Motor Speech Flashcards
(193 cards)
1
Q
The Motor System
A
*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
2
Q
Components of Motor System
A
*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
3
Q
Brain
A
*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
4
Q
Cerebrum
A
*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)
5
Q
Cerebral Cortex
A
*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
6
Q
Brainstem
A
*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
7
Q
Cerebellum
A
*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
8
Q
Types of Neurons
A
–Motor neurons
–Sensory neurons
–Interneurons
–Efferent neurons
–Afferent neurons
9
Q
Other Nervous System cells
A
–Glial cells
–Schwann cells
–Microglia
–Oligodendroglia
–Astrocytes
10
Q
Tracts
A
–Bundles of axons found in the CNS
11
Q
Nerves
A
–Bundles of axons found in the CNS
12
Q
Neurotransmitters
A
–Small substance released at end points once charge reaches axon’s terminal ramifications
–Two important neurotransmitters in the motor system: acetylcholine and dopamine
13
Q
Summary of Motor System Components
A
*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
14
Q
Desire to Move
A
*Starting place for any voluntary movement
*Taking desire and turning it into movement is often done easily but is extremely complex
15
Q
Primary and Association Cortices
A
*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
16
Q
Basal Ganglia and Cerebellum
A
*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
17
Q
Thamalmus
A
*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
18
Q
Primary Motor Cortex
A
*Receives neural motor impulses that have been processed, smoothed, and coordinated by basal ganglia, cerebellum, and thalamusP
19
Q
Descending Motor Tracts
A
*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
20
Q
Cranial and Spinal Nerves
A
*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
21
Q
Neuromuscular Junction
A
*Point where axons of lower motor neurons make synaptic connections with muscle cells
22
Q
Summary of Motor System
A
*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
23
Q
Assessment Questions Foundations:
A
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?
24
Q
Goals of a Motor Speech Evaluation
A
*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
25
Speech Production Components and Disorders
*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
26
Assessment component: Respiration
*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
27
Assessment component: Phonation
*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
28
Assessment component: Resonance
*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
29
Assessment component: Articulation
*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)
30
Assessment component: Prosody
*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
31
Standardized Test for Dysarthria
*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
32
Standardized Test for
Apraxia of Speech
*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
33
Conducting a Motor Speech Evaluation
*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
34
Muscle Strength
*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
35
Speed of Movement
*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)
36
Range of Movement
*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
37
Accuracy of Movement
*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
38
Motor Steadiness
*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
39
Muscle Tone
*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
40
Instructions for the Motor Speech Examination
*Evaluation takes 30-40 minutes
*Short version
–Evaluation takes 10-15 minutes
41
Background Information and
Medical History
*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
42
Face and Jaw Muscles at Rest and During Movement
*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?
43
Tongue at Rest and During Movement
*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?
44
Velum and Pharynx at Rest and During Movement
*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?
45
Laryngeal Function
*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?
46
Auditory-Perceptual Evaluations of the Motor Speech Mechanism
In many cases, the clinician’s ear is the best instrument for evaluating motor speech deficits
47
Phonatory-Respiratory System
*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
48
Resonation System
*Assesses velopharyngeal function
*Specific tasks
–Take deep breath and say /u/ as long as possible
–Same task as above, but clinician squeezes nose
49
Combined Systems (Phonation, Respiration, Resonation, Articulation)
*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
50
Stress Testing of the Motor Speech Mechanism
*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
51
Testing for Nonverbal Oral Apraxia
*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
52
Testing for Apraxia of Speech
*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
53
Analysis of Connected Speech
*Clinician records patient reading a standard reading passage
*Rate patient performance on the qualities listed (e.g., Are vowels and consonants produced clearly?)
54
Summary of AOS
*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
55
Definition of Flaccid Dysarthria
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
56
Neurologic Basis of Flaccid Dysarthria
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
57
Cranial Nerves of Speech Production
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
58
Trigeminal nerve (V)
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
59
Facial Nerve
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
60
Glossopharyngeal cranial nerve
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
61
Vagus Cranial Nerve
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
62
Accessory Cranial Nerve
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
63
Hypoglossal cranial nerve
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
64
Spinal Nerves
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
65
Causes of Flaccid Dysarthria
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
66
Physical Trauma
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
67
Brainstem Stroke
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
68
Myasthenia Gravis
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
69
Gillian Barre Syndrome
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
70
Polio
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
71
Other Causes of Flaccid Dysarthria
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
72
Progressive bulbar palsy
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)
73
Speech Characteristics of Flaccid Dysarthria
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
74
Resonance
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
75
Articulation
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”
76
Phonation
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
77
Respiration
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
78
Prosody
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
79
Key Evaluation Tasks for Flaccid Dysarthria
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
80
Treatment of Motor Speech Disorders
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
81
Treatment of Flaccid Dysarthria
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
82
Damage to Trigeminal Nerve
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
83
Damage to Vagus Nerve
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
84
Damage to the Facial (VII) and Hypoglossal (XII) Cranial Nerves
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
85
Summary of Flaccid Dysarthria
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
86
Neurologic Basis of Spastic Dysarthria
Bilateral damage to upper motor neuron tracts
87
Role of UMN’s in Spastic
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
88
Significance of Bilateral Damage
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
89
Causes of Spastic Dysarthria
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
90
Stroke
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
91
Amyotrophic Lateral Sclerosis (ALS)
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
92
TBI
Can produce widespread injury to brain, causing bilateral damage to pyramidal and extrapyramidal systems
93
Multiple Sclerosis
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
94
Speech Characteristics of Spastic Dysarthria
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
95
Articulation (Spastic)
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
96
Phonation (Spastic)
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
97
Resonance (Spastic)
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
98
Prosody (Spastic)
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
99
Respiration (Spastic)
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
100
Additional Characteristics of Spastic Dsyarthria
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
101
Spastic Dysarthria VS Flaccid Dysarthria
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
102
Key Evaluation Tasks for Spastic Dysarthria
Conversational speech and reading
Assesses resonance, articulation, prosody
Alternate motion rate (AMR) task
Demonstrates slow rate of phoneme production
Vowel prolongation
Evokes phonatory deficits
103
Treatment for Spastic Dysarthria
Patient specific
Primary treatment goals target:
Phonation
Articulation
Prosody
Resonance
Respiration usually not significantly affected
104
Treatment of Phonation Deficits
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
105
Traditional Articulation Treatment
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
106
Treatment of Prosody Deficits
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
107
Treatment of Resonance Deficits
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
108
Summary
Spastic dysarthria
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
109
Definitions of Unilateral Upper Motor Neuron Dysarthria
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
110
Neurologic Basis of Unilateral Upper Motor Neuron Dysarthria
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
111
Causes of Unilateral Upper Motor Neuron Dysarthria
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
112
Stroke
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
113
Tumors
Not a common cause of this dysarthria
Brain tumor can cause focal, unilateral upper motor neuron damage resulting in this dysarthria
114
Traumatic Brain Injury
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
115
Speech Characteristics of Unilateral Upper Motor Neuron Dysarthria
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
116
UMN Dysarthria: Articulation
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
117
UMN Dysarthria: Phonation
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
118
UMN Dysarthria: Resonance
Hypernasality
Unilateral upper motor neuron damage may cause mild muscular weakness in velum
119
UMN Dysarthria: Prosody and Respiration
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
120
Key Evaluation Tasks for Unilateral Upper Motor Neuron Dysarthria
Medical records
Conversational speech or reading paragraph
AMR tasks
Prolonged vowel
121
Treatment for Unilateral Upper Motor Neuron Dysarthria
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
122
UMN Dysarthria Summary
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
123
Definitions of Ataxic Dysarthria
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
124
Neurologic Basis of Ataxic Dysarthria
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
125
Neural Pathways to and from the Cerebellum
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
126
The Cerebellum and Speech
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
127
Causes of Ataxic Dysarthria
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
128
Degenerative Diseases
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
129
Stroke
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
130
Toxic Conditions
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
131
Traumatic Head Injury
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
132
Tumors
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
133
Speech Characteristics of Ataxic Dysarthria
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
134
Ataxic Dysarthria: Articulation
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
135
Ataxic Dysarthria: Prosody
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
136
Ataxic Dysarthria: Phonation
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
137
Ataxic Dysarthria: Resonance
Hypernasality
Seldom serious problem in ataxic dysarthria
Hyponasality
Intermittent
Caused by timing errors between muscles of velum and other muscles of articulation
138
Ataxic Dysarthria: Respiration
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
139
Key Evaluation Tasks for Ataxic Dysarthria
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
140
Treatment of Ataxic Dysarthria
Damage affects speed, force, and timing of movements of articulators, resulting in uncoordinated movement
Most evident speech errors related to articulation and prosody
141
Treatment of Ataxic Dysarthria: Respiration
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
142
Treatment of Ataxic Dysarthria: Prosody
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
143
Treatment of Ataxic Dysarthria: Articulation
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
144
Summary of Treatment of Ataxic Dysarthria
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
145
Definitions of Hyokinetic Dysarthria
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
146
Neurologic Basis of Hypokinetic Dysarthria
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
147
Characteristics of Parkinsonism
Distinctive collection of symptoms
Resting tremor
Bradykinesia: slow, reduced range of movement
Rigidity
Spasticity
Akinesia: delay in initiation of movements
Postural reflexes
148
Causes of Parkinsonism
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
149
Causes of Hypokinetic Dysarthria
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
150
Speech Characteristics of Hypokinetic Dysarthria
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
151
Key Evaluation Tasks for Hypokinetic Dysarthria
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
152
Treatment of Hypokinetic Dysarthria
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
153
Pharmacologic Treatments of Parkinsonism
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
154
Surgical Treatments for Parkinsonism
Complicated and invasive
Used when patient incapacitated and medications ineffective
Two general types
Ablative surgery (thalamotomy and pallidotomy)
Deep brain stimulation
155
Stem-Cell Implantation
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
156
Behavioral Treatments for Parkinsonism
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
157
Summary of Hypokinetic Dysarthria
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
158
Definitions of Hyperkinetic Dysarthria
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
159
Neurologic Basis of Hyperkinetic Dysarthria
Many disorders that cause hyperkinetic dysarthria associated with damage to basal ganglia
160
What Causes Hyperkinetic Movement?
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
161
Causes of Hyperkinetic Dysarthria
Chorea
Myoclonus
Tics
Essential tremor
Dystonia
Other causes: degenerative diseases, traumatic head injury, stroke, and infections
162
Chorea
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
163
Speech Characteristics of Hyperkenetic Dysarthria of Chorea
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
164
Myoclonus
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
165
Tic Disorders
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
166
Essential (or Organic Tremor)
Benign hyperkinetic movement disorder that causes tremulous movements in affected body parts
Idiopathic
Most common hyperkinetic movement disorder
167
Dystonia
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
168
Speech Characteristics of Hyperkinetic Dysarthria of Dystonia
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
169
Key Evaluation Tasks for Hyperkinetic Dysarthria
Vowel prolongation
Alternate motion rates (AMRs)
Conversational speech and reading
Careful observation of associated involuntary movements
170
Treatment of Hyperkinetic Dysarthria
Diverse treatment options
Based on medical or behavioral interventions
171
Medical Treatments (Hyperkinetic Dysarthria)
Pharmacologic
Drugs that suppress involuntary movements that cause speech deficits
Botox: most successful
Deep brain stimulation
172
Behavioral Treatments for Huntington’s Disease
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
173
Behavioral Treatment for Dystonia
Sensory tricks: idiosyncratic strategies that can suppress involuntary movement for a time
Bite blocks: to stabilize jaw during speech
Easy onset of phonation
174
Behavioral Treatments for Tic Disorders
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
175
Summary of Hyperkinetic Dysarthria
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
176
Definitions of Mixed Dysarthria
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
177
Neurologic Basis of Mixed Dysarthria
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
178
Causes of Mixed Dysarthria
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
179
Treatment of Mixed Dysarthria
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
180
Summary
Mixed dysarthria
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
181
Definition of Apraxia of Speech
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
182
Overview of Motor Sequencing
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
183
Neurological Basis of Apraxia of Speech
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
184
Causes of Apraxia of Speech
Disorders that damage motor speech programmer
Caused by:
Stroke (most common)
Degenerative disease
Trauma
Tumor
185
Speech Characteristics of Apraxia of Speech
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
186
Speech Characteristics of Apraxia of Speech
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
187
Assessment of Apraxia of Speech
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
188
Differential Diagnosis of Apraxia of Speech
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
189
Additional Diagnostic Considerations
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
190
Treatment of Apraxia of Speech
Mostly behaviorally based procedures to help select and sequence speech sounds correctly
Mostly 1:1 intensive treatments
191
Guiding Principles of Treating Apraxia of Speech
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
192
Specific Treatments
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
193
Summary Apraxia of speech
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
