Spastic Dysarthria

1.  What is spastic dysarthria due to?
Due to bilateral damage of the upper motor neuron tracts of the pyramidal and extra- pyramidal tracts (has an effect on both sets of lower motor neurons)

2.  Describe the speech and the reason why it sounds that way.
Speech is slow effortful and has a harsh vocal quality
Increased tone, but also has weakness, reduced range of motion and decreased fine motor control in many of the same muscles.

3.  Describe the role of upper motor neurons in spastic dysarthria.
Role of Upper motor neurons in Spastic Dysarthria:
Review of anatomy:
 UMN are part of CNS.
  They originate in the cortex and brainstem.
  UMN are grouped into pyramidal and e-pyramidal tracts.
 UMN (pyramidal-direct pathway from cortex and course down to the LMN)- UMN are divided:
  Cortex to cranial nerves (corticobulbar tract)
  Cortex to spinal nerves (corticospinal tract)
  Pyramidal tract is responsible
   for transmitting neural impulses for discrete skilled movements     down to the lower motor neurons, which sends them to the      muscles. Speech is a discrete skilled mvmt.
  Damage to parts of the pyramidal system serving speech will result in    weakness and slowness in the musculature, i.e., weak slow movements of    the tongue, lips, velum etc.

 UMN (extrapramidal-indirect pathway from cortex to LMN)
  Originate in the cortex and brainstem with numerous interconnections    including the reticular formation and the red nucleus.
  UMN of extrapyramidal system eventually synapse w/ LMN of cranial    and spinal nerves.
  Extrapayramidal system is responsible for
   Maintaining posture, regulating reflexes and monitoring muscle     tone (done at the same time the pyramidal is transmitting its neural     impulses) Normally, the pyramidal and e-pyramidal work together     resulting in allowing complex movements effortlessly.
  Damaged to Extra and pyramidal systems
   Weak and slow muscle mvmt (pyramidal )
   Weakness, increased muscle tone (spasticity) and abnormal     reflexes (ex-pyramidal)
 
 

4.  Describe the effects of the difference between bilateral damage and unilateral damage to the UMN.
Spastic dysarthria: bilateral damage to both pyramidal and ex-pyramidal systems that innervate speech.  (affects tongue, lips, velum, larynx)
Significance of bilateral damage:
 Speech production muscles will be weak, slow,(weak and slow mostly in the tongue and lips) spastic (most noticeable in laryngeal muscles and maybe velum – causing incomplete VP closure during the production of non-nasals) and have abnormal reflexes.

(Unilateral damage causes unilateral upper motor neuron dysarthria.  This is not as serious because most of the cranial n. serving speech (except lower face and tongue) receive bilateral innervation from the UMN of pyramidal and exPyramidal system)

5.  Describe the different etiologies of spastic dysarthria.
Etiologies of Spastic Dysarthria

Stroke: Most common cause of spastic dysarthria.
Must have either 2 or more strokes (bilateral) in cerebral hemispheres or one in the brainstem (right and left pyramidal and expyramidal tracts are very close in the brain stem).

ALS
ALS results in progressive degeneration of LMN and UMN.
Some people begin with involvement in LMN and exhibit flaccid dysarthria and weakness in the legs and muscle atrophy
Some begin with UMN involvement demonstrate spastic dysarthria, hyperactive gag and jaw reflexes and swallowing disorders.
Eventually both UMN and LMn are affected and result in mixed dysarthria.

Head Injury:
 HI can produce widespread damage (stretched and torn axons, lacerated brain tissue and blood vessel hemorrhage)

Multiple Sclerosis
 MS is a suspected immunological disorder that results in the inflammation or complete destruction of the myelin sheath covering the axons. MS can affect myelin anywhere w/in CNS (cerebral hemispheres, cerebellum, brainstem, and spinal cord) so depending on where the damage is..this will be the dysarthria exhibited i.e., ataxic dysarthria, mixed dysarthria).

Other:
Brainstem tumor, cerebral anoxia, viral or bacterial infections in the cerebral tissue
 
 

6. Describe the speech characteristics of Spastic D

Speech Characteristics:
I.Articulation:
Imprecise Consonants (not helpful diagnostically—common characteristic among dysarthrias)
1.  Abnormally short voice onset time for voiceless consonants
2.  Incomplete articulatory contact
3.  incomplete consonants clusters
Vowel distortions
**II Phonation
Harsh vocal quality “friction of air” characteristic
 Harshness occurs when air leaks through a partially open glottis.  Perhaps caused by purposeful partial abduction of vf to help prevent spastic muscle tone in larynx from closing the glottis too tightly during speech.  They let some subglottic air leak through their tense, partly abducted vf.
Strained-strangled Vocal quality (noticeable characteristic, but not always present)
 Sound created by subglottic air being forced through a narrow, tightly constricted larynx due to spasticity of vf causing tight hyperadduction of the vf
III Resonance
Hypernasality caused by spasticity in the velum which slows and reduces its range of movement (not as severe as that seen in Flaccid d. and does not include nasal emission as in Flaccid d.)
**IV.  Prosody
Monopitch (one of the most obvious characteristics)  caused by overall tenseness of laryngeal muscles resulting in a reduced ability to contract and relax (contracting and relaxing vf is what helps us vary our pitch)
Monoloudness  caused by overall tenseness in laryngeal muscles (by increasing and decreasing vf tension, the larynx can precisely regulate the amount of subglottic air that passes through the glottis.
Short phrases-probably due to speaking through a tight larynx.  The energy required to force air through the tightly adducted vf is great so they shorten their utterances. Frequent inhalations interrupt the rhythm of speech
Slow rate of speech caused by reduced speed and range of movement in articulators.  Weakness in articulators may contribute to slower speaking rate. Slowed rate may be the result of speaking against tight adduction of the vf
V. Respiration
Not really a problem, but there may be some abnormal respiratory movmts.  Deviant movemtns can cause reduced inhalation and exhalation, uncoordinated breathing patterns and reduced VC.

7.  Of the speech Characteristics what are the most definitive?
Phonation and Prosody are the most definitive in spastic D

8.  What are some defining Non-speech characteristics of Spastic Dysarthria and how might they be treated?

Additional Defining NON-speech  Characteristics:

1.  Emotional liability known as the pseudobulbar effect may be due to damage to areas that inhibit emotions
 Crying is more common than laughing
 Embarrassing to person. Distressing to family
 Treatment limited.  Drugs ineffective. Effect lessens with recovery
2.  Drooling: most prominent in Spastic D. probably due to impaired oral control of saliva and possibly to swallowing.
 Client often reports that the injury resulted in the production of too much saliva. Embarrassing
 Treatments: behavioral –cuing to swallow.  Drugs. Surgery

Spastic dysarthia vs Flaccid D.

9.  Define bulbar and pseudobulbar palsy
 Definitions:
bulbar palsy:  atrophy and weakness in muscles innervated through the medulla. (tongue, velum, larynx and pharynx); a name for flaccid dysarthria
pseudobulbar palsy:  (false bulbar palsy) means weakness and slowness to the same muscles.  (tongue, velum, larynx, and pharynx); a name for spastic dysarthria

10.  Describe the difference between Spastic and Flaccid dysarthria.
Difference betw. Spastic and flaccid dysarthria

The distinction between the two is their different etiologies.  Bulbar palsy: lower motor neuron; pseudo bulbar palsy: UMN

1.  Spastic D Bilateral damage to upper motor neurons of the pyramidal and extrapyramidal systems.
Flaccid D. damage to lower motor neurons
CHECK MEDICAL REPORTS FOR SITE AND TYPE OF LESION.

2.  Hypernasality is more severe in Flaccid D. and has nasal emissions.  Hypernasality may appear more intermittent in Spastic D.

3.  Spastic D may have a tight, strained strangled voice quality (but not always: it may more frequently have a harsh vocal quality instead)

4.  Spastic D. : may have pseudobalbar effect (emotional liability) and drooling.

11.  What are the key evaluation tasks and what are you looking for?
Key evaluation tasks:
1.  conversation/reading: hypernasality, imprecise consonants, monopitch/loudness, reduced stress, short phrases,
2.  AMR: slow
3.  Vowel prolongation will evoke the phonatory deficits (harsh voice quality, strained-strangled voice quality, low pitch

12.  What are some possible areas of focus for treatment?
TX
Possible areas of focus:
1.  decreasing hyperadduction of the vf
2.  increasing articulatory precision (artic. Therapy)
3.  prosody (more natural intonation
4.  hypernasality (lifts etc.)
5.  Respiration is usually not affected.

13.  What is the treatment for the processes that may be affected by Spastic D.
Phonation:
1.  Hyperadduction: (Duffy says little success in reducing hyperadduction)
 Forget any exercise that does not include speech
Easy onset of phonation to make softer glottal closures.
Yawn-sigh: (similar to the above)
Perhaps begin with yawn sigh to initiate easy onset of phonation.

Articulation: (weakness, reduced speed of movement, and reduced range of movement)
Working on imprecise articulation.
What is the purpose of tongue/lip stretching and strengthening exercises?
To reduce hyper-tonicity and increase speed and ROM; watch out—may be counterproductive and increase hyper-tonicity.
Increase intelligibility:
1.  Client Reads words.  Clinician (not looking) tries to identify words.  If unable to understand, tell the client what was wrong with the production.
**2.  Exaggerated consonants: overarticulation
**3.  Minimal contrast drills (just like articulation)
 
Treatment of Prosody
**Contrastive stress drills
**Teaching appropriate phrasing
Pitch range exercise and intonation markings (on read passages) might work if the client is able to demonstrate ability to reduce tenseness in vf during conversation enough to make pitch changes.

Treatment of resonance (sluggish velum)
Pharyngeal flap
Gelfoam injections
Palatal lift (hyperactive gag reflex may make this difficult)

Exercises (only after surgical tx when closure can be achieved)
Biofeedback with nasal mirror for nasal emission; use of See Scape
Increased loudness (use visual feedback voice light and VU meter or a sound level meter)
 This may work simply because the person opens their mouth which will increase intelligibility and encourages overarticulation.