Dementia: A Focused Review

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Educational Objectives

After reading this article, you will be familiar with:

• The differences between the dementias and their causes
• Differential diagnosis of the dementias
• Treatment strategies for the dementias
• Future direction of clinical studies

Who will benefit from reading this article?
Psychiatrists, child and adolescent psychiatrists, psychologists, primary care physicians, nurse practitioners, and other health care professionals. To determine whether this article meets the continuing education requirements of your specialty, please contact your state licensing and certification boards.

When discussing the concept of cognitive impairment, many terms are used, including dementia, amnestic disorder, cognitive impairment not dementia (CIND), cognitive impairment associated with normal aging, mild cognitive impairment, vascular cognitive impairment, and vascular cognitive impairment not dementia (VCIND). Although definitions of such terms are clinically important, there is significant uncertainty about associating a given cognitive syndrome with specific neuropathology.¹

Definitions

DSM-IV-TR defines dementia as the development of multiple cognitive deficits that include memory impairment and at least 1 of the following cognitive disturbances: aphasia, apraxia, agnosia, or a disturbance in executive functioning. The cognitive deficits must be sufficiently severe to cause impairment in occupational or social functioning and must represent a decline from a previously higher level of functioning. Amnestic disorder includes the inability to learn new information or to recall previously learned information, and deficits can consist of faulty encoding, faulty consolidation, faulty retrieval, or confabulation. The ability to immediately repeat a sequential string of information, such as a digit span, is generally not impaired in amnestic disorder.

CIND is a clinical syndrome that consists of a measurable or evident decline in memory or other cognitive abilities with little impact on day-to-day functioning. However, criteria are not met for dementia as defined by DSM-IV-TR. Cognitive impairment associated with normal aging includes memory retrieval deficiencies, decreased psychomotor speed, decreased reaction time, decreased performance on executive tasks, and decreased visuospatial skills. Although some cognitive impairment is present with normal aging, increasing age does not automatically mean losing all cognitive abilities.

Mild cognitive impairment can be divided into amnestic and nonamnestic subtypes: each subtype has deficits in a single domain or in multiple domains. Key features of the amnestic subtype of mild cognitive impairment include a subjective memory complaint also noticed by an informant, objective deficits in cognition for age, normal functional activities, preserved general cognition, and the absence of dementia. Although Alzheimer dementia most commonly develops in patients with mild cognitive impairment, other types of non-Alzheimer dementia, such as Lewy body dementia, can also occur.²

Vascular cognitive impairment is a heterogeneous group of conditions in which vascular factors are associated with or are the cause of cognitive deficits of any severity. Vascular cognitive impairment is likely the prodrome of vascular dementia and it generally affects executive functions.¹

VCIND is a clinical syndrome of cognitive impairment of a presumed vascular cause, but it is not severe enough to fulfill the criteria for dementia.^3,4

Assessment of patients with cognitive impairment

In the evaluation of cognitive impairment, there is no routine workup. The workup must be individualized for each patient. Assessment begins with a thorough medical, neurological, and psychiatric evaluation, followed by collateral information from caregivers. Current medications (eg, benzodiazepines, anticholinergics, β-blockers, corticosteroids, and opioids) may be contributing to cognitive impairment.^5-9 Neuropsychological testing can help establish the baseline level of cognitive functioning, monitor changes in cognitive functioning over time, differentiate various types of dementia, identify cognitive strengths and weaknesses, guide therapeutic interventions, and de-termine functional capacity. Laboratory studies (Table 1) should be viewed as complementary to––not a substitute for––a complete evaluation.

Differential diagnosis for dementia

Before making a diagnosis of a specific disease process, a proactive and detailed investigation for any possible cause is warranted. Table 2 lists some considerations for the differential diagnosis of dementia.

Delirium may be confused with dementia, although both delirium and dementia can coexist. In delirium, the disturbance of consciousness occurs over a short period (hours to days) and fluctuates over the course of a day. In dementia, the disturbance is more gradual/insidious and generally does not fluctuate, as in delirium. In the early and middle stages of dementia, the patient maintains alertness and attention, but in delirium, attention to the environment is decreased and the level of arousal is altered. Although attention can be impaired in the late stages of dementia, a fluctuating level of consciousness may indicate a superimposed delirium.⁶ Table 3 lists some considerations for the differential diagnosis of delirium.

Major depression can lead to cognitive impairment and must be distinguished from dementia, although both major depression and dementia can coexist. Aphasia, apraxia, and anomia are not features of depression-induced cognitive impairment. Initial symptoms include dysphoria and anhedonia, followed by cognitive impairment. In major depression, “I don’t know” is a common answer to questions about cognition.⁵ Neuropsychological features include impaired performance on tasks that involve effortful processing, memory improvement with cueing, and tendency to abandon tasks because of poor motivation. Elderly depressed patients who have residual cognitive impairment even after improvement of depression usually have an early stage of dementia, and cognitive impairment is exaggerated when depression is superimposed.

Normal pressure hydrocephalus includes a classic triad of dementia, gait disturbance, and urinary incontinence. The apraxic gait disturbance is often the initial presentation, and patients appear to be “glued” to the floor.¹⁰ Patients may present for a psychiatric evaluation with complaints of memory loss, apathy, or depression. In many instances, the cause is unknown. Risk factors include a history of brain hemorrhage, brain surgery, head injury, or meningitis. Neuropsychological features include slowed information processing and difficulty with memory retrieval. Neurosurgical treatment with a shunt is indicated for some patients. However, this treatment is controversial, and serious complications can occur—such as infection, intracerebral hemorrhage, or blockage of the shunt.^11-13