CSDS 213: Exam 2 Unit 5

Cause of Spastic Dysarthria

Caused by BILATERAL damage to Upper Motor Neurons (UMN): These are located in both the pyramidal and extrapyramidal tracts.

Pyramidal

characterized by muscle contraction that are slow and weak

Extrapyramidal

characterized by increased muscle tone (spasticity), weakness, and abnormal oral reflexes

Damage to pyramidal and extrapyramidal equals

Speech characteristics are result of muscles that show weakness and slowness (notable in lips and tongue)

AND

spasticity (most notable in the larynx), results in hyperadduction of VFs and possible incomplete VP closure

UMN tract and its role in Spastic Dysarthria

UMN tracts in the pyramidal system start in the primary motor cortex, then travel down the pyramidal system where the become lower motor neurons, then on to the muscles

Damage anywhere along corticospinal and corticobulbar tracts can cause weak slow movements

Extrapyramidal tract is more complex

When one system is damaged, the other is almost always damaged as well

For spastic dysarthria to occur the damage must be bilateral - damage to both sides of the pyramidal and extrapyramidal systems

unilateral upper motor neuron damage results in

a different dysarthria (UUMN) which is mild cause they are still receiving innervation from the other side

Causes of bilateral upper motor neuron damage (SD)

Stroke

Amyotrophic Lateral Sclerosis

Traumatic Brain Injury

Multiple Sclerosis

Brainstem Tumors

Anoxia/Cerebral Anoxia

Viral/Bacterial Infection

Stroke

A single stroke can cause SD ONLY if it occurs in the brainstem

Multiple strokes (at least 2) involving BOTH cerebral hemispheres can cause SD

A single stroke in 1 hemisphere if there is already pre-existing damage to the other hemisphere from an earlier stroke, head injury, tumor, etc. can cause SD

ALS

A degenerative neuro disease that can cause SD

The cause is unknown, with an average life expectancy of 22 months after Dx

Causes progressive degeneration of UMNs and LMNs

Symptom development depends on whether UMNs or LMNs are predominantly involved, but eventually both are. Ultimately, it often results in a Mixed Dysarthria because all areas of the motor speech mechanism are impacted.

Traumatic Brain Injury (TBI)

Brain damage resulting from a traumatic head injury can be diffuse (widespread)

Due to diffuse damage, patients may experience spastic dysarthria or mixed dysarthria

Multiple Sclerosis (MS)

Progressive inflammation and destruction of the myelin sheaths (MS)

When this damage occurs to UMNs, bilaterally, may cause spastic dysarthria

Because damage may be widespread, it can also cause ataxic dysarthria or mixed dysarthria

Brainstem Tumors

Can cause damage similar to a Brainstem CVA by compressing or dmamaging UMNs from both hemispheres

Anoxia/Cerebral Anoxia

Lack of oxygen to the cells

(when this happens to cells in the brain, it's going to impact all the cells in the brain at the same time - could result in spastic dysarthria)

Viral/Bacterial Infection

Infections in the cerebral tissue can damage UMNs bilaterally if it is widespread enough

Speech Characteristics of Spastic Dysarthria

Articulation

Phonation

Resonance

Prosody

Respiration

Other Problems (non-speech characteristics that can help with the diagnosis)

Articulation

Imprecise consonant production = most common issue (but very common in other dys)

Vowel distortions can be heard with SD

Phonation

Harsh vocal quality = most common phonatory characteristic (tense and breathy)

Strained-strangled vocal quality - good diagnostic marker (spastic/spasmodic dysphonia)

Low pitch - common in all dys but most obvious in SD

Resonance

Hypernasality (often without nasal emission) = generally not as severe as with flaccid dysarthria, which often includes nasal emission

(caused by slow and incomplete VP movement)

Prosody

Monopitch and decreased intonation is one of the most obvious characteristics of SD (vocal folds have to be able to stretch and relax, vocal folds have to have bigger amplitude for loudness)

Monoloudness

Short phrases = most evident during conversational speech (trying to push so much air through to create voice - using a lot more pressure and energy to push air through)

Slow rate of speech due to slow speed and ROM of articulatory movements, and weakness

Respiration

Least likely to be impacted

Other problems - Pseudobulbar affect

uncontrollable crying or laughing that can accompany UMN damage in the brainstem

(not a result of anything happening in the environment, usually more often during the initial impact and decreases over time)

Other problems - drooling

can occur in other dysarthrias, but most common in SD

Due to poor saliva management in the oral cavity and/or decreased rate of swallowing

What are the 3 shared characteristics between flaccid and spastic dysarthria?

Hypernasality (usually worse in flaccid and accompanied by nasal emission)

Imprecise consonants

Slow articulatory movements

Info for Differential diagnosis

Site of lesion

Degree of hypernasality

Vocal quality

Oral Reflexes

Pseudobulbar affect/drooling

Rate of speech/Vocal quality

Site of lesion

if you have case history that identifies the site of lesion you can often know just from that - does it indicate its UMN or LMN

Degree of hypernasality

more severe in flaccid and accompanied by nasal emission, in spastic it is not as severe and can be intermittent so only occurs on some phonemes

Vocal quality

D is more strained and strangled. In FD it is more breathy. Although both may be described as “harsh”.

Oral reflexes

may be reduced or absent in FD. SD may have hyper-reflexes.**

Pseudobulbar and drooling

more likely in SD than in other dysarthrias

Rate of speech/vocal quality

Slow rate of speech AND harsh/strained vocal quality = only in SD

Treatment for phonation problems

Head and neck relaxation (stretches, massage, etc.): passive/active

Easy onset of phonation

Yawn-sigh

Head and Neck relaxation

Passive stretch: patient is just trying to relax/breathe, and the therapist is moving them through the stretch (move head forward, back, left and right till you feel resistance)

Active stretch: patient is doing it themselves, moving through those motions

Easy onset of phonation

gently initiate phonation on the vowel with a little /h/ right at the beginning

Yawn-sigh

stretches out the musculature then has some easy onset

Treatment for articulation problems

Stretching exercises

Traditional Articulation Treatments

Passive Tongue Stretching exercises

Wrap their tongue in gauze and then grab the tongue

Pull the tongue straight out till you feel resistence

Hold the tongue out for 10 seconds

Move it right or left til resistance and hold for ten seconds

Then do the other side and hold it for 10 seconds

Active tongue stretching exercises

Stick their tongue out as far as they can

Elevate it like trying to touch their nose

And then down to their chin

Then right and the left sides

Hold each position for 10 seconds

Then elevate the back of their tongue to the palate like for a k sound

Can also add having them push their tongue into their cheeks on each side

This kind of active stretch might actually increase hypertonicity in some patients - monitor it, if it is increses tonicity stop immediately and do passive exercises

Active Lip stretching exercises

Have them do rounding and elongation (smile and pucker) - hold each for 10 seconds

Could do puffing up the cheeks - intraoral pressure

Open their mouth as wide as they can

Squeezing the lips tightly together

This can also increase hypertonicity

Passive lip stretching exercises

Use gauze, grab one lip at a time

Pull out till you feel resistance, hold it for 10 seconds

Switch lips

Traditional Articulation Treatments

Intelligibility drills

Phonetic placement

Exaggerated consonants

Minimal contrast drills

Treatment for Prosody Problems

Pitch range exercises

Do these because they don’t have the movement for pitch changes from the tension

Intonation profiles

Contrastive stress drills

Chunking utterances into syntactic units

Treatment for Resonance Problems

Surgical or prosthetic management

Behavioral Speech Therapy for hypernasality/Modification of Speech

Visual feedback

Reduce rate of speech

Increase loudness

Surgical or prosthetic management

Posterior Wall Augmentation

Pharyngeal flap - taking a flap of skin from the pharynx and reinserting it on the pharyngeal wall

Palatal lift - prosthetic like a retainer (People with SD, if they have hyperactive reflexes they may not be able to tolerate this)

Treatment for hypernasality

Not going to treat it unless they demonstrate good oral resonance - that they can close the VP port on some speech act***

If they can’t, then they are not capable of VP closure, so there isn’t anything we can do to help them with therapy, so we refer them for a medical treatment that might help them get the closure

Visual feedback

Having them repeat words, phrases, and sentences without nasal phonemes

Using a mirror under their nose

A feather under their nose

Seascape - a visual feedback device, looks like a thermometer with a ball and a tube that is held to the nostril and shows that there is air escaping from the nose

Reduce rate of speech

can increase intelligibility and lessen the perception of hypernasality

Provides more time for the articulators and muscles to get into the right spot

Increase loudness

louder speech can mask hypernasal resonance and increase intelligibility

Establishing a target loudness for them to maintain