NEUROCOGNITIVE DISORDERS.pptx

NEUROCOGNITIVE
DISORDERS(NCDs)
BY GEOFRY OUMA

INTRODUCTION
• NCDs include those in which a clinically significant deficit in cognition
or memory exists, representing a change from a previous level of
functioning.
• NCDs begin with delirium, followed by syndromes of major NCD, mild
NCD, and their etiological subtypes.
• The major or mild NCD subtypes are;

Major and mild NCD subtypes
NCD due to Alzheimer’s disease.
Vascular NCD.
NCD with Lewy bodies.
NCD due to Parkinson’s disease.
Frontotemporal NCD.
NCD due to traumatic brain injury.
NCD due to HIV infection.
NCD due to Huntington’s disease.

NCD due to Prion disease.
NCD due to another medical condition.
NCD due to multiple etiologies.
Unspecified NCD.

Delirium
• Charactized by disturbance in attention and awareness and a change
in cognition that develop rapidly over a short period(APA, 2013).
• The duration of delirium is usually brief(e.g. 1 week; rarely more than
1 month) and, upon recovery from the underlying determinant, the
symptoms usually diminish over a 3-to-7-day period, but in some
instances it may take as long as 2weeks.
• The age of the client and duration of the delirium influence rate of
symptom resolution.
• Delirium may transition from into a more permanent cognitive
disorder( e.g. major NCD) and is associated with high mortality rate.

DSM-5 TR DIAGNOSTIC CRITERIA
A. The disturbance in attention(i.e reduced ability to focus, sustain and
shift attention) accompanied by reduced awareness of the
environment.
B. The disturbance develops over a short period of time, usually hours
to few days, represents a change from baseline attention and
awareness and tends to fluctuate in severity during the course of
the day.
C. An additional disturbance in cognition e.g. Memory deficit,
disorientation, language, visuospatial ability, or perception.

D. The disturbance in A and C are not better explained by another
preexisting, established or evolving NCD and do not occur in the
context of a severely reduced level of arousal, such as coma.
E. There is evidence from history, physical examination, or laboratory
findings that the disturbance is a direct physiological consequence of
another medical condition, substance intoxication or withdrawal( i.e
due to drug abuse or medication), or exposure to a toxin, or is due to
multiple etiologies.

SYMPTOMATOLOGY OF
DELIRIUM
• Disorders of perception i.e illusions and hallucination.
• Disorders of speech reflected by rambling’, irrelevant, pressured and
incoherent speech.
• Disorders of attention and concentration i.e. Reduced ability to focus,
sustain and shift attention.
• Disorders of consciousness such as inattention, confusion, catatonic
stupor.
• Sleep disorders such insomnia and hypersomnolence.
• Psychomotor disorders such as catatonic stupor.

Predisposing factors
• Delirium mostly occurs in individuals with serious medical, surgical or
neurological conditions. Examples of the conditions that have been
known to precpitate delirium are
• Systemic infections, febrile illness, metabolic disorders (such as
hypoxia, hypercarpnea, or hypoglycemia), hepatic encephalopathy,
head trauma, seizures, migraine and headaches, brain abscess, stroke,
postoperative states and electrolyte disturbances.
• Substance intoxication delirium e.g. Due to alcohol, cannabis, cocaine.
• Substance withdrawal delirium and medication induced delirium.

Neurocognitive disorder
• NCD is classified in the DSM-5(APA,2013) as either mild or major, with
the distinction primarily being one of severity of symptomatology.
• Mild NCD has been known in some settings as mild cognitive
impairment, and is particularly critical because it can be used to
prevent or slow progression of the disorder.
• Major NCD constitutes what was previously described as dementia in
the DSM-IV-TR(APA,2000)

DSM-V-TR DIAGNOSTIC CRITERIA
MAJOR NCD
A. Evidence of a significant cognitive impairment from a previous level
of perfomance in one or more cognitive domains( complex
attention, executive function, learning and memory, language,
perceptual-motor, or social cognition) based on;
1. concern of the individual, a knowledgeable informant, or the
clinician that there has been a significant decline in cognitive function
and;
2. a substantial impairment in cognitive performance, preferably
documented by standardized neuropsychological testing’ or in its
absence another quantified clinical assessment.

B. The cognitive deficits interfere with independence in everyday
activities (i.e., at a minimum, requiring assistance with complex
instrumental activities of daily living such as paying bills or managing
medications).
C. The cognitive deficits do not occur exclusively in the context of a
delirium.
D. The cognitive deficits are not better explained by another mental
disorder e.g. MDD, schizophrenia.

MILD NCD DSM-V-TR
DIAGNOSTIC CRITERIA
A. Evidence of modest cognitive decline from a previous level of
perfomance in one or more cognitive( complex attention, cognitive
execution, learning and memory, language, perceptual motor or
social cognition ) based on;
1. concern of the individual, a knowledgeable informant, or the
clinician that there has been a mild decline in cognitive function and;
2. a modest impairment in cognitive performance, preferably
documented by standardized neuropsychological testing’ or in its
absence, another quantified clinical assessment.

B. The cognitive deficits do not interfere with capacity for
independence in everyday activities (i.e., complex instrumental
activities of daily living such as paying bills or managing medications
are preserved but greater effort, compensatory strategies, or
accomodation may be required).
C.The cognitive deficits do not occur exclusively in the context of a
derilium.
D. The cognitive deficits are not better explained by another mental
disorder such as MDD or Schizophrenia.

MILD OR MAJOR NCD DUE TO AD
• Alzheimer’s disease is characterized by syndrome of symptoms identified
as mild or major NCD.
• AD develops in stages.
• Onset of symptoms is slow and insidious, and the course of the disorder is
generally progressive and deteriorating’.
• Memory impairment is an early and prominent feature.
• Refinement of diagnostic criteria now enables clinicians to use specific
clinical features of the disease with considerable accuracy.
• Examination by CT or MRI scan reveals a degenerative pathology of the
brain that includes atrophy, widened cortical sulci, and enlarged ventricles.

• Microscopic examinations reveals numerous neurofibrillary tangles
and senile plaques in the brains of client with AD.
• These changes apparently occur as a part of the normal aging
process.
• However, in clients with AD , they are found in dramatically increased
numbers and their profusion is concentrated in the hippocampus and
certain parts of the cerebral cortex.

AD symptoms progression stages
I. No apparent symptoms- there is no apparent decline in memory.
II. 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. Maintaining organization with lists and a
structured routine provide some compensation. These symptoms
often are not observed by others.
III. Mild cognitive decline- there is inteference with work perfomance
which becomes noticeable to coworkers. The individual may get
lost when driving his or her car. Concentration may be interrupted.

• There is difficulty in recalling names or words, which becomes
noticeable to family and close associates. A decline occurs in the
ability to plan or organize.
Iv. Mild-to-moderate cognitive decline- at this stage of AD, the
individual may forget major events in personal history, such as his or
her own child’s birthday; experience declining ability to perfom tasks
such as shopping and managing personal finances; or be unable to
understand ccurrent news events. He or she may deny that the
problem exists by covering up memory loss with confabulation(creating
imaginary events to fill in memory gaps). Depression and social
withdrawal are common.

V. Moderate cognitive decline- at this stage, individuals lose the ability
to perfom some activities of daily living(ADLs) independently such as
hygiene, dressing, 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 retain knowledge about self. Frustrations,
withdrawal and self-absorption are common.
VI. Moderate to severe cognitive decline- at this stage the individual
with AD maybe unable to recall recent major life events or even the
name of his or her spouse. Disorientation to sorroundings is common,
and the person maybe unable to recall the day, season or the 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 seems to be worsening in the late
afternoon and evening- a phenomenon termed sundowning,
communication becomes more difficult with increasing loss of
language skills. Institutional care is usually required at this stage.
VII. Severe cognitive decline- in the end stagesof 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

DSM-V-TR AD CRITERIA
A. The criteria for major or mild NCD are met.
B.There is insidious onset and gradual progression of impairment in one
or more cognitive domains( for major NCD, at least two domains are
impaired).
C.Criteria are met for either probable or possible AD as follows;
• For major NCD, probable AD is diagnosed if either of the following is
present; otherwise possible AD should be diagnosed;
1. Evidence of a causative AD genetic mutation from family history or
genetic testing.

2. All three of the following are present:
-clear evidence of decline in memory and learning and at least one
other cognitive domain( based on detailed history or serial
nueropsychological testing).
-steadily progressive, gradual decline in cognition, without extended
plateaus.
-no evidence of mixed etiology(i.e absence of other neurodegenerative
or cerebrovascular disease, or another neurological, mental, or
systemic disease or condition likely contributing to cognitive decline).

• For mild NCD, probable AD is diagnosed if there is evidence of causative AD
genetic mutation from either family history.
• Possible AD is diagnosed if there is no evidence of causative AD genetic
mutation from either family history or genetic testing and all three of the
following are present;
-clear evidence of decline in learning and memory
-steadily progressive, gradual decline in cognition, without extended
plateaus.
-no evidence of mixed etiology(i.e absence of other neurodegenerative or
cerebrovascular disease, or another neurological or systemic disease or
condition likely contributing to cognitive decline).

• D. The disturbance is not better explained by cerebrovascular disease,
another neurodegenerative disease, the effects of a substance, or
another mental, neurological, or systemic disorder.

Etiology of AD
• The exact cause of AD is uknown. Several hypotheses have been supported
by varying amounts of quality data. These hypotheses include;
- 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
inferiomedial forebrain area(Cumming’s and Mega, 2003). This decrease in
the production of acetylcholine reduces the amount of neurotransmitter
that is released to the cells in the cortex and hippocampus, resulting in the
disruption of the cognitive processes. Other neurotransmitters implicated in
the pathology and clinical symptoms of AD include norepinephrine,
serotonin,dopamine and the amino acid glutamate.

• It has been proposed that in NCD, excess glutamate leads to
overstimulation N-Methyl-D-arspatate(NMDA) receptors, leading to
increased intracellular calcium and subsequent neuronal
degeneration and cell death.
• Plaques and tangles- an overabundance of structures called plaques
and tangles in the brains of individuals with AD. The plaques are
made of protein called amyloid beta, which is a fragment of amyloid
precursor protein(APP). Plaques are formed when these fragments
clump together and mix with molecules and other cellular matter.
- Tangles are formed from a special kind of protein called tau protein,
whose function is to provide stability to the neuron.

• In AD,the tau protein is chemically altered. Strands of the protein
becomes tangled together, interfering with the neuronal transport
system. It is not known whether plaques and tangles cause AD or are
as a consequence of AD process. It is thought that plaques and
tangles contribute to the destruction and death of neurons, leading to
memory failure, personality changes, inability to carry out ADLs, and
other features of the disease.
• Head trauma- those with head trauma are at risk for AD.
• Genetic factors- there is clearly a familial pattern in those with AD.
Some families exhibit a pattern of inheritance that suggests possible
autosomal dominant gene transmission.

• Some studies indicate that early onset cases are more likely to be familial
than late onset cases, and that from a third to half of all cases may be of
genetic form.
• Some research indicates that there is a link between AD and gene
mutations found on chromosome 21, 14 and 1( Alzheimer’s Disease
Education and Referral, ADEAR,2012).
• Mutation on chromosome 21 causes formation of abnormal APP.
Mutations on chromosme 14 cause abnormal presenilin 1(ps-1) to be
made, and mutations on chromosome 1 leads to formation of presenilin
2(ps-2). Each of these mutation leads to formation of amyloid beta protein,
a major component of the plaques associated with AD.

• Two genetic variants have been identified as risk factors for late-onset
AD. The apolipoporetion E epsilon-4 found on chromosome 19 was
identified in 1993. its exact role in dvt of AD is not yet
clear(ADEAR,2012).
• A second genetic variant, the SORLI gene, was identified in
2007(Rogaeva et al., 2007). The researchers believe thet the altered
gene function results in increasing production of the toxic amyloid
beta and subsequently plaques associated with AD.

VASCULAR NCD
• In vascluar NCD, the syndrome of cogintive symptoms is due to
significant cerebrovascular disease. The blood vessels of the brain are
affected and progressive intellectual deterioration occurs.
• Vascular NCD is the second most common NCD, ranking of NCD.
• Vascular NCD differs from AD in that it has more abrupt onset and
runs a highly variable course.
• In vascular NCD, progression of the symptoms occur in ‘steps’ rather
than as gradual deterioration, that is, at times, the symptoms seem to
clear up and the individual exhibits fairly lucid thinking

• Memory may seem better, and the client may become optimistic that
improvements is occuring, only to experience further decline in functioning
in a flactuating pattern of progression. This irregular pattern of decline
appears to be an intense source of anxiety for the clients with this disorder.
• In vascular NCD, clients suffer small strokes that destroy many areas of the
brain.
• The pattern of deficit is variable, depending on which region of the brain
have been affected. Certain focal neurological signs commonly seen in
patients with vascular NCD, includes weakness of the limbs, small-stepped
gait, and difficulty with speech. The disorder is more common in men than
women.

Etiology of vascular NCD
• The cause of vascular NCD is directly related to interruption of blood
flow to the brain.
• Symptoms results from death of nerve cells in regions nourished by
diseased vessels.
• Various conditions and diseases that interfere with blood circulation
have been implicated.
• High BP is thought to be one of the most significant factors in the
etiology of multiple strokes or cerebral infarcts.
• HTN leads to the demage of inner linings of the blood vessels.

• This can result in rupture of the blood vessel with subsequent
haemorrhage or an accumulation of fibrin in the vessel with
intravascular clotting and inhibited blood flow.
• NCD can also result from infracts related to occlusion of blood vessels
by particulate matter that travels through the bloodstream to the
brain.
• These emboli may be solid(e.g., clots, cellular debris, platelet
aggregates, gaseous(e.g.,air, nitrogen), or liquid(e.g.,fat, following soft
tissue trauma or fracture of long bones).

DSM-V-TR DIAGNOSTIC CRITERIA OF
VASCULAR NCD
A. The criteria for either mild or major NCD are met.
B. The clinical features are consistent with vascular etiology, as
suggested by either of the following;
- One of the cognitive deficits is temporarily related to one or more
cerebrovascular events.
- Evidence for decline is prominent in complex attention( including
processing and speed) and frontal executive function.
C. There is evidence of the presence of cerebrovascular disease from
history, physical examination, and/or neuroimaging’ considered
sufficient enough to account for neurocognitive defeicits.

D. The symptoms are not better explained by another brain disease or
systemic disorder.
Probable vascular NCD is diagnosed if one of the following is present,
otherwise, possible vascular NCD should be diagnosed;
-clinical criteria are supported by neuroimaging evidence of signficant
parenchymal injury attributed to cerebrovascular disease(neuroimaging
supported).
-the neurocognitive syndrome is temporarily related to one or more
document cerebrovascular events.

- Both clinical and genetic(e.g.,cerebral autosomal dominant
arteriopathy with subcortical effects and leukoenencephalopathy)
evidence of cerebrovascular disease is present.
Possible vascular NCD is diagnosed when clinical criteria are met but
neuroimaging is not availabe and the temporal relationship of the
neurocognitive syndrome with one or more cerebrovascular events is
not established.

Frontotemporal NCD
• Symptoms of frontotemporal NCD occur as a result of shrinking of the
frontal and temporal anterior lobes of the brain.
• This type of NCD was identified as pick’s disease in DSM-IV-TR.
• The cause of frontotemporal NCD is uknown but a genetic factor
appears to be involved .
• Symptoms tend to fall into two clinicall patterns;
-behavioral and personality changes and;
-speech and language problems.

DSM-TR DIAGNOSTIC CRITERIA FOR
FRONTOTEMPORAL NCD
A. The criteria are met for either mild or major NCD.
B. The disturbance has insidious onset and gradual progression.
C. Either 1 or 2;
1) behavioral variant
a) Three or more of the following behavioral symptoms; behavioral
disinhibition, apathy or inertia, loss of empathy or sympathy,
perseverative/stereotyped/compulsive/ritualistic behavior,
hyperorality and dietary changes.
b) Prominent decline in social cognition and/or executive abilities.

2. Language variant- prominent decline in language ability, in the form
of speech production, word finding’, object naming’, grammar, or word
comprehension.
D. Relative spearing of learning ,memory and percptual-motor function.
E. The disturbance is not better explained by cerebrovascular disease
another neurodegenerative disease, the effects of a substance, or
another mental,neurological or systemic disorder.

NCD due to Traumatic brain injury
• DSM-5 criteria states that the disorder is caused by an impact to the head
or other mechanisms of rapid movement or displacement of the brain
within the skull, with one or more of the following’; loss of conciousness,
posttraumatic amnesia, disorientation and confusion or neurological
signs(e.g, positive neuroimaging demonstrating injury, a new onset of
seizures or a marked worsening of a preexisting seizure disorder, visual
field cuts, anosmia, hemiparesis.
• Amnesia is the common neurobehavioral symptom following head trauma.
• Other symptoms include confusion and changes in speech, vision and
personality. Depending on the severity, the symptoms may subside or
remain permanent.

DSM-5 DIAGNOSTIC CRITERIA
A. The criteria are met for major or mild neurocognitive disorder.
B. There is evidence of a traumatic brain injury—that is, an impact to the head or other
mechanisms of rapid movement or displacement of the brain within the skull, with
one or more of the following:
1. Loss of consciousness.
2. Posttraumatic amnesia.
3. Disorientation and confusion.
4. Neurological signs (e.g., neuroimaging demonstrating injury; visual field cuts; anosmia;
hemiparesis; hemisensory loss; cortical blindness; aphasia; apraxia; weakness; loss of
balance; other sensory loss that cannot be accounted for by peripheral or other causes).
C. The neurocognitive disorder presents immediately after the occurrence of the
traumatic brain injury or immediately after recovery of consciousness and persists
past the acute post-injury period.

Neurocognitive Disorder With Lewy Bodies
• Clinically, Lewy body NCD is fairly similar to AD; however, it tends to
progress more rapidly, and there is an earlier appearance of visual
hallucinations and parkinsonian features.
• This disorder is distinguished by the presence of Lewy bodies—
eosinophilic inclusion bodies—seen in the cerebral cortex and
brainstem.
• These patients are highly sensitive to extrapyramidal effects of
antipsychotic medications.
• The disease is progressive and irreversible, and may account for as
many as 25 percent of all NCD cases.

DSM-V-TR DIAGNOSTIC CRITERIA
• A. The criteria are met for major or mild neurocognitive disorder.
• B. The disorder has an insidious onset and gradual progression.
• C. The disorder meets a combination of core diagnostic features and suggestive diagnostic features for either probable or
possible neurocognitive disorder with Lewy bodies.
• For probable major or mild neurocognitive disorder with Lewy bodies, the individual has two core features, or one suggestive
feature with one or more core features. For possible major or mild neurocognitive disorder with Lewy bodies, the individual
has only one core feature, or one or more suggestive features.
• 1. Core diagnostic features:
• a. Fluctuating cognition with pronounced variations in attention and alertness.
• b. Recurrent visual hallucinations that are well formed and detailed.
• c. Spontaneous features of parkinsonism, with onset subsequent to the development of cognitive decline.
• 2. Suggestive diagnostic features:
• a. Meets criteria for rapid eye movement sleep behavior disorder.
• b. Severe neuroleptic sensitivity.
• D. The disturbance is not better explained by cerebrovascular disease, another neurodegenerative disease, the effects of a
substance, or another mental, neurological, or systemic disorder.

Neurocognitive Disorder Due to Parkinson’s
Disease
• NCD is observed in as many as 60 percent of clients with Parkinson’s
disease (Bourgeois et al., 2008). 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 is characteristic. In some instances,
the cerebral changes that occur in NCD due to Parkinson’s disease
closely resemble those of AD.

• A. The criteria are met for major or mild neurocognitive disorder.
• B. The disturbance occurs in the setting of established Parkinson’s disease.
• C. There is insidious onset and gradual progression of impairment.
• D. The neurocognitive disorder is not attributable to another medical condition
and is not better explained by another mental disorder.
• Major or mild neurocognitive disorder probably due to Parkinson’s disease
should be diagnosed if 1 and 2 are both met. Major or mild neurocognitive
disorder possibly due to Parkinson’s disease should be diagnosed if 1 or 2 is met:
• 1. There is no evidence of mixed etiology (i.e., absence of other
neurodegenerative or cerebrovascular disease or another neurological, mental,
or systemic disease or condition likely contributing to cognitive decline).
• 2. The Parkinson’s disease clearly precedes the onset of the neurocognitive
disorder.

Neurocognitive Disorder Due to HIV Infection
• Infection with the human immunodeficiency virus-type 1 (HIV-1) can
result in a NCD called HIV-1-associated cognitive/motor complex. A
less severe form, known as HIV-1-associated minor cognitive/motor
disorder, also occurs. The severity of symptoms is correlated to the
extent of brain pathology.
• The immune dysfunction associated with HIV disease can lead to
brain infections by other organisms, and the HIV-1 also appears to
cause NCD directly.

• In the early stages, neuropsychiatric symptoms may be manifested by
barely perceptible changes in a person’s normal psychological
presentation. Severe cognitive changes, particularly confusion,
changes in behavior, and sometimes psychoses, are not uncommon in
the later stages.
• With the advent of the highly active antiretroviral therapies (HAART),
incidence rates of NCD due to HIV infection have been on the decline.
However, it is possible that the prolonged life span of HIV-
infected patients taking medications may actually increase the
numbers of individuals living with HIV-associated NCD.

B. There is documented infection with human immunodeficiency virus
(HIV).
C. The neurocognitive disorder is not better explained by non-HIV
conditions, including secondary brain diseases such as progressive
multifocal leukoencephalopathy or cryptococcal meningitis.
D. The neurocognitive disorder is not attributable to another medical
condition and is not better explained by a mental disorder.

Substance/Medication-Induced Neurocognitive
Disorder
• NCD can occur as the result of substance reactions, overuse, or abuse
(Davis, 2012). Symptoms are consistent with major or mild
neurocognitive disorder, and persist beyond the usual duration of
intoxication and acute withdrawal (APA, 2013).
• Substances that have been associated with the development of NCDs
include alcohol, sedatives, hypnotics, anxiolytics, and inhalants.
Drugs that cause anticholinergic side effects, and toxins such as lead
and mercury, have also been implicated.

B. The neurocognitive impairments do not occur exclusively during the
course of a delirium and persist beyond the usual duration of
intoxication and acute withdrawal.
C. The involved substance or medication and duration and extent of
use are capable of producing the neurocognitive impairment.
D. The temporal course of the neurocognitive deficits is consistent with the
timing Of substance or medication use and abstinence (e.g., the deficits
remain stable or improve after a period of abstinence).
E. The neurocognitive disorder is not attributable to another medical
condition or is not better explained by another mental disorder.

Neurocognitive Disorder Due to Huntington’s
Disease
• Huntington’s disease is transmitted as a Mendelian dominant gene.
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) usually occurs between age 30 and 50 years. The client
usually declines into a profound state of cognitive impairment and
ataxia (muscular incoordination).
• The average duration of the disease is based on age at onset. One
study concluded that juvenile-onset and late-onset clients have the
shortest duration (Foroud, Gray, Ivashina, & Conneally, 1999).
• In this study, the median duration of the disease was 21.4 years.

DSM-V DIAGNOSTIC CRITERIA
B. There is insidious onset and gradual progression.
C. There is clinically established Huntington’s disease, or risk for
Huntington’s disease based on family history or genetic testing.
condition and is not better explained by another mental disorder.

Neurocognitive Disorder Due to Prion Disease
• This disorder is identified by its insidious onset, rapid progression,
and manifestations of motor features of prion disease, such as
myoclonus or ataxia, or biomarker evidence (APA, 2013).
• Five to 15 percent of cases have a genetic component. The clinical
presentation is typical of the syndrome of mild or major NCD, along
with involuntary movements, muscle rigidity, and ataxia.
• Symptoms may develop at any age in adults, but typically occur
between ages 40 and 60 years. The clinical course is extremely rapid,
with the progression from diagnosis to death in less than 2 years
(Rentz, 2008).

B. There is insidious onset, and rapid progression of impairment is
common.
C. There are motor features of prion disease, such as myoclonus
or ataxia, or biomarker evidence.
condition and is not better explained by another mental disorder.

Neurocognitive Disorder Due to Another Medical
Condition
• A number of other general medical conditions can cause NCD. Some
of these include hypothyroidism, hyperparathyroidism, pituitary
insufficiency, uremia, encephalitis, brain tumor, pernicious anemia,
thiamine deficiency, pellagra, uncontrolled epilepsy, cardiopulmonary
insufficiency, fluid and electrolyte imbalances, CNS and systemic
infections, systemic lupus erythematosus, and multiple sclerosis
(Black & Andreasen, 2011; Puri & Treasaden, 2011).

B. There is evidence from the history, physical examination, or
laboratory finding that the neurocognitive disorder is the
pathophysiological consequence of another medical condition (e.g.,
multiple sclerosis).
C. The cognitive deficits are not better explained by another mental
disorder (e.g., major depressive disorder) or another specific
neurocognitive disorder (e.g., major neurocognitive disorder due to
Alzheimer’s disease).

Major or Mild Neurocognitive Disorder Due to
Multiple Etiologies
B. There is evidence from the history, physical examination, or
laboratory findings that the neurocognitive disorder is the
pathophysiological consequence of more than one etiological
process, excluding substances (e.g., neurocognitive disorder due to
Alzheimer’s disease with subsequent development of vascular
neurocognitive disorder).
C. The cognitive deficits are not better explained by another mental
disorder and do not occur exclusively during the course of a
delirium.

BIOPSYCHOSOCIAL MANAGEMENT
ASSESSMENT
- From the client history, nurses should assess the following areas of
concern:
(1) type, frequency, and severity of mood swings, personality and
behavioral changes, and catastrophic emotional reactions;
(2) cognitive changes, such as problems with attention span, thinking
process, problem solving, and memory (recent and remote);
(3) language difficulties;
(4) orientation to person, place, time, and situation; and
(5) appropriateness of social behavior.

• The nurse also should obtain information regarding current and past
medication usage, history of other drug and alcohol use, and
possible exposure to toxins.
• Knowledge regarding the history of related symptoms or specific
illnesses (e.g., Huntington’s disease, AD, or Parkinson’s disease) in
other family members might be useful.
• Physical examination- Assessment of physical systems by both the
nurse and the physician has two main emphases:
(1) signs of damage to the nervous system and

(2) evidence of diseases of other organs that could affect mental
function. Diseases of various organ systems can induce confusion, loss
of memory, and behavioral changes.
These causes must be considered in diagnosing cognitive disorders. In
the neurological examination, the client is asked to perform maneuvers
or answer questions that are designed to elicit information about the
condition of specific parts of the brain or peripheral nerves. Testing will
assess mental status and alertness, muscle strength, reflexes, sensory
perception, language skills, and coordination.

Mental Status Examination for Neurocognitive Disorder- MMSE is a
tool used to check for the mental cognitive ability e.g., orientation,
memory, attention, calculation, language and command.
Important tool for diagnosis of major or mild NCD.
History collection is not involved in MMSE.
Normal score ranges from 25-30, score of 18-24 represents mild
cognitive impairment, score of 11-18 represents moderate cognitive
impairment while a score of less than 10 represents severe cognitive
impairement.

Treatment
• Acetylcholinestrase inhibitors such as donezepil, rivastigmine,
galantamine for treatment of cognitive impairment.
• NMDA receptor antagonist such as memantine to treat cognitive
impairment.
• Antipsychotics such as risperidone, quetiapine, olanzapine for
treatment agitation, aggression, hallucinations, thought disturbances,
wandering’.
• Antidepressants such as setraline, paroxetine, nortriptyline for
treatment of deppression.

• Antanxiety(benzodiazepines)- such as lorazepam, oxazepam for
treatment of anxiety.
• sedatives/hypnotic(benzodiazepines) such as tamazepam for
treatment of insomnia.
• Sedative/hypnotic(non-benzodiazepines) such as zolpidem for
treatment of insomnia.
• Psychotherapy – CBT, individual psychotherapy, occupational
psychotherapy and family psychotherapy.
• Maintain strict schedule for routine activities e.g., breakfast time.

• Give the pt repetitive stimuli to the patient to increase mental activity
or through games and activities.
• High protein diet.
• Supportive and individual therapy.
• Relaxation and family therapy.

NEUROCOGNITIVE DISORDERS.pptx

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NEUROCOGNITIVE DISORDERS.pptx