STEP 7

1. Why he has bizarre behaviour?

Dementia is the loss of mental functionssuch as thinking, memory, and reasoningthat
is severe enough to interfere with a persons daily functioning. Dementia is not a disease
itself, but rather a group of symptoms that might accompany certain diseases or conditions.
Symptoms also might include changes in personality, mood, and behavior. Dementia is
irreversible when caused by disease or injury, but might be reversible when caused by
drugs, alcohol, hormone or vitamin imbalances, or depression.
Dementia develops when the parts of the brain that are involved with learning, memory,
decision-making, and language are affected by any of various infections or diseases. The
most common cause of dementia is Alzheimers disease, but there are numerous other
known causes. Most of these causes are very rare.
http://www.clevelandclinic.org/health/health-info/docs/2300/2340.asp
Dementia can cause changes in the behaviour of a person. Such changes are very common, but
they can place enormous stress on families and carers. It can be upsetting when someone who
has previously been gentle and loving behaves in a strange or aggressive way.
Causes of behaviour change

Dementia affects people in different ways. Understanding why someone is behaving in a
particular way may help families and carers to cope.

There are many reasons why a persons behaviour may change. Dementia is a result of changes
that take place in the brain which affect the persons memory, mood and behaviour. Sometimes
behaviour may be related to these changes taking place in the brain. In other instances, the
behaviour may be triggered by changes in the persons environment, health or medication.


Where to begin talk to your doctor

Always discuss concerns about behaviour changes with the family doctor, who will be able to
check whether there is a physical illness or discomfort present and can provide some advice. The
doctor will also be able to advise if there is an underlying psychiatric illness.


Changed behaviours are not deliberate

Coping with changed behaviours can be very difficult and is often a matter of trial and error.
Always remember that the behaviour is not deliberate.

Anger and aggression are often directed against family members and carers because they are
closest. The behaviour is out of the persons control and they may be quite frightened by it. They
need reassurance, even though it may often not appear that way.


Ways to cope with changed behaviours

Suggestions for coping with changed behaviours include:
Provide a calm, unstressed environment in which the person with dementia follows a
familiar routine this can help to avoid some difficult behaviours.
Try to keep the environment familiar. People with dementia can become upset if they find
themselves in a strange situation or among a group of unfamiliar people where they feel
confused and unable to cope.
If behaviour becomes difficult, do not attempt any form of physical contact such as
restraining the person, leading them away or approaching them from behind. Leave them
alone until they have recovered or call a friend or neighbour for support.
Dont take changed behaviour personally.
Try not to raise your voice. Speak slowly in a calm and reassuring voice.
Avoid punishment. The person may not remember the event and is therefore not able to
learn from it.
Try to remain detached; do not become provoked or drawn into an argument.

http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Dementia_changed_behaviours
Facts About Dementia
The term "dementia" is used to describe patients with impaired intellectual capacity. Dementia
patients may also be labeled as having "presenile" or "senile" dementia, "chronic" or "organic
brain syndrome," "arterio-sclerosis," or "cerebral atrophy." Dementia is not a normal part of the
aging process. Dementia can be caused by abnormal disease processes and can affect younger as
well as older persons.
Symptoms of Dementia
Short-term memory loss
Inability to think problems through
Inability to complete complex tasks
Confusion
Difficulty concentrating
and paranoid, inappropriate or bizarre behavior
Possible Causes of Dementia
Deteriorating intellectual capacity may be caused by a variety of diseases and disorders. The
National Institute on Aging states that some 100 conditions which mimic serious disorders are
actually reversible. These are sometimes called "pseudodementias," and are often treatable.
Examples of conditions causing reversible symptoms of dementia are:
Reactions to medications: Older persons taking prescription drugs may suffer adverse
reactions, including confusion. Sedatives, hypnotics, neuroleptics, antihypertensives and
antiarthritic medications are among the most common. All medications, including
over-the-counter drugs and herbal remedies, should be monitored by a physician to
reduce the possibility of side effects.
Emotional distress: Depression or major life changes such as retirement, divorce or loss
of a loved one can effect one's physical and mental health. A physician should be
informed about major stressful events. Severe delusional states should also be diagnosed
by psychiatrists.
Metabolic disturbances: Problems including renal failure, liver failure, electrolyte
imbalances, hypoglycemia, hyperglycemia, hepatic disease or pancreatic disorders can
provoke a confusional state, changes in sleep, appetite or emotions.
Vision and hearing: Undetected problems of vision or hearing may result in
inappropriate responses. This could be misinterpreted as dementia because an individual
is unable to perceive surroundings or understand conversations. Hearing and eye
examinations should be performed.
Nutritional deficiencies: Deficiencies of B vitamins (folate, niacin, riboflavin and
thiamine) can produce cognitive impairment. Special attention should be given to patients
who have difficulty in chewing, swallowing, or digesting food. Loss of taste and smell,
loss of appetite, poorly fitting dentures or even difficulty shopping or preparing food may
lead to nutritional deficiencies.
Endocrine Abnormalities: Hypothryroidism, hyperthyroidism, parathyroid disturbances
or adrenal abnormalities can cause confusion which mimics dementia.
Infections: Older persons can develop infections which produce a sudden onset of a
confusional states. They should be brought to the attention of a physician. Confusion
caused by an infection is often treatable.
Subdural Hematoma (blood clot on the surface of the brain): Clots can form which
create collections of fluid that exerts pressure on the brain. These clots can be treated by
draining the fluid before it has caused permanent damage.
Normal Pressure Hydrocephalus: The flow and absorption of spinal fluid, which is
manufactured inside the brain, is interrupted. When the fluid is not absorbed properly, it
builds up inside the reigning creates pressure. Surgery can be performed to drain the
spinal fluid into the bloodstream to relieve the pressure.
Brain tumors: Tumors in the brain can cause mental deterioration. Benign tumors can be
surgically removed. For other tumors, a combination of surgery and
radiation/chemotherapy can help patients.
Atherosclerosis (hardening of the arteries): Intellectual impairment can result when a
series of small strokes occur (multi-infarct dementia). Although damage from small
strokes is typically a irreversible, built up atherosclerotic placques can be surgically
removed or medically treated in order to prevent future strokes from occurring. If action
is taken early enough the person can be helped.
Irreversible Cognitive Impairment Conditions
Traumatic brain injury: Traumatic brain injury can occur at any age. Trauma from a
fall or an accident can precipitate personality, cognitive or behavior changes. If brain
injury is mild, previous functioning may be restored over time. In cases of moderate to
severe head trauma, brain impairment may be lasting. Careful attention should be paid to
any blows to the head. Head injuries should be examined by an neurologist or
rehabilitation specialist.
Cerebral degenerative diseases: If dementia is caused by a degenerative disease, a
progressive cognitive deterioration cannot be reversed. The most common irreversible
dementia is Alzheimer's disease. Other degenerated diseases which can also cause
dementia include dimension with Lewy's bodies, Parkinson's disease, Huntington's
chorea and Picks disease. Other causes of intellectual impairment include stroke, loss of
oxygen to the brain, Creutzfeld-Jakob's disease, Binswanger disease, AIDS and multiple
sclerosis
http://www.blhc.org/dementia.aspx
There are several situations that could cause dementia:
Diseases that cause degeneration or loss of nerve cells in the brain such as Alzheimer's,
Parkinson's and Huntington's.
Diseases that affect blood vessels, such asstroke, which can cause a disorder known as
multi-infarct dementia.
Toxic reactions, like excessive alcohol or drug use.
Nutritional deficiencies, like vitamin B12 and folate deficiency.
Infections that affect the brain and spinal cord, such as AIDS dementia complex and
Creutzfeldt-Jakob disease.
Certain types of hydrocephalus, an accumulation of fluid in the brain that can result from
developmental abnormalities, infections, injury, or brain tumors.
Head injury -- either a single severe head injury or chronic smaller injuries that often
occur from boxing.
Illnesses other than in the brain, such as kidney, liver, and lung diseases, can all lead to
dementia.
Alzheimer's disease causes 50% to 60% of all dementias. But researchers have found that
two nervous diseases, which were originally incorrectly diagnosed as Alzheimer's, are
emerging as major causes of dementia: Lewy body disease andPick's disease.

How dementia impacts behaviour
In the initial stages, patients appear so normal that people around them forget that they are
suffering from a disease that has affected their brain. While theoretically people know that the
patients have a disease, they do not correlate the apparently inconsistent or inconsiderate
behaviour of the patients with the disease. Caregivers may assume that the patient is being
uncooperative or stubborn or just not trying hard enough, and therefore get irritated or sad or
angry. Patients sense this emotion and this, too, affects their behavior.
The intention of this page is to give caregivers some idea on how behavior is impacted by
problems that dementua patients faceains. It is by no means an exhaustive list; it only aims to
help caregivers orient themselves to dementia behavior so that they set realistic expectations and
can think of ways to handle behaviors that could harm the patient and others around them.
The brain gets damaged in dementia
How dementia affects the ability to do things
How dementia affects the emotional state of the patient
What caregivers can remember about dementia behaviour
The brain gets damaged in dementia
In order to see how dementia affects behaviour, we need to understand that the diseases that
cause dementia affect the brain, and that the patients problems occur because of these organic
changes to the brain.

The brain is a very complex organ,
with billions of cells (neurons) that
communicate with each other so that
we can do things.
Different parts of the brain perform
different tasks.
Dementing diseases affect the brain.
The parts of the brain affected, and
how the damage increases over time,
depends on the disease causing the
dementia.
Image courtesy for image on
left: National Institute on
Aging/National Institutes of
Health
The damage to the brain increases as dementia progresses. The damage may become more
severe, and more areas of the brain may also get damaged.
To illustrate the increasing damage to the brain, the image panel below uses images of brains of
patients with Alzheimers Disease, the leading cause of dementia. Image courtesy for images
below: National Institute on Aging/National Institutes of Health

Images showing Pre-clinical Alzheimers Disease, Mild Alzheimers Disease and Severe
Alzheimers Disease




How dementia affects the ability to do things

Explanation Impact on behaviour

Image courtesy: National Institute
on Aging/National Institutes of
Health
Different patients have
damage in different parts
of the brain
When the disease
progresses, it may affect
different parts in different
people
Different patients will
face different types of
problems.
For example, some may
have more problems
walking, while others may
have more problems while
speaking.
Over time, the patients
ability to do things will
get worse.

Image courtesy: National Institute
on Aging/National Institutes of
Health
As dementia progresses,
the damage to the brain
increases. More areas of
the brain may get
impacted.
Visible symptoms
increase depending on the
areas of the brain affected,
and the severity of the
damage. As more and
more parts of the brain are
impacted, the patients
ability to perform
activities of daily living
keeps decreasing.
Communication is often
impacted. Memory loss is
common in many types of
dementia. Major
personality changes are
seen in some types of
dementia. There is an
overall deterioration.
In the final stages, the
patient is fully dependent
and often unable to
communicate

Every task we do has
multiple steps. Inability to
do any step results in
inability to complete a
task
If the dementing disease
has affected the patients
ability to do part of a task,
the patient will not be able
to do that task
independently and will
need assistance

Every task requires
coordination of various
parts of our body and the
ability to pay attention.
Multiple parts of the brain
have to function properly
to perform this.
For example, to light the
gas stove, we need to
position the lighter near
the burner and click its
button at the exact
moment that we turn the
corresponding knob of the
gas stove.
As dementia progresses,
at least some parts of the
brain required for this
coordination and focus
are likely to be damaged
Patients will no longer be
able to do complex tasks
that require precision and
coordination. Attempts to
do such tasks are likely to
lead to frustration or
accidents

All of us have some
fluctuation in our abilities
over days, depending on
our mood and health and
energy.
In dementia patients, we
often find fluctuations in
the abilities to do a
specific task or remember
something. Fluctuations
in cognitive ability are
particularly common in
Lewy Body Dementia
To persons interacting
with dementia patients, it
seems strange to see the
person able to remember
something on one day,
and not be able to
remember it later. When
they see the patient do
something on one day and
not be able to do it the
very next day, people
begin thinking the person
is not trying hard enough.
It is helpful to know that
such fluctuations may be
characteristic of their
dementia.

Often, patients get
disoriented because of
problems like loss of
memories, visio-spatial
problems, discomfort with
too much stimulus or
noise, inability to
understand objects around
them, etc.
This leads to multiple
problems, such as
The patient may
wander and forget
the way back
home
The patient may
consider himself/
herself as younger
and expect a
different home,
and may not
recognize the
children and
grandchildren, or
mistake the
daughter for the
wife
The patient may
keep insisting he/
she wants to go
home
The patient may be
anxious about not
knowing where the
toilet is

Patients often cannot
communicate what they
want. They may have
problems remembering
the right word, or may not
know the meaning of
words others use. They
may not be able to frame
sentences.
Patients may also have
problems knowing what
they are feeling; they may
not realize they are
hungry or thirsty or hot or
cold, or even that they are
unwell or in pain.
They may not be able to
tell caregivers what they
want. They may not be
able to indicate that they
are unwell or are in pain.
So their needs remain
unfulfilled. This may also
frustrate, distress, or anger
them, even if they dont
know how to express it.
If they are ill, their illness
will affect their ability to
do things, but caregivers
may not understand why
the patient is acting
differently today. Also,
the caregiver may not
realize that the patient
needs rest/ treatment.

In many types of
dementia, recent
memories are lost, and
patients often revert to
older memories, or
(unconsciously) try to fill
gaps in their memories
using their imagination
Patients cannot recognize
people or places, and may
not even recognize their
home and family

Often, patients are unable
to create new memories.
They may also have
problems understanding
complex instructions or
concepts.
This affects their ability to
learn new things, use new
devices, and adjust to new
places. They may also get
stressed when they meet
new persons or see new
things, and start avoiding
such situations

In many types of
dementia, the part of the
brain that tells people how
to interact socially is not
damaged initially. This
social interaction ability
deteriorates at a slower
pace in most patients
Patients may cover up for
memory loss and other
problems by giving
evasive answers, thus
masking the problem in
the presence of guests

In some types of
dementia, people become
disinhibited or are unable
to behave in socially
correct ways because the
part of the brain that
regulates behavior is
damaged. The patients
personality changes.
Emotions may also get
flattened and the patient
may show apathy. Such
problems are typical in
behavior-variant fronto-
temporal dementia.
Often, this leads to
embarrassing situations
where people may assume
the patient has bad
character or is
inconsiderate and
insensitive. For example,
the patient may made rude
remarks (even sexual
comments), yell or abuse.
Or the patient may laugh
when others are crying. Or
the patient may lose
interest in everything and
not show any reaction to
emotions of persons
nearby.

In some forms of
dementia, notably Lewy
Body Dementia, patients
may suffer from
hallucinations.
Delusions and paranoia
are also present in some
forms of dementia
Patients who hallucinate
may sometimes realize
they are hallucinating, but
at other times, they may
be confused or frightened
because they believe what
they are seeing or hearing.
Hallucinations may make
familiar tasks difficult
when they cannot
distinguish between
reality and hallucination
(for example, if they see a
road split into four, they
cannot drive). People near
them may not realize that
the patient is hallucinating
and hence confused/
frightened.
Delusions and paranoia
also affect how the patient
interacts with others. They
may accuse people of
stealing their possessions
or even of trying to kill
them. It is difficult to
make the patient
understand what is real
and what is delusion, or to
calm down a paranoid
patient.

Repetitive behavior and
compulsive behavior are
common in many forms
of dementia. (this is also
called perseveration).
Such behavior may occur
for many reasons, such as
forgetting having said or done
the thing earlier, boredom,
anxiety, agitation, etc.
Common examples are the
patient may say the same
thing repeatedly, ask the
same question, make the
same gesture, do the same
action, etcetera. Often,
such repetitive behavior is
harmless, but at times it
may be problematic (like
the patient insisting on
eating breakfast multiple
times) or even harmful
(taking medication
mutliple times) or
exhausting (such as
packing/ unpacking a
suitcase or pacing). It can
also be annoying or
distressing for caregivers
if they dont understand it
is happening because of
dementia and dont know
how to cope with it.

In many instances,
dementia patients show
changed behavior in the
evenings/ night, called
sundowning. While
causes for such behavior
are not fully understood,
they are expected to be
related to day time
activities, exhaustion,
body clock, food cycles,
intake of liquid foods near
dinner time, and so on.
Patients start acting
agitated as evening
approaches. They may be
restless and start pacing.
They may seem more
agitated and anxious.
Sleeplessness is another
problem. They may walk
up and down all night,
mumbling or even
shouting at times. All this
can be very tiring for the
patients and their
caregivers

http://dementia-care-notes.in/dementia/dementia-behaviour/

2. What are the correlation between the age with the patien problems?
Risk factors that can't be changed
Age. The risk of Alzheimer's disease, vascular dementia and several other dementias
increases significantly with age. However, dementia isn't a normal part of aging.
Family history. People with a family history of dementia are at greater risk of developing it.
However, many people with a family history never develop symptoms, and many people
without a family history do. If you have specific genetic mutations, you're at significantly
greater risk of developing certain types of dementia. Tests to determine whether you have
such genetic mutations are available, but only for the disorders in which the specific
mutation is known, for example, Huntington's disease.
Down syndrome. By the time they reach middle age, most people with Down syndrome
develop the plaques and tangles characteristic of Alzheimer's disease, according to studies.
Many, but not all, also develop dementia.

Risk factors you can change
To reduce your risk of dementia, you can take steps to control the following factors.
Alcohol use. Consuming large amounts of alcohol appears to increase the risk of dementia.
Although studies have shown that moderate amounts of alcohol one drink a day for
women and two for men especially red wine, have a protective effect, abuse of alcohol
puts you at increased risk of developing dementia.
Atherosclerosis. This buildup of fats and other substances in and on your artery walls
(plaques) is a significant risk factor for vascular dementia because it interferes with blood
flow to your brain. This can lead to stroke. Studies have also shown a possible link between
atherosclerosis and Alzheimer's disease.
Blood pressure. Blood pressure that's too high, and also possibly too low, can put you at
risk of developing Alzheimer's disease and vascular dementia.
Cholesterol. High levels of low-density lipoprotein (LDL) cholesterol, the "bad"
cholesterol, can significantly increase your risk of developing vascular dementia. Some
research has also linked it to an increased risk of developing Alzheimer's disease.
Depression. Although not yet well understood, late-life depression, especially in men, may
be an indication for the development of Alzheimer's-related dementia.
Diabetes. If you have type 2 diabetes, you're at increased risk of developing both
Alzheimer's disease and vascular dementia.
High estrogen levels. High levels of total estrogen in women have been associated with
greater risk of developing dementia. This can be determined through a blood test.
Homocysteine blood levels. Elevated blood levels of homocysteine a type of amino acid
produced by your body may increase your risk of developing Alzheimer's disease and
vascular dementia. When working properly, your body breaks down homocysteine using
vitamins B-6, B-12 and folic acid. If this isn't happening properly, it may be because you
don't metabolize these vitamins well, or you don't have enough of them in your diet. Blood
tests can determine whether you have elevated homocysteine levels.
Smoking. Smoking likely increases the risk of developing dementia because it puts you at a
higher risk of atherosclerosis and other types of vascular disease.
http://www.mayoclinic.com/health/dementia/DS01131/DSECTION=risk-factors
Age
The greatest known risk factor for Alzheimers is advancing age. Most individuals with
the disease are age 65 or older. The likelihood of developing Alzheimers doubles about
every five years after age 65. After age 85, the risk reaches nearly 50 percent. One of the
greatest mysteries of Alzheimer's disease is why risk rises so dramatically as we grow older.
Aging is the main risk factor for all types of dementia. Some diseases that cause dementia
(such as early-onset Alzheimer's disease and some frontotemporal dementias) may run in
families.
You have a greater chance of developing vascular dementia if you:
Are male.
Have high blood pressure.
Have had a heart attack.
Have atherosclerosis, a buildup of fat andcalcium in the arteries, which can lead
tocoronary artery disease.
Have diabetes.
Have high cholesterol.
Have had a stroke or transient ischemic attack (TIA).
http://www.webmd.com/alzheimers/tc/dementia-what-increases-your-risk
3. Why doctor give haloperidol and rivastigmine?
HALOPERIDOL
Type of
medicine Antipsychotic
Used for Schizophrenia and other mental health problems affecting thoughts,
feelings and behaviours
Motor tics (involuntary body movements or twitches)
Gilles de la Tourette's syndrome (a condition with involuntary body
twitches and the urge to say obscene words or make noises)
Persistent hiccups
Short-term treatment of anxiety
Feeling or being sick
Also
called Dozic, Haldol, Serenace
Available
as
Tablets
Capsules
Oral liquid
Injection

Haloperidol is used to treat mental health problems which affect the way you think, feel
or behave. These problems may make you hear, see or sense things that are not there, or
believe things that are not true, or feel unusually suspicious.

Mental health problems like schizophrenia, are thought to be caused by over-activity of
certain areas of the brain. Haloperidol works by blocking receptors in the brain to alter
the activity in these areas. It helps to improve disturbed thoughts and behaviour and
produces a calming effect where there is aggression and agitation.

Haloperidol also acts on receptors in the brain that control feelings of sickness and it is
sometimes used to provide relief from nausea and vomiting. It can also be used for
hiccups that do not go away
Before taking haloperidol
Before taking haloperidol make sure your doctor or pharmacist knows:
If you are pregnant, trying for a baby or breast-feeding.
If you have liver or kidney problems.
If you have any heart or circulation problems.
If you have breathing problems.
If you suffer from Parkinson's disease.
If you have epilepsy, depression, myasthenia gravis (a muscle weakening disease), prostate
problems or glaucoma.
If you have ever had jaundice (yellowing of the skin and whites of the eyes) or a problem
with your blood.
If you have phaeochromocytoma (a growth affecting the adrenal glands).
If you know you have low amounts of calcium, potassium or magnesium in your blood.
If you have ever had a subarachnoid haemorrhage(bleeding in the brain).
If you are taking other medicines, including those available to buy without a prescription,
herbal or complementary medicines

http://www.patient.co.uk/medicine/Haloperidol.htm

Indications
Haloperidol is indicated for the treatment of schizophrenic patients who require prolonged
parenteral antipsychotic therapy also used in Tourette's syndrome and Severe hyperactivity.
Haloperidol is indicated to treat psychotic disorders and symptoms such as hallucinations,
delusions, and hostility and to control muscular tics of the face, neck, hands, and shoulders.
It is also used to treat severe behavioral problems in children and in hyperactive children
(short-term use).

A phenyl-piperidinyl-butyrophenone that is used primarily to treat schizophrenia and other
psychoses. It is also used in schizoaffective disorder, delusional disorders, ballism, and
tourette syndrome (a drug of choice) and occasionally as adjunctive therapy in mental
retardation and the chorea of huntington disease. It is a potent antiemetic and is used in the
treatment of intractable hiccups. (From AMA Drug Evaluations Annual, 1994, p279)

Contraindications
Since the pharmacologic and clinical actions of Haloperidol Decanoate 50 and Haloperidol
Decanoate 100 are attributed to Haloperidol (haloperidol) as the active prescription,
Contraindications, Warnings, and additional information are those of Haloperidol, modified
only to reflect the prolonged action. Haloperidol is contraindicated in severe toxic central
nervous system depression or comatose states from any cause and in individuals who are
hypersensitive to Haloperidol or have Parkinsonis disease.
Side Effects
Haloperidol side effects that you should report to your health care professional or doctor as
soon as possible:
- confusion;
- constipation;
- difficulty breathing or fast breathing;
- difficulty urinating or loss of bladder control;
- drowsiness;
- dry mouth;
- eye pain or discoloration;
- fast, irregular, or pounding heartbeat;
- fever;
- fine worm-like tongue movements;
- headache;
- restlessness;
- restlessness or pacing;
- seizures or convulsions;
- severe muscle stiffness;
- shuffling walk;
- skin rash;
- slow, jerky movements;
- tremor;
- unusual bleeding or bruising;
- unusual face, mouth, or jaw movements;
- unusual tiredness or weakness;
- weight gain;
- yellowing of the skin or eyes;
http://www.genrxinfo.net/drugs/Haloperidol.htm
Drug Interactions
Haloperidol has been reported to interfere with the anticoagulant properties of phenindione
in an isolated case, and the possibility should be kept in mind of a similar effect occurring
when haloperidol is used with other anticoagulants.

Haloperidol may antagonize the action of epinephrine and other sympathomimetic agents
and reverse the blood-pressure-lowering effects of adrenergic-blocking agents such as
guanethidine. Enhanced CNS effects have been reported when haloperidol is used in
combination with methyldopa.

As with all antipsychotic agents, haloperidol should not be used alone where depression is
predominant. It may be combined with antidepressants to treat those conditions in which
depression and psychosis coexist.

If concomitant antiparkinson medication is required, it may have to be continued after
stopping haloperidol if its excretion is faster than that of haloperidol in order to avoid the
development or aggravation of extrapyramidal symptoms.

Haloperidol inhibits the metabolization of tricyclic antidepressants, thereby increasing
plasma levels of these drugs.

In pharmacokinetic studies, mild to moderately increased haloperidol levels have been
reported when haloperidol was given concomitantly with the following drugs: quinidine,
busipirone, fluoxetine. It may be necessary to reduce the haloperidol dosage.

When prolonged treatment with enzyme-inducing drugs such as carbamazepine,
phenobarbital, rifampin is added to haloperidol therapy, this results in a significant reduction
of haloperidol plasma levels. Therefore, during combination treatment, the haloperidol dose
should be adjusted, when necessary. After stopping such drugs, it will be necessary to
reduce the dosage of haloperidol.

Haloperidol may impair the antiparkinson effects of levodopa. If an antiparkinson agent is
used concomitantly with haloperidol, both drugs should not be discontinued simultaneously,
since extrapyramidal symptoms, previously controlled by antiparkinson agents, may occur
due to the slower excretion rate of haloperidol.

The physician should keep in mind the possibility of an increase in intraocular pressure
when anticholinergic drugs, including antiparkinson agents, are administered concomitantly
with haloperidol.

When haloperidol is used to control mania in cyclic disorders, there may be a rapid mood
swing to depression.

The antiemetic action of haloperidol may obscure signs of toxicity due to overdosage of
other drugs or mask the symptoms of some organic diseases, such as brain tumor or
intestinal obstructions.

Severe neurotoxicity (rigidity, inability to walk or talk) may occur in patients with
thyrotoxicosis who are also receiving antipsychotic medication, including haloperidol.

Carcinogenicity studies in mice (18 months) and rats (24 months) showed a significant
increase in mammary gland neoplasia and total tumor incidence in female mice at 1.25 and 5
mg/kg/day and in pituitary gland neoplasia in female mice at 5 mg/kg. A significant dose-
related increase in pituitary gland hyperplasia was observed in female rats at 1.25 and 5
mg/kg/day. The potential significance of these findings in man is not known. Neuroleptic
drugs elevate prolactin levels; the elevation persists during chronic administration. Tissue
culture experiments indicate that approximately one-third of human breast cancers are
prolactin dependent in vitro, a factor of potential importance if the prescription of these
drugs is contemplated in a patient with a previously detected breast cancer. Although
disturbances such as galactorrhea, amenorrhea, gynecomastia, and impotence have been
reported, which are presumed to be linked to elevated prolactin levels, the clinical
significance of elevated serum prolactin levels is unknown for most patients. An increase in
mammary neoplasms has been found in rodents after chronic administration of neuroleptic
drugs. Neither clinical studies nor epidemiologic studies conducted to date, however, have
shown an association between chronic administration of these drugs and mammary
tumorigenesis. The available evidence is considered too limited to be conclusive at this
time.

Occupational Hazards: Effects on driving ability and use of machinery: Some degree of
sedation or impairment of alertness may occur, particularly with higher doses and at the start
of treatment and may be potentiated by alcohol. Patients should be advised not to drive or
operate machinery during treatment, until their susceptibility is known.
www.news-medical.net/health/Haloperidol-Pharmacokinetics.aspx

Pharmacodynamics
Haloperidol is a psychotropic agent indicated for the treatment of schizophrenia. It also
exerts sedative and antiemetic activity. Haloperidol principal pharmacological effects are
similar to those of piperazine-derivative phenothiazines. The drug has action at all levels of
the central nervous system-primarily at subcortical levels-as well as on multiple organ
systems. Haloperidol has strong antiadrenergic and weaker peripheral anticholinergic
activity; ganglionic blocking action is relatively slight. It also possesses slight antihistaminic
and antiserotonin activity.
Pharmacokinetics

Haloperidol blocks postsynaptic dopamine D1 and D2 receptors in the mesolimbic system
and decreases the release of hypothalamic and hypophyseal hormones. It produces calmness
and reduces aggressiveness with disappearance of hallucinations and delusions.

Absorption Readily absorbed from the GI tract (oral).

Distribution Crosses the blood-brain barrier; enters breast milk. Protein-binding: 92%.

Metabolism Hepatic via oxidative N-dealkylation and reduction of the ketone group;
undergoes enterohepatic recycling.

Excretion Urine and faeces; 12-38 hr (elimination half-life).

http://www.drugsupdate.com/generic/view/59

RIVASTIGMINE
Pharmacodynamics.
Rivastigmine is an acetylcholinesterase inhibitor that facilitates cholinergic neurotransmission by
slowing the degradation of acetylcholine released by functionally intact cholinergic neurons.
Thus, rivastigmine may have an ameliorative effect on cholinergic-mediated cognitive deficits
associated with Alzheimer disease. Rivastigmine is a carbamate derivative that binds to the steric
site of the acetylcholinesterase and dissociates slowly; thus, it provides a longer duration of
action than tacrine and donepezil, which are short-acting agents, because binding to
acetylcholinesterase is hydrolyzed within minutes. In addition to acetylcholinesterase,
rivastigmine inhibits butylcholinesterase, and as a result of this dual inhibition, it can optimize
cholinergic function. Rivastigmine markedly inhibits cerebrospinal fluid acetylcholinesterase
after a single oral dose of 3 mg; it also has central nervous system selectivity over the peripheral
inhibition of acetylcholinesterase.
An oral 3 mg dose decreases acetylcholinesterase activity in cerebrospinal fluid by
approximately 40% within the first 1.5 hours after administration. Activity of the enzyme returns
to baseline levels about 9 hours after the maximum inhibitory effect has been achieved. In
patients with Alzheimer disease, inhibition of acetylcholinesterase in cerebrospinal fluid by
rivastigmine was found to be dose-dependent up to 6 mg given twice a day (the highest dose
tested).
Alterations in the clinical and cognitive status of patients receiving rivastigmine are paralleled by
changes in regional cerebral blood flow as measured by SPECT. These values are enhanced in
responders and reduced in nonresponders.
Various studies indicate that rivastigmine improves cognition and activities of daily living in
patients with dementia associated with Parkinson disease, resulting in a clinically meaningful
benefit (Moretti et al 2007).
Pharmacokinetics.
Important points pertaining to pharmacokinetics include the following:
Rivastigmine is rapidly and completely absorbed. Peak plasma concentrations are
reached in approximately 1 hour. As a consequence of the drugs interaction with its
target enzyme, the increase in bioavailability is about 1.5-fold greater than that expected
from the increase in dose.
Rivastigmine is weakly bound to plasma proteins (approximately 40%). It readily crosses
the blood-brain barrier.
Rivastigmine is rapidly and extensively metabolized (half-life in plasma approximately 1
hour) primarily through cholinesterase-mediated hydrolysis to the decarbamoylated
metabolite. Total plasma clearance of rivastigmine was approximately 130 L/h after a 0.2
mg intravenous dose, and it decreased to 70 L/h after a 2.7 mg intravenous dose.
Unchanged rivastigmine is not found in the urine; renal excretion of the metabolites is the
major route of elimination. Following administration of 14-C-rivastigmine, renal
elimination was rapid and essentially complete (greater than 90%) within 24 hours. Less
than 1% of the administered dose is excreted in the feces. No accumulation of
rivastigmine or the decarbamoylated metabolite is present in patients with Alzheimer
disease.
Transdermal rivastigmine maintains steady drug levels in the bloodstream as compared to
fluctuations with the capsule form of the drug (Mercier et al 2007). Transdermal
rivastigmine enables maintenance of a lower peak of drug concentration, fewer
gastrointestinal side effects, and an efficacy similar to the oral capsules of rivastigmine
(Salmon 2008). Despite the advantages of transdermal rivastigmine, the effects of
environmental factors such as fever or skin abrasions or tears on drug pharmacokinetics
are unknown, and the need for titration to the target dose is not eliminated (Guay 2008).
http://www.medmerits.com/index.php/article/rivastigmine/P1
Indications
Indications include the symptomatic treatment of mild to moderately severe Alzheimer
dementia and mild to moderate dementia related to Parkinson disease. Ongoing studies
are examining the effect of rivastigmine in patients with severe Alzheimer disease.
Contraindications
Rivastigmine is contraindicated in patients with known hypersensitivity to rivastigmine,
other carbamate derivatives, or to any excipients used in the formulation. Another
contraindication is severe liver impairment.
Side effect

Rivastigmine may cause side effects. Tell your doctor if any of these symptoms are severe or do
not go away:
nausea
vomiting
loss of appetite
heartburn or indigestion
stomach pain
weight loss
diarrhea
constipation
gas
weakness
dizziness
headache
extreme tiredness
lack of energy
tremor or worsening of tremor
increased sweating
difficulty falling asleep or staying asleep
confusion
Some side effects can be serious. The following symptoms are uncommon, but if you experience
any of them, call your doctor immediately:
fainting
black and tarry stools
red blood in stools
bloody vomit
vomiting material that looks like coffee grounds
difficulty urinating
painful urination
seizures
depression
anxiety
aggressive behavior
hearing voices or seeing things that do not exist)
uncontrollable movements and muscle contractions
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a602009.html


Haloperidol is a neuroleptic and a butyrophenone. Due to its strong central antidopaminergic
action, it is classified as a highly potent neuroleptic. It is approximately 50 times more potent
than chlorpromazine (sold under the brand name Thorazine, among others) on a weight basis
(50 mg chlorpromazine is equivalent to 1 mg haloperidol).
Haloperidol possesses a strong activity against delusions and hallucinations, most likely due to
an effective dopaminergic receptor blockage in the mesocortex and the limbic system of the
brain. It blocks the dopaminergic action in the nigrostriatal pathways, which is the probable
reason for the high frequency of extrapyramidal-motoric side-effects (dystonias, akathisia,
pseudoparkinsonism). It has minor antihistaminic and anticholinergic properties, therefore
cardiovascular and anticholinergic side-effects such as hypotension, dry mouth, constipation,
etc., are seen quite infrequently, compared with less potent neuroleptics such as chlorpromazine.
Haloperidol also has sedative properties and displays a strong action against psychomotor
agitation due to a specific action in the limbic system. However, in some cases Haloperidol may
worsen psychomotor agitation via its potent Dopamine receptor antagonism. Dopamine receptor
antagonism, notably of the D2 receptor subtype, can cause akathisia, psychomotor agitation,
anxiety, and restlessness, which may worsen the condition of some patients.
The peripheral antidopaminergic effects of haloperidol account for its strong antiemetic activity.
There, it acts at the chemoreceptor trigger zone (CTZ). Haloperidol is useful to treat severe
forms of nausea/emesis such as those resulting from chemotherapy. The peripheral effects lead
also to a relaxation of the gastric sphincter muscle and an increased release of the hormone
prolactin, with the possible emergence of breast enlargement and secretion of milk (galactorrhea)
in both sexes.
Haloperidol adalah antipsychotic khas. Dalam kelas butyrophenone obat-obatan yang
antipsychotic dan memiliki farmakologi efek yang mirip dengan phenothiazines.
Haloperidol adalah antipsychotic tua yang digunakan dalam pengobatan skizofrenia, lebih akut,
perawatan akut psikotik Serikat dan igauan. Ester decanoate berkelanjutan digunakan sebagai
panjang bertindak injeksi yang diberikan setiap 4 minggu untuk orang-orang dengan skizofrenia
atau penyakit terkait yang telah miskin sesuai dengan obat dan menderita kambuh lebih sering
penyakit, atau untuk mengatasi kekurangan yang melekat dengan rekan diberikan secara lisan
yang meledak dosis meningkatkan risiko atau intensitas efek samping. Di beberapa negara, ini
bisa menjadi disengaja di bawah perintah perawatan masyarakat.
Haloperidol dijual di bawah nama dagang Aloperidin, Bioperidolo, Brotopon, Dozic,
Duraperidol (Jerman), Einalon S, Eukystol, Haldol, Halosten, Keselan, Linton, Peluces,
Serenace, Serenase, dan Sigaperidol. Dalam medis slang, haloperidol kadang-kadang disebut
vitamin H.
Haloperidol ditemukan oleh Paul Janssen. Dikembangkan pada tahun 1958 oleh perusahaan
Belgia Janssen Pharmaceutica dan diserahkan kepada uji klinis pertama di Belgia pada tahun
yang sama. Setelah ditolak oleh perusahaan AS Searle karena untuk efek samping, itu kemudian
dipasarkan di AS oleh McNeil laboratorium. Disetujui oleh US Food and Drug Administration
pada tanggal 12 April 1967.
Komprehensif meninjau haloperidol telah menemukan untuk menjadi agen yang efektif dalam
perawatan gejala yang berkaitan dengan skizofrenia.
Haloperidol juga digunakan dalam pengendalian gejala:
Psikosis akut, seperti obat psikosis (LSD, psilocybin, amfetamin, ketamine dan
phencyclidine), psikosis terkait dengan demam tinggi atau penyakit metabolik
Akut fase manik sampai obat-obatan lini pertama yang secara bersamaan tertentu seperti
litium atau valproate efektif
Hiperaktif, agresi.
Akut delirium
Sebaliknya tak terkendali parah perilaku gangguan di anak-anak dan remaja
Agitasi dan kebingungan yang terkait dengan otak sclerosis
Ajuvan perawatan alkohol dan opioid penarikan
Pengobatan gangguan neurologis seperti tic gangguan, sindrom Tourette, dan chorea
Pengobatan parah mual/emesis (pasca-operasi, efek samping dari radiasi dan kanker
kemoterapi)
Ajuvan pengobatan sakit kronis parah, selalu bersama-sama dengan analgesik
Terapeutik percobaan dengan gangguan kepribadian seperti gangguan kepribadian batas
Juga digunakan dalam pengobatan terselesaikan cegukan
Beberapa minggu atau bahkan berbulan-bulan perawatan mungkin diperlukan sebelum
pengampunan skizofrenia jelas.
Di beberapa klinik penggunaan atipikal neuroleptics (misalnya clozapine, risperidone,
olanzapine, ziprasidone) umumnya pilihan atas haloperidol, karena obat ini memiliki insiden
lumayan rendah extrapyramidal efek samping. Masing-masing obat-obatan ini, namun, memiliki
spektrum sendiri berpotensi serius-efek samping (misalnya, agranulocytosis dengan clozapine,
berat badan dengan peningkatan risiko diabetes dan stroke). Neuroleptics atipikal juga jauh lebih
mahal dan baru-baru ini telah menjadi subyek meningkatkan kontroversi mengenai keampuhan
mereka dibandingkan dengan produk-produk yang lebih tua dan efek samping.
Haloperidol dianggap sangat diperlukan untuk mengobati psikiatri situasi darurat, meskipun
obat-obatan atipikal baru telah mendapatkan peran yang lebih besar dalam beberapa situasi
seperti diuraikan dalam serangkaian ulasan konsensus yang diterbitkan antara tahun 2001 dan
2005. Mendaftarkan diri di dunia kesehatan organisasi daftar dari penting obat.
Seperti biasa dengan neuroleptics yang khas, haloperidol jauh lebih aktif terhadap "positif" gejala
psikotik (delusi, halusinasi dll) daripada terhadap "negatif" Gejala (sosial penarikan, autism dll).
Dengan pengecualian dari clozapine sangat efektif, efektivitas haloperidol melawan gejala positif
telah tidak telah mengungguli oleh Anti-kejang obat baru.
UK multi-tahun studi oleh Alzheimer penelitian Trust menyarankan bahwa ini dan obat-obatan
anti-psychotic lain neuroleptic umumnya diberikan Alzheimer pasien dengan masalah-masalah
kelakuan yang ringan sering membuat kondisi mereka yang lebih buruk. Studi menyimpulkan
bahwa
Kontroversial non-medis menggunakan
Ada beberapa laporan dari pembangkang Soviet, termasuk staf medis, penggunaan haloperidol di
Uni Soviet untuk tujuan hukuman atau hanya untuk istirahat para tahanan akan. Pembangkang
terkenal yang diberikan haloperidol sebagai bagian dari Pengadilan memerintahkan perawatan
adalah Sergei Kovalev dan Leonid Plyushch. Account Plyushch di barat, setelah ia diizinkan
meninggalkan Uni Soviet pada tahun 1976, yang berperan dalam pengutukan Barat memicu
Soviet praktek di dunia Psychiatric Association's 1977 pertemuan. Penggunaan haloperidol di
Uni Soviet sistem jiwa adalah lazim karena itu salah satu obat-obatan psikotropika beberapa
diproduksi dalam kuantitas di Uni SOVIET.
Haloperidol telah digunakan untuk efek menenangkan selama deportasi Alien Amerika Serikat
imigrasi dan Penegakan Bea Cukai (ICE). Selama 2002-2008, federal imigrasi personil dulu
haloperidol tenang 356 deportees. Tahun 2008, diikuti pengadilan tantangan atas praktek,
haloperidol diberikan kepada tahanan hanya 3. Setelah tuntutan hukum, para pejabat AS berubah
prosedur sehingga melakukannya hanya dengan rekomendasi dari personel medis dan di bawah
perintah pengadilan.
Haloperidol is a typical antipsychotic. It is in the butyrophenone class of antipsychotic
medications and has pharmacological effects similar to the phenothiazines.
Haloperidol is an older antipsychotic used in the treatment of schizophrenia and in the treatment
of acute psychotic states and delirium. A long-acting decanoate ester is used as an injection given
every 4 weeks to people with schizophrenia or related illnesses who have a poor compliance with
medication and suffer frequent relapses of illness, or to overcome the drawbacks inherent to its
orally administered counterpart that burst dosage increases risk or intensity of side effects. In
some countries, injections of antipsychotics such as haloperidol can be ordered by a court at the
request of a psychiatrist.
Haloperidol is sold under the tradenames Aloperidin, Bioperidolo, Brotopon, Dozic,
Duraperidol (Germany), Einalon S, Eukystol, Haldol, Halosten, Keselan, Linton,
Peluces, Serenace, Serenase, and Sigaperidol

RIVASTIGMINE
Rivastigmine (sold under the trade name Exelon) is a parasympathomimetic or cholinergic
agent for the treatment of mild to moderate dementia of the Alzheimers type and dementia due
to Parkinson's disease. The drug can be administered orally or via a transdermal patch; the latter
form reduces the prevalence of side effects,
[1]
which typically include nausea and vomiting.
[2]

The drug is eliminated through the urine, and appears to have relatively few drug-drug
interactions.
[2]

Administration
Rivastigmine tartrate is a white to off-white fine crystalline powder that is both lipophilic
(soluble in fats) and hydrophilic (soluble in water). Like other cholinesterase inhibitors, it
requires doses to be increased gradually over several weeks; this is usually referred to as the
titration phase.
[2]
Oral doses of rivastigmine should be titrated with a 3 mg per day increment
every 2 to 4 weeks.
Rivastigmine is classified as Pregnancy category B, with insufficient data on risks associated
with breastfeeding. In cases of overdose, atropine is used to reverse bradycardia. Dialysis is
ineffective due to the drug's half-life.
[edit] Pharmacodynamics
Rivastigmine is a cholinesterase inhibitor that inhibits both butyrylcholinesterase and
acetylcholinesterase (unlike donepezil, which selectively inhibits acetylcholinesterase). It is
thought that rivastigmine works by inhibiting these cholinesterase enzymes, which would
otherwise break down the brain chemical acetylcholine.
[6]

[edit] Indication
The U.S. Food and Drug Administration has approved rivastigmine capsules and the
rivastigmine patch for the treatment of mild to moderate dementia of the Alzheimers type and
for mild to moderate dementia related to Parkinson's disease. It has been used in more than 6
million patients worldwide.
[citation needed]

Rivastigmine has demonstrated significant treatment effects on the cognitive (thinking and
memory), functional (activities of daily living) and behavioural problems that are commonly
associated with Alzheimers
[7][8][9][10]
and Parkinson's disease dementias.
[11]

[edit] Efficacy
In patients with either type of dementia, rivastigmine has been shown to provide meaningful
symptomatic effects that may allow patients to remain independent and be themselves for
longer. In particular, rivastigmine appears to show marked treatment effects in patients showing
a more aggressive course of disease, such as those with a younger age of onset, a poor nutritional
status, or those experiencing symptoms such as delusions or hallucinations.
[12]
For example, the
presence of hallucinations appears to be a predictor of especially strong responses to
rivastigmine, both in Alzheimers and Parkinson's disease patients.
[13][14]
It has been proposed
that these effects might reflect the additional inhibition of butyrylcholinesterase, which is
implicated in symptom progression and might provide added benefits over acetylcholinesterase-
selective drugs in some patients.
[12][15]
Multi-infarct dementiamay be slight improvement in
executive functions and behaviour. There are no firm evidences supporting usage in
schizophrenia patients.
Its efficacy is similar to donepezil and tacrine. Doses below 6 mg/d may be ineffective. The
effects of this kind of drugs in different kinds of dementia (including Alzheimer's dementia) are
modest, and it is still unclear which AcCh(ButCh) esterase inhibitor is better in Parkinson's
dementia, though rivastigmine is well-studied.
[edit] Side effects
Side effects may include nausea and vomiting.
[2]

It has been postulated that the strong potency of rivastigmine, provided by its dual inhibitory
mechanism, leads to more nausea and vomiting during the titration phase of oral rivastigmine
treatment.
[2]
This enforces the importance of taking oral forms of these drugs as prescribed with
food.
[4]
However, rates of nausea and vomiting are markedly reduced with the once-daily
rivastigmine patch (which can be applied at any time of the day, with or without food).
In a large clinical trial of the rivastigmine patch in 1,195 patients with Alzheimers disease, the
target dose of 9.5 mg/24 hour patch provided similar clinical effects (e.g. memory and thinking,
activities of daily living, concentration) as the highest doses of rivastigmine capsules, but with
three times fewer reports of nausea and vomiting.
[1]
.
[edit] Pharmacokinetics
When given orally, rivastigmine is well absorbed with a bioavailability of about 40% in the 3 mg
dose. Pharmacokinetics are linear up to 3 mg BID but non-linear at higher doses. Elimination is
through the urine. Peak plasma concentrations are seen in about one hour, with peak CSF
concentrations at 1.43.8 hours. When given by once-daily transdermal patch, the
pharmacokinetic profile of rivastigmine is much smoother, compared with capsules, with lower
peak plasma concentrations and reduced fluctuations.
[16]
The 9.5 mg/24 h rivastigmine patch
provides comparable exposure to 12 mg/day capsules (the highest recommended oral dose).
[16]

The compound does cross the blood-brain barrier. Plasma protein binding is 40%.
[17]
The major
route of metabolism for rivastigmine is by its target enzymes via cholinesterase-mediated
hydrolysis. Elimination bypasses the hepatic system so hepatic cytochrome P450 (CYP)
isoenzymes are not involved.
[18]
It has been suggested that this means there is a low potential for
drug-drug interactions (which could lead to adverse effects) between rivastigmine and the many
common drugs that use the cytochrome P450 metabolic pathway.
[2]

[edit] Synthesis

R. Amstuz, M. Marzi, M. Boelsterli, M. Walsinshaw, Helv. Chim. Acta 73, 739 (1990).


4. What are the correlation between of hypertension and DM which the patien on
symptom?
Hypertension
Hypertension (HT) and dementia are common disorders in the elderly. HT in the elderly
is associated with increased occurrence rates of dementia including Alzheimer's disease
(AD) and vascular dementia (VaD). In connection to this, some studies have suggested
that HT in old age correlates with the pathogenesis of dementia. Since HT is potentially
reversible, a number of randomized trials have examined whether antihypertensive
treatment may help in preventing dementia occurrence. We review five studies, all using
subjects 60 years or older, which investigated different antihypertensive pharmacological
treatments. Data from two trials (Syst-Eur, PROGRESS) open the way toward the
prevention of dementia (AD or VaD) by antihypertensive treatments. In the Syst-Eur
study, with the dihydropyridine calcium antagonists, a reduction in both types of
dementia was demonstrated (risk reduction 55%). The PROGRESS study showed that the
use of angiotensin-converting enzyme inhibitors (ACEIs), with or without diuretics,
resulted in decrease incidence of stroke-related dementia (risk reduction 19%), but
dementia without stroke was not reduced. In contrast, the SHEP trial, treatment with a
chlorthalidone-based antihypertensive regimen, did not significantly reduced the
incidence of dementia. The SCOPE study (candesartan or hydrochlorothiazide versus
placebo) and the HYVET-COG study (indapamide or perindopril versus placebo) found
no significant difference between the active treatment and placebo group on the incidence
of dementia. We found conflicting results regarding treatment benefits in dementia
prevention. Recent clinical trials and studies on animal models suggest that blockades of
RAS system could have reduced cognitive decline seen in Alzheimer's disease and
vascular dementia. Future trials primarily designed to investigate the effects of
antihypertensive agents on impaired cognition are needed.
In general, the risk of HT, which is defined as a systolic blood pressure (SBP)
140mmHg and/or a diastolic blood pressure (DBP) 90mmHg, increases with
advancing age. In fact, the prevalence of HT in individuals 60 years and older is double
that of those aged 4959 years. In Framingham study, 90% of all 65-year-old men and
women with normal BP later developed HT. This condition carries a very high risk for
cerebrovascular disease (CVD) as well as coronary heart disease (CHD). Dementia is one
of the most important neurological disorders in the elderly. Many studies have identified
HT as marker for the pathogenesis of dementia AD and VaD, while longitudinal studies
have suggested that HT is associated with a higher incidence of dementia in old age. It
has been observed that long-standing HT may lead to severe atherosclerosis and impaired
cerebrovascular autoregulation, which in turn is thought to correlate with dementia. For
these reasons, several studies have investigated whether antihypertensive treatment may
retard cognitive decline or dementia. Although the importance of lowering BP in HT
subjects is well known, the relationship between HT and cognitive function is
controversial.
To this date, the associations between BP and dementia have been inconclusive.
Considering that the incidence of dementia among the elderly population is rising rapidly
worldwide and accumulating evidence that HT may contribute to the development of
both AD and VaD, there is a reason to believe effective management of HT may translate
into major health benefits through the protection of dementia. HT has long been known to
cause CV. Midlife HT ranks as an important modifiable risk factor for late-life cognitive
decline, mild cognitive impairment (MCI) and VaD. In longitudinal cohort studies,
elevated BP is associated with cognitive decline although some cross-sectional studies
showed mixed relationships between higher BP and cognition, with many studies
showing no correlation or even J- or U-shaped associations. Findings from these
prospective cohort studies for DBP and cognitive decline are less consistent; however,
many have reported a similar inverse relation. The data on the role of BP and HT in later
life are not consistent, leaving open the issue of BP treatment in elderly people. The
controversy about the association between HT in the elderly and dementia arises because
the longitudinal relationship between BP and cognitive change is sensitive to the effects
of age, duration of followup and hypertensive treatment status, comorbidity with CVD
and CHD, and possibly subclinical dementia. More recently, a total of 668 community-
dwelling Japanese individuals without dementia, aged 65 to 79 years, were followed up
for 17 years, and examined the associations of late-life and midlife HT with the risk of
AD and VaD. During the followup, 123 developed AD, and 76 subjects experienced
VaD, and the age- and sex-adjusted incidence of VaD significantly increased with
elevated midlife BP levels regardless of late-life BP levels. There were not a significant
association between BP levels and AD. Li et al. followed a total of 837 subjects with
MCI for 5 years, 298 subjects converted to AD, while 352 remained MCI at the end of
the followup. Subjects with HT increased the risk of dementia conversion. Given their
results, treatment of HT was associated with a reduced progression in MCI to AD
dementia.
R. S. Vasan, A. Beiser, S. Seshadri et al., Residual lifetime risk for developing
hypertension in middle-aged women and men: the Framingham Heart Study, Journal of
the American Medical Association, vol. 287, no. 8, pp. 10031010, 2002
Diabetes mellitus
People with diabetes are at increased risk of having a heart attack or stroke at an early age, but
that's not the only worry. Diabetes appears to dramatically increase a person's risk of developing
Alzheimer's disease or other types of dementia later in life, according to a new study conducted
in Japan.
In the study, which included more than 1,000 men and women over age 60, researchers found
that people with diabetes were twice as likely as the other study participants to develop
Alzheimer's disease within 15 years. They were also 1.75 times more likely to develop dementia
of any kind.
"It's really important for the [public's] health to understand that diabetes is a significant risk
factor for all of these types of dementia," says Rachel Whitmer, Ph.D., an epidemiologist in the
research division of Kaiser Permanente Northern California, a nonprofit health-care organization
based in Oakland, California.

Whitmer, who studies risk factors for Alzheimer's but wasn't involved in the new research,
stresses that many questions remain about the link between diabetes and dementia. The new
study was "well done" and provides "really good evidence that people with diabetes are at
greater risk," she says, "but we really need to look at other studies to find out why."
Diabetes could contribute to dementia in several ways, which researchers are still sorting out.
Insulin resistance, which causes high blood sugar and in some cases leads to type 2 diabetes, may
interfere with the body's ability to break down a protein (amyloid) that forms brain plaques that
have been linked to Alzheimer's. High blood sugar (glucose) also produces certain oxygen-
containing molecules that can damage cells, in a process known as oxidative stress.
In addition, high blood sugar -- along with high cholesterol -- plays a role in the hardening and
narrowing of arteries in the brain. This condition, known as atherosclerosis, can bring about
vascular dementia, which occurs when artery blockages (including strokes) kill brain tissue.

"Having high glucose is a stressor to the nervous system and to the blood vessels," says David
Geldmacher, M.D., a professor of neurology at the University of Alabama at Birmingham. "The
emerging information on Alzheimer's disease and glucose shows us that we do need to remain
vigilant on blood sugar levels as we get older."
Studies dating back to the late 1990s have suggested that people with diabetes are more likely to
develop Alzheimer's disease and other types of dementia, but the research has been marred by
inconsistent definitions of both diabetes and dementia.
The authors of the new study, led by Yutaka Kiyohara, M.D., an environmental medicine
researcher at Kyushu University, in Fukuoka, sought to address this weakness by using the gold
standard of diabetes diagnosis, an oral glucose tolerance test. This involves giving a person a
sugar-loaded drink after they have fasted for at least 12 hours, and then measuring how much
glucose remains in their blood two hours later.

At the beginning of the study, the tests showed that 15% of the participants had full-fledged
diabetes, while 23% had prediabetes, also known as impaired glucose tolerance.
The participants were all dementia-free when the tests were done, but over the next 15 years 23%
received a diagnosis of dementia. Slightly less than half of those cases were deemed to be
Alzheimer's disease, with the remainder roughly split between vascular dementia and dementia
due to other causes. (The diagnoses were confirmed with brain scans of living patients and brain
autopsies in deceased patients.)
Both diabetes and prediabetes were associated with an increased risk of dementia diagnosis,
although the association was weaker for prediabetes. And the link persisted even after the
researchers took into account several factors associated with both diabetes and dementia risk,
such as age, sex, blood pressure, and body mass index.

http://edition.cnn.com/2011/09/19/health/diabetes-doubles-alzheimers

Demensia Tipe Alzheimer
Walaupun penyebab demensia tipe Alzheimer masih tidak diketahui, telah
terjadi kemajuan dalam mengerti dasar molekular dari deposit amiloid yang
merupakan tanda utama neuropatologi gangguan. Faktor genetik dianggap
berperan dalam perkembangan gangguan dalam sekurangnya beberapa kasus.
Dukungan tambahan tentang peranan genetik adalah bahwa angka persesuaian
untuk kembar monozigotik adalah lebih tinggi dari angka untuk kembar
dizigotik.
Neuropatologi. Observasi makroskopis neuroanatomik klasik pada otak dari
seorang pasien degan penyakit Alzheimer adalah atrofi difus dengan pendataran
sulkus kortikal dan pembesaran ventrikel serebral. Temuan mikroskopis klasik
dan patognomonik adalah bercak-bercak senilis, kekusutan neurofibriler,
hilangnya neuronal (kemungkinan sebanyak 50 persen di korteks), dan
degenerasi granulovaskular pada neuron. Kekusutan neurofibriler bercampur
dengan elemen sitoskeletal, terutama protein tau berfosforilasi, walaupun
protein sitoskeletal lainnya juga ditemukan. Kekusutan neurofibriler adalah ti-
dak unik pada penyakit Alzheimer, karena keadaan tersebut juga ditemukan
pada sindroma Down, demensia pugilistik (punch-drunk syndrome), Kompleks
demensia-Parkinson dari Guam, penyakit Hallervorden-Spatz, dan otak orang
lanjut usia yang normal. Kekacauan neurofibriler biasanya ditemukan di
korteks, hipokampus, substansia nigra, dan lokus sereleus.
Plak senilis, juga dikenal sebagai plak amiloid, adalah jauh lebih indikatif
untuk penyakit Alzheimer, walaupun keadaan tersebut juga ditemukan pada
sindroma Down dan, sampai derajat tertentu, pada penuaan normal. Plak senilis
terdiri dari protein tertentu, beta/A4 dan astrosit, prosesus neuronal distrofik, dan
mikroglia. Jumlah dan kepadatan plak senilis yang terdapat pada otak orang
yang telah meninggal (postmortem) telah dihubungkan dengan beratnya
penyakit pada orang yang terkena tersebut.
Protein prekursor amiloid. Gen untuk protein prekursor amiloid adalah pada
lengan panjang dari kromosom 21. Melalui proses penyambungan diferensial,
sesungguhnya terdapat empat bentuk protein prekursor amiloid. Protein beta/A4,
yang merupakan kandungan utama dari plak senilis, adalah suatu peptida
dengan 42 asam amino yang merupakan produk penghancuran protein prekursor
amiloid. Pada sindroma Down (trisomi 21), terdapat tiga cetakan protein
prekursor amiloid, dan pada penyakit di mana terjadi mutasi pada kodon
717 dalam gen protein prekursor amiloid, suatu proses patologis menghasilkan
deposisi protein beta/A4 yang berlebihan. Pertanyaan apakah proses pada
protein prekursor amiloid yang abnormal adalah penyebab utama yang penting
pada penyakit Alzheimer masih belum terjawab; tetapi, banyak kelompok
peneliti secara aktif mempelajari proses metabolik normal dari protein prekursor
amiloid dan prosesnya pada pasien dengan demensia tipe Alzheimer dalam
usaha untuk menjawab pertanyaan tersebut.
Kelainan neurotransmiter. Neurotransmiter yang paling berperan dalam
patofisiologis adalah asetilkolin dan norepinefrin, keduanya dihipotesiskan
menjadi hipoaktif pada penyakit Alzheimer. Beberapa penelitian telah
melaporkan data yang konsisten dengan hipotesis bahwa suatu degenerasi
spesifik pada neuron kolinergik ditemukan pada nukleus basalis Meynerti
pada pasien dengan penyakit Alzheimer. Data lain yang mendukung adanya
defisit kolinergik pada penyakitAlzheimer adalah penurunan konsentrasi
asetilkolin dan kolin asetiltransferase di dalam otak. Kolin asetiltransferase
adalah enzim kunci untuk sintesis asetilkolin, dan penurunan konsentrasi kolin
asetiltransferase menyatakan penurunan jumlah neuron kolinergik yang ada.
Dukungan tambahan untuk hipotesis defisit kolinergik berasal dari observasi
bahwa antagonis kolinergik, seperti scopolamine dan atropine, mengganggu
kemampuan kognitif, sedangkan agonis kolinergik, seperti physostigmine dan
arecholine, telah dilaporkan meningkatkan kemampuan kognitif. Penurunan
aktivitas norepinefrin pada penyakit Alzheimer diperkirakan dari penurunan
neuron yang mengandung norepinefrin di dalam lokus sereleus yang telah di-
temukan pada beberapa pemeriksaan patologis otak dari pasien dengan
penyakit Alzheimer. Dua neurotransmiter lain yang berperan dalam patofisiologi
penyakit Alzheimer adalah dua peptida neuroaktif, somatostatin dan
kortikotropin, keduanya telah dilaporkan menurun pada penyakit Alzheimer.
Penyebab potensial lainnya. Teori kausatif lainnya telah diajukan untuk
menjelaskan perkembangan penyakit Alzheimer. Satu teori adalah bahwa
kelainan dalam pengaturan metabolisme fosfolipid membran menyebabkan
membran yang kekurangan cairan-yaitu, lebih kaku-dibandingkan normal.
Beberapa peneliti telah menggunakan pencitraan spektroskopik resonansi
molekular (molecular resonance spectroscopic; MRS) unt uk memeriksa
hipotesis tersebut pada pasien dengan demensia tipe Alzheimer. Toksisitas
aluminium juga telah dihipotesiskan sebagai faktor kausatif karena kadar
aluminium yang tinggi telah ditemukan dalam otak beberapa pasien dengan
penyakit Alzheimer.
Suatu gen (E4) telah dihubungkan dalam etiologi penyakit Alzheimer. Orang
dengan satu salinan gen menderita penyakit Alzheimer tiga kali lebih sering
daripada orang tanpa gen E4. Orang dengan dua gen E4 mempunyai
kemungkinan menderita penyakit delapan kali lebih sering dan pada orang
tanpa gen E4.
Demensia Vaskular
Penyebab utama dari demensia vaskular dianggap adalah penyakit vaskular serebral
yang multipel, yang menyebabkan suatu pola gejala demensia. Demensia vaskular
paling sering pada laki-laki, khususnya pada mereka dengan hipertensi yang telah ada
sebelumnya atau faktor risiko kardiovaskular lainnya. Gangguan terutama mengenai
pembuluh darah serebral berukuran kecil dan sedang, yang mengalami infark dan
menghasilkan lesi parenkim multipel yang menyebar pada daerah otak yang luas.
Penyebab infark mungkin termasuk oklusi pembuluh darah oleh plak arteriosklerotik atau
tromboemboli dari tempat asal yang jauh (sebagai contohnya, katup jantung). Suatu
pemeriksaan pasien dapat menemukan bruit karotis, kelainan unduskopi, atau
pembesaran kamar jantung
5. Explain about organic mental
GANGGUAN MENTAL ORGANIK
DEFINISI
Gangguan mental organik adalah gangguan mental yang berkaitan dengan
penyakit/gangguan sistemik atau otak yang dapat didiagnosis tersendiri. Termasuk
gangguan mental simtomatik, di mana pengaruh terhadap otak merupakan akibat
sekunder dari penyakit/gangguan sistemik di luar otak (ekstra cerebral).
Yang termasuk dalam gangguan mental organik adalah :
1. Sindrom gangguan psikopatologik (misalnya demensia)
2. gangguan yang mendasari (misalnya penyakit Alzheimer)

apa saja gambaran utama dari gangguan mental organic?
a. gangguan fungsi kognitif daya ingat, daya pikir, daya belajar
b. gangguan sensorium gangguan kesadaran dan perhatian
c. sindrom dengan manifestasi yang menonjol dalam bidang persepsi, isi pikiran,
suasana, perasaan,dan emosi
d. onset sangat berpengaruh dalam penentuan diagnosis
PPDGJ III

F00 F09 GANGGUAN MENTAL ORGANIK`
(TERMASUK GANGGUAN MENTAL SIMTOMATIK)
F00 DEMENSIA PADA PENYAKIT ALZHEIMER
F01 DEMENSIA VASKULAR
F02 DEMENSIA PADA PENYAKIT LAIN YDK
F03 DEMENSIA YTT
F04 SINDROM AMNESIK ORGANIK BUKAN AKIBAT ALKOHOL dan ZAT
PSIKOAKTIF LAINNYA
F05 DELIRIUM BUKAN AKIBAT ALKOHOL dan ZAT PSIKOAKTIF
LAINNYA
F06 GANGGUAN MENTAL LAINNYA AKIBAT KERUSAKAN dan
DISFUNGSI OTAK dan PENYAKIT FISIK
F07 GANGGUAN KEPRIBADIAN dan PERILAKU AKIBAT
PENYAKIT,KERUSAKAN DAN DISFUNGSI OTAK
F08 GANGGUAN MENTAL ORGANIK ATAU SIMTOMATIK YTT
PPDGJ III

6. Demensia (definition,etiologi,classification, risk factor,criteria diagnostic,
management terapy, DD)
Definisi :
Demensia merupakan sindroma yang ditandai oleh berbagai gangguan fungsi kognitif
tanpa gangguan kesadaran. Fungsi kognitif yang dapat dipengaruhi pada demensia adalah
inteligensia umum, belajar dan ingatan, bahasa, memecahkan masalah, orientasi, persepsi,
perhatian, dan konsentrasi, pertimbangan, dan kemampuan sosial. Kepribadian pasien
juga terpengaruhi.
SINOPSIS PSIKIATRI , KAPLAN DAN SADOCK
Etiology : There are many causes of dementia, including neurological disorders such
as Alzheimer's disease, blood flow-related (vascular) disorders such as multi-infarct
cognitive impairment, inherited disorders such as Huntington's disease, and
infections such as HIV. The most common causes of dementia include:

Degenerative neurological diseases, such as Alzheimer's, frontotemporal lobar
degenerations, dementia with Lewy bodies, Parkinson's, and Huntington's
Vascular disorders, such as multi-infarct dementia, which is caused by multiple
strokes in the brain
Infections that affect the central nervous system, such as HIV dementia complex
and Creutzfeldt-Jakob disease
Chronic drug use
Depression
Certain types of hydrocephalus, an accumulation of fluid within the brain that can
result from developmental abnormalities, infections, injury, or brain tumors
Alzheimer's disease accounts for 50 percent to 70 percent of all dementia. However,
many patients with Alzheimers disease also have evidence of co-existing
cerebrovascular disease, usually consisting of multiple small areas of ischemic
changes (often call "mini-strokes") on MRI and on post-mortem examination of the
brain. Thus, many of these patients can be considered to have a "mixed" dementia.
Frontotemporal lobar degenerations, of which several types are known, account for
a substantial number of dementias, especially among those in their 50s and 60s.
Dementia with Lewy bodies has also been diagnosed with increasing frequency in
recent years. These patients have clinical signs of parkinsonism as well as dementia;
its relationship to the dementia of Parkinsons disease is still incompletely
understood.
http://www.clevelandclinic.org/health/health-info/docs/2300/2340.asp

DEMENSIA
DEFINISI
Demensia merupakan sindroma yang ditandai oleh berbagai gangguan fungsi kognitif tanpa
gangguan kesadaran. Fungsi kognitif yang dapat dipengaruhi pada demensia adalah inteligensia
umum, belajar dan ingatan, bahasa, memecahkan masalah, orientasi, persepsi, perhatian, dan
konsentrasi, pertimbangan, dan kemampuan sosial. Kepribadian pasien juga terpengaruhi.
SINOPSIS PSIKIATRI , KAPLAN DAN SADOCK
Demensia adalah keadaan dimana seseorang mengalami penurunan kemampuan daya ingat dan
daya pikir, dan penurunan kemampuan tersebut menimbulkan gangguan terhadap fungsi
kehidupan sehari-hari. Bentuk gangguan yang sangat menyolok adalah penurunan perilaku yang
secara lengkap disebut perilaku sosial (social skill) dan perilaku ini dapat dirinci lebih lanjut
menjadi:
ADL (Activity of Daily Living yaitu kemampuan seseorang untuk mengurus dirinya sendiri)
dimulai dari bangun tidur, mandi, berpakaian dan seterusnya sampai pergi tidur kembali,
pokoknya segala kegiatan orang untuk mengurus kebutuhannya sendiri.
Perilaku Okupasional yaitu perilaku yang dilaksanakan seseorang untuk menjalankan
kehidupannya untuk bekerja dan mencari nafkah, yaitu sekolah, bekerja, berorganisasi,
menjalankan ibadah, mengisi waktu luang.
Partisipasi sosial yaitu perilaku seseorang untuk hidup bermasyarakat seperti mematuhi
kewajiban sebagai warga masyarakat, misalnya mengurus KTP, SIM, Kerja Bakti,
berorganisasi sosial, menghadiri undangan dan sebagainya.
(Kecerdasan pada usia lanjut dan demensia,FKUI,Prof.Dr.dr.SM.Lumbantobing)


ETIOLOGI
Demensia mempunyai banyak penyebab tetapi demensia tipe Alzheimer dann demensia vaskular
secara bersama-sama berjumlah sebanyak 75 persen dari semua kasus. Penyebab demensia
lainnya yang disebutkan dalam DSM-IV adalah penyakit Pick, penyakit Creutz-Feldt-Jakob,
penyakit Huntington, penyakit kinson, human immunodeficiency virus (HIV) dan trauma kepala.




Dari segi etiologi dibedakan antara demensia reversibel dan irreversibel. Untuk
demensia reversible penyebabnya adalah :
1

1. Drugs
Antidepresi, antiansietas, sedatif, antiaritmia, antihipertensi, antikonvulsan, obat-obat
jantung termasuk digitalis, obat-obat antikolmergik.
2. Emosi/depresi
Depresi, shizofrenta, mania, psikosis.
3. Metabolik / endokrin
Penyakit tiroid, hipoglikemi, hipernatremi dan hiponatremi, hiperklasemi, gagal ginjal,
gagal hati, penyakit Cushing, penyakit wilson.
4. Eye/ear nutrisi
Difensiasi tiamin, difensiasi vitamin B12 (anemia pernisiosa), Difensiasi asam fosfat,
difensiasi vitamin B6 (pellagra).
5. Trauma
Trauma kranioserebal, hematon subdural akut dan kronis.
6. Tumor
Glioma, meningioma, tumor metastatis.
7. Infeksi
Meningitis dan ensefalitis bakterialis, meningitis dan ensefalitis Akibat jamur, meningitis
akibat kriptokokus, meningitis dan Ensefalitis viral, abses otak, neurosifilis, AIDS.
8. Autoimun
Lupus eritematosus diseminata, multiple sklerosis. Dan di samping itu ada juga
arterioseklerosis dan alkohol.
Untuk dementia yang irreversibel penyebabnya adalah:
1
1. Penyakit degeneratif
Penyakit Alzaimer, dementia Frontotemporal, penyakit Huntington, penyakit Parkinson,
penyakit Lewy bodies, atrofi olivopontoserebelar, amiotropik lateral sklerosis/ dementia
parkinsonism kompleks.
2. Penyakit vaskular
Infrak multipel, emboli serebral, arteritis, anoksia skunder akibat henti jantung, gagal
jantung atau keracunan karbon monoksida.
3. Trauma
Trauma kranioserebral berat
4. Infeksi
Sub akut spongiform ensefalopati (creutzfeldt-jacob disease), post ensefalitis,
Leukoensefalopati multifokal progresif.

FAKTOR RESIKO
Tipe Alzheimer
- Usia 65 thn
- Wanita
- Sanak saudara tingkat pertama
- Punya riwayat cedera kepala
- Sindroma down
Tipe Vaskular
- paling sering ditemukan pada usia antara 60 dan 70 thn
- lebih sering pada laki-laki dr pd wanita

Kaplan.H.I, Sadock. B.J, Sinopsis Psikiatri : Ilmu Pengetahuan Perilaku Psikiatri Klinis, edisi
ketujuh, jilid satu. Binarupa Aksara, Jakarta 1997. hal 502-540.


KLASIFIKASI
a. Demensia tipe alzheimer
SINOPSIS PSIKIATRI PPDGJ-III
Perkembangan defisit kognitif yang
dimanifestasikan oleh baik :
1) Gangguan daya ingat ( gangguan
kemampuan dalam mempelajari
informasi baru dan untuk mengingat
informasi yang telah dipelajari
sebelumnya )
2) Satu ( atau lebih ) gangguan kognitif
berikut :
a) Afasia ( gangguan bahasa )
b) Apraksia ( gangguan kemampuan
untuk aktivitas motorik walaupun
fungsi motorik adalah utuh )
c) Agnosia ( kegagalan untuk
mengenali atau mengidentifikasi
benda walaupun fungsi sensorik
adalah utuh )
d) Gangguan dalam fungsi eksekutif (
yaitu merencanakan,
Terdapatnya gejala demensia
Onset bertahap ( insidious onset )
dengan deteriorasi lambat. Onset
biasanya sulit ditentukan
waktunya yang persis, tiba orang
lain sudah menyadari adanya
kelainan tersebut. Dalam
perjalanan penyakitnya dapat
terjadi suatu taraf yang stabil (
plateau ) secara nyata
Tidak adanya bukti klinis, atau
temuan dari pemeriksaan khusus,
yang menyatakan bahwa kondisi
mental itu dapat disebabkan oleh
penyakit otak atau sistemik lain
yang dapat menimbulkan
demensia ( misalnya
hipotiroidisme, hiperkalsemia,
defisiensi vitamin B12, defisiensi
mengorganisasi, mengurutkan dan
abstrak )
Defisit kognitif dalam kriteria A1 dan A2
masing menyebabkan gangguan yang
bermakna dalam fungsi sosial atau
pekerjaan dan menunjukkan suatu
penurunan bermakna dari tingkat fungsi
sebelumnya
Perjalanan penyakit ditandai oleh onset
yang bertahap dan penurunan kognitif
yang terus-menerus
Defisit kognitif dalam kriteria A1 dan A2
bukan salah satu dari berikut :
1) Kondisi sistem saraf pusat lain yang
menyebabkan defisit progresif dalam
daya ingat dan kognisi ( misalnya,
penyakit serebrovaskular, penyakit
Parkinson, penyakit Huntington,
hematoma subdural, hidrosefalus
tekanan normal, tumor otak )
2) Kondisi sistemik yang diketahui
menyebabkan demensia ( misalnya,
hipotiroidisme, defisiensi vitamin B
12

atau asam folat, defisiensi niasin,
hiperkalsemia, neurosifilis, infeksi HIV
)
3) Kondisi akibat zat
Defisit tidak terjadi semata-mata selama
perjalanan suatu delirium
Gangguan tidak lebih baik diterangkan
oleh gangguan aksis I lainnya ( misalnya,
gangguan depresif berat, skizofrenia )
niasin, neurosifilis, hidrosefalus
bertekanan normal, atau
hematoma subdural
Tidak adanya serangan apoplektik
mendadak, atau gejala neurologik
kerusakan otak fokal seperti
hemiparesis, hilangnya daya
sensorik, defek lapangan pandang
mata, dan inkoordinasi yang
terjadi dalam masa dini dari
gangguan itu ( walaupun
fenomena ini dikemudian hari
dapat bertumpang tindih )

b. Demensia vaskular
SINOPSIS PSIKIATRI PPDGJ-III
Perkembangan defisit kognitif yang
dimanifestasikan oleh baik :
1) Gangguan daya ingat ( gangguan
kemampuan dalam mempelajari
informasi baru dan untuk mengingat
informasi yang telah dipelajari
sebelumnya )
2) Satu ( atau lebih ) gangguan kognitif
berikut :
a) Afasia ( gangguan bahasa )
b) Apraksia ( gangguan kemampuan
Terdapatnya gejala demensia
Hendaya fungsi kognitif biasanya
tidak merata ( mungkin terdapat
hilangnya daya ingat, gangguan
daya pikir, gejala neurologis fokal
). Daya tilik dari ( insight ) dan
daya nilai (judgment) secara
relatif tetap baik
Suatu onset yang mendadak atau
deteriorasi yang bertahap, disertai
adanya gejala neurologis fokal,
untuk aktivitas motorik walaupun
fungsi motorik adalah utuh )
c) Agnosia ( kegagalan untuk
mengenali atau mengidentifikasi
benda walaupun fungsi sensorik
adalah utuh )
d) Gangguan dalam fungsi eksekutif (
yaitu merencanakan,
mengorganisasi, mengurutkan dan
abstrak )
Defisit kognitif dalam kriteria A1 dan A2
masing menyebabkan gangguan yang
bermakna dalam fungsi sosial atau
pekerjaan dan menunjukkan suatu
penurunan bermakna dari tingkat fungsi
sebelumnya
Tanda dan gejala neurologis fokal (
misalnya, peninggian refleks tendon
dalam, respon ekstensor plantar, palsi
pseudobulbar, kelainan gaya berjalan,
kelamahan pada satu ekstremitas ) atau
tanda laboratorium adalah indikatif untuk
penyakit serebrovaskular ( misalnya,
infark multipel yang mengenai korteks dan
substansia putih di bawahnya )yang
dianggap berhubungan secara etiologi
dengan gangguan
Defisit tidak terjadi semata selama
perjalanan delirium
meningkatkan kemungkinan
diagnosis demensia vaskuler.
Pada beberapa kasus, penetapan
hanya dapat dilakukan dengan
pemeriksaan CT-Scan atau
pemeriksaan neuropatologis

c. Demensia karena kondisi medis umum lain
SINOPSIS PSIKIATRI
Perkembangan defisit kognitif yang dimanifestasikan oleh baik :
1) Gangguan daya ingat ( gangguan kemampuan dalam mempelajari informasi
baru dan untuk mengingat informasi yang telah dipelajari sebelumnya )
2) Satu ( atau lebih ) gangguan kognitif berikut :
a) Afasia ( gangguan bahasa )
b) Apraksia ( gangguan kemampuan untuk aktivitas motorik walaupun fungsi
motorik adalah utuh )
c) Agnosia ( kegagalan untuk mengenali atau mengidentifikasi benda walaupun
fungsi sensorik adalah utuh )
d) Gangguan dalam fungsi eksekutif ( yaitu merencanakan, mengorganisasi,
mengurutkan dan abstrak )
Defisit kognitif dalam kriteria A1 dan A2 masing menyebabkan gangguan yang
bermakna dalam fungsi sosial atau pekerjaan dan menunjukkan suatu penurunan
bermakna dari tingkat fungsi sebelumnya
Terdapat bukti dari riwayat penyakit, pemeriksaan fisik, atau temuan laboratorium
bahwa gangguan adalah akibat fisiologis langsung dari salah satu kondisi medis
yang tertulis di bawah ini
Defisit tidak terjadi semata selama perjalanan delirium

d. Demensia menetap akibat zat
SINOPSIS PSIKIATRI
Perkembangan defisit kognitif yang dimanifestasikan oleh baik :
1) Gangguan daya ingat ( gangguan kemampuan dalam mempelajari informasi
baru dan untuk mengingat informasi yang telah dipelajari sebelumnya )
2) Satu ( atau lebih ) gangguan kognitif berikut :
a) Afasia ( gangguan bahasa )
b) Apraksia ( gangguan kemampuan untuk aktivitas motorik walaupun fungsi
motorik adalah utuh )
c) Agnosia ( kegagalan untuk mengenali atau mengidentifikasi benda walaupun
fungsi sensorik adalah utuh )
d) Gangguan dalam fungsi eksekutif ( yaitu merencanakan, mengorganisasi,
mengurutkan dan abstrak )
Defisit kognitif dalam kriteria A1 dan A2 masing menyebabkan gangguan yang
bermakna dalam fungsi sosial atau pekerjaan dan menunjukkan suatu penurunan
bermakna dari tingkat fungsi sebelumnya
Defisit tidak terjadi semata hanya selama perjalanan suatu delirium dan menetap
melebihi lama yang lazim dari intoksikasi atau putus zat
Terdapat bukti dari riwayat penyakit, pemeriksaan fisik, atau temuan laboratorium
bahwa defisit secara etiologis berhubungan dengan efek menetap dari pemakaian
zat ( misalnya, suatu obat yang disalahgunakan, medikasi )



e. Demensia karena penyebab multipel
SINOPSIS PSIKIATRI
Perkembangan defisit kognitif yang dimanifestasikan oleh baik :
3) Gangguan daya ingat ( gangguan kemampuan dalam mempelajari informasi
baru dan untuk mengingat informasi yang telah dipelajari sebelumnya )
4) Satu ( atau lebih ) gangguan kognitif berikut :
e) Afasia ( gangguan bahasa )
f) Apraksia ( gangguan kemampuan untuk aktivitas motorik walaupun fungsi
motorik adalah utuh )
g) Agnosia ( kegagalan untuk mengenali atau mengidentifikasi benda walaupun
fungsi sensorik adalah utuh )
h) Gangguan dalam fungsi eksekutif ( yaitu merencanakan, mengorganisasi,
mengurutkan dan abstrak )
Defisit kognitif dalam kriteria A1 dan A2 masing menyebabkan gangguan yang
bermakna dalam fungsi sosial atau pekerjaan dan menunjukkan suatu penurunan
bermakna dari tingkat fungsi sebelumnya
Terdapat bukti dari riwayat penyakit, pemeriksaan fisik, atau temuan laboratorium
bahwa gangguan memiliki lebih dari satu penyebab ( misalnya, trauma kepala
ditambah penggunaan alkohol kronis, demensia tipe Alzheimer dengan
perkembagan demensia vaskular selanjutnya )
Defisit tidak terjadi semata selama perjalanan delirium

f. Demensia yang tidak ditentukan
SINOPSIS PSIKIATRI
Kategori ini digunakan untuk mendiagnosis demensia yang tidak memenuhi
kriteria tipe spesifik yang dijelaskan dalam bagian ini. Contohnya adalah
gambaran klinis demensia yang tidak terdapat bukti cukup untuk menegakkan
etiologi spesifik




1) Dari segi gambaran klinik :
Demensia global
Global : menyeluruh. Kemunduran fungsi diseluruh bidang
Demensia afasik
Afasia : tidak bisa berbahasa. Kemunduran terutama di bidang bahasa.
Demensia visuoperseptif.
Kemunduran terutama di bidang visual, memahami rangsang visual (penglihatan )
2) Dari segi anatomi dibedakan antara ;
Demensia kortikal
Demensia yang terjadi karena kerusakan di daerah korteks otak
Demensia subkortikal
Demensia yang terjadi karena kerusakan di daerah subkorteks, misalnya di daerah
ganglia basal.
3) Dari segi etiologi dan perjalanan penyakit
Demensia yang reversibel
Demensia irreversibel
Neurogeriatri, FKUI, Prof. Dr. dr. S.M. Lumbantobing, SpS(K), SpKJ
FOO DEMENSIA PADA PENYAKIT ALZHEIMER
F00.0 Demensia pada penyakit Alzheimer dengan onset dini
F00.1 Demensia pada penyakit Alzheimer dengan onset lambat
F00.2 Demensia pada penyakit Alzheimer, tipe tak kh atau tipe campuran
F00.9 Demensia pada penyakit Alzheimer YTT
FOI DEMENSIA VASKULAR
F01.0 Demensia vaskular onset akut
F01.1 Demensia multi-infark
F01.2 Demensia vaskular subkortikal
F01.3 Demensia vaskular campuran kortikal dan subkortik
F01.8 Demensia vaskular lainnya
F01.9 Demensia vaskular YTT
F02 DEMENSIA PADA PENYAKIT LAIN YDK
F02.0 Demensia pada penyakit Pick
F02.1 Demensia pada penyakit Creutzfeldt-Jakob
F02.2 Demensia padapenyakit Huntington
F02.3 Demensia pada penyakit Parkinson
F02.4 Demensia pada penyakit human immunodeficiency virus (HIV)
F02.8 Demensia pada penyakit lain YDT YDK
F03 DEMENSIA YTT
Karakter kelima dapat digunakan untuk menentukan demensia pada
FOO - F03 sebagai berikut :
.x0 Tanpa gejala tambahan
.xl Gejala lain, terutama waham
.x2 Gejala lain, terutama halusinasi
.x3 Gejala lain, terutama depresi
.x4 Gejala campuran lain
PPDGJ III
MENURUT SINOPSIS PSIKIATRI KAPLAN
DEMENSIA TIPE ALZHEIMER (DAT)
Alzheimer adalah penurunan konsentrasi asetilkolin dan kolin asetiltransferase di dalam otak
Demensia alzheimer adalah demensia progresif dimana semua kausa reversibel yang diketahui
telah disingkirkan. Dua tipe, senilis dengan kemunculan umur 65 tahun atau lebih dan presenilis
dengan usia kemunculan setelah 65 tahun. Perbedaan antara keduanya tidak bersifat
konvensional yang tidak didasari ats perbedaan riil apapun selain usia kemunculan
EPIDEMIOLOGI DAN FAKTOR RESIKO
DAT lebih sering terjadi pad wanita. Angka DAT itu sendiri itu lebih rendah pada negara non
industri, tapi ini mungkin suatu artefak akibat rendahnya perawatan media dan oleh karena itu
kurangnya kepekaan dalam membuat diagnosis tersebut. Usia pun mempengaruhi terjadinya
DAT.
DEMENSIA MULTI INFARK (MID)
Biasanya demensia ini berjalan progresif secara bertahap dengan infark rekuren. Pasien akan
menemukan suatu secra spesifik dmn fungsi merekak menjadi lebih buruk dan akan membaik
seddikit beberapa hari berikutnya sa,pai terjadi infark berikutnya. Seringkali terdapat tanda
neurologik. Gangguan kognisi dapat bersifat bercak dengan area tertentu intak.
Demensia ini lebih jarang daripada tipe DAT, lebih sering pada pria daripada wanita.
Kemunculan pada umur lebioh muda. Faktor resiko termasuk hipertensi, penyakit jantung, dan
faktor resiko lain untuk sttroke.
PENYAKIT PICK
Secara klinis mirip benar dengan DAT. Tapi klobus kanan jelas terkena, dan tanda frrontal dari
perilaku disinhibisi dapat muncul dini. Gliosis reaktif terjadi di lobus frontal dan temporal.
PENYAKIT CREUZFELDT-JAKOB
Disebabkan oleh virus lambat menular. Kemunculannya biasa terjadi di usia 40 atau 50an. Tanda
pertama berupa keluhan somatik samar ataubrasa cemas tak jelas. Termasuk atasia, tanda
ekstrapiramidal, koreoatetosis, dan disatria.
PENYAKIT HUNTINGTON
Penyakit dominan autosom dengan penetrasi lengkap (kromosom 4) ditandai oleh gerak
koreoatetoid dan demensia. Seseorang dengan orang tua yang memiliki huntington memiliki
peluang 50% menderita p[enyakit ini.
PENYAKIT PARKINSON
Gangguan gerak idiopatik dengan kemunculan biasanya pada usia lanjut, ditandai oleh
bradikinensia, tremor istirahat, tremor menggulung-pil, fasies mirip topeng, rigiditas, cara
berjalan perlahan-lahan. Gangguan intelektual ini sering terjadi dan 40-80% menjadi demensia.

GEJALA KLINIS
Pada stadium awal demensia, pasien menunjukkan kesulitan untuk mempertahankan kinerja
mental, fatigue, dan kecenderungan untuk gagal jika suatu tugas adalah baru atau kompleks
atau memerlukan penggeseran strategi pemecahan maslah. Ketidakmampuan melakukan tugas
menjadi makin berat dan menyebar ke tugas-tugas harian, seperti berbelanja, saat demensia
berkembang.
Akhirnya, pasien demensia mungkin memerlukan pengawasan dan bantuan yang terus menerus
untuk melakukan bahkan tugas yang paling dasar dalam kehidupan sehari-hari. Defek utama
dalam demensia melibatkan orientasi, ingatan, persepsi, fungsi intelektual, dan pemikiran, dan
semua fungsi tersebut menjadi secara progresif terkena saat proses penyakit berlanjut.
Perubahan afektif dan perilaku, seperti kontrol impuls yang defektif dan labilitas emosional,
sering ditemukan, seperti juga penonjolan dan perubahan sifat kepribadian premorbid.
Gangguan Daya Ingat
Gangguan ingatan biasanya merupakan ciri yang awal dan menonjol pada demensia, khususnya
pada demensia yang mengenai korteks, seperti demensia tipe Alzheimer. Pada awal perjalanan de-
mensia, gangguan daya ingat adalah ringan dan biasanya paling jelas untuk peristiwa yang baru
terjadi, seperti melupakan nomor telepon, percakapan, dan peristiwa hari tersebut. Saat perjalanan
dimensia berkembang, gangguan emosional menjadi parah, dan hanya informasi yang
dipelajari paling baik (sebagai contohnya, tempat kelahiran) dipertahankan.
Orientasi
Karena daya ingat adalah penting untuk orientasi terhadap orang, tempat, dan waktu, orientasi
dapat terganggu secara progresif selama perjalanan penyakit demensia. Sebagai contohnya, pasien
dengan demensia mungkin lupa bagaimana kembali ke ruangannya setelah pergi ke kamar mandi.
Tetapi, tidak masalah bagaimana beratnya disorientasi, pasien tidak menunjukkan gangguan pada
tingkat kesadaran.
Gangguan Bahasa
Proses demensia yang mengenai korteks, terutama demensia tipe Alzheimer dan demensia
vaskular, dapat mempengaruhi kemampuan berbahasa pasien. Pada kenyataannya, DSM-IV me-
masukkan afasia sebagai salah satu kriteria diagnostik. Kesulitan berbahasa mungkin ditandai
oleh cara berkata yang samar-samar, stereotipik, tidak tepat, atau berputar-putar. Pasien mungkin
juga memiliki kesulitan dalam menyebutkan nama suatu benda.
Perubahan Kepribadian
Perubahan kepribadian pasien demensia merupakan gambaran yang paling mengganggu bagi
keluarga pasien yang terkena. Sifat kepribadian sebelumnya mungkin diperkuat selama perkem-
bangan demensia. Pasien dengan demensia juga mungkin menjadi introvert dan tampaknya
kurang memperhatikan tentang efek perilaku mereka terhadap orang lain. Pasien demensia yang
mempunyai waham paranoid biasanya bersikap bermusuhan terhadap anggota keluarga dan
pengasuhnya. Pasien dengan gangguan frontal dan temporal kemungkinan mengalami perubahan
kepribadian yang jelas dan mungkin mudah marah dan meledak-ledak.
Psikosis
Diperkirakan 20 sampai 30 persen pasien demensia, terutama pasien dengan demensia tipe
Alzheimer, memiliki halusinasi, dan 30 sampai 40 persen pasien memiliki waham, terutama
dengan sifat paranoid atau persekutorik dan tidak sistematik, walaupun waham yang kompleks,
menetap, tersistematik dengan baik juga dilaporkan pada pasien demensia. Agresi fisik dan
bentuk kekerasan lainnya adalah sering pada pasien demensia yang juga mempunyai gejala
psikotik.
Gangguan Lain
Psikiatrik. Di samping psikosis dan perubahan kepribadian, depresi dan kecernasan adalah gejala
utama pada kira-kira 40 sarnpai 50 persen pasien demensia, walaupun sindroma gangguan depresif
yang sepenuhnya mungkin hanya ditemukan pada 10 sampai 20 persen pasien demensia. Pasien
dengan demensia juga menunjukkan tertawa atau menangis yang patologis-yaitu, emosi yang
ekstrim tanpa provokasi yang terlihat.
Neurologis. Di samping afasia pada pasien demensia, apraksia dan agnosia adalah sering, dan
keberadaannya dimasukkan sebagai kriteria diagnostik potensial dalam DSM-IV. Tanda
neurologis lain yang dapat berhubungan dengan demensia adalah kejang, yang terlihat pada kira-
kira 10 persen pasien dengan demensia tipe Alzheimer dan 20 persen pasien dengan demensia
vaskular, dan presentasi neurologis yang atipikal, seperti sindroma lobus parietalis nondominan.
Refleks primitif-seperti refleks menggenggam, moncong, mengisap, kaki-tonik, dan palmomental
mungkin ditemukan pada pemeriksaan neurologis, dan jerks mioklonik ditemukan pada 5 sampai
10 persen pasien.
Pasien dengan demensia vaskular mungkin mempunyai gejala neurologis tambahan-seperti nyeri
kepala, pusing, pingsan, kelemahan, tanda neurologis fokal, dan gangguan tidur-mungkin
menunjukkan lokasi penyakit serebrovaskular. Palsi serebrobulbar, disartria, dan disfagia juga le-
bih sering pada demensia vaskular dibandingkan demensia lain.
Reaksi katastropik. Pasien demensia juga menunjukkan penurunan kemampuan untuk menerapkan
apa yang disebut oleh Kurt Goldstein sebagai perilaku abstrak. Pasien mempunyai kesulitan dalam
generalisasi dari suatu contoh tunggal dalam membentuk konsep, dan dalam mengambil perbedaan
dan persamaan di antara konsep-konsep. Selanjutnya, kemampuan untuk memecahkan masalah,
untuk memberikan alasan secara logis dan untuk membuat pertimbangan yang sehat adalah
terganggu. Goldstein juga menggambarkan suatu reaksi katastropik, yang ditandai oleh agitasi
sekunder karena kesadaran subjektif tentang defisit intelektualnya di bawah keadaan yang me-
negangkan. Pasien biasanya berusaha untuk mengkompensasi defek tersebut dengan
menggunakan strategi untuk menghindari terlihatnya kegagalan dalam daya intelektual, seperti
mengubah subyek, membuat lelucon, atau mengalihkan pewawancara dengan cara lain. Tidak
adanya pertimbangan kontrol impuls yang buruk sering ditemukan khususnya pada demensia yang
terutama mempengaruhi lobus frontalis. Contoh dari gangguan tersebut adalah bahasa yang
kasar, humor yang tidak sesuai, pengabaian penampilan dan higine pribadi, dan mengabaikan
aturan konvensional tingkah laku sosial.
Sindroma "sundowner." Sindroma downer ditandai oleh mengantuk, konfusi, ataksia dan terjatuh
secara tidak disengaja. Keadaan ini terjadi pada pasien lanjut usia yang mengalami sedasi berat
dan pada pasien demensia yang bereaksi secara menyimpang bahkan terhadap dosis kecil obat
psikoaktif. Sindroma juga terjadi pada pasien demensia jika stimuli eksternal, seperti cahaya dan
isyarat yang menyatakan interpersonal adalah menghilang.
Onset yang perlahan-lahan dengan perjalanan yang memburuk secara progresif, tidak adanya
tanda neurologis, tidak adanya riwayat trauma atau penyakit serebrovaskular, hasil tes darah yang
normal, dan bukti atrofi kortikal pada CT scan berarti diagnosis demensia tipe Alzheimer. Karena
tidak terdapat ciri psikotik atau gangguan mood, diagnosis dicatat tanpa komplikasi. Beratnya
demensia dinyatakan sebagai moderat karena pasien memerlukan suatu pengawasan.

DIAGNOSIS
adanya penurunan daya ingat dan daya pikir, yang sampai mengganggu kegiatan harian
seseorang seperti mandi, berpakaian, makan, kebersihan diri, BAK, dan BAB.
Tidak ada gangguan keasadaran
Gejala dan disabilitas sudah nyata untuk paling sedikit 6 bulan
(PPDGJ III)

Diagnosis

Diagnosis difokuskan pada 3 hal:
Pembedaan antara delirium dan demensia
Bagian otak yang terkena
Penyebab yang potensial reversibel
Perlu pembedaan dan depresi (ini bisa diobati relatif mudah)
Pemeriksaan untuk mengingat 3 benda yg disebut
Mengelompokkan benda, hewan dan alat dengan susah payah
Pemeriksaan laboratonium, pemeriksaan EEC
Pencitraan otak amat penting CT atau MRI

F00 DEMENSIA PENYAKIT AZLZHEIMER
o Terdapat gejala demensia
o Onset bertahap (insidious onset) dengan deteriorasi lambat.. inset biasanya sulit
ditentukan waktunya yang persis, tiba2 orang lain sudah menyadari adanya
kelainan tersebut. Dalam perjalanan penyakitnya dapat terjadi suatu taraf yang
stabil (plateau) secara nyata
o Tidak adanya bukti klinis, atau temuan dari pemeriksaan khusus, yang
menyatakan bahwa kondisi mental itu dapat disebabkan oleh penyakit otak/
sistemik lain yang dapat meneimbulkan demensia.
o Tidak adanya serangan apoplektik mendadak, atau gejala neurologik kerusakan
otak fokal seperti hemiparesis, hilangnya daya sensorik, defek lapangan pandang
mata, dan inkordinasi yang terjadi dalam masa dini dari dari gangguan itu.
F00.0 DEMENSIA PADA PENYAKIT ALZHEIMER DENGAN ONSET DINI
Onsetnya sebelum usia 65 tahun
Perkembangan gejalanya cepat dan progresif
Adanya riwayat keluarga yang mengalami demensia alzheimer merupakan faktor
penyokong diagnosis tetapi tidak harus dipenuhi
F00.1 DEMENSIA PADA PENYAKIT ALZHEIMER DENGAN ONSET LAMBAT
o Sama tersebut diatas, hanya onsetnya sesudah berusia 65 tahun dan perjalanan
penyakitnya lamban dan biasanya dengan gangguan daya ingat sebagai gangguan
utamanya
o F00.2 TIPE TAK KHAS ATU TIPE CAMPURAN
Yang tidak cocok dengan pedoman untuk F00.0 atau F00.1, tipe campuran adalah
demensia alzheimer + vaskuler
o FOO.3 DEMENSIA PADA PENYAKIT ALZHEIMER YTT
F01 DMENSIA VASKULER
Terdapat gejala demensia
Hendaya fungsi kognitif biasanya tidak merata (mungkin terdapat hilangnya day
ingatan, gangguan daya pikir, gejala neurologis fokal). Daya tilik diri(insight) dan
daya nilai (judgment) secara relatif tetap baik.
Suatu onset yan mendadak atau deteriorasi yang bertahap, disertai adanya gejala
neurologis fokal, meningkatkan kemungkinan diagnosis demensia vaskuler. Pada
beberapa kasus, penetapan hanya dapat dilakukan dengan px CT-Scan atau
pemeriksaan neuropatologis
F01.0 DEMENSIA VASKULER ONSET AKUT
o Biasanya terjadi secara cepat sesudah serangkain stroke akibat trombosis
serebrovaskuler, embolisme, atau perdarahan. Pada kasus-kasus yang jarang,
suatu infark yang besra dapat sebagai penyebabnya
F01.1 DEMENSIA MULTI INFARK
o Onsetnya lebih lambt, biasanya setelah serangkaina episode iskemnik minor yang
menimbulkan akumulasi dariu infark pada parenkim otak.
F01.2 DEMENSIA VASKULER SUBKORTIKAL
o Fokus kerusakan akibat iskemik pada substansia alba di hemisferi serebral, yang
dapat diduga secara klinis dan dibuktikan dengan CT_Scan. Korteks serebri
biasanya tetap baik, walaupun demikian gambaran klinisnya masih mirip dengan
dmensia pada penyakit alzheimer.
F01.3 DEMENSIA VASKULAR CAMPURAN KORTIKAL DANM
SUBKORTIKAL
Komponen campuran kortikal dan subkortikal dapat diduga dari gambaran klinis,
hasil pemeriksaan, atau keduanya.
F01.8 DEMENSIA VASKULAR LAINNYA
F01.9 DEMENSIA VASKULAR YTT
F02 DEMENSIA PADA PENYAKIT LAIN YDK
F02.0 DEMENSIA PADA PENYAKIT PICK
o Gejala yang progresif
o Gambaran neuropatologis
o Manifestasi gangguan perilaku pada umumnya mendahului gangguan daya ingat
F02.1 DEMENSIA PADA PENYAKIT CREUTZFELDT-JAKOB
o Trias yang sangat mengarah pada penyakit ini:
o Progresif merusak
o Penyakit piramidal dan ekstrapiramidal dengan mioklonus
o Elektroensefalogram yang khas (trifasik)
F02.2 DEMENSIA PADA PENYAKIT HUNTINGTON
Ada kaitan antara gangguan gerakan koreiform, demensia, dan RPK dengan peny
huntington
Gerakan koreiform yang involunter, terutama pada wajah, tangan, dan bahu, atau
cara berjalan yang khas merupakan manbifestasi dini dari gejala ini. Biasanya
mendahului gejala demensia.
Gangguan fungsi lobus frontalis pada tahap dini, dengan daya ingat relatif masih
terpelihara, sampai pada saat selanjutnya.
F02.3 DEMENSIA PADA PENYAKIT PARKINSON
Berkembang pada seseorang dengan penyakit parkinson yang sudah parah, tidak
ada gambaran klinis khusus yang di tampilkan....
F02.4 DEMENSIA PADA PENYAKIT HIV
o Demensia yang berkembang pada seseorang dengan penyakit HIV.
F02.8 DEMENSIA PADA PENYAKIT LAIN YDT YDK
Terjadi sebagai manifestasi atau konsekuensi beberapa macam kondisi somatik
dan serebral lainnya
F03 DEMENSIA YTT
o Digunakan bila kriteria umum untuk diagnosis dmensia terpenuhi, tetapi tidak
mungkin di identifikasikan pada salah satu tipe tertentu (F00.9-F02.9)

TERAPI
Terapi

Pertama perlu diperhatikan keselamatan pasien, lingkungan dibuat senyaman mungkin, dan
bantuan pengasuh perlu.
Koridor tempat jalan, tangga, meja kursi tempat barang keperkuannya
Tidak diperbolehkan memindahkan mobil dsb.
Diberi keperluan yang mudah dilihat, penerangan lampu terang, jam dinding besar,
tanggalan yang angkanya besar
Obat:
Nootropika:
o Pyritinol (Encephabol) 1 x 100 - 3 x 200 mg
o Piracetam (Nootropil) 1 x 400 - 3 x 1200 mg
o Sabeluzole (Reminyl)
o Ca-antagonist:
o Nimodipine(Nimotop 1- 3 x 30 mg)
o Citicholine (Nicholin) 1 - 2 x 100 - 300 mg i.v./i.m.
o Cinnanzine (Stugeron) 1 - 3 x 25 mg
o Pentoxifylline (Trental) 2 - 3 x 400 mg (oral), 200 - 300 mg infuse
o Pantoyl-GABA
Acetylcholinesterase inhibitors
o Tacnne 10 mg dinaikkan lambatlaun hingga 80 mg. Hepatotoxik
o Donepezil (Aricept) centrally active reversible cholinesterase inhibitor, 5 mg 1x
/hari
o Galantamine (Riminil) 1 - 3 x 5 mg
o Rivastigmin (Exelon) 1,5, 3, 4, 5, 6 mg
o Memantine 2 x 5 mg 10 mg


Membantu penderita demensia dan keluarganya:
1. Mempertahankan lingkungan yang familiar akan membantu penderita tetap
memiliki orientasi. Kalender yang besar, cahaya yang terang, jam dinding dengan
angka-angka yang besar atau radio juga bisa membantu penderita tetap memiliki
orientasi.
2. Menyembunyikan kunci mobil dan memasang detektor pada pintu bisa membantu
mencegah terjadinya kecelekaan pada penderita yang senang berjalan-jalan.
3. Menjalani kegiatan mandi, makan, tidur dan aktivitas lainnya secara rutin, bisa
memberikan rasa keteraturan kepada penderita.
4. Memarahi atau menghukum penderita tidak akan membantu, bahkan akan
memperburuk keadaan.
5. Meminta bantuan organisasi yang memberikan pelayanan sosial dan perawatan,
akan sangat membantu.
Obat Untuk Dementia
a. Cholinergic-enhancing agents
Untuk terapi dementia jenis Alzheimer, telah banyak dilakukan penelitian.
Pemberian cholinergic-enhancing agents menunjukkan hasil yang cukup
memuaskan pada beberapa penderita, namun demikian secara keseluruhan tidak
menunjukkan keberhasilan sama sekali. Hal ini disebabkan oleh kenyataan,
bahwa dementia Alzheimer tidak semata-mata disebabkan oleh defisiensi
kolinergik. Dementia ini disebabkan juga oleh defisiensi neurotransmitter lainnya.
Sementara itu, kombinasi kolinergik dan noradregenik ternyata bersifat kompleks,
pemberian obat kombinasi ini harus hati-hati karena dapat terjadi interaksi yang
mengganggu system kardiovaskuler
b. Choline dan lecithin
Defisit asetilkolin di korteks dan hipokampus pada dementia Alzheimer dan
hipotesis tentang sebab hubungannya dengan memori mendorong para peneliti
untuk mengarahkan perhatiannya pada neurotransmitter. Pemberian precursor,
choline dan lecithin merupakan salah satu pilihan dan memberi hasil cukup
memuaskan, namun demikian tidak memperlihatkan hal yang istimewa. Dengan
choline ada sedikit perbaikan terutama dalam fungsi verbal dan visual. Dengan
lecithin hasilnya cenderung negative, walaupun dengan dosis yang berlebih
sehingga kadar dalam serum mencapai 120% dan dalam cairan serebrospinal naik
sampai 58%.
c. Neuropeptida, Vasopresin, dan ACTH
Pemberian neuropeptida, vasopresin, dan ACTH perlu memperoleh perhatian.
Neuropeptida dapat memperbaiki daya ingat semantic yang berkaitan dengan
informasi dan kata-kata. Pada lansia tanpa gangguan psiko-organik, pemberian
ACTH dapat memperbaiki daya konsentrasi dan memperbaiki keadaan umum.
d. Nootropic Agents
Dari golongan nootropic substances, ada dua jenis obat yang sering dipergunakan
dalam terapi dementia, ialah nicerogoline dan co-dergocrine mesylate. Co-
dergocrine mesylate memperbaiki perfusi serebral dengan cara mengurangi
tahanan vascular dan meningkatkan konsumsi oksigen otak. Obat ini memperbaiki
perilaku, aktivitas, dan mengurangi bingung, serta memperbaiki kognisi. Dalam
suatu penelitian multisenter, diperoleh suatu kesimpulan, bahwa antara
nicergoline dan co-dercogrine mesylate, apabila diberikan kepada penderita
dementia, akan mempunyai khasiat yang mirip, terutama terhadap perbaikan
fungsi kognitifnya. Di sisi lain, nicergoline tampak bermanfaat untuk
memperbaiki perasaan hati dan perilaku.
e. Dihydropyrdine
Pada lansia dengan perubahan mikrovaskuler dan neuronal, L-type calcium
channels menunjukkan pengaruh yang kuat. Lipophilic dihydropyridine
bermanfaat untuk mengatasi kerusakan susunan saraf pusat pada lansia.
Nimodipin bermanfaat untuk mengembalikan fungsi kognitif yang menurun pada
lansia dan dementia jenis Alzheimer. Nimodipin memelihara sel-sel endothelial
atau kondisi mikrovaskuler tanpa dampak hipotensif, dengan demikian sangat
dianjurkan sebagai terapi alternatif untuk lansia terutama yang mengidap
hipertensi esensial
DELIRIUM
Definisi
Delirium adalah keadaan yang yang bersifat sementara dan biasanya terjadi secara
mendadak, dimana penderita mengalami penurunan kemampuan dalam memusatkan
perhatiannya dan menjadi linglung, mengalami disorientasi dan tidak mampu berfikir
secara jernih.
http://www.medicastore.com
Merupakan suatu sindroma bukan penyakit yang ditandai oleh suatu gangguan kesadaran
yang biasanya terlihat bersamaan dengan gangguan kognitif secara global. Dan biasanya
merupakan tanda prognostic yang buruk.
(KAPLAN)

Etiologi
Penyebab delirium:
Alkohol, obat-obatan dan bahan beracun
Efek toksik dari pengobatan
Kadar elektrolit, garam dan mineral (misalnya kalsium, natrium atau magnesium)
yang tidak normal akibat pengobatan, dehidrasi atau penyakit tertentu
Infeksi akut disertai demam
Hidrosefalus bertekanan normal, yaitu suatu keadaan dimana cairan yang
membantali otak tidak diserap sebagaimana mestinya dan menekan otak
Hematoma subdural, yaitu pengumpulan darah di bawah tengkorak yang dapat
menekan otak.
Meningitis, ensefalitis, sifilis (penyakit infeksi yang menyerang otak)
Kekurangan tiamin dan vitamin B12
Hipotiroidisme maupun hipertiroidisme
Tumor otak (beberapa diantaranya kadang menyebabkan linglung dan gangguan
ingatan)
Patah tulang panggul dan tulang-tulang panjang
Fungsi jantung atau paru-paru yang buruk dan menyebabkan rendahnya kadar
oksigen atau tingginya kadar karbon dioksida di dalam darah
Stroke.

Penyakit intrakranial
Epilepsi atau keadaan pasca kejang
Trauma otak (terutama gegar otak)
Infeksi (meningitis.ensetalitis).
Neoplasma.
Gangguan vaskular
Penyebab ekstrakranial
Obat-obatan (di telan atau putus),
Obat antikolinergik, Antikonvulsan, Obat antihipertensi, Obat antiparkinson. Obat
antipsikotik, Cimetidine, Klonidine. Disulfiram, Insulin, Opiat, Fensiklidine,
Fenitoin, Ranitidin, Sedatif(termasuk alkohol) dan hipnotik, Steroid.
Racun
Karbon monoksida, Logam berat dan racun industri lain.
Disfungsi endokrin (hipofungsi atau hiperfungsi)
Hipofisis, Pankreas, Adrenal, Paratiroid, tiroid
Penyakit organ nonendokrin.
Hati (ensefalopati hepatik), Ginjal dan saluran kemih (ensefalopati uremik),
Paru-paru (narkosis karbon dioksida, hipoksia), Sistem kardiovaskular (gagal
jantung, aritmia, hipotensi).
Penyakit defisiensi (defisiensi tiamin, asam nikotinik, B12 atau asain folat)
Infeksi sistemik dengan demam dan sepsis.
Ketidakseimbangan elektrolit dengan penvebab apapun
Keadaan pasca operatif
Trauma (kepala atau seluruh tubuh)
Karbohidrat: hipoglikemi.
(KAPLAN)
EPIDEMIOLOGI
Merupakan suatu gangguan yang umum.
10-15% pasien di bangsal bedah umum dan 15-25% pasien di bangsal medis umum
mengalami delirium di RS selama di rawat.
30% pasien ICU dan rawat jalan intensif dan 40-50% pasien yg dalam pemulihan setelah
pembedahan fraktur mengalami delirium.
20% pasien luka bakar berat dan 30% pasien AIDS mengalami delirium saat di rawat di RS.
Penyebb delirium pasca operasi : stres pembedahan, jalur pasca operasi, insomnia, medikasi
nyeri,dll.
Faktor resiko utama delirium : USIA LANJUT.
30-40% pasien uasia lanjut yang di rawat di RS delirium .
faktor presdisposisi lain : usia muda (anak-anak), cedera otak yang telah ada
sebelumnya(demensia,vaskuler, tumor), riwayat delirium, ketergantungan alkohol, diabetes, dll.
Adanya delirium menandakan PROGNOSIS BURUK.
Angka mortalitas tiga bulan pada pasien yang mengalami delirium : 50%.

FAKTOR RESIKO
Usia lanjut, usia 30-40 tahun.
Riwayat cedera otak, seperti demensia, penyakit kardiovaskuler, tumor.
Ketergantungan alcohol.
Riwayat kondisi medis umum, seperti diabetes, kanker, gangguan sensoris (kebutaan),
malnutrisi.
(KAPLAN)

KLASIFIKASI
Menurut PPDGJ III
F05 Delirium bukan akibat alkohol dan psikoaktif lain nya
F05.0 Delirium, tak bertumpang tindih dengan demensia
F05.1 Delirium, bertumpang tindih dengan demensia
F05.8 Delirium lainya.
F05.9 DeliriumYTT.


GEJALA KLINIS
Kesadaran (Arousal)
Dua pola umum kelainan kesadaran telah ditemukan pada pasien dengan delirium, satu pola
ditandai oleh hiperaktivitas yang berhubungan dengan peningkatan kesiagaan. Pola lain ditandai
oleh penurunan kesiagaan. Pasien dengan delirium yang berhubungan dengan putus zat
seringkali mempunyai delirium hiperaktif, yang juga dapat disertai dengan tanda otonomik,
seperti kemerahan kulit, pucat, berkeringat, takikardia, pupil berdilatasi, mual, muntah, dan
hipertermia. Pasien dengan gejala hipoaktif kadang-kadang diklasifikasikan sebagai depresi,
katatonik atau mengalami demensia.
1

Orientasi
Orientasi terhadap waktu, tempat dan orang harus diuji pada seorang pasien dengan delirium.
Orientasi terhadap waktu seringkali hilang bahkan pada kasus delirium yang ringan. Orientasi
terhadap tempat dan kemampuan untuk mengenali orang lain (sebagai contohnya, dokter,
anggota keluarga) mungkin juga terganggu pada kasus yang berat Pasien delirium jarang
kehilangan orientasi terhadap dirinya sendiri.
Bahasa dan Kognisi
Pasien dengan delirium seringkali mempunyai kelainan dalam bahasa. Kelainan dapat berupa
bicara yang melantur, tidak relevan, atau membingungkan (inkoheren) dan gangguan
kemampuan untuk mengerti pembicaraan Fungsi kognitif lainnya yang mungkin terganggu pada
pasien delirium adalah fungsi ingatan dan kognitif umum Kemampuan untuk menyusun,
mempertahankan dan mengingat kenangan mungkin terganggu, walaupun ingatan kenangan
yang jauh mungkin dipertahankan. Disarnping penurunan perhatian, pasien mungkin mempunyai
penurunan kognitif yang dramatis sebagai suatu gejala hipoaktif delirium yang karakteristik.
Pasien delirium juga mempunyai gangguan kemampuan memecahkan masalah dan mungkin
mempunyai waham yang tidak sistematik, kadang kadang paranoid.
Persepsi
Pasien dengan delirium seringkali mempunyai ketidak mampuan umum untuk membedakan
stimuli sensorik dan untuk mengintegrasikan persepsi sekarang dengan pengalaman masa lalu
mereka. Halusinasi relatif sering pada pasien delirium. Halusinasi paling sering adalah visual
atau auditoris walaupun halusinasi dapat taktil atau olfaktoris. Ilusi visual dan auditoris adalah
sering pada delirium.
Suasana Perasaan
Pasien dengan delirium mempunyai kelainan dalam pengaturan suasana Gejala yang paling
sering adalah kemarahan, kegusaran, dan rasa takut yang tidak beralasan. Kelainan suasana
perasaan lain adalah apati, depresi, dan euforia.
Gejala Penyerta : Gangguan tidur-bangun
Tidur pada pasien delirium secara karakteristik adalah tergangga Paling sedikit mengantuk
selama siang hari dan dapat ditemukan tidur sekejap di tempat tidurnya atau di ruang keluarga.
Seringkali keseluruhan siklus tidur-bangun pasien dengan delirium semata mata terbalik. Pasien
seringkali mengalami eksaserbasi gejala delirium tepat sebelum tidur, situasi klinis yang dikenal
luas sebagai sundowning.
1

Gejala neurologis
Gejala neurologis yang menyertai, termasuk disfagia, tremor, asteriksis, inkoordinasi, dan
inkontinensia urin.

Gambaran Delirium Demensia
Riwayat Penyakit akut Penyakit kronik
Awal Cepat Lambat laun
Sebab Terdapat penyakit lain (infeksi,
dehidrasi, guna/putus obat
Biasanya penyakit otak kronik (spt
Alzheimer, demensia vaskular)
Lamanya Ber-hari/-minggu Ber-bulan/-tahun
Perjalanan sakit Naik turun Kronik progresif
Taraf kesadaran Naik turun Normal
Orientasi Terganggu, periodik Intak pada awalnya
Afek Cemas dan iritabel Labil tapi tak cemas
Alam pikiran Sering terganggu Turun jumlahnya
Bahasa Lamban, inkoheren, inadekuat Sulit menemukan istilah tepat
Daya ingat Jangka pendek terganggu nyata Jangka pendek & panjang terganggu
Persepsi Halusinasi (visual) Halusinasi jarang kecuali
sundowning(eksaserbasi gejala
delirium sebelum tidur)
Psikomotor Retardasi, agitasi, campuran Normal
Tidur Terganggu siklusnya Sedikit terganggu siklus tidurnya
Atensi &
kesadaran
Amat terganggu Sedikit terganggu
Reversibilitas Sering reversibel Umumnya tak reversibel
Penanganan Segera Perlu tapi tak segera

Catatan: pasien dengan demensia amat rentan terhadap delirium, dan delirium yang bertumpang
tindih dengan demensia adalah umum

DELIRIUM VS DEMENSIA
Pada kasus delirium akan terjadi gangguan pada proses pikir, sedangkan pada demensia
akan mengalami respon kognitif yang maladaptip
Karakteristik Delirium dan demensia


Delirium

Demensia

Onset

- Biasanya tiba-tiba

- Biasanya perlahan

Lama

- Biasanya singkat/ < 1
bulan

-biasanya
lama
dan
progressif
- Paling banyak dijumpai
pada usia > 65 th

Stressor

- Racun,
infeksi,
trauma,
hipertermia

- Hipertensi, hipotensi,
anemia. Racun, defisit
vitamin, tumor
atropi
jaringan otak

Perilaku

- Fluktuasi tingkat
kesadaran
- Disorientasi
- Gelisah
- Agitasi
- Ilusi
- Hilang daya ingat
- Kerusakan penilaian
- Perhatian menurun
- Perilaku
sosial tidak sesuai

- Halusinasi
- Pikiran tidak teratur
-Gangguan
penilaian
dan
pengambilan keputusan

- Afek labil

- Afek labil
- Gelisah
- Agitasi


Membedakan Delirium Dengan Demensia
Delirium Demensia
Terjadi secara tiba-tiba Terjadi secara perlahan
Berlangsung selama beberapa minggu Bisa menetap
Berhubungan dengan pemakaian obat atau gejala
putus obat, penyakit berat, kelainan metabolisme
Bisa tanpa penyakit
Hampir selalu memburuk di malam hari
Sering bertambah buruk di malam
hari
Tidak mampu memusatkan perhatian Perhatiannya 'mengembara'
Kesiagaan berfluktuasi dari letargi menjadi
agitasi(cemas)
Kesiagaan seringkali berkurang
Orientasi terhadap lingkungan bervariasi
Orientasi terhadap lingkungan
terganggu
Bahasanya lambat, seringkali tidak dapat
dimengerti & tidak tepat
Kadang mengalami kesulitan dalam
menemukan kata-kata yg tepat
Ingatannya bercampur baur, linglung
Ingatannya hilang, terutama untuk
peristiwa yang baru saja terjadi

DIAGNOSIS
1. Onset gejala yang tiba-tiba.
2. Pemeriksaan gangguan kognitif dengan MMSE (Mini Mental State Examination).
3. Adanya penyakit fisik yang diketahui, riwayat trauma kepala, ketergantungan alcohol atau
zat lain dapat meningkatkan diagnosis.
4. Lab: EEG (Elektro Ensefalo Gram) menunjukkan perlambatan umum aktivitas.
(KAPLAN)
Menurut PPDGJ III
F05 DELIRIUM, BUKAN AKIBAT ALKOHOLK dan ZAT PSIKOAKTIF LAINNYA
Pedoman diagnostik
Gangguan kesadaran dan perhatian:
o Dari taraf kesadaran berkabut sampai dengan koma
o Menurunnya kemampuan untuk mengarahkan, memusatkan, mempertahankan,
dan mengalihkan perhatian.
o Gangguan kognitif secara umum:
o Distorsi persepsi, ilusi dan halusinasi seringkali visual
o Hendaya daya pikir dan pikiran abstrak, dengan atau tanpa waham yang
bersifat sementara, tetapi sangat khas terdapat inkoherensi yang ringan
o Hendaya daya ingat segera dan jangka pendek, namun daya ingat jangka
panjang relatigf masih utuh
o Disorientasi waktu. Pada kasus yang berat terdapat juga disorientasi
tempant dan orang
o Gangguan psikomotor
Hipo/ hiper aktivitas & pengalihan aktivitas yang tidak terduga dari satu
ke yang lain.
Waktu bereaksi yang lebih panjang
Arus pembicaraan yang bertambah atau berkurang
Reaksi terperanjat meningkat
gangguan siklus tidur bangun
o insomnia/ pd kasus yg berat tidak bisa tidur sama sekalui / terbaliknya
siklus tidur bangun; mengantuk pada siang hari
o gejala yang memburuk pada malam hari
o mimpi yang menggangu/ mimpi buruk, yang dapat berlanjut menjadi
halusinasi setelah bangun tidur
o gangguan emosional: mis depresi, anxietas atau takut, lekas marah, euforia, apatis, atau
rasa kehilangan akal.
o Omset biasanya cepat, perjalanan penyakitnya hilang timbul sepanjang hari, dan keadaan
itu berlangsung kurang dari 6 bulan.

F05.0 DELIRIUM, TAK BERTUMPANG TINDIH DENGAN DEMENSIA
Delirium yang tidak bertumpang tindih dengan demensia yang sudah ada sebelumnya
F05.1 DELIRIUM, BERTUMPANG TINDIH DENGAN DEMENSIA
Kondisi yang memenuhi kriteria di atas tetapi terjadi pada saat sudah ada demensia
F05.8 DELIRIUM LAINNYA
F05.9 DELIRIUM YTT

pedoman diagnostic
gangguan kesadaran dengan penurunan kemampuan untuk memusatkan,
mempertahankan, atau mengalihkan perhatian
perubahan kognisi atau perkembangan gangguan persepsi yang tidak lebih baik
diterangkan demensia yang telah ada sebelumnya, yang telah ditegakkan, atau yang
sedang timbul.
Gangguan timbul setelah suatu periode waktu yang singkat (biasanya beberapa jam
sampai hari) dan cenderung berfluktuasi selama perjalanan hari
Teradpat bukti-bukti dari riwayat penyakit, PF, atau temuan laboratorium bahwa
gangguan adalah disebabkan oleh akibat fisiologis langsung dari kondisi medis umum.
PF : denyut jantung, temperature, tekanan darah, pernafasan, pembuluh darah karotis,
kulit kepala& wajah, leher,mata, mulut, tiroid, jantung, paru-paru, pernafasan, hati,
system saraf
Pemeriksaan laboratorium : pemeriksaan standar (kimia darah),hitung darah lengkap
dengan diferensial sel darah putih, tes fungsi tiroid, tes serologis untuk sifilis, tes
antibody HIV, urinalisis,EKG,EEG,sinar-x dada,skrining obat dalam darah dan urin.
kaplan
DD
Delirium harus dibedakan dengan kelainan kognitif global.
Tabel 1. Kriteria DSM-IV untuk delirium
Gangguan kesadaran
Penurunan derajat kewaspadaan
Tidak bisa memusatkan perhatian
Tidak bisa menggeser perhatian
Gangguan kognitif
Defisit memori
Disorientasi
Gangguan bahasa
Berkembang dalam waktu pendek
Jam dan hari
Fluktuatif, sundowning
Hal-hal tersebut di atas berubah berdasar kondisi medik, intoksikasi, dan atau pengobatan
a. Demensia
Demensia berbeda karena onsetnya adalah gradual (biasanya tahun), dan persisten. Demensia
tidak menyebabkan penurunan kewaspadaan sampai late stages (dapat diketahui dari
anamnesa). Pasien dengan dengan demensia mudah menjadi delirium, walaupun demikian,
kondisi akut pada pasien demensia bisa delirium atau kondisi akut lainnya. Demensia lewy
bodies bisa disertai dengan halusinasi dan psikosis.
b. Depresi
Depresi bisa terjadi mimic hypoactive deliriumdengan penolakan yang jelas, retardasi
psikomotor, melambatnya pembicaraan, apatis, dan pseudodemensia. Depresi tidak
mempengaruhi derajat kesadaran.
c. Psikosis
Psikosis bisa terjadi mimic hyperactive delirium. Psikosis fungsoinal berbeda karena
halusinasi suara. Lebih banyak khayalan, dan lebih sedikit fluktuatif.
d. CVA
CVA jarang disertai dengan delitium, atau salah dianggap sebagai delirium. Contohnya,
aphasia mungkin salah dianggap sebagai kebingungan. Juga kelainan difus pada atensi
karena stroke pada daerah temporooccipital, parietal, prefrontal, atau region sub kortikal pada
hemisfer kanan. Keadaan akut mungkin memperburuk tanda neurologis fokal karena CVA
lama.
http://medical-free.blogspot.com/2008/06/delirium.html
terapi
Terapi diawali dengan memperbaiki kondisi penyakitnya dan menghilangkan faktor
yang memberatkan seperti:
Menghentikan penggunaan obat
Obati infeksi
Suport pada pasien dan keluanga
Mengurangi dan menghentikan agitasi untuk pengamanan pasien
Cukupi cairan dan nutrisi
Vitamin yang dibutuhkan
Segala alat pengekang boleh digunakan tapi harus segera dilepas bila sudah
membaik, alat infuse sesederhana mungkin, lingkungan diatur agar nyaman.
Obat:
o Haloperidoi dosis rendah dulu 0,5 1 mg per os, IV atau IV
o Risperidone0,5 3mg perostiap l2jam
o Olanzapine 2,5 15 mg per os 1 x sehari
o Lorazepam 0,5 1mg per Os atau parenteral (tak tersedia di Indonesia),
Perlu diingat obat benzodiazepine mi bisa memperburuk delirium
karena efek sedasinya.
http://www.idijakbar.com/prosiding/delirium.htm

Organic Mental Disorders


An organic mental disorder is a permanent or temporary dysfunction in the brain that is
caused by physiological problems with the brain. The causes range from heredity to an injury
of the brain to a disease that affects brain tissue or changes the chemical or hormonal levels of
the brain. The symptoms of organic mental disorders vary depending on the underlying issue
of what caused the imbalance or malfunction of the brain, but they can be difficult to deal
with.

While there may or may not be a cure for the disorder depending on the exact physiological
cause, therapy and counseling may be options that can be helpful for dealing with the
symptoms that accompany organic mental disorders. From hallucinations to delusions to
personality problems, there is a wide range of problems that may develop because of a
physical problem with the brain.

Definition of Organic Mental Disorders

Organic mental disorders affect the brain's chemistry and hormonal balance in a negative way,
causing mild to serious problems for those afflicted. From social problems to internal
emotional problems, the effects of organic mental disorders can be difficult to overcome.
Getting help with any of the many organic mental disorders is possible, with therapy being a
popular way for people to deal with the root cause of the problem.

Causes
Disorders associated with OBS include:
Brain injury caused by trauma
Bleeding into the brain (intracerebral hemorrhage)
Bleeding into the space around the brain (subarachnoid hemorrhage)
Blood clot inside the skull causing pressure on brain (subdural hematoma)
Concussion

Breathing conditions
Low oxygen in the body (hypoxia)
High carbon dioxide levels in the body (hypercapnia)

Cardiovascular disorders
Abnormal heart rhythm (arrhythmias)
Brain injury due to high blood pressure (hypertensive brain injury)
Dementia due to many strokes (multi-infarct dementia)
Heart infections (endocarditis, myocarditis)
Stroke
Transient ischemic attack (TIA)

Degenerative disorders
Alzheimer's disease (also called senile dementia, Alzheimer's type)
Creutzfeldt-Jacob disease
Diffuse Lewy Body disease
Huntington's disease
Multiple sclerosis
Normal pressure hydrocephalus
Parkinson's disease
Pick's disease

Dementia due to metabolic causes
Drug and alcohol-related conditions
Alcohol withdrawal state
Intoxication from drug or alcohol use
Wernicke-Korsakoff syndrome (a long-term effect of excessive alcohol
consumption or malnutrition)
Withdrawal from drugs (especially sedative-hypnotics and corticosteroids)

Infections
Any sudden onset (acute) or long-term (chronic) infection
Blood poisoning (septicemia)
Brain infection (encephalitis)
Meningitis (infection of the lining of the brain and spinal cord)
Prion infections such as mad cow disease
Late-stage syphilis

Other medical disorders
Cancer
Kidney disease
Liver disease
Thyroid disease (high or low)
Vitamin deficiency (B1, B12, or folate)
Other conditions that may mimic organic brain syndrome include:
Depression
Neurosis
Psychosis

Symptoms of / Reasons for Organic Mental Disorders
Hallucinations
Inability to perform in social situations
Depression
Confusion
Changes in personality

Types of Organic Mental Disorders

Organic Hallucinosis - People suffering from this may experience many different types
of hallucinations that can hamper their ability to lead a normal life.
Organic Catatonic Disorder - These are characterized by problems dealing with motor
skills or malfunctioning muscles.
Organic Delusional Disorder - Someone who insists that something is true even when
it's not may be suffering from organic delusional disorder.
Organic Mood Disorder - Deep emotional problems may be caused by organic mood
disorder, which can cause depression or mania.
Organic Anxiety Disorder - Those who have problems with anxiety in public places.
Organic Dissociative Disorder - This is characterized by problems with awareness,
identity, memory, perception, or a combination thereof.
Organic Emotionally Labile Disorder - Those who suffer from wild mood swings in
both directions.
Organic Personality Disorder - Organic personality disorders deal with problems that
cause people to not fit in well with the majority of society in an extreme fashion.
Postencephalitic Syndrome - This is brought on during the late stages of Parkinson's
Disease as the nerves break down.
Postconcussional Syndrome - These are problems that may occur after a concussion due
to a blow to the head.
Unspecified Organic Disorder - Those organic disorders that are not mentioned above
may be classified as unspecified, but they are just as serious.

Treatment for Organic Mental Disorders

The treatment methods are going to vary depending on what type of mental disorder you are
dealing with, but for the most part, a professionally guided therapy program and counseling
are recommended for long term success with treating organic mental disorders even though
there may be no cure.

For many, pursuing online therapy allows them to get the help they need while still being able
to function in their day to day life. The therapy can be just as intense online - and just as
helpful. The trained therapists here at GoMentor.com can assist you with any of the organic
mental disorders that may have developed because of a disease.

Exams and Tests
Tests depend on the disorder, but may include:
Blood tests
Electroencephalogram (EEG)
Head CT scan
Head MRI

http://health.nytimes.com/health/guides/disease/organic-brain-syndrome/overview.html

DEMENTIA

Definition & Symptoms

Dementia is a syndrome (a group of related symptoms) associated with an ongoing decline of the
brain and its abilities. This includes problems with:
memory loss
thinking speed
mental agility
language
understanding
judgement

People with dementia can become apathetic or uninterested in their usual activities, and have
problems controlling their emotions. They may also find social situations challenging, lose
interest in socialising, and aspects of their personality may change.
A person with dementia may lose empathy (understanding and compassion), they may see or
hear things that other people do not (hallucinations), or they may make false claims or
statements.
As dementia affects a person's mental abilities, they may find planning and organising
difficult.Maintaining their independence may also become a problem. A person with dementia
will therefore usually need help from friends or relatives, including help with decision making.
Your GP will discuss the possible causes of memory loss with you, including dementia. Other
symptoms can include:
increasing difficulties with tasks and activities that require concentration and planning
depression
changes in personality and mood
periods of mental confusion
difficulty saying the right words
Most types of dementia can't be cured, but if it's detected early there are ways you can slow it
down and maintain mental function.
Read more about about the symptoms of dementia.

causes dementia and its symptoms

In a healthy brain, mass and speed may decline in adulthood, but this miraculous machine
continues to form vital connections throughout life. However, when connections are lost
through inflammation, disease, or injury, neurons eventually die and dementia may result.
The prospect of literally losing one's self can be traumatic, but early intervention can
dramatically alter the outcome. Understanding causes is the first step.
In the past twenty years, scientists have greatly demystified the origins of dementia.
Genetics may increase your risks, but scientists believe a combination of hereditary,
environmental, and lifestyle factors are most likely at work.
Dementia can be caused by:
Medical conditions that progressively attack brain cells and connections, most
commonly seen in Alzheimer's disease, Parkinson's disease, or Huntington's disease.
Medical conditions such as strokes that disrupt oxygen flow and rob the brain of
vital nutrients.Additional strokes may be prevented by reducing high blood pressure,
treating heart disease, and quitting smoking.
Poor nutrition, dehydration, and certain substances, including drugs and
alcohol. Treating conditions such as insulin resistance, metabolic disorders, and
vitamin deficiencies may reduce or eliminate symptoms of dementia.
Single trauma or repeated injuries to the brain. Depending on the location of the
brain injury, cognitive skills and memory may be impaired.
Infection or illness that affects the central nervous system, including Creutzfeldt-
Jakob disease and HIV. Some conditions are treatable, including liver or kidney
disease, depression-induced pseudodementia, and operable brain tumors.

Causes

Dementia is caused by damage to brain
cells. This damage interferes with the ability of
brain cells to communicate with each other.
When brain cells cannot communicate normally,
thinking, behavior and feelings can be affected.
The brain has many distinct regions, each of
which is responsible for different functions (for
example, memory, judgment and movement).
When cells in a particular region are damaged,
that region cannot carry out its functions
normally.

Take our interactive Brain Tour.
Different types of dementia are associated with particular types of brain cell damage in particular
regions of the brain. For example, in Alzheimer's disease, high levels of certain proteins inside
and outside brain cells make it hard for brain cells to stay healthy and to communicate with each
other. The brain region called the hippocampus is the center of learning and memory in the brain,
and the brain cells in this region are often the first to be damaged. That's why memory loss is
often one of the earliest symptoms of Alzheimer's.
While most changes in the brain that cause dementia are permanent and worsen over time,
thinking and memory problems caused by the following conditions may improve when the
condition is treated or addressed:
Depression
Medication side effects
Excess use of alcohol
Thyroid problems
Vitamin deficiencies

Dementia risk and prevention
Some risk factors for dementia, such as age and genetics, cannot be changed. But researchers
continue to explore the impact of other risk factors on brain health and prevention of dementia.
Some of the most active areas of research in risk reduction and prevention include cardiovascular
factors, physical fitness, and diet.
Cardiovascular risk factors: Your brain is nourished by one of your body's richest networks of
blood vessels. Anything that damages blood vessels anywhere in your body can damage blood
vessels in your brain, depriving brain cells of vital food and oxygen. Blood vessel changes in the
brain are linked to vascular dementia. They often are present along with changes caused by other
types of dementia, including Alzheimer's disease and dementia with Lewy bodies. These changes
may interact to cause faster decline or make impairments more severe. You can help protect your
brain with some of the same strategies that protect your heart don't smoke; take steps to keep
your blood pressure, cholesterol and blood sugar within recommended limits; and maintain a
healthy weight.
Physical exercise: Regular physical exercise may help lower the risk of some types of dementia.
Evidence suggests exercise may directly benefit brain cells by increasing blood and oxygen flow
to the brain.
Diet: What you eat may have its greatest impact on brain health through its effect on heart
health. The best current evidence suggests that heart-healthy eating patterns, such as the
Mediterranean diet, also may help protect the brain. A Mediterranean diet includes relatively
little red meat and emphasizes whole grains, fruits and vegetables, fish and shellfish, and nuts,
olive oil and other healthy fats.

Types of Dementia

Dementia is a general term for loss of memory and other mental abilities severe enough to
interfere with daily life. It is caused by physical changes in the brain.

Type of Dementia

Characteristics
Alzheimer's
disease
Most common type of dementia; accounts for an estimated 60 to
80 percent of cases.
Symptoms: Difficulty remembering names and recent events is
often an early clinical symptom; apathy and depression are also
often early symptoms. Later symptoms include impaired
judgment, disorientation, confusion, behavior changes and
difficulty speaking, swallowing and walking.
New criteria and guidelines for diagnosing Alzheimer's were
published in 2011 recommending that Alzheimer's disease be
considered a disease with three stages, beginning well before the
development of symptoms.
Brain changes: Hallmark abnormalities are deposits of the
protein fragment beta-amyloid (plaques) and twisted strands of
the protein tau (tangles) as well as evidence of nerve cell damage
and death in the brain.
Learn more about Alzheimer's disease.
Vascular dementia Previously known as multi-infarct or post-stroke dementia,
vascular dementia is the second most common cause of dementia
after Alzheimer's disease.
Symptoms: Impaired judgment or ability to plan steps needed to
complete a task is more likely to be the initial symptom, as
opposed to the memory loss often associated with the initial
symptoms of Alzheimer's. Occurs because of brain injuries such
as microscopic bleeding and blood vessel blockage. The location
of the brain injury determines how the individual's thinking and
physical functioning are affected.
Brain changes: Brain imaging can often detect blood vessel
problems implicated in vascular dementia. In the past, evidence
for vascular dementia was used to exclude a diagnosis of
Alzheimer's disease (and vice versa). That practice is no longer
considered consistent with pathologic evidence, which shows that
the brain changes of several types of dementia can be present
simultaneously. When any two or more types of dementia are
present at the same time, the individual is considered to have
"mixed dementia" (see entry below).
Learn more about vascular dementia.
Dementia with
Lewy bodies
(DLB)
Symptoms: People with dementia with Lewy bodies often have
memory loss and thinking problems common in Alzheimer's, but
are more likely than people with Alzheimer's to have initial or
early symptoms such as sleep disturbances, well-formed visual
hallucinations, and muscle rigidity or other parkinsonian
movement features.
Brain changes: Lewy bodies are abnormal aggregations (or
clumps) of the protein alpha-synuclein. When they develop in a
part of the brain called the cortex, dementia can result. Alpha-
synuclein also aggregates in the brains of people with Parkinson's
disease, but the aggregates may appear in a pattern that is
different from dementia with Lewy bodies.
The brain changes of dementia with Lewy bodies alone can cause
dementia, or they can be present at the same time as the brain
changes of Alzheimer's disease and/or vascular dementia, with
each abnormality contributing to the development of dementia.
When this happens, the individual is said to have "mixed
dementia."
Learn more about dementia with Lewy bodies.
Mixed dementia In mixed dementia abnormalities linked to more than one type of
dementia occur simultaneously in the brain. Recent studies
suggest that mixed dementia is more common than previously
thought.
Brain changes: Characterized by the hallmark abnormalities of
more than one type of dementia most commonly, Alzheimer's
and vascular dementia, but also other types, such as dementia
with Lewy bodies.
Learn more about mixed dementia.
Parkinson's disease As Parkinson's disease progresses, it often results in a progressive
dementia similar to dementia with Lewy bodies or Alzheimer's.
Symptoms: Problems with movement are a common symptom
early in the disease. If dementia develops, symptoms are often
similar to dementia with Lewy bodies.
Brain changes: Alpha-synuclein clumps are likely to begin in an
area deep in the brain called the substantia nigra. These clumps
are thought to cause degeneration of the nerve cells that produce
dopamine.
Learn more about Parkinson's disease.
Frontotemporal
dementia
Includes dementias such as behavioral variant FTD (bvFTD),
primary progressive aphasia, Pick's disease and progressive
supranuclear palsy.
Symptoms: Typical symptoms include changes in personality
and behavior and difficulty with language. Nerve cells in the
front and side regions of the brain are especially affected.
Brain changes: No distinguishing microscopic abnormality is
linked to all cases. People with FTD generally develop symptoms
at a younger age (at about age 60) and survive for fewer years
than those with Alzheimer's.
Learn more about frontotemporal dementia.
Creutzfeldt-Jakob
disease
CJD is the most common human form of a group of rare, fatal
brain disorders affecting people and certain other mammals.
Variant CJD (mad cow disease) occurs in cattle, and has been
transmitted to people under certain circumstances.
Symptoms: Rapidly fatal disorder that impairs memory and
coordination and causes behavior changes.
Brain changes: Results from misfolded prion protein that causes
a "domino effect" in which prion protein throughout the brain
misfolds and thus malfunctions.
Learn more about Creutzfeldt-Jakob disease.
Normal pressure
hydrocephalus
Symptoms: Symptoms include difficulty walking, memory loss
and inability to control urination.
Brain changes: Caused by the buildup of fluid in the brain. Can
sometimes be corrected with surgical installation of a shunt in the
brain to drain excess fluid.
Learn more about normal pressure hydrocephalus.
Huntington's
Disease
Huntingtons disease is a progressive brain disorder caused by a
single defective gene on chromosome 4.
Symptoms: Include abnormal involuntary movements, a severe
decline in thinking and reasoning skills, and irritability,
depression and other mood changes.
Brain changes: The gene defect causes abnormalities in a brain
protein that, over time, lead to worsening symptoms.
Learn more about Huntingtons disease.
Wernicke-
Korsakoff
Syndrome
Korsakoff syndrome is a chronic memory disorder caused by
severe deficiency of thiamine (vitamin B-1). The most common
cause is alcohol misuse.
Symptoms: Memory problems may be strikingly severe while
other thinking and social skills seem relatively unaffected.
Brain changes: Thiamine helps brain cells produce energy from
sugar. When thiamine levels fall too low, brain cells cannot
generate enough energy to function properly.
Learn more about Wernicke-Korsakoff syndrome.

Dementia treatment and care

"I thought my life was over. I knew about dementia but I never thought it could happen to
me." This sentiment reflects the denial, disbelief, and dismay common after a dementia
diagnosis.
While dealing with dementia is a challenge, the following strategies can ease your journey:
Take care of yourself emotionally. As you deal with the symptoms of dementia,
make sure you get the emotional support you need. Turn to close family members and
friends, join a dementia support group, or talk to a therapist, counselor, or clergyman.
Make important decisions early. Avoid future medical, financial, and legal confusion
by communicating your wishes and creating a plan. Designate a Power of Attorney for
money and legal matters. Discuss and document treatment and end-of-life preferences
with your doctors and family members. Create a Living Will and appoint someone you
trust to make decisions for you in case you can no longer make them for yourself.
Although these conversations may be difficult, making your wishes known is
empowering.
Watch for treatable changes. Depression, sleep disturbances, and medication
interactions can make the symptoms of dementia worse and limit independence.
Treating them may require some experimentation with lifestyle changes and
medication, but can be well worth the effort.
Create a dementia-friendly environment. Think happiness, independence, safety,
and accessibility. Preserve your health and autonomy for as long as possible by taking
simple actions: encourage memories with pictures and familiar objects; remove
tripping hazards; increase lighting; and organize a caregiving network. Planning and
flexibility can keep you one step ahead of changing needs.
Emphasize joy. When you sense the mind is half-gone, try to see it as half-present.
With appropriate support and understanding, people with dementia are capable of
experiencing and providing enjoyment and connection - even through the final stages
of the disease.

Demensia Alzheimer

Definition
Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve
cells, or neurons, resulting in loss of memory, thinking and language skills, and
behavioral changes.
These neurons, which produce the brain chemical, or neurotransmitter, acetylcholine,
break connections with other nerve cells and ultimately die. For example, short-term
memory fails when Alzheimer's disease first destroys nerve cells in the hippocampus, and
language skills and judgment decline when neurons die in the cerebral cortex.
Two types of abnormal lesions clog the brains of individuals with Alzheimer's disease:
Beta-amyloid plaquessticky clumps of protein fragments and cellular material that
form outside and around neurons; and neurofibrillary tanglesinsoluble twisted fibers
composed largely of the protein tau that build up inside nerve cells. Although these
structures are hallmarks of the disease, scientists are unclear whether they cause it or a
byproduct of it.
Alzheimer's disease is the most common cause of dementia, or loss of intellectual
function, among people aged 65 and older.
Alzheimer's disease is not a normal part of aging.
Origin of the term Alzheimer's disease dates back to 1906 when Dr. Alois Alzheimer, a
German physician, presented a case history before a medical meeting of a 51-year-old
woman who suffered from a rare brain disorder. A brain autopsy identified the plaques
and tangles that today characterize Alzheimer's disease.

What is Alzheimer's disease?

Alzheimer's disease (AD) is a slowly progressive disease of the brain that is characterized by
impairment of memory and eventually by disturbances in reasoning, planning, language, and
perception. Many scientists believe that Alzheimer's disease results from an increase in the
production or accumulation of a specific protein (beta-amyloid protein) in the brain that leads to
nerve cell death.
The likelihood of having Alzheimer's disease increases substantially after the age of 70 and may
affect around 50% of persons over the age of 85. Nonetheless, Alzheimer's disease is not a
normal part of aging and is not something that inevitably happens in later life. For example,
many people live to over 100 years of age and never develop Alzheimer's disease.
Cause of Alzheimer

The cause(s) of Alzheimer's disease is (are) not known. The "amyloid cascade hypothesis" is the
most widely discussed and researched hypothesis about the cause of Alzheimer's disease. The
strongest data supporting the amyloid cascade hypothesis comes from the study of early-onset
inherited (genetic) Alzheimer's disease. Mutations associated with Alzheimer's disease have been
found in about half of the patients with early-onset disease. In all of these patients, the mutation
leads to excess production in the brain of a specific form of a small protein fragment called
ABeta (A). Many scientists believe that in the majority of sporadic (for example, non-inherited)
cases of Alzheimer's disease (these make up the vast majority of all cases of Alzheimer's disease)
there is too little removal of this A protein rather than too much production. In any case, much
of the research in finding ways to prevent or slow down Alzheimer's disease has focused on
ways to decrease the amount of A in the brain
Risk factor

Who develops Alzheimer's disease?
The main risk factor for Alzheimer's disease is increased age. As a population ages, the
frequency of Alzheimer's disease continues to increase. Ten percent of people over 65 years of
age and 50% of those over 85 years of age have Alzheimer's disease. Unless new treatments are
developed to decrease the likelihood of developing Alzheimer's disease, the number of
individuals with Alzheimer's disease in the United States is expected to be 14 million by the year
2050.
There are also genetic risk factors for Alzheimer's disease. Most patients develop Alzheimer's
disease after age 70. However, 2%-5% of patients develop the disease in the fourth or fifth
decade of life (40s or 50s). At least half of these early onset patients have inherited gene
mutations associated with their Alzheimer's disease. Moreover, the children of a patient with
early onset Alzheimer's disease who has one of these gene mutations has a 50% risk of
developing Alzheimer's disease.
There is also a genetic risk for late onset cases. A relatively common form of a gene located on
chromosome 19 is associated with late onset Alzheimer's disease. In the majority of Alzheimer's
disease cases, however, no specific genetic risks have yet been identified.
Other risk factors for Alzheimer's disease include high blood pressure (hypertension),coronary
artery disease, diabetes, and possibly elevated blood cholesterol. Individuals who have
completed less than eight years of education also have an increased risk for Alzheimer's disease.
These factors increase the risk of Alzheimer's disease, but by no means do they mean that
Alzheimer's disease is inevitable in persons with these factors.
All patients with Down syndrome will develop the brain changes of Alzheimer's disease by 40
years of age. This fact was also a clue to the "amyloid hypothesis of Alzheimer's disease"
Symptoms of Alzheimer's

The onset of Alzheimer's disease is usually gradual, and it is slowly progressive. Memory
problems that family members initially dismiss as "a normal part of aging" are in retrospect
noted by the family to be the first stages of Alzheimer's disease. When memory and other
problems with thinking start to consistently affect the usual level of functioning; families begin
to suspect that something more than "normal aging" is going on.
Problems of memory, particularly for recent events (short-term memory) are common early in
the course of Alzheimer's disease. For example, the individual may, on repeated occasions,
forget to turn off an iron or fail to recall which of the morning's medicines were taken. Mild
personality changes, such as less spontaneity, apathy, and a tendency to withdraw from social
interactions, may occur early in the illness.
As the disease progresses, problems in abstract thinking and in other intellectual functions
develop. The person may begin to have trouble with figures when working on bills, with
understanding what is being read, or with organizing the day's work. Further disturbances in
behavior and appearance may also be seen at this point, such as agitation, irritability,
quarrelsomeness, and a diminishing ability to dress appropriately.
Later in the course of the disorder, affected individuals may become confused or disoriented
about what month or year it is, be unable to describe accurately where they live, or be unable to
name a place being visited. Eventually, patients may wander, be unable to engage in
conversation, erratic in mood, uncooperative, and lose bladder and bowel control. In late stages
of the disease, persons may become totally incapable of caring for themselves. Death can then
follow, perhaps from pneumonia or some other problem that occurs in severely deteriorated
states of health. Those who develop the disorder later in life more often die from other illnesses
(such as heart disease) rather than as a consequence of Alzheimer's disease.
Ten warning signs of Alzheimer's disease
The Alzheimer's Association has developed the following list of warning signs that include
common symptoms of Alzheimer's disease. Individuals who exhibit several of these symptoms
should see a physician for a complete evaluation.
1. Memory loss
2. Difficulty performing familiar tasks
3. Problems with language
4. Disorientation to time and place
5. Poor or decreased judgment
6. Problems with abstract thinking
7. Misplacing things
8. Changes in mood or behavior
9. Changes in personality
10. Loss of initiative
It is normal for certain kinds of memory, such as the ability to remember lists of words, to
decline with normal aging. In fact, normal individuals 50 years of age will recall only about 60%
as many items on some kinds of memory tests as individuals 20 years of age. Furthermore,
everyone forgets, and every 20 year old is well aware of multiple times he or she couldn't think
of an answer on a test that he or she once knew. Almost no 20 year old worries when he/she
forgets something, that he/she has the 'early stages of Alzheimer's disease,' whereas an individual
50 or 60 years of age with a few memory lapses may worry that they have the 'early stages of
Alzheimer's disease.'
Mild cognitive impairment
The criteria for dementia are conservative meaning that a patient must have had considerable
decline in the ability to think before a diagnosis of dementia is appropriate. The progression of
Alzheimer's disease is so insidious and slow that patients go through a period of decline where
their memory is clearly worse than its baseline, yet they still do not meet criteria for dementia.
This transitional syndrome is called Mild Cognitive Impairment (MCI). Individuals affected with
MCI have cognitive impairment that is demonstrated on formal neuropsychological testing but
are still able to function well. Formal neuropsychological testing usually means that the patient is
administered a battery of standardized tests of memory and thinking. Some of these tests are
something like the IQ tests we may have taken in school. When these tests were developed they
were administered to hundreds or thousands of people so that statistics are available to say how a
person's score compares to a sample of healthy persons of the same age. If a person scores in the
top 50%, it means that he or she did better than at least 50% of other normal people who took the
test. Persons with lower scores - often in the bottom 7% - are considered to have MCI.
There are several forms of MCI. Perhaps the most common is associated with impairment in
memory but not in the ability to plan and reason. Persons with this type called "amnestic MCI"
(amnestic comes from "amnesia" and means no memory) have a high risk of developing
Alzheimer's disease over the next few years. Persons with preserved memory but impaired
reasoning or impaired judgment (call non-amnestic MCI) have a lower risk of developing
Alzheimer's disease.
As treatments are developed that decrease the risk of developing Alzheimer's disease or slow its
rate of progression (as of June 2007, no such medication has been approved by the FDA),
recognition of amnestic MCI will be increasingly important. It is hoped that medications will be
developed that will slow the rate of progression of MCI to Alzheimer's disease or completely
prevent the development of Alzheimer's disease.
The most common early symptom of Alzheimer's is difficulty remembering newly learned
information.
Just like the rest of our bodies, our brains change as we age . Most of us eventually notice some
slowed thinking and occasional problems with remembering certain things. However, serious
memory loss, confusion and other major changes in the way our minds work may be a sign that
brain cells are failing.
The most common early symptom of Alzheimer's is difficulty remembering newly learned
information because Alzheimer's changes typically begin in the part of the brain that affects
learning. As Alzheimer's advances through the brain it leads to increasingly severe symptoms,
including disorientation, mood and behavior changes; deepening confusion about events, time
and place; unfounded suspicions about family, friends and professional caregivers; more serious
memory loss and behavior changes; and difficulty speaking, swallowing and walking.
People with memory loss or other possible signs of Alzheimers may find it hard to recognize
they have a problem. Signs of dementia may be more obvious to family members or friends.
Anyone experiencing dementia-like symptoms should see a doctor as soon as possible. If you
need assistance finding a doctor with experience evaluating memory problems, your local
Alzheimer's Association chapter can help. Early diagnosis and intervention methods are
improving dramatically, and treatment options and sources of support can improve quality of
life. Two helpful support resources you can tap into are ALZConnected, our messages boards
and online social networking community, andAlzheimer's Navigator, a web tool that creates
customized action plans, based on answers you provide through short, online surveys.
Alzheimer's and the brain
Microscopic changes in the brain begin long before the first signs of memory loss.
The brain has 100 billion nerve cells (neurons). Each nerve cell connects with many others to
form communication networks. Groups of nerve cells have special jobs. Some are involved in
thinking, learning and remembering. Others help us see, hear and smell.
To do their work, brain cells operate like tiny factories. They receive supplies, generate energy,
construct equipment and get rid of waste. Cells also process and store information and
communicate with other cells. Keeping everything running requires coordination as well as large
amounts of fuel and oxygen.
Scientists believe Alzheimer's disease prevents parts of a cell's factory from running well. They
are not sure where the trouble starts. But just like a real factory, backups and breakdowns in one
system cause problems in other areas. As damage spreads, cells lose their ability to do their jobs
and, eventually die, causing irreversible changes in the brain.
The role of plaques and tangles



Plaques and tangles tend to spread through the cortex as Alzheimer's progresses.

Two abnormal structures called plaques and tangles are prime suspects in damaging and
killing nerve cells.
Plaques are deposits of a protein fragment called beta-amyloid (BAY-tuh AM-uh-loyd) that
build up in the spaces between nerve cells.
Tangles are twisted fibers of another protein called tau (rhymes with wow) that build up inside
cells.
Though most people develop some plaques and tangles as they age, those with Alzheimer's tend
to develop far more. They also tend to develop them in a predictable pattern, beginning in areas
important for memory before spreading to other regions.
Scientists do not know exactly what role plaques and tangles play in Alzheimer's disease. Most
experts believe they somehow play a critical role in blocking communication among nerve cells
and disrupting processes that cells need to survive.
It's the destruction and death of nerve cells that causes memory failure, personality changes,
problems carrying out daily activities and other symptoms of Alzheimer's disease.
Treatment

Dementia is a condition of mental decline that causes progressive memory impairment and
problems with learning, judgment, communication, and quality of life. Alzheimers
disease, a progressive brain disorder, is the most common form of dementia. While there is
no cure for Alzheimer's disease and no treatment to reverse or halt its progression, there are
medicines available that can help treat symptoms in some people with Alzheimer's disease.
If Alzheimers disease is diagnosed earlier, treatment may enable people to carry out their
daily activities and independent living for a longer period of time and may prolong the time
that patients can be managed at home. Health care providers may also use other medicines
to help manage other troubling symptoms of Alzheimer's disease, including depression,
sleeplessness, and behavioral problems such as agitation and aggression.
Planning and medical/social management can help ease the burden on both patients and
family members. Exercise, good nutrition, activities, and social interaction are important.
A calm, structured environment also may help the person with Alzheimer's disease to
continue functioning as independently as possible.
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How Is Alzheimer's Disease Treated?
Your doctor will determine the best treatment for the Alzheimers patient based on various
factors, including:
The patients age, overall health, and medical history
Extent of the disease
The patients tolerance for specific medicines and therapies
Expectations for the course of the disease
The patient and his or her caregivers opinions or preferences
What Drugs Are Used to Treat Alzheimer's Disease?
Cholinesterase inhibitors (Aricept, Cognex, Exelon, Razadyne).Cholinesterase
inhibitors curb the breakdown of acetylcholine, a chemical in the brain important for
memory and learning. These types of medications help increase the levels of acetylcholine
in the brain. These drugs may slow the progression of symptoms for about half of people
taking them for a limited time, on average 6 to 12 months.
Aricept is the only treatment approved by the FDA for all stages of Alzheimers disease:
mild, moderate, and severe. It is available as tablets to swallow or tablets to dissolve in the
mouth. Cognex was the first of these drugs to be FDA approved, but it is used less
commonly than the other medications. Exelon is approved for use in mild to moderate
Alzheimers dementia and is available as a skin patch, capsules, and liquid form. Razadyne
(formerly Reminyl) is also approved for mild to moderate Alzheimers dementia and is
available as an extended-release capsule, immediate-release tablet, and liquid forms.
Common side effects are usually mild for these medications and include diarrhea,
vomiting, nausea, fatigue, insomnia, loss of appetite, and weight loss. Cognex use may
cause liver damage, so your doctor will need to perform tests to monitor liver function.
Namenda. Namenda is approved to treat moderate-to-severe Alzheimer's disease. Namenda
works by a different mechanism than other Alzheimer's treatments; it is thought to play a
protective role in the brain by regulating the activity of a different brain chemical called
glutamate. Glutamate also plays a role in learning and memory. Brain cells in people with
Alzheimers disease release too much glutamate. Namenda helps regulate glutamate
activity. Namenda is the only drug for Alzheimers that works this way. It may improve
mental function and performance of daily activities for some people. Namenda may have
increased benefit when used with Aricept, Exelon, Razadyne, or Cognex. Side effects of
Namenda include tiredness, dizziness, confusion, constipation, and headache.

Demensia Vaskuler

Definition
Vascular dementia is the second most common form of dementia, accounting for up to 40
percent of dementia cases in older adults. Vascular dementia is caused by reduced blood
flow to the brainusually from a stroke or series of strokes. While the strokes may be
unnoticeably small, the damage can add up over time, leading to memory loss, confusion,
and other signs of dementia. With these guidelines, however, it may be possible to
prevent further blockages and compensate for brain damage that has already occurred.
What is vascular dementia?
Vascular dementia refers to a subtle, progressive decline in memory and cognitive functioning. It
occurs when the blood supply carrying oxygen and nutrients to the brain is interrupted by a
blocked or diseased vascular system. If blood supply is blocked for longer than a few seconds,
brain cells can die, causing damage to the cortex of the brainthe area associated with learning,
memory, and language.
Depending on the person, and the severity of the stroke or strokes, vascular dementia may come
on gradually or suddenly. Currently, there is no known cure, but the good news is that making
certain lifestyle changes and using practical strategies may help prevent strokes, compensate for
cognitive loses, and slow its development.

Causes of vascular dementia
Stroke, small vessel disease, or a mixture of the two can cause vascular
dementia. Most commonly there is a blockage of small blood vessels somewhere in the vast
system of arteries that feeds the brain and enters through the base of the skull. Blockages may be
caused by plaque build-up on the inside of the artery wall, or by blood clots which have broken
loose and clogged a tributary further downstream. Clots can form as a result of abnormal heart
rhythms, or other heart abnormalities. Also, a weak patch on an artery wall can balloon outward
and form an aneurysm, which can burst and deprive the brain cells of oxygen.
It is estimated that about 50 percent of the cases of vascular dementia result from hypertension,
or high blood pressure. Less common causes of vascular dementia are associated with
autoimmune inflammatory diseases of the arteries such as lupus and temporal arteritis, which are
treatable with drugs that suppress the immune system.

Sign and symptoms
Vascular dementia affects different people in different ways and the speed of the progression
varies from person to person. Some symptoms may be similar to those of other types of dementia
and usually reflect increasing difficulty to perform everyday activities like eating, dressing, or
shopping.
Behavioral and physical symptoms can come on dramatically or very gradually, although it
appears that a prolonged period of TIAsthe mini-strokes discussed aboveleads to a gradual
decline in memory, whereas a bigger stroke can produce profound symptoms immediately.
Regardless of the rate of appearance, vascular dementia typically progresses in a stepwise
fashion, where lapses in memory and reasoning abilities are followed by periods of stability, only
to give way to further decline.
Common mental and emotional signs and symptoms of vascular dementia
Slowed thinking
Memory problems; general forgetfulness
Unusual mood changes (e.g. depression, irritability)
Hallucinations and delusions
Confusion, which may get worse at night
Personality changes and loss of social skills


Common physical signs and symptoms of vascular dementia
Dizziness
Leg or arm weakness
Tremors
Moving with rapid, shuffling steps
Balance problems
Loss of bladder or bowel control


Common behavioral signs and symptoms of vascular dementia
Slurred speech
Language problems, such as difficulty finding the right words for things
Getting lost in familiar surroundings
Laughing or crying inappropriately
Difficulty planning, organizing, or following instructions
Difficulty doing things that used to come easily (e.g. paying bills or playing a favorite
card game)
Reduced ability to function in daily life

Diagnosis
Because vascular cognitive impairment may often go unrecognized, many experts recommend
professional screening with brief tests to assess memory, thinking and reasoning for everyone
considered to be at high risk for this disorder. Individuals at highest risk include those who have
had a stroke or a transient ischemic attack (TIA, also known as a "ministroke"). Additional high-
risk groups include those with high blood pressure, high cholesterol, or other risk factors for
heart or blood vessel disease.
Professional screening for depression is also recommended for high-risk groups. Depression
commonly coexists with brain vascular disease and can contribute to cognitive symptoms.
If brief screening tests suggest changes in thinking or reasoning, a more detailed assessment is
needed. Core elements of a workup for vascular dementia typically include:
A thorough medical history, including family history of dementia
Evaluation of independent function and daily activities
Input from a family member or trusted friend
In-office neurological examination assessing function of nerves and reflexes, movement,
coordination, balance and senses
Laboratory tests including blood tests and brain imaging
According to a 2011 scientific statement issued by the American Heart Association (AHA) and
the American Stroke Association (ASA), and endorsed by the Alzheimer's Association and the
American Academy of Neurology (AAN), the following three criteria suggest the greatest
likelihood that mild cognitive impairment (MCI) or dementia is caused by vascular changes:
1. The diagnosis of dementia or mild cognitive impairment is confirmed by neurocognitive
testing, which involves several hours of written or computerized tests that provide
detailed evaluation of specific thinking skills such as judgment, planning, problem-
solving, reasoning and memory
2. There is brain imaging evidence, usually with magnetic resonance imaging (MRI),
showing evidence of either:
a. A recent stroke, or
b. Other brain blood vessel changes whose severity and pattern of affected tissue are
consistent with the types of impairment documented in neurocognitive testing
3. There is no evidence that factors other than vascular changes are contributing to cognitive
decline.
The guidelines also discuss cases where the diagnosis may be less clear-cut, such as the common
situation where vascular changes coexist with brain changes associated with other types of
dementia.
Vascular dementia prevention and treatment
There is not yet a known cure for vascular dementia, so prevention is important. The best way to
prevent vascular dementia is to lower your risk of stroke. This means getting high blood pressure
under control, avoiding cigarettes, and controlling cholesterol levels and diabetes.
But even if you or a loved one have already been diagnosed with vascular dementia, its not too
late to do anything about it. If you treat the risk factors that led to vascular dementia, you may be
able to slow the progression of the disease and possibly reverse some of the symptoms. The most
important thing is minimize your risk of having another stroke and making the dementia worse.
While there are not yet any approved medications for the treatment of vascular dementia, a
number of medications used to treat the cognitive symptoms of Alzheimers disease appear to
work for vascular dementia, too.
Prevent and treat vascular dementia by reducing your risk for stroke
Know your blood pressure. If high, work with your doctor to lower it.
Find out from your doctor if you have atrial fibrillation.
If you smoke, stop.
If you drink alcohol, do so in moderation.
Find out if you have high cholesterol. If so, work with your doctor to control it.
If you are diabetic, follow your doctor's recommendations carefully to control your
diabetes.
Include exercise in the activities you enjoy in your daily routine.
Enjoy a lower sodium (salt), lower fat diet.

Medical Care

The mainstay of management of vascular dementia is the prevention of new strokes. This
includes administering antiplatelet drugs and controlling major vascular risk factors. Aspirin has
also been found to slow the progression of vascular dementia.
Recent guidelines from the American Psychiatric Association provide both treatment principles
and possible specific therapies.
Drug treatment is primarily used to prevent further worsening of vascular dementia by treating
the underlying disease such as hypertension, hyperlipidemia, and diabetes mellitus. Antiplatelet
agents are indicated.
Pentoxifylline and, to a more limited extent, ergoloid mesylates (Hydergine), may be useful for
increasing cerebral blood flow. In the European Pentoxifylline Multi-Infarct Dementia Study,
which is a double-blinded, placebo-controlled, multicenter study, treatment with pentoxifylline
was found to be beneficial for patients with multi-infarct dementia. Significant improvement was
observed in the scales used for assessing intellectual and cognitive function.
Neuroprotective drugs such as nimodipine, propentofylline, and posatirelin are currently under
study and may be useful for vascular dementia. Nicardipine is a dihydropyridine calcium channel
blocker that was studied on the treatment of cognitive deterioration of vascular origin.
Preliminary studies showed decrease in cognitive deterioration in patients with cerebrovascular
disease.
[21]

Increasing evidence supports the involvement of the cholinergic system in vascular dementia,
similar to that seen in Alzheimer dementia. However, no cholinesterase inhibitors have been
approved to date for the treatment of vascular dementia, despite positive results in clinical trials
with this medication.
The general management of dementia includes appropriate referral to community services,
judgment and decision-making regarding legal and ethical issues (eg, driving, competency,
advance directives), and consideration of caregiver stress.
Agitation and psychosis are common in older adults with dementia and are challenging to
manage. Relatively few studies have examined the use of antidepressants for the treatment of
agitation and psychosis in dementia; however, the selective serotonin reuptake inhibitors (SSRIs)
sertraline and citalopram appear to be associated with a reduction in symptoms of agitation when
compared with placebo.
[22]
Both appear to be reasonably well tolerated when compared with
placebo, typical antipsychotics, and atypical antipsychotics. However, more studies are needed to
determine if SSRIs, trazodone, or other antidepressants are safe and effective treatments for
agitation and psychosis in dementia.
http://emedicine.medscape.com/article/292105-treatment