1. Prof.Dr.dr. H. Rusdi Lamsudin, M.Med.Sc Neurologist
Medical Doctor, Faculty of Medicine, UGM, 1971
Neurologist, Unair-UGM, 1978
Master of Medical Sciences, New Castle Univ, Australia, 1986
Head of Executive Board Muhammadiyah Hospital, Yogyakarta,
Vice Dean, Faculty of Medicine Muhammadiyah Yogyaakarta University,
PhD, UGM, 1996
Short-course, Unit Stroke & Neuro-Intensive, Insburck, Austria,1997
Head of Stroke Unit, Sardjito Hospital, Yogyakarta,
Head of Neurology Department Faculty of Medicine, UGM,
Dean of Faculty Medicine, Indonesia Islamic University, Yogyakarta, ,
Head of Neurology Department YARSIS Hospital, Surakarta
President IIMA,

2. DEMENTIA Epidemiology, Economic-Impact and Clinical’s Aspect
Prof Dr. dr. Rusdi Lamsudin MMedSc
Neurologist
Department of Neurology
YARSIS HOSPITAL
Faculty of Medicine
Indonesian Islamic University

3. Overview Epidemiology Economic Impacts Definition
Clinical presentation
Diagnosis
Differential Diagnosis
Etiology
Workup
Non-pharmacologic Treatments
Drug Treatments
Terminal Care

4. EPIDEMIOLOGY

5. Epidemiology Dementia affects 17–25 million people worldwide
Estimated 4 million in the US and an estimated 800,000 people in the UK [Ritchie, 1995; Keefover, 1996].
It affects predominantly elderly people, The prevalence of dementia in people over the age of 65 is 5% and in people over 80, it is 20%.
It has been estimated that 26% of women and 21% of men over the age of 85 have some form of dementia, of whom approximately 50% have Alzheimer’s disease (AD) [Melzer, 1997].

6. Epidemiology In case of AD:
Age specific prevalence rates almost double with every additional 5 years of age from 1% of 65, rising to about 8-10% at age 80 and %at age 90
African-Americans and Hispanics may have a higher risk than Caucasians-Americans. It also occurs less frequently in Asians than Americans

7. Growth of numbers of people with dementia
The World Alzheimer Report (2009) estimated:
35.6 million people living with dementia worldwide in 2010
Increasing to 65.7 million by 2030
115.4 million by 2050

8. Economic Impact

9. Worldwide cost of dementia
The societal cost of dementia is already enormous.
Dementia is already significantly affecting every health and social care system in the world.
The economic impact on families is insufficiently appreciated.
The total estimated worldwide costs of dementia are US$604 billion in 2010.
These costs are around 1% of the world’s GDP
0.24% in low income
1.24% in high income

10. Worldwide costs of dementia
The World Alzheimer Report (2010) estimated that:
If dementia care were a country, it would be the world’s 18th largest economy

11. Definition

12. Definition
a syndrome characterized by progressive decline of intellectual ability from a previously attained level
the decline in mental inability usually involves variable deterioration in  speech  memory  judgment  mood
without alteration of consciousness
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13. Definition Multiple Cognitive Deficits: Cognitive Disturbances:
Memory dysfunction
especially new learning, a prominent early symptom
At least one additional cognitive deficit
aphasia, apraxia, agnosia, or executive dysfunction
Cognitive Disturbances:
Sufficiently severe to cause impairment of occupational or social functioning and
Must represent a decline from a previous level of functioning

14. Clinical Presentation

15. Clinical Presentation
onset of dementia it is usually insidious
dementia is often progressive (degenerative disease) but may be static (post-traumatic brain injury)
initial presentation may include slight forgetfulness, attention and concentration deficits, and increasing repetitiousness or inconsistencies in usual behavior
later presentation may display impaired judgment, inability to abstract or generalized, and personality change with rigidity, perseveration, irritability, and confusion; affective disturbances may be prominent with loss of personality and self-care
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16. Impairment of 2 or more cognitive domain1
Memory loss 2
Language 3
Abstract thinking & Judgment 4
Praxis (learned motor behavior) 5
Spatial processing 6
Personality 7
Social conduct

17. Risk Factors for Dementia
Gender: male
Age: years
Prior stroke
Hardening of the arteries
Heart disease
High blood pressure
Diabetes
Cholesterol problems
Atrial fibrillation
Smoking
Education
Race
Family history (CADASIL-cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy )

18. Most common causes of dementia
Alzheimer’s disease
Vascular dementia
Lewy body dementia
Frontotemporal dementia

19. Established risk factors for dementia
Age
Female sex
Head trauma
Low level of education

20. Risk factors for dementia
Coronary artery disease
High dietary saturated
fat and cholesterol
Serum cholesterol
Hyperhomocysteinemia
Smoking
Diabetes mellitus
Hypertension
Apolipoprotein E status
All these are vascular risk factors!

21. Diagnosis and Diffeerential Diagnosis

22. Differential Diagnosis:TopTen (commonly used mnemonic device: AVDEMENTIA)
1. Alzheimer Disease (pure ~40%, + mixed~70%)
2. Vascular Disease, MID (5-20%)
3. Drugs, Depression, Delirium
4. Ethanol (5-15%)
5. Medical / Metabolic Systems
6. Endocrine (thyroid, diabetes), Ears, Eyes, Environ.
7. Neurologic (other primary degenerations, etc.)
8. Tumor, Toxin, Trauma
9. Infection, Idiopathic, Immunologic
10. Amnesia, Autoimmune, Apnea, AAMI

23. Comparison of the Clinical Features
Dementia
Depression
Delirium
Insidious/slow and often unrecognized; depends on cause
Coincides with major life changes; often abrupt, but can be gradual
Sudden/abrupt; depends on cause; often at twilight or in darkness
Clinical Features: ONSET
COURSE, PROGRESSION, ATTENTION, MEMORY, THINKING

24. Neurologic Diseases Associated with Intellectual Dysfunction
DISEASE PHYSICAL SIGNS CLINICAL FEATURES
Creutzfeldt-Jakob Myoclonus , cerebellar signs, Subacute course; EEG has specific abnormalities, eye movement abnormalities brain biopsy diagnostic
Huntington's disease Choreiform movements, Often positive family history; caudate atrophy corticospinal signs by CT or MRI
Multiple sclerosis Brainstem signs, optic atrophy, Usually long-standing disease; episodic illness corticospinal signs with remissions; often extensive white matter abnormalities by MRI
Wilson's disease Extrapyramidal signs , hepatic Onset in adolescence or young adult life, dysfunction, Kayser-Fleischer psychiatric disorders rings
Progressive Failure of vertical downgaze, Eye movement abnormalities; differentiate from supranuclear extrapyramidal signs Parkinson's disease; unresponsive or only palsy transiently responsive to levodopa
* = invariably present; all other physical signs are neither invariably present nor pathognomonic.
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25. Etiologic Diagnosis of Progressive Dementias in Adults
Neurodegenerative Diseases
Alzheimer’s disease
Parkinson’s disease
Diffuse Lewy body disease
Progressive supranuclear palsy
Multisystem atrophy
Huntington’s disease
Frontotemporal dementias – e.g. Pick’s disease

26. Etiology contd. Structural Disease or Trauma Vascular Disease
Normal pressure hydrocephalus
Neoplasms
Dementia pugilistica
Vascular Disease
Vascular dementia
Vasculitis
Heredometabolic Disease
Wilson’s disease
Other late-onset lysosomal storage diseases

27. Etiology contd. Demyelinating or Dysmyelinating Disease
Multiple sclerosis
Infectious Disease
Human immunodeficiency virus, type 1
Tertiary syphilis
Creutzfeldt-Jakob disease
Progressive multifocal leukoencephalopathy
Whipple’s disease
Chronic meningitis – e.g. Cryptococcal

28. DELIRIUM Acute brain dysfunction characterized by:
Global symptoms (affecting both cerebral hemispheres) including impairment of consciousness and attention
Primary physiological changes with potential for reversibility
‘waxing and waning’ symptoms – usually worse in evening
Life-threatening conditions underlying the syndrome

29. Symptoms of Delirium Common symptoms of a delirium include:
Waxing and waning levels of consciousness
Poor attention and disorientation
Disturbed memory (long and short term)
Psychosis
Sleep dysregulation
Fearfulness with agitation and aggression
Seriously impaired insight and judgment

30. Epidemiology of Delirium
Very Common % med/surg inpatients (30%+ if elderly)
30% of Adult Burn Patients
80%of delirious patients have pre-existing dementia
Predisposing Factors:
old age, postcardiotomy, s/p burns
prexisting brain damage
drug withdrawal states
AIDS

31. Causes of Delirium Often multifactorial
Infections, trauma, brain diseases
Cardiac diseases, lung disease, hypoxia, hypoglycemia
Toxins, or intoxications
Medication effects
Substance withdrawals (e.g. DTs)
Endocrinopathies
In elderly dementia patients: UTI, dehydration and pneumonia are the most common causes

32. DELIRIUM - TREATMENT Must look for medical cause(s) and treat
Symptoms can be helped by antipsychotic drugs such as haldoperidol or risperidone (especially psychosis, agitation)
Consider anticholinesterases for anticholinergic delirium
Comfort measures include reorientation strategies, reducing stimulation, frequent reassurance

33. Delirium vs Dementia (summary)
General rules of thumb:
Delirium Dementia
acute chronic
reversible irreversible
physiological structural
primary attention primary memory
deficits deficits
Delirium and dementia can coexist; in fact delirium is very common in demented patients
CAUSES OF DELIRIUM:
Infectious - encephalitis, meningitis, UTI
- also systemic infections with sepsis, fever
Withdrawal
Acute Metabolic - electrolyte changes, dehydration, blood sugsr changes, acidosis, hepatic or renal failure
Trauma
CNS pathology - seizures, tumors, strokes, etc.
Hypoxia
Deficiencies - b12, thiamine
Endocrine
Acute Vascular
Toxins,Drugs
Heavy Metals
I WATCH DEATH

34. Work-up

35. Workup History Physical Examination Laboratory studies medslides.com
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36. History - etiology
the most important component of the initial evaluation
adequate history with help of a family member is critical
description of
cognitive, memory, and behavior problems
effect on daily life - difficulty with driving, work, or family relationships
details on temporal course of illness
chronic
progressive (Alzheimer or other neurodegenerative disease)
stepwise (multi-infarct)
static (traumatic injury, episode of severe hypotension)
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37. History - treatable causes
Vascular dementia - presence of cardiovascular risk factors (smoking, HTN, chol, diabetes)
Normal pressures hydrocephalus - triad of dementia, gait, incontinence with a prior history of meningitis or subarachnoid hemorrhage
Mass lesion - history of head trauma, unexplained focal neurologic deficit, unilateral headache worsening over time
Parkinson’s disease - resting tremor and rigidity
Wilson’s disease - hepatocellular disease and dementia
HIV and neurosyphilis - high-risk sexual behavior
hereditary - family history dementia, Down’s syndrome, psychiatric disorders
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38. History - treatable causes
B12 deficiency - previous gastric surgery
B12, thiamin, niacin deficiency - inadequate nutrition, alcohol abuse
medications - opiates, sedative-hypnotics, analgesics, anticholinergics, anticonvulsants, corticosteroids, centrally acting anti-hypertensives, psychotropics
symptoms of hypothyroidism, pituitary insufficiency
occupational history - exposure to toxic substances (aniline dyes, heavy metals)
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39. Diagnostic Criteria For Dementia Of The Alzheimer Type (DSM-IV, APA, 1994)
Multiple Cognitive Deficits
1. Memory Impairment
2. Other Cognitive Impairment
Deficits Impair Social/Occupational
Course Shows Gradual Onset And Decline
Deficits Are Not Due to:
1. Other CNS Conditions
2. Substance Induced Conditions
Do Not Occur Exclusively during Delirium
F. Not Due to Another Psychiatric Disorder

40. Mental Status Examination
Examination should be geared to both the detection of focal lesions and to signs of general brain dysfunction
immediate memory testing (three object recall, recite digits forward and backward, recall a short story)
remote memory testing (recall of historical events, family milestones, or recent local or international news)
reproducible drawings
discern similarities among objects
decision-requiring tasks (finding a stamped letter or seeing a fire in a theater)
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41. Mini-Mental Status Tests
Score
Recall:
Ask for 3 objects repeated above. Give one point for each. Language:
2 Name a pencil and watch (2 points).
Repeat the following: "No ifs ands or buts."
Follow a 3-stage command: "Take a paper in your right hand: fold it in half, and put it on the floor." (3 points).
Read and obey the following: "Close your eyes."
Write a sentence.
Copy design.
Total Score: [ ] Maximum Score: 30
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42. Physical and Neurologic Examinations
Check for focal evidence of neovascular risk factors - carotid bruits, signs of alcoholism, hepatocellular injury, renal insufficiency, other systemic illnesses
specific neurologic abnormalities
frontal lobe release signs (grasp, suck, snout, root)
visual field cut and extraocular movement limitations
abnormal pupillary reactions
extrapyramidal features (carditis dyskinesis, tumors, asterixis, Korea, monoclonal disc, it)
sensory deficit and gait disorder
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43. Screening Laboratory Studies
1. Complete blood count and sedimentation rate
2. Chemistry panel (electrolytes, calcium, albumin, BUN, creatinine, transaminase)
3. Thyroid-stimulating hormone (TSH)
4. VDRL test for syphilis
5. Urinalysis
6. Serum B12 and folate levels
7. Chest x-ray
8. Electrocardiogram
9. Head computed tomography (CT)
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44. Neuroimaging Head CT or MRI is appropriate in the presence of
1) history suggestive of a mass lesion
2) focal neurologic signs or symptoms
3) dementia of abrupt onset
4) history of seizures
5) history of stroke
MRI with gadolinium contrast enhancement is superior to CT for the diagnosis of multi-infarct dementia and problems referrable to the posterior fossa
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45. Other Ancillary Studies
Lumbar puncture
routine LP for initial evaluation of dementia is not justified
may be indicated when other clinical findings suggest an active infection or vasculitis and as part of the evaluation of normal pressure hydrocephalus
sugar, protein, cell count, cultures, gamma globulins, the serology for stiffness should be obtained
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46. Other Ancillary Studies
Electroencephalogram (EEG)
usually normal or with nonspecific rhythm slowing
indicated in patients with episodic altered consciousness and in whom seizures may be suspected
may occasionally raise suspicion of a particular etiology:
focal, delta slowing is seen with tumor
unilateral attenuation of voltage may suggest an extracranial mass such as subdural hematoma
excessive beta activity may be consistent with drug ingestion
Creutzfeldt-Jakob disease has a highly specific EEG pattern
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47. Other Ancillary Studies
Formal neuropsychologic evaluation
appropriate for more specific information when the diagnosis is in doubt
also helpful in providing additional information about the nature of impairment following focal brain injury
Speech analysis
may improve patient and family communication with therapy
Formal psychiatric assessment
may be desirable if depression in addition to dementia is suspected
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48. Studies of Limited or Uncertain Utility
Cerebral blood flow and metabolism measurements
PET and SPECT scans have no routine use at present
Brain biopsy
rarely justified for non-neoplastic or noninfectious diseases
Progressive multifocal leukoencephalopathy or Creutzfeldt-Jakob disease is diagnosed by biopsy
Noninvasive neurovascular studies (carotid ultrasound, Doppler flow studies)
if MRI or CT demonstrates infarction, or
clinical course or physical examinations is suggestive of cerebralvascular disease
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49. Treatment

50. General Treatment Principles For Dementia
Treatment Of Underlying Disease Process (Primary Treatment)
Management Of Behaviors and Symptoms (Secondary Treatment)
Caregiver Support and Education

51. Primary Treatment Strategies (for progressive dementias)
1. Prevention
Identify risks and mitigate
Develop neuroprotective strategies for those at risk
2. Slow or halt progression of illness
Understanding pathophysiology leads to treatment ideas
5 year delay in onset ---> 1/3 decrease in prevalence
Delaying institutionalization by 1 month saves $1.2 billion/yr
3. Reverse symptoms
Compensate through augmentation of remaining neurons or other systems
Reversal of destructive processes & regeneration of tissue

52. Symptomatic Management and Counseling
Improving mental functioning
Management of confusion and agitation
Maintaining the patient at home
Risk factor reduction and attention to underlying etiologies
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53. Improving Mental Functioning
no established treatment for Alzheimer’s disease or for patients with multi-infarct dementia
findings of degeneration of cholinergic neurons and depletion of choline-acetyl transferase in Alzheimer's disease have led to attempts at improving cholinergic transmission
lecithin supplements (dietary choline repletion)
tacrine (a centrally active, reversible cholinesterase inhibitor)
There is no evidence to support the use of: restorative therapy with nerve growth factor, protective therapy with antioxidants, preventive therapy with drugs that inhibit beta amyloid formation, and “cerebral vasodilators” (papaverine, dihydroergotoxine) to improve memory
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54. Management of Confusion and Agitation
The chronic use of sedatives and psychoactive agents in the confused patient should be avoided unless persistent extreme agitation hampers care
The lowest possible doses should be used and for the shortest time possible
thioridazine (10 to 25 mg qhs)
haloperidol (0.5 to 1 mg bid or tid ) often a first choice in the setting of delusions and hallucinations; must be careful to avoid long-term use because of the risk of inducing tardive dyskinesia
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55. Management of Confusion and Agitation
Avoid regular use of sedative/hypnotic agents for sleep
Beta-blocking agents and anticholinergics may exacerbate confusion
Patients with depression may improve with a tricyclic compound with low anticholinergic side effects  desipramine (25 to 50 mg qhs)
A recent study of nursing home patients demonstrated substantial improvement in many patients when chronically prescribed psychotropic drugs were discontinued or reduced in dose
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56. Maintaining the Patient at Home
An important task is helping the family maintain and care for the patient at home
The goal is to sustain the highest level of function possible:
facilitate and promote an orderly home situation
regular routine use of calendars, television, newspapers, and other means of orientation
limit the use of potentially dangerous appliances
provide convenient toilet facilities
advice against driving when early impairment of judgment and spatial concepts is present
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57. Maintaining the Patient at Home
Families can often find help in local support groups, day care and group therapy services, and social service agencies
When care at home begins to exhaust and strain the family, sensitive counseling can do much to help a family cope with the difficult decision regarding institutionalization
some dementing diseases are infectious (eg, HIV infection) and that the bodily fluids and tissues of such patients require special handling to avoid transmission. It is particularly important to emphasize when home care is rendered by lay persons
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58. Risk factor reduction and attention to underlying etiologies
Central to an effective outcome :
control of cerebrovascular risk factors as hypertension, diabetes mellitus, smoking , hyperlipidemia , and coronary artery disease
endarterectory deserves consideration when a vascular etiology is strongly suspected and a significant stenosis is found
Avoidance of toxins, correction of vitamin deficiencies, discontinuation of causative drugs, initiation of hormonal replacement therapy in cases of deficiency, and treatment of underlying infectious etiologies
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59. Improving Support for Families and Other Caregivers
Who are the AD Caregivers? (slide 37)
Demands of Caregiving (slide 38)
Technology and Caregiving (slide 39)
National Support for Caregivers (slide 40)
How to Contact the ADEAR Center (slide 41)
Slide 36

60. Support for Caregivers
Demands of Caregiving
AD takes a huge physical and emotional toll. Caregivers must deal with changes in a loved one’s personality and provide constant attention for years. Thus, caregivers are especially vulnerable to physical and emotional stress.
Peer support programs can help link caregivers with trained volunteers. Other support programs can offer services geared to caregivers dealing with different stages of AD.
Slide 38

61. Treatment of AD…

62. Tacrine Cholinesterase inhibitor
1 systematic review with 5 RCTs, 1434 people, weeks
No difference in overall clinical improvement
Some clinically insignificant improvement in cognition
Significant risk of LFT abnormalities: NOT USED

63. Donepezil Aricept Cholinesterse inhibitor
Easy titration (start 5/day, then 10)
Side effects: GI (nausea, diarrhea)
Can be associated with bradycardia…
Main effect seems to be lessening of rate of decline, delayed time to needing nursing home/more intensive care

64. Other agents… Rivastigmine Galantamine Cholinesterase inhibitors
?more side effects, more titration required
Future directions:
Prevention of delirium in at risk patients (cholinergic theory of delirium)
Behavioral effects in those with severe dementia?
Treatment of Lewy Body dementia
Treatment of mixed Vascular/AD dementia

65. Comments about cholinesterase inhibitor studies…
Highly selected patients (mild-moderate dementia)
?QOL improvements…
Not known: severe dementia and mild CI

66. Memantine NEJM april 2003 Moderate to severe AD (MMSE 3-14)
N-methyl D aspartate (NMDA) receptor antagonist; theory that overstimulation of NMDA receptor by glutamate leads to progressive neurodegenerative damage
28 week, double blinded, placebo controlled study; 126 in each group; 67% female, mean age 76, mean MMSE 7.9

67. Memantine…
Found less decline in ADL scores, less decline in MMSE (-.5 instead of –1.2)
Problem: significant drop outs (overall 28% dropout rate) in both groups; data analyzed did not account for drop outs, followed those “at risk”

68. Selegiline Unclear benefit
Less than 10mg day, selective MAO B inhibitor
Small studies, not very conclusive

69. Vitamin E (alpha tocopherol)
NEJM 1997: selegiline, vit E, both , placebo for tx of AD
Double blind, placebo controlled, RCT with mod AD; 341 patients
Primary outcome: time to death, institutionalization, loss of ADLS, severe dementia
Baseline MMSE higher in placebo group
No difference in Primary outcomes; adjusted for MMSE differences at baseline and found delay in time to NH from 670 days with vit E to 440 days with placebo

70. Ginkgo Biloba
1 systematic review of 9 double blind RCTs with AD, vascular, or mixed dementia
Heterogeneity, short durations
High withdrawal rates; best studies have shown no sig change in clinician’s global impression scores

71. Other treatments
NO good evidence to support estrogens or NSAIDS

72. Other treatments… Behavioral/agitation: Nonpharmacologic strategies
Reasons for NH placement:
Agitation
Incontinence
Falls
Caregiver stress

73. ?Antipsychotics
NO data to support any significant benefit for treating behavioral symptoms of dementia with antipsychotic agents
Small group of patients with active psychoses, disturbing hallucinations, or aggressive behaviors who may have some benefit

74. Antipsychotics: Side Effects: Warnings: Sedation
Anticholinergic effects
Prolonged QT
Edema
Orthostasis
Weight gain
Confusion
Warnings:
FDA black box warning for increased mortality (OR ), and increased ?increased stroke risk

75. Prevention?
HTN and DM linked to future development of ALL types of dementia (not just vascular)…
Large initial studies of treating systolic hypertension in the elderly (SHEPS and others) demonstrated decreased risk of development of cognitive impairment over time in those patients in the original treatment group!
Decreased risk included vascular AND alzheimer type dementias…
Cholinesterase inhibitors seem to work as well (or as poorly) for both vascular and alzheimer type of dementias…
What is the link? Both common in elderly, may be that one “unmasks” the other…

76. Conclusion
International studies make it clear that dementia occurs in every country of the world. Dementia affects 1 in 20 people over the age of 65 and 1 in 5 over age of 80
Worldwide there are an estimated 35.6 million people with dementia. By 2050 the number will rise to over 115 million. For at least the last 15 years, the majority of people with dementia worldwide have been living in developing regions of the world. They account already for over 60% of all cases. By this portion will have risen to 71%.

77. Conclusion cont’
The worldwide cost of dementia will exceed 1 per cent of global GDP in 2010, at US$604 billion. If dementia care a country, it would be the world’s 18th largest economy
The costs of caring for people with dementia are likely to rise even faster than the prevalence- especially in the developing world, as more formal social care systems emerge, and rising incomes lead to higher opportunity costs.

78. Conclusion cont’
Dementia is a progressive, degenerative brain syndrome that affects memory, thinking, behavior and emotion
The progressive syndrome of dementia is define as loss of memory plus impairment in at least one other cognitive function, such as aphasia, apraxia, agnosia and disturbance in executive function, which is severe enough to interfere with activities of daily living and represent decline (DSM-IV, 1994

79. Conclusion cont’
Dementia presents with variety of clinical manifestations regardless of aetiology, and in most cases it caused by organic barain disease. It characterized by three main symptomatic domains as; 1) activities- inability to perform activities of daily life, 2) behaviours-psychiatric symtoms/behavioural disturbances and 3) cognition- neuropsychological impairment

80. Conclusion cont’
There are four main types of dementia: 1) Alzheimer’s disease (60% of cases), 2) Vascular dementia (30-40%; including about 20% where dual pathology exists), 3) Dementia with Lewy bodies (15% of cases), and 4) Fronto-temporal dementia (5% of cases).

81. Conclusion cont’
The treatments options for dementia include both pharmacological and nonpharmacological therapeutic approaches. These can be further subdivided into therapies for cognitive impairment and neuropsychiatric disturbances (psychiatric symptoms and behavioural disturbances).

82. Conclusion cont’
The quality of life patients with dementia is paramount and long-term care of the patient requires continued education and communication with clinicians, primary carers, care staff and family members.