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OCTH 731 exam 2
| Question | Answer |
|---|---|
| an agent, force, or mechanism that causes trauma | trauma |
| repeated or chronic exposure to multiple traumatic incidents that occur within a relational system, often in early childhood, which impacts development and self-awareness; continuous emotional maltreatment, absence of caregiving, compromised attachment | complex trauma |
| etiology - multiple exposures beginning in early childhood or adolescence, inconsistent or absent protective caregiving, abuse, uncontrollable and unpredictable context, transgenerational, neglect | complex trauma |
| risk factors-parental demographics, psychiatric disorders, unrealistic expectations, transgenerational trauma, substance abuse, poor family support, disability, "trigger" events, poverty, parental characteristics, transient caregivers in home | complex trauma |
| 678,000 victims in 2018; sexual abuse occurs more in females, who are more likely to suffer from emotional abuse and neglect; boys more likely to experience physical trauma; kids under 1 most vulnerable | complex trauma |
| African-American/Hispanic/multi-racial and gay/lesbian/bisexual, $15,000 annual income, unemployed and no diploma are risk factors for | elevated ACE scores |
| 3 main types of ACEs are common: household dysfunction, neglect, and abuse | ACEs |
| ____ are highly interrelated, where 1 occurs there are usually others | ACEs |
| children in ____ ____ are more susceptible to ACEs in different parts of the brain | sensitive periods |
| 7 domains id and describe signs and symptoms associated with this diagnosis - attachment and relationships, physical health, emotional responses, dissociation, maladaptive behavior, cognition, self-concept and future orientation | complex trauma |
| attachment: child has a safe environment, sense of protection, able to regulate affect and behavior; majority of population | secure attachment |
| attachment: persistent caregiver rejection, distrusting of emotions, avoid establishing meaningful relationships | avoidant attachment |
| attachment: inconsistent parents, detachment/neglect -> intrusive | ambivalent attachment |
| attachment: traumatized by repeated exposure to unpredictable, uncontrollable stress, consistently absent caregiver | disorganized attachment |
| brain structures affected by attachments with what diagnosis: prefrontal cortex, amygdala, hippocampus, hypothalamic-pituitary-adrenal axis, neurotransmitters | complex trauma |
| responsible for panic and fear, attention, memory, and social cues | hippocampus and amygdala |
| outcomes - probs of personal boundaries, chronic feelings of distrust and suspicion, social isolation, poor ability to est healthy relationships, difficulty atoning to others' emotional states, self-harming, substance abuse, inappropriate sexual stim | poor attachment |
| internal states of arousal; identifying emotions in themselves and others; alexithymia; traumatized kids are avoidant of emotional situations; result of exposure to inconsistent displays of affect and behavior, responses to displays of emotion | emotional responses |
| inability to process and integrate info and experience; how it looks: numbness, distractibility, limited expressive speech, inattention, blank stares, "out of body" feeling, static posture, poor ability to connect with others | dissociation |
| patterns are reflective of adaptation to significant stress in traumatized kids; increased likelihood of feelings of depression, anxiety, poor concentration | maladaptive behavior |
| may present as: delayed language dev., probs. with object constancy, visual perceptual probs., lack of persistent curiosity, difficulty understanding complex visual-spatial patterns, confusion, rigidity, perfectionism, hypervigilance, self-doubt | executive functioning impairments |
| model for complex trauma | SW Michigan Children's Trauma Assessment Center Model |
| criteria: experiencing, witnessing, or learning about death, violence, or injury esp. toward caregiver, 1 or more times; intrusive thoughts, avoidance, or neg. emotional reactions to reminders of traumatic event; physiological dysregulation | complex trauma |
| criterion: ACE experience, witnessed and prolonged; dysregulation; cognition and behavior; personal id and relationships; PTSD symptoms; duration of disturbance; functional impairment | complex trauma |
| kids presenting with ____ ____-related symptoms are at risk of being misdiagnosed with a variety of disorders and functional difficulties | complex trauma |
| common co-occurrences: ADHD, depressive disorders, ODD, reactive attachment disorder, psychotic disorders, specific phobias, learning/academic difficulties, juvenile delinquency | complex trauma |
| prognosis directly related to extent of exposure, interventions, and resiliency factors; ACEs increase probability of future health and behavioral problems; ACE score of 6 or more consistent with shorter life span by 20 years | complex trauma |
| decreased frontal cortical volume, structural changes in white matter, connectivity, amygdala volume, hippocampal volume, cortisol, neuroendocrine changes, strong connection with early trauma and brain dev. and function | complex trauma |
| ability of an individual to recover from adverse or traumatic events in a manner that is adaptive and nonpathologic; factors to promote - parents understand trauma, support, needs are met | resiliency factors |
| psychopharmacological intervention, in addition to psychosocial modalities, constitute best practice; weekly psychotherapy, family therapy, play therapy, self-management, expressive therapies, pharmacotherapy, community outreach | complex trauma |
| impact on occ. performance - ADLs: bathing, toileting, feeding and eating, personal hygiene and grooming, sexual activity; try to feel some sort of control through their occupational performance | complex trauma |
| impact on occ. performance - IADLs: health management, education, play and leisure, rest and sleep, work, social participation | complex trauma |
| persistent and maladaptive symptoms of inattention, hyperactivity, and impulsivity | ADHD |
| age of onset - 7; 4:1, boys:girls | ADHD |
| etiology: combo of genetic and environmental factors, tho specific underlying causes are unknown; prematurity; coexisting conditions; characteristics of sociocultural environment; dopamine receptors are less efficient | ADHD |
| neurological imaging: reduced circulation, accelerated maturity of motor cortex, causes differences with concentration and less "brain energy", decreased glucose metabolism during activity | ADHD |
| incidence and prevalence steadily increasing since 2000, stabilizing in recent years; estimates fluctuate due to differences in survey methodologies; discerning it from normal kid behavior is difficult; prevalence higher in special populations | ADHD |
| type of ADHD: fails to give close attention to details, trouble holding attention, does not seem to listen, does not follow through on instructions, trouble organizing tasks, reluctant to do tasks that require mental effort, easily distracted | inattentive type |
| type of ADHD: fidgets, runs about or climbs, unable to play and take part in leisure activities quietly, "on the go", talks excessively, blurts out answer before question completed, trouble waiting their turn, interrupts or intrudes on others | hyperactive and impulsive type |
| several inattentive and/or hyperactive-impulsive symptoms must be present prior to 12 years of age; symptoms must be evident and impacting function in more than 1 context; symptoms interfere with or reduce quality of indiv.'s social functioning | diagnosis of ADHD |
| type of ADHD: if enough symptoms of inattentive, but no hyperactive-impulsive, were present for past 6 months | predominately inattentive |
| type of ADHD: if enough symptoms of hyperactive-impulsive, but not inattentive, were present for past 6 months | predominately hyperactive - impulsive |
| type of ADHD: if enough of both symptoms were present for past 6 months | combined presentation |
| symptoms change over time, so presentation may change over time too | ADHD |
| severity of ADHD: few, if any symptoms, beyond those required to make diagnosis and no more than minor impairment in functioning | mild |
| severity of ADHD: symptoms of functional impairment in between, may not show clinically significant impairment | moderate |
| severity of ADHD: reserved for cases with many symptoms in excess of those required for diagnosis, or several symptoms that are especially severe, or marked impairment resulting from symptoms | severe |
| signs and symptoms: EF dysfunction - inhibiting behavior, using visual imagery, talking to oneself, controlling emotions and motivations, planning and problem-solving; doing vs knowing - performance problem rather than a knowing problem | ADHD |
| what percent does ADHD appear to delay executive functioning development | 30% |
| age of ADHD: disruptive behavior, aggression toward other kids, hyperactivity, conduct problems, inattentive and overactive | preschool |
| age of ADHD: unfinished tasks, trouble with school, criticism from teacher/parent/peers, low self-esteem, depression, and conduct disorders can develop here | middle childhood |
| age of ADHD: higher rates of anxiety, depression, oppositional behavior, social failure, substance abuse | adolescence |
| age of ADHD: trouble at work, relationships; difficulty following directions, remembering, concentrating; emotional and social problems | adulthood |
| treatment: behavioral or medications - stimulants, non-stimulants, anti-depressants | ADHD |
| implications: teaching skills inadequate, design prosthetic environments to compensate for EF deficits, compassion and willingness of others to make accommodations, creates a diminished capacity, reverse engineer EF system | ADHD |
| impact on occ. performance: individualized plan with general overall goals - improve occ. performance, enhance self-esteem, address any family difficulties, prevent school failure | ADHD |
| impact on occ. performance: environmental supports, instructional strategies, behavioral intervention and support, SIT and activities, importance of emotional support, self-monitoring, movement therapies, external motivation | ADHD |
| impact on occ. performance: ADLs, IADLs, health management, rest and sleep, education, work, play, leisure, social participation | ADHD |
| hostile/oppositional behavior persists through time and causes significant impairment to QOL of individual regarding their relationships and their family and social environment | oppositional - defiant disorder |
| signs: hostility towards adults and peers, refuse responsibility for actions; push limits, ignore demands/orders, acting out deliberately; behavior repeatedly negative, hostile, and challenging | ODD |
| etiology: temper characteristics more significantly influenced by genetic factors; environmental factors - maternal depression, dysfunctional family relationships, high intra-familiar hostility, parental addiction to drugs/alcohol, sociocultural disadv. | ODD |
| low prevalence, incidence varies regarding age and sex of child, onset is typically around preschool age, prior to adolescence it is more frequent in males than females, after puberty prevalence is equal between genders, rare after early adolescence | ODD |
| signs and symptoms: ongoing patterns of being uncooperative, defiant, and hostile toward authority figures; significant issues in main life contexts involving family, school, and peer groups due to regularity, frequency, and severity of behaviors | ODD |
| symptoms more persistent in what gender with ODD: ill temper, highly reactive, barely soothable, intense motor activities | males |
| diagnosis: behaviors last at least 6 months including 4 of the following: frequent tantrums, easily annoyed, angry/resentful, argues with authority figures, defy rules, deliberately annoy others, blame others for mistakes, spiteful/vindictive | ODD |
| ODD can eventually go on to develop into what disorder | conduct disorder |
| kids with this disorder are at risk of anxiety, major depression, ADHD, substance abuse, suicide attempts | ODD |
| risk factors: temporal - high levels of emotional reactivity, psychological - parallels between insecure attachments and disruptive behavior disorders, environmental - ACEs, genetic - overlap between symptoms of other disorders and this | ODD |
| treatment: psychological treatments, psychopharmalogical treatments | ODD |
| occ. performance: stress reduction/coping strats., play and/or leisure exploration, development of routines, general routines and habits, sensory integration, ADL and other skill development, relationships and employment | ODD |
| developmental disorder of neurobiological origin that is lifelong | autism spectrum disorder |
| characterized by impairments with social interaction and cues, communication, high sensitivity to changes, may be overly dependent on routines, restricted and repetitive behaviors, unusual responses to sensory info | ASD |
| etiology: no single, clearly defined cause; complex combination of biological, genetic, and environmental factors | ASD |
| brain volume: dense layers of abnormal neurons, accelerated brain growth in frontal and temporal lobes; frontal and temporal lobes affect EF, social, emotional, and language deficits; slower growth = better development | ASD |
| increasing focus on internal world, decreases from 2-6 months of age, lack of interest in people, more attention to objects than people, brain shaped and specialized to attend to nonsocial world | eye contact differences in ASD |
| hypothesis for brain connectivity: underconnectivity in long-range connections, overconnectivity in short-range connections | ASD |
| genetic etiology: account for neurobiological differences, 1 of most heritable neuropsychiatric disorders, >100 genes associated with this, comorbid conditions - Fragile X and Tuberous Sclerosis | ASD |
| environmental etiology: combine with genetic predisposition to cause or prevent, parental age at conception, toxin exposure, premature/low birth weight, maternal factors | ASD |
| symptoms: difficulty in social situations - delays in language dev., abnormalities in language use, echolalia, incorrect pronoun use; restrictive and repetitive behaviors - preocc. with routines and/or patterns, obsession with specific topics, rigidity | ASD |
| symptoms of ASD typically emerge at around what age(s) | 12-36 months |
| symptoms: cog. impairment, language comprehension low, hyperactivity, short attention span, impulsivity, aggressiveness, food selectivity, tantrums, high pain threshold, motor deficits, sleep disorders, no fear, giggling/weeping, self-injurious behavior | ASD |
| CHAT, ASQ, Screening Tool for Autism in 2-year-olds, Australian Scale for Asperger Syndrome, PDDST-1, M-CHAT | ASD |
| at what months are children screened for ASD | 18 and 24 months |
| screening: typically done by PCP, history, medical history, physical/neurological exam, parent interview, language assessment, cognitive assessment, other dev. areas, audiological testing, formal and informal, others dep. on circumstance | ASD |
| diagnosis: impairment in social communication and interaction; restricted and repetitive behavior, interests, and/or activities; must be present in early dev.; causes clinically significant impairment; can not be better explained by other disorder | ASD |
| specifiers for diagnosis: with or without accompanying intellectual impairment, with or without accompanying language impairment | ASD |
| severity: level 1 - requiring support, level 2 - requiring substantial support, level 3- requiring very substantial support | ASD |
| rates have steadily increased since 1960s; possible reasons for higher rate of diagnoses - awareness, early id, availability of services; boys:girls - 5:1, prevalence increases with SES | ASD |
| course: intellectual disability; language - early joint attention, symbolic play, receptive language, spontaneous language; motor skills - hand-eye coordination, hand preference, imitation | ASD |
| treatment: not typically medical intervention; intensive early intervention to reduce problem behaviors and increase language, social, sensory, motor, and cognitive skills; most beneficial time - 0 to 3 years | ASD |
| treatment: pharmacologic - psychotropics for comorbid conditions; complementary and alternative - may aid in associated problems rather than cure; developmental approaches - OT, PT, SLP; behavioral therapy | ASD |
| occ. performance: mental functions - emotional regulation, attention/EFs, major depression, anxiety, aggression, high complexity of task=poorer performance; digestive system functions - high risk for GI problems | ASD |
| occ. performance: sensory function and pain - visual perception a relative strength, inefficient physical and emotional responses to sensory stimuli, whole vs. parts of a figure; urinary and repro functions - sexual behavior, maturation challenging | ASD |
| occ. performance areas: ADLs, IADLs, health maintenance, education, play and leisure, employment | ASD |
| first introduced by dr. A. Jean Ayres (an OT) in mid-1970s, Ayres Sensory Integration Theory with assessment and treatment methods | Sensory Processing Disorder |
| take in, organize, and interpret info from environment through our senses and create a meaningful response | sensory processing |
| neurophysiologic condition where sensory input from body or environment is poorly detected, modulated, or interpreted resulting in atypical responses to sensory messages that manifest as problems with motor and psychological responses | SPD |
| etiology: no specific cause; strong correlations in research to genetics, prenatal conditions, perinatal complications, and environmental factors | SPD |
| etiology: low birth weight (< 4.5 pounds), prematurity (<36 weeks), maternal illness, maternal use of meds, single parent, low SES, maternal alcohol use, smoking, maternal illicit drug use, paternal illicit drug use | SPD |
| 1 in 20 demonstrate symptoms associated with sensory processing difficulties; 5-16.5% of school-age kids have sensory processing difficulties affecting participation in ed and daily activities; increased prevalence in those with Fragile X, ADHD, ASD | SPD |
| subtype of SPD: predisposition to respond too much, too soon, or for too long to sensory stimuli most people find fine | sensory over - responsiveness |
| subtype of SPD: predisposition to be unaware of sensory stimuli, to have a delay before responding, responses are muted or responds with less intensity compared to average person | sensory under - responsiveness |
| subtype of SPD: driven to obtain sensory stimulation, getting stimulation results in disorganization, does not satisfy drive for more | sensory craving |
| subtype of SPD: poor perception of body position, poorly developed movement patterns that depend on core stability, appears weak and poor performance | postural disorder |
| subtype of SPD: difficulty thinking of, planning, and/or executing skilled movements especially novel movement patterns | dyspraxia |
| signs and symptoms: respond to stim more intensely; anxiety or discomfort in situations that wouldn't normally; transitions challenging; avoidant of change; compulsive and perfectionist habits; aversions to anything messy | sensory over - responsiveness |
| signs and symptoms: exhibit less of a response to sensory info than situation demands, take longer to react; high tolerance for pain; can be socially withdrawn; can be quiet and self-contained; tend to go overlooked | sensory under - responsiveness |
| signs and symptoms: nearly insatiable craving for sensory experience; may seem as tho they can't get enough stim., can be demanding and aggressive; may be frequently injured; "thrill-seekers" | sensory craving |
| signs and symptoms: difficulty stabilizing body during movement or at rest to meet demands of a given motor task, lack body control to maintain good standing/sitting | postural disorder |
| red flags: poor m. tone and/or seems weak compared to others, often slumps over, unable to contract mm. and pull against another force, difficulty using both hands at same time, difficulty crossing middle of body to complete a task | postural disorder |
| signs and symptoms: difficulty with organizing and integrating sensory info, learning rules of movement synergies, taking advantage of perceptual cues, solving movement problems in new situations, stationary tasks can be overly challenging | dyspraxia |
| signs and symptoms: behaviors - prefers fantasy games, prefers talking to doing, prefers sedentary activities, messy or sloppy eating, frustrated when unable to do things, may be bossy, needs to stick to rules/routines | dyspraxia |
| diagnosis: Diagnostic Classification of MH and Developmental Disorder of Infancy and Early Childhood, Revised; Diagnostic Manual for Infancy and Early Childhood of Interdisciplinary Council on Developmental and Learning Disorders; Psychodynamic DSM | SPD |
| course influenced by many factors - home life, nutritional status, early id, appropriate interventions; comorbidities - ADHD, ASD | SPD |
| treatment: occasional prescriptions for meds to treat various symptoms, OT uses a SIT approach | SPD |
| occ. performance: varies with difficulty; play, ADLs, IADLs, education, rest and sleep, health management, work, social participation | SPD |
| characterized by significant impairment in both intellectual functioning and adaptive behavior, as expressed in conceptual, social, and practical adaptive skills; originates before age 18 | intellectual disability |
| measured by IQ score; -2 SD indicates impairment; mild IQ - 55 to 69, moderate IQ - 40 to 54, severe IQ - 25 to 39, profound IQ - below 25; superior level IQ - 130+ | cognitive functioning |
| severity level of ID: 3rd to 6th grade skill level in reading, writing, and math; may be employed and live independently; preschool - often unimpaired; school - academic skills of 6th grade possible; adult - can learn social and vocational skills | mild |
| severity of SPD: basic reading and writing skills, functional self-care skills, requires some oversight; preschool - impaired social skills; school - academic skills up to 4th grade with modification; adult - unskilled or semiskilled vocation | moderate |
| severity of SPD: functional self-care skills, requires oversight of daily environment and activities; preschool - severely impaired communication; school - limited academic skills; adult - needs complete support and supervision | severe |
| severity of SPD: may be able to communicate verbally or nonverbally, requires intensive overnight; preschool - dependent for care; school - functional skills training; adult - dependent on care | profound |
| prenatal causes: chromosomal abnormalities, inborn errors of metabolism, developmental disorders of brain formation, environmental influences | intellectual disability |
| perinatal causes: anoxia - complete deprivation of oxygen, low birth weight, syphilis and herpes simplex, mechanical injuries at birth | intellectual disability |
| postnatal causes: psychosocial, child abuse and neglect, traumas/infections | intellectual disability |
| 4 commonalities in inborn errors of metabolism: inherited, issues with metabolism, can lead to ID, if not treated can cause brain damage and developmental delays | prenatal cause of ID |
| prenatal causes of ID: maternal malnutrition and infection, Fetal Alcohol Exposure, lead exposure, illicit drug exposure, exposure to radiation, Rubella | environmental influences |
| perinatal causes of ID: anoxia, mechanical injuries at birth, syphilis and herpes simplex | intellectual disability |
| postnatal causes of ID: nutritional problems, adverse living conditions, inadequate healthcare, lack of early cog. stim., child abuse and neglect, TBI, meningitis or encephalitis, lead poisoning | environmental and psychosocial problems |
| incidence and prevalence: 1% around the world (almost 2x higher in low- and middle-income countries); reduced rate than previous estimates; males 1.5x more likely to be diagnosed; sex-linked genetic disorders resulting in disorder | intellectual disability |
| signs and symptoms: early symptoms - GM/FM skill dev., language, problem-solving, memory, social skill dev.; functional presentation dep. on severity level and co-occurring diagnoses | intellectual disability |
| core symptoms: intellectual functioning - reading, writing, math, abstract thinking; adaptive limitations - comm., self-care, home living, social/interpersonal skills, leisure, health and safety, self-direction, functional academics, comm. resource use | intellectual disability |
| diagnosis: intellectual functioning - verbal comprehension, working memory, perceptual reasoning, abstract thought; how well a person meets community standards; onset during a developmental period | intellectual disability |
| course: time, interventions, supports may change severity levels; life expectancy - mild=no difference, severe/profound=shorter; goals - manage condition and achieve highest potential | intellectual disability |
| impact on prognosis: stigma - isolation, self-esteem, social exclusion, discrimination, anxiety and/or depression; strengths-based interventions - gain adaptive behavioral skills through remediation, AT | intellectual disability |
| treatment: used for co-occurring conditions; psychotropic meds for MH; those with neuromuscular dysfunction may use Botox, baclofen, etc. to address m. tone; indiv. supports - therapies, ed., training programs, consults, organization involvement | intellectual disability |
| occ. performance: ADLs, IADLs, health management, education, work, play/leisure/social participation | intellectual disability |
| formerly called cerebral paralysis, painting in the Lourve first depiction of it, mid-1800s medical investigations began | cerebral palsy |
| complex, heterogeneous condition; movement, m. tone, and coord. are primarily affected; brain-based, non-progressive, permanent condition; lesion in immature brain that results in disorders of posture and voluntary movement | cerebral palsy |
| etiology: prenatal or perinatal origin; motor impairment may be accompanied by problems with sensory function, cognition, speech, and seizures (less common) | cerebral palsy |
| injury occurs when the brain is still developing; can occur during prenatal, perinatal, or postnatal periods up to age 3; abnormal m. tone and astereotypical patterns of movement which develop in an effort to compensate for lack of voluntary control | cerebral palsy |
| etiology: 85-90% injury occurred in utero; infection, trauma, or hypoxia; post-delivery CVAs; second most common neurologic impairment in childhood, following intellectual disability | cerebral palsy |
| occur when the brain does not grow properly or fully develop; ex. cerebral dysgenesis and microencephaly | congenital malformations |
| I & P: most common cause of motor limitations and childhood disability globally; more common in males (4:1); 1 in 500 live births; has increased in middle- and low-income areas; non-Hispanic black children have higher prevalence | cerebral palsy |
| increased survival rates of very low birth weight and premature infants; 15x more prevalent in twins, higher in triplets; infants smaller and premature are at a greater risk, common in multiple births | stable incidence of cerebral palsy |
| signs and symptoms: tone abnormalities, reflex abnormalities, atypical posture, delayed motor dev., atypical motor performance, associated disorders | cerebral palsy |
| symptom of CP: degree of resistance when a m. is stretched; hyper-, hypo-, dys-; involuntary or irregular m. contractions triggered by several factors - physiological changes, startle, emotional state, sleepiness, concentration on cog. tasks | tone abnormalities |
| symptom of CP: abnormal tone - retained primitive reflexes and delay in acquisition of righting and equilibrium reactions | reflex abnormalities |
| symptom of CP: delay in attainment of motor milestones; present at birth but not recognized until milestones achieved; motor abnormalities affected - asymmetrical hand use, unusual gait or crawling, uncoord. reach, difficulty with speech | delayed motor dev. and performance |
| diagnosis: 1. injury results in one of 3 periods; 2. once injury occurred no worsening; 3. abnormal m. tone and stereotypical patterns of movement; 4. mm. and nn. connecting them with spinal cord are normal; 5. lifelong disability | cerebral palsy |
| areas affected: cerebral cortex - spasticity; basal ganglia - athetosis; cerebellum - ataxia | cerebral palsy |
| classifications: spastic, dyskinetic/athetoid, ataxic | cerebral palsy |
| classification: spastic - monoplegia, diplegia, hemiplegia, and quadriplegia | cerebral palsy |
| type of spastic CP: increased m. tone especially antigravity mm.; paucity of movement; lack of selective m. activation | hypertonia |
| type of spastic CP: low m. tone, floppy, more often is transient (changes with age), may be associated with ataxia, may be associated with developmental delay | hypotonia |
| life expectancy associated with severity of motor, cognitive, visual impairment; mild-moderate - normal life span; severe - management of feeding and swallowing is important; ID is strongest predictor of survival | cerebral palsy |
| goal: gain motor control to poss. extent; positioning for max. indep. min. effects of abnormal m. tone/pain; instruct handling techniques; strats. to accomplish ADLs; recommend AE and AT to increase occ. performance; improve feeding and speech | cerebral palsy |
| medical management: gait analysis/monitoring, monitor skeletal changes, orthotic devices, monitor food intake; focus is on techniques to decrease spasticity and dystonia; oral meds to reduce spasticity | cerebral palsy |
| surgical management: pump implanted in abdominal wall that administers baclofen; botox into specific m., reduction in spasticity for 3-6 months; selective dorsal rhizotomy | cerebral palsy |
| occ. performance: body function - neuroMSK and movement-related functions; sensory function - visual difficulties, sensory processing difficulties; mental function - global and specific | cerebral palsy |
| occ. performance: ADLs; health management; rest and sleep - pain, dystonia, respiratory issues; education; work - environmental mods; play and leisure - motor limits; social participation | cerebral palsy |
| common link between all types of this disorder are decreased strength, m. cramping, decreased gross motor skills | muscular dystrophy |
| inability to rise up off the floor without using the UEs to walk up the thighs to assist with hip extension; child rolls onto hands and knees, bear weight by using hands to support while raising post., use hands to "walk" up legs to assume standing pos. | gower manuever |
| depressed area on the post. axillary fold, seen when the patient abducts shoulders to 90 degrees and flexes elbows to 90 degrees, pointing bilateral hands upwards | valley sign |
| MD subtype: x-linked recessive inherited condition, only men; ABSENCE/DEFICIENCY of dystrophin causing fragile m. cells; symptoms - delayed motor dev., proximal weakness, increased fatigue; age of onset - symptoms arise at 3-4 years | Duchenne MD |
| MD subtype: observed - waddling gait, enlarged calf mm., increased falls, failure to learn to run or jump; most are wheelchair dependent by 12-15 years; contractures on top of w/c use leads to contractures of 90 degrees + later on; most limiting | Duchenne MD |
| MD subtype: affects voluntary skeletal mm. and cardiac and pulmonary mm.; up to 1/3 have cognitive impairment; 90% have valley sign; life expectancy ~30 years | Duchenne MD |
| MD subtype: SHORTER than normal dystrophin protein levels causing partially functional m. cells; x-linked recessive inherited condition; age of onset - onset of symptoms vary from 5-60 but often between 6-18 | Becker MD |
| MD subtype: observed - delayed ambulation, difficulty climbing stairs, "toe-walking", m. cramps, fatigue; facial mm. are not affected; heel cord contractures and lumbar lordosis develop to compensate for pelvic weakness | Becker MD |
| MD subtype: progression of m. wasting/weakness - prox. to dist., symmetric; starts in pelvic girdle and thighs then to trunk and UE; calves and forearms preserved until later stages; slower rate than DMD; life expectancy - ~40-50 years | Becker MD |
| MD subtype: OVER 50% of id'd subtypes of MD; classified by age of onset, rate of progression, type of inheritance; most are autosomal recessive inheritance with a childhood onset; others are autosomal dominant with a late adolescence/adult onset | Limb - Girdle MD |
| MD subtype: signs - symm. or asymm. m. weakness; starts in pelvis and shoulders; waddling gait; slow variable m. wasting; m. cramping; enlarged calves; severe lordosis with scoliosis; prox. m. weakness; positive Gower sign; cardiopulm. complications | Limb - Girdle MD |
| MD subtype: TEEN OR ADULT ONSET; 50% live >50 years; autosomal dominant inherited disorder, both males and females; m. weakness progression is slow; 30% die from cardiac complications | Myotonic MD |
| MD subtype: weakness begins in face, LEs, forearms, hands, neck (distal), worse in cold weather; delayed relaxation after contraction; affects other organs including eyes, heart, GI system, respiratory system | Myotonic MD |
| MD subtype: 3rd most common type; autosomal dominant inherited; affects men and women; onset between 7-20; early onset = more severity and faster progression; weakness is not symmetrical | Facioscapulohumeral MD |
| MD subtype: facial, shoulder, upper arm musculature affected initially; difficulty with or unable to close eyes; asymm. smiling; drooping of corners of mouth at rest; atrophy of facial mm. mass; winged scapula; may progress to pelvic mm., affecting gait | Facioscapulohumeral MD |
| MD subtype: less common; x-linked recessive inheritance; onset - by age 10; cardiac complications, frequent pacemaker placement which is a major cause of early death; have ave. lifespan with early intervention and medical management | Emery - Dreifuss MD |
| MD subtype: generally symm. m. contractures appear before m. weakness is recognized; heel cords, elbows, post. neck | Emery - Dreifuss MD |
| etiology: Duchenne, Becker, and Emery-Dreifuss fall under this categoty | x - linked |
| etiology: Emery-Dreifuss and Limb-Girdle fall under this category | autosomal recessive |
| etiology: Emery-Dreifuss, Limb-Girdle, Facioscapulohumeral, and Myotonic fall under this category | autosomal dominant |
| diagnosis: present or complain of symptoms including m. weakness, increased falls, m. cramps, increased fatigue; testing to confirm or rule out - genetic testing, EMG testing, m. biopsy | muscular dystrophy |
| treatment: no cure or specific tx. to reverse or stop progression; focus on symptoms management, enhancing QOL, increasing life expectancy, maintaining independence as long as possible - respiratory, skin integrity, pain, and nutrition | muscular dystrophy |
| treatment: OT/PT - HEP, baseline for ADLs, mobility; prevent/slow loss of strength, ROM, and function; assess/monitor for equipment needs, splints, orthotics for stability and prevention of contractures | muscular dystrophy |
| treatment: corticosteroids - decrease m. damage, immunosuppressants - delay m. degen., anticonvulsants - control m. activity, antibiotics - respiratory infections | muscular dystrophy |
| surgical management: focus on corrective and preventative procedures - contracture release, scoliosis repair, cardiac stability, respiratory assist, spinal stabilization, pacemaker placement, tracheostomy (vent), feeding tubes | muscular dystrophy |
| occ. performance: ADLs - strength and fatigue, health management - rate of progression, education, work, play, leisure, social participation - anger and frustration | muscular dystrophy |
| etiology: Cornelia de Lange Syndrome, Prader-Willi Syndrome, William's Syndrome | genetic |
| etiology: Cri-du-Chat Syndrome, Down Syndrome, Klinefelter's Syndrome, Turner's Syndrome, Fragile X Syndrome | chromosomal |
| etiology: Galactosemia, Hunter Syndrome, Phenylketonuria, Tay-Sachs Disease | inborn errors of metabolism |
| etiology: microcephalus and hydrocephalus | brain formation |
| periventricular leukomalacia, hypoxic-ischemic encephalopathy, intraventricular hemorrhage, IVH grade 1-2, IVH grade 3-4 | injuries to brain resulting in CP |
| associated disorders: cognitive impairment, orthopedic conditions, seizure disorder, visual impairments, oral motor and communication disorders, gastrointestinal, pulmonary | cerebral palsy |
| type of CP: monoplegia - 1 limb; diplegia - trunk and LEs, UEs to a lesser degree; hemiplegia - 1 total side, UE usually more than LE; quadriplegia - all 4 limbs, head, and trunk; motor cortex | spastic |
| type of CP: disorder of balance and control in timing of uncoordinated movements seen with weakness; wide-base gait with tremor; cerebellar involvement; least common type | ataxia |
| type of CP: impairment of power of voluntary movement; basal ganglia | dyskinesia |
| level of CP: uses no assistive devices; can walk indoors and outdoors with no limits; can run and jump; decreased speed, balance, and coordination | level 1: walks without limitations |
| level of CP: limited in outdoor activities; ability to walk indoors and outdoors and climb stairs with a railing; difficulty with uneven surfaces and inclines; minimal ability to run and jump | level 2: walks with limitations |
| level of CP: walks with assistive mobility device indoors and outdoors on level surfaces; may be able to do stairs with a railing; may propel manual wheelchair | level 3: walks using a hand-held mobility device |
| level of CP: self-mobility severely limited even with assistive devices; uses wheelchairs most of the time and may propel their own power wheelchair | level 4: self - mobility with limitations |
| level of CP: physical impairments that restrict voluntary control of movement and ability to maintain head and neck position against gravity; all areas of motor function impaired; cannot sit or stand on own; no independent mobility | level 5: transported in a MWC |
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emma.scarmon-coyotes
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