SPH 378 Notes Semester 2 Exam Notes

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NEUROGENIC/MOTOR SPEECH DISORDERS
INTRODUCTION
Common Neuropathologies of Speech and Language Revision
1. Cerebro-vascular Accidents (CVA) Stroke
2. Intracranial tumours
3. Hydrocephaly
4. Infections
5. Toxaemia
6. Metabolic disorders
7. Feeding disorders
8. Degenerative diseases
9. Traumatic brain injuries (TBI)
Symptom development
Rapid
• Over minutes/hours→ occlusive vascular disease (large arteries)
Rapid and uninterrupted

• Over days/weeks → infection, rapidly growing tumours
Gradual
• Over months/years, punctuated with periods of remission ranging from weeks to months →
occlusive vascular disease (smaller arteries)
Gradual and uninterrupted

• Over months/years → slowly, progressive degenerative disease
• E.g. Alzheimer’s disease
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Definitions of Specific Neurogenic Communication Disorders Revision
Language Disorders
Definitions and Common Aetiologies of Neurogenic Language of Disorders
1. Aphasia
a. Broca’s Aphasia
b. Wernicke’s Aphasia
c. Global Aphasia
2. Right Hemisphere Syndrome
3. Traumatic Brain Injury
4. Dementia
Speech Disorders
Motor Speech Disorders
“… speech disorders resulting from neurologic impairments affecting the motor planning,
programming, neuromuscular control, or execution of speech.” (Duffy, 2013, p. 4)
“First, motor refers to the part of the nervous system that controls voluntary movements.
Neuroanatomists call this portion of the nervous system the “motor system.” Speech is
communication through the use of vocal symbols, sometimes also defined as the physical production
of language. Disorders means an abnormality of function; the plural form of the word indicates that
there is more than one abnormality in this condition. Motor speech disorders, therefore, are a
collection of speech production deficits that are caused by the abnormal functioning of the motor
system.” (Freed, 2020)
• Developmental and/or Acquired Disorders

• Can co-occur with Language Disorders
Dysarthria /Anarthria
“… a collective name for a group of speech disorders resulting from disturbances in muscular control
over the speech mechanism due to damage of the central or peripheral nervous system. It
designates problems in oral communication due to paralysis, weakness, or incoordination of the
speech musculature”
Speech Subsystems and Musculature involved

Speech acquisition and refinement is dependent upon the development and growth of the
subsystems of speech production.
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]
• Anatomy of speech production is a “performance” anatomy (Bosma, 1975) – structures are

formed through use. The eventual size and shape of structures are determined by their
different functions, e.g. aerodigestive system -> chew and swallow.
• Changes (growth and development) happen slowly – time to adapt and refine.
• Speech functions depend on maturation of the speech production system.
Speech-motor control must adapt to the (anatomical and) physiological changes.
Definition and Principles of Motor learning:

Motor learning is defined as the “process of acquiring the capability for producing skilled actions”
(Schmidt, 1988, p. 345).
• experience and practice

• speed, effectiveness, accuracy and generalisation
• precursors to motor learning
• modelling rather than instruction
• motor skills vs. motor learning
• variation
• feedback
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• rate
• habituation
Speech is the externalized expression of language and speech sensorimotor control can be defined
as the motor-afferent mechanisms that direct and regulate speech movements (Netsell, 1988, p.
247; Van der Merwe in McNeil, 2010, p. 4).
As a motor skill, speech is “goal directed” and “afferent-guided”, and it meets the general
requirements of a fine motor skill, e.g. (i) it is performed with accuracy and speed, (ii) uses
knowledge of results, (iii) is improved by practice, (iv) demonstrates motor flexibility in achieving
goals, and (v) relegates all of this to automatic control, where “consciousness” is freed from the
details of action plans (Netsell, 1988, p. 250; Van der Merwe in McNeil, 2010, p. 4).
Speech-motor events have to be coordinated and produced in such a way that the desired acoustic
result is achieved.
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Dyspraxia / Apraxia
“A neurologic speech disorder reflecting an impaired capacity to plan or program sensorimotor
commands necessary for directing movements that result in phonetically and prosodically normal
speech. It can occur in the absence of physiologic disturbances associated with the dysarthrias and
… any components of language.”
Models of Communication And Speech Production

Caruso, A.J., & Strand, E.A. (1999).
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Van der Merwe, A. (2010).
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1. Cognitive and Linguistic Aspects of the Framework
2. Motor Aspect of the Framework
a. Sensorimotor Planning
b. Sensorimotor Programming
c. Sensorimotor Execution
3. Speech Movements
Motor-Speech Disorders vs. Other Communication Disorders

Other Neurologic Disorders
Other Neurologic Speech Disturbances
• Several disturbances of speech neither clearly represent nor traditionally have been defined
as MSDs. They are nonetheless neurologic in origin and distinct in their clinical
characteristics. These deficits include, but may not be limited to, acquired neurogenic
stuttering, palilalia, echolalia, some forms of mutism, foreign accent syndrome, and
aprosodia associated with right hemisphere dysfunction.
Cognitive, Linguistic, and Cognitive-Linguistic Disturbances

• Changes in speech resulting from language and other cognitive deficits (e.g., aphasia,
akinetic mutism, and other cognitive and affective disturbances that attenuate or inhibit
speech) are sometimes difficult to distinguish from MSDs.
• In addition, because they often co-occur with MSDs, they can complicate examination and
diagnosis.
Sensory Deficits
• The effect of congenital deafness, for example, on the development of speech can be
profound; even deafness acquired in adulthood can result in some degradation of speech.
The effects of hearing loss on speech production, however, are distinguishable in many ways
from MSDs.
• Tactile, kinesthetic, and proprioceptive sensations are also important to the development
and maintenance of normal speech, and their malfunction has been implicated in certain
MSDs. Therefore, it is important to think of motor speech processes and disorders as
sensorimotor, and not just motor, in nature.
Nonneurologic Disturbances
Some influences on speech are not fully captured by cognitive-linguistic or motor speech processes.
Some are localized in the body but not in the nervous system. Others reside in the “mind” but are
neither neuromotor nor specifically cognitive-linguistic in character.
Musculoskeletal Defects (e.g., Laryngectomy, Cleft Lip and Palate, Fractures, Abnormal Variants of
Cavity Size and Shape)
The integrity of muscle, cartilage, and bone is important to normal speech; injury, disease,
congenital absence, loss to aging or poor care (e.g., teeth), or surgical removal of muscle, cartilage,
or bone can alter speech. Other physical influences, such as abnormal variations in the size and
shape of primary speech structures or the effects of systemic illness, also can alter speech in ways
that exceed, mask, or exacerbate the effects of focal neuropathologies on speech.
Nonneurologic or Nonpsychogenic Voice Disorders

Certain voice disorders could actually be subsumed under the musculoskeletal defects just
described. They are given separate recognition here, however, because they can be misinterpreted
as reflecting neuropathology. These disorders include, for example, dysphonias associated with head
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or neck neoplasms, vocal abuse, or hormonal disturbances. Their diagnosis may be established by
history or during direct laryngeal examination, and experienced clinicians often can hear that the
dysphonia is not neurologic.
Psychogenic and Related Nonorganic Speech Disorders

• Speech can undergo change as a result of abnormal psychiatric states (e.g., schizophrenia,
depression, conversion disorder). It can also change as a result of faulty subconscious
“learning” or compensation in response to various physical, neurologic, or psychologic
influences, sometimes in people who are otherwise psychologically healthy. The speech
manifestations of these disorders can be difficult to distinguish from those stemming from
neurologic disease.
• Because these problems reside in the mind, they are arguably neurologic if one believes that
the mind and brain are inextricably linked. Because they are not fundamentally neuromotor
in nature, however, it is important to distinguish them from MSDs.
• Psychogenic and related nonorganic voice and speech disorders are not uncommon in
medical practices, and not infrequently they accompany neurologic abnormalities. Their
recognition and management are important in medical speech pathology practices.
Normal Variations In Speech Production

Age-Related Changes in Speech
• Normal aging is associated with changes in speech and language that are physiologically,
acoustically, and perceptually detectable. They include, at the least, changes in pitch, voice
quality and stability, loudness, speech breathing patterns, rate, fluency, and prosodic
variations.
• Because neurologic disorders often are overlaid on an aging nervous system and because
some speech changes associated with aging are similar to those associated with dysarthria,
the identification of a speech characteristic as abnormal and possibly indicative of dysarthria
requires an awareness of the range of normal for a given age and general physical condition.
Unfortunately, many of these judgments depend on subjective clinical experience, because
objective measures either are not easily obtained in clinical settings or are associated with
extreme variability of normative data.
Gender
• The speech of men and the speech of women are perceptually distinguishable, and the
differences can influence the detection of abnormalities, at least with some methods of
analysis. For example, acoustic indices of laryngeal abnormalities may differ among men and
women with the same neurologic disease, and some of the acoustic heterogeneity within
specific categories of dysarthria may be explained by gender.
• Whether gender differences influence the clinical perceptual diagnosis of motor speech
disorders is uncertain, but it is nonetheless important to keep them in mind.
Variations in Style
• Speech varies as a function of personality, emotional state, and speaking role.
• Such variations often and justifiably go unnoticed by clinicians and researchers intent upon
recognizing abnormality, but sometimes they must be identified explicitly for accurate
differential diagnosis.
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Basic Definitions (Adult vs Paediatric)
Motor speech disorders (MSDs) can be defined as speech disorders resulting from neurologic
impairments affecting the planning, programming, control, or execution of speech. MSDs include the
dysarthrias and apraxia of speech.
Dysarthria is a collective name for a group of neurologic speech disorders that reflect abnormalities
in the strength, speed, range, steadiness, tone, or accuracy of movements required for the
breathing, phonatory, resonatory, articulatory, or prosodic aspects of speech production. The
responsible neuropathophysiologic disturbances of control or execution are due to one or more
sensorimotor abnormalities, which most often include weakness, spasticity, incoordination,
involuntary movements, or excessive, reduced or variable muscle tone.
For the purpose of this introductory chapter, we will define apraxia of speech as a neurologic speech
disorder that reflects an impaired capacity to plan or program sensorimotor commands necessary
for directing movements that result in phonetically and prosodically normal speech. It can occur in
the absence of physiologic disturbances associated with the dysarthrias and in the absence of
disturbance in any component of language.
Unlike dysarthria, the existence of apraxia of speech as a distinct clinical entity often is ignored
outside the speech pathology literature. Consequently, its distinctive clinical manifestations
frequently are buried within categories of aphasia or under the generic heading of “dysarthria”. This
is unfortunate, because the nature of apraxia of speech is different from that of aphasia and
dysarthria; its localization is quite different from that for most types of dysarthria; and its
management is different from that for dysarthria and aphasia.
Prevalence and Distribution of Disorders

Motor speech disorders are associated with various congenital and acquired conditions that involve
the central and/or peripheral nervous or related systems.
The most common conditions existing in the paediatric and adult population are cerebral palsy and
cerebrovascular accidents.
An analysis of the adult patient caseload recorded at the Mayo-clinic (USA) between 1987-90 and
1993-2001 showed that motor speech disorders represented a significant portion (41%) of the
acquired speech, voice, language and cognitive conditions seen (Duffy, 2005, p. 7-8).
The research showed that motor speech disorders (dysarthria and apraxia) account for 57% of the
acquired neurogenic communication disorders (Duffy, 2013, p. 6).
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Categorizing Motor Speech Disorders
(Duffy, 2013, p. 9-11; Johns, 1985, p. 98-99; Love, 2000, p. 11-14)
Motor speech disorders can be described according to different dimensions, e.g. neurological or
etiological characteristics, or symptoms and signs of speech production.
The following neurological and aetiological variables should be considered (Duffy, 2013, p. 10-11):
a) age of onset,
b) course,
c) site of lesion,
d) (neurological) diagnosis,
e) pathophysiology,
f) speech components involved,
g) severity, and
h) perceptual characteristics
a) Age of onset
MSDs can be congenital (or developmental) or acquired. This distinction can influence management
decisions and prognosis. However, time of onset in acquired disorders is almost always relatively
clear, and it rarely challenges clinical diagnosis beyond a careful history and neurologic examination.
Clinicians should recognize the distinction, but it is not usually difficult to establish.
b) Course
MSDs can be congenital (e.g., cerebral palsy); chronic or stationary (e.g., cerebral palsy in adults;
patients who have reached a plateau after a stroke); improving (e.g., during spontaneous recovery
from a stroke or closed head injury); progressive or degenerative (e.g., amyotrophic lateral sclerosis
or PD); or exacerbating-remitting (e.g., multiple sclerosis). Monitoring MSDs over time may actually
help establish the course of disease or help eliminate diagnoses incompatible with a particular
course. In many cases, by the time a patient is seen for speech evaluation, the course is already
established. Nonetheless, the course of a problem has an important influence on management
decisions.
c) Site of lesion
Lesions associated with MSDs can include such diverse loci as the neuromuscular junction, the
peripheral and cranial nerves, the brainstem, the cerebellum, the basal ganglia, the pyramidal or
extrapyramidal pathways, and the cerebral cortex. Establishing the lesion site is a primary goal of
neurologic evaluation and one to which distinguishing among MSDs can contribute. Conversely,
knowledge of the lesion site can predict certain speech deficits. Incompatibility of speech findings
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with known or postulated lesion sites can raise doubts about presumed localization or suggest the
presence of additional lesions or even different diseases. For example, the presence of a mixed
hypokinetic-spastic-ataxic dysarthria in someone with a diagnosis of PD should raise questions about
the neurologic diagnosis or suggest the presence of neurologic dysfunction beyond that explainable
by PD alone.
d) Neurologic diagnosis
Broad categories of neurologic disease include degenerative, inflammatory, toxic-metabolic,
neoplastic, traumatic, and vascular etiologies. Within each of these broad categories, more specific
diagnoses are applied. By itself, an MSD usually is not diagnostic of a particular neurologic etiology
or specific disease. Because many diseases can affect multiple or variable portions of the nervous
system, it is neither particularly useful nor feasible to classify MSDs by disease (e.g., the dysarthria of
multiple sclerosis, or the dysarthria of stroke). At the same time, some dysarthria types are found
very commonly in some neurologic diseases and rarely or never in others (e.g., when PD causes
dysarthria, its type is hypokinetic; when myasthenia gravis causes dysarthria, its type is always
flaccid). Therefore, identification of a specific MSD may provide confirmatory evidence for disease
diagnosis.
e) Pathophysiology.
It is presumably the underlying pathophysiology (e.g., weakness, spasticity) that determines the
distinctive pattern of speech deficits associated with each MSD. Therefore, the presence of certain
speech abnormalities, or patterns of them, suggests one or more pathophysiologic disturbances and
vice versa.
Variables relevant to the speech disorders themselves include the following:
f) Speech components involved

MSDs can be categorized according to the speech subsystems that are affected. Knowing whether
speech breathing, phonation, resonance, or articulation is impaired can contribute to speech
diagnosis and often influences management.
g) Severity
Severity, by itself, does not differentiate among MSDs, because each one can vary along the full
severity continuum. It can raise questions about diagnosis, however. For example, speech
characteristics that suggest profound weakness are usually accompanied by physical findings that
confirm the weakness. If the physical examination is incompatible with underlying weakness, it may
be necessary to consider another cause (e.g., psychogenic or maladaptive speaking strategies).
Severity is relevant to management decisions. Coupled with information about diagnosis and the
course of disease, severity helps determine when management is necessary, whether it will be short-
term or long-term, whether it should focus on improving speech or developing augmentative forms
of communication, and so on.
h) Perceptual characteristics.
We have established that the perceptual characteristics of speech are crucial to differential diagnosis
and management. Because of its firm grounding in clinical research, because it has been heuristically
valuable to the acoustic and physiologic study of MSDs, and because it is so salient to daily clinical
activity, the perceptually based classification scheme of DAB forms the framework around which
MSDs are discussed in the textbook.
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I C F / ICF-CY Model and Neurogenic Communication Disorders
Interactions between the elements are dynamic but do not necessarily have a predictable one-to-
one relationship. It is possible to have an impairment that does not limit activity participation.
Influences on Health & Well-Being:

1. Health Condition:
• affects body functions or structures to varying degrees
• limits ability to engage in activity (what person can do)
• restricts participation in range of typical occupations (what person does do)
2. Environmental Factors:
• physical environment (space)
• social (values / beliefs / attitudes / inclusion)
• culture
• political / organisational
3. Personal Factors:
• attitudes to illness / wellness
• attitude to disability
• expectations
Model Descriptors
“Body Function and Structure” – Impairment (1º/2º)
• loss or abnormality of body structure, physiological or psychological function
“Activity”
• nature and range of individual’s functionality, e.g. walking (mobility), speaking
(communication), tooth brushing (self-care)
• activity can be limited in terms of duration and quality
• activity limitations / limitations in environment is possible
“Participation”
• Societal level: inclusion / access to resources
• nature and extent of a person’s involvement in life roles / society
“Environmental Factors”
• physical / social and attitudes
• individual
o home, school, workplace
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o objects / equipment used in daily life
• services and systems
o social / health / housing
o communication / transport systems
o media / law / legal services
o official / unofficial rules and legislation
“Personal Factors”
• e.g. age, race, gender, culture, beliefs and values, educational and social background,
experiences, personality, character style, aptitudes, lifestyle habits, upbringing, coping
styles, profession, past and current experience. (List by group from Netherlands)
Application: Example
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Will not be asked, but it is
assumed that you already
ANATOMY AND PHYSIOLOGY OF RESPIRATION know and understand this.
SPH 121: ANATOMY and PHYSIOLOGY OF RESPIRATION
1. Introduction
Humans must breathe to maintain body systems that are dependent on efficient oxygen exchange.
As humans, we also use the respiratory system to provide an energy source for oral communication.
Respiration is defined as “the exchange of gases between an organism and its environment. We
bring oxygen to the cells of the body to sustain life by breathing in, the process of inhalation, and
eliminate waste products by breathing out, or exhalation” (Seikel, King & Drumright, 2010, p. 35).
The lungs are found within the thorax, which has the first rib and clavicle as its superior border and
the twelfth rib as its inferior border. The lateral and anterior aspects are made up of the ribs and
sternum. The thorax is suspended from the vertebral (spinal) column.
2.1 The support structure of respiration

1) Vertebral column
The functional unit of the vertebral column is the vertebra (plural = vertebrae) or
vertebral column segment. The vertebral column has five divisions: cervical (C1 –
C7), thoracic (T1 – T12), lumbar (L1 – L5), sacral (S1 – S5) and coccygeal (coccyx).
The vertebrae are numbered sequentially from superior to inferior by section, so

that the uppermost cervical vertebra is C1, the second is C2, and so forth to C7.
Likewise for the thoracic vertebrae, the lumbar vertebrae and the sacral
vertebrae. The coccygeal vertebrae are considered to be a fused unit, and are
therefore known as the coccyx.
The vertebral column is composed of 33 segments of bone with a rich set of fossa
and protuberances clearly designed for function. Although vertebrae have roughly
the same shape, their form and landmarks vary depending on the location and
the area they serve, their attachments (such as the ribs), and their neural load.
• C2 also called the axis – vertebra on which skull pivots
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• T1-T12 form posterior point of attachment for ribs and provide basis for respiratory
framework
• L1-L5 provide direct and indirect attachment for posterior fibres of diaphragm, back
muscles, abdominal muscles
Landmarks of vertebra:
• Spinous process
• Transverse processes (on both sides)
• Corpus (body)
• Vertebral foramen (opening through which spinal cord tracts pass)
• Intervertebral foramina (openings through which spinal nerves exit/enter spinal cord)
• Superior and inferior articular facets (allows for limited movement between vertebrae)
The vertebral column houses the spinal cord, with spinal nerves emerging and entering the spinal
cord through spaces between the vertebrae.
The ribs of the rib cage articulate with the spinal column in a fashion that permits the rib cage some
limited movement for respiration.
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2) Pelvic (hip) girdle and pectoral (shoulder) girdle
The vertebral column is central to the body, and if we are to interact physically with our
environment, we must attach appendages to this column. The lower extremities are attached to this
axis by means of the pelvic girdle, and the upper extremities are attached through the pectoral
girdle.
3) Ribs and rib cage

Ribs are capable of a degree of movement so that the rib cage
can rock up in front and flare out via lateral rotation, being
hinged on the vertebral articulation with the rib cage.
Ribs are of three general classes: true ribs, false ribs and
floating ribs. The true (or vertebrosternal) ribs consist of the
upper ribs (1 – 7), all of which form a more or less direct
attachment with the sternum. The false (or vertebrochondral)
ribs (8 – 10) are also attached to the sternum through cartilage,
although this chondral portion must run superiorly to attach to
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the sternum. The floating (or vertebral ribs) (11 – 12) articulate only with the vertebral column.
The rib cage is made up of 12 pairs of ribs (12 on each side of the body) which are attached
posteriorly to the vertebral column. Each rib generally consists of four components: the head, neck,
shaft and angle.
The elastic properties of cartilage permit the ribs to be twisted on the long axis (torqued) without
breaking. Thus, the rib cage is quite strong (being made up predominantly of bone), but capable of
movement (being well-endowed with resilient cartilage).
The rib cage provides a point of attachment for the muscles that provide strength, rigidity, continuity
and mobility to rib cage. It also serves a protective function (heart and lungs) and provides the basis
for respiration.
The cartilaginous attachment of the ribs to the sternum permits the ribs to rotate slightly during
respiration, allowing the rib cage to elevate during inhalation (ribs slope slightly downward at rest).
This elevation of the rib cage provides an increase in lung capacity for respiration.
The sternum has three components:

• manubrium sterni: attached to clavicle and first rib
• corpus (body): ribs 3-7 directly attached, ribs 8-9 indirectly attached
• xiphoid (ensiform process)
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4) The soft tissue of the thorax and airways
Deep to the rib cage lays the core of respiration. Gas exchange for life occurs within the lungs
(spongy, elastic tissue that is richly perfused with vascular supply and air sacs). Healthy, young lungs
are pink, whereas older lungs that have undergone the stresses of modern, polluted life are
distinctly gray.
Communication between the lungs and the external environment is by means of the airways, which
includes the oral and nasal cavities, larynx, trachea and bronchial tubes.
a. The trachea
The trachea is a flexible tube, which is approximately 11cm in length and composed of a series of 16
to 20 tracheal rings (hyaline cartilage rings) that are connected by continuous mucous membrane
lining, which provides both continuity and flexibility. The cartilage provides support, while the
membrane allows for freedom of movement. The tracheal rings are open in the posterior aspect,
which allows for expansion and contraction of the diameter of the ring. Increase and decrease of the
diameter of the ring is largely controlled by the trachealis muscle.
This trachea runs from the inferior border of the larynx for about 11cm, where it bifurcates (divides)
at a point known as the carina trachea, to become the left and right main stem bronchi (or bronchial
tubes), which serve the left and right lungs respectively.
b. The lungs
The lungs consist of blood, arterial and venous network, connective tissue, respiratory pathway and
specialized tissue. The right lung consists of three lobes (superior, middle and inferior lobes), while
the left lung has two lobes (superior and inferior lobes). The space on the left side is taken up by
heart and mediastinal structures or “middle space” (oesophagus, trachea, blood vessels).
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The main stem bronchi bifurcate to form lobar (intermediate) bronchi which serve the lobes of the
lungs. Further branching occurs until the final division ends in the terminal bronchioles, which
becomes the alveolar duct, which communicates with the alveoli.
The alveolar lining is made up of two types of cells:

a) Type I pneumocytes – directly involved in gaseous exchange
b) Type II pneumocytes – secrete surfactant which reduces surface tension, so promoting the
inflation of the alveoli
Communication between the external and internal environment is thus by means of the trachea and
the bronchial tree (in the lungs).
c. Filtering structures
The airway has multiple filtering functions to safeguard the lungs against pollutants. The following
structures serve to protect the lungs against pollutants:
• Nostril hairs
• Mucous membrane lining the upper airway system
• Cilia
• Beating epithelia
• Lymphatic system
2.2 The movement of air though the system

The lungs are covered with pleural linings which, in conjunction with the thoracic wall, provide the
mechanism for air movement through muscular action. When the diaphragm contracts, the lungs
are pulled down because of the association between the pleurae and the diaphragm. Diaphragmatic
contraction expands the lungs, drawing air into them through the bronchial passageway.
2.3 Muscles of inhalation

As with many voluntary functions, inhalation is a graded activity. Depending on the needs of your
body, you are capable of quiet inhalation, which requires only one muscle, and forced inhalation,
which calls on many more muscles.
1) The primary muscle of inhalation – Thorax

The primary muscle of inhalation is the diaphragm (the dividing line between the thorax and the
abdomen). The fibres of the diaphragm pull on the central tendon, resulting in the downward
motion of the diaphragm during inhalation. This movement expands the lungs in the vertical
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dimension and distends the abdomen simultaneously. The diaphragm is innervated by the phrenic
nerve (arising from the cervical plexus of spinal nerves).
2) Accessory muscles of inhalation

Although the diaphragm is the major contributor to inhalation, it needs assistance to meet the needs
of your body for forced inhalation. Generally, muscles of the thorax and neck that elevate and
expand the rib cage and serve some accessory function for inhalation.
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2.4 Muscles of forced exhalation
To inflate the lungs, you need to expand the cavity that holds them so air can rush in. To do this, you
either increase the long dimension by contracting the diaphragm, or you can elevate the rib cage
with just a little bit more effort. Forced exhalation reverses this process by pulling the thorax down
and in and by forcing the diaphragm higher into the thorax.
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PHYSIOLOGY
Respiration requires muscular effort, and the degree to which an individual can successfully control
that musculature determines, in large part, the efficiency of respiration itself. Respiration is the force
behind speech production.
Humans are capable of quiet respiration as well as forced inhalation and exhalation. Quiet
inhalation will utilise the diaphragm and often the external intercostals, but forced inhalation will
use many of the accessory muscles. Exhalation may be passive, driven by the forces of torgue,
elasticity, and gravity. Muscles that reduce the size of the thorax can also be used; they compress
the abdomen or pull the rib cage down, subsequently forcing the air out of the lungs beyond that
which is expired in passive exhalation.
Terminology:
• Torque – twisting of the chondral portion of the ribs, while the osseous portion does not
move
• Elasticity – lungs are highly elastic and tend to expand as soon as the compression (which
occurs during inhalation) is released
• Gravity – causes the ribs to be pulled back after they have been expanded during inhalation,
maximizes lung capacity by pulling down abdominal viscera
During the process of inhalation:

• The rib cage is raised against gravity
• The chondral portions of the ribs are twisted
• The viscera are compressed
• The alveoli are inflated against the resistance of the surface tension
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During exhalation:
• The forces of gravity and elasticity drives the process of exhalation
• The muscles relax and the lungs are deflated (muscles reduce the size of thorax)
• The rib cages is pulled downwards and the diaphragm is pushed higher into the thorax
• Untorquing of ribs occurs
• When passive expiratory forces reach resting level, the respiratory cycle is repeated.
3.1 Respiration for life

It is obvious that respiration is vital. The goal of respiration is:
• oxygenation of blood
• elimination of carbon dioxide
1) The basic process of gas exchange has four stages:

ventilation, distribution, perfusion and diffusion.
a) Ventilation – refers to the actual movement of air in the airway. It occurs as a result of the action
of the diaphragm and the muscles of respiration.
b) Distribution – the air is distributed to over the 300 million alveoli where the oxygen-poor vascular
supply from the right pulmonary artery is perfused to the 6 billion capillaries that supply those
alveoli.
c) Perfusion is the migration of fluid through a barrier
d) Diffusion – gas exchange across the alveolar-capillary membrane (i.e. migration or mixing of one
material, e.g. oxygen, through another)
2) Respiratory cycle
During quiet respiration, adults will complete between 12 and 18 cycles of respiration per minute. A
cycle of respiration is defined as one inhalation and one exhalation.
The following figure displays the volume of two cycles of quiet respiration.
This quiet breathing pattern is known as quiet tidal respiration and it involves about 500ml (½ litre)
of air with each cycle. A quick calculation will reveal that humans process something on the order of
6000-8000 ml (6 – 8 litres) of air every minute. Because these values are based on quiet, sedentary
breathing, they will increase during strenuous work.
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3.2 Volumes and capacities
Respiration is the product of a number of forces and structures, and for us to make sense of them,
we need to define some volumes and capacities of the lungs.
1) Volumes
Volumes indicate arbitrary partitioning of the respiratory system so that we may get an accurate
estimate of the amount of air each compartment can hold. Different volumes include:
2) Capacities
Capacities are the more functional units of respiration. It refers to combinations of volumes that
express physiological limits. Different capacities include:
3) Effect of age on volume

As humans age, tissue changes. Vital capacity (VC) is a function of body weight, age, and height. The
following graph illustrates the effect of age on selected volumes and capacities in healthy males.
Note that the total lung capacity (TLC) remains the same across the adult lifespan, but vital capacity
(VC), inspiratory capacity (IC), and expiratory reserve volume (ERV) diminish. Functional residual
capacity (FRC) increases as one ages because it reflects the loss of inspiratory capacity with aging.
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VC increases steadily with body growth up to about 20 years of age, holds constant through about
age 25, and then begins a steady decline. As age increases, VC decreases by about 100ml per year in
adulthood.
Females have smaller VC throughout the life span (males tend to be taller).
3.3 Pressures of the respiratory system

There are five specific pressures for nonspeech and speech function.
Volumes and pressures vary as a direct function of the forces acting

on the respiratory system. With the vocal folds open, oral pressure,
subglottal pressure and alveolar pressure are roughly equivalent.
Intrapleural pressure will remain constantly negative, increasing in
negativity during inhalation. These pressures are all measured
relative to atmospheric pressure.
During inhalation, expansion of the thorax decreases the already

negative intrapleural pressure, and the increased lung pressure
volume results in a negative alveolar pressure. Air from outside the
body will flow into the lungs as a result of the pressure difference
between the lungs and the atmosphere. During exhalation, this
pressure differential is reversed, with air escaping the lungs to
equalize the positive alveolar pressure with the relatively negative atmospheric pressure.
3.4 Effects of posture on speech

Body posture and position are significant contributors to the efficiency of respiration and any
condition that comprises posture also compries respiration. As the body is shifted from an erect,
sitting posture to supine, the relationship between the physical structures of respiration and gravity
changes.
In a sitting position, gravity is pulling the abdominal viscera down (supporting inhalation), as well as
pulling the rib cage down (supporting exhalation). In supine position, the body gravity pulls the
abdominal viscera toward the spine. The result of this is spread of viscera toward the thorax and
further distension of the diaphragm into the thoracic cavity. In supine position, gravity supports
neither exhalation nor inhalation; muscles of inhalation must elevate both the abdomen and rib cage
against gravity.
Although VC is not affected, the ability to completely inflate the lungs is. Subsequently the RLV is
significantly reduced from approximately 38% of VC in sitting position to 20% in supine, arising from
the shift in viscera and effects of gravity on the rib cage. The elastic forces that would normally
inflate the lungs to that of 38% point only inflate them to 20%, leaving muscular effort to account for
the additional 18%.
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3.5 Pressures of speech
The respiratory system operates at two levels of pressure virtually simultaneously. The first level is
the relatively constant supply of subglottal pressure required to drive the vocal folds (i.e.
phonation). The second level of pressure is one requiring micro-control. As we maintain constant
pressure needed for phonation (first level of pressure), humans can rapidly change the pressure for
linguistic purposes such as syllable stress.
To maintain constant pressure for speech, we must first charge the system. During normal
respiration, inhalation takes up approximately 40% of the cycle, while exhalation takes up 60%.
The respiratory cycle for speech is markedly different. Long, drawn-out exhalation to produce long
utterances is needed, and you need a very short inhalation to maintain the smooth flow of
communication. When humans breathe in for speech, they actually spend only 10% of the
respiratory cycle on inhalation and about 90% breathing out. This however does not change the
amount of air humans breathe in and out.
The following figure illustrates how humans modify their respiratory cycle during speech compared
with nonspeech respiratory cycle.
During the speech, the speaker rapidly inhales a markedly larger volume of air than during quiet tidal
respiration, and then slowly exhales the air during speech. Note that the inhalation occurs with the
same timing in both speech and nonspeech, but that the expiratory phase is proportionately longer
during speech. In the final portion of the trace, the speaker is called on to speak on expiratory
reserve volume (i.e. using muscles of exhalation to continue speaking beyond the point at which the
person would normally take a breath).
The checking action is used to maintain a constant flow of air for precise control of sub-glottal
pressure. That is, humans check (impede) the flow of air out of the inflated lungs by means of
muscles that got it there in the first place – the muscles of inhalation. The checking action is
extremely important for respiratory control of speech, because it directly addresses a person’s
ability to restrain the flow of air. The checking action thus permits humans to maintain the constant
flow of air through the vocal tract, which in turn lets humans accurately control the pressure
beneath the vocal folds that have been closed for phonation. This is very important for vocal
intensity and frequency of vocal fold vibration.
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Class notes
OVERVIEW OF THE SUBSYSTEMS OF SPEECH PRODUCTION AND SPEECH

INTELLIGIBILITY
Speech is a complex motor act, dependent on the precise and coordinated interaction between
respiration, phonation, resonance, articulation subsystems of speech production, resulting in
appropriate prosody (supra-segmental characteristics of speech). When one or any combination of
the five components is affected due to a neuro-motor disturbance, the result could be dysarthria.
(Please refer to the self-study guidelines on p. 9.)
a) Respiration:
• Speech production is dependent on a sufficient, steady and controlled flow of air, and the
build-up of sub-glottal pressure in order to initiate vocal fold motion and start (continuous)
vibrations (based on the Bernoulli-effect) and speech production (specifically phonation).
• Damage to the central nervous system and/or nerves that innervate the respiratory muscles
may result in weakness (paresis)/paralysis, and therefore the generation of a smaller supply
of air, insufficient pressure affecting phonation, or uncontrolled/unsteady airflow available
for speech production. This has implications for length of utterances (volume), loudness
(pressure), inhalation duration, voice quality, pitch and stress changes, and eventually
prosody.
b) Phonation:
• Normal voicing (phonation) depends on the complete/adequate adduction and controlled
ad- and abduction of the vocal folds, and enough sub-glottal air pressure to allow the vocal
folds to vibrate (Bernoulli-effect). The movement (ad- and abduction) requires just the right
amount of tension in the vocal folds (and laryngeal structures as a whole) for clear
phonation to occur.
• Neuro-motor damage may impair voice quality and reduce the ability to change pitch,
loudness and length/steadiness of phonation during phonation, e.g.
o Spastic Dysarthria – too much (hyper) adduction and phonation with a forced,
“strain-strangled” quality.
o Flaccid Dysarthria – weak (hypo) adduction and breathy phonation.
c) Resonance:
• Resonance is the production of phonemes, and ultimately continuous speech (co-articulated
phonemes), with the appropriate oral or nasal tonality by occluding or opening the
velopharyngeal port. This requires raising and depressing the velum together with the
contraction and narrowing of the pharynx respectively.
• In order to accomplish the appropriate tonality, the muscles of the velum and pharynx need
to respond quickly and in a coordinated way to the different resonance requirements of
speech.
• Weak, slow, fluctuating/unsteady or inadequate velar and/or pharyngeal muscle contraction
may cause hypernasality, and is the result of damage to the (motor) cortex, activation
pathways (direct/indirect), control circuits (cerebellar/basal ganglia) of speech-motor
control, and/or the different nerves innervating the velum and pharynx.
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d) Articulation:
• Refers to the shaping of the vocal airstream in different ways, e.g. allowing unrestricted flow
(vowels), blocking (plosives), tightly or slightly restricting (fricatives), or redirecting the
airstream (nasals).
• The articulators achieve the different changes in the airstream at specific places in the vocal
tract by producing movements with the precise timing, direction, speed, strength and
placement required for a specific phoneme.
• Neuro-motor damage may affect the lips, tongue, jaw, velum, pharynx and the vocal folds,
and the site of lesion in the nervous system and severity of damage usually determine the
degree and which articulators are most severely affected.
• Articulation errors include inaccurate consonant production, distortion of vowels,
inappropriate silences and irregular articulation breaks.
e) Prosody:
• Refers to the “melody” of speech and contributes to the meaning of an utterance through
use of stress and pitch, i.e. speech intelligibility. There is also a link between prosody and
loudness, pitch and rate.
• Stress is accomplished by changing the pitch, loudness, and duration of syllables within
words to give it added importance or to clarify meaning.
• Intonation is the use of pitch changes and stress to communicate, e.g. questions, statements
and exclamations.
• Adding prosody to an utterance is not a simple task. It depends on the complex interaction
and coordinated involvement of respiration, phonation, resonance and articulation, e.g. to
change loudness, pitch, or duration of a syllable. E.g.
o Weakness and slow muscles movements of respiration, phonation, resonance and
articulation impair the strength and timing of contractions and may result in
monopitch and monoloudness of speech.
o Involuntary movements impair voluntary and controlled movements of speech, and
may result in irregular pitch variations, sudden increases or decreases in loudness,
and prolonged intervals between syllables and words.
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Class Powerpoint
Respiration
What is Speech?
Speech is …
• … movement made audible
• … a fine motor function/movement
• … an interruption/distortion of airflow
• … a shared function (ventilation) – speech breathing
• … which starts with respiration and depends on the characteristics of the structures.
• Humans “hijacked” the act of O2-exchange for oral communication.
Speech Breathing is …
• … the process by which forces are supplied to the speech production apparatus to generate
the sound of oral communication
• … the creation of pressures (+/(+/--; act ./
• … the displacement of structures
• … the generation of flows within the breathing apparatus
• “(the) functional capacity of the breathing apparatus (which) lies in its capacity for
movement”
Extra definition: The term “speech breathing” is usually used when referring to the manner in which
the breathing pump is utilized for the production of the airflow necessary for phonation. When
utilizing breathing for the purpose of speech, the rate and volume of inhalation, and the rate of
exhalation during the utterance seem to be governed largely by the speech controlling system and
its requirements with respect to phrasing, loudness, and articulation.
We speak on exhalation, and the longer our inhalation, the more words we can produce clearly as
we breathe out. In addition, the deeper we breathe in, the more force, or louder, we can project our
voice. Proper upright posture and alignment of our trunk, neck and head facilitates efficient
respiration and clear and audible phonation.
The Breathing Apparatus
Speech is a whole-body movement – down to the feet.
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Biomechanical alignment: “how your blocks are stacked”; you need stability to get mobility.
• Biomechanical alignment is the ideal state of the body, where our joints and muscles are
positioned for maximum function.
• Basically, good posture. Good posture allows for stability.
• Babies have poor postural control
• Why is biomechanical alignment NB?
o It allows for the optimal length-tension relationship between structures.
o Not overextended or too “floppy”/relaxed
Structures involved in Speech Production
Bony Thorax
• Vertebrae and vertebral column
• Ribcage and connection to vertebral column
• Pectoral girdle (shoulder girdle)
• Sternum
• Pelvic girdle
Visceral Thorax
• Airway – mouth, nose, trachea and bronchi
• Lungs
• Mediastinum
Muscles of Respiration
• Diaphragm (primary muscle of inhalation)
• Accessory muscles of inhalation and exhalation
• Muscles of postural control
Diaphragm
• Primary
• Inspiratory
• Muscle
NB: Muscle attachments
Look at the attachments and think about how the

structures they are attached to, can affect their
movement.
Will not ask names of muscles, but it is your library and is

NB to know as an SLT.
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Ribcage wall muscles (1)
Ribcage wall muscles (2)
You can still speak whilst being upside down and moving etc. Why? Because you have intact
neurology.
Abdominal Wall Muscles
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Velopharyngeal closure
• To produce most speech sounds, the air and sound need to be directed into the mouth and
blocked from entering the nasal cavity. This is done through closure of the velopharyngeal
valve. The velopharyngeal valve consists of the following structures: Velum (soft palate) and
pharyngeal walls.
o Laryngeal constrictor (the pharyngeal walls)
▪ Superior, middle, inferior pharyngeal constrictors
▪ Superior pharyngeal constrictor is most NB in velopharyngeal closure
• The function of the velopharyngeal mechanism is to create a tight seal between the velum
and pharyngeal walls to separate the oral and nasal cavities for various purposes, including
speech. Velopharyngeal closure is accomplished through the contraction of several
velopharyngeal muscles including the levator veli palatini, musculus uvulae, superior
pharyngeal constrictor, palatopharyngeus, palatoglossus, and salpingopharyngeus. The
tensor veli palatini is thought to be responsible for eustachian tube function.
• Closes and opens so that we don’t sound hypernasal or hyponasal.
Velopharyngeal Dysfunction and Speech

Velopharyngeal dysfunction causes a leak of sound and/or air into the nose during speech. It can
cause several speech problems, including:
• Hypernasality, where there is too much sound in the nose during speech
• Nasal emission of air when making certain speech sounds
• Weak consonants because of the leak of air through the nose
• Making speech sounds in the throat due to the lack of air in the mouth
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Volumes and Capacities
Lung Volumes and Capacities
Influence of Body Position
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Normal Respiration and Speech Breathing
Normal Breathing
• During rest tidal breathing inspirations and expirations ±equal duration.
• Any force generated at resting position is by muscle activation only.
• Active and passive forces
o Passive arise from natural recoil of muscles, lung tissue, lining of alveoli, etc.
o Active - ±20 muscles in chest wall dependent on/limited by strength of respiratory
muscles and amount of air in lungs.
Speech Breathing
• Process by which the respiratory apparatus provides the energy or driving force required to
the speech production apparatus to generate the sounds of speech production for oral
communication.
• Capacity for tidal breathing – not necessarily able to generate volumes and pressures for
voluntary voice production/sustained sub-glottal air pressure to support speech.
• Speech breathing is quick, deep inhalations and slow, controlled exhalations.
• Speech breathing disorder = dysfunction of lower airway (lungs and chest wall) - does not
include function of larynx, articulators or resonators.
• I.e. respiratory apparatus not able to supply adequate driving force to generate pressures,
volumes and flows to support speech production (MAY only have a speech breathing
problem).
Speech Breathing Control Variables

Pressure – sum of all the active and passive forces acting on the breathing apparatus
Volume – air in lungs
Shape – chest wall configurations
Airflow – control of the air as it flows through the larynx and supra laryngeal area.
Normal vs Disordered Breathing
VC = vital capacity
IRV = inspiratory reserve

volume
ERV = expiratory reserve

volume
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Respiration Components/Problems (Speech Breathing Control Variables)
Component / Problem 1 – Volume of Air
Memorize these triangles.
Problem is at the top, reason is at

the bottom.
We are still just looking at the

contribution of respiration.
BGL = Breath Group Length
KNOW:
1. What is problem?
2. What does it sound
like?
3. Where does the
problem lie?
• Short BGL = short utterances; sound cartoonish.
• Less air to produce long utterance and keep VF’s vibrating.
• Can’t create space for inhalation due to muscles being affected.
Component / Problem 2 – Pressure
• Very soft speech.

• May have normal prosody, but cannot speak louder. Listener might struggle to understand.
The combination of reduced inhalatory volume and exhalatory pressure

causes.
Reduced Vital Capacity (VC)
i.e. VC = all lung volumes, except residual volume
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Component / Problem 3 - Inspiratory Duration
• Shape of chest wall.

• Normal speech breathing is quick, deep inhalations and slow, controlled exhalations.
• Inhalation here is slow and might be audible.
• Problem: abdominal muscles not making diaphragm stable so that it can contract.
Component / Problem 4 – Control of Air Flow
• All 4 subsystems are involved.

• Sound like: poor speech intelligibility.
• Problem: resonance and articulation not well controlled due to laryngeal and supra-
laryngeal insufficiency.
• Reduced vital capacity in isolation does not significantly impact on speech intelligibility
(Hardy, 1983)
• HOWEVER, the degree to which upper airway structures are involved determines how big
the impact of reduced VC is on speech intelligibility, i.e. in the presence of additional
laryngeal, velopharyngeal and/or oral involvement VC does have an impact
• Reason: air wastage due to inefficient valving of the air at laryngeal and supra-laryngeal
levels (Hardy, 1983).
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Speech Breathing Disorders in specific Conditions/Populations
Parkinson’s Disease:
• Max [a] phonation measures phonation and respiration (volume of air).

• Parkinsons have problems with steadiness of movement of respiration.
• Diaphragm not contracting consistently, so problem with inhalation duration. Poor control
of movement.
Cervical Spinal Cord Injury:
• Muscles are weak and spastic.
Cerebral Palsy:
• They speak like you would blow out a candle.

• LNFS = little or no functional speech.
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Cerebellar Disease:
• In TBI – whiplash effect.

• Uncoordinated voluntary movements.
• Ataxia.
Mechanical Ventilation:
• No variation in pressure so can’t change loudness.
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FRAMEWORK FOR ANALYSIS OF PERCEPTUAL SPEECH CHARACTERISTICS
The following “steps” may help guide observations and description of what speech sounds like:
1. What do I see? Where do you see it? (“Big picture”)

• posture
• systematic observation of body as a whole, hips/pelvis, ribcage, shoulders/shoulder girdle,
neck, head, face
• (a)symmetry
• tightness/reduced movement, floppiness, excessive/unnecessary movement
2. What do I hear? (Subsystems)

• respiration (volume, pressure, inhalation duration, airflow control)
• phonation (clarity, pitch, tone, loudness)
• resonance (nasality)
• articulation (clarity, place, manner)
• prosody (rate, pitch, loudness, intelligibility)
3. What is interfering? (Link to anatomy, physiology and neurology)

• respiration – muscles (groups), forces, control
• phonation – intrinsic, extrinsic laryngeal muscles, general movement, vocal fold integrity
• resonance – muscles of velopharyngeal closure
• articulation – muscles of lips, mandible, tongue, cheeks, velum (neuromuscular
characteristics)
Biomechanical alignment is important because it ensure the optimal length-tension relationship

between structures.
CLINICAL SYNDROMES OF THE SPEECH MOTOR SYSTEM

Motor Speech Disorders are a group of speech disorders associated with neurological impairment
affecting the motor control of speech muscles or motor programming of speech movements. Motor
Speech Disorders encompass numerous types of Dysarthria and Apraxia of Speech.
1. Spastic Dysarthria 6. Mixed Dysarthria
2. Flaccid Dysarthria 7. Unilateral Upper Motor Neuron Dysarthria
3. Ataxic Dysarthria 8. Developmental (Verbal) Apraxia of Speech
4. Hyperkinetic Dysarthria 9. Acquired Apraxia of Speech
5. Hypokinetic Dysarthria
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1. Spastic Dysarthria
Neuromuscular Characteristics: NB: Know these tables.
• Muscle tone NB: Site of lesion and
• Muscle strength neuromuscular
• Range of movement characteristics for all
• Speed of movement dysarthrias.
• Accuracy of movement
• Steadiness/smoothness of movement
Introduction
• Spastic dysarthria is caused by damage to neurons of the cortex (know where cortex is)
• Typically associated with bilateral damage to the direct and indirect activation tracts of the
CNS
• Characterized by extremely poor articulation, a strained voice quality, and a low-pitched
voice
• May manifest in any or all of the respiratory, phonatory, resonatory, and articulatory
subsystems of speech subsystems (more than one), but it is generally not confined to a
single component
• Primary deviant speech characteristics reflect the effects of excessive muscle tone and
weakness on speech
• Weakness of muscles is part of all dysarthrias.
• Also refer to UUMN dysarthria, p.18.
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Effects on the Subsystems of Speech Production
• Upper motor neuron = in the cortex.

• Agonistic and antagonistic muscles – both are stiff and contracted.
• This will affect articulation, respiration, everything. “Tug-of-war” between muscles.
• Diaphragm cannot expand; not full volume of air in lungs.
• Articulation: slow, limited range of movement, strained – due to increased muscle tone.
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2. Flaccid Dysarthria
• Flaccid dysarthria is associated with damage to brainstem, lower motor neurons or motor
cranial nerves
• Characterized by hypernasal speech, poor articulation, and a breathy voice
• May manifest in any or all of the respiratory, phonatory, resonatory, and articulatory levels
of speech
• Primary deviant speech characteristics can be traced to muscular weakness and reduced
muscle tone and their effects on the speed, range, and accuracy of speech movements.
Neuromuscular Characteristics:
• Muscle tone
• Muscle strength
• Range of movement
• Speed of movement
Only found in
flaccid dysarthria.
Lower motor neuron = in the cranial nerves.
Definitions:
• Muscle atrophy
o Muscle atrophy is the wasting or thinning of muscle mass. It can be caused by disuse
of your muscles or neurogenic conditions.
• Fasciculations
o Muscle twitches can have causes that aren't due to underlying disease.
o A fasciculation, or muscle twitch, is a spontaneous, involuntary muscle contraction
and relaxation, involving fine muscle fibers.
o Flaccid: There may be specific parts of the oropharyngeal musculature affected,
identified by eliciting syllables of “ka”, “la”, and “ma”, which involves CN IX/X, XII,
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and VII, respectively. Fasciculations in these muscles, but especially the tongue,
suggests motor neuron disease.
• Fibrillations
o Fine, rapid twitching of individual muscle fibers with little or no movement of the
muscle as a whole.
o If a motor neuron or its axon is destroyed, the muscle fibers it innervates undergo
denervation atrophy. This leads to hypersensitivity of individual muscle fibers to
acetyl choline so that they may contract spontaneously.
Effects on the Subsystems of Speech Production: Hyperkinetic Dysarthria
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3. Ataxic Dysarthria
Ataxic dysarthria is associated with damage to the cerebellar control circuit. It may manifest itself in
any or all of the respiratory, phonatory, resonatory, and articulatory levels of speech, but the
characteristics are more prominent in articulation and prosody. Describe movement patterns as
“uncoordinated voluntary movements”.
• NB: Know that damage is in the cerebellar control circuit.

• NB: Know that characteristics are more prominent in articulation and prosody.
• Muscle tone is not increasing or fluctuating, it is just not quite right (not normal enough for
integrity of muscles to do their job).
• These are the clumsy children with bad handwriting (in children, not necessarily adults).
• Accuracy of movement: inaccurate (uncoordinated voluntary movements); explains bad
handwriting.
o When they WANT to move (voluntary), it is not very accurate.
• Speed and timing and direction of movement is affected – so when asked to do a voluntary
movement you’ll see (overshooting or undershooting; they will do it too fast/slow, not in the
correct direction so too far/near).
• Can be hypernasal due to timing of movement being off.
• **Overshooting and undershooting (if you see this, immediately thing Ataxia).
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• Shallow inhalations due to timing and overshooting/undershooting (rib cage movement).
• They have a bit of a spastic+flaccid combination (phonation).
• Monoloudness (or excessive loud or excessively soft).
• Problems with rhythm of movement.
• Ataxia vs stuttering
o Stuttering: Will have problems with same sound; consistently.
o Ataxia: problem on a syllable now, later not on same syllable. Rhythm and timing are
not correct. Not consistent.
o There is not a site of lesion in stuttering.
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Hyperkinetic and Hypokinetic Dysarthria
1. Muscle tone
2. Muscle strength
3. Range of movement
4. Speed of movement
5. Accuracy of movement
6. Steadiness/smoothness of movement
NB: Use these characteristics to differentiate between the two.
Difference between Hyperkinetic and Hypokinetic Dysarthria
• This is from the ASHA website.
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4. Hyperkinetic Dysarthria (Predominantly Quick or Slow)
Too much movement.
Hyperkinetic dysarthria is caused by damage to the caudate and putamen and is associated with
diseases of the basal ganglia control circuit. It is characterized by irregularities in the rate, pitch,
and loudness of speech, frequent stoppages of speech and tics. It may manifest in any or all of the
respiratory, phonatory, resonatory, and articulatory levels of speech, and it often has prominent
effects on prosody. Describe movement patterns as “involuntary movements”.
Important Information: Hyperkinetic Dysarthria
• Excessive muscle contractions; uncontrolled tics.

o Out of control.
• Huntington’s disease and Tourette syndrome are examples.
• Muscle tone and steadiness NB to diagnose Hyperkinetic.
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Distorted vowels: VF’s are open but you have tremors; no smooth controlled exhalation.
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5. Hypokinetic Dysarthria
Hypokinetic dysarthria is caused by damage to the substantia nigra (as in Parkinson’s) and is
characterised by a weak voice with many hesitations intermixed with brief rushes of speech. It may
manifest itself in any or all of the respiratory, phonatory, resonatory, and articulatory levels of
speech, but is more evident in voice, articulation, and prosody. Its primary deviant speech
characteristics reflect the effects of rigidity, reduced force and range of movement, and slow
individual, but sometimes fast repetitive movements of speech.
Posterchild: Parkinson’s disease.
Substantia nigra
Have movement arrests/stops.
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Not really important.
6. Mixed Dysarthria
Mixed dysarthria occur when both upper and lower motor neurons are damaged. This typically
occurs as the result of disease. Amyotrophic lateral sclerosis (ALS)/Motor Neuron Disease/Lou
Gehrig's Disease is the disease that most frequently cause mixed forms of dysarthria.
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7. Unilateral Upper Motor Neuron Dysarthria
Unilateral Upper Motor Neuron dysarthria is caused by damage to the upper motor neurons that
carry impulses to the cranial and spinal nerves on one side only (unilateral). It may manifest itself in
any or all of the articulatory levels of speech. Its primary deviant speech characteristics reflect the
effects of weakness, and even incoordination, on speech. Usually does not have forthright problems
with mandibular, velopharyngeal, laryngeal or lingual speech movements (i.e. subtle and may
manifest in function). Redundancy in innervation of structures minimalizes the effect of the
damage on speech, chewing, swallowing and upper airway protection functions.
• Muscle tone
• Muscle strength
But only on the one side of the face, opposite to the site of lesion
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8. Childhood Apraxia of Speech/Developmental (Verbal) Apraxia of
Speech/Developmental Verbal Dyspraxia and Developmental Oral Apraxia
Childhood Apraxia of Speech (CAS) [Developmental Apraxia of Speech (DAS), or Developmental
Verbal Dyspraxia (DVD)] has been described as a defect of articulation in the absence of obvious
muscular disturbance (no NMC) of the speech mechanism, to execute voluntarily the expected
programming and motor gestures needed for articulation. This means that movements of speech,
which is of the tongue, lips, or palate, appear normal for involuntary/automatic and spontaneous
movement such as smiling or licking the lips, but are inadequate for the complex and rapid
movements used for articulation. The disability in DAS is one of voluntary motor planning,
programming, combining and sequencing of speech movements rather than one of motor force and
control in both speech and non-speech acts (Love, 2000, p. 8).
Oral apraxia/Non-speech apraxia is the inability to perform voluntary movements of the tongue,
pharynx, lips, cheeks and velum due to a problem with the (sensorimotor) planning, programming,
combining and sequencing of movements of these structures. Automatic movements of the
muscles may be preserved.
Verbal apraxia is the inability to produce speech voluntarily because of a problem with
(sensorimotor) planning, programming, combining and sequencing muscle movements of the
tongue, pharynx, lips, cheeks and velum to produce speech, although automatic movements of the
muscles may be preserved.
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9. (Acquired) Apraxia of Speech
NO Neuromuscular Characteristics present!!!
• Muscle tone
• Muscle strength
**If you see any neuromuscular characteristics, you are not looking at Apraxia of Speech.
That is because AOS reflects a problem with the sensorimotor planning of speech movements, not
execution that is visible in the quality of the movements like dysarthria.
Introduction
Apraxia of Speech is an impairment of the central motor programming (and planning) for voluntary
production of phonemes and the sequencing of muscles movements required to produce speech.
Acquired apraxia is associated with damage to Broca’s area and other cortical-motor areas, i.e. the
result of pathology in the left cerebral hemisphere. It does not have the neuromuscular dimension
like the dysarthrias or the linguistically based speech errors associated with aphasia, but the clinical
manifestations of AOS are believed to reflect a disturbance in the programming of movements of
speech only. AOS can exist independent of impairments in verbal comprehension, reading
comprehension, and writing. Clinical features of AOS convey the impression that muscles are
capable of normal function and that the appropriate message has been formulated, but that it is
either difficult to enact the planned message or that the perceptual characteristics of sounds that
emerge are not what is intended
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Effects on the Subsystems of Speech Production
• When you ask them to do something (voluntary) they might not be able to. But when they
do something automatically it might still be intact.
• NB: Voice onset time (important to know for test).
o What is wrong with person if they have voice onset time?
• Can have respiratory apraxia (when you just ask them to breathe)
• Resonance can be affected when you ask them to say a specific sound (because it is
voluntary).
• Vowels are affected – something associated with Apraxia.
Video (classic apraxia)

He does not have a respiratory system that is affected and does not have low muscle tone (no
neuromuscular characteristics)
• P-t-k
o Can do “p” and “t” because it is only one sound (one plan).
o Frontal sounds are learned first.
o Struggles with “k” – it is not so visible and requires more sophisticated movement.
o He learned the plan in the process (could pronounce the “k” after a few tries).
o Could not do p-t-k; they are in different places in the mouth and it is more planning.
Sequencing becomes a problem.
o Planning messes up the execution; execution is not the problem.
o Problem is with sequencing.
o He has verbal apraxia, not oral or limb apraxia.
• Person with Dysarthria will not say it so long, slower.
o Person with Apraxia will improve with repetition, but dysarthria will get worse.
o P-t-k: will also struggle.
o Person with dysarthria has the plan, but when it is done it is done messy (not
correct).
NB: you will get a case with a site of lesion or picture ; “OPE shows no neuromuscular problems”.
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Table: Mayo Clinic Perceptual Classification of Dysarthrias
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Knowledge check
1. You are approached by the daughter of a client regarding information in her father’s hospital
file. Explain “dysarthria” and “apraxia of speech” as neurogenic speech disorders and how it
differs from “aphasia” to her.
2. Explain the poor speech intelligibility of people with dysarthria given the role of respiration in
speech production. Consider the site of lesion, specific anatomy and physiology of the
subsystem, the neuromuscular characteristics and their role in speech production as guidelines
for the answer. Respiration in persons with:
a. Spastic dysarthria
b. Flaccid dysarthria
c. Hyperkinetic dysarthria
3. Name and explain the four variables/components of speech breathing.
4. Describe the anticipated perceptual fallouts for each of the four variables/components and the
anatomical correlates of each of the problems.
Spastic dysarthria
1. Define spastic dysarthria in your own words.
2. Which nerve tracts must be damaged/affected for a diagnosis of spastic dysarthria?
3. What are the most common causes of spastic dysarthria?
4. How does damage to the pyramidal and extrapyramidal tracts contribute to the symptoms
of spastic dysarthria?
5. Explain the pseudobulbar palsy and the “pseudobulbar affect”.
6. Which prominent speech production symptoms are associated with spastic dysarthria?
Flaccid dysarthria
1. Define flaccid dysarthria in your own words.
2. Which nerve tracts must be damaged/affected for a diagnosis of flaccid dysarthria?
3. Why are cranial nerves also known as the “final common pathway”?
4. Which six paired cranial nerves are involved in speech production?
5. What role do the spinal nerves play in speech production?
Apraxia of Speech
1. Define apraxia of speech (AOS) in your own words.
2. Where are the site(s) of lesion for AOS?
3. What are the most common causes of AOS?
4. Which neuromuscular characteristics are present/prominent in AOS?
5. Which prominent speech production symptoms are associated with AOS?
6. Are there any co-morbidities to look out for, i.e. additional conditions, or other
communication disorders that can co-occur with AOS?
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Videos
• Why is biomechanical alignment NB?
o it allows for the optimal length, tension, relationship between structures.
Video 1: Spastic dysarthria
See?
- arm is actually stiff, it just looks floppy -> feel their arm or hand
- bad posture, not biomechanically aligned
- arm -> holding onto arms; has hemiplegia
Hear?
- low volume -> low pressure; no loudness variation; monoloudness
- not smooth phonation; strained/tensed/forced; strained strangled voice
- respiration: audible inhalation, short utterances due to spasticity (too much tension in the
muscles; muscles are contracting too much and not enough freedom of movement)
- prosody: slow speech rate (increased muscle tone is restricting speed and range of
movement and muscle tone is also restricting movement); low intelligibility
- articulation: struggles with speech sounds because of the stiffness in the tongue muscles
- resonance: hypernasal
What is interfering?
- Respiration (volume on air, pressure, inhalation durations, control of air)
- Phonation: intrinsic muscles (spastic, too much muscle tone)
- Resonance: hypernasal (not complete velopharyngeal closure or not fast enough and not
accurate enough; too much muscle tone)
The stroke caused the "messages" from the cortex to be distorted or incorrect.
**neuromuscular characteristics/parameters
1. Muscle tone
2. Muscle strength The face has tonic and
3. Speed of movement phasic muscles (shorter and
4. Range of movement smaller but can fire
5. Accuracy of movement constantly so won’t get
6. Steadiness of movement tired).
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ASSESSMENT – PRINCIPLES, OSME AND CRANIAL NERVES
Case Study: Application and SNAPPS Preparation
A twenty-seven-year-old entrepreneur is referred to you for management four weeks after he was
seriously injured during a rugby match. On admission to the hospital he was unconscious and
presented with respiratory problems. A tracheostomy was performed next to the rugby field to
manage the immediate respiratory distress and the patient was fed via nasogastric tube for 10 days
after admission. The man was in an induced semi-coma for one week after the incident and no
assessment could be conducted. He has since showed a marked recovery. His twin brother, who is
also his business partner, accompanies him to the consultation.
The following medical assessment information is available:

• Vital signs are normal and tracheostomy tube removed
• Right hemiparesis with moderately increased muscle tone visible in trunk and limbs (right)
• Markedly reduced breath support for speech – 2-3 syllable utterances
Poor voicing during speech production attempts – soft, monotonous, with audible hypernasality
• Hypertonic tongue and severe drooling from right side of mouth

• “Good” receptive language skills
1. Which of the following aims and principles will apply to this case?
2. Which of the following components of assessment will apply to this case?
3. Which of the above speech assessments would you recommend in this case? Also select the
most appropriate tasks/activities you would use, and justify your choices.
4. Which of the above speech assessments would you recommend in this case? Also select the
most appropriate tasks/activities you would use, and justify your choices.
Notes made in class

• Muscle tone: if the muscle is spastic or flaccid, the muscle is not active, so it is weak. That
muscle is not really doing anything. It is not receiving proper signals from the brain. The
muscle doesn’t start at “neutral”; it cannot actively perform. There is no force within the
muscle that allows for strong and accurate movement within the muscle.
• With flaccid muscles, you have a deficit in muscle energy, so you need so much more energy
and effort to move that muscle.
• Assessment is about determining baseline (to compare and look for changes or progress or
even tract negative changes). Sometimes you need to repeat baseline (reassess).
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AIMS, PRINCIPLES AND PROCESS OF ASSESSMENT
Assessment – Examinations and Procedures
“Identifying a speech problem as neurologic and the localizing it within the nervous system is similar
to a neurologist’s effort to localize a disease and establish a neurologic diagnosis. The differences
between the two enterprises are that speech may be only one of a number of neurologic problems
and that speech diagnosis is usually not diagnostic of specific neurologic disease. However, these
differences sometimes blur. Speech difficulty is sometimes the presenting complaint and the only
detectable neurologic abnormality, and its diagnosis may permit localization and may narrow
disease diagnostic possibilities. Speech examination is thus an important component of many
neurologic examinations.” (Duffy, 2013, 2020, p. 61).
Aims/Goals and Purposes of Examination

“In many ways the goals of a motor speech evaluation are no different from the goals of any speech-
language evaluation. Haynes and Pindzola (2011) said that a speech-language evaluation is done to
(i) understand a patient’s problem and to (ii) establish the beginning level of treatment.”
“The purposes of the motor speech examination often vary as a function of practice site and stage of
care. Sometimes the priority is to establish the speech diagnosis and its implications for localization
and neurologic diagnosis. Under other circumstances, formulating treatment recommendations
takes precedence.” (Duffy, 2013, 2020, p. 61)
1. Problem detection / confirmation

 Does a functional speech/communication problem exist?
 “Is there a problem with the person’s speech?”
2. Problem description
 Features of speech and related structures and functions
 “If there is a problem, what is the best way to describe it?”
3. Determine diagnostic possibilities – 6 questions (Duffy, 2013, p. 62; Freed, 2012, p. 49)
a. Neurological? (I.e. result of neurological disorder)
b. Organic vs psychogenic?
c. Onset: Sudden or gradually over time?
d. Recently acquired vs longstanding?
▪ Spontaneous recovery; plasticity of the brain
e. Motor speech disorder vs aphasia vs other?
f. Dysarthria? Type(s)?
4. Differential diagnosis
5. Determine the diagnosis(es)
 Single diagnosis, or order of possibilities
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6. Implications of the diagnosis (ICF)
 Localisation, disease and functional communication problems
7. Determine severity – 3 reasons (Duffy, 2013, p. 62)
a. Matched against complaints
b. Prognosis and treatment decision-making
c. Baseline to measure changes
8. Determine need to refer client to other members of multi-disciplinary team
a. Physical – doctor, PT, OT, dietician, medical specialist
b. Psychological – psychologist, counsellor, psychiatrist, pastoral support
c. Financial/social – SW
9. Determine focus of treatment (Yorkston, Beukelman, Strand & Hakel, 2010)
General Process/Course
Principles of Clinical Evaluation

1. Establishing a knowledge base
2. Speech evaluation forms part of any neuro examination
3. ICF Framework
a. Impairment
b. Speech activities
c. Participation
4. Timing
5. Use consistent procedures / materials
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COMPONENTS OF ASSESSMENT
Components of the Clinical Examination
A.
B.
C.
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PRELIMINARY Ax: CASE HISTORY (History incorporating the ICF and ICF-CY Frameworks
Case History
a. Adult: (Based on Duffy, 2013, p. 65-66)
i. Introduction and obtaining of permission for intervention
ii. Goal setting
iii. Basic biographical and background information
iv. Onset and course of speech deficit
v. Medical history – known aetiology(s) and/or site of lesion
vi. Associated or related deficits/disorders
vii. Perception of deficit/disorder
viii. Consequences of deficit/disorder (Strictly ICF-guided)
ix. Awareness of diagnosis and prognosis
x. Intervention (to date)
xi. Expectations and needs (ICF based)
b. Paediatric (Based on Strand & McCauley, 1999, p. 81)

i. Introduction and obtaining of permission for intervention
ii. Developmental history – Pre-morbid
iii. Communication history and skills
iv. Family history
v. Medical history – known aetiology(s) and/or site of lesion
vi. Associated or related deficits/disorders (ICF-CY based)
vii. Motor skills – gross motor, fine motor, oral-motor
viii. Psychosocial skills
ix. Current medical status
x. Other observations
xi. Intervention (to date)
xii. Support system (ICF-CY based)
PHYSICAL Ax: STRUCTURAL-FUNCTIONAL ORAL-SENSORIMOTOR and CRANIAL NERVES

Physical Examination
1. Examination of the speech mechanism during non-speech activities
a. Structural-functional status; and
b. Neuromuscular characteristics
2. Oral-motor behaviour (reflexes)
3. Oral-sensory capacities
4. Cranial nerve testing
1. Speech Mechanism Examination (Usually during non-speech activities)

This examination has a dual purpose, namely to (i) determine the structural-functional status of the
speech mechanism, and (ii) identify the neuromuscular features that influence speech production.
a. Structural-functional Status
Other Terms:
oral-peripheral evaluation (OPE), motor speech assessment, oral-facial evaluation, oral-sensorimotor
examination/evaluation (OSME)
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Rationale:
• oral mechanism is observed and evaluated during non-speech ánd speech activities in order
to determine its neural, structural and functional integrity
• information is then integrated with case history information – ICF/ICF-CY based – ,
perceptual speech characteristics and speech intelligibility measures
Objectives:
• provides information regarding the shape, size and symmetry of structures (structural-
functional status);
• the strength, speed, range, steadiness and accuracy of oro-facial movements (specifically
the face, lower jaw, lips, tongue and soft palate);
• the (changes) in muscle tone in rest (neurological tone), during sustained postures and
during activity; and
• sensory integrity (structural and functional)
Observations and results of the OSME provide evidence that confirms or rejects hypotheses based of
other speech findings.
(Refer to Appendix D – OSME Form).
Oral-Facial Structures:
1. Face – cheeks
2. Mandible (incl. teeth)
3. Lips
4. Tongue
5. Velopharynx (velum)
a. at rest
b. sustained posture
c. movement (function)
6. Larynx
 Generally direct observations of laryngeal functions are difficult without specialist
equipment like a flexible naso-endoscopy. Laryngeal functions can be observed
indirectly by means of the following non-speech activities:
i. Can the person produce a strong, sharp cough?
ii. Can the person produce a sharp glottal stop?
iii. Is audible inhalation (stridor) present?
b. Neuromuscular Characteristics
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1. Muscle tone
2. Muscle strength
3. Range of movement
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4. Speed of movement
5. Accuracy of movement
6. Steadiness of movement
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2. Oral-Motor Behaviour
Reflexes (Refer to Appendix D – Oral Reactions) and Oral-motor Skills
 present, absent, age appropriate
 normal or primitive/unrefined
 oral motor skills related to non-speech (e.g. saliva control) and speech activities
 accuracy and speed of movement relating to absence or presence of groping behaviour
 gag reflex: you can ask about it and if they experience it, but don’t ask for a demonstration.
 Reflexes: only babies up until 6 months (maybe even cut it down to 3 months).
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3. Oral-sensory Capacity (Subjective) (NEVER in isolation)
• Light touch
• Two-point discrimination
• Pain and temperature
• Stereognosis
4. Cranial Nerve Testing

• Cranial nerves make up part of the peripheral nervous system and are also known as the
“final common pathway” (FCP).
• The FCP for speech includes the paired cranial nerves that supply muscles of phonation,
resonance, articulation and prosody, and the paired spinal nerves that innervate muscles
of respiration. In this way oral musculature is provided with crucial sensory and motor
information.
• Cranial nerves consist of efferent motor fibres that arise from nuclei in the brainstem and
afferent sensory fibres that originate in the peripheral ganglia.
• Motor or efferent parts of the cranial nerves are formed by axons of nerve cells “within” the
brain. Groups of these nerve cells form the nuclei of origin from the cranial nerves.
• The nuclei of origin of the cranial nerves receive impulses from the cerebral cortex through
the corticobulbar tracts.
• The majority of corticobulbar fibres to the motor cranial nerve nuclei cross the midline
(decussate) before reaching the nuclei.
• There is bilateral innervation for all cranial nerve motor nuclei except portions of N.
Trigeminal, N. Facial and N. Hypoglossus.
• Sensory or afferent parts of the cranial nerves are formed by axons of nerve cells “outside”
the brain. They are situated on the nerve trunks or actually in the sensory organ itself, e.g. in
the nose, ear or eye. The central processes of these cells enter the brain and terminate by
synapsing with cells that are grouped together to form the nuclei of termination. These cells
have axons that cross the midline, ascend and synapse on other sensory nuclei (e.g.
thalamus). These axons of the resulting cells then terminate in the cerebral cortex (sensory
cortex).
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Robbins-Klee Paediatric OSME (Cranial Nerve Framework)
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Anatomy Innervation Function Testing
 Biggest of cranial nerves  Innervation is bilateral and Oral-motor and Speech: 1. Open mouth wide
 Originates in pons symmetrical (Only ipsilateral  chewing/mastication, i.e. 2. Bite down hard – palpitate
 Motor and Sensory  Motor fibres of N. jaw movement and closure masseter, temporalis
branches connect to lateral Trigeminal innervate:  role in the sensorimotor 3. Resistance against movement –
pons o masseter control of jaw movements open and close
 Motor nuclei are limited to o temporalis during speech
pons and sensory nuclei run o lateral and medial  provides reflex control for
from mesencephalon to pterygoids “biting”
spinal cord o tensor tympani
 Consists of three branches o tensor veli palatini Sensory:
of which only the o mylohyoid  pain transfer
ophthalmic and maxillary o anterior digastric  temperature and tactile
branches have sensory muscle from face, forehead and
innervation from N. mucosa of nose, mouth and
Trigeminal nerve Trigeminal, and mandibular • Sensory fibres of N. teeth
(V) branch have both motor Trigeminal have three main  deep pressure and
and sensory innervation. branches: kinaesthetic information
o Ophthalmic – from teeth, gums, hard
innervates upper palate and
face: skin of temperomandibular joint
forehead, scalp,
eyes and nose
o Maxillary – maxilla
and maxillary sinus;
mucosa of the
mouth (upper lip);
nasal cavity, palate
and nasopharynx;
teeth (upper), and
cheeks
o Mandibular – motor
fibres to tensor veli
palatini, tensor
tympani and jaw
muscles; sensory
fibres from scalp,
mandible, mucosa
of mouth, and
anterior 2/3 of
tongue
 Mixed motor and sensory  Innervation is bilateral and Motor: 1. Frown
nerve with autonomic symmetrical  facial expression – 2. Close eyes with resistance
component  Upper face receives orbicularis oculi, occipito 3. Puff cheeks
 A complex nerve made up ipsilateral and contralateral frontalis, zygomatic, 4. Close lips tightly/Purse lips
by 3 nuclei: innervation buccinator, orbicularis oris 5. Smile
a) main motor nucleus,  Lower face receives most of  articulation and oral 6. Salivation
b) parasympathetic nuclei the corticobulbar fibres, but movement – platysma, 7. Sensation of temperature,
(autonomic) – superior from the opposite stylohyoid, portion of the taste, texture and shape
salivatory and lacrimal hemisphere (i.e. digastric, and submental 8. Reaction to ordinary/loud
nuclei, and contralateral innervation) muscles sounds
Facial Nerve (VII) c) nucleus of the tractus  hearing – stapedius
solitarius (joined by
taste fibres from N. V, Sensory:
IX and X)  taste from anterior 2/3 of
 Originates within the pons tongue (chorda tympani)
near the reticular formation and taste buds in soft and
hard palate
 floor of the mouth
 cornea
Autonomic:
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 reflex response to corneal
irritation
 submandibular and
sublingual salivary glands
 nasal and palatine glands
 Complex nerve, mixed  Innervation is bilateral and Motor: 1. Phonate /a/ for pharyngeal and
motor and sensory with symmetrical  Stylopharyngeus – velar movement (elevation)
autonomic component  Both efferent and afferent elevation of velum, pharynx 2. Swallow
 nuclei in medulla fibres decussate, i.e. and larynx, and narrowing 3. Saliva secretion
o nucleus ambiguus contralateral innervation of pharynx 4. Sensation – taste from
(motor),  Motor nucleus – receives  Combined with N. Vagus posterior tongue; pain, touch,
o inferior salivatory corticobulbar fibres from important for swallowing pressure and temperature from
nucleus both hemispheres – fauces, velum, upper pharynx
(autonomic), and innervate: Autonomic (secretomotor): 5. Gag – reflex
o nucleus of the o stylopharyngeus  Saliva secretion from
tractus solitarius (with N. Vagus and parotid gland
(sensory) – also Accessory)
fibres from N. o fibres to superior Sensory:
Glossopharyngeus
Fascialis and Vagus and middle  Taste from posterior 1/3 of
nerve (IX)  Works with N. Vagus and pharyngeal tongue and part of the
Accessory which makes constrictor velum
independent functioning  Inferior salivatory nucleus  Pain, touch, pressure and
difficult to determine (autonomic with temperature from posterior
secretomotor fibres) receive 1/3 of tongue, fauces,
information from velum, upper pharynx and
hypothalamus, olfactory Eustachian tubes
system and oral cavity (glossopharyngeal
(taste) – innervate: neuralgia)
o parotid gland
 Tractus solitarius (sensory
nucleus) receives taste
information through Reflex:
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afferent fibres that  Reflex connections
decussate and run to the between pharyngeal
contralateral thalamic and sensory and motor neurons
hypothalamic nuclei – in medulla mediate the gag
innervate: reflex
o Posterior 1/3 of the  Strong connection with N.
tongue and part of Vagus
the velum
• nuclei in medulla • Innervation is bilateral and Motor:

o nucleus ambiguus asymmetrical – also • intrinsic laryngeal muscles – 1. Palatal arches symmetry at rest
(motor), ipsilateral and contralateral abduction and adduction of and elevation in function
o dorsal nucleus • SLN innervates sensation vocal folds (voicing, 2. Phonate /a/ and /u/ for voicing,
(parasympathetic), above the level of vocal coughing, swallowing) maximum phonation time and
and folds and cricothyroid • pharyngeal constrictor – resonance (adduction of vocal
o nucleus of the muscle narrowing of pharynx folds) (Distinguish between
tractus solitarius • RLN innervates mucosa (resonance, coughing, respiration and phonation)
(sensory) – also (sensory) under level of swallowing) 3. Vary pitch and loudness
fibres from N. vocal folds, intrinsic • palatal muscles 4. Cough or glottal coup
Fascialis and laryngeal muscles and the (palatopharyngeus, - 5. Swallow
Vagus nerve (X) Glossopharyngeus inferior pharyngeal glossus, 6. Sensation – taste from tongue
• Axon from nucleus constrictor salpingopharyngeus, base; pain, touch, pressure and
ambiguus has pharyngeal • Both efferent and afferent levator veli palatini and temperature from pharynx and
and laryngeal branch fibres decussate, i.e. musculus uvulae) – larynx
• Pharyngeal branch -> taste contralateral innervation elevation of velum
and motor • Motor nucleus (nucleus (resonance, swallowing)
• Laryngeal branch -> ambiguus) – receives • laryngeal mucosa
superior laryngeal nerve corticobulbar fibres from
(SLN), recurrent laryngeal both hemispheres – Parasympathetic:
nerve (RLN) (NB innervates: • organs
asymmetrical course: right o intrinsic laryngeal
recurrent laryngeal nerve muscles
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passes behind carotid and o pharyngeal Sensory:
sub-clavicular arteries, and constrictor • Taste from base of tongue
end in larynx; left recurrent o palatal muscles – • Pain, touch, pressure and
laryngeal nerve passes palatopharyngeus, - temperature from pharynx,
under around the aorta, glossus, larynx, thoracic and
ascends between trachea salpingopharyngeus, abdominal viscera
and oesophagus and ends levator veli palatini
in larynx) and musculus Reflex:
uvulae (NOT tensor • Gag reflex – connection
veli palatini) with N. Glossopharyngeus
o laryngeal mucosa
• Dorsal nucleus
(parasympathetic) –
innervates:
o intestines
o pancreas
o stomach
o oesophagus
o trachea
o smooth muscles and
mucosal glands of
bronchi
o kidneys, liver and
heart
• Tractus solitarius (sensory
nucleus) receives taste
information via afferent
fibres from inferior ganglion
– innervates:
o epiglottis and
valleculae (tongue
base)
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o pharynx
• Pain, touch, pressure and
temperature from tympanic
membrane, and pain from
the pharynx, larynx, thoracic
and abdominal viscera
• Mediate sensation of
nausea and hunger
• The spinal accessory nerve • The cranial root joins the • The spinal accessory • When testing cranial nerve XI,
consists of a cranial and a vagus to innervate the uvula nerve’s primary function is the spinal part is evaluated.
spinal root. and the levator palatini. as a motor to the muscles • The accessory part is accessory
• The nucleus of the cranial • As previously mentioned, (including the to the vagus and cannot be
root is found in the nucleus the spinal root innervates sternocleidomastoid) that tested alone.
ambiguus of the medulla. the sternocleidomastoid help turn, tilt, and thrust • Initially, look at the size and
• It receives corticonuclear and trapezius muscles. the head forward or raise symmetry of the
fibers from both cerebral the sternum and clavicle if sternocleidomastoid muscles
hemispheres. the head is in a fixed and palpate them. (Do this on
• These fibers then join the position. yourself and others to become
glossopharyngeal, vagus, • It provides innervation also familiar with normal muscle
Accessory nerve
and spinal accessory nerves. to the trapezius muscle, size and firmness.)
(XI) • The spinal root’s nucleus is which is responsible for • Ask the patient to turn the
located in the spinal shrugging the shoulders. head to one side and hold it
nucleus of the anterior gray there while you try to push it
column of the spinal cord. back to the middle.
• The fibers pass through the • Put one hand on the patient’s
lateral white column and cheek and the other on the
eventually form a nerve shoulder to brace the patient.
trunk, which joins the Gently push against the cheek
cranial root to pass through and observe and palpate the
the foramen magnum. sternocleidomastoid on the
opposite side of the neck.
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• The spinal root then • Next have the patient try to
separates from the cranial thrust the head forward while
root, however, to find its you gently resist the movement
way to the with your hand against the
sternocleidomastoid and forehead. Again, observe and
trapezius muscles. palpate the
sternocleidomastoid muscle.
• Finally, ask the patient to shrug
his or her shoulders while you
press down on the shoulders.
You should feel the shoulders
elevate against your gentle
resistance.
• The hypoglossal nerve runs • The hypoglossal nerve • The hypoglossal nerve 1. Observation for atrophy or
under the tongue and innervates the intrinsic innervates the muscles fasciculations as well as
controls tongue muscles of the tongue. responsible for tongue symmetry on protrusion;
movements. • It also innervates four movement. 2. assessment for lateralization,
• The nucleus, called the extrinsic tongue muscles: • The four intrinsic muscles protrusion, elevation,
hypoglossal nucleus, is the genioglossus, of the tongue control retraction (to observe range of
located in the medulla hyoglossus, chondroglossus, tongue shortening, movement);
beneath the lower part of and styloglossus. concaving (turning the tip 3. assessment of movement
the fourth ventricle. • With the branches from the and lateral margins against resistance for strength
Hypoglossal (XII) • It receives fibers from both ansa cervicalis, cranial nerve upward), narrowing, testing on lateral, protrusion,
cerebral hemispheres, with XII contributes to the elongating, and flattening. and elevation movement;
one exception. innervation of the • The extrinsic muscles 4. articulation testing
• The cells serving the sternothyroid, sternohyoid, innervated account for
genioglossus muscle receive and omohyoid muscles, thus tongue protrusion
only contralateral fibers. contributing to the (genioglossus), drawing the
• The nerve fibers pass elevation and depression of tongue upward and
through the medulla and the larynx. backward (styloglossus),
emerge in the groove and retraction and
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between the pyramid and depression of the tongue
the olive. (hyoglossus).
• Other apparent branches of • The hyoglossus also acts
the hypoglossal are not with the chondroglossus to
connected with the elevate the hyoid bone,
hypoglossal nuclei but thus participating in
rather are derived from the phonation.
ansa cervicalis of cervical
vertebrae C1, C2, and C3.
• Ansa means “loop,” and
some branches of these
spinal nerves form a loop
and join the hypoglossal
nerve to help innervate the
sternothyroid, sternohyoid,
and omohyoid muscles.
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ASSESSMENT – PERCEPTUAL AND SUBSYSTEMS 1
“In many ways the goals of a motor speech evaluation are no different from the goals of any
speech-language evaluation. Haynes and Pindzola (2011) said that a speech-language evaluation is
done (i) to understand a patient’s problem, and (ii) to establish the beginning level of treatment.”
“The purposes of the motor speech examination often vary as a function of practice site and stage
of care. Sometimes the priority is to establish the speech diagnosis and its implications for
localization and neurologic diagnosis. Under other circumstances, formulating treatment
recommendations takes precedence.”
“The clinician’s ear is the best instrument for evaluating deficits of the motor speech mechanism.
Based on acoustic characteristics of a patient’s speech, the clinician can make a quick, accurate
diagnosis, but it does take experience. Furthermore, this is a relevant way of evaluating the speech
“product”, because what the listener/ communication partner hears provides the ultimate
judgement of whether speech is defective and to what degree, i.e. speech intelligibility.”
Subsystems of Speech Production
Know the anatomy and

physiology.
Why do Ax’s?
• To test what the patient CAN do.
Do it more than once to make
sure you don’t base it on single
time.
• Neurogenic disorder: do it more
than once because can have
more than one problem (not just
e.g. polyp that will have same
result every time).
• 3-5 repetitions.
a) Respiratory-Phonatory Subsystems
• Respiratory and phonatory components are best assessed together - normal phonation
depends on adequate sub-glottal pressure.
• Starts with observations – visual and auditory – followed by specific measurements.
Components measured include:
o influence of the four different respiratory components on phonation
o the quality of phonation
o length/duration of phonation
o pitch of phonation
o loudness of phonation.
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• These functions can provide useful diagnostic information (differential diagnosis), and often
indicate specific intervention goals.
• Starts with observations – visual and auditory – followed by specific measurements.
Components measured include:
o loudness
o length/duration of phonation
o pitch of phonation
o quality of phonation
• These functions can provide useful diagnostic information, and often indicate specific
intervention goals.
Activities, Measures and Tasks
Tasks:
a) Specific observations (subjective):
 posture and chest wall configuration before and during phonation/speech
production (inhalation duration) (biomechanical alignment)
 respiratory rate before and during phonation/ speech production
b) Breathing pattern
 clavicular, thoracic, abdominal
c) Breathing rate
 fast, shallow, forced (before and during phonation/speech production)
 “Relax. I am going to determine your breathing pattern.” Count the number of
breaths per minute. Norm = 12-18.
b) Describe and/or assess:
 quality,
 pitch, and
 loudness of phonation
c) Maximum phonation time (volume)
a. Relax. Take a deep breath and say /a/ as long, steadily, and clearly as possible.
b. Other tasks:
i. Water bubble manometry
ii. Speech tasks/activities
▪ Ask to name days of week/months of year/count until they run out of
breath
▪ Would you ask person with severe artuc problems to do speech activities
to test volume? NO. because you wont know if it is artic of volume.
▪ Short BGL/utterances, telegraphic speech.
d) Pitch variation (vocal fold and laryngeal mobility)
a. “Relax. Take a deep breath and say /a/ … (Rising and falling scale)
b. Know the physiology of the cartilages that move, whole larynx move up and down
for pitch changes; up + forward for higher pitch; observe whether you can see the
movement of the larynx.
e) Loudness variation (pressure)
a. “Relax. Take a deep breath and say /a/ … (Crescendo and decrescendo).
f) Cough/ glottal coup
a. (Differentiate – respiratory vs laryngeal deficit).
b. Cough with phonation, vocal fold closure with vibration for phonation, can listen to
quality+pressure+adduction+effort)
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c. Coughing is adduction of vocal folds, so good adduction, soft cough means lack of
pressure.
d. Person with spastic dysarthria will not be able to relax vocal folds again for
phonation.
g) S-z ratio (respiratory vs laryngeal deficits) (Norms and calculation)
a. (Differentiate between respiratory and laryngeal deficits) (Norms and calculation)
b. “Relax. Take a deep breath and say /s/ as long and clearly as possible.” (Repeat with
/z/).
c. Do again when voiced /z/ is longer than voiceless /s/; stroke px’s might struggle.
d. Do again to optimize Ax opportunity.
h) Answer the following questions – observations:
a. Is there a delay (latency period) between the signal to phonate and the initiation of
phonation? (Why? What does it mean? AOS or dysarthria?)
b. Is there a delay (latency period) between the initiation of phonation and the
production of sound? (Why? What does it mean? AOS or dysarthria?)
i) Assess duration and depth of inhalation during phonation/speech production (compliment
Task a)
a. (shape of breathing apparatus – duration of inhalation)
b. Sniff-test
i. Quick sniffing of the nose, can ONLY do that if diaphragm can contract
effectively, such as for speech, model the task). Shallow + slow = problem.
c. Other tasks:
i. Water bubble manometry
ii. Speech tasks/activities
j) Waterbubble Manometry
 Norm:
▪ 5 cm deep – pressure
▪ 5 s duration – volume
▪ Conditions:
▪ Blow bubbles at 5 cm
▪ Sustain for 5s
▪ Controlled – water should
not spill
Overview of the Respiratory Components (Triangles), Correlates, Measurements & Tasks
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Check and ensure the following:
• The correct name of each assessment tasks/activities/procedures
• You understand and can describe each of the assessment tasks/activities/procedures
• You always use the correct terminology to describe the different tasks/activities/procedures
• Purpose/aim of each task/activity/procedure
• Interpretation of results of each task/activity/procedure – also know norms
• Performance/results that could be expected for the different types of MSDs (and aphasias)
for the different tasks/activities/procedures, i.e. what result to anticipate to confirm your
hypothesis.
DIFFERENTIATING: Respiration vs Phonation
• S-z ration might be normal for someone with respiration problems; paired with max a
phonation you can determine respiration (volume of air) problems.
• Loudness – more respiration, pitch- more phonation; both need volume
• Both can give info about closure, but glottal coup will give info about closure and vibration
(vibrate smoothly). Cannot cough? Adduction + pressure (respiratory problem) problems.
For soft cough you can also ask them to “hik” to determine the adduction + pressure.
b) Resonance Subsystem
• “This portion of the assessment focuses on the velopharyngeal competence. Incomplete
closure of theVP-port will result in hypernasality, a symptom most frequently linked with
spastic, flaccid and hypokinetic dysarthria. Velar movement and voice quality are also
evaluated through other tasks of the motor speech assessment; therefore the findings of the
following two tasks should be combined with the previous results to arrive at the most
accurate description of the patient’s velopharyngeal function.”
• Focuses on the velopharyngeal competence
o Incomplete closure of the port will result in hypernasality caused by inappropriate
nasal emissions – symptom most frequently linked with spastic, flaccid and
hypokinetic dysarthria
• Velar movement and voice quality are also evaluated using other tasks of motor speech
evaluation
• Findings of ALL tasks should be considered to arrive at the most accurate description of the
patient’s velopharyngeal function.
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• Velum has a partner – the pharynx. Superior laryngeal constrictor – velopharyngeal closure.
• Hyponasality: not part of dysarthria. The resonance might be affected but will not be
hyponasality as a typical picture. Hyponasality means there’s something blocking like the
adenoids or their nose is blocked.
• Knowledge and understanding of the relevant anatomy and physiology is important:
o Understand and explain the mechanism of velopharyngeal closure. How is closure
achieved?
Activities, Measures and Tasks

a) OSME – evaluate velar function by listening to resonance
b) Flutter Test (Appropriate?)
a. “Take a deep breath and say /u/ for as long as possible.” (Alternate occluding and
leaving nostril opening during phonation)
b. Is there a difference between production (/u/) (high vowel, most affected by closure
of velum) when nostrils are open/unoccluded vs. occluded? You take your hand with
glove, and you close one nostril, then alternate between occluding one nostril and
both. Should not be nasal, should not be any change in quality as there should not
have air escaping through nose. Ask the patient to blow their nose before doing the
test. This speaks to your nasal resonance.
c) Cold mirror (Accuracy/reliability?)
a. Not reliable/preferred due to many false positives
b. “Take a deep breath and say /u/ for as long as possible.” (Hold the mirror under the
persons nose during phonation.)
c. Does the mirror fog up during phonation? (Positive physiological sign for nasal
emission – confirmed by hypernasal speech quality)
d) Party Blower (with front end cut off) (Appropriate?)
a. To maintain airflow; air should only go through mouth; party blower will not stay
straight if air is escaping though nose; problems with volume would have already
been detected and will be able to sustain for short period.
c) Articulation Subsystem
In addition to the speech sound assessment in OSME and continuous speech assessment:
a) Articulation Test - repertoire of speech sounds in specific language(s)
a. Full articulation assessment to determine repertoire of speech sounds in specific
language(s).
b) Maximum intra-oral pressure
a. List of all the plosives to target: listen for clarity. Not just in isolation; in word.
c) Maximum force of closure
a. Bilabials - you need lip approximation.
(Refer to articles on SUNLearn).
d) Prosody (Focus is on production of prosodic/supra-segmental speech characteristics)

Are they able to speak in an auditory interesting way, or is it monotonous.
Respiration: pressure + volume problems.
a. Speech rate
o e.g. marked slow, fast, affecting speech intelligibility?
o Too fast/too slow. Too fast: blurred speech production.
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b. Stress contrasts
o Pitch, loudness, duration of the stress.
o “The cat sits on the mat.” – Don’t use this; make up your own.
o Use this to change meaning – put stress on different words.
c. Intonation
o (Questions, assertions, exclamations)
o e.g. You did whát?
Good for yóú, girl.
Oh my, oh my!
o Try to make it within the person’s field of interest. You want to look at inflection in
the end.
o Assertion: “But I do think it is important”. / “But I think it is important”.
o Exclamation: Ask px to akt surprised/object loudly.
Which types of speech tasks/activities are needed to ensure assessment is functional?
e) Diadochokinesis – Combined Systems

Combination of Systems
• Two measurements of importance:
o Alternating Motion Rate (AMR), and
o Sequential Motion Rate (SMR)
▪ Alternating Motion Rate assesses the patient’s ability to move the
articulators in a rapid, smooth repetitive manner
▪ Sequential Motion Rate assesses the patient’s ability to move the
articulators in a rapid, smooth sequence of motions
• Measurements are known as diadochokinetic rate measurements.
o What is the diadochokinetic rate? The diadochokinetic (DDK) rate is a measurement
that speech-language pathologists (SLPs) can make. These professionals help people
with communication problems
• SMRs are more difficult to perform accurately than AMRs.
• AMRs provide information about the rate and rhythm of syllable repetition.
• SMRs provide information on the sequencing, smoothness and rate of production.
• SMRs highlights symptoms of Apraxia of Speech (AOS).
o Not unusual for individuals with AOS to complete AMR task successfully and
struggle to complete even first attempt at the SMR sequence.
o Mistakes with sequence of syllables, phoneme replacements and articulatory
groping behaviour during production of a speech sequence.
o However, not ALL individuals with AOS are able to complete the AMR task
successfully, i.e. many have difficulty with both tasks.
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NB: Know the tasks inside out. Be able to write down the instruction.
Alternating Motion Rate (AMR)

• Careful consideration of AMRs can provide a clinician with information about the type of
Dysarthria
o Task: “Take a deep breath and say /p, p, p/ as long, as fast and as
evenly/clearly as possible.” (Repeat the task with /t/ and /k/ respectively.)
o Evaluate: Speed/rate and rhythm
o Observations: Listen for changes in loudness, pitch and articulation. (Must be
performed in a controlled manner)
o If they do it too slowly, ask to say it faster. You want to put stress on the system.
Does the articulation fall apart now that they say it faster? Must be in a controlled
manner.
o Spastic and Flaccid Dysarthria – slow and regular AMRs.

o Hyperkinetic and Ataxic Dysarthria – slow and irregular AMRs, e.g. excessive
variations in loudness.
o Hypokinetic Dysarthria – often more rapid AMRs than normal, e.g. blurred
articulation.
o AOS – possible that can perform task in a normal manner after a number of
repetitions. Why? (Only one movement plan.) Not in severe cases.
For person with apraxia vs dysarthria: Apraxia might improve. Once you’ve broken plan, you might
be able to repeat. 2min later they might be back to square 1. Person with dysarthria wont improve,
they have a problem with execution – actually performing the motion.
Sequential Motion Rate (SMR)

• SMRs highlights the symptoms of Apraxia of Speech (AOS)
o Task: “Take a deep breath and say /p, t, k/ as long, as fast and as
evenly/clearly as possible.”
o Evaluate: Sequencing, smoothness and rate
o Observations: Listen for changes in loudness, pitch and articulation. (Must be
performed in a controlled manner).
o AOS – delays in the beginning of the task (latency period between the signal to phonate
and the initiation of phonation), phoneme substitutions, incorrect sequencing of
syllables, and articulatory groping for the correct phoneme placement.
o Groping = seeking. Groping around in the oral space trying to figure out where
to produce the sound. Articulatory groping behaviour.
o Dysarthrias – will continue to perform poorly with rate, rhythm, articulation and other
subsystems affected as in AMRs. Problem remains execution of speech movements.
More difficult to perform. Apraxia struggles; 3 different plans in the correct sequence.
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f) Connected / Contextual Speech
Contextual (Connected) Speech – Speech Intelligibility (Is there any deterioration?)
Contextual speech: like a speech sample. Start during case history already. Record the speech
sample.
a. Spontaneous speech (Conversational speech), e.g. narratives (re-telling vs generating new
narrative) and conversations.
b. Narrative
c. Reading tasks, e.g. word lists, rhymes, poems, songs, magazine/newspaper articles, etc.
a. If px is able to read, might be illiterate or has/had dyslexia. But good example of
structured connected speech.
b. Poem/song/rap or children’s rhymes – already have rhythm built in. Good task to
use.
d. Descriptions, e.g. everyday objects, procedures or steps to follow, giving directions, etc
Conclusion: intelligible – intelligible with some difficulty – unintelligible. What is interfering?

(Subsystems involved)
g) Stress Testing – “Performance Load Tests” • Not the same as prosody.

• You place person under
Stress Testing – “Performance Load Tests” stress in terms of speech
production to see how
Not the same as “stress contrasts” – (distinguish from prosody stress shift). system performs.
a. Increased phonemic complexity • AOS: Will show clear
a. e.g. CVC, CCVC, CCVCC, CCCVC, etc./VCV, VCCV, VCVC, etc. fallout here.
b. e.g. CV vs. CVC vs CCVC (clusters) vs. CCCVC vs. CVCC etc. • Myasthenia gravis (flaccid
c. Grading it – making it systematically more difficult. dysarthria) will show clear
fallouts.
d. You can model and they imitate, it’s not about generating the
• In prosody you are looking
language, only speech. at shifts in stress.
b. Monosillabic vs. Multisillabic words
a. e.g. five, fire, firefly, firebrigade, firefighting-fit, etc.
b. Butter vs butterfly vs butterfly wing
c. Kom vs komkommer vs komkommerslaai
d. Here we look at the correct programming and taxing the system (volume +
articulation).
c. Increased utterance length
a. Start with simple phrase or sentence.
b. Grade and control by considering number of syllables and phonemic complexity.
c. Everything combined + volume.
Refer to the Kent, Kent and Rosenbek (1987) article on SUNLearn.
• Undershooting+overshooting - ONLY for ataxic dysarthria. For artic, they overdo the
direction, distance and timing. So it affects the pronunciation.
• For ax tasks: start with respiration+phonation, then resonance, then artic, prosody,
connected speech, ddk's + stress testing. It will then all make sense because you can link it to
what you've already seen.
• Atrophy, fasciculation + fabrillations = will only see in tongue (velum is bilaterally
innervated).
• Gait: a person's manner of walking.
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DIFFERENTIAL DIAGNOSING
Definition
“The process of narrowing possibilities and reaching conclusions about the nature of the deficit.”
 Brodley, Lane & Strough (1999)
 Abdo et al. (2010)
 Sackett et al. (1991)
• Won’t ask any definitions again.

• Broca’s aphasia goes hand in hand with AOS due to site of lesion. The one affects
language production, the other has problem with planning.
General Guidelines (Duffy, 2013, p. 356-357)

1. Speech evaluation should always attempt to make a diagnosis possible.
2. When results cannot go beyond description, reasons should be stated explicitly.
3. Diagnosis should not be made if one cannot be determined.
4. Speech diagnosis should be related to known neurologic diagnosis or lesion localization.
5. Remember, different speech disorders can co-exist.
6. Examination can lead to conclusion that speech is normal.
a. Speech could have changed – still within normal limits. Formulate list of diagnostic
possibilities.
b. Change has occurred outside motor system, e.g. Mood.
c. Perception of abnormality due to psychological factors
d. Speech is normal, but traumatic event (physical/psychological) has generated
complaint f change.
e. Referral agent mistook a developmental disorder as a new symptom of neurological
disease.
7. Diagnostic label/possibilities make communication easier. However, be careful!
Distinguishing between Dysarthrias
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Distinguish between AOS and Aphasia
Distinguish between AOS and Dysarthria

DYSARTHRIA APRAXIA
ETIOLOGY
• Dysarthric errors result from a disruption of • Apraxia results from an impaired ability to
muscular control due to lesions of either the generate the motor programs for speech
central or peripheral nervous systems. In this movements rather than from the disordered
way, the transmission of messages transmission of controlling messages to the
controlling the motor movements for speech speech musculature. Apraxia is a
is interrupted. Because it involves problems planning/programming problem, not a
with the transfer of information from the movement problem like dysarthria.
nervous system to the muscles, dysarthria is
• Apraxia occurs following damage to Broca's
classified as a neuromotor disorder.
Area, or Brodmann's area 44, which is located
• Central Nervous System Lesions on the third gyrus of the left frontal lobe.
Damage to the pyramidal tract causes spastic Thus, apraxia is always the result of a central
dysarthria. Lesions of the substantia nigra cause nervous system lesion. It is a cortical
hypokinetic dysarthria. Disruption of feedback problem, not a motor impulse transmission
loops involving the cerebellum cause ataxic problem like dysarthria
dysarthria.
• Peripheral Nervous System Lesions

Finally, damage to any part of the peripheral
nervous system serving the muscles of speech
causes flaccid dysarthria.
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TYPES OF ERRORS
• Errors are consistent and predictable. • Inconsistent and unpredictable
• Different error patterns occur in spontaneous
speech versus repetition
• Spontaneous speech contains fewer errors
than repetition tasks.
• There are no islands of clear speech; no • There are islands of clear speech; when
matter what the speaking task or materials producing over-learned material or material
used, the patient will exhibit the same that has become automatic, the patient will
amount and types of errors. speak clearly.
• Errors are mainly distortions and omissions. • Substitutions are the most common type of
Distortions are the most common type of error, with others normally being
error in dysarthria approximations of the targeted phoneme
• Other types of errors found in apraxic speech,
listed from most to least common, include:
Repetitions
Additions
Transpositions
Prolongations
Omissions
Distortions
• Errors are often perseveratory or anticipatory
in nature. As in stuttering, the anticipation of
errors causes dysfluent speech.
• Groping, trial and error types of articulatory
movements. This is probably related to the
anticipation of errors.
SPEECH SOUNDS AFFECTED

• Consonants consistently imprecise, with the • Vowels are easier to produce than
production of final and initial consonants consonants.
being equally impaired. • Single consonants are easier than blends.
• Vowels are not affected as much although, • Final consonants are easier than those in the
due to problems with tongue movement, initial position. This may occur because initial
they may sound too much alike. consonants are affected by anticipatory
errors. Also, perhaps once an apraxic gets
speech started with the production of a
vowel, production continues in a more
automatic fashion.
• Fricative and affricates are the most difficult
phonemes for apraxics to produce. (These
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sounds require very complex articulatory
movements.)
ASPECTS OF SPEECH AFFECTED

• All aspects of speech, including articulation, • Apraxia is mainly a disorder of articulation.
phonation, resonance, prosody, rate and Some prosodic problems may occur as a
respiration, may be affected by dysarthria. result of the hesitations caused by the
Dysphagia frequently accompanies dysarthria apraxic speaker's anticipation of errors.
However, problems with voice, resonance,
etc., are not symptomatic of this disorder.
ADDITIONAL PROBLEMS
• Changes in muscle tone may accompany • As lesions of Broca's area do not cause
dysarthria. The movements of the soft palate, changes in muscle tone, apraxia may occur
lips, tongue and jaw may be impaired not without such symptoms. Therefore, apraxia
only during speech, but also in the context of of speech may occur without concomitant
vegetative functions. As such, changes may swallowing problems. The movement of the
affect the oral and pharyngeal stages of the velum, lips, tongue and jaw will only be
swallow, dysarthria and dysphagia often co- impaired during speech. Of course, a stroke
occur. may damage Broca's area and motor tracts or
• Diadochokinesis will be slow. However, it will other areas involved in swallowing
be normal within the limitations of the simultaneously. In such a case, dysphagia and
neuromuscular disorder; the patient may apraxia would be seen in the same patient.
distort or omit phonemes but syllables will be • Diadochokinesis will be slow and abnormal;
produced in the correct order. syllables may be produced out of order.
EFFECTS OF UTTERANCE COMPLEXITY

• Utterance complexity does not directly affect • Increases in utterance complexity cause
the degree of imprecision present in a increases in the complexity of apraxic
dysarthric patient's speech. Such a patient symptoms. For example, it is much easier for
will produce single syllable and multi-syllabic a patient with apraxia to produce single
words with approximately the same amount syllable versus multisyllable words and
of distortion. sentences.
EFFECTS OF SPEECH RATE

• As the rate of a dysarthric's speech increases, • As the rate of an apraxic's speech increases,
the intelligibility of that person's speech will the intelligibility of that person's speech may
decrease proportionally. In order to improve actually increase probably to the same
iltelligibility, the dysarthric must learn to slow overlearned response as with automatic
rate by articulating complex words syllable by speech-days of the weeks etc.
syllable. • Noting the effect of increased rate on speech
intelligibility may be one way to help
differentiate between dysarthria and apraxia.
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THERAPY
• For many clinicians therapy for dysarthria is • Although some recommend compensatory
strictly compensatory. If motor pathways are techniques most apraxics benefit more from
damaged, they cannot be repaired. The therapy that focuses on retraining more than
dysarthric patient must learn to use on compensation. Melodic Intonation
techniques that increase the intelligibility of Therapy (Sparks and Holland, 1976) is one
his/her speech. technique that is frequently used with apraxic
patients. It is believed that, through the use
of melody and rhythm, this method
stimulates the creation of more neuronal
connections in the right hemisphere. This
may allow the "potential Broca's area"
located in the right hemisphere to begin
generating motor programs that control
speech production. Duffy (1995) describes
the type of patient for whom MIT might help
best.
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Practice case: Flaccid Dysarthria
Case
1. Associated or related deficits/disorders – Other contributing factors
a. Do you have any associated or related deficits/disorders?
i. Often people with aphasia/dysarthria/apraxia have dysphasia
2. Perception of deficit/disorder
a. Describe how you perceive your condition?
b. How did CVA affect relationships?
c. Wife’s perceptions
3. Intervention (to date)
a. What intervention have you received?
i. Who else are you seeing? This will give an idea of the overall picture.
4. Expectations and needs (ICF based)
a. What are your expectations?
i. He is a professional.
ii. Also, you want to know for referrals.
Medical history: in this case we have enough information; the case explains the stroke. But you
might also need to ask about blood pressure.
Px’s who come to you are not able to speak; so will not necessarily be able to give much information.
Brainstem stroke = no hemiplegia. And it says he can walk.
Might have balance problem due to Cranial nerve 8.
Goal setting: goals for sessions. “This is why I see you”. Mutual goal setting.
Activities: can’t talk on the phone or run a meeting
Participation: can’t participate in his role like before.
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TREATMENT AND HABILITATION (GENERAL)
Management Issues and Decisions
a) Focus of intervention should be on communication rather than speech (only).
b) Purpose of intervention is to maximise the effectiveness, efficacy and naturalness of
communication. Specific intervention goals should be identified, namely:
i. restore function,
ii. compensation, or
iii. adjustment.
c) Identify factors which may influence intervention decisions, namely:
i. medical diagnosis and prognosis;
ii. impairment, limitations and restrictions (ICF) (including those from society);
iii. environment and communication partners;
iv. motivation and needs;
v. associated problems; and
vi. the health care system.
d) Determine the therapy focus, e.g. component(s) targeted or prioritised.
e) Plan the duration and termination of intervention.
General Approaches to Treatment

a) Medical Intervention – pharmacological, surgical
i. Parkinsons - medication for speech.
b) Prosthetic Intervention – perceptual normalcy, speech modification, biofeedback
i. Biofeedback: feedback from your body.
ii. Speech bulbs for cleft.
iii. Resonance often require prosthesis. Hard to fix.
c) Behavioural management – speech-orientated, communication-orientated
i. Speech Therapist field.
ii. Most of 10b is behavioural based.
d) Augmentative and alternative communication (AAC)
i. Px may need all 5 at different stages, or only 1.
ii. Not therapy approaches, just approaches to treatment.
e) Counselling and support
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Rationale and Principles of Behavioural Management, and Principles of Motor
Learning
Rationale for Behavioural Management

Neural plasticity justifies intervention, because …
a. the brain is not a static organ
b. organisation of the cortex is not fixed (flexibility/adaptation)
c. neural adaptation/recovery occurs with muscle use
d. the nervous system is capable of recovery and reorganisation after injury
The brain is not a static organ

• The brain’s structure and function can be altered as a function of intracellular changes,
changes in intercellular and synaptic interconnections, biochemical or genetic level
modifications and, most relevant in this context, behavioural training.
Organisation of the cortex is not fixed (flexibility/adaptation)

• Adaptive changes in the nervous system, a process known as neural adaptation or
neuroplasticity, result from learning that occurs through muscle use and changes in patterns
of behavior.
• Neuroplasticity is the mechanism through which an injured brain reorganizes itself to
reacquire or compensate for lost or impaired abilities, either naturally or through
rehabilitation.
• Although plasticity is more evident in the young, studies of healthy old animals have
demonstrated benefits from motor skill training and participation in social environments;
The adult cortex can be reorganized by experience, learning, and physical action,
presumably because of neuroplasticity (see the next section). Under some circumstances,
and to varying degrees, such plasticity can occur at all levels of the nervous system, not just
the cerebral cortex.
Neural adaptation/recovery occurs with muscle use

• Motor activity is a powerful driver of cortical reorganization (neuroplasticity) in normal skill
acquisition and after neurologic injury. The neural adaptation induced by movement can
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permit an increase in the firing rate of motor units or the recruitment of previously
underused motor units, with a subsequent increase in strength and power and better
coordinated activation of muscle groups. The notion of motor plasticity recognizes a two-
way interaction in which repeated motor performance influences cortical reorganization,
with subsequently improved motor performance.
The nervous system is capable of recovery and reorganisation after injury

• There are certainly limits on the degree to which the adult nervous system can recover from
injury. For example, studies of experimentally lesioned rats document persisting impairment
of qualitative aspects of movement, even when the ability to achieve movement goals
recovers.
• More germane, and unfortunately, clinicians are regularly reminded of these limitations in
their daily practices. Nonetheless, some recovery of function after injury very often occurs.
• Some of what happens during recovery reflects natural physiologic responses that are
independent of volitional behaviour, such as resolution of edema, certain synaptic changes,
or recruitment of other brain areas to perform certain functions, all of which can occur
within hours of injury; genetic factors may also influence aspects of plasticity. Other changes
are more related to sensorimotor and cognitive activity. For example, functional magnetic
resonance imaging (fMRI) data suggest that reorganization within the CNS is evident in
patients who have recovered from hemiparesis caused by cortical stroke; findings
demonstrate increased activity in a larger region of the motor cortex than is normally
activated, as well as increased activity in the sensorimotor cortex in the unaffected
hemisphere, ipsilateral premotor cortex, and the contralateral cerebellar hemisphere.
Principles of Behavioural Management

a) Motor reorganisation after injury requires use (functional movement)
b) Compensation requires that speech production becomes conscious
c) Increasing physiological support often should be the initial focus of treatment
i. Do proper Ax and determine which system needs tx first.
d) Principles of Motor Learning* should dictate the structure of the treatment plan, e.g. speech
and communication orientated treatment
i. Use for session plans.
e) Medical and Speech diagnoses are relevant to management intervention
f) In general, management should start early, but not in all cases
i. if not medically stable, WAIT.
g) Compile baseline data is necessary to establish therapy goals and to measure change
i. Do the ax more than once to give enough opportunity for data points.
ii. Use every time you see px to determine baseline.
h) Organisation of sessions is instrumental – Duffy (2013), p. 395-396
i. frequency (therapy),
ii. ordering tasks (session plan), (depends on px whether you start or end with most
difficult task)
iii. error rates (not so challenging that success cannot be achieved, but still requiring
more than average effort),
▪ But it is also supposed to be hard, without overwhelming them. Be flexible
iv. fatigue, and
v. individual vs. group therapy (purpose of each).
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Principles of Motor Learning:
(Explain each. Why are these principles important? How are they linked to the approaches?)
NB
1. Nothing improves speech like speech.
▪ But has to be functional.
2. Drill is essential.
▪ Being repetitive without being boring
3. Formal instruction and demonstration improve performance.
▪ Px is learning to do it consciously.
4. Self-learning should be encouraged.
5. Feedback (consistent, accurate and honest) is essential.
▪ Never say "good job".
▪ Let px take video of what they are doing and take it home.
▪ Mirror work, visual and auditory feedback.
▪ Give specific feedback.
6. Specificity of training is of utmost importance.
7. Consistent and variable practice is valuable.
▪ Repetition without repetition/being boring.
8. Improve muscle strength.
▪ Respiration muscles - do with physio + OT. Flaccid, Ataxic and Hypokinetic
dysarthria.
9. Speed-accuracy trade-off.
▪ Write in rationale for session plan. Will use pacing board to try and slow down
(decrease speed) for speed-accuracy trade-off.
In test: You will get a case. You want to see which principles are being honoured for the px's
treatment.
Motor learning includes 3 stages:

 Cognitive
NB  Associative
 Automatic
Hierarchy to determine goals:

• Start with the aspect/subsystem/component that will bring about most overall improvement
• Identify the aspect/subsystem/component that will be readily modified with minimum input
• Reduce speech impairment – target specific subsystem(s)
• Reduce or eliminate ineffective or overcompensation
• Develop effective speech/communication compensatory behaviour
• Use functional prostheses to normalise function
• Use functional prostheses to improve function
• Improve interaction
• Conserve communication skills
• Use Augmentative and Alternative Communication (AAC)
• Guide and support significant others or caregivers, e.g. optimise interaction
Choice of above mentioned goal(s) determined by:

• Individual’s communication needs.
• Severity of communication handicap.
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• Nature of underlying impairment, e.g. neurological damage due to TBI, progressive
condition.
• Motivation and cooperation of individual and caregivers/SOPs.
Treatment for the Specific Types of Dysarthria (Subsystems)

Later in notes.
Treatment for Apraxia/Dyspraxia

Later in notes.
MEET YOUR PATIENTS:

(Go through the following Case Studies and apply the above information as required).
Case Study 1: Application and SNAPPS Preparation

A twenty-seven-year-old entrepreneur is referred to you for management four weeks after he was
seriously injured during a rugby match. On admission to the hospital he was unconscious and
presented with respiratory problems. A tracheostomy was performed next to the rugby field to
manage the immediate respiratory distress and the patient was fed via nasogastric tube for 10 days
after admission. The man was in an induced semi-coma for one week after the incident and no
assessment could be conducted. He has since showed a marked recovery. His twin brother, who is
also his business partner, accompanies him to the consultation.
The following medical assessment information is available:

• Vital signs are normal and tracheostomy tube removed
• Right hemiparesis with moderately increased muscle tone visible in trunk and limbs (right)
• Markedly reduced breath support for speech – 2-3 syllable utterances
• Poor voicing during speech production attempts – soft, monotonous, with audible
hypernasality
• Hypertonic tongue and severe drooling from right side of mouth
• “Good” receptive language skills
1. You are chairing a case discussion of your patient (Case 1) in the adult neuro out-patient clinic
at Tygerberg Hospital where you work. Outline your plan for the patient to your colleagues
and justify your choices. Follow points 6.1 and 6.2 on p. 39 of the Class Notes.
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Case Study 2: Application and SNAPPS Preparation
1. The patient’s wife is a physiotherapist. Explain to her the principles of motor learning which
will guide your treatment plan.
2. By following the Hierarchy to determine Treatment Goals on p. 41 of the Class Notes, and the
specific techniques in Unit 10b, compile a treatment plan for your patient.
(This is a very „big” question, but it would be worth it working out an answer. It will offer you an
opportunity to learn, apply and check the new information covered in Unit 10. Work together on this
in preparation for the first contact session at the end of July, indicated in the course guidelines. I will
confirm the date with you closer to the time. So, please don’t wait too long.)
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TREATMENT AND HABILITATION (SUBSYSTEMS)
Respiration (Speech-breathing)
The overarching goal for treatment of respiratory impairments in dysarthria is to attain a steady sub-
glottal air pressure level, which allows for non-fatiguing production of speech with adequate
loudness and breath group length. When selecting preliminary respiratory interventions strategies, it
is always best to use information about the client's respiratory pattern and determine first whether
the respiratory patterns are primary respiratory impairments (neuromotor disorder), compensatory
strategies (appropriate adjustments), maladaptive strategies (inappropriate/non-productive), or
some combination.
Treatment Focus:
i. respiratory support (prosthetic support),
ii. behavioural compensation and control, and Don’t have to know the tables.
iii. instrumental bio-feedback
Specific Treatment Strategies, Techniques and Goals:
“+” may be appropriate; “++”, uniquely appropriate, but not necessarily for all patients;
“-” contraindicated, rarely necessary, or uncertain.
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Phonation
The goal for treating phonatory impairments is to increase respiratory support, velopharyngeal
competence and decrease laryngeal weakness that is preventing the client from forcefully adducting
the vocal folds. The clinician begins by assessing non-speech reflex patterns and begins working to
transition from reflexive to voluntary phonation.
Treatment Focus:
i. (compensation for) laryngeal deficit, and
ii. optimise respiration and resonance
Other Suggestions:
Have family members or caregivers use a phonation diary to report the times when reflexive
phonation occurs. The diary can illustrate changes over a specified time. For more complete details
see Yorkston, K. M., Beukelman, D. R., Strand, E. A., & Bell, K. R. (1999). Management of motor
speech disorders in children and adults, p. 343-344.
• Neck turning - towards paralysis. You are compacting the tissue.

• Massaging - controversial. No evidence.
• Soft onset can be used (breathy onset).
• Reflexive phonation - basically coughing.
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Resonance
The goal of managing velopharyngeal inadequacy is to dampen effects of the nasal cavity to reduce
overall loudness. One common way to determine velopharyngeal inadequacy is to compare speech
with the nares occluded versus not occluded. This comparison will give details on how the
velopharyngeal inadequacy is affecting speech intelligibility, loudness, phrase length, and
articulatory precision.
Treatment Focus:
i. reduce the effect of the velopharyngeal deficit, and
ii. improve speech intelligibility by optimising respiration and articulation
Speaking in supine position - only practical in acute phase. Velum is pulled by gravity in direction of
tongue. Biofeedback.
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Articulation
The goal for articulation treatment is usually to improve accuracy and precision of sound production.
However, this is usually accomplished by focusing on functions other than those directly related to
place and manner as in the typical types of articulation therapy. Usually articulation is remediated by
slowing the rate and modifying prosody therefore there is usually less time spent with articulation
remediation.
Treatment Focus:
i. accuracy and precision of speech production,
ii. improved speech intelligibility by optimising respiration, phonation and resonance, and
iii. modification of speech rate and prosody
Also refer to the “Bite block” under Prosthetic Treatment.
• Immediately put it into a word after doing exercises.

• Integral stimulation - what we're all going to do.
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Prosody and Naturalness of Speech
The goal of prosody and naturalness is to maximize the accuracy of prosodic patterns and their
naturalness. The theory is that working on stress should be done earlier in the treatment sessions
once the individual's respiration and articulation have been determined to be sufficient to support
connected utterances. Yorkston, Beukelman, and Bell (1988, p. 464) defined naturalness as "a
perceptually derived, overall description of prosodic adequacy. Speech is considered natural if it
conforms to the listener's standards of rate, rhythm, intonation and stress patterns, and if it
conforms to the syntactic structure of the utterance being produced."
The most common way to manage prosodic deficits is by acoustic analysis. Viewing the fundamental
frequency, intensity, and durational contours of words and phrases may provide information about
how a speaker is signalling stress and the source of perceived unnaturalness too, as well as providing
feedback during management.
Treatment Focus:
i. accuracy and naturalness of prosodic patterns
"Conducting" the px's speech; being the conductor like in a choir.
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Speech Rate
The goal of rate modification is to facilitate articulatory precision and intelligibility by allowing time
for full range of movement, improved coordination and improved linguistic phrasing. It has been
stated that reducing rate may also be easier to achieve than other motor goals because of the
physiologic limitations imposed by the different dysarthrias. There are different ways to decrease
rate through prosthetic devices or more natural methods. However, it is important to remember
that rate reduction should always improve intelligibility. If it does not, the strategy should not be
used because it will reduce the naturalness of the individual’s speech.
Treatment Focus:
Articulatory precision and speech intelligibility by allowing time for:
i. full range of movement,
ii. improved coordination, and
iii. improved linguistic phrasing
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Overview of Medical-Surgical and Medical-Pharmacological Treatment
Medical intervention should always be done in collaboration with members of the (multidisciplinary)
team which includes the speech pathologist, ENT, plastic surgeon, and/or neurologist. It is important
to remember that the speech pathologist must beforehand assess speech carefully and determine
the need for medical or surgical intervention. Sometimes pharmacological management may be all
that an individual will need. Some neurological diseases commonly associated with dysarthria are
effectively managed by drugs and the benefits can include improved speech. Other times, however,
surgical intervention is needed such as surgery for pharyngeal flap or sphincter pharyngoplasty. But
again, it is important to remember that in some cases there may be improvement but no resolutions
and sometimes there can be a development of new deficits.
Treatment Focus:
Improve speech by positively influencing (i.e. improve) intelligibility, rate and naturalness of an
individual’s speech directly or indirectly.
Specific Treatment Strategies, Techniques and Goals: Medical-Surgical
Specific Treatment Strategies, Techniques and Goals: Medical-Pharmacological
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Overview of Prosthetic Treatment
The goal of prosthetic management is to enable individuals to improve speech or assist them in their
communication. There are several mechanical and electronic devices available that may give
temporary or permanent relief. Some prosthetic devices can directly modify what happens in the
vocal tract during speech therefore helping to promote perceptual normalcy. Other devices can help
to modify speech after it has been produced. Prosthetic devices are also available that will help to
modify the manner of speech production. These devices may alter rate or prosody in usually an
abnormal way. It is important to remember that prosthetic devices can be used temporarily and
used only until physiological recovery or the effects of behavioural management allow them to be
discarded.
Treatment Focus:
i. normalise or improve speech, and
ii. support communication
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APRAXIA
Apraxia of Speech (AOS) definition:

“AOS is a neurologic speech disorder that reflects an impaired capacity to plan or program
sensorimotor commands necessary for directing movements that result in phonetically and
prosodically normal speech. It can occur in the absence of physiologic disturbances associated with
the dysarthrias and in the absence of disturbances in any component of language.”
Motor Planning
“During the planning phase of the production of articulated speech … a gradual transformation of
(phonemes) to a code that can be handled by a motor system has to take place.”
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The Brain and Planning
• Planning is mediated at the “highest level” of the motor hierarchy.
• Motor planning of speech (and other) movement is the responsibility of the “association areas.”
• Premotor cortex
• Supplementary motor area
• Prefrontal and parietal association areas
• Caudate circuit of Basal Ganglia
• Broca’s and Wernicke’s areas
Primary Cortices Premotor and Supplementary Motor Areas
Association Cortices
• Pre-frontal Area: Formulate integrated behaviour

• Association Areas -> premotor cortex and SMA: organize movement in medial stage
• Premotor Cortex, SMA and BG: Neuronal processing and direct planning
• Parietal Association Cortex: Integration of sensory modalities and planning, e.g. sensory
memory store for internal feedback
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So what?
• “The extensive connections between cortical motor and sensory areas suggest that the
planning phase requires a complex coalition between these neural structures and thus
between motor and sensory information.”
• “Motor planning is goal orientated, and motor goals for speech production can be found in
the spatial and temporal specifications of movements for sound production.”
o Spatial: place + manner of articulation.
Management
• Primary goals of treatment: (for session plans)
o Effectiveness
o Efficiency
o Naturalness of communication
• AOS treatment focuses on:
o Re-establishing plans or programmes
o Improve ability to select, activate or set parameters, e.g. duration, speed, force.
Approaches
• Medical intervention
o Pharmacological, e.g. seizures, Dopamine
o Surgery
• Prosthetic treatment
o Self-generated rate reduction, e.g. metronome vs finger tapping, “pace board”
• Behavioural management
o Speaker vs. communication-orientated
• AAC
• Counselling and support
Rationale for Behavioural Management

• Neural plasticity justifies intervention, because …
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o the brain is not a static organ
o organisation of the cortex is not fixed (flexibility/adaptation)
o neural adaptation/recovery occurs with muscle use
o the nervous system is capable of recovery and reorganisation after injury
(Class notes, p. 39)
Principles of Behavioural Management

• Motor reorganisation after injury requires use (functional movement).
• Compensation requires that speech production becomes conscious.
• Increasing physiological support often should be the initial focus of treatment.
• Principles of Motor Learning* should dictate the structure of the treatment plan, e.g. speech
and communication orientated treatment.
• Medical and Speech diagnoses are relevant to management intervention.
• In general, management should start early, but not in all cases.
• Compile baseline data is necessary to establish therapy goals and to measure change.
• Organisation of sessions is instrumental.
o frequency (therapy),
o ordering tasks (session plan),
o error rates (not so challenging that success cannot be achieved, but still requiring
more than average effort),
o fatigue, and
o individual vs. group therapy (purpose of each).
Important Considerations
• Baseline data, stimuli selection and ordering
• Physiological Support
• Principles of motor learning dictate treatment
• Imitation
o Volitional response
o Stimuli provide model/map
o Simplify drill –cognitive, linguistic
o Pure imitation will not resolve AOS.
o You have to do GRADING. Which phoneme(s) are you going to target. Phonemic
complexity. Semantic complexity. Communicative value. What are you going to
select. First make sure you have the sensory aspect. 8 step integral stimulation.
• Intra-or inter-systemic re-organisation
o E.g. Rote counting, progressive approximations, phonetic placement, minimal pairs,
non-speech activities (“magnet effect”)
• Gestural re-organisation
o E.g. non-speech movements like tapping for rate, rhythm and stress
Principles of Motor Learning

Principles of motor learning dictate treatment
• nothing improves speech like speech,
• drill is essential,
• formal instruction and demonstration improves performance,
• self-learning should be encouraged,
• feedback (consistent, accurate and honest) is essential,
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• specificity of training is of utmost importance,
• consistent and variable practice is valuable,
• improve muscle strength, and
• speed-accuracy trade-off
Techniques (Duffy, 2013, Ch. 18)

• Integral Stimulation (Rosenbek, Lemme, Ahern, Harris & Wertz, 1973)
• Sound Production Treatment (Wambaugh, et al., 1996)
• PROMPT (Chumpelik, 1984; Square-Storer& Hayden, 1989)
o A lot of kinaesthetic cues (touching). Lot of tactile info to help child find pattern.
• Melodic Intonation Treatment (Sparks, Helm & Albert, 1974)
• Biofeedback (Vibrotactile stimulation) (Rubow, Rosenbek& Collins, 1984)
• Moto-Kinesthetic Speech Training Method (Stinchfield & Young, 1938)
• Association Method (McGinnis, Kleffner& Goldstein, 1956)
• Sensory-Motor Approach (McDonald, 1964)
• Touch-Cue Method (Bashir, Grahamjones& Bostwick, 1984)
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Not for the test.
DEVELOPMENTAL APRAXIA
A brief history …
• First described by Hadden (1891), doctor, case of ‘Charles M’
• Orton (1937) descriptions of speech disorder consistent with characteristics of CAS
• Late 1950’s –60’s Morley and colleagues (UK)
• 1960’s –70’s McGinnis, Johnson and Mycklebust (US)
• Classic studies: Rosenbek and Wertz (1972); Rosenbek et al. (1974); and Yoss and Darley
(1974).
• Next 15 years the “era of controversy and strongly held opinions”.
• Research base expanded slowly with more general acceptance of disorder more resources
and involvement of variety of disciplines.
• Caruso , Crary , Hall, Jordan, Love, Maas, Marquardt, McCauley, McNeil, Robin, Shriberg ,
Strand, Van der Merwe, Velleman
Is CAS just a name, just a label?
(Mis)nomers and (Mis)interpretations: “Developmental” or “Childhood”

• “Progress over time” or “state of emergence”
• “Delayed” or “disordered” communication development
• “Acquired” vs. "congenital"
• May NEVER be normal, i.e. not just a maturational issue.
• Impact throughout the developing speech processing and language systems (Also others,
e.g. cognition?)
• Not merely to distinguish time of origin.
• Children: soft neurological signs. No clear site of lesion, even on scans. Adults: hardcore site
of lesion signs; can be seen on scans. Clear frontal-parietal lesions.
“Apraxia” and or dyspraxia

• Praxis, or conceptualisation, planning and programming of skilled voluntary movement
• “Loss of communication skills”
• Implies (purely) neurological basis for problem.
• Planning, programming and learning of fine motor movements and refining skills (control).
• Rather lack of development of communication skills.
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• A clear neurological origin for the disorder has not (yet) been documented.
“Speech ” vs. verbal ” vs. oral

• Use "speech" to support motor base.
• “Verbal” supports both speech and language bases of disorder.
• “Oral” refers to additional feature.
• Planning and programming of movement implicated, but not limited to it.
• Speech acquisition and processing? Language and metalinguistic implications?
• NEVER in isolation. Speech is more than an oral gesture.
• Verbal: speech as outcome, produce sound etc.
• Non-verbal: movement (pucker, lick lips, touch your nose w tongue tip)
Definition of CAS
• “A neurological childhood (pediatric) speech sound disorder, in which the precision and
consistency of movements underlying speech are impaired in the absence of
neuromuscular deficits(e.g. abnormal reflexes or muscle tone).
• CAS may occur as a result of a known neurological impairment, in association with complex
neurobehavioral disorders of known or unknown origin, or as an idiopathic neurogenic
speech sound disorder.
o idiopathic - no known cause.
• The core impairment in planning and/or programming spatio-temporal parameters of
movement sequences results in errors in speech sound production and prosody.” ASHA
(2007, p. 6)
o 6 months of age - no Canonical babbling - can diagnose CAS.
• CAS - high prevalence with ASD children.
• Worster-Drought syndrome (WDS) also associated with CAS.
o Worster-Drought syndrome (WDS) is a type of cerebral palsy (movement disorder)
that affects the muscles around the mouth and throat.
Definition unpacked (Lof, 2012)

• CAS is a neurological disorder
o (still) labelled as "speech-motor disorder".
• CAS is a problem with precision and consistency of movements underlying speech
o difficulties in hitting the exact targets
• CAS is present in the absence of neuro-muscular abnormality(e.g. abnormal reflexes,
abnormal muscle tone)
o not dysarthria –may co-exist, but rarely
o not focused on nerve-to-muscle connection
o not tone or muscle weakness
• CAS as a result of known neurological impairment, in association with complex
neurobehavioral disorders of known or unknown origin, or as an idiopathic neurogenic
speech sound disorder
o Causes?
o Can co-occur with autism, Fragile X (“complex neurobehavioral disorder”)
o Idiopathic means “unique to the individual”, or it could mean “we just don’t know”
(and we may never know!)
• CAS primary impairment of planning and/or programming of spatio-temporal parameters
of movement sequences
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o Core impairment.
o "Time" and "space" for performing the movements of speech.
o Movement sequences –problem getting order and timing of the movements right
and making transitions.
• CAS causes speech and prosody errors
o Prosody and the supra-segmental aspects of speech, particularly applying stress to
syllables and words.
Some uncertainty still remains

• Is the disorder a speech and language-based problem? Or a combination of both?
o It is a combination of both.
• Some of the best “definitions” are the insights from children themselves:
• “My mouth won’t cooperate with my brain.” (K., 13 years)
• “I am thinking the right sounds, but my mouth does something else.” (P.Y. explaining a
frustrating session to a student.)
• “My brain just isn’t cooperating with my mouth today!” (P.H., 12 years)
Characteristics re-visited
Speech Characteristics of CAS

1. Speech sound errors – sound class and manner of production
o Stops and nasals (mostly “resolved” first).
o Fricatives, affricates and consonant clusters (persist).
o Vowels and liquids (variant).
o Classes involving more complex oral gestures.
o Plosives + nasals: respond easiest to tx because you can feel them.
o Vowels: no other speech disorder vowels are affected. CAS use schwas.
o Speech acquisition is markedly slower.
2. General developmental pattern observed in children with OAS; speech acquisition may take
place at a (much) slower rate and possibly only with intensive therapy.
3. Irregular mistakes (“Errors of complication”)
o Additions – make speech more complicated by adding extra phonemes, e.g.
/æplsaks/ (applesauce), /kəloud/ (cloud), /kwink/ (queen), /klæt/ (cat), /sutskeis/
(suitcase), /biblou (below)
o Prolongations – occurs with vowels and continuous consonants, e.g. /s:æd/ (sad),
/hæ:pi/ (happy)
i. Prolongations affects vowels.
o Repetitions of sounds and syllables – “trial and error groping kinds of repetitions” or
“perseverative” errors, e.g. /ststeiɚz/ (stairs), or /hæmbɚgɚgɚ/ (hamburger)
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oNon-phonemic productions–glottal plosives, bilabial fricatives, subtle voicing errors
(“voicing” and “devoicing errors”)
4. Hierarchy of errors (Rosenbek & Wertz, 1972)
1. Omissions (most prominent), followed by
2. Substitutions,
3. Distortions,
4. Additions,
5. Repetitions,
6. Prolongations
o Two and three feature errors, e.g. /mIfn/, /mIvn/ for mitten (combinations of place,
manner, voicing errors) –3s, 4s, 5s and 6s most common for imitated speech tasks
o Single feature errors – 1s and4s in spontaneous speech
o Age groups
− Younger: 1s and 2s
− Older: 3s and simplified consonant blends
o Kaufman (1995, p. 2) suggests errors of omission as a criterion for children at risk for
OAS: “The child who deletes sounds from words beyond the age of three.”
5. Voicing errors
o Voiced for unvoiced substitutions
o Subtle voicing and “detuning errors”
o Prevocalic voiceless consonants are often voiced, and final voiced stops are devoiced
6. Vowel and diphthong errors
o Inconstant and varying vowel omissions and incorrect articulation of vowels
o Variability in vowel accuracy is proposed as marker for differential diagnosis of CAS,
e.g./aI/→/a/, /æ/→/a/
o Vowel distortion = CAS.
o Neurogenic stuttering - will not stutter on same sound or syllable every time (or
within same word), inconsistent.
7. Difficulty with phoneme and syllable sequencing
o Great difficulty “joining consonants and vowels in even simple words” (Hadden,
1891), e.g. play → /pəl…/ or /ləp…/
o Diadokokinesis tasks – Rate of Alternating Movements vs. Rate of Successive
Movements
o Increase in errors with increase in complexity and length of utterance
o Metathesis (sound shift), bv. fish→ /ʃIf/, mask→/mæks/, snow→/soun/
8. Inconsistency and variability of errors comparison of errors over time, i.e. day to day and
word/sentence to word/sentence
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9. Speech Intelligibility
o Factor that changes over time in positive direction.
o Associated with maturation.
10. Nasality and nasal emissions (resonance)
o Not structural or functional, probably rather due to poor motor control
(incoordination) of the velopharyngeal mechanism
o Nasal assimilation, or nasals followed by stops, e.g. /rIŋk/
11. Groping, or still-posturing of articulators
o Also called “trial-and-error” movements.
o Noticeable increase in frequency with multi-syllabic words.
o More prevalent in older children –side effect of therapy? (Awareness of required
placement and desire to perform correctly).
12. Prosody
o Excessive-equal stress with emotive conditions, e.g. happy, sad, angry perceived as
“neutral” and questions attempts as “happy”
o Longer utterance duration – longer voice onset time, and vowel and fricative
duration.
13. Dysfluency
o Repetition of sounds and/or syllables disappears as articulation improves.
o Rather “irregularities of rhythm”.
o However, stuttering can co-occur (Hall etal., 2007, p. 49).
o Stuttering has rhythm.
14. Prognosis
o Does not progress with traditional/conventional therapy.
o Very slow progress –the most frustrating aspect of CAS.
o Skills and experience of clinician and motivation of child.
o Length of intervention –3-10 years.
o Improves but may persist into adulthood - degree dependent.
o It does not spontaneously resolve.
Unusual Aspects
A. Communication development characterised by:
• Single utterances conveying multiple meanings.
• Apparent "loss" of words (Word Recall).
o Motor programming problems may interfere with “storage”, i.e. deficiency in
phonological memory necessary for storage and retrieval.
o Inconsistent anomia. Have similarities with Broca's aphasia.
• Use of gestures.
o Pointing, pulling, idiosyncratic gesture system.
o Sequence of gestures can indicate syntactic knowledge/development - iconic,
metaphorical, deictic and "beats".
• “Mouth sounds”.
o Refers to vocalizations, sound imitations and grunting noises used to support
communication efforts.
o They can feel the sounds. Proprioceptive feedback.
• Over-learned Verbal Routines.
o Environmental sounds, emotional responses, songs, rhymes and poems.
• Affected language skills
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o Problems with receptive language reported – semantic and syntactic problems, e.g.
pronouns. (number agreement, use, substitution, omission), verb omission, SVO
order errors.
o Receptive consistently superior to expressive.
B. Motor and Praxis Problems

Findings suggestive of Neurological Involvement:
• Limb apraxia.
• Clumsiness.
• Poor tactile perceptual abilities.
o OT will tell you about this.
• Slowness in learning activities of daily living (manipulation/handling of objects).
• Gross and fine motor problems.
• Problems in constructive manipulatory play.
• Handwriting problems.
C. Other
• Non-speech Oral Apraxia.
• Auditory Processing Problems.
o No problems with hearing acuity–pure tone stimuli.
o Problems with processing complex sequences of information in which ideas are
hierarchically related to each other.
• Feeding and swallowing problems.
• Personality and Behaviour
o Quiet , friendly shyness.
o Frustration, confidence, comorbidities.
• Cognitive Abilities
o Intelligence within normal range ––“dull normal to superior”.
o Expect differences between verbal and non-verbal skills.
o Academic learning problems reading, spelling and writing.
Differential Diagnosis: A skill and an art

Need for Accurate Diagnosis
“One significant value in correctly diagnosing a child with DAS is that the diagnosis often radically
changes the direction of the therapeutic management and opens the door to a variety of techniques
not usually employed with the typical child with developmental phonological disability.” (Love, 1992,
p. 98)
• Impact on family–emotional, financial?

• Impact on child?
Misclassification?
Epidemiology:
• 5% of preschool children have phonological disorders of unknown origin.
• Estimated prevalence of CAS is 1 to2% in 1,000 livebirths–“low prevalence” disorder.
• Ratio of males to females estimated to be 2:1.
• Higher in children with comorbidities
• Average (USA) clinician should have 1-2 cases of DAS for every 100 children with speech
sound disorders on their caseload!
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• Probable80% “false positive” diagnoses of CAS –about80% of children have unfair apraxia
label!!
ICF/ICF - CY Perspective
Framework for DD
Core Elements:
1. Case History
2. Speech Sound System Assessment
3. Oral-Structural-Functional Examination
4. Motor-Speech Examination
5. Language Assessment
1. Case History
• Any “neurological events” that might suggest neurological damage.
• Family history of speech or language impairments.
• Past and/or current problems with feeding, chewing, swallowing and/or drooling (may
suggest possible co-existing oral apraxia).
**NB for early intervention clinic.
2. Sound System Assessment

• Describe phonetic and phonemic inventories.
• Compare with normative data.
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• Compare with characteristics, e.g. observations regarding word and syllable shapes.
o Vowel Accuracy –attention to regional, social dialectal variation in vowels.
o Consistency and variability of errors.
o Children without DAS usually improve across trials and with a model, while children
with DAS are more likely to show degraded performance across trials.
3. Oral Structural Functional Exam

• Rule out/ identify oral apraxia.
• Rule out dysarthria based on neuromuscular characteristics:
o abnormal muscle tone
o reduced muscle strength
o range,
o accuracy,
o strength,
o speed, and
o steadiness of movement
• At rest and in movement.
o each articulator in isolation
o coordinated movement
4. Motor Speech Examination

• Imitate utterances of increasing length and phonetic complexity
o Speech praxis
o Vowel and consonant distortions
o Timing and sequencing errors
o Dysprosody
o Compare performances when varying rate, and providing tactile and gestural cues
o Oral groping (and associated movements)
o Inconsistency
• Problems with transitions
o DDK-focus on consistency and accuracy (not speed).
o Multisyllabic words, and/or as words get progressively longer.
o Bad coarticulation.
• Conversational speech for…
o Overall intelligibility (% of words understood).
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PAEDIATRIC TRAUMATIC BRAIN INJURY
Definitions
• Insult to the brain caused by an external physical force.
• Diffuse Axonal Injury (DAI) –tearing and shearing of microscopic brain cells.
• Acquired brain injury is an insult to the brain that has occurred after birth, e.g. closed/open
head injury, stroke, near suffocation, infections in the brain, anoxia.
• NB: biochemical and biophysical changes that happen. Brain metabolism gets disturbed in
TBI. Shaking + tearing of brain issue. Neurological storm that happens post TBI. Not our field
but we need to understand the process that it sets in motion.
Biomechanics of TBI
• Impact or direct blow to the head.
o Head can be fixed.
o Head can move in a linear plane.
• Inertial forces result in straining of the underlying neural elements.
o Rotational force -when the brain is the centre of the rotational axis.
o Angular force -when the neck is the centre of the rotational force.
▪ Whiplash.
• Hypoxic injuries to the brain due to cessation of oxygenation, e.g. suffocation, strangulation,
drowning.
• Brain: contra coup, but also some twisting. So axons often get twisted off.
Common Mechanism of TBI

Mechanism – Acceleration/Deceleration
Mechanism – Acceleration/Deceleration (side to side) Coup-Contra-coup effect
Ataxic dysarthria = often result

of motor vehicle accident.
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Common Mechanism of TBI (cont.)
• Differential movement of partially tethered brain within the skull.
• Results in:
o Bruising of the brain surface against rough areas of the skull.
o Stretching and twisting of nerve axons.
o
• Minimum force needed for mild TBI is 40km/h
• Most pathophysiology of mild TBI renders neurons dysfunctional rather than destroyed as in
Diffuse Axonal Injury (DAI).
• In mild TBI there is metabolic dysfunction with rapid reversal to normal within days.
Brain Behaviour Relationships
Have this as handout

for clinic for caregiver.
Paediatric Traumatic Brain Injury

• Children’s brains do not reach their adult weight of 3 pounds until age of 12 years.
• Brain, and most importantly, frontal lobe region does not reach full cognitive maturity till
mid-twenties.
• Frontal Lobe houses executive skills, these include: judgement, problem solving, mental
flexibility, etc.
• Frontal Lobe is very vulnerable to injury.
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• Damage to the Frontal Lobe anywhere along the developmental continuum can impact
executive skill functioning.
Nature of PTBI
• Varies with age
• Infants:
o inflicted injuries
o more likely to suffer falls
o child abuse
• Non-accidental Injuries (NAIs) –child usually < 1 year more severe than accidental injury
• Preschool:
o falls from furniture/play equipment
o pedestrian accidents
o linked to environmental factors –family / social
• Older children
o sporting or pedestrian accidents
o linked to their own actions
• Paediatric TBI occurs more frequently on holidays/weekends
• More common in socially disadvantaged families
• Pre-existing learning/behaviour problems
Severity
• Mild:
o 13 to 15PGCS (Paediatric Glasgow Coma Score);
o LOC (Loss of Consciousness) < 20min;
o PTA (Post Traumatic Amnesia) < 24 hours
• Moderate:
o 9 to 12 PGCS;
o LOC 20 min to 36 hours;
o PTA 1 to 7 days
• Severe:
o 8 and less PGCS;
o LOC > 36 hours;
o PTA > 7 days
Symptoms
• Acute Symptoms:
o headache
o nausea
o dizziness
o fatigue
o insomnia
o sleeping too much, drowsiness
o light/noise sensitivity
o sadness
o mental slowing, mentally foggy
o poor concentration, memory problems
• Complaints are highly nonspecific.
• Most severe symptoms are evident within minutes.
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• Delayed symptom onset is rare.
• Combination of physical and cognitive symptoms is most common.
• Measurable improvement within hours.
• Gradual symptom recovery over 7 to 10 days in 80 –90% of cases.
• Children and adults show similar rate and course of symptom recovery.
• More severe forms of complicated mild TBI may be at risk of slower recovery.
• Headache is the symptom that tends to linger longest.
• ‘Post-concussion Syndrome’ –persistent complaints after mild TBI.
Cognitive Symptoms – MPTBI

• Acute Cognitive Symptoms –evidence on tests of orientation, immediate memory, working
memory and delayed memory for measurable impairment in cognitive functioning.
• Improvement is measurable within minutes to hours.
• Expected complete recovery in the first week in most cases.
• Look at cognitive responsibilities for the child's age. Take that into consideration. What is the
expectation for child's age - what should they be able to do?
Implications – Physical
• Tired all the time/Tires more quickly
And implications for
• Continuing headache (maybe accompanied by nausea)
language and speech (and
• May also be bothered by noise or light
perhaps even hearing).
• Less active
• Dizziness
• Ringing in the ears
• Slurred speech
• Changes in balance, difficulty grasping objects
• Bothered by light and noise
• Sleep changes, e.g. can’t sleep, nightmares
Implications –Thinking
• Memory, especially short-term memory.
• Difficulty learning new information.
• Trouble paying attention and staying on task.
• Misses instructions.
• Multi-tasking or splitting and dividing attention –“executive skills” –can be very challenging.
Implications – Emotional and Behavioural

• Impulsivity
• Worried and moody.
• Flat affect or little change in emotion.
• Spends more time alone.
• Easily upset, e.g. teary, agitated, aggressive.
• Self-centered – finding it hard to take another’s point of view.
• Difficulty exercising good social judgement.
• Difficulty following daily routine at school and/or home.
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Implications – Personality
• Depression
• Social skills problems.
• Mood swings.
• Problems with emotional control.
• Inappropriate behaviour.
• Inability to inhibit remarks.
• Inability to recognize social cues.
• Problems with initiation.
• Reduced self-esteem.
• Difficulty relating to others.
• Difficulty maintaining relationships.
• Difficulty forming new relationships.
• Stress/anxiety/frustration and reduced frustration tolerance.
Assessment
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Can be part of promotion campaigns.
Myths about PTBI
• Children “Grow into Their Brain Injuries” as children grow, more is expected, children with a
history of brain injury may not be able to meet the demands ...
• Impact of an injury may not become apparent till years post injury and … not be attributed
to an earlier blow to the head.
Recovery
• Neuropsychological recovery in uncomplicated mild TBI in pre-schoolers – indistinguishable
from healthy controls 5 years after injury.
• No long term consequences of uncomplicated mild TBI in children 23 years after injury.
• 7 to 8% of mild TBI remain symptomatic.
• Uncomplicated mild TBI does affect cognitive function slightly in pre-schoolers – back to
normal at 12 months.
• In line with principle: less severe injury at early age, the better the outcome.
• No difference between mild TBI with or without LOC by one week.
• In mild TBI Post Traumatic Amnesia (PTA) is associated with more severe effects and slower
recovery in the acute phase (up to 72 hours) – not predictive of outcome.
• Complicated mild TBI may increase risk for slow recovery but not predictive of outcome.
• Moderate and severe TBI injury –related factors predict outcome (LOC, PTA, GCS) but…
• Injury-related factors do not predict final outcome in mild TBI.
• Persistent symptoms in mild TBI are associated with previous neurological or psychiatric
history and other life stressors.
• Complicated mild TBI which includes PTA, LOC, EEG abnormalities, pathological reflexes, and
fractures may cause persistent mild neuropsychological dysfunction.
• “The only cure for Brain Injury is prevention”.
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CEREBRAL PALSY
Definition
• “Cerebral Palsy describes a group of permanent disorders of the development of
movement and posture, causing activity limitation, that are attributed to non-progressive
disturbances that occurred in the developing fetal or infant brain. The motor disorders of
CP are often accompanied by disturbances of sensation, perception, cognition,
communication, and behaviour (and feeding), by epilepsy, and by secondary
musculoskeletal problems.”
o Problematic?
o Definition:
▪ “motor disorders”= movement disorders
• Gross and fine motor movement. Feeding + speech have
components of both.
▪ “group of permanent disorders”
▪ “development of movement and posture”
▪ “non-progressive disturbances”
• Does not get worse/deteriorate, BUT is does change as individual
changes.
▪ “developing fetal or infant brain”
• Cut-off time for diagnosis.
• Acquired CP: up to 2-3 years after birth, anything that happens such
as near drowning etc.
• Infants with CP don't help kick in birthing process.
▪ “sensation, perception, cognition, communication, and behaviour (and
feeding)”
• Due to site of lesion – brain.
• Also tactile (proprioceptive) problems.
• Proprioceptors are sensors that monitor change in a body’s position
or the position of its parts, and these include muscle and joint
sensors, such as muscle spindles and GTOs. Vestibular sense falls
into this category because it provides information about the body’s
position in space.
• Proprioception is the sense of muscle and joint position.
• CVI (Cerebral visual impairment): brain doesn't see. Info is not
received or interpreted. Structures are normal. In CP CVI is very
prevalent. SNHL also very prevalent.
• Conductive HL also, due to Eustachian tube (due to movement
problems).
▪ “epilepsy and secondary musculoskeletal problems”
• CP is one of the most frequent causes of motor disability in children.
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Just extra info.
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CP as “Developmental disorder”
• Influence of accompanying disorders on general development.
o Sensory – vision, hearing, other
o Cognitive
o Behaviour
o Other
• Activity limitations.
• Participation restrictions.
• Multi-, inter-and trans-disciplinary intervention.
• Think ICF.
Implications for carers and SO’s
Aetiologies and prevalence of CP
Pre-Natal
• Preterm birth status –bleeding, encephalopathy.
• In utero growth retardation.
• Multiples.
• Cerebral malformation and stroke.
o IVH (baby stroke).
o Intraventricular hemorrhage (IVH) of the newborn is bleeding into the fluid-filled
areas, or ventricles, surrounded by the brain.
• Infections during pregnancy, e.g. rubella, cytomegalovirus, toxoplasmosis.
• Mechanical trauma.
• Radiation and substance abuse.
• Poor maternal nutrition.
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Peri-Natal
• Birth asphyxia –anoxia/hypoxia.
• Mechanical (birth) trauma.
• Placenta privia
o Not getting enough oxygen during birth.
• Infection, e.g. herpes simplex, HIV.
Post-Natal
• Trauma
o First 2 (2-3 in some definitions) years after birth.
• Infections, e.g. meningitis, encephalitis
• Asphyxia, e.g. near-drowning
• Neoplasms of CNS.
o Growths that displaces brain tissues can cause disturbances in growth or
development of brain structures.
• Severe and longstanding infantile jaundice –kernicterus and hyperbilirubinaemia
• Idiopathic.
o Unknown.
38-40 weeks is normal term.

Preterm:
1. Late preterm = 34-36+6
2. Preterm = 28-33 weeks
3. Micro prems = (24) - 27 weeks
Preterm birth - high risk of brain bleeding.
Classification of CP
Components:
1. Motor abnormalities
• Nature and typology
o Typology: distribution (where?)
• Functional motor skills
2. Accompanying/associated Impairments
• Musculo-skeletal problems
• Neuro-developmental problems
3. Anatomical and Neuro-Imaging findings

• Anatomical distribution
• Specific neuro-imaging findings –CT/MRI
4. Causation and Timing
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UMN in Extrapyra- Most
Cerebellum
cortex. midal common.
• No flaccid or hypokinesia.
• Hypokinesia: not CP. Usually brain structures missing. Beyond diagnosis of CP.
Child should stretch out arms to be picked up. Flexors are

usually spastic (muscle that bends are stiff).
Extensors can also be stiff (arms are stiff).
"Stormy" movement - big

excessive movements.
• Dystonia: extreme positions with limbs. Head is kind off also a "limb" - it responds like a 5th
limb. Extreme positions and they get stuck there (2 patterns). Just spasticity - nothing extreme.
• Choreoathetosis is a movement disorder that causes involuntary twitching or writhing. It’s a
serious condition that can affect your posture, walking ability, and everyday movement. More
severe cases can cause permanent disability.
• Choreoathetosis combines the symptoms of chorea and athetosis. Chorea causes fast,
unpredictable muscle contractions like fidgeting, or arm and leg movements. Chorea mostly
affects the face, limbs or trunk of the body. Athetosis causes slow writhing movements, typically
of the hands and feet.
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• Monoplegia and Triplegia are scarce.
Classification of CP (cont.)
A. Spastic CP
• Most common type in USA, UK, Europe, Aus.
• Increased muscle tone –limited movement.
• Hyperreflexia.
o Some like biting reflex - tonic bite (extreme closure of jaw).
• Abnormal patrons of posture and movement.
• Pattern always same regardless of position.
• Resistance to external movement.
• Spasticity vary -alertness, position.
• Level of stiffness can change –anxiety, pain, emotional state, surface, sensory input.
• Retain primitive reflexes – Moro, grasp, suck.
Middle picture:
Diplegia (increased muscle tone in

lower limbs), scissoring of lower
limbs.
Difficult to put nappies on this child.

Hip adductors.
Hemiplegia - flexion,
stifness.
Spastic CP. Extension in trunk, flexion in

arms.
Too much time laying down. They work

into gravity. End up looking like surface
they lay on.
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B. Dyskinetic CP
• Abnormal patrons of movement and posture.
• Involuntary, uncontrolled, recurring and often stereotypical movements –whole body.
• (Unwanted) twisting action that occurs with volitional activity –unwanted/aimless
movements.
• Includes choreo-athetosis and dystonic CP
• Choreo-athetosis is dominated by:
o Hyperkinesia–increased movements, “stormy “in nature
o Tend to present more hypotonic
• Distonic CP is dominated by:
o Hypokinesia–reduced activity, “stiff” movement, extreme positions
o Tone changes quickly –more hypertonic
Do what child is doing if you are unsure whether spastic

or dyskinetic. Is it extreme position (can’t move any
further). Dystonia - open hand. Spasticity - closed
hands.
Extreme asymmetry.
C. Ataxic CP
• Loss of coordinated volitional movement.
• Problems with force, rhythm and accuracy of movement.
• Predominantly quadriplegia –affects whole body.
• Can walk –wide stance and unsteady.
• Problems with arm and hand control.
• Overshooting –direction, speed, force.
• Tend to present with lower muscle tone.
• Low prevalence –±5% of cases.
• They always find some external source of something to lay against or move from.
Video: Boy is not looking at food whilst eating - if he looks, he will fall on his face. He fixes his eyes
on something stable because body fails him.
Classification of function
• Gross Motor Function Classification System (GMFCS)
o http://www.canchild.ca/en/measures/gmfcs.asp
• Manual Ability Classification System
o (MACS & Mini-MACS)
▪ The Manual Ability Classification System (MACS) described how children
aged 4–18 years with CP use their hands when handling objects in daily
▪ activities.
▪ Mini-MACS is an adaptation of MACS for children aged 1–4 years.
o http://www.macs.nu/
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• Communication Function Classification System (CFCS)
o http://www.cfcs.us
• Eating and Drinking Ability Classification System (EDACS)
o http://www.sussexcommunity.nhs.uk/get-
involved/eating_drinking_classification.htm
A child will generally have the same level across all instruments.
Gross Motor Function Classification System (GMFCS)

The gross motor function of children and young people with cerebral palsy can be categorised into 5
different levels using a tool called the Gross Motor Function Classification System.
Will be able to kick a ball

but might fall.
There’s an extra fitting

connected to frame,
other than level 3.
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**In the test: We will receive a case and the GMFCS level will be provided.
Manual Ability Classification System (MACS)
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Mini-MACS
Communication Function Classification System (CFCS) for Individuals with Cerebral Palsy
The purpose of the CFCS is to classify the everyday communication performance of an individual
with cerebral palsy into one of five levels. The CFCS focuses on activity and participation levels as
described in the World Health Organization’s (WHO) International Classification of Functioning,
Disability, and Health (ICF).
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Accompanying impairments
1. Musculo-skeletal Problems
o CP is disorder of movement.
2. Seizure disorders
3. Sensory Impairments (see Reference List)
a. Visual problems– cerebral visual impairment
b. Hearing problems–conductive, sensorineural
4. Intellectual Disability
5. Feeding and Swallowing problems
6. Saliva Control (oral-sensorimotor)
7. Communication
Middle ear not getting ventilated via Eustachian

tube - middle ear infection.
Deterioration of auditory nerve.
Not a typical comorbidity, Acquired language

but can occur. Right disorder, so not in
hemiplegia - higher child with CP.
incidence of AOS. Unless they
require it later.
Often GI issues: in practice, child won't eat. Constipation and Gastro-oesophageal reflux.
Oesophagus can be spastic.
Feeding classification – EDACS

People with cerebral palsy cannot use the range of physical movement available to most of us.
Difficulties may occur in the development of walking, speech and hand function. The movements
involved in biting, chewing and swallowing are frequently affected. Children and young people with
cerebral palsy may have problems eating enough food to grow and to stay healthy because it is
challenging to move their mouths to eat and drink efficiently. Some of them will have problems with
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frequent chest infections because particles of food or drink enter their lungs when they swallow.
These difficulties continue throughout their lives.
EDACS describes five distinct levels of ability using the key features of safety and efficiency:
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RANDOM CLASS NOTES
• Phasic bite: babies, phases, up down up down of jaws.
• Tonic bite: abnormal (don't test for it; it is deviation), elicited centrally (in the front). Baby
bite down on spoon and get stuck there. Increased muscle town. CN 5 is indicated -
something there is not right. Not damaged, otherwise it would be flaccid. Damage to CN is
flaccid. CN 5 damage = mouth that is open. Because muscles not being innervated. Tonic bite
= adults with TBI, Children with cerebral palsy.
• Lower Motor damage is CN damage. CN = lower motor neuron.
• Hypokinetic dysarthria: Range of movement: tremor's, rigidity, pausity of movement.

Struggle with control of airflow so reduced max a. Normal nasality. Make note if they have
hypernasality - might have mixed dysarthria.
• Flaccid dysarthria: All CN's related to speech therapy.
• LNFS: Little or no functional speech; 30 or less intelligible words. Complex communicational

needs.
• Plan the duration and termination of intervention: motivation. "Let us try 5 visits and see if
we can see any difference".
• Biofeedback: feedback from your body.
• Undershooting+overshooting - ONLY for ataxic dysarthria. For artic, they overdo the
direction, distance and timing. So it affects the pronunciation.
• AOS vs Brocas aphasia vs Spastic dysarthria - differential diagnosis. Damage is in same

region.
• AOS - some cannot say anything (moderate to severe, might have LTNFS); might only be able
to do root tasks (such as counting).
• AAC: for initial treatment to take away initial pressure, OR/AND when patient can't speak or
communicate. AAC - px has definite way of saying what they want to say, it won’t get lost.
• For ax tasks: start with respiration+phonation, then resonance, then artic, prosody,
connected speech, ddk's + stress testing. It will then all make sense because you can link it to
what you've already seen.
• Atrophy, fasciculation + fabrillations = will only see in tongue (velum is bilaterally

innervated).
• Gait: a person's manner of walking.
• Heart Attack (Myocardial Infarction): A heart attack (medically known as a myocardial

infarction) is a deadly medical emergency where your heart muscle begins to die because it
isn't getting enough blood flow. This is usually caused by a blockage in the arteries that
supply blood to your heart.
• Article: Aetiology of childhood AOS: a clinical practice... NB for self-study.
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• Physiological disturbances = neuromuscular characteristics (so for AOS when comorbid with
dysarthria).
• There is variability among people with regards to brain mapping. Different exact areas in
brain are affected for different people.
• Keep landmarks in mind because they might pop up in report or on scan.
• Stroke: motor + sensory areas are very close together. Always ask "Are sensory area
affected?".
Video 1 of AOS:
• Starting falling out at counting (at 16), backwards counting - not as natural, have to think
about it. Variety of tasks.
• Was impulsive, started talking before target was given. Test perceptual understanding.
• Right hemiparesis
• Started making weird mistakes that could be language related.
• When had to bring in hand - bigger plan - struggled. Limb apraxia?
• If receptive lang is very bad - AOS is not main problem. Then you work on Aphasia rather.
• Eating - very similar to speaking movements. Look for dysarthric component - range of
movement etc.
Video 2 of AOS: (young guy)

• ahhh, eeeehhh, ooohhhh
• AMR fallout (kah kah kah kah)
• Delayed onset, groping behaviour
• TV - yes, television - no
• Had problems with single words and phonemes.
• more severe
Video 3 CAS (boy)

• Prosody: not a lot of flexion in voice. monotonous. Very nasal.
• thick, thicker, thickening
• zip, zipper, zippering
• please, pleasing, pleasingly
• jab, jabber, jabbering
CAS: Inconsistently constantly comes up. Errors are not very predictable. Do not follow typical
errors.
CAS vs Stuttering: CAS does not have consistency, stuttering has consistency.
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TEST
• NB Unit 6b Neurology (Cranial nerve innervation summary); afferent control etc.
• Learn and know this.
• Know structures + their innervation.
• NB Class notes, for test as well
• Diadochokinesis is an NB term.
• Test: will focus is on differentiating and differential diagnosis. Very NB.
• Differentiate between different subsystems (put together Ax protocol for specific patient
with appropriate selection of Ax tasks).
• Treatment approaches are NB. Know by heart: the 3 pages making decisions around
treatment (principles, hierarchy, considerations, bigger approaches, communication vs
speech approaches, pharmacological vs surgical. Not expected to know techniques for
dysarthria.
• Know what focus for each subsystems would be. bigger goals, Unit 10 - focus area for
treatment (pharmacological, external pacing), not tables.
• Might ask to discuss specific treatment approach and might ask to compare 2 approaches.
Know the notes on treatment inside out - use for rationale and justification.
• NB: Expected results.
• Will have a look at classification - NBBBB. Know the site of lesion and neuromuscular
characteristics
• Ax: go back to everything regarding Ax. CN's, Case History, OSME.
• Test: Apply differential diagnosis.
• Will not write on childhood Apraxia (CAS). Just understand diff characteristics.
• Cerebral Paulsy: NBBBB for test.
• Unit 10a: Know 3 pages by heart. Treatment and habilitation. Also NB for
prevention+promotion next year.
• You will write about the assignment.
Test format
• 100 marks
• On sunlearn
• Variety of formats
• 50% on shorter format (1-5 marks)
• 50% longer than 5 marks (10-20 marks)
• Matching
• MCQ
• Ordering items.
• Fill in short answers.
• Essay type questions (15-20 marks).
• Negative marking for OVERselecting items for MCQ.
• Will not tell you how many to select, you need to know.
• 50% linked to cases (application); main focus is differential diagnosis (aphasia vs dysarthria
vs apraxia)
• NB Assignment – learn for the test.
145
L. Barnard 20972237
Rosenbek's 8 Step Continuum
146
L. Barnard 20972237
Melodic Intonation Therapy
147
L. Barnard 20972237

SPH 378 Notes Semester 2 Exam Notes

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SPH 378 Notes Semester 2 Exam Notes

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3

Rapid and uninterrupted

Gradual and uninterrupted

• Developmental and/or Acquired Disorders

Speech Subsystems and Musculature involved

• Anatomy of speech production is a “performance” anatomy (Bosma, 1975) – structures are

Speech-motor control must adapt to the (anatomical and) physiological changes.

Definition and Principles of Motor learning:

• experience and practice

Models of Communication And Speech Production

Motor-Speech Disorders vs. Other Communication Disorders

Cognitive, Linguistic, and Cognitive-Linguistic Disturbances

Nonneurologic or Nonpsychogenic Voice Disorders

Psychogenic and Related Nonorganic Speech Disorders

Normal Variations In Speech Production

Prevalence and Distribution of Disorders

Variables relevant to the speech disorders themselves include the following:

f) Speech components involved

Influences on Health & Well-Being:

2.1 The support structure of respiration

The vertebrae are numbered sequentially from superior to inferior by section, so

• C2 also called the axis – vertebra on which skull pivots

3) Ribs and rib cage

The sternum has three components:

The alveolar lining is made up of two types of cells:

2.2 The movement of air though the system

2.3 Muscles of inhalation

1) The primary muscle of inhalation – Thorax

2) Accessory muscles of inhalation

During the process of inhalation:

3.1 Respiration for life

1) The basic process of gas exchange has four stages:

c) Perfusion is the migration of fluid through a barrier

3) Effect of age on volume

3.3 Pressures of the respiratory system

Volumes and pressures vary as a direct function of the forces acting

During inhalation, expansion of the thorax decreases the already

3.4 Effects of posture on speech

OVERVIEW OF THE SUBSYSTEMS OF SPEECH PRODUCTION AND SPEECH

The Breathing Apparatus

Speech is a whole-body movement – down to the feet.

Structures involved in Speech Production

NB: Muscle attachments

Look at the attachments and think about how the

Will not ask names of muscles, but it is your library and is

Ribcage wall muscles (2)

Abdominal Wall Muscles

Velopharyngeal Dysfunction and Speech

Influence of Body Position

Speech Breathing Control Variables

Volume – air in lungs

Shape – chest wall configurations

Normal vs Disordered Breathing

IRV = inspiratory reserve

ERV = expiratory reserve

Memorize these triangles.

Problem is at the top, reason is at

We are still just looking at the

BGL = Breath Group Length

Component / Problem 2 – Pressure

• Very soft speech.

The combination of reduced inhalatory volume and exhalatory pressure

Reduced Vital Capacity (VC)

i.e. VC = all lung volumes, except residual volume