08 Cognitive Disorders

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The American Psychiatric Publishing Textbook of Psychiatry, Fifth Edition. Edited by Hales RE, Yudofsky SC,

Gabbard GO. 2008 American Psychiatric Publishing, Inc. All rights reserved. www.appi.org2

CHAPTER 8 Topic Headings

DELIRIUM

DefinitionClinical Features

DSM-IV-TR Diagnosis of Delirium

Delirium Subtypes

Etiopathogenesis

Neuronal Integrity

Role of Oxygen

Cardiovascular and Respiratory Reserves

Oxygen Demand and AnemiaAnoxia

Additional Selective MechanismsNeurotransmitter Roles

Melatonin

Neuroanatomic Loci

Epidemiology

Inpatient Studies

Diagnostic and Liaison Challenges

Clinical Evaluation

History

Medication Review

Interview and ObservationRating Scales

Neurological Examination

Laboratory Tests

Electroencephalography

Differential Diagnosis

Risk Factors: Precipitants and Baseline Vulnerability

Prognosis

MortalityMorbidity

Permanent Cognitive Dysfunction

Duration

Treatment and Prevention

Nonpharmacological Interventions

Pharmacotherapy

Cholinergic Modulation

PreventionDelirium: Summary

DEMENTIAClinical Features of the Dementias

DSM-IV-TR Classification of Dementias

Cortical Versus Subcortical Dementias

Cortical Dementias

Subcortical Dementias

Dementias With Cortical and Subcortical Features

Epidemiology

Comorbidity and Differential Diagnosis

Mild Cognitive Impairment

DeliriumMood Disorders

Amnestic Disorders

Substance Abuse/Dependence

Psychotic Disorders and Mental Retardation

(continued)


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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

EtiologyClinical Features

Selected Amnestic Disorders

Differential Diagnosis

Treatment

Mild Cognitive ImpairmentPostconcussion Syndrome

CONCLUSION


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CHAPTER 8 Tables and Figures

Table 81. DSM-IV-TR diagnostic criteria for delirium due to . . . [indicate the general medical condition]

Table 82. Range of reported frequencies of clinical features of delirium

Figure 81. Hypothesized delirium cascade: dopamineoxygen link.

Figure 82. Gaudreau and Gagnon delirium circuit hypothesis.

Table 83. Evaluation of delirium

Figure 83. Comparison of electroencephalogram, constructional apraxia, and mental status in delirium.

Table 84. Delirium versus dementia

Table 85. Delirium differential beyond dementia

Figure 84. Interrelationship of baseline and precipitating factors in delirium.

Figure 85. Lorazepam and the probability of transitioning to delirium.

Table 86. Risk factors for delirium

Figure 86. Delirium and mortality in intensive care unit patients.

Table 87. Risk factors for delirium and intervention protocols

Table 88. Reports of atypical antipsychotics in the treatment of delirium

Table 89. Diagnostic features of the dementias

Table 810. Cortical and subcortical dementia types

Table 811. Established and proposed risk factors for dementia of the Alzheimers type

(continued)


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CHAPTER 8 Tables and Figures (continued)

Figure 87. Histopathology images: F-amyloid plaques, neuritic plaques, and neurofibrillary tangles in

Alzheimers disease.

Figure 88. Schematic view of the main pathological events in Alzheimers disease.

Figure 89. T2 magnetic resonance image of vascular dementia, multi-infarct type, in a patient with

diabetes mellitus and hypertension.

Figure 810. Histopathology images: Lewy body variant of Alzheimers disease.

Table 812. Potentially reversible etiologies of dementia

Table 813. Psychiatric differential diagnosis of dementia

Table 814. Laboratory tests for dementia workupFigure 811. Magnetic resonance image of hippocampal volume in a healthy control subject and a patient with

Alzheimers disease and hippocampal atrophy.

Figure 812. Fluorodeoxyglucose positron emission tomography study of a healthy older control subject

and a patient with Alzheimers disease (AD).

Figure 813. Fluorodeoxyglucose positron emission tomography study of a patient with late-stage

Alzheimers disease.

Table 815. Dementia pharmacotherapy

Table 816. DSM-IV-TR diagnostic criteria for amnestic disorder due to . . . [indicate the general medical condition]Table 817. DSM-IV-TR diagnostic criteria for substance-induced persisting amnestic disorder

Table 818. Causes of amnestic disorders

Summary Key Points


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TABLE 81. DSM-IV-TR diagnostic

criteria for delirium due to . . .[indicate the general medical

condition]

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 81).


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TABLE 82. Range ofreported frequencies of

clinical features of delirium

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 82.

Source. Modified with permission from Meagher DJ,

Trzepacz PT: Delirium Phenomenology Illuminates

Pathophysiology, Management, and Course. Journal of

Geriatric Psychiatry and Neurology11:150156, 1998.

Includes data from Voyer et al. 2006.


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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 81.

FIGURE 81. Hypothesized

delirium cascade: dopamine

oxygen link.

ATP = adenosine triphosphate;Ca+ = calcium; DA = dopamine;O2 = oxygen; TH = tyrosinehydroxylase.


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FIGURE 82. Gaudreau and

Gagnon delirium circuit

hypothesis.

Gaudreau and Gagnon (2005) proposed a neural circuit, as shown in Figure 82, 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.

ACh = acetylcholine; DA = dopamine;GABA = K-aminobutyric acid;Glu = glutamate.

Source. Reprinted from Gaudreau JD, Gagnon P:

Psychogenic Drugs and Delirium Pathogenesis: The

Central Role of the Thalamus. Medical Hypotheses

64:471475, 2005. Copyright 2005, Elsevier, Inc. Used

with permission.


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TABLE 83. Evaluation

of delirium

In the evaluation of delirium, a thorough history provides the majority of diagnostic information

(Table 83). Several factors can obscure the clinical picture in the delirious patient, however, and

thus a meticulous approach is indispensable.


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The American Psychiatric Publishing Textbook of Psychiatry, Fifth Edition. Edited by Hales RE, Yudofsky SC,Gabbard GO. 2008 American Psychiatric Publishing, Inc. All rights reserved. www.appi.org

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FIGURE 83. Comparison of

electroencephalogram,

constructional apraxia, and

mental status in delirium.

Utilizing electroencephalography,

Romano and Engel (1944) first

demonstrated that delirious

patients had progressive

disorganization of rhythms and

generalized slowing (Figure 83).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 andattention deficits but not with

psychomotor subtype.


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TABLE 84. Delirium

versus dementia

Most frequently, delirium needs to be distinguished from dementia (Table 84). 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 deliriumtends 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.


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TABLE 85. Delirium differential beyond dementia

Other possibilities to consider in the differential diagnosis of delirium include drug intoxication and

withdrawal, schizophrenia, catatonia, and Bells mania (Table 85).


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FIGURE 84.

Interrelationship of baseline

and precipitating factors in

delirium.

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 84).

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

275:852857, 1996. Copyright 1996, American

Medical Association. Used with permission.


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FIGURE 85.

Lorazepam and

the probability of

transitioning to

delirium.

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 85).

Source. Reprinted from Pandharipande P,

Shintani A, Peterson J, et al: Lorazepam

Is an Independent Risk Factor forTransitioning to Delirium in Intensive Care

Unit Patients. Anesthesiology104:2126,

2006. Copyright 2006, Lippincott Williams

& Wilkins. Used with permission.


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TABLE 86. Risk factors for delirium

Prospective studies have identified many precipitants and baseline risks for delirium (Table 86). Two

of the most frequently reported risk factors are preexisting cognitive decline and advanced age.

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. W ilson 1972.


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FIGURE 86. Delirium and mortality in intensive care unit patients.

Research using multivariate and logistic regression analyses has demonstrated that delirium

independentlyincreased mortality risk in study samples. For example, Ely et al. (2004a) found a 6-monthmortality hazard ratio of 3.2 for ICU patients who had been delirious while on the ventilator (Figure 86).

Source. Ely et al. 2004a.


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TABLE 87.

Risk factors

for delirium

and

intervention

protocols

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 87).

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

EnglandJournal ofMedicine 340:669676,

1999. Copyright 1999,

Massachusetts Medical

Society. All rights

reserved.

(continued)


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TABLE 87. (continued)


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TABLE 88. Reports of atypical antipsychotics in the treatment of delirium

At least 19 English-language reports are available regarding atypical antipsychotics in the treatment of

delirium (Table 88). 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.

Source. Reprinted from Seaman J: Diagnosis and Treatment of Delirium in 2006. Psychiatric Times 23(6):12, 2006. Copyright 2006, CMP Media LLC. Used with

permission.


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TABLE 89. Diagnostic features of the

dementias

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 rolefunctioning and represent a significant

decline (Table 89). Although the dementias

share core features, specific dementia

syndromes differ in terms of the sequence

of presentation of these and additional

associated clinical features.

(continued)

Source. Adapted from American Psychiatric Association 2000.


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TABLE 89. (continued)

Source. Adapted from American Psychiatric Association 2000.


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TABLE 810. Cortical and

subcortical dementia types

A distinction is made between

dementias with primarily cortical and

those with primarily subcortical

pathology (Table 810). Whereas all

dementias exhibit the same coreclinical features, cortical and

subcortical dementias often differ in

their specific clinical presentation.


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TABLE 811. Established and

proposed risk factors for dementia

of the Alzheimers type

Dementia of the Alzheimers 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 811.


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FIGURE 87. Histopathology images: F-amyloid

plaques, neuritic plaques, and neurofibrillarytangles in Alzheimers disease.

The neuropathology of Alzheimers disease includes F-amyloid deposits, neuritic plaques, and

neurofibrillary tangles (Figure 87)

A, Four recognized stages of neuritic plaque developmentrevealed by the Bielschowsky silver technique. Top left:

Diffuse plaque composed mostly ofF-amyloid (AF) peptide

without increased density of neurites. Top right: Primitiveplaque consisting of AF peptide accumulation and increasednumbers of nonenlarged neurites. Bottom left: Mature plaque

with a densely stained central AF core surrounded by greatlyenlarged dystrophic neurites. Bottom right: Burned-out (end-stage) plaque consisting of an isolated mass of AF.B, The classic mature neuritic plaque, about 100 Qm indiameter, containing a pale staining amyloid core at its centerthat is surrounded by a halo of dystrophic (enlarged) neurites.Bielschowsky silver technique.

C, A mature neuritic plaque with enlarged dystrophic neuritesbut no amyloid core.

D, High magnification view of neurofibrillary tangles, whichappear coarse and stain darkly by the Bielschowsky silvertechnique.

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.


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FIGURE 87. (enlarged)

(continued)

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.


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FIGURE 87. (enlarged)

Source. Reprinted from Davis RL, Robertson DM (eds): Textbook of Neuropathology, 3rd Edition, Baltimore, MD, Williams & Wilkins, 1997. Copyright 1997, W illiams & Wilkins.

Used with permission.


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FIGURE 88. Schematic view of the main

pathological events in Alzheimers disease.

Neurofibrillary tangles (NFTs)intraneuronal bundles of phosphorylated tau proteinsare 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 Alzheimers disease are represented schematically in

Figure 88 (Felician and Sandson 1999).

Amyloid precursor protein (APP) (1) is released into the mediaafter cleavage by E-secretase to form the soluble EAPP (2).

Conversely, APP may be internalized (3) and cleaved by F- andK-secretases to form F-amyloid (AF) fragments (4). The proteinAF aggregates (5) in fibrillar nonsoluble material to compose thecore 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), anddisruption of structures involved in ion homeostasis such as ion-motive adenosine triphosphatases (8). Inflammatory responseswith reactive glial cells (9) lead to production of cytokines andcomplement. Possibly playing key roles are membranereceptors such as class A scavenger receptor or receptor for

advanced glycation end products (10). Global decrease occursin neurotransmitters, including acetylcholine (11). Potential

pharmacological targets:AF protein metabolism (15) andaggregation (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 Alzheimers Disease. Journal of Neuropsychiatry and Clinical

Neuroscience 11:1931, 1999. Copyright 1999 American Psychiatric Press, Inc.


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FIGURE 89. T2 magnetic

resonance image of vascular

dementia, multi-infarct type,

in a patient with diabetes

mellitus and hypertension.

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 Alzheimers 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 89;

Choi et al. 2000).

The bilateral, symmetrical pattern of white matterlesions is characteristic of small vessel arterialdisease. Enlarged sulci are consistent with

associated parenchymal loss.

Source. Reprinted with permission from Yock DH: Imaging of CNSDisease:

A CT and MRI Teaching File. St. Louis, MO, MosbyYear Book, Inc., 1991.


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FIGURE 810. Histopathology images: Lewy body variant of Alzheimers disease.

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 Alzheimers disease

neuropathology (Figure 810) (Gomez-Isla et al. 1999).

In this patient with dementia, the number of plaques and tangles in the neocortex was borderline for the diagnosis ofAlzheimers disease. Left, The substantia nigra showed a moderate degree of nerve cell loss and small numbers ofLewy 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.


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TABLE 812. Potentiallyreversible etiologies of dementia

Reversible dementias are estimated to account for 1%10% of dementias. Examples of potentially

reversible dementias are shown in Table 812.


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TABLE 813. Psychiatric differential diagnosis 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 813.


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TABLE 814. Laboratory

tests for dementia workup

Laboratory tests may be modified on a case-by-case basis. Tests to consider are shown in Table 814.

Serum drug levels of medications associated with altered mental status (e.g., tricyclics,

anticonvulsants, digitalis, antiarrhythmics) should be obtained if clinically indicated.


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FIGURE 811. Magnetic resonance image of hippocampal volume (arrows) in a healthy control

subject (left) and a patient with Alzheimers disease and hippocampal atrophy (right).

Neuroimaging is increasingly routine in the evaluation of dementia. CT is generally more readily available

and of lower cost than MRI, although MRIs superior resolution has led to its greater use in dementia

evaluation. In cases of suspected dementia of the Alzheimers type, hippocampal atrophy may serve as a

sensitive early marker for cognitive decline (Figure 811) (Jack et al. 2000; Petersen et al. 2000).

Source. Reprinted with permission from FosterNL, Minoshima S, Kuhl DE: Brain Imaging in Alzheimer Disease, inAlzheimer 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.


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FIGURE 812. Fluorodeoxyglucose positron emission tomography study of a healthy

older control subject and a patient with Alzheimers disease (AD).

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 812 and 813). Functional neuroimaging techniques may reveal a specific pattern of

parietal and temporal deficits in dementia of the Alzheimers type that could lead the physician to

consider earlier treatment with antidementia pharmacotherapy.

The patient demonstrates bilateral temporal and parietal hypometabolism with some involvement of theposterior cingulate gyrus and relative preservation of primary cortex and basal ganglia. Metabolic activity isgreatest in the visual cortex.

Source. Reprinted with permission from Valk PE, Bailey DL, Townsend DW, et al.: Positron Emission Tomography: BasicScience and Clinical Practice. London,

Springer-Verlag, 2003, pp. 343, 344.


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The American Psychiatric Publishing Textbook of Psychiatry, Fifth Edition. Edited by Hales RE, Yudofsky SC,Gabbard GO. 2008 American Psychiatric Publishing, Inc. All rights reserved. www.appi.org 36

FIGURE 813. Fluorodeoxyglucose positron emission tomography study of a patient with

late-stage Alzheimers disease.

This patient shows widespread hypometabolism that is still most pronounced in temporal and parietal cortexand maximal in the left hemisphere (right side of the image). There is relative preservation of metabolism invisual cortex and sensorimotor cortex bilaterally.

Source. Reprinted w ith permission from Valk PE, Bailey DL, Townsend DW, et al.: Positron Emission Tomography: BasicScience and Clinical Practice.

London, Springer-Verlag, 2003, pp. 343, 344.


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TABLE 815.

Dementia

pharmacotherapy

Modern pharmacotherapeutic interventions, including anticholinesterase agents in concert with

other psychopharmacological agents, should be aggressively used early in the disease process to

maintain the patients cognitive functional status (Table 815).

(continued)


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TABLE 815.

(continued)


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TABLE 818. Causes of

amnestic disorders

The most common etiologies of

amnestic disorders (Table 818)

usually involve bilateral damage to

areas of the brain involved in memory,

including the dorsomedial and midline

thalamic nuclei, the hippocampus, theamygdala, 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.


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CHAPTER 8 Key Points

DELIRIUM

Delirium is an acute brain disorder manifested by a syndromal array ofneuropsychiatric 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)


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

deficits plus amnesia that is not helped by cueing, whereas subcorticaldementias feature apathy, affective lability, depressed mood, bradyphrenia, and

decreased attention/concentration plus amnesia that is helped by cueing.

Compared with dementia of the Alzheimers 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 inmental 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 Alzheimers

type is an anticholinesterase agent with memantine.

CHAPTER 8 Key Points (continued)

(continued)


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CHAPTER 8 Key Points (continued)

AMNESTIC AND OTHER COGNITIVE DISORDERS

Amnestic disorders are characterized by an inability to learn and recallnew 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 patients age and education level but without thedeficits 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 maycontinue for 1 year in 7%15% of patients.

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08 Cognitive Disorders