Flaccid Dysarthria Flashcards
What is Flaccid Dysarthria?
- Caused by injury or disease of one or more cranial or spinal nerves involved in speech
- to the muscles involved in speech, or
- to the junction between them
What is impaired in Flaccid Dysarthria?
Reflect problems in the nuclei, axons, or neuromuscular junctions that make up the motor units of the Final Common Pathways (FCP).
May be manifest in any or all of the:
-respiratory
-phonatory
-resonatory
-and articulatory components of speech
What word is Flaccid Dysarthria?
WEAKNESS
Speech:
Continuous breathiness
Diplophonia (2 pitches in voice)
Nasal emissions
Short phrases
Hypernasality
Rapid deterioration and recovery with rest
Imprecise alternating motion rates (AMRs)
Physical Characteristics:
Weakness
Flaccidity
Atrophy
Fasciculations
hypoactive gag reflex
Rapid deterioration and recovery with rest
Hypertonia
What are the Characteristics of Flaccid Dysarthria?
Around 8% of all dysarthrias
Muscle weakness and reduced muscle tone in one or more groups of muscles
Decrease in the speed, range and accuracy of speech movements.
These are problems of EXECUTION
NOT planning or programming.
What are the 5 characteristics of Flaccid Dysarthria?
- Weakness
- Hypotonia
- Atrophy
- Fasciculations
- Progressive Weakness
Clinical Characteristics info on: WEAKNESS
WEAKNESS
Paresis – partial loss of use of the muscle group
Paralysis – total loss of muscle contraction
Can be due to damage in the cell body of the LMN, the axon of the LMN, the neuromuscular junction (synapse), or the muscle itself
Observed during single, sustained, or repetitive contractions
Clinical Characteristics info on: HYPOTONIA
Reduced Muscle Tone
- “Floppy”
- Reduced resistance to passive movement
Also display hyporeflexia
- Reduced reflexes in the affected muscles
Clinical Characteristics info on: ATROPHY
Reduction in muscle volume due to the lack of communication between the nerve and muscle
NOT an acute symptom, takes some time to take effect
Associated with more significant paresis or paralysis
Clinical Characteristics info on: FASCICULATIONS
- Visible, arrhythmic, isolated twitches in resting muscle
- Due to spontaneous action potentials in dying nerves
- Primarily seen when the LMN is damaged, not when the muscle alone is damaged
Clinical Characteristics info on: PROGRESSIVE WEAKNESS
When the neuromuscular junction is affected, muscle will weaken with sustained or repeated contraction
This is more significant than simple fatigue
- With rest or certain medications, the person will recover strength very quickly
Commonly seen in conditions like myasthenia gravis (grave muscle weakness)
CN V- Trigeminal Nerve Lesion Info
Begins in the Pons
Rarely the only CN involved in flaccid dysarthria
Significant sensory pain (trigeminal neuralgia) can affect speech
What is CN V- Trigeminal Nerve Lesion NON SPEECH Characteristics?
NON-SPEECH
- Difficulty resisting lateral pressure on jaw (unilateral)
- Jaw hangs open at rest (bilateral)
- Difficulty with chewing or drooling is sometimes reported
What is CN V- Trigeminal Nerve Lesion SPEECH Characteristics?
SPEECH
- Unilateral damage does not usually affect speech significantly
- Possibly a mildly slower rate for Puh during AMRs (vs Tuh or Kuh)
- Bilateral damage reduces precision or fully impairs labial and dental sounds and decreases precision of other consonants and vowels
CN VII- Facial Nerve Lesions Info
Begins in the lower Pons near the Abducens nerve (lateral eye movement)
Travels near CN VIII after leaving brainstem and can be impacted by acoustic neuromas
Infections (e.g., herpes zoster) can trigger Bell’s palsy
What is CN VII- Facial Nerve Lesion NONSPEECH Characteristics?
NON SPEECH
- Drooping eyebrow and unwrinkled forehead on the affected side
- Ipsilateral eye does not blink or close
- Lip may droop and not seal during eating, increased chance of biting lip
- During recovery, regeneration may cause simultaneous blink/face mvmt
What is CN VII- Facial Nerve Lesion SPEECH Characteristics?
SPEECH
- Decreased precision and rate on “puh” but not “tuh” or “kuh”
- Distortion of bilabial and labiodental consonants
- May exaggerate jaw movement to compensate for lip weakness
CN IX – Glossopharyngeal Lesions Info
Begins in the medulla alongside CN X- Vagus (nucleus ambiguus)
Usually damaged with CN X (at minimum), not in isolation
What is CN IX- Glossopharyngeal Nerve Lesion NON SPEECH Characteristics
NONSPEECH
- Asymmetric gag reflex if damage is unilateral
- Pain in the upper pharynx (glossopharyngeal neuralgia)
- Decreased pharyngeal elevation during swallow
What is CN IX- Glossopharyngeal Nerve Lesion SPEECH Characteristics
SPEECH
- Difficult to assess alone as it is primarily sensory
- But remember sensory functions include proprioception of articulators
- Motor functions have some overlap with CN X (pharyngeal plexus)
CN X- Vagus Lesions Info
Begins in medulla alongside CN IX- Glossopharyngeal (nucleus ambiguus and dorsal motor nucleus)
What are the THREE main branches of the CN X- Vagus Nerve and what is presented when damaged?
Three main branches with different effects when damaged
PHARYNGEAL
- Pharyngeal plexus with CN IX for upper pharynx
- Velum and posterior tongue movement
SUPERIOR LARYNGEAL
- Sensory and motor function for lower pharynx and cricothyroid
RECURRENT LARYNGEAL
- All other laryngeal motor function and sensory function below the vocal folds
What is the CN X- Vagus Lesion Characteristics: ORAL
NONSPEECH
- Unilateral
- Velum will hang lower on the side of the lesion and pulls toward the strong side during swallow and phonation
- Decreased gag reflex on the impaired side
BILATERAL
- Velum hangs low and does not elevate during swallow or phonation
- Absent or near-absent gag reflex
- Nasal regurgitation during swallow
SPEECH
- Hypernasality
- Weak pressure on oral consonants
What is the CN X- Vagus Lesion Characteristics: LARYNX
NONSPEECH
- Unilateral
- Decreased reflexive and volitional cough strength
- Increased chance of penetration and aspiration during swallow
- Visible reduction of movement on side of lesion during endoscopy
BILATERAL
- Respiratory stridor during inhalation if vocal folds are paralyzed adducted
- Cough sharpness severely reduced or absent
- Significant risk of aspiration if vocal folds are paralyzed abducted
SPEECH
- Breathiness, Hoarseness, Diplophonia or Aphonia
- Reduced pitch and loudness range
**Diplophonia= is the production by the voice of 2 separate tones through quasiperiodic variations in the vocal fold vibration
**Aphonia= loss of ability to speak through disease of or damage to the larynx or mouth.
What is the CN X- Speech changes in the Pharyngeal Branch?
- Hypernasality
- Weak pressure on consonants
What is the CN X- Speech changes in the Recurrent Laryngeal Branch?
Dysphonia (Hoarseness, Breathiness, Diplophonia Stridor, Aphonia)
Superior Laryngeal Branch?
Reduced pitch range
CN XII- Hypoglossal Lesion Info
Begins in medulla from a number of roots that combine after exiting the brainstem
Controls all the muscles of the tongue except palatoglossus (CN X)
Often damaged along with CN IX- Glossopharyngeal, CN X- Vagus, and/or CN XI- Spinal Accessory.
What is the CN XII-Hypoglossal Lesion NONSPEECH (Unilateral & Bilateral) Characteristics?
Unilateral
- Atrophy and fasciculations on the side of damage
- Tongue deviates to the weak side on protrusion
Bilateral
- Atrophy and fasciculation on both sides of the tongue
- Limited movement of tongue laterally and on protrusion
- Saliva accumulation and decreased bolus control during eating
What is the CN XII-Hypoglossal Lesion SPEECH Characteristics?
Decreased speed and articulatory precision of lingual consonants and vowels
Can be compensated for by excessive jaw movement
Cul-de-sac resonance effects
** Cul-de-sac resonance—occurs when sound resonates in a cavity (oral, nasal, or pharyngeal) but is “trapped” and cannot exit because of an obstruction.
Spinal Nerve Leasions
Phrenic Nerve (C3-5) innervates the diaphragm
Other cervical and thoracic nerves for accessory muscles
Damage can result in rapid, shallow breathing
Respiratory weakness alone leading to flaccid dysarthria is rare, but it happens
- Decreased loudness
- Short phrase length
What is the Summary of Common Characteristics in FLACCID DYSARTHRIA?
Hypernasality
Nasal emission
Imprecise consonants
Breathiness
Dysphonia (hoarsness)
Decreased pitch range
Decreased loudness
** Nasal air emission (air that escapes out of nose) can be heard during production of certain consonants (such as /p/, /t/, /k/, /s/, /sh/, and /ch/). When there is nasal emission, the consonants become weak or omitted.
** When there is nasal emission, the consonants become weak or omitted. In addition, the child may use abnormal speech sounds (such as a hard “uh” instead of the consonant sound /g/) because of the lack of air pressure in the mouth. Hypernasality is due to an abnormal opening between the nose and the mouth during speech.
What are the Etiologies of FLACCID DYSARTHRIA?
Degenerative Disease
Physical Trauma
- Surgery
- Head/neck injury
Brainstem stroke
Head and Neck Cancer
Guillian-Barre Syndrome
Myasthenia Gravis
Multiple Sclerosis
Amyotrophic Lateral Sclerosis
Tramatic Injury
Guillain- Bare Syndrome
Autoimmune disease of the peripheral nervous system
Onset often follows viral infection
Progressive, but quick (2-3 weeks to reach significant weakness)
Recovery period is long (30% have residual weakness after 3 years)
**A condition in which the immune system attacks the Peripheral nerves causing weakness and numbness in the limbs.
Myasthenia Gravis (grave muscular weakness)
Autoimmune disease of the neuromuscular junction
Rapidly increasing weakness with use, recovery with rest
May sound normal at first, but after counting to 100, significant dysarthria
Multiple Sclerosis
Progressive, autoimmune demyelinating disease of the brain and spinal cord
Can affect any and all sensory and motor functions
May show mixed dysarthria symptoms (flaccid, spastic, and/or ataxic)
- Flaccid first, or alone, is incredibly rare (~1.5% of cases)
Amyotrophic Lateral Sclerosis
Progressive disorder of voluntary muscles
Depending on course of progression, may show flaccid and/or spastic dysarthria symptoms
Traumatic Injury
Damage primarily to brainstem and cranial nerves
Additional damage to other areas of cerebrum and control circuits present differently
Treatments for Flaccid Dysarthria
Is the cause progressive?
Work on maintenance and compensation
Respiratory system treatments
- Postural adjustment and monitoring
- Working on maximum loudness and/or vowel duration
- Working on monitoring inhalation/exhalation rates and phrase lengths and adjusting them
Articulation treatments
- Strength training (e.g., oral-motor exercises) are frequently used, but their efficacy when used alone is limited at best
- Using a bite-block during therapy to force tongue movement and limit jaw compensation
- Make them talk, focusing on the appropriate voice/place/manner, overarticulation, rate modification
Voice treatments
- Adjust voice onset via effortful closure, easy onset, etc. as necessary
Compensation for Flaccid Dysarthria
Goal is counteracting weakness and strengthening muscles again
- BUT if the nerves aren’t firing, treatments will do nothing!
Prosthetics (e.g., palatal lift for hypernasality)
Amplifiers to compensate for reduced loudness
Surgical intervention
- Thyroplasty or injection for vocal fold paralysis
RESPIRATION
PHONATION
RESONANCE (refers to the way airflow for speech is shaped as it passes through the pharynx (throat), oral (mouth) and nasal (nose) cavities)
ARTICULATION
PROSODY
NON SPEECH
NEUROANATOMY
