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Conceptualization
Prefrontal cortex (especially dorsolateral prefrontal cortex): involved in executive function and intention formation. Default mode network (medial prefrontal cortex, posterior cingulate): supports internal thought and autobiographical memory.
Language Planning
Left inferior frontal gyrus (Broca’s area);
Posterior superior temporal gyrus (Wernicke’s area)
Middle temporal gyrus
motor planning
Supplementary motor area (SMA): initiates and sequences speech motor plans.
Premotor cortex: organizes articulatory movements.
Inferior frontal gyrus: interfaces between linguistic and motor planning
Neuromotor Action
Primary motor cortex (M1): controls muscles of the lips, tongue, jaw, and larynx.
Basal ganglia: regulates initiation and smoothness of movement.
Cerebellum: fine-tunes timing and coordination.
Brainstem nuclei (e.g., nucleus ambiguus): innervate cranial nerves for articulation
Sensory Feedback
Auditory cortex (superior temporal gyrus): processes self-generated speech sounds.
Somatosensory cortex: receives tactile and proprioceptive feedback from articulators.
Cerebellum: compares expected vs. actual output for error correction
Apraxia of Speech (AoS)
(Broca’s area), supplementary motor area, or insula; motor planning deficit; muscle strength normal; inconsistent errors; groping movements common; slow; stress equal; aware of errors
dysarthria
neuromuscular impairment; motor execution deficit; muscle strength imparied; consistent errors; groping movements rare; variable rate; monotone or harsh; not aware of errors
UMN vs LMN damage
spasticity and weakness due to disrupted motor control; damage leads to flaccidity and muscle atrophy from direct denervation
spastic vs flaccid
increased vs decreased muscle tone; shaking vs inability to contract
Spastic Dysarthria
Bilateral UMN damage; Strained voice, slow rate, monopitch; Reduced speed, increased tone; Commonly corticobulbar tracts, motor cortex
flaccid dysarthria
LMN damage, Weakness & limp muscle
UMN vs LMN damage jaw
limited movement due to spasticity vs flaccidy & jaw deviation toward lesion side
UMN vs LMN damage lips
weakness, but more visual than audible vs can’t produce /b,p,w,f,v/ vowels distorted
UMN vsLMN damage tongue
Slow, stiff movements; bilateral lesions severely impair articulation vs Atrophy, fasciculations, reduced strength and range.
unilateral UMN
mild dysarthria
bilateral UMN
Severe spastic dysarthria; slow, effortful speech
unilateral LMN
Localized weakness (e.g., facial droop)
bilateral LMN
Profound flaccid dysarthria; multiple articulators affected
basal ganglia
Basal ganglia damage disrupts motor control, speech fluency, and cognitive-emotional regulation. It can lead to hypokinetic or hyperkinetic dysarthria
Hypokinetic dysarthria
Parkinson’s most common cause; Rigidity/reduced range of motion, basal ganglia damage: Substantia nigra pars compacta
hyperkinetic dysarthria
Huntington’s; Involuntary movements; basal ganglia damage: Striatum (Putamen)
Ataxic dysarthria
dyscoordination; cerebellar damage; eg cerebellar hemispheres and vermis; timing affected/speech slurred