Speech Motor Control

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22 Terms

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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.

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Language Planning

  • Left inferior frontal gyrus (Broca’s area);

  • Posterior superior temporal gyrus (Wernicke’s area)

  • Middle temporal gyrus

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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

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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

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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

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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

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dysarthria 

neuromuscular impairment; motor execution deficit; muscle strength imparied; consistent errors; groping movements rare; variable rate; monotone or harsh; not aware of errors

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UMN vs LMN damage

spasticity and weakness due to disrupted motor control; damage leads to flaccidity and muscle atrophy from direct denervation

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spastic vs flaccid

increased vs decreased muscle tone; shaking vs inability to contract

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Spastic Dysarthria

Bilateral UMN damage; Strained voice, slow rate, monopitch; Reduced speed, increased tone; Commonly corticobulbar tracts, motor cortex

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flaccid dysarthria

LMN damage, Weakness & limp muscle

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UMN vs LMN damage jaw

limited movement due to spasticity vs flaccidy & jaw deviation toward lesion side

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UMN vs LMN damage lips

weakness, but more visual than audible vs can’t produce /b,p,w,f,v/ vowels distorted

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UMN vsLMN damage tongue

Slow, stiff movements; bilateral lesions severely impair articulation vs Atrophy, fasciculations, reduced strength and range.

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unilateral UMN

mild dysarthria

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bilateral UMN

Severe spastic dysarthria; slow, effortful speech

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unilateral LMN

Localized weakness (e.g., facial droop)

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bilateral LMN

Profound flaccid dysarthria; multiple articulators affected

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basal ganglia

Basal ganglia damage disrupts motor control, speech fluency, and cognitive-emotional regulation. It can lead to hypokinetic or hyperkinetic dysarthria

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Hypokinetic dysarthria

Parkinson’s most common cause; Rigidity/reduced range of motion, basal ganglia damage: Substantia nigra pars compacta

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hyperkinetic dysarthria

Huntington’s; Involuntary movements; basal ganglia damage: Striatum (Putamen)

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Ataxic dysarthria

dyscoordination; cerebellar damage; eg cerebellar hemispheres and vermis; timing affected/speech slurred