Delusional disorders of later life suggest a hereditary predisposition. An individual is more likely to develop it if there is another family member who also has delusional disorder or schizophrenia. At least one study has linked the development of delusional disorder to feelings of inferiority within the family. Some researchers suggest that delusional disorders are the product of specific early childhood experiences with an authoritarian family structure. Predisposing factors include social isolation (and isolation caused by vision or hearing impairment), lack of stimulating interpersonal relationships, and physical illness. Severe stress (such as a move to a foreign country) may make an individual vulnerable to developing delusional disorder. Imbalances in neurotransmitters have been shown to cause delusional symptoms, and research continues into studying the effects of such imbalances and the potential to develop delusional disorder.

Delusional disorders commonly begin in middle or late adulthood, usually between ages 40 and 55, but they can occur at a younger age. The disorders affect less than 1% of the population; the incidence is about equal in men and women.

The psychiatric history of a delusional patient may be unremarkable, aside from behavior related to his delusions. He’s likely to report problems with:

• social and marital relationships

• depression

• sexual dysfunction

• social isolation

• hostility

• accepting treatment.

Gathering accurate information from a delusional patient may prove difficult. His responses and behavior
during the assessment interview provide clues that can help to identify his disorder. Family members may confirm your observations—for example, by reporting that the patient is chronically jealous or suspicious. He may deny feeling lonely, relentlessly criticizing or placing unreasonable demands on others.

When assessing the patient, look for:

• unusual communication patterns —he may be evasive, overly talkative with grandiose themes, or make contradictory, jumbled, or irrational statements

• expressions of denial, projection, and rationalization (Once delusions become firmly entrenched, the patient will no longer seek to justify his beliefs. However, if he’s still struggling to maintain his delusional defenses, he may make statements that reveal his condition, such as “People at work won’t talk to me because I’m smarter than them.”)

• accusatory statements—these are characteristic of the delusional patient

• pervasive delusional themes (grandiose or persecutory)

• nonverbal cues, such as excessive vigilance or obvious apprehension when people enter the room.

• Violent behavior

• Suicide

• Legal problems

For characteristic findings in patients with this condition, see Diagnosing delusional disorders.

Assessment also includes:

• neurologic evaluation

• psychological evaluation

• laboratory blood and urine tests, which are used to exclude organic causes of delusions, such as amphetamine-induced psychoses, electrolyte imbalances, hyperadrenalism, pernicious anemia, and thyroid disorders.

Therapy options that have shown effectiveness consist of:

• individual therapy

• cognitive behavioral therapy to recognize and change inappropriate thought patterns

• family therapy

• mobilization of support system for the isolated elderly patient.

• In dealing with the delusional patient, be direct, straightforward, and dependable. Whenever possible, elicit his feedback. Move slowly and matter-of-factly and respond without anger or defensiveness to his hostile remarks.

• Respect the patient’s privacy and space needs. Don’t touch him unnecessarily.

• If the patient allows, take steps to reduce social isolation. Gradually increase social contacts after he has become comfortable with the staff.

• Watch for refusal of medication or food, resulting from the patient’s irrational fear of poisoning.

• Monitor the patient carefully for the adverse effects of antipsychotic drugs: drug-induced parkinsonism, acute dystonia, akathisia, tardive dyskinesia, and malignant neuroleptic syndrome.

• If the patient is taking clozapine, stress the importance of returning weekly to the hospital or an outpatient setting to have his blood count monitored.

• Involve the patient’s family in treatment. Teach them how to recognize an impending relapse, and suggest ways to manage symptoms. These include tension, nervousness, insomnia, decreased concentration ability, and apathy.

• Remember to consider cultural and religious beliefs. Beliefs that may be considered delusional in one culture may be culturally sanctioned in another.

Alzheimer’s is the most common dementia in individuals age 65 and older. At least 50% to 60% of all dementias currently seen are caused by Alzheimer’s disease. In the United States, slightly more than 5 million individuals have Alzheimer’s disease and 4.9 million of those individuals are over age 65. The incidence of Alzheimer’s dementia increases as people age. It’s estimated that 2% of the population ages 65 to 75 have Alzheimer’s dementia, which increases to 42% of the population by age 85 and older.

Alzheimer’s disease is the fifth leading cause of death among older American adults.

The cause of Alzheimer’s dementia is unknown and can only be diagnosed with complete accuracy by the microscopic examination of brain tissue after death. Researchers continue to investigate the influence of biologic, environmental, and genetic factors in attempt to identify the cause of the disease. Studies show that there’s a familial pattern with early-onset cases of Alzheimer’s dementia. Researchers have found that after death, the brain tissue of Alzheimer’s patients exhibits abnormal clusters of beta-amyloid proteins that form plaques, which are found outside and around the neurons in the hippocampus. When the brain tissue is stained, neurofibrillary tangles (twisted nerve cell fibers) are also evident. These tangles impair communication between neurons. It isn’t known if these plaques and tangles are the cause of or the result of the disease, however. Other gross changes in the brain include thickening of the leptomeninges, enlarging ventricles, shrinking of the hippocampus and gyri, widening sulci, and generalized atrophy. There are also lower levels of acetylcholine in the brains of individuals with Alzheimer’s dementia.

The patient with Alzheimer’s dementia typically exhibits four stages of progressive decline in intellectual function, personality changes, behavioral changes, and impairment in judgment. These stages consist of the following:

• Preclinical Alzheimer’s dementia—The hippocampus structure is affected and shrinks over time resulting in both short- and long-term memory loss.

• Stage 1 (mild Alzheimer’s dementia)—The cerebral cortex continues to shrink and additional cognitive losses occur. The patient is usually cooperative and can follow basic instructions. The patient may show signs of:

– memory disturbance, and inability to recall events, which is noticed by others

– apathy

– poor judgment and problem-solving skills

– new carelessness in habits and personal appearance

– poor concentration and short attention span

– disorientation to time

– mild aphasia

– inability to retain new memories

– gradual withdrawal from activities

– wandering and becoming easily lost

– denial of or hiding impairment

– suspiciousness

– irritability

– uncharacteristic motor behavior.

• Stage 2 (moderate Alzheimer’s dementia)—Continued impairment is characterized by:

– language disturbance with impaired word finding and circumlocution (talking around a topic)

– increased apraxia, agnosia, and aphasia

– continuous repetitive behaviors such as pacing

– disorientation to person, place, and time

– worsening irritability

– depression

– delusions and psychosis (possibly)

– inability to perform normal activities without assistance

– altered sleep-wake cycles and wandering at night (possibly)

– motor skill lack of coordination with poor balance and gait.

• Stage 3 (severe Alzheimer’s dementia)—Marked by pervasive plaques and tangles in the brain with severe cognitive impairment. This final stage is characterized by:

– inability to recognize family and friends

– frequent inability to communicate at all (incoherence)

– decreased response to stimuli

– less voluntary movement, leading to complete immobility

– frequent urinary and fecal incontinence

– frequent aspiration

– swallowing problems

– emaciation.

• Loss of ability to care for self

• Increased trauma from falls, wandering, and environmental hazards

• Increased risk of infection caused by aspiration and immobility

• Reduced lifespan

• Increased caregiver and family stress

• Increased societal costs

The diagnosis of Alzheimer’s dementia requires that alternative causes of dementia, some of which may be reversible, must be excluded. Other such causes include the following:

• metabolic disorders, such as vitamin B₁₂, B₁, and B₃ deficiencies

• endocrine disorders, such as hypothyroidism or hypoglycemia

• vascular disorders

• infections that affect the central nervous system, such as human
immunodeficiency virus, Creutzfeldt-Jakob disease, and syphilis

• substance abuse such as with chronic drug and alcohol abuse

• brain injury, such as tumors, hydrocephalus, and trauma

• Huntington’s disease

• Parkinson’s disease

• Pick’s disease, a degenerative disease of the frontal and temporal lobes of the brain.

Tests to aid in diagnosis include:

• cognitive assessment evaluation

• functional dementia scale

• EEG

• computed axial tomography of the head

• magnetic resonance imaging of the head

• cerebrospinal fluid analysis, which may show beta-amyloid deposits

• laboratory tests:

– serum electrolytes

– serum glucose, calcium, blood chemistry

– serum thyroid function tests

– vitamin B₁₂ level

– serum ammonia level

– toxicology screen for drugs or alcohol

– urinalysis

– blood gas analysis.

Once alternative causes of Alzheimer’s dementia have been excluded, a diagnosis can be made if the patient’s symptoms match the criteria in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. (See Diagnosing dementia of the Alzheimer’s type, page 60.)