from mixed dysarthria through acquired AOS

Question 1

mixed dysarthria lesion and clinical presentations (much of what is known based on ALS)

Answer 1

progressive degeneration of UMNs and LMNs; weakness as prominent motor symptom; symptoms may first appear in limbs (spinal), bulbar (CNs), or mixed (brainstem and MNs)

Question 2

mixed dysarthria perceptual

Answer 2

prolonged intervals and phonemes, inappropriate silences, flaccid + spastic effect; add’l from sheet: abnormal pitch, monopitch, harsh voice, breathy, strained, hypernasal, nasa emission, monoloudness, audible inspiration, slow rate, short phrases, reduced stress, excess and equal stress, imprecise consonants, distorted vowels, intelligibility

Question 3

mixed dysarthria etiologies

Answer 3

degenerative (most common, esp. ALS, Friedrich’s ataxia,), demyelinating (MS), vascular, toxic-metabolic, traumatic, neoplasm, infectious or autoimmune

Question 4

mixed dysarthria disease example

Answer 4

ALS: absence of muscle nourishment, progressive, no cure; hypoglossal MNs disproportionately affected); 1-5 years life expectancy; reduced intelligibility; especially lower lip, tongue, jaw movement, can use instrumental measures and speech characteristics as first disease markers and to separate stages of ALS (Green, Yunusova, et al.)

Question 5

ataxic dysarthria lesion and clinical presentations

Answer 5

bilateral damage to cerebellum (and connections to thalamus and cerebral hemisphere)/cerebellar pathways in brainstem/generalized cerebellar disease; disordered contractions of agonist/antagonist muscles; lack of coordination; jerky movements; dysrhythmia, dysmetria (over-, undershooting), intention tremor, wide gait

Question 6

ataxic dysarthria perceptual

Answer 6

imprecise consonant, articulatory breakdown, distorted vowels, excess and equal stress, prolonged phonemes and intervals, slow rate, harshness, monopitch, monoloudness, excessive loudness variation; scanning speech (choppy, out-of-sync); articulation and prosody most prominent

Question 7

ataxic dysarthria etiologies

Answer 7

degenerative, vascular, demyelinating, cerebellar, tumors, TBI, stroke, toxicity

Question 8

ataxic dysarthria disease example

Answer 8

Friedrich’s ataxia: autosomal recessive; loss of coordination, fatigue, vision impairment, heart condition, most common childhood onset type

Question 9

roles of cerebellum

Answer 9

connect to cerebral cortex; auditory and proprioceptive feedback; connections to brainstem and indirect activation pathways; cooperation with basal ganglia

Question 10

inputs to cerebellum and outputs from cerebellum

Answer 10

input from cortex, vestibular system, spinal cord, brainstem, and relay neurons in pons; output to cortex, primary motor and premotor cortex via deep cerebellar nuclei via thalamus: cortex->cerebellar cortex->relay nuclei->thalamus

Question 11

Weismer, Yunusova, Bunton

Answer 11

instruments must be sensitive to dysarthria, tell us about the movement of speech motor systems, functional communication implications, and feasibility of implementation and interpretation

Question 12

basal ganglia components and fx

Answer 12

caudate, putamen, globus pallidus, substantia nigra, subthalamic nucleus; integrate motor info. for complex movements, plan and execute complex movements, movement selection, motor learning, postural support/muscle tone for skilled, voluntary movement, regulate amplitude, velocity, initiation

Question 13

BG effect on direct pathways (corticospinal; voluntary)

Answer 13

excitatory by mechanism of disinhibition (not letting gate close)

Question 14

BG effect on indirect pathways

Answer 14

inhibits unwanted movements (tics, tremors, etc.)

Question 15

hypokinetic and hyperkinetic

Answer 15

hypo: too much inhibition; not enough excitation; not enough inhibition; too much excitation

Question 16

hypokinetic dysarthria lesions and clinical presentations

Answer 16

not enough direct pathway excitation; damage to basal ganglia (substantia nigra) and fiber tracts; neurotransmitter imbalance; reduced movements; muscle rigidity, resting tremor, bradykinesia, hypokinesia, postural instability, acceleration of speech, walk (much of this from PD)

Question 17

hypokinetic dysarthria perceptual

Answer 17

monopitch/monoloud/reduced stress contrasts, imprecise consonants, breathy, reduced vocal intensity, fast rate, short rushes of speech; add’l from sheet: harshness, variable rate, inappropriate silence, repeated phonemes/syllables

Question 18

hypokinetic dsyarthria etiologies

Answer 18

degenerative, vascular, trauma, infectious, virus, stroke, antipsychotic, dementia

Question 19

hypokinetic dysarthria disease example

Answer 19

PD (majority): dopaminergic neurons loss in substantia nigra; resting tremor, slow movements, rigid, masked face, usually later in life, progression between 5-15 years

Question 20

hyperkinetic dysarthria lesion and clinical presentations

Answer 20

basal ganglia lesion (esp. caudate/putamen); abnormal, rhythmic, or irregular involuntary movements (hyperkinesia): myoclonus–single jerk, tics, tremor, dyskinesia, athetosis–writhing, ballism–fast/irregular/gross, chorea–rapid/involuntary/purposeless, dystonia–abnormal posture from excessive muscle contraction

Question 21

hyperkinetic dysarthria perceptual

Answer 21

inappropriate silences, voice stoppages, prolonged intervals, excessive loudness variation or alternating loudness, irregular articulation, vowel distortions, imprecise consonants, strained, harsh, transient breathiness, audible inspiration; prosody and rate (+ interruptions) most noticeable

Question 22

hyperkinetic dsyarthria etiologies

Answer 22

degenerative, Huntington’s Chorea, dystonia, toxic, medication, tumors

Question 23

hyperkinetic dysarthria subtypes

Answer 23

chorea (rapid, random movements); dystonia (slow, sustained movements)

Question 24

hyperkinetic dysarthria disease example

Answer 24

Huntington’s Chorea: inherited, degenerative, abnormal movements, often starts in 40s, survival 15 yrs., caudate nucleus atrophy

Question 25

UUMN dysarthria lesion and clinical presentations

Answer 25

more anatomic; UMN unilaterally; hemiplegia, impaired skilled movements, UMN system damage, unilateral facial weakness, lingual weakness; primary sign is weakness and incoordination of tongue and lower half of face on opposite side of lesion; effects more “focal” due to unilateral nature; TEMPORARY (often) and milder symptoms

Question 26

UUMN dysarthria perceptual

Answer 26

imprecise consonants, irregular articulation (clumsy), dysphonia, slowed rate; add’l from sheet: abnormal pitch, pitch breaks, monopitch, harsh, hoarse, breathy, strained, hypernasal, hyponasal, nasal emissions, loudness, monoloudness, slow rate, short phrases, increased rate, reduced stress, variable rate, prolonged intervals, irregular breakdowns

Question 27

anarthria

Answer 27

speechlessness due to severe loss of neuromuscular control over speech

Question 28

neurogenic and psychogenic speech disorders

Answer 28

should not see motor-based problems of movement or speech-like production (check stimulability): anarthria, neurogenic mutism, aprosodia

Question 29

acquired apraxia of speech

Answer 29

impaired capacity to plan or program (or activate appropriate programs or parameters) sensorimotor commands for speech that occurs in the absence of physiologic disturbances (neuromuscular weakness) and language components; lesion unidentified, probably left hemisphere; may co-occur with muscle weakness (non-speech) and language-based impairments; abnormal rate and prosody; possible limb apraxia; 3 most common = artic errors, rate and rhythm, prosody

Question 30

history of AOS

Answer 30

originally considered linguistic/phono disorder, BUT then artic issues more distortions than substitutions; now generalized motor program with generalized instructions for class of related movements, but parameters can be manipulated

Question 31

motor program

Answer 31

OLD: abstract code or structure stored in brain to execute movement in the absence of sensory feedback; for skilled movement, not new or unlearned; retrieval/unpacking/command stages; reaction time increases with movement complexity; BUT 1) too many codes to store, and 2) only applies to practiced movements (storage and novelty issues)
NEW: (generalized) motor programs as memory representations that encode relations among various kinds of info. based on past experiences

Question 32

Ziegler et al. article

Answer 32

AOS as disconnection of movements from the mind; functional/intact basic motor system, preserved access to abstract mental or phono representations of speech; speech and language production linked

Question 33

Is mixed dysarthria rare?

Answer 33

No

Question 34

hyperkinesia

Answer 34

increase in (excessive) involuntary muscle movements

Question 35

spasticity

Answer 35

result of hyperactive stretch reflexes caused by excitatory and inhibitory imbalance

Question 36

which pathways for bradykinesia and hyperkinesia?

Answer 36

bradykinesia: direct; hyperkinesia: indirect