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what is hyperkinetic Dysarthria
Disease of the basal ganglia or extra pyramidal pathway. It means too much movement; it produces involuntary movements (excessive involuntary movements: chorea, myoclonus, tics, dystonia and essential tremor); the impression is that it interferes with normal speech production and that if involuntary movements could be eliminated, speech production might be normal.
The movements are unpredictable and variable.
- a group of various MSD
- can be:
- Hyperkinetic Dys of the ___ type.
- chorea, tics, tremor, dystonia,
What can cause hyperkinetic Dysarthria?
Any condition that causes too much Dopamine to be released into the basal ganglia
Has an excitatory effect
Progressive genetic disorder of the basal ganglia
Child has a 50% chance of inheriting the disease
Symptoms appear at about 35 - 40 y/o
15yr life expectancy
Chorea, dementia, emotional instability, cognitive decline, personality changes
associated with hyperkinetic dysarthria of the chorea type.
choreic movements interfere with voluntary actions
Hyperkinetic Dysarthria of the Chorea Type
most subsystem impacted in Hyperkinetic Dysarthria?
(abnormal excessive involuntary movement)
Orofacial dyskinesia: face
Tardive Dyskinesia : (specific to face) late onset/common side effect of using antipsychotic drugs
Too much movement
single or repetitive, brief sharp jerk of the body
Simple or Complex, non-purposeful under partial voluntary control
Complex: has a purpose: Ex. scratching, throwing, chewing, word
When the person involuntarily swears (inappropriate derogatory comments)
Diagnosis for Tourette Syndrome
Most commonly associated with Tourette syndrome. Must have tics for 1yr, have a motor and vocal tics and never a period of more than 2 months when they didn’t have the ticks, client must report significant impairment to get diagnosis.
Quick, irregular, rapid, involuntary purposeless movements. Variable tone present in the muscles. Seen in Huntington’s disease, encephalitis.
Dance like movements. appear smooth and coordinated (they are unpredictable)
- Abrupt contractions of the muscles of trunk or head.
- Can effect the whole or half (hemi Ballismus) of the body (depends on nuclei damaged).
Damage to the sub-thalamic nucleus.
Abnormal muscle contractions cause involuntary writhing movements.
Seen in people with CP
Involuntary abnormal postures that occur with co-contraction of antagonist muscles.
Can appear focally. Ex. mouth
A sudden involuntary movement
Tonic: a prolonged or continuous spam
Clonic: a short repetitive spam
Forceful closing of the eyes
The most common involuntary movement.
The origin can be at the cerebellum or a pathway (cerebellar pathway).
Resting: Body is in repose
Postural: Body part is maintained against gravity
Action: During movement
Terminal: As the body nears the target
Distinctive Speech Characteristics: of the Chorea type
- Prolonged intervals between words and sounds
- Variable rate
- Inappropriate silences
- Excess loudness variations
- Prolonged phonemes
- Sudden inhalations/exhalations
- Voice stoppages
- Transient breathiness
(in order from most common)
Hyperkinetic Dysarthria of the dystonia-type
- Affects Articulation the most
- Slower movements than Chrorea
- (waxing and weaning)
AMRs help you best observe the dystonia
- Deviant speech characteristics:
- Distorted vowels
- Harsh vocal quality
- Irregular articulatory breakdowns
- Strained-strangled vocal quality
- Inappropriate silences
- Excess loudness variations
- Voice stoppages
- Audible inspiration Voice tremor
- Alternating loudness
(in order of most common)
non speech characteristics of hyperkinetic Dysarthria of the dystonia type
- Anterior spillage
- facial grimacing
- Mouth opening, closing
- lip pursing or retraction
- rotary tongue movements & protrusion
- (due to sustained muscle spasms)
- Neck torsion
- elevation of larynx
- slower movements that chorea
Who does it primarily manifest?
weakness and coordination specially in central face and tongue
Most common cause Stroke
can be masked by other co-occurrences
often temporary and mild in nature
UUMN Dysarthria patient complaints:
- Slurred, thick, or slow speech
- Chewing and swallowing difficulties Pseudobulbar crying or laughter
UUMN Dysarthria Clinical signs:
- imprecise consonants (most pervasive)
- Slow AMRs (2nd most common)
- Irregular & imprecise AMRs
- Irregular articulatory breakdowns
- Reduced strength/endurance/speed of lip and tongue movement
- Harsh vocal quality may be present
- Reduced loudness
- Mild vocal fold spasticity
Resonance: mostly not affected
Prosody: affected by slower rate
- mild incoordination issues with phonation reduced loudness
- Loudness decay
- Short phrases
- reduced vowel duration
UUMN Dysarthria: Subsystems affected?
What are the most common mixed dysarthrias?
Ataxic/Spastic (MS, most caused by stroke)
Hypokinetic/Spastic (associated with degenerative disease)
What determines the prominent components of mixed dysarthria?
Severity and extent of damage
remember is can change over time.
ALS and Mixed Dysarthria
- Progressive degeneration of motor neurons.
- Most common MND
- death is usually to respiratory failure
a mixed UMN and LMN disease
- Prosodic excess
- Distinguishing Deviant Speech Characteristics:
- Prolonged intervals
- Prolonged phonemes
- Inappropriate silences
- *all impact prosody
- (bad date)
Multiple Sclerosis (MS)
most common demyelinating disease
Can occur anywhere in CNS
most do not have dysarthria
- Most common speech complaints:
- Loudness control, harshness and impaired articulation
MS and mixed dysarthria
- Deviant Speech Characteristics: MS
- Impaired loudness*
- Defective articulation
- Impaired emphasis
- Impaired pitch control*
- Inappropriate pitch level
- Sudden articulatory breakdowns*
- Reduced Pitch Variability +
- Slow rate of Speech +
- * characteristic of Ataxic
- + characteristic of Spastic
TBI and mixed Dysarthria
60% the dysarthria resolves, 10% have chronic dysarthria.
Any kind can present due to diffused damage.
tend to see: Flaccid/Spastic
- Reduced vocal intensity
- Slowed rate of speech
- Syllable lengthening
Wilson's Disease and Mixed Dysarthria
prevents metabolism of dietary copper
- reduced stress
- Cognitive, motor and psychiatric problems
Apraxia of speech
Impaired planning or programming the voluntary movements for speech production
Nonverbal oral apraxia
Impaired planning or programming of nonverbal oral movements Apraxia of speech
- Inability to sequence nonverbal, voluntary movements of the tongue lips, jaw, and other oral structures:
- protruding the tongue, whistling, biting the lower lip and puffing out the cheeks
left hemisphere damage
often co-occurs with aphasia
does not affect spontaneous or reflexive orofacial movements
The Motor Speech Programmer Network
Broca’s area & supplementary motor area
May be a primary storehouse and integrative processor for previously acquired, highly practiced speech routines
Often identified as a lesion site in people with AOS
has been identified as a site of damage from stroke in people with AOS
Sometimes the only site of damage
Has a role in the acquisition of new speech routines
No damage to the left insula may be a good prognosis sign
Lesion here have been associated with AOS
known role in motor control
Lesions of stroke induced AOS are usually located in the:
- Left posterior frontal lobe
- Left parietal lobeLeft
- Basal Ganglia
A disturbance in the performance of the movements needed to use an object, make a gesture or complete a sequence of individual movements; Apraxia of speech is one of the ideomotor apraxias; a deficit in carrying out the motor plan needed to use the object or make a gesture.
Deficits in performing purposeful limb movements that can not be explained impairments in strength, mobility, sensation, or coordination
Usually affects both r/l limbs
May interfere with writing/nonverbal communication (gestures)
Apraxia for phonation
Can’t produce voicing upon command.
Can’t coordinate respiration and phonation to get the sound out.
Usually resolves on its own. 1-2 weeks
Etiologies of Apraxia
Stroke: most common cause
Degenerative diseases: not commonly associated with AOS
Primary progressive AOS
Demyelinating: MS (occasionally)
site of lesion for Apraxia
Anything that damages the Motor Speech Programmer Network
SMR, imitation of graded in complexity syllables, words, multisyllabic words and sentences are most sensitive to AOS
Apraxia: distorted sound substitutions and additions. Dysarthria is rarely associated with additions or substitutions and distortions are closer to the intended phoneme.
Articulation distortions are not helpful in distinguishing
Fluency abnormalities common in apraxia/uncommon in aphasia
Difference in performance of SMRs (more diff.)/ARMs (apraxia)
More diff. with volitional speech than automatic (apraxia). Dysarthria shows no difference.
Narratives more diff. than pic description, conversation is easier (have control): Apraxia
Do better if they can see and hear the model and repeat immediately (apraxia )
Syllable lengths effects (longer syllables are more difficult): Apraxia
Syllabicity effects: more powerful influence on AOS than word frequency effects
Syllable length effects, syllable boundary effects, word complexity effect (pg. 279)
See box 11-3 pg. 278 for all salient characteristic of AOS
The clustering of several of these characteristics help distinguish AOS from Dysarthria
Variability is considered by many to be a hallmark of AOS
Apraxia: Patient Perceptions & Complaints
My speech won’t come out right
I know what I want to say
Similar to people with aphasia
Speech is not fluent
Try to be more careful to reduce errors
More diff. with longer multisyllabic words
Apraxia and Articulation
Recognize errors and try to fix them
Grouping for articulatory postures
Describe as stutter
Praxia and Rate and Prosody
Issues are present even when the articulatory errors are not present
Disturbances are a defining feature of AOS
Rate: is generally slower and more variable than normal
Apraxia and Fluency
Problem worsen under conditions of stress or fatigue
Apraxia and task variables
SMR’s more difficult than AMR’s
Automatics should be less difficult than conversation speech
more familiar easier than novel speech
more complex, more difficult
Masked by aphasia
Tend to co-occur
Limited to a few utterances May or many not be meaning full (ex. stereotypie)
Ask them to count, imitate CVC syllables, sing, AMRs
Use overlearned/or automatically produced (less demand on programming abilities)
Look for a threshold at which patients succeed and fail on tasks
Apraxia of phonation (muteness)
Usually an early and transient problem, when confined to broca’s area.
Persistence for longer than 2wks should raise suspicions about a different diagnosis. (e.g., severe aphasia)
Display frustration and confusion
Non-verbal oral apraxia Usually present with apraxia of phonation
What is the goal of therapy for AOS?
to reestablish the motor plan/program for speech production. Help activate the program and to obtain effective/efficient communication.
What are the principles of motor learning?
We should be using this
Practice is very important, but must be the correct movements
Trying to create a new motor plan
Hands on assistance that is gradually faded
Relies on modeling, experience, and practice/drill of the movements
*DAB: people have lost the pre-program of speech, so intensive practice is needed. Hundreds!
Massed versus Distributed Practice
- Massed practice (one target, over and over again)
- Results in good learning of a single motor pattern but doesn’t generalize easily to other contexts
- Distributed practice (working on multiple targets in a single session)
- Results in slower learning that is better generalized and retained
Random versus Blocked Trials
- Random (variable) practice:
- (stimulus is mixed up, each stimulus is repeated 30-40 times, may work on same stimulus several times, its random) Stimuli are mixed up throughout a session
- Better for development of motor learning (per literature)
- Blocked (consistent) practice:
- One stimulus is practiced repeatedly followed by repeated practice of a second stimulus and so on (never working on the same stimulus more than once)
- You work on stimulus for 5 minutes, and then move on to the next stimulus.
Varying the Context in Apraxia Treatment
Varying the contexts facilitates motor learning
Select a particular movement sequence with different co-articulatory contexts and different manners of production
Vary prosody and loudness
Always model new contexts and alterations in prosody
a behavioral management and motor approach.
Research to support it’s use with kids with Apraxia of Speech
Most commonly used method for speakers with moderate or severe apraxia
Emphasizes multiple input modes Tactile, visual, auditory Gestures can be added as cues if needed Involves a hierarchy of steps
The eight-Step Continuum
you can start at any point in the continuum. Most clinician begin at step 4(1: most powerful cueing) at each-step you need to include 30-40 repetitions of skill. You move up and down the continuum based on the feedback you get from your client.
- 1. Watch and listen
- Clinician says word first, then both say word together
- 2. Watch and listen
- Clinician says word first, then clinician mouths word while client says it
- 3. Watch and listen
- Clinician says word, client repeats independently (you can add a delay time here. makes it more difficult)
- 4. Watch and listen
- Clinician says word, client repeats independently multiple times
- 5. Written word cue
- Clinician presents target word on paper; client reads aloud with written cue If you don’t read, use a picture
- 6. Written word no cue
- Clinician presents target word on paper; client reads aloud without written cue
- 7. Response to question
- Clinician asks Q to elicit target word
- 8. Role play
- Role play with clinician, family, friends to evoke target word in conversational contexts
Sound Production Treatment for Apraxia
(other more commonly used approach for indv. with adults)
Improve accuracy of spatial targeting and timing at the syllable level (GOAL)
Good efficacy data Emphasis is a minimal pairs approach
Steps for Sound production Treatment:
1. Modeling & Imitation Target is /p/: Say, “Pie/bye”, if able to produce /p/, give another repetition. If they CAN’T, you go to step
2. Repeat step 1 with a written cue point to word while modeling target production, if correct, give feedback and have them repeat it gain. If no, go to step 3
3. Integral stimulation” Focus only on the target sound: /p/ Using the single item, Pie “watch me, listen to me, and say it with me”. if correct give feedback and do again. If missed go to step 4
4 Articulatory Placement & Model Specific to the speakers perceived errors. Model the word and ask them to repeat it If correct give feedback and do again, if missed provide feedback and go to step 5
- 5. Isolated Sound Production
- modeling: repeat the sound only if correct, give feedback and go to next minimal pair.
- If incorrect, move on to another pair.
Ten exemplars counts as one trial. (you will have 10 minimal pairs).
Continue treatment until 90% of the trained items are produced correctly in 3 out of 4 sessions.Sentence level means working at the target sound at the phrase completion.Ex. Clinician: “I came home and ate__” Child: “pie”
Multiple Input Phoneme Therapy (MIPT) for Apraxia
For adults with severe acquired apraxia who have few verbal stereotypies
Sterotypies serve as initial stimuli
Clinician and client produce utterance while tapping on arm
Clinician fades voice but mouths words and continues to tap arm
Introduce new words with same initial phoneme as stereotypies
Efficacy of Apraxia Treatment
Must consider available evidence
Integral stimulation and sound production treatment have strongest evidence to date
Other treatments appear to be beneficial