Dementia with Lewy Bodies

David Weisman, M.D.,1 and Ian McKeith, M.D.2

ABSTRACT

Synucleinopathies, with and without dementia, encompass a wide range of diseases

including Parkinson’s disease, multiple system atrophy, rapid eye movement (REM) sleep
behavior disorder, and dementia with Lewy bodies (DLB). DLB is a neurodegenerative
disorder resulting in slowly progressive and unrelenting dementia until death. Prevalence
studies suggest that it is the second most common dementing illness in the elderly. The
neuropathologic findings of DLB show a wide anatomic range. Lewy bodies and Lewy-
related pathology are found from the brain stem to the cortex and, in many cases, associated
with concurrent Alzheimer’s disease pathology. A recent international consortium on DLB
has resulted in revised criteria for the clinical and pathological diagnosis of DLB
incorporating new information about the core clinical features and improved methods for
their assessment. The presentation of DLB is typically one of cortical and subcortical
cognitive impairments, with worse visuospatial and executive dysfunction than Alzheimer’s
disease. There may be relative sparing of memory especially in the early stages. Core clinical
features of DLB include fluctuating attention, recurrent visual hallucinations, and parkin-
sonism. Suggestive features include REM sleep behavior disorder, severe neuroleptic
sensitivity, and low dopamine transporter uptake in the basal ganglia on functional neuro-
imaging. Additional supportive features that commonly occur in DLB, but with lower
specificity, include repeated falls and syncope, transient, unexplained loss of consciousness,
severe autonomic dysfunction, hallucinations in other modalities, systematized delusions,
depression, relative preservation of medial temporal lobe structures on structural neuro-
imaging, reduced occipital activity on functional neuroimaging, prominent slow wave
activity on electroencephalogram, and low uptake myocardial scintigraphy. Management
of DLB includes pharmacological and nonpharmacological interventions for its cognitive,
neuropsychiatric, motor, and sleep disturbances.

KEYWORDS: Dementia with Lewy bodies, Lewy body variant, dementia, a-synuclein

D ementia with Lewy bodies (DLB) is the sec-
ond most common cause of dementia in the elderly.
Lewy bodies are neuronal inclusions classically associ-
ated with idiopathic Parkinson’s disease. Over the past
two decades, research has suggested that Lewy bodies,
found in up to 30% of autopsied brains, play a significant
role in the spectrum of dementing disorders that have
come to be known as DLB.1
The neuropathologic findings of DLB show a
wide anatomic range. Lewy bodies and Lewy-related
changes are found from the brain stem to the cortex and,
in many cases, associated with concurrent Alzheimer’s
disease pathology. Thus, DLB is probably best thought
of as a spectrum, with a wide range of Lewy body
involvement in the brains of patients with dementia
(Fig. 1). Clinicopathologic studies have identified three

1
Department of Neurosciences and the Alzheimer’s Disease Research
Center, University of California, San Diego; 2University of Newcastle
upon Tyne, Wolfson Research Centre, Newcastle General Hospital,
Newcastle, United Kingdom.
Address for correspondence and reprint requests: David Weisman,
M.D., University of California, San Diego Alzheimer’s Disease Re-
42
search Center, 9500 Gilman Drive, La Jolla, CA 92093.
Dementia; Guest Editor, Jody Corey-Bloom, M.D., Ph.D.
Semin Neurol 2007;27:42–47. Copyright # 2007 by Thieme
Medical Publishers, Inc., 333 Seventh Avenue, New York, NY
10001, USA. Tel: +1(212) 584-4662.
DOI 10.1055/s-2006-956754. ISSN 0271-8235.
 DEMENTIA WITH LEWY BODIES/WEISMAN, McKEITH 43

Figure 1 Relationship of DLB to Alzheimer’s disease and Parkinson’s disease. Diagram is not drawn to epidemiologic scale. AD,
Alzheimer’s disease; LBV, Lewy body variant of AD; DLBD, diffuse Lewy body disease; PDD, Parkinson’s disease with dementia; PD,
Parkinson’s disease; LB, Lewy bodies.

dementia types in which clinical phenomenology may be
related to Lewy bodies. These are:
1. Parkinson’s disease with dementia: Patients with
Parkinson’s disease who become demented at least
1 year after the onset of motor symptoms.
2. Diffuse Lewy body disease: Patients with dementia
and diffuse cortical Lewy bodies pathology without
other significant pathological abnormalities.
3. Lewy body variant of Alzheimer’s disease: Patients
with clinical dementia whose brains display both
cortical Lewy bodies and Alzheimer-type neuro-
pathologic changes. This is the most common form
of Lewy body dementia, occurring in 70% of
patients with DLB.1
Parkinson’s disease,4 Spillantini et al showed that both
Parkinson’s disease and cortical Lewy bodies contained
a-synuclein.5 Alpha-synuclein is a 140 amino acid
protein of unknown function. It is currently believed
that abnormal protein processing gives rise to the cyto-
plasmic collections of a-synuclein, which then coalesce
to form Lewy bodies.6 Using immunohistochemistry,
antibodies to a-synuclein reliably identify Lewy body
pathology.
Thus, despite uncertainties in clinical phenotypes,
pathogenesis, and pathophysiology, the spectrum of
DLB and Parkinson’s disease is now recognized as

PATHOPHYSIOLOGY
The discovery of Lewy bodies within substantia nigra
neurons in patients with Parkinson’s disease was made by
Lewy in 1912.2 These Lewy bodies consist of cytoplas-
mic inclusions within monoaminergic and cholinergic
neurons of the substantia nigra, locus ceruleus, and basal
nucleus of Meynert. They have a dense eosinophilic core
surrounded by a lucent halo and are easily seen with
routine staining. In contrast to Parkinson’s disease, the
neocortical Lewy bodies seen in DLB are smaller, lack a
halo, and are difficult to see under routine staining
conditions (Fig. 2). Because of this, it has been only
20 years since Kosaka et al identified widely distributed
Lewy bodies in the cortex and subcortex of patients with
parkinsonism and dementia.3
On the heels of Polymeropoulos et al’s 1997 Figure 2 Neocortical Lewy body (at tip of arrow) abutting the
discovery that a mutation on the a-synuclein gene nucleus of a neuron (60  ). The stain is anti-a-synuclein with a
(SNCA) on chromosome 4 was associated with familial hematoxylin counterstain.
44 SEMINARS IN NEUROLOGY/VOLUME 27, NUMBER 1 2007

Table 1 Probability That the Pathological Findings Are Associated with a DLB Clinical Syndrome
Alzheimer-Type Pathology
Lewy Body-Type Pathology Braak Stage 0–II Braak Stage III–IV Braak Stage V–VI

Brain stem-predominant Low Low Low

Limbic (transitional) High Intermediate Low
Diffuse neocortical High High Intermediate
12
Data modified from McKeith et al.

belonging to a class of disorders characterized by patho-
logic a-synuclein processing at a cellular level, termed
synucleinopathies.7 Abnormal synuclein processing is
also implicated in multiple system atrophy, which shows
glial a-synuclein-positive cytoplasmic inclusions.
Although 35 to 90% (depending on pathological
definition) of DLB cases prove to have concurrent
Alzheimer-type pathology,1 the molecular relationship
between Lewy bodies and Alzheimer changes is un-
known. The pathological Alzheimer’s disease changes
that accompany DLB are plaque predominant (i.e., there
is usually significantly less tangle pathology than that
seen in typical Alzheimer’s disease brains).8
Whether Lewy bodies have direct or indirect
effects on local neurons remains unclear. Brains of
patients with Lewy bodies demonstrate severe depletion
of both cholinergic and dopaminergic markers.9 Cortical
Lewy bodies, however, do not correlate well with the
clinical severity of dementia, particularly when there is
significant superimposed Alzheimer’s disease pathol-
ogy.10,11 A recent international consortium on DLB
has proposed a new scheme for the pathological assess-
ment of Lewy bodies and Lewy neurites using a-synu-
clein immunohistochemistry and semiquantitative
grading of lesion density, with the pattern of regional
involvement being more important than total Lewy body
count.12 The new scheme takes into account both Lewy-
related and Alzheimer’s disease-type pathology to allo-
cate a probability that these are associated with the
clinical DLB syndrome (Table 1). It predicts, for exam-
ple, that patients with Lewy bodies found throughout
the neocortex (diffuse neocortical) who have minimal to
moderate Alzheimer’s disease-type pathology (Braak
stage 0 to IV) will have a high probability that their
pathological findings are associated with a DLB clinical
syndrome.
Dementia eventually occurs in 30 to 50% of all
Parkinson’s disease cases.13 Typically, the dementia
occurs 10 years after motor onset. It is characterized by
impairment in executive functions, visuospatial skills,
free-recall memory, and verbal fluency, consistent with
a pattern of frontal/subcortical dementia. The neuro-
pathology of Parkinson’s disease with dementia is con-
troversial. Cortical Lewy bodies have been reported in up
to 90%, with many having Alzheimer-type pathological
changes.14 There is also evidence that cortical Lewy body
involvement, not Alzheimer pathology, determines clin-
ical dementia.15 For the purposes of this review, how-
ever, we will focus our remarks on neocortical Lewy body
disease (i.e., Lewy body variant and diffuse Lewy body
disease).
CLINICAL PRESENTATION
Dementia with Lewy bodies usually presents in late
adulthood, between the ages of 60 and 90, with no
significant gender or ethnic differences in prevalence.16
The disease is a dementing disorder; thus, progressive
and disabling cognitive impairment (of enough severity
to interfere with day-to-day function) is the central
feature.17 Patients show a combination of cortical and
subcortical cognitive impairments with significant atten-
tional deficits in addition to executive and visuospatial
dysfunction (Table 2). Compared with Alzheimer’s dis-
ease, there may be relative sparing of memory especially
in the early stages.18,19 However, because the cognitive
differences are quantitative and not qualitative, the
distinction between cognitive profiles may be difficult.

Table 2 Case Presentation

A 70-year-old man noted that his coordination was ‘‘off’’ and that he was having problems balancing his checkbook for about a year.
On a recent trip to Italy he had became quite confused with difficulty driving. Increasingly, his sleep was disturbed by vivid,
and sometimes violent dreams in which his wife reported that he vocalized and thrashed around in the bed.
His examination showed full orientation and normal calculations. Language was normal. The patient remembered three of five items
on a short-term verbal memory task. He had difficulty drawing a clock and intersecting pentagons. There was mild rigidity but no
postural instability.
Comment: This case is suggestive of DLB because of the prominent visuospatial difficulties, parkinsonism (a core feature), and REM
sleep behavior disorder (a suggestive feature). This patient would meet revised consortium criteria for probable DLB.

The recent international consortium on DLB has
resulted in revised criteria for the clinical diagnosis of
DLB incorporating new information about the core clini-
cal features and improved methods for their assessment.12
Core Features
The core features of DLB include fluctuating cognition,
recurrent visual hallucinations, and spontaneous parkin-
sonism (Table 320).
Fluctuations in cognitive function due to waxing
and waning attention over minutes, hours, or days are
Table 3 Consensus Criteria for DLB
1. Central feature (essential for a diagnosis of possible or
probable DLB)
Dementia defined as progressive cognitive decline of
sufficient magnitude to interfere with normal social or
occupational function; prominent or persistent memory
impairment may not necessarily occur in the early stages
but is usually evident with progression; deficits on tests
of attention, executive function, and visuospatial ability
may be especially prominent
2. Core features (two core features are sufficient for a diagnosis
of probable DLB, one for possible DLB)
Fluctuating cognition with pronounced variations in attention
and alertness
Recurrent visual hallucinations that are typically well formed
and detailed
Spontaneous features of parkinsonism
3. Suggestive features (one or more of these in the presence of
one or more core features is sufficient for a diagnosis of
probable DLB; in the absence of any core features, one or
more suggestive features is sufficient for a diagnosis of
possible DLB; probable DLB should not be diagnosed on
the basis of suggestive features alone)
REM sleep behavior disorder
Severe neuroleptic sensitivity
Low dopamine transporter uptake in basal ganglia
demonstrated by SPECT or PET imaging
4. Supportive features (commonly present but proven to
have diagnostic specificity)
Repeated falls and syncope
Transient, unexplained loss of consciousness
Severe autonomic dysfunction
Hallucinations in other modalities
Systematized delusions
Depression
Relative preservation of mesial temporal lobe structures on
computed tomography/magnetic resonance imaging
Reduced occipital activity on SPECT/PET
Low uptake MIBG myocardial scintigraphy
Prominent slow wave activity on EEG with temporal lobe
transient sharp waves20
Data modified from McKeith et al.12
DEMENTIA WITH LEWY BODIES/WEISMAN, McKEITH 45
difficult to ascertain, even by the most experienced
clinician, but can be very helpful in identifying DLB.
When asked explicitly, caregivers may affirm daytime
drowsiness and sleep, periods of confusion, and episodes
of staring into space.21
Visual hallucinations in DLB are recurrent and
well formed. The hallucinations are a useful symptom
when diagnosing DLB because they are generally
present early in the course of the illness and do not
diminish in later periods. Functional brain imaging
demonstrates altered patterns of activation and blood
flow in the visual cortex. Harding et al showed slightly
increased numbers of Lewy bodies in the anterior and
medial temporal lobe in those with hallucinations.22
Visual hallucinations may predict a good response to
cholinesterase inhibitors.23
Extrapyramidal signs, including bradykinesia, fa-
cial masking, and rigidity, are the most frequent signs of
parkinsonism in DLB patients. Resting tremor is dis-
tinctly uncommon. Parkinsonism is usually bilateral and
occurs with the onset of dementia, although the onset
and the severity of the parkinsonism are highly variable.
There is often more axial rigidity and facial masking in
DLB than in idiopathic Parkinson’s disease. Although
conventional teaching suggests that DLB may be poorly
responsive to levodopa, small trials have shown that
DLB patients tolerate this medication and, in some
cases, show a beneficial response.24
Suggestive Features
In addition to these core items, the recent DLB
consortium identified additional clinical features sug-
gestive of DLB, including rapid eye movement
(REM) sleep disorder, severe neuroleptic sensitivity,
and low dopamine transporter uptake in basal ganglia
demonstrated by single photon-emission computed
tomography (SPECT) or positron-emission tomogra-
phy (PET) imaging.
REM sleep behavior disorder consists of partic-
ularly vivid (and sometimes violent) dreams during
REM sleep without the normal muscle atonia that
prevents movements (other than eye movements) during
dreams. Patients literally act out their dreams, mani-
fested by talking and moving, sometimes with goal-
oriented violence. Because the patients have little mem-
ory of these dreams, the history is dependent on the
patient’s bed partner. Interestingly, the sleep disorder
may be present many years before the onset of demen-
tia.12
Neuroleptic sensitivity to D2 receptor blockers
occurs in about half of DLB patients and, when present,
is considered suggestive of DLB. Because a neuroleptic
‘‘stress test’’ to aid diagnosis is dangerous in this pop-
ulation and may prove irreversibly damaging, this is not
recommended.25
46 SEMINARS IN NEUROLOGY/VOLUME 27, NUMBER 1 2007
Functional imaging of the dopamine transporter
(DAT) defines the integrity of the nigrostriatal dopa-
minergic system and, using specific ligands, provides a
marker for presynaptic neuronal degeneration. Low
striatal DAT activity occurs in DLB but not in Alz-
heimer’s disease and, thus, may be helpful in distinguish-
ing between the two disorders.26
Supportive Features
Commonly present but not specific (‘‘supportive’’)
features of DLB include repeated falls and syncope,
transient unexplained loss of consciousness, severe auto-
nomic dysfunction, hallucinations in other modalities,
systematized delusions, depression, relative preservation
of medial temporal lobe structures on structural
neuroimaging, reduced occipital activity on functional
neuroimaging, prominent slow wave activity on electro-
encephalogram (EEG), and low uptake iodine-123
metaiodobenzylguanidine (MIBG) myocardial scintig-
raphy. Scintigraphy with [I-123] MIBG, which enables
quantification of postganglionic sympathetic cardiac in-
nervation, is reduced in DLB and may have high
sensitivity and specificity in differentiating it from Alz-
heimer’s disease.27 According to the revised DLB con-
sortium criteria, two core features (or one core feature
and one suggestive feature) are sufficient for a diagnosis
of probable DLB; one core feature or one or more
suggestive features are sufficient for a diagnosis of
possible DLB.12
DIAGNOSIS
As with Alzheimer’s disease, definitive diagnosis of DLB
rests on brain autopsy following death. Generally speak-
ing, the accuracy of the clinical diagnosis of DLB is
relatively low based on the consortium for DLB diag-
nostic criteria prior to the recent revision. Using the
older criteria against neuropathology, several studies
have reported acceptable specificities (71 to 95%) but
suboptimal sensitivities (18 to 83%).17,28 There are
currently no cerebrospinal fluid or genotypic biomarkers
available to support a diagnosis of DLB in life.29
TREATMENT
The treatment of DLB generally parallels that for
Alzheimer’s disease. There are no preventatives or cura-
tive agents for DLB.
It has been suggested that acetylcholinesterase
(AChE) inhibitors may be more effective in treating
DLB due to early and prominent central nervous
system cholinergic dysfunction in these patients.30
However, only one double-blind, placebo-controlled,
multicenter trial has evaluated the safety and efficacy of
AChE inhibitors in the treatment of DLB (although
several have examined Parkinson’s disease with demen-
tia). A 5-month study of rivastigmine in DLB showed
a significant benefit of treatment on behavioral symp-
toms as assessed by the Neuropsychiatric Inventory and
on a cognitive speed score. It is not clear if there was an
actual change in cognition.
Presently AChEs are the mainstay of DLB treat-
ment. These medications, including donepezil (Aricept),
rivastigmine (Exelon), and galantamine (Razadyne ER
or Reminyl), block the breakdown of acetylcholine
within the synapse, thereby prolonging its effect on
postsynaptic receptors. The AChE inhibitors are usually
well tolerated at their standard dosing. The primary side
effects associated with treatment are gastrointestinal
(e.g., nausea, vomiting, diarrhea, anorexia, weight loss);
insomnia, vivid dreams, leg cramps, and urinary fre-
quency have also been reported.
It is common to find a patient on an AChE
inhibitor while also maintained on a centrally acting
anticholinergic agent, such as diphenhydramine for sleep,
other antihistamines for allergy, meclizine for dizziness or
vertigo, oxybutynin for bladder control, or a highly
anticholinergic tricyclic (such as amitriptyline) for de-
pression or chronic pain. A careful review of medications,
including over-the-counter agents, is essential to avoid
pharmacological contradictions.
No controlled clinical trials have evaluated the
treatment of parkinsonism in DLB, although there are
reports of small series of DLB patients whose motor
impairments were successfully treated with levodopa.31
Clinical experience suggests that levodopa is less effec-
tive in treating motor impairments in DLB than in
idiopathic Parkinson’s disease. Because the parkinson-
ism may be mild and the dopaminergic agents may
produce side effects, such as a worsening of attention
and visual hallucinations, one should only treat the
movement disorder if the symptoms interfere with
function. Antiparkinsonism drugs should be started at
the lowest possible dose and increased with caution.
Visual hallucinations and delusions may be ex-
acerbated by dopaminergic agents, so tapering of these
agents is typically the first step in managing psychosis.
The visual hallucinations may respond to AChE inhib-
itors32 or antipsychotics. Traditional neuroleptics are
best avoided. If necessary, the newer atypical antipsy-
chotic medications can be used in lowest effective dose
and cautiously. We often begin with quetiapine (Sero-
quel) 12.5 to 25 mg and titrate to an effective dose. It is
worth mentioning that hallucinations that are non-
threatening to the patient and do not disturb function
may not require any pharmacological intervention. Per-
sistent postural hypotension may respond to midodrine
(an a agonist) and fludrocortisone (a mineralocorticoid)
or a reduction in blood pressure medications. REM sleep
behavior disorder typically responds to low doses of
clonazepam prior to sleep.

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