DEMENTIA AND COGNITIVE IMPAIRMENT

EPIDEMIOLOGY, DIAGNOSIS AND TREATMENT

KEYWORD

• Clinicians should be knowledgeable about the various neurocognitive disorders, which are common and severe in
elderly adults
• Diagnosis requires careful history and skilled clinical assessment, followed by appropriate laboratory investigators
• Diagnostic imaging can be useful when interpreted by experts familiar with these conditions
• Biomarkers for most of these disorders are still being validated and are not yet recommended for clinical use
• Referral to specialists can be valuable for spesific purpose, such as neuropyschologists for objective cognitive
testing and interpretion; neurologist for diagnosis, particulary of less common disorders; geriatric pyschiatrists
when there are pyschological or behavioral changes
• Drug treatments at present provide symptomatic relief. Psychososial and other supportive therapies are essential
INTRODUCTION

 When elderly patients and their families report symptomps of memory loss  experienced clinicians know that
these concerns refer to a range of cognitive abilities not just memory.
 The clinician’s first challenge is to indentify the cognitive changes that are clinically significant.
 The second challenge is to determine the cause of cognitive impairment (underlying causes).
 This article is describes these entities and their diagnoses using the framework of the recently published fifth
editions of the American Psychiatric Association’s Diagnostic and Statistical Manual, Fifth Edition (DSM-5)
Dementia
• Typically diagnosed when cognitive impairment has become
sever enought to compromise social and/ or occupational
functioning
• Requires substantial impairment to be present in one or
more cognitive domains
• The impairment must be sufficient to interfere with
independence in everyday activities
Mild Cognitive Impairment
• A state intermediate between normal cognition and
dementia, with essentially preserved functional abilities
• Made when there is modest impairment in one or more
cognitive domains
• The impairment must represent a decline from previously
higher level should documented by history and objective
assessment
IMPACT OF DEMENTIA

 In United States, alzheimer’s disease (AD) is leading a cause of death, hospital admissions, skilled nursing facility
admissions, and home health care. The costs of health services and the informal costs of unpaid caregiving for
individuals with dementia are high and growing.
 Family caregivers also experince increased emotional stress, depression, and health problems.
 In absolute number 35,6 million people worldwide were estimated to be living with dementia in 2010, a number
expected to reach 115,4 million people by 2050.
DEMENTIA IN POPULATION

 Prevalence is a function of both incidence and duration. Because most dementia are not curable, their duration
reflects how long individuals live with their dementia.
 Thus, the public health burden dementia depends both on the development of new cases and on the survival of
those cases after onset.
PREVALENCE

 Prevalence dementia increases exponentially with increasing age and doubles every 5 years after age 65 years.
 In high countries, prevalence is 5% to 10% in those aged 65 years, and is usually greater among women then
among men, in large part because women live longer than men.
 Higher prevalence has been reported in African American and Latino/Hispanic populations than non-Hispanic
populations.
 Global systemic reviews and meta analyses suggest that prevalence of dementia is lower in sub-Saharan Africa and
higher in Latin America than in the rest of the world.
INCIDENCE

 The incidence of dementia increases steadily until age 85 or 90 years, and then continues to increase but less
rapidly. It is either similiar in men and women or slightly higher in women.
 Annual age specific rates ranged from 0,1% at age 60-64 years to 8,6% at age 95 years.
RISK AND PROTECTIVE FACTORS
Demographic Risk Factors
• Increasing age, higher among woman, lower educational levels have
been associated with higher prevalence.
Genetic Factors
• Deterministic autosomal dominant genes, apolipoprotein E*4 (APOE*4)
polymorphism on chromosome 19.
Medical Risk Factors
• Cardiovascular disease, heart failure and atrial fibrillation

Psychiatric Risk Factors

• Recurent major depression in earlier adulthood, and post traumatic
stress disorder
Head Injury
• Neurocognitive disorder can occur immediately after a traumatic brain
injury or after the recovery of consciousness at any age
Lifestyle and Environmental Risk Factors
• Smoking, heavy consumption of alcohol, and exposure to
pepticides
Protective Factors
• Brain reverse refers to structural capacity and integrity of the brain
• Cognitive reverse refers to its functional capacity
Education and Cognitive Activity
• Higher education is associated with lover prevalence of dementia

Cognitive Activity
• Several popular leisure activities have been associated with lower risk of dementia

Pharmacologic Factors
• Protective effect against dementia with the use of nonsteroidal antiinflamatory
drug, effects of the lipid-lowering HMG Co-A (3-hydroxy-3-methylglutary-co-
enzym A) reductase inhibitor (statin)
CLINICAL ASSESMENT

Family members or other caregivers

spontaneously express concern about
cognitive difficulties

Subjective Assesment Objective Assesment

Overlearned, routine activities may
be preserved but problems may be
occurring in problem solving,
multitasking, and dealing with new
situations.
• Neuropsychological assessment
• Mini-Mental State Examination
(MMSE), The Montreal Cognitive
Assessment (MoCA), or The
MiniCog.
THE CAUSAL SUBTYPES MOST LIKEY TO BE SEEN IN GERIATRIC
PSYCHIATRY SETTINGS
 ALZHEIMER’S DISEASE.

AD is neurodegenerative disease, characterized by progressive

loss of synapses and neurons, the accumulation of amyloid
plaques, neurofibrilary tangles and prominenr cholinergic deficits.
 GENETICS OF AD

Autosomal dominant mutation that cause rare cases of early – onset familial AD are the
amyloid precusor protein (APP) gene on chromosome 21, the presenilin 1 (PS1) gene n
chromosome 14 and the presenilin 2 (PS2) gene on chromosome 1.
 Individuals with Down Syndrome, caused by trisomy 21, ineitably develop Alzheimer’s
neuropathology if they live long enough.
 BIOMAKER FOR AD

 Signs of cerebral amyloid deposition, such as positron emission

tomography (PET) brain scans with amyloidtracers, and reduced levels
ofamyloid beta 42 in the cerebrospial fluid (CSF), have been proposed as
research biomakers.
The NIA-AA guidlines also describe a stage of
asymptomatic preclinical AD
 VASCULAR DEMENTIA

 In major and mild vascular neurocognitive disorders,the cognitive deficits are principally attributed to
cerebrovascular disease. Referred to variously as arteriosclerotic dementia, multi-infarct dementia, vascular
cognitive impairment, and vascular cognitive disorder, it is the second most common cause of dementia and is
frequently present in combination with AD (mixed dementia). It can result from both large and small vessel
disease, with the location of the lesions more important than the volume of
 To diagnose vascular neurocognitive disorder, there should either be a clear history of stroke or transient
ischemic attacks temporally related to the cognitive decline, or neurologic deficits consistent with sequelae of
previous strokes.
 NEUROIMAGING

 Neuroimaging (computed tomography [CT] or MRI)-based evidence of

significant parenchymal injury attributable to cerebrovascular disease can
include one or more large vessel infarcts, a single large or strategically
located infarct or hemorrhage, extensive lacunar infarcts outside the
brainstem, or extensive white matter lesions.
 GENETICS

 There are rare autosomal dominant cerebrovascular disorders, such as

CADASIL (cerebral autosomal dominant arteriopathy with subcortical
infarcts and leukoencephalopathy), which is a form of hereditary stroke
caused by NOTCH3 mutations on chromosome 19.
FRONTOTEMPORAL LOBAR DEGENERATION ( FRONTOTEMPORAL
DEMENTIA)

 Frontotemporal dementia (FTD), the third most prevalent degenerative

dementia, is characterized by prominent atrophy of the frontal and
temporal lobes, with the predominant neuropathologic proteins
containing inclusions of hyperphosphorylated or ubiquitin protein.
 GENETICS

 In familial FTD, mutations have been associated with genes encoding

proteins affecting several fundamental cellular functions, including
microtubule-associated protein tau (MAPT), granulin, C9ORF72,
transactive response DNA-binding protein of 43 kDa, valosin-containing
protein, chromatin-modifying protein 2B, and fused in sarcoma protein.
 NEUROIMAGING

 Structural MRI or CT can show distinct patterns of regional

cortical atrophy that correlate with the clinical variants of FTD.
DEMENTIA WITH LEWY BODIES (DLB)

 DLB is the second most common neurodegenerative dementia. The

underlying disease is primarily characterized by alpha-synuclein
misfolding and aggregation within the pathognomonic Lewy bodies, which
are also found in Parkinson’s disease. Onset of symptoms is between the
sixth and ninth decades, and average survival is 5 to 7 years.
 NEUROIMAGING

 To help differentiate Lewy body–related dementias (DLB and dementia in

Parkinson’s disease) from other dementias, DaT PET scans may be useful.
Generalized low uptake on SPECT and fluorodeoxyglucose PET with
reduced occipital activity also suggests DLB. wave activity on
electroencephalography with temporal lobe transient sharp waves
NEUROCOGNITIVE DISORDER CAUSED BY HUNTINGTON DISEASE

 Neurodegenerative disease caused by autosomal dominant mutation consisting of

CAG repeats on chromosome 4
 Began by damaging the striatum of basal ganglia  to the entire brain
 Usually manifests in 4th or 5th decade of life
 Had a median survival of 15 to 20 years
 Cognitive deficits and behavioral symptoms often emerge before motor
abnormalities
 Hereditary related, genetic testing is diagnostic
NEUROCOGNITIVE DISORDER CAUSED BY PRION DISEASE

 Prions : transmissible misfolded protein particles

 Causing spongiform encephalopathies
 E.g : creutzfeld-Jacob disease
 Typically diagnosed during 7th or 8th decades of life
 Rapidly progressive (less than a year of survival)
 Diagnosis with biopsy or autopsy
 MRI with specific contrast or technique may show positive results
TREATMENT

Cause
Symptomatic
specific
treatment
treatment
CAUSE SPECIFIC TREATMENT

 Currently there are no disease modifying therapies available for

neurodegenerative disorder
SYMPTOMATIC TREATMENT

 Cholinesterase inhibitor (donepezil, rivastigmine, galantamine)

 Increase cholinergic transmission at the synaptic cleft
 Said to be works well for patient with AD
 Minimal evidence of benefit in patient with MCI
 NDMA receptor antagonist (memantine)
 Approved treatment for moderate to severe dementia caused by AD
 Research shown mixed results in frontotemporal dementia
 Serotonergic agents (SSRI)
 Works with behavioral/psychiatric symptoms in frontotemporal dementia
 No improvements in cognition
 Dopamine Blocking agents
 Must be used with caution with DLB patient
 Should be used for dementia due to the risk of adverse cerebrovascular events
 Benzodiazepine
 Avoided in neurocognitive disorders
 Exception for REM sleep disorder in DLB
SUMMARY

 Clinician should be knowledgeable about the neurocognitive disorders that are

common and severe in eldery adults.
 Diagnosis requires good history taking and skilled clinical assessments.
 Drug treatments currently only provide symptomatic relief
 Psychosocial and other supportive therapies are essential
CONCLUSION
 Was there a clear question
for the study to address ?

In this article there are population studied so as to produce prevalence number that is
group of country, age, region, gender and subtype of dementia. The higher prevalence
obtained from group of countries (USA), region (hispanic and latino people), in age more
than 85 years old, and subtype of dementia is Alzheimer’s. The gender is ussually greater
among women than among men.
 Was there a comparison with an
appropriate reference standard ?

In this article describes these entities and their diagnosis using the framework’s of the
recently published fifth edition of the American Pyschiatric Association Diagnostic and
Statistical Manual, Fifth Edition (DSM-5)
 Did all patients have a
diagnostic test and
reference standard ?

No, because the authors didn’t conduct

direct research on the patients. In this
article only explain the instruments use to
establish the diagnosis of dementia.
 Is the disease status of the tested
population clearly described ?

Can’t tell, because the authors didn’t conduct direct research on the patients. And
biomarker of dementia written by this article have not been validated.
 Were all outcomes important to the
individual or population considered ?

Yes, because this article explains about various risk and protective factors and
symptomps of dementia, so that people can know that dementia causes a decrease
cognitive function.