(2) Chapter 9 - The Dysarthrias

Motor Speech Disorders and Dysphagia

dysarthrias

Neurologically based speech disorders characterized by abnormal strength, speed, range, steadiness, tone, and accuracy of movement involved in speech production; these abnormalities may be evident in respiration, phonation, articulation, prosody, and resonance; the effects of the neural damage that causes dysarthrias, unlike aphasia and apraxia of speech, are pervasive; any and all aspects of speech production may be affected

• Distinct from neurologically based language disorders, such as aphasia, and from apraxia of speech, a neurogenic disorder of motor planning (programming) of speech movements, with no muscular weakness or paralysis

• The different types of dysarthria share certain characteristics; impaired muscular control of the speech mechanism and peripheral or central nervous system pathology are common to all forms of dysarthria; differences in the nature and loci of pathology create different forms of the disorder

• Dysarthria may be progressive when associated with such degenerative diseases as amyotrophic lateral sclerosis (ALS), typically resulting in flaccid and spastic dysarthrias, and Parkinson's disease, typically causing hypokinetic dysarthria

neuropathology of the dysarthrias

• Nonprogressive neurological conditions that cause dysarthria include strokes, infections, traumatic brain injury, and surgical trauma, as well as such congenital conditions as cerebral palsy, Moebius syndrome, encephalitis, toxic effects from alcohol or drugs, and so forth

• Degenerative neurological diseases that cause dysarthria include-in addition to previously mentioned Parkinson's disease and ALS-Wilson's disease, progressive supranuclear palsy, dystonia, Huntington's disease, multiple sclerosis, myasthenia gravis, primary progressive aphasia, Pick's disease, Alzheimer's disease, progressive pseudobulbar palsy, and many others

• Neurotraumatic causes of dysarthria include penetrating head injuries, neck trauma, skull fracture, and surgical trauma

• Infectious diseases that cause dysarthria include AIDS, Creutzfeldt-Jakob disease, and central nervous system (CNS) tuberculosis

• Toxic-metabolic causes include botulism, drug toxicity or abuse, carbon monoxide poisoning, dialysis encephalopathy, and many others

Common sites of lesion include the lower motor neuron, unilateral or bilateral upper motor neuron, cerebellum, and basal ganglia (extrapyramidal system)

• Pathophysiology and neuromuscular problems include muscle weakness, spasticity, incoordination, and rigidity; there usually is a variety of movement disorders, including reduced or variable range and speed of movement, involuntary movements, reduced strength of movement, unsteady or inaccurate movement, and abnormal tone (increased, decreased, or variable)

communicative disorders associated with dysarthria

Respiratory problems

Phonatory disorders

Articulation disorders

Prosodic disorders

Resonance disorders

respiratory problems

Include forced inspirations or expirations that interrupt speech, audible or breathy inspiration, and grunting at the end of expiration

phonatory disorders

Pitch disorders characterized by abnormal pitch, pitch breaks, abrupt variations in pitch, monopitch, diplophonia, and shaky or tremulous voice

Loudness disorders characterized by too-soft or too-loud speech, monoloudness, sudden and excessive variation in loudness, progressive decrease in loudness throughout an utterance, or alter- nating changes in loudness

Vocal-quality problems characterized by a harsh, rough, gravelly voice; a hoarse voice (especially the "wet" variety); a continuously or intermittently breathy voice; a strained or strangled voice; effortful phonation; or a sudden and uncontrolled cessation of voice

articulation disorders

Include imprecise production of consonants, prolongation and repetition of phonemes, irregular breakdowns in articulation, distortion of vowels, and weak production of pressure consonants

prosodic disorders

Include a slower, excessively faster, or variable rate of speech; shorter phrase lengths; and such linguistic stress problems as reduced, even, or excessive stress

There may also be prolongation of intervals between words or syllables, inappropriate pauses in speech, and short rushes of speech

resonance disorders

Include hypernasality, hyponasality, and nasal emission

Other characteristics include slow, fast, or irregular diadochokinetic rate and palilalia (compulsive repetition of one's own utterances with increasing rate and decreasing loudness), as well as decreased intelligibility of speech

ataxic dysarthria

Results from damage to the cerebellar system; characterized predominantly by articulatory and prosodic problems, reflecting predominantly impaired timing and coordination of muscle movements; ataxia (defined as muscular incoordination and irregular movements) is a main factor co tributing to this type of dysarthria; will only appear during movement of the articulators; at rest, these structures will seem normal

• Motor symptoms created by cerebellar damage are not confined to speech production; thus, ataxia will be manifested in other motor movements; individuals with ataxic dysarthria will most likely walk with an ataxic gait; nystagmus may also be present; individuals may also overshoot or undershoot intended movements, known as dysmetria

• Neuropathology includes bilateral or generalized cerebellar lesions, degenerative ataxia (e.g., Friedreich's ataxia and olivopontocerebellar atrophy and late onset autosomal dominant and idiopathic sporadic forms of cerebellar ataxia), cerebellar vascular lesions (due to stroke), tumors, traumatic brain injury, toxic conditions (e.g., alcohol abuse and drug toxicity), and inflammatory conditions (e.g., meningitis and encephalitis), and demyelinating diseases

• The major characteristics of ataxic dysarthria include the following:

  • Gait disturbances

  • Movement disorders

  • Respiratory disorders

  • Articulation disorders

  • Prosodic disorders

  • Phonatory disorders

  • Speech quality

  • Resonance disorders

ataxic gait

The feet are broadly spread apart and step irregularly

nystagmus

Back and forth rapid eye movement

gait disturbances ataxic dysarthria

Instability of the trunk and head, tremors and rocking motions, rotated or tilted head posture, and hypotonia

movement disorders ataxic dysarthria

Overshooting or undershooting of targets; uncoordinated, jerky, inaccurate, slow, imprecise, and halting movements

respiratory disorders ataxic dysarthria

Exaggerated and paradoxical (simultaneous antagonistic) movement during speech production

articulation disorders ataxic dysarthria

Imprecise production of consonants, irregular articulatory breakdowns, and distortion of vowels

prosodic disorders ataxic dysarthria

Excessive and even stress, prolonged phonemes and intervals between words or syllables, and slow rate of speech

phonatory disorders ataxic dysarthria

Monopitch, monoloudness, and harshness

speech quality ataxic dysarthria

Impression of drunken speech

resonance disorders ataxic dysarthria

Intermittent hyponasality in some individuals (not a prominent feature)

flaccid dysarthria

Results from damage to the motor units of cranial or spinal nerves that supply speech muscles (lower motor neuron involvement; damage to the peripheral nervous system)

• A lower motor neuron (LMN) is an efferent portion of a cranial or spinal nerve; all motor plans from the CNS must pass through the LMNs to be executed by muscles; when there is damage to an LMN, motor plans sent from the brain to the muscle cannot reach the muscle or are poorly conducted along the damaged nerve; therefore, the muscles cannot be properly activated for movement; flaccidity is present for volitional and nonvolitional movement (e.g., stretch reflex) and is characterized by hypotonia and muscle weakness

• Only one major muscle group (e.g., the tongue), several muscle groups (affecting either the phonatory or articulatory systems), or all of the muscle groups involved in speech production may be affected, suggesting possible subtypes of flaccid dysarthria

• Neurological conditions causing flaccid dysarthria include such degenerative diseases as amyotrophic lateral sclerosis (ALS), motor neuron disease, progressive bulbar disease, and multiple systems atrophy (MSA); myasthenia gravis and botulism; vascular diseases and brainstem strokes; infections (e.g., polio, infections secondary to AIDS); demyelinating diseases (e.g., Guillain-Barré syndrome); and trauma due to brain, laryngeal, facial, or chest surgery

• Specific cranial nerves that may be involved in flaccid dysarthria include the trigeminal (V), facial (VII), glossopharyngeal (IX), vagus (X), accessory (XI), and hypoglossal (XII) nerves; specific spinal nerve involvement may indirectly affect speech production because of an involved respiratory system

• The major characteristics of flaccid dysarthria include the following:

  • Muscular disorders

  • Respiratory weakness

  • Phonatory disorders

  • Resonance disorders

  • Phonatory-prosodic disorders

  • Articulation disorders

  • Three disorder clusters

hypotonia

Low muscle tone

muscular disorders flaccid dysarthria

Weakness, hypotonia, atrophy, diminished reflexes, isolated twitches of resting muscles (fasciculations), contractions of individual muscles (fibrillations), and rapid and progressive weakness with the use of a muscle and recovery with rest

respiratory weakness flaccid dysarthria

Reduced subglottic air pressure (with spinal nerve involvement), weak inhalation (with damaged phrenic nerve and paralyzed diaphragm)

phonatory disorders flaccid dysarthria

Breathy voice and audible inspiration

resonance disorders flaccid dysarthria

Hypernasality, nasal emission, and short phrases

phonatory-prosodic disorders flaccid dysarthria

Short phrases, harsh voice, monopitch, and monoloudness or reduced loudness

articulation problems flaccid dysarthria

Imprecise consonants and weak pressure consonants (more pronounced with lesions of cranial nerves V, VII, and XII)

three disorder clusters flaccid dysarthria

(1) phonatory incompetence

(2) resonatory incompetence

(3) phonatory-prosodic insufficiency

hyperkinetic dysarthria

Results from damage to the basal ganglia (extrapyramidal system); it is associated with variable muscle tone and involuntary movements that interfere with speech production; any or all of the speech systems may be affected, but prosodic disturbances are dominant

• Common causes include degenerative diseases (e.g., Huntington's disease), vascular diseases (brainstem stroke), trauma (head injury), toxic or metabolic conditions (e.g., lithium toxicity, tardive dyskinesia), and many others (Tourette's syndrome, seizure disorders); spasmodic dysphonia is caused by extra movement of the vocal folds and is therefore considered a hyperkinetic dysarthria; the cause may be unknown in the majority of cases; the muscles of the face, jaw, tongue, palate, larynx, and respiration may be involved

• The major characteristics of hyperkinesias and the resulting hyperkinetic dysarthria include the following:

  • Orofacial dyskinesia

  • Myoclonus

  • Tics

  • Chorea

  • Athetosis

  • Ballism

  • Hemiballism

  • Dystonia

  • Spasm

  • Tic

  • Tremor

  • Communicative disorders

  • Respiratory problems

  • Phonatory disorders

  • Resonance disorders

  • Articulation problems

  • Prosodic disorders

orofacial dyskinesia hyperkinetic dysarthria

Abnormal, involuntary, rhythmic or nonrhythmic movements of the orofacial muscles

myoclonus hyperkinetic dysarthria

Involuntary, rapidly occurring jerks of body parts; may be of single or multiple muscles; hiccups due to diaphragmatic spasms; palatal tremor

tics hyperkinetic dysarthria

Commonly of the face and shoulders; typically patterned, rapid, and stereotyped

chorea hyperkinetic dysarthria

Purposeless, random, involuntary movements of body parts

athetosis hyperkinetic dysarthria

Slow, writhing, purposeless movements; may be a combination of chorea and dystonia

ballism hyperkinetic dysarthria

Bilateral, involuntary, and irregular movement of the extremities; can be violent

hemiballism hyperkinetic dysarthria

Unilateral, involuntary, and irregular movement of the extremities; can be violent

dystonia hyperkinetic dysarthria

Contractions of antagonistic muscles that cause abnormal postures; spasmodic torticollis (intermittent dystonia and spasms of the neck muscles); blepharospasm (forceful and involuntary closure of the eyes due to spasm of the orbicularis oculi muscle)

spasm hyperkinetic dysarthria

A muscle contraction that is sudden and involuntary

tic hyperkinetic dysarthria

A stereotyped movement that is quick and repetitive and is involuntary

tremor hyperkinetic dysarthria

Rhythmic movements, a common form of involuntary movement

communicative disorders hyperkinetic dysarthria

Specific symptoms depending on the dominant neurological condition (e.g., chorea, dystonia, athetosis, spasmodic torticollis)

respiratory problems hyperkinetic dysarthria

Audible inspiration and forced and sudden inspiration or expiration not typical of other types of dysarthria

phonatory disorders hyperkinetic dysarthria

Voice tremor, intermittently strained voice, voice stoppage, vocal noise, harsh voice, and loudness variations

resonance disorders hyperkinetic dysarthria

Hypernasality in some cases, but typically mild

articulation problems hyperkinetic dysarthria

Imprecise consonant productions, often associated with distorted vowels and hypernasality; slower rate of speech

prosodic disorders hyperkinetic dysarthria

Prolonged interword intervals, inappropriate silent periods, phoneme prolongations, and excess and equal stress; also, monopitch and monoloudness, reduced stress, and short phrases

hypokinetic dysarthria

Results from damage to the basal ganglia (extrapyramidal system); it may affect all aspects of speech, but voice, articulation, and prosody are typically the most affected; muscular rigidity and reduced force and range of movement cause the speech problems

• Has a number of causes, but the most common cause is degenerative Parkinson's disease; other causes include stroke (vascular diseases), toxic and metabolic conditions including antipsychotic or neuroleptic drug toxicity, repeated head trauma, and infections (e.g., HIV, Creutzfeldt-Jakob disease)

• Characterized by the following:

  • Tremors

  • Mask-like face

  • Micrographic writing

  • Walking disorders

  • Postural disturbances

  • Decreased swallowing

  • Respiratory problems

  • Phonatory disorders

  • Prosodic disorders

  • Articulation disorders

  • Dysfluencies

  • Resonance disorders

• The only dysarthria that creates an increased rate of speech; because the range of motion of the articulators is reduced, the structures do not move as far for speech production; therefore, the speech of an individual with hypokinetic dysarthria will often speed up until there is a breakdown; this is commonly referred to as rapid-fire articulation

• In addition to these motor speech symptoms, individuals with hypokinetic dysarthria (Parkinson's disease in particular) will also demonstrate several non-speech-motor symptoms as a result of basal ganglia damage, including:

  • Absence of arm swinging while walking

  • Bradykinesia

  • Festination

  • Hypomimia

  • Hypokinesia

  • Micrographia

  • Stooped or hunched posture

If these symptoms are present due to basal ganglia damage but are not the result of Parkinson’s disease, these symptoms are referred to as Parkinsonian; any of the other etiologies described previously (stroke, HIV, etc.) can produce Parkinsonian signs, including hypokinetic dysarthria

tremors hypokinetic dysarthria

Facial, mouth, and limb muscle tremors at rest, diminishing when moved voluntarily

mask-like face hypokinetic dysarthria

Infrequent blinking and no smiling

micrographic writing hypokinetic dysarthria

Excessively small print

walking disorders hypokinetic dysarthria

Slow to begin, then short, rapid, shuffling steps

postural disturbances hypokinetic dysarthria

Involuntary flexion of the head, trunk, and arm with difficulty changing positions

decreased swallowing hypokinetic dysarthria

Accumulation of saliva in the mouth and drooling

respiratory problems hypokinetic dysarthria

Reduced vital capacity; irregular breathing, and faster rate of respiration

phonatory disorders hypokinetic dysarthria

Monopitch, low pitch, monoloudness, and harsh and continuously breathy voice

prosodic disorders hypokinetic dysarthria

Reduced stress, inappropriate silent intervals, short rushes of speech, variable and increased rate in segments, and short phrases

articulation disorders hypokinetic dysarthria

Imprecise or distorted consonants; stops sounding more like fricatives; mushy fricatives

dysfluencies hypokinetic dysarthria

More frequently repeated phonemes and less frequently palilalia (e.g., “Yes, yes, yes, yes, yes” that fades into a mumble)

resonance disorders hypokinetic dysarthria

Atypical but mild hypernasality in about 25% of individuals

akinesia

Absence of movement; immobile posture

bradykinesia

A difficulty with the initiation of movement

festination

A type of gait characterized by short, shuffling footsteps that progressively quicken; often seem as an attempt to maintain balance

hypomimia

Diminished facial movement causing a lack of facial expression

hypokinesia

A reduced amount and range of motion

micrographia

Evolution from typical handwriting to abnormally small handwriting

spastic dysarthria

Results from bilateral damage to the upper motor neurons (direct and indirect motor pathways), creating a predominant spasticity; lesions in multiple areas, including the cortical areas, basal ganglia, internal capsule, pons, and medulla, are common

• Caused most commonly by multiple strokes that damage both the pyramidal (direct activation pathway, or DAP) and extrapyramidal (indirect activation pathway, or IAP) tracts, single stroke (if it occurs only in the brainstem and not in the cerebral hemispheres), primary lateral sclerosis (PLS), multiple sclerosis, traumatic brain injury, brainstem tumor, and viral or bacterial infection of the cerebral tissue; in children, cerebral palsy is a common etiology

• Characterized by the following:

  • Spasticity and weakness

  • Movement disorders

  • Articulation disorders

  • Prosodic disorders

  • Phonatory disorders

  • Resonance disorders

spasticity and weakness spastic dysarthria

Bilateral facial weakness, less severe lower face weakness, normal or near normal jaw strength

movement disorders spastic dysarthria

Reduced range, force, and speed of movement, loss of fine and skilled movement, and increased muscle tone

articulation disorders spastic dysarthria

Imprecise production of consonants, distorted vowels

prosodic disorders spastic dysarthria

Excess and equal stress, slow rate, reduced stress, and short phrases

phonatory disorders spastic dysarthria

Hyperadduction of vocal folds, continuous breathy voice, harshness, low pitch, pitch breaks, strained and strangled voice quality, monopitch, and monoloudness

resonance disorders spastic dysarthria

A predominant hypernasality due to inadequate closure of the velopharyngeal port

mixed dysarthrias

A combination of two or more pure dysarthrias; all combinations of pure dysarthrias are possible, although a combination of two types is more common than a combination of three or more; the symptom complex may include the major problems of the types that are mixed, but, in some cases, the symptoms of one type may be dominant; the two most common mixed forms are flaccid-spastic dysarthria and ataxic-spastic dysarthria

• Neurological diseases that produce more widespread or diffuse effects may cause mixed dysarthria; more frequently noted causes include such motor neuron diseases as amyotrophic lateral sclerosis (progressive degeneration of motor neurons), demyelinating multiple sclerosis, Friedreich’s ataxia, and the somewhat rare Wilson’s disease

mixed flaccid-spastic dysarthria

Associated with amyotrophic lateral sclerosis (ALS)

Characterized by imprecise production of consonants, hypernasality, harsh voice, slow rate, monopitch, short phrases, distorted vowels, low pitch, monoloudness, excess and equal stress or reduced stress, prolonged intervals, prolonged phonemes, a strained and strangled quality, breathiness, audible inspiration, inappropriate silences, and nasal emission

mixed ataxic-spastic dysarthria

More often associated with multiple sclerosis (MS), is characterized by impaired loudness control, harsh voice quality, imprecise articulation, impaired emphasis, hypernasality, inappropriate pitch levels, decreased vital capacity, breathiness, and sudden articulatory breakdowns

Wilson’s disease

A combination of ataxic and spastic types of dysarthria

Reduced stress, monopitch, and monoloudness may be the three most prominent symptoms

Friedreich’s ataxia

A combination of those found in ataxic and spastic types of dysarthria

unilateral upper motor neuron (UUMN) dysarthria

Results from damage to the upper motor neurons that supply cranial and spinal nerves involved in speech production; while all the previous types of dysarthria are defined physiologically, this one is defined purely in anatomic terms

• The most common cause is stroke; nonhemorrhagic or hemorrhagic strokes account for 92% of individuals with this type of dysarthria; neurosurgical trauma and multiple sclerosis are two other infrequent causes; dysarthria due to vascular disorders that produce left hemisphere lesions may coexist with aphasia or apraxia; dysarthria due to right-hemisphere lesions may coexist with right-hemisphere syndrome

• Characterized by the following:

  • Neurological impairments

  • Articulation disorders

  • Phonatory disorders

  • Prosodic disorders

  • Resonance disorders

  • Associated disorders

neurological impairments UUMN dysarthria

Unilateral lower face weakness, unilateral tongue weakness, unilateral palatal weakness, and hemiplegia/hemiparesis

articulation disorders UUMN dysarthria

Imprecise production of consonants, irregular articulatory breakdowns, and some vowel distortions and sound or syllable repetitions

phonatory disorders UUMN dysarthria

Harsh voice, reduced loudness, strained harshness, wet hoarseness, breathiness, monopitch, monoloudness, and low pitch

prosodic disorders UUMN dysarthria

Slow rate, increased rate in segments, excess and equal stress, and short phrases

resonance disorders UUMN dysarthria

Hypernasality or nasal emission, or a combination of the two

associated disorders UUMN dysarthria

Dysphagia, aphasia, apraxia, and right-hemisphere syndrome

assessment of the dysarthrias

Involves multiple procedures because of the wide range of symptoms that must be evaluated; as for any disorder of communication, assessment of dysarthria begins with taking a complete case history, examining the medical records of the patient, and interviewing the patient and the family to understand the patient's past communicative behaviors and current status

• Specific to assessing the variety of dysarthric symptoms, most clinicians do the following:

  • Record an extended conversational speech sample and a reading sample

  • Use a variety of speech tasks, including imitation of syllables, words, phrases, and sentences; production of modeled syllables, words, phrases, and sentences; and sustained phonation (vowel prolongation)

  • Assess the diadochokinetic rate or alternating motion rates (AMRs) and sequential motion rates (SMRs)

  • Assess the speech production mechanism during non-speech activities

  • Assess respiratory problems

  • Assess phonatory disorders

  • Assess articulation disorders

  • Assess prosodic disorders

  • Assess resonance disorders

  • Assess speech intelligbility

  • Assess muscle strength, speed, range, accuracy, tone, and steadiness of movement involved in speech production

  • Use such standardized tests as the Assessment of Intelligibility of Dysarthric Speech, the Quick Assessment for Dysarthria, and Frenchay Dysarthria Assessment-Second Edition; the Speech Intelligibility Test for Windows is also available for making a computerized assessment; alternatively, the clinician may use a comprehensive assessment protocol

  • Make a differential diagnosis based on a careful analysis of clusters of neurologic and speech symptoms that are predominant in specific types of dysarthria

assess the speech production mechanism during non-speech activities

Observing facial symmetry, tone, tension, droopiness, expressiveness, and so forth

Observing the movements of the facial structures as the patient puffs the cheeks, retracts and rounds the lips, bites the lower lip, and so forth

Observing the patient's emotional expressions

Taking note of the patient's jaw movements and deviation during movement and observing the tongue movements

Observing the velopharyngeal mechanism and its movements

Assessing nasal airflow by holding a mirror at the nares as the patient prolongs the vowel /i/ 

Assessing laryngeal function by asking the patient to cough, a weak cough being associated with weak adduction of the cords, inadequate breath support, or both

assess respiratory problems

Observing the patient's posture and breathing habits during quiet and during speech, taking note of rapid, shallow, or effortful breathing, signs of shortness of breath and irregularity of inhalation and exhalation, and so forth

assess phonatory disorders

Having the patient say "ah" after taking a deep breath and sustain it as steadily and for as long as the air supply lasts

Taking note of the patient's pitch, pitch breaks, diplophonia, abrupt variations in pitch, and lack of normal pitch variations

Taking note of voice tremors; assessing the presence of diplophonia; and judging vocal loudness, its appropriateness, variations, decay, and alternating changes

Judging the quality of voice, including hoarseness, harshness, and breathiness, taking note of strained or effortful voice production or sudden cessation of voice

assess articulation disorders

Evaluating consonant productions, duration of speech sounds, phoneme repetitions, irregular breakdowns in articulation, precision of vowel productions, phoneme distortions, and the adequacy of pressure consonantal productions

assess prosodic disorders

Evaluating the rate of speech, phrase lengths in selected portions of speech, stress patterns in speech, pauses in speech, and the presence of short rushes of speech

assess resonance disorders

Making clinical judgments about hyponasality and hypernasality and nasal emission

assess speech intelligibility

Making clinical judgments as to the percentage of words or phrases understood and by using a rating scale if warranted

assess muscle strength, speed, range, accuracy, tone, steadiness of movement

Systematic observations throughout the assessment session

To assess muscle integrity and function, clinicians may use a systematic protocol, such as the one provided by Hegde and Freed

goals and procedures of treatment

Treatment of dysarthria includes a wide range of techniques, partly because the communication disorders themselves have a wide range; all aspects of speech production must be addressed in treatment; goals should be individualized to suit the clusters of problems a patient exhibits; the underlying medical condition (stable, progressive) will influence the degree of improvement

Treatment goals include modifying respiratory, phonatory, articulatory, resonatory, and prosodic problems and increasing the efficiency, effectiveness, and naturalness of communication

• Treatment goals also include increasing physiological support for speech and teaching self-correction, self-evaluation, and self-monitoring skills; teaching compensatory behaviors for lost or reduced functions is important, and teaching the use of alternative or augmentative communication systems may be necessary

• Augmentative and alternative communication (AAC) devices may be recommended for those whose intelligibility is severely affected and for those diagnosed with degenerative disease, such as ALS or Huntington's disease; for these individuals, teaching the device early in the disease progression is key so that they and their caregivers can be accustomed to how the AAC device works and choose the device that might best meet their needs as the disease progresses

• Treatment procedures include intensive, systematic, and extensive trials (drill), instruction, demonstration, modeling (followed by imitation), shaping, prompting, fading, differential reinforcement, and other proven behavioral management procedures; it is generally recognized that treatment of dysarthria (and other neurogenic communication disorders) is essentially behavioral; when necessary, phonetic placement and its variations can be taught; instrumental feedback or biofeedback may be used when needed

• Some treatment strategies that are helpful for one dysarthria type may be counterproductive for another; for example, relaxation techniques that are appropriate for treating spasticity should not be used for treating flaccid dysarthria, because the muscles are already too loose and relaxed; the clinician, therefore, should be familiar with the characteristics of each dysarthria and critically appraise whether a treatment strategy is beneficial for the dysarthria being presented

specific treatment targets

In treating patients with dysarthria, the clinician needs to target specific skills:

Modification of respiration

Modification of phonation

Modification of resonance

Modification of articulation

Modification of speech rate

Modification of prosody

Modification of pitch

Modification of vocal intensity

modification of respiration

Training consistent production of subglottal air pressure with the help of a manometer or air pressure transducer; training maximum vowel prolongation; shaping production of longer phrases and sentences; teaching controlled exhalation; teaching the client to push, pull, or bear down during speech or nonspeech tasks; using resistive breathing devices to increase breath support for speech by strengthening inspiratory muscles; using a manual push on the client's abdomen; modifying postures that promote respiratory support, including using neck and trunk braces if helpful; and teaching the client to inhale more deeply and exhale slowly and with greater force during speech

modification of phonation

Using biofeedback to shape desirable vocal intensity and training the client in the use of portable amplification systems if the voice is too soft; possibly also training aphonic clients in the use of an artificial larynx and teaching the client to initiate phonation at the beginning of an exhalation

modification of resonance

Providing feedback on nasal airflow and hypernasality by using a mirror, nasal flow transducer, or nasendoscope; training the client to open the mouth wider to increase oral resonance and vocal intensity; and using a nasal obturator or nose clip

For clients with hypernasality, a continuous positive airway pressure (CPAP) machine can be used to strengthen the velum through resistance

This device, commonly used for sleep apnea, pushes air through the nose to keep the velum open

When speaking while using this device, the velum is actively resisting this pressure

modification of articulation

Training the client to assume the best posture for good articulation; using a bite block to improve jaw control and strength; using such methods as simplifying the target, instruction, demonstration, modeling, shaping, and immediate feedback in teaching correct articulation; using phonetic placement, slower rate, and minimal contrast pairs; providing instructions and demonstrations and teaching self-monitoring skills; using relaxation techniques, such as the jaw-shaking exercise to loosen up muscles of the mandible; and teaching compensatory articulatory movements (e.g., use of tongue blade to make sounds normally made. with tongue tip)

modification of speech rate

Using delayed auditory feedback (DAF), a pacing board, an alphabet board, a metronome, or hand or finger tapping, and by reducing excessive pause durations in speech