Adult Comm unit 4 Final

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Adult Comm unit 4 Final
2013-04-29 12:36:04
adult comm unit final

adult comm unit 4 final
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  1. potential cognitive deficits after RHBD & subsequent impacts on comm
    • Coarse coding deficit: LH narrows down word meaning by way of limiting potential possibilities, such as round, red as features of apple. RH widens (coarse) possibilities for word finding. RH allows for more distant possibilities from the core such as rotten as a feature of apple. May facilitate processing of unfamiliar sentences.
    • Suppression deficit: mentally activate multiple meanings of words & phrases, but then suppress what is incompatible. Ppl with RHD may sustain the mental activation of contextually inappropriate meanings for too long. Deficits in this & coarse coding can lead to difficulties in conversational comp.
    • Cognitive resources: attentional processing demands. Limits on attentional capacity. Impacts of more demanding discourse environments.
    • Social cognitive deficits: ability to use politeness conventions & info about interpersonal relationships & to reason using theory of mind. Allows ppl to understand & interpret their own & other people’s mental states, & to predict & explain their behavior. Deficits in competent social relations. Indifference. Reduced affect, self-monitoring deficits.
  2. anatomical diff b/w R & LH
    • RH: diffuse effects that are not readily reducible to specific linguistic or comm. abilities. Less discrete communicative impairments. Requires assumption, less straight-forward. Normative data is quite limited.
    • LH: focal effects on specific linguistic & comm. abilities. Discrete comm. impairments. Easily quantified, straight-forward. Normal is better defined.
  3. symptom/ assessment/ tx options
    • prosody: S- inability or reduced ability to produce or comprehend linguistic and/or affective info communicated by F0 (pitch), intensity (loudness), or duration cues in speech; impact on emotional utterances; monotone. A/T- teach patient how to use emotional intonation by explaining written descriptions of emotional tones of voice & match the description to written labels & emotional faces; working on increasing prosody together by talking in unison with clinician; contrastive stress drills.
    • discourse & pragmatics: S- deficits in overall meaning, gist, topic, theme and/or moral of narrative; issues with global coherence; overemphasis of details; issues with sarcasm, irony, figurative expressions; understanding appropriate comm., context; processing emotional faces/non-verbals; sensitivity to listener needs & situations; humor- unrestrained hilarity to difficulty appreciating humor. A- ave utterance length; appropriateness of content; ability to comprehend ambiguity & metaphors (test of lang competence); emotion & non-verbal comm. (the awareness of social inferences test); listening behaviors checklist. T- increase consistency, redundancy of info; summarize, sort or explain stimuli by theme or gist; self monitoring for typical errors; diagrams, charts, note cards, other visual representations of discourse; topic control; use as few words as possible; interpersonal skills; emotional & non-verbal processing (train comm. partner to explicitly state emotions); awareness of non-verbal behaviors; recognizing, associating, identifying discrepancies; explain diff b/w literal & contextually intended meanings.
    • reading & writing: S- difficulty processing visual info; issues of neglect. A/T- line bisection test; clock drawing test. T- depends much upon pre-morbid level; attention to left (highlighting, stickers); functional tasks (instructions, grocery lists); organizational guides; reading comp strategies.
    • Attention: S- limitations inattention needed to perform cognitive-comm tasks; alertness; ability to arouse & maintain attention; issues with divided & switching attention. A- brief test of attention, test of everyday attention
    • Memory: S- recall & recognition deficits, story memory, word list learning. A- everyday memory questionnaire, rey complex figure test & recognition trial. T- eternal memory aids (memory notebooks), assistive tech, focus on patient identified needs, spaced retrieval training.
    • executive functioning: S- planning, organization, reasoning & problem solving. A- behavioral assessment of the dysexecutive syndrome (BADS) T- problem solving activities
  4. role of SLP in dementia
    • Primary role in screening, assessment diagnosis, treatment, & research of cognitive-comm disorders, such as dementia.
    • Identification, assessment, intervention, counseling, collaboration, case management, education, advocacy, research
  5. mild cognitive impairment
    • Subtle cognitive deficits may be present up to 9 years before dementia diagnosis.
    • Transitional, pre-clinical state, a condition in b/w the cognitive changes associated with healthy aging & the more pathological changes the accompany Alzheimer’s disease.
  6. dementia diagnostic criteria
    Acquired (not congenital); persistent (not transitory); several areas of impairment; not focal, like aphasia; dementia is most common diagnosis in nursing home; over age 65, 6 30% of pop have it; over age 85, 50-60%.
  7. early signs of dementia
    Memory failure, disorientation, lapses in judgment, difficulty performing ADLs, difficulty performing mentally challenging tasks, misplacing things, apathy & loss of initiative, changes in mood.
  8. causes of dementia symptoms
    Vascular, psychiatric (depression), metabolic disorders, nutritional deficiencies, drug overdose/side-effects, infections, toxic poisoning, many are reversible.
  9. types of dementia & clinical presentations
    • Alzheimer’s disease: insidious onset; gradual, slow progression. Most common type; pervasive episodic memory impairment; relatively spared non-declarative memory function until later stages.
    • Vascular dementia: abrupt or more gradual onset; step-wise progression. Documented evidence of cerebrovascular & cardiovascular disease; memory deficits, not as striking as in AD; gait disturbances, falls, early onset of incontinence, personality & mood changes.
    • Dementia with lewy bodies & parkinson’s disease: insidious onset; relatively rapid progression. Parkinsons features; worse visuospatial & executive function impairments than AD; better memory function than AD early on.
    • Mixed dementia: variable onset, variable progression. Combo of features of AD & VaD; combo of features of AD & DLB.
    • Frontotemporal lobar degeneration: early onset, rapid progression. Early appearance of changes in behavior, social function, lang, & personality; episodic memory relatively spared in the early stages.
  10. differential diagnosis of vascular dementia vs alzheimer''s dementia
    • VaD: (onset & progression)- abrupt onset; step-wise progression. (neuroimaging findings)- evidence of multiple ischemic lesions, hemorrhagic events, & white matter lesions is required for diagnosis per DSM-IV-TR guidelines. (focal neurological signs)- present. (Hachinski ischemia scores (HIS))- score of 7 or greater. (attention)- worse performance than AD. (episodic memory imparment)- better performance on immediate & delayed verbal memory measures, compared to persons with AD. (gait alterations)- present early & are more common. (personality changes)- more likely; tend to occur earlier in the course.
    • AD: (onset & progression)- insidious onset; gradual progression. (neuroimaging findings)- evidence of hypoperfusion of the medial temporal lobe areas including the hippocampus, entorhinal & perirhinal cortices, & parahippocampal gyrus; no evicende of cerebrovascular event for probable AD diagnosis, per DSM-IV-TR guidelines. (focal neurological signs)- usually absent. (hachinski ischemia scores (HIS))- score of 4 or lower. (attention)- better performance than VaD. (episodic memory impairment)- cardinal, early-appearing, severe deficit on delayed verbal memory measures. (gait alterations)- may present later; not as common. (personality changes)- less likely than in VaD; tend to present in the middle to late stages.
  11. differential diagnosis of dementia with lewy bodies & parkinson's dementia & alzheimer's dementia
    • DLB & PD: (onset & pregression)- insidious onset; relatively rapid progression. (histopathology)- hallmark; abnormal intracellular inclusion bodies called lewy bodies, composed of alpha-synuclein protein; neuritic plaques may be present; neurofibrillary tangles are rarely present. (extrapyramidal sings & parkinsonian features)- present; tremors, rigidity, bradykinesia. (visuospatial impairments)- worse than AD. (executive function impairments)- worse than AD. (visual hallucinations & fluctuations in consciousness)- present early & are more common.
    • AD: (onset & progression)- insidious onset; gradual progression. (histopathology)- hallmark; neurofibrillary tangles & neuritic plaques, composed of beta-amyloid. (extrapyramidal signs & parkinsonian features)- rare but possible. (visuospatial impairments)- better than DLB & PD. (executive function impairments)- better than DLB & PD. (visual hallucinations & fluctuations in consciousness)- infrequent.
  12. differential diagnosis of fronto-temporal lobe dementia & alzheimer's dementia
    • FTLD: (onset & progression)- early onset to age 655 years; onset is most common in the 50s; rapid progression. (neuroimaging)- progressive atrophy of the frontal & anterior temporal lobe; semantic dementia (SD)- inferolateral temporal lobe atrophy; progressive nonfluent aphasia (PNFA)- left perisylvian area involvement [insula, brocas area, motor & premotor cortices]; frontal variant- orbitomedial frontal lobe atrophy. (histopathology)- prominent neuronal loss with microvascular or spongiform changes, severe gliosis, inclusion bodies in some cases. (episodic memory)- relatively spared especially in early stages. (social disinhibition)- early appearing & marked deterioration in socially appropriate behavior. (lang deficits)- variable depending on type; SD- semantic associatons & conceptual knowledge are dramatically affected; PNFA- agrammatism, apraxia of speech, dysarthria, verbal perseveration, mutism; frontal variant- sparse lang
    • AD: (onset & progression)- insidious onset; gradual progression. (neuroimaging)- hypoperfusion of the medial temporal lobe including the hippocampus, entorhinal & perirhinal cortices, & parahippocampal gyrus. (histopathology)- neurofibrillary tangles & neuritic plaques, composed of beta-amyloid. (episodic memory)- severely impaired in early stages. (social disinhibition)- not the cardinal symptom in  early stages; when present, social disinhibition is not as marked as in FTLD. (lang deficits)- subtle in early stages; more pronounced in middle stages; lang deficits stem from episodic memory impairment.
  13. effects of alzheimer's disease on comm in early, middle, & late stages
    • Early stages: (sounds)- used correctly. (words)- may omit a meaningful word, usually a noun, when talking in sentences; may report trouble thinking of the right word; vocab is shrinking. (grammar)- generally correct. (content)- may drift from topic; reduced ability to generate series of meaningful sentences; difficulty comprehending new info; vague. (use)- knows when to talk, although may talk too long on subject; may be apathetic, failing to initiate conversation when it would be appropriate to do so; may have difficulty understanding humor, verbal analogies, sarcasm, & indirect & nonliteral statements.
    • Middle stages: (sounds)- used correctly. (words)- difficulty thinking of words in a category; anomia in conversation; difficulty naming objects; reliance on automatisms. (grammar)- sentence fragments & deviations common. (content)- freq repeats ideas, forgets topic, talks about events of past or trivia; fewer ideas. (use)- knows when to talk; recognizes questions; may fail to greet; loss of sensitivity to conversational partner; rarely corrects mistakes.

    • ·     
    • Late stages: (sounds)- generally used correctly,
    • but errors are not uncommon. (words)- marked anomia, poor vocab, lack of word
    • comp; may make up words & produce jargon. (grammar)- some grammar is
    • preserved but sentence fragments & deviations common; lack of comp of many
    • grammatical forms. (content)- generally unable to produce a sequence of related
    • ideas; content may be meaningless & bizarre; subject of most meaningful
    • utterances is retelling of a past event; marked repetition of words &
    • phrases. (use) – generally unaware of surroundings & context; insensitive
    • to others; little meaningful use of lang; some patients are mute; some are
    • echolalic.
  14. assessment options in dementia
    • Rating scales: quick, but not sensitive; insensitive to subtle intellectual decline; not good for early stages or suspected dementia
    • Targets for rating: estimate of intellectual abilities; competence in ADLs; both.
    • Arizona battery for comm. disorders of dementia (ABCD): identify & quantify comm. deficits or persons with dementia, specifically alzheimers; 4 screening subtests speech discrimination, visual perception & literacy, visual fields & visual agnosia); 14 additional subtests to evaluate mental status, linguistic expression, verbal memory, linguistic comp, & visuospatial construction.
  15. coping with dementia
    Progressive, irreversible nature of dementia rules out restoration of lost abilities; clinical effort is rather a holding action in which the advancing effects of neurologic disease are lessened by helping the person with dementia & their caregivers control the effects on daily life.
  16. purposes of intervention in dementia
    Minimize the disruptive effects of comm. disorder on person with dementia & support caregivers; ensure the safety of person with dementia & keep them healthy; provide support & direction for person with dementia & caregivers.
  17. spaced retrieval training (SRT)
    A memory training procedure in which patients are trained to perform newly taught procedures, recognize newly taught stimuli, or remember to do something at a designated time with gradually increasing time intervals b/w training & performance.
  18. external memory aids
    Visual schedules, alarm clocks, memory wallets.
  19. TBI
    The result of abrupt external forces acting on skull & brain, as when a moving object such as a bullet, club, or baseball strikes the head, or the moving head strikes a stationary object such as an automobile dashboard, tree or sidewalk.
  20. cognitive-lang profiles associated with TBI
    Aphasia is a result in about 20-30% of all adults with closed-head injury; most other TBI patients have cognitive-comm impairment (orientation, attentional problems, visuospatial skills, problem solving/higher reasoning/executive function, personality changes, memory problems.
  21. incidence & prevalence of TBI
    About 1.4 mill US residents receive medical attention for TBI each year; the precise incidence of TBI in US is unknown; if only persons who receive treatment for TBI are counted, the incidence is likely to be about 100 per 100,000 per year; if the count includes an estimate of persons injured but not counted, the incidence may be as high as 250 per 100,000 per year.
  22. risk factors of TBI
    More men have TBI than women; twice as many males b/w 15 & 25 years have TBI than women; leading cause of neurologic injury in persons under age 50; older adults toddlers are more likely to experience them than young adults.
  23. causes of TBI
    Vehicular accidents, falls, assults, child abuse.
  24. open vs closed head injury & impacts of loss of consciousness
    Penetrating (open) head injury often does not cause unconsciousness; loss of consciousness occurs more often in closed head injury
  25. coup vs contracoup injury
    Site of blow bruising; site directly opposite to where the blow was struck
  26. potential damage that may occur in TBI
    • Shearing/Twisting: brain tissue alternatively compressed & stretched, leading to diffuse axonal injury, deafferentation, & finally collateral sprouting or dendritic proliferation
    • Tearing: of brain tissue may be caused by the uneven & sharp edges within the cranial vault
    • Contusion/Hemorrhage/Hematoma: bruising, bleeding, & accumulating blood from the impact
  27. secondary consequences of TBI
    • Edema/hydrocephalus: accumulation of fluids b/w the brain & skull, in the ventricles, or in the brain tissue (hydrocephalus) may cause brain swelling (edema)
    • Intracranial pressure: edema, hydrocephalus, & hemorrhage may cause heightened pressure inside that skull compressing & displacing brain tissue & increasing neurologic impairment
    • Brain ischemia: (insufficient oxygen supply to brain tissues) caused by physical injury to heart or lungs, pressure squeezing
    • vessels, & cerebral vasospasm (contraction of muscles surrounding a blood vessel)
    • Blood-brain-barrier: may allow normally excluded substances (proteins, neurotransmitter chemicals) to enter brain tissue)
  28. concussion & post-concussive syndrome
    • Concussion: physiologic injury to brain w/o evidence of structural alteration
    • Postconcussive syndrome: (headache, vomiting, memory loss, dizziness, double vision, blurred vision, emotional liability, sleep disturbances) persisting for weeks or months; can last a year; more common in children.
  29. purpose of glasgow coma scale
    Eye opening; motor responses; verbal responses
  30. prognostic indicators in TBI
    • Focal injuries usually have a better prognosis than diffuse injuries
    • Coma is defined as Glasgow Coma Scale (GCS) score of 8 or less; GCS assesses responsiveness in immediate post-injury period
    • GCS scores of 3-8 denote severe head injury; scores 9-12 denote moderate; scores 13-15 denote mild
    • Research studies have found the score taken 6 hrs after injury to have a relationship with recovery, however, patients may get worse after 6 hrs so they much be continuously assessed.
  31. behavior management in TBI
    • May manipulate antecedent stimuli (stimuli that elicit or maintain certain behaviors) or response contingencies (consequences for behaviors) (verbal praise, music, sweets) or extinction, selected responses elicit neither pleasurable nor aversive stimuli
    • Attend to settling events (neurologic state, physiologic state, cognitive state, emotional state, attitude & belief states, living arrangement, presences or absence of specific people, recent history of interaction, environmental stresses, time of day
  32. pharmacological intervention considerations in TBI
    Dosage must be monitored; side-effects must be carefully monitored; pharmacological tx may stimulate alertness & attention; may reduce agitated behaviors (often sedative, anticonvulsant or antipsychotic); may decrease depression or sadness (often sedative)
  33. cognitive-comm rehab considerations in TBI
    • Restorative interventions: designed to restore cognitive-comm process, seeking to promote patients’ capacity for independence in daily life by treating specific cognitive processes such as attention, memory, & lang. improvement in one cognitive-comm process is meant to improve other related abilities (improvements in sustained attention may help reading abilities)
    • Compensatory/adaptive interventions: external aids, compensatory strategies, or modified environment to increase functioning in daily life activities
  34. attention training
    • May focus on any of the types of attention discussed previously, such as selective attention or divided attention.
    • Commonly used program called attention processing training (APT) is a training sequence with the theory that working on focused attention & sustained first will assist alternating & divided
    • Strategies & environmental support, psychosocial support for deficits
  35. memory training
    • Memory drills for improving retrospective memory (retention & recall of past experiences & events) largely have been abandoned in favor of compensatory approaches
    • Restorative training of prospective memory (permits intentions formed in the past to govern present behavior, such as remembering to remember, keeping appointments, going to class), however, has shown meaningful benefits. Internal strategies (mnemonic devices, imagery, expanded rehearsal time [spaced-retrieval methods]); external aids (checklist, calendars, electronic organizers, memory books)
  36. self-awareness training
    Training caregivers & providing education about the patients deficits & providing environmental support
  37. reasoning & problem solving interventions
    Tx may entail structured practice & coaching in stimulated or actual everyday situations; positive everyday routines & time-pressure management may contribute to improved planning & problem-solving in daily life.
  38. visuospatial processing training
    Appropriate for those who have trouble discriminating visual stimuli or analyzing spatial relationships; tx may include scanning drills, figure-ground discrimination tasks, & mental manipulation of visual stimuli
  39. lang & pragmatic training
    May be treated thru tx of the underlying non-linguistic cognitive processes; may also be treated thru direct pragmatic, comm. training; appropriate comm. behaviors may be practiced & modeled in daily-life tasks; group tx may be helpful
  40. community integration in TBI
    Focus is on re-entry into family, vocational, & community settings. Preparation usually takes place in residential transitional living facilities. Carried out by an interdisciplinary team
  41. family member considerations in TBI
    Support & reassurance are important in early stages of brain-injured family member’s recovery. Family’s needs for info & direction becomes greater as the patient’s survival is assured, & issues of coping & management become salient.