Spastic Dysarthria Profile

Comprehensive vocabulary deck covering the pathophysiology, clinical characteristics, etiologies, and treatment strategies for Spastic Dysarthria as outlined in the lecture.

Spastic Dysarthria

bilateral damage to the upper motor neurons (UMN) of the direct and indirect activation pathways of the CNS, with spasticity as its hallmark.

at level of EXECUTION

DIrect pathways

Regarding the direct pathways, these are the ones that go from the motor cortex down through the corona radiata, and through the internal capsule, and through brainstem to whatever nucleus it is synapsing/innervating in the brainstem.

2 different kinds of pyramidal tracts:

1.corticobulbar: innvertaes muscles of the face

2.Corticospinal: innervates limbs like arms, legs,

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•These are predominately faciliatory tracts, meaning that when they fire, it causes something to happen, as supposed to stopping something from happening when they fire.

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•Involved In discrete movements: e.g., I say jump and you jump. I want this muscle to jump and this muscle is jumping.

Indirect pathways

In indirect pathways, still originate in motor cortex, but they synapse at a basal ganglia, cerebellum, etc, prior to either goint back to the cortex or down to the brainstem.

Indirect pathways are really important for reflexes, posture, tone, etc. e.g., basal ganglia for regulating how much movement, cerebellum for timing and coordination, etc., so tract that sends down that extra information

Damage to Pyramidal system

When you have damage to the pyramidal system, will look similar to flaccidity.

•Damage can result in weak/slow skilled movements

•Loss of fine, skilled movement

•Hypotonia

•Weakness (Distal > proximal)

•Babinski sign

•Hyporeflexia

Damage to Extrapyramidal System

When you have damage to the extrapyramidal system, that is when you will see the spasticity.

-recall, when thinking about spasticity broadly, occurs when nothing is suppressing reflex arc from activating , resulting in you getting so tight.

•Damage can result in weakness, increased muscle tone (spasticity), and abnormal reflexes

•Increased muscle tone

•Spasticity

•Clonus

•Decorticate or decerebrate posture

•Hyperactive stretch reflex

•Hyperactive gag reflex

Damage rarely occurs in isolation. Usually both tracts involved

Both tracts involved because next to eachother in brain.

Common ETIOLOGIES

1. ALS: Very common to see ALS with spastic dysarthria; typically affects lower motor neurons first before affecting UMNS, so typically onsets with flaccid first and then spastic.

2. STROKE: aka stroke in vertebrobasilar atery: There is only one vertebrobasilar artery (unlike how we have 2 MCAs, 2 ACAS), and it is located directly center in the back of the brainstem, so if you have a stroke there affects both sides instead of just one because it is in the dead center of the brain. 

   1. Brainstem strokes ABOVE the level of the nuclei cause spastic dysarthria

3. TBI: widespread injury to brain, causing bilateral damage to pyramidal and extrapyramidal systems

4. Multiple sclerosis: ; demyelinating disease; so when it demyelinates the UMNs bilaterally, that results in spastic dysarthria.

Note: most MS cases will have mixed spastic ataxic dysarthria.

Articulation Errors

Very common in spastic dysarthria

•Imprecise consonant production

•Most common articulation error

•Result of abnormally short voice onset time for voiceless consonants, incomplete articulatory contact, incomplete consonant clusters

•Vowel distortions

Incomplete articulatory contact b/c of tightness of the tongue, lack of range of motion,

Phonation

Harsh Voice Quality: Strained-strangled vocal quality

Low PITCH: increased muscle tone in larynx

Resonance

•Hypernasality

•Caused by spasticity in velar muscles, which slows and reduces range of soft palate movement and results in incomplete velopharyngeal closure during nonnasal speech sounds

•Not as severe as with flaccid dysarthria

•Generally does not include nasal emission

Prosody

•Monopitch

•Caused by overall tenseness of laryngeal muscles, resulting in reduced ability to contract/relax to vary pitch

•Monoloudness

•Caused by overall increased muscle tone in laryngeal muscles

•Short phrases

•Natural consequence of speaking through abnormally tight larynx, making it difficult to use longer utterances

•Slow rate of speech

•Caused by reduced speed and range of movement

Respiration

•Problems of respiration do not play great role in spastic dysarthria

•Abnormal respiratory movements causing

•Reduced inhalation and exhalation

•Uncoordinated breathing patterns

•Reduced vital capacity

•Phonation/prosody problems more likely result of hyperadduction of vocal folds than respiratory problem

Note: exception for this is ALS with problems with respiration

Hyperadduction: vocal folds being pushed together tightly, so everything is very tight.

Additional Characteristics of spastic dysarthria

•Pseudobulbar affect

•Uncontrollable crying or laughing that can accompany damage to upper motor neurons of brainstem

•Appears to be caused by damage to part of brain important in inhibiting emotions

•Drooling

•Due to impaired oral control of saliva or less frequent swallowing

Most common speech production errors

•Imprecise consonants

•Monopitch

•Reduced stress

•Harsh voice quality

•Monoloudness

•Low pitch

•Slow rate

•Hypernasality

•Strained-strangled quality

•Short phrases

•Distorted vowels

•Pitch breaks

•Breathy voice

•Excess and equal stress

How to evaluate Spastic Dysarthria

•Conversational speech and reading

→ Assesses resonance, articulation, prosody

•Alternate motion rate (AMR) task

→ Demonstrates slow rate of phoneme production

•Vowel prolongation

→ Evokes phonatory deficits