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40 Cards in this Set
- Front
- Back
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Attention Deficit Hyperactivity Disorder |
•A persistent pattern of: Inattention (difficulty attending to tasks, leaving tasks unfinished, appearing not to listen, losing things) Or •Hyperactivity and impulsivity (e.g., fidgety, excessive activity, difficulty with sitting still, difficulty waiting) OR both (combined subtype) •Substantial clinical presentation < 12 years •Symptoms must occur across settings |
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ADHD across the lifespan |
Can be identified around 3-4 years. Over time: often less impulsive, inattention persists. •Adolescents: impulsivity manifests in different areas (e.g., greater risk of teenage pregnancy, car accidents). •Adulthood: approx 50% have ongoing difficulties. Common symptoms in adulthood - a need to be busy, restlessness. •Inattention, hyperactivity and impulsivity may result in other difficulties (e.g., poor academic performance, learning difficulties, difficulty with peer relationships). |
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ADHD causes Biological Gene-environment |
Causes: Biological •More common in families where one person has ADHD (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). Causes: Gene-environment interaction •Environmental factors also appear to play a small role (e.g., studies found mutation involving dopamine system more likely to exhibit symptoms of ADHD if mother smoked during pregnancy). •Other possible environmental factors: maternal stress and alcohol use, parental marital instability |
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Treatment approaches |
•Psychosocial Interventions: target broader issues (i.e., academic performance, decrease disruptive behavior, improve social skills). •Biological Interventions: aim to reduce impulsivity and hyperactivity, improve attention. •Combined approach |
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ADHD Psychosocial intervention approaches |
Psychosocial intervention approaches Behavioral Interventions (Home + School) •Increase positive behaviors (e.g., stay seated, increase maths problems attempted, practice social skills etc.) •Reinforcement programs Parent Education: (e.g., responding to behaviour, making adaptions). Social Skills programs: (e.g., groups with peers) Adults: Cognitive Behaviour Therapy |
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ADHD Biological treatment approaches |
Stimulant Medication (e.g., Ritalin, Adderall) •Effectiveness for reduction in core symptoms (hyperactivity and inattention). •Work by reinforcing the brain’s ability to focus attention during problem solving tasks. •Other non-stimulant drugs can also be effective (e.g., Strattera). •Recommended temporarily + in combination with psychosocial intervention . |
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Specific Learning Disorder |
Performance that is substantially below what would be expected given the person’s: age, IQ & education. •Impairment in Reading •Impairment in Expression (writing) •Impairment in Mathematics. Long term impact: More likely to drop out of school, unemployment, suicidal thoughts and attempts (negative impacts can be mitigated by support). |
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Specific Learning Disorder |
DSM-IV-TR •Listed disorders separate disorders (i.e., reading, maths, written expression). DSM-5 •Due to significant overlap, disabilities are now combined to assist clinician take a broader view. •Diagnostic issue: IQ discrepancy vs. response to intervention. |
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Specific Learning Disorder Causes: Genetic and environmental |
Causes: Genetic and environmental •Twin and family studies suggest learning disorders run in families. •Genes appear to affect learning in general, rather than specific area (e.g., reading, writing, maths). •Genes located on chromosome 1, 2, 3, 6, 11, 12, 15 and 18 all repeatedly linked to word recognition. •Factors such as socioeconomic status, cultural expectations, parental interactions and expectations, child management practices, types of school support = impact outcomes |
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Specific Learning Disorder |
Neurological causes: 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. |
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Specific Learning Disorder |
Treatment approach: Educational interventions •Specific skill instruction (e.g., find main idea, find facts) •Strategy instruction (e.g., decision making, critical thinking) Direct Instruction (Kameenui, Fien & Korgesaar, 2013) •Involves highly scripted lesson plans, in small groups based on progress •Teaching for mastery •Progress continually assessed & plans modified |
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Autism Spectrum Disorder |
Two core features in DSM-5: •Impairment in social communication + social 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’ Level 2 = ‘Requiring substantial support’ Level 3 = ‘Requiring very substantial support’ |
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Autism Spectrum Disorder |
Changes from DSM-IV-TR Conceptualized as separate disorders: •Autistic disorder •Pervasive Developmental Disorder – not otherwise specified •Asperger’s Syndrome DSM-5 •Autism Spectrum Disorder •Social (Pragmatic) Communication Disorder – new to DSM-5 |
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Autism Spectrum Disorder 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). |
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Autism Spectrum Disorder Restricted, repetitive patterns of behavior, interests or activities (evidence of at least 2 out of the following): |
•Stereotyped or repetitive motor movements, use of objects or speech (e.g., echolalia, body movements, lining up toys, idiosyncratic phrases). •Insistence of sameness, inflexible adherence to routines or ritualised patterns of verbal and non verbal behaviour (e.g., extreme distress at small changes, taking same route each time, difficulty with transitions).
•Restricted, repetitive patterns of behavior, interests or activities (continued). •Highly restricted, fixated interests that are abnormal in intensity or focus (e.g., strong attachment or preoccupation with unusual objects, perseverative interests). •Hyper or hyporeactivity to sensory input (e.g., adverse response to sounds, textures, excessive smelling/touching objects, fascination with lights/movement). |
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Austsim Spectrum Disorder approaches and supports |
Common approaches & Supports •Behaviour intervention programs (e.g., ABA programs; ESDM program). •Allied health supports (e.g., speech therapy, psychologist, occupational therapist). •Social skills groups. Common goals •Generalize behavioral approaches to home, school and community. •Improvements in social communication (e.g., making requests, interaction with peers, joint attention and play skills). |
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Intellectual Disability |
•Characterised by significantly below-average intellectual and adaptive functioning. •Difficulties with day to day activities. •Individuals display broad range of abilities and personalities. •Impairments in a range of areas, e.g., language, social skills, reasoning (mild-severe). |
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Intellectual disability |
DSM-5: changed to ‘Intellectual Disability’/ IQ cut-off score no longer specific. 3 domains: Conceptual: e.g., poor language, reasoning and memory Social: e.g., problems with social judgement, making friendships Practical: e.g., personal care, job responsibilities •Course is chronic and prognosis varies considerably |
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Intellectual Disability Causes |
Causes 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 Genetic influences •Chromosomal disorders, single-gene disorders, mitochondrial disorders, multiple genetic mutations •Some cases of ID have no identified etiology |
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Intellectual Disability - Treatment approaches |
•No biological treatment available •Behavioural interventions/strategies + other supports •Build skills for quality of life, independence. |
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NEUROCOGNITIVE DISORDERS DSM-5 |
•DSM-5: ‘Neurocognitive Disorders’ new category for forms of dementia and amnestic disorders - with major and mild subtypes. •Prominent feature is impairment of cognitive abilities (e.g., memory, attention, perception, thinking). •Also may involve other psychological aspects (e.g., changes to behaviour and personality; anxiety and depression; paranoia, agitation, aggression). |
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Delirium |
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. |
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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 |
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Treatment |
Treatment •Address underlying causes •Antipsychotic drugs can be prescribed when cause is unknown Psychosocial management: managing agitation and anxiety; increasing familiar personal belongings and family support; including patient in treatment decisions. Prevention: appropriate medical care for illness and medication monitoring. |
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Neurocognitive Disorder |
Major Neurocognitive Disorder (previously Dementia) •Gradual deterioration of brain function which impacts memory, judgment, language and other cognitive processes Mild Neurocognitive Disorder (new to DSM-5) •Focuses on early stages of cognitive decline. Some impaired cognitive ability, but can function independently with accommodations. |
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Neurocognitive Disorders |
Examples of symptoms •Memory impairment (inability to remember events) •Agnosia: Inability to recognise and name objects •Facial agnosia: Inability to recognise faces •Decline in intellectual functioning Emotional changes: Delusions (irrational beliefs), depression, agitation, aggression, apathy. |
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Alzheimer’s Disease |
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 |
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Alzheimer’s Disease |
•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. •Certain markers for Alzheimer’s currently being investigated. |
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Vascular Neurocognitive Disorder |
•Blood vessels in the brain are blocked or damaged (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. •Risk for men is slightly higher than women. Onset: more sudden than Alzheimer’s disease. Progression: similar to Alzheimer’s disease. |
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Frontotemporal Neurocognitive Disorder |
•Damage to frontal or temporal regions of the brain - impacts personality, language and behavior. Behaviour variant: (e.g., socially inappropriate actions, apathy, poor judgments, perseverative behavior). Language variant: (e.g., word finding difficulties, word comprehension, speech production). •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 |
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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, especially accompanied with alcohol abuse or lower socioeconomic status. •Common causes: Traffic accidents, assaults, falls, suicide attempts. |
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Lewy Body Disease |
Lewy bodies: 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. |
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Parkinson’s Disease |
•Degenerative brain disorder •Characteristics: motor problems (e.g., stooped posture, slow body movements, tremors, jerkiness in walking, voice changes). •Changes in motor movements are the result of 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. |
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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, clumsy, repetitive movements such as tremors and leg weakness, apathy and social withdrawal. •Impaired thinking in later stages of infection. •New medications are limiting number of patients who experience neurocognitive disorder (now less than 10% of patients). |
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Huntington’s Disease |
•Genetic disorder that affects motor movements, resulting in involuntary movements of the limbs. •Only a portion of people with Huntington’s disease go on to display neurocognitive disorder (estimates vary, 20-80%). •Inherited disease: 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). |
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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. |
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Substance-Induced |
•Prolonged drug use, especially with poor diet, can damage the brain. •7% of individuals dependent on alcohol meet criteria for neurocognitive disorder. Chronic use of other drugs can also lead to neurocognitive disorder symptoms. •Brain damage can be permanent and cause similar symptoms as Alzheimer’s type. •Symptoms: memory impairment, language disturbance, apraxia, agnosia, executive functioning difficulties. |
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Treatments Research on 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. |
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Treatments Psychosocial treatments |
Aim to teach skills to compensate for lost abilities. •‘Memory wallets’ •Tablet computers •Cognitive stimulation (e.g., word games, practice with numbers) •Navigation Systems – ‘smart home’ •Communication skills Impact on caregivers: Higher rates of anxiety, depression and stress. Supportive counselling: cope with frustration, depression, guilt and loss. |
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Protective factors |
Prevention •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 |
