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Neurogenic Communication Disorders: An Overview

Lynette Carlson, M.A., CCC-SLP, lrcarlso@d.umn.edu

Dana Collins, Ph.D., CCC-SLP, drcollin@d.umn.edu

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, cd@d.umn.edu

  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.