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60 terms

Speech Science Mid term 2

Covers remaining topics of chestwall/ breathing, dynamic vocal tract and structural elements of the larynx
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Function(s) of the Larynx
Conduit for inhaled and exhaled air
Dynamic valve
to prevent debris/food from entering airway
constrict airway to allow increase in Ps
cough, thoracic fixing [lifting, defecation, childbirth]
Vertical displacement of larynx important for swallowing
Sound source for vocalization/speech
Thyroid Cartilage
largest, most prominent of the laryngeal cartilages. Forms the V-shaped laryngeal prominence [aka, Adam's apple] anteriorly (front)
Anterior end of each vocal fold forms an attachment to the internal surface of the thyroid cartilage
lamine (body)
Hyoid sits superiorly to superior horns
Has superior and Inferior Horns (see notecard)
-sliding/ rotation movement
Horns/ Notch of the Thyroid Cartilage
-superior horn connected to the hyoid bone via ligaments
-inferior horn articulates with the cricoid cartilage below via diarthrodial joint [aka cricothyroid joint]
-superior thyroid notch is space just above the angle of the thyroid cartilage and just below the hyoid bone
Cricoid Cartilage
ring-shaped [signet] cartilage below the thyroid cartilage
narrowest arch in the front, widens posteriorly into a tall lamina
superior surface of the lamina supports the arytenoids
ligaments attach cricoid to thyroid superiorly, and 1st tracheal ring inferiorly
numerous muscle attachments
fossa on both sides
gliding motion= ant to post Fo adjustment by changing VF length
rocking motion= adduct to abduct of VF
Crico-Thyroid Articluation
These two pieces of cartilage that compose the part of the Larynx are joined by the cricothyroid m. (pars rectus/ pars oblique).
spans the gap between cricoid and thyroid cartilages, adducts these two cartilages causing the VF's to lengthen and increase tension. Primary Fo [pitch] controller.
This is done by making the vocal ligament (connects between arytenoids and thyroid cartilage anteriorly) taut and loose--attachment on vocal process and notch)
Arytenoids
paired cartilagenous, pyramidal-shaped structures that articulate with the lamina (body) of the cricoid cartilage.
Vocal process serves as an attachment for posterior end of vocal ligament/vocal fold
Muscular process attachment point for adductors/abductor
-these cartilages have both a rocking and gliding motion
Hyoid bone
suspends the larynx to the upper VT
Lateral Cricoarythenoid m.
spans the superior rim of the cricoid to the muscular process of the arytenoid. Adducts vocal process of arytenoid, MEDIAL COMPRESSION for louder voice
primary VC adductor/ loudness controller increases cm H20 from 5 to 12-20 for instance
Posterior Cricoarythenoid m.
posterior surface of cricoid to muscular process of arytenoid. Primary and only VF abductor, so....always active when you inspire air into the lungs
primary vocal fold abductors
Thyroarytenoid m.
spans internal surface of thyroid cartilage to vocal process and anterolateral surface of arytenoids. Pulls arytenoids forward, SHORTENS and THICKENS the VFS
can increase vocal pitch/ regulate stifness of VF; dependent on patter of co activation of CTm. (antagonist)
Vocalis m.
spans inferior surface of thyroid/vocal process and inserts into vocal ligament along its length. REGULATES TENSENESS of the VFS; obliquely oriented fibers
Interarytenoids
Oblique fibers criss-cross between arytenoids from base to apex, Adducts arytenoid, narrow posterior glottal chink. Transverse fibers interconnect posterior surfaces of arytenoids. Adducts arytenoids/VF's
Dysphonia
usually caused by changes in the vocal folds
especially the mucous membrane [lamina propria] that covers the fold
upper respiratory infection [cold], neoplasms [tumors], ulcers resulting from hard glottal attack, overuse
progressive neuromotor diseases [PD, UMNS, LMN, Cerebellar Ataxia, ALS, MS, neuropathy, myasthenia gravis]
congenital malformations associated with clefting, laryngeal web
idopathic dysphonias: spasmodic adductor dysphonia & spasmodic abductor dysphonia
measured by speech-laryngeal aerodynamics, EEG
Tidal Breathing Control
Automatic breathing or involuntary breathing is controlled by brainstem, esp. medulla:
Generate rhythmic pattern of breathing (central pattern generator, or CPG)
Regulate oxygen and carbon dioxide levels in blood by adjusting respiration
Efferent control of breathing:
Signals from brainstem travel via peripheral nerves to muscle
Example:
For inspiration: medulla phrenic nerve (C3-C5) diaphragm (fibers contract)
Signals from cortical areas
Limbic areas
Motor areas
Somatosensory areas
Oppositional Breathing
Very rarely encountered
Seems to result from lack of control over sequential pattern of muscular contraction
People who do this simultaneously contract muscles of inhalation and exhalation
It's normal to contract some oppositional muscles for the purpose of control during speech production
It's abnormal to directly counteract muscular actions
Tidal Volume
volume of air inhaled and exhaled during any single expiratory cycle
Resting volume--up a little--back to resting volume
~500 cc at rest, ~1600 cc light work, ~2000 cc heavy work
Inspiratory Reserve Volume
quantity of air which can be inhaled beyond that inhaled in a tidal volume
top of tidal volume wave to max inspiration
~1500-2500 cc
Expiratory Reserve Volume
quantity of air that can be forcibly exhaled following a quiet or passive exhalation
opposite of inspiratory reserve: resting volume down to max exhalation
~1500-2000 cc
Residual Volume
quantity of air that remains in lungs and airways after maximum exhalation: air that cannot be fully extracted during the expiratory phase
trapped in the 'dead volume' space of pulmonary appartus/ trachea
~1000-1500 cc
Inspiratory Capacity
maximum volume of air that can be inhaled from the resting expiratory level
resting level to max inspiration
= tidal volume + inspiratory reserve volume
Vital Capacity
quantity of air that can be exhaled after deepest inhalation possible
air you have access to through the lungs that shrinks with age, sex, athletes vs. non, etc peaks in 3rd decade of life and begins to decline again
= tidal volume + inspiratory reserve volume + expiratory reserve volume
Males ~ 3500-5000 cc, Females ~ 2500-4000 cc
Functional Residual Capacity
quantity of air in lungs and airways at resting expiratory levels
expiratory reserve volume + residual volume
Resting level to expiratory+dead volume
males ~ 2300 cc
Total Lung Capacity
quantity of air lungs hold at height of maximum inhalation
= sum of all lung volumes
Relaxation -Pressure Curve
Expression of pressure equality points in breathing
pressures generated entirely by passive forces, + or - x-axis is alveolar pressure (passive and active forces) and y-axis is percent vital capacity
way in which to measure the pressure of air flow during points of transition
Represents pressures generated by the total respiratory system
Linear at mid-volume range
Non-linear at extremes of lung volume
can also be divided into relaxation pressure generated by the lungs and by the rib cage wall (these two lines combined= RPC)
Extended Steady Utterance
SPEECH BREATHING
deepest inspiration possible and speaking until air supply is depleted (produced throughout most of vital capacity)
Sustained vowel
Series of repeated syllables of equal stress
Sung note
alveolar pressure doesn't change; RCW/ Ab wall/ lung volume all decrease
Requires both relaxation pressure and muscular pressure
Running Speech
SPEECH BREATHING
Reading aloud
Public speaking
Conversational speaking
Highly variable, due to variation in phonetic content, prosody, and voice
Running speech occurs in the midrange of vital capacity
Why? Mechanical- breathing apparatus not as stiff here, and relaxation pressure not as extreme
.... If relaxation pressure is not as extreme, let muscular pressure will be required to counteract the effect.
Output variables
Volume: cm3 or cc, Liters; Lung volume--air within the space
Flow: cc/sec ; Liters/sec
Pressure: cmH2O; mmHg
Shape
Pressure equality
Air enters the lungs with a flow proportional to the difference between alveolar and atmospheric pressures
Patm= Palv
Alveolar pressure is equal to atmospheric pressure at three points in the respiratory cycle:
beginning of inspiration
end of inspiration
end of expiration
Moderate to Severe Spastic Quadropeligia
caused by a hypoxic ischemic injury (HIE)--blockage of artery for limited period of time, both hemispheres usually severity can vary with time and GA age; these individuals cannot sustain a 5 cm H2O in speech; dysarthria ; these individuals vital capacity production is about 2 liters where we would regularly expect 5-6 liters
Running speech Relaxation pressure/ muscular pressure
Muscular pressure during inspiratory phase:
diaphragm;
rib cage wall... but only with utterance initiations at large lung volumes
Muscular pressure during expiratory phase:
rib cage wall
abdominal wall (predominant)
As relaxation pressure becomes increasingly less positive (even negative), magnitude of positive muscular pressure increases
expiratory rib cage wall and abdominal wall muscles maintain a low level of activity during inspiration.... this enables them to be in a state of readiness to begin driving expiration (speech production) as soon as inspiration has ended
--most of the time, targeted alveolar pressure is higher (more +) than relaxation pressure..... That's why positive muscular pressure must be added throughout the breath group
Abdominal wall during Speech Breathing
Abdominal wall is predominant during expiratory phase
As abdominal wall moves inward...
Diaphragm moves headward muscle fibers elongate prep for quick and powerful inspirations
Lifts rib cage wall expiratory muscle fibers elongate prep for quick expiratory pulses
Allows expiratory efforts of rib cage wall efficient pressure change
Predominant, compared to rib cage expiratory muscles
When doing this, inspirations are short and loudness hanges for linguistic stress are quick.
Body positioning and running speech
upright: chest wall and diaphgram moving down+ RCW out 38-40% vital capacity
supine: ab and RCW in + diaphgram up 20% vital capacity (may be used as a therapy technique because AB muscles do not need to be as engaged because of passive force pushing down on ab content in order to produce speech/ breathing)
upright VC is better; and decresase with supine position; and increase (though not as high as upright) when sitting or on hands/ knees
Body positioning and tidal breathing
in upright position-- during the inspiratory phase the diaphragm, RCW, AB wall are used during exhalation the ab wall is controlled by passive forces
in supine-- inspiration is controlled by the diaphragm and RCW
expiration controlled by passive force
Cognitive-Linguistic factors
Inspirations:
Occur at sentence, clause, and phrase boundaries
Larger when followed by longer breath groups
Smaller when followed by shorter breath groups
Expirations:
Syllable number tends to dictate where within vital capacity breath group stops
End at smaller lung volumes when preceded by greater number of syllables
Medulla elements for tidal breathing
Pre Botzinger Complex-- small unit of brain for respiration
Respiratory Central Pattern Generator (rCPG)
regulate O2 adn CO2 using sensors to monitor these in blood
Consists of interneurons (neither motor/ sensory)
Local circuit (medulla)
Vental Respiratory Group (VRG)--rostal/caudal; works w/ PBC for respiration
(speech breathing is not included in these structures of the medulla) limbic--> anterior singulate cortex ('old' brain) signal from limbic system are sent to the lower resperatory (Pre Bot) certain ingrained speech utterances (affect/ emotional) speech are stored here
Afferent Control of Tidal Breathing
Afferent control of breathing:
Important for control of breathing pattern
Chemoreceptors
Central chemoreceptors
respond to changes in carbon dioxide levels in cerebral spinal fluid
Peripheral chemoreceptors
respond to changes in carbon dioxide levels in arterial blood and oxygen levels
Chemoreceptors work synergistically to stimulate adjustments in breathing
Afferent control of breathing:
Mechanoreceptors
In pulmonary apparatus
stretching of smooth muscles (such as w/ increase in lung volume)
airway irritants (smoke)
In chest wall
changes in muscle length
changes in force
In larynx and upper airway
Special Breathing acts
e.g. NOT tidal breathing
This includes breathing acts not related to the medulla/ brainstem
Can be either voluntary, highly learned and well-practiced, or emotionally-driven
Controlled by higher brain centers that override/bypass brainstem or work synergistically with it
require motor plan
Comes from subcortical (basal nucleus, cerebellum, thalamus) and cortical (frontal and parietal lobe) structures
However, reliance on motor plan decreases as behavior becomes learned and less consciously guided
Eupnea
Normal quiet breathing
Hyperpnea
Increased depth of breathing
Increased tidal volume with or without increased rate
Dyspnea
When pulmonary ventilation approximates VC volume
"air hunger"
Apnea
Cessation of breathing at end of a normal expiration
When voluntary, it's just "holding your breath"
no movement of muscles of respiration, unchanged lung volume
swallow apnea
"sleep apnea"
Apneusis
Cessation of breathing in inspiratory position
deep, gasping inspiration with a pause at full inspiration followed by a brief, insufficient release
Often caused by caused by damage to the pons or upper medulla (stroke, trauma)
Cheyne-Stokes respiration
Aka: "periodic breathing"
Gradually increased tidal volume for several breaths, followed by several breaths with gradual decreasing tidal volume
Cycle then repeats itself
Most common cause = cardiac failure
also can be seen in patients with strokes, traumatic brain injuries, brain tumors, and following administration of morphine
Biot's respiration
Form of periodic breathing characterized by repeated sequences of deep gasps followed by apnea
Causes include very high CSF pressure or destructive disease of the brain (esp. damage to the medulla oblongata due to strokes or trauma)
Generally indicates a poor prognosis
Chronic Obstructive Pulmonary Disease (COPD)
cause: exposure to toxic chemicals (eg, long-term exposure to tobacco smoke)
loss of elasticity of lung tissue, destruction of structures supporting alveoli, destruction of capillaries feeding alveoli
thus, alveoli tend to collapse during exhalation
this impedes airflow and traps air in the lungs
symptoms: shortness of breath, hyperventilation, expanded chest
increased muscular effort required to overcome increased stiffness of lungs
Pulmonary Fibrosis
scarring of the lung
gradually, alveoli become replaced by fibrotic tissue
scarring causes irreversible loss of the tissue's ability to transfer oxygen into the bloodstream
symptoms:
Shortness of breath, particularly with exertion
Chronic dry, hacking cough
Fatigue and weakness
Discomfort in the chest
Loss of appetite
Rapid weight loss
Spasmodic Dysphonia
ADDuctor type is most common; lots of activity from LCA (hyperactive), excess use of false VF, progressive neuromotor disease: unknown cause lesion?
limited treatment-- botox handout
ABDuctor type is an overactive PCA and breathy quality of voice; sublexication of arytenoid processes
Chest Voice
little or no longitudinal tension
slack vocal ligaments
thick vocal folds
large amplitudes of vibration along vocal fold margin
closed phase of duty cycle is long
vertical phase difference is apparent
vocal fundamental frequency is low
generally loud voice
Falsetto Voice
high longitudinal tension
high medial compression
tense vocal ligaments
thin vocal folds
small amplitude of vibration
incomplete glottal closure
negligible vertical phase difference
Diaphragmatic Breathing
Also called "abdominal breathing"
Doesn't mean that the individual is selectively using the diaphragm for inspiration
Thoracic Breathing
Do not necessarily demonstrate an increase in activity of rib cage wall inspiratory muscles
Females tend to do more thoracic breathing
Clavicular Breathing
May result in excessive tension in the throat and inadequate breath supply
Should be avoided- encourage clients to use diaphragmatic or thoracic breathing patterns instead
Infrequently encountered (e.g., neck/spinal cord injuries)
Glottal Chink
medial compression, but glottis is still open posteriorly
Point A of relaxation pressure point
Point A-- (actual RPC) end of expiration; recoil or relaxation pressure for lung (recoil in) and rib cage (relaxation out) [apposing forces] alone are equal, but opposite; relaxation pressure= 0, lung volume= FRC [x axis relaxation pressure/ y axis vital capacity]
Point C of relaxation pressure point
Point C-- (on lungs line and actual RPC lines) additional air volume inhaled in lungs, relax chestwall and closed glottis; rib cage by itself at equilibrium, lung recoil (movement of lung inwards) is higher and represents main contributor to chestwall positive relaxation pressure [x relaxation pressure/ y vital capacity]
Point D of relaxation pressure point
Point D--(on RPC line) inhale near 100% VC, Lungs/RC expanded well beyond their equilibrium states, relax chestwall against a closed glottis, result is a high positive relaxation pressure apparent for CW, tendency to drive CW toward point A [lungs inward too] (equilibrium volume) [ x relaxation pressure/ y vital capacity]
Point E of relaxation pressure point
Point E--( on CW and RC line) air is forcible expelled past and expiration here, relax chest wall against a closed glottis, lung stretch minimal but RC is greatly compressed [CW outward], inward contributing maximally to the high negative relaxation pressure [ x relaxation pressure/ y vital capacity]
Reinkes Edema
lamina propria is swollen; difficult to breathe
vocal nodules
usually medial ;easier to see at high pitches when folds are longitudinally stretched; usually compensated for by pulling VF apart and increasing phonation; bisection of VF because of nodule in middle creates 2 seperate F0s of the VFs
Ventilation is greatest when...
Breathy voiced quality
Continuous speaking
High-flow voiceless sounds
Loud speaking