CMD Exam 3

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oSpeech is effortless in nature oEasy, rapid, rhythmic, even flowing
oMarked by word or phrase repetitions, interjections, pauses, and revisions All people produce disfluencies some of the time
oUnusual, tense disfluencies that interfere with communication \-Most common form of fluency impairment \-Acquired/ neurogenic stuttering- in adulthood due to brain damage or emotional trauma
oRapid bursts of dysrhythmic, unintelligible/ not comprehendible speech
Primary stuttering behaviors (stuttering-like disfluencies) -b-b-b-b-b-b-b-baseball
Audible sound
Primary stuttering behaviors (stuttering-like disfluencies) -mmmmmmmotorcycle
inaudible sound
Primary stuttering behaviors (stuttering-like disfluencies) -B------------baseball
Primary stuttering behaviors
Repetition, audible sounds, and inaudible sounds
Secondary stuttering behaviors
counterproductive behaviors, become more automatic, and more distracting than primary behaviors
Myths about stuttering
People who stutter are more introverted than people who do not stutter, people who stutter are more anxious and nervous than people who do not stutter, parents of children who stutter are more anxious and sensitive than parents of children who do not stutter, people who stutter have lower intelligence than people who do not stutter, people who stutter have less self-confidence than people who do not stutter
Etiology of stuttering
Dynamic relationships between: o Inherited traits -Temperament, cognitive abilities, language abilities, attention, perception, speech motor control o External conditions -Parental expectations, relationships with others, child-rearing practices, educational experiences
development of stuttering
•Usually gradual oSometimes develops suddenly • Genetic predisposition o15% first-degree relatives • Balance between demands and capacities oNeurological development oLanguage development oEmotional constancy
Stuttering Assessment
• Interviews and case history • Speech samples • Language development • Consistency- stutter on same word (reading same passage twice) • Adaptation • Feeling and attitudes • Trial therapy
measures (stutter)
• Non-stuttering disfluencies (phrase repetitions, revisions) vs. stuttering-like disfluencies • Frequency of stuttering o 500 total words o 76 words were stuttered o (76/500) x 100= 15.2% • Percentage of each disfluency type o 76 words were stuttered o 21 words contained sound prolongations o (21/76) x100 = 27.6% prolongations
Stutter Modification (treatment)
\-client is taught to stutter less and more easily \-speech is more natural \-considerable focus on attitudes and negative reactions to speaking situations
Fluency Shaping (treatment)
\-client is taught to have stutter-free speech \-loss of speech naturalness -little to no attention given to attitudes, negative reactions, and so on
Vocal hygiene
Cause of voice disorders
• Abuse/misuse- screaming, excessive use, untrained singing, etc. • Medical- nervous system damage, cancer, virus, etc. • Psychogenic- emotional stress, unresolved psychological issues, etc.
swelling of the vocal folds
reduction of tissue
increased muscle activity
decreased muscle activity
Aphonia (vocal quality)
loss of voice
harsh voice (vocal quality)
excessive muscle tension
breathy voice (vocal quality)
partial whisper
hoarse (vocal quality)
both breathy and harsh
conversation aphonia/ dysphonia
o Psychogenic problem- no organic cause o Normal phonation in vegetative functions (coughing, gurgling, laughing)
o High pitch voice by postpubertal male o Easily corrected
Muscle tension dysphonia
o Simultaneous contractions of adductors and abductors- tension in the laryngeal muscles o Type A personalities
vocal fold paralysis
o Recurrent laryngeal nerve of the vagus (X) damage: unilateral paralysis o Move the affected fold closer to midline
spasmodic dysphonia
o Rare: 1-2 ppl per 10,000 o Basal ganglia is affected o Adductor SD: strain-strangle voice quality o Botulinum toxin (BOTOX) injections at 3–6-month intervals is the most effective treatment
o HPV o Wart-like growths o Usually disappear without treatment -If get too large may compromise airway
o 11,000 new patients each year o 75% are on the vocal folds themselves o Exposure to inhaled smoke- smoking and drinking together dramatically increases risk -15-20% require laryngectomy
contact ulcers
o Ulcers on the vocal processes of the arytenoids o Excessive slamming during low pitch, nonproductive throat clearing/ coughing, gastric reflux, intubation
vocal nodules
o Callous-like growths o 20% of patients with voice problems o “screamer’s nodules” o Form in pairs: greatest amplitude of vibration o bilateral
vocal polyps
o 10% patients with voice disorder o Blister-like growth o Unilateral
voice evaluation
•Managed by a team •Patient interview o Vocal hygiene •Judgement of quality •Instrumental evaluation o Endoscopy o Visipitch
voice therapy techniques
• Counseling • Vocal hygiene education • Yawn-sigh • Respiration training
• Surgical removal of the larynx due to cancer • Trachea redirected to stoma
laryngectomy treatments
•Esophageal speech •Electrolarynx o Handheld battery-operated device o Mechanical quality of voice •Tracheoesophageal puncture (TEP)
acquired apraxia of speech
•Disorder in planning, programming of motor speech movement caused by damage to left, frontal lobe •Speech sound errors o Based on imprecise consonants, substitute simple sounds for complex sounds •Prosodic impairment o Slow rate, prolonged consonants, and vowel, pauses between words, even stress on syllables
childhood apraxia of speech
•Causes have not yet been identified; researchers disagree •Severe speech delays o Words dominated by simple syllables shapes and early developing sounds o Vowel errors o Inconsistent speech sound production o Altered intonation and word stress
•Speech disorders due to damage to the central and/ or peripheral nervous system pathways •Involves all major subcomponents of speech production o Respiration, phonation, resonance, and articulation •Cerebral palsy causes congenital dysarthria
cerebral palsy
•A syndrome of deficits resulting from injury to the nervous system at or shortly after birth •the child’s muscles are weak, paralyzed, and/ or uncoordinated •different types •causes dysarthria in children
causes of cerebral palsy
•prenatal o anoxia (lack of 02), disease, metabolic problems •perinatal o anoxia from umbilical cord problems (strangulation) o premature separation of the placenta o brain trauma •postnatal o brain trauma
Types of dysarthria
• Flaccid- muscle weakness & atrophy, hypernasal, nasal emissions, breathiness • Spastic- muscles fight against stretching, hypertonicity, articulatory imprecision, slow rate, short phrases, harsh voice quality, reduced loudness, and pitch variation • Ataxia • Hypokinetic- Parkinson’s disease, damage to basal ganglia, hypertoned and rigid muscles, resting tremor, monopitch and loudness, accelerated movements and short rushes of speech • Hyperkinetic • mixed
Assessment of dysarthria
• oral-peripheral examination o structures and speech • look at reflexes and voluntary movement of structures during speech and non-speech tasks • speech sample/ intelligibility rating
o Difficulty or an inability to swallow o May be unable to consume enough food and liquids safely o Social impact -food  social gathering
when food enters the airway
Normal swallow

oAnticipatory- Smelling, salivate, getting ready to taste, sight- Avoid potential harm (food poisoning)

oOral- Preparatory- chewing- Transport- swallowoPharyngeal- Protection of the airway*- Esophagus opens to take in the food

oEsophageal - Bolus moves throughout esophagus in peristaltic waves

Anticipatory stage
•Before food reaches the mouth •Sensory information helps person prepare for food o Sensory info- visual & olfactory •Allow person to discriminate desirable and undesirable things to eat
•Preparatory o Food chewed and mixed with saliva (bolus) •Transport o Tongue pushes the bolus up against the palate and moved it posteriorly toward the pharynx o Size and consistency of bolus dictate lingual strength needed
•Purposes o Protect the airway o Direct bolus to the stomach •Swallow is triggered by sensory information sent to the brain •Upper esophageal sphincter opens •Velum elevates and contracts •Epiglottis covers larynx and larynx moves up and forward
•Begins when larynx lowers backward o Breathing continues •Esophageal peristalsis o Peristalsis- synchronized smooth muscle contractions
Causes of dysphagia in adults
\-stroke \-dementia \-traumatic brain injury neuromuscular disease \-cancer
Modified barium swallow study
o Barium-coated food o Fluoroscope images taken by radiologist o Can visualize pharyngeal stage & any aspiration
bedside clinical assessment
oAssess ability to take food off plate (cognitive/ motor skills) \- Level of alertness \- Oral-motor exam (lips, tongue, initiation of the pharyngeal swallow) \- Upward movement of larynx? \- Coughing? \- Gurgling sound?
Dysphagia treatments
•Positioning o Upright: direct food to esophagus •Environmental modifications o Cueing, reminders •Special spoons/cups •Change food consistency o Thickened liquids •Teach new swallowing patterns o Dry swallows
Causes of brain damage
•Cerebrovascular accident (CVA), strokeso Embolus: moving clots from another part of the body o Thrombosis: Clot from gradual accumulation of plaqueo Hemorrhages: bleeding in brain Aneurysm: weakening in the artery that bulges and breaks
tissue death
spontaneous recovery
neural reorganization
classification of aphasia
• Broca’s • Wernicke • Conduction • Anomia • Transcortical • global
Broca's aphasia
• Lesion to Broca’s area • Nonfluent, awkward verbal expression • Short phrases and sentences • Slow rate • Agrammatism • Auditory comprehension is minimally impaired Ex: Work-desk-sales
Wernicke's aphasia
• Damage to Wernicke’s area • Impaired auditory comprehension • Fluent speech • Verbal paraphasias (fork for spoon) • Neologisms oMaking up new words • Poor repetition Ex: full sentences but not clear at all Varely (ex of neologism used) “I’m doing happy”
Global aphasia
• Wide lateral damage to the left hemisphere • All parts of language processing severely impaired oNonfluent oPoor comprehension oPoor repetition
Assessment of aphasia
• Immediately following brain injury oSpontaneous recovery (SR): first few weeks • More formal assessment following SR oConversation oFormal diagnostic testing oRepetition oReading and writing
Aphasia treatment
•Empower the patient to communicate successfully •Communication tasks to activate neural plasticity mechanisms •Cues and prompts- pictures, phonemic cues, phonological rhyming, etc. •Compensatory strategies •Family support groups •Constraint-induces therapy o Inhabit use of intact language skills o Encourage use of impaired language skills •Augmentative communication systems •Supported communication for aphasia o Focuses on training of conversational partners
Traumatic Brain Injury
Head injury o Brain trauma - Neurological damage caused by injury to the head from motor vehicle accidents, falls, blast trauma, etc. o Damage to multiple parts of the brain as well as connecting fibers.
brain bruises
tearing of structures and vessels
areas of encapsulated blood \-intracranial: within the brain \-meninges: in the tissue surrounding the brain
TBI therapy
•Focuses on the deficits revealed from the assessment o i.e. memory- visual association to facilitate memory, external memory aids, written schedules o reasoning or problem solving- use scenarios
Sports concussion
Short-term period of confusion and loss of memory following injury to the head o Symptoms resolve after a period of rest when sensory stimulation is minimized o Major concern is that repeated exposure may result in progressive degenerative disease o Important for SLPs to establish cognitive function and monitor changes resulting from concussion
• Deterioration of cognitive and language abilities resulting from progressive degeneration of the brain • Alzheimer’s disease is the most frequent etiology • Other types of dementia: Vascular, Huntington’s, Frontotemporal • Progressive degeneration of both hemispheres of the brain • Problems with working memory, orientation, reasoning, judgment
Causes of dementia
• Hereditary disorders • Vascular disease • Viruses • Incidence of the disorder increases with age
Assessment of dementia
•Identifying cognitive deficits and lrvel of impairment •Neuropsychologist & SLPs to assess: o Orientation o Memory o Self-case o And other areas
dementia treatment
•Reminiscence therapy o Individually pr in a group o Use old photographs, objects, videos that have important meaning to trigger long-term memory of events o Conversation related to the event works to foster orientation and episodic memory •Spaced retrieval training o Present new or remembered information o Increase length of time interval that the information is remembered
Goals of AAC
facilitate expressive and receptive communication o Augmentative: supplementing communication o Alternative: replacement of natural speech and/or writing
Primary components of an AAC system
•Symbols o Unaided o Aided o Graphic \-Iconicity \-Transparent \-Opaque \-Translucent