Delirium, Dementia, and Amnestic and Other Cognitive Disorders

The American Psychiatric Publishing
TEXTBOOK OF PSYCHIATRY
Fifth Edition
Edited by Robert E. Hales, M.D., M.B.A., Stuart C. Yudofsky, M.D., Glen O. Gabbard, M.D.
© 2008 American Psychiatric Publishing, Inc. All rights reserved. www.appi.org
CHAPTER 8
Delirium, Dementia, and Amnestic

and Other Cognitive Disorders
James A. Bourgeois, O.D., M.D., F.A.P.M., Jeffrey S. Seaman, M.S., M.D.,
Mark E. Servis, M.D.
Slide show includes…

Topic Headings
Tables and Figures
Key Points
The American Psychiatric Publishing Textbook of Psychiatry, Fifth Edition. Edited by Hales RE, Yudofsky SC, 1
Gabbard GO. © 2008 American Psychiatric Publishing, Inc. All rights reserved. www.appi.org
CHAPTER 8 • Topic Headings
DELIRIUM Prognosis
Definition Mortality
Clinical Features Morbidity
DSM-IV-TR Diagnosis of Delirium Permanent Cognitive Dysfunction
Delirium Subtypes Duration
Etiopathogenesis Treatment and Prevention
Neuronal Integrity Nonpharmacological Interventions
Role of Oxygen Pharmacotherapy
Cardiovascular and Respiratory Reserves Cholinergic Modulation
Oxygen Demand and Anemia Prevention
Anoxia Delirium: Summary
Additional Selective Mechanisms
DEMENTIA
Neurotransmitter Roles
Clinical Features of the Dementias
Melatonin
DSM-IV-TR Classification of Dementias
Neuroanatomic Loci
Cortical Versus Subcortical Dementias
Epidemiology
Cortical Dementias
Inpatient Studies
Subcortical Dementias
Diagnostic and Liaison Challenges
Dementias With Cortical and Subcortical Features
Clinical Evaluation
Epidemiology
History
Comorbidity and Differential Diagnosis
Medication Review
Mild Cognitive Impairment
Interview and Observation
Delirium
Rating Scales
Mood Disorders
Neurological Examination
Amnestic Disorders
Laboratory Tests
Substance Abuse/Dependence
Electroencephalography
Psychotic Disorders and Mental Retardation
Differential Diagnosis
Risk Factors: Precipitants and Baseline Vulnerability
(continued)
CHAPTER 8 • Topic Headings (continued)
Clinical Evaluation
History
Mental Status Examination
Physical Examination
Laboratory Tests
Neuroimaging
Multidisciplinary Referrals
Management
Clinical Management
Pharmacotherapy
Dementia: Summary
AMNESTIC AND OTHER COGNITIVE DISORDERS
Amnestic Disorders
Epidemiology
Etiology
Clinical Features
Selected Amnestic Disorders
Differential Diagnosis
Treatment
Mild Cognitive Impairment
Postconcussion Syndrome
CONCLUSION
CHAPTER 8 • Tables and Figures
Table 8–1. DSM-IV-TR diagnostic criteria for delirium due to . . . [indicate the general medical condition]
Table 8–2. Range of reported frequencies of clinical features of delirium
Figure 8–1. Hypothesized delirium cascade: dopamine–oxygen link.
Figure 8–2. Gaudreau and Gagnon delirium circuit hypothesis.
Table 8–3. Evaluation of delirium
Figure 8–3. Comparison of electroencephalogram, constructional apraxia, and mental status in delirium.
Table 8–4. Delirium versus dementia
Table 8–5. Delirium differential beyond dementia
Figure 8–4. Interrelationship of baseline and precipitating factors in delirium.
Figure 8–5. Lorazepam and the probability of transitioning to delirium.
Table 8–6. Risk factors for delirium
Figure 8–6. Delirium and mortality in intensive care unit patients.
Table 8–7. Risk factors for delirium and intervention protocols
Table 8–8. Reports of atypical antipsychotics in the treatment of delirium
Table 8–9. Diagnostic features of the dementias
Table 8–10. Cortical and subcortical dementia types
Table 8–11. Established and proposed risk factors for dementia of the Alzheimer’s type
(continued)
CHAPTER 8 • Tables and Figures (continued)
Figure 8–7. Histopathology images: -amyloid plaques, neuritic plaques, and neurofibrillary tangles in
Alzheimer’s disease.
Figure 8–8. Schematic view of the main pathological events in Alzheimer’s disease.
Figure 8–9. T2 magnetic resonance image of vascular dementia, multi-infarct type, in a patient with
diabetes mellitus and hypertension.
Figure 8–10. Histopathology images: Lewy body variant of Alzheimer’s disease.
Table 8–12. Potentially reversible etiologies of dementia
Table 8–13. Psychiatric differential diagnosis of dementia
Table 8–14. Laboratory tests for dementia workup
Figure 8–11. Magnetic resonance image of hippocampal volume in a healthy control subject and a patient with
Alzheimer’s disease and hippocampal atrophy.
Figure 8–12. Fluorodeoxyglucose positron emission tomography study of a healthy older control subject
and a patient with Alzheimer’s disease (AD).
Figure 8–13. Fluorodeoxyglucose positron emission tomography study of a patient with late-stage
Alzheimer’s disease.
Table 8–15. Dementia pharmacotherapy
Table 8–16. DSM-IV-TR diagnostic criteria for amnestic disorder due to . . . [indicate the general medical condition]
Table 8–17. DSM-IV-TR diagnostic criteria for substance-induced persisting amnestic disorder
Table 8–18. Causes of amnestic disorders
Summary Key Points
The DSM-IV-TR diagnostic criteria for
delirium require a disturbance in
consciousness/attention and a change
in cognition that develop acutely and
tend to fluctuate (Table 8–1).
TABLE 8–1. DSM-IV-TR diagnostic

criteria for delirium due to . . .
[indicate the general medical
condition]
The disruption of attention is often considered the core symptom of delirium, but deficits can also
occur in perception, memory, language, processing speed, and executive functioning. The reported
frequencies of the clinical features of delirium are shown in Table 8–2.
TABLE 8–2. Range of

reported frequencies of
clinical features of delirium
Source. Modified with permission from Meagher DJ,

Trzepacz PT: “Delirium Phenomenology Illuminates
Pathophysiology, Management, and Course.” Journal of
Geriatric Psychiatry and Neurology 11:150–156, 1998.
Includes data from Voyer et al. 2006.
A proposed causal link between metabolic derangements and the development of delirium has been
presented in Brown (2000) and Bourgeois et al. (2003) and is summarized in Figure 8–1.
FIGURE 8–1. Hypothesized

delirium cascade: dopamine–
oxygen link.
ATP = adenosine triphosphate;

Ca+ = calcium; DA = dopamine;
O2 = oxygen; TH = tyrosine
hydroxylase.
Gaudreau and Gagnon (2005) proposed a neural circuit, as shown in Figure 8–2, whereby the
interactions between neurons utilizing dopamine, acetylcholine, glutamate, and GABA regulate the
thalamocortical glutaminergic tract. Sensory overload, confusion, psychosis, and altered arousal
levels can result when this tract is in a state of dysregulation.
FIGURE 8–2. Gaudreau and

Gagnon delirium circuit
hypothesis.
ACh = acetylcholine; DA = dopamine;

GABA = -aminobutyric acid;
Glu = glutamate.
Source. Reprinted from Gaudreau JD, Gagnon P:

“Psychogenic Drugs and Delirium Pathogenesis: The
Central Role of the Thalamus.” Medical Hypotheses
64:471–475, 2005. Copyright 2005, Elsevier, Inc. Used
with permission.
In the evaluation of delirium, a thorough history provides the majority of diagnostic information
(Table 8–3). Several factors can obscure the clinical picture in the delirious patient, however, and
thus a meticulous approach is indispensable.
TABLE 8–3. Evaluation

of delirium
Utilizing electroencephalography,
Romano and Engel (1944) first
demonstrated that delirious
patients had progressive
disorganization of rhythms and
generalized slowing (Figure 8–3).
Specifically, patients show
slowing of the peak and average
frequencies in addition to
increased theta and delta but
decreased alpha rhythms.
Interestingly, the
electroencephalographic changes
correlate with cognitive
dysfunction and memory and
attention deficits but not with
psychomotor subtype.
FIGURE 8–3. Comparison of

electroencephalogram,
constructional apraxia, and
mental status in delirium.
Most frequently, delirium needs to be distinguished from dementia (Table 8–4). Dementia has an
insidious rather than an acute onset, features chronic memory and executive disturbances, and—
unless it is Lewy body dementia or there is a superimposed delirium—tends to not fluctuate. A
nondelirious dementia patient typically has intact attention and alertness. Dementia is also
characterized by impoverished speech and thinking, as opposed to the confused or disorganized
pattern seen in delirium.
TABLE 8–4. Delirium

versus dementia
Other possibilities to consider in the differential diagnosis of delirium include drug intoxication and
withdrawal, schizophrenia, catatonia, and Bell’s mania (Table 8–5).
TABLE 8–5. Delirium differential beyond dementia
Numerous and widely varying precipitants can activate delirium in susceptible (high baseline
vulnerability) patients. In their landmark study, Inouye and Charpentier (1996) separated out baseline
risks present at admission (e.g., prior cognitive impairment) from precipitants affecting the patient after
admission (e.g., new-onset respiratory insufficiency). Robust patients with less baseline vulnerability
(“more cerebral reserve”) were more resilient to new precipitants after admission (Figure 8–4).
FIGURE 8–4.
Interrelationship of baseline
and precipitating factors in
delirium.
Source. Adapted from Inouye SK, Charpentier

PA: “Precipitating Factors for Delirium in
Hospitalized Elderly Persons: Predictive Model
and Interrelationship With Baseline Vulnerability.”
Journal of the American Medical Association
275:852–857, 1996. Copyright 1996, American
Medical Association. Used with permission.
One of the most common precipitants of delirium is medication. Numerous medications across
many classes have been noted to precipitate delirium. The commonly used benzodiazepine
lorazepam has been shown to independently increase delirium development in intensive care unit
patients (Pandharipande et al. 2006; Figure 8–5).
FIGURE 8–5.
Lorazepam and
the probability of
transitioning to
delirium.
Source. Reprinted from Pandharipande P,

Shintani A, Peterson J, et al: “Lorazepam
Is an Independent Risk Factor for
Transitioning to Delirium in Intensive Care
Unit Patients.” Anesthesiology 104:21–26,
2006. Copyright 2006, Lippincott Williams
& Wilkins. Used with permission.
Prospective studies have identified many precipitants and baseline risks for delirium (Table 8–6). Two
of the most frequently reported risk factors are preexisting cognitive decline and advanced age.
TABLE 8–6. Risk factors for delirium
Source. Benoit et al. 2005; Brown and Stoudemire 1998; Centeno et al. 2004; Culp et al. 2004; Edlund et al. 2001; Foy et al. 1995; Francis et al. 1990; Gaudreau et al.
2005; Gustafson et al. 1988; Henon et al. 1999; Inouye and Charpentier 1996; Inouye et al. 1993; Leung et al. 2005; Lundstrom et al. 2003; Marcantonio et al. 1994; Minden
et al. 2005; Pompei et al. 1994; Rockwood 1989; Rogers et al. 1989; Schor et al. 1992; Williams-Russo et al. 1992; L. M. Wilson 1972.
Research using multivariate and logistic regression analyses has demonstrated that delirium
independently increased mortality risk in study samples. For example, Ely et al. (2004a) found a 6-month
mortality hazard ratio of 3.2 for ICU patients who had been delirious while on the ventilator (Figure 8–6).
FIGURE 8–6. Delirium and mortality in intensive care unit patients.
Source. Ely et al. 2004a.
Several comprehensive, primarily nonpharmacological intervention protocols have been published.
Regrettably, only a few of these reports are methodologically robust. One large, well-designed study was
Inouye et al.’s (1999) Elder Life Program. In this prevention program, researchers selected 426 nondelirious
patients at risk for delirium and sought to address baseline cognitive impairment, sleep, mobility, vision,
hearing, and dehydration (Table 8–7).
TABLE 8–7.
Risk factors
for delirium
and
intervention
protocols
Source. Adapted with

permission from Inouye
SK, Bogardus ST Jr,
Charpentier PA, et al.:
“A Multicomponent
Intervention to Prevent
Delirium in Hospitalized
Older Patients.” New
England Journal of
Medicine 340:669–676,
1999. Copyright 1999,
Massachusetts Medical
Society. All rights
reserved.
(continued)
TABLE 8–7. (continued)
At least 19 English-language reports are available regarding atypical antipsychotics in the treatment of
delirium (Table 8–8). Only one of those 19 reports, however, was a randomized, double-blind trial
(risperidone), and it was powered as a pilot only. However, specialists in psychosomatic medicine have
been successfully using these agents in clinical practice for the past decade despite scanty literature
support and other pressures.
TABLE 8–8. Reports of atypical antipsychotics in the treatment of delirium
Source. Reprinted from Seaman J: “Diagnosis and Treatment of Delirium in 2006.” Psychiatric Times 23(6):1–2, 2006. Copyright 2006, CMP Media LLC. Used with
permission.
According to DSM-IV-TR, core features of
the dementias include multiple cognitive
deficits (anterograde and/or retrograde
memory impairment and aphasia, apraxia,
agnosia, or disturbance in executive
functioning) that cause impairment in role
functioning and represent a significant
decline (Table 8–9). Although the dementias
share core features, specific dementia
syndromes differ in terms of the sequence
of presentation of these and additional
associated clinical features.
TABLE 8–9. Diagnostic features of the

dementias
Source. Adapted from American Psychiatric Association 2000.
(continued)
TABLE 8–9. (continued)
Source. Adapted from American Psychiatric Association 2000.
A distinction is made between
dementias with primarily cortical and
those with primarily subcortical
pathology (Table 8–10). Whereas all
dementias exhibit the same core
clinical features, cortical and
subcortical dementias often differ in
their specific clinical presentation.
TABLE 8–10. Cortical and

subcortical dementia types
Dementia of the Alzheimer’s type
(DAT), the most common dementia,
is estimated to affect nearly 2 million
white Americans. Established and
proposed risk factors for DAT are
shown in Table 8–11.
TABLE 8–11. Established and

proposed risk factors for dementia
of the Alzheimer’s type
The neuropathology of Alzheimer’s disease includes -amyloid deposits, neuritic plaques, and
neurofibrillary tangles (Figure 8–7)
FIGURE 8–7. Histopathology images: -amyloid

plaques, neuritic plaques, and neurofibrillary
tangles in Alzheimer’s disease.
A, Four recognized stages of neuritic plaque development

revealed by the Bielschowsky silver technique. Top left:
Diffuse plaque composed mostly of -amyloid (A) peptide
without increased density of neurites. Top right: Primitive
plaque consisting of A peptide accumulation and increased
numbers of nonenlarged neurites. Bottom left: Mature plaque
with a densely stained central A core surrounded by greatly
enlarged dystrophic neurites. Bottom right: Burned-out (end-
stage) plaque consisting of an isolated mass of A.
B, The classic mature neuritic plaque, about 100 m in
diameter, containing a pale staining amyloid core at its center
that is surrounded by a halo of dystrophic (enlarged)
neurites. Bielschowsky silver technique.
C, A mature neuritic plaque with enlarged dystrophic neurites
but no amyloid core.
D, High magnification view of neurofibrillary tangles, which
appear coarse and stain darkly by the Bielschowsky silver
technique.
Source. Reprinted from Davis RL, Robertson DM (eds): Textbook of Neuropathology, 3rd
Edition, Baltimore, MD, Williams & Wilkins, 1997. Copyright 1997, Williams & Wilkins. Used
with permission.
FIGURE 8–7. (enlarged)
Source. Reprinted from Davis RL, Robertson DM (eds): Textbook of Neuropathology, 3rd Edition, Baltimore, MD, Williams & Wilkins, 1997.
Copyright 1997, Williams & Wilkins. Used with permission.
(continued)
FIGURE 8–7. (enlarged)
Source. Reprinted from Davis RL, Robertson DM (eds): Textbook of Neuropathology, 3rd Edition, Baltimore, MD, Williams & Wilkins, 1997. Copyright 1997, Williams & Wilkins.
Used with permission.
Neurofibrillary tangles (NFTs)—intraneuronal bundles of phosphorylated tau proteins—are an early
pathological change in the hippocampus, amygdala, and entorhinal cortex. Dementia severity is
proportional to the density of NFTs. With accumulated neuron damage, presynaptic terminal density is
decreased. The pathophysiological events in Alzheimer’s disease are represented schematically in
Figure 8–8 (Felician and Sandson 1999).
FIGURE 8–8. Schematic view of the main
pathological events in Alzheimer’s disease.
Amyloid precursor protein (APP) (1) is released into the media
after cleavage by -secretase to form the soluble  APP (2).
Conversely, APP may be internalized (3) and cleaved by - and
-secretases to form -amyloid (A) fragments (4). The protein
A aggregates (5) in fibrillar nonsoluble material to compose
the core of the neuritic plaque (6). Neurofibrillary tangles form
(7). The neurotoxicity of tau and amyloid results in oxidative
stress, with increased intracellular reactive oxygen species
(ROS), and disruption of structures involved in ion homeostasis
such as ion-motive adenosine triphosphatases (8).
Inflammatory responses with reactive glial cells (9) lead to
production of cytokines and complement. Possibly playing key
roles are membrane receptors such as class A scavenger
receptor or receptor for advanced glycation end products (10).
Global decrease occurs in neurotransmitters, including
acetylcholine (11). Potential pharmacological targets: A
protein metabolism (1–5) and aggregation (6); tau protein
metabolism (7); oxidative stress, acting via calcium channels
(8); inflammatory response (9, 10); neurotransmitter modulation
(11); and neuroprotection.
Source. Reprinted with permission from Felician O, Sandson TA: “The Neurobiology and
Pharmacotherapy of Alzheimer’s Disease.” Journal of Neuropsychiatry and Clinical
Neuroscience 11:19–31, 1999. Copyright 1999 American Psychiatric Press, Inc.
Because the cognitive deficits in multi-infarct vascular dementia follow a series of discrete lesions,
progression is stepwise, with relative stability of cognitive status between vascular insults as opposed
to the gradual progression of deficits seen in Alzheimer’s disease. Lesions are generally located in the
subcortical nuclei, frontal lobe white matter, thalamus, and internal capsule and are associated with a
characteristic appearance on MRI of periventricular hyperintensities on the T2 images (Figure 8–9;
Choi et al. 2000).
FIGURE 8–9. T2 magnetic

resonance image of vascular
dementia, multi-infarct type,
in a patient with diabetes
mellitus and hypertension.
The bilateral, symmetrical pattern of white matter

lesions is characteristic of small vessel arterial
disease. Enlarged sulci are consistent with
associated parenchymal loss.
Source. Reprinted with permission from Yock DH: Imaging of CNS Disease:
A CT and MRI Teaching File. St. Louis, MO, Mosby–Year Book, Inc., 1991.
Pathologically, the Lewy body variant is characterized by the presence of Lewy bodies (intraneuronal
eosinophilic inclusion bodies) in subcortical and cortical structures in addition to Alzheimer’s disease
neuropathology (Figure 8–10) (Gomez-Isla et al. 1999).
FIGURE 8–10. Histopathology images: Lewy body variant of Alzheimer’s disease.
In this patient with dementia, the number of plaques and tangles in the neocortex was borderline for the diagnosis of
Alzheimer’s disease. Left, The substantia nigra showed a moderate degree of nerve cell loss and small numbers of
Lewy bodies. Right, Ubiquitin immunohistochemistry revealed multiple Lewy bodies in nerve cells of the cingulate
gyrus.
Source. Reprinted from Davis RL, Robertson DM (eds): Textbook of Neuropathology, 3rd Edition. Baltimore, MD, Williams & Wilkins, 1997. Copyright 1997, Williams & Wilkins.
Used with permission.
Reversible dementias are estimated to account for 1%–10% of dementias. Examples of potentially
reversible dementias are shown in Table 8–12.
TABLE 8–12. Potentially

reversible etiologies of dementia
The patient with cognitive impairment may have psychiatric illnesses other than or in addition to
dementia. Clinical history and examination need to be focused to consider these other diagnostic
possibilities. The psychiatric differential diagnosis of dementia is shown in Table 8–13.
TABLE 8–13. Psychiatric differential diagnosis of dementia
Laboratory tests may be modified on a case-by-case basis. Tests to consider are shown in Table 8–14.
Serum drug levels of medications associated with altered mental status (e.g., tricyclics,
anticonvulsants, digitalis, antiarrhythmics) should be obtained if clinically indicated.
TABLE 8–14. Laboratory

tests for dementia workup
Neuroimaging is increasingly routine in the evaluation of dementia. CT is generally more readily available
and of lower cost than MRI, although MRI’s superior resolution has led to its greater use in dementia
evaluation. In cases of suspected dementia of the Alzheimer’s type, hippocampal atrophy may serve as a
sensitive early marker for cognitive decline (Figure 8–11) (Jack et al. 2000; Petersen et al. 2000).
FIGURE 8–11. Magnetic resonance image of hippocampal volume (arrows) in a healthy control
subject (left) and a patient with Alzheimer’s disease and hippocampal atrophy (right).
Source. Reprinted with permission from Foster NL, Minoshima S, Kuhl DE: “Brain Imaging in Alzheimer Disease,” in Alzheimer Disease, 2nd Edition. Edited by Terry RD,
Katzman R, Bick KL, et al. Philadelphia, PA, Lippincott Williams & Wilkins, 1999, p. 69, Figures 2A and 2B. Copyright 1999, Lippincott Williams & Wilkins.
Functional neuroimaging (e.g., SPECT, PET, in vivo proton MRS), although not currently widely
available, holds promise in the evaluation of the cortical pathology of dementia, particularly when
combined with genetic assessment of patients at risk for clinical dementia (Weiss et al. 2003;
Figures 8–12 and 8–13). Functional neuroimaging techniques may reveal a specific pattern of
parietal and temporal deficits in dementia of the Alzheimer’s type that could lead the physician to
consider earlier treatment with antidementia pharmacotherapy.
FIGURE 8–12. Fluorodeoxyglucose positron emission tomography study of a healthy

older control subject and a patient with Alzheimer’s disease (AD).
The patient demonstrates bilateral temporal and parietal hypometabolism with some involvement of the
posterior cingulate gyrus and relative preservation of primary cortex and basal ganglia. Metabolic activity is
greatest in the visual cortex.
Source. Reprinted with permission from Valk PE, Bailey DL, Townsend DW, et al.: Positron Emission Tomography: Basic Science and Clinical Practice. London,
Springer-Verlag, 2003, pp. 343, 344.
FIGURE 8–13. Fluorodeoxyglucose positron emission tomography study of a patient with
late-stage Alzheimer’s disease.
This patient shows widespread hypometabolism that is still most pronounced in temporal and parietal cortex
and maximal in the left hemisphere (right side of the image). There is relative preservation of metabolism in
visual cortex and sensorimotor cortex bilaterally.
Source. Reprinted with permission from Valk PE, Bailey DL, Townsend DW, et al.: Positron Emission Tomography: Basic Science and Clinical Practice.
London, Springer-Verlag, 2003, pp. 343, 344.
Modern pharmacotherapeutic interventions, including anticholinesterase agents in concert with
other psychopharmacological agents, should be aggressively used early in the disease process to
maintain the patient’s cognitive functional status (Table 8–15).
TABLE 8–15.
Dementia
pharmacotherapy
(continued)
TABLE 8–15.
(continued)
The DSM-IV-TR diagnostic classification of
amnestic disorders is based on etiology. The
criteria for amnestic disorder resulting from a
general medical condition is presented in
Table 8–16.
TABLE 8–16. DSM-IV-TR diagnostic

criteria for amnestic disorder due to . . .
[indicate the general medical condition]
The DSM-IV-TR diagnostic criteria for
amnestic disorder due to the effects of
a substance are listed in Table 8–17.
TABLE 8–17. DSM-IV-TR

diagnostic criteria for
substance-induced persisting
amnestic disorder
The most common etiologies of
amnestic disorders (Table 8–18)
usually involve bilateral damage to
areas of the brain involved in memory,
including the dorsomedial and midline
thalamic nuclei, the hippocampus, the
amygdala, the fornix, and the
mammillary bodies. Unilateral damage
may sometimes be sufficient to
produce memory impairment,
particularly in the case of left-sided
temporal lobe and thalamic structures.
TABLE 8–18. Causes of

amnestic disorders
CHAPTER 8 • Key Points
DELIRIUM
 Delirium is an acute brain disorder manifested by a syndromal array of
neuropsychiatric symptoms.
 Delirium is epidemic among hospitalized patients, especially in the elderly.
 Numerous and widely varying precipitants can activate delirium in vulnerable
patients.
 Delirium likely exerts an independent mortality risk for select populations and
serves as a “medical alarm” for many others.
 Delirium can resolve completely, resolve gradually, or lead to a permanent
cognitive disorder.
 The fundamental goal of treating delirium is to prevent and reverse delirium
and thus mitigate associated morbidity and mortality risks.
DEMENTIA
 Dementia is characterized by amnesia and one or more other impairment(s)
in cognition.
(continued)
CHAPTER 8 • Key Points (continued)
 Cortical dementias feature notable aphasia, apraxia, agnosia, and visuospatial

deficits plus amnesia that is not helped by cueing, whereas subcortical
dementias feature apathy, affective lability, depressed mood, bradyphrenia, and
decreased attention/concentration plus amnesia that is helped by cueing.
 Compared with dementia of the Alzheimer’s type, frontotemporal dementia is
characterized by executive dysfunction, disinhibition, attentional deficits, and
personality changes with relatively preserved memory and visuospatial function.
 Lewy body dementia and Lewy body variant are characterized by fluctuations in
mental status, well-formed visual hallucinations, delusions, depression, apathy,
anxiety, extrapyramidal symptoms, and neuroleptic sensitivity.
 Patients with mild cognitive impairment have memory symptoms validated by
clinical examination and/or testing that is significantly less impairing than full-
spectrum dementia; whether this condition warrants medication treatment for
cognitive symptoms is controversial.
 Neuroimaging is a routine expectation in the workup of dementia.
 A common clinical combination of medications for dementia of the Alzheimer’s
type is an anticholinesterase agent with memantine.
(continued)
CHAPTER 8 • Key Points (continued)
 AMNESTIC AND OTHER COGNITIVE DISORDERS

 Amnestic disorders are characterized by an inability to learn and recall
new information (anterograde amnesia) or an inability to recall previously
learned information (retrograde amnesia).

 Common causes of amnestic disorder include head injury, transient
global amnesia, and benzodiazepines.
 Mild cognitive impairment (MCI) is defined as cognitive decline greater
than expected for a patient’s age and education level but without the
deficits in normal functioning associated with dementia.
 MCI is a risk state for dementia, with more than half of patients with the
amnestic subtype of MCI progressing to dementia within 5 years.
 Postconcussion syndrome (PCS) involves a constellation of somatic,
psychological, and cognitive symptoms resulting from head trauma that
usually resolve within 1 month, although persistent symptoms may
continue for 1 year in 7%–15% of patients.

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The American Psychiatric Publishing

Delirium, Dementia, and Amnestic

Slide show includes…

TABLE 8–1. DSM-IV-TR diagnostic

TABLE 8–2. Range of

Source. Modified with permission from Meagher DJ,

FIGURE 8–1. Hypothesized

ATP = adenosine triphosphate;

FIGURE 8–2. Gaudreau and

ACh = acetylcholine; DA = dopamine;

Source. Reprinted from Gaudreau JD, Gagnon P:

TABLE 8–3. Evaluation

FIGURE 8–3. Comparison of

TABLE 8–4. Delirium

TABLE 8–5. Delirium differential beyond dementia

Source. Adapted from Inouye SK, Charpentier

Source. Reprinted from Pandharipande P,

TABLE 8–6. Risk factors for delirium

FIGURE 8–6. Delirium and mortality in intensive care unit patients.

Source. Ely et al. 2004a.

Source. Adapted with

TABLE 8–8. Reports of atypical antipsychotics in the treatment of delirium

TABLE 8–9. Diagnostic features of the

Source. Adapted from American Psychiatric Association 2000.

Source. Adapted from American Psychiatric Association 2000.

TABLE 8–10. Cortical and

TABLE 8–11. Established and

FIGURE 8–7. Histopathology images: -amyloid

A, Four recognized stages of neuritic plaque development

FIGURE 8–9. T2 magnetic

The bilateral, symmetrical pattern of white matter

FIGURE 8–10. Histopathology images: Lewy body variant of Alzheimer’s disease.

TABLE 8–12. Potentially

TABLE 8–13. Psychiatric differential diagnosis of dementia

TABLE 8–14. Laboratory

FIGURE 8–12. Fluorodeoxyglucose positron emission tomography study of a healthy

TABLE 8–16. DSM-IV-TR diagnostic

TABLE 8–17. DSM-IV-TR

TABLE 8–18. Causes of

 Cortical dementias feature notable aphasia, apraxia, agnosia, and visuospatial

 AMNESTIC AND OTHER COGNITIVE DISORDERS

learned information (retrograde amnesia).

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