Neurogenic Speech Disorders Week 1

WHAT IS SPEECH?

Interface between language (thoughts, ideas) and decodable sound energy we produce (acoustics)

Five Domains of Speech

Respiration, phonation, resonance, articulation, prosody

Subsystems of Speech Production:

respiratory, phonatory, articulatory, resonatory, prosody

Cognitive-linguistic

Intent to speak, Rules of language

Motor speech planning, programming, and control

Organized verbal message, Select-sequence-regular motor programs, Appropriate co-articulation timing, duration, and intensity, Sensory feedback (auditory and somatosensory)

Neuromuscular execution

Combination of respiration, phonation, articulation, prosody, and resonance to produce speech

respiration

slow, restricted, weak, or uncoordinated muscle activity used inbreathing for speech

Phonation:

sound production at the level of the larynx

Resonance

dampening or amplifying sound by changing the size, shape, and/or number of cavities (shape changes, sound changes)

Articulation:

movement of speech structures employed in producing the sounds of speech

Prosody

varying intonation, stress, and rhythm during speech

Neuro

having to do with the nerves, nervous system, neuromuscular and/or motor control system

Genic

resulting from or caused by

Speech

that thing we do most often to communicate

Disorder

something is wrong

Major Types:

The Dysarthrias

Apraxia of Speech

The Aphasias

Right hemisphere disorders

Dementia

TBI

MOTOR SPEECH DISORDERS (MSD)

There is a broad correspondence between the different structures of the human nervous system and the different types of neurogenic communication disorders• The symptoms, severity, and outcomes of neurogenic communication disorders reflect the location, extent, and nature of nervous system damage

SIMPLE MODEL OF SPOKENLANGUAGE PRODUCTION

Conceptual Processing, Language Processing: Lemma selection (MEANING)Phonological/ Grammatical Encoding (FORM)Conceptual Processing Motor Execution (i.e., speech articulation) Motor Planning / Programming

Motor Planning

: process that define and sequence articulatory goals (prior to initiation of movement)

Motor Programming

: processes that establish and prepare the flow of motor information across muscles, as well as control timing and force of movement (prior to initiation of movement)

Disordered Motor Planning/Programming: inability to group and sequence relevant muscles withrespect to each other (apraxia of speech - AOS - both acquired and developmental)

Motor Execution

processes that activate relevant muscles (during and after initiation ofmovement)• Disordered Motor Execution: deficits in physiology and movement abilities of muscles (dysarthria -both acquired and development)

Acquired:

damage to a previously intact nervous system

May be caused by a cerebrovascular accident (CVA, aka stroke), degenerativediseases, brain tumors, or traumatic brain injuries (TBIs)• New injury

Developmental

abnormal development of or damage to a developing nervous system Caused by congenital diseases or damage to the developing nervous system(different effects than damage to an already developing and intact system)

DYSARTHRIA

group of speech disorders resulting from disturbances in muscular control (weakness, slowness, or incoordination) of the speech mechanism• Caused by damage to the central or peripheral nervous system or both• Term encompasses coexisting neurogenic disorders of several or all of the basic processes of speech: respiration, phonation, resonance, articulation, and prosody

dysarthria Presents in:

25% of Cerebrovascular Accident patients

25% of Amyotrophic Lateral Sclerosis patients

30% of Traumatic Brain Injury patients

50% of Multiple Sclerosis patients• 90% of Parkinson's Disease patients• 30-90% of Cerebral Palsy patients

Arthria

to utter distinctly

dysarthria is

A disorder of movement or movement control◦ Can be categorized into different types Each type of dysarthria is characterized by distinguishable auditory perceptual (and often visual) characteristics

Each has a different underlying neuropathology The category of the dysarthria implies the location of the pathology

HOW IS MOVEMENT IMPACTED?

Range

Accuracy

Tone

Strength

Speed

Steadiness

symptoms of dysarthria May include any combination of:

Abnormal speech rhythm

Articulation inaccuracies

Audible breathing

Reduced breath support for speech

Limited jaw movement Limited tongue movement

Loudness inconsistencies

loudness reduction

Nasal resonance changes

Rapid speech rate

Slow speech rate Slurred speech Speech quality change

praxis

performance of an action; a motor plan

apraxia

impaired capacity to plan or program sensorimotor commands necessary for directing movements that result in phonetically and prosodically normal speech." Important to differentiate from dysarthria and aphasia but frequently co-occurs.• Can occur in the absence of physiologic disturbances associated w/ the dysarthria's

Can occur in the absence of disturbance in any component of language

APHASIAS

Aphasia is an acquired selective* impairment of language modalities and functions resulting from brain damage in the language-dominant hemisphere (affects production or comprehension of language and/or the ability to read or write)

COGNITIVE-COMMUNICATIONDISORDERS

Cognitive communication disorders are difficulties with any aspect of communication that is due to/affected by cognitive impairment rather than primary speech or language deficit.

neurogenic communication disorders- broadly speaking

Each neurogenic communication disorder describes an impairment whose

symptoms are mostly not seen in the other neurogenic communication

disorders.

For example, symptoms of dysarthria are generally not observed in aphasia.

However, it is possible for two different neurogenic communication disorders to

co-occur (and they often do!)

Common for a patient to present with both dysarthria and aphasia post-stroke.

Communication Problems

dysarthria and AOS can make it difficult to understand speech, decreasing the ability to communicate effectively

Social Difficulty

the communication problems caused by dysarthria and apraxia may affect relationships with family and friends and can make social situations challenging

Depression (Quality of Life - QOL)

dysarthria and apraxia may lead to social isolation and depression

Auditory-perceptual measures

What do you hear? see and feel?

Instrumental and/or Laboratory Methods

Not widely accepted or used because it is expensive and time consuming

Acoustic

Physiologic/kinematic

Visual imaging

issues with audio-perceptual measures

Subject to unreliability of judgments among clinicians

May be difficult to agree on severity

Cannot directly test hypotheses about the pathophysiology underlying the perceivedspeech abnormalities

Perceptual Classification is hard because:

Listeners must identify clinically significant features from a multidimensional acoustic signal

Salient features are not invariant; any one individual can deviate from group similarities

It is possible that subgroups exist

Intelligibility

Information is exclusively from the speech signal.

comprehensibility

information comes from speech signal plus context; sharing meaning using any and all information available

different diagnosis considerations for dysarthria

has distinct neuroanatomic and neurophysiologic substrates. Different types may reflect:-Different disease processes-Different prognoses-Different treatments

Therefore, it should be differentially diagnosed

why is the motor system important

All observable behavior is directly related to activity in the motor system.

Without the motor system, we could experience sensation, think,reason, problem solve, read, and do mental math, BUT we could notcommunicate our thoughts and abilities to anyone via verbal or gestural communication/speech.

relevant cranial nerves

trigeminal (CN V) Facial (CN VII)

Glossopharyngeal (CN IX)

Vagus (CN X)

Hypoglossal (CN XII)

Spinal Nerves

trigeminal (CN V)

emerges from the pons

Bilateral UMN innervation with input from bothhemispheres going to both nerves

three main branches of the pons

V1 Ophthalmic (sensory; innervates upper face)

VII Maxillary (sensory; innervates midface)

VIII Mandibular (motor & sensory)

sensory function of trigeminal nerve

mucous membranes of the mouth, side of the head and scalp, lower jaw, anterior twothirds of tongue

Proprioceptive

from muscles of jaw, face, lip, tongue,teeth, etc. sends information to the midbrain

motor function of trigeminal nerve

aw movements - muscles

Unilateral lesion to CNV3 mandibular branch

Jaw may be weak (ipsilateral (same side) to lesion) and may deviate to weak side when opened• Degree of masseter/temporalis contraction when patient bites down may be decreased

Bilateral lesions to CNV3 cause the jaw to hang open or move with limited range

Patient may be unable to close mouth; may move slowly or with reduced range

Patient may be unable to clench teeth strong enough for masseter/temporalis contraction to be felt

Unilateral damage to motor division (CNV3)

Seldom affects speech production (unaffected side is usually strong enough to compensate for weakened muscles)

Bilateral damage to motor division (CNV3)

Can have very serious effect on articulation; may be unable to make bilabials, labiodentals, etc. as well as lip and tongue adjustments for vowels, glides, liquids

Speech rate may be slowed (compensatory or primary)

Damage to sensory portion of mandibular branch

Imprecise articulation from reduced sensory information about articulation movements or contacts (think novocaine)

Facial Nerve (CN VII)

Emerges from the pons

It is motor and sensory in function, but only the motor component has a clear role in speech

It innervates the muscles of the upper and lower face

Upper face is innervated bilaterally by UMN

Lower face is innervated contralaterally by UMN (primarily) Facial muscles crucial for speech are those that move thelips and firm the cheeks

CN VII Motor and sensory

Motor

Supplies the stapedius muscle, stylohyoid muscle, posterior belly of diagastric,and the muscles of facial expression• Lesions can paralyze the entire ipsilateral side of the face, causing facial asymmetry

Fasciculations may be seen in the perioral area and the chin Sensory

Taste anterior 2/3 of the tongue

CN VII lesions

Common etiologies include brainstem pathologies, acoustic neuromas, heroes zostar, mononucleosis, vascular lesions and trauma.• Unilateral lesion of CN VII:•

Affected side sags and is hypotonic

Forehead may be unwrinkled, eyebrow drooped, eye open and unblinking

May see asymmetries during retraction/pursing lips; cheek puffing

bell's palsy

isolated CN 7 weakness from an undetermined etiology.

Upper and lower facial muscles affected and ability to close eye on affected sidemay be limited.86% of cases make full recovery.

nonspeech oral mech findings for bilateral lesions of CNVII

Mouth may be lax

Patient may be unable to retract/purse lips or puff the cheeks

Fasciculations may be present

Drooling may be observed

Pocketing of food

CNVII lesions- speech finding

Unilateral damage

May be more visible than audible; may have mild articulatory distortions; vowels usually fine

Bilateral damage Articulatory distortions; may have complete inability to produce sounds involving lipclosure.

Bilabials, ex., /p, b/ or labiodentals, ex., /f, v/

If doing a diadochokinetic rate would notice on the puh syllable of "puh tuh kuh"

Flutter of cheeks may be present when talking• Indicates hypotonicity - less resistance to intraoral air pressure

GLOSSOPHARYNGEAL (IX) NERVE

Bilateral UMN innervation

CN IX emerges from the medulla

Motor

Supplies the stylopharyngeus muscles

Sensory

Carries sensation from pharynx to posterior 1/3 of the tongue, including taste• Lesions often accompanied by lesions to the vagus nerve (CN X).

Often results in reduced pharyngeal sensation and a decrease in the gag reflex

Etiologies are similar to those that affect the other CNs in the lower brainstem

CN IX Lesions: Non-Speech and Speech Findings

Nonspeech oral mechanism findings

Reduced/asymmetrical gag reflex, BUT.....?• Pharyngeal elevation during swallowing may be reduced. Speech findings• Can't be assessed directly.

Vagus Never (CN X)

Bilateral UMN innervation• Emerges from the medulla Vagus (latin for wandering)

One of the most important CNs for speech production.

Divides into 3 branches:

Pharyngeal branch

Superior laryngeal branch

Recurrent laryngeal branch

pharyngeal branch

Constricts pharynx, elevates/retracts palate for speech & swallowing

Joins branches of glossopharyngeal and external laryngeal branch to make up 'pharyngeal plexus'

Superior laryngeal branch

Sensory component - Internal Laryngeal Nerve: transmits sensations from larynx, epiglottis, base of tongue, etc.

Motor component - External Laryngeal Nerve: innervates inferior pharyngeal constrictors and cricothyroid (pitch adjustments)

Recurrent laryngeal branch

Right is shorter; Left is longer because it loops around the heart

Passes down upper chest, loops around the subclavian artery (R) and aorta (L) before traveling back up the neck to enter the larynx

Innervates all of the intrinsic laryngeal muscles (except cricothyroid)

Sensory fibers carry sensations from larynx/subglottis

CN X Lesions

Etiologies include tumors, trauma from surgery, infections, stroke, Guillain-Barre syndrome, motor

neuron diseases, aneurysms.

Nonspeech oral mechanism findings

Unilateral lesions to pharyngeal branch:

Soft palate hangs lower on side of lesion

And what would happen with phonation? What about the gag reflex?

Bilateral lesions to pharyngeal branch:

Palate hangs low at rest and moves minimally/not at all during phonation

Gag reflex may be difficult to elicit (can be normal)

Nasal regurgitation may occur during swallowing

CN X Non-speech oral mech findings

Nonspeech findings for Superior Laryngeal Branch

(must visualize this on endoscopy or a rigid scope)

If recurrent laryngeal nerve branch isn't affected too, vocal cords may look normal.

In Unilateral lesions, the affected vocal cord may appear shorter than normal.

In Bilateral lesions, both cords may appear short and may be bowed.

Unilateral lesion (w/ or w/o SLN):

Affected vocal fold will be weak/paralyzed

May have dysphagia; impaired cough strength.

Bilateral lesion (w/ or w/o SLN):

Both cords will be weak/paralyzed

Dysphagia, poor cough strength

At risk for airway compromise (depending on position of paralysis of the folds)

Inhalatory stridor may occur

Pharyngeal branch affected

Unilateral lesion:

May have mild hypernasality

Bilateral lesion:

Hypernasality, nasal emission,

imprecise pressure consonants,

loudness and phrase length may be reduced

Superior laryngeal nerve (only) affected

Unilateral lesion:

Mild breathiness/hoarseness, reduced ability to after pitch

bilateral lesion: more moderate breathiness, hoarseness, decreased loudness, difficulty altering pitch

If superior laryngeal nerve and RLN affected

Breathiness or aphonia

Hoarseness

Reduced loudness

Diplophonia

Reduced pitch

Short phrases ...why?

Rapid vocal flutter

hypoglossal nerve: CN XII

Bilateral UMN innervation but with more input from contralateral hemisphere• Motor• Innervates all intrinsic and extrinsic muscles of the tongue (except for thepalatoglossus

CN XII basics

Emerges from the medulla

Innervates all the intrinsic and extrinsic muscles of the tongue

except for palatoglossus which is innervated by the pharyngeal plexus

Very important for lingual movements for speech, chewing andswallowing

Etiologies similar to those affecting other CNs (lesions in neck, surgery,trauma, infections, tumors, motor neuron diseases).• Lesions to XII often damage IX, X and XI since they travel together, butsome tumors/trauma may affect XII only.

CN XII non-speech oral mech findings

unilateral lesions:

Tongue will be weak (ipsilaterally) and will deviate to the weak side

Tongue may atrophy on weak side

May see fasciculations

Bilateral lesions:• Bilateral atrophy and fasciculations possible

Protrusion may be (very) limited in range; lateralization and elevation may beimpossible

Saliva may accumulate in the mouth; food may pocket in cheeks. Drooling may occur.

CN XII speech findings

unilateral lesions: mildly imprecise articulation (lingual control)

bilateral lesion:

mild to severe imprecision during articulation of lingual consonants

t, d, l (lingual- alveolar) th (lingual dental)

spinal nerve lesions

Usually need diffuse impairment of nerves supplying respiratory muscles to interfere significantly with breathing.• Etiologies include spinal cord injury, myasthenia gravis, ALS, Guillain-Barre' Syndrome.