motor speech diso wk 3

ataxic dysarthria

associated with damage to cerebellar control circuit

most evident characteristics in artic and prosody

primary deficit: impaired motor control

key physiologic feature: incoordination, may involve hypotonia

ataxic localization

damage to cerebellum

most often bilateral (unilaterally: RH)

influences speech mvmnts through corticocerebellar tract or extrapyramidal system

cerebellum

time components of movement

scale the force and range of muscle activity

coord sequences of muscle contractions for skilled behavior

does not directly initiate mvmnt

ataxic pt presentation

drunk speech (slurred)

stumbling over words

biting tongue/cheek when speaking or eating

speech deteriorates with alcohol

poor coord of breathing speech

ataxic

without ability to coordinate/order

clinical characteristics of ataxia

difficulty standing and walking

nystagmus

hypotonia

dysmetria

decomposition of mvmnt

evaluation tasks for ataxic dysarthria

conversational speech/reading

AMR tasks (often irreg and slow, no steady rhythm, impacts prosody)

slurred speech

result of articulatory inaccuracy

imprecise consonants, irreg artic breakdown, distorted vowels

scanning speech

excess and equal stress across syllables

syllables produced with similar duration

slow, segmented speech rhythm

etiology of ataxic dysarthria

degenerative disease

vasular disorder

trauma

tumors

toxicity

inflammation (encephalitis)

demyelinating disease (MS)

Friedrich's ataxia

rare inherited disease

spinal cord and peripheral nerves degenerate

cerebellum degenerates

onset btwn 5-15 yrs old

first sympoms: gait ataxia

respiration and ataxic dysarthria

don't need to strengthen

focusing on controlling airflow more accurately during speech

uncoord mvmnts cause speech on residual air, affecting prosody and phonation

respiration tasks

slow and controlled exhalation

speak immediately on exhalation

stop phonation early

optimal breath group (teaching how many syllables or words can be said clearly on one full inhalation)

prosody and ataxic dysarthria

rate, stress, intonation problems

slow rate = improve intelligibility

incorporate more typical stress and intonation into utterances, speech may exhibit more natural quality

rate control tasks

reciting syllables to a metronome

finger on hand tapping

cued reading material

hypokinetic dysarthria

basal ganglia control circuit pathology

most evident deficits in voice, artic, prosody

decreased range of mvmnt, or hypokinesia

rigidity, reduced force and range of mvmnt

increased speech rate

clinical characteristics of hypokinetic dysarthria

rigidity, bradykinesia, hypokinesia, akinesia = Parkinsonism

etiology of hypokinetic dysarthria

interferes with basal ganglia control circuit

degenerative diseases are most frequent

vascular disorder

trauma

toxicity

infection

normal pressure hydrocephalus

parkinsonism =/= parkinson's disease

parkinson's disease

slowing progressive, idiopathic neurologic disease

nerve cell loss in substantia nigra and dicreased dopamine in striatum

side effects of medication- dyskinesia

most almost always also develop dementia

resting tremor hallmark

idiopathic

not quite sure what the cause is

parkinson's speech

reduced loudness

repeated phonemes, palilalia, or "blurred" AMRs

reduced stress, monopitch, monoloudness, inappropriate silences, short rushes of speech, variable rate, increased rate in segmentals, increased overall rate

laryngeal findings, hypokinetic dysarthria

bowed vocal folds

tremulous arytenoids

ventricular fold mvmnt

decreased intensity, pitch/loudness variability, speed to initiate phonation, max phonation time

artic findings, hypokinetic dysarthria

reduced amplitude and velocity of lip mvmnt, tongue endurance, speech rate, variation in syllable duration

increased connected speech rate

key eval tasks for hypokinetic dysarthria

conversational speech/reading, identify prosodic abnormalities

speech AMRs- reductions in the range of mvmnt and rate abnormalities, rapid/accelerated/"blurred" speech AMRs

vowel prolongation

trtmnt of hypokinetic dysarthria

pharmacologic (meds)

sugrical

behavioral (speech therapy)

pharmacologic trtmnts for parkinsonism

replace dopamine in striatum

correct neurotransmitter imbalance by decreasing acetylcholine activity in striatum

surgical trtmnts for parkinsonism

complicated and invasive

used when pt incapacitated and medications ineffective

ablative (completely taken away)- thalamotomy, pallidotomy

deep brain stimulation

behavioral trtmnts for parkinsonism

artic: imprecise consonants, compounded errors by reduced rate- rate reduction, stretching, traditional artic tasks

phonation: activities to more fully adducted VF position

respiration: shallow breath support- cueing for complete inhalation, slow and controlled exhalation

prosody: improved by slowing rate

LSVT lee silverman voice treatment

targets increased respiratory effort

daily ahhs, think loud

1 hr/day, 4 days/wk, 4 consecutive weeks

hyperkinetic dysarthrias

group of motor speech disorders associated with basal ganglia control circuit and hyperkinetic mvmnt disorders

involve involuntary mvmnts that disrupt normal speech disruption

localization of hyperkinetic dysarthrias

basal ganglia

loss of subthalamic nucleus function (reduced inhibition, incr cortical firing, abnorm mvmnts)

loss of striatal neurons (dysreg globus pallidus output, invol mvmnts)

neurotransmitter imbalance (incr dopamine or decr acetylcholine)

mvmnt disorders characteristics

strained vocal quality, inprecise consonants, artic breakdowns, inappropriate prolonged silent intervals and prolonged phonemes

excessive loudness variation and voice stoppages

depends on type of mvmnt disorder

etiology of hyperkinetic dysarthrias

unknown

mvmnt disorders have unknown etiologies, dysarthria is result of mvmnt disorder

etiologies of hyperkinetic dysarthrias

degenerative diseases

toxic/metabolic

infectious

vascular

trauma

tourette's syndrome

huntington's disease

autosomal dominant CNS disorder, progressive and inherited disorder

severe loss of neurons in caudate nucleus and putamen

diffuse neuronal loss in cortex

symptoms: chorea, dementia, depression, personality changes

tardive dyskinesia

toxic/metabolic conditiion

caused by dopamine blocking agents

symptoms: involuntary/repetitive mvmnts, grimacing, tongue twitching, lip smacking, rapid mvmnts

neuromuscular deficits

chorea

dystonia

essential tremor

chorea

involuntary rapid, nonsterotypic, random, purposeless mvmnts of body structures

abnormalities with inhibitory BG pathways

effortful speech, invol orofacial mvmnts, chewing/swallowing problms, upatterned mvmnts

dystonia

involuntary abnorm postures resulting from excessive contraction of muscles

effortful speech, invol orofacial mvmnts, chewing/swallowing problms, slow mvmnts, strained/harsh voice quality, variability in loudness in rate

dystonic hyperadduction of the VFs

spasmodic dysphonia

dystonic mvmnts of laryngeal muscles that are triggered during speech

characterized by strained or breathy voice quality

adductor- hyperadduction of adductor laryngeal muscles, VF close too tightly

abductor- VF open too much

essential tremor

voice disorder, localization is unknown

quavering, rhythmic, waxing and waving tremor, most evident vowel prolongation

slowed articulation

key eval tasks for hyperkinetic dysarthrias

conversational speech and reading AMR tasks

sustained phonation

visual observation

trtmnt for hyperkinetic dysarthrias

behavioral: speech rate, rhythymic breathing/relaxation, speaking on exhalation

medical: deep brain stimulation, pharmacologically, botox

neurological basis of uumn dysarthria

most cranial nerves serving speech muscles recieve bilateral innervation from UMN

unilateral damage to upper motor neurons

velum, pharynx, and larynx are innervated bilaterally and should not be affected by UMN damage

unilateral upper motor neuron dysarthria

generally milder and temporary, known to co-occur with aphasia and apraxia of speech

weakness in face and tongue, sometimes other levels of speech system, sometimes shows spasticity and incoordination

apparent in artic, prosody, phonation

can be difficult to distinguish spastic or ataxis dysarthria

largely vascular etiology

UUMN speech characteristics

speech production errors, slow AMRs, harsh voice quality

depends on spastic-like or ataxic-like

associated with unilateral central face and tongue weakness

predominant stroke etiology

mild deficits

key eval tasks for UUMN dysarthria

conversational speech and reading

speech AMRs

vowel prolongation

medical records - most telling

trtmnt of UUMN dysarthria

targets traditional artic tasks

mixed dysarthrias

combination, any combination is possible, one may predominate

more present than a single dysarthria type by itself

95% of dysarthrias are combination of 2, other 5% is more than 2

most are perceptually distinguishable

can be first signs of neurological disease

most common types of mixed dysarthria

flaccid-spastic 68%

ataxic-spastic 7%

hyperkinetic-hypokinetic 4%

ataxic-hypokinetic 4%

hypokinetic-spastic 3%

ataxic-hypokinetic-spastic 2%

etiologies of mixed dysarthrias

combined neurologic events (multiple strokes)

co-occurence of 2+ neurologic diseases (stroke & PD)

degenerative disease that affect more than one portion of nervous system

trauma

motor neuron disease

spinal muscle atrophy

progressive bulbar palsy

primary lateral sclerosis or progressive pseudobulbar palsy

ALS

spinal muscle atrophy

affects LMNs only

flaccid, not mixed

progressive bulbar palsy (PBP)

LMN weakness of cranial nerve muscles

flaccid and not mixed if only confined to ___?

can be thought of as ALS with LMN components

ALS

affects motor system at all levels- motor cortex, brainstem, spinal cord- causing both UMN and LMN signs

1-5 per 100,000 population

onset 40-70 years of age

life expectancy of 1-5 years

ALS clinical profiles

fatigue, cramping, fasciculations, weakness, muscle atrophy

commonly associated with mixed flaccid-spastic dysarthria

diagnosis based on clinical profile and electrophysiologic conformation

flaccid-spastic dysarthria

strained-strangled-harsh-liquid sounding voice quality

hypernasality

imprecise consonants

slow rate

commonly associated with ALS

ataxic-spastic dysarthria

progressive supranuclear palsy (PSP)

multisystem neurodegenerative disease affects globus pallidus, substantia nigra, thalamus, subthalamic nucleus, midbrain, brainstem nuclei, cerebellum

associated with hypokinetic, ataxic, spastic dysarthrias

multiple system atrophy

neurodegenerative condition with various combinations of parkinsonism, ataxia, spasticity, autonomic dysfunction

hypo/hyperkinetic, ataxic, or spastic dysarthria may be present

multiple sclerosis

acquired demyelinating disease

characterized by demyelination and death of oligodendrocytes within lesion

ataxic and spastic dysarthria combined are most commonly associated

trtmnt of mixed dysarthria

first treat component most severely affecting speech production

treat in order: respiration, resonation, phonation, articulation, prosody- prior speech components are foundation for others

dependent on client needs

AAC for pts with ALS