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Cranial nerves involved in motor speech
CNV (trigeminal): jaw movement, chewing, speech
CNVII (facial): facial expression and lip movement
CNIX (glossopharyngeal): pharyngeal movement
CNX (vagus): phonation and resonance through laryngeal and velopharyngeal control
CNXI (accessory): head and neck
CNXII (hypoglossal): tongue movement
parts of the brain involved in motor speech
cerebrum: planning, initiating speech
brainstem: swallowing; midbrain, pons, medulla
cerebellum: coordinating smooth, well times and appropriately scaled movements
neurons: transmit signals
Upper motor neurons (UMNs)
originate in the motor cortex
travel down through the brain and spinal cord
initiate and modulate voluntary movement
Lower motor neurons (LMNs)
begin in brainstem and spinal cord
pathway to neurons in the muscles
Impacts for motor speech from lesions to the pyramidal system
lesions above the brain stem result in symptoms on the contralateral side of the body
lower half of the face and tongue receive contralateral cortical innervation only
other muscles of speech production receive bilateral motor cortex input
extrapyrmadial system
multisynaptic pathways that connect motor areas of the cerebral cortex to the lower motor neuron
have pitstops via basal ganglia, substantia nigra, red nuclei, subthalamic nuclei
control hypokinetic and hyperkinetic movement
hypokinetic signs
lack of spontaneous movement
akinesia: inability to complete a motor act, slowness in initiation and execution
bradykinesia: delayed or false starts in the commencement of movement and slowness once the motor act is initiated
hyperkinetic signs
abnormal involuntary movements
unable to successfully inhibit cortical motor activity
disrupt the rate and rhythm of motor activity
dyskinesia
abnormal involuntary movements
myoclonus
involuntary single or repetitive fast jerking movement
tics
rapid compulsive movements that may be voluntarily suppressed
chorea
purposeless rapid random movement of body part
ballismus
gross abrupt muscular contractions causing flailing movements (stroke)
athetosis
slow purposeless writhing movements (CP)
dystonia
abnormal involuntary movement from simultaneous contraction of agonist and antagonist muscle
tremor
involuntary rhythmic movement of body part
definition of dysarthria, what is it associated with
speech disorders resulting from disturbances in the CNS and/or PNS that control the muscles of speech production
associated with slowness, weakness, incoordination of muscle movements
subsystems which may be affected in dysarthria
respiratory system
phonatory system
articulatory system
resonatory system
7 types of dysarthria
flaccid
spastic
ataxic
unilateral upper motor neuron
hypokinetic
hyperkinetic
mixed
Flaccid dysarthria (lesion, characteristics)
lesion: lower motor neuron system, between brainstem and SC, cranial nerves
loss of reflexive, automatic, voluntary control of muscles
muscle weakness
breathiness, short phrases, hypernasality, imprecise consonants, harshness, monopitch
unilateral upper motor neuron dysarthria (UUMN)
lesion: upper motor neurons
spasticity and incoordination
unilateral lower facial weakness
unilateral lingual weakness
mild and transient speech difficulties
imprecise consonant production
spastic dysarthria
lesion: bilateral upper motor neuron damage
slow effortful and strained speech
imprecise consonants, distorted vowels and hypernasality
low pitch, harsh voice, strained
monopitch, monoloudness
prosodic excess
ataxic dysarthria
lesion: cerebellum and/or its connections
coordination and timing deficits rather than weakness
prosodic excess
articulatory inaccuracy
phonatory-prosodic insufficiency
hypokinetic dysarthria
lesion: extrapyramidal system
slowness or movement and/or lack of spontaneous movement
prosodic insufficiency
hyperkinetic dysarthria
lesion: extrapyramidal system (basal ganglia)
chorea or dystonia isolated to the face and larynx
slow, slurred and effortful speech
laryngeal tremor or dystonia - shaky or tight voice that closes off when speaking
Huntington’s chorea
common hyperkinetic disorder
choreiform movements
sudden, forced involuntary inspiration/expiration
random hyperadduction of vocal folds and poor resonatory-phonatory control
prosodic excess
phontaroy stenosis (harsh, strained, vocal arrests)
articulatory-resonatory incompetences
mixed dysarthria and clinical examples
lesion: more than one level of the nervous system
ALS, Multiple sclerosis, TBI
Motor speech programmer (MSP)
a network of interacting structures and pathways that temporally sequences the motor movements necessary for accurate speech
apraxia
have accessed the correct phonemes initially in the correct sequence
have the peripheral physical capacity to say the word but cannot find the phonetic shape and/or transitions from sound to sound
Key features and characteristics of apraxia of speech
articulation disturbances
fluency disturbances
rate & prosody disturbances
task variables influence
articulation distortions in apraxia of speech
consonant distortions predominate
distorted anticipatory substitutions
distorted perseverative substitutions
distorted additions
distorted sound prolongations
distorted voicing distinguishments
rate & prosody disturbances in apraxia of speech
slow overall rate
prolonged but variable vowel duration in multisyllabic words/phrases
prolonged interword intervals
difficulty altering rate on command
restricted altered pitch
altered stress
halting, effortful and irregular speech characteristics in apraxia
fluency disturbances in apraxia of speech
multiple attempts to self-correct errors
false articulatory starts and restarts
groping for articulation postures
sound & syllable repetitions
influential task variables in AOS
error higher for volitional vs automatic utterances
consonant cluster errors more frequent
auditory-visual stimuli better than single mode
speech sequential motion rates (SMRs) “pataka” harder than alternate motion rates (AMRs) “papapa”
intervention targets for aphasia, apraxia, dysarthia
aphasia: language comprehension and expression
apraxia: retraining motor sequences
dysarthria: strength, coordination and tone of muscles
neuroplasticity
the brain’s capacity to reorganise its structure and function in response to experience, learning and injury
Principles of experience-dependent neuroplasticity (8)
Use it or lose it
Use it and improve it
specificity
intensity matters
repetition matters
salience matters
Increase complexity
timing matters
principles of motor learning (practice conditions)
intensity of sessions
distribution of sessions
variability of tasks
schedule of tasks
task complexity
principles of motor learning (feedback conditions)
type of feedback: Knowledge of performance (KP) or Knowledge of results (KR)
frequency of feedback
timing of feedback
What is the effect of speech mechanism impairments and examples?
speech mechanism impairments leads to speech that sounds atypical
speech mechanism impairments: reduced range of movement, reduced speed of muscles, VF hyperadduction, velopharyngeal incompetence
atypical speech: slurred speech, imprecise consonant production, hypernasality, strained voice)
5 primary and overlapping approaches to the management of dysarthria
medical
behavioural
prosthetic
augmentative and alternative communication (AAC)
counselling and support
Goals of treating flaccid dysarthria
increasing strength and control of muscles
compensating for weakness to improve intelligibility
interventions for flaccid dysarthria
increasing respiratory support
speech breathing practice
abdominal diaphragmatic breathing
breathing against resistance
prosthetic assistance using expiratory boards or biofeedback tools
articulation therapy to target specific sounds and increase articulatory/phonatory effort
over articulation
CPAP for velopharyngeal strengthening
goals for treating spastic dysarthria
reduce spasticity and to reduce gradual appropximations of a full range of movements
Interventions for spastic dysarthria
facilitate air flow by increasing respiratory support and coordination with speech
reduce hyperadduction of VF using muscle relaxation techniques, forward focus, deconstruction exercise, vocal function exercises (sustained ‘eeee’)
palatal lift
CPAP
goals for treating ataxic dysarthria
improving of compensating for deficits of motor control and coordination
intervention for ataxic dysarthria
establish regular respiratory cycle and adding voice
starting and stopping voice in one exhalation
phonatory control
contrastive intonation and stress drills
improve consonant imprecision & vowel distortion (isolations)
goals for treating hyperkinetic dysarthria
reduce excessive and/or abnormal involuntary movements
surgical and pharmacological management most effective
behavioural techniques: bite blocks, rate reduction strategies, postural adjustments
interventions for unilateral upper motor neuron dysarthria (UUMN)
behavioural approaches that target articulation, rate and prosody
intervention for mixed dysarthria
focusing on subsystems impacted and the nature of presenting impairments
2 examples of evidence-based neuroplasticity based intervention
LSVT
BeClear
summarise what is LSVT LOUD
focuses on phonation
concomitant improvement : articulation, rate, overall intelligibility
intensive program -16 sessions
max phonatory effort, high therapeutic effort, voice awareness and use
features of LVST LOUD
Focus on voice
Focus on high effort
Focus on intensive treatment
Focus on calibration
Focus on quantification (documentation & measurements)
daily tasks in LSVT LOUD (3)
maximum duration sustained phonation
maximum fundamental frequency range
maximum functional speech loudness
hierarchical speech loudness tasks in LSVT LOUD
structural reading and spontaneous speaking
increasing in complexity with each week: words, simple phrases → sentences, simple conversation → reading/conversation → conversation
tasks in LSVT LOUD Merthods
daily tasks (hierarchical by each week)
homework tasks
carryover assignments
Goals of BeClear Treatment: Clear speech training
modifying habitual speech to enhance intelligibility
rate reduction
overarticulation
principles of neuroplasticity: Be Clear
specificity: exclusive practice of connected speech tasks
intensity: 1 hr treatment, 4x per week, for 4 weeks
Salience: meaningful communication using individualised stimuli
repetition: high level of repetition within and across treatment sessions
Components of the BeClear Treatment Protocol
Extended pre-practice: shaping and instatement, KP feedback & modelling by clinician
pre-practice: stimuli randomly selected, KP feedback & modelling
practice: functional phrases (everyday; out and about phrases) & functional speech tasks (reading, PDT, conversation); KR feedback
Home practice: functional phrases, reading aloud, PDT, conversation
6 guiding principles for management of apraxia of speech (AOS)
not all patients will be appropriate for treatment
counselling and education of patient and family regarding the nature of AOS and treatment rationale are important
repetition and drill are essential - 10 000 reps
tasks are hierarchical
self-monitoring is essential
salient treatment targets
Restorative approaches to AOS intervention
to improve/restore impairments
articulatory-kinematic
sensory cueing
rate and rhythm control
intersystemic facilitation (using other intact motor system to support speech production)
compensatory approach to treating AOS
when not responsive to retraining
AACL functional communication option AND supports
treatment stimuli for AOS
to provide greatest benefit or foundation for improvement
stimulability used but generalisation with complex untested targets
words and phrases more motivating and functional
meaningful, self-selected stimuli
hierarchical
patient-centred
DIfference between treatment for dysarthria vs apraxia
dysarthria: from underlying pathophysiology
start at word level
more collaborative
keep moving on from errors
apraxia: from severity of speech production
start at phoneme level
more clinician-led
do not accept errors
treatment selection for mild-moderate deficits vs severe deficits in AOS
mild-moderate
target rate, melodic flow
multisyllabic level
severe
postural shaping and production of functional units
sound-syllable-word level
Which treatment for AOS is considered most evidence based?
articulatory-kinematic approaches
articulatory kinematic approaches (what is articulatory, kinematic, goal and examples)
articulatory: movement of the lips, jaw, tongue
kinematic: timing, sequencing, speed and placement
how the articulators move during speech
goal is to retrain the brain to plan and execute speech movement more accurately
e.g. eight-step continuum, sound production treatment (SPT), PROMPT, rate/rhythm approaches
articulatory-kinematic approach: eight step continuum
WATCH, LISTEN, DO
progress from phoneme repetition to independent utterance
maximum support (1-2), fading cues (3-5), independent (6-8)
articulatory-kinematic approach for AOS: sound production treatment (SPT)
combine eight-step continuum with articulatory placement cueing, phonetic tasks and extensive modelling
if unable to produce: provide phonemic cards, verbal, visual or tactile cues
Sound production treatment (SPT) for Severe AOS treatment: 3 phases
Phase 1: Sound production - sustained phonation of /ah/ and variations
Phase 2: rehearse automatic responses to experience fluent speech production
Phase 3: phonemic drill and return to volitional speech
Articulatory-kinematic intervention for AOS: PROMPT (Prompts for reshaping oral muscular targets)
tactile cues
when patient produces incorrect production of phonemes, SLP will find the correct contact points for relevant phonemes and move the articulators passively. Then the patient will repeat the attempt with SLP moving articulators simultaneously
Articulatory-kinematic intervention for AOS: Rate/rhythm approaches
slowing speech rate using paced or metred speech
incorporating intonation, stress, rhythm cues
Melodic intonation therapy (MIT): incorporating singing
Contrastive stress drills