Organic Mental Disorder final- MS. Ritika soni

PRESENTER: MS. RITIKA SONI
ASST. PROFESSOR
SNC, SHIMLA

• Introduction to organic mental
illness
• Delirium, Dementia, Amnestic
disorder, Alzheimer's disease ect.
– Introduction
– Prevalence
– Etiology
– Signs and symptoms
– Diagnostic Criteria
– Management

 Organic mental disorders, also known as organic
brain syndrome ,organic brain disease, organic
mental syndrome, refers to any syndrome or
disorder of mental functions whose cause is
alleged to be known as organic (physiologic).
 Organic mental disorders, are disturbances that
may be caused by injury or disease affecting brain
tissues as well as by chemical or
hormonal abnormalities. Exposure to toxic
materials, neurological impairment, or abnormal
changes associated with aging can also cause
these disorders.

 Cognitive disorders include those in which a
clinically significant deficit in cognition or
memory exists, representing a significant
change from a previous level of functioning.
 The DSM-IV-TR (American Psychiatric
Association [APA], 2000) describes the etiology
of these disorders as a general medical
condition, a substance, or a combination of
these factors.

• An organic psychosis are characterized by
abnormal brain function with a known physical
cause characterized by an altered perception
of reality.
• American Psychiatric Association defines
organic psychosis/ organic brain syndrome as,
“a mental disorder characteristically resulting
from diffuse impairment of brain tissue function
from any cause.

• First episode
• Sudden onset
• Older age of onset
• History of drug and alcohol use disorders
• Concurrent medical or neurological disorder
• Neurological signs or symptoms like seizure
,impairment in consciousness, head injury, sensory or
motor disturbances
• Presence of confusion , disorientation ,memory
impairment or soft neurological sign.
• Prominent visual or other non auditory hallucinations.

• F00 Dementia in Alzheimer's disease
o F00.0Dementia in Alzheimer's disease with early
onset
o F00.1Dementia in Alzheimer's disease with late
onset
o F00.2Dementia in Alzheimer's disease, atypical or
mixed type
o F00.9Dementia in Alzheimer's disease, unspecified

• F01Vascular dementia
o F01.0Vascular dementia of acute onset
o F01.1Multi-infarct dementia
o F01.2Subcortical vascular dementia
o F01.3Mixed cortical and subcortical vascular
dementia
o F01.8Other vascular dementia
o F01.9Vascular dementia, unspecified

• F02Dementia in other diseases classified
elsewhere
o F02.0Dementia in Pick's disease
o F02.1Dementia in Creutzfeldt-Jakob disease
o F02.2Dementia in Huntington's disease
o F02.3Dementia in Parkinson's disease
o F02.4Dementia in human immunodeficiency virus
[HIV] disease
o F02.8Dementia in other specified diseases
classified elsewhere

• F03Unspecified dementia
A fifth character may be added to specify
dementia in F00-F03, as follows:
o F03.0 Without additional symptoms
o F03.1 Other symptoms, predominantly delusional
o F03.2 Other symptoms, predominantly
hallucinatory
o F03.3 Other symptoms, predominantly depressive
o F03.4 Other mixed symptoms

• Delirium
• Dementia
• Organic amnestic syndrome
• Other organic mental
disorders

• Delirium is an acute, transient, usually
reversible, fluctuating disturbance in
attention, cognition, and consciousness
level.
• Delirium:
Delirium is a mental state characterized by a
disturbance of cognition, which is manifested
by confusion, excitement, disorientation,
inattention and a clouding of consciousness.
Hallucinations and illusions are common.

 Delirium is a serious disturbance in mental
abilities that results in confused thinking and
reduced awareness of the environment. The
start of delirium is usually rapid — within hours
or a few days.

• Delirium may occur at any age but is more common
among the elderly.
• At least 10% of elderly patients who are admitted to the
hospital have delirium; 15 to 50% experience delirium
at some time during hospitalization.
• Delirium is also common after surgery and among
nursing home residents and ICU patients.
• When delirium occurs in younger people, it is usually due
to drug use or a life-threatening systemic disorder.

Experts have identified three types of delirium:
 Hyperactive delirium.
Probably the most easily recognized type, this may include
restlessness (for example, pacing), agitation, rapid mood
changes or hallucinations, and refusal to cooperate with
care.
 Hypoactive delirium.
This may include inactivity or reduced motor activity,
sluggishness, abnormal drowsiness, or seeming to be in a
daze.
 Mixed delirium.
This includes both hyperactive and hypoactive signs and
symptoms. The person may quickly switch back and forth
from hyperactive to hypoactive states.

 The DSM-IV-TR (APA, 2000) differentiates
between the disorders of delirium by their
etiology, although they share a common
symptom presentation.
 Categories of delirium include:
1. Delirium due to a general medical condition
2. Substance-induced delirium
3. Substance-intoxication delirium
4. Substance-withdrawal delirium
5. Delirium due to multiple etiologies

 In this type of delirium, evidence must exist (from
history, physical examination, or laboratory findings)
to show that the symptoms of delirium are a direct
result of the physiological consequences of a general
medical condition (APA, 2000).
 Such conditions include :
 Systemic infections,
 Metabolic disorders (e.g., hypoxia, hypercarbia, and
hypoglycemia)
 Fluid or electrolyte imbalances
 Hepatic or renal disease
 Thiamine deficiency
 Postoperative states
 Hypertensive encephalopathy
 Postictal states and sequelae of head trauma (APA, 2000).

 This disorder is characterized by the symptoms of
delirium that are attributed to medication side effects
or exposure to a toxin. The DSM-IV-TR (APA, 2000) lists
the following examples of medications that have been
reported to result in substance-induced delirium:
 Anesthetics
 Analgesics
 Antiasthmatic agents
 Anticonvulsants, antihistamines
 Antihypertensive and cardiovascular medications
 Antimicrobials, antiparkinsonian drugs
 Corticosteroids, gastrointestinal medications
 Histamine H2-receptor antagonists (e.g., cimetidine)
 Immunosuppressive agents, lithium, muscle relaxants
 And psychotropic medications with anticholinergic side
effects.
 Toxins reported to cause delirium include organophosphate
(anticholinesterase) insecticides, carbon monoxide,and
volatile substances such as fuel or organic solvents.

 With this disorder, the symptoms of delirium
may arise within minutes to hours after taking
relatively high doses of certain drugs such as
cannabis, cocaine, and hallucinogens.
 It may take longer periods of sustained
intoxication to produce delirium symptoms
with alcohol, anxiolytics, or narcotics (APA,
2000).

 Withdrawal delirium symptoms develop after
reduction or termination of sustained, usually
high-dose use of certain substances, such as
alcohol, sedatives, hypnotics, or anxiolytics
(APA, 2000).
 The duration of the delirium is directly related
to the half-life of the substance involved and
may last from a few hours to 2 to 4 weeks.

 This diagnosis is used when the symptoms of
delirium are brought on by more than one cause.
For example:
 The delirium may be related to more than one
general medical condition or it may be a result of
the combined effects of a general medical
condition and substance use (APA, 2000).

A useful mnemonic for remembering possible causes of
delirium is “I WATCH DEATH”.
• I nfections
• W ithdrawal drug or alcohol
• A cute metabolic conditions
• T rauma
• C NS pathology
• H ypoxia
• D efficiencies, vitamins
• E ndocrinopathies
• A cute vascular conditions
• T oxins or drugs
• H eavy metals poisoning

 Brain disorders such as dementia, stroke or
Parkinson's disease
 Previous delirium episodes
 Visual or hearing impairment
 The presence of multiple medical problems

 Delirium may last only a few hours or as long
as several weeks or months.
 People with other serious, chronic or
terminal illnesses may not regain the levels
of thinking skills or functioning that they had
before the onset of delirium. Delirium in
seriously ill people is also more likely to lead
to:
 General decline in health
 Poor recovery from surgery
 Need for institutional care
 Increased risk of death

1.Level of consciousness is often affected, with a disturbance in the
sleep–wake cycle. The state of awareness may range from that of
hyper vigilance (heightened awareness to environmental stimuli) to
stupor or semicoma.
2.Sleep may fluctuate between hyper somnolence (excessive
sleepiness) and insomnia. Vivid dreams and nightmare are common.
3. Psychomotor activity may fluctuate between agitated,
purposeless movements (e.g., restlessness, hyperactivity,
striking out at nonexistent objects) and a vegetative state
resembling catatonic stupor. Various forms of tremor are
frequently present.
4. Emotional instability may be manifested by fear, anxiety,
depression, irritability, anger, euphoria, or apathy.
Autonomic manifestations, such as tachycardia, sweating, flushed
face, dilated pupils, and elevated blood pressure, are common.

5.Reduced awareness of the environment
This may result in:
 An inability to stay focused on a topic or to
switch topics
 Getting stuck on an idea rather than
responding to questions or conversation
 Being easily distracted by unimportant things
 Being withdrawn, with little or no activity or
little response to the environment

6.Poor thinking skills (cognitive impairment)
• Orientation: in obvious cases, orientation in
person, time, and place will all be disturbed
• Attention & Concentration is impaired
• Memory disturbances are seen, particularly
recent events and impaired registration (e.g.
digit span), short-term recall (e.g. name and
address), and long-term recall (e.g. current
news items).
• Speech: the patient may mumble and be
incoherent.
• Difficulty speaking or recalling words
• Rambling or nonsense speech
• Trouble understanding speech
• Difficulty reading or writing

7.Perception: visual perception is the
modality most often affected. Illusions
and misinterpretations are frequent.
8.Insight is usually impaired.

 The symptoms of delirium usually begin quite
abruptly (e.g., following a head injury or
seizure).
 At other times, they may be preceded by several
hours or days of prodromal symptoms (e.g.,
restlessness, difficulty thinking clearly, insomnia
or hyper somnolence, and nightmares).
 The duration of delirium is usually brief (e.g., 1
week; rarely more than 1 month) and, upon
recovery from the underlying determinant,
symptoms usually diminish over a 3- to 7-day
period, but in some instances may take as long
as 2 weeks
(Sadock & Sadock, 2007).

• Impairment of the consciousness and attention (on a
continuum from clouding to coma, reduced ability to
direct,focus ,sustain and shift attention )
• Global disturbance of cognition ( perceptual distortions:
illusions and hallucinations most often visual ; impairment
of abstract thinking and comprehension with or with out
transient delusions ,but typically with some degree of
incoherence ,impairment of immediate recall and of recent
memory but relatively intact remote memory ;disorientation
for time as well as in more severe cases for place and
person.

• Psychomotor disturbances ( hypo or hyper activity and
unpredictable shifts from one to one another ;increased
reaction time increased or decreased flow of speech and
enhanced startle reactions )
• Disturbance of sleep wake cycle (insomnia or in severe cases
total sleep loss or reversal of the sleep wake cycle ;day time
drowsiness ,nocturnal worsening of symptoms ,disturbing
dream or nightmares which may continue as hallucinations
after awakening)
• Emotional disturbances .e.g. depression, anxiety or fear,
irritability ,euphoria ,apathy.
• The onset is usually rapid and the course diurnally fluctuating
and total duration of the condition much less than 6 months .

• Physical examination reveals the cause of
delirium
• Laboratory work up include CBC, electrolytes,
thyroid function tests, ECG , EEG ,chest x
ray ,blood ,urine , and CSF cultures .
• EEG: It shows a generalized slowing of
activity

• Assessment
• Client history : from the clients history ,nurses
should assess the following areas of concern.
• Type ,frequency, and severity of mood swings,
• Personalityand behavioral changes
• Catastrophic emotional reactions
• Cognitive changes such as problems with
attention span ,thinking process ,problem –
solving
• Language difficulties
• Orientation to person ,place, date and situation
• Appropriateness of social behavior

Assessment should focus on two main
areas
• Signs of damage to the nervous
system
• Evidence of diseases of other organs

Pharmacological
Intervention
Non-pharmacological
Intervention

Physical Interventions:
Environmental Interventions:
Cognitive Interventions:
Psychologic Interventions:

• Initial interventions include general measures to support cerebral
function:

• The delusions expressed by a patient
should not be directly disputed. Instead,
alternative explanations of events should
be offered, and frequent reassurance
should be given.

• 100 mg of B1 IV for thiamine deficiency and IV
fluids for fluid and electrolyte imbalances
• Symptomatic management: as many patients are
agitated , emergency psychiatric treatments may be
needed. Small doses of benzodiazepines
(lorazepam or diazepam) or antipsychotics
(haloperidol) may be given orally or parenterally.

• Educating families and patients regarding the
etiology and course of disease is an important role
for physicians.
• Educate the patient, family, and primary
caregivers about future risk factors.
• Families may worry that the patient has brain
damage or a permanent psychiatric illness.
Providing reassurance that delirium often is
temporary and is the result of a medical condition
,may be beneficial to both patients and their
families.
• Suggest that family members or friends visit the
patient, usually one at a time, and provide a calm
and structured environment. Encourage them to
furnish some familiar objects, such as photos or a
favorite blanket, to help reorient the patient and
make the patient feel more secure.

• Dementia consists of verity of symptoms
that suggest chronic dysfunction.
• Global impairment of intellect is the
essential feature, manifested as difficulty
with memory, attention, thinking, and
comprehension skills severe enough to
reduce a person’s ability to perform
everyday activities.

 Other mental function can also be
affected including mood, personality,
judgment, and social behavior.
 Although specific diagnostic criteria are
found for various dementias, such as
Alzheimer’s diseases or vascular
dementia, all dementia have certain
common elements that results in
significant impairment in social or
occupational functioning and causes a
significant decline from a previous level
of function.

 This disorder constitutes a large and growing public
health problem.
 Scientists estimate that 4.5 million people currently
have Alzheimer’s disease (AD), the most common
form of dementia, and the prevalence (the number of
people with the disease at any one time) doubles for
every 5-year age group beyond age 65 (National
Institute on Aging [NIA], 2005).
 The disease affects one in ten people age 65 and
older, one in five ages 75 to 85, and one in two age
85 and older (Laraia, 2004).
 Researchers estimate that by 2050, 13.2 million
Americans will have AD if current population trends
continue and no preventive treatments become
available.

 After heart disease and cancer, AD is the
third most costly disease to society,
accounting for $100 billion in yearly costs
(NIA, 2005). This proliferation is not the
result of an “epidemic.” It has occurred
because more people now survive into the
high-risk period for dementia, which is
middle age and beyond.

 Dementia is defined by a loss of previous
levels of cognitive, executive, and memory
function in a state of full alertness.
(Bourgeois, Seaman, & Servis, 2008).

 Primary dementia
 Secondary dementia
 Cortical dementia
 Sub cortical dementia
 Progressive dementia
 Frontotemporal dementia

1.Primary dementias are those, such as AD,
in which the dementia itself is the major
sign of some organic brain disease not
directly related to any other organic
illness.
2.Secondary dementias are caused by or
related to another disease or condition, such
as human immunodeficiency virus (HIV)
disease or a cerebral trauma.

Dementia where the brain damage primarily
affects the brain’s cortex, or outer layer. Cortical
dementias tend to cause problems with memory,
language, thinking, and social behavior

 Dementia that affects parts of the
brain below the cortex. Sub cortical dementia
tends to cause changes in emotions and
movement in addition to problem with memory
memory.

 Dementia that gets worse over time, gradually
interfering with more and more cognitive
abilities.

 FTD or frontotemporal degenerations refers
to a group of brain disorders that primarily
affect the frontal and temporal lobes of the
brain.
 Shrinkage of these lobes. Generally
associated with personality, behavior, and
language.

Stage 1.
No
Apparent
Symptoms
Stage 2.
Forgetfu
lness.
Stage 3.
Mild
Cognitive
Decline.
Stage 4.
Mild-to-
Moderate
Cognitive
Decline;
Confusion.
Stage 5.
Moderate
Cognitive
Decline;
Early
Dementia.
Stage 6.
Moderate-
to-Severe
Cognitive
Decline;
Middle
Dementia.
Stag
Sev
Cogn
Decl
La
Deme

Stage 1. No Apparent Symptoms:
In the first stage of the illness, there is no
apparent decline in memory.
Stage 2. Forgetfulness:
• The individual begins to lose things or forget
names of people.
• Losses in short-term memory are common.
• The individual is aware of the intellectual decline
and may feel ashamed, becoming anxious and
depressed, which in turn may worsen the symptom.
• These symptoms often are not observed by others.

 In this stage, there is interference with
work performance, which becomes
noticeable to coworkers.
 Concentration may be interrupted.
 The individual may get lost when driving his
or her car.
 There is difficulty recalling names or words,
which becomes noticeable to family and
close associates.
 A decline occurs in the ability to plan or
organize.

 At this stage, the individual may forget major
events in personal history, such as his or her own
child’s birthday; declining ability to perform
tasks, such as shopping and managing personal
finances; or be unable to understand current
news events.
 He or she may deny that a problem exists by
covering up memory loss with confabulation
(creating imaginary events to fill in memory
gaps).
 Depression and social withdrawal are common.

 In the early stages of dementia, individuals lose
the ability to perform some activities of daily
living (ADLs) independently, such as hygiene,
dressing, and grooming, and require some
assistance to manage these on an ongoing basis.
 They may forget addresses, phone numbers, and
names of close relatives. They may become
disoriented about place and time, but they
maintain knowledge about themselves.
 Frustration, withdrawal, and self-absorption are
common.

At this stage, the
individual may be unable
to recall recent major
life events or even the
name of his or her
spouse.
Disorientation to
surroundings is
common, and the
person may be unable to
recall the day, season,
or year.
The person is unable to
manage ADLs without
assistance. Urinary and
fecal incontinence are
common. Sleeping
becomes a problem.
Psychomotor
symptoms include
wandering,
obsessiveness,
agitation, and
aggression.
Symptoms seem to
worsen in the late
afternoon and
evening—a
phenomenon termed
sun downing.
Communication becomes
more difficult, with
increasing loss of language
skills. Institutional care is
usually required at this
stage.

 In the end stages of AD, the individual is
unable to recognize family members. He or
she most commonly is bedfast and aphasic.
 Problems of immobility, such as decubiti and
contractures, may occur.
 Stanley and associates (2005) describe the
late stages of dementia in the following
manner:
 the person becomes more:
 chair bound or bedbound. Muscles are rigid,
contractures may develop, and primitive reflexes
may be present.

 The person may have very active hands and repetitive
movements, grunting, or other vocalizations
 There is depressed immune system function, and this
impairment coupled with immobility may lead to the
development of pneumonia, urinary tract infections,
sepsis, and pressure ulcers.
 Appetite decreases and dysphasia is present; aspiration
is common.
 Weight loss generally occurs.
 Speech and language are severely impaired, with
greatly decreased verbal communication.
 The person may no longer recognize any family
members.
 Bowel and bladder incontinence are present and
caregivers need to complete most ADLs for the person.
 The sleep-wake cycle is greatly altered, and the person
spends a lot of time dozing and appears socially
withdrawn and more unaware of the environment or
surroundings.
 Death may be caused by infection, sepsis, or aspiration,
although there are not many studies examining cause of
death.

The disorders of dementia are differentiated by their
etiology, although they share a common symptom
presentation.
Categories of dementia include:
1. Dementia of the Alzheimer’s type
2. Vascular dementia
3. Dementia due to HIV disease
4. Dementia due to head trauma
5. Dementia due to Lewy body disease
6. Dementia due to Parkinson’s disease
7. Dementia due to Huntington’s disease
8. Dementia due to Pick’s disease
9. Dementia due to Creutzfeldt–Jakob disease
10. Dementia due to other general medical conditions
11. Substance-induced persisting dementia
12. Dementia due to multiple etiologies

 The onset of symptoms is slow and insidious,
and the course of the disorder is generally
progressive and deteriorating.
 Examination by computerized tomography
(CT) scan or magnetic resonance imaging (MRI)
reveals a degenerative pathology of the brain
that includes atrophy, widened cortical sulci,
and enlarged cerebral ventricles.
 Microscopic examinations reveal numerous
neurofibrillary tangles and senile plaques in the
brains of clients with AD.

FIGURE –1 Changes in the Alzheimer’s Brain. A. PET scan
showing metabolic activity in a normal brain. B. Diminished metabolic
activity in the Alzheimer’s diseased brain. C. Late stage Alzheimer’s
disease with generalized atrophy and enlargement of the ventricles and
sulci. (Source: Alzheimer’s Disease Education & Referral Center, A
Service of the National Institute on Aging. 2005. http://www.
alzheimers.org/)

Gyrus
Normal Alzheimer’s
Memory
Memory
LanguageLanguage
Ventricle
Gyrus
Sulcus
Sulcus

The exact cause of AD is unknown. Several
hypotheses have been supported by varying amounts
and quality of data. These hypotheses include:
1. Acetylcholine Alterations:
 Research has indicated that in the brains of AD
clients, the enzyme required to produce
acetylcholine is dramatically reduced.
 The reduction seems to be greatest in the nucleus
basalis of the inferior medial forebrain area.
 This decrease in production of acetylcholine
reduces the amount of the neurotransmitter that is
released to cells in the cortex and hippocampus,
resulting in a disruption of the cognitive processes.

 Other neurotransmitters implicated in the
pathology and clinical symptoms of AD
include nor epinephrine, serotonin,
dopamine, and the amino acid glutamate.
 It has been proposed that in dementia,
excess glutamate leads to overstimulation of
the N-methyl-D-aspartate (NMDA) receptors,
leading to increased intracellular calcium,
and subsequent neuronal degeneration and
cell death.

2. Plaques and Tangles.
 An overabundance of structures called
plaques and tangles appears in the
brains of individuals with AD.
 The plaques are made of a protein
called amyloid beta (Aβ ), which are
fragments of a larger protein called
amyloid precursor protein.
 Plaques are formed when these
fragments clump together and mix with
molecules and other cellular matter.
 Tangles are formed from a special kind
of cellular protein called tau protein,
whose function it is to provide stability
to the neuron.
 In AD, the tau protein is chemically
altered).
 Strands of the protein become tangled
together, interfering with the neuronal
transport system.

3.Head Trauma:
 The etiology of AD has been associated with
serious head trauma.
 Studies have shown that some individuals who
had experienced head trauma had
subsequently (after years) developed AD.
 Munoz and Feldman (2000) report an increased
risk for AD in individuals who are both
genetically predisposed and who experience
traumatic head injury.

4.Genetic Factors:
There is clearly a familial pattern with some
forms of AD.
 Some families exhibit a pattern of
inheritance that suggests possible autosomal
dominant gene transmission.
 People with Down syndrome, who carry an
extra copy of chromosome 21, have been
found to be unusually susceptible to AD

 In vascular dementia, the clinical syndrome of
dementia is due to significant cerebrovascular
disease. The blood vessels of the brain are
affected, and progressive intellectual
deterioration occurs.
 Vascular dementia is the second most common
form of dementia, ranking after AD

Etiology:
 The cause of vascular dementia is directly related to
an interruption of blood flow to the brain. Leads to
death of nerve cells.
 Hypertension leads to damage to the lining of blood
vessels. This can result in rupture of the blood vessel
with subsequent hemorrhage or an accumulation of
fibrin in the vessel with intravascular clotting and
inhibited blood flow leads to multiple small strokes
or cerebral infarcts.
 Cognitive impairment can occur with multiple small
infarcts (sometimes called “silent strokes”) over time
or with a single cerebrovascular insult that occurs in
a strategic area of the brain.
 An individual may have both vascular dementia and
AD simultaneously.

 Infection with the human immunodeficiency virus-
type 1 (HIV-1) produces a dementing illness called
HIV Associated Dementia [HAD].
 The immune dysfunction associated with HIV disease
can lead to brain infections, and appears to cause
dementia directly.
 In the early stages, neuropsychiatric symptoms may
be manifested.
 Severe cognitive changes, particularly confusion,
changes in behavior, and sometimes psychoses, are
not uncommon in the later stages.

 Serious head trauma can result in symptoms
associated with the syndrome of dementia.
 Amnesia is the most common neurobehavioral
symptom following head trauma, and a degree
of permanent disturbance may persist.
 Repeated head trauma, such as the type
experienced by boxers, can result in dementia
pugilistica, a syndrome characterized by
emotional lability, dysarthria, ataxia, and
impulsivity

 This disorder is distinctive by the presence of
Lewy bodies(abnormal baloon like clumps of
protein)—eosinophilic inclusion bodies—seen in
the cerebral cortex and brainstem
 however, it tends to progress more rapidly, and
there is an earlier appearance of visual
hallucinations and parkinsonian features.
 These patients are highly sensitive to extra
pyramidal effects of antipsychotic medications.
 The disease is progressive and irreversible, and
may account for as many as 25 percent of all
dementia cases.

 Dementia is observed in as many as 60 percent
of clients with Parkinson’s disease
 In this disease, there is a loss of nerve cells
located in the substantia nigra, and dopamine
activity is diminished, resulting in involuntary
muscle movements, slowness, and rigidity.
 Tremor in the upper extremities
 In some instances, the cerebral changes that
occur in dementia of Parkinson’s disease closely
resemble those of AD.

 Damage is seen in the areas of the basal
ganglia and the cerebral cortex.
 The onset of symptoms (i.e., involuntary
twitching of the limbs or facial muscles; mild
cognitive changes; depression and apathy)
 & is usually between age 30 and 50 years.
 The client usually declines into a profound
state of dementia and ataxia.

 Studies reveal that pathology of Pick’s
disease results from atrophy in the frontal
and temporal lobes of the brain.
 The cause of Pick’s disease is unknown, but a
genetic factor appears to be involved.
 The clinical picture is strikingly similar to
that of AD.
 Others like personality change, whereas the
initial symptom in AD is memory impairment.

 Creutzfeldt–Jakob disease is
an uncommon
neurodegenerative disease
caused by a transmissible
agent known a“slow virus”
or Prion(abnormal infectious
protein in the brain).
 Five to 15 percent of cases
have a genetic component.
 Symptoms like syndrome of
dementia, along with
involuntary movements,
muscle rigidity, and ataxia.
 Symptoms may develop
between ages 40 and 60 years.
 The clinical course is
extremely rapid, with
progressive deterioration and
death within 1 year.

 A number of other general medical
conditions can cause dementia.
 Some of these include endocrine conditions
(e.g., hypoglycemia, hypothyroidism),
pulmonary disease, hepatic or renal failure
cardiopulmonary insufficiency, fluid and
electrolyte imbalances, nutritional
deficiencies, frontal or temporal lobe
lesions, central nervous system (CNS) or
systemic infections, uncontrolled epilepsy,
and other neurological conditions such as
multiple sclerosis (APA, 2000).

DSM-IV-TR identifies the following types of substances
with which persisting dementia is associated:
1. Alcohol
2. Inhalants
3. Sedatives, hypnotics, and anxiolytics
4. Medications
a. Anticonvulsants
b. Intrathecal methotrexate
5. Toxins
a. Lead
b. Mercury
c. Carbon monoxide
d. Organophosphate insecticides
e. Industrial solvents

 The diagnosis is made according to the
specific etiological substance involved.
 For example, if the substance known to
cause the dementia is alcohol, the diagnosis
is Alcohol-Induced Persisting Dementia.

 This diagnosis is used when the symptoms of
dementia are attributed to more than one
cause.
 For example, the dementia may be related
to more than one medical condition or to the
combined effects of a general medical
condition and the long-term use of a
substance.

 Hypoxia: any condition leading to a deficiency of oxygen to the brain
 Nutritional deficiencies: vitamins (particularly B and C); protein;
 fluid and electrolyte imbalances
 Metabolic disturbances: porphyria; encephalopathies related to
hepatic, renal, pancreatic, or pulmonary insufficiencies; hypoglycemia
 Endocrine dysfunction: thyroid, parathyroid, adrenal, pancreas,
pituitary
 Cardiovascular disease: stroke, cardiac insufficiency, atherosclerosis
 Primary brain disorders: epilepsy, Alzheimer’s disease, Pick’s disease,
Huntington’s disease, multiple sclerosis, Parkinson’s disease
 Infections: encephalitis, meningitis, pneumonia, septicemia,
neurosyphilis (dementia paralytica), HIV disease, acute rheumatic
fever, Creutzfeldt–Jakob disease Intracranial neoplasms
 Congenital defects: prenatal infections, such as first-trimester
maternal rubella

Dementia symptoms vary depending on the cause, but
common signs and symptoms include:
1.Cognitive changes
 Memory loss, which is usually noticed by a spouse or
someone else
 Difficulty communicating or finding words
 Difficulty with visual and spatial abilities, such as
getting lost while driving
 Difficulty reasoning or problem-solving
 Difficulty handling complex tasks
 Difficulty with planning and organizing
 Difficulty with coordination and motor functions
 Confusion and disorientation

 Psychological changes
 Personality changes
 Depression
 Anxiety
 Inappropriate behavior
 Paranoia
 Agitation
 Hallucinations

1.Emotional lability (marked variation in
emotional expression).
2.Catastrophic reaction (when confronted with
an assignment which is beyond the residual
intellectual capacity, patient may go into a
sudden rage).
3.Thought abnormalities, e.g. perseveration,
delusions.
4.Urinary and faecal incontinence may develop
in later stages.
5.Neurological signs may or may not be
present, depending on the underlying cause.

 memory problems – regularly forgetting
recent events, names and faces
 asking questions repetitively
 increasing difficulties with tasks and
activities that require organisation and
planning
 becoming confused in unfamiliar
environments
 difficulty finding the right words
 difficulty with numbers and/or handling
money in shops
 becoming more withdrawn or anxious

Specific symptoms can include:
 stroke-like symptoms: including muscle
weakness or temporary paralysis on one side
of the body (these symptoms require urgent
medical attention)
 movement problems – difficulty walking or a
change in the way a person walks
 thinking problems – having difficulty with
attention, planning and reasoning
 mood changes – depression and a tendency to
become more emotional

 periods of being alert or drowsy,
or fluctuating levels of confusion
 visual hallucinations
 becoming slower in their physical movements
 repeated falls and fainting
 sleep disturbances

Early symptoms of frontotemporal dementia may
include:
 personality changes – reduced sensitivity to
others' feelings, making people seem cold and
unfeeling
 lack of social awareness – making inappropriate
jokes or showing a lack of tact, though some
people may become very withdrawn and
apathetic
 language problems – difficulty finding the right
words or understanding them
 becoming obsessive – such as developing fads for
unusual foods, overeating and drinking

The most common symptoms of advanced dementia include:
 Memory problems – people may not recognize close family and
friends, or remember where they live or where they are.
 Communication problems – some people may eventually lose
the ability to speak altogether. Using non-verbal means of
communication, such as facial expressions, touch and gestures,
can help.
 Mobility problems – many people become less able to move
about unaided. Some may eventually become unable to walk and
require a wheelchair or be confined to bed.
 Behavioral problems – a significant number of people will
develop what are known as "behavioral and psychological
symptoms of dementia". These may include increased agitation,
depressive symptoms, anxiety, wandering, aggression or
sometimes hallucinations.
 Bladder incontinence is common in the later stages of
dementia, and some people will also experience bowel
incontinence.
 Appetite and weight loss problems are both common in advanced
dementia. Many people have trouble eating or swallowing, and
this can lead to choking, chest infections and other problems.

 1.DSM-IV-TR Diagnostic Criteriafor
dementia of the Alzheimer’s Type:
A)The developmentof multiple cognitive
defects manifested by both,
1. Memory impairment (impair ability to
learn new information or recoll the
learn information)

2. One or more of the following cognitive
disturbances:
 Aphasia (language disturbance)
 Apraxia (impair ability to carry out motor
activity’s)
 Agnosia ( failure to recognized of identify objects)
 Disturbance in executive functioning (i.e:
planning, organizing, abstracting, sequencing)
B)Thecourse is characterized by gradual onset
and continuing cognitive decline.

2. DSM-IV-TR Diagnostic Criteria for
Vascular Dementia:
A)The development of multiple cognitive
learn new information or recall the learn
information)

2. One or more of the following
disturbances:
 Aphasia (language disturbance)
cognitive
(impair ability to carry out motor Apraxia
activity’s)
 Agnosia
objects)
( failure to recognized of identify
 Disturbance in executive functioning
(i.e:

B)Focal neurological signs and symptoms
(e.g: exaggeration of deep tendon reflex,
extensor planter response, weakness of an
extremity.
C)The defect does not occur during the onset
of a delirium.

3. DSM-IV-TR Diagnostic Criteria For
Dementia Due To Other Medical
Conditions.
information)

2. One or more of the
following cognitive disturbances:
o Aphasia (language disturbance)
o Apraxia (impair ability to carry
activity’s)
out motor
o Agnosia ( failure to recognized of identify objects)
o Disturbance in executive functioning (i.e:

E.g: HIV infection, traumatic brain injury,
Parkinson diseases, Huntington’s
diseases, pick diseases, hypothyroidism,
normal – pressure hydrocephalus, brain
tumor, etc.

4. DSM-IV-TR Diagnostic Criteria For
Dementia Due To Multiple Etiologies
information)

o Aphasia (language disturbance)
o Apraxia (impair ability to carry out motor activity’s)
o Agnosia ( failure to recognized of identify objects)
o Disturbance in executive functioning (i.e: planning,
organizing, abstracting, sequencing)
2. One or more of the
following cognitive disturbances:

• Medical History
• Laboratory evaluation-blood test, urine test to test for various
infections; hepatic and renal dysfunction; diabetes or hypoglycemia;
electrolyte imbalances; metabolic and endocrine disorders;
nutritional deficiencies; and presence of toxic substances, including
alcohol and other drugs.
• Brain imaging- EEG, CT, MRI,PET
• EEG, which measures and records the brain’s electrical activity.
• CT scan, an image of the size and shape of the brain can be
obtained.
• Magnetic resonance imaging (MRI) is used to obtain a computerized
image of soft tissue in the body. It provides a sharp detailed picture
of the tissues of the brain.
• A lumbar puncture may be performed to examine the cerebrospinal
fluid for evidence of CNS infection or hemorrhage

 Positron emission tomography (PET) is used
to reveal the metabolic activity of the brain
 In a recent study at the University of
California Los Angeles, researchers used PET
following injections of FDDNP (a molecule
that binds to plaques and tangles in vitro)
 With this test, the researchers were able to
distinguish between subjects with AD, mild
cognitive impairment, and those with no
cognitive impairment.
 With FDDNP-PET, researchers are able to
accurately diagnose AD in its earlier stages
and track disease progression noninvasively
in a clinical setting.

• Neurological Reflexes- reflexes, co-
ordination and balance, muscle tone and
strength, eye movement, speech and
sensation.
• Psychiatric Evaluation- Mental status
examination, mini mental status
examination

DRUG CLASSIFICATION FOR TREATMENT OF
Tacrine (Cognex)
Donepezil (Aricept)
Rivastigmine (Exelon)
Galantamine (Razadyne)
Memantine (Namenda)
Cholinesterase Inhibitor
NMDA Receptor
Antagonist
Cognitive impairment
Risperidone* (Risperdal)
Olanzapine*(Zyprexa)
Quetiapine*(Seroquel)
Haloperidol (Haldol)
Antipsychotic
Antipsychotic
Antipsychotic
Antipsychotic
Agitation, aggression,
hallucinations, thought
disturbances,
wandering
Sertraline (Zoloft)
Paroxetine (Paxil)
Nortriptyline (Pamelor)
Antidepressant(SSRI)
Antidepressant(SSRI)
Antidepressant(Tricyclic)
Depression
Depression
Depression

DRUG CLASSIFICATION FOR TREATMENT
OF
Lorazepam (Ativan)
Oxazepam (Serax)
Antianxiety
(Benzodiazepine)
Antianxiety
(Benzodiazepine)
Anxiety
Anxiety
Temazepam (Restoril)
Zolpidem (Ambien)
Zaleplon (Sonata)
Sedative/Hypnotic
(Benzodiazepine)
Sedative/Hypnotic
(Nonbenzodiazepine)
Sedative/Hypnotic
(Nonbenzodiazepine)
Insomnia
Insomnia
Insomnia
Trazodone (Desyrel)
Mirtazapine
(Remeron)
Antidepressant
(Heterocyclic)
Antidepressant
(Tetracyclic)
Depression and
Insomnia
Depression and
Insomnia

 Daily routine
 Nutrition & body weight
 Personal hygiene
 Toilet habits and incontinence
 Accidents
 Fluid management

 Moods and emotions
 Wandering
 Disturbed sleep
 Interpersonal relationship

• Nursing Assessment
– Assess the key areas in history, MSE and
MMSE and other examinations to get
probable symptoms and defect.

1. Risk for trauma related to impairments in cognitive and
psychomotor functioning
2. Potential for injury related to disorientation as evidence by
muscular inco-ordination.
3. Potential for violence related to hallucination
as evidence by agitation
4. Impaired Verbal Communication
5. Chronic confusion related to impairments in cognitive
processes as evidence by conversation.

5.Altered thought process related to vascular
diseases as evidenced by delusional/memory defect.
6. Disturbed self-concept related to loss of
independent functioning a evidenced by social
isolation.
7. Self Care Deficit related to impaired cognitive
functioning as evidenced by poor physical
appearance.
8.Disturbed Sensory Perception related to Dementia
Due to Lewy Body Disease as evidenced by
hallucinations.

a. Arrange furniture and other items in the room to
accommodate client’s disabilities.
b. Store frequently used items within easy access.
c. Do not keep bed in an elevated position. Pad side rails and
headboard if client has history of seizures. Keep bed rails
up when client is in bed (if regulations permit).
d. Assign room near nurses’ station; observe frequently.
e. Assist client with ambulation.
f. Keep a dim light on at night.
g. If client is a smoker, cigarettes and lighter or matches
should be kept at the nurses’ station and dispensed only
when someone is available to stay with client while he or
she is smoking.
h. Frequently orient client to place, time, and situation.
i. If client is prone to wander, provide an area within which
wandering can be carried out safely.
j. Soft restraints may be required if client is very disoriented
and hyperactive.

• Assess client’s level of disorientation and confusion
to determine specific requirements for safety.
• Institute appropriate safety measures, such as the
following:
a.Place furniture in room in an arrangement that
best accommodates client’s disabilities.
b.Observe client behaviors frequently; assign staff on
one to- one basis if condition warrants; accompany
and assist client when ambulating; use wheelchair for
transporting long distances.

c.Store items that client uses frequently within
easy access.
d.Remove potentially harmful articles from
client’s room: cigarettes, matches, lighters,
sharp objects.
e.Remain with client while he or she smokes.
f.Pad side rails and headboard of client with
seizure disorder. Institute seizure precautions as
described in procedure manual of individual
institution.
g.If client is prone to wander, provide an area
within which wandering can be carried out
safely.

 Frequently orient client to reality and
surrounding
 Use tranquilizers and soft restraints , as
prescribed by physician for clients protecting
during period of excessive hyperactivity.

• Assess client’s level of anxiety and
behaviors that indicate the anxiety is
increasing.
• Maintain low level of stimuli in client’s
environment (low lighting, few people,
simple decor, low noise level).
• Remove all potentially dangerous objects
from client’s environment.
• Have sufficient staff available to
execute a physical confrontation, if
necessary.

• Use tranquilizing medications and
soft restraints, as prescribed by
physician.
• Sit with client and provide one-to-one
observation if assessed to be actively
suicidal.

 Research reported at the 2019 Alzheimer’s
Association International Conference®
suggests that adopting multiple healthy
lifestyle choices, including healthy diet, not
smoking, regular exercise and cognitive
stimulation, may decrease the risk of
cognitive decline and dementia.

• Reminiscence Therapy
– Reminiscence therapy is defined by the
American Psychological ) as "the use of
life histories – written, oral, or both –
to improve psychological well-being.
– This form of therapeutic intervention
respects the life and experiences of the
individual with the aim to help the
patient maintain good mental health.

• Increased environment cues
– Address patient by name to facilitate
orientation of self.
– Offer environmental cues to offer
orientation of time, place and person.
– Encourage visit from family and friends.
– Provide assistive device like glasses, hearing
aid, walker etc. if needed.
– Caring a dementic patient is a burdensome
task for family members too, provide support
to the career too.

 Amnestic disorders are a group of disorders
that involve loss of memories, loss of ability
to create new memories, or loss of ability to
learn new information.
 These disorders are characterized by
problems with memory function. There are a
variety of symptoms associated with
amnestic disorders, as well as differences in
the severity of symptoms.

 The two main types of amnestic disorders
centre on whether or not the cause of the
memory problems is known.
1. Organic Amnesic Syndrome: this is
diagnosed when there is a known physical
cause of the memory problems.
2. Unspecified Amnestic Disorder: this is
diagnosed when the exact cause of the
memory loss is not fully known.

 Amnesia refers to loss of memories such as
facts, information and experiences. It is
characterized by the inability to retain or
recall past experiences. The condition may be
temporary or permanent, depending on
etiology.
 Some people with amnesia have difficulty
forming new memories.
 People with amnesia usually retain knowledge
of their own identity, as well as motor skills.

 The onset of symptoms may be acute or
insidious, depending on the pathological
process causing the amnestic disorder.
 Duration and course of the illness may be
quite variable and are also correlated with
extent and severity of the cause.

1.Retrograde amnesia: Means people
experience difficulty in recalling events that
happened or facts that they learned before
the onset of the amnestic disorder. This type
of amnesia is called retrograde amnesia.
 This type of amnesia tends to affect recently
formed memories first. Diseases such as
dementia cause gradual retrograde amnesia.

2.Anterograde amnesia
The inability to learn new facts or retain new
memories, which is called Anterograde
amnesia.
 This effect can be temporary. For example,
individual experience it during a blackout
caused by too much alcohol.
 It can also be permanent. if the area of brain
I.e. hippocampus is damaged.
 Hippocampus plays an important role in
forming memories.

3.Transient global amnesia
Transient global amnesia (TGA) is a poorly
understood condition.
 If anyone develop it, they will experience
confusion or agitation that comes and goes
repeatedly over the course of several hours.
 They may experience memory loss in the
hours before the attack, and will probably
have no lasting memory of the experience.
 Scientists think that TGA occurs as the result
of seizure-like activity or a brief blockage of
the blood vessels supplying to the brain.
 It occurs more frequently in middle-aged and
older adults.

 Infantile amnesia
Most people can’t remember the first three
to five years of life. This common
phenomenon is called infantile or childhood
amnesia.
 Profound amnesia may result in
disorientation to place and time, but rarely
to self (APA, 2000).

The exact symptoms of amnestic disorder vary depending on
its particular cause.
 In general, the symptoms associated with amnestic
disorders include:
 Loss of memory
 Confusion & Disorientation with time and space
 Lack of insight to their loss of memory
 Difficulty learning or recalling information
 Being aware of memory loss but unable to understand why
 The individual may engage in confabulation—the creation
of imaginary events to fill in memory gaps.

1. Amnestic disorder due to a general medical condition
2. Substance-induced persisting amnestic disorder
3. Dementia
4. Anoxia
5. Damage to the hippocampus
6. Head injuries
7. Trauma or stress : Severe trauma or stress can also
cause dissociative amnesia.
A specific type of D.A is called dissociative fugue,
can lead to unexpected traveling or wandering.
8. ECT : Retrograde amnesia of the weeks or months.
Some people experience Anterograde amnesia,
usually resolving within 2 weeks of the treatment.

 General medical conditions that may be
associated with amnestic disorder include
head trauma, cerebrovascular disease,
cerebral neoplastic disease, cerebral anoxia,
herpes simplex encephalitis, poorly
controlled insulin dependent diabetes, and
surgical intervention to the brain

The DSM-IV-TR identifies the following substances with
which amnestic disorder can be associated:
1. Alcohol
2. Sedatives, hypnotics, and anxiolytics
3. Medications
a. Anticonvulsants
b. Intrathecal methotrexate
4. Toxins
a. Lead
b. Mercury
c. Carbon monoxide
d. Organophosphate insecticides
e. Industrial solvents

 To lose old memories, widespread brain
deterioration. This can be caused by
Alzheimer’s disease or other forms of
dementia.
4.Anoxia
 A depletion of oxygen levels can also affect
your entire brain and lead to memory loss.
This condition is called anoxia. If the anoxia
isn’t severe enough to cause brain damage,
the memory loss can be temporary.

 Hippocampus is a part of the brain and limbic
system responsible for memory. Its activities
include forming memories, organizing
memories, and retrieving them when
needed. Its cells are most easily disrupted by
anoxia and other threats such toxins.
 When hippocampus is impaired, individual
will have difficulty in forming new memories.
If hippocampus is damaged in both halves of
brain, one can develop complete
Anterograde amnesia.

 Traumatic head injuries, as well as stroke,
tumors, and infections, can also cause
damage to your brain.
 This damage can include permanent memory
problems. Concussions commonly disrupt
memories of the hours, days, or weeks
before and after you were injured.

 Short-term alcohol use can cause blackout.
This is a temporary form of Anterograde
amnesia.
 Long-term alcoholism can cause Wernicke-
Korsakoff syndrome. If individual develop
this condition, will have difficulty in forming
new memories but may not be aware of it.

 Severe trauma or stress can also cause
dissociative amnesia. With this condition,
individual’s mind rejects thoughts, feelings,
or information that you’re too overwhelmed
to handle.
 A specific type of dissociative amnesia,
called dissociative fugue, can lead to
unexpected traveling or wandering. It can
also lead to amnesia around the
circumstances of traveling as well as
forgetting other details of one’s life.

 Individual experience retrograde amnesia of
the weeks or months before treatment.
 One could also experience Anterograde
amnesia, usually resolving within 2 weeks of
the treatment.

To treat amnesia, your doctor will focus on the underlying
cause of your condition.
 Chemically induced amnesia, from alcohol for example,
can be resolved through detoxification. Once the drug is
out of system, memory problems will probably subside.
 Amnesia from mild head trauma usually resolves without
treatment over time. Amnesia from severe head injury may
not recede. However, improvements usually occur within
six to nine months.
 Amnesia from dementia is often incurable. However, your
doctor may prescribe medications to support learning and
memory.
 If anyone have persistent memory loss, doctor may
recommend occupational therapy. This type of therapy can
help you learn new information and memory skills for daily
living. Therapist can also teach you how to use memory
aids and techniques for organizing information to make it
easier to retrieve.

The following healthy habits can lower your risk of
blackouts, head injuries, dementia, stroke, and other
potential causes of memory loss:
 Avoid heavy use of alcohol or drugs.
 Use protective headgear when you’re playing sports
that put you at high risk of concussion.
 Stay mentally active throughout your life. For
instance, take classes, explore new places, read new
books, and play mentally challenging games.
 Stay physically active throughout your life.
 Eat a heart-healthy diet, including fruits, vegetables,
whole grains, and low-fat proteins.
 Stay hydrated.

Organic Mental Disorder final- MS. Ritika soni

Organic Mental Disorder final- MS. Ritika soni

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