Neurocignitive Disorders. 1 Flashcards

1
Q

What are neurocognotive disorders?

A

Disorders in which the core feature is acquired dysfunction in a cognitive domain that occurs after “early life”

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2
Q

What are the domains of cognition?

A

Memory

Language

Executive function

Visuospatial functioning

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3
Q

What are the common neurocognitive conditions ?

A
  • delirium
  • amnesia
  • aphasia
  • dementia
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4
Q

What is delirium?

A
  1. A disturbance in awareness and attention:
    Awareness is usually assessed by one’s alertness/orientation to the environment

Attention (one’s ability to direct, focus, sustain, and shift attention) can be assessed qualitatively and/or quantitatively.

  1. An additional disturbance in a cognitive domain (e.g., memory, language thoughts/delusion, perceptual (including hallucinations ))
  2. The sudden onset of symptoms (over hrs to a few days) that typically fluctuate during the day
  3. Evidence for a direct physiological cause (I.e., a medical condition, substance intoxication or withdrawal)
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5
Q

What are the diagnostic criteria for delirium?

A

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)

D. The disturbances in criteria A or criteria C are not 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

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6
Q

What is the pathology of delirium?

A

Numerous medical conditions and drugs can induce a delirium

Delirium’s are often seen in an ICU

In order for a delirium to be induced, primitive brain structures (the brain stem) are affected

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7
Q

Describe the risk factors and course of delirium

A

Risk factors:
Non-modifiable: e.g. poor health, older age, male gender

Modifiable: e.g. immobilization, sleep disturbance, ICU setting

Symptoms persist until causal factors are treated

Resolution typically occurs within 3-7 days

Amnesia for events during delirium is common

Delirium is a poor prognostic sign for long-term survival and associated with longer ICU stays

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8
Q

How can delirium be treated?

A
  1. Treat underlying medical condition
  2. Use medications (antipsychotics) for associated symptoms (insomnia, psychosis, agitation)

Note: benzodiazepines are a risk factor for a delirium, so they are used only to treat a delirium causes specifically by alcohol withdrawal)

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9
Q

How can we use environmental support measures to treat delirium?

A

Balanced stimulation(not under or over)

Provide orienting stimuli (e.g. lighting, personal effects, sensory perception aids)

Provides for safety needs (e.g. presence of an attendant, bedrails, and possibly restraints)

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10
Q

What is a dementia?

A

Refers to multiple and severe cognitive impairment without impaired consciousness

Is usually progressive and irreversible

Is most common in the elderly (>5% incidence 65 and higher with rate doubling every five years)

Note: if problems don’t result in impairment in activities of daily living, then the disorder is refferred to as “Mild Cognitive impairment”—MCI (not a DSM term)

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11
Q

What does Ahlzeimer’s dementia involve?

A

Significant memory impairment plus impairment in at least 1 other cognitive domain

A gradual onset with steadily progressive gradual decline

Exclusion of other causes of the symptoms (e.g. stroke)

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12
Q

Give the epidemiology of Ahlzeimers dementia

A

Most common dementia with onset typically 65 and higher

No notable gender bias

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13
Q

Give the general course of Ahlzeimer’s dementia (+10 years)

A

Early stage: memory deficits (rapid forgetting) and word-finding problems

Middle stage: further decline in memory and language, visuospatial deficits, agnosias [inability to identify/comprehend meaning of stimuli ], mood changes, personality changes and psychosis

End stage: global cognitive impairment, motor deficits, death from opportunistic infections

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14
Q

Describe symptoms of Mild Ahlzeimer’s disease early stage

A

person may function independently, may have memory lapses

Friends and family begin to notice difficulties

Problems coming up with the right word or crime

Trouble remembering names names when introduced to new people

Challenges performing tasks in social or work settings

Forgetting material that one has just read

Losing or misplacing s valuable object

Increasing trouble with planning or organizing

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15
Q

Give the symptoms of Moderate Ahlzeimer’s disease (middle stage)

A
  • forgetfulness of events or about one’s own personal history
  • feeling moody or withdrawn, especially in socially or mentally challenging situations
  • being unable to recall their own address or telephone number or the high school or college from which they graduated
  • confusion about where they are or what day it is
  • the need for help choosing proper clothing for the season or the occasion
  • trouble controlling bladder and bowels in some individuals
  • Changes in sleep patterns, such as sleeping during the day and becoming restless at night
  • An increased risk of wandering and becoming lost
  • Personality and behavioral changes, including suspiciousness and delusions or compulsive, repetitive behavior like hand-winging or tissue shredding
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16
Q

Give a description (not symptoms ) moderate Ahlzeimer’s/middle stage

A

A person may have greater difficulty performing tasks, such as paying bills, but they may still remember significant details about their life

May notice person with Ahlzeimer’s confusing words, getting frustrated or angry, or acting in unexpected ways, such as refusing to bathe. Damage to nerve cells in the brain can make it difficult to express thoughts and perform routine tasks

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17
Q

What are the symptoms of severe Ahlzeimer’s disease(late stage)?

A

Individuals may:

  • need round the clock assistance with daily activities and personal care
  • lose awareness of recent experiences as well as of their surroundings
  • experience changes in physical abilities, including the ability to walk, sit and, eventually, swallow
  • have increasing difficulty communicating
  • become vulnerable to infections, especially pneumonia
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18
Q

Give a raw description (not symptoms) severe Ahlzeimer’s disease

A

Individuals lose the ability to respond to their environment, to carry on a conversation and, eventually, to control movement. They may still say words or phrases, but communicating pain becomes difficult. As memory and cognitive skills continue to worsen, significant personality changes may take place and individuals need extensive help with daily activities

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19
Q

Explain the neuroanatomical pathology of AD

A
  • Hippocampal atrophy
  • Enlarged ventricles
  • cortical atrophy
20
Q

Explain the neurochemical pathology of AD

A

Acetylcholine(ACH) is decreased. This neurotransmitter is important fir memory formation

Other neurotransmitters, such as glutamate are also affected

21
Q

Explain the neurofunctional pathology of AD

A

Reduced metabolism in posterior parts of brain (parietal and temporal lobes)

22
Q

Explain the histopathological pathology of AD

A

B-amyyloid plaques and neurofibrillary tangles

Detection of amyloid in brain by :

CSF samples
PET imaging

A definitive diagnosis of AD is only made through post-Mortem analysis of brain tissue

23
Q

Explain the genetics of early onset AD

A

Onset less than 65

Usually in 50s but as early as in 30s, only 10% of all AD cases

Possibly more rapid progression of symptoms

There is a strong genetic component to early-onset AD:

3 AD genes have been identified (located on chromosomes 1, 14 and 21)

If 1 copy of the gene is inherited, then the person will develop early-onset AD

24
Q

What are the genetics of late onset AD?

A

Onset at 65 and above

90% of AD cases

Genes have been identified as RISK FACTORS for late-onset AD but do not guarantee the disorder

Example
Apolipoprotein E (APOE) gene

Chromosome 19
1 or 2 copies of APOE e4 is associated with increased chance of developing late onset AD

An APOE test is available

25
Q

What are the main treatment of AD?

A

Drugs that increase acetylcholine (cholinesterase inhibitors) :

  • donepezil(Aricept)
  • galantamine (Razadyne)
  • rivastigmine(Exelon)

Have similar side effects (GI, hypertension)

Drugs that decrease glutamate. (NMDA-receptor blockers):
-memantine (Namenda)

Overall, AD drugs have been disappointing.
A cost-benefit analysis should be considered before Rx

26
Q

What are other interventions for AD?

A

Pharmological

For non-memory symptoms (anxiety, sleep)

Neuroleptic are inappropriately prescribed to manage these symptoms. Now there is a FDA black box warning against this off label use (increased mortality risk)

Psychosocial

External mnemonics in early stages
Safe return program for wanderers
Family support to prevent “Careguver Syndrome”

27
Q

What therapies of AD are under investigation?

A
  • Anti-amyloid drugs
  • Ginkgo biloba
  • Antioxidants
  • estrogen replacement drugs
  • nonsteroidal antigen-inflammatory drugs
  • statins
  • gene therapy
  • shunt therapy

These are not FDA approved and have shown either negative or mixed results

28
Q

Explain the differential diagnosis of AD

A

Multiple causes of dementia must be ruled out:

Vascular (clue: patient has symptoms of vascular disease plus a stepwise progression of dementia symptoms)

Frontotemporal(Pick’s)( clue: frontal signs predominate early on, such as disinhibition and personality change)

Parkinson’s (clue: patient has a dementia that starts after over 12 month of motor symptoms (rigidity, shuffling, and tremors and then develops dementia)

Huntington’s (Clue: patient has a motor disorder with characteristics choreiform and athetoid movements and often psychiatric disturbance)

Prion disease (e.g., Creutzfeldt-Jacob ) (Clue: dementia progresses rapidly over a few months with death under a year)

Consider dementia’s due to tumors, infection, etc. that may be reversible

29
Q

Explain lewy body dementia as a differential diagnosis of AD

A

Lewy body dementia

Clue: in addition to dementia, patient has:

  • fluctuating cognition
  • visual hallucinations
  • mild Parkinsonism (but usually not a tumor)

If dementia develops within 12 months of Parkinson’s an signs, then diagnose LBD (not Parkinson’s dementia)

  • Severe neuroleptic sensitivity (don’t prescribe)
  • drugs used for Parkinsonism usually don’t help motor symptoms and often worsen psychotic symptoms
30
Q

Are amnesia and dementia DSM 5 diagnoses?

A

No longer DSM 5 diagnoses

31
Q

What are the DSM 5 neurocognitive disorders ?

A
  1. Delirium
  2. Major neurocognitive disorder
  3. Mild neurocognitive disorder
32
Q

What is major neurocognitive disorder?

A

Significant decline in one or more cognitive domain:

Deficits interfere with independence in daily activities.

33
Q

What is mild neurocognitive disorders?

A

“Modest” declije in one or more cognitive domain:

Deficits do NOT interfere with the capacity for independence in daily activities

34
Q

What are the Major and mild NCD subtypes?

A

NCD Etiological subtypes
-Ahlzeimer’s

  • frontotemporal lobar degradation
  • Lewy body disease
  • traumatic brain injury
  • substance/medication use
  • HIV infection
  • another medical infection
  • vascular disease
  • prion disease
  • Huntington disease
  • Parkinson’s disease
  • multiple etiologies
  • unspecified etiology
35
Q

Based on DSM 5 definition of NCD, both amnesties patients and demented ….

A

Would get the same DSM 5 diagnosis -“NCD”. (“Major” or “Mild” depending on functional disability

On exams, the terms “dementia” and “amnesia” will be used and answer choices - students should be able to differentiate these conditions

36
Q

Describe the development of language in children across the years

A
  • 5-7 month= language -like sounds
  • 7-8 month = well-formed syllables
  • 1-2 years: first word ‘mama’, understand connection between word ‘mama’ and visual /acoustic appearance
  • 2 years: speaking in rich phrase (children language)
  • 3 years: most of the time correct use of words and grammar, they understand the rules of grammar
37
Q

How does language develop in children?

A
  • language develops spontaneously in children
  • capacity to learn language is innate
  • Ability to learn language comes from adaptations of the human brain that arose in the course of human evolution
38
Q

What is the function of the left hemisphere when it comes to language?

A

Dominant(96%)

  • language processing
  • lexicon (dictionary)
  • phonetic assembly
  • phonetic procession
39
Q

What is the role of right hemisphere ?

A
  1. Communicative and emotional prosody (stress, timing, intonation)
    • right anterior damage: wrong intonation
    • right posterior damage: difficulty in interpretation
  2. Pragmatic of language
    • damage of right hemisphere: difficulty in construction of sentences into a story
    • difficulty in understanding jokes, sarcasm
40
Q

Describe the Wernicke-Gschwind model of language

A
  • Broca’s and Wernicke’s areas are processing images of words and articulation of speech
  • The arcuate fasciculus is a unidirectional pathway from Wernicke’s to Broca’s area
  • Wernicke’s and Broca’s area interact with association ears
41
Q

What is Lewy body dementia?

A

Patient have dementia

And fluctuating cognition

Visual hallucinations

Mild Parkinsonism

If dementia develops within 12 months of Parkinson’s sings, then diagnose LBD (not Parkinson’s dementia

Severe neuroleptic sensitivity (don’t prescribe)(severe extrapyrimidal symptoms develop)

Drugs used for Parkinsonism usually don’t help motor symptoms and often worsen psychotic symptoms

42
Q

Explain Huntington as a differential of AD

A

Patient has a motor disorder with characteristic chloreiform and athetoid movements and often psychiatric disturbance

43
Q

Explain prion as a differential diagnosis of AD

A

Prisons disease (creutzfeldt-Jakob) dementia progresses rapidly over a few months with death under a year

44
Q

Explain frontotemporal dementia as a differential of AD

A

Frontal signs predominate early on, such as disinhibition and personality change

45
Q

Explain vascular dementia as a differential of AD

A

Patient has symptoms of vascular disease plus a stepwise progression of dementia symptoms

46
Q

Describe Parkinson’s dementia as a differential of AD

A

Patient has a dementia that starts after over 12 months of motor symptoms (rigidity, shuffling, and tremors and then develops dementia)