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Preschool Language > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

Prader-Willi Syndrome

A

A rare genetic disorder in which the paternal genes on chromosome 15 are deleted or unexpressed resulting in a number of physical, mental, and behavioral problems.

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2
Q

Prevalence: PWS

A

1 out of 10,000 to 15,000 live births are diagnosed with Prader-Willi
Impacts more than 400,000 worldwide
Boys and girls are impacted equally

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3
Q

Clinical Features PWS in Infancy

A 
Hypotonia
Distinct facial features: almond-shaped eyes
Thin upper lip/downturned
Head narrowing at temples
FTT (failure to thrive)
Lack of eye coordination
Poor responsiveness

Very difficult to get these children to feed, they are obese as children becasue they are insatiable, delayed motor development, hypogonadism (produce little to no hormones)

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3
Q

Clinical Feauture PWS in Childhood

A 
Excessive food craving
Weight gain (especially in trunk region)
Hypogonadism
Poor growth: small stature hands/feet
Learning disabilities (mild to moderate)
Delayed motor development
Speech problems
Behavior problems
Sleep disorders (Apnea)
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4
Q

Specific Speech and Language Deficits in PWS

A 
Speech sound errors
Hypernasality
Flat intonation
Imprecise articulation
Slow speaking rate
Abnormal pitch
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5
Q

Treatment and Care for PWS

A 
Nutrition and diet modification
Growth hormone treatment
Sex hormone treatment
Therapies: Physical Therapy, Speech Therapy, Occupational Therapy, Developmental Therapy, Nutrition, Mental Health Therapy
Environmental modification

OT reccommends swimming

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6
Q

Speech (SLP) role in PWS

A

SLP will address speech and language issues in the child with PWS
SLP will address feeding concerns in infancy

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6
Q

Prognosis for PWS

A

There is no cure for PWS
Most will require specialized care and supervision throughout their lives
Most adults will reside in residential care facility so eating habits can be monitored
Biggest health risks are complications from obesity
Therapy at home & school will be needed to address cognitive delays, communication, and behavioral delays

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7
Q

Dandy Walker

A

DW malformation is characterized by a hypoplastic or missing cerebellar vermis, enlarged 4th ventricle, and cyst of the posterior fossa

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8
Q

Prevalence/Prognosis DWS

A

DWM is estimated to occur in >1 in 25,000 live births. It is the most common congenital malformation of the cerebellum
Mortality rates have decreased over time with medical advances
Current estimates suggest 27% of individuals with DWM die early
Overall prognosis is considered to be good and hopeful for those that survive
Best prognostic factor is absence of other congenital defects

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9
Q

Associated Problems in DWS

A 
Hydrocephalus
Seizures
Polycystic Kidneys
Cardiac Anomalies
Limb and facial abnormalities
Symptoms of increased intracranial pressure
Lethargy, emesis, irritability
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10
Q

Associated Symptoms in DWS

A 
Frequent
Other CNS abnormalities/disorders may co-occur
Decreased intelligence
Unsteady gait
Nystagmus
Lack of coordination
Occasional
Vision Problems
Hearing Problems
Cleft lip/palate
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11
Q

Treatment/Management of DWS

A

Early treatment included removing the membranes of the posterior fossa (high mortality rates)
Surgical management of DWM currently includes shunting of the 4th ventricle to drain excess CSF buildup (caused by cyst formation)
Anticonvulsive therapy or medication is commonly needed
Variable symptoms are treated as needed by (including PT, OT, ST)

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11
Q

Fragile X

A

Fragile X Syndrome is an X-linked condition caused by a mutation on the FMR1 gene on the X chromosome. It is usually inherited from a mother who is a carrier of the condition.
Fragile X inheritance is complicated. The FMR1 mutation involves a region of repeating DNA bases on the gene. A FMR1 gene with 55-199 repeats is said to have a “premutation” and a gene with 200 or more repeats is said to have a “full mutation.” Premutations passed on in an egg may or may not develop into full mutations.

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12
Q

Prevalence of Fragile X

A

Fragile X is one of the most common genetic disorders
1 in 4000 males
2 in 6000 females

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13
Q

Clinical Features of Fragile X

A 
Delay in crawling, walking, or rotating
Hand clapping or hand biting
Hyperactive or impulsive behavior
Anxiety and unstable mood
Intellectual disability
Speech and Language Delay
Tendency to avoid eye contact
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13
Q

Clinical Feautures of Fragile X 2

A 
Autistic Behavior
Sensory Integration Problems
Gastro-esophageal Reflux
Recurrent Otitis Media
Seizures affect about 25% of people with Fragile X
Flat Feet
Flexible Joints
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14
Q

Clinical Features of Fragile X 3

A 
Low muscle tone
Large body size
High arched palate
Scoliosis
Large testicles
Large forehead
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15
Q

Clinical Features of Fragile X 4

A

Large ears
Prominent jaw
Long face
Soft skin

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16
Q

Treatment/Management of Fragile X

A

No specific treatment
Treatment as indicated for any accompanying health issues
OT for sensory integration
ST may be needed for problems with poor intelligibility, pragmatics, grammar, oral motor difficulties, and phonological problems

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16
Q

Prognosis for Fragile X

A

Prognosis is dependent on the degree of intellectual disability and the severity of the other associated conditions

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17
Q

NAS (neonatal Abstinence Syndrome) PRENATAL

A

A collection of symptoms found in newborns that have been exposed to addictive drugs in the womb. The drugs pass through the placenta to the infant. Once the infant is born, and is no longer receiving the drug(s), (s)he goes through withdrawal known as NAS

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18
Q

NAS POSTNATAL

A

A collection of symptoms found in the infants who are treated with drugs such as fentanyl or morphine for pain shortly after birth. They subsequently go through withdrawal when the drugs are withdrawn

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19
Q

Epidemiology of NAS

A

4.3% of pregnant women ages 15-44 reported using illicit drugs (2003)
10% of 4.1 million live births in the US have been exposed to opiates or opioids (heroin, methadone, pain pills)
NAS is more commonly seen in urban areas

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20
Q

Clinical Features of NAS

A

Signs and symptoms typically begin between 103 days after birth, but may take up to 10 days to appear
Signs and symptoms depend on the drug(s) the mother used, how long she used the drug(s), the amount, and whether the baby was premature or term

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20
Q

NAS and prenatal toxemia

A

can be prenatally toxemic, but not necessarily have NAS
woven stretchy blankets are better for NAS, proprioceptive feedback
tremors

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21
Q

Dandy Walker considerations

A

cysts are numerous and fluid-filled, resulting in massive enlargement of kidneys
phenobarbital (common anticonvulsive)
drug treatment can inhibit therapy/development

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22
Q

Fragile X considerations for therapy

A

eye contact is very overstimulating to them, do not want to do this in therapy initially. They need sensory/movement/vestibular input to organize visual stimulation.
1/3 will also have autism

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23
Q

Clinical Features of NAS list

A 
Blotchy skin coloring (mottling)
Diarrhea
Excessive sucking
Fever
Hyperactive reflexes
Increased muscle tone
Irritability
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24
Q

Common Long-term Effects of NAS

A

Boys – increased risk for ADHD and behavioral disorders
Girls – increased risk for mood disorders
Both – increased risk for mental retardation and learning impairments (Weissman, et. Al, 1999)

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25
Q

NAS Scoring System

A

May help determine when to start, titrate, or terminate therapy
Finnegan – Most common
Lipsitz
Modified scales per institution

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26
Q

Treatment/Management of NAS

A 
Swaddling
Rocking the infant
Reducing noise and lights
Breastfeeding unless contraindicated
Team: ST, OT, PT, MD, Nursing, Mental Health Professionals, Social workers
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27
Q

Drug management of NAS

A

Opioids – used for opioids and polydrug withdrawal
Phenobarbital – used for polydrug withdrawal (most common)
Methadone – used for opioid withdrawal
Morphine – used for polydrug withdrawal, helps control seizures

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28
Q

Prognosis for NAS

A

Long-term outcomes are highly dependent on whether or not the mother continues to use addictive and/or illicit drugs
Environmental support/factors impact prognosis as well

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29
Q

William’s Syndrome

A

Williams syndrome is caused by the deletion of genetic material from chromosome 7. The loss of 1 of 2 copies of elastin protein in chromosome 7 is often associated with the cardiovascular and musculoskeletal issues seen in patients.

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30
Q

Prevalence of William’s Syndrome

A

1 in every 10,000 births
Equal male to female ration
Proportionate across race
An estimated 20,000-30,000 individuals in the U.S. have WS
Unlikely for other family members to have WS but if the person who has WS plans to have children, the child has a 50% chance of also having the diagnosis

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31
Q

Clinical Features of Williams Syndrome

A 
Small upturned nose
Wide mouth
Long philtrum
Full lip
Small chin
Puffiness around the eyes
Drooping cheeks
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31
Q

More Clinical Features of William’s Syndrome

A

Dental abnormalities (slightly small, widely spaced teeth)

Starburst (lacy white pattern in children with green and blue eyes)

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32
Q

Associated Problems in William’s Syndrome (Consistent)

A 
Cardiovascular issues
Supravalvular Aortic Stenosis (Narrowing of the blood vessels)
Low birth weight
Feeding problems
Hyperacusis
Developmental Delays
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33
Q

More associated problems in William’s Syndrome (Consistent)

A

Mild to moderate learning disabilities
Overly friendly
Lack of social inhibition
Strength in expressive skills

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34
Q

Associated Problems in William’s Syndrome (frequent)

A

Hypercalcemia – elevated blood calcium level
Kidney abnormalities
Musculoskeletal issues such as low muscle tone and joint laxity: loosening of joint bones
Mental disability – 75% of WS

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35
Q

Associated Problems in William’s Syndrome

A 
High blood pressure
Irritability/colic-like
Modified diet
FTT
Low muscle tone
Distractibility
Fine motor / spatial impairment
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36
Q

Other Associated features of William’s Syndrome:
Elfin
Cocktail Party

A

Williams syndrome is also sometimes called:
Elfin syndrome – inappropriate to use. Adult stature is slightly smaller than average and facial features become more apparent with age
Cocktail Party syndrome – inappropriate to use. Clients have excellent speech, appear to have strong social skills, fixated eye contact, and extreme friendliness. Many people with WS prefer talking to older individuals rather than peers.

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37
Q

Treatment of William’s Syndrome

A

Modified diet, monitor calcium level
Heart surgery
PT (joint issues, delays, low muscle tone)
ST (feeding as infants, social skills intervention, cognition, receptive language, expressive vocabulary +, ability to tell narratives +) Therapy most effective when accessing strengths

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37
Q

Prognosis for William’s Syndrome

A 
No cure
Usually unable to live independently
Most people with WS will have a shorter lifespan due to complications of:
Heart failure
Kidney disease
Death (from anesthesia)
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38
Q

Fetal Alcohol Syndrome

A

Caused by women who drink during their pregnancy
Common misconceptions: The amount or alcohol, type of alcohol, or timeline of pregnancy make no difference, alcohol use can always be damaging

39
Q

Prevalence of FAs

A

1 in 500 babies are born with FAS

1 in 100 babies have disabilities resulting from prenatal alcohol exposure (FAE)

40
Q

Clinical Features of FAS

A 
Symptoms range from mild to severe
Abnormal facial features
Smooth philtrum
Small head size
Shorter than average height
Low body weight
Poor coordination
Hyperactive behavior
Problems with the heart, kidneys, and bones
Difficulty paying attention
Poor memory
Difficulty in school (math especially)
Learning disabilities
Speech and language delays
Intellectual disability or low IQ
Poor reasoning and judgment
Sleep problems as baby
Sucking problems as baby
Vision and hearing issues
Difficulty feeding as infants
41
Q

Treatment for FAS

A

Medical care  all the care needed for a typical child plus other professionals depending on their specific impairments (pediatrician, PCP, audiologist, immunologist, neurologist, ophthalmologist, OT, PT, SLP)
Medication  stimulants, antidepressants, neuroleptics, anti-anxiety pills
Behavior and education therapy  friendship training, specialized math tutoring, executive functioning training, parent-child interaction therapy, behavior management training
Alternative approaches  biofeedback, auditory training, relaxation therapy, yoga, exercise, acupuncture, energy healing, vitamins, animal assisted therapy

42
Q

Facial Features of FAS

A 
Epicanthal folds in inner medial corners of eyes
Flat nasal bridge
Small palpebral fissures under eyes
Railroad track ears
Upturned nose
Smooth philtrum
Thin upper lip
43
Q

Prognosis for FAS

A

No cure for FASDs

Early intervention has been shown to improve the child’s development

44
Q

Down Syndrome

A

Individuals with Down syndrome have 47 chromosomes instead of the usual 46

45
Q

Prevalence of Down Syndrome

A 
Most common genetic condition
 1 in every 691 births
 6,000 born each year in the U.S.
 > 400,000 in the U.S.
 all races and SES
46
Q

Most common clinical features of Down

A 
Flattened facial features
Small head
Short neck
Protruding tongue
Upward Slanting eyes
Unusually shaped ears
47
Q

Often present clinical features of Down

A 
Poor muscle tone
Broad, short hands
Single crease in palm
Relatively short fingers
Excessive flexibility
48
Q

Associated clinical features of Down

A 
Heart defects
Eye problems
Hearing problems
Dementia
Obesity
Leukemia
Mild-severe Intellectual
49
Q

Noted associated problems in Down

A

tend to have higher incidence of reflux, secondary to heart problems
more reflux tends to correlate with more ear infections (otitis media)
Trisomy 21 most common genetic variation

49
Q

Treatment of Down

A

No specific treatment
 May need surgery due to associated factors
 Early intervention services should include:
Speech and language therapy
Physical therapy
Occupational therapy

50
Q

Speech Issues in Down

A

May not say first words until 2 or 3 years.
 Understand relationships between words and concepts by 10-12 months but are lacking the neurological and motor skills to speak.
 Many pre-speech and pre-language skills are needed first:
Imitation
Turn taking
Visual skills
Auditory skills
Tactile skills
Oral motor skills
Cognitive skills

51
Q

Prognosis for Down

A

In 1983 the life expectancy was 25 compared to 60 today.
Increased risk of Dementia with aging.
Individuals with Down syndrome live fulfilling lives as long as they have good education programs, home environments, health care, family support, friends, and community.

52
Q

Smith-Magenis

A

SMS is a chromosome microdeletion/mutation syndrome that is characterized by a very distinct series of physical, developmental and behavioral features
Includes varying levels of mental retardation, cranio-facial abnormalities, sleep disturbances and self-injurious behaviors

53
Q

Prevalence of SMS

A

SMS occurs 1 in 25,000 births; equal in male and females
Thought to be under diagnosed or misdiagnosed as :Williams syndrome, VCFS, PWS, DS (especially in the newborn period due to infantile hypotonia)

53
Q

Frequent Clinical Features (75%) of SMS

A 
OTOLARYNGOLOGIC:
   Middle ear and laryngeal anomalies
   Hoarse, deep voice
CRANIOFACIAL/SKELETAL:    
   Brachycephaly
   Midface hypoplasia
   Relative prognathism with age
   Broad, square-shaped face
   Everted, "tented" upper lip
   Deep-set, close-spaced eyes
   Short broad hands
   Dental anomalies
54
Q

Frequent Clinical Features of SMS

A

NEURO/BEHAVIORAL:
Cognitive impairment/ developmental delay
Generalized complacency/ lethargy (infancy)
infantile hypotonia
Sleep disturbance
 Inverted circadian rhythm of melatonin
Stereotypic behaviors

55
Q

Frequent clinical features of SMS

A 
Self-injurious behaviors
Speech delay
Hyporeflexia
Signs of peripheral neuropathy
Oral sensorimotor dysfunction (early childhood)
56
Q

Common Clinical Features (>50%) of SMS

A 
COMON FEATURES >50%
Hearing loss
Short stature
Scoliosis
Hyperacusis
Tracheobronchial problems
Velopharyngeal insufficiency
57
Q

Clinical Features (<50%) of SMS

A 
Cardiac defects
Thyroid function abnormalities
 Immune function abnormalities
Renal/urinary tract abnormalities
Seizures
Forearm abnormalities
Cleft lip/palate
Retinal detachment
58
Q

Specific Behavioral Issues in SMS

A
  • Arm Hugging
  • Hand Squeezing
  • Hyperactivity and attention problems
  • Prolonged Tantrums
  • Sudden moodiness
  • Explosive Outbursts
58
Q

Treatment of SMS

A

Early childhood intervention programs, special education, vocational training later in life, SLP, PT, OT, behavioral therapy, and sensory integration therapies
Gastroenterologists and nutritionists
Use of psychotropic medication
Therapeutic management of the sleep disorder

58
Q

SLP and Smith-Magenis

A

Early childhood: swallowing, feeding, oral sensorimotor development, oral motor movements
Further development: use of sign language and total communication programs

58
Q

Prognosis for SMS

A

Early intervention is key
People with SMS can expect to accomplish many of things their “typical” peers do—attend school, achieve in their outside areas of interest, be successfully employed, even move away from their family home
Need a significant amount of support from their families and from school, work, and residential service providers to achieve these goals
Appear to have a normal life expectancy, but no supporting research

59
Q

Laundau-Kleffner

A

Characterized by the sudden or gradual onset of aphasia in an otherwise typically developing child

60
Q

Prevalence of L-K

A

Around 160 cases have been reported between 1957-1990, though exact prevalence is difficult to ascertain due to frequent misdiagnosis

61
Q

Prognosis of L-K

A

Prognosis is characterized by immense variation.
Aphasia may last for days or years. Recovery may be full, or some language difficulties may persist.
However, most will outgrow seizures by the age of 15, and early intervention often leads to better outcomes.

62
Q

Velocardial Facial Syndrome

A

Missing a small part of chromosome 22 at the q11 region.
Unknown cause of deletion, but this is one of the most frequent chromosome defects in newborns.
10% inherited
Most “sporadic”
10% of individuals with VCFS do not have a deletion in the chromosome 22q11 region.
Other chromosome defects
Maternal diabetes
Fetal alcohol syndrome
Prenatal exposure to Accutane®

63
Q

VCFS/Digeorge

A

digeorge is a sequence, not a syndrome. can present with digeorge sequence but not have VCFS.
VCFS is a syndrome and it has genetic markers

63
Q

Prevalence of VCFS

A

Many do not present with obvious anomalies at birth.
1/3 of individuals do not have CHD or overt clefts of the palate.
Other associated problems may go unnoticed as they require special procedures (ultrasound, MRI).
1 in 1600 to 1 in 2000

64
Q

Features of VCFS

A

Many of the findings in VCFS are very common among other multiple anomaly syndromes
Most common/consistent features:
behavioral
cognitive
vascular
BDs & LDs will not be evident until later in life and may go unrecognized for many years.
Important to recognize the psychiatric manifestations of this syndrome at all developmental stages

65
Q

Cognitive Issues in VCFS

A

Children perform worse than would be expected by their cognitive level on tasks requiring:
 shifts of attention
cognitive flexibility
working memory
visuospatial and numerical abilities
When present, intellectual disabilities are usually relatively mild
The cognitive profile:
Relative strengths in the areas of reading, spelling, and rote memory
Relative weaknesses in the areas of visuospatial memory and arithmetic
Changes with development
Usually a decline in IQ as move into adulthood

66
Q

Common speech problems in VCFS

A

Delayed development of speech and language skills
Hypernasal speech due to velopharyngeal dysfunction
Articulation disorders
Voice disorders and laryngeal anomalies
Language impairment
Pragmatic and social skills difficulties

67
Q

Possible Concomitant Disorders in VCFS

A 
ADHD
Oppositional defiant disorder
Specific and social phobias
Generalized anxiety disorder
Separation anxiety disorder
Obsessive-compulsive disorder
Major depressive disorder and dysthymia
Autism spectrum
By late adolescence and early adulthood, this picture seems to change as up 1/3 of the patients with VCFS develop psychotic disorders mostly resembling schizophrenia and schizoaffective disorder”
68
Q

Treatment of VCFS

A

Specific treatment for VCFS is determined based on the following:
Child’s age, overall health, and medical history
The extent of the disease
Child’s tolerance for specific medications, procedures, or therapies
Expectations for the course of the disease
Parent opinion or preference
Heart defects will be evaluated by a cardiologist.
A plastic surgeon and a speech pathologist evaluate cleft lip and/or palate.
Speech and gastrointestinal specialists evaluate feeding difficulties.
Immunology evaluations should be performed in all children with this deletion.
In severe cases where immune system function is absent, bone marrow transplantation is required.
Many will benefit from early intervention to help with muscle strength, mental stimulation, and speech problems

69
Q

Prognosis for VCFS

A

Small minority will not survive the first year of life.
Majority will have a treatable heart condition and immune system disorder that will not be significant enough to interfere with survival.
Most progress into adulthood with normal growth.

69
Q

Angelman and the difference between PWS

A

Both Angelman Syndrome and Prader­Willi Syndrome occur as a result of severe reductions of a gene on chromosome 15. What’s the difference? In AS, the abnormality is on the maternally ­derived chromosome 15, and for PWS, the abnormality is on the paternally­derived chromosome 15.

70
Q

Consistent Clinical Features of Angelman

A

Developmental delay
Movement or balance disorder (usually ataxia)
Behavioral uniqueness (frequent smiling, easily excitable, hand­flapping movements)
Speech impairment (none or minimal use of words)

71
Q

Frequent Clinical Features of AS

A

Delayed, disproportionate head
growth (microcephaly by 2 yrs.)
Seizures (before 3 yrs.)
Abnormal EEG (in first 2 yrs.)

72
Q

Associated Clinical Features of Angelman

A 
Flat occiput
Occipital groove
Protruding tongue
Tongue thrusting; suck/swallowing disorders
Feeding problems
Prognathia
73
Q

Associated clinical features of Angelman’s 2

A 
Wide mouth
Wide­spaced teeth
Frequent drooling
Strabismus
Hypopigmented skin
Hyperactive LE deep tendon reflexes
 Uplifted, flexed arm position
Wide­based gait
74
Q

Associated clinical features of Angelman’s 3

A 
Increased sensitivity to heat
Abnormal sleep­wake cycles/ diminished need for sleep
Excessive chewing/mouthing behaviors
Attraction to/fascination with water and/or crinkly items such as paper
Abnormal food related behavior
Obesity (in older children)
Scoliosis
Constipation
74
Q

Diagnosis of Angelman’s

A

AS results from severe reduction of the UBE3A gene on the maternally­ derived chromosome 15.
 If clinical features are present, genetic testing should be performed.
 Most common diagnosis is between 2­ 5 years of age. This is because this is when the characteristic behaviors become most evident.
Other common misdiagnoses include Autism Spectrum Disorders and Cerebral Palsy.

74
Q

Treatment for AS

A

Consistent behavioral intervention and stimulation to over­ come developmental challenges
Behavioral treatment programs have been shown to benefit abnormal sleep/wake cycles
ABA has been found to be an effective instructional method
Anticonvulsant medication may be necessary to treat seizures

75
Q

SLP Treatment of AS

A

Hand­flapping motions are thought to result from inability to communicate effectively
Conversational speech will never develop in highest functioning individuals
 Individuals with AS have much better comprehension than expression
Severe seizures may inhibit reaching first stages of communication, such as establishing eye contact
Most common aim for treatment is teaching sign language
Other options include picture based communication boards or speech generating devices
Carryover is key! SLP must collaborate with parents and other professionals in order to help the child learn to functionally communicate

76
Q

Prognosis for AS

A

Mobility issues become a more predominant concern as the child ages, and is often associated with concerns of obesity.
 If severe ataxia is present, the child may lose his or her ability to walk if ambulation is not encouraged.
Scoliosis may develop in adolescence, especially if the individual is non­ ambulatory.
 Lifespan is not dramatically shortened.

77
Q

Cure for AS

A

A cure for AS has been found in mice!

With a recently received grant, the Foundation for Angelman Syndrome Therapeutics is beginning their first human study

78
Q

Asperger’s syndrome

A

An autism spectrum disorder
¨ Characterized by difficulty with social interaction, repetitive patterns of behavior and interests
¨ Demonstrate limited empathy for peers

78
Q

Prevalence of Asperger’s

A

The incidence of Asperger syndrome is not well established.
However, experts in population studies estimate that 2 in 10,000 children have the disorder.
The prevalence of Autism Spectrum Disorders in 2007 was estimated at 1 in 150 children.
The prevalence of Asperger syndrome has been estimated by studies to be 1 in 500 children.
Boys are 3 to 4 times more likely to be diagnosed with AS than girls.

78
Q

Possible Causes of Asperger’s

A

Unknown
¨ Possible genetic basis (passed down primarily from father)
¨ Harmful substance consumption during pregnancy
¨ Common in Silicon Valley children (parents have very organized minds)

79
Q

Common Social Features of Asperger’s

A

Difficulties with peer relationships (Possible carry-over to parent and family relationships)
Inappropriate attempts to initiate social interactions and make friends
Need for and adherence to structure, routine, rituals, and/or schedules
Socially inappropriate behavior
Failure to understand social cues
Inability to understand and follow social norms
Inability to “put himself in the other person’s shoes”

80
Q

Nonverbal Communication Features of Asperger’s

A

Limited use of gestures
Inability to use or understand body language
Awkward or inappropriate use of non-verbal communication
Flat affect or inappropriate facial expressions
Inability to read the facial expressions of others
Lack of eye contact

81
Q

Sensory Features of Asperger’s

A

Possible sensitivities to sound, touch, taste, sight, smell, pain, temperature, and food textures
Can be hypo-sensitive to some stimuli and hyper-sensitive to others.

82
Q

Speech & Language Features of Asperger’s

A

No language development delay
Possible advanced vocabulary
Abnormalities in production of speech and language
Pedantic speech
Odd pitch (monopitch), intonation (incorrect or absent), prosody, & rhythm
Difficulties with abstract language- makes literal interpretations
Difficulties with the social rules of language
Interruptions, irrelevant information, maintaining topic, turn
talking, “monologing”
Unusually formal or idiosyncratic ways that are not understood
Lack a “filter”- Says whatever comes to mind
Amount of speech depends on emotional state

82
Q

Common Activities/Interests in Asperger’s

A

Has an “obsessive” interest that causes: exclusion of other activities, is narrow or limited to a very specific topic, that may be uncommon for age especially in terms of amount and type of facts the child knows, and that may overrule his or her desire for social relationships.
Child may also lack interactive play.

83
Q

Treatment for Asperger’s

A

Focuses on:
OT/PT for motor coordination and sensory integration
Social skills intervention
Intervention for anxieties, repetitive and
obsessive behaviors, and co-occurring disorders

84
Q

SLP treatment for Asperger’s

A

Initiation of social interactions
Use and understanding of verbal and nonverbal communication in various settings
Education of parents and teachers

85
Q

Prognosis for Asperger’s

A

Very good prognosis of a fully functional and independent life similar to that of a neurotypical individual especially with social skills intervention
Difficulties in social interactions may persist throughout life which may result in bullying, problems in romantic relationships, depression, loneliness, and difficulties keeping a job.

85
Q

Autism

A

Pervasive developmental disorder of unknown etiology with suspected genetic and environmental triggers.
Affects the brain’s normal development of social and communication skills.
Appears in the first 3 years.
Stereotypical behaviors (self stimulation) and perseveration of interest on an object are often observed.
Unusual response to sensory stimuli

86
Q

Prevalence of Autism

A

It is estimated that between 1 in 80 and 1 in 240 with an average of 1 in 110 children in the United States have an ASD.
Estimate 6 out of 1000 children will have autism
Boys are 4x more likely than girls
Comorbidity is common with:
Intellectual disability
Seizure disorders
Anxiety, depression
Hyperactivity, obsessive compulsive disorder

87
Q

Diagnosis of Autism

A

The diagnosis of autism requires disturbances in each of three domains:
 social relatedness
 includes marked impairment in non-verbal communication, peer relationships and social-emotional reciprocity.
communication/play
 includes either a delay or total lack of spoken language and lack of developmentally-appropriate make-believe or social play.
restricted interests and activities
 includes encompassing preoccupations, adherence to non- functional routines or rituals, stereotypies and motor mannerisms.

88
Q

Specific Assessment Tools for Autism

A

Checklist for Autism in Toddlers (CHAT) or modified checklist (M-CHAT)
Autism Screening Questionnaire.
Autism Diagnostic Interview - Revised (ADI-R)
Autism Diagnostic Observation Schedule (ADOS)
Childhood Autism rating Scale (CARS)
Gilliam Autism Rating Scale
Pervasive Developmental Disorders Screening Test - Stage 3

89
Q

Treatment of Autism 1

A
  • SLP- communication, social interactions, improved eating (esp. tolerance)
  • OT/PT- coordination, motor control
  • OT- sensory integration
  • MDs and psychiatrists- medicines for related
90
Q

Treatment of Autism 2

A

Applied Behavioral Analysis (ABA) Skinner- 1930s
This program is for younger children with an autism spectrum disorder. Uses a one-on-one teaching approach that reinforces the practice of various skills. The goal is to get the child close to normal developmental functioning.
Treatment and Education of Autistic and Related Communication Handicapped Children (TEACCH) Erick Schopler- 1970s
It uses picture schedules and other visual cues that help the child work independently and organize and structure their environments. Do not expect children to achieve typical development with treatment.

91
Q

Treatment of Autism 3

A

Early Start Denver Model (ESDM) Rogers & Dawson- 2000s
encompasses a developmental curriculum that defines the skills to be taught at any given time and a set of teaching procedures used to deliver this content.
Pivotal Response Training (PRT) Koegel & Koegel-1970s
Child directed, goal of PRT is to produce positive changes in the pivotal behaviors, leading to improvement in communication skills, play skills, social behaviors and the child’s ability to monitor his or her own behavior. by focusing on critical, or “pivotal,” behaviors that affect a wide range of behaviors

92
Q

Treatment for Autism 4

A

Floortime (DIR) Greenspan-1980s
is to help the child reach six developmental milestones that contribute to emotional and intellectual growth: self-regulation and interest in the world, intimacy or a special love for the world of human relations, two-way communication, complex communication, emotional ideas, emotional thinking

Preschool Language (3 decks)

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