity for detecting mild cognitive impairment among
The Healthy Brain Checklist
all tests in the published literature. It can be administered by office
This short, check-box form can be completed by patients at
staff and is attractively reimbursed by Medicare and most private
registration in less than two minutes.
payers. It requires Internet connectivity at the point of care and a
licensing fee. Instructions for establishing an account with a free
Use it to identify early stage problems and to document medical
trial are available at:
necessity for an assessment.
Download at www.ocvitalaging.org/physician
• mini-mental state exam (mmse) – This was the original
standard for primary care assessment but is somewhat outdated and no longer reimbursed by Medicare and other payers. The primary advantage is that its 30-point scale is well known. The disadvantages are that it was designed to assess dementia (not mild cognitive impairment) and it is not sensitive for detecting subtle decline. Furthermore, it must be scored manually and there are no published norms to adjust for patient age and education
level. It takes about ten minutes to administer. The testing materials
section 5 Diagnosis
and scoring instructions can be purchased through:www.parinc.com.
Regardless of the results of the memory assessment (normal or abnormal), it is important to follow the guidelines that promote
• Clock Drawing Test - This is another well-known standard for
ongoing cognitive vitality for your patients.
assessing severe impairment and dementia (not mild cognitive impairment). The scoring is somewhat more subjective than the
Normal Assessment result
MMSE and it has equally poor sensitivity for detecting subtle decline.
If the patient does not show objective evidence of memory or cognitive
It is not generally reimbursed but it is free to use and usually quick
impairment, and that is clinically consistent with the physician's
to administer, taking from 3 to 6 minutes. A key point of difference
is that this tool tests visuo-spatial skills whereas most of the more
1. Reassure the patient and educate them about risk factors
common tools assess memory.
they should manage, and share the brochure "Risk Factors for
• montreal Cognitive Assessment (moCA) – This is a combination of
many brief neuropsychological tests that have been assembled into
2. Advise the patient to use the risk factor identification tool for
a battery with a 30-point scale like that of the MMSE. It is a relatively
Alzheimer's disease and related disorders (ADrD) at the OCVA
new test with growing validation for detecting dementia but minimal
website (www.OCVitalAging.org). This will make them aware of
data showing an ability to detect mild cognitive impairment. For use
their risks, as well as how best to manage them, according to
in a clinical setting, the MoCA requires the purchase of a licensing
agreement. Instructions for administering and scoring the MoCA are
3. Schedule the patient for re-assessment in 12 months to assure
that they remain cognitively healthy.
Abnormal Assessment result
2. refer to Usual Channels for Neuropsychological evaluation
If the patient shows objective evidence of memory or other cognitive
If you currently refer patients with memory complaints to a particular
impairment, then the cause of the problem should be diagnosed and
source for neuropsychological evaluation, there is no compelling
treated by using one of the following two options:
reason to disrupt that established approach. However, you might
1. Order ADRD Diagnostic Work-Up
consider using a simple, office-based assessment to determine which
Following the National Institute of Neurological and Communicative
patients should be referred.
Diseases and Stroke/Alzheimer's Disease and Related Disorders
The most important aspect of these guidelines is that you are vigilant
Association (NiNCDs-ADrDA) diagnostic guideline for ADRD will
in identifying subtle complaints and ushering the patient forward
generate an accurate diagnosis in more then 90% of cases.
along some constructive pathway toward a high standard of care.
These diagnostic guidelines are summarized in the following pages:
3. refer to OCVA memory Assessment service
You may wish to refer your patients to the OCVA Memory Assessment
• ADRD Diagnostic Work-Up Guidelines (Section 5.1)
Service at Hoag Hospital. Through this pathway, your referred
• Other Diagnostic Work-Up Guidelines (Section 5.2)
Select Appropriate Cognitive Assessm
patients will be assessed with the MCI Screen and the test results will be provided to you so that you can decide appropriate next steps in
2. Refer to an ADRD Specialist
accordance with those results. The OCVA has also assembled a panel
OCVA maintains a list of specialists who can accept referrals as needed.
of experts who can receive specialty referrals as needed.
To obtain the list, please contact the program Education and Screening
For more information, please contact:
Education and Screening Coordinator
Delivering an Alzheimer's Diagnosis
Differential Diagnostic Work-up
In recognition of the growing importance of Alzheimer's disease, the
5.1 for Alzheimer's Disease and related
National Alzheimer's Association held four regional town hall meetings
with more than 800 participants, including 300 people living with the disease. The outcome of the meetings, summarized as The 2008
routine ADrD diagnostic tests include:
Report: Voices of Alzheimer's Disease, identified diagnostic challenges and dissatisfying interactions with the medical community as key
a. Blood tests to exclude potentially contributing causes of
challenges to address.
cognitive impairment, including: • Chemistry panel: hyponatremia, hypocalcemia, hypercalcemia,
Several specific insights were voiced by the meeting participants and
hypokalemia, renal dysfunction, hepatic dysfunction,
published by the Alzheimer's Association as Principles for a Dignified
hyperglycemia, hypoglycemia, protein wasting.
Diagnosis. These insights from families and patients with Alzheimer's disease provide suggestions on how to improve the diagnostic
• CBC with differential: anemia, leukopenia, leukemia,
challenges and process that both patients and physicians face. These
thrombocytosis, thrombocytopenia, megaloblastosis,
lymphocytopenia, lymphocytosis, monocytosis, acute infection.
• Fasting lipid panel: low HDL (<45), high LDL (>100).
• Talk to me (a patient) directly, the person with dementia.
• Vitamin D-1,25(OH)2, B12, folate: vitamin deficiencies.
• Tell the truth.
• Homocysteine: homocysteinemia (>14).
• Test early.
• TSH, free T4: hypothyroidism, hyperthyroidism.
• Take my concerns seriously, regardless of my age.
• Deliver the news in plain but sensitive language.
b. Urinalysis: proteinuria, glucosuria, ketonuria, hematuria,
• Coordinate with other care providers.
c. Non-contrast MRI with volumetric assessment of hippocampus
• Explain the purpose of different tests and what you hope to learn.
(CT if MRI not possible). Radiologic interpretations consistent
• Give me tools for living with this disease.
with a diagnosis of:
• Work with me on a plan for healthy living.
• Recognize that I am an individual and the way I experience this
• Relatively greater atrophy in the hippocampus, medial temporal or
disease is unique.
• Alzheimer's is a journey, not a destination.
• Amount of ischemic vascular disease does not explain any
As a healthcare professional who touches patients' lives, you
might be interested in reading the short document Principles for a
• Absence of hydrocephalus, masses, or hemorrhages.
• Subtle amounts of atrophy may be missed. Therefore a negative
You may download the Principles for a Dignified Diagnosis document at
CT or MRI report (e.g., normal, age-related changes, mild
generalized atrophy) does not exclude Alzheimer's disease if there is objective cognitive impairment.
• Extensive ischemic white matter disease.
• Well-placed lacunar infarcts or hemorrhages in the hippocampus
• Large infarct of the anterior, middle or posterior cerebral artery.
5.2 Other Differential Diagnostic Work Up
• Medium to large cerebral hemorrhages, or residua thereof.
Tests that can be used to further confirm cognitive impairment not
Traumatic Brain Injury
due to Alzheimer's disease (AD) depend upon the patient's underlying
• Focal or asymmetric patterns of atrophy, especially in inferior
medical conditions and risks for possible:
frontal or anterior temporal lobes.
• Small, petechial hemorrhages, especially in the white matter.
• Radiation therapy, chemotherapy, anticonvulsants,
• Diffuse axonal injury, seen as focal areas of white matter
anticholinergics, antipsychotics, and chronic abuse or
demyelination, and blood residua.
dependence upon benzodiazepines, tranquilizers, anxiolytics or
Normal Pressure Hydrocephalus
• Ventriculomegaly greater than the degree of cortical atrophy.
Action: Withdrawal, reduction or substitution of the potentially
• Periventricular white matter increases in signal intensity
Organ and systemic Disorders
• Ballooning of the 3rd ventricle.
• Thinning of the corpus callosum.
• Lead, mercury, carbon monoxide, organophosphate
insecticides, toluene, industrial solvents.
if the routine ADrD diagnostic tests do not identify the
• Immunologic Disorders
etiology, then there are two possibilities:
• Systemic lupus, temporal arteritis, cerebral arteritis.
1. The objectively established cognitive impairment is a false
• Serum protein- and immuno-electrophoresis, specialized
positive result and the patient does not have a progressive
studies for cerebral vasculitis and immunodeficiency
2. The routine ADRD diagnostic tests were not sensitive enough
Action: Refer to rheumatology or immunology.
(a false negative result), and more specialized ADRD diagnostic
• Severe Pain Syndromes: MR of the spine or other affected body
testing is needed.
part, EMG/NCV studies.
There are five approaches to differentiating between these two
Action: Refer to pain specialty.
• Metabolic Syndrome
a. Repeat the same cognitive test now. Look for variability in
The US National Cholesterol Education Program Adult Treatment
performance to identify whether the previous result was a false
Panel III (2001) requires at least three of the following:
positive or false negative.
• Central obesity: Waist circumference ≥ 102 cm or 40 inches
b. Repeat cognitive testing with the same tests in 4 to 6 months
(male), ≥ 88 cm or 36 inches (female) or body mass index >
to look for change. This will establish whether there is a
progressive cause of cognitive impairment or not.
• Fasting Lipid Panel:
c. Refer to a neuropsychologist for a more comprehensive battery
of tests (if not already done) that can help better determine if
- Triglycerides: ≥ 150 mg/dl (≥ 1.7 mmol/L).
there is evidence of a progressive cognitive impairment and can
- HDL-C < 40 mg/dL (male), < 50 mg/dL (female).
help differentiate AD from non-AD causes.
- Blood Pressure ≥ 130/85 mm Hg
d. Refer to an ADRD specialist.
• Fasting plasma glucose ≥ 6.1 mmol/L (110 mg/dl).
Action: Refer to endocrinology, internal medicine, diabetology.
hallucinations, visual problems, executive dysfunction, aprexia.
• Diabetes or Pre-diabetes: Fasting glucose, HgbA1c.
• Frontal Temporal Lobe Disease: Usually age of onset is 50-60
Action: Refer to diabetology, endocrinology.
years old. Primarily affects frontal and temporal lobes. Loss of language, apraxia, personality changes, disinhibition or other
• Thyroid Disorders: Hypothyroidism, hyperthyroidism
behavioral abnormalities, and flat or inappropriate affect are early
• Cerebrovascular disease: Small and large strokes, subdural,
subarachnoid, cerebral, and intraventricular hemorrhages.
• Hungtington's Disease: Usually age of onset is 30-40 years old.
• Orthostatic blood pressures, carotid/transcranial Doppler,
Choreoathetosis, executive dysfunction, memory loss.
MR angiography, sedimentation rate, PT/PTT, coagulopathy studies.
• Creutzfeld-Jakob Disease: Movement disorder, insomnia,
Action: Refer to stroke neurology.
inattention, fatigue, and rapidly progressive dementia are characteristic. Any age can be affected. Abnormal periodic EEG
• Cardiovascular Disease: (Coronary artery disease, Arrhythmia,
Valvular Disease, Congestive Heart Disease, Cardiomyopathy): CRP, ECG, Cardiac Doppler, Holter monitor and other appropriate
• Traumatic Brain Injury: Can be progressive if multiple head injuries
or very severe single head injury with loss of consciousness.
Action: Refer to cardiology.
• Epilepsy: EEG studies.
• Sleep Disorders (Sleep Apnea, Myoclonus, REM Behavior Disorder,
Action: Refer to neurology or epileptology.
• CNS Infection (HIV, Cryptococcus, cysticercosis, neurosyphyllis)
Action: Refer to sleep specialist.
Action: Refer to infectious diseases.
• Pulmonary Disease (COPD, restrictive lung disease, other hypoxic
• CNS Demyelination (Multiple Sclerosis, Kufs disease,
Adrenoleukodystrophy, Metachromatic leukodystrophy, other
Action: Refer to internal medicine or pulmonology.
• Kidney Disease: GFR, urinalysis.
Action: Refer to neurology.
Action: Refer to nephrology.
• Liver Disease: Liver enzymes, hepatic encephalopathy.
Disorders Affecting The Central Nervous system
• Depression, Anxiety, Obsessive Compulsive Disorder: appropriate
history or standardized scale evaluation.
Action: Refer to psychiatry.
• Other Psychiatric Disorders
Action: Refer to psychiatry.
• Parkinson's Disease: Movement disorder followed by executive
dysfunction, visual-spatial deficits and memory loss at least several years later.
• Lewy Body Disease: Marked fluctuation in level of confusion,
loss of balance, difficulty walking, REM behavior disorder, visual
such as mental/physical exercise, and diet, as well as psychosocial
section 6 Treatment
intervention, careful management of co-morbid conditions such as
Optimal treatment follows accurate diagnosis of any underlying
diabetes and hypertension, and integrating community resources for
medical conditions. Guidelines for performing an accurate
patients and families.
diagnosis of conditions that impair memory are available in sections
For more details on the psychosocial components of optimal treatment,
5 of this guideline.
Treating Alzheimer's disease and related disorders (ADrD) requires a
• Psychosocial treatment of AD (Section 6.3)
robust approach that includes:
Community resources that support appropriate psychological
• Identification and treatment of common medical conditions
interventions are available at:
• Pharmacologic treatment
• Non-pharmacologic treatment
Pharmacologic Treatment strategies
identifying and Treating Common medical Conditions
6.1 for Alzheimer's Disease
Untreated, or not well-controlled common medical conditions, such as thyroid disease, vitamin deficiency, heart disease, and diabetes frequently cause memory loss. Similarly menopause and testosterone
For a full discussion of the background for the pharmacologic
deficiency, various medications, and depression can also cause
treatment strategies given below, please see Section 6.2
memory loss. It is important to make sure that these conditions are
"Background for Pharmacologic Treatment of Alzheimer's Disease."
well controlled and monitored regularly. Treatment guidelines for those
Also please note that the indicated treatment efficacy will differ
conditions are widely available from a variety of sources.
from patient to patient, and may not be expected for all patients
with Alzheimer's disease (AD).
Pharmacologic Treatment of ADrD
Like many other diseases, early detection and treatment of ADRD is
Overall Treatment strategy
the key to successful treatment outcomes. For Alzheimer's disease
Although there is considerable variability between patients with AD,
(AD), there is a substantial body of evidence showing disease-delaying
there is a substantial body of evidence showing disease-delaying
effects using combined therapy of a cholinesterase inhibitor (Exelon®,
effects using combination therapy of a cholinesterase inhibitor
Razadyne®, Aricept®) and memantine (Namenda®). Because these
(Exelon®, Razadyne®, Aricept®) and memantine (Namenda®). Because
effects occur at all clinical stages of AD, it is imperative to initiate
these effects occur at all clinical stages of AD, it is imperative to initiate
combined therapy as early as AD is detected, and continue patients on
combination therapy as early as AD is detected, and to continue
combined therapy until they reach the hospice terminal stage of AD.
patients on combination therapy until they reach the hospice terminal
For more details, please review:
Available evidence on the efficacy of the cholinesterase inhibitors in
• Pharmacologic treatment of AD (Section 6.1)
delaying AD progression indicates that:
• Rationale for Pharmacologic treatment of AD (Section 6.2)
• Aricept® is likely to provide disease-delaying effects for 1-3 years.
Non-Pharmacologic Treatment of ADrD
• Razadyne® is likely to provide disease-delaying effects for
Non-pharmacologic interventions have been recognized as
important components of an optimal treatment strategy. Such
• Exelon® is likely to provide disease-delaying effects for 1-4 years.
interventions include, but are not limited to, life style modifications
Therefore, after 1-3 years of treatment with Namenda plus Aricept
Aricept Dosing schedule
or Razadyne, patients may benefit by switching to Namenda plus the
Exelon patch, particularly if more rapid decline has recently occurred.
® (donepezil HCl) Tablet
Aricept is a prescription medication to treat mild, moderate and severe
step 1: set and manage expectation About Treatment
AD. It is available in 5, 10, and 23 mg/day in tablet form. The starting
Before starting new medications, it is always helpful for patients and
dose is 5 mg/day and can be increased to 10 mg/day after 4-6 weeks of
family members to understand what to expect from these treatments.
treatment and good tolerability. Similarly it can be increased to 23 mg/
Frequently patients and caregivers have unrealistic expectations and
day after at least 3 months of treatment and good tolerability.
don't realize that "not getting worse" means that the medications are working. Since AD is a progressive degenerative disease, "stabilizing"
the symptoms can be a positive outcome. Patients should also understand that finding the right combination of medications and dosages is a process that may take months. Finally, physicians should
Stop Aricept: related side
eﬀects should resolve
make it clear that some percentage of patients may not respond in any
No side eﬀect /
within 3-5 days.
meaningful way to the treatment.
Wel tolerated for 4-6 weeks
• If side eﬀects resolve
Therefore, setting the right expectations will help patients and family
(Aricept-related), then use
members approach the treatment process with a constructive mindset
inhibitor or go back to the
and a realistic idea about the course ahead.
step 2: start Cholinesterase inhibitor
• If side eﬀects do not resolve,
they are not Aricept-related,
(Aricept®, exelon®, razadyne®)
No side eﬀect / Wel tolerated
and medical evaluation to
It is important to choose the correct cholinesterase inhibitor and
for 3 months or longer.
identify the cause of the side eﬀects is indicated.
its maximum, well-tolerated dose within the approved range. This
process may take weeks to months, and it is always recommended to objectively measure the treatment effect on memory and function after achieving a stable optimal dose.
For more details, please see:
• Aricept Dosing Schedule• Exelon Dosing Schedule• Razadyne Dosing Schedule
Loss of eﬀect
Consider switching to other
after 1-3 years?
step 3: Add memantine (Namenda®)
After reaching the optimal dose of the chosen cholinesterase inhibitor,
add Namenda and find the maximal dose, from 5 to 20 mg, that is well
*Take at dinner or bedtime.
tolerated without side effects. After achieving a stable optimal dose, it
If nightmares or vivid dreams
is always recommended to objectively measure the treatment effect on
occur, then take it in the a.m.
memory and function.
For more information, please see:
• Namenda Dosing Schedule
exelon Patch Dosing schedule
razadyne er Dosing schedule
® (rivastigmine transdermal system)
Razadyne® ER (galantamine hydrobromide extended-release)
Exelon Patch is a prescription medication to treat mild to moderate AD. It is available in 4.6 and 9.5 mg/day. The starting dose is 4.6 mg/
Razadyne ER is a prescription medication to treat mild to moderate
day and can be increased to 9.5 mg/day after a minimum of 4 weeks of
AD. It is available in 8, 16 and 24 mg/day. The starting dose is 8 mg/
treatment and good tolerability.
day and can be increased to 16 mg/day after a minimum of 4 weeks of treatment and good tolerability. Similarly, it can be increased to 24 mg/day after a minimum of 4 weeks of treatment and good tolerability.
Remove Exelon patch:
side eﬀects should
resolve within 2 days.
• If side eﬀects resolve
No side eﬀect / Wel tolerated for
(Exelon-related), reapply the
a minimum of 4-6 weeks
patch over the abdomen.
Stop Razadyne ER:
This will reduce the actual
No side eﬀect / Wel tolerated
Related side eﬀects
dose to 3.1 mg and 6.7 mg in
for a minimum of 4 weeks
should resolve within
4.6 mg and 9.5 mg patch,
respectively. If not well tolerated, then use alternate
• If side eﬀects resolve
(Razadyne-related), then use alternate
• If side eﬀects do not resolve,
they are not Exelon-related,
and medical evaluation to
or go back to the prior
identify the cause of the side
No side eﬀect / Wel tolerated
eﬀects is indicated.
for a minimum of 4 weeks
Loss of eﬀect
• If side eﬀects do not
after 1-4 years?
resolve, they are not
Consider switching to other
medical evaluation to
identify the cause of the
*Apply the patch to the upper body (chest, shoulder,
side eﬀects is indicated.
Stay on Exelon Patch
back) each a.m., and remove the previous day's patch. Rotate the site to avoid skin irritation.
Loss of eﬀect
Consider switching to other
after 1-3 years?
*Take after breakfast or dinner to avoid GI upset.
Stay on Razadyne ER
Namenda Dosing schedule
Namenda Dosing schedule
(Possible alternative approach)
(Recommended by manufacture)
Alternatively, because the terminal elimination half-life is 60-80 hours,
Namenda (memantine HCl) is a prescription medication to treat
Namenda may be given as a once a day drug. Also, the time to steady
the symptoms of moderate to severe AD. It is available in 5 and
state is 3 weeks. For this reason, Namenda may be better tolerated by
10 mg tablets.
changing dose every 2 weeks instead of every week during titration.
One 5 mg tablet in am
Stop Namenda: Related
side eﬀects should
resolve within 3-14 days.
No side eﬀect /
• If side eﬀects resolve
Wel tolerated for 2 weeks
(Namenda-related), then the
One 5 mg tablet in am & one 5 mg tablet at night*
dose should be reduced by
5mg. If this does not work, patient may not be able to
• If side eﬀects do not resolve,
One 10 mg tablet in am & one 5 mg tablet at night
they are not Namendarelated, and
No side eﬀect /
Wel tolerated for 2 weeks
medical evaluation to
identify the cause of the side eﬀects is indicated.
One 10 mg tablet in am & one 10 mg tablet at night
No side eﬀect /
Wel tolerated for 2 weeks
*For patients with severe renal impairment, 5 mgtwice daily is the recommended dose.
*Take in am. If experiences
drowsiness, take at bed time.
step 4: monitor Cognition and Function every 3 to 6 months
Depending on the structure of any given practice, reimbursement
for performing cognitive assessment may be an important
After optimizing the doses of both the cholinesterase inhibitor and
consideration in the selection of the most appropriate assessment
namenda, schedule follow-up visits every 3-6 months and measure
tool. The MCI Screen is generally reimbursed by Medicare and
memory and function. See patients earlier if problems develop.
most major insurers, the MOCA and the Clock Drawing Test may
Regular monitoring is critical for:
each be reimbursed in some situations, and the MMSE is almost
• Measuring treatment efficacy
universally not reimbursed.
• Deciding if treatment modification is indicated
step 5: evaluate Unexpected Changes
• Identifying co-morbid conditions (see step 5)
Sudden or subacute changes, or development of symptoms that are
• Educating patients and families about the importance of staying
out of sequence with that expected by FAST staging, are not typical of
AD progression. The most common reasons for such changes are:
Quite often, there is a misconception among patients and families
• Infection: Urinary Tract infection, aspiration pneumonia.
that the treatment is not working because the patient is not getting
• Trauma: Unobserved falls, particularly if head injury occurred.
better. However, in degenerative disorders such as AD, "being stable"
• Metabolic: Dehydration due to altered patterns of eating and
or "getting worse at a slower rate" is a positive treatment effect that
improves quality of life and can substantively reduce healthcare costs.
• Iatrogenic: Compliance problems, anticholinergics, anti-anxiety,
Regular monitoring can be quickly and accurately done within the
constraints of a routine follow-up visit.
• Exacerbation of an existing medical condition.
• Development of a new medical condition.
Assessment tools such as the Functional Assessment Staging
• Environmental: Changes in residence, light level, noise level,
(FAST), the Dementia Severity Rating Scale and the Clinical
routine, caregiver, sleeping pattern or activity level.
Dementia Rating Scale can be used. The FAST staging instrument which takes several minutes to complete, assesses the patient's
Additional Information on Cholinesterase Inhibitors
level of severity and provides a variety of useful other pieces of information, such as the patient's developmental age, approximate
MMSE score, and expected duration per FAST stage for untreated
Optimal Dosing of Aricept (donepezil): The primary mechanism of action
AD. The Clinical Dementia Rating Scale takes more time to
is likely to be acetylcholinesterase inhibition. However, clinically, this
administer in clinical practice (about 10 to 20 minutes) and is more
effect is observed to disappear within 1-2 years. One should find
widely used in clinical research settings.
the highest dose among 5, 10 or 23 mg that causes no side effects.
Because all of the Aricept 23 mg studies are 6 months, there are
Cognitive assessment tools such as MCI Screen, MOCA, MMSE
no published data to indicate that 23 mg prolongs the duration of
and Clock Drawing can be used (see section 4). Note that these
tests differ greatly in their sensitivity and specificity. For example,
Potential Aricept Side Effects: Side effects occur in 9-19% of patients
the MMSE and Clock Drawing tests are not sensitive for detecting
and are dose dependent. Loss of appetite, nausea, diarrhea, dizziness,
or monitoring the mild cognitive impairment stage of AD, and
syncope, lightheadedness and nightmares are the most common.
should be restricted to patients in the dementia stage. The MOCA
These side effects usually resolve within 3-7 days of stopping Aricept
is intermediate in sensitivity and specificity, and the MCI Screen
because the elimination half-life is 70 hours. If side effects resolve,
has the highest sensitivity and specificity for discriminating
Aricept can be restarted at the next lower dose, and the side effects
normal aging from mild cognitive impairment and dementia. The
usually do not reappear.
MCI Screen has also been well validated as an effective tool for monitoring changes in mild cognitive impairment and dementia.
For more information: www.aricept.com
Additional Information on Memantine
Optimal Dosing of Exelon Patch: The optimal dose is the highest well-
tolerated dose, ranging from 3.1 mg to 14.3 mg per day. The dose of
the patch is approximately 1/3 lower when applied over the abdomen
Optimal Dosing of Namenda: The optimal dose of Namenda is the highest
compared to the upper body (i.e., 4.6 and 9.5 mg patches applied to the
one from 5 to 20 mg daily that is well tolerated. Because of Namenda's
abdomen give 3.1 and 6.7 mg doses respectively). The FDA approved
72-hour half-life, it can be given once daily without difficulty. It usually
doses are 4.6 and 9.5 mg daily. However, the phase III FDA clinical trial
does not cause drowsiness, so it can be given in the a.m. If it causes
showed further improvement in cognition for doses up to 19 mg daily,
drowsiness, give at bedtime.
but there were more side effects above the 9.5 mg dose. When patients
Potential Namenda Side Effects: Side effects occur in about 5% of
tolerate the 9.5 mg dose, then one can try increasing the dose to 14.3
patients, are dose dependent, and almost always occur within 3 to
mg (see below).
7 days after a dose increase. The most common ones are agitation,
Potential Exelon Patch Side Effects: Side effects occur in 5-6% of patients
irritability, confusion or a general worsening of function. If a side effect
and are dose dependent. Skin irritation is the most common one,
occurs, then lower the dose by 5 mg and continue that lower dose. If
followed by loss of appetite. These side effects usually resolve within
side effects are mild, they may resolve on their own over a few weeks
two days of stopping the patch because the elimination half-life is 3
without lowering the dose.
hours. If side effects resolve, the patch can be restarted at a lower dose,
For more information: www.namenda.com
and the side effects usually do not reappear.
For more information: www.exelonpatch.com
Background For Pharmacologic
6.2 Treatment of Alzheimer's Disease
Abeta42, the 42-amino acid breakdown product of the amyloid
Optimal Dosing of Razadyne ER (Galantamine ER): The primary mechanism
precursor protein, self-aggregates to form oligomeric clusters of
of action is likely to be the presynaptic nicotinergic receptor
Abeta42. There is an extensive body of research supporting a major
modulation, which increases multiple neurotransmitters to a mild
role for oligomeric Abeta42 in the pathogenesis and clinical expression
degree, and stimulates three neuroprotective mechanisms—reduced
of Alzheimer's disease (AD).1-4 Human post-mortem studies have
cholinergic neuron damage, increased degradation of amyloid
shown that patients receiving acetylcholinesterase (Ache) inhibitors
precursor protein along the non-amyloidogenic pathway (sAPP-alpha),
have lower levels of cortical Abeta42 than those not receiving AchE
and reduced glutamate-mediated excitotoxicity. One should therefore
inhibitors.5 Furthermore, animal models of AD have shown that
find the highest dose, from 8 to 24 mg, without side effects.
AchE inhibition reduces Abeta42 production. Studies from the
Potential Razadyne ER Side Effects: Side effects occur in about 4% of
Karolinska Institute have shown that cerebrospinal fluid levels of
patients and are dose dependent. Loss of appetite, nausea, diarrhea,
AchE and butyrylcholinesterase, which correlate very well with brain
dizziness, syncope, lightheadedness and bradycardia are the most
cholinesterase levels, remain inhibited by at least 50% below baseline
common. These side effects usually resolve within 2-5 days of stopping
after 1 year of Exelon treatment of AD patients.6 Also, the type of AchE
Razadyne ER because the elimination half-life is about 14-24 hours (for
inhibited by Exelon favors protection against synaptic damage.7 In
the non-extended release form of Razadyne, half-life is 7 hours). If side
contrast, after 3 months of treatment, cerebrospinal fluid AchE levels
effects resolve, Razadyne ER can be restarted at the next lower dose,
are 200% above baseline with Aricept, and are no longer reduced
and the side effects usually do not reappear.
by Razadyne. AchE-R, the neuroprotective, or read-through, form of AchE, is reduced relative to AchE-S, the form associated with synaptic
For more information: www.razadyneer.com.
damage. The neuroprotective/neurodestructive ratios of Exelon, Aricept, and Razadyne are 1.4, 0.6 and 0.4 respectively.7
The longest prospective clinical study was done at Harvard by Atri et al.,8
Longer duration studies of galantamine (Razadyne) also support
in which AD patients at all clinical stages received either no treatment
that it may delay AD progression. A 3-year open label extension of a
(N=144, 1990-95), cholinesterase inhibitor (Chei) therapy only (N=122,
randomized, double-blind trial of Razadyne vs. placebo showed a 50%
1998-2005), or Namenda plus a CheI (N=116, 1998-2005) for up to four
reduction in the rate of cognitive decline compared to expected rate of
years. Rates of cognitive and functional decline were carefully statistically
decline on placebo using a matched patient sample.17
analyzed. The Namenda plus CheI group showed a 33% delay in the rate
Longer duration studies of Aricept indicate that it may delay AD
of functional decline in AD patients starting with minimal functional
progression for up to 3 years in certain subgroups. The rate of
impairment (equivalent to mild cognitive impairment), a 60% delay in AD
conversion from MCI to AD dementia over 3 years was reduced in a
patients starting with mild dementia, and a 50% delay in AD patients who
subset of depressed AD patients.18 A 1-year, open label extension in
were moderately severely demented. This finding was consistent with
severe AD patients treated with Aricept found that they did not decline
a 12-month, quantitative, volumetric MRI study in mild to moderately
in behavior or functional abilities, but that these benefits were lost if
demented AD patients, in which monotherapy with either Namenda9 or a
treatment was discontinued for 1 month or longer.19 A 1-year, double-
CheI10 delayed the rate of hippocampal atrophy.
blind, placebo-controlled trial of MCI patients treated with Aricept
In contrast to the disease-delaying effect of combined therapy, the Atri
showed no difference in functional abilities and overall severity over the
et al. study showed that AD patients receiving no treatment showed
2 years, but did show a slight reduction in rate of cognitive decline.20 A
the same rate of decline as patients receiving CheI monotherapy. An
3-year open label extension of mild-to-moderate AD patients treated
independent study by the Pfizer global research team provided further
with Aricept showed cognitive and functional decline over the study
information about the treatment effect of CheI monotherapy.11 They
that did not differ between patients initially treated during the first six
performed a meta-analysis of randomized, placebo-controlled, CheI
months of the study (the duration of the randomized part of the trial)
trials for up to 12 months, and found no difference between placebo and
with Aricept or placebo.21 Another 3-year open label extension study of
Aricept or Razadyne in the rate of cognitive decline. There was only one
AD patients treated with Aricept found small but statistically significant
double-blind, placebo controlled, randomized trial of Exelon lasting 12
reductions in the rates of cognitive and functional decline, but not
months, which suggested a delay in rate of cognitive decline.
global decline.22 Another open-label study of Aricept for up to 4 years
Longer duration studies of rivastigmine (Exelon) support that it may
found reduced rates of cognitive and functional decline for the first 2
delay AD progression, at least in certain sub-populations. A re-analysis
years, but no change in rates of institutionalization at 3 years.23 Overall,
in 2010 of the randomized, placebo-controlled, Exelon study lasting up
Aricept appears to slightly delay cognitive and/or functional decline for
to 4 years found a 25% reduction in the rate of conversion from MCI
not longer than 2-3 years.
to AD for Exelon-treated patients, particularly females.12,13 A 5-year
Although the above findings are not absolute, they suggest that the
open label extension study of Exelon in 32 AD-treated patients showed
largest disease-delaying effect among the CheIs is with Exelon, both
stabilization in cognition, function and severity for 2-3 years. Of the 8
in terms of amount and duration of delay (i.e., the only CheI with
patients who remained in the study at 5 years, 2/3 of them had started in
5-year data for at least some patients). The evidence for Aricept and
the high dose Exelon group.14 A 2-year study comparing Exelon to Aricept
Razadyne suggests a smaller disease-delaying effect that can last for
found that moderate-to-severe AD patients under 75 years old declined
up to 2-3 years. More importantly, the Harvard study indicates that
less in severity and functional abilities on Exelon. AD patients over 75
combined therapy with Namenda and a CheI delays rate of cognitive
years old responded the same to Exelon and Aricept over 2 years.15 Two
and functional decline at all clinical stages of AD by 33% to 60%, which
open label extension studies, each lasting two years, compared the
means that one should attempt to detect AD as early as possible and
course of Exelon-treated AD patients vs. the expected cognitive decline
maintain combined therapy as long as possible. A reasonable strategy,
from historical, untreated AD controls. Both studies found clinically
therefore, would use any of the CheIs with Namenda during the first
meaningful reductions in the rate of cognitive decline on Exelon that
two to three years, depending upon the patient's course, and switch to
influenced overall severity.16 These longer duration Exelon studies
one of the other CheIs and Namenda when patients begin to show a
provide the strongest support for a disease-delaying effect among the
more rapid decline.
care manager who can assess family needs, help caregivers navigate
Psychosocial interventions in mCi
the health care system and community resources, and serve as a coach
and early Alzheimer's Disease
has been shown to improve caregiver quality of life, social support,
mastery of caregiving, and confidence.41,42 Additionally, quality of care,
Psychosocial interventions are a key component of treatment for
as measured by adherence to guidelines, was dramatically higher in
the non-cognitive symptoms of MCI and early Alzheimer's disease.
patients who were assigned a care manager than those who were not.42
According to two recent literature reviews, 35-85% of individuals with MCI exhibit behavioral abnormalities.24,25 Individuals with MCI
exhibit an average of 2.3 neuropsychiatric disturbances, with some
Caregiver education has proven benefits for both the caregiver and
experiencing as many as 9.6 symptoms.26 There is no typical profile of
person with MCI or early AD. Studies have investigated a variety of
neuropsychiatric disturbances in MCI or mild AD as these symptoms
educational programs, which vary in content (e.g., caregiver self-care,
are heterogeneous and unpredictable.27 Across studies, depression,
behavior management), format (single- or multiple-session), and
apathy, anxiety, and irritability are the most common neuropsychiatric
complexity (i.e., offered independently or as part of a multicomponent
symptoms in MCI.24,25 Compared to cognitively intact older adults,
intervention). Key outcomes for caregivers include significant
persons with mild AD were at significantly greater risk for apathy (Odds
improvements in knowledge of Alzheimer's disease,43 ability to
Ratio = 42) and depression (OR = 17).28 Neuropsychiatric disturbances,
cope with the dementia,43 depression,44,45 anger,46 burden,45 use of
like the cognitive and functional symptoms of MCI and AD, worsen with
adaptive coping strategies,44 self-efficacy46 and response to difficult
behaviors.45 Additionally, caregiver education can also significantly
Psychosocial interventions to alleviate neuropsychiatric symptoms
reduce the actual frequency of behavior problems,47 with key patient
are critical given their deleterious consequences, including increased
outcomes including stabilization,43 and significantly reduced agitation
risk of conversion from MCI to AD,30 greater functional dependence,31
heightened risk for institutionalization,32 shorter survival time,33 and higher levels of burden and depression among caregivers.34
Early-Stage Groups Early stage groups that incorporate education and support for
evidence Base for Key early Psychosocial interventions
both individuals with MCI or early Alzheimer's disease and their care partners have proven beneficial in the literature. While early
Caregiver Counseling and Support
stage groups vary, they typically include parallel support sessions
In a series of studies, Mary Mittelman and her colleagues at New
for persons with early memory loss and their care partners, and an
York University demonstrated that early access to a combination of
educational component. A recent randomized controlled clinical trial
counseling (i.e., 2 family and 4 individual sessions), a caregiver support
demonstrated that participation in an early stage group can improve
group, and ad hoc telephone consultation lowered the rate of nursing
quality of life for the person with MCI or early AD, as evidenced in
home placement by 28.3%, delayed institutionalization by 557 days,35
significantly reduced depression and behavioral symptoms, improved
and resulted in other significant benefits for caregivers, including
family communication, enhanced feelings of self-efficacy, and better
reduced depression,36 better self-rated health,37 improved satisfaction
emotional and social functioning.49
with support network,38 and greater tolerance for a loved one's memory and behavior problems.39
Cognitive StimulationA number of studies have now demonstrated that cognitive
stimulation can have additive effects over and above those accrued
Effective management of MCI and early AD requires an integrated
by the acetylcholinesterase inhibitors and Namenda. In Requena et
approach to care that encompasses medical care, psychosocial
al.,50 persons with mild AD who received a combination of cognitive
interventions, community services, and family resources.40 Access to a
stimulation and 10 mg of Aricept showed less decline on measures
of overall mental status (MMSE), cognitive functioning (ADAS-
examples – Psychosocial interventions as a
Cog), and functional abilities (FAST) across 2 years than their peers
Component of Treatment in mCi and early AD
receiving no treatment or medication alone. Subsequently, Niu et al.51
demonstrated that cognitive stimulation significantly improved apathy
1. A 56-year-old male corporate executive with multiple domain
and depression/dysphoria in persons with mild-to-moderate AD. In
MCI who can no longer work or drive, is spending a lot of time
MCI, a 4-week cognitive intervention that included activity planning,
sleeping at home, and exhibits depressed affect. Patient is receiving
self-assertiveness training, relaxation techniques, stress management,
acytelcholinesterase inhibitor and anti-depressant. Patient has high
use of external memory aids, memory training, and motor exercise,
degree of insight into how MCI has affected him. Caregiver is highly
resulted in significant improvements on measures of activities of daily
motivated to seek services for patient and self.
living, mood, and verbal and nonverbal episodic memory.52 Options
• Refer patient for individual counseling
for cognitive stimulation include computer-based programs and
• Refer patient and caregiver to early stage support group
participation in an early stage day program.
• Educate couple regarding need for meaningful, purposeful, and
pleasurable activity, and suggest options such as volunteering and early stage day program
Given the changes in motor53 (e.g., walking speed, standing balance) and higher level functional abilities54 that are already evident in MCI
• Educate couple regarding benefits of cognitive stimulation and
and early AD, in addition cognitive decline and neuropsychiatric
options, including at-home computer-based programs and early
symptoms such as depression, exercise can play an important role in
stage day program
maintaining physical, mental and emotional well-being. In MCI, walking
• Promote exercise for positive benefits on cognition and mood
150 minutes per week for 6 months resulted in significant improvement
2. A 75-year-old homemaker with amnestic MCI being cared for by her
on the ADAS-Cog,55 better than that achieved by Aricept alone over
81-year-old spouse who is physically frail and has multiple chronic
the same period.56 Aerobic exercise (e.g., treadmill, stationary bike)
health conditions. Patient will not acknowledge memory loss, is
sufficient to elevate heart rate to 75-85% of reserve improved cognitive
resistant to services, and husband feels overwhelmed.
function, particularly executive skills, in women with MCI.57 In AD,
• Refer for care management support to assist caregiver to
physical activity has also been associated with reduced depression,58
assess both patient's and caregiver's needs, assist with patient's
better physical health52 and longer survival time.59 Among older
resistance and problem-solving, and coordinate care and
adults, other health benefits of exercise have been documented for
community resources for patient and/or caregiver
depression,60 quality of life,61 falls,62 cardiovascular function,63 and disability.64
• Promote use of caregiver support group and educational
opportunities related to caregiving
Purposeful and Pleasurable Activities
3. A 65-year-old man with early AD, living alone, estranged from
Given the gradual loss of ability to engage in previously meaningful
family, and relying on support of neighbor. Patient retains some
work and leisure activities, and the high frequency of apathy and
insight into his condition, but insists on living alone, has been the
depression in MCI and early AD, it is critical to encourage affected
victim of a scam, and continues to drive short distances. It appears
individuals to become involved in purposeful and pleasurable activities.
patient may be missing medications. Patient has minimal resources.
Simply increasing the frequency and intensity of pleasurable activities
• Refer to Adult Protective Services due to self-neglect for possible
in AD has been shown to alleviate depression.65 In MCI and early AD,
conservatorship and coordination of services.
individuals may be able to continue participating in some activities
• Report patient to DMV for driving evaluation/license revocation.
relatively independently with encouragement and support (e.g., appropriate transportation) by caregivers. Early stage day programs, however, offer a venue for meaningful, pleasurable activities, cognitive stimulation, and peer support, while relieving the caregiver.
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Orange County Vital Aging Program
HOW TO CREATE A STRUCTURAL SUMMARY Rapid Reference 4.1 Preparing the Transparency Template HOW TO CREATE A STRUCTURAL 1. Photocopy the templates from Appendixes 5a and 5b onto an 8'' x 11'' SUMMARY FOR THE RORSCHACH transparency. Do not enlarge or reduce the size of the form. (It's ofteneasiest to take the book to a full-service photocopy store where you canpurchase a single transparency and have them photocopy it for you.)
Differential Diagnosis of NICO Lesions Wesley E. Shankland, II, D.D.S., M.S., Ph.D. TMJ & Facial Pain Center The diagnosis and treatment of orofacial pain are challenges to the clinician as well as frustrating to the one afflicted. At least two reasons account for these observations. Anatomically, the orofacial region is one of the most highly innervated areas of the human body, especially the oral cavity. Referred pain patterns, collateral innervation, and multiple innervations of structures all confuse a person's perception as to the location of the pain generator (i.e., a lesion or injured structure). This honest confusion complicates the doctor's diagnostic attempts.