Dementia

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In many ways, the frustration experienced bypatients struggling with mild cognitive impairment(MCI) is matched by the frustration ofclinicians facing the challenge of managing thisheterogeneous condition. The prognosis can bevariable, and no proven therapies exist.

Defined as a clinical syndrome involving progressive deterioration in multiple areas of cognitive functioning, dementia is a major cause of disability, institutionalization, and increased mortality among the elderly. Although it can occur in younger persons too, dementia is typically associated with aging. It is often seen as a disease that cannot be prevented or cured. However, there is increasing evidence that some types of dementia can be successfully treated or even reversed.

In patients with dementia who are physically aggressive and dangerous to themselves or others, the use of intramuscular haloperidol or lorazepam may be appropriate. Because haloperidol causes less drowsiness and cognitive impairment than lorazepam, it is preferred in patients with dementia and delirium. The usual dose of haloperidol for elderly patients with dementia is 0.5 to 1 mg; this dose can be repeated every 25 to 30 minutes until the patient is no longer dangerous to self or others. If benzodiazepine or alcohol withdrawal is suspected, lorazepam is the preferred medication. Physical restraints may be appropriate until the medication takes effect.

Given the lack of a good evidence base for pharmacological treatment of neuropsychiatric symptoms of dementia, are there any effective treatments for such problems as agitation, aggression, delusions, hallucinations, repetitive vocalizations, and wandering? A recent review suggests that nondrug interventions that address behavioral issues and unmet needs may be helpful, as may caregiving interventions and the use of bright light therapy.

Theories about the causes of Parkinson disease (PD) are as tangled as the neurofilament proteins of Lewy bodies. However, investigators are teasing out threads of evidence that increasingly implicate environmental factors--perhaps aided and abetted by genetics--as contributors to this common neurodegenerative disorder.

How do you know whether a patient with end-stage dementia is experiencing pain or suffering when the patient has lost the ability to communicate verbally? Experts say a clinician should have a high index of suspicion that a patient with end-stage dementia is experiencing pain or suffering.

By now, many clinical researchers and practitioners recognize the strong association between cognitive impairment and type 2 diabetes, which, in its early stages, is characterized by hyperinsulinemia and insulin resistance. Although this relationship has not been observed uniformly, more than 20 large-scale epidemiologic studies have reported a link between type 2 diabetes and in creased risk of cognitive impairment and dementia, including Alzheimer disease (AD), the most common type of dementia.

Many physicians, including psychiatrists, may shy away from seeing elderly patients with symptoms of dementia because they imagine that there are a large number of alternative diagnoses and that differential diagnosis is complicated. In fact, however, the number of possible diagnoses in most situations is relatively small and the diagnosis of dementia in older patients is certainly feasible in primary care psychiatry.

The numbers of patients with Alzheimer disease (AD), as well as those with severe cognitive impairment caused by traumatic brain injury and stroke, are continuing to increase. This article includes some nonconventional treatment approaches for which the evidence is limited.

Agitation in the Elderly

While dementia is marked by such cognitive deficits as disorientation, memory loss and changes in intellectual functioning, these are not the symptoms that cause the most distress to caregivers.

Signals

Patients with Alzheimer disease (AD) often have Lewy body pathology (LBP). Although the exact significance of LBP is unknown, LBP appears to be more common in persons with familial AD related to gene mutations of presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein. To examine the genetics of LBP, the team from Puget Sound HCS, led by James B. Leverenz, MD, associate professor at the University of Washington in Seattle, reviewed 25 familial AD cases that included 9 known PSEN1 mutations and 14 familial AD cases that included a single PSEN2 mutation. The brain stem, limbic cortex, and neocortex were examined for LBP.

Physicians who use electroconvulsivetherapy (ECT) need tobe vigilant for unstable medicalconditions before and during the courseof treatment. This brief review is intendedto highlight some basic principlesand specific concerns that maybe encountered in the use of ECT inpatients who have comorbid medicalillness.