-patient's description of the problem

-date of onset

-pattern of onset (sudden/gradual)

-nature of symptoms (constant, fluct)

-associated cognitive, lang, swallow, motor

-known medical diagnoses

-med/surgic hx

-meds

-impact on daily functions

-impact on/impressions of sig others

- compensatory strategies that help

- history

- oral motor exam

- intelligibility testing

- perceptual evaluation of speech

- instrunmental ax

-diagnostic therapy probes

flashlight

gloves

tongue depressors

stopwatch

laryngeal mirror

-structural integrity (structures, inflammation, colour etc)

-localization of damage (UMN vs LMN)

-Symmetry

Scerity of physical change/damage (not speech)

By Subsystems (respiratory, phonatory, articulatory, resonatory, prosody)

By Structure (face, lips, teeth, tongue, soft palate, larynx, lungs)

By Cranial Nerve

-strength/force of muscle contraction

-steadiness

-muscle tone

-speed of non speech movement

-range of non speech movement

-accuracy of non speech movement

-coordination of rapid, repeated non speech movements

-ident dysarthria types

-be able to use descriptors assoc with characterizing dysarthria

-dysarthrias are recog by how they sound

- can be dist from normal speech and non-neurologic speech disorders

-not all ppl with dysarthria sound the same and the diffs go beyond variations in severity

-when they sound the same, similarities logically reflect lesion loca, and presumably, common underlying pathophysiology

yes

-aids in the diagnosis of neurological problem

flaccid

spastic

hypokinetic

hyperkinetic: chorea

hyperkinetic - dystonia

ataxic

mixed

unilateral UMN

- specific damage to isolated nerves or muscles

OR

-multiple peripheral nerves (bulbar palsy)

- regular rate of repetition

- non speech ddks may be low for specific affected muscles/ articulators

-imprecise

What types of phonatory-prosodic insufficency would you see in flaccid dysarthria?

-a very large tumour or sig degenerative disease

- UMN disorder (bilateral damage to pyramidal and extrapyramidal system)

imprecise

slow

labored

-reduced inhalatory and resp volumes

-shallow breathing

-paradoxical breathing

-reduced utterance length per BG

What are the phonatory characteristic of spastic dysarthria?

larngeal stenosis (valve hyperadduction)

harsh quality (strangled)

low, pitch, reduced range, pitch breaks

reduced modulation of voice amp

monopitch

monoloudness

intermittent voice arrests

short phrases

excess and equal stress on sylls 

-less severe

- spastic hemiplegia one side only 

-rel to tongue and face (unilat innervated pts)

- articulators are slow

- reduced ROM

- tongue may deviate

- imprecise consonants

-usually transient/short term

imprecise consonants

repeated phonemes- dysfluencies

palilalia

-dysphonia

-breathiness

-harshness

-reduced loudness

-inc overall rate

-variable (festinating) rate

- increased rate in segments

-inappropriate silences

- reduced stress

- monopitch

- monoloudness

- short rushes of speech

-reduced vital capacity

-reduced amplitude of chest movement

damage to the inhibitory loop of the BG

BY:

-poss destruction of the subthalamic nucleus (increasing thalamic and cortical excitory firing)

-loss of striatal neurons

-imbalance between excitatory cholinergic and inhibitory dopaminergic neurotransmitters

-altered discharge to thalamocortical pathways (lesions to cerebellar structures like the dentate nucleus and red nucleus)

Chorea (Rapid, random, dancelike movments of a body part, can be present at rest and during sustained movement, can be subtle or large)

Dystonia (slow hyperkinesia, excessive co-contraction of antagonistic muscles, an ex is torticollis)

Rhythmic

Essential

Phsyiological

resting - when body part relaxed

postural - against gravity 

action - on initiation of movement

terminal - at end of movement, as target reached

(TRAP)

postural and action

(may involved head, hands, upper body, voice)

unpredictable (irregular artic breakdowns)

imprecise artic

vowel distortions

irregular VP incompetence

nasal emissions or VP air wastage

- irregular variations in loudness and voice quality

- harsh, strained-strangled quality

-random hyperadduction of the vfolds, voice arrest

- transient breathiness

suddent involuntary inspirations or expirations

sniffing/grunting/throat clearing etc

irregular breakdowns

prolonged, inappropriate silences

irregular prosodic excess

excess and = stress

-irreg, unpredictable interruptions

- rapid or variable rate

-dropped movement segments

- unexpected pauses

-damage to the cerebellum or cerebellar control circuit pathways

-most commonly associated with bilateral lesions or generalized cerebellar disease

hypotonia (dec res to passive movement)

dysmetria (inability to control movement range or trajectory)

intention tremor

sequencing and speed movement errors

-complaints of sounding drunk

-complaints of difficulty coordinating speech and breathing

-complaints of biting tongue during speech or eating

-imprecise, slow artic breakdown

-inconsistent probs

-prolongation of phonemes

-telescoping (syllable or series of sylls run together with transient acceleration)

hoarse and breathy or harsh (even to strain-strangled)

voice tremor

monotony

pitch breaks

- scanning speech - excess and =

intermittend periods of explosive inflection

poorly modulated pitch and loudness

overall monopitch and monoloudness

prolonged phonemes

-TBI

- more than one neurologic event or co-occurence of two diseases

- ALS

-MS

- Progressive Supranuclear Palsy

- Multiple System Atrophy

spastic and flaccid

(severly imprecise artic, reduced intelli)

(slow rate or speech)

(short phrases)

(marked hypernasality)

(severe harshness, strained-strangled voice quality, often very low pitch)

(severely disrupted prosody)

hypokinetic

spastic

ataxic

massive cell loss in the motor system, frontal lobes, BG, cerebellum

survival is 6-7 yrs

paralysis of vertical gaze

no tremor

prominent frontal lobe dysfunction

does not resp to antiparkinsonian drugs

hypokinetic 

spastic

ataxic

- helps to think about differential diagnosis, neurologic localization

-provides framework (structure, terminology) for clinic and research in motor speech disorders

-not perceptual only framework, so encourages to think across domains (perception, physiology, neurophysiology)

-methodological issues - 38 different pieces?, patterns?

-dimensions are non-unique, their physchometric properties arent known

-no further research elaborated on the reln bet dysarthria type and side of lesion (ie: just a clinical tool with minimal scientific backup)

-representation of etiologies in original dysarthria groups - some only have one cause (eg, mixed als only etc)

-not enough subtypes

-questionable relevance for det tx

-cannot be applied to developmental dysarthria

-independent of the course of the disease (acute, degenerative, chronic)

-doesnt deal at all with severity

-had to assign 1-7 in severity for (imprecise consonants, monopitch, hypernasality, excess loudness variation, harsh oice, short phrases, distorted vowels, inappropriate silences)

-Used 28 DAB samples

-17 experienced SLPs - average accuracy was only 19% (and only 1% for flaccid, up to 55% for hyperkinetic)

-grad students after 5 hrs training were 56% accurate

- 5 listeners and 35 original DAB speakers

-intrajudge reliability was about 80%

- interjudge was 50-80 (lowest reliability for mixed)

-diffs  - ataxic were often described as fast rate although DAB says the are slow

-Bizareness - prominent in Z and K not in DAB

-47 speakers (hypokin, mixed, flaccid and spastic)

-judges - 10 grad students and 10 experienced SLPs

- 38 perceptual features on 7 pt scale

-intrarater agreement vs interrater agreement (complete was within 1 pt, within 2 more pts)

-fouund  less than 1 diff with most features

-found more than 1 pt diff with harsh voice. strain-strangled voice, breathy voice, voice stoppages, intelligibility and bizareness

- high agreement for pitch breaks, voice stoppages, nasal emisison, grunt, inapprop silence, short rushes of speech, irreg artic, repeated phonemes, intelligibility

- no diffs bet grad students and SLPs

Dab system cannot be a sole tool for the clinical differential diagnoses

ways to improve perceptual judgements must be ident

ID of the pattern instead of specif dimensions might produce diff results

Problem (state soln)

hard to pick up on errors b/c were so focussed on verbal content

Dont look at the speaker

spring

-when displaced want to return to its resting position

-stretch results in elastic recoil (the force that brings the spring to it's rest position)

P times V = Constant

As volume increases, pressure decreases

pressure

flow

high

out

decreases

active

passive

wont have enough loudness

will have short units of speech

-simultaneous finely graded activity of insp and exp muscles

-quick inhalations and long exhalations

-high level of control (to spk in phrases of diff durations, pause w/o taking breaths, speak in diff body positions, during running etc)

-difficulty with generating or maintaining the appropriate pressure due to weakness of the resp muscles

- inappropriate use of the resp syst (inhaling to a higher than necessary lung volume)

- unpredictable activity of the respiratory system

- poss in all types of dysartrhia

- can be compensatory (abdomen compensates for rib cage in PD, paradoxical breathing in hyperkinetic disorders, overdrive in VP imp)

-subglottal pressure generation

-lung volume / vocal level (loudness)

-phrasing / pausing (breath groups)

-respiratory shape

-fatigue, dyspnea with speaking

-loudness (decreased - soft voice, variable)

-Breath group duration (short phrases)

- Pause duration, placement and frequency

-Prosody (stress)

-tremor

-low pitch

-hypernasal

- v short bgs

-unintelligible

- 2-3 wd phrases only

-one wd at a time

not moving really at all

inspiratory musculature involved

intercostals and abdominals are rigid, diaphragm only one working well

- u tube manometer

water bubble manometer

-hand-held spirometer

SPL meter

should be 70db 6-12 inches from the mouth

-do in quiet, and in noisy environ

clavicular breathing

paradoxical breathing

checking action

supine

which muscles are supported / compromised in Supine position?

what would you do for each client?

diaphragm - compromised, b/c gravity is usually helping it

abdominals - gravity is now supporting them 

*if someone has diaphragmic issues never put them in supine position for testing

*if abdominals are affected, put in supine and see if that helps

-inc subglottal pressure

- inc breath group duration

- use appropriate lung volume range

- increase speech intensity

-improve breathing efficiency

-reduce fatigue during speaking

- med issues always first

- manage laryngeal, VP, artic probs first ONLY if breathing patterns are maladaptive and compensating for upper airway probs

- manage both at the same time

- manage breathing first

non speech tidal breathing

sustained phonation

single wds

strings of wds (#s, days of the week)

Phrases of diff duration

stress-varying

postural adjustments

when the expiratory muscles are impaired ( so the binder helps suck them in)

the binder pushes to get the air out

-if they are cognitively intact enough

- they could use a tray on the wheelchair to help push the air out

-tell them to breathe in normally and then lean forward and push

-hand (work on awareness)

-UTube or digital manometer (Adequate subglott press)

-Respitrace or respiratory magnetometers (EMGs)

How could you use the utube or digitial manometer for feedback?

show maintaining of subglot press for dif ammts of time 

-can do with kids, cog imp,its a simple task)

BUT doesnt necessarily translate to speech

Good starting point for extremely severe clients, not for maintaining

How could you use a magnetometer for feedback?

-teaching using speech tools

-teach speaking in shorter breath groups

-teach about pausing and stress in normal speech and reading (not every pause = inhalation, pausing and inhaling at clause boundaries)

-contrastive stress drills

-expressing emotions

write parahraph then ask them to read with a feeling

-inc strength (ability to produce force)

-inc endurance (ability to sustain force)

-lead to changes in muscle size, alters motor commands and changes patterns of activation within and accross muscles

How do you train strength vs endurance?

strength- heavy loads , small number reps , lots of recovery time, high intensity

endurance - light loads but large number of reps 

-abdominal and intercostal muscles are skeletal muscles, similar to limb muscs

- strength training inproves motor perf in skeletal muscles

-inc inspiratory volume (therefore BG length, loudness)

-shorten inspirations

-improve ability to hold inspiratory effort (checking action)

-reduce speaking related dyspnea

-dec effort req during speech breathing

-breath against resistance

-patient inspires repeatedly through device for 2 min, one min recover, then 8-10 times

- showed to benefit those with muscular dystrophy, spinal cord injury, spinal muscular atrophy, larnygeal papilloma, bilateral VF paralysis

- importatn to carry it over to speech (BG length, loudness)

-dev better control over the expiratory phase (inc BG length, loudness)

-prolong expiratory flow

-decrease speaking-rel dyspnea and fatigue

-carry over to speech!!!! constanct SG pressure, loudness, BG length

frog breathing

-to compensate for weak inspiratory muscles

-each inspiration inc lung volume by 50-75 cc

-repeated 8 to 10 times up to a normal size tidal breath

-takes about 5 sec to complete

-speech ratings

-voice ratings

-transcription

-identification / counts of behaviour (eg: errors, # of stuttering events)

-gold standard

-validity

-easy to perform

-cheap

-robustness

-reliability

-perception is tricky by nature (phonemic restoration, discrim vs ident, prosodic effects, McGurk)

-multidimensional nature of speech/voice and interdependency of dimensions

-different refs for normal

-lack of agreement on what descriptors are most imp

-deps on method of judgement (broad, narrow)

-dep on who the judge and the speaker are

-know what your analysis is for

-simplify (reduce dimensions)

-train judges

-use referece samples

- use the same ass samples within and across patients

-stay tuned to research - look for new ways

-explore more correspondence bet instrunment and perceptual analysis

-to control phonation - rapid, vibratory, quasi-periodic motions of the VF

-to control artic (laryngeal devoicing gesture for consonants, laryngeal height for vowels)

Why do the VFs vibrate?

largely due to aerodynamic (Bernoulli) and elastic (passive) forces arising from small variations in the glottal area nad pressure changes below and between VF.

-phonemic distinction (presence, absence or phonation identified sound classes, vowel distinctions)

-prosody (intonation, stress, phrasal junctures)

-Speaker ident (sex,dialect, social status)

- paralinguistic information (emotions)

the physiological implementation of voicelessness

happens under muscular control

large, long, motion cycle of VF

Fo is a physical property, repetition rate of recurring waveshape

Pitch - a percieved frequency (infuenced by intensity and sound characteristics)

What is normal F0 for:

infants (distress)

infants (non distress)

Toddler (1 yr)

Toddler (2 yrs)

Child (6 yrs)

Child (11 yrs)

Adult

infant distress - 400 - 440

infant non dist - 340

toddler 1 - 400

toddler 2 - 320

child 6 - 290

child 11- 220

adult - males 120, fem 220

- anaylsed within a breath group

- usually a falling Fo - declination line

- reset of F0 after each breath group

-stressed syllables are above declination line

hypoadduction impairments

hyperadduction impairment

phonatory instability impairment

long term instability

mixed impairment

phonatory coordination impairment

- inadequate VF closure

- reduced loudness

- breathy or hoarse voice (laryngeal paralysis, PD, TBI, progressive supranuclear palsy, Shy-Drager Syndrome

pitch level

pitch breaks

monopitch

excessive loudness variation

loudness decay

harsh voice

hoarse (wet) voice

breathy voice

strained-strangled voice

long term instability 

wow -1-3 hz

tremor - 3-10 hz

flutter - 15-18 hz

non-speech:  cough, laugh, sign (volitional versus involuntary/reflexive)

Phonation

Rapid vowel repetitions ( i-i-i-)

acoustic anaylsis

visualization of VF (stroboscopy, indirect laryngostcopy)

aerodynamic assessment (measure of laryngeal resistance)

grunting

laughing

controlled coughing

postural adjustments (phonating in supine, head turn)

combining respiratory and laryngeal behaviors - speech initiation at the begining of exhalation

grunt

hmmmmmmmm

aaaaaa (no tongue shaping needed)

then just keep shaping 

What is the tx for hypoadduction?

who could you use if for?

goal is to enhance VF adduction

useful for patients with unilateral or bilateral VF weakness (paresis) or glottal incompetence 

(TBI with brainstem confusion, brainstem stroke, Shy-Drager Syndrome, PSP)

clasping hands together and squeezing palms togehter as hard as possible

interlacing hands and puling outward

sitting in char, grasping the bottom with both hands, pulling upward

to decrease adduction forces and improve airflow through the glottis

useful for those with spastic dysarthria (UMN disease), CP, hyperkinetic disorders (like huntingtons)

may occur as a compensatory mechanism for managing weakness at the laryngeal or velopharyngeal level

-easy onset of phonation (yawn sigh, chewing) relaxed phonation shaped into various sounds

-laryngeal massage, relaxation

-decrease of laryngeal resistance with increased pitch, head rotation, initiation of utterances at high lung volumes

surgical options - recurrent laryngeal nerve resection (induced unilateral VF paralysis), botox

Do most studies find support for biofeedback?

what are some examples of biofeedback methods?

yes

only 3 out of 18 didnt find any

(microphone, surface EMG, fibroscopic laryngoscopy, visipitch, anivox, speech viewer, dr speech

-voice amplifiers

-speech enhancer (CP, MS, TBI, Myasthenia Gravis, vent/trach, spasmodic dysphonia, stroke, PD, paralysed vocal cords)

-Delayed auditory feedback DAF - slows speaking rate, inc in intensity and speech intelligibility

-pacing board (syllable by syllable tapping)

-alphabet board (first letter pointing)

goal: to achieve better speech with increased loudness through reorganization of neural control processes

voice focus - 'think loud' is used at the system trigger for improving vocal effort

single focus - global parameter that seems to engage multiple speech systems

high phonatory and physical effort - inc effort is needed to override rigidity and hypokinesia

sensory calibration/perception - speaker must learn to identify the appropriate amount of effort

quantification - quantified feedback by the clinician is key to motivating speakrs 

doing anything that intensly will get a result

doesnt work on artic at all

does loud voice generalize to artic?

other side effects of PD

-intensive tx - daily practice needed

tx is administerd four times per week for 16 sessions in one month

- can even have web-based delivery

What principles are lsvt based on?

use it or lose it

use it and improve it

neuroplasticity

intellectually and emotionally

- boot camp style

- lots of emotional language 

follows principles of motor learning (intensity)

How was success judged in LSVT?

what types of PD patients were used?

intelligibility judged by patients and carers , subjective measures

only rel mild PD patients were used

unconcealed allocation

small N

Underrepresentation of females

diff patients were examined by different means (laryngoscopy, perceptual analysis, aerodynamic measures)

No statistical comparison between LSVT and other therapies like RET

Some judgements (intelligibility) done by patients and carers only (not blind)

methodological quality is poor

* some things here cant be avoided, some can

why it works?

who the approach works for in PD

Why it would work for MS, DS and other disorders

Does it affect intelligibility

Is it better/diff than other therapies

* Respiratory, coordination and voice control training, with emphasis on prosody

* Prosody based therapy

How does prosody based therapy work?

who made it?

Johnson and Pring (1990)

10 sessions over 4 wks

S1 and S2 - est a relaxed diaphragmatic breathing pattern, coordinate breathing and phonation

S3 - improve voice loudness and loudness contrasts (repeating short phrases for imagined listeners at different distances away)

S4 - use of stress patterns (contrastive stress drills)

S5-7 - Pitch excercises using visipitch

S8 - clear speech practice

S9- vocal loudness (SPL meter)

S10- rate control

-if she's in supine, put in upright to help the diaphragm

-spastic/hyperaduction - can do easy onsets, inc duration of bgs through appropriate use of voice and respiration, teach prosody, rate

-if she cant raise pitch, then train to inc loudness, will give similar perceptual effect

-LSVT or other

-work on inc loudness

-work on pacing

- work on voice

-awareness training (i heard from your fam that you're hard to understand, you know why? play tape)

-clear speech (voice control and effort), work on making clear speech, sit with back to client

1) tensor veli palatini - CN V

2) levator veli palatini - CN X

3) Palatoglossus - CN X

4) Palatopharyngeus CN X

5) Uvula X

6) Superior Pharyngeal Constrictor X

open vs closed

elevation and port size

body/head position

degree of opening 

fast rates - reduction in magnitude of velar movment (undershoot)

inc nasal airflow and nasalance at slow speaking rates but not at fast rates

diffs in temporal measures of VP function at different rates

multistage lowering

magnitude of VP movement is less - could use in therapy

more movement in slow rates - sometimes sounds really hypernasal

velum

lateral pharyngeal walls

posterior pharyngeal walls

consistently inadequate closure - too much/ too little opening

inappropriate timing (delayed closure)

inconsistence closure

worsening over time (fatigue) worsening in complex sequences

-7 pt rating scale

-phonation, single words, phrases, paragraph reading

-nasal emissions - pressure consonants (loaded sentences) weak sounding consonants

-hypernasality

-hyponasality

-test with nares occuluded

-notice face - facial grimacing

-presence and degree of the VP problem

-measures of oral pressure and nasal flow

-oral pressure - normal is 5-10cm h20 for pressure consonants

-nasal flow - normal is less than 30cc.sec for non nasals

-VP orifice area: normal under .o2 for non nasal consonants

-speech sample - use syllables with bilabials, if labial weakness - use alveolars, vary complexity

timing relns between intraoral pressure and nasal flow

-measures differentiate speakers with varying degress of VPI

-use words like hamper and jumper, bc have to go from all energy out nose to non v fast

-for speakers with mild impairment and interpittent VP insufficiency

-artic drills

-speaking rate intervention (slower or faster)

-reducing loudness (phonatory, respiratory tx)

-clear speech (larger movements for decreasing oral resistance)

-if indicated, strengthening using CPAP (continuous positive airways pressure) 

try slower speech, helps with coordination etc

or 

speak louder tends to inc clarity and slow speech down

blows air through the nose 

use speech to talk against the constant positive pressure in the nose

'strengthen the speech environment'

See Scape - detects flow, low tech

Nasometer (Kay-Pentax, Inc.) - detecting acoustic energy

Endoscopy

-consistent VP insufficency

-adequate resp support

-presence of voluntary phonation

-can tolerate the lift (desensitization may be required)

cooperation

non-spastic

no severe swallowing disorder

course of the disease (degenerative)

* ALS might have hightened reflexes so can't put stuff in their mouth

-blowing

-sucking

-swallowing

-gagging

-electrical stimulation

-tactile stimulation

kids have to dev their phonological system on top of having apraxia, but have lots of neuroplasticity

adults already have their system, but less neuroplasticity

- lack of agreement with what exactly constitutes planning and programming

- lives in between psycho-linguistic processing and speech production in speech models

-lack of agreement about AOS essential characteristics

-rarely exists in the pure form

motor planning - defines motor goals (eg lip rounding, velum elevation)

motor programming - commands for different muscle groups, depending on the speficic artic situation, accounts for muscle tone, direction and ROM

(Intention to speak)

morphemes

phonological encoding

phonological words

phonetic encoding

gestural scores

implementation

speech movements

(Actual execution)

-Broca's area

-Left insula - subcortical structure, along the cortico-bulbar pathways

-Left frontal and parietal regions

-arcuate fasciculus

-basal ganglia 

-reduced ability to perform skilled learned movements (especialy on command)

-effortful, groping articulation (slow)

-difficult in movement initiation

-articulatory inconsistencies on repeated productions

-prosodic disturbances (misalignment of stress)

-preserved automatic speech

- increased difficulties with increased complexities or at higher speaking rates

-clients aware of difficulties

-break down if rate increased

1) oral non-verbal apraxia

2) Constructional apraxia

3) Dressing apraxia

4) Ideational apraxia

5) Ideomotor apraxia

6)Left-sided apraxia

7)Oculomotor apraxia

What are oral movement tasks (examples)?

In what apraxia would they be affected?

-DDKs

-Work Repetition - inc complexity

-Show me how - limb/oral apraxia - make a fist, play the piano, salute, kiss, blow

-polysyllabic word naming - complexity (telephone, potatoes)

-sucessive repetitions 

-spontaneous speech (grandfather passasge etc)

speaking on command, automantic speech, singing

Main Q - where does speech break down?? (automatic speech, imitation, spontaneous production) (sylls, words, multisyll wds, phrases, sentences, conversation)

What perceptual features are you looking for in an assessment of AOS?

-

-slow rate

-prolonged segment duration and inter-segment durations (think, intrusive schwa)

-errors consistent in type (additions, substitutions, distortions)

-phonetic analysis (place, manner of artic, voicing)

-prosodic abnormalities

-rate manipulation

-mostly durational cues

-vowels, inter-segmental pauses, fricatives, VOTs

aphasia - disruption of linguistic processes

dysarthria- paresis, ataxia, akinesia, rigidity, dyskinesia, tremor

AOS - motor programming disorder

AOS- always slow rate, increase in rate leads to increase in errors

Aphasia - normal rate, can inc rate without errors

AOS - long vowel durations

Aphasia - normal vowel durations

AOS - inaccuracy in placement

Aphasia- no distortions, substitutions are not distorted

AOS- consistent location and type of errors

Aphasia - inconsistence location and type of errors 

AOS - drill helps - need to access motor programs

Aphasia - drills useless

AOS - yes, difference, auto phrases will be ok

Dysarthria- NO, all speech the same 

motor planning and coordination are affected

articulatory breakdowns are irregular

articulation and prosody disorders are prominent

oral mechanism exam may be normal

AMRs - irregular in ataxia but regular in AOS

Islands of effort free speech - unusual in ataxia and VERY unusual in AOS

Automantic speech - no better than volitional in ataxic

Groping - ataxic speakers rarely grope for artic postures and do not usually attempt to correct artic errors

Substitution - not as freq in ataxia as AOS

-focus on accuracy of articulatory positioning and transitioning between segments (regain pts or artic)

-focus on rhythmic, temporal or prosodic aspects

-inter-systemic reorganization (use of gestures, finger counting etc)

phonetic derivation - speech from non speech

progressive approximation - sh and th from s

phonetic pmacement - teach how sounds are made, manipulate oral structures, dev onomatopoetic assoc

miimal contrasts - tea sea

Wambaugh et al, 1996

- for consonants

- minimal contrasts is the unique features

-hierarchy - modeling and repeating of contrastive words, graphic (letter) cuing, integral stimulation, phonetic placmeent cueing and repeated practice

What is Integral Stimulation and Repeated Practice (rosenbeck et al , 1973)

AOS tx on emphasizing regaining pts of artic and dequencing

8 steps:

-simultaneous productions (watch,listen,say with me)

-patients response is delayed

-imitation without simultaneous cues from clinician

-multiple repetitions without cues

-stimulit in a printed form, no cues

-delayed oral reading

-responding to questions

-role play

-created by deborah hayden

-prompts for restructuring oral musculature phonetic targets

-articulation + rate control

-Oral/Facial Prompt

-tactile/kinesthetic feedback

-minimal pairs

* to do with structuring in hierarchines of ling complexity and cog complexity and enhancing feedback

Goal is to facilitate temporal schemata

- Melodic Intonation Therapy

-Metronomic Pacing / Finger Tapping

- Contrastive stress techniques

-Emotional stress

-Prolonged speaking

Electroarticulography - about $3000, request it! 

BUT everyone needs an artificial palate with electrodes embedded

-To Elicit Vocalizations - use automatic speech tasks, social response situations, singing, shape phonation from a cough, yawn, laugh, push gently on stomach during the exhalation phase of breathing

-To Shape Syllables from Phonation - humming to nasal context

-To shape words based on the existing sound repertoire - fine to fire, five

-Shape words from stereotypic utterances - Multiple Input Phoneme Therapy

-Use cues - audit, visual, written, tactile

-focus on speech 

-choose targets wisely

-prosodic tx may be viewed as supporting artic but may also serve own purpose

-cueing hirarych and hierarchy of difficulty

-severity

-stimulability (BUT some studies show that tx of non stim sound resulted in much broader generalization)

-difficulty 

-frequency of occurence

-isolated sound versus syllables

-too many sounds at once may be a problem

-functionality

-co-existent aphasia?

-course/nature of the disease (degenerative)

-corticobasal degen

-PSP

ALS

PPA

Ps - subglottal air pressure

Po - intraoral air pressure

Vg - glottal airflow

Vo - oral airflow

Vn- nasal airflow

14

therefore about 140000 muscular events per phoneme (motor units)

put in order

motor program

language

motor exectuion

ideas

ideas (cognition)

language

Motor program

motor execution

 a speech disorder resulting from damage to neural mechanism that regulate speech movements

OR

a collective name for a group of neurologic speech disorders resulting from abnormalities in the speed, strength, range, steadiness, tone or accuracy of movement req for control of the respiratory, phonatory, resonatory, articulatory and prosodic aspects of speech production (duffy)

-weakenss of speech muscles

-changes in movment speed

changes in movement size

spasticity

excessive, reduced, or variable muscle tone

incoordination (kind of like 'inaccurate movements')

involuntary movements

-cog, ling and cog-ling deficits (aphasia, akinetic mutism) - we would still do

-purely sensory deficits (hearing loss)

-musculoskeletal deficits of non-neurologic nature (laryngectomy, cleft ) - we still do

- physchogenic, nonorganic disorders (depression, shizophrenia)

-normal aging

What is the prevalence of dysarthria in?

lacunar strokes (deep)

TBI

PD

ALS

lacunar -30%

TBI - 25%

PD - 60%

ALS - 25%, later on 70%

age of onset

course

site of lesion

neurological diagnosis

pathophysiology

speech subsystem involved

severity

premotor cortex

supplementary motor area

Primary language cortex

Broca's area

primary motor cortex

primary sensory cortex

fissure of rolando

supramarginal gyrus

initiation, maintenance, inhibition and learning of complex motor behaviours

(continuation of movement too)

-controls voluntary musculature on the contralateral side

- somatotopically organized (spatial organization by region of the body)

-the # of motorneurons allocated to a musc depends on the degree of control needed for that muscle

Functions!

patterns used for swallowiong may be in one region , but for ex: genioglossus has more than one use, so if brain damage, then gg may be unusable for one thing but not for another 

cell

axon

axon terminal

Contained in the CNS

Originate in the cortex

Terminate at the cranial or spinal nerve nuclei

Corticospinal and Corticobulbar

innervate LMNs on the opposite side of the body

the indirect motor system (brainstem motor pathways)

regulates reflexes

-imput to LMNs though multiple synpses

spasticity

hyperreflexia

weakness

emotional lability

loss or reduction in skilled movment

hemiplegia (paralysis in one side of the body) or hemiparesis (weakness in one side of the body)

Bainski's sign

Unilateral UMN dysarthria OR Spastic Dysarthria

Where are the LMNs

Where do they originate

Where to they terminate

wHat do they do?

contained in CNS and PNS

also called final common pathway

Originate in branstem and spinal ford and terminate at the muscle

carry out UMN commands for voluntary movements 

hypotonia

atrophy

hyporeflexia

weakness

fasciculations

Flaccid dysarthria

-autoimmune, inflammatory disease caused by the attack on the myelin sheath of peripheral nerves by antibodies or white blood cells

- weakness then paralysis starting in extremities

-diffs with eye movments, facial movements, speaking, swallowing

- very slow heard rate or low blood pressure

controls flow of info to cortex

sensory relay - processes all sensory info except olfaction

functions - attn, memory, learning, abstract thinking, goal oriented beh, language, conciousness, emotion

ventral anterior

and 

ventral lateral

(faciliate movement assoc with BG)

contralateral hemianasthesia 

hyperalgeasia after some time

(touch, pain info impaired)

1 caudate nucleus

2 putamen

3 caudate nucleus and putamen= striatum

4 globus pallidus

5 subthalamic nucleus

6 substantia nigra (prod dopamine)

sends input to the striatum, prod dopamine, excites the direct pathway, inhibits the indirect pathway (faciliates or stops motion)

putamen

globus palladus

1) info from the association cortex

2)info reaches the striatum (caudate and putamen) 

3)striatum inhibits the GP Interna (part of the lentiform)

4)GP interna now inhibited - when excited it inhibits the thalamus

5)Thalamus is now allowed to get all excited (VA and VL esp assoc with movement)

6)The thalamus sends the info back to the frontal motor cortex

7)Motor cortex- pre-central gyrus, humunculous, tongue part

8) Upper Motor Neuron Fibres (cortico-bulbar tract) project down through internal capsule

9)Continue ipsi until reach the hypoglossal nucleus in the medulla -where they decussate then synapse

10) continue bilaterally and exit through hypoglossal canal

1)motivation ares of cortex become excited

2)motivation/assoc cortex sends info to striatum. Caudate recieve info from multimodal addoc cortices/eye controlling motor ares. Putamen reiceves more divers info from sensory auditory and visual areas

3)Striatum will inhibit the globus pallidus internus (which tonically inhibits the thalamus), thus when the GPi is inhibited, it allows the thalamus to get excited

4)Thalamus is now disinhibited

5)Thalamus presents the frontal motor cortes with appropriate motor programs for desired movmenet

6)Cortico-bulbar tract goes down through the internal capsule

7)then at nuclei, excited lower motor neurons

1) association cortex sends info to striatum

2) straitum sends inhibitory info to GP Ex (GPe tonically inhibits the the STN)

3)SubThalamic Nucleus is now allowed to be excited

4)Sub Thalamic Nucleus in turn excited the a)GP interna and b) influences the substantia nigra pars reticulata

5) GP interna inhibits the thapalmus b) SN does something too, together they form a sort of 2 way brake

6)Thalamus relays this info to the motor cortex and the beh is inhibited (the cortex no longer has thalamic permission to run the motor programs, and movement is halted)

the striatum doesnt inhibit the GPi.

Therefore GPi always excited and thalamus always inhibited

output of GP int to thalamus increased 

-facilitaes or inhibits motor activity

-temporal sequencing of movements

-assist in motor learning (together with the supplementary motor cortex)

-cognitive- memory

rigidity - inc musc tone

hypokinsesia - poverty of movement

bradikinesia - slow initiation and speed of movement

tremor at rest - rhythmic, involuntary, oscillatory movements

L-DOPA - facilitates dopamine production in the SN

Pallidotomy (lesion to GPi)

Deep brain stim - insertion of one or more electrodes into the thalamus 

-fetal/stem cell transplant

-all these txs dont usually fix speech

Ballism - violent, flailing movements of larger amplitued, lesions to subthalamic nucleus

Dystonia - persistent posture of a body part which can result in grotesque movements and distored postures of the body

-when initiating a movement, frontal and parietal cerebral motor cortex also sends a copy of the movement to cerebellum, via relay neurons in the pons. This gives the cerebellum info to compare with the motion feedback it gets from the body

-cerebelllum compares performed movements iwth what the desired movement was (so it can make corrections)

1)spinal cord relays proprioceptive info regarding movements that are happening

2)Medulla (inferior olive) helps dev memory in the cerebellum (helping us to master new complex movements)

3)major parts of the cerebellum do diff things (cerebrocerebellum spinocerebelum, vestibulocerebellum)

4)PUrkinje cells in the cerebellum (all 3 aresa) modulate inhibition of movement (these cells are on the surface of the cerebellum, in the cerebellar cortex)

5)purkinje cells are inhibitory to deep cerebellar cells

cerebrocerebellum - higher functions like SPEECH!!!, and fined tunes motions of the hands 

Spinocerebellum - recieves direct input from the spinal cord , Distal movements (walking)

Vestibulocerebellum - oldest part, concerned with posture and equilibrium

cortex - via pontine nucleus - cerebellum (dentate nucleus) - thalamus - cortex

initial movements are 'trimmed' by Purkije cells which have an inhibitory function

disorganization, decomp of movement

hypotonia

weakness

dysmetria - difficulty scaling and timing of movements (DDK tasks)

intention tremor

ataxia

What is acetylcholine (ACh)

resp for?

responsible for much of the stimulation of muscles (makes them contract)

also involved in cog function (memory)

ACh- based neurotransmitter system

there are a cholinergic system, cholinergic drugs

-autoimmune disorder (the body produces antibodies to block Ach receptors), inhibits the effects of ACh

-Weakness, fatigues - head and neck muscles are severely effected (speech, swallowing, breathing, eye movements)

-no atrophy and fasciculations

-TX - removal of the thymus

-Cholinergic txs useful

alpha motor neurons 

Force generation

(motor)

gamma motor neurons

(muscle tone)

a single nerve impulse produces a single contraction that is called 'muscle twitch'

a simple twitch gives only 20-30% of the max tension possible - musc will start to relax before the max is reached

if a second stimulus is given before a muscle relaxes the musc will shorten further, building up more tesnsion than a simple twitch - this is called SUMMATION

-increase of rate of firing (temporal summation)

-engage greater number of motor units (spatial summation)

What are the two types of contraction

which one is used for speech?

isotonic - the musc shortens or lengthens keeping a constant tension

isometric - muscle doesnt shorten, held at same length, tension buids up, no movement

ISOTONIC more in speech

-we can change neural structure

-we can change fibre types

-we can change innervation

*therapy can trigger changes!

physiologically - the max tension that a muscle or grp of muscles can generate by contraction under specific condition to resist or repel a load

physically - to muscle force, a quantity which tends to change the velocity of the external load

-determined by various neural, structural, mechanical and metabolic factors

the gamma motor system

also controls position in space and provides proprioceptive feedback to the cortex

lack on inhibition of the stretch reflex

movement triggers and involuntary contraction opposing the movement

UMN issue

lack of inhibition to the gamma system results in spasticity

loss of inhibition in the gamma motor neurons

leads to

chronic contraction of intrafusal fiber

leads to 

chronic contraction of extrafusal fibers

*pathalogical reflexes intact

*no atrophy

resistance to externally imposes joint movement

can be due to simultaneous co-contraction of agonists and antagonists

tone disruption

weakness

1) signals from the brain (motor commands, voluntary movements)

2)signals fomr the brainstem - CPGS

3)Sensory signals from feedback

4) Reflexes