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------=_NextPart_01C5BA16.295154D0 Content-Location: file:///C:/752BCE74/PsycGR20050914ppt_files/pres.xml Content-Transfer-Encoding: quoted-printable Content-Type: text/xml; charset="utf-8" ------=_NextPart_01C5BA16.295154D0 Content-Location: file:///C:/752BCE74/PsycGR20050914ppt_files/slide0004.htm Content-Transfer-Encoding: quoted-printable Content-Type: text/html; charset="us-ascii" Clinical Management of Dementia
Clinical Management of Behavioral and Psychological Symptoms in Dementia
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Speaker Disclosure of
Financial Relationship
•Consultant for:
•
•
•Grant support from:
•
•
•Discussion of off-label or investigational use  
•
• Yes ___   No ___
•
<= span style=3D'font-size:88%;font-weight:normal;visibility:hidden'>•
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3
The University= of Medicine and Dentistry of New Jersey–Center for Continuing and Outreach Education (UMDNJ-CCOE) and DiMedix are joint sponsors of the 2005 Neuroscience Grand Rounds.
Primary control and responsibility for curriculum = development resides with the 2005 Neuroscience Grand Rounds Curriculum Development Steering = Committee and UMDNJ-CCOE.
= ;
The views pres= ented in this educational activity are those of the authors/faculty and do not necessarily reflect those of the educational provider or the commercial supporter.
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4
Steering Committee
•Peter Buckley MD, Medical College of Georgia
•Jose M. Canive, MD, Albuquerque VA Medical Center
•John G. Csernansky, MD, Washington University School of Medicine
•Carl Eisdorfer, PhD, MD, University of Miami School of Medicine
•Alan I. Green, MD, Dartmouth Medical School
•Joseph H. Henry, MD, University of Miami School of Medicine
•James W. Jefferson, MD, University of Wisconsin Medical School
•Marc Laruelle, MD, Columbia University
•Jeffrey A. Lieberman, MD, University of North Carolina Scho= ol of Medicine 
•Matthew Menza, MD, University of Medicine and Dentistry of = New Jersey
•John W. Newcomer, MD, Washington University School of Medicine
•Stephen M. Strakowski, MD, University of Cincinnati College= of Medicine
•Richard M. Steinbook, MD, University of Miami School of Medicine
•Marvin S. Swartz MD, Duke University School of Medicine = ;
•&#= 13;
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5
Activity Reviewers
•Giovanni Caracci, MD
•Associate Dean for Education
•Vice Chair for Education and Training
•Department of Psychiatry
•UMDNJ-New Jersey Medical School
•Newark, New Jersey
•Kenneth R. Kaufman, MD, MRCPsych
•Professor of Psychiatry and Neurology
•UMDNJ-Robert Wood Johnson
•  Medical School
•New Brunswick, New Jersey
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Objectives
•Summarize the behavioral and psychological = <= span style=3D'font-size:88%'>symptoms of dementia (BPSD)
•Describe the prevalence and burden of BPSD
•Review the classes of medications that may = = be used to treat BPSD
•Summarize the evidence for antipsychotics in <= span style=3D'font-size:88%'>the treatment of dementia-related = psychosis/agitation
•
<= span style=3D'font-size:88%;font-weight:normal;visibility:hidden'>•
<= span style=3D'font-size:88%;font-weight:normal;visibility:hidden'>•
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Objectives (cont’d)
•Dis= cuss the adverse effects of various antipsychotic therapies that may im= pact selection of the appropriate agent in the elderly
<= span style=3D'font-weight:normal;visibility:hidden'>•
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Outline
=
<= span style=3D'font-size:156%'>•Definition
<= span style=3D'font-size:156%'>•Prevalence
γ= 2;Aging and Dementia
γ= 2;Behavioral and Psychiatric Symptoms <= /span>
<= span style=3D'font-size:156%'>•Impact on Caregivers and Patients
<= span style=3D'font-size:156%'>•Treatment/Management
γ= 2;Focus on Antipsychotic Therapy
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Dementia & Delirium
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Dementia and Delirium
•Dementia
•C= ognitive loss that impairs social or occupational
• functional capacity
•Consequence of a number of specific conditions
•Typically progressive in course
•
•Delirium
•Also compromise cognition
•Consequence of factors that impair attention and <= /span>consciousness
•May be reversible
Dementia and delirium may coexist
Dement= ia is the general designation for cognitive dysfunction that interferes with social= or occupational functioning.1&nb= sp; Dementia itself is not a disease, but is rather a syndrome or set = of symptoms associated with certain diseases or conditions including Alzheimer’s disease (AD, the most common type of dementia), vascular dementia, mixed AD and vascular dementia, Lewy body dementia, frontotempo= ral dementia, Huntington disease, Parkinson’s disease, Pick disease, and Creutzfeldt-Jakob disease.  = The decline in cognitive function is typically gradual and progressive.
Deliri= um, characterized by a disturbance of consciousness and a change in cognition that develops over a short period of time, can result from medical illnes= ses including urinary tract infection, fecal impaction, dehydration, endocrine abnormalities, and congestive heart failure, or from drug therapy, particularly polypharmacy or medications with significant anticholinergic activity.2-4  Oth= er agents that may cause or exacerbate loss of mental capacity include opiat= es, sedative-hypnotics, analgesics, anticholinergics, anticonvulsants, corticosteroids, centrally acting hypertensives, psychotropics, and alcohol.  Through appropriate identification and treatment of the underlying etiology, resolution of delirium may be achieved.
Dement= ia and delirium may coexist.  For example, patients with dementia may experience an acute decline in cognit= ion (delirium) due to a medical illness or polypharmacy.





Ref= erences:
1. Alzheimer’s Association. Alzheimer’s Disease and Related Dementias Fact Sheet;  1999.   Available at: http://www.alz.org/Resources/FactSheets.asp. Accessed April 1, 2004; 2. Z= araa AS. Pharmacologic management of agitation and psychosis in older demented patients. Geriatrics. 2003;58:48-53; 3. Tune LE. Anticholinergic effects of medication in elderly patients. J Clin Psychiatry. 2001;62(suppl 21):11-14; 4. Desai AK, Grossberg GT. Recognition and management of behavioral disturbances in dementia. Primary Care Compan= ion J Clin Psychiatry. 2001;3:93-109.


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Dementia and Cognitive Decline
•Mem= ory loss (recent memory in particular)
<= span style=3D'font-weight:normal'>•Language impairment (aphasia)
<= span style=3D'font-weight:normal'>•Performance deficit (apraxia)
<= span style=3D'font-weight:normal'>•Recognition problems (agnosia)
<= span style=3D'font-weight:normal'>•Executive function
<= span style=3D'font-weight:normal'>•Personality changes
In pat= ients with dementia, short-term memory is affected early in the course of illness.  Visuospatial deficits and execut= ive function impairments also appear early in the illness.  As the disease advances, all cog= nitive functions are impaired. Language impairment, performance deficit, recogni= tion problems, and personality changes result as the disease progresses.















Ref= erences:
Bonner LT, Peskind ER. Pharmacologic treatments of dementia. Med Clin North Am. 2002;86:657-674.
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Behavioral and Psychologica= l Symptoms of Dementia (BPSD)
•Term used since 1996 to describe= symptoms of disturbed perception, thought content, mood, or behavior = that frequently occur in patients with dementia
•BPSD occurs in up to= 90% of dementia patients = ;
Fin= kel SI et al. Int Psychogeriatr. 1996;8(suppl 3):497-500; Finkel SI. Clinician. 1998;16:33-42.
Until = 1996, dementia was defined as a constellation of symptoms called behavioral disturbances. The term “disturbances,” however, was felt to be too general = and was seen as hampering efforts to reach a clearer understanding of dementi= a. A consensus conference, convened by the International Psychogeriatric Association (IPA) Task Force on BPSD, agreed that a more descriptive term= was needed and coined the term “behavioral and psychological symptoms of dementia” (BPSD)—a cluster of symptoms of disturbed perception, thought content, mo= od, or behavior that frequently occurs in patients with dementia.1,2<= /font>
Studie= s have shown that BPSD occurs in up to 90% of nursing home residents with dementia.2  The occurrence and worsening of = BPSD result in patient and caregiver suffering, significant loss of quality of life for both the patient and caregiver, institutionalization, and increa= sed costs of care.3  = This makes the early identification and appropriate treatment of BPSD essentia= l to help reduce the immense social, health, and economic burdens associated w= ith dementia.









Ref= erences:
1. Finkel SI, Costa e Silva J, Cohen G, Miller S, Sartorius N.  Behavioral and psychological sig= ns and symptoms of dementia: a consensus statement on current knowledge and implications for research and treatment.=  
Int Psychogeriatr. 1996;8(suppl 3):497-500; 2. Finkel SI. The si= gns of the behavioural and psychological symptoms of dementia. Clinician.<= /i> 1998;16:33:42. Grossberg GT. The ABC of Alzheimer’s disease: behavi= oral symptoms and their treatment. Int Psychogeriatr.  2002;14(suppl 1):27-49.

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Estimate of Mental Illness Prevalence in Those Aged 55+ in US
•Anxiety disorders 11.4 %
•M= ood disorders   4.4 %
•Depressive symptoms
in community 8%-20% <= /div>
•Depressive symptoms in
primary care setti= ngs 37%
•Schizophrenia    0.6%
•Severe cognitive impairment    6.6%
•M= ild cognitive impairment        = ;         17%-34%
US Surgeon General. In: Report on Mental Health= 1999; Available at: ht= tp://www.surgeongeneral.gov/library/mentalhealth/toc.html.  Accessed March 4, 2004; Petersen = RC et al. Arch Neurol= . 2001;58:1985-1992.
To sta= rt, the prevalence of mental illness in the US adult population ≥ 55 years = of age will be briefly reviewed.
Accord= ing to the US Surgeon General’s Report on Mental Health 1999, there are a variety= of mental disorders that contribute significantly to the total burden of men= tal illness.1 These include anxiety disorder, mood disorder, major depression, schizophrenia, and disorders that cause cognitive impairment.=
Most s= triking among the population ≥55 years of age are the high prevalence rates for depression (as high as 20% in the community and 37% in the primary care setting) and mild cognitive impairment (ranging from 17% to 34% in population-based studies).2
Althou= gh not the focus of this presentation, mild cognitive impairment is a condition that= is gaining attention. Mild cognitive impairment—a transitional clinical state between the cognition of normal aging and mild dementia—is considered to be an indicator of progression to AD.  Among patients with mild cogniti= ve impairment, 15% to 20% will convert to AD each year.2








Ref= erences:
1. US Surgeon General. Older adults and mental health. In: US Surgeon General’s Report on Mental Health 1999. Available at: http://www.surgeongeneral.gov/library/mentalhealth/toc.html.  Accessed March 4, 2004; 2. Peter= sen RC, Doody R, Kurz A, et al. Current concepts in mild cognitive impairment= . Arch Neurol. 2001;58:1985-1992.
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Prevalence of Behavioral and Psych= ological Symptoms in Dementia
•Range varies w= ith disease stage
•Agitation 4%-63%
•Delusions 0%-20%
•Hallucinations 3%-20%
•Paranoia 0%-20%
•Behavioral disorder 4%-38%
•Emotional lability 3%-18%
•Depression 8%-34%
Eisdorfer C et al. Am J Psychiatry. 1992;149:190-194.
The pr= evalence of behavioral and psychological symptoms varies depending on the stage of AD.  Based on an analysis fr= om a registry of patients with AD (n=3D324), using the Global Deterioration Sc= ale, it was found that in early stage AD (stage 2), 52% of the  patients experienced some BPSD, increasing to 77.1% by stage 6.
The sl= ide shows the range of prevalence for specific BPSD symptoms, depending on the disease stage.

















Ref= erences:
Eisdorfer C, Cohen D, Paveza GJ, et al. An empirical evaluation of = the Global Deterioration Scale for staging Alzheimer’s disease. Am J Psychiatry. 1992;149:190-194.

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Life Expectancy at Age 65
OASDI. Available at: http://www.ssa.gov/OACT/TR= .  Accessed April 4, 2004.
11.9
15.5
19.6
20.9
22.7
18.2
20.1
13.4
0
5
10
15
20
25
1940
1997
2040
2075
Year Cohort Turns 65 Years of Age
3D"Text
Life Expectancy (years)
Beyond Age 65
Male
Female
This s= lide illustrates the increasing life expectancy among those 65 years of age.  In 1940, the life expectancy was= 11.9 years for men and 13.4 years for women.&= nbsp; By 1997, the life expectancy increased to 15.5 and 19.6 years, respectively. By 2075, the average life expectancy after age 65 is projec= ted to increase to 20.1 and 22.7 years, respectively.
Accord= ing to these projections, the Federal Old-Age and Survivors Insurance and Disability Insurance (OASDI) Trust Funds will be exhausted by the year 2042.<= br>














Ref= erences:
Old Age Survivor and Disability Insurance (OASDI).  2004 Annual Report of the Boa= rd of Trustees of the Federal OASDI Trust Funds.  Available at: http://www.ssa.gov/OACT/TR.  Accessed April 4, 2004.
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------=_NextPart_01C5BA16.295154D0 Content-Location: file:///C:/752BCE74/PsycGR20050914ppt_files/slide0008_image012.gif Content-Transfer-Encoding: base64 Content-Type: image/gif R0lGODlhNgAgAHcAMSH+GlNvZnR3YXJlOiBNaWNyb3NvZnQgT2ZmaWNlACH5BAEAAAAALAAABAAH ABcAgQAAAADM//8A/wECAwIUjI+py40Ao5y02out2Lz7D4ZiVwAAOw== ------=_NextPart_01C5BA16.295154D0 Content-Location: file:///C:/752BCE74/PsycGR20050914ppt_files/slide0009.htm Content-Transfer-Encoding: quoted-printable Content-Type: text/html; charset="us-ascii" Clinical Management of Dementia
Projected Incidence of Dementia
in the US by Age: 1980-2050
Data derived using 2000 US Census Bureau middle-series estimate of population growth. Reproduced w= ith permission. Hebert LE et al. Arch Neurol. 2003;60:1119-1122<= /b>. Copyright  © 2002. American Medical Association. All rights reserved.]
In 2050
13.2 million
8.0 million
4.8 million
0.4 million
0
2
4
6
8
10
12
14
2000
2010
2020
2030
2040
2050
Years
3D"Text
Persons With AD
(mi= llions)
65-74
75-84
85+
Total
In 200= 0, the AD patient population in the United States totaled 4.5 million people. Over = the next 50 years, assuming that the age-, race-, and education-specific risk= of disease remains constant and that the longevity of the US population continues to increase, the number of people with AD is expected to increa= se almost 3-fold, to 13.2 million by 2050.
A bett= er understanding of the underlying biology of AD and the discovery of modifi= able risk factors are critical for managing this looming public healthcare cri= sis.













Ref= erences:
Hebert LE, Scherr PA, Bienias JL, Bennett DA, Evans DA. Alzheimer disease in the US population: prevalence estimates using the 2000 census.= Arch Neurol. 2003;60:1119-1122.

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file:///C:/752BCE74/PsycGR20050914ppt_files/slide0009_image030.gif Content-Transfer-Encoding: base64 Content-Type: image/gif R0lGODlhFQA9AHcAMSH+GlNvZnR3YXJlOiBNaWNyb3NvZnQgT2ZmaWNlACH5BAEAAAAALAEAAQAS ADoAggAAAADM/5nMAMwAZv/MAAECAwECAwECAwNZCLo6wzA6F+uc8upN4a5ZB3rPaJ5oqq5s675w zBJ0jdY2hO987/MR4GknKxqPyKRyaRKwBM4KdEqtWq/YKKSKsjK/4LA4HCgHUmYzKl2OsN/wuPwM eaPVkQQAOw== ------=_NextPart_01C5BA16.295154D0 Content-Location: file:///C:/752BCE74/PsycGR20050914ppt_files/slide0010.htm Content-Transfer-Encoding: quoted-printable Content-Type: text/html; charset="us-ascii" Clinical Management of Dementia
Causes of Dementia
•Alzheimer’s dementia =
•Vascular dementia
•Lewy body dementia
•Frontotemporal dementia
•Huntington disease
•Parkinson’s disease
•Pick disease
•Creutzfeldt-Jakob disease=
Alzheimer’s Association; 1999.  Available at: http://www.alz.org/Resources/FactSheets.asp.
Dement= ia is the general designation for mental deterioration characterized by a loss of intellectual abilities of sufficient degree to interfere with social or occupational functioning. Dementia itself is not a disease, but is rather= a syndrome or set of symptoms associated with certain diseases or condition= s. Although nearly all dementias involve memory loss once they become sufficiently advanced, memory may not be noticeably affected in the earli= est stages of some of the non-Alzheimer disorders. In these disorders, the cognitive decline is characterized by other abnormalities of thinking, not necessarily involving memory.
Estima= tes of the prevalence of dementia are complicated by the fact that different types of dementia may occur in overlapping fashion. Although AD is the most common type of dementia, other progressive neurodegenerative dementias also exis= t. These include vascular dementia, also known as multi-infarct dementia, mi= xed AD and vascular dementia, Lewy body dementia, frontotemporal dementia, Huntington disease, Parkinson’s disease, Pick disease, and Creutzfeldt-Jakob disease.









Ref= erences:
Alzheimer’s Association. Alzheimer’s Disease and Rel= ated Dementias Fact Sheet; 1999. &nb= sp; Available at: http://www.alz.org/Resources/FactSheets.asp. Accessed April 1, 2004.

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Alzheimer’s Dementia
•Accounts for almost 60% of all dementias
•Affects over 4 million Americans  =
•Diagnosis: rule out other etiologies
–Careful history, thorough physical and neurologic = exam, lab tests
•Insidious onset and gradual progression
–Onset generally late in life
–Impaired memory, thinking, and behavior
–Average duration from onset of symptoms to death: = 8 to = 10 years
•
American Psychiatric Association. Am= J Psychiatry. 1997;154(suppl 5):1-39; Alzheimer’s Association; 1999.  Available at: http://www.alz.org/Resources/FactSheets.asp.
AD, a = degenerative disease of the brain, is the most common cause of dementia, accounting for almost 60% of all dementias and affecting over 4 million Americans.1=   Diagnosis of AD is a process of elimination to rule out other etiologies of dementia, requiring careful history, thorough physical and neurologic exams, and laboratory tests.1,2   AD generally occurs late in life, most commonly in the 60s, 70s, 80s, and beyond.  Symptom onset is insidious, with gradual decline in memory, thinking, and behavior.  Average duration from onset of symptoms to death is approximately 8 to 10 years (range 3 to 20 years).















Ref= erences:
1. Alzheimer’s Association. Alzheimer’s Disease and Rela= ted Dementias Fact Sheet; 1999.  Available at: http://www.alz.org/Resources/FactSheets.asp. Accessed April 1, 2004;  2. American Psychiatric Association. Practice guideline for the treatment of patients with Alzheimer’s disease and other dementias of late life.  Am J Psychiatry. 1997;154= (suppl 5):1-39.
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Vascular Dementia
•Pure vascular dementia accounts for 15%-20% of all= = dementias
<= span style=3D'font-size:75%;font-weight:normal'>•Another 20= % have both vascular dementia and AD
•Loss of cog= nitive function due to ischemic, hypoperfusive, or hemorrhagic brain disease
(mini-infarcts) •Onset appe= ars to be relatively sudden, as it may take several strokes for symptoms to appear  •Treatment = of high blood pressure and other vascular risk factors may modify progression<= /div>
Cohen D et al. J Gerontol. 1993;48:M255-M260; Alzheimer’s Associati= on; 1999.  Available at: http://www.alz.org/Resources/FactSheets.asp.
Vascul= ar dementia, or multi-infarct dementia, is the second most common form of dementia.1
Pure v= ascular dementia is defined by the loss of cognitive function due to ischemic, hypoperfusive, or hemorrhagic brain lesions as a result of cerebrovascular disease or cardiovascular pathology. While pure vascular dementia accounts for 15% of all dementias, a further 30% of individuals have both vascular dementia and AD.2
Becaus= e the strokes are small and the damage done to brain tissue is limited at first, sympto= ms come on gradually and may not be immediately noticeable. Symptoms are var= ied and usually reflect increasing difficulty to perform everyday activities. Once symptoms become apparent, precautions to prevent additional strokes = by controlling blood pressure and other vascular risk factors may slow the progression of vascular dementia.1












Ref= erences:
1. Alzheimer’s Association. Alzheimer’s Disease and Related Dementias Fact Sheet; 1999.&= nbsp; Available at: http://www.alz.org/Resources/FactSheets.asp. Accessed April 1, 2004; 2. Cohen D, Eisdorfer C, Gorelick P, et al. Psychopathology associated with Alzheimer's disease and related disorders. J Gerontol.= 1993;48:M255-M260.

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Parkinson’s Disease
•Progressive disorder of the CNS =
•Affects >1 million Americans =
•Characterized by tremors, stiffness in the = limbs and joints, speech difficulties, and = <= span style=3D'font-size:88%'>difficulty initiating physical movement  = ;
•Late in the disease course, some patients <= /span><= span style=3D'font-size:88%'>develop dementia and eventually AD
Alzheimer’s Association: 1999.    Available at: http://www.alz.org/Resources/FactSheets.asp.
Parkin= son’s disease is a progressive neurologic disorder of the central nervous system (CNS) that affects over 1 million Americans. Parkinson’s disea= se results from degeneration of neurons in a region of the brain that contro= ls movement. This degeneration creates a shortage of the neurotransmitter dopamine, which causes tremors, stiffness in the limbs and joints, speech difficulties, and difficulty initiating physical movement. Late in the co= urse of the disease, some patients develop dementia and, eventually, AD.















Ref= erences:
Alzheimer’s Association. Alzheimer’s Disease and Rel= ated Dementias Fact Sheet; 1999.  Available at: http://www.alz.org/Resources/FactSheets.asp. Accessed April 1, 2004.
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Lewy Body Dementia
•~20% of patients with AD show diffuse Lewy body = disease postmortem
•Diagnosis requires dementia plus at least 1 of the= = following:
–Recurrent hallucinations
–Spontaneous parkinsonism
–Fluctuations in cognition
•Although initial symptoms may be mild, severe cognitive impairment eventually develops
•Parkinson’s disease may not be clinically ma= nifest
Alzheimer’s Association; 1999.  Available= at: http://www.alz.org/Resources/FactSheets.asp;
Honig LS. Avai= lable at: http://ci.columbia.edu/c1182/web/sect_5/c1182_s5_5.html.
Lewy b= ody dementia clearly overlaps with AD. Dementia with Lewy body disease is present in a= bout 20% of AD patients, as diagnosed by postmortem pathology.1
Diagno= sis of Lewy body dementia requires both dementia and 1 or more of 3 key features: (1) recurrent, well-formed visual hallucinations; (2) spontaneous parkinsonism (ie, increased tone, gait disorder, rest tremor, postural instability, and sometimes orthostatic hypotension); and (3) fluctuations in cognition, including changes in attention and alertness and frequent fainting spells= .2  Although initial symptoms of Lew= y body dementia may be mild, affected individuals eventually develop severe cognitive impairment.
Lewy b= odies are also found in the brains of people with Parkinson’s disease (PD). Some people who are initially diagnosed with PD later go on to develop a demen= tia that closely resembles Lewy body disease.











Ref= erences:
1. Alzheimer’s Association. Alzheimer’s Disease and Related Dementias Fact Sheet; 1999.&= nbsp; Available at: http://www.alz.org/Resources/FactSheets.asp. Accessed April 1, 2004; 2. Honig LS. Recognition of vascular dementia, dementia wi= th Lewy bodies, and frontotemporal dementia. Available at: http://ci.columbi= a.edu/c1182/web/sect_5/c1182_s5_5.html. Accessed April 10, 2004.
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Frontotemporal Dementia
and Pick Disease
•Onset at 45-65 years of age
•Atrophy of frontal and anterior temporal lobes and= degeneration of the striatum
–Pathologic changes include microvacuolation, glios= is of = astrocytes, and prominent cell loss
–Pick disease: ballooned cells (Pick bodies) also present
•Relative preservation of memory, visuospatial skil= ls, = and motor performance compared with AD =
•Prominent/early language impairment and behavioral= deficits
American Psychiatric Association. Am= J Psychiatry. 1997;154(suppl 5):1-39;  Fago JP. Hosp Pract. 2001;36:59-66,69;  Snowden JS et al. Br J Psychiatry. 2002;180:140-143.
Compar= ed with AD, frontotemporal dementia (FTD) has an earlier onset, usually occurring bet= ween 45 and 65 years of age.1  Neuroimaging reveals that in FTD, there is atrophy of the frontal = and anterior temporal lobes and degeneration of the striatum, with relative sparing of the parietal and occipital lobes.1,2  Neuropathologic changes include microvacuolation, gliosis of astrocytes, and prominent cell loss in the frontotemporal lobes.  In Pi= ck disease, a form of FTD, characteristic Pick bodies are also present.= 2,3
Clinic= ally, FTD is differentiated from AD by the fact that patients with FTD have a relative preservation of memory, visuospatial skills, and motor performance.1=   Although some memory loss occurs, memory is usually not as affected as executive function or language. Additionally, visuospatial skills and manual dexterity remain relatively intact so that patients are often still able to work during the early sta= ge of disease.  FTD is characte= rized by prominent language impairment and behavioral symptoms early on.1,= 2  Obsessional behaviors, loss= of social inhibitions, depression, anxiety, and somatization are also common= .









Ref= erences:
1. Snowden JS, Neary D, Mann DMA. Frontotemporal dementia. Br J Psychiatry. 2002;180:140-143; 2. American Psychiatric Association. Practice guideline for the treatment of patients with Alzheimer’s disease and other dementias of late life.  Am J Psychiatry. 1997;154= (suppl 5):1-39; 3. Fago JP. Dementia: causes, evaluation, and management. Hosp Pract. 2001;36:59-66, 69.
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Huntington Disease (HD)
•Inherited, degenerative brain disease, usually = beginning in mid-life •Early symp= toms include involuntary movement of the limbs or facial muscles, difficulty concentrating, and = depression   = •Other sympt= oms include personality change, hallucinations, delusions, slurred speech, and impaired judgment •Children have a 50% chance of inheriting the gene = that causes HD
Wood BE et al. Psychiatr Serv. 2002;53:703-705;  Honig LS. Available at: http://ci.columbia.edu/c1182/web/sect_5/c1182_s= 5_5.html.
Huntin= gton disease (HD) is an inherited, degenerative brain disease that causes both physical and mental disabilities that usually begins in mid-life.1
Early = symptoms vary from person to person and include involuntary movement of the limbs or fa= cial muscles, difficulty concentrating, and depression. Other symptoms include personality change (eg, disinhibition and substance and alcohol abuse), psychosis (ie, hallucinations and delusions), verbal output decline (spontaneous speech), chorea, and gait change.2
Childr= en born to a person with HD have a 50% chance of inheriting the gene that causes HD.&n= bsp; A genetic test is available to confirm a diagnosis of HD and to identify carriers of the HD gene.1













Ref= erences:
1. Wood BE, Kim KK, Harpold GJ. Psychiatric management of Huntington’s disease in extended care settings. Psychiatr Serv.<= /i> 2002;53:703-705; 2. Honig LS. Recognition of vascular dementia, dementia = with Lewy bodies, and frontotemporal dementia. Available at: http://ci.columbia.edu/c1182/web/sect_5/c1182_s5_5.html. Accessed April 1= 0, 2004.
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Creutzfeldt-Jakob Disease (CJD)
•Rare, fatal prion protein disord= er
•Causes rapid progress= ive dementia and other neuromuscular disturbances
•Bovine spongiform encephalopathy (“mad cow disease”) is a variant
of CJD
Alzh= eimer’s Association; 1999.  Available= at: http://www.alz.org/Resources/FactSheets.asp.
Creutz= feldt-Jakob disease (CJD) is a rare, fatal brain disorder that causes rapid progressi= ve dementia and other neuromuscular disturbances. It is caused by a pathogen called a "prion," which is short for "proteinaceous infect= ious particle."  It consists of protein that transforms normal prote= in molecules into infectious ones.
Early = symptoms include failing memory, changes in behavior, and lack of coordination. The disease typically progresses rapidly, and is characterized by pronounced mental deterioration, involuntary movements, and severe difficulties with sight, muscular energy, and coordination.
Recent= ly, a new variant of CJD (vCJD) that has been linked to bovine spongiform encephalopathy (mad cow disease) has heightened awareness of this disease= .












Ref= erences:
Alzheimer’s Association. Alzheimer’s Disease and Rel= ated Dementias Fact Sheet; 1999.  Available at: http://www.alz.org/Resources/FactSheets.asp. Accessed April 1, 2004.
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Behavioral and Psychologi= cal Symptoms of Dementia
(BPSD)
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Psychological Symptoms
Occurring in Dementia
<= span style=3D'font-weight:normal'>•Delusions
<= span style=3D'font-weight:normal'>•Hallucinations
<= span style=3D'font-weight:normal'>•Misidentifications
<= span style=3D'font-weight:normal'>•Depression
•Sleeplessness
<= span style=3D'font-weight:normal'>•Anxiety
Finkel SI et al. Int Psychogeriatr.= 1996;8(suppl 3):497-500.
The ps= ychological symptoms of dementia are mainly assessed on the basis of interviews with patients and caregivers. It is estimated that approximately 90% of people with dementia experience psychological symptoms that may or may not be directly linked to cognition. These include delusions (false beliefs, eg, that possessions are being stolen), auditory or visual hallucinations, misidentifications (not recognizing family, friends, or locations), depression, sleeplessness, and anxiety (repeatedly asking questions about= an upcoming event or fear of being left alone).
Delusi= ons have been reported in up to 73% of those with dementia, hallucinations in 15% to 49= %, misidentifications in 23% to 50%, and depression in up to 80%.










Ref= erences:
Finkel SI, Costa e Silva J, Cohen G, Miller S, Sartorius N.  Behavioral and psychological sig= ns and symptoms of dementia: a consensus statement on current knowledge and implications for research and treatment. Int Psychogeriatr. 1996;8(suppl 3):497-500.
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Behavioral Symptoms Associa= ted = With Dementia
•Aggression
•Wandering
•Restlessness
•Agitation
•Culturally inappropriate behavior
•Sexual disinhibition
•Hoarding
•Pacing
•Screaming
•Crying
•Cursing
•Apathy
•Repetitive questioning
•Shadowing (stalking)
Fin= kel SI et al. Int Psychogeriatr. 1996;8(suppl 3):497-500.
The be= havioral symptoms of dementia are typically identified by directly observing wheth= er patients exhibit disturbed behaviors, such as physical aggression, wander= ing, restlessness, agitation, culturally inappropriate behavior, sexual disinhibition, hoarding, pacing, screaming, crying, cursing, apathy, repetitive questioning, and shadowing or stalking.1
Among = those with dementia, 90% are expected to develop significant behavioral problems at = some point in the course of their illness, irrespective of the level of cognit= ive impairment.2  Alt= hough the cognitive disturbances of dementia have received the most attention in terms of targeted pharmacotherapy, behavioral disturbances cause consider= ably greater morbidity and may be more amenable to treatment with drugs.2=
Behavi= oral symptoms that require constant supervision or involve aggressive acts place a grea= ter burden on caregivers than simply assisting with activities of daily livin= g.1 Even nonaggressive behavioral symptoms can increase caregiver distress because the demands they make on the caregiver’s time and attention= are less predictable than those of routine daily care.








Ref= erences:
1. Finkel SI, Costa e Silva J, Cohen G, Miller S, Sartorius N.  Behavioral and psychological sig= ns and symptoms
of dementia: a consensus statement on current knowledge and implications for research and treatment. 
Int Psychogeriatr. 1996;8(suppl 3):497-500; 2. Desai AK, Grossbe= rg GT. Recognition and management of behavioral disturbances in dementia. J Primary Care Companion J Clin Psychiatry. 2001;3:93-109.
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Jost BC, Grossberg GT. J Am Geriatr Soc. 1996;44:1078-1081. Reprinted with permission.=
Peak Frequency of Behavioral and Psychological Symptoms as AD Progresses
100
80
60
40
20
0
-40
-30
-20
-10
0
10
20
30
Months Before Diagnosis<= /span>
3D"Text
Prevalence= (% of patients)
=
Months After Diagnosis
Sexually inappropriate behavior
Suicidal
ideation
Agitation
Diur= nal
rhythm
Irritability
Wandering
Aggression
Hallucinations
Delusions
Accusatory
behavior
Paranoia
Depression
Anxiety
Social
withdrawal=
Mood
change
Socially unacceptable behavior
Jost a= nd Grossberg studied the prevalence and time of onset for behavioral and psychological symptoms in patients with AD.  As seen on this slide, onset of BPSD may occur more than 30 months before or= up to 20 months after the initial diagnosis of AD. At the early stages, soci= al withdrawal, depression, and paranoia are more common. Suicidal ideation, which is relatively rare in the disease itself, may also occur, along with anxiety and changes in the person’s daily routine.
The mo= re problematic behavioral symptoms, such as irritability, wandering, aggression, hallucinations, delusions, and sexually and socially inappropriate behavi= or, usually occur after the initial diagnosis of AD.  In fact, for the majority of pat= ients, the behavioral symptoms prompt the diagnosis because families can no long= er ignore inappropriate behavior.











Ref= erences:
Jost BC, Grossberg GT. The evolution of psychiatric symptoms in Alzheimer’s disease: a natural history study.
J Am Geriatr Soc. 1996;44:1078-1081.
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ipCjONkLkzvtmGSP5ngB5CtSrkakelbGaIODYOK24JhHGIlGAQA7 ------=_NextPart_01C5BA16.295154D0 Content-Location: file:///C:/752BCE74/PsycGR20050914ppt_files/slide0023.htm Content-Transfer-Encoding: quoted-printable Content-Type: text/html; charset="us-ascii" Clinical Management of Dementia
Etiology of BPSD
•Biologic substrate
•Psychological factors
•Social and environmental aspects
•Medical/medication problems
IPA BPSD educational pack—modul= e 3: etiology. Available at:
http://www.ipa= -online.org/ipaonlinev3/ipaprograms/bpsdrev/toc.asp; Zaraa AS. Geriatrics. 2003;58:48-53.
Althou= gh the exact etiology of BPSD is unknown, available evidence suggests that a combinati= on of biologic, psychological, and social and environmental factors may be responsible for the onset of BPSD.1,2 The relative contributio= n of each factor appears to vary for a particular symptom or group of symptoms. Although behavioral and psychological symptoms in patients with dementia = may be due to the disease process itself, BPSD including agitation and psycho= tic symptoms may also be caused by concomitant medical problems that must be recognized and treated appropriately.2
The ne= xt few slides will examine each of these causal sources of BPSD.














Ref= erences:
1. International Psychogeriatric Association (IPA) BPSD educational pack—module 3: etiology.  Available at: http://www.ipa-online.org/ipaonlinev3/ipaprograms/bp= sdrev/toc.asp.  Accessed March 3, 2004; 2. Zaraa= AS. Pharmacologic management of agitation and psychosis in older demented patients. Geriatrics. 2003;58:48-53.
------=_NextPart_01C5BA16.295154D0 Content-Location: file:///C:/752BCE74/PsycGR20050914ppt_files/slide0024.htm Content-Transfer-Encoding: quoted-printable Content-Type: text/html; charset="us-ascii" Clinical Management of Dementia
Possible Biological Basis for BPSD=
•Neurotransmitter changes
–Acetylcholine
–Dopamine
–Norepinephrine
–Serotonin
–Glutamate
•HPA axis overactivity
–Disturbed diurnal cycle
•Neuropathology
Grossberg GT. Int Psychogeriatr. 2002;14(suppl 1):27-49; IPA BPSD educational = pack—module 3: etiology. Available at: http://www.ipa-online.org/ipaonlinev3/ipaprograms/bpsdrev/toc.as= p;
Pomara N et al.