maggie praxis 4 Flashcards
Dysarthria
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?
Broca’s
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
