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Neurogenic speech

disorders

Dr. Szabó Edina


University of Debrecen, Medical and
Health Scienc Center Faculty of
Medicine, Dep. of Phisycal Medicine
and Rehabilitation
Animal difference

Soul (church model)

Toolmaking ability

Thinking skills/Ability
of thinking

Modeling capabilities

2
Darwin's theory of language origin

 Darwin about animal


intelligence

 Ancient human cognitive


function

 Vocalization:
rudimentary song

 Articulated language
3
Cerebral lateralization

 Evolutionary background
 Speech and hemispheres
Left: verbal-logical Phineas Gage (1848)
Right: visual-synthetic
Right: primitive forms of
knowledge is kept
 Research of Gazzaniga (1983)
Testing split-brain patients

4
The brain without language
 How can the human mind
function without a functioning
language system? (Lecours és
Joanette, 1980)
 The case of Brother John
Different stages of aphasia
Abilities remained intact even under
attack: thinking, music, sound, face
detection, use of objects, spatial
orientation, mechanical intelligence,
working memory, episodic memory,
self-presentation
Changed skills: cognitive operations
that require symbolic representation
5
He could behave as a human being !
The brain structure I.

6
The communication of the brain

The basic structural and functional unit of


the nervous system is: the neuron

Parts: cell body, nucleus, extensions


(dendrites), axon (endings), myelin sheath

7
8
Blood supply of the brain

9
Introduction to the
clinical aphasiology
11
Cerebral infarction II.

12
Cerebral infarction III.

13
14
15
Hemorrhagic stroke I.

16
Hemorrhagic stroke II.

17
The communication-centered
definition of aphasia
The aphasia is
neurogenic
communication
disorder, which hides
the competence of
the person, which is
manifested in
conversations.
(Aura Kagan, Aphasia
Institute)

18
Etiology of aphasia

Hemorrhagic stroke
Cerebral infarction
Primary brain tumors or metastases
Trauma (concussion, skull fracture)

19
Symptoms of aphasia
Fluency disorder: nonfluent vs.
fluent aphasia
Understanding disorder
Agrammatism/paragrammatism
Perseveration
Paraphase: semantic, phonemic
Neologism
Verbal automatism
20
Syndroms of aphasia (Boston school)

Classical classification (BDAE, WAB)


Evaluation of the spontaneous
speech, speech repetition,naming and
the understanding
Localization principle: which language
areas of the brain are responsible for
different functions (FTP lobes parts of
perisylvian)

21
Global aphasia
 Nonfluent speech
 Verbal automatism
 Perseverations
 Severe understanding disorder

22
Paul Broca and the Broca lesion

23
Broca aphasia
 Nonfluent speech
 Agrammatism (missing suffixes, parts of
sentences, suffixes)
 Phonemic paraphases
 Word finding difficulties
 Faulty speech repetition
 Mild, or moderate understanding
disorder
 Monotonous intonation

24
Carl Wernicke and the Wernicke lesion

25
Wernicke aphasia

Fluent, but empty speech


Meaningless, jargon words
Phonemic and semantic
paraphases
Severe understanding disorder

26
Conduction aphasia

Spontaneous speech: Fluent, but


with a lot of phonemic paraphase
The faulty repetition of words and
phrases
A striking difference between
spontaneous speech and speech
repetition

27
Anomic aphasia

Fluent spontaneous speech


Word finding disorder
Circumscription
Mild understanding disorder
Adequate speech repetition

28
Transcortical aphasias

TMA: nonfluent speech, adequate


speech repetition

TSA: disorder of understanding


words and sentences, speech
repetition is good

Mixed TA: severe impairments in


all language functions, repetition is
slightly better
29
Atypical aphasias

Crossed aphasia
Subcortical aphasia
Bilingual aphasia

30
 They do not understand him, but
he knows what he wants to say

 World is narrowing or completely


closing up around him

 Becomes shipwrecked among


people

 He needs help, he needs to


learn to express himself again!

31
The affected
 There is no exact data in
Hungary

 If U.S. rates are considered,


we have more than 40 000
people suffering from
aphasia

 It's probably just a gentle


estimate, as the main cause,
stroke, is higher in Hungary
than in the U.S.

32
The affected
 Even more frightening picture
when we look at the range of
indirectly affected:

 Families are also included in


this figure: 160 000 (40 000 * 4)

 Tertiary affected people 640 000


(40 000 * 16)

With quaternary affetced people, the proportion is 25%, so it suggests that a quarter
of the population can be in direct conctact with an aphasia affected person in
Hungary (40 000 * 64)

Therefore, a quarter of our society must learn to communicate with them, to


develop them 33
Motor speech
disorders

 The speech is one of the most impressive


motor activity
 The control of speech movements in
childhood is possible
 The adults are forced to pay attention to
their speech movements as a result of a
cerebral accident
 Two large groups: the apraxia and
dysarthria
34
What is considered as motor
speech disorder?
The speech production deficit which develops
as a consequence of neuromuscular and /
or motor control system impairment
Sometimes occurs collectively with other
language impairments (eg aphasia)
Other oral movements can be damaged
besides speech, for example the smiling,
chewing, etc..

35
Determination of speech motor
system

Four Subsystems of Speech


Production:

Respiratory system
Phonatory system
Resonatory system
Articulatory system
36
Frequency of motor speech
disorders
Reliable estimates are rare, but ...
51% of adult speech disorders are
motor aphasia, dysarthria with 46%,
5% apraxia.
Among children 5 % of
developmental communication
disorders are due to motor
dysfunction

37
What about nonfluent aphasias?
Why not discuss the motor speech
disorder?
Nonfluent speech in aphasia is just
one component of a more complex
communication disorder
Differential diagnosis of motor
speech disturbances: always
understanding difference

38
What about stuttering?

Dysfluentia
Subcortical laesio, injury of basal
ganglions
Neurogen dysfluentia/neurogenic
stuttering

39
The common definition of motor
speech disorders according to their
characteristics

We talking about motor planning /


programming deficit when we
experience inability to select
appropriate muscle groups,
difficulty to sychronize them:
Apraxia
Muscles suffers physiological or
motor function injuries: Dysarthria
40
How can we classify motor
speech disorders?

After etiology:
Acquired:
– Can be caused by cerebrovascular
accident (stroke), degenerative diseases,
traumatic brain injury or brain tumor
Developmental:
– Can be caused by congenital disease or
injury caused to the developing nervous
system
41
Apraxia
 The failure of articulatory gestures in normal conversion, wrong
linguistic representation (even in imitation tasks!)

 Features: slow speech (rarely entire speech), sound distortions,


prolonged vowels (extended release), reduced prosody,
inconsistent defects, speech starting problems, searching
articulatory gestures

 Speech disorder is a result of neurological damage: left frontal


cortex, stroke near Broca’area then it is called kinetic /
ideomotor apraxia and when the left parietal cortex is damaged
it’s kinesthetic / ideativ apraxia
 Can appear due to cerebral injuries, illnesses, after infections.

42
Dysarthria
 Neuromuscular disorder which affetcs
execution of speech movements,
regulation of muscle tone, reflexes,
movement kinematic aspects
 It is characterized by a slow, erratic
sounds harsh, raspy or whispering
voice, consistent mistakes,or other
features depending on the type of
dysarthria
 Three primal features (depending on
model) spasticity, dyskinesia, ataxia.
 Its common causes are progressive
neurological disease and stroke. 43
Etiology, symptoms,
and classification of
dysarthria
Definition of dysarthria

Darley, Aronson, Brown (1975):

 Muscular control weakness, complex


muscle (neurogenic) dysfunction.

 Consequence of organic injury in the


central or peripheral nervous system

Cséfalvay Zsolt, 2007

45
The speech control
cranial nerves

 Nervus trigeminus (V.)


 Nervus facialis (VII)
 Nervus
glossopharyngeus
(IX.)
 Nervus vagus (X.)
 Nervus accesorius
(XI)
 Nervus hypoglossus
(XII.)
46
Cséfalvay Zsolt, 2007
Bulbar (or flaccid) dysarthria

(a) lesion in the peripheral motor


neuron (involement of cranial
nerves)

(b) muscle weakness (flaccid


muscles)
Cséfalvay Zsolt, 2007
47
Etiology of bulbar (flaccid) dysarthria

Injury to the nuclei of 5, 7, 9, 10, 11,


12 th. cranial nerves or the bulbar
nuclei
Monopathia: affects only one nerve
Polypathia: more nerves are
concerned

Cséfalvay Zsolt, 200748


Etiology of bulbar (flaccid)
dysarthria

Physical injury: surgery, cranial


injury and neck injuries
Brainstem stroke (brainstem
vascular involvement)
Myasthenia gravis

Cséfalvay Zsolt, 2007


49
Etiology of bulbar (flaccid) dysarthria

Guillain Barré syndroma (progressive


inflammatory disease,
demyelinization)
Tumor (near the brain stem)
Muscular dystrophy (progressive
degeneration of muscle tissue)
Progressive bulbar paralyses.

Cséfalvay Zsolt, 2007 50


Symptoms of bulbar dysarthria
Resonance disorder : hypernasality

Artikulation disorder: slow


artikulation

51
Symptoms of bulbar dysarthria

 Phonation
disorder:phonation
incompetence
(insufficient
closing of vocal
cords) - dysphonia

52
Symptoms of bulbar dysarthria

Respiratory Disorder: C., Th nerve


problems only (diaphragm, damage
to intercostal muscle movement,
lack/insufficient subglottic
pressure, poor sound intensity

Prosodic disorder

Cséfalvay Zsolt, 2007


53
Symptoms of bulbar dysarthria
(Summary)

 n. trigeminus laesio: artikulation disorder,


resonance disorder
 n. facialis laesio: artikulation disorder
 n. vagus laesio: resonance disorder,
phonation disorder
 n. hypoglossus laesio: artikulation
disorder
 Unilateral injury: milder symptoms
 Bilateral injury – severe symptoms

Cséfalvay Zsolt, 2007 54


Spastic dysarthria

Bilateral central motor neuron


involvement

Cséfalvay Zsolt, 2007


55
Etiology of Spastic dysarthria

 Stroke

 Cerebrocranial trauma

 Sclerosis multiplex (when central


motoneuron is affected)

 Tumor

Cséfalvay Zsolt, 2007


56
Symptoms of spastic dysarthria

 Spastic slow articulation (especially


consonants)
 Spastic dysphonia (due to hyperadduction
of vocal cords)
 Hypernasality – the spasticity slows down
and limits the movement of soft palate
muscles
 Dysprosodia: limited range of voice and
volume, short phrases, slow speech rate
 Rarely: respiratory problems
Cséfalvay Zsolt, 2007
57
Accompanying symptoms of spastic
dysarthria

(1) spastic laughter, crying (which is


difficult to control voluntarily)
(2) hypersalivation (which may be the
control of salivary dysfunction, or as
a result of less frequent swallowing)

Cséfalvay Zsolt, 2007


58
Ataxic (cerebellar)
dysarthria
Etiology
 Laesio of
the
cerebellum
or
cerebellar
tracks

Cséfalvay Zsolt, 2007 60


Etology of ataxic dysarthria
Degenerative disease:
Cerebellar ataxia,
Friedreich ataxia (hereditary
spinocerebellar disease),
Olivopontocerebellar degeneration
Stroke – blood supply dysfunction in the
areas of the cerebellar
Toxic injury (chemical substances, alcohol,
drugs)
Cranial trauma - cerebellar
Tumor ( eg. astrocytoma)
Cséfalvay Zsolt, 2007
61
Symptoms of ataxic dysarthria

 Disorder of speech cordination


(artikulation, prosody)
 Vague, indistinct articulation: "Boozer"
articulation, irregular intervals (more
syllable words)
 Mild hyponasality
 Mild dysphonia

Cséfalvay Zsolt, 2007


62
Hyperkinetic dysarthria
Hyperkinetic dysarthria

 Hyperkinetic disorder: excessive


involuntary movement (chorea,
myoclonus, dystonia, essential tremor)

 Etiology: Basal ganglia injury and areas


around the BG (eg Huntington's
disease).

Cséfalvay Zsolt, 2007


64
Symptoms of hyperkinetic dysarthria

Involuntary movements of (resp.,


phon., artik., reson.) muscles
Choreatic hyperkinesia –due to
simultaneous or successive
involvement of muscles (lip muscles
and phonation muscles are involved)

Cséfalvay Zsolt, 2007 65


Symptoms of Hyperkinetic dysarthria
CHOREA:
 Long intervals between syllables and
words
 Variable speech rate
 Inadequate breaks (silence)
 Variable volume
 Prolonged vowels
 Fast, and short inhalation, exhalation
and phonation intervals

Cséfalvay Zsolt, 2007 66


Hypokinetic dysarthria

 Occur due to pathological changes in


BG, their connection with other areas
of CNS

Cséfalvay Zsolt, 2007


67
Etiology of Hypokinetic dysarthria

 Parkinson‘s disease

 Postencephalopatic parkinsonism

 Craniocerebral trauma (BG, substantia


nigra)

Cséfalvay Zsolt, 2007


68
Symptoms of hypokinetic
dysarthria

Dysprosodia: monotone speech


(limited vocal range and volume)

Long pauses (due to akinesia)

Fast speech rate.

Cséfalvay Zsolt, 2007


69
Symptoms of hypokinetic dysarthria

Articulation disorder:

 "blurry" articulation ,
atypic dysfluency: repetition
(initial phonemes)
 palilalia (very fast repetition of
words)

Cséfalvay Zsolt, 2007


70
Symptoms of hypokinetic dysarthria

Dysphonia: Due to incomplete


closure of the vocal cords (breathy
voice quality, rough, raspy voice)
Mikrophonia: low sound level
Respiratory disorder: rapid, shallow
breathing
Resonance abnormalities: mild
symptoms (hypernasality)
Cséfalvay Zsolt, 2007
71
Mixed dysarthria

Etiology:
Sclerosis multiplex/multiple
scerosis
Multisystemic atrophy (Shy-Drager
sy, progressive supranuklear
paralysis, olivopontocerebellar
atrophy
ALS
Wilson's disease
Cséfalvay Zsolt, 2007 72
Symptoms of mixed dysarthria

 SM: ataxic-spastic form (phonatio-


articulation disorder)
Wilson‘s disease (BG involvement)
hypokinetic form, later spastic-
ataxic form
ALS: initial stage

Cséfalvay Zsolt, 2007


73
How we can identify motor
speech disorders? Tests
 Frenchay Dysarthria Test
 Apraxia Battery for Adults-2nd edition
 Assessment of Intelligibility in
Dysarthric Speakers (AIDS)
(computerized version called CAIDS)
 Sentence Intelligibility Test
 TOCS+ for children by Megan Hodge is
this website:
http://www.tocs.plus.ualberta.ca/videodemo.h
tm
These testing procedures are not adapted in
Hungary for motor speech disorders

74
Diagnostic

 A comprehensive assessment of
communication disorder following a detailed
diagnostic protocol
 At present, the differential diagnosis is based
on the professional perceptual, acoustic
monitoring, psychological testing as there are
no objective acoustic and physiological
indicators available
 The diagnosis itself should include the
damage rate, the rate of mistakes, the rate of
"false positive" responses and the rate of
corrections
75
Diagnostic process

Assessment of the oral motorium

 Testing of phonatio and prolong phonatio


 The examination shall include, detailed
diagnostics of the individual subsystems:
respiration, phonation, resonance,
articulation and prosody
 Cognitive / Communication Skills Mapping
 observe compensatory strategies used by
patients
76
The examination
 Examination is carried
out during speech and
at rest
 Speech muscles of the
peripheral nervous
system (specific tasks)
 Examination of cranial
nerves: V.,VII., IX., X.
XI. a XII. (neurological
examination)

Darley, Aronson, Brown:


Examination of motor speech
77
disorders
Examination of the facial muscles at
rest (VII. n. facialis)

 Is the face symmetrical?


 Can you move your lips?
 Can you show your teeth?
 Eyes:open,or partially shut?
 The face rigid, mask-like?
 Are forehead muscles symmetrical
when raising
eyebrows/wrinkling/frowning?

 Is the nose symmetrical?


78
Examination the facial muscles in
motion (VII. n. facialis)

Is the smile symmetrical?


Looking for the right position when
smiling (apraxia?)
Pouching of lips
Close lips
Puffing up cheeks
Muscle strength

79
Examination the lower jaw muscles in
resting position (V. n. trigeminus)
Is the jaw symmetric?

Is there deviation during resting?

80
Examination of the lower jaw muscles
during spontaneous movements

There is a deviation jaw when the


mouth is open?
Looking for the right position whilst
opening (apraxia)?
Is there possible side movement?
Is there strong resistance against
pressure?

81
Examination of the tongue muscles at
rest (XII. n. hypoglossus)

Is the size and shape of the tongue


normal?
In the located in the middle of the
mouth?
Is the shape of the tongue
symmetrical?
Is there fasciculation muscle of the
tongue?
Can it remain inactive?
82
The examination of the tongue muscle
movements (XII. n. hypoglossus)

Can the tongue move out?


Can the patient stick his tongue
out?
Can he resist lateral pressure to the
tongue?
Can patient produce lateral
movements?

83
Examination of the velum, pharynx
and larynx at rest and during exercise
(X. n. vagus)

Does velum elevates during fonation


?
Is velum symmetrical?
Can we trigger gag reflex?

84
Examination of the larynx
(X. n. vagus)

 Is patient able to
produce a loud
cough?
 Able to develop
adequate
subglottic
pressure?
 Can we hear
inhalation
stridor?

85
Summary
 Must be able to distinguish between disorder of
motor planning (apraxia) and disorder of motor
execution (dysarthria)
 Dysarthria: we must be able to determine the
type of dysarthria
 Be able to determine how damage to the motor
subsystems affect intelligibility of speech
 We have to know if the disease is acquired or
developmental
 Disorder emerged suddenly or gradually
 Set up the treatment plan accordingly

86
From diagnosis to therapy
A detailed
diagnostic
protocol is
an
opportunity
for better
trauma-
specific
treatment
plan
87
Vocalization and swallowing

Lungs provides air flow


Glottis: vocal phonation and
positioning
Resonator areas: synchronized
orientation
Swallow: Preoral, oral, pharyngeal
and oesophageal stages
Swallowing apnea, opening the top
of the esophagus
88
Dysphonias

Organic dysphonia

Functional dysphonia

89
Functional dysphonia
Change in the tone (usually hoarseness),
overuse of voice, larynx is less strainable
without primary structural difference in
the larynx itself. All complaints are
usually accompanied by paresthesia

Phonoponozis

Phononeurosis
90
Mészáros Krisztina
Phonoponozis I.

Definition:

Improper use of sounds, vocal


dysfunction due to overuse of the
phonatory apparatus

Mészáros Krisztina 91
Phonoponozis II.
Complaints:

Gradually formed, altered, hoarse


voice, becomes asymptomatic after
relaxing, urged to croak and
swallowing, globus sensation,
foreign body sensation, pain
sensation in the neck, sore throat,
and cough.
92
Mészáros Krisztina
Phonoponozis III.
Symptoms:
Changed, usually hoarse voice, but not
aphonic. Hard start-up sound, almost
normal range of voice, prolonged sound
shorter, limited volume.
Decreased, tight vocal movements, irregular,
tight thoracic breathing. Face, tongue, jaw,
neck under tension, neck veins visible
during speech.
Larynx: false vocal cords distend due to
straining, congestion in free margins of
the vocal cords.
vocal knots, margin oedema appear, and
failure of glottic closure at the back of the
larynx
93
Mészáros Krisztina
Phonoponozis IV.
Treatment:

Voice Therapy and in cases of


existing tough vocal cord knots ,
surgical removal is recommended.

94
Mészáros Krisztina
Juvenilis dysphonia I.
Definition:

Formed in childhood, improper voice


use, excessive use of the phonation
apparatus due to vocal dysfunction.

95
Mészáros Krisztina
Juvenilis dysphonia II.
Complaints:

Hoarseness, deepening of the voice,


croaking

96
Mészáros Krisztina
Juvenilis dysphonia III.
Symptoms:
A sharp, deep-pitched, hoarse voice.
Urge to croak, hard starting volume.
Fast speech, rhythm, inaccurate
articulation, irregular, tight thoracic
breathing. Face, tongue, jaw, neck
are tense, neck veins distended
during speech.
Larynx: loose watery vocal cords,
vocal bunch knots, failure of glottic
closure. 97
Mészáros Krisztina
Juvenilis dysphonia IV.
Treatment:

Voice therapy and in cases of


existing tough vocal cord knots,
surgical removal is recommended.

Mészáros Krisztina 98
Phononeurosis

Voice production disorder of


psychogenic origin, sudden and
severe voice symptoms.

Psychogenic aphonia: inability to


produce sounds, immediate
psychiatric treatment and voice
therapy.

99
Mészáros Krisztina
Dysodia
The functional voice disorders.
Respiratory defects
Incorrect setting of the articulation
area
4-6 hours of overstraining
Caffeine, drugs
Early singing lessons
Ignoring vocal hygene
recommendations
100
Mészáros Krisztina
Gastro-oesophageal reflux
disease in phoniatry
implications

101
The most common aspects in phoniatry
of the GERD

Dysphonia
Pharyngitis
Dysphagia
excess flow of mucus in the back of
throat
Stimulated cough
Chronic Bronch.
Asthma bronch.
102
Mészáros Krisztina
Top phoniatric result
Hoarseness

Etiology:
The acid-induced vagal reflex
triggered recurrent coughing reflex.
There is direct acid effect on the
pharynx, larynx.

103
Mészáros Krisztina
Diagnostic, anamnesis
 Substernal burning  Feeling of mucus
sensation, pain flow in the throat
 Nocturnal  Frequent throat
regurgitation pains
 Coughing, wheezing  Jugular
 Aspiration discomfort
 Morning hoarseness  Heartburn (rarely)
 Croaking

Mészáros Krisztina
104
Diagnostic, examination

oto-nasal laryngological
examination
laryngial video-stroboscopy
Auditory Sound Scan
examination of sound retention
time and vocal range
Analysis of sound dynamics
105
Stroboscop evidence
 The congestion of inter-ary region of the
vocal cords, false vocal cords slight
oedema of the vocal cords.
 Pronounced hyperplasia of the inter-ary
region, contact granuloma.
 In general, the glottis level of
vasoconstriction, decreased vocal cord
vibration parameters, harsh sound start.
 In addition to harsh sound start,
hypotonic vibration in front of the vocal
cords
106
Mészáros Krisztina
GERD and the phoniatry
Varying degrees of hoarseness
Vocal holding time shortens
Sound stage renal
Decreased ability of raising volume
20% of phoniatric patients affected
by clinical symptoms, 14% was
proven in during gastroenterologic
examination
Mészáros Krisztina
107
Treatment

Gastroenterology areas: Medication


and lifestyle counseling.

Phoniatric Therapy: Sound Therapy


treatment to the added functional
components.

Mészáros Krisztina
108
Thank you
for your
attention!

109

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