Flaccid Dysarthria Flashcards
A Lesion in ______ can cause flaccid dysarthria
LMN system
UMN involves all of pathway above or below the level of the synapse?
above
LMN involves the pathway above or below the synapse to the muscle fiber?
below
In the UMN system, do fibers leave the brain stem?
No, fibers never leave the brain stem
*except for the cortico-spinal tract
T or F
Deficits are the similar when they occur in the LMN or UMN systems
False.
Deficits are very different if they occur in the LMN or UMN system
What results in because it all comes together in the LMN system.severe damage in the UMN system?
need 2 lesions that take out both bilateral tracts to have severe damage
Is there severe damage if there is 1 lesion in the UMN system?
No.
If just one lesion, something can get through to the LMN system
With the LMN system, it takes ____ lesion(s) to wipe out the function?
1
* because it all comes together in the LMN system
Where do lesions that result in flaccidity occur?
Anywhere along the motor unit
Do symptoms vary according to where the lesion/damage is?
Yes.
Symptoms vary according to where damage occurs
Primary unique deficit in flaccidity is..
Weakness to muscles.
Can happen to any muscle.
Weakness refers to…
…reduced strength/force of muscle contraction
Most things can be explained on basis of weakness
If the palate too weak to close, the patient will have…
hypernasality
UMN system damage results in what kind of dysarthria?
Spastic dysarthria.
Primary unique deficit is spasticity.
Can also have some weakness but weakness is not defining character.
What is the primary unique deficit of spastic dysarthria?
Spasticity
What is the only dysarthria with PNS involvement?
Flaccid dysarthria
2 other names for PNS
LMN and FCP – refer to same as PNS
When motor units are damaged…
…muscle looses its ability to contract
If all of the LMN input (nerve impulse) is lost to a muscle what occurs?
paralysis
It there is only partial loss of LMN input what occurs?
paresis
What is paresis?
There’s still some input to muscle, but contraction is weakened, therefore weaker muscle movement
Other defining characteristics of Flaccid Dysarthria (4):
- Hypotonia & weak reflexes
- Atrophy
- Fasiculations & fibrillations. Fasiculations don’t occur immediately after insult – takes a while to see them (1-3 weeks after nerve supply is gone). They’re quick, jerky movements in resting muscles. Difference between fasiculations & fibrillations - fasiculations are visible, fibrillations aren’t.
- Progressive muscle weakness – in all flaccid dyarthria fatigue is a factor. But in some disorders, there is a quick weakening with use. The muscle fatigues quickly when used. This occurs in neuromuscular junction dz, such as Myasthenia Gravis.
Where the damage occurs on the motor unit determines…
the type of characteristics
ATROPY & FASICULATIONS ARE ONLY SEEN IN LMN or UMN INVOLVEMENT?
LMN INVOLVEMENT
Hypotonia & weak reflexes:
Weak muscles leads to hypotonia (reduced muscle tone).
This affects speed, range/accuracy of muscle movements.
Reflexes may be diminished or completely gone.
With flaccidity in muscles, muscle doesn’t contract so you get flabby muscle
Atrophy:
Muscle starts to waste away, loses mass/bulk when nerve fibers are damaged
Fasiculations & Fibrillations:
Quick, jerky movements in resting muscles
Do fasiculations occur immediately after insult?
No.
It takes a while to see them (1-3 weeks after nerve supply is gone)
What is the difference between fasiculations & fibrillations?
Fasiculations are visible, Fibrillations aren’t
What are some etiologies of Flaccid Dysarthria (8):
- Neuromuscular Junction Dz ( e.g. Myasthenia Gravis)
- Vascular disorders (e.g. Wallenberg’s lateral medullary syndrome)
- Infectious processes (e.g. polio)
- Demyelinating Dz - such as Guillian Barre dz –
- Muscle diseases – such as Muscular Dystrophy
- Degenerative dz – such as motor neuron dz (e.g. ALS)
- Anatomic anomalies such as Arnold Chiari malformation
- Radiation treatment
Neuromuscular Junction Dz (e.g. Myasthenia Gravis):
Chronic dz characterized by rapid weakness of voluntary movement of muscles & improvement with rest
AcH receptors are destroyed in MG so receptors aren’t receptive to AcH, which triggers muscle contraction
When you let the muscle rest, it functions more normally.
Myasthenia Gravis occurs in men _____ and in women _____.
Men: after age 50
Women: between 20-40 years of age
Main characteristics of Myasthenia Gravis (3):
- drooping eyelids
- weak facial muscles
- flaccid dysarthria
What is the “Tensilon” test given for Myasthenia Gravis?
Injections of tensilon give after pt shows signs of fatigue when talking
Pt should show rapid improvement.
To have pt do stress test for this – count to 100, etc.
Vascular disorders:
Brain stem stroke that affects cranial nerve nuclei can cause flaccid dysarthria
Other vascular syndromes, such as Wallenberg’s lateral medullary syndrome, may result in flaccid dysarthria
Infectious processes-polio:
polio is viral dz in which LMN cell bodies may be affected
Demyelinating Dz - such as Guillian Barre dz:
unknown cause, loss of myelin occurs in some nerves.
Facial & oropharyngeal muscles are affected 1st, often results in flaccid dysarthria & dysphagia
Muscle diseases – such as Muscular Dystrophy:
Genetic, inherited, and degenerative.
Muscle fibers degenerate.
Flaccid dysarthria is frequent symptom.
Degenerative dz- motor neuron dz
groups of disorders – motor neurons degenerate
Degenerative dz- ALS:
most common type of motor neuron dz
Affects both UMN and LMN system
Results in mixed dysarthria with flaccid component
Anatomic anomalies – Arnold Chiari malformation:
Congenital (occurs at birth)
Results in distortion of brain stem which may result in impairment of cranial nerves.
Often don’t see symptoms till adulthood.
Flaccid dysarthria is one symptom.
Radiation treatment:
Used for CA tx
Can have side effects leading to neuropathy (any dz of the nerve) with resulting flaccid dysarthria
What is neuropathy?
any dz of the nerve
All symptoms of damage in Flaccid Dysarthria are due to lesions in the LMN or UMN system?
LMN system
Cranial Nerve V (Trigeminal Nerve):
Originates at pons
Provides sensory information about jaw, face, lip and tongue
Provides motor function to jaw
3 branches of Cranial Nerve V (Trigeminal):
- Sensory opthalmic branch
- Sensory maxillary branch
- Motor & sensory mandibular branch
The Sensory opthalmic branch of the Trigeminal Nerve (CN V) innervates…(1)
upper face
The Sensory maxillary branch of the Trigeminal Nerve (CN V) innervates…(1)
midface
The Motor & sensory mandibular branch of the Trgeminal Nerve (CN V) innervates…(3)
- jaw muscles
- tensor tympani
- tensor veli palatini (tenses & flattens velum)
T or F
If Cranial Nerve V (Trigeminal Nerve) is damaged, usually other cranial nerves are damaged
True.
Rarely is it damaged alone
Unilateral damage (LMN) to Cranial Nerve V (Trigeminal) symptoms:
Jaw deviates to side of weakness or may be easily pushed to one side.
May not feel much muscle contraction of masseter when pt bites down
Bilateral damage (LMN) to Cranial Nerve V (Trigeminal):
Jaw may hang open at rest
Pt may not be able to close jaw or may move it slowly or have reduced ROM
If examiner tries to open or close jaw & have pt resist this, pt may not be able to resist the movement
Pt complaints with LMN damage to Cranial Nerve V (Trigeminal):
Complaints related to jaw weakness, i.e. difficulty chewing, drooling, etc
Sensory complaints of decreased sensation from face, cheek, tongue, teeth, palate
–>Asses by having pt close eyes & touch face
How do you asses for effects on speech of Vth nerve (Trigeminal) damage:
Have pt read or converse – listen to speech
Do AMR’s (puh, etc.; tuh, etc.; kuh, etc.) – should be more imprecision/slowness for puh
If Myasthenia Gravis present, may be progressive weakness in jaw opening
Unilateral damage to Vth (Trigeminal) does/does not affect speech significantly?
Does not
Bilateral damage to Vth (Trigeminal) does/does not affect speech?
Does
Symptoms of bilateral damage to Vth (trigeminal) Nerve:
- Patient may try to hold jaw closed to compensate
- Speech rate may be slow.
- Sensory impairment may affect articulation due to reduced sensory information regarding movements of articulators.
- ->Pt with sensory problem may exaggerate artic movements to compensate
What does Cranial Nerve VII (Facial Nerve) do?
Only concerned with motor components for speech.
It innervates lip muscles to aid in producing bilabials and labiodentals
It helps to firm cheek muscles to allow build-up of intraoral air pressure.
Sensory portion carries info for taste from anterior 2/3 of tongue
Bell’s palsy:
Common condition affecting VIIth nerve
Results from unilateral VIIth damage
Affects upper and lower facial muscles – difficulty opening eyes
Most have full recovery
Usually due to viral infection
Symptoms of (LMN) unilateral lesion to Cranial Nerve VII (Facial Nerve) (7):
- At rest, affected side sags & is hypotonic
- Forehead may be unwrinkled
- Eyebrow drooped
- Eye open and unblinking
- Tip of nose & corner of mouth may be drawn toward affected side
- Drooling may occur
- If pt smiles, face will show more movement toward the good side
Symptoms of Bilateral lesions (LMN) to Cranial Nerve VII (Facial Nerve):
*more rare than unilateral
Symptoms include:
- Damage isn’t so striking because there is facial symmetry.
- At rest, mouth is lax, space between lips more than normal.
- Pt may not be able to retract lips or puff out cheeks.
- Drooling may occur.
- Pt may complain of not being able to move lips well in speech & that food spills out of mouth.
What is synkinesis?
An abnormal contraction of muscle next to the muscle that is normally moving
What can cause synkinesis?
VIIth nerve damage can result in abnormal movements of face – synkinesis
How do you asses for VIIth (Facial) nerve damage effects on speech (6):
- Use conversation, reading, AMRs & stress testing
- May see “flutter in cheek” - due to less resistance to intraoral pressure.
- May be poor bilabial closure with more imprecision on “puh” than “tuh”, etc.
- May be some slowness, but precision more affected than speed.
- Do stress testing for Myasthenia Gravis
- For both unilateral and bilateral, look for pt compensation
Assessing for unilateral damage to VII (Facial) Nerve effects on speech (3):
- Damage may be mild distortion of some sound, especially bilabials & labiodentals
- Visible symptoms may be more apparent than speech symptoms
- Vowels not usually affected
Assessing for bilateral damage to VII (Facial) Nerve effects on speech:
- Pt may not be able to make bilabials & labiodentals at all
- Vowels may be distorted if pt can’t round or spread lips
Pt compensations with unilateral damage to VII (Facial) Nerve:
- Pt may prop up sagging side or assist in movement
2. May have exaggerated jaw closure to try to make bilabial sounds
Pt compensations with bilateral damage to VII (Facial) Nerve:
- May substitute lingual alveolar sounds for bilabials i.e. t/p
Glossopharyngeal Nerve (IXth):
- Motor fibers originate in the reticular formation of medulla and pass through posterior fossa and into phayrnx to innervate the stylopharyngeus muscle (raises pharynx in speech & swallowing)
- Sensory fibers bring info from pharynx & posterior 1/3 of tongue. It is this component that makes us gag. Damage here may result in decreased gag reflex
Is the Glossopharyngeal Nerve (IX) usually damaged alone or with another nerve?
IXth nerve rarely damaged alone
Damage usually affects Vagus as well
How do you assess for Glossopharyngeal Nerve (CN IX) damage?
- By eliciting gag reflex
- Check symmetry of reflex.
- Reduced gag may implicate either sensory or motor part of nerve.
- Sensory part affected if pt reports decreased sensation in the area.
- Note – not always a reliable test of IXth nerve function as some pts experience normal gag reflex after IXth damage.
- IXth nerve damage may cause reduced pharyngeal elevation during swallowing due to poor innervation for stylopharyngeus.
- May also be pain in pt’s throat going down to back of lower jaw. Can be triggered by swallowing or sticking out tongue.
- Speech signs – damage to IXth cannot be assessed directly through speech tasks.
Vagus Nerve (CN X) (location):
- Exits at lower level of medulla along with IXth and XIth nerves.
- Has 3 branches
The 3 branches of the Vagus Nerve (CN X):
- Pharyngeal
- Superior laryngeal branch
- Recurrent laryngeal branch
Location of the Pharyngeal Branch of the Vagus Nerve (CN X):
-goes to pharynx & palate
Location of the Superior Laryngeal Branch of the Vagus Nerve (CN X):
– goes to larynx & pharynx
Location of the Recurrent Laryngeal Branch of the Vagus Nerve (CN X):
– goes to upper chest & loops around blood vessels, then travels back up to larynx
Pharyngeal branch of Vagus innervates (3 areas):
- Muscles of Pharynx (except stylopharyngeus which is innervated by IXth)
- Muscles of Soft Palate (including the levator palatini) (except tensor veli palatini which is innervated by Vth) - results in palatal constriction and elevation in speech & swallowing. (Hypernasality may result if damage occurs here.)
- Palatoglossus Muscle – contraction can either depress soft palate or pull sides of tongue up and back
Superior laryngeal branch of the Vagus Nerve innervates (internal & external branches):
- Internal part brings sensation from larynx & base of tongue.
- External part innervates inferior pharyngeal constrictor muscles & cricothyroid muscle. (Damage can result in pitch problems.)
Recurrent laryngeal branch of the Vagus Nerve innervates:
- all intrinsic laryngeal muscles except cricothyroid
- Sensory fibers bring sensory info from vocal folds & larynx
Lesion to the Vagus Nerve that are above separation of the 3 branches will affect:
All muscles supplied by the specific nerve below the level of lesion
i.e.
the pharyngeal & palatal muscles innervated by the pharyngeal branch
cricothyroid muscle innervated by superior laryngeal
branch
AND
all other intrinsic laryngeal muscles innervated by recurrent laryngeal branch
Lesions of the Vagus Nerve below the pharyngeal branch but still high enough to affect other 2 branches will….
Not affect pharyngeal & palatal muscles, but will cause paralysis or weakness to cricothyroid & other intrinsic laryngeal muscles
Lesions of superior laryngeal branch of the Vagus Nerve but not recurrent branch will affect:
Cricothyroid muscles but not other intrinsic laryngeal muscles
Lesions of the Vagus Nerve affecting only recurrent laryngeal nerve will cause:
Weakness or paralysis of the other intrinsic laryngeal muscles (except cricothyroid) on the side of the lesion
Unilateral pharyngeal lesions above the origin of the 3 branches of the Xth nerve will cause (3 things):
- Soft palate hangs lower on side of lesion
- Soft palate pulls toward nonparalyzed side in phonation
- Gag reflex may be diminished.
Bilateral pharyngeal lesions above the origin of the 3 branches of the Xth nerve will cause (3 things):
- Soft palate hangs low in pharynx at rest & moves little during phonation.
- Gag reflex may be diminished or absent
- May be nasal regurgitation in swallowing
Speech signs of damage to the Xth Nerve (Vagus):
Can affect:
- phonation
- resonance
- articulation
- prosody
- But phonation & resonance are the most affected*
-When pharyngeal branch is affected unilaterally there is only mild or no hypernasality, may be nasal emission during pressure consonants
When pharyngeal branch of the Vagus Nerve (CN X) is affected bilaterally (4):
- Can be severe hypernasality & marked nasal emission
- Imprecise pressure consonants due to inability to build up intraoral pressure
- May be reduced intensity
- May be facial grimacing as they try to hold back air from nares
CN X (Vagus): How do you tell if articulation problem is due to general weakness or to inability to impound oral pressure?
Pinch off nostrils and have pt speak. This allows the pressure to be maintained & can listen for weakness in articulators
CN X (Vagus): Unilateral lesions below pharyngeal branchbut above superior laryngeal & recurrent laryngeal nerve can cause (6):
- Breathiness
- Aphonia
- Reduced loudness
- Diplophonia
- Reduced pitch
- Pitch breaks
CN X (Vagus): Lesions of superior laryngeal nerve cause (unilateral and bilateral damage):
- only slight, subtle changes in voice
- If unilateral: may cause mild breathiness or hoarseness & some problems with pitch changing
- Bilateral lesions can cause marked ability to change pitch
CN X (Vagus): Unilateral recurrent laryngeal nerve lesions only causes:
breathy-hoarse voice & decreased loudness
CN X (Vagus): Bilateral recurrent laryngeal nerve lesions cause (2):
- Inhalatory stridor but voice may be OK because folds are adducted closed enough to midline
- Airway may be compromised – this is serious
Accessory Nerve (CN XI) (location and function):
- Exits along with IXth and Xth nerves.
- Is sensory and motor.
- Aids in innervation to uvula, levator palatini (elevates soft palate) and intrinsic laryngeal muscles.
- Important in head & neck movement.
- Damage can be caused by neck surgery as well as those things mentioned affecting Xth nerve.
- Effect on speech is negligible
Nonspeech signs of Accessory Nerve (CN XI) damage:
Reduced shoulder elevation on side of lesion, weakened head turn on side opposite of lesion
Bilateral lesions to Accessory Nerve (CN XI) can cause:
Head drooping with some mild effects on phonation & respiration
Hypoglossal Nerve (CN XII) (Location and Function):
- Originates in medulla.
- Innervates all intrinsic & extrinsic tongue muscles except palatoglossus (innervated by Xth).
- Is essential for tongue movement, chewing & swallowing.
- Often seen with damage to IX, X, XI
- Can be damaged by anything that causes damage to these other nerves, as well as neck surgery or trauma
Nonspeech signs of unilateral (LMN) damage to the Hypoglossal Nerve (CN XII) (2):
- Tongue may deviate to weak side & to side of lesion upon tongue protrusion.
- Will have problems curling tongue tip on weak side and with pushing tongue into cheek with resistance (on weak side)
Nonspeech signs of bilateral (LMN) damage to the Hypoglossal Nerve (CN XII) (5):
- Tongue may atrophy & have bilateral fasiculations.
- Tongue may not be able to protrude at all or with limited ROM but will be symmetrical in its excursion.
- Food may be squirreled in cheek & pt may not be able to move food around well in mouth.
- Pt may complain of tongue feeling heavy
- May be drooling due to tongue weakness.
Speech signs of damage to the Hypoglossal Nerve (CN XII) (3):
- Main characteristic is imprecise articulation & first problems may be with lingual phonemes, i.e. t, d, s, sh, ch, r, l.
- May be resonance problems due to tongue falling back into pharynx. May sound like hypo or hypernasality but it isn’t. It is due to tongue position.
- May be exaggerated jaw movement to compensate for tongue weakness.
How do you assess Hypoglossal Nerve (CN XII) damage?
By looking at lingual consonants in connected speech & AMRs
In AMRs “puh” should be OK but the others won’t. “Kuh” may be more affected than “tuh” because it is harder to get the back of the tongue up. In normal speakers, rate of producing “kuh” is slower than “tuh”.
What is Bulbar Palsy?
- A condition that occurs when there are several cranial nerves damaged
- Can be caused by any of the etiologies we have discussed as well as disorders that typically affect multiple nerves, such as ALS, Myasthenia Gravis and brain stem tumors
Multiple Cranial Nerve Lesions:
- Can cause Bulbar Palsy
- Nonspeech signs are similar to ones mentioned for single nerve damage but with a more severe effect
- Damage to more than one cranial nerve frequently occurs because they are close together
Distinguishing features (related to speech & respiration) of Flaccid Dysarthria (Duffy) (8):
- Hypernasality
- Nasal Emission
- Continuous breathiness
- Audible inspiration (stridor)
- Isolated articulatory imprecision
- Atrophy
- Fasiculations
- Diplphonia
