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
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
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)
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??
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).
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
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)
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
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
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
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
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
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)
14
Q
Autism Spectrum Disorder
Core features in the DSM- 5
A
Two core features:
- impairment in social communication and interaction
- 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
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
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)
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
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
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
Delirium
Characteristics
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
Delirium
Causes
- 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
Delirium Treatment
- 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
Major Neurocognitive Disorder (previously dementia)
Gradual deterioration of brain function which impacts memory, judgment,
language and other cognitive processes
29
Mild Neurocognitive Disorder
| new to DSM- 5
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
Alzheimer's Disease
Definition
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
Alzheimer's disease
Prevalence
- 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
Alzheimer's disease
Measures
- Mental State exam
- ADNI
- 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
Vascular Neurocognitive Disorder
- 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
Frontotemporal Neurocognitive Disorder
incl. pick's disease
- 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
Traumatic Brain Injury
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
Lewy Body Disease
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
Parkinson's disease
- 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
HIV infection
- 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
Huntington's Disease
- 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
Prion Disease
- 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
Substance induced
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
Neurocognitive disorders
Causes
- 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
Neurocognitive disorders
Prevention and Treatment
Goals
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
Neurocognitive disorders
Biological treatments
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
Neurocognitive disorders
Psychosocial treatments
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
Neurocognitive disorders
Protective Factors
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
PSYC212
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