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Neurogenic Communication Disorders: An Overview
Lynette Carlson, M.A., CCC-SLP, [email protected]
Dana Collins, Ph.D., CCC-SLP, [email protected]
Neurogenic Communication Disorders
Context
SLP working with Physician
Topics Overview Neurogenic Communication Disorders
Cognitive-Linguistic Motor Speech
Assessment
Treatment
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Overview of Neurogenic Communiation Disorders
Aphasia
Cognitive-Communication Disorders
Dysarthrias
Apraxia of Speech
Language and Cognition
Language Modalities Cognitive Components
Comprehension Auditory Graphic/Visual
Expression Verbal Graphic/Visual
Attention Memory Executive functions
Language is a symbol system for exchange of ideas
Language
Comprehension
Graphic/Visual
Content
Form
Use
Auditory
Content
Form
Use
Expression
Graphic/Visual
Content
Form
Use
Verbal/Vocal
Content
Form
Use
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Cognition supports Communication
Attention
Perception
Memory
Executive Functions
Language
Effective Commun
ication
Acquired Cognitive-Linguistic Disorders Focal Lesions
Left aphasia Right cognitive-communication disorder in RHD
Multiple lesions More than one location of injury
cognitive communication deficits, may include aphasia
The resulting disorder depends on the damage patterns in the brain and the etiology of the damage.
May also have motor speech disorders dysphagia hearing, fluency, voice disorders
Aphasia and Left Hemisphere Lesions Means “without language”
Acquired language disorder typically due to focal damage of left cerebral hemisphere
May impair multiple communication modalities Auditory comprehension Visual comprehension Verbal Expression Written/graphic expression
Etiology= left cerebral hemisphere damage Stroke Accidents diseases, tumors, etc
Incidence and prevalence
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Aphasia: Associated Deficits Agnosia
Prosopagnosia
Acalculia
Agrammatism
Agraphia
Alexia
Aphasia: Associated Deficits
Anomia
Paraphasia
Hemiplegia/ hemiparesis
Body scheme disturbance
Diaschesis
Perceptual Disorders (Brookshire pp 60-61)
Homonymous Hemianopsia “same part, half blind”
Neurological Visual Impairment
Hemineglect
Hemispatial Neglect
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Language Centers: The Perisylvian Zone Broca’s Area Wernicke’s Area Transcortical Motor area Transcortical Sensory area Arcuate Fasciculus
http://www.educ.utas.edu.au/users/tle/Journal/ARTICLES/2006/clip_image006.jpg
The Mind and the Brain: http://www.ling.upenn.edu/courses/Fall_2001/ling001/neurology.html
Types of Aphasia: Based on site of lesion
Nonfluent Aphasia (aka anterior aphasias)
Broca’s Transcortical Motor Global
Fluent Aphasia (aka posterior aphasias)
Wernicke’s Anomic Conduction Transcortical Sensory
Broca’s Aphasia posterior inferior frontal lobe
Auditory Comprehension Usually pretty good, but not intact.
Verbal Expression Impaired, telegraphic aggrammatism Fair word retrieval Trouble repeating
Visual Comprehension Varies.
Graphic Expression Impaired Reflects verbal skills Can’t necessarily use AAC
May also have right unilateral UMN dysarthria, apraxia of speech, dysphagia. May have right hemiparesis; few sensory deficits
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Global Aphasia perisylvian zone
Auditory Comprehension Profound deficit May seem to get the gist of the message
Verbal Expression Profound deficit May have stereotypical utterances, literal & verbal paraphasias
Visual Comprehension Profound deficit
Graphic Expression Profound deficit May perseverate on a pattern.
Everything is so impaired, you don’t have a distinctive pattern. Right hemiplegia; sensory deficits Attentive, alert, socially appropriate (unlike dementia)
Transcortical Motor Aphasia Ant Sup Frontal Lobe
Auditory Comprehension Usually pretty good
Verbal Expression Dysnomia Difficulty initiating and organizing responses 1-word responses Repetition is good compared to other verbal skills
Visual Comprehension May be okay
Graphic Expression Impaired Reflects verbal skills
Some right hemiplegia; no sensory deficits
Wernicke’s Aphasia temporal lobe, Wernicke’s area
Auditory Comprehension Severe deficits
Verbal Expression Fluently articulated but paraphasic speech (paragrammatic speech) Paraphasia in repetition tasks Press of speech Dysnomia
Visual Comprehension Severe deficits
Graphic Expression
Reduced insight into deficits; some sensory deficits; generally no right hemiplegia
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Transcortical Sensory Aphasia Auditory Comprehension Impaired
Verbal Expression well articulated; irrelevant, paraphasic Dysnomia NO press for speech Good repetition skills relative to other skills
Visual Comprehension Impaired oral reading preserved
Graphic Expression Impaired
Hallmark: remarkable ability to repeat in the context of features of severe Wernicke’s. Spared memorized material. Some sensory deficits and right hemiparesis
Conduction Aphasia arcuate fasciculus Auditory Comprehension Usually good Is aware of the errors made in verbal expression
Verbal Expression Repetition is disproportionately impaired Fluency limited to short runs of speech Dysnomia; Literal paraphasias
Visual Comprehension Usually good
Graphic Expression Usually impaired
Some sensory deficits
Anomic Aphasia FRONTAL Like a mild transcortical motor aphasia Respond to initial phoneme cues
ANGULAR GYRUS At times, fail to retrieve word AND fail to recognize word if SLP says it.
INFERIOR TEMPORAL Severe dysnomia Near normal reading and writing and auditory comprehension
Residual Aphasia Word retrieval deficits left over after passing through more severe aphasia.
No right hemiparesis or sensory deficits Auditory comprehension usually is good in context NO PARAPHASIAS! Reading and writing vary.
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Transcortical Mixed
Auditory Comprehension impaired
Verbal Expression Echolalic Tend not to speak unless spoken to
Visual Comprehension impaired
Graphic Expression impaired
Subcortical Aphasia: Site of Lesion
Cognitive-Communication Disorders and Right Hemisphere Dysfunction
Attentional/Perceptual Deficits Executive Function deficits Affective Limitations Communication Impact
RH Impairment can affect any of these
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Right Hemisphere Dysfunction: Attention/Perceptual Deficits
Left visual field cut Left neglect Denial of illness/injury Inattention Constructional deficits Facial Recognition deficitis Spatial disorientation
Right Hemisphere Dysfunction: Executive Function Deficits
inferences and abstraction reasoning and problem solving theory of mind generating alternatives organization
Right Hemisphere Dysfunction: Affective Deficits
Insight, awareness affect, expression emotional content “big picture”
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Right Hemisphere Dysfunction: Cognitive-Communication Deficits
Impaired Discourse Comprehension and Expression Impaired Prosody recognition and usage Impaired social communication Deficits in using abstract or complex information
Deficits across modalities secondary to extralinguistic limitations
RHD (BDAE)
Cognitive-Communication Disorders Secondary to Multifocal Lesions
More than one location of injury cognitive communication deficits, may include aphasia
The resulting disorder depends on the damage patterns in the brain and the etiology of the damage. TBI Dementia Tumor Encephalopathy Etc.
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Effects of Multi-focal lesions Deficits depend on sites of lesion Sensory Motor Behavioral Affective Communication
Language Cognition
Effect varies with site,severity, etiology…
Impaired memory Impaired attention Irrelevant speech Confabulations Circumlocutions Tangents Fragments Non-cohesiveness Impaired pragmatics Impaired organization
Concrete Egocentric Labile/agitated Impaired organization Impaired insight Impaired reasoning Impaired problem solving Aphasia Impaired self-regulation
Dysarthria
“ 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,” (Darley, Aronson, & Brown, 1969; 1975).
Examples DDK task Reading a passage
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Apraxia of Speech (AOS)
“a motor speech disorder resulting from impairment of the capacity to program sensorimotor commands for the positioning and movements of muscles for the volitional production of speech,” (Duffy, 2005).
Example Reading a passage
Major types of Motor Speech Disorders (MSDs) (Duffy, 2005)
Type Localization Neuromotor Basis Dysarthria
Flaccid Lower motor neuron Weakness Spastic Bilateral upper motor
neuron Spasticity
Ataxic Cerebellum Incoordination Hypokinetic Basal Ganglia Rigidity or reduced ROM
Hyperkinetic Basal Ganglia Abnormal movements Unilateral Upper Motor Neuron
Unilateral Upper motor neuron
Weakness, incoordination, spasticity
Mixed More than one More than one Undetermined ? ?
Apraxia Left dominant hemisphere
Motor planning or programming
Classifying MSDs
Perceptual methods - gold standard of differential diagnosis of MSDs
Perceptual characteristics were associated with lesions in different portions of CNS and PNS
Confirmed by later acoustic and physiologic studies and visual and tactile inspection of speech mechanism
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How are MSDs classified according to speech characteristics?
Affected subsystem Respiration, phonation, articulation,
resonance, prosody Severity Important for management and confirmation
of physical findings Perceptual characteristics Important for classification and diagnosis/
treatment
Flaccid Dysarthria Etiology: Damage to LMNs of the
cranial or spinal nerves in the peripheral nervous system (Duffy, 2005).
Neuromuscular signs: Muscle weakness and hypotonia
Reduction in voluntary, automatic and reflexive movements
Possible development of muscle atrophy, fasciculations and fibrillations.
Damage to spinal nerves may affect control of breathing
Speech Characteristics: Hypernasality Slow imprecise
articulation possibly accompanied by nasal emission and shortened phrases
Decreased loudness and monopitch
Breathiness, audible inspirations and hoarseness in voice
Spastic Dysarthria
Speech Characteristics: Due to Increased muscle tone
weakness, reduced range of motion, decreased fine motor control (also affecting respiration)
Imprecise articulation, slow rate, distorted vowels
Harsh, strain-strangled voice quality, monopitch, monoloud
Possible hypernasality Short phrases, excess
and equal stress
Etiology: Damage to Bilateral (UMNs) involving the direct and/or indirect activation pathways in the central nervous system (Duffy, 2005).
Neuromuscular signs:
Control of breathing patterns may be affected and result in reduced vital capacity.
DAP-causes loss of fine, skilled movements especially in the speech muscles, hypotonia, weakness, diminished reflexes and presence of Babinski sign.
IAP- causes an increase in muscle tone, spasticity, hyperactive reflex responses (clonus, stretch, gag) and abnormal postures.
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Unilateral Upper Motor Neuron (UUMN) Dysarthria
Etiology: Damage to UMN on one side of the brain, especially the frontal lobe (Duffy, 2005).
Neuromuscular signs: Weakness in the lower face with a
possible facial droop on opposite side of the lesion
Weakness in the lips, and tongue on the opposite side of the lesion may also be present in the
extremities of the body on the opposite side of the lesion
Severe damage will result in hemiparesis
Speech Characteristics:
Imprecise consonants, irregular articulatory breakdown, and slow rate
Harsh or strained voice quality
Mild hypernasality Increased rate of speech in
segments excess and equal stress, and
reduced loudness
Ataxic Dysarthria
Etiology: bilateral or generalized disease or focal lesions to the lateral hemispheres, posteromedial or paravermal regions of cerebellum (Duffy, 2005)
Neuromuscular signs: Deficits in controlling timing,
force, range, and direction of voluntary movement,
Broad-based gait and difficulty with walking and standing
Intention tremors
Hypotonia of muscles
Speech characteristics: Imprecise consonants,
distorted vowel production, and irregular articulatory breakdowns
Excess and equal stress throughout speech production as well as prolonged phonemes and intervals between phonemes
Harsh voice quality accompanied by monopitch and monoloudness
Hypokinetic Dysarthria Etiology: Damage to the Basal
Ganglia Control Circuit
Neuromuscular signs: Tremor Rigidity (excessive muscle tone) Overall slowness of initiation and
control of movement Loss of postural reflexes and an
abnormal posture Lack of facial expression (masked
facies) and reduced blinking at rest Shuffling gait and reduction of arm
swing during walking Sensory deficits
May have difficulty in ability to monitor their speech
Speech Characteristics:
Monopitch, monoloudness, and reduced stress
Imprecise consonant production
Inappropriate silences and short phrases
Harsh, breathy voice quality and low pitch
Variable rate of speech with short rushes or blurred speech in segments, increased rate overall
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Hyperkinetic Dysarthria Etiology: Damage to the basal ganglia
and cerebellar control circuits and associated brainstem structures (Duffy, 2005).
Neuromuscular signs: Abnormal excessive involuntary
movements, which can be quick or slow or present in combination. orofacial dyskinesias, chorea, tics,
myoclonus, athetosis, tremor, dystonia, and spasms.
Difficulty controlling breathing/sudden or forced inspirations and exhalations
Movements may be irregular or sustained in nature.
Speech Characteristics: Harsh strain-strangled voice
quality Imprecise articulation and
with vowels distortions and velopharyngeal incompetence.
Difficulty controlling pitch, loudness, stress, duration and rate of speech (prosody) due to involuntary movements
Mixed Dysarthrias Etiology: Damage to combination the
Upper and Lower Motor Neurons, the basal ganglia control circuit, the cerebellar control circuit and the associated brainstem structures.
Neuromuscular signs UMNs (spastic) will cause spasticity in
the muscles, hyperactive reflexes and slow movements.
LMNs (flaccid) will cause low tone in the face, reduction in reflexes(absent gag), muscle weakness, atrophy, and fasciculations, especially in the tongue.
Speech Characteristics: Spastic Imprecise articulation
Poor prosody which includes monopitch (low), monoloudness, and reduced stresa
Harsh or strain-strangled voice quality Hypernasality (not as perceptible as
flaccid dysarthria) Flaccid Hypernasality Slow imprecise articulation possibly
accompanied by nasal emission and shortened phrases
Decreased loudness and monopitch Breathiness, audible inspirations and
hoarseness in voice
AOS
Etiology: distinguished from aphasia and dysarthria because it is usually caused by focal damage to the left cerebral hemisphere (e.g., tumors, trauma, stroke) (Duffy, 2005).
Neuromuscular signs: Spasticity and Weakness (hemiparesis)
which affects the right side of the body, lower face, and tongue
May also have sensory deficits, hyperactive stretch reflexes, and Babinski sign on the right
Non-verbal apraxias (limb, oral) may also be present
Speech Characteristics:
Articulation errors are inconsistent and may include vowel and consonant distortions, as well as substitution, deletion, addition, repetition and prolongation of sounds
Placement errors and groping (trial and error movements) for the correct articulatory posture is frequently observed
Automatic speech is better than linguistically complex speech
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Assessment Comprehensive
Speech Language Voice Fluency Hearing *Swallowing
Varies by setting, Pt status, concerns to address
Examining for neurogenic communication disorders
Differential diagnosis Rule out other communication disorders Referral for other presenting symptoms Recommendations
Case review, interview, observations, formal testing
Assessment varies on setting and patient status
Assessing Langauge
Four modalities
Sample tests Western Aphasia Battery Boston Diagnostic Aphasia Batter Minnesota Test for Differential Diagnosis of Aphasia Aphasia Diagnostic Profiles Boston Assessment of Severe Aphasia
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Examining Cognitive-Communication
Attention, Memory, Executive Functions, Perception, Affect Examples
• Mini Inventory of Right Brain Injury-2 • Burns Brief Inventory of Communication and Cognition • Brief Test of Head Injury • Scales of Cognitive Ability for Traumatic Brain Injury • Rivermead Behavioural Memory Test-3 • Functional Assessment of Verbal Reasoning and
Executive Strategies
A Motor Speech Exam includes: Patient history Structural – functional exam Motor speech exam Examine physiological parameters
Respiration Phonation Resonance Articulation Prosody
Identification of perceptual speech characteristics Examining Neuromuscular Condition
Dysarthria Assessment
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Apraxia Assessment
Methods for Classifying MSDs
Instrumental methods Acoustic methods-CSL, MDVP, Nasometer Physiologic methods-EMG, Kinematics, Pressure/Flow
measures Visual imaging methods-Videostroboscopy, Nasoendoscopy,
Laryngoscopy, Diagnostic Imaging
Treatment Restore function Maximize function
AAC Options
Address quality of life
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Treatment varies with stage of recovery:
Early Middle Later Behavior mgmt Sensory stimulation Environmental control Pharmacological mgmt
Orientation training Behavior management Component training Compensatory Training Support networks
Compensatory training Support networks
Recovery & Neuroplasticity Lifelong ability of the brain to reorganize as a result of
experience (Kolb and Gibb, 2008) Mechanisms underlying change
Biochemical Physiologic Structural
NP Principles
Intensive Stimulation Involve multiple modalities Use stimuli that evoke positive emotion,
capture attention Work for error-free learning Behavior modification works
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Repetition Reduce demands on impaired systems Build elaborate encoding (many ways to learn) Work with themes, semantically related
material Prep, prime them for the task
Suggested Resources American Speech-Language-Hearing Association, www.asha.org
Department of Communication Sciences and Disorders, UMD, 174 Chester Park, 218-726-7974, [email protected]
Robert F. Pierce, Speech-Language-Hearing Clinic, 156 Chester Park, 218-726-8199
Brookshire, Robert(2003).. Introduction to Neurogenic Communication Disorders, Seventh Edition. St. Louis: Mosby
Duffy, J. (2005). Motor Speech Disorders: Substrates, Differential diagnosis, and Management. Elsevier Mosby
Freed, D. B. (2000). Motor speech disorders: diagnosis and treatment. Singular Publishing: San Diego.
Suggested Resources
Love, R., & Webb, W. (2001). Neurology for the Speech-Language Pathologist, 4th edition. Butterworth-Heinemann, Boston, MA.
Myers, P. (1999). Right Hemisphere Damage: Disorders of Communication and Cognition. Singular Publishing.
Silver, J., McAllister, T., and Yudofsky, S. (2011). Textbook of Traumatic Brain Injury: 2nd Edition. American Psychiatric Publishing
Yorkston, K., Buekelman, D. R., Strand, E., and Bell, K. (1999). Management of motor speech disorders in children and adults, 2nd edition. Pro Ed: Austin, TX.
Yorkston, K., Miller, R., & Strand, E. (2004). Management of speech and swallowing in degenerative diseases, 2nd edition. Pro Ed: Austin, TX.