final review Flashcards
what do slps and auds do and what are the requierements for each
slp: speech, language, voice etc
-masters, 9 mo fellowship, 400 hrs supervised clinical work, praxis, ccc-slp
aud: balance and hearing
-doctorate, 1820 hrs fellowship, ccc-a
5 principles of brain organization
plasticity, hierarchical org, sensitive period, specialisaztion, interconnectivity
3 traditional language domains
content: semantics–meaning and vocab
form: syntax (sentences), morphology (words), phonology (sounds)
use: pragmatics (social skills etc)
grices maxims
quantity: how much
quality: truthfulness
relevance: on topic
manner: how you say it
joint attention
6-9 months
simultaneous focus on same object
overextension
16 mo
one word for all things in the category
overextension
16 mo
one word for all things in the category
decontextualized language
preschool
outside of hear and now
what’s the purpose of differents types of assessments?
screenings: short, to see if further testing is needed
standarized tests: to diagnose someone
questionaires: other contexts you cant see
observational: you do it
developmental language disorder
impaired comprehension and or use of spoken, written, and/or other symbol system (semantics, syntax, pragmatics)
-what’s hard: telling a narrative, reading, writing, talking, understanding facial expressions, anticipating emotions of others
-cause: we don’t know
-prevalence: 7% of kindergarteners
autism spectrum disorder
difficulties in 2 areas: social communication/interaction, repetitive behaviors and restricted interests
causes: we don’t know
intelletual disability
deficits in: intellectual functining and adaptive behaviors– must be identified by age 18
-compensatory treatment: strategies other than language (pictures etc)
-remedial treatment: treating the language directly
aphasia
acquired disorder of loss of language. can affect all language modalities (reading, writing, speaking, listening)–damage ot left hemisphere (stroke, TBI)
fluent vs nonfluent aphasia
f: longer phrases
logorrhea (excessive talkitiveness)
paraphasias (wernicke’s–comprehension)
nf: short phrases, agrammatisms, labored/effortful speech (broca’s–expression)
right hemisphere dysfunction
damage to right hemishpere of brain
-anosognosia (deficit in self awareness)
-social comminication problems (fine speech and language, bad grice’s maxims)
-left neglect
-difficulty with problem solving, reasoning, abstract thought
( someone with RHD will not have aphasia!!!)
traumatic brain injury
injury to brain from external impact (3 types)
open, closed, polytrauma
symptoms of an mTBI
-blurred vision
-slurred speech
-dizziness
-vomiting
-confusion
-ringing in ears
-nausea
-headaches
ssd disorders
impairment of they sound system that is a significant problem with speech sound production causing it differ from they demographic
articulation disorders vs phonological
articulation: correct perceptual target, can’t position articulators
phonological: incorrect perceptual target, consistent rule-based errors
apraxia vs dysarthria
apraxia: motor programming, inconsistent errors
-slow rate of speech
-distorted sounds
-imparied prosody (stress issues)
dysarthria: motor execution, consistent errors and distortion
who is most at risk for a voice disorder?
people who talk a lot
women
perceptual measures of voice
loudness: intensity
pitch: frequency
quality: how it sounds (gravely, etc)
how is pitch impacted by the shape of the vf?
if they are longer/thinner (stretched) there will be higher pitch
if they are short/thicker (not stretched) the pitch will be lower
three categories within voice disorders and what types fall under them?
neurogenic: problem with the nervous system
-spasmodic dysphonia
-vocal fold paralysis
structural: structurally wrong with vf
-nodules, polyps, granulomas
-laryngectomy
functional:no neurogenic/structural cause
-mutational falsettor
-muscle tension dysphonia
vocal nodules
bilateral
caused by phonotrauma
develop gradually over time
callous-like
treatment: behavioral voice therapy
vocal polyps
unilateral, fluid or blood fillded/vasular
caused by phontrauma
can develop in single instance
blister like
treatment; surgery, bvt
granulomas
large, unilateral lesions
posterior portion of vocal fold!
caused by GERD/phonotrauma
treatment: GERD management and bvt
granulomas
large, unilateral lesions
posterior portion of vocal fold!
caused by GERD/phonotrauma
treatment: GERD management and bvt
laryngectomy
partial or total removal of larynx
mutational falsetto
cause: psychology
higher voice than expected for age
treatment: laryngeal resposturing/bvt
muscle tension dysphonia
cause: excess tension
treatment: laryngeal reposturing/bvt
spasmodic dysphonia
cause: laryngeal nerve misfiring
2 types:
abductor: seperated too often—breathy
adductor: come together too often—strained, strangled
treatment: botox injection
vocal fold paralysis
cause: nerve damage
treatment: surgery– implants or repositioning of folds
fluency disorders
atypical disruption ot the forward flow of speech
core features of stuttering
repetitions (re-re-repetition)
prolongation (prolooooongation)
blocks (bl–ock)
secondary behaviors of stuttering
-learned
blinking, starter devices, head jerk, avoiding social situation
risk factors for a fluency disorder
family history
gender (more males!)
neuroanatomical differences (deficits in the white matter tracts that support orofacial movement)
high self awareness to speech
traumatic event
treatments: fluency shaping vs stuttering modification
fs: eradicate disfluencies (make them have less stuttering instances)
sm: change the idsfluencies ot make them easier (addresses thoughts and feelings)
how to talk to someone who stutters
focus on what they are saying not how they are saying it
what about children and disfluency
5% of children go through a disfluent stage (75% will recover)
dysphagia
unsafe or inefficient swallowing
3 phases of the swallow
(what’s going on, so what could go wrong?)
**oral: **preparatory–mastication, create a bolus,
transportation–stripping action (bolus hits the posterior pharyngeal wall)
pharyngeal:hyolaryngeal elevation, vocal fold closure, epiglottic closure, reflexive cough, bolus enters the upper esophageal sphincter
esophageal:peristalsis moves bolus to stomach
what can go wrong in the oral phase?
lips don’t close, food isn’t chewed right, not enough saliva, residue in their mouth, initiation of swallow is slow
what could go wrong in the pharyngeal phase?
penetration or aspiration because of inadequate hyolaryngeal elevation/epiglottis closure, no reflexive cough
-if hyolaryngeal elevation/epiglottic closure isn’t happening food could get stuck/pool in the vellecula (right above epiglottis)
penetration vs aspiration
penetration: food hits the larynx
aspiration: food enters the trachea/lungs
pediatric feeding disorders
persistent failure to eat adequately
associated difficulties of pediatric feeding disorder
prematurity/nicu
low birth weight
craniofacial abnormalities
low muscle tone
developmental disabilities
inadequte nutrition
sensory issues
prenatal exposure to drugs/alcohol
assessment of dysphagia 3 types
clinical/bedside swallow exam: (kinda like a screening), just the clinician with the patient
videofleuroscopy/modified barium swallow study (MBS): x-ray, good image of the whole study
FEES: camera down nose, can’t see the oral or esopageal pahse, but you can see the residue etc
pathway of energy through the ear
outer: acoustic energy to mechanical energy at the tympanic membrane (which vibrates the ossicular chain)
middle: mechanical energy
inner: mechanical to hydraulic
nerve: electrical energy to the brain
outer ear structures
pinna/auricle
EAC
middle ear structures
ossicles: malleus, incus, stapes
eustachian tube
tympanic membrane (ear drum)
purpose of eustachian tube
equalizes/relieves pressure in the middle ear
inner ear
vestibule and semicircular canals
cochlea
auditory nerve
conductive hearing loss
damage to outer or middle ear
causes:
-congenital blockage
-cerumen blockage or foreign object in auditory canal
-perforated tympanic membrane
-otitis media
-malformations of the auter and or middle ear
conductive hearing loss
damage to outer or middle ear
causes:
-congenital blockage
cerumen blockage or foreign object in auditory canal
-perforated tympanic membrane
-otitis media (middle ear infection)
-malformations of the auter and or middle ear
sensorineural
causes:
-illness, drug use in pregnancy
-in-utero infections
-menengitis
-problems at birth
-noise exposure
-unknown cause (57%)
any infection if doesn’t specify that its part of the outer/middle ear
presbycusis
sensorinerual loss due to aging
gradual decline
starts early in adulthood
initially affects high frequency sounds
tinnitus
ringing, roaring, buzzing in the ears
loss vs impariment/disability
hearing loss: objective
hearing impariment/disability: up to the patients opinion (because of their lifestyle), how much it affects their life
hearing tests: behavioral v objective
behavioral: requires patient to do something (raise hand etc) when they hear a tone
-better for adults
objective: what their system is doing (otoacoustic emissions and tympanometry)
-better for infants
otoacoustic emissions
ojective measure
elecrto-acousitcal testing
cochlear functioning (screens all babies)
echo of the cochlear
tympanometry
objective measure
tests the acoustic flow of energy theough the outer and middle ear
amplification
hearing aids: amplify sounds
assistive listening devices: FM systems
cochlear implants
bypasses damaged portions of the ear to directly stimulate the auditory nerve
qualification for cochlear implants
children: bilateral profound hearing loss/deaf, implant early is better
adults: profound hearing loss/deaf, hearing aids don’t help
