NCP Dementia of Alzheimer's Type / Vascular Dementia


Early Onset (At or Below Age 65)
290.10 Uncomplicated
290.11 With delirium
290.12 With delusions
290.13 With depressed mood
Late Onset (After Age 65)
290.0 Uncomplicated
290.3 With delirium
290.20 With delusions
290.21 With depressed mood

(Note: DAT should also be coded on Axis III, 331.0.)


290.40 Uncomplicated
290.41 With delirium
290.42 With delusions
290.43 With depressed mood

Note: In the presence of vascular dementia, the specific underlying medical cause, such as stroke, should be coded on Axis III.

(For dementias due to other general medical conditions, refer to DSM-IV for specific code listing.)

Dementia of the Alzheimer’s type is a specific degenerative process occurring primarily in the cells located at the base of the forebrain that send information to the cerebral cortex and hippocampus. It is the most common form of dementia and is characterized by a steady and global decline. In comparison, vascular dementia reflects a pattern of intermittent deterioration related to multiple infarcts to various areas of the brain. Although the etiologies differ, these two forms of dementia share a common symptom presentation and therapeutic intervention.



These forms of dementia reflect a chronic organic mental disorder with progressive cognitive losses caused by damage to various areas of the brain, depending on underlying pathology. Personality change is common and may be manifested by either an alteration or accentuation of premorbid characteristics with primary deficits in memory and planning and a predisposition to confusion.

Biological Theories

Vascular dementia reflects a pattern of intermittent deterioration in the brain. Symptoms fluctuate and are determined by the area of the brain that is affected. Deterioration is thought to occur in response to repeated infarcts of the brain. Predisposing factors include cerebral and systemic vascular disease, hypertension, cerebral hypoxia, hypoglycemia, cerebral embolism, and severe head injury.

Several studies have shown that antibodies are produced in the brains of individuals with Alzheimer’s disease. Although the triggering mechanism is not known, the reactions are actually autoantibody production, suggesting a possible alteration in the body’s immune system. Although the exact cause of Alzheimer’s disease is unknown, several hypotheses have been supported by varying amounts and quality of research data. The exception is research on environmental causes, such as the ingestion of aluminum, which to date have not been supported by research findings. Research has revealed that, in DAT, the enzyme required to produce acetylcholine is dramatically reduced, especially in the areas of the brain where the senile plaques and neurofibrillary tangles occur in the greatest numbers. This decrease in acetylcholine production reduces the amount of neurotransmitter that is released to cells in the cortex, hippocampus, and nucleus basalis, resulting in a disruption of memory processes. Additionally, the neuritic plaques that accumulate are composed of beta-amyloid, an insoluble protein that is an abnormal breakdown product of the cell membrane constituent amyloid precursor protein (APP). Furthermore, the formation of the customary plaques and tangles appears to be related to the cholesterol-transporting protein, apolipoprotein-E (ApoE), which has been associated with an earlier-than-average age of onset for the common form of Alzheimer’s disease for individuals who carry the ApoE4 genetic variant.

Thus, genetics appears to play a role. Studies suggest a familial pattern of transmission that is four times greater than in the general population. Familial, or early-onset Alzheimer’s, has been linked to defects of genes on chromosomes 1, 14, or 21, with some families exhibiting a pattern of inheritance that suggests possible autosomal-dominant gene transmission. Furthermore, Down syndrome (extra chromosome 21) may have some relationship to Alzheimer’s disease. At autopsy, both have many of the same pathophysiological changes, and a high percentage of individuals with Down syndrome who survive to adulthood develop Alzheimer’s lesions by age 50. (Incidentally, these individuals carry two copies of the gene for APP.)

Current research suggests that Alzheimer’s disease may actually be a lifelong process, with changes in the brain developing decades before the onset of dementia. Other researchers theorize that a rich education may increase a person’s reserve of brain cells or connections between nerve cells, either of which could reduce the risk of dementia.



Feeling tired; fatigue may increase severity of symptoms, especially as evening approaches

Day/night reversal; wakefulness/aimless wandering, disturbance of sleep rhythms

Lethargy; decreased interest in usual activities, hobbies; inability to recall what is read/follow plot of television program; possibly forced to retire

Impaired motor skills; inability to carry out familiar, purposeful movements

Content sitting and watching others

Main activity may be hoarding inanimate objects; repetitive motions (e.g., fold-unfold-refold linen), hiding articles, or wandering


Possible history of systemic/cerebral vascular disease, hypertension, embolic episodes (predisposing factors)

Ego Integrity

Behavior often inconsistent; verbal/nonverbal behavior may be incongruent

Suspicious or fearful of imaginary people/situations; clinging to significant other(s)

Misperception of environment, misidentification of objects/people, hoarding objects; belief that misplaced objects are stolen

Multiple losses; changes in body image and self-esteem

Emotional/ability (cries easily, laughs inappropriately); variable mood changes (apathy, lethargy, restlessness, short attention span, irritability); sudden angry outbursts (catastrophic reactions)

May deny significance of early changes/symptoms, especially cognitive changes, and/or describe vague, hypochondriacal reports (e.g., fatigue, diarrhea, dizziness, occasional headaches)

May conceal limitations (e.g., make excuses for not being able to perform tasks; thumbing through a book without reading it)

Feelings of helplessness; strong, depressive overlay; delusions; paranoia


Urgency (may indicate loss of muscle tone)

Incontinence of urine/feces

Prone to constipation/impaction, with diarrhea


Hypoglycemic episodes (predisposing factor)

Lack of interest in/forgetting of mealtimes; dependence on others for food cooking and preparation at table, feeding, using utensils

Changes in taste, appetite; denial of hunger/refusal to eat (may be trying to conceal lost skills)

Loss of ability to chew (silent aspiration)

Weight loss; decreased muscle mass; emaciation (advanced stage)


May be dependent on SO to meet basic hygiene needs

Appearance disheveled, unkempt; body odor present; poor personal habits

Clothing may be inappropriate for situation/weather conditions

Misinterpretation of, or ignoring, internal cues, forgetting steps involved in toileting self, or inability to find the bathroom


Concealing inabilities (may make excuses not to perform task, may thumb through a book without reading it)

Family members may report a gradual decrease in cognitive abilities, impaired judgment/ inappropriate decisions, impaired recent memory but good remote memory, behavioral changes/individual personality traits altered or exaggerated

Loss of proprioception sense (location of body/body parts in space)

Primitive reflexes (e.g., positive snout, suck, palmar) may be present

Facial signs/symptoms dependent on degree of vascular insults

Seizure activity (secondary to the associated brain damage) may be reported/noted

Mental status (may laugh at or feel threatened by exams)

Disoriented to time initially, then place; usually oriented to person until late in disease process

Impaired recent memory, progressive loss of remote memory

May change answers during the interview

Difficulty in comprehension, abstract thinking

Unable to do simple calculations or repeat the names of three objects, short attention span

Hallucinations, delusions, severe depression, mania (advanced stage)

May have impaired communication: difficulty with finding correct words (especially nouns); conversation repetitive or scattered with substituted meaningless words; speech may become inaudible; gradually loses ability to write (fine motor skills) or read


History of recent viral illness or serious head trauma, drug toxicity, stress, nutritional deficits (may be predisposing/accelerating factors)

Incidental trauma (falls, burns, etc.); presence of ecchymosis, lacerations

Disturbance of gait

Striking out/violence toward others

Social Interactions

Possibly fragmented speech, aphasia, and dysphasia

May ignore rules of social conduct/inappropriate behavior

Prior psychosocial factors (individuality and personality influence present altered behavioral patterns)

Family roles possibly altered/reversed as individual becomes more dependent


Family history of DAT (4 times greater than general population); incidence of primary degenerative dementia is more common in women (who live longer) than in men; vascular dementia occurs more often in men than in women

May present a total healthy picture except for memory/behavioral changes

Use/misuse of medications, OTC drugs, alcohol


Note: Although no diagnostic studies are specific for Alzheimer’s disease, these studies are used to rule out reversible problems that may be confused with these types of dementia.

Antibodies: Abnormally high levels may be found (leading to a theory of an immunological defect).

ApoE4: Screens for the presence of a genetic defect associated with the common form of DAT.

CBC, RPR, Electrolytes, Thyroid Studies: May determine or eliminate treatable/reversible dysfunctions (e.g., metabolic disease processes, fluid/electrolyte imbalance, neurosyphilis).

Vitamin B12: May disclose a nutritional deficit, if low.

Folate Levels: Low level can affect memory function.

Dexamethasone Suppression Test (DST): Rules out treatable depression.

ECG: Rules out cardiac insufficiency.

EEG: May be normal or show some slowing (aids in establishing treatable brain dysfunctions), they may also reveal focal lesions (vascular).

Skull X Rays: Usually normal but may reveal signs of head trauma.

Vision/Hearing Tests: Rule out deficits that may be the cause of or contribute to disorientation, mood swings, altered sensory perceptions (rather than cognitive impairment).

Positron-Emission Tomography (PET) Scan, Brain Electrical Activity Mapping (BEAM), Magnetic Resonance Imaging (MRI): May show areas of decreased brain metabolism characteristic of DAT. (In the future, scans may become a screening tool to reveal early changes, such as plaque formation or development of neurofibrillary tangles, for those at risk of developing dementia.)

CT Scan: May show widening of ventricles, or cortical atrophy.

CSF: Presence of abnormal protein from the brain cells is 90% indicative of DAT.

Tropicamide (Mydriacyl) Pupil Response Test: Hypersensitive to drugs that block the action of acetylcholine. Pupil dilation response to the eyedrops seems equal in clients with mild or early-stage DAT as in severe stage; therefore, this test may provide an early screening tool but is still being researched.

Alzheimer’s Disease–Associated Protein (ADAP): Postmortem studies have yielded positive results in more than 80% of DAT patients. Adaptation of ADAP for live testing is being investigated.


1. Provide safe environment; prevent injury.
2. Promote socially acceptable responses; limit inappropriate behavior.
3. Maintain reality orientation/prevent sensory deprivation/overload.
4. Encourage participation in self-care within individual abilities.
5. Promote coping mechanisms of client/significant other(s).
6. Support client/family in grieving process.
7. Provide information about disease process, prognosis, and resources available for assistance.


1. Adequate supervision/support systems available.
2. Maximal level of independent functioning achieved.
3. Coping skills developed/strengthened and SOs using available resources.
4. Disease process/prognosis and client expectations/needs understood by SO.
5. Plan in place to meet needs after discharge.