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Cranial nerve V
Trigeminal- Facial sensation
Innervation- Motor and Sensory
Cranial Nerve VII
Facial- facial expression, taste (anterior 2/3 tongue), tears/saliva
Innervation- Motor and Sensory
Cranial Nerve IX
Glossopharyngeal- Taste (posterior 1/3 tongue), swallowing, saliva production
Innervation- Motor and Sensory
Cranial Nerve X
Vagus- parasympathetic control (hear, lungs, gut), voice, swallowing
Innervation- Motor and Sensory
Cranial Nerve XI
Accessory- shoulder shrug, head turning (trapezius, SCM)
Innervation- Motor
Cranial Nerve XII
Hypoglossal- tongue movement
Innervation- Motor
Which type of motor neurons are affected in flaccid dysarthria?
lower motor neurons
How can CN 5 be affected in flaccid dysarthria?
trigeminal neuralgia
unilateral lesion of mandibular branch
bilateral lesion
trigeminal neuralgia
pain in one or more sensory divisions of CN 5
can be triggered by movement- patients may avoid lip, face, or jaw movement to avoid pain
unilateral lesion of mandibular branch of CN 5
jaw deviates to the weak side when opened
limited effect on speech- stronger side is good at compensating for damage
may have decreased masseter/temporalis contraction- weaker jaw movements when chewing
bilateral lesion of CN 5
unable to close or lateralize jaw
decreased mass ester/temporalis contraction
loss of sensation to face and tongue
inability to elevate jaw can cause devastating impact on articulation
unilateral lesion of CN 7 in flaccid dysarthria
facial droop ipsilaterally; eye droop
asymmetrical facial expression
decreased/ absent lip movement- may not affect speech much but might cause distortion
bilateral lesion of CN 7 in flaccid dysarthria
facial droop on both sides
decreased/absent lip movement
symmetrical facial expression
may be harder to see the problem visually
speech effects- distortion of labial sounds, cheek flutter during speech
unusual movements to watch for- synkinesis, hemifacial spasm, facial myokymia
synkinesis
movements of muscles next to intended muscles
facial myokymia
similar to fasciculations but more prolonged
how is CN 9 affected in flaccid dysarthria?
possible reduction in gag relex
lesion affects of CN 10 affected in flaccid dysarthria?
pharyngeal branch lesion- hypernasality/ nasal emission
changes to phonation
SLN only affected- mild hoarseness, decrased pitch range (cricothyroid affected)
RLN only affected- breathy/hoarse voice, inhalitory stridor if lesion is bilateral (muscles for adduction/abduction)
pharyngeal banch of the vagus nerve
motor innervation- most of pharynx and soft palate (not tensor palatini)
pharyngeal constriction/ VP closure
superior laryngeal nerve branch (SLN)
external laryngeal nerve- motor innervation to cricothyroid and inferior pharyngeal constrictor
internal laryngeal nerve- sensory innervation to base of tongue and larynx
Recurrent laryngeal nerve branch (RLN)
motor and sensory innervation to all intrinsic laryngeal muscles except cricothyroid which is vulnerable during thyroid surgery
how is CN 11 affected in flaccid dysarthria?
damage to the spinal part results in problems with head control and indirectly affects speech
unilateral lesion of CN 12 in flaccid dysarthria
decrease in tongue bulk on side of lesion
weakness
tongue deviate to weak side
speech effect- may have articulatory imprecision
bilateral lesion of CN 12 in flaccid dysarthria
tongue atrophy
faciculations
symmetric but limited protrusion
significant articulation problems for speech
which cranial nerve is most often damaged in flaccid dysarthria?
CN 10- Vagus
What is the order of cranial nerves that are most to least damaged in flaccid dysarthria
CN 10
CN 7
CN 12
CN 5
which cranial nerve is least often damaged in flaccid dysarthria
CN 5
distinctive speech characteristics in flaccid dysarthria
hyper nasality- leads to distorted labial or lingual phonemes and distorted vowels
breathiness
nasal emission
audible insiration
short phrases
less disctinctive speech characteristics of flaccid dysarthrias that are also seen in other types of dysarthria
imprecise consonants
monopitch
harsh or hoarse voice
monoloudness
a study by Leveque et al. (2022) found that participants with spinal and bulbar muscular atrophy (SBMA) had
lower motor neuron problems
spastic dysarthria results from damage to
upper motor neurons
what is the hallmark characteristic of spastic dysarthria
spasticity- excess muscle tone, decreased muscle strength
spastic dysarthria may affect what speech subsystem
any
characteristics of direct activation pathway damage in spastic dysarthria
loss of impairment in fine, discrete movements
weakness with increased muscle tone (spasticity)
pathological reflexes re-emerge
Babinski sign
oral reflexes
characteristics of indirect activation pathway damage in spastic dysarthria
increased muscle tone/ spasticity- legs resist bending, arms resist extension
hyperactive reflexes- hyperactive stretch reflex can lead to clonus, looks like rhythmic tremor due to a muscle kept under tension)
characteristics of direct AND indirect pathway damage in spastic dysarthria
spasticity with weakness- more distal than proximal
decreased ROM and slowness of movement
abnormal reflexes
bilateral UMN symptoms in limbs in spastic dysarthria shows
bilateral involvement
clinical findings of spastic dysarthria- pseudobulbar palsy results from
UMN bilateral lesions of corticobulbar fibers
looks like LMN cranial nerve problems
nonspeech oral mech findings in spastic dysarthria
drooling
mild weakness
symmetry observed but face is held in a somewhat fixed, subtle smile or pout
clinical findings of spastic dysarthria- emotional lability
may seem to be on the verge of tears when talking
may fluctuate between crying and laughing
inner emotional state may not match emotional expression
distinctive speech features of spastic dysarthia
low pitch
slow rate
strained strangled voice quality
other speech characteristics of spastic dysarthria
short phrases
monopitch
monoloudness
articulation problems- imprecise consonants, distorted vowels
hypernasality
excess and equal stress
increased duration of phoneme to phoneme transitions
reduced speech and range of tongue and jaw movements
reduced rate and slope of second formant transitions
smaller vowel space, and centralization of vowel formants
unilateral upper motor neuron disease
primarily articulation problems secondary to weakness, spasticity, and/or incorrdination
unilateal direct and indirect activation pathway damage to unilateral upper motor neuron disease
contralateral innervation- most of the body
bilateral innervation (except hypoglossal/facial)- most cranial nerves
clinical characteristics of unilateral upper motor neuron disease
contralateral hemiplegia sometimes with sensory deficits
weakness and spasticity, reflexes exaggerated/ abnormal
often contralateral lower face weakness
patient perceptions of speech characteristics in unilateral upper motor neuron disease
aware of their problems
significant improvement in a first two days after stroke
slow, slurred speech
drooling, chewing, and swallowing problems
clinical symptoms of unilateral upper motor neuron disease
loss of voluntary control
initial muscle paralysis flaccid with emergence of spasticity within several weeks
contralateral hyperactive reflexes
altered reflexes- Babinski sign emergence and loss of abdominal and cremasteric reflexes
no atrophy in paralyzed muscles
clinical findings of unilateral upper motor neuron disease
language and/or cognitive problems likely
imprecise consonants; slow, imprecise AMRs
irregular articulatory breakdowns- unclear reason
phonatory problems depending on where the damage is- CN 10= phonatory prob