SPHY205 Introduction to Motor Speech Disorders (Acquired)

Motor Speech & Its Place in Communication

• Motor speech = complex, learned motor activity involving:

  • Planning & programming the movement sequences.

  • Execution & control of actual muscular contractions.

• Embedded within the broader communication chain:

  • Concept → lexical/grammatical selection → phonological encoding → motor planning/programming → neuromuscular execution.

• Model of information flow:

  • LANGUAGE SYSTEMS (cognition/linguistics) ➜ MOTOR SPEECH SYSTEM (planning → programming → execution).

  • Damage anywhere in this cascade can impair the final spoken output.

Speech Sub-Systems & Their Communicative Roles

• Respiration – air supply; supports loudness & phrase length.

• Phonation – vocal‐fold vibration; generates sound/voice.

• Articulation – shaping speech sounds via tongue, lips, jaw, palate.

• Resonance – oro/nasal balance; governs nasality.

• Prosody – rhythm, rate, stress, intonation ⇒ contributes to naturalness & communicative intent.

• Clinical exercise:
  • Tongue-twister “She sells sea-shells by the sea-shore” vs.
  • Yelling at the footy
  ⇒ Different tasks tax respiration, articulation, prosody to different degrees.

Neuro-Anatomical Foundations of the Speech Motor System

Core Structures

• Cerebrum

  • Primary motor cortex (initiation/execution of voluntary movement).

  • Premotor & supplementary motor cortices (planning, sequencing).

  • Primary sensory cortex (somatosensory feedback).

• Basal ganglia – selects intended mvmt, suppresses competing mvmt; neurotransmitter-driven.

• Cerebellum – real-time error detection, timing, scaling, coordination; key to motor learning.

• Brainstem – houses cranial-nerve nuclei; conduit for UMN–LMN synapses.

• Spinal cord & nerves – postural/respiratory support.

Functional Divisions of the Motor System

1. Direct Activation Pathway (DAP) – pyramidal tract, part of Upper Motor Neuron (UMN) system.
   • \text{Primary motor cortex} \rightarrow \text{corticobulbar/corticospinal fibres} \rightarrow \text{CN & SN nuclei}.
   • Facilitates fast, skilled, consciously controlled movements (= turns motor activity \uparrow).

2. Indirect Activation Pathway (IAP) – extrapyramidal tract, also UMN.
   • Originates largely in brainstem; multiple interconnections.
   • Regulates posture, tone, reflexes (= turns motor activity \downarrow).

3. Control Circuits

   • Basal Ganglia Circuit: cortex ⇄ basal ganglia ⇄ thalamus; balances initiation vs. inhibition.
     • Damage → \text{hyperkinesia} (too much movement) or \text{hypokinesia} (too little).

   • Cerebellar Circuit: cortex ⇄ cerebellum ⇄ brainstem/spinal cord; supplies predictive/feed-forward adjustments.

4. Final Common Pathway (FCP) – Lower Motor Neuron (LMN) system.
   • Includes all \text{cranial nerves} & \text{spinal nerves} supplying speech musculature.
   • “Last link in the chain” (Duffy, 2020, p.29).

Cranial Nerves Critical for Speech

• V Trigeminal – face sensation & jaw movement.

• VII Facial – facial expression; taste (ant. 2\/3 tongue).

• IX Glossopharyngeal – pharyngeal elevation; taste (post. 1\/3).

• X Vagus – larynx & pharynx motor/sensory.

• (XI) Accessory – supports head/shoulder posture, influences resonance.

• XII Hypoglossal – intrinsic & extrinsic tongue muscles.

Sensorimotor Integration

• Speech production is non-linear & overlapping; constant afferent (sensory) feedback fine-tunes efferent (motor) commands.

• Effective speech depends on the synchronous operation of all above subdivisions.

Acquired Motor Speech Disorders (MSDs)

• Definition (Duffy 2020, p.3): “speech disorders resulting from neurological impairments affecting the planning, programming, control, and/or execution of speech.”

• Common neurological aetiologies:
  • Stroke
  • Degenerative e.g., Parkinson’s, Huntington’s, MND, Friedreich’s ataxia
  • Trauma
  • Demyelinating e.g., multiple sclerosis
  • Drug toxicity

Dysarthria vs. Apraxia of Speech (AOS)

Detailed Classification of Motor Speech Disorders

By Clinical Course

• Congenital vs. Acquired.

• Chronic V Stationary ; Improving ; Progressive V Degenerative; Exacerbating-remitting

By Lesion Type/Site

• Structural (e.g., glossectomy) vs. Neurological (e.g., hypoglossal lesion).

By Perceptual Characteristics (Darley, Aronson & Brown 1969)

• Foundation for many modern auditory-perceptual taxonomies.

Modern Neuro-Topological Scheme

• Flaccid Dysarthria – LMN; execution; \text{weakness}.

• Spastic Dysarthria – bilateral UMN; execution; spasticity; results in stiff and rigid speech patterns that can lead to imprecise articulation.

• Ataxic Dysarthria – cerebellum; control;

• Hypokinetic Dysarthria – basal‐ganglia control; control; rigidity; reduced ROM, scaling deficits.

• Hyperkinetic Dysarthria – basal-ganglia control; control; involuntary movements

• Unilateral UMN Dysarthria – unilateral UMN; execution/control; mixed mild weakness & incoordination.

• Mixed Dysarthria – multiple loci; execution and/or control; combined pathophysiology.

• Apraxia of Speech – dominant hemisphere (often left frontal/insula); planning/programming.

Hallmark Perceptual Features Clinicians Must Monitor

• Articulation: imprecise consonants, distorted vowels, irregular breakdowns, prolonged phonemes.

• Resonance: hypernasality, nasal emission.

• Phonation: strained-strangled, breathy, harsh/rough, reduced or excessive loudness variation.

• Prosody: monoloudness, monopitch, equal & excess stress, variable rate, prolonged intervals.

• Respiration: short phrases, rapid fatigue.

• Sequencing: escalating difficulty with longer words/utterances (esp. in AOS).

Illustrative Clinical Scenarios

• Rapid-fire tongue-twisters stress articulatory timing ⇒ may expose Ataxic features.

• Yelling in a stadium demands sustained respiration & laryngeal valving ⇒ challenges Flaccid/Spastic systems.

Integrative Summary & Clinical Significance

• Speech depends on a distributed neural architecture operating at conscious & subconscious tiers.

• Sensorimotor integration underpins intelligibility & naturalness; any breakdown can yield MSD.

• Differential diagnosis hinges on mapping perceptual signs to neuro-anatomical knowledge.

• Comorbidities (aphasia, dysphagia, cognitive-linguistic deficits) are common; holistic assessment essential.

• Understanding pathophysiology informs evidence-based management (e.g., LSVT for Hypokinetic, contrastive stress for AOS, posture/breathing drills for Flaccid).

Key References

• Duffy, J.R. ( 2020 ) Motor Speech Disorders: Substrates, Differential Diagnosis & Management (3^{rd} ed.).

• Darley, F.L., Aronson, A.E., & Brown, J.R. ( 1969 ). “Differential Diagnostic Patterns of Dysarthria”, JSHR, 12(2), 246–269.