maggie praxis 4 Flashcards Preview

praxis > maggie praxis 4 > Flashcards

Flashcards in maggie praxis 4 Deck (50):


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


Communication problems in dysarthria include

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


Ataxic dysarthria

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


Ataxic dyarthria physical characteristics

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


Ataxic dysarthria communication characteristics

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


Neuropathology of ataxia

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


Flaccid dysarthria

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


Flaccid dysarthria neuropathology

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


Specific CNs which may be involved in flaccid dysarthria

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


Physical characteristics of flaccid dysarthria

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


Communication characteristics of flaccid dysarthria

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


Hyperkinetic dysarthria

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


Causes of Hyperkinetic dysarthria

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


Physical characteristics of hyperkinetic dysarthria

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


Hypokinetic dysarthria

Results from damage to basal ganglia (extrapyramidal system)


Causes of hypokinetic dysarthria

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


Physical characteristics of hypokinetic dysarthria

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)


Communication characteristics of hypokinetic dysarthria:

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


Spastic dysarthria

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


Physical characteristics of spastic dysarthria

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


Communications characteristics of spastic dysarthria

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


Mixed dysarthrias

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


Mixed flaccid-spastic

associated with ALS


Characteristics of mixed flaccid-spastic

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


Mixed ataxic-spastic

associated with MS


Characteristics of mixed ataxic-spastic

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


Unilateral Upper Motor Neuron Dysarthria

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


Causes of UUMN dysarthria

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


Physical characteristics of UUMN dysarthria

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


Communication characteristics of UUMN dysarthria

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


Assessment of dysarthria

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)


Treatment of dysarthrias

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


Tx procedures dysarthria

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


Dementia is associated with

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


Rt hemisphere syndrome

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


Tx of patients with TBI

Cognitive rehabilitation and direct communication training`


Cognitive rehab following TBI

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


Communication Tx following TBI

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.


Apraxia is often associated with lesions in what area?



Porch Index of Communicative Ability

Samples speech & language skills to only a limited extent


Apraxia of speech (AOS)

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


Locus of AOS

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


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

False. They typically have a reduced rate


Characteristics of AOS

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


Assessing AOS

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)


Tx of AOS

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


Progression of Tx of AOS

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


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

loss of skilled movement
-decreased muscle tone


UMN indirect activation pathway controls

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


LMN function

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