CH5-Spastic Dysarthria

Question 1

What is Spastic Dysarthria?

Answer 1

• perceptually distinct MSD
• caused by bilateral damage to the direct & indirect activation pathways of CNS

Question 2

What is the localization of

Spastic Dysarthria?

Answer 2

• UMN pathways

Question 3

Clinical Features of

Spastic Dysarthria

Answer 3

• excessive muscle tone (hypertonicity)
• weakness of speech
• predominantly problem of neuromuscular execution

Question 4

Direct Activation Pathway Damage-

UMN lesions

&

Spastic Paralysis

Answer 4

• direct activation pathways damage = impairment of fine, discrete movements
• Acute lesions = reduced muscle tone & weakness are evident but evolve to increased tone & spasticity.
  
  • weakness more pronounced in distal than proximal muscles.
  • reflexes tend to be diminished initially but become more pronounced over time.
• associated with positive Babinski sign

Question 5

What reflex is a lesion in the direct activation

pathway associated with?

Answer 5

• Positive Babinski Sign - a pathologic reflex
  
  • present in adults associated with CNS damage
  • reflects the release of a primitive reflex from CNS inhibition
  • normal in infants
  • Elicited by applying pressure from sole of foot on side of heel forward to the little toe and across to great toe
    
    • normal response = planting of toes
    • babinski response = estension of great toe & fanning of other toes

Question 6

What reflexes are common in bilateral

UMN disease?

Answer 6

Pathologic oral reflexes

suck, snout, palmomental and jaw jerk reflexes

Question 7

Name phonatory abnormalities of

Spastic Dysarthria

Answer 7

Associated with UMN involvement

• strained
• strained-harsh
• strained-strangled voice quality
• grunt at end of expiration

strained voice quality can also be present in some hyperkinetic dysarthrias

Question 8

Effects of

damage to indirect activation

pathways

Answer 8

• affects inhibitory role in motor control
• lesions = lead to overactivity (positive signs) such as :
  
  • increased muscle tone
  • spasticity
  • hyperexcitable reflexes
    
    • signs are interrelated

Question 9

Characteristics of

Spastic Dysarthria

Answer 9

Characteristics:

• combined effects of weakness and spasticity
• slowed movement
• reduction in range & force
• manifests in any/all respiratory, phonatory, resonatory, & articulatory parts of speech

Question 10

What do you phonatory abnormalities do you hear?

Answer 10

• Strained voice quality
  
  • Often present during vowel prolongation in people with spastic dysarthria
  • Note that duration is not notably short as it is with LMN vocal fold weakness or paralysis

Question 11

Name phonatory abnormality associated with spastic dysarthria in sound clip

Answer 11

• strained or strained-strangled voice quality
• often present during vowel prolongation in people with spastic dysarthria

Question 12

Listen for phonatory abnormality

associated with

spastic dysarthria

Answer 12

Grunt at end of expiration

• Following one, two, three, what time, and each vowel prolongation

Most often evident in people with spastic dysarthria

Other abnormalities are also present:

• markedly strained voice quality
• monopitch and monoloudness
• slow rate
• imprecise articulation

Question 13

Relationship of spastic paralysis

to

spastic dysarthria

Answer 13

Several of general principles and observations about spastic paralysis can be usefully applied to clinical conceptions of spastic dysarthria

• people w. spastic paralysis have:
  
  • decreased skilled movement
  • weakness from direct activation pathway damage
  • increased muscle tone
  • spasticity from indirect activation pathway damage.
• major abnormalities that affect movement include
  
  • spasticity, wakness, reduced ROM, slowness of movement
• which are also most salient features of disordered movement in spastic dysarthria.

Question 14

Etiologies

of Spastic Dysarthria

Answer 14

Damages to direct & indirect activation pathways bilaterally cause spastic dysarthria

• all categories cause bilateral CNS motor system damage & spastic dysarthria w/ varying frequency.
• Degenerative & vascular disorders are predominant causes.
  
  • Vascular Disorders-13%
  • Degenerative Disease - 58% -
  • Congenital Disorders-4%
  • Inflammatory Disease-3.5%

Question 15

Patient Perceptions

&

Complaints

-Spastic Dysarthria

Answer 15

• frequent complaint:
  
  • speech is slow or effortful
  • patient confirms it feels as if they are speaking against resistance (not often associated with other dysarthria types)
  • fatigue with speaking (sometimes with accompanying deterioration of speech
    
    • exception of myasthenia gravis (MG).
    • more frequent complaint in spastic vs. flaccid.
  • pts. often say they must speak more slowly to be understood, but admit they cannot speak faster.
  • may complain of nasal speech, though more associated with flaccid dysarthria
  • Swallowing - common; includes oral and pharyngeal phases of swallowing. Persistent = lesion often in brainstem.
  • drooling - more complaints than other dysarthria types
  • gagging when brushing teeth
  • pseudobulbar effect- difficulty controlling expression of emotions (laughter & crying)

Question 16

Non Speech Oral Mech Clinical findings

in Spastic Dysarthria

Answer 16

• nonspeech -
  
  • dysphagia (common, sometimes severe)
  • drooling d/t decreased swallowing frequency/poor control of secretions
  • reflexive swallowing - slowed jaw, lip & facial movement; occassionally audible with “clunking” character.
  • nasiolabial folds at rest = smoothed/flattened; fixed subtle smiling/pout posture.
  • reflexive/emotional facial movment frequently emerge slowly but may then overflow & be excessive.
  • psuedobulbar effect (pathologic laughing or crying)
• oral mech
  
  • normal jaw strength
  • jaw clonus - shivering or rapid tremor-like appearance. (evident as mouth opens for a yawn/jaw relaxed after teeth clenched)
  • bilateral weakness in face
  • decreased range of lip retraction & pursing
  • lower facial weakness is not as pronounced as with LMN lesions.
  • tongue is full & symmetric, ROM reduced, weakness apparent on strength testing.
  • AMRs show reduced ROM.
  • palate symmetric - may move slowly or minimally on phonatin
  • hyperactive gag reflex
  • cough and glottal coup may be normally sharp if respiratory & laryngeal movments not too slowed.
  • pathologic oral reflexes common:
    
    • sucking, snout, palmomental, and jaw jerk reflexes are present.
    • unambiguous and easily elicited = suggestive of UMN involvement.

Question 17

Acoustic & Physiologic Findings

in Spastic Dysarthria

Answer 17

• Respiration -
  
  • PLS- reduced voluntary respiratory msucle activation & dysfunction
  • reduced inhalatory & exhalatory respiratory volumes = shallow breathing; paradoxical breathing, restricted respiratory intake, reduced vital capacity.
  • hyperadduction usually present = normal expiratory capacitymust work against laryngeal resistance to airflow
• Laryngeal function -
  
  • normal at rest, bilateral hyperadduction of true & false vocal folds duriing speech amy be apparent.
  • pseudobulbar palsy/multiple bilateral strokes = acoustic evidence of increased shimmer & jitter
• Velopharyngeal function -
  
  • sluggish palate or not at all during vowel prolongation
  • palatal immobility
  • slow movmeent
  • incomplete velopharyngeal closure during videoflouroscopy & nasoendoscopy
• Articulation, Rate & Prosody -supported that movement rate is slow & movment range & precision are reduced.

Question 18

Vascular Disorders

associated with

Spastic Dysarthria

Answer 18

• lacunes/lacunar infarcts - small, deep strokes in small penetrating arteries of basal ganglia, thalamus, brainstem, and deep cerebral white matter.
• Binswanger’s disease (subcortical arteriosclerotic encephalopathy) - term for patients with vascular dementia; major leasions in subcoritcla white matter, with relative sparing of cortex adn basal ganglia; bilateral lesions can affect UMN pathways adn lead to spastic dysarthria.
• Moyamoya disease - chronic, progressive, nonatherosclerotic occlusive vascular disease that most frequently affects children, adolescents, and young adults.; can cause stroke, intracranial hemorrhage, including speech and language deficits d/t association with stenosis of distal internal carotid arteries & first branches.
• Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) - genetic small vessel vascular disease associated with mutations in NOTCH3 gene. presents early in adulthood. Main features are migrain with aura, recurrent small subcortical strokes, cognitive & mood disturbances, dysarthria is common. bilateral lesions, associated with spastic dysarthria.

Question 19

Degenerative Disease

associated with

Spastic Dysarthria

Answer 19

Primary lateral sclerosis (PLS)-

• can present as spastic dysarthria (with or without dysphagia); dysarthria present in many cases
• infrequent subcategory of motor neuron disease

Progressive pseudobulbar palsy -

• aka for when spastic dysarthria is primary manifestation of neurodegenerative disease
• also designated as progressive spastic dysarthria - for patients that it can be the presenting sign of motor neuron disease, including ALS, or variant/focal presentation of PLS
• PLS - life expentancy about 10 yrs. vs. shorter for ALS.

Question 20

Congenital Disorders

associated with

Spastic Dysarthria

Answer 20

• Cerebral Palsy* - often associated with dysarthria, can be severe.
• can be spastic in type, more frequent that other types. but does not correspond to type of CP. (Spastic CP does not = spastic dysarthria)

Sometimes dysarthria & associated oromotor deficits are predominant or only manifestations of a congenital /developmental neuromotor disorder.

• congenital suprabulbar palsy (paresis) = group of disorders associated with UMN abnormalities affective bulbar muscles (bilaterally) among which spastic dysarthria can be prominent manifestation. aka Worster-Drought syndrome.
  
  • diverse causes include stroke, anoxia, epilepsy, meningoencephalitis, neuronal migration disorders leading to structural abnormalities such as agenesis, cortical dysplasia; underdiagnosed
  • frequent co-occurrence of quadriparesis, developmental delay, and epilepsy.
  • other terms: congenital bilateral perisylvian syndrome, opercular syndrome, foix-chavany-marie syndrome.
  • some/all could be causally relevant to childhood apraxia of speech.

Question 21

Inflammatory Diseases

associated with

Spastic Dysarthria

Answer 21

leukoencephalitis - inflammatory demyelinating desease that affects white matter or brain or spinal cord.

• acute hemorrhagic leukoencephalitis - white matter of both hemispheres is destroyed, with similar changes in brain steam and cerebellar peduncles.
• destruction associated with necrosis of small blood vessels and surrounding brain tissue with inflammatory reactions in meninges.
• tendency for large focal lesions to form in cerebral hemispheres.
• bilateral & multifocal effects of white matter disease can affect UMN pathways and cause spastic dysarthria or mixed dysarthrias.

Question 22

Speech Clinical findings

in

Spastic Dysarthria

Answer 22

• conversational speech & reading, AMRs, and vowel prolongation most useful task for eliciting salient & distinguising characteristics of spastic dysarthria.
  
  • associated w/ impaired movement patterns not weakness of individual muscles.
    
    • associated with deficits in all speech valves & components of speech system, not always equally. –> effects intelligibility.
    • slowness reduced range of individual & repetitive movments, reduce force of movement
    • excessive or biased muscle tone or spasticity.
    • hyperadduction during phonation.

Question 23

Clusters of Deviant Clinical findings

associated with

Spastic Dysarthria

Answer 23

1. prosodic excess - excess & equal stress & slow rate
   
   • slowness of indiv. & repetitive movements
   • slow movemnts = reduce speech rate & contribute to excess & equal stress by reducing speech of muscular adjustments necessary for rapid pitch, loudness, duration.
2. articulatory-resonatory incompetence - represented by imprecise consonants, distorted vowels, hypernasality
3. prosodic insufficiency - consits of monopitch, monoloudness, reduced stress, short phrases
   
   • reflects reduced vocal variability with stressed syllables left unstressed, reduced pitch/loudness. decreased range of movement.
4. Phonatory stenosis- low pitch, harshness, strained-strangled voice, pitch breaks, short phrases & slow rate.
   
   • seems as voiced produced through narrowed glottis with secondary reduction of phrase length & speech rate.
5. Other -
   
   • breathiness = vocal fold weakness
   • slow rate esp. during connected speech tasks