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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.
DOI: 10.1176/appi.books.9781585623402.292211

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Delirium, dementia, and amnestic and other cognitive disorders are classified as cognitive disorders in DSM-IV-TR (American Psychiatric Association 2000). As a group, they represent psychiatric disturbances formerly described as exclusively due to "organic" as opposed to "functional" etiological factors. As research into the etiology and treatment of other psychiatric disorders has progressed, the artificial distinction between organic (an anachronistic term in current clinical practice) and functional psychiatric illness has blurred substantially. Nonetheless, these cognitive disorders generally have clear structural and functional disturbances in brain function as their primary causes. Psychological factors are still very relevant in the patient's experience of symptoms and his or her behavioral and emotional response to illness. Delirium, dementia, and the other cognitive disorders make clear the need for psychiatric evaluation based on the biopsychosocial model of psychiatric illness.

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FIGURE 8–1. Hypothesized delirium cascade: dopamine–oxygen link.ATP = adenosine triphosphate; Ca+ = calcium; DA = dopamine; O2 = oxygen; TH = tyrosine hydroxylase.

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.

FIGURE 8–3. Comparison of electroencephalogram, constructional apraxia, and mental status in delirium.

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.

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.

FIGURE 8–6. Delirium and mortality in intensive care unit patients.Source. Ely et al. 2004a.

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 amyloid core surrounded by greatly enlarged dystrophic neurites. Bottom right: Burned-out (end-stage) plaque consisting of an isolated mass of A amyloid. 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 8–8. 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: -amyloid 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.

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.

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. A, The substantia nigra showed a moderate degree of nerve cell loss and small numbers of Lewy bodies. B, 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.

FIGURE 8–11. Magnetic resonance image of hippocampal volume (arrows) in a healthy control subject (A) and a patient with Alzheimer's disease and hippocampal atrophy (B).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.

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.
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TABLE 8–1. DSM-IV-TR diagnostic criteria for delirium due to . . . [indicate the general medical condition]
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TABLE 8–2. Range of reported frequencies of clinical features of delirium
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TABLE 8–3. Evaluation of delirium
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TABLE 8–4. Delirium versus dementia
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TABLE 8–5. Delirium differential beyond dementia
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TABLE 8–6. Risk factors for delirium
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TABLE 8–7. Risk factors for delirium and intervention protocols
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TABLE 8–8. Reports of atypical antipsychotics in the treatment of delirium
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TABLE 8–9. Diagnostic features of the dementias
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TABLE 8–10. Cortical and subcortical dementia types
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TABLE 8–11. Established and proposed risk factors for dementia of the Alzheimer's type
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TABLE 8–12. Potentially reversible etiologies of dementia
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TABLE 8–13. Psychiatric differential diagnosis of dementia
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TABLE 8–14. Laboratory tests for dementia workup
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TABLE 8–15. Dementia pharmacotherapy
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TABLE 8–16. DSM-IV-TR diagnostic criteria for amnestic disorder due to . . . [indicate the general medical condition]
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TABLE 8–17. DSM-IV-TR diagnostic criteria for substance-induced persisting amnestic disorder
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TABLE 8–18. Causes of amnestic disorders
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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.

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 DAT, FTD is characterized by executive dysfunction, disinhibition, attentional deficits, and personality changes with relatively preserved memory and visuospatial function.

LBD and LBV are characterized by fluctuations in mental status, well-formed visual hallucinations, delusions, depression, apathy, anxiety, extrapyramidal symptoms, and neuroleptic sensitivity.

MCI patients 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 DAT is an anticholinesterase agent with memantine.

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.

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.

PCS is 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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Sample questions:
1.
A range of frequencies of various clinical features of delirium have been reported. Which of the following clinical features is least often reported in delirium?
2.
Changes in selected neurotransmitters have been reported to occur in delirium. Which of the following neurotransmitter changes is widely accepted to play a role in delirium?
3.
Dementia, in contrast to delirium, has which of the following clinical features?
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