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105 Cards in this Set

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Lexical-Semantic Processing
*Using words and their meanings to understand and produce language
*Examples of errors under this category may include
-word-finding and word choice errors (paraphasias)
-impaired understanding of the meaning of words (word recognition
-impaired ability to follow commands or comprehend questions).
-impairments in accessing the phonological representation of words (resulting in phonemic paraphasias)
-trouble discriminating speech sounds which will affect comprehension.
Morphosyntactic Processing
*Using a rule based system to assemble words into sentences. Type of errors may include:
-poor/limited sentence structure
-the omission of certain parts of speech and tense markers (my name Jason, He talk yesterday, substituting he for she, etc.)
Difference Between Primary Progressive Aphasia (PPA) and Acute Onset Aphasia
*PPA is completely a separate entity from aphasia of an acute onset (i.e. from a stroke)
*Acute aphasia is completely not related to the development of PPA.
*PPA is a degenerative disease similar to Alzheimer's, except that only language deficits are present in the early stages.
*Cognitive deficits eventually are present.
Major differences:
-PPA:slow, gradual onset. Progressive deterioration. Not caused by a stroke, tumor, infection, but by atrophy of language areas. Eventually, cognitive impairments become apparent.
World Health Organization (WHO) International Classification of Functioning, Disability and Health
*Structure and function (impairment)
*Activities (disability):
*Participation (handicap):
*Environmental factors:
Structure and Function (WHO)
impairment
-Something is wrong with the brain and brain functions. aka. tumor on vocal cord. function is inability to voice.
In brain, structure is cellular damage language parts of the brain and impairment is inability to find correct words or phonemic pattern (function).
Activities (WHO)
disability
-Functional consequences of impairment, reduction of personal activities, specific task. aka. telling the nurse what you need / using the phone. (ADL=activities of daily living, IADL=instrumental activities of daily living).
Participation (WHO)
handicap
Impact of impairment and activity on social roles/life activities.
aka. things that affect daily life. Can't work. Problems engaging in daily life and its roles.
Environment (WHO-book differentiates this)
Wrapped up with participation. Can help or hinder a person's role.
aka. ADA wheelcahir access to building can limit participation. The amount of support from others or lack therof (need to be sent to subacute nursing facility).
Why is ICF important?
International Classification of Functioning
-helps us understand 'the big picture' and view the complexity of aphasia.
-Highlights the dynamic interaction of multiple factors in which aphasia can impacte each person's life.
-Makes us consider each individual uniquely.
-Wording "individual" with aphasia, aphasic does not refer to person.
aka. word finding goal helps patient talk to nurse, oral motor=structure and function, slow down and articulate=goes under activities. can't separate cognition and language much.
Intensive Care
medically unstable. Goal is life preservation. length of stay (LOS) less than a week. SLP is diagnostician and consultant to physicians.
Acute Care
typical hospital floor. Goal is differential diagnosis and stabilization. LOS 3-7 days. SLP consult and reccomends, screens, corrects diet, communicates with family.
Inpatient Rehabilitation Unit
medically stable, and can tolerate 2-3 hours of therapy. LOS 2-3 weeks. SLP's assess and give treatment (restore (impairment), adapt (activity/ participation)
team approach
Skilled Nursing Facility
for those who cannot tolerate intense therapy in inpatient. SLP treats, educates family, adaptive & restorative treatment.
Long Term Care - LTC
Limited nursing and rehab services. Goal is adaptive treatment. improve quality of life and manipulate environment.
Home Health
SLP-improves and maintains ind. functional abilities. (from daily restorative to less frequent focusing on environment) See where breakdowns happen at home.
Outpatient
4-12 weeks and is the least expensive setting. SLP helps to carry over strategies into real life. may target vocational goals. Insurance loves this option because it's cheapest.
Managed Care
System designed to reduce huge healthcare cost (fee for service). Diagnosis related group (DRG) determins reimbursement for Medicare by diagnosis. Resource Utilization Group (RUG) determines reimbursement based on nursing needs of patient.
Functional measures, functional outcomes & documentation. (word goals well to get reimbursed)
Aphasia
*"Aphasia is a selective impairment of the cognitive system specialized for comprehending and formulating language" aka. acquired language impairment breakdown in the brain circutry that underlies language function.
(speaking, listening, reading, writing-not motor deficit)
*Symbolic processing disorder (form and interpret symbols)
*May involve any or all modalities.
-Neurogenic. has to be acquired, have language then loose it.
-May have associated attn and memory problems.
-Reduced efficiency forming, producing speech, access to stored info and retention.
Neurogenic Causes of Aphasia
*Stroke / CVA (Ischemic, hemorrhagic)
*TBI (open / closed headwound)
*Tumors
*Progressive dementias (fronto-temporal, primary progressive, don't confuse with anomia)
*Infections
Aphasia is NOT...
*Apraxia: impairment of programing and positioning / sequencing. (groping, periods of error free speech, but coexists in aphasia)
*Dysarthria-impairment in ability to use muscles for speech.
*Not a problem of sensory function (aka agnosia; impaired ability to recognize /perceive a stimulus). bilateral hemisphere.
*Problem of intellect
*Part of being confused /psyciatric disturbed.
Language and Aphasia
*Language is cognitively based.
*Shared code to represent concepts though the use of symbols and rule based combinations of symbols.
4 Interrelated Components for Communication
*Language (content, semantics, form & structure, phonology, morphology, syntax. form/content/use)
*Speech
*Cognitive domains (attention / reasoning, memory)
*Pragmatics
Language
form/content/use.
-Phonology=phonemes / sounds. segmenting sound elements within words. suprasegmental is processing intonation, stress, pauses.
*Morphology-word endings that change meaning (ed. ing)
*Syntax-rules for word combination that allow us to understand passive/active sentences.
*Lexical (content) word forms in various modalities that rely on previously heard / seen words-something represents word in brain.
*Semantic - concept or meaning that words represent based on our network of info.
Speech
Motor output (distinguish between motor speech disorder and language impairment)
Cognitive Components
*Memory allows us to encode, store and retrieve info. Working memory (formerly short term) made up of attention span, capacity (7-12 pieces of info), time limit, mental manipulation of info.
*Long term Memory: info that was processed in working memory that is stored. Types include declarative (knowledge based on semantic / factual or episodic /autobiographical) or Nondeclarative (aka procedural. habitual and require little effort to recall).
*Memory processes: encoding / storage and retrieval. process of keeping info in active memory, storing in long term memory, then retrieving it through encoding (internal representations of info: association, rehearsal, catagories, chuncking) or retrieval (transfer info from long term to consciousness). To remember.
Components of Attention
*Sustained: ability to sit and focus on a certain task.
*Selective: prioritize to what you pay attention.
*Divided-listen to two things at once
*Alternating-alternate attention between two or more tasks.
(person w aphasia can be overwhelmed and may require one person at a time to focus).
Executive Functioning
High level set of abilities for generating, selecting, planning and monitoring behavior (planning, organizing, inhibition, reasoning, cognitive flexibility, problem solving, self monitoring)
Pragmatics
Rules of social use of language. Allows us to adjust language to different partners. State intent (request, greet). Take turns / initiate topic selection n maintenance. Use of conversational repair (repeat, elaborate, simplify).
Auditory Phonological Analysis
-discriminate sounds of speech input into words, syllables, and determine suprasegmental aspects.
Phonological Input Buffer
provides temporary storage (holding spot)
Phonological Input Lexicon
Library of spoken words previously heard
Acoustic Phonological Conversion
Allows translating what is heard directly into phonemes (needed to repeat aloud unfamiliar words)
Phonological Output Lexicon
Library of spoken words previously produced
Phonological Output Buffer
Temporarily stores phonemes of given word while the motor speech plans are being processed
Orthographical System (written word)
-Abstract letter ID: visual recognition of letters in fonts/ formats
-Orthographic input lexicon: stores the letter strings that correspond to oour vocab of written words
-Letter to Sound rules: used to translate graphemes into phonemes on a letter by letter basis (used to read unfamiliar words)
-Sound to letter rules: translate phonemes into graphemes (used in spelling unfamiliar words)
-Orthographic output lexicon: stores spelling of written vocab we previously used
-Orthographic Output Buffer-temporarily holds spelling while a word is being prepared to be written.
Classifying Aphasia
-Uni dimensional framework. Expressive and receptive as well as semantic and syntactic components are considered inseparable. Hildred Schule introduced this.
-Dichotomus=fluent / nonfluent, expressive / receptive
-Multidimensional=multiple forms of aphasia corresponding to a different underlying site of lesion and having charateristic list of features (lesion method).
-don't focus on ID type of aphasia. focus on strengths and weaknesses. No two are the same.
Words to Describe Aphasia
*Naming-word finding
*Fluency-on a scale 1-10
*Comprehension-follow directions and answer yes/no ?
*Repetition-repeating is a good way to do therapy.
Anomia
Difficulty finding words: names of people, objects, locations, concepts, actions.
-excessive pausing
-circumlocutions (describe, define, sound effect of target word)
Types of Fluent Aphasia
*Wernickes : Transcortical Sensory (wernikes aphasia with good repetition)/ Conduction : Anomic Aphasia
Types of Non Fluent Aphasia
Global Aphasia
Brocas Aphasia / Transcortical Motor Aphasia (like brocas with good repetition)
Paraphasias (anomia)
Errors in naming
phonemic-literal. sound errors involve substitutions, additions, oppissions, and/or rearrangements of target word phonemes (dog/bog)
semantic-word choice error that is semantically related to target word (mother=father, fork=knife)
random-substitutions that lack apparent semantic relations to the target words (dog=bottle)
jargon: production of entire sentences in which all content words and in some cases functior words (articles / prepositions) are replaced by neologisms (substitution of a non-word / new word)
Fluency
Phrase length inthe speech production as well as characteristics of melodic line, articulatory agility, speech rate, and grammatical form.
-fluent is without effort despite presence of sounds, words, or grammatical errors. normal phrase length.
-Nonfluent is with effort, halting, slow rate with little melodic features. short phrase length.
Paragrammatism
Substitution of inappropriate syntactic elements. Empty speech. Fluent speech lacking informational content.
Agrammatism
aka. Telegraphic speech
Breakdown in morphosyntactic processing. short utterances, omission of articles, conjunctions, plurals, tense markers. difficulty with complex sentences and questions.
Comprehension
Ability to understand verbal and written language (sign too)
*Breakdowns at various levels of complexity.
-Discriminating sounds
-Semantic processing
-Morpho-syntactic (can't understand word endings and combinations, esp. before /after or tenses)
*Rule out hearing loss
Repetition
Ability to repeat spoken language. compare to pts. spontaneous speech.
4 Classifications of Aphasia
Comprehension, Fluency, Repetition, Naming
Sulci
crevices or infoldings
-Sylvia fissure separates temporal from parietal and frontal
-Central sulcus runs from the separation of the hemispheres toward the sylvian fissure
Gyri
bumps or ridges
-Precentral gyrus=motor strip
-Postcentral gyrus=sensory strip
Stuff about Brain / Nerves to know
CNS/PNS
Grey matter is cell bodies. cerebral cortex is grey matter along w subcortical structure (thalmus & basal ganglia)
white matter is bundles of axons.
Supramarginal and Angular Gyrus
parietal lobe, and associated with comprehension of written language.
Brocas Area
inferior frontal gyrus. associated w/phonological representation, production of speech sounds, syntactic processing.
Wernickes Area
Posterior aspects of superior temporal lobe. Associated w comprehension of phonologic, semantic, and morphosyntactic linguistic processes.
Fiber Tracts
White matter. Integrate receptive and expressive language processes.
-Superior longitudinal fasiculus connects the frontal lobe to the parietal temporal and occipital cortices (cells that are wired together fire together)
-arcuate fasciculus connects wernikes and brocas.
Subcortical Structures of Note
Thalamus-major relay station. plan, memory, executive function. SO MANY deficits if there is a stroke here.
Basal ganglia-influences motor systems
Vascular supply-Internal Carotid
(from neck)
*Anterior and lateral blood supply to brain
*Main source of blood for anterior cerebral and mesial (inside middle deep part of frontal lobe) cerebral arteries (ACA, MCA)
*ACA: medial and orbital sectors of frontal lobe
*MCA: inferior and lateral sectors of temporal lobe. Lateral sectors of frontal, parietal and occipital lobes. (includes perisylivan language zones, brocas and wernikes, and lenticulostriate areteries to deep structures like the basal ganglia. these are vunerable to emboli and drops in blood pressure. MCA is our key blood vessel to language aeas and oxygenates perisylvian area. Does have superior and inferior branches.
emboli
traveling clot
Vascular supply-Vertebral
Both vertebrals join together to form the basilar artery.
PCA-posterior cerebral artery feeds the medial occipital, temporal lobe, and subcortical structures (thalamus) also feeds brainstem (survival functions and cranial nerve pathway).
Circle of Willis
our "little alien". aka. the joined system of anterior and posterior blood supply to prevent uneven blood flow.
Watershed Area
Edges of the three main territories of the ACA MCA and PCA (near sylvian fissure / temporal lobe). dual blood supply. more resistant to infarction (damage) from emboli (clot that forms, or apiece of fatty plaque that breatks off and blocks artery.) It is more vunerable to drops in blood pressure.
Broca's Aphasia
Nonfluent, effortful, relatively spared comprehension.
-agrammatism (verbal and written)
-Word finding better than sentence formation (syntactic processing and putting words together is difficult)
-Listener often able to guess and the speaker with Brocas can give feedback about accuracy.
- Often occurs with apraxia of speech, right hemiplegia (bc area is close to motor strip of left brain)
-Lesion: inferior frontal gyrus (brocas area) gen. in the anterior portion of brain by motor strip.
Transcortical Motor
similar to brocas except much better repetition abilities. non fluent, relatively spared comprehension. lesion is superior and anterior to Brocas /watershed area in generally the anterior portion of the brain.
Wernike's Aphasia
Fluent, marked comprehension, naming, and repetition deficits.
-Marked by paraphasias, empty speech.
-Paragrammatism
-Poor auditory comprehension of their own words
-Meaningless, stereotypic utterances
-Logorrhea, jargon
-can be misdiagnosed as psychiatric patients.
-May not have hemiplegia
-Lesion is Posterior portion of superior temporal gyrus.
Transcortical Sensory
Like Wernickes except better repetition, poor comprehension. Fluent, intact repetition, echolalia (most output is repetition).
Lesion is posterior and inferior to wernickes*
Conduction Aphasia
Fluent, relatively intact comprehension, poor repetition.
-impaired repetition, good spontaneous expression, occasional word finding problems with phonemeic paraphasias, good awareness and attempts at self correction.
Lesion at supramarginal gyrus and underlying white matter tracts (between brocas and wernikes). fairly rare.
Global Aphasia
Signifigant impairment in all modalities. Little to no verbal output, may perseverate on a word or sound, sensory and motor problems.
Lesion is entire perisylvian area including brocas, wernikes. anterior and posterior branch of LMCA. (no nothing).
Transcortical Mixed
isolation. similar to global, but with better repetition.
-Nonfluent speech, fluent repetition.
Lesion is whatershed areas around brocas and wernikes. This is obvious. can't say a word, but can repeat.
Anomic Aphasia
Isolated impairment in naming with fluent speech and good comprehension. Word finding deficits and empty speech, circumlocutions, fillers, generic terms (it, things) aka. decent words but not lot of nouns. May have some word recognition difficulties.
Lesion is at angular gyrus, posterior parieto-temproal juncture.
Subcortical Aphasia
Lesions to non-cortical structures in brain (beneath cortex of L hemisphere.) Deficits can change dramatically over time. unpredictable nature of symptoms, may have more sensory and motor impairment (basal ganglia, thalmus)
Crossed Aphasia
Term used to describe aphasia in right hemisphere lesions. Language dominance located in R hemisphere. Less than 4 percent of patients have crossed aphasia. (lefties)
Why should you be careful with labeling aphasia?
-symptoms may change as patient progressess
-no two patients are the same
-Most people fit into multiple categories, if they do (brocas) they will have different strengths and will respond to therapy differently.
-Different tests may categorize a person differently, could be the raters too.
-Diagnosis doesn't give basis to treat, but just gives an idea what might be affected to catagorize the patient. as a therapist, describe a pt. strength and weakness.
Where is Memory Located?
All over the brain.
Frontal lobe (encoding and retrieval strateties, working memory)
-Deep in medial temporal lobe (hippocampus, declarative and anterograde memories-new learning memory. it's sensitive to oxygen deprivation.)
-Basal ganglia / caudate nucleus (procedural memory-aka tying a shoe)
-Modality and domain specific regions (semantic memories)
Executive Functioning
Frontal lobes and its pathways.
CVA
Cerebrovascular Accident (CVA)-disruption of blood to the brain.
-Most common cause of aphasia and right hemisphere disorders.
-More individuals are surviving stroke, affectingthe costs of care.
-WHO defined as rapidly developing signs of focal or global disturbance of cerebral function-symptoms last over 24 hours w/no apparent cause.
-1/4 men 1/5 women have stroke if they live to 85.
-TIA brief focal cerebral event that develops reapidly and resolves w/n 24 hours (most 2-3 hours).
Ischemic
*Deficient blood due to a complete or partial occlusion of arteries (adema=swollen brain)
-Cells unable to maintain cellular funtion and to remove toxic waste.
-Results in necrosis (cell death) and an infarct (area of dead brain tissue) develops with loss of tissue bulk.
-Ischemic penumbra=surrounding zone of ischemia around the inner zone of infarction.
-Lacun=small ischemic stroke in a small penetrating artery (lenticulostriate arteries in BG)
Hemorrhagic
Rupture of blood vessles within the cranium and floods the brain tissue. Blood is not brain cells friends. it destroys tissue.
*Blood displaces / compresses and destroys brain tissue, arteries, cranial nerves due to aneyrysms, arteriovenus malformations (AVM's), trauma (carotid dissection)
-Anerysm-weakening of artery or vessel wall
*Intracerebral hemorrhage (ICH) is within the brain tissue, intraparenchyma=inside brain.
*Subarachnoid hemorrhage (SAH) blood spills into the arachnoid space around the brain
*Subdural hematoma (SDH) between the dura layers protecting the brain (above the arachnoid mater) outside brain.
*Higher mortality, but less permanent brain damage if treated successfully.
Thrombotic
(Ischemic Stroke)
Build up of fatty plaque (atherosclerotic plaque)
-Atherosclerosis=a disease of the artieries in which fatty materials deposited in the vessel wall, resulting in narrowing and eventual impairment of blood flow.
-Thse deposits form lesions in which the body responds by lying down fibrin material, platelyet adheasion and traps the blood cells forming a thrombosis (clot that forms inside a blood vessel or heart cavity). Arteries become hard. (Diabetes=brittle).
Embolic
(Ischemic Stroke)
Blood clot that moves through the bloodstream until it lodges in a narrowed vessel and blocks circulation
-common source is from the heart (atrial fibrilation=irregular heart beat that causes blood to pool in heart and a greater chance of clots)
-other body parts:
DVT=deep vein thrombosis, or poor circulation.
Stroke Signs
Slurred speech
Impaired language
trouble swallowing
trouble communicating/ understanding
numbness
motor dysfunction
double vision
weakness
gait/posture instability
Risk Factors
Smoking (raise blood pressure)
Heart disease
Obesity
Cancer
Substance Abuse (cocaine)
high cholesterol
diabetes
genetic
10-20% higher chance of a stroke if you had a TIA within a year. 30-60% of stroke within 5 years.
If symptoms resolve, it's a TIA and won't show on brain scan.
If there are symptoms there will be permanent damage.
Diaschisis
Temporary suspension of functions that depend on structures remote from an infarct
Infarct
area of dead brain tissue.
Edema
swelling
Stroke Imaging
-CT: computer Assisted Tomography. Radiation is used to diagnose hemorrhages. does not allow for immediate visualization of ischemic infarct and may not show tiny lesions. Docs rec CT first to rule out bleed. Blood is very bright.
MRI-magnetic resonance imaging, shows sharper image w/o radiation
-MRA: images blood vessels.
Carotid endarterectomy (CEA)
Surgical removal of thrombotic material from carotid artery.
-decreases stenosis (narrowing) and improves blood flow.
-May stroke during procedure, but is necessary bc carotid might be fully blocked.
Aneurysm Clipping
Surgical procedure to stabilize an aneurysm
Craniotomy
Opening the cranium. Procedure to access brain and remove hematomas (clots) or relieve pressure / perform aneurysm clipping.
Medications to Treat Stroke
t-PA (tissue plasminogin activator) clot buster. use within 3 hrs of stroke to decrease evidence of bleeds. thins blood, so be careful of recent surgery n head trauma.
-Anticoagulants: blood thinner to prevent clotting and attemt to return blood flow (heparin, Cumadin=generic warfardin, or rat poison.)
INR (international normalized ratio) is how thin is blood. need between 2-3.
-Antiplatelets: prevents platelets from adhering
-Vasodilators: relaxes arterial walls
-Antihypertensives: reduce blood pressure.
Meningioma Tumor
(may result in stroke)
benign, slow growing
low occurance rates
does not invade cortical tissue
may result in transient aphasia
Glioblastoma Multiforme
(may result in stroke)
rapidly growing, very invasive growth of glial cells
survival avg. 1-6 years
Infection
Infection may cause neurogenic language disorders.
Inflammation of brain.
Other Cognitive Communication Disorders
Deficits NOT considered to be aphasia (underlying cog impairments):
TBI
Dementia
Right hemisphere disorders (non dominant language hemisphere)
Alexia
loose ability to read
Agraphia
loose ability to write
apraxia
motor planning disorder.
dysarthria
motor speech disorder.
PPA
Primary Progressive Aphasia: type of frontotemporal degeneration in left frontal lobe and insular cortex. single symptom, but does not reflect brain pathology.
-degenerative cognitive condition, not from trauma.
-aphasia may be first symptom of neurologic disease (CNS)

-Agrammatic output, motor speech impairments, anomia
-aphasia without dementia, (trouble word finding, comprehension, read/write, cog, executive function, attention)
-other mental functions are preserved
-When cog. functions are evident of another disorder, the diagnosis changes from aphasia. ex. aphasia plus dementia.
-considerable variability in criterion for PPA in published studies.
Area: left perisylvian region. Presence of Tau
Variants of PPA
Progressive non fluent aphasia (PNFA)
Logopenic Progressive Aphasia (LPA)
Semantic Dementia (SD)
Progressive NON FLUENT Aphasia
-Atrophy in left frontal lobe and insular cortex
-Deficit at level of articulatory programming and accessing lexical representations, disruptions in syntax and grammar.
-Understands single words and simple sent, however, complex syntax may be difficult.
-Associated with corticobasal degeneration and progressive supranuclear palsy.
Presence of Tau protein (dementia).
Logopenic Progressive Aphasia
*Atrophy in left posterior temporal cortex and inferior parietal lobe
*Logopenic=without words.
*hesitant, anomic, poor repetition, phonological errirs, impaired sentence comprehension, halting anomic quality of spontaneous speech with marked hesitations
*Disturbance in accessing phonological lexicon and inpaired phonological working memory
*Motorspeech behaviors, single word comprehension, word meaning preserved
*Auditory-verbal short term memory (AVSTM) trouble following conversations, individual cannot "hold" onto info long enough to decipher meaning.
*underlying pathology associated with Altzheimers (tangles and plaques)
Semantic Dementia
*FLUENT-motor speech preserved
*Accurate grammar
*severe anomia with semanti memory impairment (poor single world comprehension even when presented in other modalities)
*Semantic paraphasias (table for chair)
*Pathologically associated of ubiquitin protein (in absence of tau)
How to Recognize PPA
Patients are aware of problems before family and friends, and are usually able to cover it up.
-frusteration and depression common
-language demands for job or ADLs are affected, but not daily routines (rote).
-associated with a specific stressful event or highly demanding episode.
-50% of pts with PPA developed nonaphasic impairments 5 years after. (dysarthria, dysphagia, facial weakness, apraxia, rigidity/ tremors)
-Death avg/ 7 years (3-17 range).
(dementia or Alzheimers are not aware)
Neuroimaging and PPA
-sometimes normal
-some reveal atrophy: decreased blood flow, decreased glucose
-left perisylvian and anterior temporal and inferior parietal lobe atrophy. some have right abnormalities, but left is greater
PPA and Autopsy
*cellular changes do not correspond to well known specific or clinical findings.
-some have picks disease
-20-30% Alzheimers
-tau, changes in glia
PPA Treatment
*Consider patients motivation, and resources (cognitive, financial)
*Behavioral treatment can focus on proactive strategies, educate family, give sense of purpose and control
*Traditional aphasia intervention is good for short term treatment for those with PPA
*the condition is not reversible by therapy, but can provide relief
*family counseling is integral in success and coping.
*frequent followup to establish pattern of decline
*treatment adjusted often
*AAC introduced early
*Family involved