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maggie praxis 4 Flashcards

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1
Q

Dysarthria

A

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

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2
Q

Communication problems in dysarthria include

A

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

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3
Q

Ataxic dysarthria

A

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

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4
Q

Ataxic dyarthria physical characteristics

A

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

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5
Q

Ataxic dysarthria communication characteristics

A

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

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6
Q

Neuropathology of ataxia

A

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

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7
Q

Flaccid dysarthria

A

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

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8
Q

Flaccid dysarthria neuropathology

A

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

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9
Q

Specific CNs which may be involved in flaccid dysarthria

A

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

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10
Q

Physical characteristics of flaccid dysarthria

A

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

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11
Q

Communication characteristics of flaccid dysarthria

A

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

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12
Q

Hyperkinetic dysarthria

A

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

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13
Q

Causes of Hyperkinetic dysarthria

A

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

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14
Q

Physical characteristics of hyperkinetic dysarthria

A

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

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15
Q

Hypokinetic dysarthria

A

Results from damage to basal ganglia (extrapyramidal system)

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16
Q

Causes of hypokinetic dysarthria

A

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

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17
Q

Physical characteristics of hypokinetic dysarthria

A

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)

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18
Q

Communication characteristics of hypokinetic dysarthria:

A

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

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19
Q

Spastic dysarthria

A

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

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20
Q

Physical characteristics of spastic dysarthria

A

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

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21
Q

Communications characteristics of spastic dysarthria

A

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

22
Q

Mixed dysarthrias

A

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

23
Q

Mixed flaccid-spastic

A

associated with ALS

24
Q

Characteristics of mixed flaccid-spastic

A

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

25
Q

Mixed ataxic-spastic

A

associated with MS

26
Q

Characteristics of mixed ataxic-spastic

A

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

27
Q

Unilateral Upper Motor Neuron Dysarthria

A

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

28
Q

Causes of UUMN dysarthria

A

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

29
Q

Physical characteristics of UUMN dysarthria

A

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

30
Q

Communication characteristics of UUMN dysarthria

A

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

31
Q

Assessment of dysarthria

A

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)

32
Q

Treatment of dysarthrias

A

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

33
Q

Tx procedures dysarthria

A

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

34
Q

Dementia is associated with

A

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

35
Q

Rt hemisphere syndrome

A

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

36
Q

Tx of patients with TBI

A

Cognitive rehabilitation and direct communication training`

37
Q

Cognitive rehab following TBI

A

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

38
Q

Communication Tx following TBI

A

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.

39
Q

Apraxia is often associated with lesions in what area?

A

Broca’s

40
Q

Porch Index of Communicative Ability

A

Samples speech & language skills to only a limited extent

41
Q

Apraxia of speech (AOS)

A

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

42
Q

Locus of AOS

A

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

43
Q

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

A

False. They typically have a reduced rate

44
Q

Characteristics of AOS

A

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

45
Q

Assessing AOS

A

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)

46
Q

Tx of AOS

A

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

47
Q

Progression of Tx of AOS

A

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

48
Q

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

A

loss of skilled movement

-decreased muscle tone

49
Q

UMN indirect activation pathway controls

A

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

50
Q

LMN function

A

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

praxis (20 decks)

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