Definition of childhood dysarthria:  a neurogenic speech impairment caused by dysfunction of the motor control centers of the immature brain and is marked by disturbances of the speech muscles in speed, strength, steadiness, coordination, precision, tone, and range of motion.
 

The childhood dysarthrias of cerebral palsy (UMN):
Definition of cerebral palsy: a non-progressive disorder of motion and posture due to brain insult or injury occurring in the period of early brain growth, generally under three years of age.

Cerebral palsy also includes disturbances in cognition, perception, sensation, language, hearing, emotional behavior, feeding and seizure (to complicate the picture)

Three major types of dysarthria in Cerebral palsy:
 a.  spastic
 b.  dyskinetic (athetosis)
 c.  ataxic

Spastic syndromes:
 a.  are overwhelmingly the most common type of motor disorder in CP.
 b.  associated with low birth weight, hypoxia, and ischemia (reduced cerebral    blood flow)
 Types:
 1.  Spastic hemiplegia
  Characteristics:
  a.  arm and leg on one side of the body show signs of clasp-knife spastic     paresis
  b.  Corticospinal tract is affected; Corticobulbar fibers may or may not be     affected
  c.  A prominent cranial nerve sign is XII nerve involvement with      deviation of the tongue to the side of the body opposite the cerebral    lesion
  d.  If dysarthria is present in hemiplegia, bilateral control of the speech     musculature permits rapid resolution of dysarthria.
  e.  May have mild phonologic delay, language and cognitive problems
  f.  Early left-hemisphere lesions: language functions are taken over by    right hemisphere but may leave visual-spatial functions of right     hemisphere somewhat compromised because language processing is    assuming neuronal space.
  g. Left hemiplegia: language is not impaired but may have right-    hemisphere damage

2.  Spastic paraplegia: usually only affects the legs.  Speech and language are ok.

3.  Spastic diplegia:
  a. all extremities are affected, but lower limbs are involved more      than upper
  b.  Respiratory muscles may be affected.
  c.  Severity of dysarthria: mild to sever affecting all muscles (respiratory,    laryngeal, articulatory, and palatopharyngeal
  d.  dysphagia and drooling may be present
  e.  Cognitive may be affected, but not necessarily.
  f.  flexion and adduction of the hips  and scissoring (crossing of the legs    during walking, a widely known clinical sign of child spasticity), toe    walking
4.  Spastic quadriplegia:
  a.  displays approximately equal motor involvement in all four limbs: the     most sever of all the spastic syndromes.
  b.  Usually both corticospinal and corticobulbar fibers are compromised
  c.  Usually respiratory, laryngeal, articulatory and palatopharyngeal     muscles are involved.
  d.   Dysphagia, drooling, and lower facial paralysis with sensory loss of     the lips and chin may be present
  e.  Usually have a significant degree of cognitive impairment and speech     and language delay although some may be cognitively intact

Speech impairment in Spastic syndromes:
a.  Usually occurs where there is bilateral involvement of the corticobulbar system
b.  Four major abnormalities of voluntary movement:
 1.  spasticity
 2.  weakness
 3.  limited ROM
 4.  slowness of movement
c.  The speech mechanism:  The oral movements of spastic individuals characterized by muscle weakness, articulatory instability and accuracy in finding target articulation points rather than due to spastic hypertonus of the speech muscles.
d.  Speech performance:
 1.  Respiratory function: These children do have abnormal respiratory functions; however, they are mild and don’t by themselves interfere with speech production; it is only when laryngeal, velopharyngeal or articulatory dysfunctions interact with the respiratory dysfunctions that overall speech function may become clinically impaired. For instance, a child may use more air volume per syllable than the normal child, but this may be due to poor laryngeal valving resulting in limited respiratory support for speech.
 2.  Layngeal function:  May exhibit monopitch/monoloudness; struggle-strangle voice quality; sometimes aphona
 3.  Velopharyngeal function: hypernasality and nasal emission is common in the spastic population.  Management of velopharyngeal impairments not only resolves resonance but also improves articulation and airflow throughout the speech mechanism improving overall speech performance
 4.  Articulatory function:  phoneme acquisition follows similar course in both normal and cerebral palsied.  Imprecision in fricative and affricative production and difficulty achieving extreme articulatory gestures.

Dyskinetic syndromes:
 Athetosis is gthe most common dyskinetic syndrome in CP.  It may appear as a pure form or a mixed (majority) such as choreoathetosis or dystonic athetosis. Dyskinetic syndromes are less common than spastic syndromes. Athetosis, often with choreoathetosis is now predominantly caused in cerebral palsy by perinatal anoxia.

 Athetoid Syndrome:
 a.  hypotonia an slow motor development (hypotonia may progress to normal tone or a mixed hypertonic-athetoid condition with maturity)
 b.  Failure to achieve sitting balance
 c.  the MORO reflex and the asymmetric tonic neck reflex (ATNR) are abnormal
  MORO reflex: If you produce a loud sound, the reflex is pathologic if there is a persistent symmetrical adduction and upward movement of the arms with fingers splayed followed by a flexion of arms in clasp manner.
  ATNR reflex:  The reflex is elicited by turning the infant’s head to each side for 5 seconds.  (repeated 5 times).  The reflex is pathologic if there is obligatory extension and flexion of lims for more than 60 seconds.
 d.  Dysphagia and frooling: chronic dysphagia and dysarthria are common; In general, severity of the dyskinetic involvement of the limbs is correlated with the severity of the speech mechanism involvement.
 e.  Cognitive deficits may or may not accompany the motor disability

 Speech mechanism Impairment in athetosis:
 a.  Respiratory function: Cerebral damage of the periaqueduct area is common in hypoxic-ischemic disorders of neonates who develop either athetosis or spasticity.  The damage may delay or disrupt the development of higher neural centers that control respiration in cerebral-palsied children.  The result may be a disturbance in the normal slowing of the breathing rate that comes with age and a disorder in the regulation of breathing patterns. (Respiration remains at a fast rate and irregular)
  Belly breathing:  Belly breathing is produced by the contraction of the diaphragm with little or no thoracic expansion. During the first 6 months, abdominal area movement is greatest during inspiration.  (The thoracic expansion does not have enough support in the infant initially). With development, around 6 mo, mid-thoracic movements can be seen during inspiration. With ability to sit, there is normal extension of the vertebral column and thorax against gravity.  Rotation patterns of the body develop and elongate the abdominals and the intercostals.  In athetoid children, lack of stability and extension of the vertebral column as well as delayed head balance and sitting posture result in breathing patterns of the neonate that persist into later childhood.
  Paradoxical or reverse breathing: Identified by the depression of the upper chest during inhalation and flaring of the lower rib margins. It is usually attributed to a lack of strength of the upper chest and neck muscles to counteract the forceful contraction of the diaphragm. During inspiration these muscles do not fix the rib cage against negative intrathoracic  pressure created by the downward movement of the diaphragm. The result is a rib cage of limited size and reduced volume of air during inhalation. Reversed breathing appears more often in athetoid CP. There is move involvement in the thoracic wall muscles as compared to abdominal muscles.  The diaphragm provides for a tendency toward the flared ribs.
Although reversed breathing may contribute to limitations in pitch and loudness  and elevated Fo due to increased subglottal air pressure. The substitution of voiced consonants for their voiceless cognates seems to result from an attempt to conserve respiratory effort.

Laryngeal Function Laryngeal dysfunction is common.
 a.  monotony of pitch
 b.  low and weak intensity
 c.  inability to adduct the vocal folds to midline of the glottis
 d. breathy quality
 e.  some have a hyperadduction of the vf with a lack of phonation (the hyperadduction may be as a result of a generalized hypertonic muscle contraction.)

Articulatory dysfunction:
 a.  large ranges of jaw movement (may act as a facilitator to tongue movement; Tongue height for articulatory targets varied with the ability of the ability to control jaw movement)
 b.  inappropriate positioning of the tongue for phonetic segments because of a reduced range of tongue movement (reduced anterior – posterior tongue movement, which distorts positions for the vowels); inability to shape the tongue for consonant productions
 c.  instability of velar elevation (moves inappropriately and more slowly)
 d.  prolonged transition times for articulatory movements(Limited range of tongue movements and grossness of tongue shaping appeared to be the causes of abnormally long transition times between articulatory movements.
 e.  retrusion of the lower lip

Causes of Athetoid Dysarthria
Both speech and neurologic literature have implied that the dysrthria of athetosis in CP is caused by variable, irregular, and even random involuntary movements of the speech muscles. (Conventional view) However, newest research proposes that a pattern of abnormal voluntary motor commands for speech is generated by athetoids rather than a set of involuntary movements.  The researchers assume that inappropriate commands arise in athetosis because cerebral lesions preclude normal sensorimotor integration for generating appropriate motor commands for speech. Disruption of the internal sensorimotor feedback system for appropriate motor commands leads to the generation of faulty movements that are perceived by others as involuntary. In summary the dysarthria appears to be caused to faulty programming of voluntary movements rather than the result of random involuntary movements.

Children with spasticity are slightly superior to those with athetosis in respiratory functions and articulatory functions.
Childhood dysarthrias of the cerebral palsies remain the most common childhood motor speech disability.

Ataxic Syndromes:
An uncommon syndrome in CP
The disorder in ataxic cerebral palsy is primarily one of incoordination and the most significant sign is a wide-based, lurching, staggering gait.
Other classic signs include
 a.  hypotonia
 b. action tremor
Etiology: cerebellar malformation, metabolic disturbances, birth trauma, and genetic
Mixed ataxic-spastic children are a frequent subtype.  They usually have spastic signs in the lower limbs and are labeled as ataxic diplegics.

Speech Mechanism
Similar to those of adults
Speech signs:  speech retardation, inconsistency of substitutions and omissions of sounds, scanning speech, and dysrhythmia and associated disorders of intonation and stress.
Ten deviant perceptual speech dimensions in adult ataxia (might also be present in children): imprecise consonants, irregular articulatory breakdown, distorted vowels, excess and equal stress, prolonged phonemes, slow rate, monopitch, monoloudness, and harsh voice.
Note: severity of articulation disorder may be related more to general intellectual levels than to the degree of oromotor disability; ataxia may present as a mild disorder and even be difficult to separate from general developmental phonological impairment.

LMN

Much more likely (10x’s) to have UMN disorders.
LMN are less likely to have childhood dysarthria, but if they do it is in the later stages of the disease.

Poliomyelitis cause by viral involvement in the brain stem and spinal cord was once a common cause.
There are a few children with myasthenia gravis (neuromuscular juncture)

Speech signs:  all can be classified as flaccid dysarthria.
Hypernasality, imprecise consonants, breathiness, monopitch, harsh voice, short phrases, monoloudness. (Not all children have all of these characteristics)

Signs of LMN disorders:
1.  Weak muscles: muscles that are incapable of contracting to a desired strength and then relaxing. Seen in the lips, face, tongue, jaw and velopharynx
2.  Hypotonia: reduction of muscle tone (may be present in the absence of weakness)Lips and tongue, vocal fold (weak cough response; breathy)
3.  Fatigue: inability to perform a sustained repetitive motor act; poorly sustained rates of diadochokinetic syllables
4.  Other: absent tenden reflexes, lack of a Babinski sign, presence of atrophy, tongue fasciculations, lack of clonus,

LMN Dysarthrias
Important signs of lower motor neuron disorder in children include
 a.  weakness,
 b.  fatigability,
 c.  hypotonia
 d.  atrophy
 e. fasciculations
With individuals with nerve palsies of V, VII, X, and XII there is weakness and paralysis
Hypernasality is the major presenting speech sign in LMN disorders.
Major speech signs of flaccid dysarthria in addition to hypernasality include imprecise consonants, continuous breathiness, nasal emissions, audible expiration, harsh voice, short phrases and monopitch.
 

Disorders of Anterior Horn Cell and Cranial Nerve Motor Neuron
1.  Juvenile Progressive Bulbar Palsy (Fazio-Londe Disease)
rare; facial paralysis, dysphagia, flaccid dysarthria; All lower cranial nerve nuclei may be affected; the ocular nerve is usually spared; hypernaslity, dysphagia, tongue and face weakness
2.  Moebius Syndrome: (Congenital Facila Diplegia) rare; facial pralysis; Mild distortions were sometimes presents

Disarthrias of peripheral and cranial nerve action.
1.  Guillain-Barre Syndrome: SLP may perform a dysphagia evaluation or the effects of respiratory weakness on speech.  AAC may be used temporarily until recovery (65% recover completely)
2.  Bell Palsy (Facial Nerve Palsy) There may be partial or complete paralysis of one side of the face. A mild dysarthria may result from slurring of the bilabial phonemes
3.  Masticator and hypoglossal paralyses: Chewing muscles are innervated by cranial nerve V.  Isolated damage to XII is marked by unilateral atrophy and fasciculation of the tongue.
4.  Vocal Fold paralysis: X nerve damage; The symptoms of the flaccid vocal folds near the midline or in the paramedian position are harshness and reduced loudness.  If fixed in an adducted position, the voice will be harsh and breathy as well as reduced in loudness. In addition, diplophonia, short phrases, and inhalatory stridor will be heard. May be congenital or acquired (growths, trauma, inflammatory illness).
5.  Palatal paralysis: Unilateral lesions of the cranial nerve X often result in weakness of the palate and pharynx also. In mild cases: hypernasality, in severe cases: hypernasality and audible nasal emissions.
6.  Familial Dysautonomia (Riley-Day Syndrome): fundamental defect is thought to be due to an imbalance between the parasympathetic and sympathetic portions of the autonomic nervous system. Seen predominately in Jewish children is characterized by dysphagia, failure to produce and overflow of tears, hypoactive or absent tendon reflexes, moderate hypotonia, poor motor coordination, postural hypotension, emotional lability.
Motor speech disorder: hypotonic; speech: flaccid dysarthria

Dysarthria in disorders of the neuromuscular Junction
Generalized myasthenia gravis occurs as the result of a failure in transmission because of reduced availability of acetylcholine at the junction. Causes muscle weakness after sustained muscle contraction. The Vagus nerve is sometimes the first to be affected:  hupernasiality.  Fatigability is the cardinal symptom. Drug therapy

Dysarthria in disorders of muscles: Two types dystrophy or myopathy

Duchenne Muscular dystrophy: Most common type of muscular dystrophy. X-linked heredity and mostly affects boys. Caused by a protein deficiency that results in a loss of muscular strength.  A significant diagnostic sign is enlargement of the calf muscle as well as other muscle groups.  Infiltration of fat and connective tissue replaces muscle fiber. Dysarthria (flaccid) may appear in the last stages.  An alternate communication device may be effective in the later stages of disease.

Myotonic dystrophy: an autosomal dominate progressive muscular disorder.  It is marked by an abnormal persistence of voluntary muscular contraction.  The child is unable to relax a contracted muscle quickly or release a gripped object rapidly.  There may be facial paralysis. Early sucking a swallowing difficulties resolve; the myopathic facies is common: atrophy of the facial muscles gives the child a long, lean appearance and an expressionaless face.  Eyelid ptosis, flaccid facial musculature and an open bite. The most common symptoms reportedly are velopharyngeal incompetence and hypernasal speech; Therapy: for hypernasality (lifts, flap surgery, therapy)

Infantile facioscapulohumeral (FSH) Muscular dystrophy: Uncommon; severe weakness that leads to death.  Facial weakness and ptosis; hypernasal speech, bulbar muscle weakness, and respiratory insufficiency; sensorineural hearing loss.  Therapy: palatal lift

Myopathies:  Diseases of abnormal changes in the muscle itself or the membranes of the  muscles; rare; the predominating symptom is muscle weakness.  If congenital: hypotonia with progressive muscular weakness. If cranial nerves innervating the bulbar muscles ar involved, speech functions may be disturbed. Flaccid dysarthria.
 
 
 
 
 
 

Assessment:
1.  oral motor abilities (vouluntary nonspeech movements, feeding and dyspahgic behavior, primitive oral reflexes and oral-sensory capacities
2  speech production subsystems (respiration, laryngeal, velopharyngeal, articulatory, and speech intelligibility
cognitive/linguistic functions:

Oral motor evaluation:
1.  modified feeding: A small morsel of food (bolus) is selectively placed in the oral cavity.  The small morsel challenges the child to perform precise movements with the tongue and lips, articulators
 Provides a gross clinical assessment of the cranial nerves involved in speech and predicts their degree of motor involvement.
 Evidence of dysphagia provides significant signs of neurological damage
 Cranial nerves are assessed through chewing and swallowing activities during the modified feeding:
 a.  Facial nerve: flaccid facial muscles, flaccid lips, open mouth posture and drooling;
 b.  hypoglossal:  neurological impairment: unable to shape, cup, point protrude, retract, lateralize or elevate the tongue tip in trying to manipulate the bolus
  UMN tongue will deviate to side opposite lesion; in spasticity, speed, strength, range and coordination of the tongue are limited.
  LMN tongue deviates to the side of the lesion. Tongue atrophy
 c. trigeminal nerve responsible for biting and chewing.
 d.  Glossopharyngeal: indications that the velum is not elevating during the swallow.
2.  Love – Hagerman – Tiami clinical dysphagia examination
assess: biting, sucking, swallowing, chewing soft food and hard food.

3.  Abnormal oral reflexes and deviant oral motor behavior
a.  Jaw thrust is a forceful, downward extension of the mandible; are elicited by presentation of food; can interfere with efficient removal of food or liquid from the spoon, bottle or cup.
b.  Tongue thrust is a forceful protrusion of the tongue from the mouth; may be repetitive; only abnormal after 18 mo; may interfere with adequate transport of food and liquid through the oral cavity
c.  Lip retraction: the upper lip appears pulled upward and the lips are retracted in a smile; interferes with appropriate use of the lips in feeding
d.  Tonic bite reaction: is stimulated by touching the jaws, teeth, or gums; the feeding utensils cannot be manipulated in the oral cavity easily
e.  Tongue retraction: tongue is pulled back; interferes with removal of food from utensils and efficient oral transit.
f.  Nasal regurgitation is the backward flow of liquid through the nasal cavity; associated with abnormal function of the velopharynx
 

4.  Oral-Motor assessment Scales
 a.  Prespeech Assessment Scale:  assess pre-speech behaviors below 2 years: feeding, respiration, phonation, and sound play are evaluated
 b.  Preschool Oral Motor Examination: assess oral reflexes and a protocol for observing the young child with abnormal motor patterns
 c.  Evaluation of Basic and Early Skilled Speech Movements:  assesses oral ands speech behaviors, examining back, elbow, sitting, standing and hand postures

5.  Oral-sensory capacities
 Tests are not widely used by SLPs because research indicates that this ability and speech performance is not related.
 Tactile sensitivity: assessed using a two-point discrimination using a esthesiometer in the speech-science laboratory.
 Oral-stereognostic testing: another procedure to test the loss of oral-sensory capacities.
  Stereognosis is the ability to recognize three-dimensional forms through the senses by placing small acrylic forms representing geometric shapes into the mouth of a child and the child identifies the shape.

6.  Radiologic examination: for signs of dysphagia
 Young CP population often demonstrates recurrent aspiration with secondary infection to the young.  Dysphagia may lead to inadequate fluid and calorie intake, malnutrition; at risk for gastroesophageal reflux and associated esophagitis.

7.  Oral-Motor evaluation of the speaking child
 The Robbins-Klee protocol: a 86 item test that assess the structure and function of the vocal tract from lips to respiration-laryngeal complex. Both speech and nonspeech aspects are assessed.   It is the motor speech examination that provides a standardized assessment of the oropharyngeal mechanism in childhood dysarthrics and suspected developmental verbal dyspraxics.

 Respiratory dysfunction: goal is to determine how much the respiratory problem affects speech performance and what limitations it imposes for improvement; clinical impression of breath-control
 a. Prolongation of a neutral vowel: Two tasks (a) routine phonation time (b) maximum-effort phonation time; this will provide an estimate of what expiratory reserve the child possesses when phonation is produced at high levels of breath support; The duration of prolonged phonation under the two conditions reveals the child’s ability to use the respiratory system to drive the vocal tract under various conditions as well as the ability of the laryngeal system to modify the airstream.
 b.  Counting from one to ten under the two conditions (a) Count until I tell you to stop; (b) take a deep breath and count as long as you can; tells you how many syllables may be uttered on a breath group and for speaking at high levels of lung volume
 c.  Comparing voiced CV repetitions with voiceless CV repetitions The mean number of syllables produced per second for voiced and voiceless CV repetitions should be calculated so that comparisons can be made between the speech tasks.  Generally, voiced CV syllables are easier to produce than are voiceless CV syllables, and counted morphemes are more difficult than vowel prolongation in voiced/voiceless tasks.
 d.  Producing Contextual Speech in Reading or Conversation  Obtain mean length of utterance per inhalation for the counting task; compare with mean length of utterance for counting; comparison of these two measures will reveal how demands of length and complexity are affected by respiratory limitations
 e.  Inspiring and expiring of a deep breath The ability to increase lung volume and to control expired air serves as a test of the capacity of the respiratory system without confounding respiration by vocal tasks.  Timing of the inspiratory and expiratory phase is useful because the ability to increase the inspiratory lung volume before an utterance generally increases the length of the expired breath group and more syllables can be uttered in the breath group.
 Signs of poor respiratory function
  a.  short utterances with audible or visible inhalations between each     utterance
  b.  slowing of speech over time
  c. strained vocal quality at the end of phrases
 Signs of impaired respiratory control
  a.  reduced syllable repetitions
  b.  decreased overall rate
  c. uncontrolled exhalations
  d.  unsuccessful in varying loudness
  e.  consistently soft or breathy voice (may also be due to poor velopharyngeal or lip valves

Rapid rates of inhalation of more than 30 times per minute generally compromise breath control for speech

Laryngeal Dysfunction:
The five tasks above can also tell us about laryngeal functioning because of the interdependence of the respiratory and laryngeal systems.
1. Prolongation of neutral vowel: tests laryngeal control
2.  Difference between voiced and unvoiced CV repetitions point to problems with adduction and abduction of vocal folds; a slow, weak breathy or strained sound when asked to imitate a machine gun and say “ah-ah-ah-ah” as fast as he can.
 -child with hypotonic muscles (athetoid) may extend the trunk and neck to help
 -child with continuous breathy indicate hypofunctioning
3. Reduced pitch and loudness ranges; Low pitches suggest weakness  (LMN); hoarse, harsh, or struggle-strained qualities are common to spastic disorders.

Velopharyngeal dysfunction:
1.  prolong /s/; requires firm velopharyngeal seal
2.  counting 1-10; contains plosives and fricatives
3.  testing for consistent nasal emission when counting
4.  Instrumentation: videofloroscopic

Articulation:
Use sentence tests because motor complexity in sentence production usually is increased over single words and the results of the sentence testing may provide a clearer picture of what problems the motor impaired child faces in motor control; Examine for phonological processes

Instrumental:
Spectrograms: evidence of disturbed articulatory movements
Videofluoroscopic; velopharyngeal competence
EMG: timing of articulatory gestures of lip, jaw and tongue
Strain gauge sensors placed on the mandible or tongue may yield precise information of the velocity and force used in articulation

Speech intelligibility: there are assessments available: Yorkston and Beukelman:  Assessment of Intelligibility of Dysarthric Speech.
 

Cognitive-Linguistic assessment:
Neuropsychological developmental assessment
 
 

Issues in speech management of childhood dysarthria
1.  Prespeech oral-motor training and early intervention: Research shows that motor coordination for speech activities is different than it is for nonspeech activities such as feeding programs.  However, it does not completely contradict the need for prespeech muscle training of lips, tongue, jaw, and soft palate in motor activities as chewing, swallowing, sucking, blowing, an oral muscle diadochokinesis.

2.  Early intervention:
 a.  Appripriate early management of dysphagia and abnormal oral reflexes has several advantages for children at risk: nutritional intake, difficult feedings will be easier, control of oral movement will be made more normal.  The improved oral-motor control then can be utilized for improved speech production when speech has its onset.
 b.  Neurodevelopmental therapists currently are providing leadership in prespeech feeding management; the neurodevelopmental approach is becoming the therapy of choice for neurologically impaired at risk infants.
 Prefeeding Skills (Morris & Klien, 1987) a comprehensive program
 c. Pre-speech sound-making during the period of oral motor training feeding is critical to attaining more normal speech.  Sound making must be imitated, reinforced, stimulated. Optimal program should give equal weight to feeding therapy and stimulation of developmental sequences of early vocal utterances.
3.  Later Oral-motor management
Oral motor exercises: conflicting research findings; Hixon and Hardy deny that training in non-speech activities have any effect on motor control for speech, however, recent research shows that select activities may benefit specific dysarthrias.  Limited prominence is given to oral exercises in current dysarthia management programs
4.  Drooling:  It appears that a problem as extreme as constant drooling may demand surgery.
5.  Technology:
 a.  Biofeedback: promising; techniques have been employed in combination with other techniques to create a total speech management program
 b.  Communication Aid:
  -increase attention, reduce frustration and raise motivational levels
  -improve language comprehension and help organize language
  -Use computers or other assistive communication devices at necessary points in overall speech management plan, but when possible aim for oral speech with limited assistance form communication aids
  - Decision Matrix for election of communication technology;

Therapy:
1.  Seating for adequate respiratory performance: the child must have appropriate support the results in normal neck elongation, head and shoulder alignment and firm trunk support and stability of the spine.The most appropriate position is a seated posture in which the upper extremities, head control, eye contact and vocalization are enhanced.  A seat belt will secure the pelvis in the correct position.  A child’s individual ability to generate adequate breath support in various positions is important since the location of muscle weakness is a large component of neurologic impairment.
 -Expanding physiological breath support for speech: Phonatory drills requiring maximal levels of performance provide practice for expanding physiological support for speech
 -Speaking within respiratory limits: Ascertain the child’s ability to increase air intake (instruction in deep inhalation); use dry spirometer of provide feedback for improvement; sustain a vowel (the child takes a breath then phonates watching in a mirror for the relationship between respiratory patterns of inhalation/exhalation and thoracic/abdominal patterns;
 Some recommend that the best strategy for developing adequately high levels of lung volume is to put off training until the child is producing connected speech.
 Sometimes improvement of articulation production is obtained by better valving with more efficient use of available air via  palatal lifts, flaps
 Measurement of breath support and increasing expiratory control is mandatory in a well-organized therapy plan: The ability to generate subglottal pressure within the range of 5-10 cm of water for more than 5 sec.; oral manometers can be purchased by medial supply houses.
 -Speech phrasing:  The goal is to produce short patterns of utterance between more-frequent-than normal inspirations.  The use of short utterances within well-timed inhalations between phrases usually allows the dysarthric child to communicate without the loss of intelligibility that occurs when speaking without breath support. May have to convince the child of the benefits.
 

Laryngeal dysfunction:
 -Hypo- and hyperfunctional Voice symptoms: are resistant to modification; suggest trial therapy
 Adolescent voice management: Ear training; tape recordings trial therapy.  Result will be increased intelligibility;
 Loudness symptoms: Pushing/pulling technique; digital pressure; voice amplifiers; use of palatal lift may improve valving to the total vocal tract
 Pitch and stress symptoms: Auditory/visual biofeedback is helpful in allowing monitoring; use of visi-pitch as biofeedback; Variation in intonation should be taught to increase pitch flexibility; practicing pitch contours has been helpful; develop stress patterns to maximize speech naturalness

Velopharyngeal dysfunction:
Pharyngeal flap surgery: Hardy finds this surgery disappointing for dysarthric populations and recommends palatal lift prosthesis.  Due to paralysis of muscles surgeons are reluctant to perform the surgery because there is limited if any successful outcomes.
Palatal lift prosthesis: the most viable approach:
 1. It allows the child to develop and maintain sufficient intraoral air pressure to produce consonantal sounds
 2. Aerodynamic aspects of the vocal tract are improved so there is an increase in the duration of utterances on one expiration: increased vocal output
 3. Tongue postures for vowel production become more normal after placement
 4.  Allows more normal velopharyngeal closure to occur reducing hypernasality
 5.  Due to the improvement of the aerodynamic and mechanical aspects of the vocal mechanism, loudness is improved.
 Contraindications for palatal lift:
  - if speech musculature is severely motor involved, it is unlikely that the    lift, even with reduced hypernasality will make speech intelligible
  -UMN with hyperactive gag reflex makes fitting and tolerance for the lift    difficult
  -Motor involvement may preclude independent insertion, removal, and    cleansing of the prosthesis.
 Role of SLP: help in fitting of the prosthesis; work closely with prosthodontist;
  Make decisions regarding whether hypernasality is improved; make sure    hyponasality is not occurring due to poor fitting; make referrals to     prosthodontist for adjustments when needed.
Traditional approach to improving resonance (minimal resonance difficulty)
 1.  oral nasal balance
 2.  auditory discrimination between oral/nasal sounds
 3. reduce nasal emission

Articulatory Muscle dysfunction:
 Hardy suggests the need to move quickly from training CV syllables to training speech sounds in words and syllables.
Guidelines for selection of Target sounds:
 1.  errors that are stimulatible
 2. Sounds that are produced correctly in at least one position
 3.  Distorted sounds corrected before sound substitutions or omissions
 4.  More visible sounds
 5.  Earlier developing sounds

Phonological processes approach has proven successful in isolated cases

Hardy’s suggestion to management guidelines:
 1.  train errors in initial positions; postvocalic positions will be easier to obtain later
 2.  train articulatory distortion that fall short of target points because prognosis for achieving focal contacts is good
 3.  referred training in articulatory omissions and distortions that are based on motor involvement, since these are more difficulty until articulatory distortions are managed.
 4.  use a multiple auditory-visual stimulation approach rather than auditory stimulation alone
 5.  train voice/voiceless contrast by slowing the speech and concentrating on correct production of voiceless phonemes; critical because many use voiced for voicless consonants.

Dr. Harmon: suggests using a distinctive feature approach

Neurologic Symptoms in Articulation
Rule of thumb: it is more common for children with dyskinetic dysarthria to have difficulty finding appropriate focal articulation because of involuntary movement patterns that may be reflected in their oral musculature;
Spastics: have difficulty in initiating movement and display problems in coordination and force articulation They can find focal articulation but have weak and uncoordinated articulatory movement.
LMN: demonstrate muscle weakness but can reach focal articulation points easily while lacking force for articulation resulting in moderate phoneme distortion

Compensatory Articulation:
Slp may refine a compensatory production the child is using
 for a particular sound

Frustration in articulation therapy:
Training may be difficult and frustrating; may need to give the child a short vacation after prolonged therapy;
Some SLPs become frustrated with slow progress
Therapy may be a lifelong process with refresher courses along the way.