International Psychogeriatrics (2018), 30:2, 273–280 © International Psychogeriatric Association 2017

doi:10.1017/S1041610217001855

CASE REPORT
Case series of mild behavioral impairment: toward an
understanding of the early stages of neurodegenerative
diseases affecting behavior and cognition
...........................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................

Alicja Cieslak,1 Eric E. Smith,1 John Lysack1,2 and Zahinoor Ismail1,3

1
Department of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Calgary, Canada
2
Division of Neuroradiology, Cumming School of Medicine, University of Calgary, Calgary, Canada
3
Department of Psychiatry, Mathison Centre for Mental Health Research & Education, University of Calgary, Calgary, Canada

ABSTRACT

Mild behavioral impairment (MBI) is characterized by later life acquired, sustained, and impactful
neuropsychiatric symptoms (NPS) of any severity that cannot be better accounted for by other formal medical
and psychiatric nosology. MBI is an “at risk” state for incident cognitive decline and dementia, and for some,
MBI is the index manifestation of neurodegeneration, observed in advance of cognitive impairment. Initially
described in Frontotemporal Dementia (FTD), MBI evolved to describe a preclinical stage of all cause
dementia, and has been operationalized in the International Society to Advance Alzheimer’s Research and
Treatment-Alzheimer’s Association (ISTAART-AA) proposed research diagnostic criteria. Here, we describe
three cases in which patients diagnosed with a variety of dementing conditions initially presented with NPS to
the Cognitive Neurosciences Clinic at the University of Calgary, Canada. All patients described in our series
were given a final diagnosis of dementia; the etiology supported by clinical, cognitive, and neuroimaging
findings. In all three cases, the progression to dementia was preceded by NPS that meet criteria for MBI.
With these examples, we are able to illustrate that MBI can represent a premonitory stage of dementia of
different etiologies. These cases demonstrate early use of the MBI checklist (MBI-C). The cases presented
in this series serve as examples of NPS as early manifestations of dementia. Our case examples include both
FTD and AD, and demonstrate that before a diagnosis of a neurodegenerative disease is considered, often
patients will be diagnosed with and treated for a psychiatric condition. These early NPS can be characterized
within the domains outlined in the ISTAART-AA MBI criteria, and detected with the MBI-C, which may
help clinicians consider neurodegenerative disease in the differential diagnosis of later life onset psychiatric
symptomatology.

Key words: mild behavioral impairment, neuropsychiatric symptoms, frontotemporal dementia, Alzheimer’s disease, preclinical dementia,
prodromal dementia

Introduction by other formal medical and psychiatric nosology.

MBI is an “at risk” state for incident cognitive
Mild behavioral impairment (MBI) is increasingly decline and dementia, and for some, MBI is
recognized as a premonitory stage of dementia. the index manifestation of neurodegeneration,
Initially, conceived as a descriptor of pre-FTD observed in advance of cognitive impairment.
behavioral changes (Taragano et al., 2009), the The International Society to Advance Alzheimer’s
construct has evolved to describe a preclinical stage Research and Treatment-Alzheimer’s Association
of all cause dementia (Ismail et al., 2016). MBI (ISTAART-AA) has published proposed research
is characterized by later life acquired, sustained, diagnostic criteria for MBI which operationalize
and impactful neuropsychiatric symptoms (NPS) the relationship between mild cognitive impairment
of any severity that cannot be better accounted for (MCI) and MBI, in that MBI can occur in advance
of MCI, or in concert with MCI, or even after MCI
Correspondence should be addressed to: Zahinoor Ismail, 3280 Hospital Dr. NW, (but by definition, in advance of formal dementia
TRW Building First Floor, Mathison Centre, Calgary AB, T2N 2Z6, Canada. diagnosis) (Ismail et al., 2016).
Phone: +1 403 210 6900. Email: zahinoor@gmail.com. Received 16 Feb 2017;
revision requested 4 Apr 2017; revised version received 20 Jun 2017; accepted However, the measurement of NPS in pre-
20 Aug 2017. First published online 11 October 2017. clinical populations remains challenging and
274 A. Cieslak et al.
underappreciated, where screening priorities are
for cognitive symptoms and not neurological or
neuropsychiatric ones (Ismail and Mortby, 2017).
NPS have been long described in dementia, and
rating scales for NPS in neurodegenerative diseases
are dementia focused, generally with a short 2–
4 week reference range, and are silent on the
natural history and onset, course, and duration of
symptoms. Thus, it is not yet common practice
to consider formal neurodegenerative disease NPS
scales in preclinical populations, when formal
psychiatric and neurological illnesses are usually the
subject of concern. An MBI specific rating scale has
been developed, the MBI checklist (MBI-C, www.
MBItest.org) which is based on the ISTAART-AA
MBI criteria. The goal of the MBI-C is to assist
in the assessment of later life onset NPS, with
neurodegenerative disease in mind.
Given the novelty of the MBI concept and the
importance of considering NPS preceding all cause
dementia (and not just FTD), we present a series
of three cases from the Cognitive Neurosciences
Clinics at the University of Calgary, Canada, which
illustrate clinical manifestations of MBI. For all
cases, MBI diagnosis was made in accordance
with the ISTAART-AA MBI criteria, based on
clinical history from patient and informant. The
MBI-C was used to detect and describe the NPS
in this clinical setting, and was completed by
the informant. Case 1 presents the clinical case
of a 57-year old man who met MBI criteria
for affective dysregulation and impulse dyscontrol
and who went on to develop Frontotemporal
Dementia (FTD). Case 2 presents the clinical
case of a 78-year old man who met the MBI
criteria for decreased motivation and went on to
develop probable Alzheimer’s disease. Finally, case
3 presents the clinical case of a 64 year-old woman
who presented with co-morbid MBI and MCI,
meeting the MBI criteria for decreased motivation
and affective dysregulation and who progressed
to probable Alzheimer’s disease. Informed consent
letters were obtained from all patients or their
formally designated substitute decision makers.
Case 1: Affective dysregulation and impulse
dyscontrol
A 57 year-old male initially manifested behavioral
symptoms at the age of 54. He presented with a
three-year history of anxiety, irritability, and anger,
followed one year later by problems with attention
and planning. Ultimately, a clinical diagnosis of
FTD was made, according to the International
Behavioral Variant FTD Criteria Consortium
clinical diagnostic criteria for behavioral variant
FTD (Rascovsky et al., 2011).
Symptom presentation
The patient’s wife first noticed changes in his
personality about three years prior to clinic
assessment, one year after they had moved from
overseas. The patient became short-tempered and
easily frustrated. It seemed to the patient’s wife that
his angered responses were out of proportion to
the situation. For instance, he smashed and broke
their computer after having difficulty in operating
it during an online video call. There were multiple
other examples of the patient causing physical
damage to their home in periods of frustration,
for instance by punching holes in walls. This
behavior was out of keeping with his premorbid
personality.
The patient’s wife initially discounted the
changes as situational, given their move and
change in living situation, but these personality
changes persisted and were followed by cognitive
symptoms. Eventually, the patient also became
easily distractible and less attentive, having a harder
time keeping track of information and remembering
details of conversations. He remained functional
with respect to activities of daily living and as far
as his wife was aware he remained able to perform
work duties without complaints from coworkers or
supervisors as to his work performance. The patient
worked as a manager at a home renovation and
supplies store. His wife reported the one oddity
she noticed was that he had started to bring items
home from work. She would find these items in
the pockets of his clothes. The patient told his
wife that he had forgotten to put these items back
before leaving work, but it was unclear if this
was due to forgetfulness or if it was new-onset
shoplifting.
Clinical assessment
Cognitive testing on initial assessment included the
Consortium to Establish a Registry for Alzheimer’s
Disease (CERAD) battery in which he scored
121. His Mini-Mental Status Exam (MMSE) score
was 28/30. His Montreal Cognitive Assessment
(MoCA) score was 26/30. He drew a normal clock.
His Frontal Assessment Battery score was 17 out
of 18. His Geriatric Depression Scale (GDS) score
3/15. All scores were within normal limits.
Neuroimaging ordered at initial assessment
included a non-contrast CT scan of the head, which
showed mild atrophy of the frontal lobes bilaterally.
There were contraindications to performing MRI.
An FDG PET scan of the brain, done within two
months, showed hypometabolism in the frontal and
temporal lobes and to a milder degree in the left
insular cortex supportive of early changes related to
FTD (Figure 1).

Figure 1. (Colour online) Case 1 (a) Non-contrast CT head showing mild atrophy of the frontal lobes bilaterally (b) FDG PET scan brain
showed hypometabolism in the frontal and temporal lobes and to a milder degree in the left insular cortex.
Neuropsychiatric symptoms
At initial consultation, clinical assessment of NPS
using the neuropsychiatric inventory questionnaire
(NPI-Q), revealed moderate levels of disinhibition
while levels of agitation and irritability were rated
as mild. Administered at the same time, the MBI-
C showed moderately severe symptoms of agitation,
aggressiveness, argumentativeness, and impulsivity.
Disinhibition and loss of empathy were noted to
be present and mild in the severity rating. Thus,
at initial consultation, the patient met ISTAART-
AA criteria for MBI, exhibiting symptoms in
the MBI domains of affective dysregulation and
impulse dyscontrol. Neuroimaging showed changes
consistent with FTD and in conjunction with
further clinical decline served to support of a final
diagnosis of FTD.
MBI case reports 275
Treatment
The patient showed improvement in his NPS with
the initiation of serotonin reuptake inhibitors but
continued to experience cognitive symptoms.
Case 2: Decreased motivation
A 78 year-old man presented with a four-
year history of cognitive decline, predominantly
affecting short-term memory, but complicated by
accompanying depressive symptoms. The patient
was given a diagnosis of Alzheimer’s dementia
based on NIA-AA criteria (McKhann et al., 2011),
possibly of the frontal variant type. Cholinesterase
inhibitors were initiated. There was improvement of
the patient’s behavioral symptoms and stabilization
of his cognitive performance.
276 A. Cieslak et al.
Symptom presentation
The patient’s wife noted a change in her husband
in the spring four-years prior, when he stopped
attending cancer support group meetings. He had
been attending these meetings for over a decade
before that. In fact, this was a support group that
he had started and watched grow with success. He
was proud of this achievement and his wife became
worried that he no longer showed interest in
remaining involved. He became socially withdrawn
on many fronts, but not overtly sad, which again
was unusual for him as his wife described him as a
previously socially engaged person.
Clinical assessment
Around the same time, his wife noted that he
was more forgetful. His cognitive screening tests
at that time, including the MMSE and MOCA,
were within normal range and he was treated for
depression, with little effect. One year later, his
cognitive symptoms became worse and began to
interfere with daily function. Neuropsychological
testing revealed deficits in attention, episodic
memory and visuospatial function. His wife
reported needing to increasingly provide him
with reminders to take his medications, attend
appointments, and eventually maintain hygiene.
Repeat assessments showed a measurable decline
in cognitive testing. Over the course of the year, his
cognitive screening test scores declined to 25/30 on
his MMSE, 17/30 on the MoCA, and 83 on the
CERAD battery. His GDS score was 0.
Neuroimaging included an MRI brain, which
showed predominantly temporal lobe atrophy and
a mild degree of chronic small vessel disease. FDG
PET scan of the brain one year after he developed
cognitive symptoms showed hypometabolism in the
frontal lobes, including the insular cortex with a
less prominent degree of hypometabolism in the
temporal lobes and the inferior parietal lobes,
posterior cingulate gyrus and the convexity of the
temporal lobes (Figure 2).
Neuropsychiatric symptoms
Retrospectively, the patient would have met
ISTAART-AA criteria for MBI at the time of
initial presentation to primary care, where he
demonstrated late life onset of apathy and social
withdrawal, one-year prior to the emergence of
cognitive symptoms. While he exhibited symptoms
in the MBI domain of decreased motivation/drive,
with a lack of alternative explanations, the most
convenient and related psychiatric diagnosis was
provided – depression. He was treated with
antidepressants, but with little effect.
Case 3: Decreased motivation and MCI
A 64 year-old woman presented with a four-year
history of insidious cognitive decline that was
accompanied by symptoms consistent with apathy
by two years, but initially diagnosed and treated
as depression. A diagnosis of probable Alzheimer’s
dementia based on NIA-AA criteria was later made
(McKhann et al., 2011).
Symptom presentation
Four years into the disease course, the patient
began to show signs of dependency on others, and
her husband took over managing the household
finances. In the year following her loss of inde-
pendence with respect to financial management,
the rate of her decline accelerated as she displayed
loss of insight, a steeper decline in daily function,
and was unable to participate actively during clinic
visits due to the degree of her cognitive impairment.
During cognitive clinic visits, she perseverated
on somatic complaints like neck and shoulder
pain.
Clinical assessment
Cognitive screening tests revealed impairment in
multiple domains including orientation, attention,
recall, language, and construction. Cognitive
screening tests included a CERAD battery on
which she scored 67, MMSE on which she
scored 22/30 and the Rowland Universal Dementia
Assessment Scale (RUDAS) on which she scored
16/30, well below the dementia cut-off of 23. She
scored 5/15 on the GDS.
Neuroimaging included an MRI of the brain
and an FDG PET scan (Figure 3). The MRI brain
showed marked generalized atrophy with bilateral
parietal lobe predominance. The FDG PET scan
showed hypometabolism of the parietal lobes and
to the lesser extent the temporal lobes, more
prominently on the right then the left, a consistent
with changes of neurodegenerative disorder of the
Alzheimer’s type.
Neuropsychiatric symptoms
Retrospectively, the patient would have met
ISTAART-AA criteria for MBI concurrent with
MCI, exhibiting symptoms in the domain of
decreased motivation/drive with initial presentation
of behavioral and cognitive symptoms at age
60. Similar to case 2, in the absence of
alternative nosological options, a diagnosis of
depression was given, and treated unsuccessfully
with antidepressant medications.
 MBI case reports 277

Figure 2. (Colour online) Case 2 (a) MRI brain showed predominantly temporal lobe atrophy and a mild degree of chronic small vessel
disease. (b) FDG PET scan brain showed hypometabolism in the frontal lobes, including the insular cortex with a less prominent degree of
hypometabolism in the temporal lobes and the inferior parietal lobes, posterior cingulate gyrus, and the convexity of the temporal lobes.

Discussion early NPS are given psychiatric diagnoses, which

This series of case reports aimed to illustrate that
when NPS emerge in later life, and result in
what is now defined as MBI, they can represent
a premonitory symptom of dementia. We present
narrative examples of neurodegenerative diseases
affecting cognition that were preceded by NPS as
outlined by the MBI criteria. These cases illustrate
that early NPS occur in different forms of demen-
tia, including but not exclusive to FTD. While
FTD is more traditionally associated with early
neuropsychiatric features, other dementias can also
present early with NPS (Taragano et al., 2009).
Often, patients with neurodegenerative disease and
then evolve into clearer pictures of FTD, AD, or
other dementias (Woolley et al., 2011). However,
being given inappropriate psychiatric diagnoses
can result in potential exposure to unnecessary
medications or delays in the care and management
of the underlying neurodegenerative disease (Jalal
et al., 2014).
Several recent longitudinal studies have suppor-
ted the consideration of later life onset psychiatric
symptomatology as prodromal manifestations of
dementia. A Finnish case-control study of 27,948
pairs assessed linkages between psychiatric illness
and dementia risk. The findings were that the
width of the time window between the exposure
278 A. Cieslak et al.

Figure 3. (Colour online) Case 3 (a) MRI brain showed generalized atrophy with parietal lobe predominance. (b) FDG PET scan showed
hypometabolism of the parietal lobes and to the lesser extent the temporal lobes, more prominently on the right then the left.

(psychiatric syndrome) and the outcome (AD)
affected the results. The authors determined that
having a mental disorder was associated with
higher risk of AD with a five-year time window
but not with a ten-year window, and suggested
that: “some of the disorders may represent
misdiagnosed prodromal symptoms of AD, which
underlies the importance of proper differential
diagnostics among older persons” (Tapiainen et al.,
2017). Similarly, a 28-year follow-up of the
Whitehall II cohort study in the United Kingdom
assessed depression and dementia incidence in
10,308 participants. Late-phase, but not early-
phase depressive symptoms, had a higher risk of
dementia, suggesting that depressive symptoms are
a prodromal feature of dementia or that they share
common etiology (Singh-Manoux et al., 2017).
A 14-year Australian study of 4,922 cognitively
healthy men assessed baseline risk factors for
development of dementia. The association between
depression and dementia was only apparent during
the initial five years of follow-up, suggesting that

depression was more likely a marker of incipient
dementia rather than a modifiable risk factor
(Almeida et al., 2017).
The MBI construct and MBI-C fit nicely into
the discussion raised by these important recent
publications, and that age of onset, the degree to
which symptoms are sustained, and time frames are
essential to accurate diagnosis and understanding
of psychiatric illness. The goal of the MBI-C is
case detection, based on an explicit translation of
the ISTAART-AA MBI criteria. It consists of 34
questions representing the MBI domains of apathy,
emotional dysregulation, impulsivity and agitation,
social cognition, and psychosis and is generally
completed by an informant. The MBI-C uses
non-dementia language intended for functionally
independent adults, a reference range of six-
months, and a stipulation that symptoms are
acquired in later life (Ismail et al., 2017).
To illustrate the applicability of the MBI-C to
the different types of dementia, our cases include
patients with different dementia types, a classic
behavioral variant FTD presentation, a frontal
AD, and an early onset AD. The MBI-C is
not meant to supplant the NPI, but rather to
complement it. The NPI and NPI-Q are the gold
standards for measurement of NPS in dementia,
and for detecting change over time. The NPI
and NPI-Q have been seminal in the evolution of
our understanding of neurodegenerative disease,
and are instrumental in the ongoing assessment
of dementia. We hope the MBI-C will further
establish the importance of recognizing NPS in
dementia, and extend this awareness earlier in the
disease course. The MBI-C may also serve as
an educational tool to emphasize the difference
between chronic symptoms and sustained new-
onset psychiatric symptoms in older adults and
encourage clinicians to think of neurodegenerative
diseases in the differential diagnosis when symp-
toms emerge in late life.
Validation of the MBI-C will allow examination
of the patterns of NPS among the different types
of dementia. In this case report, we show how the
MBI-C can be used as a tool in MBI diagnosis,
and early identification of preclinical dementia. For
example, in our first case, the patient presented
with angry outbursts, irritability, and tendency
to violent expression of anger, representing the
MBI domain of impulsivity and agitation. His
wife described a distinct change in personality
as he progressed to developing FTD. In the
latter two cases, both patients developed early
symptoms consistent with apathy (representing the
MBI domain of drive and motivation, with the
addition of emotional dysregulation in the third),
and eventually developed Alzheimer’s disease.
MBI case reports 279
Just as we see different patterns of cognitive
impairment in the different forms of dementia, it
may be that we will also see different patterns of
early NPS in different pathologies. If we are able to
identify these patterns with the MBI-C, we will be
able to predict with higher sensitivity the etiology
of the dementing illness. For instance, could MBI
with predominant early apathy be the equivalent of
amnestic MCI in predicting the course of illness?
Future research is needed which investigates the use
of the MBI-C to examine whether particular MBI
domains are predominantly present among specific
dementia etiologies. It will be important to link
these early NPS to neurobiology. The ISTAART
group of researchers have explored models that help
conceptualize the neurobiology of neuropsychiatric
disease in dementia, and these models will help
address issues around early detection of identifying
dementia and identifying NPS treatment targets
(Geda et al., 2013; Rosenberg et al., 2015;
Lanctôt et al., 2017). Models include the frontal-
subcortical circuitry, cortico–cortical networks, and
the monoaminergic system; neuroimaging and
biomarkers have implicated all these models in
the neurobiology underlying NPS in AD (Geda
et al., 2013). The MBI-C will be advantageous in
identifying the NPS that manifest at the earliest
stages of AD and as such provide further insight
into the neurobiology of AD. Using neuroimaging
and biomarkers for lesion localization in con-
junction with detecting behavioral changes earlier
with the MBI-C may allow for more accurate
attribution of behavioral symptomology to lesion
location.
A further diagnostic strength of the MBI-C
is that it can be applied as patients evolve in
their dementing illness. Measuring the change that
occurs in behavior will add to the information
gained in measuring cognitive decline, and assist
in overall illness prognostication. Understanding
the evolution of NPS among the different types
of dementia may lead to improved understanding
and management of NPS and cognition in these
patients.
Similar arguments for the utility of identifying
MCI are relevant to identifying patients with
MBI. Early identification of neurodegenerative
illness allows an approach to studying prevention
of progression to dementia and to investigating
future disease modifying agents earlier in the
disease course (Petersen et al., 2001). Furthermore,
we suspect that earlier treatment of behavioral
symptoms might lead to improved functional
outcomes for the patient and may affect the
management of caregiver stress and burden,
consequently improving the patient’s quality of life
(Fischer et al., 2012).
280 A. Cieslak et al.
In summary, NPS can often emerge in later
life, and may predict or precede the cognitive
impairment and dementia. Current psychiatric
nosology does not adequately frame these NPS as a
dementia precursor. The construct of MBI aims to
identify the importance of symptom natural history,
and that later life onset of symptoms require closer
consideration for alternative etiologies. The MBI-
C is a tool designed for MBI case detection,
and may have utility into increasing detection and
awareness of later life onset NPS and their link to
neurodegenerative disease.
Conflict of interest
None.
Acknowledgments
This work was supported through the Alzheimer
Society of Calgary via the Hotchkiss Brain Institute.
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