Measures of Tongue Function: Normative Data & Clinical ...
| |ICCD 2016 |
| |Iowa Conference on Communicative |
| |Disorders |
| |Cedar Falls, Iowa |
|[differential diagnosis of Motor Speech Disorders] |
| |
| |
Motor Speech Disorders
The evolution of a classification system
Prior to the classification system first introduced by Darley, Aronson, & Brown (1969), the dysarthrias were considered a single diagnosis.
The implication was that this diagnosis had homogeneous features.
Distinctions were made between dysarthria and aphasia, even dysarthria and apraxia of speech.
Parallels
Autism
No longer really considered a unitary diagnosis
Autism spectrum
Further definition
Asberger’s Syndrome
Differential diagnosis
Evolution of a discipline
A need to better understand and define clinical populations.
Evaluation
More accurate diagnosis
Treatment
Guide our treatment decisions
Darley, Aronson, & Brown
Pivotal articles (1969)
“Motor Speech Disorders” text (1975)
Defined and identified the dysarthrias
Initial sample = 212 patients
Lesion site
Perceptual characteristics
Motor characteristics
Benefits & Drawbacks
Assists with confirmation of lesion site
Can rule out other potential diagnoses
Clinical “shorthand”
Similar to aphasia syndromes
Guides treatment decisions
Understanding the underlying pathology results in selecting the appropriate treatment
Reliability has been questioned
Corresponding lesion data
Clinical knowledge
Not confirmed empirically
Take home message…
Clinically useful
Evolution continues
Our understanding of neuropathology will never be static
New discoveries
New procedures
For now, the system is a useful one that will continue to be refined
Hyperkinetic
Myriad of movement disorders
The Dysarthrias
“A collective name for a group of neurologic speech disorders resulting from abnormalities in the strength, speed, range, steadiness, tone, or accuracy of movements required for control of the respiratory, phonatory, resonatory, articulatory, and prosodic aspects of speech production. The responsible pathophysiologic disturbances are due to central or peripheral nervous system abnormalities and most often reflect weakness; spasticity; incoordination; involuntary movements; or excessive, reduced or variable muscle tone.”
(Duffy, 2013 p. 4)
Prevalence of MSD
Based on a sample > 14, 000 people referred for a speech/language evaluation at Mayo Clinic from 1993-2008
Other neurologic speech disorders - 0.4%
Apraxia of Speech – 3.9%
Nonaphasic cognitive-communication disorders – 16.8 %
Aphasia – 25.8%
Dysarthria – 53%
Definition revisited:
Key features of the dysarthrias
Neurologic basis
Disorder of movement
Categorized based on
Lesion
Physical characteristics (OME findings)
Speech characteristics
| | | | |
|DYSARTHRIA |Lesion |Physical signs |Speech |
| | | | |
|FLACCID | | | |
| | | | |
|SPASTIC | | | |
| | | | |
|ATAXIC | | | |
|HYPOKINETIC | | | |
| | | | |
|HYPERKINETIC | | | |
| | | | |
|MIXED | | | |
| | | | |
Flaccid Dysarthria
Results from injury/damage to cranial and/or spinal nerves
Final common pathway
Lower motor neuron
Reflexive, automatic, and voluntary activities are ALL affected when the lesion resides in the FCP.
Can impact all subsystems of speech
Primary characteristics can be traced to weakness
Which of the Cranial and/or spinal nerves might be implicated?
Etiologies
Surgical
Nonsurgical
Neuropathies
Tumor/Neoplasm
Myasthenia gravis
Degenerative
Vascular
Anatomic malformation
Demyelinating
Other
Lesion analysis
Trigeminal
Innervation properties
Three branches (sensory)
Motor component
Signs
Sensory loss
Jaw deviation (unilateral)
Jaw may hang open (bilateral)
How do you test?
Speech signs
Imprecision in connected speech
Most affected with bilateral lesions
Facial
Innervation properties
Sensory
Motor
Which would be most devastating to speech?
Signs
Facial droop
Drooling (possibly)
Pocketing
Testing
Speech signs
Imprecision in connected speech
Related to facial weakness
What sounds would be most affected?
Glossopharyngeal
Innervation properties
Sensory
Motor
Signs
Testing
Speech signs
Vagus
Innervation properties
Sensory
Motor
Signs
Velar signs
Testing
Speech signs
Phonation
Respiration
Resonance
Spinal Accessory
Innervation properties
Motor
Signs
Shoulder weakness
Testing
Speech signs
Hypoglossal
Innervation properties
Motor
Signs
Tongue deviation
Atrophy
Testing
Speech signs
Imprecision with articulation
Compensation with the mandible
Spinal nerve lesions
Damage to spinal nerves C-1 through C-5
Primary damage to respiration
How does that interfere with speech?
Signs
Rapid/shallow breathing
Exaggerated thoracic expansion
Flaccid dysarthria related to isolated damage to spinal nerve lesions is rare
Primary Characteristics
Weakness
Hypotonia and reduced reflexes
Fasciculations and fibrillations
Darley, Aronson & Brown (1969)
Hypernasality
Articulatory Imprecision
Breathiness
Monopitch
VPI
Audible inspiration
Harsh vocal quality
Short phrases
Monoloudness
***********************************************************************************
Spastic Dysarthria
Secondary to damage of the direct and indirect pathways of the CNS (UMN system)
Direct pathway
Pyramidal tract
Corticobulbar tracts
Interacts with cranial nerves
Corticospinal tracts
Interacts with spinal nerves
Facilitatory action
Leads to skilled discrete movements
Indirect pathway
Extramyramidal
Regulates reflexes, maintains posture, tone
Inhibatory nature
Clinical Characteristics
Difficulty with fine, discrete movements
Initially decreased tone
Weakness
Develops into increased tone, spasticity
Those muscles utilized in fine movements most affected
Decreased reflexes initially, then more pronounced
Babinski sign
Oral motor reflexes
Suck
Snout
Jaw jerk
Etiologies
Vascular
Brainstem stroke
Bilateral effects
Cerebral stroke can’t have the same impact, unless there is previous damage, or perhaps midline shift/compression from a hemorrhagic stroke
Lacunar infarcts
Multi-infarct dementia
Not a common problem with DAT
Inflammatory
Leukoencephalitis
Degenerative disease
Primary lateral sclerosis
Traumatic Brain Injury
Multiple Sclerosis
Neoplasm
Oral Mechanism
Dysphagia
Drooling
Pseudobulbar affect
Normal jaw strength
Facial movements may be slow then move into excess/extreme
Hyperactive reflexes
Speech Characteristics
Impairments noticed most by looking at muscle movement rather than isolated muscles
?« speed
?«range
?«force
?ªmuscle tone
Darley, Aronson, & Brown (1969a)
Imprecise artic
Monopitch
?« stress
Harshness
Monoloudness
Low pitch
Slow rate
Hypernasality
Strained-strangled quality
Short phrases
Distorted vowels
Pitch breaks
Breathy quality
Excess and equal stress
***********************************************************************************
Ataxic Dysarthria
Cerebellum
Two cerebellar hemispheres
Vermis
Ipsilateral contribution
Unlike the cerebral hemispheres which have contralateral contributions
With median lesions, effects may be bilateral
How does the “circuit” function?
The “circuit”
Notice of movement-cerebral hemispheres
Monitors the movement via feedback from the muscles/joints that conduct the movement.
Regulates movement in an ongoing fashion based on both ends of this circuit.
Clinical Characteristics
Ataxic dysarthria typically manifests with diffuse cerebellar damage
Any signs/symptoms from unilateral lesions tend to improve rapidly
Disordered gait
Truncal instability, titubation
Rotated head postures
Occular motor abnormalities
Ataxic dysarthria
Etiologies
Degenerative Diseases
Hereditary Ataxias
Multiple Sclerosis
Paroxysmal Ataxic Dysarthria
Vascular Disorders
Aneurysms
AVMs
Occlusion in the vertebrobasilar system
Neoplasm
Trauma
Toxic/metabolic conditions
Alcoholic cerebellar degeneration
Severe malnutrition
Vitamin deficiencies
Pharmacological
Antiseizure drugs
Lithium
Valium
Hypothyroidism
Normal Pressure Hydrocephalus
Oral Mechanism
Most aspects of the OME can be entirely normal
Size
Strength
Symmetry
Face, jaw, tongue, palate
Rest, and during sustained postures
Gag
Reflexive swallow
OME abnormalities
Irregular AMRs
Observe the regularity of movement of the tongue, lips, and jaw
AMRs and connected speech
Systemic problem
Affects the entire system rather than isolated impairment from muscles/muscle groups
Speech
Imprecision with artic
Irregular artic breakdown
Distorted vowels
Excess and/or equal stress
Prolonged phonemes/pauses
Slow rate
Harshness
Monopitch
Monoloudness
Reduced/irregular breathgroups
Darley, Aronson, & Brown 1969
Artic imprecision
Excess/equal stress
Irregular artic breakdowns
Distorted vowels
Harsh quality
Prolonged phonemes
Prolonged intervals
Monopitch
Monoloudness
Slow rate
Loudness variations
Voice tremor
***********************************************************************************
Hypokinetic Dysarthria
Pathology of the basal ganglia control circuit
Rigidity
Reduced force/range
Decreased mobility a/o range lead to the name “hypokinetic”
The only dysarthria which has
“rapid” speech rate as one of the perceptual characteristics.
Depletion or reduction of the neurotransmitter, dopamine.
Parkinson’s disease that best reflects hypokinetic dysarthria.
Basal Ganglia Control Circuit
Functions
Regulate muscle tone
Movements that support goal directed activity
Postural adjustments
Adjust movements to the environment
Assists in learning new movements
Damage results in reduced movement a/o a failure to inhibit involuntary movement
Hypokinetic dysarthria most reflects reduced movement
Clinical Characteristics
Resting tremor
4-7 Hz
Limbs
Pill-rolling
Jaw, lips, and tongue
Rigidity
Resistance to passive stretch
Decreased movement
Bradykinesia/Akinesia
Slow movement
Freezing
Shuffling gait
Micrographia
Masked facies
Reduction in:
Arm movement while walking
Gestures
Blinking
Head movement
Swallowing frequency
Loss of postural reflexes
Reduced “righting” response
Stooped posture
Difficulty initiating movment
While lying down
Sitting to standing
Etiologies
Damage to the basal ganglia
Degenerative
Vascular
Traumatic
Inflammatory
Neoplastic
Toxic
Metabolic diseases
Oral Mechanism
Immediate revealing features
Masked facies
Flat affect
Respiratory signs
Infrequent swallowing
May result in drooling
Size, strength, and symmetry may be normal
AMRs may be slowly initiated a/o rapid and restricted in range
Speech Characteristics
Monopitch
Monoloudness
Reduced intensity
Breathy quality
Reduced stress
Short phrases
Variable rate
Short rushes of speech
Imprecise consonants
***********************************************************************************
Hyperkinetic Dysarthria
Another dysarthria type that manifests secondary to damage to the basal ganglia control circuit
May effect all or isolated speech subsystems.
Involuntary movement is the hallmark feature
Rhythmic
Irregular
Fast
slow
Abnormal
What constitutes abnormal?
Involuntary movements when steadiness is expected
Hyper-in this case does not mean fast
Excessive, extra
Many forms
Classified based on speed and periodicity
Classification
Dyskinesia
Myoclonus
Tics
Chorea
Ballism
Athetosis
Dystonia
Spasm
Tremor
Etiologies
Degenerative
Vascular
Traumatic
Inflammatory
Toxic
Metabolic disease
***********************************************************************************
Mixed Dysarthrias
Mixed dysarthrias
Combination of dysarthrias
Two or more
Diffuse damage
Etiologies
Degenerative
ALS
MS
PSP
Toxic metabolic
Wilson’s disease
Hepatocerebral degeneration
Hypoxic encephalopathy
Vascular Disorders
Trauma
Neoplasm
Infectious diseases
***********************************************************************************
Apraxia of Speech
“A neurologic speech disorder that reflexts an impaired capacity to plan or program sensori-motor commands necessary for directing movements that result in honetically and prosodically normal speech. It can occur in the absence of physiologic disturbances associated with the dysarthrias and in the agsence of disturbance in any component of language.”
(Duffy, 2013, p. 4)
Apraxia of speech is secondary to a disturbance of the motor programming system.
Central impairment
Can occur without muscle impairment
Normal function is apparent
High variability
The motor speech programmer executes the motor movements/sequences necessary to convey language
Speech ‘vs’ Language
Primarily left hemisphere lesions
Motor speech area
Brocca’s area
Supplementary motor cortex
Insula
Variability in lesion locations
Dronkers, 1993
Etiologies
AOS is secondary to primarily focal lesions
vascular
Tumors
Focal/discrete trauma
Surgical
Other
Degenerative conditions
Occasionally have focal effects
Clinical Characteristics
May exhibit right sided weakness
May also have sensory deficits
Hyperactive reflexes
Limb apraxia
Concomitant aphasia
Brocca’s type
Can exist in a “pure” form
Few documented cases
Assessment findings
Oral mechanism
May have rt. weakness
May result in dysarthria that is not the same as AOS
Nonverbal oral motor apraxia
Difficulty performing oral tasks.
Sequential AMRs
Most sensitive task to the effects of AOS.
Specific Speech Characteristics
Slow rate
Prolonged consonants/vowels
Many pauses
Inter/intrasegmental
Disruptions in prosody
Equal stress
Decreased pitch/intonation contours
False starts
Effortful/laborious speech
Repetitions
***********************************************************************************
Factors that influence speech production
Walking
Injurious Falls
One-third of Americans aged 65+ fall each year.
Every 14 seconds, an older adult is treated in the E.R. for a fall, every 29 minutes an older adult dies after a fall.
Annually, falls result in more than 2.4 million injuries in emergency departments, resulting in over 772,000 hospitalizations and over 21,700 deaths.
In 2012, the costs related to falls was over $36 billion, with an expectation to reach over 59 billion annually by 2020.
Aging
Affects gait patterns
Change in skeletal structure
Reduced muscle mass/strength
Results in a higher incidence of neuropathology.
Often with deleterious cognitive and motor effects.
Increasing incidence of falls
Fear of falling
Multitasking
Bombarded today by competing stimuli
Cell phones
Talking or texting
Music
Environment
Walking while talking
Sharing tasks may become more difficult when systems become compromised.
Statement of the Problem
Injurious falls are a major medical concern.
Individuals with neurologic compromise may be at a greater risk.
There are known factors that contribute to fall risk.
Physical decline
Cognitive decline
Pharmacological effects
Environmental factors
What other factors may be influential?
Cognitive load…
GAITRite™ System
Analysis of gait conducted using the GAITRite™ System
14’ portable carpet
16,128 embedded sensors to capture footfalls instantly
Measures include temporal and spatial parameters
Procedures
Each of the groups completed the following:
Montreal Cognitive Assessment
Beck Depression Index
Gait Measures
Baseline (walking, no talking)
Low load (counting by ones)
Medium load (subtracting by 3s)
Originating number varied/attempt
High load (alpha-numeric sequence)
D-7, E-8, F-9…
Gait conditions were counterbalanced to account for order effect.
Each walk was completed twice to control for learning
The average was used for analysis.
Dependent measures
Functional ambulation profile (FAP)
Ratio of step length to leg length to step time; FAP score is derived from a formula that includes several critical gait parameters found to be highly related to fall risk. (Nelson et. al, 1999)
Velocity
Centimeters/second
Stride length
Centimeters
Double support time
The percentage of time per ambulation cycle with both feet on the ground.
Parkinson and Healthy Elderly
Twenty six participants with Parkinson Disease: Peak medication time
Age: Mean = 67.44 (41-91)
Hoehn & Yahr Stage:
22-Stage 2, 3-Stage 3, 1-Stage 4
Thirteen healthy elderly participants
Age: Mean – 68.07
Matched for education level
No significant differences across groups
Stride length or Velocity
Data were collapsed and a condition effect was revealed Baseline > High load
A significant difference and interaction was revealed for Double Support
The healthy adult group significantly increased their Double Support time
The group with PD did not
High vs. Low Medication State
We recruited the same twenty six participants several months later. We asked that they be within 30 minutes of their next medication administration. The same procedures were followed, and we added the Functional Ambulation Profile (FAP) score as a predictor of fall risk.
No differences between conditions or High/Low medication states
Step velocity
Step length
Double support
FAP
Dopaminergic replacement medication did not alleviate the effect of cognitive load.
These results were shared at the World Congress on Parkinson Disease in Paris 2009
Current Study
A double blind, randomized control study to investigate the effects of cognitive enhancing medication on performance in individuals with Parkinson disease.
Participants were randomly assigned to a drug (Rasagiline vs. Placebo).
Prior to taking the drug, baseline measures were collected on all experimental tasks (Pre-treatment).
Gait
Additional measures
After 30 days, participants received an increased dose
Participants receiving Rasagiline were given a higher dosage for the next 30 days.
Participants receiving the placebo received additional placebo tablets.
After 60 days, final data collection occurred (Post-treatment).
Gait
Additional measures
Walking while talking
Individuals with neurological compromise are at an increased risk for falls during the multitask of talking while walking.
Automatic speech doesn’t carry as great a risk.
Increased cognitive load will have deleterious effects especially in high fall risk conditions
Low light
Descending stairs
Giving directions
Mental calculations
Tracking conditions
Obstacles
Environmental variations
Cranial Nerve Information Sheet
|Cranial Nerve |Type |Function |
|I – Olfactory |Sensory |Smell |
|II – Optic |Sensory |Vision |
|III - Oculomotor |Motor |Eye movement |
|IV - Trochlear |Motor |Eye movement (superior oblique) |
|V - Trigeminal |Sensory |Facial sensation – 3 branches |
| | |Opthalamic |
| | |Maxillary |
| | |Mandibular |
| | |Anterior tongue sensation |
| |Motor |Muscles of mastication |
|VI - Abducens |Motor |Eye Movement - lateral rectus |
|VII - Facial |Sensory |Taste - anterior 2/3 tongue |
| |Motor |Facial expression |
|VIII - Vestibulocochlear |Sensory |Hearing |
| | |Balance |
|IX - Glossopharyngeal |Sensory |Pharyngeal sensation |
| |Motor |Pharyngeal muscles |
|X - Vagus |Sensory |Pharynx, larynx, esophagus |
| |Motor |Muscles of palate, pharynx, and larynx |
|XI- Spinal Accessory |Motor |Shoulder, head movement |
|XII - Hypoglossal |Motor |Tongue movement |
For the purpose of screening, the functions listed above are the primary functions of the cranial nerves. This is not meant to serve as an exhaustive list of cranial nerve functions.
© Stierwalt, J.A.G., (2003) Cranial Nerve Information Sheet
Cranial Nerve Screening
|Cranial Nerve |Function |Screening Task |
|I – Olfactory |Sensory - Smell |odors |
|II – Optic |Sensory - Vision |vision chart/acuity |
|III- Oculomotor |Motor – Eye movement |"follow the moving finger" |
|IV - Trochlear |Motor – Eye movement (superior oblique) |look at the nose |
|V - Trigeminal |Sensory - facial sensation/anterior tongue |Have the individual close their eyes: touch |
| | |the face |
| |Motor - muscles of mastication |Palpate muscles that clench the teeth |
|VI - Abducens |Motor - lateral rectus |look to the side |
|VII - Facial |Sensory - taste |sweet, sour, bitter, salt |
| |Motor - facial expression |smile, raise the eyebrows |
|VIII - Vestibulocochlear |Sensory - hearing |a tuning fork |
| |balance |look for vertigo |
|IX - Glossopharyngeal |Sensory - pharynx sensation |gag reflex |
| |Motor – pharyngeal muscles |gag reflex |
|X - Vagus |Sensory –pharynx, larynx, esophagus |Check phonation |
| |Motor - muscles of palate, pharynx, and larynx|Assess vocal quality |
|XI- Spinal Accessory |Motor – Shoulder, head movement |shoulder shrug and/or turning the head to |
| | |resistance |
|XII - Hypoglossal |Motor - tongue movement |Assess tongue movement |
© 2003 Julie A.G. Stierwalt, Ph.D.
Bibliography
|Ball, L. J., Bernthal, J. E., & Beukelman, D. R. (2002). Profiling communication characteristics of children with |
|developmental apraxia of speech. Journal of Medical Speech-Language Pathology, 10, 221-230. |
|Ball, L. J., Beukelman, D. R., & Pattee, G. L. (2002). Timing of speech deterioration in people with amyotrophic lateral|
|sclerosis. Journal of Medical Speech-Language Pathology, 10, 231-236. |
|Barkmeier, J., Jordan, L. S., Robin, D. A., & Schum, R. L. (1991). Inexperienced Listener Ratings of Dysarthric Speaker |
|intelligibility and Physical Appearance. In C. A. Moore (Ed.), Dysarthria and apraxia of speech: Perspectives on |
|management (pp. 65-75). Baltimore: MD, Paul H. Brookes Publishing Co., Inc. |
|Beukelman, D. R., Fager, S., Ullman, C., Hanson, E., & Logemann, J. (2002). The impact of speech supplementation and |
|clear speech on the intelligibility and speaking rate of people with traumatic brain injury. Journal of Medical |
|Speech-Language Pathology, 10, 237-242. |
|Burkhead, L.M., Sapienza, C.M., & Rosenbek, J.C., (2007). Strength-training exercise in dysphagia rehabilitation: |
|Principles, procedures, and directions for future research. Dysphagia, 22, 251-265. |
|Clark, H.M. (2003), Neuromuscular treatments for speech and swallowing: A tutorial. American Journal of Speech |
|Language Pathology, 12, 400-415. |
|Daniel, B. (1982). A soft palate desensitization procedure for patients requiring palatal lift prostheses. The Journal |
|of Prosthetic Dentistry, 48(5), 565-566. |
|Dromey, C. (2003). Spectral measures and perceptual ratings of hypokinetic dysarthria. Journal of Medical |
|Speech-Language Pathology, 11(2), 85-94. |
|Dronkers, N. F. (1996). A new brain region for coordinating speech articulation. Nature, 384(14), 159-161. |
|Freed, D. (2000). Motor Speech Disorders: Diagnosis and Treatment. San Diego, CA: Singular Thompson Learning. |
|Hageman, C. F., Simon, P., Backer, B., & Burda, A. N. (2002, November). Comparing MIT and motor learning therapy in a |
|nonfluent aphasic speaker. Symposium conducted at the annual meeting of the American Speech-Language-Hearing |
|Association, Atlanta, GA. |
|Hanson, E. K., Yorkston, K. M., & Beukelman, D. R. (2004). Speech supplementation techniques for dysarthria: A |
|systematic review. Journal of Medical Speech-Language Pathology, 12(2), ix-xxix. |
|Hartelius, L., Carlstedt, A., Ytterberg, M., Lillvik, M., & Laakso, K. (2003). Speech disorders in mild and moderate |
|Huntington disease: Results of dysarthria assessments of 19 individuals. Journal of Medical Speech-Language Pathology, |
|11(1), 1-14. |
|Hixon, T.J., Weismer, G., & Hoit, J.D., (2008). Preclinical Speech Science: Anatomy, Physiology, Acoustics, Perception.|
|Plural |
|Horiuchi, M., Maki,F., Yanagisawa, T., Sugihara, H., Takahashi, Y., Ohashi, K. (2002). Therapeutic efficacy of |
|transcranial magnetic stimulation for ALS and spinocerebellar degeneration, International Congress Series, 1235, |
|525-532. |
|Hustad, K. C., & Garcia, J. M. (2002). The influences of alphabet supplementation, iconic gestures, and predictive |
|messages on intelligibility of a speaker with cerebral palsy. Journal of Medical Speech-Language Pathology, 10, 279-286.|
|Hustad, K. C., & Sassano, K. (2002). Effects of rate reduction on severe spastic dysarthria in cerebral palsy. Journal |
|of Medical Speech-Language Pathology, 10, 287-292. |
|Kent, R.D., Duffy, J.R., Weismer, G.,& Stuntebeck, S. (2000) Ataxic Dysarthria. Journal of Speech Language Hearing |
|Research, 143, 1275-1289. |
|Kent, R. D., Kent, J. F., & Rosenbeck, J. C. (1987). Maximum performance tests of speech production. Journal of Speech |
|and Hearing Disorders, 52, 367-387. |
|Klasner, E. R., Yorkson, K. M., & Lillvik, M. (2002). Everyday listeners’ perspective on amyotrophic lateral sclerosis |
|and Huntington disease dysarthria: Barriers and strategies in understanding distorted speech samples. Journal of Medical|
|Speech-Language Pathology, 10, 293-298. |
|Klockgether, T. (2000). Handbook of Ataxia Disorders: Neurological Disease and Therapy. New York: Marcel Dekker. |
|LaPointe L.L., Stierwalt J.A.G., Maitland C.G. (2010). Cognitive loading and injurious falls in Parkinson disease. |
|International Journal of Speech, Language Pathology |
|Lasker, J.P., Stierwalt, J.A.G., & Hageman, C. F.(2005, November) Enhancing conversation skills in aphasia/apraxia using|
|a multimodal approach.Technical session at American Speech Language Hearing Association, San Diego, CA. |
|Lefkowitz, K, & Netsell, R. (1994). Correlation of clinical deficits with anatomical lesions: Post-traumatic speech |
|disorders and MRI. Journal of Medical Speech-Language Pathology, 2(1), 1-15. |
|Liss, J. M., Kuehn, D. P., & Hinkle, K. P. (1994). Direct training of velopharyngeal musculature. Journal of Medical |
|Speech-Language Pathology, 2(3), 243-251. |
|Ludlow, C., Hoit, J., Kent, R., Ramig, L., Shrivastav, R., Strand, E., et al. (2008). Translating principles of neural |
|plasticity into research on speech motor control recovery and rehabilitation. Journal of Speech, Language and Hearing |
|Research, 51, 240-258. |
|McHenry, M. A. (2002). A comparison of nasalance and velopharyngeal orifice area in dysarthria. Journal of Medical |
|Speech-Language Pathology, 10, 299-306. |
|McKeever, S. L., & Miller, R. M. (2002). Glossopharyngeal breathing to improve functional vital capacity and speech |
|production in a patient with flaccid dysarthria. Journal of Medical Speech-Language Pathology, 10, 307-312. |
|McNeil, M., Rosenbek, J., & Arorison, A. (Eds.) (1984). A Neurobiologic View of the Dysarthrias. The dysarthrias: |
|Physiology, acoustics, perception, management. 53-88. |
|Mitsumoto, H., Chad, D. A., & Pioro, E. P. (1998). Amyotrophic lateral sclerosis. Philadelphia, PA: F. A. Davis Company.|
|Netsell, R. W. (1994). Instrumentation and special procedures for individuals with dysarthria. American Journal of |
|Speech-Language Pathology, (p. 9-11). |
|Netsell, R., & Daniel, B. (1979). Dysarthria in adults: Physiologic approach to rehabilitation. Archives of Physical |
|Medicine and Rehabilitation, 60, 502-507. |
|Raymer, A. M., Haley, M. A., & Kendall, K. L. (2002). Overgeneralization in treatment for severe apraxia of speech: A |
|case study. Journal of Medical Speech-Language Pathology, 10, 313-318. |
|Schmidt, R.A., & Bjork, R.A. (1992). New conceptualizations of practice: Common principles in three paradigms suggest |
|new concepts for training. Psychological Science, 3, 207-217. |
|Schulz, G.M., Dingwall, W.O., & Ludlow, C.L. (1999). Speech and oral motor learning in individuals with cerebellar |
|atrophy. Journal of Speech Language Hearing Research, 42, 1157-1175. |
|Solomon, N. P., Lorell, D. M., Robin, D. A., Rodnitzky, R. L., & Luschei, E. S. (1995). Tongue strength and endurance in|
|mild to moderate Parkinson’s disease. Journal of Medical Speech-Language Pathology, 3(1), 15-26. |
|Spencer, K. A., Yorkston, K. M., & Duffy, J. R. (2003). Behavioral management of respiratory/phonatory dysfunction from |
|dysarthria: A flowchart for guidance in clinical decision making. Journal of Medical Speech-Language Pathology, 11(2) |
|xxxix-lxi. |
|Stierwalt, J., Hageman, C. F., & LaPointe, L. L. (2004, August-September). The motor learning guided approach to apraxia|
|of speech. Symposium conducted at the meeting of the World Congress of the International Association of Logopedics and |
|Phoniatrics, Brisbane, Australia. |
|Stierwalt, J.A.G., LaPointe, L. L., Maitland, C.G., & Toole, T. (2008). Effects of cognitive-linguistic load on |
|parameters of gait in Parkinson disease. Journal of Medical Speech-Language Pathology, 16, 4, 259-266. |
|Stierwalt, J.A.G., & Youmans, S.R. (2007). Tongue measures in individuals with normal and impaired swallowing. |
|American Journal of Speech Language Pathology, 16(2), 148-156. |
|Strand, E. (1997). Amyotrophic lateral sclerosis: Diagnosis and management for the clinician. Journal of Medical Speech |
|Language Pathology, 5(2) 153-154. |
|Strand, E., & Sullivan, M. (2001). Evidence-based practice guidelines for dysarthria. Journal of Medical Speech-Language|
|Pathology, 9(4), 258-274. |
|Thompson, E. C., Murdoch, B. E., & Stokes, P. D. (1996). Tongue function in subjects with upper motor neuron type |
|dysarthria following cerebrovascular accident. Journal of Medical Speech-Language Pathology, 3(1), 27-40. |
|Thompson-Ward, E. C., Murdoch, B. E., & Stokes, P. D. (1997). Biofeedback rehabilitation of speech breathing for an |
|individual with dysarthria. Journal of Medical Speech-Language Pathology, 5(4), 277-288. |
|Vogel, D., & Cannito, M.P. (Eds.). (2001). Treating disordered speech motor control. Austin, TX: ProEd. |
|Warlow, C. (1991). Handbook of neurology. Oxford: Blackwell Scientific Publications. |
|Webster, D. B. (1999). Neuroscience of Communication (2nd ed.). San Diego, CA: Singular Thompson Learning. |
|Yorkston, K. M., Klasner, E. R., Bowen, J., Ehde, D. M., Gibbons, L. E., Johnson, K. et al. (2003). Characteristics of |
|multiple sclerosis as a function of the severity of speech disorders. Journal of Medical Speech-Language Pathology, |
|11(2), 73-84. |
|Yorkston, K. M., Spencer, K. A., & Duffy, J. R. (2003). Behavioral management of respiratory/phonatory dysfunction from |
|dysarthria: A systematic review of the evidence. Journal of Medical Speech-Language Pathology, 11(2), xiii-xxxviii. |
................
................
In order to avoid copyright disputes, this page is only a partial summary.
To fulfill the demand for quickly locating and searching documents.
It is intelligent file search solution for home and business.
Related download
Related searches
- measures of economic growth
- measures of managerial effectiveness
- four measures of organizational effectiveness
- measures of validity in research
- definition of measures of effectiveness
- measures of relative position calculator
- measures of position calculator
- measures of central tendency calculator
- measures of central tendency worksheets
- measures of central tendency pdf
- describe the measures of central tendency
- three measures of central tendency