WEEK 12 Flashcards

Neurodevelopment and Neurocognitive Disorders

1
Q

Typical childhood development

A
  • Significant brain changes occur in early years
  • critical development in all areas
  • follows a sequential pattern
  • Disruption in early development may disrupt
    later development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Attention-Deficit/Hyperactivity Disorder

- definition

A
A persistent pattern of:
- inattention OR 
- hyperactivity and impulsivity  
OR 
- both (combined subtype)
  • Substantial clinical presentation less than 12 yrs.
  • symptoms must occur across settings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ADHD across the lifespan

A
  • can be identified 3- 4
  • adolescents: impulsivity manifests in different areas ( eg. car accidents, teen pregnancy)
  • Adulthood: approx. 50% have ongoing difficulties- need to be busy
  • inattention, hyperactivity and impulsivity may result in other difficulties (poor academic performance, relationships etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ADHD diagnostic issues

A
  • debate: are some children being misdiagnosed? Over diagnosis?
  • valid data suggests 5-7% of children meet criteria for ADHD

Gener differences:

  • boys 3 x more likely
  • reason for gender difference is largely unknown (differences in presentation?)
  • focus of research on boys- DSM 5 criteria not applicable to girls??
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ADHD Causes

Biological

A
  • genetic influence- multiple genes are responsible
  • Mutations occur which create extra copies on one chromosome or deletion of
    genes = copy number variants (CNVs). Research has focused on gene associated
    with dopamine (GABA, norepinephrine and serotonin also involved).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ADHD Causes

Gene- environment interaction

A
  • environmental factors play a small role (eg. mother smoked during pregnancy- mutation involving dopamine- exhibit symptoms of ADHD)
  • eg. maternal stress, parental marital instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ADHD Causes

Psychologica/ social influences

A
  • Negative response from parents, teachers and peers= contribute to low self esteem and negative self image
  • impact on friendships (rejection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ADHD

Psychosocial treatment

A
  • target broader issues
    (i.e., academic performance, decrease disruptive
    behaviour, improve social skills)
  • Increase positive behaviours

Reinforcement programs:

  • parent education
  • social skills programs
  • ADULTS: CBT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ADHD

Biological treatment

A

Stimulant medication

  • reduction in core symptoms (hyperactivity and inattention)
  • reinforce the brains ability to focus attention during problem solving tasks
  • non stimulant drugs can be effective
  • recommended temporarily with psychosocial intervention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Specific Learning Disorder

A

Performance that is substantially below what would be expected given the person’s: age, IQ and education

  • impairment in reading
  • impairment in expression (writing)
  • impairment in maths
  • 5-15 % of youth

Long term impact:

  • drop out of school
  • unemployment
  • suicidal thoughts and attempts

DSM- 5
- disabilities are now combined to assist clinician take a broader view
diagnostic issue: IQ discrepancy vs response to intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Specific Learning Disorder
Causes

Genetic and Environmental

A
  • twin and family studies suggest learning disorder run in FAMILY
  • Genes affect learning in general rather than specific area
  • SES
  • cultural expectations
  • parental interactions and expectations
  • types of school support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Specific Learning Disorder
Causes

Neurological Causes

A

Structural & functional
differences found in brains of people with SLD using
brain imaging.

Reading:
- Specific areas of the left hemisphere –
involved with word recognition (dyslexia).

Maths disorders: Intraparietal sulcas (left hemisphere)
– critical for development of sense of numbers.

Written expression: No current evidence for specific
brain differences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Specific Learning Disorder
Causes

Treatment approach

A
  • education interventions (specific skill instruction eg. find main idea, facts) (strategy instruction eg. decision making, critical thinking)
  • direct instructions (highly scripted lesson plans, teaching for mastery, progress continually assessed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Autism Spectrum Disorder

Core features in the DSM- 5

A

Two core features:

  1. impairment in social communication and interaction
  2. restricted and repetitive patterns of behaviour, interests or activities
    - Impairments are present in early childhood and limit daily function
  • Level of severity:
    1: requiring support
    2: requiring substantial support
    3: requiring very substantial support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Autism Spectrum Disorder

DSM- 5 criteria

A

SOCIAL COMMUNICATION: (Must meet all 3 criteria for DSM-5 diagnosis)

  • Deficits in social-emotional reciprocity (e.g., atypical social
    approach, difficulty with back & forth conversation)
  • Deficits in non-verbal communicative behaviours used for social interaction (e.g., poor integrated verbal/non-verbal
    behaviors) .
  • Deficits in developing, maintaining and understanding
    relationships (e.g., difficulty with imaginative play, making friendships)

RESTRICTED INTERESTS
(evidence of at least 2 out of the following)

  • Stereotyped or repetitive motor movements, use of objects or speech
  • insistence of sameness, inflexible adherence to routines or ritualised patterns of verbal and non verbal behaviour
  • highly restricted, fixated interests that are abnormal in intensity or focus
  • Hyper or hyporeactivity to sensory input
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Autism Spectrum Disorder

Stats

A
  • 1 in 59 school aged children
  • male: female: 4: 1
  • co- morbidities are common
  • range of IQ scores (approx. 31% have intellectual disability)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Autism Spectrum Disorder

Genetic influence

A
  • highly complex genetic component
  • families with 1 autistic child- 20% chance of having another child
  • older parents age may be associated with autism

Neurobiological influences:

  • possible role of amygdala
  • possible role of oxytocin: role in how we bond with others and social memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Autism Spectrum Disorder

Intervention approaches

A
  • most focus on teach new adaptive skills and reducing problem behaviours to make functional progress
  • behaviour intervention programs
  • allied health supports
  • social skills groups
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Intellectual Disability

characteristics

A
  • significantly below average intellectual and adaptive functioning
  • difficulties with day to day activities
  • individuals display broad range of abilities and personalities
  • impairments in range of areas (eg. language, social skills, reasoning)
20
Q

Intellectual Disability

DSM- 5

A

IQ cut off no longer specific

3 Domains:

  • Conceptual (eg. poor language, reasoning and memory)
  • Social (eg. problems with social judgement)
  • Practical (eg. personal care, job responsibilities)

age of onset: below 18 yrs
1-3% of general population
90% fall within mild ID range (IQ: 50-70)
course is chronic

21
Q

Intellectual Disability

Causes

  • environmental
  • prenatal
  • perinatal
  • postnatal
A

Environmental: e.g., deprivation, abuse, neglect

Prenatal: e.g., exposure to disease/drugs in womb

Perinatal: e.g., labour difficulties and delivery

Postnatal: e.g., Infections, head injury

22
Q

Intellectual Disability

Genetic Influences

A

Chromosomal disorders, single-gene disorders,
mitochondrial disorders, multiple genetic mutations

  • Some cases of ID have no identified etiology

Chromosomal Conditions:
- Chromosomal abnormalities can lead to ID (e.g., Down Syndrome or Fragile x)

23
Q

Intellectual Disability

Treatment Approaches

A
  • No biological treatment available
  • Behavioural interventions/strategies + other supports
  • Build skills for quality of life, independence.
24
Q

Neuro-cognitive Disorders

characteristics

A

DSM 5: new category for
forms of dementia and amnestic disorders - with major and mild subtypes

Prominent feature is impairment of cognitive abilities

may also involve other psychological aspects (eg. mood)

25
Q

Delirium

Characteristics

A

Delirium: temporary state of confusion and disorientation

Presentation: confused, disorientated, cannot focus or sustain attention, impaired memory and language

May develop over hours or days and can vary throughout day. Subsides quickly.

  • Most common amongst older adults, people undergoing
    medical procedures, cancer or AIDS patients.
  • May result in longer lasting effects than once thought
26
Q

Delirium

Causes

A
  • Intoxication by drugs
  • Withdrawal from alcohol and sedatives
  • Infections
  • Head injury or brain trauma
  • Improper use of prescribed medication
  • Children: high fevers, certain medications
  • Sleep deprivation or excessive stress
  • Often occurs during the course of Dementia
27
Q

Delirium Treatment

A
  • assess underlying causes
  • antipsychotic drugs when cause is unknown

Psychosocial Management: managing agitation and anxiety; increase familiar personal belonging and family support; including patient in treatment decisions

Prevention: appropriate medical care for illness and medication for monitoring

28
Q

Major Neurocognitive Disorder (previously dementia)

A

Gradual deterioration of brain function which impacts memory, judgment,
language and other cognitive processes

29
Q

Mild Neurocognitive Disorder

new to DSM- 5

A

Focuses on early stages of cognitive decline. Some impaired cognitive
ability, but can function independently with accommodations

Eg.

  • alzheimer’s disease
  • Parkinson’s disease
  • Huntington disease
30
Q

Alzheimer’s Disease

Definition

A

Impairment of: memory, orientation, judgment and reasoning (develops steadily and gradually).

Examples: forgetting important events, losing objects, decreased interest in others/activities, social isolation.

May become
agitated, confused, depressed, anxious.

  • Aphasia: Difficulty with language
  • Apraxia: Impaired motor functioning
  • Agnosia: Failure to recognise objects
  • Difficulty with planning, organisation and sequencing
31
Q

Alzheimer’s disease

Prevalence

A
  • around 50% of neurocognitive disorders are the result of Alzheimer’s
  • Slower decline in early and end stage, rapid in middle stages
  • early onset: 40-50, usually presents: 60- 70

Average survival time is 4- 8 years

Buffer period: people with a high level of education decline more rapidly once symptoms start BUT intellectual achievement may be associated with the delay of onset
–> ‘Cognitive reserve hypothesis’ - increased synapses = more neuronal death required before dementia is obvious.

32
Q

Alzheimer’s disease

Measures

  • Mental State exam
  • ADNI
A
  • Simplified Mental State Exam is currently used to assess language
    and memory difficulties
  • Alzheimer’s Disease Neuroimaging Initiative (ADNI): Research using
    brain scans and chemical tracers may soon allow clinicians to
    identify Alzheimer’s disease before cognitive ability declines
    significantly
33
Q

Vascular Neurocognitive Disorder

A
  • Blood vessels in brain are blocked or damages (strokes)
  • Nutrients and oxygen no longer carried to areas of brain tissue
  • Multiple sites can be damaged, thus impairments differ from person to person
  • Results in decline in processing speed and executive function.
  • 70 to 75 years = 1.5% of people; Over 80 years = 15% of people.
  • Risk for men is slightly higher than women.

Onset: more sudden than Alzheimer’s disease.

Progression: similar to Alzheimer’s disease

34
Q

Frontotemporal Neurocognitive Disorder

incl. pick’s disease

A
  • Damage to frontal or temporal regions of the brains- impacts personality, language and behaviour
  • Behaviour variant (eg. socially inappropriate behaviours)
  • Language variant (eg. word finding difficulties)
  • Pick’s disease:
  • an example of rare neurological condition which fits into this category. Accounts for 5% of people with neurocognitive disorders. - Similar symptoms to Alzheimer’s disease
  • Course 5-10 years, Early onset: around 40-50 years
  • Genetic component
35
Q

Traumatic Brain Injury

A

Severe trauma to the head causing sustained injuries can lead to neurocognitive disorder

Symptoms:
- Executive dysfunction, problems with learning and memory

At risk:
- Teens and young adults (alcohol use, low SES)

Common causes:

  • Traffic accidents
  • assaults
  • falls
  • suicide attempts
36
Q

Lewy Body Disease

A

lewy bodies are microscopic deposits of a protein that damage brain cells over time

Symptoms: impairment in alertness and attention, visual hallucinogens, and motor impairments

Overlap with presentation of neurocognitive
disorders due to Parkinson’s disease

37
Q

Parkinson’s disease

A
  • degenerative brain disorder

Characteristics:
- motor problems

Cause:
- damage to dopamine pathways. Lewy bodies are also present in the brain

Course varies widely: some individuals function well with treatment

75% who survive 10 years with Parkinson’s develop
neurocognitive disorder

38
Q

HIV infection

A
  • Human immunodeficiency virus type 1 (HIV-1) causes AIDS, can
    also cause neurocognitive disorder. HIV infection appears to be responsible for the neurological impairment

Symptoms:

  • Cognitive slowness
  • Impaired attention
  • Forgetfulness
  • social withdrawal
  • Impaired thinking in later stages of infection
  • new medication- limit number of patients who experience neurocognitive disorder (now less than 10%)
39
Q

Huntington’s Disease

A
  • Genetic disorder that affects motor movements, resulting in involuntary movements of limbs
  • Only a portion of people with Huntington’s disease go on to
    display neurocognitive disorder (estimates vary, 20-80%)
  • approximately 50% of children of parents with Huntington’s disease will develop it
  • Genetic linkage analysis techniques have identified deficit
    on chromosome 4 and have now identified the gene
    (Huntington’s Disease Collaborative Research Group)
40
Q

Prion Disease

A
  • Rare progressive disorder caused by “Prions”

Prions:
- proteins that can reproduce themselves and cause damage to brain cells leading to decline

  • no known treatment
41
Q

Substance induced

A

prolonged drug use, especially with poor diet, can damage the brain

  • 7% of individuals dependent on alcohol meet criteria for
    neurocognitive disorder
  • Brain damage can be permanent and cause similar symptoms as Alzheimer’s type

Symptoms:

  • memory impairment
  • language disturbance
  • apraxia, agnosia
  • executive functioning difficulties
42
Q

Neurocognitive disorders

Causes

A
  • Caused by a variety of underlying disorders (Alzheimer’s,
    Huntington’s disease, head trauma, substance abuse & others)

Neurofibrillary tangles: tangled, strandlike filaments within
brain cells

Amyloid plaques: gummy protein deposits

  • Both forms of damage accumulate over time and may be responsible.

Alzheimer’s:
- Appears to be more than one genetic cause.
Deterministic genes: if you have one of these genes, nearly 100% chance of developing. These are rare.

Susceptibility genes: Only slight increase of developing
Alzheimer’s disease. More common in general population

43
Q

Neurocognitive disorders

Prevention and Treatment
Goals

A

Goals:
- Attempt to prevent certain conditions, such as
substance abuse/strokes.
- Delay onset of symptoms to provide better quality of
life.
- Support individuals and caregivers cope with
deterioration.

44
Q

Neurocognitive disorders

Biological treatments

A

Stem cells: Benefits of transplanting stem cells into brain are being researched.

Medication: used to enhance cognitive abilities; possible short term improvement, not effective in the long term. There are side effects to consider.

Ginkgo biloba: initial studies suggested modest improvements in memory,
however other studies have not replicated the effect.

Vitamin E: High dose delayed progression compared to placebo, however high
doses found to increase mortality. Not recommended.

Antidepressants: SSRI (& other drugs) alleviate depression and anxiety accompanied with cognitive decline

45
Q

Neurocognitive disorders

Psychosocial treatments

A

Aim to teach skills to compensate for lost abilities

  • ‘memory wallets’
  • tablet computers
  • cognitive stimulation
  • navigation symptoms

Impact on caregivers: Higher rates of anxiety, depression and stress.

Supportive counselling: cope with frustration, depression, guilt and loss

46
Q

Neurocognitive disorders

Protective Factors

A

Prevention
Fratiglioni, Winblad & von Strauss (2007)
- Large study using medical records of 1810
participants older than 75 years - 13 year follow up.

Three major recommendations (protective factors)

  • Control blood pressure
  • Do not smoke
  • Lead active physical and social life