motor speech disorders exam 3

what percent of dysarthrias does ataxic account for?

11.4%

most eivdent characteristics of ataxic dysarthria?

-incoordination

-reduced tone

-slow and inaccurate force, ramge, timing, and direction of movement

-problem with motor control (discoordination)

Where is the location of damage with ataxic dysarthria?

cerbellar control circuit

what makes up the cerebellar control circuit?

cerebellar hemispheres and its connections (anterior, posterior, and flocculondular lobes)

function of cerebellum

controls equilibrium and balance ipsillaterally

function of the anterior lobe of the cerebellar control circuit

posture, gait, and truncal tone

function of the posterior lobe of the cerebellar control circuit

skilled voluntary movements, muscle tone

vermis

Connects the two hemispheres of the cerebellum

3 primary roles of the cerebellum

1. timing of components of movement

2. scaling size of muscle actions

3. coordinating sequences of movement for scaled motor behavior

where does the cerebellum recieve info from?

the frontal lobe (primary and premotor regions) & descending corticospinal and corticobulbar tracts

where does the cerebellum send info to?

the primary motor cortex, brainstem, and spinal motor nuclei

function of the cerebellar control circuit

controls continuous corrective modifications to coordinate appropriate movements - receives information before execution and modifies appropriately

result of damage to the flocculondular lobe

truncal ataxia, nystagmus

truncal ataxia

difficulty/inability to maintain steady posture of trunk

nystagmus

Involuntary rapid eye movements

result of damage to the anterior lobe

gait ataxia

gait ataxia

characterized by unsteady walking with a wide base of support; uncoordinated

result of damage to the posterior lobe (ipsilateral)

limb ataxia

hypotonia

intention tremor

incoordination

dysmetria

dyssynerey/decomposition of movements

dysdiodokinesia

dysdiodokinesia

abnormal timing and velocity of AMRs

intention tremor

worsening of action tremor as the limb approaches a target in space

result of damage to the cerbellar control circuit

-breakdown is in speech motor control (not execution)

-perception is in lack of muscle control

-dysphagia is less common with ataxia

titubation

rhythmic consistent tremor of body or head

dysmetria

disturbance in trajectory or inability to control range of movement

movement decomposition

errors in sequence and speed of movement

mild facial weakness

weakness often limited to the lower face

what are the top three etiologies of ataxic dysarthria?

1. degenerative (36.7%)

2. vascular (20.3%)

3. undetermined (13.4%)

how does the patient describe their speech with ataxic dysarthria?

-speech is slurred (sound drunk)

-rapid fatigue

-unccordinated breathing and speaking (sometimes)

nonspeech oral mech findings of ataxic dysarthria

-normal size, strength and symmetry

-possible irregular AMRs

Note: interpret findings with caution

speech oral mech findings of ataxic dysarthria

-repetitions of words/phrases reveal fatigue, irregular artic breakdowns, and prosodic abnormalities

-assessed using convos, reading, and AMRs

distinguishing speech characteristic of ataxic dysathria

speech AMRs; errors are in timing, force, range, reduced speed, and tone

alternating motion rates (AMRs)

evaluates the speed, regularity, and coordination of a person's oral articulators by measuring how fast and steadily they can repeat a single syllable; ask the client to take a deep breath and repeat "puh, puh, puh"

AMR norms for healthy older adults

Puh (/pa/): 4.1-8.1 syllables per second

Tuh (/ta/): 3.6-8.2 syllables per second

Kuh (/ka/): 3.2-8.1 syllables per second

Puh Tuh Kuh (/pataka/ - SMR): 2.5-9.0 syllables per second

deviant clusters for ataxic dysarthria

1. articulatory inaccuracy

2. prosodic excess

3. phonatory-prosodic insufficiency

articulatory inaccuracy (ataxic)

-imprecise consonants

-irregular articulatory breakdowns

-vowel distortions

prosodic excess (ataxic)

-excess and equal stress

-prolonged phonemes

-prolonged intervals

-slow rate

phonatory-prosodic insufficiency (ataxic)

-harshness

-monopitch

-monloudness

respiratory and laryngeal function with ataxic dysarthria

-possible reduced respiratory function

-incoordination of timing of exhalation and phonation

-paradoxical and irregular movements in rib cage and abdomen

-initiaiton of speech is with reduced lung volume

-reduced pitch and loudness

-unsteadiness during vowel production

acoustic and physiologic findings with ataxic dysarthria

-slow rate (reliable preditcor of intelligibility)

-longer syllables and sentence duration

-reduced rate of feedback

-rhythm issues

-increased VOT

speech characteristics of ataxic dysarthria

irregular artic breakdowns (imprecise consonants, vowel distortions)

prosodic disturbances (prolonged phonemes, slow are, excess and equal stress)

phonation (harsh, monopitch, monoloundess)

what causes spastic dysarthria?

result of damage to the UMNs that impacts the direct and indirect activation pathways

What areas of speech can spastic dysarthria impact?

respiration, phonation, articulation, resonance, and prosody (all aspects)

basic description of spastic dysarthria

a combination of weakness and spasticity; reflects excessive muscle tone

corticobulbar tract stimulates...

the cranial nerves

corticospinal tract stimulates

the spinal nerves

bulbar speech muscles include:

lower face and portions of the tongue

indirect activation pathway (IAP) function

regulates reflexes, maintains posture & tone, and provides framework for skilled movement; most acitivites are inhibitory

IAP location

originates in the cortex of each cerebral hemisphere; synapses occur between the cortex and brainstem/spinal cord

clinical characteristics of UMN damage: DAP

-stimulates movement in the FCP

-loss of fine, skilled movements

-increases tone and spasticity

-hyporreflexia (positive Babinski)

clinical characteristics of UMN damage: IAP

-affects inhibition of impulses (overactivity)

-increased muscle tone, spasticity, hyperexcitable reflexes, weakness, reduced ROM, and slowness of movements

top 4 etiologies of spastic dysarthria

1. degenerative (58%)

2. vascular (13%)

3. undetermined (11%)

4. demyelinating (3%)

vascular disorders (spastic)

-stroke

-vascular dementia (Binswanger Disease)

-myoamoya

-CADASIL

degenerative diseases (spastic)

-ALS/Motor neuron disease

-Primary Lateral Sclerosis (PLS)

-Progressive pseudobulbar palsy (PSP)

leukoencephalitis (inflammatory disease - spastic)

demyelinating disease due to the destruction of white matter in the brain and/or spinal column

congenital disordersd (spastic)

cerebral palsy

patients reports with spastic dysarthria

-speech is slow and effortful (talking against resistance)

-fatigue when speaking

-nasality

-oral and pharyngeal dysphagia

-emotional lability

nonspeech oral mech findings with spastic dysarthria

-dysphagia/oral discretions

-flattened nasolabial folds

-"on the verge of tears" expression

-jaw clonus

-hyperactive gag reflex

-reduced soft palate movement

-pathologic oral reflexes

jaw clonus

involuntary jerking motion of the jaw

speech oral mech findings with spastic dysarthria

-imapired movement patterns rather than weakness

-deficits at all the speech valves and components of the speech system

-described by slowness, reduced range of individual and repetitive movements, reduced force of movement, and/or excessive muscle tone

deviant clusters for spastic dysarthria (4)

1. prosodic excess

2. articulatory-resonatory incompetence

3. prosodic insufficiency

4. phonatory stenosis

prosodic excess (spastic)

excess and equal stress, slow rate

articulatory resonatory incompetence (spastic)

imprecise consonants, distorted vowels, hyper nasality

prosodic insufficiency (spastic)

mono pitch, mono loudness, reduced stress, short phrases

phonatory stenosis (spastic)

low pitch, harshness, strained-strangled voice, pitch breaks, short phrases, slow rate

resonance findings with spastic dysarthria

-absence of control with velopharyngeal function (resonance)

-soft palate may move sluggishly

-indicates systemic relationship between voicing and velopharyngeal function w/o rapid control of phonatory valve

articulation, rate, and prosody findings with spastic dysarthria

-reduced articulatory range and precision

-voicing of voiceless consonants

-reduced vowel prolongation

-reduced prolongation of sibilants /s/

-reduced lingual and lip movement

-prosodics effected (rate, range, and strength of movement)