MSD midterm Study Guide

5 speech domains

RRAPP

Respiratory

Resonance

Articulation

Phonation

Prosody

Describe 5 speech domains

Respiration: breathing support for speech. Air from the lungs provide the power needed to speak 

Resonance: Sound quality and amplification. Sound travels through the throat, mouth, and nose which shapes how the voice sounds. Ex. Hypernasal- too much sound/air coming through the nose vs hyponasal- not enough sound goes through the nose sound “stuffy” saying nasal sounds 

Articulation: speech sound production. The lips, tongue, teeth and jaw move to form clear speech sounds. When the articulator is not moving in the correct place it can change the sound. Getting each phoneme intact 

Phonation: The VF in the larynx vibrate to create sounds - hypophonia weak, breathy speech. diplophonia - double pitches at the same time 

Prosody:Rhythm and expression of speech. Includes pitch stress, rate, intonation, that add meaning and emotion to speech ex. Monotone voice 

Two general types of MSD

Dysarthria: neurologic in origin, speech disorders that reflect abnormalities in the RATSSS of movements required for the aspects of speech production (RRAPP)

Apraxia of Speech: a neurologic speech disorder that reflects an impaired motor planning and programming sensorimotor commands necessary for directing movements that result in phonetically and prosodically normal speech

List 6 types of dysarthria

FAUSHH

Flaccid

Ataxic

Unilateral Upper Motor Neuron

Spastic

HYPERkinetic

HYPOkinetic

Describe 6 types of dysarthria

Flaccid: Weak muscle tone affecting speech clarity (muscle weakness); characterized by breathiness

Ataxic: Poor coordination causing irregular speech rhythm (muscle incoordination); characterized by slurred speech

Spastic: Muscle stiffness leading to slow, slurred speech (muscle spasticity); characterized by strained voice

UUMN (unilateral upper motor neuron): Upper motor neuron weakness, incoordination, or spasticity; affects execution or control of speech production

Hyperkinetic: Involuntary movements disrupting speech (involuntary movements); characterized by variable rate and volume

Hypokinetic: Limited movement resulting in rapid soft speech (muscle rigidity); characterized by mumbled words

Localization for each 6 types of dysarthria

Flaccid: Lower motor neuron (final common pathway, motor unit)

Ataxic: Cerebellum (cerebellar control circuit)

Spastic: Bilateral upper motor neuron (direct and indirect activation pathways)

Hyperkinetic: Basal ganglia control circuit (extrapyramidal)

Hypokinetic: Basal ganglia control circuit (extrapyramidal)

UUMN: Unilateral upper motor neuron

Neurologic- Specifics of 6 types dysarthria

Flaccid: Weakness

Ataxic: Incoordination

Spastic: Spasticity

Hyperkinetic: Involuntary movements

Hypokinetic: Rigidity; reduced range of movement; scaling problems

UUMN: Upper motor neuron weakness, incoordination, or spasticity

How movement is affected (salient features)- RATSS

Range 

Accuracy

Tone 

Strength

Speed 

Steadiness

What are the salient features that we need to be aware of when assessing MSDs

ROM, Accuracy, Tone, Strength, Speed, Steadiness (RATSSS)

What + how each salient feature may be impacted

Range: reduced or variable

Accuracy: inaccurate, either consistently or inconsistently 

Tone: increased, decreased, or variable 

Strength: reduced consistently, but sometimes progressively 

Speed:  reduced or variable 

Steadiness: unsteady - rhythmic or arhythmic

Complications associated with/ MSDs

Communication problems, social difficulty, depression (QOL)

What are issues with audio-visual perceptual measures?

Audio- Visual

• unreliability of judgments among clinicians 

• Difficult to agree on severity 

• Can’t directly test hypotheses about the pathophysiology underlying the perceived speech abnormalities 

Perceptual: 

• Listeners must identify clinically significant features from a multidimensional acoustic signal 

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

• Possible subgroups exist

What disorders are the result of an issue with certain processing components

Apraxia

What disorders are the result of an issue with motor execution

Dysarthria

Names (numerical + names) and function (what they control/do in general) of each speech cranial nerves

1. CN V (5): Trigeminal- Chewing and sensation. Controls the muscles of mastication (jaw opening/closing) and provides sensation to the face, lips, teeth, tongue (anterior 2/3 for general sensation), and oral cavity. Helps with jaw stability for speech.- facial innervation

2. CN VII (7): Facial- controls facial expressions, crucial for speech moves the lips and firms the cheeks. Innervates Upper and Lower face. Motor in function. Lesions can cause facial asymmetry. 

3. CN IX (9): Glossopharyngeal- Swallowing and sensation. Controls part of the pharynx, provides taste and sensation from the posterior 1/3 of the tongue, contributes to the gag reflex, and assists with swallowing.

4. CN X(10) Vagus- mixed innervation most important for speech production Voice, swallowing, and resonance. Controls the soft palate, pharynx, and larynx (vocal folds). Responsible for phonation (voice), resonance, swallowing, and airway protection. Major nerve for speech and swallowing.

5. CN XI(11): Accessory- Head and neck movement. Controls the sternocleidomastoid and trapezius muscles for head turning and shoulder elevation. Helps provide head and neck stability during speech and swallowing.

6. CN XII (12): Hypoglossal- Tongue movement. Controls the intrinsic and extrinsic muscles of the tongue. Essential for articulation, bolus manipulation, chewing, and swallowing. 

7. Spinal nerves: Control muscles of the neck, shoulders, and respiration. 

The phrenic nerve (C3–C5) controls the diaphragm, which provides the breath support needed for speech. 

Intercostal and other spinal nerves help control the chest and abdominal muscles used for breathing during speech.

Example of degenerative

ALS

Example of inflammatory

Encephalitis

Example of toxic-metabolic

Drug toxicity/hypoglycemia

Example of Neoplastic

Cancer (astrocytomas)

Example of Trauma

TBI

Example of Vascular

Stroke

Describe the direct activation pathway/pyramidal system (UMN)

 Axons don’t synapse w/ other cells until they’re at the final destination, crucial to voluntary movement activity 

What happens when direct activation pathway is damaged

Small lesions can have big effects (weakness/loss/reduction of skills movements) UMN innervate the LMNs on the opposite side of the body, some UMN have bilateral innervation

Describe the indirect activation pathway(extrapyramidal system (UMN system).

Subconscious automatic muscle (posture, muscle tone, movements that support + accompany voluntary movements.

What happens if indirect pathway is damaged?

Unilateral: mild spasticity, slow movements, hyperadduction of VF. Bilateral: ridgid muscle tone hyperflexia, dysphagia, disinhibition

Describe the function of the cerebellum

 Integrates and coordinate execution of smooth, directed movements

What happens if the cerebellum is damaged?

Ataxic dysarthria

Describe the basal ganglia

Plans and programs postural + supportive components of motor activity.

What happens if the basal ganglia is damaged?

Hyperkinetic, Hypokinetic dysarthrias

Medical conditions associated with MSDs

Flaccid: stroke affects CN, brainstem injuries— Myasthenia Gravis, Guillian-Barre syndrome

Spastic: bilateral stroke, TBI— MS, Cerebral palsy

Ataxia- cerebellar stroke or tumor, TBI, MS

Hyperkinetic- Huntingtond diease, tourettes, dystonia

Hypokinetic- Parkinson’s Disease, Parkinsonism

UUMN- small stroke, TBI, brain tumor

What are the SLPs’ roles and goals with MSDs?

description

establishing diagnostic possibilities

diagnosis of MSD (a dysarthria or apraxia of speech diagnosis)

Establishing implications for localization and disease diagnosis (the parts of the brain that can be damaged based on what we’re seeing)

specifying severity

Know the five main parts of an MSD evaluation.

Case history

oral mech

perceptual assessment of speech

assessment of ICE (Intelligibility, Comprehensibility, and Efficiency) 

estimate of functional communication effectiveness/psychosocial impact 

Chart review and case history – what are they, what might they entail, what information might they give us?

Medical history, basic data, tells us why they are here, details of injury, course of symptoms, reported changes, patient perception of deficits/diagnosis/prognosis, management to date, history of communication issues, informal assessment of speech characteristics. 

What do we assess during the oral motor mechanism? Why?

RATSSS (range of motion, accuracy, tone, strength, speed, steadiness) ; the changes in those aspects help us determine which type of dysarthria it is (ex: reduced tone = flaccidity, excess tone = spasticity) 

What are the primary tasks of a speech assessment.

vowel prolongation, alternating motion rates, sequential motion rates, contextual speech, speech stress testing

What tasks can be completed to assess each of the speech systems? RRAPP

Respiration: vowel prolongation, connected speech task 

Resonance: connected speech task, vocal stress test 

Articulation: connected speech task, AMRs (alternating motion rates), SMRs (sequential motion rates), vocal stress test 

Phonation: vowel prolongation, connected speech 

Prosody: connected speech task 

What is intelligibility

Intelligibility: the degree to which the listener can understand the acoustic signal produced by a speaker. 

What is comprehensibility

Comprehensibility: the degree to which a listener understands speech on the basis of the auditory signal plus all other information what may contribute to understanding what has been said (gestures, facials, etc). 

What is efficiency

Efficiency: the rate at which intelligible or comprehensible info is conveyed 

How do we assess intelligibility?

AIDS (assessment of intelligibility of dysarthric speech), connected speech task

Flaccid Dysarthria- Hallmark characteristics

Primary or hallmark characteristics: weakness, breathy speech, reduced strength, no cog deficits 

Flaccid - etiologies

Damage to LMN

Flaccid- Motor, sensory, non-speech, and speech impact of trigeminal nerve (CN V) lesions:

jaw weakness, reduced sensation from face, jaw, lips, tongue. Articulatory imprecision

Flaccid-Motor, sensory, non-speech, and speech impact of facial nerve (CN VII) lesions:

unilateral facial weakness, Mild articulatory distortions

Flaccid-Motor, non-speech, speech, unilateral and bilateral damage impact of vagus nerve (CN X) lesions

weakness of velopharyngeal and laryngeal muscles, hypernasality, nasal emission, breathiness

Flaccid- Motor, non-speech, and speech impact of hypoglossal nerve (CN XII) lesions

tongue weakness, Imprecise articulation.

What happens when there are spinal nerve lesions?

reduced respiratory support for speech.

Flaccid DAB cluster

Respiration	Breathy voice due to poor respiratory support; reduced loudness
Phonation	Breathy voice (most characteristic), hoarse voice, diplophonia (occasionally), reduced vocal intensity
Resonance	Hypernasality, nasal air emission, weak intraoral pressure due to velopharyngeal weakness
Articulation	Imprecise consonants, consonant distortions, slow or weak articulatory movements, especially with labial and lingual sounds
Prosody	Monopitch, monoloudness (less common than in other dysarthrias), short phrases due to reduced breath support

Flaccid- Any cog deficits

NO

Spastic- Hallmark characteristics

Spasticity, increased tone,

Slow speech rate

Slow, regular AMR’s

Reduced variability of pitch & loudness

Harsh, strained-strangled voice

Reduced range of movements

Spastic-Oral reflexes of importance for spastic dysarthria

Snout reflex, sucking reflex, palmomental reflex 

Spastic- Etiologies associated with spastic dysarthria

Damage to bilateral LMN

Spastic- Non-speech symptoms/signs

hypertonia, hyperflexia, clonus (rhythmic oscillating), pseudobulbar effect, dysphagia, drooling, slow AMRs  

Spastic- Speech symptoms

Prosodic excess - excess and equal stress, slow rate

Prosodic insufficiency - monopitch, monoloudness, short phrases, reduced stress

articulatory-resonatory incompetence - imprecise consonants, distorted vowels, hypernasality

Phonatory stenosis - low pitch, harshness, strained-strangled voice, pitch breaks, short phrases, slow rate

Spastic- DAB cluster

Respiration	Reduced breath support, short phrases
Phonation	Strained-strangled voice quality (hallmark), harsh voice, low pitch
Resonance	Hypernasality (may be present, usually less severe than in flaccid dysarthria)
Articulation	Imprecise consonants, slow and regular alternating motion rates (AMRs), vowel distortions may occur
Prosody	Slow speech rate, equal and excess stress, monopitch, monoloudness

Difference between Spastic + Flaccid

Site of lesion	Flaccid	Spastic
Muscle tone	Decreased (hypotonia/flaccid)	Increased (hypertonia/spasticity)
Weakness	Severe weakness	Weakness with stiffness
Reflexes	Decreased or absent	Hyperactive
Muscle appearance	Atrophy and fasciculations may be present	No atrophy or fasciculations (unless there is concurrent LMN damage)
Speech rate	Variable; may be slow	Slow
Voice quality	Breathy, weak, may be hoarse	Strained-strangled, harsh
Pitch	May be low or breathy	Often low, monopitch
Loudness	Reduced	Reduced, monoloudness
Resonance	Hypernasality with nasal emission	Mild-moderate hypernasality
Articulation	Imprecise consonants due to weakness	Imprecise consonants due to weakness and spasticity

Prosody	May have short phrases	Slow rate, equal/excess stress
Oral mechanism exam	Weakness, reduced ROM, atrophy, fasciculations	Slow movement, increased resistance, spasticity, exaggerated jaw jerk

Ataxic-hallmark characteristic

 Irregular and inconsistent articulatory breakdown

Irregular AMR

Vowel distortions

Prolonged phonemes

Excess & Equal stress

Excess loudness variation

Poor coordination of breathing with speech

What does the cerebellum control + how is it connected to the rest of the brain

It controls movement and coordination, connected to the brain stem (3 cerebrum penducles), controls movement for RRAPP

Primary characteristics of ataxic dysarthria and cerebellar damage

• Cognitive deficits 

• articulatory inaccuracy - imprecise consonants, irregular articulatory breakdowns, distorted vowels

• prosodic excess - excess and equal stress, prolonged phonemes, prolonged intervals, slow rate

• phonatory-prosodic insufficiency - harshness, monopitch, monoloudness

Ataxic- speech symptoms

imprecise articulation, hypernasality, strained voice

Ataxic- non speech

facial weakness, difficulty chewing and swallowing

Ataxic- etiologies

Damage to cerebellum

Ataxic- primary characteristic (DAB)

• articulatory inaccuracy - imprecise consonants, irregular articulatory breakdowns, distorted vowels

• prosodic excess - excess and equal stress, prolonged phonemes, prolonged intervals, slow rate

• phonatory-prosodic insufficiency - harshness, monopitch, monoloudness

Hyperkinetic- hallmark characteristics

Abnormal rhythm or irregular & unpredictable, rapid or slow involuntary movement

Hyperkinetic- etiologies

 Damage to basal ganglia, Huntingtons disease, Tourtette 

What is unique about hyperkinetic dysarthria

Has a group of speech disorders cause by different dykinesias 

general understanding of each of the types of dyskinesias discussed

• Chorea: quick, irregular, unpredictable movements from one body part to another looks like break dancing 

• Dystonia: sustained involuntary muscles contractions in one or more body parts 

• Tremors 

• Tics

Hypokinetic- hallmark

·       Fast rate

·       Rapid, blurred AMRs

·       Reduced stress

·       Monopitch, monoloudness

·       Inappropriate silences

·       Breathiness

reduced loudness

Hypokinetic- etiologies

Damage to basal ganglia

Hypokinetic- speech characteristics

• Respiration: reduced loudness (monloudness), Short phrased bc reduced breath 

• Phonation: breathy, monloudness + monopitch 

• Resonance: normal

• Articulation: imprecise consonant, short rushes of speech 

• Prosody: flat

Hypokietic- non speech

• Reduced facial expression

• Micrographia (small handwriting) 

Hypokinetic- Deficits for salient features

Reduced loudness variation, pitch variation

Hypokinetic- DAB

Articulation: imprecise consonant, reduced movement amplitude 

Breathing/Phonation: monloudess + monpitch, reduced stress, breathy 

UUMN- characteristics

Imprecise articulation (the most common feature)

Slow speech rate

Harsh, strained, or hoarse voice quality

Reduced loudness (may be mild)

Mild hypernasality (occasionally present)

Irregular articulatory breakdowns (less common)

Mild dysphagia

UUMN- changes to speech musculature

Contralateral lower facial weakness (weakness on the side opposite the lesion)

Contralateral tongue weakness, with possible tongue deviation away from the side of the lesion when protruded

Reduced strength and speed of speech muscles

Mildly reduced range of motion (ROM)

Generally normal muscle tone or only slight increase

No significant muscle atrophy

No fasciculations (because lower motor neurons are intact)

Oral reflexes may be slightly hyperactive, but severe reflex changes are uncommon

UUMN- clinical characteristics

History of a unilateral stroke (most common cause)

Contralateral lower facial weakness

Contralateral tongue weakness

Possible mild dysphagia (difficulty swallowing)

Mild hemiparesis or hemiplegia (weakness or paralysis on one side of the body)

Emotional lability may be present in some cases

Generally mild neurological deficits compared with bilateral UMN lesions

Speech deficits are usually mild and often improve over time

No muscle atrophy or fasciculations (LMNs remain intact)

UUMN- common etiologies

• Unilateral stroke (CVA) — most common cause

  • Often involves the internal capsule or motor cortex

• Traumatic brain injury (TBI)

• Brain tumor

• Neurosurgical injury

• Less commonly, other unilateral focal brain lesions

UUMN- common size of lesion

• Usually a small, unilateral lesion

• Lesion affects the upper motor neuron (corticobulbar) pathways supplying the speech musculature

• Because the lesion is unilateral and most cranial nerve nuclei receive bilateral cortical innervation, speech deficits are typically mild

Severity

this can be a helpful sign when determining diagnosis

Severity

Usually mild (hallmark feature) to moderate

Speech deficits

Speech deficits are often subtle and may be difficult to detect.

Articulation

Articulation is typically the most affected speech subsystem.

Patients are often..

highly intelligible, with only slight reductions in speech clarity.

Symptoms often..

improve over time, especially after a stroke, due to neurological recovery and compensation.

Non-speech oral mech exam finding

Contralateral lower facial weakness

Contralateral tongue weakness, with possible deviation away from the side of the lesion

Mild weakness of the lips and tongue

Reduced speed of oral movements

Slightly reduced range of motion (ROM)

Generally normal muscle bulk (no atrophy)

No fasciculations

Muscle tone usually normal or mildly increased (spasticity may be minimal)

Oral reflexes may be slightly hyperactive

Possible mild dysphagia

Speech impact

Speech Impact

• Usually mild dysarthria

• Speech is generally intelligible, with only slight reductions in clarity.

• Articulation is the primary speech subsystem affected.

• Communication is often only mildly impaired, especially in quiet, familiar settings

Primary speech finding

• Imprecise consonants (hallmark feature)

• Slow speaking rate

• Harsh, strained, or hoarse voice quality

• Reduced loudness (may be mild)

• Mild hypernasality (occasionally present)

• Irregular articulatory breakdowns (less common)

• Mild monopitch or monoloudness may occur but are not prominent

UUMN- best way to diagnose

an oral mech exam 

Tricky: the symptoms are more mild due to bilateral innervation of the UMNs 

UUMN- Common physical findings

• Contralateral lower facial weakness (central facial paresis)

• Contralateral tongue weakness, with possible deviation away from the side of the lesion

• Mild hemiparesis or hemiplegia on the side opposite the lesion

• Reduced strength, speed, and range of motion of oral structures

• Possible mild dysphagia

• Normal muscle bulk (no atrophy)

• No fasciculations

• Muscle tone usually normal or mildly increased

• Possible mildly exaggerated oral reflexes