spaud 101 final exam

brainstem stroke affects on dysphagia

(oral stage difficulty, delayed/absent pharyngeal swallow)

\*incomplete laryngeal elevation/ closure and reduced upper esophageal sphincter opening (aspiration, inability for bolus to enter esophagus)

dementia affects on dysphagia

(reduced oral awareness, food help in mouth, pharyngeal swallow delay)

prematurity affects on dysphagia

swallow abilities - 30-40 weeks gestation

weak facial muscles, under developed lungs

uncoordinated or week suck (reflexes 3-8 weeks before birth)

cerebral palsy affects on dysphagia

degree of motor deficit important

cognitive difficulties inadequate velopharyngeal closure

larynx doesnt elevate, pharyngeal peristalsis

childhood language disorders

significant difficulties with cognitive or linguistic abilities that support language. Limitation in language form, content, or use that interfere with participation in social academic activities.

patterns of language impairment

content (semantics), form (syntax, morphology, phonology), use (pragmatics)

impairments of language form

infants/toddlers (normal is 2 by 2)

\-low frequency of vocalization

\-lack of syllable productions in babbling

preschoolers (2-5)

\-immature or disordered phonology

\-grammatical morphology errors

school-age children (5-18)

\-difficulties with complex sentences

\-poor narratives and expository texts

impairments of language content

infants/toddlers (0-2)

\-understands few words in context

\-less than 50 words by 2

preschoolers (2-5)

\-restricted vocabulary size

\-reduced comprehension of basic concepts

school-age children (5-18)

\-incoherent stories

\-difficulties with figurative language

immpairments of language use

infants/toddlers

\-lack of intentionality

\-restricted range of communicative functions (appear to be passive observers)

Indicators of language disorders in children

\-test scores

\-language sample measures

\-negative social, psychological, educational, and vocational consequences

diagnostic conditions characterized by a language disorder

\-specific language impairment (SLI)

\-neurodevelopmental disorders

Specific language development

\-significant developmental delays despite normal cognitive functioning, normal childhood experiences, normal hearing and vision, no signs of neurological impairment.

\-approximately 7% of the school-age children

intellectual disability

\-significantly subaverage general intellectual functioning (IQ below 70)

\-significant limitations in adaptive functioning (self-care, home living, social/interpersonal skills)

\-2% of the population

autism spectrum disorder

pervasive impairments in reciprocal social interaction skills, communication skills, stereotypical behaviors, interests, and activities

\-1% of the population

specfic learning disorder

\-difficulty in the acquisition and use of listening, speaking, reading, writing, reasoning, or mathematical abilities

\-cannot be explained by intellectual disabilities, sensory problems, neurological disorders, or poor instruction

\-many professionals believe that learning disorders in the areas of speaking and listening are language disorders

transdisciplinary team approach

one professional is coordinator of care

multidisciplinary team approach

everyone does their own assessment

norm-referenced standardized testing

testing against their peers

Assessment of infants and toddlers

\-Known etiologies easiest to diagnose

\-Prediction: Which delays will lead to normal development and which will not?

\-Parent report is very important (asks how often they have longer sentences, ask questions, and use grammatical morphemes)

Assessment of Preschoolers

(using language samples of at least 100 udderances) Mean length of utterance, syntactical structures, vocabulary knowledge

Assessment of School-Age Children

\-usually referred by teacher because of academic performance

\-narrative analysis (read and retell - looking for form, content, or use issues)

clinician-centered approaches

\-behavioral principles (stimulus, response, reward)

\-structured activities

child-centered approaches (MILEU)

\-language facilitation through play

\-modeling, self-talk, parallel talk

expansion language simulation

\-repeat the child’s utterance and complete it

extenstion language simulation

\-adds information to what has been said (ex. blue truck -> big blue truck)

recast language simulation

say the same meaning in a different form (statement becomes a question)

build-ups and breakdowns language simulation

expansion + breaking utterance into component parts

intervention for school-age children

literature based intervention - pre-reading discussions, multiple readings of the books, reinforcing concepts (mini-lessons focusing on semantics)

service delivery: legal issues

section 504 - illegal to discriminate against individuals with disabilities

PL 99-457 (birth to 3) - help families address children’s needs (infant parent programs)

IDEA (3 to 21) - free appropriate public education, less restrictive environment

causes of brain damage

\-Cerebrovascular Accident (CVA)

\- Strokes

\-Head Injury

\- Traumatic Brain Injury

\-Growths

\- Neoplasms (tumors)

\-Progressive Deterioration (Dementia)

cerebrovascular accident causes

embolus-moving clots from another part of the body

thrombosis-clot from gradual accumulation of plaque (more common and more recoverable than hemorrhages)

hemorrhages-bleeding in the brain

aneurysm-weakening in the artery that bulges and breaks

stroke immediate affects

(most prominant 3-5 days after stroke)

\-edema-swelling of brain tissue

\-infarct-tissue death

\-spontaneous recovery- neural reorganization

TBI immediate affects

\-contusions-brain bruising (seen on surface of the brain)

\-lacerations- tearing of structures and vessels

\-hematomas-areas of encapsulated blood (intracranial-within the blood, meninges-in the tissue surrounding the brain)

aphasia

acquired language disorder that results from brain damage, usually to the left hemisphere.

\-naming problems (verbal/literal paraphasias, circumlocution)

\-fluency problems

\-auditory comprehension problems

\-agrammatism (function words/ closed class words)

Broca's Aphasis

\-nonfluent, awkward verbal expression

\-short phrases and sentences

\-slow rate

\-agrammatism

\-auditory comprehension is minimally impaired (good receptive, poor expressive)

\-caused by a lesion to broca area (in posterior inferior frontal lobe)

wernickies aphasia

\-impaired auditory comprehension

\-fluent speech (normal intonation, stress patterns)

\-verbal paraphasias

\-"jargon aphasia"

\-poor repetition

\-reading and writing areas impacted

\-damage to wernickies area

automatic sequences

\-"how are you?"

\-"doing good"

circumlocution

talking around a word

conduction aphasia

\-arcuate fasciculus damaged (connects wernickies to brocas)

\-minimally impaired auditory comprehension

\-good spontaneous speech (fluent ex. hellos and goodbyes)

\-hallmark is poor repetition

\-literal paraphasias (phonemic paraphasias)

\-aim for correction

\-should be conductive reading+writing

anomic aphasia

\-"without words"

\-inferior parietal/posterior temporal lobe damaged

\-word-finding problems (difficulty finding names of objects, pictures, and concepts. paraphasias and circumlocution)

\-fluent speech

\-good comprehension (good receptive)

transcortical aphasia

\-"watershed strokes"

\-widespread damage to the frontal lobe (transcortical motor)

\----good conversation but difficulty initiating utterances

\-widespread damage to parietal lobe (transcortical sensory)

\----poor auditory comprehension but good repetition (looks like wernickies but can repeat phrases. EVERYTHING is a repetition task for people with this aphasia)

global aphasia

\-wide lateral damage to the left hemisphere (typically to larger arteries)

\-all parts of language processing severely impaired

\-nonfluent, poor reading+writing skills, poor comprehension, poor repetition, hardest to work with

aphasia assessment

\-immediately following brain injury

\-spontaneous recovery (SR)

\-more formal assessment after SR: focusing on expressive, receptive, reading, and writing,

\---conversation, informal diagnostic testing, repetition, reading+writing

\-faster we get them into rehab, better we can take advantage of neuroplasticity

aphasia intervention

empower the patient to communicate successfully -> communication tasks to activate neural plasticity mechanisms ->cues and prompts (pictures, phonemic cues, phonological rhyming) -> compensatory strategies ->family support groups

\-"life participation model"

right hemisphere stroke

\-emotional recognition impaired

\-demonstrate sensory neglect

\-narrative and conversational discourse skills impaired \\n -over-detailed

\-don’t remain of topic

\-visual neglect

\-"walky-talkies"

\-lack deficit awareness

brain injury

\-lack of deficit awareness

\-cognitive processing, pragmatics, word finding are most prominent deficits

dementia

\-Alzheimers disease is most frequent etiology

\-progressive degeneration of both hemispheres of the brain

\-problems with working memory, orientation, reasoning, judgment

generating sound

\-object requires mass

\-requires elasticity

\-example: guitar string or vocal folds (stiff= higher pitch, less tension= lower pitch)

wavefrom (graph) terminology

simple vs. complex waves

simple vs. complex waves

simple waves

\-vibrates at a single frequency

\-rarely occurs in real world

\-pure-tone

complex waves

\-vibrations that contain 2 or more frequencies

\-nearly all sounds in real world are complex

\-speech, music, applause

sound propagation

\-vibrations cause molecules in air to move

\-molecules bump into other molecules making them move

\-sound travels at roughly 350 meters per second (roughly 7783 mph)

\-as you move further from the sound source the amplitude decreases due to friction in the air

the ear

outer ear

\-funnels sound waves

middle ear

\-amplifies waves

inner ear

\-turns waves into electrical impluses

auditory nervous system

auditory nerve, brainstem, auditory cortex

sound propagation through the ear

\-acoustic sound in the ear canal

\-sound waves impinge on the TM which vibrates

\-causes the ossicular chain to move

\-moves the oral window

outer ear

pinna

\-visible flap of cartilage attached to the head

external auditory meatus (external ear canal)

\-oil gland secrete cerumen (ear wax) - used to protect middle ear pinna

middle ear

tympanic membrane (ear drum)

\-an elastic membrane that separates the outer ear from the middle ear

\-converts the acoustic wave into a mechanical wave

ossicular chain

\-malleus -connected to tympanic membrane

\-incus

\-stapes-connected to oval window

eustachian tube

\-connected to throat, helps equalize pressure in middle ear.

inner ear

\-hollowed-out portion of the temporal bone

\-starts at oval window, ends at the round window

contains three sensory organs

\-cochlea (hearing)

\-vestibule (balance)

\-semicircircular canals (balance)

cochlea

\-hollow tube with 2 1/2 turns

\--starts at the oval window

\--ends at the round window

\-has 3 sections

\--scala vestibuli (SV) - filled with perilymph

\--scala media (SM) - filled with endolymph

\--scala tympani (ST) - filled with perilymph

basilar membrane

\-separates the scala tympani from scala media

\-moves in a wavelike manner

\-loud sounds create large waves

\-soft sounds create small waves

\-tonotopic

\--high pitches are at beginning of membrane

\--low pitches are at the end of membrane

organ of corti

\-tonotopic organization

\--traveling wave (determined by amplitude and frequency of the sounds)

\--hair cells

\-outer verses inner

\-shearing motion

\-depolarization (mechanically gated let channels)

\-transduction of energy (cranial nerve VIII-CNS (primary auditory cortex of temporal lobe)) tonotopically organized

the traveling wave

1. response always begins at the base of cochlea
2. amplitude grows as it travels apically


3. reaches a peak at a point determined by frequency of the sound
4. vibration then dies out rapidly

auditory nerve

\-8th cranial nerve

\-contains 30000 neurons that conduct information in one direction (afferent=neurons from cochlea to brain which conduct sensory information) (efferent=neurons from brain to cochlea which provides feedback for protective functions)

auditory pathway

cochlea->cochlear nucleus (lower brainstem)->superior olivary complex->lateral leminiscus nucleus->inferior colliculus nucleus->medial genticulate body->auditory complex

efferent

down from brain

afferent

up to the brain

conductive hearing loss

air conduction - loss

bone conduction - WNL

AB-gap - sig.

sensorineural healing loss (SNHL)

ac- loss

bc- loss

ab gap-not sig.

mixed hearing loss

ac-loss

bc-loss

ab gap-sig.

units of measurement

\-sound pressue level (dB SPL)

\-hearing level (dB HL)

\-sensation level (SL)

\-presentation level (patients threshold)

audiogram

graph representing levels of hearing

x-axis = frequencies

y-axis = intensity level (in dB HL)

"Normal" hearing level set to 0 dB HL

(0 dB HL is at top of graph)

possible causes of conductive hearing loss

\-outer ear (external auditory meatus occluded ex. cotton swab or wax)

\-middle ear (otitis media ex. tubes from ear infection. otosclerosis ex. when ear bones get arthritis)

possible causes of sensorineural hearing loss

cochlea "sensory"

\-prenatal (anoxia, trauma, fetal alcohol syndrome)

\-perinatal (disruption during birth process)

\-postnatal (meningitis, high fevers, noise exposure, aging)

8th nerve lesion "neural"

\-acoustic neuromas (tumor) (ofter starts as tinnitus)

\-acoustic neuritis (inflammation)

degrees of hearing loss threshold values

normal (-10-25 dB HL)

mild (26-40 dB HL)

moderate (41-55 dB HL)

moderately severe (55-70 dB HL)

severe (70-90 dB HL)

profound (90+ dB)

speech audiometry

speech recognition threshold

\-using equally stressed bisyllabic words ex. hotdog, cupcake

word recognition score

\-50 word lists that are phonetically balanced. use a carrier phrase ex. "say the word couch"

Auditory Brainstem Response (ABR)

\-testing newborns

\-localization of brain lesion sites on auditory pathway

\-noncooperative individuals

Otoacoustic Emissions (OAEs)

\-found more in females

\-"echo" from OHCs of cochlea

\-evoked vs. spontaneous

audiologic rehabilitation

for those who need to modify communication skills as a result of aqcuired hearing impairments

audiologic habilitation

children or those who are listening and learning to use speech and lainguage skills for the first time

steps in hearing aid process

1. consultation - test hearing, discuss options, earmold impression
2. fitting - determining hearing aid specifications
3. aural rehabilitation (AR) groups

hearing aid fitting goals

\-provide audibility for sounds that cannot be heard due to hearing loss (accomplished by ampllifier - measured by gain)

\-ensure that output of the device does not reach intensities that will cause discomfort or damage to the person

difficult listening environments

reverberations - sound reflects from hard surfaces

\-carpeting/drapes + softer surfaces (less reverberation)

\-reverberation time - the amount of time it takes for an intense sound to decrease by 60 dB after the source is turned off

signal-to-noise ratio (SNR)

\-signal intensity minus noise intensity

cochlear implant

external :

\- microphone

\-speech processor

\-transmitter

internal:

\-receiver

\-electrode array

learning to hear

detection

\-document softest sound that can be heard w/o amplification

discrimination

\-ability to determine whether two sounds are same or different

identification

\-occurs after a child has learned the symbolic representation of the sound

ossicular chain

malleus, incus, stapes

dysphagia

difficulty or inability to swallow, may be unable to consume enough food and liquids safely

aspiration

when food enters the airway

4 stages to the swallow

anticipatory, oral, pharyngeal, esophageal

anticipatory stage

not completely voluntary, before food reaches the mouth, sensory information helps a person prepare for food (visul, olfactory information), allows someone to discriminate desirable and undesirable things to eat.

oral stage (part one)

voluntary

prepatory-food is chewed and mixed with saliva (bolus)

lips sealed; larynx/pharynx are at rest,

Masticated in a rotary lateral manner,

sensory input about food: taste, texture, temperature and bolus size,

back of tounge is elevated-bolus in oral cavity.

oral stage (part two)

voluntary

transport-tongue pushes bolus up against palate and moves it posteriorly towards pharynx

(size and consistency of bolus dictate lingual strength needed)

\-oral phase is over when bolus passes anterior faucial pillars

Pharyngeal stage

voluntary but more automatic than oral stage

brainstem and sensorimotor cortex are crucial (medulla in brainstem has nerves that control motor movements of larynx/pharynx/tongue)

Physiological events occur simultaneously

\-velum elevates and contracts (so there is no nasal regurgitation)

\-larynx closes then moves up and forward (we should not be breathing during this process)

\-epiglottis covers larynx (flips to protect airway)

\-swallow is triggered by sensory info sent to brain

\-pharyngeal peristalsis (wave-like contraction where superior, medial, and inferior pharyngeal constrictor muscles contract)

\-upper esophageal sphincter opens

esophageal stage

begins when larynx lowers backward, breathing resumes \n -upper esophageal sphincter contracts \n -bolus moves through esophagus in peristaltic waves (synchronized smooth muscle movements)

causes of dysphagia in adults

\-cerebrovascular accident

\-brainstem stroke

\-dementia

\-TBI

\-neuromuscular disease

\-cancer

cerebrovascular accident affects of dysphagia

\-left hemisphere damage (oral stage difficulty, delay in pharyngeal swallow initiation (aspiration)

\-right hemisphere damage (oral stage difficulty, reduced pharyngeal peristalsis (food getting "stuck" in throat)

TBI affects on dysphagia

varies according to location and severity of injury

cognitive deficits: choosing food, rule of eating, maintaining attention + may have reduced tongue control, difficulty chewing

nueromuscular disease affects on dysphagia

multiple sclerosis, ALS, Parkinson's Disease

progressive disease-muscular movements weak and uncoordinated, difficulty at all levels of the swallow

cancer affects on dysphagia

automatic structure may change from surgery

radiation irritates tissue of mouth and throat

medications lower immune system painful infections of the mouth

assessment of dysphagia questions

\-are the muscles of the tongue, lips, and jaw functioning?

\-can patient elevate larynx?

\-can patient feed themselves?

\-what foods can patient eat safely?

dysphagia 1, 2, 3, 4

puree, cottage cheese texture, soft solids, regular diet

noinstrumental clinical exame (NICE)

bedside clinical assessment (ability to take food off plate- cognitive/motor skills)

\-level of alertness, oral-motor exam (lips, jaws, tongue, initiation of the pharyngeal swallow), upward movement of larynx? coughing? gurgling sound?