Motor Speech Disorders Quiz 1

Disorders of speech resulting from neurologic impairment affecting the planning, programming, control or execution of speech.

They encompass apraxia of speech and the dysarthrias.

They are NOT language, cognitive‐communication, or swallowing problems.

A group of motor speech disorders resulting from

disturbances in muscular control or execution over the

speech mechanism

Due to damage of the central or peripheral nervous

system◦Result from paralysis, paresis, incoordination, involuntary

movements, or excessive or variable tone of the speech musculature

inadequate loudness

Hoarseness, harshness, breathiness, diplophonia, strained-strangled quality

hypernasality

Distortion (or substitution or omission)

Monopitch, monoloudness, excess & equal stress, rate too fast/too slow

StrokeTraumaInfectious processesTumorsProgressive neural diseasesDemyelinating diseases (e.g., Guillain‐Barré - an acute form of polyneuritis, often preceded by a respiratory infection, causing weakness and often paralysis of the limbs) Muscle diseases (e.g., muscular dystrophy - a hereditary condition marked by progressive weakening and wasting of the muscles.)

Toxic agents

A neurogenic speech disorder

results from impairment of the capacity to program sensorimotor

commands to position and move muscles for the volitional

production of speech

in the absence of paralysis, paresis, incoordination, involuntary

movements, or excessive or variable tone of the speech musculature

Frequently co‐occurs with aphasia

May co‐occur with dysarthria

Etiology: most often stroke◦ Except for the progressive form: primary progressive

apraxia of speech (PPAOS) for which we don’t know the etiology

DYSARTHRIA

Problem with muscular control or execution

Paralysis, paresis, incoordination, involuntary movements, excessive or variable tone

AOS

Problem with motor planning

NO paralysis, paresis, incoordination, involuntary movements, excessive or variable tone

◦ Still considered “gold standard”◦ Relies on clinician’s ability to analyze speech by listening to it

◦ Information from the medical history and from careful visual and tactile observation provides confirmatory evidence

◦ Most widely used method clinically◦ Can be unreliable if used by someone not trained and practiced in listening

critically to disordered speech

◦ Ultimate outcome of treatment is how well the speaker is able to be understood by a listener (if speaking is a realistic goal)

Acoustic

Uses instrumentation to analyze speech waveform

Studies have shown that a fixed set of acoustic measurements

does not necessarily correlate highly with perceived severity of

dysarthria

Little consensus about selection of measures that correlate with

perceptual ratings of quality

Generally used to explore speech impairment in greater detail, with quantifiable, reliable measurements

Used to confirm perceptual judgments◦ Useful for providing feedback in some forms of treatment, in

objectifying progress, although changes in the acoustic signal don’t always yield big payoffs in improved intelligibility

Uses instrumentation to study movements of speech structures and

the airstream, muscle contractions, biomechanical activity, &

relationships between neural activity and movement

Includes EMG, EGG, spirometry, nasal accelerometry

Physiologic activity can be imaged with fMRI, PET, SPECT, TMS, MEG

Generally used to try to correlate perceptual judgments with what’s happening physically in order to refine our understanding of the relationships

May serve as feedback during some forms of treatment, or to objectify progress, although changes in physiologic measurements don’t always yield big payoffs in improved intelligibilit

◦ Instrumental visual image is interpreted perceptually, so

really combines instrumental & perceptual methods ◦ Include

◦ Videofluoroscopy

◦ Nasendoscopy◦ Laryngoscopy◦ Videostroboscopy

Darley, Aronson, & Brown (DAB; also called the Mayo Classification System)

- lesion site

◦ Peripheral Dysarthrias

◦ Myopathic (muscle weakness) ◦ Myoneural (connecting muscles & nerves) ◦ Lower motor neuron

◦ Central Dysarthria

◦ Spastic ◦ Dyskinetic ◦ Ataxic

◦ Mixed Dysarthria

◦ Congenital/developmental

◦ Acquired

◦ Chronic/static◦ Improving◦ Progressive/degenerative

◦ Exacerbating‐remitting

Description of speech features

establishing diagnostic possibilites

Establishing a diagnosisEstablishing possibilities for localization and disease diagnosis

Specify severity

Normal or abnormal?

◦ Neurologic?◦ If not, organic or psychogenic?◦ Recent onset or longstanding?

◦Is it a MSD?◦ If so, dysarthria or apraxia of speech? ◦ If dysarthria, what kind of dysarthria?

◦ Process of elimination◦ List all possibilities that it could be and look for evidence to rule in or rule

out◦ Sometimes it’s as valuable to rule things out as to get a definitive diagnosis

R/O dysarthriaR/O apraxia vs dysarthria R/O malingering Evaluate and treat speech

◦ State implications of diagnosis

◦ What does it imply for localization?

◦ If a neurologic dx has been made, is the speech dx compatible with it? ◦ REMEMBER:

We diagnose the speech problem, not the medical) condition that causes the speech problem

However, sometimes it may be appropriate to state what medical condition the MSD is usually associated with, especially if the medical dx is uncertain or is for a condition that is not usually associated with what you’ve observed◦ e.g., “The patient demonstrates a mixed flaccid‐spastic dysarthria which is most often

associated with amyotrophic lateral sclerosis and a slow, insidious onset, not with the sudden onset typical of stroke.”

Match to patient’s complaints; gross mismatches may suggest psychogenic

etiology

Influences prognosis & management decisions

Initial estimates serve as baselines against which improvement or deterioration

are measured

◦Introduction, discuss patient’s purpose

◦Basic data (review for accuracy)

◦ Address & phone

◦ Age◦ Education◦ Occupation

◦ Marital/family status (hearing loss of spouse)◦ History of childhood speech & language problems

◦ When did it start?◦ Sudden or gradual?◦ Better, worse, or same now?◦ Any other problems start at the same time? Before? After

◦ Eating/swallowing◦ Change in emotional expression? Laugh or cry more easily?◦ Any medications?◦ Dental status◦ Hearing status◦ Visual acuity (If glasses are prescribed, pt. should wear them) ◦ Other medical problems?

◦ Describe in own words◦ Noticed any changes?

◦ Useful for determining extent of disability and barriers to participation

◦ Do people have trouble understanding you? When? What do you do?

◦ Do you ever have to write to make yourself understood? Has your problem affected your work? Does it prevent you from doing anything?

◦ What have you done to compensate? How has it worked?◦ Have you had any help? When/how long? What was done? Did it

work?◦ Do you think you need help with your speech now?

◦ Find out how much they understand so you know how to share info ◦ What have you been told about the cause of the problem?◦ In view of the diagnosis, what’s going to happen?

Salient features: features that contribute most directly to diagnosis

◦Strength: reduced, usually consistently but sometimes progressively

◦ Speed: reduced or variable (except in hypokinetic dysarthria, when it is increased but accompanied by reduced ROM)

Examination of speech mechanism

◦ Range of motion (ROM): reduced or variable

◦Steadiness: unsteady, either rhythmic or arrhythmic

◦ Tremor, hyperkinesias◦ Tone: a normal property of muscle that establishes its

appearance as neither too taut nor too flabby; a constant state of readiness◦ May be increased, decreased, or variable

◦Accuracy: inaccurate, either consistently or inconsistently

◦Not always present◦ Not diagnostic of MSDs, but are clues that help confirm or

refute a diagnosis

◦ Include:

◦ Atrophy◦ Fasciculations◦ Uninhibited laughing/crying ◦ Pathologic reflexes◦ Etc.

◦ relax, look forward (or close eyes), let

lips part to breathe quietly through

mouth.

◦Look for:

◦ Asymmetry◦ Expressionless, masklike, and unblinking◦ Abnormal, spontaneous, involuntary movements ◦ Tremors of lips, around mouth or chin

◦Lip retraction◦Lip rounding or pursing

◦Sustained mouth opening

◦Cheek puffing

Expressiveness: observe emotions, try to elicit spontaneous smile and compare with voluntary lip retraction; look for difficulty inhibiting laughter or crying

AMRs*: as rapidly and steadily as possible; observe rate, range, regularity of movement, involuntary movements◦ Lip pursing◦ Lip retraction

◦ Cheek puffing*AMR = alternating motion rate

◦ Hang lower than normal?

◦ Involuntary movements?

◦ Mouth opening as wide as possible

◦ Deviation?◦ Resistance to opening? To closing?◦ Normal bulk of masseter and temporalis when biting down?

◦ AMRs: open and close rapidly

◦ Some spontaneous movement is common◦ Look for atrophy, fasciculations, or large‐scale involuntary

movements

◦ Protrusion

◦ If deviates, repeat and note if consistent to one side, since mild deviation is natural but inconsistent re: side

◦ Lateralization

◦ Inside mouth◦ Outside mouth

◦ Protrusion

◦ If deviates, repeat and note if consistent to one side, since mild deviation is natural but inconsistent re: side

◦ Lateralization

◦ Inside mouth◦ Outside mouth

◦ Side‐to‐side

◦ Slow, one side at a time

◦ AMR

◦ Frontal◦Lateral inside & outside mouth

◦ SP hang low?◦ Symmetric faucial arches?

◦ Involuntary movements?

◦ Prolong /ɑ/

◦ Elevation? Symmetric?

◦ Evidence of nasal airflow on mirror?

Staccato / ɑ /

Evidence of nasal airflow on mirror during /s:/ or rep. of /pΛ/

If real question, use videofluoroscopy

◦ Cough

◦ Sharpness◦Coup de glotte (glottal coup): sharp glottal stop or grunting

sound

◦ Sharpness◦Inhalatory stridor?◦Consider requesting laryngeal exam, pursuing EGG or

acoustic analysis

◦ Quiet breathing

◦ Posture? ◦ SOB? Rapid, shallow, labored? ◦ Abdominal/thoracic movements limited in ROM? ◦ Shoulder movements? ◦ Neck extension/retraction? ◦ Regular rate?

◦ Sharpness of cough or glottal coup ◦ Weak cough with reduced ROM of abdominal thoracic excursion: respiratory weakness

◦ Manometer ◦ Maintain a stream of bubbles at depth of 5 cm for 5 sec

Not involved in speech production, but can be confirmatory evidence about

localization

Normal reflexes: presence is reflection of normal NS function; absence reflects

PNS pathology◦ Gag/pharyngeal reflex: back of tongue, PPW, faucial pillars

Afferent path CN IX (glossopharyngeal)

Motor path CN IX & X (vagus)

Characterized by palatal elevation, tongue retraction, sphincteric contraction of

pharyngeal walls

In general, significant only if absent or asymmetric (hypoactive on less responsive side)

present during infancy but tend to

disappear during NS maturation

Presence beyond infancy associated with CNS pathology, especially in frontal lobe cortical and subcortical regions◦ Be cautious if presence is weak or equivocal – a small percentage of

“normal” adults exhibit primitive reflexes

“release phenomenon” – reduction of cortical inhibitory influence on lower brain centers

stroke upper lip with tongue blade, beginning at lateral aspect and moving medially; do on both sides

No response in normal adults

Pursing lips: positive or pathologic result; can be confirmatory of UMN

disease, esp. diffuse damage to premotor cortex; frequently seen in dementia

When very strong, may purse lips as object approaches mouth, or turn mouth toward tactile stimulation at corner of mouth or cheek: called rooting reflex

light tap of finger on philtrum or tip of nose; or pressure of index finger on midline of upper lip and philtrum

◦ No response in normal adults

◦ Positive or pathologic response: protrusion and elevation of lower lip and depression of lateral angle of mouth

◦ Goal – test for nonverbal oral apraxia ◦ Focus on ability to perform without off-target approximations, frank errors, or frustrating

awareness that performance is incorrect with accompanying attempts at self-corrections

◦ Elicit with spoken command first, give model if necessary

◦ Often improve on imitation ◦ Able to perform reflexively or unconsciously, so be on the lookout so you can compare performance

◦ Pitch◦ Loudness◦ Quality◦ Duration◦ Steadiness◦ Observe face for movements

AKA diadochokinetic rates

Determine:

speed and regularity of reciprocal movements of jaw, lips, anterior and posterior tongue

Precision of artic movements

Adequacy of VP closure

Respiratory and phonatory support for sustained speech tasks

/pΛ/, /tΛ/, /kΛ/

◦ Ability to move quickly from 1 artic position to another

◦ Useful when AOS is suspected◦ /pΛtΛkΛ/, buttercup, coffeepot, etc.

◦ Conversational and narrative speech

◦ Oral reading of standard passage

◦ Use if

◦ LMN weakness of unknown cause is present◦ Pt. complains of changes in speech as day progresses or with physical

effort◦ Count as precisely as possible; continue without rest for 2-4 minutes ◦ Repeated readings of Grandfather Passage (or other passage)

◦ If AOS is suspected

◦ If mute or barely able to speak, ask to sing familiar tunes or use automatic speech tasks

◦ Frenchay Dysarthria Assessment - 2

◦ Apraxia Battery for Adults - 2◦ Apraxia of Speech Rating Scale

Degree to which a listener understands the auditory signal produced by the

speaker

Degree to which a listener understands the auditory signal PLUS all info associated with it (e.g., gestures, facial expressions, prosody, familiarity with context, etc.)

Rate at which intelligible or comprehensible information can be conveyed

intelligibility or comprehensibility

◦be specific about the level of speech and context

◦Measures designed to elicit the patient’s perspective about the impact of the disorder and whether treatment is making a difference

◦Valuable for assessing the limitations to activity and participation

◦Dysarthria Impact Profile◦ Measures the psychosocial impact of acquired dysarthria from the speaker’s perspective in the areas of:◦ Self-perception◦ Self-concept

◦ Self-esteem

◦ Developed for use by community-dwelling adults with any communication disorder

Produced by LMN lesion (bulbar palsy) ◦ Nuclei of spinal or cranial nerves◦ Axons◦ Myoneural junction

LMN lesion: all movement is affected (reflexive, automatic, & voluntary)

Reduced muscle tone & ROM

Atrophy & fasciculations

◦ Fasciculations: visible, arrhythmic twitches or dimplings in resting m. 2° spontaneous motor unit discharges; results from n. degeneration or irritation

Weakness of muscle contraction

◦Neuromuscular junction diseases

◦Myasthenia gravis (MG)

Autoimmune disease that destroys acetylcholine (ACh) receptors on

muscles, making them less responsive to the ACh that triggers

contraction

Abnormally rapid weakening of voluntary muscles with use,

improvement with rest (which replenishes ACh supply)

Tensilon injection improves performance immediately after stress testing

◦ Botulism ◦ Botulinum toxin blocks release of ACh at presynaptic membrane

◦ Paralyzes affected muscles

◦ Brainstem stroke

◦ Polio (poliomyelitis) (myelitis: inflammation of spinal cord) ◦ Herpes zoster (shingles - an acute, painful inflammation of the nerve ganglia, with a skin eruption often forming a girdle around the middle of the body. It is caused by the same virus as chickenpox.) ◦ Opportunistic infections assoc with AIDS ◦ Encephalitis ◦ Meningitis

◦ Guillain-Barré: demyelinization of spinal & cranial nerves

particularly at the base of the skull

◦ Muscular dystrophy: degeneration of m fibers and proliferation of connective tissue

◦ Poliomyositis: disease of striated muscles associated with infections

- myositis: inflammation of muscles

◦ Progressive bulbar palsy: LMN weakness of CN muscles; dysarthria &

dysphagia are predominant signs

◦Radiation therapy for carcinoma ◦Surgery/other trauma ◦Idiopathic mononeuropathies (neuropathy - dysfunction of peripheral nerves causing numbness & weakness)

◦ Bell’s palsy: CNVII

◦ Trigeminal ◦ Maxillary branch – sensory info ◦ Mandibular branch – jaw movement

◦ Unilateral damage:◦ jaw deviates to weak side when opened ◦ No perceptible impact on speech

◦ Bilateral damage:◦ jaw hangs open◦ Profound effect on bilabials, labiodentals, lingualveolar, and lip and tongue

adjustment for many vowels and glides

◦ Facial◦ Perioral fasciculations

◦ Unilateral

◦ Effects more visible than audible ◦ Face sags on affected side, no wrinkles or NL fold ◦ Pocketing of food on affected side ◦ Reduced retraction & puffing, cheek flutter

◦ Bilateral ◦ Effects more audible than visible ◦ Face looks symmetric, but weakness is present ◦ Distortions of bilabials, labiodentals, and vowels that require lip rounding or spreading

◦ Vagus – important branches for speech:

◦ Pharyngeal branch◦ Superior laryngeal branch ◦ Recurrent laryngeal branch

◦ Unilateral

Soft palate lower on weak side at rest, pulls up toward strong side on phonation,

reduced gag on weak side

Superior laryngeal n.: vf shorter

Recurrent laryngeal n.: vf fixed in paramedian position

Both sup. & rec. : paralyzed in abducted position

May hear hypernasality, stridor or breathiness

◦ SP low at rest, minimal or no movement on phonation, absent gag ◦ Superior laryngeal n.: bowed vfs◦ Recurrent laryngeal n.: both cords in paramedian position◦ Both superior & recurrent: both cords in abducted position◦ Hypernasality, nasal emission, breathiness, stridor

◦ (Spinal) accessory nerve◦ Unilateral: generally no effect on speech ◦ Bilateral

◦ May affect respiration, phonation, and resonance mildly, but can’t be separated from CNX effects

◦ Hypoglossal

◦ Unilateral

◦ Tongue atrophy & fasciculations ◦ Deviation to weak side on protrusion ◦ Imprecise articulation

◦ Bilateral ◦ Tongue atrophy & fasciculations ◦ Minimal ROM ◦ Pocketing of food, difficulty handling saliva ◦ Imprecise articulation of all lingual sounds

◦ Hypernasality, nasal emission, continuous breathiness, stridor

◦May also hear:◦ Hoarseness, harshness, diplophonia, monopitch, monoloudness, short

phrases, imprecise articulation

◦ Everything we hear can be traced to weakness

Bilateral UMN lesions; pseudobulbar palsy◦ Because most speech LMNs are bilaterally innervated

from UMNs, bilateral UMN lesions are generallyrequired to produce spastic dysarthria UMN ◦ Unilateral UMN lesions don’t generally have a major, long-term effect on speech, but we will discuss possible effects later

◦ Vascular

Single brainstem stroke in vertebrobasilar artery distribution◦ R & L UMN pathways in close proximity

Bilateral cerebral hemisphere strokes◦ R & L UMN pathways not close in cerebral hemispheres ◦ Usually caused by 2 separate strokes◦ Lacunar infarcts

◦ Small deep infarcts in penetrating arteries

◦ Inflammatory disease

◦ Leukoencephalitis

Inflammation of white matter of brain or spinal cord

Causes necrosis of small blood vessels & surrounding

brain tissue

◦ Degenerative disease

◦ Primary lateral sclerosis

◦ Rare motor neuron disease ◦ Onset usually in 50s ◦ Dysarthria is often the first symptom

◦ Hyperactive reflexes◦ Pathological reflexes◦ Chewing and swallowing problems ◦ Pseudobulbar affect◦ drooling

Strained-strangled voice quality, harshness, low pitch, reduced pitch variation,

reduced loudness variability

Hypernasality

Imprecise articulation

Slow rate, slow but regular AMRs

All can be traced to spasticity, slowness of movement, reduced ROM, & somewhat to weakness

◦ Slow rate◦ Harsh, strained-strangled voice quality◦ Reduced variability of pitch and loudness ◦ Slow regular AMRs

The palmomental reflex or Marinesco-Radovici Sign or Kinn reflex or Marinesco Reflex is a primitive reflex consisting of a twitch of the chin muscle elicited by stroking a specific part of the palm.

The jaw jerk reflex or the masseter reflex is a stretch reflex used to test the status of a patient's trigeminal nerve and to help distinguish an upper cervical cord compression from lesions that are above the foramen magnum. caused by striking the chin when the mouth is open.

a condition caused by inflammation of a nerve or nerves secondary to injury or infection of viral or bacterial etiology.

Post-polio syndrome (PPS) is a condition that can affect polio survivors decades after they recover from their initial poliovirus infection. Unlike poliovirus, PPS is not contagious.

Moyamoya disease is a rare, progressive cerebrovascular disorder caused by blocked arteries at the base of the brain in an area called the basal ganglia.

- causes weakness and numbness

CADASIL (Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy) is an inherited form of cerebrovascular disease that occurs when the thickening of blood vessel walls blocks the flow of blood to the brain.