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COSD Ch. 8 notes

by: Maycie Tidwell

COSD Ch. 8 notes COSD 10303

Maycie Tidwell
GPA 3.8

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These notes cover what we learned in chapter 8
Survey of Communication Disorders
Class Notes
COSD, communication disorders
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This 10 page Class Notes was uploaded by Maycie Tidwell on Thursday March 31, 2016. The Class Notes belongs to COSD 10303 at Texas Christian University taught by Watson in Spring 2016. Since its upload, it has received 26 views. For similar materials see Survey of Communication Disorders in Nursing and Health Sciences at Texas Christian University.

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Date Created: 03/31/16
COSD Ch. 8 notes 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 Pyramidal Tract: Direct Activation Pathway  Originates in primary motor cortex  Responsible for rapid, discrete, volitional movement of articulators for speech production  Connects the outer layer of the brain (i.e., cortex) to the neurons that control muscle activation Extrapyramidal Tract: Indirect Activation Pathway  Regulating reflexes and maintaining posture and muscle tone  Provides necessary framework to facilitate movement carried out by pyramidal system Basal Ganglia  Regulate motor function and maintain posture and muscle tone Subcortical & Lower Brain Structures  Thalamus  Basal Ganglia  Brainstem  Cerebellum Basal Ganglia:  Direct paths increase/facilitate mvmt (e.g., Parkinsons –reduced slow movements)  Indirect paths decrease/inhibit mvmt (e.g., Huntington’s Chorea – involuntary movements) *You need this in order to move correctly and control your movements Cerebellum:  Maintain muscle tone  Coordinate fine motor and complex motor activities  Participate in motor learning  Ataxia Peripheral Nervous System:  Twelve pairs of cranial nerves  Most originate in the brainstem  Especially important for speech production  Thirty-one pairs of spinal nerves  22 of them are important for speech breathing  Helps the CNS communicate with the body Spinal cord:  Neuronal cell bodies protected by a myelin sheath.  Receives sensory info and contains motor neurons supplying muscles Motor Speech control:  Motor speech production process  Movement plan/program retrieved from memory  Sent to motor control areas (i.e., primary motor cortex)  Transmitted to muscles and structures of the speech mechanism  Nerve impulses modified throughout the process to ensure precise, smooth muscle movements  Internal and external sensory information allows monitoring and modification of movements NEUROGENIC SPEECH DISORDERS:  CAUSES  CEREBRAL PALSY  THE DYSARTHRIAS  APRAXIA OF SPEECH  Related to problems of movement can affect all speech processes  Planning  Coordination  Timing (when saying word “cat” we have to time the “c” then “at”)  Execution  Heterogeneous group of disorders Causes of Neurogenic speech disorders:  Stroke is leading cause  TBI (car accidents, sports injuries, any brain injuries)  Anoxia, especially in pre-, neo-, and post-natal brain injury  Brain tumors  Infections and neurotoxins  Degenerative diseases (diseases that wont be cured or get better)  Multiple sclerosis, amyotrophic lateral sclerosis (ALS), Parkinson’s and Huntington’s diseases, myasthenia gravis The Dysarthria’s:  A group of neuromuscular impairments that affect speed, range, direction, strength, and timing of motor speech movements  All speech processes may and may result in unintelligible speech  Slow or rapid rate  Range and strength may decrease  Timing may be erratic  Difficulty in motor speech control NOT planning  Not a language disorder**** it results in speech problems Types of Dysarthria’s: Different types result of lesions to different parts of CNS or PNS  Flaccid—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  Spastic—Hypertonia, rigid or stiff muscles, too much tone in muscles (working too hard)  Lesions to bilateral upper motor neurons  Ataxic—Hypotonia and poor coordination (reduced muscle tone and poor timing, etc)  Hyperkinetic—Increased involuntary movement (tremors and tics) (results from damage to basal ganglia)  Hypokinetic—Decrease or lack of movement (Parkinson’s has this)  Mixed Dysarthria—Extremely varied symptoms See Table 10.1 in text Examples of Dysarthria’s:  Flaccid Dysarthria  Bulbar Palsy  Progressive Bulbar Palsy Tongue Fasciculations(video)  Myasthenia Gravis – neuromuscular junction  Muscular Dystrophy – muscle degeneration  Living with Muscular Dystrophy (video)  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)  Toastmaster Speech - Ataxic Dysarthria  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  Michael J. Fox on Parkinsons  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  Youngster with Dystonia  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  Documentary on Huntington's Dance  Mixed Dysarthria  Amyotrophic Lateral Sclerosis (ALS)  Mixed spastic-flaccid dysarthria  Living with ALS  Traumatic brain injury (TBI) Typically spastic-ataxic dysartyhria Parkinson’s Disease: (Hypokinetic Dysarthria)  Degenerative disease affecting 1- 2 % of people over 50  Life expectancy after Dx is 15 years  No known cause (environmental & genetic?)  Hypokinetic dysarthria in 90%  Due to damage to basal ganglia and reduced range  Reduced loudness  Fast rate of speech  Disfluencies  Imprecise articulation  Breathy, harsh/hoarse, pitch and loudness variability Assessment of People with Dysarthria:  Team approach  Goals:  Determine if there is significant long term problem  Describe impairment  Identify functions not impaired  Establish goals and baseline for intervention  Form prognosis  Oral peripheral exam and samples of speech in several contexts 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  Articulation  Use of gestures and AAC with severe involvement Cerebral Palsy:  Result of brain injury early in fetal or infant development  Range of severities, physical manifestations, and possible cognitive deficits  Over 500,000 people in U.S., most under age 21  Developmental, non-progressive and noninfectious  More predictable motor patterns than other neurogenic motor disorders Types of CP: Spastic or hypertonic  Too much muscle tone in opposing muscles  “exaggerated stretch reflex”  Approx. 60% of population with CP Athetoid or dyskinetic  Slow, involuntary writhing type movement  Approx 30% of population with CP Ataxic  Uncoordinated movement and disturbed balance  Approx. 10% of population with CP Motor Speech Problems Associated with CP:  Developmental dysarthria  All aspects of speech production may be affected:  Breathing may be rapid and shallow  Hypertonic voicing  Hypernasality  Articulatory difficulties  Prosodic difficulties  Other factors  intellectual, auditory, information processing, swallowing, and language deficits Etiology of CP:  Higher incidence among extremely low and high weight newborns, nonwhite in U.S., born to older mothers, males  Most common causes:  anoxia & hemorrhages  infections and toxins  accidents during pregnancy Life Span Issues with CP:  Added stress for family—chronic grief  Confirmation may take a few years as child’s condition changes  Early intervention usually focuses on motor movement and communication, possibly AAC  Inclusion or special classes  Competitive employment and independent living or in supervised environment Assessment of people with CP:  Team effort  Communication concerns differ with type of CP, severity, and age of individual  Thorough oral peripheral examination  Potential for augmentative/alternative communication (AAC)  Alternative / Augmentative Communication  Thorough description of speech and language abilities Intervention for people with CP:  Correct or compensate for faulty motor patterns  Motor patterns usually targeted within process of speech production (Systems approach)  Possible prosthetic devices or intra-oral surgery  Electropalatograph- used to train tongue movement  Target sounds based on ease of production  Work with PT to facilitate movement patterns  Possible use of AAC  Linguistic and social competence as important as use of device  Consult with parents about expectations Apraxia of Speech:  Impairment in volitional or voluntary motor placement and sequencing  Acquired neurological impairment of the ability to program and execute volitional speech (Broca’s area)  Difficulties with speech-sound articulation and prosody  Not result of muscle or linguistic deficits  Speech characterized by groping attempts to find the correct articulatory position  Make repeated attempts because aware of errors  Aphasia vs. Apraxia  Children may also exhibit developmental apraxia Assessment of people with Apraxia of Speech:  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 Management of Acquired Apraxia of Speech:  Integral Stimulation: “watch me, listen to me, do what I do”  Hierarchy of cuing  Melodic Intonation Therapy (MIT)  Prosody, emphasizing melody, rhythm and stress patterns  Contrastive stress  Used with mild to moderate


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