Motor Speech Disorders - Vocabulary Flashcards (Exam Notes)

Vocabulary-style flashcards covering key terms and concepts from the MSD lecture notes.

Motor Speech Evaluation

A comprehensive exam including history; oral mechanism at rest or during nonspeech; perceptual assessment of speech characteristics; intelligibility assessment; and estimates of functional communication and psychosocial impact of MSD.

Dysarthria

Group of neurological speech disorders produced by damage to the CNS or PNS.

Apraxia (AOS)

Neurological speech disorder that reflects an impaired capacity to plan or program sensorimotor commands necessary for directing movements.

Purpose of Motor Speech Examination

Describe and characterize the features of speech and structure/ functions.

Spastic Dysarthria — Clinical Characteristics

Spasticity (hypertonia) and spastic weakness or paralysis.

Spastic Dysarthria — Etiologies

Vascular disorders; trauma; toxins; demyelinating; degenerative disease (e.g., PLS, ALS).

Spastic Dysarthria — Lesion Site

Bilateral damage to Upper Motor Neuron pathways (pyramidal and extrapyramidal tracts).

Spastic Dysarthria — Slow Articulatory Movements

A characteristic feature: slow articulatory movements.

Ataxic Dysarthria — Clinical Characteristics

Poor timing, control, and coordination.

Ataxic Dysarthria — Etiologies

Any process that damages the cerebellum or cerebellar control circuit.

Ataxic Dysarthria — Lesion Site

Damage to the cerebellum or neural tracts that connect the cerebellum to the rest of the CNS.

Ataxic Dysarthria — Speech Characteristics

Drunken speech; poor coordination of movements.

Hyperkinetic Dysarthria — Clinical Characteristics

Extra involuntary movements.

Hyperkinetic Dysarthria — Etiologies

Any process that damages the circuitry associated with hyperkinesias; degenerative processes included.

Hyperkinetic Dysarthria — Lesion Site

Damage to Basal Ganglia Control Circuits and other portions of CNS (basal ganglia, thalamus, cerebral cortex).

Hyperkinetic Dysarthria — Speech Characteristics

Too much movement.

Hypokinetic Dysarthria — Clinical Characteristics

Problems with rigidity, reduced force, reduced range of movement, and slow/fast repetitive movements.

Hypokinetic Dysarthria — Etiologies

Any process that interferes with basal ganglia control circuit; degenerative diseases.

Hypokinetic Dysarthria — Lesion Site

Damage to basal ganglia control circuits and their structures (striatum; lentiform nucleus; substantia nigra and subthalamic nuclei).

Hypokinetic Dysarthria — Speech Characteristics

Too little movement.

UUMN Dysarthria — Clinical Characteristics

Loss/impairment of fine, skilled movements; hyperreflexia; unilateral lower facial weakness; increased muscle tone; spasticity.

UUMN Dysarthria — Etiologies

Vascular; tumor; trauma; degenerative disease; multiple possible causes; undetermined neurological diagnosis.

UUMN Dysarthria — Lesion Site

Unilateral Upper Motor Neurons; damage to either right or left UMNs but not both.

UUMN Dysarthria — Speech Characteristics

Slow movements on one side.

Mixed Dysarthria — Clinical Characteristics

Intelligibility; occur more frequently than single dysarthria types.

Mixed Dysarthria — Etiologies

Degenerative; vascular; trauma; demyelinating; tumor; multiple possible causes.

Mixed Dysarthria — Lesion Site

Progressive degeneration of upper and lower neuron system.

Mixed Dysarthria — Speech Characteristics

Any combination of dysarthrias.

Apraxia — Clinical Characteristics

Absence of auditory processing deficits; awareness of errors; self-repairs; frustration; visible/auditory groping of tongue, lips, and mandible.

Apraxia — Speech Characteristics

Distortions; inconsistent errors.

Apraxia — Etiologies

Stroke; neurodegenerative conditions; inflammatory and toxic-metabolic processes; tumors and trauma.

Apraxia — Lesion Site

Damage to motor speech programmer; unilateral, left hemisphere lesion.

Apraxia — Treatment (three aims)

1) Reestablish plans/programs; 2) Improve ability to select/activate them; 3) Set parameters for speech movements in context.

Communication-Oriented Approaches

Efforts to improve communication even if speech does not change; relevant to Dysarthria and AOS.

Speaker-Oriented Approaches

Aim to improve intelligibility, efficiency, and naturalness; applicable to AOS.

Compensatory Strategies

Reduce impact of dysarthria on speech/communication without changing underlying neuromotor deficits.

Restorative Strategies

Reduce severity of dysarthria by restoring lost motor abilities.

CN V — Trigeminal

Sensory and motor; elevation of mandible.

CN VII — Facial

Sensory and motor; controls muscles of mastication, including lips.

CN VIII — Auditory

Sensory: sense of hearing.

CN IX — Glossopharyngeal

Sensory and motor; contributes to pharyngeal movement.

CN X — Vagus

Sensory and motor; movements of pharynx and larynx; sensory function of pharynx, larynx, trachea, bronchi, and lungs.

CN XI — Spinal Accessory

Accessory and motor; controls movements of neck muscles; positioning of the larynx.

CN XII — Hypoglossal

Motor; controls tongue movements.

Spinal Nerves

Nerves extend from the CNS; cranial nerves subserve the head and neck; innervate the rest of the body.

Neurogenic Mutism

Lack of speech due to underlying brain damage.

Neurogenic Mutism — Etiologies

Surgery; dementia; TBI; seizures; nervous system diseases; medications.

Psychogenic Disorders

Caused by traumatic events.

Hyperfunctional Disorders

Too much function (overuse).

Factitious Disorders

Lying about disorder or symptoms for gain.

Differentiating MSDs vs Hyperfunctional Disorders

Use medical history (psychosocial history): e.g., when did you notice the issue and what were you doing at the time?

Aphasia + Apraxia with comprehension/expression limitation

If someone has aphasia and apraxia and is unable to comprehend and express, start treating comprehension and expression for quality of life; patient cannot express what they do not understand.

Upper Motor Neuron

Efferent: exiting brain; Motor.

Sensory

Afferent: entering the brain.

Conversion Disorders

Caused by a traumatic event; anxiety; body exhibits symptoms without a medical cause (e.g., stuttering during a speech task).

Locked-in Syndrome

Understanding but no way of expressing; eye blinking but no other facial expression.

Significant Speech Disorder

Start treating language or speech; speech becomes more functional.

Instrumental Examination

Not required; the same information can be obtained by other means.

Confirmatory Signs

Defining clue.

Salient Features

Abnormal characteristics.

Articulatory-Kinematic Approaches

Aim to improve spatial and temporal aspects of movement to improve articulatory accuracy.

Rate/Rhythm Approaches

Rate reduction; introduce timing or rhythm (metronome, pacing, finger tapping, oral reading).

Augmentative and Alternative Communication (AAC)

Symbols, aids, strategies, and techniques used as a supplement or alternative to oral language.

Intersystemic Facilitation/Reorganization

Gestures, rhythmic vibrotactile stimulation, singing.