How does flaccid dysarthria occur?
- produced by a LMN lesion & causes damage to cranial & spinal nerves
Etiologies of flaccid dysarthria:
- brainstem stroke
- guillian barre syndrome: demylenization of spinal & cranial nerves
- myasthenia gravis: autoimmune disease that destroys Ach receptors on muscles
- muscular dystrophy: degeneration of m fibers & connective tissue
Flaccid Dysarthria
◦Best distinguishing features for flaccid dys.:◦Hypernasality, nasal emission, continuous breathiness, stridor◦May also hear:◦Hoarseness, harshness, diplophonia, monopitch, monoloudness, short phrases, imprecise articulation◦Everything we hear can be traced to weakness
Spastic dysarthria
Oral Motor Exam:
- pathological oral reflexes (suck, snout, jaw jerk reflex)
- drooling
- pseudo bulbar affect
- slow, regular AMRs
Articulation:
- imprecise articulation w/ distorted vowels
Resonance:
- hyper nasality
Prosody:
- short phrases
- monopitch & monoloudness
- excess & equal stress
- slow rate
phonation:
- low pitch
- strained strangled voice
- pitch breaks
How does spastic dysarthria occur?
- bilateral UMN damage
etiologies of spastic dysarthria:
- ALS:
- TBI
- Multiple sclerosis
how does ataxic dysarthria occur?
cerebellar damage
ataxic dysarthria
oral motor exam:
- hypotonia
- slow voluntary movements
- jerkiness of movement
- wide-based gait
- intention tremor
- dysmetric jaw, face & tongue AMRs
articulation:
- irregular, transient articulatory breakdowns
- vowel distortions
prosody:
- excess, equal stress
phonation:
- excess loudness variations
hypokinetic dysarthria occurs by:
damage to basal ganglia
hypokinetic dysarthria caused by:
- anti-psychotic medications
- head trauma
- associated with parkinson's
hypokinetic dysarthria:
oral motor exam:
- limited ROM
- resting tremor
- masked facies
articulation:
- Bradykinesia: reduced speed of muscles
- hesitations & false starts
- slow speech
- rigidity
- reduced loudness
- imprecise consonant production
- reduced pitch variability
- festinating speech
prosody:
- Monopitch & monoloudness
- palalia
phonation:
- hoarseness
- low volume
hyperkinetic dysarthria occurs by:
damage to the basal ganglia
- may be unilateral or bilateral damage
hyperkinetic dysarthria
articulation/speech:
- irregular consonant & vowel distortions
- slow, irregular AMRs
resonance:
- intermittent hypernasality
prosody:
- inappropriate silences
- excess loudness variations
- excessive/variable stress patterns
phonation:
- voice stoppages
- strained-harsh voice
- audible inspiration
- tremor like voice
unilateral UMN dysarthria
Articulation:
- imprecise artic
- slow rate, slow AMRs
Resonance: WNL
Phonation:
- sometimes hoarseness/harshness
- occasional reduced loudness
ALS
- spastic-flaccid dysarthria
atrophy & fasciculations
strained strangled voice
slow rate
Dysarthria vs AOS vs paraphasias
dysarthria vs AOS vs paraphasias
AOS
MSD resulting from disturbed planning or programming of volitional speech actions/patterns in the absence of paralysis, paresis, or incoordination
AOS speech characteristics
◦Slow rate of speech◦Articulatory groping◦Errors of phoneme distortion and substitution ◦Syllable segmentation◦Disturbed prosody –misassigned/abnormal stress◦Initiation of speech and artic. transitions are particularly difficult◦Prolonged cons., vowels, and inter sound, syllable, and word durations
AOS vs paraphasias
AOS◦Errors mostly initial◦Errors more related to phonetic complexity◦Sequencing errors rare◦Additions rare◦Abnormal fluency◦Syllable segmentation
Paraphasia◦Errors can be anywhere◦Errors less related to phonetic complexity◦Sequencing errors common◦Additions common◦Normal fluency◦No syllable segmentation
Severe AOS
Speech characteristics depart from less severe form◦Reduced variability of articulatory characteristics:◦Limited speech sound repertoire◦Speech may be limited to a few meaningful or unintelligible utterances◦Imitation of isolated sounds may be in error, and errors may be limited in variety◦Errors may be highly predictable◦Automatic speech may not be better than volitional◦Muteness may be present, but rarely for longer than 1 or 2 weeks if 2°AOS◦Usu. accompanied by severe aphasia and nonverbal oral apraxia
Primary Progressive AOS(PPAOS)
AOS of insidious onset, gradual progression & prolonged course in which AOS is the first, only, or most salient feature & in which criteria are not met for diagnosis of another neurodegenerative disease
PPAOS speech features
• Slow overall speech rate• Lengthened segments between words• Sound distortions• Increased sound distortions or distorted sound substitutions as utterance length or complexity increases• Syllable segmentation within multisyllabic words
types of PPAOS
• Type 1: predominantly articulatory abnormalities• Distortions & distorted substitutions, repeated sounds, attempted self-correction• More evident when aphasia is present & > AOS• Tends to be association with widespread involvement in premotor, prefrontal, temporal-parietal lobes, caudate, & insula• Type 2: predominantly prosodic abnormalities• Segmentation of words & syllables• More evident in PPAOS without aphasia• Tends to be associated with involvement in premotor cortex & midbrain atrophy• Type 3: no clear difference in prominence of articulatory vs. prosodic abnormalities