speech disorders final

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  1. CNS
    • Brain (cerebrum, cerebellum, subcortical structures, brainstem)
    • Spinal cord
  2. PNS
    • Contains nerve fibers that connect the CNS to the muscles & sense organs
    • 12 pairs of cranial nerves; 31 pairs of spinal nerves; sensory receptors.
  3. neurons & neural transmission
    • Neurons: smallest unit of nervous system. It contains dendrites (receive info from other neurons); cell body; axon (pass the info to other neurons); some axons are covered with myelin sheath (white fatty substance), myelin electrical insulation & faster conduction
    • neural transmission: synapse- point of comm. b/w neurons or b/w neuron & muscles; synaptic cleft- space b/w axon & dendrite or muscle fibers; a chemical transmitter released by the axon of one neuron drifts across the synaptic cleft & stimulate the dendrite of another neuron or stimulate the muscle fibers.
  4. 6 lobes of cerebrum
    frontal, parietal, occipital, temporal, insular, limbic
  5. important areas
    • Frontal: broca’s area (44)- important for speech motor planning; precentral gyrus (4, 6)- site of initiation of voluntary motor movement; supplementary motor area- precise role not known, overall believed to contribute to motor control; motor strip & SMA gives rise to the corticospinal & conticobulbar tracts, which allows for contralateral innervation
    • Parietal: primary receptor site for somatic (body) sense; postcentral gyrus (3, 1, 2)- sensory counterpart to motor strip
    • Temporal: site of auditory reception; important for auditory & receptive lang processing; heschl’s gyrus (41)- all auditory info in projected here; wernicke’s area (22)- damage here results in disturbances of spoken lang decoding
  6. insula & limbic lobe functions
    • Insula: present beneath frontal, parietal, & temporal opercula. Possible roles- perception, motor control, self-awareness, cognitive functioning, & interpersonal experience
    • Limbic lobe: present in medial surface of each hemisphere. Functions- homeostasis, olfaction, memory, emotion
  7. functions of important subcortical structures
    • Thalamus: motor control; receives auditory, somatosensory, & visual sensory signals; relays sensory signals to the cerebral cortex; controls sleep & awake states
    • Basal ganglia: related to control of background movement (postural & supportive aspects) & initiation of movement; possibly coordinates slower components of speech
    • Cerebellum: automatic motor coordinating center- coordinates motor commands with sensory inputs to control movement; controls balance, posture, & synergy of voluntary movement (mainly proprioception); probably coordinates rapid speech movements
  8. cranial nerve, origin, & function
    • Trigeminal (V): bilateral; pons; jaw movement, face, mouth, jaw sensation
    • Facial (VII): upper face (bilateral), lower face (contralateral); pons; facial movement, hyoid elevation, stapedius reflex, salivation, lacrimation, taste
    • Glossopharyngeal (IX): bilateral; medulla; pharyngeal movement, pharynx & tongue sensation, taste
    • Vagus (X): bilateral; medulla; pharyngeal, palatal & larygeal movement, pharyngeal sensation, control of visceral organs
    • Accessory (XI): bilateral; medulla; shoulder & neck movement
    • Hypoglossal (XII): contralateral > bilateral; medulla; tongue movement
  9. role of spinal nerves in speech process
    31 pairs; exit thru spinal column; for speech, these serve the respiratory apparatus- innervate muscles of chest wall
  10. speech motor control-Neuroanatomical & Functional Divisions
    • Final common pathway (FCP): consists of cranial nerves & spinal nerves. These neurons are called lower motor neurons (LMN)
    • Direct activation pathway (pyramidal tract): direct connection to final common pathway (the neurons in this pathway are called UMN). Consists of corticobulbar & corticospinal tracts
    • Indirect activation pathway (extrapyramidal tract): multiple synapses b/w cortex & FCP. The neurons in this pathway are also called UMN. Consists of- corticoreticular tract (b/w cortex & reticular formation), corticorubral tract (b/w cortex & red nucleus), vestibulospinal tract, rebrospinal tract, reticulospinal, & related tracts. They provide input to LMN. They might possibly play a role in regulating automatic (subconscious) muscle activities (tone & posture) & movements that accompany voluntary activities, their precise role in speech not clear.
    • Control circuits: they do not have direct contact with LMNs.
    • Basal ganglia control circuit: fibers from cortex (supplementary motor area & brocas area) project to basal ganglia. Basal ganglia will smooth these movements (tone & posture). They are then sent back to cortex via thalamus. The cortical planning areas modify movement plan based on this input from basal ganglia. The motor commands are then sent to motor cortex. The basal ganglia control circuit is also considered as part of the extrapyramidal system
    • Cerebellar control circuit: fibers from cortex (supplementary motor area & brocas area) project to cerebellum. The cerebellum will smooth these movements based on feedback from muscles. They are sent back to cortex via thalamus. The cortical planning areas modify the movement plan based on this input from cerebellum. The motor commands are then sent to motor cortex.
  11. speech motor control-Theoretical Framework
    • Motor planning: neuroanatomical structures primarily involved- broca’s, wernicke’s, prefrontal cortex, area 6, supplementary motor area (SMA). The dominant hemisphere plays a primary role in motor planning process. At this state the phonological units corresponding to the planned uttereance are converted into motor plans. this stage is articulator specific
    • Motor programming: neuroanatomical structures primarily involved- SMA, basal ganglia, lateral cerebellum, fronto-limbic system & motor cortex. Programming is probably controlled by both hemispheres. This stage is muscle specific. At this stage the spatiotemporal & force parameters (such as muscle tone, velocity, direction, range of movements) & sequence of motor programs for muscle of each articulator are specified.
    • Motor execution: neuroanatomical structures primarily involved- SMA, cerebellum, basal ganglia, motor cortex, thalamus, brainstem, peripheral nerves & motor units. During this stage the hierarchy of motor plans & programs are delivered to the muscles by the LMN (final common pathway). The timely movements of muscles manifests as speech
  12. motor speech disorders
    • A motor speech disorder is caused by neurological impairments interfering with motor planning, motor programming, & neuromuscular execution related to speech.
    • Dysarthria: traditionally was considered a motor execution disorder. Lately some types (parkinson’s disease) are considered to have an impairment at the motor programming level.
    • Apraxia: impaired motor planning
  13. 6 major types of dysarthria & the areas of damage
    • spastic- UMN
    • flaccid- LMN
    • ataxic- cerebellar system
    • hypokinetic- extrapyramidal system
    • hyperkinetic- extrapyramidal system
    • mixed- mulpitle motor systems
  14. spastic dysarthria
    • Most commonly caused by strokes & degenerative diseases. Comes from bilateral UMN damage.
    • Speech characteristics: excess & equal stress, slow rate of speech; strained-strangled-harsh voice quality; imprecise consonant artic; hypernasal; lower vocal pitch; poor respiratory support
  15. flaccid dysarthria
    • Caused by damage to cranial nerves- damage could be due to diff reasons (stroke, degeneration, TBI)
    • Facial VII: bilateral facial nerve damage- inhibited jaw movement, paralysis of lip muscles, weak sounds
    • Glossopharyngeal IX: hypernasal, dysphagia
    • Vagus X: hypernasal, nasal emission, vocal fold paralysis (breathiness, monoloudness), dysphagia
    • Accessory XI: no direct effects on speech, shoulder/head droop
    • Hypoglossal XII: imprecise artic of sounds that depend on tongue movement
  16. ataxic dysarthria
    • Caused by damage to cerebellum. Volitional movements are slow & awkward.
    • Speech characteristics: drunkin speech; impaired force, timing & amplitude of movements; irregular artic breakdown; alternate b/w normal & hypernal speech
  17. hypokinetic dysarthria
    • Caused by damage in & around basal ganglia; associated with degenerative disordered (parkinson’s disease)
    • Speech characteristics: slow initation of volitional speech movements (bradykinesia); rigidity of speech muscles; tremor in speech & respiration muscles; strainied & breathy voice quality, soft, quiet speech; highly variable artic, periods of suddenly rushed speech, & long periods of silence.
  18. hyperkinetic dysarthria
    • Commonly caused by damage to basal ganglia; key feature- involuntary movements.
    • Fast Hyperkinesia (study only Chorea): rapid, unpatterened, unsustained involuntary movements of the trunk, limb, face, tongue, diaphragm [huntington’s chorea]
    • Slow Hyperkinesia (study only Athetosis): continuous, arrhythmic, slow & writhing type of movements that cease during the sleep. Although usually seen in limbs, the muscles of  face, neck & tongue may be affected. [cerebral palsy]
    • Speech characteristics of this type: prolonged intervals b/w consonants; excessive variation in loudness; abnormal silent intervals; variable stress patterns; irregular artic breakdown; sudden forced inspiration-expiration
  19. mixed dysarthria
    Caused by combo of neurologic events or diseases that affect more than one system. Combo of spastic & flaccid is common. Each person will be diff with a diff combo of symptoms.
  20. apraxia
    Apraxia of Speech AOS
    • means action. Motor planning is impaired. 
    • A motor speech disorder in which planning of speech movements are impaired. During motor planning stage, the phonological units corresponding to the planned utterance are converted into motor plans. can co-occur with (broca’s) aphasia & orofacial apraxia
  21. AOS types
    AOS causes
    • Aka verbal apraxia. Childhood apracia of speech (CAS), developmental apraxia of speech DAS, developmental verbal dyspraxia DVD; acquired apraxia of speech. Causes in children usually unknown 
    • Vascular (stroke is leading cause of apraxia in adults); degenerative; traumatic; tumor; other (seizure disorder, multiple causes). Neuropathology: usually a pathologic condition in lang-dominant hemisphere; damage usually in posterior frontal lobe, around broca’s area; damage can sometimes be in parietal lobe
  22. AOS speech characteristics
    • Highly variable errors (hallmark feature- inconsistency in errors); groping during speech; occasional instances of error-free fluent speech. Artic error patterns: substitution errors most common; clusters are more commonly misarticulated; affricates & fricatives are commonly misarticulated; consonant errors more common than vowel errors; syllable transpositions; errors increase as word length increases.
    • Prosody (rate, stress) is usually affected due to artic errors & groping, & attempts to avoid errors
    • Fluency is affected due to false starts, syllable repeptitions, attempts to avoid errors & groping
    • Influence of task: automatic speech (counting, days of week) may be more fluent (& less erroneous) than more thoughtful speech; errors in both imitative & spontaneous speech responses; higher error rate for nonsense words than meaningful words
  23. oral mechanism exam
    • Trigeminal (V): observe jaw at rest, biting, lateral movemnt of jaw, opening mouth, say /pa ta ka/ repeatedly
    • Facial (VII): observe face at rest, smile, raise eyebrows, puff cheeks, closing eyes tightly, frowning
    • Glossopharyngeal (IX): swallowing tasks, gag reflex
    • Vagus (X): observe soft palate at rest, say non nasal sounds, grunting, voluntary cough, swallowing (look for laryngeal elevation), prolong /a/, note voice quality
    • Hypoglossal (XII): observe tongue at rest, lateral 7 vertical movement of tongue, move tongue in & out, try to touch nose with tongue tip, lick lip (circular motion)
    • Dysarthria: look for strength, speed, range, steadiness, tone, & accuracy of oral movements
    • Apraxia of speech: ddetermine if there is co occuring orofacial apraxia (important observation groping while performing nonspeech related oral movements)
  24. dysarthria speech eval
    apraxia of speech eval
    • Assess: pitch, loudness, voice quality, resonance, respiration, prosody, artic, overall speech intelligibility
    • Production of speech movements in isolation & sequence; production of words with increasing phonogical complexity; production of phonologically complex phrases & sentences; overall speech intelligibility
  25. dysarthria intervention
    • Some conditions can be medically treated (Parkinson’s disease); surgical tx is sometimes used to fix paralyzed structures; prosthetic management in some cases (palatal lift appliance to reduce hypernasality); AAC may be appropriate for severe patients or degenerative patients; counseling will often be a large part of tx for degenerative diseases.
    • Specific treatment approaches: intelligibility drills; open mouth approach (to enhance intelligibility); exaggerated artic (to enhance intelligibility); reducing rate of speech (delayed auditory feedback, metronome, pacing board); adequate breath support for speech (inhaling at appropriate linguistic breaks & considering fewer words per breath); feedback (using mirror to show range of movements, clinician’s verbal feedback); provide strategies for listeners to facilitate the comm.
  26. AOS intervention
    • Concentrating on artic; focus on sequencing; focus on volitional motor movements; tx should be intense, frequent, & may take a long time; tx will progress thru a hierarchy; tx of prosody; goal is successful comm., not perfection
    • Things to keep in mind: use automatic speech to practice successful oral motor control; the easiest targets will be visible, short, & artic simple; some clients will try to speak in normal rate, tx should focus on finding them a new, slower rate that will improve intelligibility; work on increasing the delay b/w clinician model & client production; explore the use of diff contexts to find facilitative context; use diff type sof cues to help client; AAC may be appropriate for severe cases; provide strategies for listeners to facilitate the comm.
    • Specific tx approaches: controlling rate & rhythm; constraint-induced therapy; PROMPT (prompts for restructuring oral muscular phonetic targets)- clinician will touch patient’s face to give them tactile cues about which oral muscles to move while producing an utterance; melodic intonation therapy (MIT); 8 step continuum approach
  27. disfluency 
    onset age of stuttering
    lifetime incidence of stuttering
    • An interruption of speech that may be seen as either normal or abnormal; even typically fluent speakers can be momentarily disfluent.
    • b/w 2-5 years old
    • Most studies estimate that around 10% of all individuals stutter at some point in their lives
  28. prevalence of stuttering in school-age children
    • About 2.5% of preschool and school age children stutter; this is true across races & ethnic groups
    • There are about 72 million children in the US; 2.5% of them stutter; 2.5 kids out of every 100 kids will stutter; roughly 1.8 million kids who stutter in the US; 3 boys stutter for every girl who stutters.
  29. familial distribution of stuttering
    A large proportion of people who stutter have relatives who stutter; there is also high concordance for stuttering in identical twins (when one twin stutters, the other one does too); these findings point to a genetic basis
  30. therapy goals of stuttering 
    factors to determine if someone stutters
    • A fluency component; a lang enrichment component; an emotion regulation component; a social skills component 
    • Type of disfluency; freq of disfluency; duration of disfluency; level of effort, tension, & avoidance; self-concept as a communicator
  31. type of disfluency
    • Sould/syllable repetitions; sound prolongation; monosyllabic whole word repetition; multisyllabic whole word repetition; incomplete phrases
    • Primary symptoms of stuttering: audible sound prolongations; silent prolongations (silent blocks); repetitions (part word or monosyllabic, whole word repetitions)
  32. freq of disfluency 
    duration of disfluency 
    self-concept as a communicator
    • People who produce more than 10 or more disflueincies per 100 words tend to be judged as people who stutter. People who produce 2 or fewer disfluencies per 100 words tend not to be judged as people who stutter. Freq can play a general role in determining whether or not one stutters, however, these rules are not hard & fast. 
    • The ave duration of a stuttering-like disfluency is about 1 second. For the most severe stuttering, blocks may last longer than a minute. 
    • Sometimes people who stutter mildly have an exceptionally poor self-concept about their ability to communicate.
  33. secondary symptoms of stuttering
    • People who stutter may do things to avoid stuttering. This usually involves a repertoire of behaviors learned by the person, that are designed to limit the presence of stuttering, hide the presence of stuttering, or assist the person to quickly stop stuttering
    • Gross movements of body (head movement, movement of arm/hands/leg/shoulder); finer movement of body (eye/brow movement, nostril flare, finger/toe movement); breath stream/laryngeal (sudden inhalation before speech, sudden exhalation before/after speech, non-speech vocalizations, pitch changes, volume changes); verbal accessories (starters, retrials, circumlocutions, postponements/stalling, substitutions)
  34. what makes a good clinician
    Empathy, warmth (unconditional positive regard), genuineness (congruence), a preference for evidence-based practice, commitment to continuing education, critical thinking, creative, accurate empathy, non-possessive warmth, genuineness, ability to listen, ability to adjust to quickly-changing circumstances, ability to make quick & accurate behavioral observations
  35. 4 purposes of eval
    • investigate whether or not a person stutters- especially in a young child
    • if the person really does stutter, than another purpose is to characterize the person’s stuttering- core behaviors, secondary behaviors, freq, duration, severity of behaviors, feelings & attitudes about communicating verbally.
    • Assess various factors that may cause or contribute to the persistence of stuttering- trajectory of person’s stuttering; person’s level of awareness about stuttering behaviors; health & family history; history of tx; internal environment/temperament; external environment; expressive lang ability, receptive lang ability, phonological ability, artic ability, reading ability; beliefs about stuttering; motivation for seeking tx; impact of stuttering on the person.
    • Investigate whether or not a client who stutters is a good candidate for therapy
  36. fluency assessment
    • Collect speech sample & exam them. Conversational speech sample (2 100 word samples); reading sample (100 words)
    • Examine types of disfluency, types of secondary stuttering behaviors, freq of core/secondary behaviors, duration of stuttering moments, assessment of speech rates, consistency of disfluency
    • Types of core stuttering behaviors: go thru speech sample & identify disfluencies, coding them on transcript; code each stuttering moment by type; make as many passes thru sample as you need to be sure you’ve identified, correctly-coded each moment of stuttering
  37. consistency of disfluency
    Aka amount of adaptation. Means does stuttering occur with the same freq, same type, same duration, in repeated trials of the same speaking task. Good for diagnosing neurogenic stuttering.
  38. tx goals for stuttering
    Eliminate secondary features; identify/awareness of secondary features; reduce tension in focal points; freq of stuttering; improve self-concept about talking; develop fluency-inducing lifestyle; reduce freq of stuttering; reduce abnormality of stuttering; reduce negative feelings about stuttering & speaking; reduce negative thoughts & attitudes about stuttering & speaking; increase overall comm. abilities; create an environment that facilitates fluency
  39. tx options for stuttering
    • Tx elements: behavioral therapy, cognitive therapy, prosthetic therapy, pharmaceutical/drug therapy.
    • Behavioral therapy: 2 types- indirect & direct (direct- fluency shaping techniques; stuttering modification techniques)
    • Indirect therapy: stuttering & speech production are rarely talking about explicitly. Principles of positive reinforcement & negative reinforcement are applied as the child speaks. The client indirectly learns (thru reinforcement) to extinguish bad speech behaviors, & to acquire/develop/strengthen fluency-inducing speech behaviors. Indirect therapy can be used for borderline stuttering (preschool), mild school-age stuttering.
    • Direct tx: stuttering is talked about explicitly. The anatomy & physiology of speaking are discussed explicitly. The client learns to dissect & explicitly modify their speech patterns.
    • Direct therapy: (fluency shaping)- involves teaching fluency-inducing techniques that allow the client to initiate utterances successfully, & keep the utterances moving forward successfully. (stuttering modification)- involves teaching the client techniques aimed at allowing the client to control & modify moments of stuttering in a way that makes the stuttering less severe; allowing the client to escape from moments of stuttering in a manner that neutralizes the speech behaviors that triggered the stuttering & reinforces speech behaviors that will extinguish stuttering
    • Cognitive therapy: parent counseling; cognitive restructuring (changing thought patterns about speaking, communicating, & stuttering); self-help (an informal sort of cognitive restructuring but still crucially important); client counseling on lifestyle change (life coaching); people who stutter may also seek psychoanalysis/psychotherapy to deal with issues that potentially intersect with their stuttering
    • Prosthetic therapy: usually involves electronic devices designed to trick the system into fluent speaking; delayed auditory feedback DAF, altered auditory feedback AAF (speecheasy), masking, metronomes, computer software with biofeedback-type displays that may facilitate fluent speech production
    • Pharmaceutical: prescription meds aimed at alleviating symptoms of stuttering
    • Other types of tx: hypnosis; regulated breathing
  40. cluttering
    • History: Documented in Europe since 1717. Adults with stuttering only- 55%; stuttering & cluttering- 40%; cluttering only- 5%.
    • Rate abnormality symptoms: An excessive number of disfluencies, the majority of which are not typical of people who stutter. The freq placement of pauses & use of prosodic patterns that do not conform to syntactic & semantic constraints. Inappropriate (usually excessive) degrees of coartic among sounds, especially in multisyllabic words.
    • 4 essential characteristics for a dx: excessive number of whole word or phrase repeptitions; poorly organizaed thinking (speaks before clarifying thoughts); short attention span & poor concentration; lack of complete awareness of problem
    • assessment: speech & lang performance tasks (speech samples, artic tests, lang tests [comprehension & production]); computer-based cluttering assessment tool (uses speech natureness scale); self-awareness measures (self appraisal questionnaires); other (oral exam, audiological eval, samples of motor skills)
    • supplementary assessment tools: cluttering symptoms summary checklist (4 mandatory symptoms, 6 most common facultative symptoms, other facultative symptoms); checklist for possible cluttering (total score); cluttering tx planning profile (speech & motor coordination, lang & cognition, behavioral/pragmatic, developmental)
    • therapy: (increase awareness & self-monitoring skills; improve rate (& artic & speech intelligibility); improve linguistic & narrative skills; improve fluency skills; improve meta-cluttering skills; improve phonatory & respiratory behaviors; improve family, friend, & employer support; improve collaboration with other team members; foster transfer & maintenance); (modifying speech rate & regularity (delayed auditory feedback DAF, self-monitoring with DAF, window reading, breathing modifications, drone-type speaking style, oral motor syllable training program, exaggerated mouth movements); (promoting relaxation & mental imagery (positive self-talk & affirmation); increase awareness of cluttering (video/audio tape, lang of fluency, vibro-tactile feedback, counseling & attitude change, group sessions, interpersonal/listening skills); improving attention span).
  41. neurogenic stuttering
    • What is it: speech dysfluencies acquired secondary to neurologic disease/impairment or insult to the CNS. Aka acquired stuttering, cortical stuttering. Develops in adulthood after adolescence- sudden onset. May occur in isolation or comorbidly with—AOS (trying to reach or correct artic movements o perceptual goals); dysarthria/hypokinetic (difficulty initiating movements due to motor deficits [rigidity, bradykinesia, akinesia]); aphasia (deficits in word retrieval & verbal formulation, trying to revise linguistic errors
    • Symptoms: neurogenic stuttering provides strong evidence for a neurogenic basis for developmental stuttering. Heterogeneous (symptoms differ b/w individuals). Characterized by sound/syllable repeptitions, prolongations, & blocks that disrupt normal rhythm & flow of speech (sound/syllable repeptions most freq). freq ranges from mild to severe. Can be transient or permanent. No pattern on types of words that increase stuttering (content vs function words have  equal probability)
    • Etiology & anatomy: most common etiologies include CVA & TBI (dysfluencies usually present w/in one month post-onset. Degenerative diseases [parkinsons, progressive supranuclear palsy, dementia, motor neuron disease], seizures, metastiatic brain tumors anoxia, bilateral thalamotomy, drug abuse, neurosurgery). Multi-focal & diffuse/bilateral lesions more likely to result in permanent symptoms than single/unilateral lesions. Multiple lesion sites (predominance of left hemi lesions; also associated w/lesions in the right hemi, basal ganglia, supplementary motor area, thalamus, midbrain, pons; spared structures- cranial nerves, occipital lobe)
    • How to assess: speech samples taken under many speaking conditions; client info (background, case history); client reactions to speaking & stuttering; indirect assessments to determine malingering.
    • Neurogenic vs developmental stuttering: where are dysfluencies located (not restricted to initial syllables, occur w/o utterances; occur on both content & function words); which tasks exacerbate or reduce dysfluencies (DAF, choral reading, singing, etc do not improve dysfluencies; no consistent diff b/w spontaneous speech vs imitation); is there an adaptation effect (no improvement with repeated readings); anxiety, avoidance and/or secondary behaviors (common to express awareness & annoyance; no significant anxiety or avoidance of speaking situations; secondaries usually limited to mild facial grimacing)

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