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COSD Exam 4 Study Guide

by: Maycie Tidwell

COSD Exam 4 Study Guide COSD 10303

Maycie Tidwell
GPA 3.8

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This is a study guide reviewing the concepts that will be tested on the fourth exam.
Survey of Communication Disorders
Study Guide
COSD, Survey, communication, disorders
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This 15 page Study Guide was uploaded by Maycie Tidwell on Tuesday April 5, 2016. The Study Guide belongs to COSD 10303 at Texas Christian University taught by Watson in Spring 2016. Since its upload, it has received 19 views. For similar materials see Survey of Communication Disorders in Nursing and Health Sciences at Texas Christian University.

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Date Created: 04/05/16
COSD 10303: Survey of Communication Disorders Review for Exam 4 Chapter 7: Fluency Disorders 1) What is the difference between the incidence and the prevalence of stuttering? What are the incidence and prevalence of stuttering? What does that mean in terms of recovery from stuttering? Prevalence and Incidence:  Reported lifetime incidence—5%  Vast majority (80%) spontaneously recover  1% of population do NOT spontaneously recover  Male to female ratio = 3 to 1 (girls recover more often)  50% report that they have a relative who stuttered  Recent research indicates that stuttering may be linked to a gene or genes (e.g., chromosomes 3 and 12) Stuttering rates: 5% lifetime incidence 20% persistence rate 1% population prevalence * The longer you’ve been stuttering, the less likely you will spontaneously recover. 2) How can stuttering affect one’s life in school, at work, and in one’s social interactions? Effects of Stuttering:  World Health Organization  Handicap or a handicapping condition: can be, but it doesn’t have to be.  TQ: T or F, stuttering is a handicapping disability. FALSE. (it can be)  “the disadvantages that result from reactions to the audible and visible events of a person’s stuttering, including those of the person who stutters”  Can have a negative effect on variety of daily activities  Children’s school performance  Workplace  Social interactions 3) What are three ways a person who stutters wants a communication partner to react or not react? What Some Persons Who Stutter Tell Us:  How they want their conversational partners to react  Don’t finish sentences  Maintain normal eye contact  Don’t say, “ Think before you talk.”  Don’t say, “Just relax”  Don’t say, “Take a big breath before you speak.” 4) What is meant by the statement “stuttering is more than what you hear the speech of a person?” Stuttering is more than what you hear: -Head: cognitive -Heart: Affective (lead to embarrassment, shame and guilt) -Speech: behavior • * Affected by age, environment (including how others react to his stuttering), time stuttered, previous treatment, cultural background 5) What are normal (other) disfluencies and how do they differ from stuttered disfluencies? Be able to give or recognize examples of all disfluency types. Normal Disfluencies (not stuttering):  Seen in all children  Typically observed when begin combining words (2 -3 years)  Whole word Reps. (with no tension and very few repetitions) and phrase repetitions  Interjections  Revisions  Phrase repetitions ex: “Can I, can I go?” 6) Where in speech does stuttering typically occur? (e.g., on initial words of a sentence) Basic Characteristics of Stuttering:  Loci of Stuttering for Adults  Initial words  Consonants  Longer words  Words used less frequently Ex: “Survey of Communication disorders is a necessary course for SLP majors.” Initial, consonant. Consonant, longer. Consonant. Consonant. 7) Do all children stutter?  NO. 8) Around what age does developmental stuttering appear? Onset and Development of Stuttering:  Onset between 2 and 4 years  Development can be gradual, but not always (only for some kids)  Development can also be sudden!  Severity increases as child ages  General trends regarding:  Stuttering behaviors  Reactions to stuttering(differs with child depending on temperament)  Conditions that appear to promote stuttering 9) What is neurogenic stuttering? How is it different from developmental stuttering? Developmental vs. Neurogenic Stuttering:  Neurogenic stuttering  Associated with disease or trauma  Disfluencies on function and content words  Stuttering typically widely dispersed throughout an utterance  Developmental stuttering  Disfluencies on content words  Secondary behaviors  Stuttering typically on initial syllables 10) What is thought to be the cause of stutter? What do we know does NOT cause stuttering? No Definitive Etiology (Cause):  Evidence of genetic component (runs in families)  Neurophysiological difference  May be exacerbated by environmental things, but not causes by.  Evidence of differences in brain structures and function  NO evidence for  Neurosis  Learning it from others  Environment does NOT CAUSE stuttering Theories and Conceptualizations of Stuttering:  Organic Theory: physical cause  Theory of cerebral dominance  Modified vocalization hypothesis  Discoordination between muscles of phonation  New developments in medical technology  Studying the central nervous system  Preliminary findings: stuttering linked to failure of neurophysiological system that integrates motor, linguistic, and cognitive processes  Behavioral Theory: learned response to external conditions  Wendell Johnson—diagnosogenic theory- NO SUPPORT FOR THIS THEORY (not wanting to make it worse by mentioning it to child)  Originally diagnosed by lay person (parents)  Stuttering begins in the parent’s ear  Behaviors the child exhibits are, by and large, hesitations and repetitions normally seen in children  Stuttering disorder occurs after being diagnosed  Parents react with increased criticism and punishment  Psychological Theory: neurotic symptom with ties to unconscious needs and internal conflicts- NO SUPPORT FOR THIS THEORY.  Current conceptual models:  Covert repair hypothesis  Demands and capacities model (DCM)- demands exceed capacities of child.  EXPLAN model  Failure in interactions between the PLAN and Execution of speech  What are the three factors that are thought to interact to cause stuttering (as discussed in class)?  What is the organic theory of stuttering?  What is the diagnosogenic theory? Is there evidence that this theory may be true? 11) What do we mean when we say stuttering may be a disability but not a handicap?  Stuttering is a disability but it is not a handicap because it does not hinder people from doing what they want to do. 12) Describe the basic procedures used in the indirect and direct treatment approaches in treatment of children who stutter? Stuttering Intervention for Young Children:  Indirect approach: Stuttering is mild and has just started  We change the environment  GOAL: facilitate fluency through environmental manipulation  No explicit discussion with child  Information sharing and counseling with parents  Direct approach: Stuttering is moderate to severe and has been present for over a year  Direct/explicit attempts to modify child’s speech  “hard” vs. “easy” speech  Teach strategies that help increase easy speech  Lidcombe Approach:  For preschoolers who stutter  Evidence based treatment  Behavioral treatment (operant)  Focuses on speech, not feelings/emotions  Treatment done by parents  Goal of treatment: no stuttering  Teaches the parents how to do verbal contingencies during conversation with child  Speech language pathologist trains the parent/caregiver to provide safe and accurate feedback  5 to 1 ratio (5 praises for each correction)  What is the therapy approach most often used at the Miller Speech and Hearing Clinic for young preschool children who stutter? Why does Watson believe it is so effective? 13) Describe the goals and basic procedures associated with fluency shaping and stuttering modification approaches to stuttering treatment. Therapy Techniques with Older Children and Adults:  Fluency-Shaping Techniques  Prolonged speech (slowed down)  Light articulatory contacts and gentle voicing onsets  Pausing/Phrasing  Response-contingent stimulation  Stuttering Modification: teaches the person to change the way they stutter  Cancellation phase  Pull-out phase  Preparatory sets  Best technique for people with a lot below the water line (high waterline)  Elements of several techniques can be used simultaneously 14) How effective is stuttering treatment for preschool-age children, school age children, and adults? Effectiveness of Stuttering Intervention:  Studies link success to early diagnosis and treatment  Cautious optimism in school-aged children  Improvement rate of 60 to 80% regardless of therapy used  Prolonged speech and/or gentle voicing onsets tend to yield superior benefits 15) Describe 4 aspects of fluent Speech. Fluent Speech:  Effortless  Smooth and rapid  Continuous, uninterrupted  Forward flow 16) What is meant be the “iceberg” of stuttering? The Iceberg of Stuttering: the things above the water waterline are what you SEE (overt issues). And the covert issues are what are below the water line. 17) Explain the 7 tips that are often shared with parents of young children who stutter. 7 tips when talking to your child who stutters: 1. Reduce your pace 2. Asking questions(don’t ask complicated questions or bombard them with Qs) (give child time to respond) 3. Full listening (its okay to tell them you don’t have time to listen sometimes) 4. Taking turns when talking (helps their fluency, everyone gets an equal turn) 5. Building confidence (focus on strengths other than talking, use descriptive praise) 6. Special times with child (5 minutes a day, one-on-one, no distractions, undivided attention, use one skill and see how it goes, make special time for each of your children) 7. Normal rules apply (discipline the child as normal) 18) What are four “speaking/vocalizing” conditions that people who stutter often report they stutter less? Ways to increase fluency: -accents -acting/characters -yelling -singing - airy voice (Marilyn Monroe) Chapter 10: Motor Speech Disorders 1) What are the structures of the brain important for motor speech function? Physiological subsystems:  Nervous system  Respiratory system  Auditory system  Articulatory/resonating system  Phonatory system Nervous System:  Brain  Spinal cord  Associated nerves and sense organs  Neuron  Basic unit of nervous system  Three parts  Body  Axon (away from cell body)  Dendrite (toward cell body)  Synapse  Space between axon and dendrite  Lower motor neuron responsible for muscle activation  Central Nervous System  Brain  Cerebrum  Cerebellum  Brainstem  Spinal Cord  Peripheral Nervous System  Cranial nerves  Spinal nerves Brain:  Cerebrum: -Right and left hemispheres -For 98% of pop L is dominant for most receptive / expressive language and for motor speech production -Hemispheres composed of white fibers covered by a gray cortex of cell bodies -Gyri (hills), fissure or sulci (valleys) 4 lobes: -Frontal  Primary motor cortex  Separated from parietal by central sulcus (fissure of Rolando) -Parietal  Somatosensory cortex -Temporal -Occipital  Cerebellum  Brainstem 2) What are the major differences between cerebral palsy, dysarthria, and apraxia? Dysarthria: Difficulty in motor speech control NOT planning Not a language disorder**** it results in speech problems CP: Developmental dysarthria. Results from brain abnormality. Range of severities, physical manifestations, and possible cognitive deficits. 3 types: Spastic, Athetoid or Ataxic.  Apraxia: Problems with programming of movement, not the result of a muscle or language problem. Impairment in volitional or voluntary motor placement and sequencing. Acquired neurological impairment of the ability to program and execute volitional speech. 3) Name and describe some of the causes of neurogenic speech disorders. a. Stroke: when blood flow to an area of brain is cut off. When this happens, brain cells are deprived of oxygen and begin to die. When brain cells die during a stroke, abilities controlled by that area of the brain such as memory and muscle control are lost. STROKE IS LEADING CAUSE OF NEUROGENIC DISORDERS. b. TBI: traumatic brain injury (causes forms of dysarthria). TBI’s cause the brains’ axons are severely damaged which is called axonal shearing. c. Anoxia: lack of oxygen at birth. d. Brain tumors: e. Infections and neurotoxins: they disrupt brain development in the womb. Can come from bacterial and viral infections such as HIV, mercury, lead, alcohol, or drugs. f. Degenerative diseases: characterized by progressive, often irreversible deterioration, and loss of function in the organs or tissues. Diseases that won’t be cured or get better. i. Multiple sclerosis: mixed dysarthria Amyotrophic lateral sclerosis (ALS): mixed dysarthria Parkinson’s: degenerative neurological disease. No known cause. (hypokinetic dysarthria) Huntington’s diseases Myasthenia gravis 3) Describe the main types of cerebral palsy (CP). (Table 10.3) What are the speech characteristics/deficits of persons with these types of CP? a. Spastic Cerebral Palsy:  Too much muscle tone in opposing muscles “exaggerated stretch reflex”  Approx. 60% of population with CP b. Athetoid Cerebral Palsy:  Slow, involuntary writhing type movement  Approx 30% of population with CP c. Ataxic Cerebral Palsy:  Uncoordinated movement and disturbed balance  The problem is in the cerebellum (seems like you’re drunk)  Approx. 10% of population with CP 4) What are the main causes of CP?  Higher incidence among extremely low and high weight newborns, nonwhite in U.S., born to older mothers, males  Most common causes: o Anoxia (lack of oxygen at birth) & hemorrhages (brain bleed at birth) o infections and toxins o accidents during pregnancy 5) Is cerebral palsy (CP) static or progressive? Do the characteristics change as a person with CP ages?  Static, non-progressive and non infectious  It does not get worse over time, but exact symptoms can change over time. 6) What are the treatment options for someone with CP?  Correcting or compensating for faulty motor patterns a. Motor patterns usually targeted within process of speech production (Systems approach) b. Possible prosthetic devices or intra-oral surgery c. Electropalatograph- used to train tongue movement d. Target sounds based on ease of production e. Work with PT to facilitate movement patterns f. Possible use of AAC i. Linguistic and social competence as important as use of device ii. Consult with parents about expectations 7) Describe the major types of dysarthria. What are the speech characteristics of the different dysarthrias? (Table 10.1) What are the possible causes of these dysarthrias? Examples of Dysarthria’s:  Flaccid Dysarthria  Bulbar Palsy  Progressive Bulbar Palsy Tongue Fasciculations(video)  Myasthenia Gravis – neuromuscular junction  Muscular Dystrophy – muscle degeneration  Spastic Dysarthria  Weakness and loss of inhibitory control  Typically bilateral upper motor neuron lesions due to strokes  Pseudobulbar Palsy  Ataxic Dysarthria  Damage to cerebellum or cerebellar control circuitry  Incoordination and reduced muscle tone  Not due to muscle weakness  Movements are jerky, inaccurate, and not smooth  You often appear drunk  Very hard to understand the speech (slurred)  Hypokinetic Dysarthria  Slow and reduced range of motion due to rigidity or increased resistance to stretch  Feel stiff and have hard time getting movement going and then have trouble stopping movement  Parkinson’s Disease – reduced dopamine  Hyperkinetic Dysarthria  Due to damage to basal ganglia, specifically indirect pathways  Leads to unwanted movement  Tremor: Rhythmic mvmt of limbs, head voice  Tics: Rapid, patterned mvmts that can be suppressed for brief periods with effort  Motor (e.g., eye twitching) or vocal (e.g., throat clearing)  Dystonia  Slow hyperkinesia  Slow, sustained abnormal posturing (e.g., body twisting)  Excessive pitch/loudness variations, irregular breakdowns in artic, variable rate and inappropriate silences  Chorea (“Dance”)  Appear to move continuously and fast  Variable speech rate, irregular articulatory breakdowns, prosody abnormalities  Huntington’s Chorea  Inherited, appears between 3- and 50  Movement worsens over time  Significant mood and personaligy changes  Survival rate is about 20 years  Mixed Dysarthria  Amyotrophic Lateral Sclerosis (ALS)  Mixed spastic-flaccid dysarthria  Traumatic brain injury (TBI) Typically spastic-ataxic dysartyhria 8) What is the difference between hypotonia, hypertonia, hypokinetic, and hyperkinetic? Hypotonia: weakness, and reduced reflexes, and can lead to wearing down of muscles (cranial and spinal nerves) Lesions to lower motor neurons or muscle unit. Reduced muscle tone and poor timing, etc. Hypertonia: rigid or stiff muscles, too much tone in muscles (working too hard) Lesions to bilateral upper motor neurons. Hypokinetic: Decrease or lack of movement (Parkinson’s has this). Hyperkinetic: Increased involuntary movement (tremors and tics) (results from damage to basal ganglia) 9) What are the goals of an assessment for a dysarthric patient? Goals:  Determine if there is significant long term problem  Describe impairment  Identify functions not impaired  Establish goals and baseline for intervention  Form prognosis 10) What are some things that you might do for intervention? What are the components of the systems approach? Intervention for people with Dysarthria:  Basic principles  Teach compensatory strategies  Foster purposeful control  Monitor and record change  Begin early to forestall formation of “bad” habits  Provide information and support  Evidence-based practice does not support non-speech oral motor treatments (you can’t really strengthen their oral speech muscles)  LSVT for Parkinson’s disease  Maintain the client’s speech abilities even as the client’s overall function decreases  Systems approach  Respiration  Phonation  Resonance: An example of a resonance disorder would be hyper nasality.  Articulation  Use of gestures and AAC (computer that speaks for you) with severe involvement 11) What are the differences between dysarthria and apraxia of speech? Dysarthria:  Speech sound distortions  Highly consistent speech sound errors  Little audible or silent groping  Rapid or slow rate Apraxia:  Speech sound substitutions  Inconsistent speech sound errors  Audible and silent groping  Slow rate: characterized by repetitions, prolongations, and additions 12) What are some of the assessment procedures to determine apraxia?  Nature of impairment requires SLP to assess  Imitation of words and sentences  Reading aloud  Spontaneous speech  Rapid repetition of short syllables—DDK rates  Other aspects of speech should also be assessed 13) What are some intervention strategies for apraxia? Management of Acquired Apraxia of Speech:  Integral Stimulation: “watch me, listen to me, do what I do” o Hierarchy of cuing  Melodic Intonation Therapy (MIT) o Prosody, emphasizing melody, rhythm and stress patterns  Contrastive stress (emphasizing different parts of words) - Used with mild to moderate BONUS: I learned about a website that allows you to register to get an AAC for you child if they have a severe communication impairment. The AAC device allows people to express their needs and wants and talk to others through a talking computer keyboard device. Overview: • Aphasia: difficulty with Thinking of the thoughts / words • Apraxia: difficulty with Planning the movement & send a message from the brain to the muscles • Dysarthria: difficulty with Executing the movements


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