The document discusses neurocognitive disorders such as delirium, major neurocognitive disorder (dementia), and mild neurocognitive disorder. Delirium is characterized by disturbances in attention, awareness and cognition that develop over a short period of time and fluctuate in severity. Major neurocognitive disorder involves a significant decline in cognition that interferes with daily life while mild neurocognitive disorder involves a modest decline that does not interfere with independence. The causes, diagnosis, treatment and prognosis of these disorders are explained.
2. • The Neurocognitive Disorder category encompasses the group of
disorders in which the primary clinical deficit is in cognitive function,
and that are acquired rather than developmental, they represent a
decline from a previously attained level of functioning.
• Although cognitive deficits are present in many if not all mental
disorders (e.g., schizophrenia, bipolar disorders), only disorders
whose core features are cognitive are included in the NCD category.
3. Introduction
• Cognition refers to tasks that include:
• memory
• language
• orientation
• judgment
• problem-solving
• planning
• ability to have interpersonal relationships
• praxis (perform actions)
• Cognitive disorder is when regular trouble in
these areas disrupts daily functioning.
• Causes of cognitive disorders include head
injury, medical conditions, substance abuse, and
aging.
4. Classification of Neurocognitive
disorders
• Three groups:
• Delirium,
• Major or Minor Neurocognitive Disorders
(Dementia)
• Amnestic disorders.
• Within Major or Minor Neurocognitive Disorders:
Alzheimer’s disease, Vascular dementia, Multi-
infarct dementia, Frontotemporal, Creutzfeldt-Jacob
disease (mad cow disease), Huntington’s disease,
Parkinson’s disease, Human Immunodeficiency
Virus (HIV) disease, etc.
5. History of Neurocognitive
disorders
• No longer referred to as organic because name
implies that non-organic disorders or functional
mental disorders (e.g. depression) have no
biological basis.
• ICD-10 still uses the term ‘organic’.
6. • DSM-5 recognizes a less severe level of cognitive impairment, mild
neurocognitive disorder, which can also be a focus of care, and which
in DSM-IV was subsumed under "Cognitive Disorder Not Otherwise
Specified."
7. Delirium
• The essential feature of delirium is a disturbance of attention or
awareness that is accompanied by a change in baseline cognition that
cannot be better explained by a preexisting or evolving
neurocognitive disorder (NCD).
• Usually involves perceptual disturbances, abnormal psychomotor
activity, and with sleep cycle impairment.
8. • Confusion, or, as it is also known, ‘clouding of the sensorium’, is the
cardinal symptom of delirium and is present in all cases. Patients may
appear dazed, their attention wanders, and they often seem to drift
off.
9. Epidemiology
Prevalence:
• 1% of those aged >55 years
• 13% of those aged >85 years
• General Medical inpatients 10-30%
• Institutionalized elderly 44%
10. Predisposing Factors
• Age (>65 yrs)
• Male
• Dementia or history of cognitive impairment
• History of delirium
• Sensory impairment
• Decreased oral intake
• Coexisting medical conditions e.g Neurological, stroke, Metabolic,
Fractures or traumas
• Drugs (Use of psychoactive drugs, Anticholinergics, alcohol)
11. Precipitating
• Most of the Predisposing factors but also
• Use of narcotics
• Hypoxia, anaemia
• Surgery (Orthopaedic, cardiac)
• Environmental (admission to ICU, Physical restraints, use of bladder
catheter, pain)
12. Aetiology
Major causes are CNS disease, systemic disease and either intoxication
or withdrawal from pharmacological or toxic agents. These include:
• Seizure
• Migraine
• Head trauma, brain tumour, Stroke
• Electrolyte imbalance
• DM
• Infections: Sepsis, malaria
• Medications: Analgesics, Antibiotics, Steroids
14. Diagnosis
Diagnostic Criteria (DSM V)
A. A disturbance in attention (i.e., reduced ability to direct, focus,
sustain, and shift attention) and awareness (reduced orientation to the
environment).
B. The disturbance develops over a short period of time (usually hours
to a few days), represents a change from baseline attention and
awareness, and tends to fluctuate in severity during the course of a
day.
C. An additional disturbance in cognition (e.g., memory deficit,
disorientation, language, visuospatial ability, or perception).
15. • D. The disturbances in Criteria A and C are not better explained by
another preexisting, established, or evolving neurocognitive disorder
and do not occur in the context of a severely reduced level of arousal,
such as coma.
E. There is evidence from the 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 a drug of abuse or to a medication), or
exposure to a toxin, or is due to multiple etiologies.
16. Specify whether:
• Substance intoxication delirium
• Substance withdrawal delirium
• Medication induced delirium
• Delirium due to another medical condition
• Delirium due to multiple aetiologies
17. Specify if:
• Hyperactive: The individual has a hyperactive level of psychomotor activity
that may be accompanied by mood lability, agitation, and/or refusal to
cooperate with medical care.
• Hypoactive: The individual has a hypoactive level of psychomotor activity
that may be accompanied by sluggishness and lethargy that approaches
stupor.
• Mixed level of activity: The individual has a normal level of psychomotor
activity even though attention and awareness are disturbed. Also includes
individuals whose activity level rapidly fluctuates.
19. Associated Factors
• Disturbance in the sleep–wake cycle. Individuals with delirium are
often somnolent during the daytime or awake and agitated at night.
They may have difficulty falling asleep and marked confusion on
arousal.
• Emotional disturbances. Individuals with delirium are often
emotionally labile. They may be extremely agitated and frightened or
withdrawn and apathetic. Periods of irritability, belligerence, or
euphoria can occur.
20. • Abnormal electroencephalogram (EEG) findings. EEG abnormalities
are common in patients with delirium, usually showing either
generalized slowing or fast wave activity. But delirium may occur
without EEG changes.
• Sundowning: State of confusion occurring in the late afternoon and
spanning into the night. Sundowning can cause a variety of behaviors,
such as confusion, anxiety and aggression.
21. • Psychotic disorders e.g Schizophrenia
• Bipolar and depressive disorders with psychotic features
• Acute Stress Disorder
• Malingering and Factitious disorder
22. Treatment
• Delirium is a reversible condition and should be treated as a medical
emergency
• Primary goal is to treat the underlying cause
• Provide physical, sensory, and environmental support
• Address and minimize contributing factors
23. Behavioural Interventions
• Provide orienting environmental cues (clocks, calendars, names of
care providers)
• Provide adequate social interaction
• Have the patient use eye glasses and hearing aids appropriately
• Mobilize the patient as soon as possible
• Ensure adequate intake of nutrition and fluids
• Psychoeducation
24. Pharmacotherapy
• Recommended for behavioural disturbance/agitation, psychotic
features and insomnia
• I.M Haloperidol (in low dosages) a drug of choice for agitation, when
patient is calmer oral Haloperidol can be used.
• SGA also used: Risperidone, Olanzapine, Quetiapine, Aripiprazole
• Avoid Phenothiazines because these drugs ae associated
with significant anticholinergic activity.
• As much as possible avoid Benzodiazepines and anticholinergics as
they may increase confusion or paradoxically increase disinhibition.
25. Prognosis
• The older the patient and the longer the patient has been delirious,
the longer the delirium takes to resolve.
• Delirium may progress to stupor, coma, seizures, or death, particularly
if the underlying cause remains untreated. Mortality among
hospitalized individuals with delirium is high, and as many as 40% of
individuals with delirium, particularly those with malignancies and
other significant underlying medical illness, die within a year after
diagnosis.
26. Other Specified Delirium
• This category applies to presentations in which symptoms characteristic of delirium that
cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning predominate but do not meet the full criteria for delirium
or any of the disorders in the neurocognitive disorders diagnostic class.
• The other specified delirium category is used in situations in which the clinician chooses
to communicate the specific reason that the presentation does not meet the criteria for
delirium or any specific neurocognitive disorder. This is done by recording “other
specified delirium” followed by the specific reason (e.g., “attenuated delirium
syndrome”).
• An example of a presentation that can be specified using the “other specified”
designation is the following:
Attenuated delirium syndrome: This syndrome applies in cases of delirium in which
the severity of cognitive impairment falls short of that required for the diagnosis, or in
which some, but not all, diagnostic criteria for delirium are met.
27. Unspecified Delirium
• This category applies to presentations in which symptoms
characteristic of delirium that cause clinically significant distress or
impairment in social, occupational, or other important areas of
functioning predominate but do not meet the full criteria for delirium
or any of
the disorders in the neurocognitive disorders diagnostic class.
• The unspecified delirium category is used in situations in which the
clinician chooses not to specify the reason that the criteria are not
met for delirium, and includes presentations for which there is
insufficient information to make a more specific diagnosis (e.g., in
emergency room settings).
28. Major and Mild Neurocognitive
Disorders (NCD)
• The DSM-IV-TR referred to these disorders as Dementia, and ICD-
10 still uses this description.
• Although the DSM-5 now refers to these disorders as Neurocognitive
Disorders (NCD), the term dementia is still retained to certain extent
(APA, 2013).
• The APA (2013) states that the term dementia is a customary
description of degenerative disorders for older adults, however, the
term neurocognitive disorders is more inclusive as it includes
neurocognitive disorders that affect younger people as well (APA,
2013).
• The APA (2013) views these disorders as unique when compared to
the other DSM-5 categories as the underlying pathology and
aetiology can be easily determined.
• The primary diagnosis would be Major or Mild NCD, followed by an
aetiological subtypes (e.g. Alzheimer’s disease, Parkinson’s disease,
HIV infection, etc.)
29. Major and Mild Neurocognitive
Disorders
DSM‐5 defines Major and Minor Neurocognitive disorders.
• Major Neurocognitive disorders involve significant decline in one or more
areas of cognition, which interferes with complex instrumental activities of
daily living (paying bills, cooking, etc.). these disorders are further classified
by severity (mild, moderate, or severe) and as with or without behavioral
disturbance (e.g., wandering agitation, aggression, marked
apathy, etc.).
• Mild Neurocognitive disorders, also called Mild Cognitive Impairment
(MCI), involve measurable decline that is of concern to the individual and an
informant, and are objectively measurable on cognitive testing, but do not
interfere with capacity for independent functioning.
30. Major and Mild Neurocognitive
Disorders
• To understand the clinical picture of these disorders, it is necessary to
note which neurocognitive domains are affected. The DSM-5 describes
these as follows (APA, 2013):
• Complex attention: Sustained, divided and selective attention as well
as processing speed.
• Executive functioning: Planning, decision making, working memory
error detection and correction, inhibition and mental flexibility.
• Learning and memory: All memory registers (e.g. short-term,
semantic, autobiographical) and implicit learning.
• Language: Expressive and receptive language.
• Perceptual-motor: This includes visual perception, visuo-constructional
abilities, perceptual-motor, praxis and gnosis.
• Social cognition: Recognition of emotions and theory of mind.
31. Major Neurocognitive Disorder (Dementia)
• Dementia refers to a disease process marked by progressive cognitive
impairment in clear consciousness.
• In dementia, cognitive deficits should be apparent even with clarity of
consciousness.
32. • Dementia is caused by a variety of pathologies, each of which has
specific diagnostic criteria,
including:
• Alzheimer’s disease;
• vascular dementia;
• Parkinson’s disease;
• frontotemporal lobar degeneration;
• Lewy body dementias;
• dementia secondary to enduring effects of alcohol or other toxic
exposures.
33. • The potential reversibility of dementia is related to the underlying
pathological condition and to the availability and application of
effective treatment.
34. Epidemiology
Prevalence
• 5% in those aged >65year
• 20-40% in those aged >85 year
• 15-20% in General Outpatients
• 50% in chronic care facilities
35. In terms of the type of dementia
• Dementia of Alzheimer’s Type (DAT): 50-60%
• Vascular Dementia: 15-30%, Common in the 60-70 year age group,
M>F
• Frontotemporal lobar degeneration is the third most prevalent
dementia under the age of 65 years.
36. NCD, cont.
• Aetiology
• Dementias are sub-categorized according to
presumed aetiology, and include:
• Dementia of the Alzheimer’s Type
• Vascular Dementia
• Mixed vascular and Alzheimer’s type
• Lewy Body Dementias
• Pick’s Disease
• Frontotemporal Dementia
• Dementia Due to Other General Medical
Conditions
• Substance-Induced Persisting Dementia
• Dementia Due to Multiple Aetiologies
• Dementia Not Otherwise Specified
37. Diagnostic Criteria (DSM V)
• Major Neurocognitive Disorder
Diagnostic Criteria
• A. Evidence of significant cognitive decline from a previous level of performance 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).
38. 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.,
major depressive disorder, schizophrenia).
Specify whether due to:
• Alzheimer’s disease
• Frontotemporal lobar degeneration
• Lewy body disease
• Vascular disease
• Traumatic brain injury
• Substance/medication use
39. • HIV infection
• Prion disease
• Parkinson’s disease
• Huntington’s disease
• Another medical condition
• Multiple aetiologies
• Unspecified
40. Specify:
• Without behavioural disturbance: If the cognitive disturbance is not accompanied
by any clinically significant behavioral disturbance.
• With behavioral disturbance (specify disturbance): If the cognitive disturbance is
accompanied by a clinically significant behavioral disturbance (e.g., psychotic
symptoms, mood disturbance, agitation, apathy, or other behavioral symptoms).
Specify current severity:
• Mild: Difficulties with instrumental activities of daily living (e.g., housework,
managing money).
• Moderate: Difficulties with basic activities of daily living (e.g., feeding, dressing).
• Severe: Fully dependent.
41. Mild Neurocognitive Disorder
• A. Evidence of modest cognitive decline from a previous level of performance 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 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
accommodation may be required).
42. 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., major depressive disorder, schizophrenia).
43. Specify whether due to:
• Alzheimer’s disease
• Frontotemporal lobar degeneration
• Lewy body disease
• Vascular disease
• Traumatic brain injury
• Substance/medication use
• HIV infection
44. • Prion disease
• Parkinson’s disease
• Huntington’s disease
• Another medical condition
• Multiple aetiologies
• Unspecified
45. Specify:
• Without behavioral disturbance: If the cognitive disturbance is not
accompanied by any clinically significant behavioral disturbance.
• With behavioral disturbance (specify disturbance): If the cognitive
disturbance is accompanied by a clinically significant behavioral
disturbance (e.g., psychotic symptoms, mood disturbance, agitation,
apathy, or other behavioral symptoms).
46. Neurocognitive Disorder Due to
Alzheimer’s Disease
• Accounts for nearly half of neurocognitive disorders
• Clinical Features
• Typically develop gradually and steadily
• Memory, orientation, judgment, and reasoning deficits
• Additional symptoms may include
• Agitation, confusion, or combativeness
• Depression and/or anxiety
47. NCD, cont.
• Major risk factors are:
• family history
• genetic factors
• head injury
• Onset of Alzheimer’s is subtle - initial memory
impairment and gradual deterioration of
cognitive abilities.
• Pathology is associated with parietal and
temporal regions of the brain.
48. • More common in less educated individuals
• More educated individuals decline more rapidly after onset; this suggests that education
simply provides a buffer period of better initial coping
• Slightly more common in women
• Possibly because women lose estrogen as they age; estrogen may be protective
49. Alzheimer’s Disorder: Extent of
Deficits
• Range of cognitive deficits
• Aphasia – difficulty with language
• Apraxia – impaired motor functioning
• Agnosia – failure to recognize objects
• Difficulties with
• Planning, Organizing
• Sequencing
• Abstracting information
• Negative impact on social and occupational functioning
50.
51. • Features of brains with Alzheimer’s disease
• Neurofibrillary tangles (strand-like filaments)
• Amyloid plaques (gummy deposits between neurons)
• Brains of Alzheimer’s patients tend to atrophy
52. Vascular Neurocognitive Disorder
Vascular
• Cerebrovascular disease is second most common
cause of dementia.
• Injury or brain disease infarctions (death/damage of
vessels) due to obstruction in blood supply lesions
and changes to brain structures.
• Abrupt onset and fluctuating course.
• Risk factors: Hypertension, diabetes, advanced age,
stroke, alcoholism, cardiovascular risk factors (smoking,
obesity).
• Disorder more common in men.
• Compared to Alzheimer’s Type, more likely to have
depression, affective changes, disturbance of gait, and
confusion.
53. Frontotemporal Neurocognitive
Disorder
• Broadly refers to damage to the frontal or temporal regions of the
brain, affecting
• Personality
• Language
• Behavior
• Two types of impairment
• Declines in appropriate behavior
• Declines in language
• Example: Pick’s disease
55. Neurocognitive Disorder Due to
Pick’s Disease
• Rare neurological condition which accounts for 5% of all dementia
diagnoses
• Produces a cortical dementia like Alzheimer’s
• Occurs relatively early in life (around 40s or 50s)
• Little is known about what causes this disease
56. Neurocognitive Disorder Due to
Traumatic Brain injury
• Accidents are leading cause
• Symptoms last for at least one week after head injury, including
problems with executive function, learning, memory
• Memory loss is the most common symptom
• May be found in athletes who experience repeated blows to the head
(e.g., football players)
• Head injury-related dementia is characterized by emotional lability,
dysarthria (speech impairment) and impulsivity
57. Neurocognitive Disorder Due to
Lewy Body Disease
• Lewy bodies = microscopic protein deposits that damage brain over
time
• Symptoms onset gradually
• Symptoms include impaired attention and alertness, visual
hallucinations, motor impairment
• Similar to Alzheimer’s but more rapid.
58. Micrograph of brain cells containing a Lewy body
which is an abnormal aggregation of protein
Lewy bodies can be more easily
detected using special antibody
staining against the α-synuclein
protein
Tau protein and tangles
within a neuron cell
59. What Clues Can Suggest DLB?
Fluctuation – good days and bad days
REM sleep behavior disorder
Difficulty with complex mental activities
Day-time sleepiness
Medication sensitivity – tranquilizers and neuroleptics
Motor dysfunction
Vivid hallucinations/Delusions
Autonomic dysfunction
Abnormal brain imaging
60. DLB Contd
REM sleep disorder
• Acting out dreams
• Sometimes injured by falling out of bed
• Sometimes injure sleep mate
61. DLB (Difficulty with Complex Mental
Activities)
• Executive function severely impaired
• Visuospatial dysfunction
• Decline in attention
• Memory often relatively spared in the early stage
62. Cognitive Fluctuation (DLB)
• Most difficult to define and identify
• Fluctuation of MMSE scores by >5 points up
& down over 6-month period
• Family members say:
• “appears drowsy, but awake”, “looks dazed”
• “not aware of what is going on”
• “can be fine one day and confused the next”
• Minutes, hours or days between periods
REM sleep behavior disorder
Difficulty with complex mental activities
Fluctuation – good days and bad days
Day-time sleepiness
Medication sensitivity
Vivid hallucinations/Delusions
Motor dysfunction
Autonomic dysfunction
Abnormal brain imaging
63. DLB (Motor Dysfunction)
• Fine motor skills are lost
• Rigidity
• Parkinson symptoms
• Tremor
• Slowness of movement (bradykinesia)
• Shuffling gait
• Loss of balance
• Falls
REM sleep behavior disorder
Difficulty with complex mental activities
Fluctuation – good days and bad days
Day-time sleepiness
Medication sensitivity
Vivid hallucinations/Delusions
Motor dysfunction
Autonomic dysfunction
Abnormal brain imaging
64. Neurocognitive Disorder Due to
Parkinson’s Disease
• Parkinson’s disease
• Degenerative brain disorder
• Dopamine pathway damage
• 1 out of 1,000 people are affected worldwide
• Chief difficulty: motor problems
• Tremors, posture, walking, speech
• Not all with PD will develop dementia
• 75% survive 10+ years after diagnosis
65. Neurocognitive Disorder due to
HIV Infection
• HIV-1 can cause neurological impairments and dementia in some
individuals
• Cognitive slowness, impaired attention, and forgetfulness
• Apathy and social withdrawal
• Typically occurs in later disease stages
• Now occurs in <10% of individuals with HIV; HAART decreases risk
66. Neurocognitive Disorder Due to
Huntington’s Disease
• Huntington’s Disease = genetic autosomal dominant disorder
• Caused by a gene on chromosome 4
• Manifests initially as involuntary limb movements (chorea), usually
later in life
• Somewhere between 20-80% display neurocognitive disorder
• Dementia follows a subcortical pattern
67. Neurocognitive Disorder Due to
Prion Disease
• Disorder of proteins in the brain that reproduce and cause damage
• No known treatment, always fatal
• Can only be acquired through cannibalism or accidental transmission
(e.g., contaminated blood transfusion)
• Example: Creutzfeldt-Jakob disease
• Affects one out of 1,000,000 persons
• Linked to mad cow disease
68. Substance/Medication-Induced
Neurocognitive Disorder
• Results from prolonged drug use, especially in combination with poor
diet
• May be caused by alcohol, sedative, hypnotic, anxiolytic or inhalant
drugs
• Brain damage may be permanent
• Symptoms similar to Alzheimer’s
• Deficits may include
• Memory impairment
• Aphasia, apraxia, agnosia
• Disturbed executive functioning
70. Physical and mental status exams
Physical and mental status exams
• Physical exams are used to evaluate possible etiologies for dementia.
• Neurologic exam should look for symptoms of parkinsonism, gait changes,
and other focal neurological findings.
• Mild AD is not associated with physical findings.
• Later stages of AD: extrapyramidal signs, myoclonus, and gait disturbance
may occur.
• A mini mental state exam (MMSE) or a Montreal Cognitive Assessment
(MoCA) is used to screen for MCI or more severe impairment in patients with
subjective complaints of memory difficulty.
• MMSE has been the “gold standard” although it may not be sensitive to
mild changes in highly educated individuals (24 is considered a cut‐off score
for normal cognition).
71. Medical Treatment of
Neurocognitive Disorders
• Few primary treatments exist
• Most treatments attempt to slow progression of deterioration, but
cannot stop it
• Future directions
• Glial cell-derived neurotrophic factor, stem cells: may slow deterioration
• Some drugs target cognitive deficits
• Cholinesterase-inhibitors: Aricept, Exelon, Reminyl
• Long-term effects not well demonstrated
72. Medical Treatment of
Neurocognitive Disorders
• Exploratory treatments
• Ginkgo biloba to improve memory – findings are mixed
• Drugs to treat associated symptoms
• SSRIs for depression and anxiety
• Antipsychotics for agitation
• All are only modestly effective for short periods
• Currently testing vaccines on genetically altered mice
73. • Acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine,
and tacrine) and the N‐methyl‐d‐aspartate (NMDA) antagonist
memantine.
• Cholinesterase inhibitors have been found to improve cognitive
functioning for up to a year, followed by decline along a parallel path.
Approved for all disease stages.
74. • • Stopping treatment tends to put patients back on their original path
of decline.
• Memantine: approved for moderate to severe AD only. results in a
modest improvement in
functional measures. May be an additive effect of memantine and a
cholinesterase inhibitor.
• rivastigmine has an additional indication for dementia of
Parkinson’s disease
75. Psychosocial Treatment of
Neurocognitive Disorders
• Aims of psychosocial treatments
• Enhance lives of patients and their families
• Teach compensatory skills
• Use memory enhancement devices, if needed
• Example: “Memory wallets” containing statements about one’s life
• Cognitive stimulation can delay onset of more severe symptoms
76. Psychosocial Treatment of
Neurocognitive Disorders
• Caregivers get instructions on how to handle problematic behavior,
including
• Wandering
• Socially inappropriate behavior
• Aggressive or rebellious behavior
• Caregivers also under great deal of stress, may need their mental
health treatment
77. Major or Minor Neurocognitive Disorder Due to
Another Medical Condition (Amnestic
Disorders)
• The amnestic disorders ae coded in the DSM-5 as "major or
minor neurocognitive disorders due to another medical condition.
• All of these disorders cause impairment in memory as the major
sign ad symptom
78. Amnestic disorders (ICD-10)
• Clinical picture
• Memory impairment in the absence of other
cognitive impairments.
• Characterised by:
• inability to learn new information (anterograde
amnesia) or
• inability to recall knowledge stored from before
onset of disorder (retrograde amnesia)
• Short-term and recent memory are affected.
• Onset can be sudden or gradual.
79. • Classified according to aetiology
• Amnestic Disorder Due to a General Medical Condition
• Substance-Induced Persisting Amnestic Disorder
• Amnestic Disorder Not Otherwise Specified
80. Amnestic disorders, cont.
• Aetiology
• Main brain areas implicated in amnestic disorders:
• temporal lobes
• midline nuclei of the thalamus
• Hippocampus
• mamillary bodies
• amygdala (left more implicated than right).
• Frontal lobe symptoms include confabulation and
apathy.
81. Amnestic disorders, cont.
• Aetiology, cont.
• Possible causes of amnestic disorders:
• systemic conditions (such as thiamine or Vitamin B1
deficiency) (e.g. Korsakoff’s syndrome)
• hypoglycaemia (low blood sugar)
• brain-related conditions like hypoxia (low oxygen)
• seizures and epilepsies
• surgical procedures to the brain/head injury
• infections (e.g. herpes simplex encephalitis)
• tumours
• cerebro-vascular diseases
• substance-related conditions (e.g. alcohol,
neurotoxins, sedatives, and over-the-counter-drugs)
• multiple sclerosis
82. Amnestic disorders, cont.
• Treatment and management
• Primary approach = treat underlying cause:
• If underlying cause is primary, systemic or cerebral,
can use thiamine, antiretroviral medication, or aspirin.
• Despite variety of pharmaco-therapeutic trials, no
drug treatments have proved effective in amnestic
disorders.
• Rehabilitation for mild cases of amnesia involves
memory techniques and tools.
• Emotional and social support for difficulties in
occupational and social functioning.
• Many people gradually recover; psychotherapy,
counselling help individual adjust to illness and
recovery.
Editor's Notes
Technology Tip: Alzheimer's Association. The Alzheimer's Association web site contains information on local chapters, coping strategies for caregivers, and scientific progress towards effective treatment and understanding of this disorder. http://www.alz.org/
This shows the PET scan of a brain afflicted with Alzheimer’s disease (left) compared to a normal brain (right).
Technology Tip: More information on Pick’s disease can be found here: www.ninds.nih.gov/disorders/picks/picks.htm
Technology Tip: For more information on traumatic brain injury, visit the following sites: www.cdc.gov/ncipc/tbi/TBI.htm
Round eosinophilic intra-cytoplasmic inclusion bodies
Specific stains can be used to detect the deranged protein, alpha synuclein
Can be found in brainstem areas as well as cortical areas and hippocampus
Amyloid plaques similar to AZD can also be seen, but are not as numerous and AZD hallmark of neuro-fibrillary tangles are rare or non-existent
Here are the remarkable symptoms and let’s take a closer look at a few of them.
Difficulty appears when there is a step approach to tasks, e.g. making a shopping list, going to the store, finding the items and checking out, then following a recipe. Visuospatial tasks are those that require eye-hand coordination such as copying a drawing or tracing a path with your finger
Wake-sleep cycles are abnormal
Can do a task one day and not the next
Combined with visuospatial dysfunction, this problem can make it hard to feed oneself. Can’t button buttons. Patient appears lethargic and slowed down. Extreme fall risk.
Technology Tip: For more information on Parkinson’s disease visit the following site: www.mayoclinic.com/health/parkinsons-disease/DS00295
Technology Tip: For more information on AIDS dementia, visit the following sites: http://www.ninds.nih.gov/disorders/aids/aids.htm
http://www.emedicinehealth.com/dementia_due_to_hiv_infection/article_em.htm
Teaching tip: Reminder: HAART = highly active antiretroviral therapies
Technology Tip: For more information on Huntington’s Disease, visit the following sites: www.ninds.nih.gov/disorders/huntington/huntington.htm, www.nlm.nih.gov/medlineplus/huntingtonsdisease.html
Technology Tip: For more information on Creutzfeldt-Jakob Disease, visit the following sites: www.mayoclinic.com/health/creutzfeldt-jakob-disease/DS00531