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Motor Speech Dis.

Exam 2

Flaccid Dysarthria Site of Lesion Lower Motor Neuron (Cranial Nerves)
Flaccid Dysarthria Etiology Results from impairment to Final common pathway
Flaccid Dysarthria Associated Disorders Bell's Palsy, Bulbar Palsy, Myesthenia Gravis
Flaccid Dysarthria Neurologic Characteristics -fasciculations (quivering) -atrophy (very weak muscles) -flaccid paralysis -hyporeflexia/ -Hypotonia (muscle fibers are completely paralyzed for both reflexes and voluntary movements)
Flaccid Dysarthria Speech -Vocal Cord Paralysis- unilateral or bilateral -Breathiness -Inspiratory Stridor- vocal cords open so breather in and hear breath -Short Phrases -Monotony of pitch and loudness
Flaccid Dysarthria Resonance -hypernasality- air through nose -nasal emission
Flaccid Dysarthria Articulation -imprecise consonant articulation -possible inadequate intraoral pressure -can be unintelligible
Flaccid Dysarthria Swallowing -may have significant problems
Flaccid Dysarthria Other Problems DAB Clusters •Phonatory incompetence •Resonatory incompetence •Phonatory prosodic insuffienciency - Myesthenia Gravis • Reduced acetylcholine • Eye movement: ptosis, diplopia • Progressive muscle weakening with use: Gets better with rest
Spastic Dysarthria Site of Lesion Upper Motor Neuron of corticobulbar tract
Spastic Dysathria Etiology CVA, tumor, trauma -unilateral damage has mild effect -bilateral damage is more devastating
Spastic Dysarthria Associated Disorder Pseudobulbar Palsy
Spastic Dysarthria Neurologic Characteristics -slow movement/reduced range of movement -spastic paralysis • Unilateral: -nasolabial flat/tongue deviates to weak side • Bilateral (Pseudobulbar): -poor tongue and lip mobility/reduced velar movement/hyperreflexia (gag) -pseudobulbar laugh/cry
Spastic Dysarthria Speech -harsh, strained, strangled -audible grunts -low F0
Spastic Dysarthria Resonance -hypernasality (WITHOUT nasal emissions)
Spastic Dysarthria Articulation -imprecise consonant articulation -slow -can be unintelligible
Spastic Dysarthria Swallowing -difficulty with oral transit and aspiration even with unilateral damage
Spastic Dysarthria Other Problems -DAB characteristics • Prosodic excess • Prosodic insufficiency • Articulatory-resonatory incompetence
Ataxic Dysarthria Site of Lesion Cerebellum or damage to pathways to/from the cerebellum
Ataxic Dysarthria Etiology Stroke, tumor, trauma, MS, alcoholic degeneration, degenerative diseases
Ataxic Dysarthria Neurologic Characteristics -disruption of coordinated movement failure to coordinate sensory data with motor performances, staggering or reeling gait -decomposition of movement  breakdown of coordination
Ataxic Dysarthria Neurologic Characteristics II -dysmetria- overshoots/undershoots -dysdiadochokinesia- inability to perform rapid alternating movement of muscles [ppp kkk ggg] -rebound- inability to predict or stop/ dampen movement -hypotonia- decreased muscle tone
Ataxic Dysarthria Neurologic Characteristics III -intention tremor- hand tremors when you have intention to do something -nystagmus- abnormal rhythmic oscillation of eyes -pendular reflexes -abnormal response to a stimulus -slow movement -positive Rhomberg- cant stand with eyes closed and on one leg
Ataxic Dysarthria Neurologic Characteristics IV -intention tremor- hand tremors when you have intention to do something -nystagmus- abnormal rhythmic oscillation of eyes -pendular reflexes -abnormal response to a stimulus -slow movement -positive Rhomberg- cant stand with eyes closed and on one leg
Ataxic Dysarthria Speech -may be normal or excessive loudness or pitch variation -may be coarse voice tremor
Ataxic Dysarthria Resonance -Velopharyngeal functioning is intact
Ataxic Dysarthria Articulation -imprecise consonant articulation (DAB) -vowel distortion -difficulty with continuous articulation sounds: /r,l/ diphthongs -timing errors = distortion
Ataxic Dysarthria Prosody -prolongation of intervals -speech may have explosive or scanning quality
Ataxic Dysarthria Other Problems -Excess and equal stress (prominent DAB feature) -emphasizes stressed and unstressed syllables -may seem like DRUNK -prolongation of intervals -speech may have explosive or scanning quality
ALS Site of Lesion Mixed UMN and LMN
ALS Etiology Unknown, degeneration of UMN and LMN
ALS Neurologic Characteristics -fasciulations -atrophy of tongue muscles -slow movement -reduced range -spasticity usually present unless LMN damage is well advanced -weakness of oral musculature
ALS Speech characteristics (symptoms similar to pseudobulbar palsy) -harsh, strained, strangled (may show predominantly bulbar signs) -breathiness -inspiratory stridor
ALS Resonance -hypernasality -nasal emission not prominent
ALS Articulation -imprecise consonant articulation -vowel distortion -slow -unintelligible in later stages
ALS Swallowing -varies with stages -aspiration with LMN damage -dysphasia parallels loss of speech
ALS Other Problems Stages: S1: no speech dis. S2: obv. Speech disorder but still intelligible S3: Reduced intell. S4: Speech supplemented- natural speech is no longer functional S5: No functional speech -respiration is very affected
MS Site of Lesion Mixed Spastic and Ataxic - Progressive demyelinating disease
MS Neurologic Characteristics Early: -diplopia (blurred vision) -transient parasthesias -mild weakness Later -marked gait difficulty -dysarthria -significant weakness
Hypokinetic Dysarthria Site of Lesion Basal Ganglia- reduces movement -idiopathic (doesn’t know where it comes from) degenerative changes in Substantia Nigra causing deficiency in the neurotransmitter dopamine
Hyperkinetic Dysarthria Site of Lesion Basal Ganglia- failure to inhibit involuntary movement -seen in association with a variety of extrapyrimdal disorders
Hypokinetic Dysarthria Associated Disorder Parkinson's
Hyperkinetic Dysarthria Associated Disorder Huntington’s Chorea (opposite of parkinson’s  too much movement that you have no control over) - Dystonia
Hypokinetic Dysarthria Neurologic Characteristics -dementia -dampens/modulates -resting tremor- pill rolling -rigidity -bradykinesia= reduced speed of movement -akinesia/hypokinesia =lacking spontaneous movement, slowness in initiation and execution of all voluntary movement
Hypokinetic Dysarthria Neurologic Characteristics II -masked facies -stooped leaning posture -festination- little steps, barely go far, will see increase in rate but reduced in range -dementia
MS Speech -harshness -impaired loudness -pitch control impaired
Hyperkinetic Dysarthria Neurologic Charqacteristics -dementia -involuntary movement -choreic movements • Rapid, coordinated but pointless -limbs are hypotonic -posture cannot be maintained
Hyperkinetic Dysarthria Neurologic Characteristics II -facial grimacing -tongue protrusion -may be triggered by attempt to speak -continuous, arrhythmic, slow movements-stop during sleep
Hypokinetic Dysarthria Speech -hoarseness -breathiness -monotony- not much variation -higher than normal F0
Hyperkinetic Dysarthria Speech -harsh strained, strangled -Voice stoppages -pitch breaks -excess loudness variation -decreased F0 -tremor palatal myoclonus
MS Resonance Possible hypernasality
Hypokinetic Dysarthria Resonance Possible hypernasality with brain stem involvement
Hyperkinetic Dysarthria Resonance Hypernasality
MS Articulation Variable
Hypokinetic Dysarthria Articulation Imprecise = less range in movement
Hyperkinatic Dysarthria Articulation -dysarthria amount depends on oral mechanism -variable articulation -imprecise consonants -distorted vowels -place and voicing errors -prolonged phonemes
Hypokinetic Dysarthria Respiration Decreased Intensity
Hyperkinetic Dysarthria Respiration Excessive loudness
MS Prosody -impaired emphasis (DAB term) -excess or equal stress
Hypokinetic Dysarthria Prosody -pallilalia- I’m good. I’m good. I’m good. -festination of rate- speech is sped up
Hyperkinetic Dysarthria Prosody -overall prosodic deviations -slow rate
MS Other problems Charcot’s triad: nystagmus, diplopia, and dysarthria
Hyperkinetic Dysarthria Other Problems -myoclonus- twitching -ballism- flailing limbs -tics- brief, unsustained, recurring, compulsive movements - swallowing is a complaint -Athetosis: CP -Lingual-facial-buccal dyskinesia:slow writhing movements -Essential tremor-voice
Assessment is the process by which decisions about intervention are made
Description is the characterization of the features of a disorder
intellegibility degree to which the acoustic signal (i.e., utterance produced) is understood by the listener
Comprehensibility degree to which a listener understands an utterance produced by a speaker in a particular communication context
You are asked to see a patient for "slurred speech." On exam you note this is tongue deviates to the left, with atrophy and fasciculations. Where in the nervous system is the damage most likely to be? left hypoglossal nerve - The presence of atrophy and fasciculations is only seen in flaccid paralysis (LMN disease). LMNs innervate ipsilateral muscles
Cerebellar Damage Positive Rhomberg Intention Tremor
UMN damage Positive Babinski Emotional Lability
LMN Damage Fasciculations Hyporeflexia
Basal Ganglia Damage Resting Tremor Festination
Abnormal Oral Motor Develeopment in CP Spastic and dyskinetic cerebral palsy are characterized by persistent primitive reflexes which interfere with a childs's ability to reach appropriate developmental oral-motor milestones
Apraxia is different from Dysarthria 1. consistency (dysarthria) vs. variability (apraxia) of errors 2. apraxic errors cannot be explained on the basis of weakness or incoordination
Apraxia is inconsistent Inconsistency is a hallmark of apraxia of speech. However, errors can be predicted on the basis on phonetic and syllabic complexity.
Dysarthria a collective name for a group of related speech disorders that are due to disturbances in muscular control (weakness, slowness, or incoordination) of the speech mechanism due to damage to the central or peripheral nervous system or both
Frenchay Dysarthria Assessment 7 sections: -first 6 sections assess function of reflexes, respiration and various articulators (for speech and nonspeech tasks) -last section assesses intelligibility -typical profiles available for various types of dysarthria
Assessment of Intelligibility of Dysarthric Speech (AIDS) -designed to provide a clinician-judged technique for measuring intelligibility in a clinical setting -provides objective measure of sentence and single word intelligibility during a reading or imitative speaking task
AIDS measurers obtained Single word intelligibility (50 words) Transcription Forced choice Sentence intelligibility Transcription Speaking rate Rate of intelligible speech Communication efficiency ratio
AIDS tasks *sentences vary from 5 - 15 words -also allows measurement of speaking rate -can get a measure of intelligibility (intelligible WPM) -may be useful in distinguishing mild from normal speakers (when single word production seems OK)
AIDS measures Intelligibility (%) Speaking rate (WPM) Rate of Intelligible Speech (IWPM) Rate of Unintelligible Speech (UWPM) Communication Efficiency Ratio
Cerebral Palsy -most common childhood handicapping condition in the US -brain injury either during gestation or before 3 years of age -incidence = 1.5-3/1000 live births estimates of dysarthria secondary to CP = 31-88% associated with low birth weight/prematurity
Hallmarks of Cerebral Palsy (Primitive postural reflex) -Tonic neck reflex ('fencing posture’) -Positive supporting reaction -Infant makes automatic stepping movements when suspended vertically -Moro reflex (startle reflex) -Sucking and rooting response -Will turn toward stimulus and begin sucking
Hallmarks of Cerebral Palsy persistence of primitive reflexes delays in achieving developmental milestones infant may display poor feeding ability, irritability, or disordered sleep patterns; later on, may evidence poor balance and an early hand preference
Cerebral Palsy Spastic Syndrome -spastic hemiplegia/hemiparesis dysarthria and dysphagia not usually a big problem arm>leg -spastic diplegia (Little’s disease) difficulty sitting, walking, running - little difficulty with hands and fine motor -spastic quadriplegia (limb weakness)
Cerebral Palsy Spastic Syndrome Neurologic Characteristic -weakness -movement velocity deficits -increased muscle tone with hyperactive stretch reflexes and +Babinski -persistence of primitive reflexes -distal portions of arms and legs usually more affected than trunk
Cerebral Palsy Dyskinetic Syndrome -basal ganglia play role in initiating and regulating movement lesions of BG typically result in involuntary movement, with both reductions dysarthria and dysphagia are common
Cerebral Palsy Dyskinetic Syndrome Speech irregular articulatory breakdowns inappropriate silences prolonged intervals and speech sounds excessive loudness variation voice stoppage may be velopharyngeal incompetence
Cerebral Palsy Ataxic Syndromes influences both posture and voluntary movement cerebellum receives info from the cortex re: initiation of movement so that it can make appropriate adjustments in muscle activity
Cerebral Palsy Ataxic Syndrome Neurologic Characteristics errors in rate, range, force and direction of movement overshoot or undershoot spatial targets wide-based ataxic gait hypotonia
Cerebral Palsy Ataxic Syndrome Speech Characteristics reflect impaired coordination may have difficulty coordinating respiratory activity with other aspects of speech
Apraxia an acquired disorder caused by damage to cerebrum, characterized by loss of the ability to execute or carry out learned purposeful movements, but not caused by incoordination, sensory loss, or deficits of comprehension. MOTOR PLANNING
Apraxia of Speech Disorder of speech resulting from neurologic impairment affecting the motor programming of speech (Darley, Aronson & Brown, 1975)
Motor Speech Processing 3-stage/process division of the motor system planning programming execution
Factors Affections Errors in AOS Syllabicity effects Syllable frequency/length/boundary Clusters within syllables tend to be more difficult than cluster across boundaries (e.g., stake vs. mistake) Word complexity More segments/syllable or syllables/word = more errors
Stage 1: Birth -3 months infant possesses a pool of reflexes, or automatisms, that subserve survival rooting reaction suckle-swallow reflex reflexive closure of vocal folds
Stage 2: 4 - 12 months Cortical control emerges, and patterns become less automatic. Modification of early patterns results in greater variability. Separation of tongue and lip movements from jaw movement appears in feeding but not in sound play.
Stage 3: 12 - 24 months Higher levels of cortical control and sensory integration provide further modification of feeding movements. Previously meaningless oral movements become associated with verbal language. Feeding development involves
Stage 4: 24 - 36 months Both feeding and speech movements can be executed at voluntary or automatic levels. New movements are learned at the cortical level, although the execution of automatic and routine feeding and speech patterns are mediated at a subcortical level.
Beyond Stage 5 High-level systems of fine movement control refine speech production above the level of movement control necessary for feeding. Adult-like stability of speech motor control is probably not achieved until at least 8 years of age
Connection between Feeding and Speech Possible correlations between motor skill development for feeding and for speech Patterns of sucking, swallowing, biting and chewing may provide basic movement patterns that are modified for speech.
Connection between Feeding and Speech II Possible that the organization of sensory information guides flexible and fluent movement patterns feeding may provide a multisensory environment with frequent opportunities to organize and reorganize sensorimotor control.
Connection between Feeding and Speech III Abnormal oral-motor development affects the emergence of the normal components that lead to efficient feeding and speech
Stability Oral stability Depends on development of neck and shoulder girdle stability and control Facilitates efficient movement for feeding and speech



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