Motor Speech Disorders

Speech Disorders Overview

Flaccid Dysarthria

  • Characteristics:

    • Slow, labored articulation

    • Distorted lingual consonants

    • Marked hypernasality due to velopharyngeal weakness

    • Hoarse or breathy voice resulting from phonatory weakness

  • Severity Varies: Severity of symptoms depends on the cranial or spinal nerves involved.

  • Definition:

    • Flaccid Dysarthria arises from damage to the lower motor neurons (LMN) of cranial or spinal nerves, leading to:

    • Paralysis

    • Weakness

    • Hypotonia

    • Atrophy

    • Hypoactive reflexes

  • Core Speech Characteristics: These characteristics relate to underlying causes in:

    • Respiration

    • Phonation

    • Articulation

    • Prosody

    • Resonance

  • Common Causes: Any condition disrupting neural impulses along LMNs which control speech subsystems, such as:

    • Brainstem Cerebrovascular Accidents (CVA)

    • Tumors

    • Infections

    • Physical or surgical trauma

Causes and Conditions for Flaccid Dysarthria

  • Disruption of Motor Impulses: Results in muscle weakness, decreased tone, or paralysis leading to impaired speech systems.

  • Physical Trauma:

    • Most common cause of flaccid dysarthria, which can occur from:

    • Direct trauma (e.g. motor vehicle accidents, falls, sports injuries, closed head injuries)

    • Surgical trauma (e.g. carotid plaque removal, cardiac surgeries, head/neck tumor removal, dental/oral surgery)

  • Brainstem CVA:

    • Bulbar Palsy from ischemic or hemorrhagic strokes affecting cranial nerve nuclei in the brainstem leading to LMN cell body damage.

    • Proximity of cranial nerves means one stroke can affect multiple cranial nerves (CNs).

  • Myasthenia Gravis:

    • Autoimmune disorder affecting the neuromuscular junction leading to acetylcholine receptor blockage.

    • Symptoms include reduced loudness and breathy voice, with features worsening with repetition.

    • Diagnostic Clue: Fatigue testing (counting from 1 to 100 or long reading).

  • Guillian-Barre Syndrome:

    • An inflammatory demyelinating disorder, often post-vaccination that affects motor neurons more than sensory neurons.

    • Speech features include flaccid weakness and loudness, short phrases.

    • Approximately 5% morbidity in acute stages, but full recovery can take weeks or months.

  • Poliomyelitis:

    • Rare due to vaccinations, it is a viral infection that destroys LMN cell bodies affecting cervical and thoracic spinal nerves, resulting in respiratory weakness.

    • Speech characteristics: labored breathing during speech, short phrases, using residual air, decreased vocal loudness; can impact CNs in 10-15% of cases.

  • Other Causes:

    • Tumors, muscular dystrophy, progressive bulbar palsy

  • Diagnosis:

    • Based on a cluster of characteristics affecting speech subsystems:

    • Resonance: Damage to the pharyngeal branch of the vagus (X) nerve causing velum weakness, decreased intraoral pressure, leading to air loss through the nasal cavity, hypernasality, nasal emissions, weak pressure consonants, and short phrases.

    • Articulation: Damage to the facial (VII) and hypoglossal (XII) nerves, leading to reduced lip and tongue control; trigeminal (V) damage may cause jaw elevation weakness.

    • Phonation: Damage to the laryngeal branch of the vagus (X) nerve resulting in phonatory incompetence, marked by breathy voice or inhalatory stridor.

  • Respiration Issues: Damage to cervical or thoracic spinal nerves results in insufficient inhalation, poor exhalation, and reduced subglottic pressure causing loudness issues and short phrases.

  • Prosody: Poor pitch and loudness due to weak laryngeal and articulatory control resulting in monopitch, monoloudness, and lack of stress variation.

Treatment Approaches

  • Treatment Targets: Dependent on the damaged cranial nerve; need to consider comorbidities.

  • Exercises: Non-speech oral strengthening exercises are ineffective; instead, focus on speech tasks that require fine coordination, timing, and agility.

  • Trigeminal (V) Nerve Damage:

    • Unilateral damage has minimal effect on speech.

    • Bilateral damage causes severe jaw weakness with poor articulator contact, leading to shorter phrases and slower rate; treatment may include jaw sling/splinting or kinesiotaping for stabilization.

Key Takeaways:

  • Speech-focused Goals: Speech-focused, functional goals are prioritised over nonspeech drills.

  • Treatment for Resonance Deficits: Velopharyngeal support (CPAP, palatal lift) is highly effective.

  • Collaboration: ENT collaboration is critical for addressing vocal fold weakness.

  • Support: Respiratory support and articulatory precision exercises improve overall speech intelligibility.

Additional Points on Flaccid Dysarthria

  • agus (X) Nerve Damage:

    • Affects glossopharyngeal (IX) and accessory (XI) nerves due to proximity; resonance treatments include surgical pharyngeal flap or palatal augmentation, and prosthetic palatal lift to improve speech.

    • Phonation Treatments: Effortful closure and breath control techniques are recommended, including sustained breath holding and head turns to the weak side.

  • Prosody Treatments: Include studying pauses and employing natural syntax along with pitch range exercises and contrastive stress drills.

Spastic Dysarthria

  • Definition: Caused by bilateral damage to upper motor neuron (UMN) tracts resulting in spastic paralysis or paresis of speech muscles, leading to stiff articulators with restricted range of motion (ROM).

  • Hyperreflexia: Exaggerated reflexes as part of spasticity; common in bilateral damage to pyramidal and extrapyramidal tracts.

  • Characteristics of Spastic Dysarthria: Damage from both major UMN pathways leads to characteristics such as:

    • Weak, slow, and imprecise movements of the tongue, lips, and velum.

    • Increased tone (spasticity) and abnormal reflexes such as exaggerated gag, jaw jerk, and bruxism.

Etiology of Spastic Dysarthria

  • Causes include:

    1. Stroke/CVA: Common cause where multiple CVAs may affect both left and right tracts or a unilateral CVA may have pre-existing damage leading to bilateral impacts.

    2. Amyotrophic Lateral Sclerosis (ALS): Progressive neurodegenerative disease impacting both UMNs and LMNs. Average life expectancy is roughly 22 months post onset.

    3. Traumatic Brain Injury (TBI): Common due to widespread damage from coup/countercoup injuries, axonal shearing that affects both tracts leading to possible mixed spastic-flaccid dysarthria.

    4. Multiple Sclerosis (MS): Autoimmune demyelinating condition disrupting UMN transmissions leading to spasticity and possibly resulting in other dysarthrias depending on CNS area impacted.

Common Speech Production Errors in Spastic Dysarthria

  • According to Darley et al. (1969), the following are the fourteen most common errors:

    • Imprecise consonants

    • Monopitch

    • Reduced stress

    • Harsh vocal quality

    • Monoloudness

    • Low pitch

    • Slow rate

    • Hypernasality

    • Strained-strangled voice

    • Short phrases

    • Distorted vowels

    • Pitch breaks

    • Continuous breathy voice

    • Excess and equal stress

  • Drill Examples:

    • Intelligibility drills

    • Phonemic placement training

    • Exaggeration of consonants

    • Minimal contrast drills

Key Characteristics Affected by Spastic Dysarthria

  • Areas Most Affect:

    • Least Affected: Respiration

    • Most Affected: Articulation, phonation, resonance, and prosody.

  • Articulation:

    • Imprecise Consonants: Most frequent error; leads to:

    • Short vocal onset for voiceless sounds

    • Incomplete articulatory contact

    • Incomplete clusters/blends

    • Vowel distortions reflecting abnormal tone in articulators.

    • Treatment:

    • Stretching or Beckman oral-motor exercises for tone regulation and traditional articulation drills.

  • Prosody:

    • Monopitch: Results from tense muscles unable to vary pitch.

    • Monoloudness: Limited loudness control leading to short phrases due to tight larynx and frequent inhalations.

    • Slow Rate: Often due to weak right articulators, requiring effortful speech; treatment includes pitch-range exercises, contrastive stress drills, and chunking utterances.

Additional Symptoms and Distinguishing Characteristics

  • Pseudobulbar Affect: Uncontrolled laughing or crying stemming from UMN damage to emotional control centers; may not reflect true emotions.

  • Drooling: Resulting from poor oral control of saliva due to fewer swallow triggers.

  • Phonation Issues:

    • Harsh or strained voice from air leaks through partially open glottis, low pitch due to increased laryngeal muscle tone; treatment includes relaxation techniques and easy phonation onset exercises.

  • Respiration: Not primarily affected, but can exhibit:

    • Smaller vital capacity and uncoordinated breathing leading to phonation-related problems.

Key Distinctions

  • Bulbar Dysarthria vs. Pseudobulbar Palsy:

    • Flaccid dysarthria is associated with damage to lower motor neurons (LMNs), while spastic dysarthria involves damage to upper motor neurons (UMNs).

  • Spastic Dysarthria Treatment Focus: Emphasizes reducing muscle tension and improving control rather