Spastic Dysarthria Flashcards
Cause of SD
caused by bilateral damage to both the pyramidal and extrapyramidal neural pathways
Upper motor Neuron - pyramidal system
- corticospinal tract
- corticobulbar tract
Upper motor Neuron - extrapyramidal system
UMNs = motor fibers in CNS
- motor tract
- to get the signals to the lower neurons
Motor neuron - UMN damage
Cause spasticity
- hypertonicity
- hyperreflexia
- unilateral damage > UUMN dysarthria
- bilateral damage > spastic dysarthria
Motor neuron - LMN damage
Cause flaccidity
- hypotonicity
- hyperreflexia
- flaccid dysarthria
What is spasticity?
UMN damage = spasticity
- a type of hypertonicity
- unregulated reflexive contraction
- some UMN control our reflexes when we don’t want them
- UMNs can override reflexes
Neurological basis of SD - Damage UMNs
- motor neurons in CNS
- bilateral damage
- pyramidal and extrapyramidal tracts that serve speech muscles
Neurological basis of SD - pyramidal system
- originate in PMC (primary motor cortex)
- synapse with LMNs at brainstem
- direct activation pathway
- corticobulbar tract serves most speech muscles
- bilateral damage = weakness and slowness of speech muscles on both sides
Neurological basis of SD - extrapyramidal system
- fibers originate in cortex and brainstem
- make numerous connections
- eventually synapse with LMNs
- indirect activation pathway
- maintains posture, regulate reflexes, monitors muscle tone
- works in parallel with pyramidal system
Signs of UMN lesions - SD
bilateral damage to both pyramidal and extrapyramidal and extrapyramidal fibers that innervates speech muscles
combination of symptoms
- weakness
- slow movements
- spasticity
- hyperreflexia
- spastic paralysis
Etiologies - stroke
- most common cause of SD
- single stroke in brainstem
- or single stroke with or following one in the other hemisphere
- or pre-existing condition on other side
- no such thing as a spastic/UUMN mixed dysarthria
Etiologies - TBI
- cortical
- subcortical
- brainstem
- hemorrhages
- hematomas
- herniation - compressed tissues
Etiologies - brainstem tumors
compress UMNs or CN nuclei
Etiologies - cerebral anoxia
possible widespread damage to both sides
Etiologies - viral or bacterial infections
e.g. meningitis
- itis: information
Speech characteristics - articulation
imprecise consonants
- incomplete articulatory contacts
- incomplete clusters
vowel distortion
Speech characteristics - phonation
harsh voice quality
- fricative through partially open glottis
“strained-strangled”
low pitch
- spasticity of TA muscle
Speech characteristics - resonance
hypernasality
Speech characteristics - prosody
- monopitch
- monoloudness
- short phrases
- slow speech rate - reduced speed of articulators
Additional characteristics
Psudobulbar effect
- “emotionally labile” : very emotional, even with the smallest thing
- UMN damage
Drooling
Positive babinski sign
- bilateral in SD
- spastic on both feet
- sign of upper motor neuron
babinski sign
big toe juts out, the other toes faint out
Key evaluation tasks
Conversational speech and reading
AMRs
- rhythm can be regular or irregular
- speech is slow and regular
Vowel prolongation
- strength strangled voice
Treatment for phonatory deficits
easy onset
- visi-pitch: start out quiet and put more pressure latter
Yawn-sigh
- used to improve pitch, loudness, and quality in hyper funciton
- laryngeal elevation, tongue high and forward, VFs tight, pharynx constrcited
- yawn-sigh is designed to counteract this
– add voice after sigh (mid or low vowels)
– /h/ word
