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Major Mental Illness > Neurocognitive Disorders > Flashcards

Neurocognitive Disorders Flashcards

1
Q

Neurocognitive disorders arise out of….

A

changes in brain structures, function or chemistry

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2
Q

Mild Neurocognitive Disorder

A

encompasses cognitive problems that are not reaching levels that impair everyday functioning, but still require clinical attention.

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3
Q

Issues with Mild Neurocognitive Disorder

A
  • the DSM 5 dx by definition is meant to be disorders that do not affect functioning, but according to assessment it actually does.
  • individuals with this dx are suppose to be likely for ALZ, but many dont go onto to develop this
    - some people may be worried that they are going to develop it. are we purposefully scaring them>
  • whats the point of this dx if we dont even have a way of treating ALZ?
  • does Mild minimize the actual dx? -especially since it does affect functioning….
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4
Q

Clinical signs of brain damage

A
  • inability to engage in neurogenesis- ability to make new neurons is limited (destruction of neurons means the end)
  • inability to engage in self-appraisal
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5
Q

Mini Mental Status Exams

A
  • a brief quantitative cognitive measure on adults

- is your best bet to figure out whether you need to refer for a neurological

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6
Q

Damage of brain tissues

A
  • is related to the extent of the damage and involve a wide range of outcomes dependent on :
    • nature, location, and extent of neural damage
    • premorbid competence, and personalty of individual
    • individual’s life situation

Additionally….

 - you can have: 
     - limited damage = profound deficits 
     - profound damage = limited deficits
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7
Q

some issues that arise from brain damage

A
  • personality issues
  • attention
  • language
  • EF
  • psychosis
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8
Q

Diffuse versus local damage (brain injuries)

A

Focal brain injury = typically large and identified as “macrosopically” (not needing a microscope)
- visible gash on the skull/bruises = immediate attention!

diffuse injury= are typically microscopic
- go unnoticed and proper tests may not get ordered unless there are other symptoms that raise attention.

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9
Q

Delirium

A

a state of acute brain failure that lies between normal wakefulness & stupor

  • sudden onset and involves fluctuating states of reduced awareness
  • confusion, disturbed concentration, and cognitive dysfunction( attention, memory, thinking)
  • Reversible but may evolve into permanent neurocognitive or other neurological disorder
  • Can specify for its cause: substance intox, withdrawal, medication-induced – especially dangerous when associated with alcohol abuse
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10
Q

Risks of developing Delirium

A
  • age ( both elderly and children are at a higher risk )
  • drug intoxication, or withdrawal
  • head injury or infection
  • individuals with recent cardiac surgery (10-51%)
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11
Q

Continuum Level of Consciousness

A

Alert-wake –> Delirium –> Stupor –> Coma

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12
Q

Delirium as a poor prognosis

A

correlated with:

  • with morbidity (dead within 6 months)
  • with cognitive decline
  • with longer hospital stay
  • comorbid heart problems

** true medical emergency

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13
Q

Treatment for Delirium

A

Medications: Benzos or antipsychotics

tx:
Family Support
behavioral tx to assist in orientation ( where is the kitche? where is the TV?)

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14
Q

Major Neurocognitive Disorder (formerly known as Dementia)

A
  • involved marked deficiencies in cognitive abilities (attention, learning, memory, language, social cognition)
  • loss & decline of previous baseline functioning
  • characterized by a gradual pattern of decline
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15
Q

Criteria for Dementia

A

Memory impairment with at least one of the following:

  • agnosia (difficulties with identifying objects)
  • apraxia ( motor issues)
  • aphasia (language production)
  • Executive functioning
  • Social cognition - difficulty identifying emotions

*symptoms must cause significant impairment in social/occupational functioning and represent a decline form premorbid (previous functioning)

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16
Q

changes between Delirum DSM IV to DSM 5

A
  • “Consciousness” changed to “level of awareness”
  • In addition to memory, orientation, and language deficits, DSM5 adds domains of executive ability and visuospatial impairment
  • “Cognitive Deficits” replaced with “Cognitive Decline,” as the latter emphasizes a previous higher level of functioning
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17
Q

Memory during Dementia

A
  • memory becomes affected and individual presents with the inability to learn new knowledge/ new skills, spatial control, judgment and reasoning, motor control, and judgment/reasoning
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18
Q

Socially inappropriate behaviors in Dementia

A
  • patients may engage in crude jokes (racial ) or engage in sexual inappropriateness
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19
Q

Attention in Dementia

A

unaffected…consciousness stable….usually slow

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20
Q

Causes of Dementia

A
  • Syphillis, AIDS, parkinsons, intercranial tumors, abscess, dietary deficiency, severe and repeated head injury , TBI, lead/mercury exposure
  • most common cause:
    Alzheimers
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21
Q

3 major types of Dementia

A
  1. Alzheimer’s Dementia (cortical dementia )
  2. Lewy Body Dementia
  3. Vascular Dementia

2&3 presented with mixed presentation along with ALZs

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22
Q

Vascular Dementia

A

• Based on a history of small strokes associated with hypertension; or bleeding in the brain
• Stepwise deterioration of function, with each small stroke making it worse
• A lot of overlap with Alzheimer’s
- Vascular pathology in people with Alzheimer’s, and the reverse also true

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23
Q

Lewy Body Dementia

A

2nd - lewy body dementia (23%) (66% also with AD)

  • Associated with visual hallucinations
  • There are no delusions
  • Progressive cognitive decline

Textbook on lewy body dementia:

· Variations in alertness, recurrent hallucinations, and parkinsonian symptoms

· Lewy Bodies are intraneuron inclusion bodies first identified in the substantia nigra of patients with Parkinson’

Lewy bodies are abnormal aggregations (or clumps) of the protein alpha-synuclein. When they develop in a part of the brain called the cortex, dementia can result.

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24
Q

Alzheimer’s Disease

A

1st alzheimer’s disease ( cortical dementia) 70%

-The most common type

Textbook on Alzs:

  • Slow and progressive course terminating in delirium and death
  • Reduction of acetylcholine activity
  • Accumulation of amyloid plaques between neurons in the brain
    - Protein fragments that are naturally produced
  • Average of 3-7 years from diagnosis to death
  • Age is major risk factor
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25
Q

Sundowning

A

the idea that as a day progresses people get worse and worse

Occurs more in ALZ

(although limited evidence)

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26
Q

2nd most common neurodegenerative disease

A

Parkinson’s Disease

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27
Q

Parkinson’s Disease Prevalence

A
  • Affects about 3% over the age of 80
  • affects about 1% of people between 65-69
  • mostly found in men
  • About 75% of individuals go onto show signs of dementia
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28
Q

Parkinsons Disease

A
  • a movement disorder characterized by tremors or rigid movements
  • caused by loss of dopamine neurons

**smokers & coffee drinkers –> less likely to develop parkinsons

29
Q

Treatment of Parkinson’s Disease

A
  • There are no treatments to slow or stop the brain cell damage caused by Parkinson’s disease dementia.
  • Current strategies focus on helping symptoms.
    - Cholinesterase inhibitors
    - Antipsychotics ( but should be used with caution)
30
Q

Huntingtons Disease

A
  • rare GENETIC degenerative disorder of the nervous system due to overproduction of dopamine in the basal ganglia/nigrostriatal
    • genetic mutation on Chromosome 4
    • if your parents have it…you have a 50% chance of getting it
  • Patients usually go onto develop dementia
  • Chronic, progressive chorea (jerky involuntary movements affecting especially the shoulders, hips, and face)
31
Q

Huntington’s Disease Prevalence

A
  • affects men and women equally
  • Begins mid life (age 40)
  • death occurs about 10-20 years after the first symptoms appear
32
Q

Alzheimer’s is more than just a memory impairment….

A

it involves multiple cognitive components

  • Disorientation
  • Poor judgment
  • neglect of personal hygiene
  • psychosis (although not everybody gets psychosis)
33
Q

How can you differentiate between psychosis and ALZ induced psychosis?

A
  • important to consider when the disease began
  • SCZ psychosis is very bizarre (aliens are in my belly)
  • ALZ psychosis is more paranoid & jealous (some body is taking money out of my bank account! / my husband is cheating on me ! )
34
Q

Alois Alzheimer

A

found that an unusual disease of the cerebral cortex affected a woman in her 50’s

  • he coined the term i assume?
35
Q

Course of ALZ

A
  • the course takes months and years…
  • eventually they become less connected to the environment and are reduced to a vegetative state
  • upon dx of ALZ, people live about 3-7 years
36
Q

Assessments to use in ALZ

A

**never brought either of these into class

CRAT Battery

Dementia Battery

37
Q

inheriting APOE-4 allele

A
  • from both parents –> significantly increases risk of late onset of ALZ
  • even if ALZ is not developed, you may have many memory impairments
  • approx. 55% of people develop ALZ with two copies
  • approx 65% of people with one copy

**35% have no APOE gene and still get ALZ

38
Q

APOE-2 Allele

A

is a protective allele to the late onset of ALZ

*APOE-3 is a neutral allele and doesnt decrease or increase chances of ALZ

39
Q

Early onset of ALZ

A
  • due to Amyloid Precursor Protein Gene ( APP)
    - Located on chromosome 21 (same as down syndrome)
    - Mothers of children with DS had a 4.8% risk of developing alzheimer’s when they were compared with mother of children with other mental retardation
    - APP is associated with earlier type of onset of ALZ (40-60 )
  • due to Ps1 and Ps2 genetic mutations
40
Q

Other factors that may influence influence onset of ALZ (4)

A
  • lack of exercise
  • diabetes (insulin levels are low in brain areas affected by ALZ)
  • obesity
  • exposure to metals (lead/ aluminum )
41
Q

Risk factors of developing ALZ

A
  • age ( your brain starts to shrink at 18 )
    • after 80 years old = 50% of getting ALZ
  • females are more likely to get ALZ
  • loneliness study
    - those who were lonely has 2xs the risk of getting ALZ
  • being a smoker
  • less yrs of education/ less income
  • head trauma
  • pass episodes of depression
    - depression + genetic predisposition = 7xs mo. likely
42
Q

Impact of ALZ

A

4.5 million have AD by 2000

will go as high as 13.5 million by 2050

3rd most expensive disease to treat next to cardiovascular disease & cancer

43
Q

Clinical course and behavioral presentation for ALZ: MILD

A

faltering recent memory
navigational disturbance
naming and speech ( language disturbance)
remote memory usually intact (temporal lobe is affected)
Insight–good to fair

44
Q

Clinical course and behavioral presentation for ALZ: MODERATE

A

more rapid short term memory loss
frontal lobe signs
Trdisorders of visuospatial orientation calculation, comprehension
judgment
insight becomes poor
may display significant emotional lability.

45
Q

Clinical course and behavioral presentation for ALZ: SEVERE

A 
more rapid decline of memory
usually disoriented to time and place
more bxial and mood issues
 poor hygiene, and grooming
 few (activities of daily living) ADL’s intact
cannot make decisions
needs assistance
46
Q

Mechanisms of Alz’s Disease ( how does it start?)

A
  • The disease process usually starts in the mesial temporal area of the brain spreading eventually to the rest of the cerebral cortex (prefrontal/parietal/occipital) , relatively sparing the motor strip until late stage
  • Amyloid plaques
    - accumulation of amyloid plaques between nerve cells neurons in the brain –> protein fragments that the body produces normally → it is a sticky substance that divided. And when it divides improperly it creates Beta Amyloyd (which is toxic to the brain)

Accumulation of beta amyloid causes neuronal death.
Some people say its the cause..others say its the consequence…nobody knows.

  • Neurofibrillary tangles
    - consist of twisted fibers inside the brain cells.
    - consist of Tau which forms a microtube that transports nutrients in cell
    - the tau proteins harden = the microtube collapses and interfers with numerous intercellular functions
  • reduction in ACH in ALZ –> neural damage
47
Q

Treatment of ALZ

A
  • Drug treatments include cholinesterase inhibitors :
    - Aricept –> increases ACH & slows down cognitive decline
    - Memantine–> blocks NMDA (glutamate)

**both drugs together = good cognitive effects

  • behavioral treatments (skinnerian)

**atypical antipsychotic medication would increase these issues, a low dosage of antipsychotic is OK

48
Q

ALZ behavior

A
  • they wonder off
  • sexually promiscuous
  • psychosis & agitation
49
Q

Overall… when it comes to ALZ, early detection is KEY !….but how do we predict it?

A
  • we can often detect the size of the hippocampal to predict neurocognitive deficits
  • even though some individuals with APOE-4 alleles dont go onto develop ALZ they tend to work harder on memory tasks compared to controls
  • difficult to detect neurocognitive deficits because brain scans are not diagnostic
50
Q

Neuropsychological profiling considerations in ALZ

A
  • thorough clinical interview with trusted individuals (family, friends) to assess premorbid function
  • assessments to determine type and level of dementia impairment
  • screening battery should have –> memory tests, complex constructions, naming tacks, word fluency, digit span, copying shapes, word list memory
  • CRAT & dementia battery
51
Q

Anstey, Mack, & Cherbuin (2009) Alcohol consumption as a risk factor for dementia and cognitive decline: meta-analysis of prospective studies

A
  • Meta-analysis of alcohol consumption as a risk factor for dementia and cognitive decline
    o Included people with Alzheimer’s Dementia, Vascular Dementia, or Any Dementia
  • Heavy drinkers did not have an increased risk of any dementia compared with nondrinkers
    o This may reflect a sampling bias – very heavy drinkers may be less likely to participate or to achieve follow-up
    o Samples used were old – so heavy drinkers may have been screened out due to cognitive impairment
  • Light to moderate intake of alcohol associated with reduction in risk of AD, VaD, and Any Dementia, compared with alcohol abstinence
  • Unclear if results show a protective effect of alcohol consumption throughout adulthood or if there is a specific benefit to alcohol in late life
52
Q

Weintraub et al. (2009). The Alzheimer’s Disease Centers’ Uniform Data Set (UDS): The neuropsychologic test battery

A
  • The Neuropsychological Test Battery from the Uniform Data Set, includes brief measures of:
    o Dementia Severity (Mini Mental Status Examination (MMSE)
    o Attention (digit span F & B)
    o processing speed (Digit symbol, Part A of Trail Making Test)
    o executive functions (Part B of Trail Making Test)
    o episodic memory (Logical memory Story A w/ immediate & delayed recall)
    o language
    • Fluency (animal & vegetable list)
    • Naming (Boston Naming Test)
  • Sample based on date gathered by the Clinical Dementia Rating Scale and the Functional Assessment Questionnaire
  • UDS gathers data annually on 918 variables
  • Decline in episodic memory considered a hallmark of early AD
53
Q

HIV- 1 infection (HIV Dementia)

A
  • HIV penetrates the CNS
  • Individuals with HIV are prone to rare infections (parasites)
  • They can have a NC disorder due to infection and HIV can INDIRECTLY cause a neurocognitive disorder
54
Q

HIV Dementia Features

A
  • involves brain changes (atrophy) , swelling of the brain
  • Features include:
    • dementia within a year at times
    • apathy
    • withdrawal
    • psychosis
55
Q

in HIV, prevention is important (if you can afford it)

A
  • medication has prolonged lives
  • medication reduces neurocognitive disorder, but individuals can still show mild deficits
  • claims up to 20 million deaths
56
Q

Vascular Dementia Profile

A
  • mimics ALZ
  • sometimes accompanied by a mood disorder

Clinically, it is more optimistic than ALZ because decrease elasticity can be managed.

you can decrease risk of future risk via medical management ( i assume bc its mostly due to strokes/bleeding in the brain)

57
Q

Vascular Dementia Prevalence

A
  • occurs after age 50

- affects more men than woman

58
Q

Traumatic Brain Injury (TBI) - most common types

A
  • MVA
  • sport injuries
  • veterans have also been exposed, but muddied by PTSD
59
Q

Sustained injuries in TBI …

A
  • are not always going to have full recoveries
  • close head injury- brain damage is indirect bc inertia forces cause the brain to come into contact with the interior of the skull ( coupe contecoupe –> the soft tissue inside is still moving )
  • Brain sheering – being twisted relative to brain stem
60
Q

Head injury outcomes

A
  • unconsciousness - how long is a good indicator of the damage.
      - Retrograde amnesia→ inability to consolidate long term storage ( lost memory from before the event) 
   - Anterograde amnia→ post tx amnesia inability to store memories that occured during and after the trauma
  • personality changes ( think Phineas Cage)
    • impulsivity changes…crude…
61
Q

Residual damages after a MILD TBI

A

Concussions…contrusions… G force ( acceleration by gravity that you feel on a roller coaster)

- creating small tears in delicate areas 
- repeated concussions --> looks like ALZ 
- cognitive functioning tends to deteriorate even after a concussion
62
Q

Post concussive syndrome

A

a complex disorder in which symptoms like headaches and dizziness last for weeks and sometimes months after the injury.

66% of NFL (ted johnson) experience 1 concussion in their career

those with +3 were 5xs more likely to be diagnosed with mild cognitive problem
- also more likely to dx with depression

63
Q

TBI - treatment

A
  • long term rehabilitation : requires assessment and provides goals to compensate and deal with issues impaired
  • Medication - drugs that improve memory
    • Aricept (same as ALZ)
64
Q

TBI Outcomes

A
  • chronic headache, dizziness, impaired concentration, anxiety
  • occupational impairment –> loss of adult life
  • 22% develop epilepsy due to scar tissue (seizures within 2 yrs of injury)
65
Q

decades after TBI

A

sucidality

personality changes

depression

global IQ drop

66
Q

TBI in children

A

children with TBI are more aversely affected …

–especially if they have not developed motor/language skills (low baseline to begin with )

  • if TBI is mild –> emerge without long lasting effects
67
Q

b12 vitamin

A

correlated with lower brain atrophy ( maybe good to know for TBI?)

68
Q

Variables associated with favorable outcomes of TBI

A
  • short/brief periods of unconsciousness
  • minimal cognitive impairment
  • prior mental illness/impairment = worse outcome
  • high intellectual abilities prior to TBI
  • Motivation to recovery = good to learn compensatory mechanism
  • better social support/ better life = good
  • early learning = good

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