Motor Speech

Question 1

The Motor System

Answer 1

*Parts of the nervous system that control voluntary movement
*Allows thought to be turned into movement
*Extremely complex
*Type of disorder dependent on location and extent of damage to motor system

Question 2

Components of Motor System

Answer 2

*One of several subdivisions of nervous system
*Organized into:
–Central nervous system (CNS)
*Brain and spinal cord
–Peripheral nervous system (PNS)
*12 pairs of cranial nerves and 31 pairs of spinal nerves

Question 3

Brain

Answer 3

*Most complex and important part of nervous system
*Nearly all activity in nervous system originates in or is processed by brain
*Voluntary motor commands to muscles originate in brain
*Receives sensory information from body and controls cognitive functions
*Divided into:
–Cerebrum
–Brainstem
–Cerebellum

Question 4

Cerebrum

Answer 4

*Largest and most prominent part of brain
*Split into two hemispheres by longitudinal fissure
*Organized into four areas called “lobes”
–Frontal lobe
–Temporal lobe
–Parietal lobe
–Occipital lobe
*Most obvious feature is deep convolutions known as gyri (singular = gyrus)
*Prominent sulci:
–Lateral sulcus
–Central sulcus
*Prominent gyri
–Precentral gyrus (primary motor cortex, motor strip)
–Postcentral gyrus (primary sensory cortex, sensory strip)

Question 5

Cerebral Cortex

Answer 5

*Vital part of nervous system
*Surface of cerebrum
–If laid flat, span surface area of 340 sq. in.
–Thickness of two to five mm
*Often described as “gray matter” of brain
*Performs higher cognitive activities
–Language, motor planning, problem solving, sensory perception

Question 6

Brainstem

Answer 6

*Divided from top to bottom:
–Midbrain
–Pons
–Medulla
*Between cerebrum and spinal cord
*Cranial nerve nuclei: points where cranial nerves attach to brainstem
*Important because:
–Acts as passageway for descending and ascending neural tracts that travel between cerebrum and spinal cord
–Controls certain integrative and reflexive actions (respiration, consciousness)
–Conveys motor impulses from CNS to muscles of larynx, face, tongue, pharynx, and velum
*Cranial nerves project out from CNS

Question 7

Cerebellum

Answer 7

*Most important function
–Coordinates voluntary movements so muscles contract with correct amount of force and at appropriate times
*Attached to back of brainstem
*Makes neural connections with cerebral cortex and many other parts of CNS

Nervous System
*Contains many different types of cells
*Neurons
–Most important cells in nervous system
–Three primary components
*Cell body
*Dendrites
*Axon

Question 8

Types of Neurons

Answer 8

–Motor neurons
–Sensory neurons
–Interneurons
–Efferent neurons
–Afferent neurons

Question 9

Other Nervous System cells

Answer 9

–Glial cells
–Schwann cells
–Microglia
–Oligodendroglia
–Astrocytes

Question 10

Tracts

Answer 10

–Bundles of axons found in the CNS

Question 11

Nerves

Answer 11

–Bundles of axons found in the CNS

Question 12

Neurotransmitters

Answer 12

–Small substance released at end points once charge reaches axon’s terminal ramifications
–Two important neurotransmitters in the motor system: acetylcholine and dopamine

Question 13

Summary of Motor System Components

Answer 13

*Nervous system divided into CNS and PNS
–CNS includes brain and spinal cord
–PNS includes spinal and cranial nerves
*Brain
–Organized into cerebrum (four lobes), brainstem, and cerebellum
*Neurons
–Most important cells of nervous system
–Means by which neural impulses are transmitted from one part of the nervous system to another

Question 14

Desire to Move

Answer 14

*Starting place for any voluntary movement
*Taking desire and turning it into movement is often done easily but is extremely complex

Question 15

Primary and Association Cortices

Answer 15

*Primary cortex
–Comprised of
*Cortices that first analyze sensory information
–Primary auditory cortex
–Primary visual cortex
–Primary sensory cortex
*Cortex that receives planned motor impulses from cortical and subcortical areas of the brain
–Primary motor cortex
–Planning for voluntary movement does not originate in primary motor cortex

*Association cortex
–“Makes sense” of sensory impulses initially analyzed by primary cortices
–Not a single region of brain, but divided into four areas of cortex
–Formulates initial planning of a voluntary movement
–Sends rough sequence of motor impulses down to subcortical structures for further processing and refining

Question 16

Basal Ganglia and Cerebellum

Answer 16

*Link the association cortex with the primary motor cortex
*Cerebellum:
*Takes rough motor impulses from the association cortex, smoothes them out, coordinates them, and sends them (via thalamus) up to primary motor cortex

Question 17

Thamalmus

Answer 17

*Important subcortical gray matter structure
*Doorway through which subcortical systems of nervous system communicate with cerebral cortex
–Receives neural inputs of planned motor movements from basal ganglia and cerebellum
–Sensory impulses from the body pass through thalamus on way to cortex
*Believed to use sensory information to further refine motor impulses

Question 18

Primary Motor Cortex

Answer 18

*Receives neural motor impulses that have been processed, smoothed, and coordinated by basal ganglia, cerebellum, and thalamusP

Question 19

Descending Motor Tracts

Answer 19

*Pyramidal system
–Carries impulses that control voluntary, fine motor movements
–Works at a conscious level
*Extrapyramidal system
–Carries impulses that control postural support needed by fine motor movements
–Works at more of an unconscious level, automatic in function

Question 20

Cranial and Spinal Nerves

Answer 20

*Upper motor neurons
–Motor fibers within the CNS
–Damage to upper motor neurons often results in spasticity
*Lower motor neurons
–Motor fibers in the cranial and spinal nerves
–Damage to lower motor neurons results in muscle paralysis or paresis

Question 21

Neuromuscular Junction

Answer 21

*Point where axons of lower motor neurons make synaptic connections with muscle cells

Question 22

Summary of Motor System

Answer 22

*Motor system
–Important, very complex component of nervous system
–Consists of primary and association cortex, basal ganglia, cerebellum, thalamus, pyramidal and extrapyramidal tracts, and neuromuscular junction
–Damage at any level of motor system may result in movement disorder

Question 23

Assessment Questions Foundations:

Answer 23

Does the problem seem to be the result of a neurologic Suggested questions for the SLP to ask about a motor speech evaluation (Duffy (2013), Swigert (2010):
– Is there a problem with the patient’s speech?
– If there is a problem, what is the best way to describe it?
– Does the problem seem to be the result of a neurologic disorder?
– If it seems to be neurologic in origin, did it appear suddenly or slowly?
– Is the problem related strictly to speech production, or is it more of a problem with language, such as aphasia?
– If it is a problem of speech production, do most of the problems seem to be related to the sequencing of phonemes?
– If there are no phoneme sequencing errors, what are the characteristics of the patient’s speech errors and any associated motor problems?

Question 24

Goals of a Motor Speech Evaluation

Answer 24

*Two basic methods of evaluating motor speech disorders
–Instrumentation: relies on sophisticated devices to objectively measure components of speech production
–Perceptual analysis: relies on clinician’s ears (and eyes) to judge
*Most clinicians do not have access to sophisticated instruments

*Hayes and Pindzola (2011) stated two goals of any speech-language evaluation
–Understand a patient’s problem
–Determine beginning level of treatment

*Clinician collects relevant background information about patient
Patient performs numerous tasks to assess the function of motor speech systemSuggested questions for the SLP to ask about a motor speech evaluation (Duffy (2013), Swigert (2010):
–Is there a problem with the patient’s speech?
–If there is a problem, what is the best way to describe it?
–Does the problem seem to be the result of a neurologic disorder?
–If it seems to be neurologic in origin, did it appear suddenly or slowly?–Is the problem related strictly to speech production, or is it more of a problem with language, such as aphasia?

–If it is a problem of speech production, do most of the problems seem to be related to the sequencing of phonemes?
–If there are no phoneme sequencing errors, what are the characteristics of the patient’s speech errors and any associated motor problems?
*Clinicians will likely make an accurate diagnosis by answering these questions

Question 25

Speech Production Components and Disorders

Answer 25

*Five components necessary for normal speech production
–Respiration, phonation, resonance (what you are hearing?/clarity of speech?), articulation, prosody (patterns of stress/intonation)
*When one or any combination affected by neuromotor disturbance, motor speech disorder will result (dysarthria or apraxia of speech)
*Location in nervous system determines type of motor speech disorder

*Dysarthria
–Speech production deficit resulting from neuromotor damage to PNS or CNS
*Apraxia of speech

–Motor speech disorder often associated with damage to left hemisphere of brain*Dysarthria and apraxia of speech are not:
–Language disorders
–Cognitive disorders
–Results of abnormal anatomical structures, sensory loss, or psychological disturbance

Question 26

Assessment component: Respiration

Answer 26

*Primary function for speech production
–Provides subglottic (below) air pressure needed to set vocal folds into vibration (pressure is building up and vocal folds burst open, then the force comes thru quickly, the fold come back together -cycle)
*Speech production is dependent on full, steady supply of air
–Nerve damage means weak muscles to move air in and out of lungs, which leads to less air for speech production, resulting in:
*Short phrases
*Reduced loudness and breathy voice

Question 27

Assessment component: Phonation

Answer 27

*Production of voiced phonemes through vocal-fold vibrations in larynx
–Normal phonation: complete adduction (come together) of vocal folds; sufficient subglottic air pressure
–Neuromotor damage to nerves that innervate the vocal-fold adductor muscles can have several effects on speech production
*Flaccid dysarthria, spastic dysarthria, neuromotor damage to laryngeal muscles

Question 28

Assessment component: Resonance

Answer 28

*Proper placement of oral or nasal tonality onto phonemes during speech accomplished by raising and lowering of velum
–Oral resonance
*Produced when velum is raised and closes off nasal cavity from vocal air stream
–Nasal resonance
*Produced when velum is lowered and oral cavity is blocked by the lips or tongue
–Damage to nerves innervating velar muscles may cause hypernasal quality

Question 29

Assessment component: Articulation

Answer 29

*Shaping of vocal air stream into phonemes
–Accomplished by different structures within vocal tract: “articulators”
*Correct articulation requires articulators to perform movements that have appropriate timing, direction, force, speed, and placement for any given phoneme
*Neuromotor damage to articulators may affect lips, tongue, jaw, velum, or vocal folds
–Results in articulation errors (e.g., imprecise consonants or distorted vowels)

Question 30

Assessment component: Prosody

Answer 30

*Melody of speech, using stress and intonation to convey meaning
–Accurate and clear prosodic features require coordinated participation of phonation, respiration, resonance, and articulation
*Neuromotor damage can affect prosody
–Monopitch and monoloud quality
–Involuntary movements can result in irregular pitch variations, loudness, and prolonged intervals

Question 31

Standardized Test for Dysarthria

Answer 31

*There are few published standardized tests for dysrathia
*Frenchay Dysarthria Assessment-2—aids in differential diagnosis among the dysarthrias
*Assessment of Intelligibility of Dysarthric Speech—provides an objective assessment of single-word and sentence intelligibility
*Speech Intelligibility Test for Windows—computer version of the above test

Question 32

Standardized Test for
Apraxia of Speech

Answer 32

*Apraxia Battery for Adults-Second Edition—designed to diagnose apraxia of speech in adolescents and adults.
*It is the only published adult apraxia test
*Contains six subtests
*Provides info on severity, treatment suggestions, and changes over time
*Some researchers assert a number of test items assess disorders other than apraxia

Question 33

Conducting a Motor Speech Evaluation

Answer 33

*Five components of speech production need to be carefully assessed
–Also constantly assess six salient features:
*Muscle strength
*Speed of movement
*Range of motion
*Accuracy of movement
*Motor steadiness
*Muscle tone

Question 34

Muscle Strength

Answer 34

*Accurate speech
–Requires adequate strength to perform speech production tasks
*Decreased muscle strength
–Can affect respiration, articulation, resonance, phonation, prosody
*Muscle strength assessed by:
–Asking patient to press tongue against tongue blade or to count aloud from 1 to 100

Question 35

Speed of Movement

Answer 35

*Accurate speech
–Requires very rapid muscle movements of tongue and vocal folds
*Reduced speed of movement characteristic of most dysarthrias
–Exception: hypokinetic dysarthria
*Speed assessed by tasks concentrating on:
–Alternate motion rates (AMR)
–Sequential motion rates (SMR)

Question 36

Range of Movement

Answer 36

*Accurate speech
–Requires range of movement of articulators
*Reduced range of movement may cause:
–Inability to open jaw or completely adduct vocal folds
–Prosody to be affected
*Assessed by:
–Asking patient to extend or hold articulators in various positions

Question 37

Accuracy of Movement

Answer 37

*Clear speech
–Requires accurate movements of articulators
*With strength, speed, range, direction, and coordinated timing
*Reduced accuracy of movement may cause:
–Distorted consonants; intermittent hypernasality
*Assessed through:
–Conversational speech; spoken paragraph reading

Question 38

Motor Steadiness

Answer 38

*Normal speech requires the ability to hold a body part (articulator) still
*Reduced motor steadiness may cause:
–Tremors
–Large, involuntary movements that interfere with voluntary movements
*Assessed by asking patient to:
–Hold a position or prolong a vowel

Question 39

Muscle Tone

Answer 39

*Normal speech requires muscle tone ready for quick movements
*Reduced muscle tone may cause:
–Decreased muscle tone: weakness or paralysis
–Increased muscle tone: spasticity or rigidity
*Assessed by:
–Inferring when listening to patient’s speech
–Looking at affected body parts

Question 40

Instructions for the Motor Speech Examination

Answer 40

*Evaluation takes 30-40 minutes
*Short version
–Evaluation takes 10-15 minutes

Question 41

Background Information and
Medical History

Answer 41

*First portion is obtaining background information and medical history
*Thoroughness is important, as clues may be gathered from:
–Rate of onset
–Site of lesion
–Current status of problem

Question 42

Face and Jaw Muscles at Rest and During Movement

Answer 42

*Looking for:
–Abnormal muscle tone or strength
–Asymmetrical facial features
–Restricted range of movement

*Specific tasks
–Is mouth symmetrical?
–Can patient’s lips be forced open?
–Does face have expressionless, masklike appearance?
–When patient looks up, is there wrinkling on both halves of forehead?
–Is smile symmetrical?
–Can patient pucker lips?

–Can patient puff out cheeks and hold air in oral cavity as you squeeze the cheeks?
–Does jaw hang loosely or deviate to one side when mouth is wide open?
–Is patient able to move jaw to right and left?
–Can patient keep jaw closed while examiner attempts to open it?
–Can patient keep jaw open while examiner attempts to close it?

Question 43

Tongue at Rest and During Movement

Answer 43

*Involves function of hypoglossal cranial nerve (XII)
*Specific tasks
–Does size of tongue appear normal at rest?
–Is tongue symmetrical and still at rest?
–Are fasciculations present when the tongue is at rest?
–Is patient able to protrude tongue completely?
–Can patient keep tongue tip at midline while examiner pushes tongue to left and right?
–Is patient able to touch upper lip with tongue tip?
–Can patient keep tongue tip pressed against inside of cheek as examiner pushes the cheek inward?
–Can patient move tongue from side to side?

Question 44

Velum and Pharynx at Rest and During Movement

Answer 44

*Many of these muscles innervated by vagus cranial nerve (X)
*Difficult to see these structures clearly
*Specific tasks
–Does velum rise symmetrically each time patient says /a/?
–Is there pharyngeal gag reflux when back wall of pharynx is touched?

Question 45

Laryngeal Function

Answer 45

*Larynx cannot be observed directly
–Need instrumentation
*Laryngeal mirror
*Flexible nasoendoscope
*Specific tasks
–Can patient produce sharp cough?
–Can patient produce sharp glottal stop?
–Is inhalatory stridor present?

Question 46

Auditory-Perceptual Evaluations of the Motor Speech Mechanism

Answer 46

In many cases, the clinician’s ear is the best instrument for evaluating motor speech deficits

Question 47

Phonatory-Respiratory System

Answer 47

*Specific tasks
–Deep breath and say /a/, holding as long and steadily as clearly can
–Latency period between signal to say /a/ and initiation of phonation?
–Quality, pitch, loudness, and phonations

Question 48

Resonation System

Answer 48

*Assesses velopharyngeal function
*Specific tasks
–Take deep breath and say /u/ as long as possible
–Same task as above, but clinician squeezes nose

Question 49

Combined Systems (Phonation, Respiration, Resonation, Articulation)

Answer 49

*Alternate motion rate (AMR)
*Specific tasks
–Take deep breath and say “puh, puh, puh” as long, as fast, and as evenly as possible
–Sequential motion rate (SMRs)
–Make three sounds together

Question 50

Stress Testing of the Motor Speech Mechanism

Answer 50

*Screening for myasthenia gravis
–Patient asked to count quickly from 1 to 100
*Relatively rapid rate of deterioration of articulation, resonance, and phonation while counting, and with typical recovery, after rest there will be a recovery
*Otherwise, performance may decline if muscles taxed again

Question 51

Testing for Nonverbal Oral Apraxia

Answer 51

*Nonverbal oral apraxia of speech: disruption in sequencing of oral movements that are nonverbal
–May be present with or without apraxia of speech
*Specific tasks
–Have patient perform voluntary, nonverbal oral movements without demonstrating beforehand

Question 52

Testing for Apraxia of Speech

Answer 52

*Sequencing difficulty, pauses, distortions
*Specific tasks
–Repeat or read words of increasing complexity, beginning with same CVC syllable
–Repeat words with simple CVC consisting of identical initial and final consonants
–Count from 1 to 20 and backward
–Read sentences, including spontaneously and on demand

Question 53

Analysis of Connected Speech

Answer 53

*Clinician records patient reading a standard reading passage
*Rate patient performance on the qualities listed (e.g., Are vowels and consonants produced clearly?)

Question 54

Summary of AOS

Answer 54

*Two methods to evaluate motor speech disorders
–Instrumentation and perceptual analysis
*Obtain thorough background history and medical information
*Evaluate respiration, phonation, resonance, articulation, and prosody
*Examine six processes that are foundation for all voluntary movements
–Muscle strength, speed of movement, range of movement, accuracy of movement, motor steadiness, and muscle tone
*Evaluation allows clinician to:
–Fully describe patient’s speech production abilities, answer pertinent questions about the patient’s deficits, and arrive at correct diagnosis

Question 55

Definition of Flaccid Dysarthria

Answer 55

Caused by impairments of lower motor neurons in cranial or spinal nerves (damage to PNS)
Paralysis, weakness, hypotonicity, atrophy, and hypoactive reflexes of involved speech subsystem musculature
Weakness in speech or respiratory musculature results in distinctive qualities

Characterized by:
Slow-labored articulation
Marked degrees of hypernasal resonance
Hoarse-breathy phonation

Question 56

Neurologic Basis of Flaccid Dysarthria

Answer 56

Caused by damage to lower motor neurons (part of PNS)
Final common pathway: last and only “road” neural impulses from upper motor neurons travel to reach muscles
Caused by any disorder that disrupts flow of neural impulses along lower motor neurons that innervate muscles of respiration, phonation, articulation, prosody, or resonance

Question 57

Cranial Nerves of Speech Production

Answer 57

Six pairs of cranial nerves play vital role in speech production
Referred to as “cranial nerves of speech production”
Trigeminal, facial, glossopharyngeal, vagus, accessory, hypoglossal
Lower motor neurons inside these nerves transmit motor impulses from upper motor neurons to muscles used in speech production

Damaged nerve or combination of nerves determines specific characteristics
Damage may be from:
Brainstem stroke
Growing tumor
Viral or bacterial infections
Physical trauma
Surgical accidents

Question 58

Trigeminal nerve (V)

Answer 58

Attached to brainstem at level of pons, divided into three main branches (ophthalmic, maxillary, and mandibular)
Mandibular branch most important for speech and innervating muscles in lower jaw and velum
Damage to trigeminal nerve can be unilateral or bilateral

Question 59

Facial Nerve

Answer 59

Branches out from brainstem just below trigeminal nerve, dividing into cervicofacial and temporofacial branch
Damage to facial nerve:
Can cause weakness or paralysis in all muscles on same side of face, resulting in drooping of the eyelid, mouth, cheek, and other structures

Question 60

Glossopharyngeal cranial nerve

Answer 60

Originates in brainstem at medulla, coursing out to pharynx
Innervates stylopharyngeus and superior pharyngeal constrictor muscles
Damage also affects vagus nerve
Plays role in speech resonance and phonation by shaping pharynx into appropriate positions needed to produce various phonemes correctly

Question 61

Vagus Cranial Nerve

Answer 61

One of most important cranial nerves for speech production
Three branches
Pharyngeal branch
Damage can affect movement of velum, resonance
External superior laryngeal nerve branch
Damage can affect pitch
Recurrent nerve branch
Damage of recurrent branch causes breathy phonation

Question 62

Accessory Cranial Nerve

Answer 62

Originates in medulla just below vagus nerve
Works in conjunction with vagus nerve, helping innervate intrinsic muscles of velum, pharynx, and larynx
Damage to cranial components of accessory nerve will affect vagus nerve as well and vice versa

Question 63

Hypoglossal cranial nerve

Answer 63

Provides motor innervation for all intrinsic and most extrinsic muscles of tongue
Damage to hypoglossal cranial nerve
Results in weakness of tongue or paralysis
Primary characteristic of hypoglossal nerve damage
Imprecise articulation, phoneme distortion, or slow lingual movements

Question 64

Spinal Nerves

Answer 64

Many important for motor speech production
Phrenic nerve one of most important nerves of respiration
Damage generally must be widespread to significantly impair respiration
Exception: injury to phrenic nerve
Paralyzed diaphragm, decreased loudness; shortened, breathy or strained vocal quality

Question 65

Causes of Flaccid Dysarthria

Answer 65

Caused by anything that disrupts flow of motor impulses along cranial or spinal nerves that innervate muscles of speech production
Conditions that damage lower motor neurons
Physical trauma, brainstem stroke, myasthenia gravis, Guillain-Barré syndrome, and polio
Other causes
Tumors, muscular dystrophy, progressive bulbar palsy

Question 66

Physical Trauma

Answer 66

Surgical trauma with accidental cut of cranial nerve
Carotid endarterectomy
Cardiac surgery
Removal of head and neck tumors
Dental surgery
Head and neck injury
Motor vehicle accidents, blows to head, and falls

Question 67

Brainstem Stroke

Answer 67

Known as cerebrovascular accident (CVA)
Occurs with interruption of blood flow to brain as artery breaks or is blocked
Can affect cranial nerves directly
Degree of impairment depends on number of lower motor neurons that are lost to a stroke
Possible for single brainstem stroke to damage more than one cranial nerve

Question 68

Myasthenia Gravis

Answer 68

Affects neuromuscular junction
Caused by antibodies that block/damage muscle tissue
Temporary treatment
Injection of edrophonium chloride (Tensilon)

Symptoms
Rapid fatigue of muscular contractions over short time, with recovery after rest
Hypernasality; decreased loudness; breathy voice quality; decreased articulatory precision
Assessment
Stress test involving asking patient to count from 1 to 100 or to read lengthy paragraph

Question 69

Gillian Barre Syndrome

Answer 69

Results in demyelization
Frequently occurs after certain kinds of infections and immunizations
Symptoms
Flaccid dysarthria, dysphagia
Recovery
High recovery rate, lasting weeks or months
5% die in acute stages

Question 70

Polio

Answer 70

An infectious viral disease that attacks cell bodies of lower motor neurons
Most frequently affects cervical and thoracic spinal nerves, causing:
Labored inhalation during speech; shortened speech phrases; speaking on residual air; decreased loudness
Can also affect cranial nerves

Question 71

Other Causes of Flaccid Dysarthria

Answer 71

Tumors growing in or near brainstem
Muscular dystrophy
Causes progressive degeneration of muscle tissue
Can result in weakness in many muscles served by cranial nerves

Question 72

Progressive bulbar palsy

Answer 72

Can affect both upper and lower motor neurons, although often present only in lower motor neurons
With lower motor neuron damage, causes flaccid dysarthria
With upper and lower motor neuron involvement, causes mixed dysarthria (flaccid-spastic)

Question 73

Speech Characteristics of Flaccid Dysarthria

Answer 73

Not all individuals with flaccid dysarthria demonstrate deficits in all areas
Severity level within each area varies for each patient
Important to look for clusters of symptoms when trying to diagnose particular type of dysarthria

Question 74

Resonance

Answer 74

Reflects bilateral damage to pharyngeal branch of vagus nerve because innervates most muscles of velum
Hypernasality: most noticeable error
Nasal emission: weak velopharyngeal closure
Weak pressure consonants: decreased intraoral air pressure
Shortened phrases: wasted air that escapes through nasal cavity during speech

Question 75

Articulation

Answer 75

Imprecise consonant production
Large range of severity, from mild distortion to complete unintelligibility
Damage to facial and hypoglossal nerves
Bilateral damage to facial nerve
Damage to trigeminal nerve
– Difficulty elevating jaw sufficiently to bring articulators into contact with each other
May need to elevate jaw by hand or use “jaw sling”

Question 76

Phonation

Answer 76

Phonatory incompetence
Incomplete adduction of vocal folds during phonation
Caused by damage to recurrent branch of vagus nerve
Can result in breathy voice quality or whisper; weak or paralyzed adductor and abductor muscles
Combined presence of hypernasality and phonatory incompetence is strongest confirmatory sign of flaccid dysarthria as correct diagnosis

Question 77

Respiration

Answer 77

Weakened respiration may or may not be a component of flaccid dysarthria
Decreased inhalation or impaired control of exhalation during speech with damage to cervical and thoracic spinal nerves responsible for innervating diaphragm and intercostal muscles
Symptoms
Reduced loudness, shortened phrase length, strained vocal quality if speaking on residual air to prolong phrase length, monoloudness, monopitch
May inhale frequently while speaking, which can adversely affect prosody
May be difficult to determine whether due to poor laryngeal valving or weakened respiration

Question 78

Prosody

Answer 78

Weakened laryngeal muscles that are unable to make many fine vocal-fold adjustments necessary for normal pitch and loudness variations
Symptoms: monopitch, monoloudness
Not unique to flaccid dysarthria, so not definite diagnostic markers for flaccid dysarthria

Question 79

Key Evaluation Tasks for Flaccid Dysarthria

Answer 79

Conversational speech and reading
Can evoke errors of resonance (hypernasality), articulation (imprecise consonants), respiration (shortened phrase length), and prosody (monopitch, monoloudness)
Alternate motion rate (AMR) task
Will highlight a slowed rate of phoneme production

Prolonged vowel
Helpful in eliciting breathy voice quality heard in phonatory incompetence; also useful for observing respiratory weakness
Speech stress test
Necessary in suspected cases of myasthenia gravis

Question 80

Treatment of Motor Speech Disorders

Answer 80

The traditional approach to treating motor speech disorders is to
Use assessment data to identify deficits
Begin working with patients using appropriate treatment goals
Increase complexity of tasks as patients improve
Work toward generalization of improvements

Rosenbek (2017) refined this approach with six additional recommendations:
Help patients recognize differences in their speech
Help patients have a willingness to change their speech for the better
Work closely with patients when setting goals of treatment

Increasingly insist that patients are talking therapeutically in their sessions, eventually even while engaged in small talk
Ensure patients are learning to listen, evaluate, and self-correct their speech
Be sure to progressively add cognitive-linguistic load to treatment tasks to ensure patients are working toward generalization

Question 81

Treatment of Flaccid Dysarthria

Answer 81

Treatments for flaccid dysarthria are presented according to which cranial nerve or combination of nerves are damaged
Needs and abilities of patients vary greatly
Nonspeech oral strengthening exercises
Value of these open to question
General rule to follow: if improving speech production is the goal, treatment activities should concentrate directly on speech production

Question 82

Damage to Trigeminal Nerve

Answer 82

Unilateral damage
Negligible effect on speech production
Bilateral damage
Rare
Can leave jaw muscles very weak or, in severe cases, cause inability to close jaw
May need jaw sling to compensate

Question 83

Damage to Vagus Nerve

Answer 83

Affects glossopharyngeal and accessory cranial nerves
Close proximity to each other
Treatment for resonance
Velar strength-training procedure; modification of speech; reduce rate; more open-position mouth during speech; increase loudness
Treatments for phonation
Pushing and pulling procedures, holding breath, hard glottal attack, head turning and sideways pressure on the larynx
Treatments for prosodic deficits
Pitch range exercises, intonation profiles, contrastive stress drills, chunking utterances into syntactic units

Question 84

Damage to the Facial (VII) and Hypoglossal (XII) Cranial Nerves

Answer 84

Affects speech production primarily by decreasing lip strength and range of movement
Traditional articulation drills often recommended
Treatment for respiratory weakness
Correct posture, compensatory prosthetic devices, speaking immediately on exhalation, cueing for complete inhalation

Question 85

Summary of Flaccid Dysarthria

Answer 85

Flaccid dysarthria
Caused by any process that damages lower motor neurons used in speech production; lower motor neurons are found in certain cranial and spinal nerves
Speech characteristics of flaccid dysarthria include hypernasality, imprecise consonants, and breathy voice quality

Treatment for flaccid dysarthria
Can include tasks that attempt to strengthen weakened muscles; however, may be more productive to work on strategies that concentrate directly on increasing intelligibility of patient’s speech

Question 86

Neurologic Basis of Spastic Dysarthria

Answer 86

Bilateral damage to upper motor neuron tracts

Question 87

Role of UMN’s in Spastic

Answer 87

Bilateral damage to upper motor neurons of pyramidal/extrapyramidal neural pathways
Pyramidal system:
Damage can result in weak/slow skilled movements
Extrapyramidal system:
Damage can result in weakness, increased muscle tone (spasticity), and abnormal reflexes

Question 88

Significance of Bilateral Damage

Answer 88

Damage must be bilateral, affecting both left and right tracts of pyramidal and extrapyramidal systems
Results in combination of what would be expected if each system damaged unilaterally
Weakness and slowness, particularly in tongue and lips
Spasticity most noticeable in laryngeal muscles
Abnormal reflexes

Question 89

Causes of Spastic Dysarthria

Answer 89

Any injury that causes bilateral damage to upper motor neurons of pyramidal and extrapyramidal systems
Strokes
Degenerative diseases
Traumatic head injury
Infections of brain tissue
Tumors

Question 90

Stroke

Answer 90

Most common cause of spastic dysarthria
Will result in spastic dysarthria only when:
Two or more strokes occur in certain combinations in the cerebrum or a single stroke occurs in brainstem

Question 91

Amyotrophic Lateral Sclerosis (ALS)

Answer 91

Degenerative neurologic disease of unknown cause
Terminal, with average life expectancy of 22 months from time of onset
Causes spastic dysarthria when upper motor neuron involvement predominant
Eventually affects both upper and lower neurons, resulting in flaccid-spastic mixed dysarthria

Question 92

TBI

Answer 92

Can produce widespread injury to brain, causing bilateral damage to pyramidal and extrapyramidal systems

Question 93

Multiple Sclerosis

Answer 93

Suspected immunologic disorder resulting in inflammation or complete destruction of myelin sheath covering axons
With bilateral involvement to upper motor neurons, it can result in spastic dysarthria

Other Causes^^^
Brainstem tumor
Cerebral anoxia
Brain damage from lack of oxygen in blood
Viral infection in cerebral tissue
Bacterial infection in cerebral tissue

Question 94

Speech Characteristics of Spastic Dysarthria

Answer 94

Speech errors in spastic dysarthria result of:
Spasticity (stiffness)
Slowness
Weakness in vocal-tract muscles
Components of speech
Articulation, phonation, resonance, and prosody usually affected more than respiration

Question 95

Articulation (Spastic)

Answer 95

Articulation errors
Very common in spastic dysarthria
Imprecise consonant production
Most common articulation error
Result of abnormally short voice onset time for voiceless consonants, incomplete articulatory contact, incomplete consonant clusters
Vowel distortions

Question 96

Phonation (Spastic)

Answer 96

Harsh vocal quality
Most common phonatory error
Occurs when air leaks through partially open glottis during phonation
Strained-strangled vocal quality
Tight hyperadduction of vocal folds
Low pitch
Result of increased muscle tone in larynx

Question 97

Resonance (Spastic)

Answer 97

Hypernasality
Caused by spasticity in velar muscles, which slows and reduces range of soft palate movement and results in incomplete velopharyngeal closure during nonnasal speech sounds
Not as severe as with flaccid dysarthria
Generally does not include nasal emission

Question 98

Prosody (Spastic)

Answer 98

Monopitch
Caused by overall tenseness of laryngeal muscles, resulting in reduced ability to contract/relax to vary pitch
Monoloudness
Caused by overall increased muscle tone in laryngeal muscles
Short phrases
Natural consequence of speaking through abnormally tight larynx, making it difficult to use longer utterances
Slow rate of speech
Caused by reduced speed and range of movement

Question 99

Respiration (Spastic)

Answer 99

Problems of respiration do not play great role in spastic dysarthria
Abnormal respiratory movements causing
Reduced inhalation and exhalation
Uncoordinated breathing patterns
Reduced vital capacity
Phonation/prosody problems more likely result of hyperadduction of vocal folds than respiratory problem

Question 100

Additional Characteristics of Spastic Dsyarthria

Answer 100

Pseudobulbar affect
Uncontrollable crying or laughing that can accompany damage to upper motor neurons of brainstem
Appears to be caused by damage to part of brain important in inhibiting emotions
Drooling
Due to impaired oral control of saliva or less frequent swallowing

Question 101

Spastic Dysarthria VS Flaccid Dysarthria

Answer 101

Bulbar palsy
Atrophy and weakness in muscles innervated through medulla, including tongue, velum, larynx, and pharynx
Caused by damage to lower motor neurons
Pseudobulbar palsy
Weakness and slowness in same muscles
Caused by damage to upper motor neurons

Cause of damage
Spastic dysarthria: bilateral damage to upper motor neurons of pyramidal and extrapyramidal systems
Flaccid dysarthria: damage to lower motor neurons
Hypernasality
In spastic dysarthria not as severe and without nasal emission

Phonation
Spastic dysarthria: tight, strained-strangled; Flaccid dysarthria: breathy
Reflexes
Spastic dysarthria: hyperreflexes
Flaccid dysarthria: reduced or absent oral reflexes

Slow speech rate combined with harsh or strained-strangled voice only occurs in spastic dysarthria
Pseudobulbar affect and drooling associated with spastic dysarthria more than any other dysarthria

Question 102

Key Evaluation Tasks for Spastic Dysarthria

Answer 102

Conversational speech and reading
Assesses resonance, articulation, prosody
Alternate motion rate (AMR) task
Demonstrates slow rate of phoneme production
Vowel prolongation
Evokes phonatory deficits

Question 103

Treatment for Spastic Dysarthria

Answer 103

Patient specific
Primary treatment goals target:
Phonation
Articulation
Prosody
Resonance
Respiration usually not significantly affected

Question 104

Treatment of Phonation Deficits

Answer 104

Harsh or strained-strangled vocal quality caused by hyperadduction of vocal folds
Increased muscle tone in muscles of larynx cause vocal folds to involuntarily adduct too tightly during phonation
Exercises
Head and neck relaxation; easy onset of phonation; yawn-sigh exercises

Symptoms: weakness, reduced speed of movement, reduced range of movement
Imprecise consonant production: primary articulation error in spastic dysarthria
Stretching exercises
Tongue-stretching
Lip-stretching
Traditional articulation exercises

Question 105

Traditional Articulation Treatment

Answer 105

Recommended for imprecise consonant productions
Concentrate on increasing patient awareness of articulation errors and practicing best phoneme productions
Intelligibility drills, phonetic placement, exaggerating consonants, minimal contrast drills

Question 106

Treatment of Prosody Deficits

Answer 106

Activities that help patient regain vocal-tract flexibility needed to appropriately vary pitch and loudness
Pitch range exercises
Intonation profiles
Contrastive stress drills
Chunking utterances into syntactic units

Question 107

Treatment of Resonance Deficits

Answer 107

Hypernasality caused by slowness and reduced range of movement
Surgical and prosthetic treatments
Pharyngeal flap procedure, Teflon injections, palatal lift
Decreasing velar hypertonicity
Behavioral-based treatments
Visual feedback, increase loudness

Question 108

Summary
Spastic dysarthria

Answer 108

Caused by any process resulting in bilateral damage to pyramidal and extrapyramidal systems
Results in muscle weakness and slowness of articulators during speech (bilateral pyramidal damage) and increased muscle tone (spasticity) in articulators (bilateral damage to extrapyramidal system)

Spastic dysarthria (cont’d.)
Characterized by imprecise consonants, monopitch, monoloudness, reduced stress, and harsh vocal quality
Treatment concentrates on reducing increased muscle tone by relaxation and stretching; traditional articulation exercises can target imprecise consonant production

Question 109

Definitions of Unilateral Upper Motor Neuron Dysarthria

Answer 109

Motor speech disorder caused by damage to upper motor neurons on one side of brain that supply cranial and spinal nerves involved in speech production
Characterized by weakness in lower face, lips, and tongue on opposite side of lesion, resulting in deficits, specifically imprecise consonants

Question 110

Neurologic Basis of Unilateral Upper Motor Neuron Dysarthria

Answer 110

Most cranial nerves serving speech muscles (except lower face and tongue) receive bilateral innervation from upper motor neurons
Speech deficits after unilateral upper motor neuron damage usually less severe than with bilateral damage
Unilateral damage to upper motor neurons can cause obvious speech deficits
Damage to muscles of lower face and tongue
Cranial nerves serving these innervated primarily by upper motor neurons only on one side of brain
Severe cases of unilateral damage
Lower face and tongue may be paralyzed on affected side
Since upper motor neurons bilaterally innervate velum, pharynx, and larynx:
They should not be affected by unilateral upper motor neuron damage as sufficiently innervated from unaffected side
Reality: unilateral upper motor neuron damage appears to affect function of bilaterally innervated structures

Question 111

Causes of Unilateral Upper Motor Neuron Dysarthria

Answer 111

Any condition that damages upper motor neurons on one side of brain after damage to either left or right hemisphere
Pathologies causing focal lesions are most common cause

Question 112

Stroke

Answer 112

Most frequent cause of unilateral upper motor neuron dysarthria
Stroke causing this dysarthria can occur almost anywhere in brain that contains upper motor neurons: many cortical and subcortical areas, brainstem, internal capsule
Strokes involving frontal lobe are leading cause of unilateral upper motor neuron dysarthria

Question 113

Tumors

Answer 113

Not a common cause of this dysarthria
Brain tumor can cause focal, unilateral upper motor neuron damage resulting in this dysarthria

Question 114

Traumatic Brain Injury

Answer 114

Not a common cause, as most traumatic brain injury results in diffuse damage affecting both hemispheres
Possible to have head injury with lesion restricted primarily to one side of brain
Damage affects upper motor neurons unilaterally either at cortical, subcortical, or brainstem level

Question 115

Speech Characteristics of Unilateral Upper Motor Neuron Dysarthria

Answer 115

In most cases, results in mild or moderate speech production errors
Often short-term for mildly impaired patients, with recovery over days or weeks
More serious cases
Co-occurs with other disorders, such as aphasia, apraxia, limb hemiparesis, visual deficits, or cognitive impairments
Co-occurring speech and language disorders may be difficult to clearly diagnose this dysarthria because patient’s output may be limited
Dysarthria may take “back seat” to other deficits

Question 116

UMN Dysarthria: Articulation

Answer 116

Unilateral upper motor neuron dysarthria primarily a disorder of articulation
Affects tongue and lower face much more than any other speech structure
Causes of articulation deficits due to:
Weakness
Reduced range of motion
Decreased fine motor control of tongue
Imprecise consonant production: primary difficulty
Irregular articulatory breakdowns
Slow alternate motion rates (AMRs)
Irregular AMRs

Question 117

UMN Dysarthria: Phonation

Answer 117

Mild to moderate harsh vocal quality
Suggests larynx sometimes can be affected by unilateral upper motor neuron damage even though bilaterally innervated
Reasons for harsh vocal quality
Result of mild vocal-fold weakness or spasticity
Previously unknown lesion present with new
Dysphonia
General medical condition not attributed to upper motor neuron damage

Question 118

UMN Dysarthria: Resonance

Answer 118

Hypernasality
Unilateral upper motor neuron damage may cause mild muscular weakness in velum

Question 119

UMN Dysarthria: Prosody and Respiration

Answer 119

Rarely impaired in this dysarthria
When prosody affected, most likely cause is slightly slow rate of speech
Respiration rarely affected due to widely distributed innervation of intercostal muscles and bilateral innervation of diaphragm

Question 120

Key Evaluation Tasks for Unilateral Upper Motor Neuron Dysarthria

Answer 120

Medical records
Conversational speech or reading paragraph
AMR tasks
Prolonged vowel

Question 121

Treatment for Unilateral Upper Motor Neuron Dysarthria

Answer 121

Often other coexisting deficits are allotted bulk of treatment time
Articulation may be so minor that SLP may decide not to treat it
Intelligibility drills
Phonetic placement
Exaggerating consonants
Minimal contrast drills

Question 122

UMN Dysarthria Summary

Answer 122

Cause: damage to upper motor neurons on only one side of brain
Almost exclusively disorder of articulation
In left hemisphere co-occurs with aphasia and apraxia; in right hemisphere co-occurs with visual and cognitive deficits associated with injury to that side of brain
Treatment: traditional articulation tasks

Question 123

Definitions of Ataxic Dysarthria

Answer 123

Motor speech disorder often due to damage to cerebellum or its neural pathways
Results in speech errors that are primarily articulatory and prosodic, giving speech unsteady, slurred quality

Question 124

Neurologic Basis of Ataxic Dysarthria

Answer 124

Caused by damage to cerebellum or neural pathways that connect cerebellum to other parts of central nervous system
“Ataxia”: widespread incoordination; Greek word for “lack of order”
Cerebellum
Primary function: coordinate timing and force of muscular contractions
Processes sensory information from all over body and integrates information into execution of movement

Question 125

Neural Pathways to and from the Cerebellum

Answer 125

Cerebellum
Attached to brainstem
Communicates with rest of CNS through three bundles of neural tracts called cerebellar peduncles

Inferior peduncle allows cerebellum to:
Receive sensory information from entire body about position of body parts
Recognize what body is doing during movement and whether motor impulse to muscles is accomplishing intended result
Monitor timing and force of movements while performed

Middle peduncle allows cerebellum to:
Receive preliminary information from cortex regarding planned movements
Coordinate planned movements by integrating sensory information from body with individual’s experience of what appropriate movement should be, smoothing and refining according to current conditions

Superior peduncle allows cerebellum to:
Have main output to rest of CNS
Send its processed motor impulses to motor areas of cortex, completing corticocerebellar control circuit

Cerebellar control circuits: neurons that course through three cerebellar pathways
Not called upper motor neurons because do not synapse with lower motor neurons

Question 126

The Cerebellum and Speech

Answer 126

Two ways cerebellum influences speech movements
Through corticocerebellar control circuit
Planned motor impulses of planned speech act sent from cortex to cerebellum
Cerebellum coordinates and refines preliminary movements
Coordinated motor impulses then sent to thalamus for more refinement before sent to motor cortex and then to muscles
Two ways cerebellum influences speech movements (cont’d.)
Through its connections to extrapyramidal system
Makes rapid adjustments in timing and force of movements to compensate for unexpected changes in circumstances of movement

Question 127

Causes of Ataxic Dysarthria

Answer 127

Causes of Ataxic Dysarthria
Damage to cerebellum or its control circuits causing difficulties coordinating voluntary movements
Cerebellar ataxia: movement deficits of timing, force, range, and direction
Vermis: midpoint of cerebellum between cerebellar hemispheres upon which speech coordination is highly dependent

Question 128

Degenerative Diseases

Answer 128

Autosomal dominant cerebellar dysfunction of late onset
Hereditary disease usually beginning in middle age
Idiopathic sporadic late-onset cerebellar ataxia
Similar to autosomal dominant cerebellar dysfunction, but does not include as many neurologic symptoms
Friedreich’s ataxia
Progressive hereditary disease affecting spinal cord as well as cerebellum
Olivopontocerebellar degeneration
Progressive cerebellar disorder that runs in families

Question 129

Stroke

Answer 129

Stroke
Cerebellum has rich arterial blood supply
Arteries serving cerebellum:
Superior cerebellar, anterior inferior cerebellar artery
Ataxic dysarthria can result in:
Blockage to arteries serving cerebellum, ruptured aneurysms, arteriovenous malformations
Cerebellar signs: limb ataxia, problems with balance, visual deficits, ataxic dysarthria

Question 130

Toxic Conditions

Answer 130

Toxic conditions
–Most treatable with ataxic dysarthria resolving as toxic levels decrease
Lead and mercury poisoning
Long- and short-term alcohol consumption
Exposure to chemicals such as acrylamide and cyanide
–Toxic levels that may not be irreversible
Phenytoin (Dilantin): antiseizure drug

Metabolic conditions
Vitamin E or B12 deficiency
Severe cases of hypothyroidism
Hereditary disorders such as Wilson’s disease

Question 131

Traumatic Head Injury

Answer 131

Trauma to cerebellum tends to be diffuse, as with most head injuries
Cerebellar peduncles especially vulnerable to twisting and rotational forces because cerebellum essentially an appendage attached to brainstem

Question 132

Tumors

Answer 132

Extent of ataxic dysarthria depends on location and size of tumor
Tumor can affect cerebellar function by:
Growing in cerebellar tissue, perhaps directly destroying and compressing cerebellum
Growing near cerebellum, thereby compressing cerebellar tissue
Interfering with functions of cerebellar control circuits

Metastatic tumors: among most common
Formed when primary tumor sheds cancerous cells that seed a secondary (metastatic) tumor
Low-grade actrocytoms
Slow-growing type of tumor appearing frequently in cerebellum, especially in children
Hemangioblastomas
Benign tumors of proliferated blood vessels found occasionally in cerebellum

Other Possible Causes
–Not common
Viral infections invading cerebellum
Infections such as trichinosis, typhus, and syphilis
Bacterial abscess near cerebellum that compresses surrounding brain tissue

Question 133

Speech Characteristics of Ataxic Dysarthria

Answer 133

Movements appear poorly coordinated
Problems controlling timing/force for speech
Slurred, monotonous articulation
Primarily disorder of articulation and prosody
Scanning speech:
Term to describe ataxic dysarthria, describing slow, deliberate production of syllables, with each syllable in word receiving equal stress

Question 134

Ataxic Dysarthria: Articulation

Answer 134

Articulation deficits significant problem
Imprecise consonant production
Most prevalent speech error
Distorted vowels
Imperfect articulation gives ataxic dysarthria slurred quality
Caused by cerebellar damage disrupting timing, force, range, and direction of movements
Irregular articulatory breakdowns
Imprecise consonant and vowel productions vary from utterance to utterance
Decomposition of movement: manifestations of cerebellar dysfunction, where instead of smooth coordinated movements, they are distinct and jerky

Question 135

Ataxic Dysarthria: Prosody

Answer 135

Equal and excess stress
Distinguishing characteristic of ataxic dysarthria
Prolonged phonemes and prolonged intervals between phonemes
Slow movement on both single and repetitive motion tasks; hypotonia
Monopitch and monoloudness
Caused by hypotonia of speech muscles

Question 136

Ataxic Dysarthria: Phonation

Answer 136

Few phonatory deficits noted in ataxic dysarthria
Harsh vocal quality
Caused by decreased muscle tone in laryngeal and respiratory structures, preventing full contraction of these muscle groups
Voice tremor

Question 137

Ataxic Dysarthria: Resonance

Answer 137

Hypernasality
Seldom serious problem in ataxic dysarthria
Hyponasality
Intermittent
Caused by timing errors between muscles of velum and other muscles of articulation

Question 138

Ataxic Dysarthria: Respiration

Answer 138

Uncoordinated movements in respiratory muscles, contributing to speech deficits
Paradoxical movements: movements that occur when muscles work against each other rather than in coordination
Paradoxical movements of intercostal muscles and diaphragm
Leads patient to speak on residual air, which can lead to increased rate of speech, decreased loudness, and harsh vocal quality

Question 139

Key Evaluation Tasks for Ataxic Dysarthria

Answer 139

Speech alternate motor tasks
Slower than normal, difficulty maintaining steady rhythm with repetition
Severe cases: speed up abruptly then unexpectedly slow down
Reading, conversational speech, and repeating sentences containing numerous multisyllabic words

Question 140

Treatment of Ataxic Dysarthria

Answer 140

Damage affects speed, force, and timing of movements of articulators, resulting in uncoordinated movement
Most evident speech errors related to articulation and prosody

Question 141

Treatment of Ataxic Dysarthria: Respiration

Answer 141

Do not need to address strengthening respiration
Concentrate on controlling airflow more accurately during speech, as uncoordinated movements of respiratory muscles cause speech on residual air, affecting prosody and phonation

Tasks to help improve breath control during speech
Slow and controlled exhalation
Speak immediately on exhalation
Stop phonation early
Optimal breath group: teaching how may syllables or words can be said clearly on one full inhalation

Question 142

Treatment of Ataxic Dysarthria: Prosody

Answer 142

Prosodic problems involve:
Rate, stress, and intonation
By slowing rate, can improve intelligibility
By incorporating more typical stress and intonation into utterances, speech may exhibit more natural quality

Rate control
–Slow, irregular rate characteristic of ataxic dysarthria, but may attempt to speak too rapid for speech capabilities
Articulators are not given enough time to reach target positions
Listener not given enough time to assimilate spoken message

Rate control tasks
Reciting syllables to a metronome
Finger or hand tapping
Cued reading material
Used with written sentences or paragraphs
–Clinician points to word or syllable at desired rate
–Slash marks or spaces to indicate necessary pauses when reading

Stress and intonation
–Concentrate on developing more natural pitch and loudness variations in connected speech
Stress and intonation exercises
Contrastive stress drills
Pitch range exercises
Intonation profiles
Chunking utterances into syntactic units

Question 143

Treatment of Ataxic Dysarthria: Articulation

Answer 143

May improve with slowed rate
Need to concentrate directly on improving production of phonemes
Articulation tasks
Intelligibility drills
Phonetic placement
Exaggerating consonants (overarticulation)
Minimal contrast drills

Question 144

Summary of Treatment of Ataxic Dysarthria

Answer 144

Summary
Ataxic dysarthria caused by any process resulting in damage to cerebellum or cerebellar control circuits
Common causes include degenerative diseases and stroke
Articulation and prosody most significantly affected

Speech characteristics include imprecise consonant production and irregular articulatory breakdowns
Treatment concentrates on:
Controlling respiration for speech
Increasing articulatory accuracy
Developing optimal rate and intonation in connected speech

Question 145

Definitions of Hyokinetic Dysarthria

Answer 145

Caused by any process that damages basal ganglia (extrapyramidal system)
Speech characteristics: harsh vocal quality, reduced stress, monoloudness, imprecise consonants
May manifest in any or all levels of speech
Most evident in voice, articulation, and prosody
Reflects effects of rigidity, reduced force and range of movement, and slow but sometimes fast repetitive movements

Question 146

Neurologic Basis of Hypokinetic Dysarthria

Answer 146

Unique, as only dysarthria with:
Increased rate as symptom
Mainly one causative factor (parkinsonism)
Symptoms affect muscles of speech
Symptoms caused by dysfunction to basal ganglia or to basal ganglia’s neural connections to other parts of CNS
Hypokinetic (less motion

Question 147

Characteristics of Parkinsonism

Answer 147

Distinctive collection of symptoms
Resting tremor
Bradykinesia: slow, reduced range of movement
Rigidity
Spasticity
Akinesia: delay in initiation of movements
Postural reflexes

Question 148

Causes of Parkinsonism

Answer 148

Caused by dysfunction in basal ganglia
Depends on balanced interaction of several neurotransmitters, including dopamine (inhibitory) and acetylcholine (excitatory)
Reduction of dopamine in striatum
Causes too much acetylcholine
Thought to be primary cause of rigidity, bradykinesia, and other symptoms of parkinsonism
Varied causes of reduced dopamine

Question 149

Causes of Hypokinetic Dysarthria

Answer 149

Parkinsonism: collective term for different disorders sharing many similar symptoms
Major causes of hypokinetic dysarthria
Idiopathic Parkinson’s disease
Neuroleptic-induced parkinsonism
Postencephalitic parkinsonism
Traumatic head injury
Toxic metal poisoning
Stroke

Question 150

Speech Characteristics of Hypokinetic Dysarthria

Answer 150

Quite distinctive
Most noticeable errors: prosody and articulation
Most errors result of bradykinesia, akinesia, and muscle rigidity
In severe cases tremors cause tremulous phonations

Prosody: monopitch, reduced stress, and monoloudness most common
Articulation: imprecise consonants, repeated phonemes, palilalia
Phonation: harsh/breathy quality, aphonia, low pitch
Respiration: sometimes noted
Resonance: if present, mild hypernasality
Significant individual differences

Question 151

Key Evaluation Tasks for Hypokinetic Dysarthria

Answer 151

Conversational speech and reading
Evoke many errors of prosody
Detect short rushes
Speech alternate motion rates (AMRs)
Highlight articulation errors
Vowel prolongations
Assess vocal quality

Question 152

Treatment of Hypokinetic Dysarthria

Answer 152

Divided into three categories
Pharmacologic
Most widely used
L-Dopa
Surgical
Ablation procedures (making lesion in basal ganglia)
Deep brain stimulation
Behavioral: speech-language therapy

Question 153

Pharmacologic Treatments of Parkinsonism

Answer 153

Replacing dopamine in striatum
Problem: direct dosages of dopamine unable to reach striatum
Precursor of dopamine, L-dopa used to reach striatum and then converted to dopamine
Correct neurotransmitter imbalance by decreasing acetylcholine activity in striatum
Anticholinergic drugs
Sometimes combined with L-dopa treatment

Question 154

Surgical Treatments for Parkinsonism

Answer 154

Complicated and invasive
Used when patient incapacitated and medications ineffective
Two general types
Ablative surgery (thalamotomy and pallidotomy)
Deep brain stimulation

Question 155

Stem-Cell Implantation

Answer 155

Stem cells unique as can transform themselves into different types of cells
Found naturally in embryos, in adult tissues, and can be grown in labs
Significant amount of research concentrated on using stem cells to treat parkinsonism
Results preliminary but encouraging
Few human trials conducted

Question 156

Behavioral Treatments for Parkinsonism

Answer 156

Behavior- and instrumentation-based tasks important part of clinical treatment plan
Articulation
Most common deficit: imprecise consonants due to reduced range of motion in articulators
Compounded by increased rate
Treatment types
Rate reduction, stretching, traditional articulation tasks

Phonation
Adduct vocal folds only partially or have harsh or breathy vocal quality
Combined with poor respiratory support; results in significantly reduced loudness
Activities to more fully adducted position
Pushing and pulling procedure; hard glottal attack; voice amplifiers; instrumental biofeedback; Lee Silverman Voice Treatment

Respiration
Shallow breath support can cause shortened phrases and decreased loudness
Respiratory treatments
Speaking immediately on exhalation
Cueing for complete inhalation
Slow and controlled exhalation
Stop phonation early
Optimal breath group

Prosody
Improved by slowing rate
Intonation profiles
Contrastive stress drills
Chunking utterances into syntactic units

Question 157

Summary of Hypokinetic Dysarthria

Answer 157

Caused by processes that damage basal ganglia
Closely associated with parkinsonism
Idiopathic Parkinson’s disease most common cause
Speech characteristics vary widely among individuals
Treatment involves targeting articulatory precision, phonatory effort, and natural prosody

Question 158

Definitions of Hyperkinetic Dysarthria

Answer 158

Perceptually distinguishable group of motor speech disorders manifested in any or all levels of speech
Most caused by dysfunction in basal ganglia
All produce involuntary movements that interfere with normal speech production
“Hyperkinetic”: “too much movement”
Each hyperkinetic movement disorder has its own involuntary motions

Question 159

Neurologic Basis of Hyperkinetic Dysarthria

Answer 159

Many disorders that cause hyperkinetic dysarthria associated with damage to basal ganglia

Question 160

What Causes Hyperkinetic Movement?

Answer 160

Basal ganglia not well understood
Complex mechanisms within basal ganglia not well understood
Different disorders associated have nearly opposite effects on movement (example: Parkinson’s and Huntington’s)
Cause more complicated than a simple imbalance of one or two neurotransmitters

Question 161

Causes of Hyperkinetic Dysarthria

Answer 161

Chorea
Myoclonus
Tics
Essential tremor
Dystonia
Other causes: degenerative diseases, traumatic head injury, stroke, and infections

Question 162

Chorea

Answer 162

Movement disorder distinguished by random involuntary movements of limbs, trunk, head, and neck
Choreic motions
Appear dancelike, smooth, and coordinated, but actually unpredictable, purposeless, and sometimes jerky or abrupt

Sydenham’s chorea
Rare disorder affecting children after rheumatic fever
Huntington’s disease
Progressive inherited disorder
Stroke: rare for stroke to cause chorea
Tardive dyskinesia
Caused by taking certain antipsychotics

Question 163

Speech Characteristics of Hyperkenetic Dysarthria of Chorea

Answer 163

Degree of chorea influences how severely speech is affected
Distinctive speech errors include:
Prolonged intervals between syllables and words; variable speech rate; inappropriate silences; excess loudness variations; prolonged phonemes; rapid, brief inhalations or exhalations of air; voice stoppages; and intermittent breathy voice quality

Question 164

Myoclonus

Answer 164

Hyperkinetic movement disorder distinguished by involuntary and brief contractions of part, whole, or group of muscles in same area
Muscle contractions may appear singly, in repeating irregular pattern, or rhythmically
Can appear as part of many conditions:
Kidney failure, epilepsy, cerebral anoxia, strokes, traumatic head injury, and progressive neurologic diseases

Question 165

Tic Disorders

Answer 165

Tic: rapid movement that can be controlled voluntarily for a time, but performed frequently due to compulsive desire
Cause traced to mild brain damage or toxic reactions to medications in some cases, but no identifiable CNS disorder in most cases

Question 166

Essential (or Organic Tremor)

Answer 166

Benign hyperkinetic movement disorder that causes tremulous movements in affected body parts
Idiopathic
Most common hyperkinetic movement disorder

Question 167

Dystonia

Answer 167

Hyperkinetic movement disorder of muscle tone
Causes involuntary, prolonged muscle contractions that interfere with normal movement or posture
Slower, more sustained quality than seen in chorea, with contractions that wax and wane during ongoing movement
Sensory tricks may be helpful

Disorders that have dystonia as a characteristic:
Spasmodic torticollis
Drug-induced dystonia
Meige syndrome
Spasmodic dysphonia

Question 168

Speech Characteristics of Hyperkinetic Dysarthria of Dystonia

Answer 168

Articulation: imprecise consonants, distorted vowels, irregular articulatory breakdowns, prolonged phonemes
Prosody: monopitch, monoloudness, inappropriate silences, shortened phrases
Phonation: harsh vocal quality, strained-strangled quality, excess loudness variation
Respiration and resonance: less impacted

Question 169

Key Evaluation Tasks for Hyperkinetic Dysarthria

Answer 169

Vowel prolongation
Alternate motion rates (AMRs)
Conversational speech and reading
Careful observation of associated involuntary movements

Question 170

Treatment of Hyperkinetic Dysarthria

Answer 170

Diverse treatment options
Based on medical or behavioral interventions

Question 171

Medical Treatments (Hyperkinetic Dysarthria)

Answer 171

Pharmacologic
Drugs that suppress involuntary movements that cause speech deficits
Botox: most successful
Deep brain stimulation

Question 172

Behavioral Treatments for Huntington’s Disease

Answer 172

Early stages: maintain normal prosody and optimal rate
Middle stages: rate of speech, rhythmic breathing and relaxation, speaking on exhalation
Progressive dementia: work closely with caregivers

Question 173

Behavioral Treatment for Dystonia

Answer 173

Sensory tricks: idiosyncratic strategies that can suppress involuntary movement for a time
Bite blocks: to stabilize jaw during speech
Easy onset of phonation

Question 174

Behavioral Treatments for Tic Disorders

Answer 174

Behavioral treatments have been effective in some cases
Habit reversal training
Relaxation therapy may be helpful when combined with other treatment procedures
Exposure response prevention
Comprehensive behavioral intervention for tics

Question 175

Summary of Hyperkinetic Dysarthria

Answer 175

Collection of separate dysarthrias, each associated with hyperkinetic movement disorder
Caused by involuntary movements interfering with voluntary attempts at speech
Effects of each disorder on speech production vary
Many associated with damage to basal ganglia
Most common treatment is drug-based

Question 176

Definitions of Mixed Dysarthria

Answer 176

Motor speech disorder
Occurs when neurologic damage extends into two or more parts of motor system
Characterized by combination of characteristics in single (pure) dysarthria

Question 177

Neurologic Basis of Mixed Dysarthria

Answer 177

Neurologic damage crossing anatomical boundaries, affecting various components of motor system
Any combination of pure dysarthrias
Prominence of each pure dysarthria within mixed dysarthria varies significantly among individuals
Prominence of one dysarthria type can change over time

Question 178

Causes of Mixed Dysarthria

Answer 178

Caused by various disorders affecting two or more parts of motor system
Examples include:
Single or multiple strokes
Brain tumors
Traumatic head injuries
Degenerative diseases
Infectious diseases

Multiple sclerosis
Progressive demyelinating disease
Can occur in brainstem, cerebellum, cerebral hemispheres, and spinal cord
Can cause any pure or any combination of mixed dysarthria
Ataxic-spastic most common

Multisystems atrophy
Collective term for group of degenerative disorders, many including parkinsonian symptoms
Shy-Drager syndrome
Progressive supranuclear palsy
Olivopontocerebellar atrophy

Amyotrophic lateral sclerosis (ALS)
Progressive degeneration of any of four areas of motor neurons
Often progresses from affecting two motor neuron groups to all four
Mixed dysarthria predominates throughout much of this disorder

Wilson’s disease
Very rare hereditary disease preventing normal metabolism of dietary copper
Penicillamine successful in treating most patients
Dysarthria one of earliest signs
Ataxic-spastic-hypokinetic present in many

Friedreich’s ataxia
Rare, inherited, progressive disorder
Causes neuron degeneration in cerebellum, brainstem, and spinal cord
Untreatable, fatal
Ataxic-spastic dysarthria most prevalent mixed dysarthria

Question 179

Treatment of Mixed Dysarthria

Answer 179

Treating mixed dysarthria challenging
Many speech errors
Difficult to determine where to start

General rule: first treat component most severely affecting speech production
Dworkin (1991) suggested when elements of mixed dysarthria affect speech production equally, treat in following order:
Respiration, resonation, phonation, articulation, prosody
Rationale: prior speech components foundation for others
Other caveats:
Given multiple problems in single component of speech production, treat most severe first
Patient may have strong preference for what needs to be treated initially
Patient’s attention or memory deficit may make working on one deficit too difficult

Augmentative communication for patients with ALS
Communicative stages of patient with ALS
Responsibility of SLP changes within each stage
Progression variable

Question 180

Summary
Mixed dysarthria

Answer 180

Mixed dysarthria occurs with damage to more than one portion of motor system
Extent and location of neurologic damage determine combination of pure dysarthrias to be components of mixed dysarthria
One speech components may be more noticeable

Many conditions cause mixed dysarthria
ALS and MS are common degenerative diseases that cause mixed dysarthria
Treatment sequence is to first treat component contributing most to speech deficits
If elements equally affected, use sequence of respiration, resonation, phonation, articulation, prosody

Question 181

Definition of Apraxia of Speech

Answer 181

Pure apraxia of speech rare
Disorder of motor timing and sequencing
Not caused by:
Muscle weakness
Abnormal muscle tone
Reduced range of movement
Decreased muscle steadiness

Question 182

Overview of Motor Sequencing

Answer 182

Two main types of apraxia
Ideational apraxia
Uncommon; disturbance in conception of object or gesture
Ideomotor apraxia
Disturbance in performance of movements needed to use object, make gesture, sequence movements
Typically affects voluntary movements
Subcategories: limb apraxia, nonverbal oral apraxia, apraxia of speech

Question 183

Neurological Basis of Apraxia of Speech

Answer 183

Motor speech programmer
Neural network in brain that sequences motor movements needed to produce speech
First analyzes linguistic, motor, sensory, and emotional information
Near perisylvian area of left hemisphere

Question 184

Causes of Apraxia of Speech

Answer 184

Disorders that damage motor speech programmer
Caused by:
Stroke (most common)
Degenerative disease
Trauma
Tumor

Question 185

Speech Characteristics of Apraxia of Speech

Answer 185

Primarily disorder of articulation and prosody
Slow, labored, halting speech
Instances of groping
Some say inconsistent speech errors, but research suggests fairly consistent for location and type in repeated trials

Question 186

Speech Characteristics of Apraxia of Speech

Answer 186

Severe and mild apraxia demonstrate fewest characteristics
Errors of:
Articulation: most common
Prosody: frequently abnormal
Respiration: may have difficulty taking deep breath on command
Resonance and phonation: seldom issues

Question 187

Assessment of Apraxia of Speech

Answer 187

Sequential motion rate task (SMRs)
Sensitive assessment, especially when compared with alternating motion rate (AMR) tasks
Conversational speech and reading aloud
Determine effects of prosody
Repeating words of increasing length
Reading or repeating low-frequency, multisyllabic words in isolation or sentences

Question 188

Differential Diagnosis of Apraxia of Speech

Answer 188

Diagnosis only when determined significant number of patient’s speech errors match those known to apraxia of speech
Four categories of behaviors determine correct diagnosis
Primary clinical characteristics
Nondiscriminitive clinical characteristics
Behaviors usually found in disorders other than apraxia of speech
Behaviors that rule out presence of apraxia of speech

Question 189

Additional Diagnostic Considerations

Answer 189

Rule out other conditions that cause movement difficulties similar to those seen in apraxia
Muscle weakness
Sensory loss
Comprehension deficit
Incoordination
Differentiating between apraxia of speech and aphasia
Three situations present difficulties when making differential diagnosis
Pure apraxia of speech, aphasia alone, or aphasia and apraxia of speech
Apraxia of speech from literal paraphasic errors of aphasia
Apraxia of speech from nonfluent language errors of Broca’s aphasia

Differentiating between apraxia of speech and dysarthria
Speech errors in apraxia increase as word length and complexity increase; errors of dysarthria fairly constant
Muscle range of motion, tone, coordination, and strength are within normal limits in apraxia of speech; at least one muscle quality impaired in nearly all dysarthrias
–Apraxia of speech primarily affects articulation and prosody; dysarthria can affect all five
–Apraxia of speech can have articulatory groping
–Apraxia usually occurs with damage to perisylvian area of language dominant hemisphere; dysarthria can be result of diverse damage
–Apraxia of speech co-occurs more frequently with aphasia than dysarthria
–Patient with apraxia of speech produce automatic speech and emotional speech with few errors, while those with dysarthria typically demonstrate same errors regardless of whether overlearned or emotional in nature

Question 190

Treatment of Apraxia of Speech

Answer 190

Mostly behaviorally based procedures to help select and sequence speech sounds correctly
Mostly 1:1 intensive treatments

Question 191

Guiding Principles of Treating Apraxia of Speech

Answer 191

Goal: help patient relearn motor sequences to produce phonemes accurately
Not all patients candidates for therapy
Treatment:
Sequenced to maintain success
Repetitive and intensive drill
Patients learn to self-monitor
Concentrate on functional words

Question 192

Specific Treatments

Answer 192

Articulatory kinematic treatments
Concentrate on improving timing and placement of articulatory movements through modeling, positioning of articulators, and repetition
Rate and rhythm procedures
Assume apraxia of speech primarily result of timing errors
Alternative and augmentative communication
Recommended with limited verbal communication
Intersystemic facilitation and reorganization treatment
Patient’s communicative strengths used to assist verbal speech

Question 193

Summary Apraxia of speech

Answer 193

Disorder of motor sequencing
Not caused by muscle weakness, abnormal muscle tone, reduced range of movement, or decreased muscle steadiness
Subcategory of ideomotor apraxia
Disturbance in performance needed to complete action
Numerous potential causes: stroke most common
Primarily disorder of articulation and prosody
Motor speech programmer
Neural network to control sequencing of speech movement
When diagnosing, important to eliminate condition that cause speech errors similar to those in apraxia of speech
Many treatments available