Unit III
Unit III
ELDERLY
NEUROCOGNITIVE DOMAINS
The criteria for neurocognitive disorders are based on defined cognitive domains. The domains
defined below, along with guidelines for clinical thresholds, form the basis on which NCDs, their
levels, and their subtypes maybe diagnosed.
Executive function: planning, decision making, Mild: Increased effort for multistage projects;
working memory, responding to feedback, error difficulty multitasking or resuming interrupted
correction, over-riding habits, inhibition, mental task; increased fatigue from extra effort for
flexibility planning, organizing, decision making; large
social gathering more taxing or less enjoyable
due to increased effort for following shifting
conversations
Learning and memory: immediate, recent – Mild: difficulty recalling recent events; relies
including free recall, cued recall & recognition increasingly on lists and calendar; occasional
memory, long-term – semantic & reminders to keep track of evens in books or
autobiographical, implicit learning movies; occasionally may repeat self over a
week to same person; lose track of whether bill
have been paid
RISK FACTORS
1. Age
2. Genetic factors
3. Lower educational attainment
4. Chronic comorbid diseases: Vascular diseases, CHD, HT
5. Metabolic syndrome: visceral obesity, elevated triglycerides and LDL
6. Diabetes & Hyperlipidaemia
7. Tobacco and alcohol use
EVALUATION
1. Medical history and physical examination
2. Mental status examination
3. Neuropsychological assessment
4. Ability to repeat a list of words or digits
5. Ability for free and cued recall
6. Recognition memory
7. Memory for facts
8. Memory for personal events or people
9. Implicit learning
INTERVENTION
Pharmacological
There is no cure for dementia nor are there any disease-modifying drugs available to combat
dementia. Certain drugs and only in some cases, address the symptoms of dementia by slowing down,
in the short term, the progression of cognitive loss. These drugs commonly referred to as anti-
dementia drugs, can only ever be prescribed by a medical doctor and the choice of drug will largely
depend on the dementia sub-type.
How these drugs operate relates to the presence of Acetylcholine in the brain. The latter is a
neurotransmitter or brain chemical required to facilitate communication between nerve cells in the
brain. It becomes depleted with dementia. For this reason, it is often treated with a brand of drugs
called Acetylcholine Inhibitors, developed to boost levels of Acetylcholine in the brain.
Non-pharmacological
ALZHEIMER’S DISEASE
INTRODUCTION
The most common early symptom is difficulty in remembering recent events. As the disease
advances, symptoms can include problems with language, disorientation (including easily getting
lost), mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition
declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately
leading to death. Although the speed of progression can vary, the typical life expectancy following
diagnosis is three to nine years.
Familial Alzheimer's disease is an inherited and uncommon form of Alzheimer's disease. Familial AD
usually strikes earlier in life, defined as before the age of 65. FAD usually implies multiple persons
affected in one or more generation. Sporadic Alzheimer's disease (or Nonfamilial Alzheimer's disease)
describes all other cases, where genetic risk factors are minor or unclear.
DIAGNOSIS
Possible Alzheimer’s disease is diagnosed if there is no evidence of causative genetic mutation but if
all the following are present:
AETIOLOGY
Genetic causes
Neuropathological causes
1. Aβ plaques
2. Amyloid pathology
3. Neuronal fibrillary tau tangles
SYMPTOMS
Cognitive deficits
Neuropsychiatric symptoms
1. Agitation
2. Apathy
3. Depression
4. Delusions
5. Sleep disorders
1. Social withdrawal
2. Mood swings
3. Aggression
4. Wandering
5. Loss of inhibition
6. Distrust in others
RISKS FACTORS
1. Down syndrome
2. Inflammation due to trauma, sepsis or infection
3. Cerebral hypoperfusion
4. Traumatic brain injury
5. Cerebrovascular diseases such as ischemia
6. Cardiovascular diseases such as HT and heart attacks
7. Poor diet and obesity
8. High LDL
9. Sedentary lifestyle
EVALUATION
INTERVENTION
Pharmacological
There is no cure for dementia in Alzheimer’s disease nor are there any disease-modifying drugs
available to combat dementia. Certain drugs and only in some cases, address the symptoms of
dementia by slowing down, in the short term, the progression of cognitive loss. These drugs
commonly referred to as anti-dementia drugs, can only ever be prescribed by a medical doctor and the
choice of drug will largely depend on the dementia sub-type.
How these drugs operate relates to the presence of Acetylcholine in the brain. The latter is a
neurotransmitter or brain chemical required to facilitate communication between nerve cells in the
brain. It becomes depleted with dementia. For this reason, it is often treated with a brand of drugs
called Acetylcholine Inhibitors, developed to boost levels of Acetylcholine in the brain.
Non-pharmacological
VASCULAR DEMENTIA
INTRODUCTION
Vascular dementia refers to changes to memory, thinking, and behavior resulting from conditions that
affect the blood vessels in the brain. Cognition and brain function can be significantly affected by the
size, location, and number of vascular changes.
Symptoms of vascular dementia can begin gradually or can occur suddenly, and then progress over
time, with possible short periods of improvement. Vascular dementia can occur alone or be a part of a
different diagnosis such as Alzheimer's disease or other forms of dementia. When an individual is
diagnosed with vascular dementia, their symptoms can be similar to the symptoms of Alzheimer's.
Vascular dementia is caused by different conditions that interrupt the flow of blood and oxygen supply
to the brain and damage blood vessels in the brain. People with vascular dementia almost always have
abnormalities in the brain that can be seen on MRI scans. These abnormalities can include evidence of
prior strokes, which are often small and sometimes without noticeable symptoms. Major strokes can
also increase the risk for dementia, but not everyone who has had a stroke will develop dementia.
Other abnormalities commonly found in the brains of people with vascular dementia are diseased
small blood vessels and changes in the white matter of the brain.
DIAGNOSIS
Vascular dementia is diagnosed when the criteria for MCI is met, the clinical features are consistent
with a vascular etiology, there is evidence of the presence of cerebrovascular disease from history,
physical examination, or neuroimaging, and the symptoms are not better explained by another brain
disease or systemic disorder.
For a diagnosis of probable vascular dementia, the onset of the cognitive deficits must be temporally
related to one or more cerebrovascular events. Also, evidence for decline should be prominent in
complex attention, including processing speed, and frontal-executive function.
Possible vascular dementia is diagnosed if the clinical criteria are met but neuroimaging is not
available and the temporal relationship of the neurocognitive syndrome with one or more
cerebrovascular events is not established.
AETIOLOGY
SYMPTOMS
1. Confusion
2. Trouble paying attention and concentrating
3. Reduced ability to organize thoughts or actions
4. Decline in ability to analyze a situation, develop an effective plan and communicate that plan
to others
5. Slowed thinking
6. Difficulty with organization
7. Difficulty deciding what to do next
8. Problems with memory
9. Restlessness and agitation
10. Unsteady gait
11. Sudden or frequent urge to urinate or inability to control passing urine
12. Depression or apathy
RISKS FACTORS
1. Increasing age
2. History of heart attacks, strokes, or ministrokes
3. Abnormal aging of blood vessels – atherosclerosis
4. High LDL, obesity
5. High BP, diabetes
6. Smoking
7. Atrial fibrillation
EVALUATION
INTERVENTION
Pharmacological
Non-pharmacological
Delirium is a common and serious acute neuropsychiatric syndrome with core features of inattention
and global cognitive dysfunction. The etiologies of delirium are diverse and multifactorial and often
reflect the pathophysiological consequences of an acute medical illness, medical complication or drug
intoxication. Delirium can have a widely variable presentation, and is often missed and
underdiagnosed as a result. At present, the diagnosis of delirium is clinically based and depends on the
presence or absence of certain features. Management strategies for delirium are focused on prevention
and symptom management.
Clinical experience and recent research have shown that delirium can become chronic or result in
permanent sequelae. In elderly individuals, delirium can initiate or otherwise be a key component in a
cascade of events that lead to a downward spiral of functional decline, loss of independence,
institutionalization, and, ultimately, death. Delirium affects an estimated 14–56% of all hospitalized
elderly patients. At least 20% of the 12.5 million patients over 65 years of age hospitalized each year
in the US experience complications during hospitalization because of delirium.
TYPES OF DELIRIUM
Hyperactive delirium
This may be the easiest type to recognize. People with this type may be restless and pace the room.
They also may be anxious, have rapid mood swings or see things that aren't there. People with this
type often resist care.
Hypoactive delirium
People with this type may be inactive or have reduced activity. They tend to be sluggish or drowsy.
They might seem to be in a daze. They don't interact with family or others.
Mixed delirium
Symptoms involve both types of delirium. The person may quickly switch back and forth from being
restless and sluggish.
DIAGNOSIS
Disturbance in attention, i.e., reduced ability to direct, focus, sustain, and shift attention, accompanied
by reduced awareness of the environment. The disturbance needs to have developed over a short
period of time and should represent a change from baseline attention and awareness, and usually
fluctuates in severity during the course of a day. Other additional disturbances in cognition, such as
memory deficit, disorientation, perception may be present.
The diagnosis is made if these symptoms are not better explained by another preexisting, established,
or evolving neurocognitive disorder and do not occur in the context of a severely reduced level of
arousal, such as coma. Further, there needs to be evidence from the history, physical examination, or
lab findings that the disturbance is a direct consequence of another medical condition.
AETIOLOGY
SYMPTOMS
Cognitive deficits
RISKS FACTORS
EVALUATION
INTERVENTION
Pharmacological
1. Olanzapine
2. Risperidone
3. Quetiapine
4. Haloperidol
Non-pharmacological