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COSD chapter 9 notes

by: Maycie Tidwell

COSD chapter 9 notes COSD 10303

Maycie Tidwell
GPA 3.8

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These notes cover what we learned in chapter 9!
Survey of Communication Disorders
Class Notes
COSD, Survey, communication, disorders
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This 13 page Class Notes was uploaded by Maycie Tidwell on Thursday April 14, 2016. The Class Notes belongs to COSD 10303 at Texas Christian University taught by Watson in Spring 2016. Since its upload, it has received 8 views. For similar materials see Survey of Communication Disorders in Nursing and Health Sciences at Texas Christian University.

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Date Created: 04/14/16
COSD Ch. 9 notes ** TEST Q: matching Aphasia (left hemisphere) Right Hemisphere Injury TBI Dementia Cerebrum:  Right and left hemispheres ▯ -For 98% of pop L is dominant for most receptive / expressive language and for motor speech production ▯ - If you’re right handed, then your L hemisphere is for language ▯ - Also most left handed people are also L hemisphere for language 4 Modalities of Language:  Expressive Language: -Writing and Speaking  Receptive Language: -Understanding/listening and Reading ***BUT THE separation between L and R hems. Are not as clean as it looks. A lot crosses over. 4 lobes of brain:  Frontal  Parietal  Temporal  Occipital Language Processing:  Brocas’ Area ▯ Frontal lobe ▯ Production of language (not a speech disorder)  Wernicke’s Area ▯ Left temporal lobe ▯ Comprehension of language Cranial Nerves: Nerves specifically important for motor speech and hearing LANGUAGE DEVELOPMENT THROUGH THE LIFESPAN:  Unless there is neuropathology, adults continue to refine communication skills  Use o Adults are skilled conversationalists o Narratives improve until the seventies  Content o Some words fade and others are added o Deficits in accuracy and speed of word retrieval/naming  Form o Continue to acquire some aspects of syntax o Complex sentence construction declines with advanced age Aphasia:  Aphasia—“without language”  Stroke is the primary cause  Result of localized brain damage o Aphasic population is very diverse o Auditory comprehension & word retrieval deficits common in all  Affects over 1 million people in the U.S.  Can cross all modalities o Listening, speaking, reading, writing, &/or related language functions  Several types but individuals rarely have only one Deficits and Characteristics of Aphasia:  Expressive deficits: o Reduced vocabulary o Omission/addition/substitution of words o Stereotypic speech (Repeating words) o Delayed or reduced output of speech o Hyperfluent speech (say a lot with no meaning)  Language comprehension deficits  Range of severity based on o Cause o Location and extent of injury o Age of injury (young people recover better) o Age and general health of client  Disorder can be categorized into syndromes based on similarity in patterns of behavior  Often accompanied by apraxia and/or dysarthria (motor speech problems)  Seizures in about 20% of aphasic adults  Depression may be present Accompanying Deficits:  Hemiparesis: hemi means half, paresis means Weakness  Hemiplegia: Paralysis  Hemisensory impairment: Loss of the ability to perceive sensory information (can’t feel pain)  Hemianopsia: visual processing difficulties affecting ability to read (blindness in R visual field)  Dysphagia: when paresis, paralysis and/or sensory impairment affects chewing or swallowing  Agnosia: Deficit in understanding sensory information (e.g., visual agnosia in the Man who Mistook his Wife for a Hat)  Agrammatism: Omission of grammatical elements  Agraphia: Writing difficulties  Alexia: Reading problems  Anomia: Naming problems  Jargon: Meaningless speech with typical intonation. Aka Fluent aphasia   Neologism: A novel word (e.g., pen>”badle;” chair> “ponty”)  Paraphasia: Word and phoneme substitutions o Phonemic (sounds): hiss for kiss, Loose for juice o Verbal: husband for wife, walkside for sidewalk  Verbal stereotype: Expression repeated over and over (e.g., naked lady; obscenties) Types of Aphasia: Fluent Aphasia (not good)  o Word substitutions, neologisms, and often verbose verbal output o Lesion in posterior part of L hemisphere Wernicke’s Aphasia (Maisy has this) o Rapid speech, jumbled content o Poor auditory and visual comprehension o Verbal paraphasia or unintended words and neologisms o Jargon o Mild to severe impairment in naming and imitative speech o Maisy’s speech ▯ Anomic Aphasia o Word retrieval difficulties o Fluent spontaneous speech with word retrieval difficulties o Mild to moderate auditory comprehension problems ▯ Conduction Aphasia o Paraphasia (can be to the point of incomprehensible) o Anomia o Only mild auditory comprehension problems o Poor repetitive or imitative speech ▯ Subcortical Aphasia o Fluent expressive speech o Paraphasias and neologisms o Repetition, listening, and reading unaffected o Cognitive deficits and reduced vigilance Nonfluent Aphasia:  Slow, labored speech  Word retrieval and syntactic problems  Site of lesion in or near the frontal lobe in L  Broca’s Aphasia (most common non fluent) (Carl has this)  Broca’s area: Motor planning and working memory  Short sentences with agrammatism  Anomia  Slow labored speech and writing  Problems with imitation  Articulation and phonological errors  Transcortical Motor Aphasia  **Difficulty initiating speech  Mild comprehension deficit  Good verbal imitative abilities  Global or Mixed Aphasia  **Profound impairment in all modalities  Most severely debilitating aphasia  Limited spontaneous expressive ability or stereotypes  Naming and imitation affected  Auditory and visual comprehension deficits ***TEST Q: know the difference between fluent and nonfluent and focus on Wernicke’s and Broca’s Aphasia. Causes of Aphasia:  Stroke or cerebrovascular accident (CVA) o Effect ½ million annually in U.S. of whom approx 100,000 become aphasic o Ischemic—Complete or partial occlusion of arteries  Cerebral arteriosclerosis, embolism, and thrombosis o Transient ischemic attack (mini strokes) o Hemorrhagic—Burst blood vessel  Aneurysm and arteriovenous malformation  Head injury, infections, disease, and tumors Indicators of Stroke:  Risk factors:  Smoking, alcohol use, poor diet, lack of exercise, high blood pressure, high cholesterol, diabetes, obesity and history of strokes  Loss of consciousness, headache, weak or immobile limbs, slurred speech  Ischemic strokes (most common) – complete to partial blockage o Cerebral arteriosclerosis – thickening and build up o Embolism – traveling (en route) o Thrombosis – does not travel o Loss of consciousness, headache, weak or immobile limbs, slurred speech o Series of “ministrokes” (transient ischemic attacks)  Hemorrhagic stroke o Aneurysm – bulging of artery wall o Arterivenous malformation – tangle of arteries and veins (malformed) Patterns of Recovery:  Ischemic o Improvement within the first weeks after injury o Recovery slows down after 3 months  Hemorrhagic o More severe after injury o Most rapid recovery at the end of the first month and into second month Damage from Stroke:  Injury to left hemisphere results in aphasia o Right- handed and some left-handed  Injury to right hemisphere results in aphasia in few cases o Usually in left-handed who right hemisphere is more important for language Primary Progressive Aphasia:  Degenerative disorder of language  Mental functions and activities of daily living preserved  Takes at least 2 years to develop  Not dementia  No loss of cognitive function  Progresses from primarily motor speech disorder to inability to speak – comprehension remains mostly intact Life Span Issues:  Mostly middle-aged and beyond  Risk increased with history of o Smoking o Alcohol use o Poor diet o Lack of exercise o High blood pressure o High cholesterol o Diabetes o Obesity o TIAs / previous strokes  First indications o Loss of consciousness o Headache o Weak or immobile limbs o Slurred speech  Can be temporary or permanent  Hospitalization o One third die from the stroke o Long, deep coma is indicator of possible poor recovery o Acute care followed by rehabilitation services when client’s condition permits  Aphasia may be accompanied by neuromuscular deficits, seizures, & dementia o They do not cause aphasia  Behavior, emotional, & social changes and possible personality changes  Spontaneous recovery o Fastest recovery during the first few weeks and months after incident o Recovery slows, usually ceasing after 6 months o Recovery better and faster in  Younger  Less severely affected  Good health  Left-handed o Usually the earlier treatment the better Assessment for Aphasia:  Medical history—Previous health and current neurological reports  Interview with client and family—SLP receives and gives information  Oral peripheral exam  Hearing testing  Speech and language observation and testing o Initially informal at bedside  Counseling is ongoing  Formal testing postponed until patient is stable  Address  Overall communication skills  Expressive language  Receptive language  All modalities across all aspects of language  Listening, expressive output, reading, writing, gestures  Standardized tests are available  Observation/interpretation of client behavior Testing for Aphasia:  All areas of language  Receptive and expressive  Selection of formal tests ▯ Tests vary with model of aphasia ▯ Interpretation of client behavior during testing Intervention for Aphasia:  Goal: Aid recovery and provide compensatory strategies (TEST Q)  Determined by assessment and client/family needs  Cross-modality generalization (e.g., comprehension and production)  Conversational techniques  “Bridging” between cerebral hemispheres (e.g., using R brain with gesture)  Multimodality stimulation  AAC  Neural plasticity  Involve family members Right Hemisphere Injury (RHI):  Group of deficits resulting from right cerebral hemisphere injury  Characteristics o Neglect information from left side o Unrealistic denial o Impaired judgment and self-monitoring o Lack of motivation o Inattention  Can have a strong impact on communication Language Characteristics of RHI:  Both receptive and expressive  Pragmatics most impacted—Topic maintenance, use of contextual cues  Poor auditory and visual comprehension o May be very concrete (e.g., problems with humor) o Poor judgment in identifying and using important information (e.g., includes irrelevant information) o Paralinguistic deficits with problems in comprehending and producing emotional language Additional Deficits:  Attentional deficits o Left visual neglect  Visuospatial deficits o Poor visual discrimination o Poor scanning and tracking o Difficulty recognizing faces (including family members), remembering routes, reading maps RHBD (ASHA, 2008):  Swallowing – 52%  Memory – 41%  Problem solving – 40% Assessment for RHI:  Visual scanning and tracking  Auditory and visual comprehension  Direction following  Response to emotion  Naming and describing  Writing  Observation is essential for pragmatics  Portions of aphasia batteries, standardized measures for RHD, and nonstandardized measures can be used Intervention fro RHI:  Begins with visual and auditory recognition (needed for more complex tasks)  Respond appropriately in conversation  Track increasingly complex information  Use time restraints in conversational turn  Sequencing and explaining actions (organize linguistic information)  Synthesize skills within conversation  Target nonlinguistic markers (e.g., eye contact, body language, gestures) TBI:  Disruption in normal functioning caused by a blow or jolt to the head or penetrating injury  Leading causes o Falls o Motor vehicle accidents o Blows to the head  Assaults  Caused by blow or jolt to head or a penetrating head injury (e.g., falls, motor crashes, sports, assaults)  Highest risk: 0-4 years and 15-19 years  1.4 million people sustain TBI annually  5.3 million Americans require long-term help post-TBI (2% of US pop)  Twice as many males  Diffuse injury to the entire brain o Infection o Bruising and laceration of brain o Edema o Hypoxia (lack of oxygen) o Intracranial pressure o Infarction (death of tissue deprived of blood) o Hematoma (focal bleeding)  May have sensory, motor, behavioral, and affective disabilities  Epilepsy, hemisensory impairment, and hemiparesis/hemiplegia may occur Characteristics of People with TBI:  Inability to resume daily living tasks and interests  Affects Cognitive areas: orientation, memory, attention, reasoning/problem solving, executive function (i.e., planning, executing and monitoring goal-directed behavior)  Language impacted in 3 of 4 TBIs – anomia & comprehension  Most disturbed language area is pragmatics (e.g., errors in judgment and inability to inhibit behavior)  Deficits may also include o Speech (1/3 have dysarthria) o Voice o Swallowing o Psychosocial/personality changes  Severity related to initial levels of consciousness and post- traumatic amnesia Life Span Issues with TBI:  Most are young, result of vehicular accident  Several stages of recovery  Initially, nonresponsive and require full assistance  Gradually respond to stimuli and recognize some individuals  Confusion and agitation  Inappropriate, incoherent, emotional language  Later, can remain alert and hold short conversations  Oriented to person and place, not time  Inappropriate, unaware, unrealistic, and uncooperative  In later stages of recovery, can initiate and carry out tasks  May consistently behave in a socially inappropriate manner  Periodic depression and irritability  Most will have lingering deficits, especially in pragmatics Assessment for TBI:  Interdisciplinary o Neurological, psychiatric, and psychological reports are very important for SLP  Ongoing and varies with stage of recovery o Observation o Few specifically designed tests o Sampling of pragmatic behaviors Intervention for TBI:  Cognitive rehabilitation—designed to increase functioning abilities in everyday life o Restorative o Compensatory approaches  Varies with stage of recovery o Initially orientation, stimulation, & recognition o Next memory, executive function, vocabulary, and language form o Then higher language functions, pragmatics, and independence Dementia:  Impairment of intellect and cognition due to neurogenic causes o 15% of elderly with 20% respond to treatment, increasing incidence with more elderly o After age 65, many more cases (e.g., nearly half of those admitted into long-term care facilities)  Includes several conditions and syndromes  Memory deficits, poor reasoning, impaired abstract thinking, inability to attend to relevant information, impaired communication, and personality changes Types of Dementias:  Cortical—Visuospatial deficits, memory problems, judgment and abstract thinking disturbances, and language deficits in naming, reading and writing, and auditory comprehension o Alzheimer’s (60 -80% of all dementias) & Pick’s  Subcortical—Deficits in memory, problem solving, and language; related motor problems o Multiple sclerosis o AIDS-related encephalopathy o Parkinson’s o Huntington’s Alzheimer’s Disease:  Affects 13% of those over 65 o 50% of those over 85 th  5.5 million people in US; 6 leading cause of death (CDC, 2013)  More common in women by 2-3:1  Cause may be genetic and environmental  Twisted neuro-filaments in neurons especially in temporal lobe and associational pathways o Resultant brain atrophy  Memory, especially short term, most affected Language Characteristics of Alzheimer’s Disease:  Initially word-finding, off-topic comments, and comprehension difficulties  Later paraphasia and delayed word-finding  With more advanced, vocabulary and sentence production difficulties  In most advanced o Naming and syntactic errors o Minimal comprehension o Jargon, echolalia, or mutism Life Span Issues of Alzheimer’s:  Person usually unaware  Early memory loss, especially new information o Word-retrieval and higher language difficulties o Initiate little communication  Gradual vocabulary decrease, comprehension reduction, and pragmatic skills deterioration o Frequent repetitions and ritualized or high usage phrases  Nursing home o Meaningless language, echolalia or mutism o Motor functioning impaired Assessment for People with Alzheimer’s:  MRI may confirm early suspicions  SLP identifies changes in language functioning as disease progresses ▯ History and neurological  Particularly interested in memory deficits  Detail client’s strengths and weaknesses Intervention for Alzheimer’s:  Goal: Maintain client at highest level of performance and help others maximize client’s participation  Team effort  Target o Word memory with associational tasks o Auditory attending and comprehension o Verbal responding o Formation of sentences 3 Approaches of Intervention for Alzheimer’s:  Cognitive rehabilitation ▯ Individualized goals (e.g., recalling name of family member) ▯ Implement strategies based on goals  Cognitive training ▯ Structured practice to improve specific cognitive functions (e.g., attention, memory)  Cognitive stimulation ▯ Less direct, often in groups, general enhancement of cognitive and social functioning More intervention for Alzheimer’s:  Errorless learning ▯ Memory intervention technique ▯ Use cues / instructions to prevent / reduce mistakes ▯ New neural pathways ▯ Reduce cues with time (vanishing cues)  Spaced retrieval ▯ Prompts to recall info occurs at spaced or delayed intervals


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