maggie praxis 4

Question 1

Dysarthria

Answer 1

Neurologically based speech disorder. Many different types. Common to all: impaired muscular control of the speech mechanism and peripheral or central nervous system pathology

Question 2

Communication problems in dysarthria include

Answer 2

respiratory, articulatory, phonatory, resonatory, and prosodic disturbances caused by weakness, incoordination, or paralysis of speech musculature

Question 3

Ataxic dysarthria

Answer 3

Results from damage to cerebellar system. Characterized predominantly by articulatory & prosodic problems

Question 4

Ataxic dyarthria physical characteristics

Answer 4

gait disturbances, over- or undershooting of targets; uncoordinated, jerky, inaccurate, slow, imprecise movemnts

Question 5

Ataxic dysarthria communication characteristics

Answer 5

Artic: imprecise consonants; irregular artic. breakdowns & vowel distortions
Prosody: excessive & even stress; prolonged phonemes and intervals btw words or syllables; slow rate of speech. Phonatory: monopitch, monoloudness, and harshness
Speech quality: drunken sounding

Question 6

Neuropathology of ataxia

Answer 6

cerebellar lesions, Friedrich’s ataxia, TBI, alcohol and drug abuse, meningitis and encephalitis (inflammatory conditions)

Question 7

Flaccid dysarthria

Answer 7

LMN damage. Results from damage to motor units of cranial or spinal nerves that supply speech muscles

Question 8

Flaccid dysarthria neuropathology

Answer 8

myasthenia gravis; vascular diseases & brainstem strokes; infections (e.g. polio and AIDS); dymyelinating disease (e.g. Guillain-Barre syndrome); progressive bulbar palsy & ALS (degenerative diseases); surgical trauma during brain, laryngeal, facial, or chest surgery

Question 9

Specific CNs which may be involved in flaccid dysarthria

Answer 9

trigeminal (V), facial (VII), glossopharyngeal (IX), vagus (X), and hypoglossal (XII) nerves

Question 10

Physical characteristics of flaccid dysarthria

Answer 10

weakness, hypotonia, atrophy, diminished reflexes; twitches of resting muscles (fasciculations) and contractions of individual muscles (fibrillations); rapid and progressive weakness w/ use and recovery with rest

Question 11

Communication characteristics of flaccid dysarthria

Answer 11

Respiration: weakness in combination w/ cranial nerve weakness; Phonatory: breathy voice, audible inspiration, short phrases; Resonance: hypernasality, imprecise consonants, nasal emission, short phrases; Phonatory-prosodic: harsh voice, monopitch, and monoloud

Question 12

Hyperkinetic dysarthria

Answer 12

Results from damage to basal ganglia (extrapyramidal system). Associated w/ involuntary movements and variable muscle tone. Prosodic disturbances are dominant

Question 13

Causes of Hyperkinetic dysarthria

Answer 13

etiology often unknown; include vascular, traumatic, infectious , neoplastic, and metabolic factors; Huntington’s disease

Question 14

Physical characteristics of hyperkinetic dysarthria

Answer 14

abnormal & involuntary movements of orofacial muscles; myclonus (involuntary jerks), tics of face and shoulders, tremor, chorea; abrupt & severe contractions of the extremities; writhing, involuntary movements (athetosis); spasms; dystonia (contractions of antagonistic muscles); spasmodic torticollis; blepharospasm

Question 15

Hypokinetic dysarthria

Answer 15

Results from damage to basal ganglia (extrapyramidal system)

Question 16

Causes of hypokinetic dysarthria

Answer 16

Parkinson’s, Alzheimer’s, multiple or bilateral strokes, repeated head trauma, inflammation, tumor, antipsychotic or neuroleptic drug toxicity, hydrocephalus

Question 17

Physical characteristics of hypokinetic dysarthria

Answer 17

Resting tremors of face, mouth, and limb muscles which DIMINISH when moved voluntarily; mask-like face w infrequent blinking and no smiling; micrographia (small writing); walking disorders (slow to start, then short, rapid, shuffling steps); postural problems such as involuntary flexion of head, trunk, arm, and difficulty chanting positions; decreased swallowing (drooling)

Question 18

Communication characteristics of hypokinetic dysarthria:

Answer 18

Phonatory: monopitch, low pitch, monoloudness, harsh and continuously breathy voice
Prosody: reduced stress, inappropriate silent intervals, short rushes of speech, variable and increased rate in segments, short phrases
Artic: imprecise consonants, repeated phonemes, resonance disorders and mild hypernasality
Respiratory: reduced vital capacity, irregular breathing, faster rate of respiration

Question 19

Spastic dysarthria

Answer 19

Results from bilateral damage to upper motor neurons. Lesions in multiple areas, including cortical areas, basal ganglia, internal capsule, pons, and medulla are common

Question 20

Physical characteristics of spastic dysarthria

Answer 20

spasticity and weakness, especially bilateral facial weakness, though jaw strength may be normal and lower face weakness may be less severe; reduced range and slowness of movement, loss of fine and skilled movement and increased muscle tone; hyperactive gag reflex; hyperadduction of VFs and inadequate velopharyngeal port closure

Question 21

Communications characteristics of spastic dysarthria

Answer 21

Prosody: excess & equal stress, slow rate, monopitch, monoloudness, reduced stress, and short phrases
Artic: imprecise consonants & distorted vowels
Phonatory: continuous breathy voice, harshness, low pitch, pitch breaks, STRAINED-STRANGLED quality, short phrases, slow rate
Resonance: predominant hypernasality

Question 22

Mixed dysarthrias

Answer 22

Combination of two or more pure dysarthrias. Most common mixed types are: flaccid-spastic and ataxic-spastic

Question 23

Mixed flaccid-spastic

Answer 23

associated with ALS

Question 24

Characteristics of mixed flaccid-spastic

Answer 24

imprecise consonants, hypernasality, harsh voice, slow rate, monopitch, short phrases, distorted vowels, low pitch, monoloudness, excess & equal stress and reduced stress, strained-strangled quality, breathiness, etc

Question 25

Mixed ataxic-spastic

Answer 25

associated with MS

Question 26

Characteristics of mixed ataxic-spastic

Answer 26

impaired loudness control, harsh voice quality, imprecise articulation, impaired emphasis, hypernasality, inappropriate pitch levels, and sudden artic breakdowns

Question 27

Unilateral Upper Motor Neuron Dysarthria

Answer 27

Result from damage to upper motor neurons that supply cranial and spinal nerves involved in speech production

Question 28

Causes of UUMN dysarthria

Answer 28

vascular disorders produce lft-hemisphere lesions may coexist w/ aphasia or apraxia; dysarthria due to rt-hemisphere lesions may coexist with rt hemisphere syndrome

Question 29

Physical characteristics of UUMN dysarthria

Answer 29

unilateral lower face weakness, unilateral tongue weakness, unilateral palatal weakness, and hemiplegia/hemiparesis

Question 30

Communication characteristics of UUMN dysarthria

Answer 30

Artic: imprecise consonants and irregular artic breakdowns Phonatory: harsh voice, reduced loudness, strained harshness Prosody: slow rate, increased rate in segments, excess and equal stress, monopitch, monoloudness, low pitch, and short phrases Resonance: predominantly hypernasality Other: dysphagia, aphasia, apraxia, and rt hemisphere syndrome

Question 31

Assessment of dysarthria

Answer 31

1) Record extended conversational speech and reading sample; 2) Use variety of speech tasks (e.g. imitations of syllables, words, phrases, and sentences), sustained vowel prolongation; 3) Diadochokinetic rate or alternating motion rations and sequential motion rates; 4) Assess speech production mech during nonspeech activities (e.g. oral mech exam, coughing, nasal airflow); 5) Assess respiration, phonation, articulation, prosody, and resonance, and intelligibility; 6) Standardized tests (e.g. Assessment of Intelligibility of Dysarthric Speakers & Frenchay Dysarthria Assessment)

Question 32

Treatment of dysarthrias

Answer 32

techniques to modify respiratory, phonatory, articulatory, and resonatory problems are all necessary

Question 33

Tx procedures dysarthria

Answer 33

Intensive, systematic, and extensive drill, instruction, demonstration, modeling, shaping, prompting, fading, differential reinforcement, and other proven behavioral management procedures. When necessary, phonetic placement and instrumental feedback or biofeedback may be used

Question 34

Dementia is associated with

Answer 34

Wernicke-Korsakoff syndrome (associated with alcoholism), Alzheimer type, frontotemporal dementia, Parkinson's, Huntington's infection, and other (vascular disease, multiple CVAs, TBI)

Question 35

Rt hemisphere syndrome

Answer 35

Symptoms: attentional and affective symptoms; communication deficits found in 50% of cases. Treatment often addresses problems such as impaired attention, impulsive behavior, pragmatic communication impairments and visual neglect

Question 36

Tx of patients with TBI

Answer 36

Cognitive rehabilitation and direct communication training`

Question 37

Cognitive rehab following TBI

Answer 37

Clinicians may train the following: attention, visual processing, and memory

Question 38

Communication Tx following TBI

Answer 38

Involves direct behavioral procedures. Systematic reinforcement of attending behaviors, appropriate discourse, topic maintenance, self-correction, etc. to decrease inappropriate behaviors. Goals should be functional w/ initial focus on effectiveness of communication NOT grammatical correctness. Family members should be involved.

Question 39

Apraxia is often associated with lesions in what area?

Answer 39

Broca's

Question 40

Porch Index of Communicative Ability

Answer 40

Samples speech & language skills to only a limited extent

Question 41

Apraxia of speech (AOS)

Answer 41

Neurogenic speech disorder. A basic disorder of volitional movement in the absence of muscle weakness, paralysis or fatigue.

Question 42

Locus of AOS

Answer 42

caused by damage or injury to speech-motor programming areas (e.g. Broca's) in the dominant hemisphere

Question 43

T/F patients with AOS have rapid rate of speech?

Answer 43

False. They typically have a reduced rate

Question 44

Characteristics of AOS

Answer 44

Consonants more impacted than vowels; increased frequency of errors on longer words; groping behaviors; automatic productions easier than volitional productions; awareness of errors; speech sound substitutions common, particularly substitution of voiceless phoneme for voiced (e.g. "pet" for "bet"); may make several unsuccessful attempts to self-correct

Question 45

Assessing AOS

Answer 45

Repetitive production of single- and multiple syllables (e.g. "puh-ta-kuh", multisyllabic words); imitative production of progressively longer words, phrases, and sentences; picture description tasks; assess oral reading; assess overall movement of limbs; administer standardized tests (e.g. Apraxia Battery for Adults)

Question 46

Tx of AOS

Answer 46

Auditory-visual stimulation, oral-motor repetition, & phonetic placement

Question 47

Progression of Tx of AOS

Answer 47

Carefully sequenced to move from automatic simple productions to less automatic, more spontaneous productions

Question 48

damage to UMN direct activation pathway causes (spastic dysarthria) problems

Answer 48

loss of skilled movement | -decreased muscle tone

Question 49

UMN indirect activation pathway controls

Answer 49

UMN indirect activation pathway controls Control posture, tone, & movements supportive of voluntary movement

Question 50

LMN function

Answer 50

LMN function Produce muscle actions for reflexes & muscle tone. Carries out UMN commands for voluntary movements & postural adjustments