Language Final

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  1. What is located in the CNS?
    • Cerebrum: brain hemispheres
    • Diencephalon: deep in brain hemispheres, appears at the upper end of the brianstem, thalamus, subthalamus, hypothalaums, epithalamus. 
    • Brainstem: Top of spinal cord
    • Cerebellum: Behind brain stem
    • Spinal Cord: Cord
  2. What are the 4 lobes?
    • Fronal 
    • Parietal 
    • Temporal 
    • Occipital
  3. Describe the Ventricles
    • Fluid filled space in the center of the brain and brain stem 
    • Can expand, but this is bad with a TBI
  4. Describe a neuron
    • Cell body
    • Dendrites (receive info)-many of them
    • Axon (transmits) Most covered in myelin
  5. Describe Gray and white matter
    • Gray: Neurons, Glial Cells (like glue- surround neurons and hold them in place and supply nutrients and oxygen and insulate neurons from each other. 
    • What matter: Myelinated Axons (tract)
  6. Describe the parts of the protective envelope.
    • Skull
    • Vertebrae
    • Meninges (enclose the CNS)
  7. What are the 3 main parts of the Meninges?
    • Dura Mater (elastic and strong)
    • Arachnoid (conforms to skull)
    • Pia Mater (conforms to brain)
  8. What are the characteristics of the Dura mater?
    • Durable, slightly elastic with two surfaces
    • Outer surface attaches to inside of skull and inner surface attaches to the arachnoid.
  9. What are the characteristics of the arachnoid layer
    • Cob web like sheet of tissue (does not conform to brain surface)
    • Creates a space called the subarachnoid space filled with cerebrospinal fluid and is a shock absorber. Has blood vessels.
  10. What are the characteristics of the pia mater
    • Fragile
    • Adheres tightly to the brain surface.
  11. What is the incidence of TBI?
    • Estimates: 95-200 per 100,000 people
    • But the true incidence is unknown.
  12. What are the outcomes for Adults with TBI?
    • No hospital: 75%
    • Died: 4%
    • Disabled: 8%
    • Full Recovery: 13%
  13. What are risk factors associated with TBI?
    • Age
    • Sex
    • Substance Abuse
    • Poor academic performance
    • SES
    • HIstory of TBI
    • Participation in High Risk sports (boxing, motorcycling, bicycling, snowmobiling, rock climbing) 
    • Personality
  14. Compare and contrast Traumatic Brain Injury
    • Open head injury (penetrating): Bullet Wounds, similar to focal lesions -one place
    • Closed head injury: Blows or collisions that cause diffuse damage, affecting large areas of the brain.
  15. For Penetrating Brain Injuries, what are the two sub types and compare and contrast them.
    • High Velocity Missle: high kinetic energy creates a pressure wave. Destroys tissue on both sides of the projectile's track and diffuse bleeding and tissue disruption occurs. Also may cary foreign material into brain. 
    • Low velocity missile: Destroys tissue adjacent to the projectile's tract and carries foreign material into the brail. If strikes skull opposite point of entry, may ricochet.
  16. For non-penetrating Brain injuries, what are the two sub types and compare and contrast them.
    • Nonacceleration: Usually less severe injury with deformation of the skull and impression trauma. 
    • Acceleration: Brain and brian stem suffer difuse damage. Linear acceleration head (head is struck by a force aligned with the center axis of the head). (angular acceleration- head is struck off center, causing it to rotate and move at an angle away from the point of impact.
  17. what is a hemorrhage. what type of brain injury does it go with?
    • bleeding. 
    • non-penetrating.
  18. What is a hematoma, what are the sub types and what type of brain injury is it associated with?
    • accumulation of blood
    • Epidural: between the dura mater and the skull (above the dura, 20-30 die from their head injuries) Depends on whether bleeding is from an artery or a vein and depends on location.
    • Subdural: Beneath the dura mater above the arachnoid
    • Subarachnoid: within the subarachnoid space
    • Intracerebral: within the brain.
  19. What are the primary consequences of TBI?
    • Impact brain and meninges
    • Caused by mechanical effects of: Compression, stretching, shearing, abrasion, laceration
  20. What are the secondary Consequences of TBI?
    • Cerebral edema (swelling)
    • Traumatic hydrocephalus (fluid in brian)
    • Elevated intracranial pressure 
    • Ischemic brain damage (temp reduction of oxegen)
    • Alterations in the blood-brain barrier
  21. Secondary consequences can be ....
    worse than initial.
  22. what is the severity of the TBI?
    • Nature and severity of the TBI determines nature and severity of the patient's symptoms
    • Nature and severity of the TBI usually determines nature and severity of the patient's recovery.
  23. Describe the history of the hemispheres according to dax, broca and jackson.
    • 1836: Dax- Momory for words resides in the left brain hemisphere (for right handers)
    • 1860: Broca- Left hemisphere of the brain is responsible for articulate speech (for right handers) after studying patients with brain injury
    • 1874: jackson- Left hemisphere is for language and the right hemisphere is for visual recognition, discrimination, and recall
  24. Describe the history in the 1900's
    • Early 1900- Collaborative hemishperes
    • Left side damage: socially appropriate, impaired comprehension and production of language 
    • Right side damage: Socially inappropriate, intact comprehension and production of language,
    • 1960s
    • Left Hemisphere: Rational, analytic and specialized for processing sequential, time-related material (auditory stimuli)
    • Right hemisphere: intuitive, holistic, specialized for processing nonlinear spatially distributed arrays of information (visual stimuli)
  25. Zaidel states that the adult right hemisphere possesses grammatical competence equivalent to what?
    a 5 year old child - 1978
  26. What is the current take on the hemispheres collaborate?
    Contemporary neural netowrk models of hemispheric specialization are moving away from the appealing but simplistic concept of isolated and specialized brian hemispheres to emphasize the ways in which the hemispheres collaborate to accomplish mental functions and to produce and regulate behavior. Although what is know about the right hemisphere is largely descriptive, with little sense of cause and effect, investigators slowly are becoming more sophisticated about its role in communication, cognition, and behavior.
  27. Only ___ of adults who suffer a right hemisphere brain injury develop communication impairments. The likely candidates to do so are:
    • 1/2
    • Cortical lesions
    • History of familial left handedness
    • Low education levels.
  28. What are the 6 general characteristics of RHS?
    • Insensitive to others/ preoccupied with self
    • Oblivious to social conventions
    • Unconcerned about physical and mental impairments
    • Verbose, tangential, and rambling in speech
    • Insensitive to the meaning of implied or abstract material
    • Unable to grasp the overall significance of complex events.
  29. What are the cognitive and behavioral symptoms associated with RHS?
    • Left hemispatial neglect
    • Do not respond to stimuli on the side of the body opposite the side of brain injury
    • More common and most severe after parietal lobe damage
    • Majority recover 
    • Related to prognosis of daily life function
  30. what are the 5 common signs of left neglect
    • Failure to respond to items left of body
    • Self care for the right side only
    • Failure to move/attend to the left arm/leg
    • Bumping into items on the left side 
    • Reading/writing right side only
  31. What is Anosognosia and describe it as it relates to RHS?
    • Denial of illness
    • More common with right parietal lobe injury
    • some acknowlege but indifferent/minimize
    • Some are in complete denial- No paralysis, sensory loss, visual field blindness.
  32. Compare right hemisphere injury and left hemisphere injury
    • Right:
    • Respond quickly and impulsively
    • make frequent errors and correct with more lines
    • Leave out details on the left hand side
    • Fragmented, disorganized, and crowded drawing.
    • Left: 
    • Respond cautiously and slowly
    • Do not make frequent errors (get false starts, hesitations, self corrections)
    • Proportions and dimensions are accurate
    • Incomplete, clumsy, but coherent drawing
  33. Define Topographic impairment and Geographic Disorientation
    • Topographic impairment: distorted internal representations of external space. (failure to recognize landmarks)
    • Geographic disorientation: confuse geographic location of familiar people, places, or things (recognize immediate surroundings but not where they are)
  34. What are the visuoperceptual impairments associated with RHS?
    difficulty recognizing objects, pictures, or drawings presented in unusual formats.
  35. What is prosopagnosia?
    Difficulty with facial recognition
  36. Individuals with RHS are insensitive to: and fail to communicate:
    • emotional tone of facial expressions, body language, situation
    • emotional tone by speech prosody, facial expression, body language
  37. What are the cognitive and behavioral symptoms-in relation to attention- that are associated with RHS?
    • Arousal: physiologic/behavioral readiness to respond.
    • Vigilance: ongoing sensitivity to stimulation
    • Orienting: direction toward a stimulus
    • sustained: maintenance over time
    • Selective: maintenance in presence of competing stimuli
    • Alternating: moving from stimulus to stimulus
    • Divided: performing more than 1 activity at a time
  38. What are the communication impairments associated with RHS?
    • Diminished speech prosody
    • Excessive, confabulatory, tangential and sometimes inappropriate connected speech
    • Impaired comprehension of narratives and conversations (insensitivity to relationships, premature assumptions, failing to judge the appropriateness of events/situations, failing to appreciate implied meanings.
  39. Describe the prosody of someone with RHS?
    • Lacks normal variability in pitch and ludness.
    • Reduced spontaneity and variety in non-verbal movements
    • Slow rate
    • Reduced empathetic stress
    • Diminished pitch variability/restricted intonation
  40. Describe narrative productions for RHS
    • Use more words but produce less information
    • Fragmented and lack of cohesion and do not have an overall point
    • Dont establish relationships among events
    • permit personal expereinces and opinions to intrude into the narrative
  41. What are the pragmatic impairments of RHS
    • Turn taking
    • Topic maintenance
    • social conventions
    • eye contact
    • begin/end conversations abruptly 
    • talk excessively without regard for their listener
    • dont stay on topic well
    • interject irrelevant, tangential, and inappropriate comments
    • Dont make conversational repairs
    • yeilding the floor to conversational partners
  42. Define aphasia
    Communication disorder caused by brain damage and characterized by complete or partial impairment of language comprehension, formulation, and use; excludes disorders associated with primary sensory deficits, general mental deterioration, or psychiatric disorders.
  43. What do localizationists do?
    • accumulate informaation about brain-behavior relationships
    • If a pattern is found, then function is assigned to that region (localization of function)
  44. What is phernology, when did it occur, and what is its history with localizationists?
    • Early 1800s 
    • Mapping of the brain
    • Hyperdeveloped brain regions pressed outward on the skull creating bumps and ridges. 
    • The bumps and ridges could be analyzed. 
    • Fell into scientific disrepute in the late 1830s except in the us and england we needed until the late 1800s.
  45. What did broca claim in the 1860's
    Broca claims that loss of articulate speech (for right-handers) is caused by damage to the posterior inferior frontal lobe of the left hemispheres.
  46. What did wernicke claim in 1874
    Wernicke claims that loss of language functions (for right-handers) is caused by damage to the posterior temporal love of the left hemisphere
  47. What did the antilocalizationist movement focus on
    the brain operating as an integrated whole
  48. What is cerebral dominance?
    • Left-hemisphere is responsible for language for right-handed people.
    • Right-hemisphere is responsible for language for left handed people.
  49. Left hemisphere is dominant for language in _______,
    Left hemisphere is dominant for language in about 85% of adults who are left handed (~100% for those who are right handed)
  50. Explain the research associated with cerebral dominance?
    • 1. Injected sodium amytal into the carotid arteries of left handed adults.
    • 2. Anesthetized the brain hemisphere on the side of the injection

    • *18% stopped talking when the right side was injected
    • *69 % stopped talking when the left side was injected
    • 13% stopped talking when either side was injected (both sides working together for language)
  51. Due to the number of language specific areas that are being found daily, it can be concluded that
    domains like language do not live within well defined borders.
  52. What are the language areas of the brain?
    • Perisylvian region
    • Brocas area
    • Wernicke's area
    • Primary auditory cortex
    • Arcuate fasciculus
    • Angular gyrus
    • Primary visual cortex.
  53. Where is the perisylvian region and what happens with damage?
    Area surrounding the Sylvian fissure in the left hemisphere

    almost always results in a language impairment
  54. Where is Borca's Area?
    Posterior inferior frontal lobe, presumed role in planning and organizing speech movements
  55. Where is Wernicke's Area?
    • Posterior superior left temporal lobe
    • Storage and retrieval of words and their meanings
    • Knowldege and retrieval of grammatical linguistic rules. 

    AKA auditory association cortex.
  56. Where is primary auditory cortex?
    • Top surface of each temporal love in the sylvian fissure
    • Perception and discrimination of auditory stimuli

    • AKA Heschl's gyrus
    • Input for wernikes
  57. Arcuate Fasciculus
    • Band of nerve fibers connecting the midtemporal lobe to lower regions of the frontal lobe via the parietal lobe
    • Wernicke's and Broca's areas communicate.
  58. Where is the angular gyrus?
    • Junction of the temporal, parietal, and occipital lobes.
    • Important for processes involved in reading and writing.
  59. Describe comprehension of speech?
    • 1. Ears to primary auditory cortex
    • 2. Auditory Cortices encode acoustic signal
    • 3. Sent to Wernicke's area (left hemisphere)
    • 4. Interpretend
  60. Describe comprehension of writing
    • Identical to speech except:
    • 1. eyes to visual cortex
    • 2. Visual cortex encodes visual cortex
    • 3. sent to Wernike's area
    • 4. Interpreted
  61. Describe spontaneous speech
    • 1. Wernicke's area constructs an utterance (phonologic, syntactic, semantic)
    • 2. Sent to Broca's area via Arcuate Fasisculus
    • 3. Broca's area codes an action plan
    • 4. Action plan sent to Primary Motor cortex.
    • 5. Sent to pyramidal system to Cranial nerves
    • 6. Speech muscles are activated
    • 7. Wernicke's area monitors the speech
  62. Describe the 10 steps of Repetition
    • 1. Ears to primary auditory cortex
    • 2. Auditory Cortices encode acoustic signal
    • 3. Sent to Wernicke's area (left hemisphere)
    • 4. Interpreted
    • 5. Sent to Broca's area via Arcuate Fasciculus
    • 6. Broca's area codes an action plan
    • 7. Action plan sent to Primary Motor cortex
    • 8. Sent to pyramidal system to cranial nerves
    • 9. Speech muscles are activated
    • 10. Wernicke's area monitors the speech.
  63. Describe the 10 steps of Oral reading
    • 1. Eyes to visual cortex
    • 2. Visual cortex encodes visual signal
    • 3. Sent to Wernicke's area (left hemisphere)
    • 4. Interpreted
    • 5. Sent to Broca's area via Arcuate Fasciculus
    • 6. Broa's area codes an action plan
    • 7. Action plan sent to Primary motor cortex
    • 8. Sent to pyramidal system to Cranial nerves
    • 9. Speech muscles are activated
    • 10. Wernicke's area monitors the speech
  64. Describe the process of writting?
    • 1. Wernicke's generates the message (syntactically acceptable, spelling)
    • 2. Sends it to the premotor cortex (via the arcuate fasciculus) to get the correct arm/hand movemenets
    • 3. Eyes and Wernicke's are a monitors productions
    • 4. Wernicke's not satisfied, then erase, revise, and other repair.
  65. What is What is a literal paraphasia>
    • Phnemic
    • Phonological errors (foon for spoon)
  66. What is a verbal paraphasia?
    • Semantic
    • Unintentional incorrect word substitution 
    • Semantic: production is usually related (fork when want spoon)
    • Unrelated: Production has no clear relationship (she to eat soup)
    • Perseverative: production is a previously used word (I ate the soup with the shore then I left the shoe and drove away in the shoe
  67. What are the 3 classifications of aphasia?
    • Fluency 
    • Auditory comprehension
    • Repetition
  68. Describe fluent aphasia
    • Damage posterior (behind) to the central sulcus
    • Speak smoothly with little effort
    • Speech rate, intonation, emphatic stress similar to speaker without aphasia.
    • Front half of the language dominant hemisphere.
  69. Describe nonfluent aphasia
    • Damage anterior to the central sulcus
    • Speak slowly with great effort
    • Pausing between syllables and words
    • Diminished/absent intonation & stress patterns
  70. Describe the location of broca's aphasia
    • Broca's Area
    • Mohr et al. (1978) found that a lesion confined to Broca's area led to "transient speech apraxia" (mutism and effortful articulation that rapidly improves)
  71. Broca's Aphasia requires ...
    • A large lesion to the sylvian region
    • *Operculum (a part of the cortex that covers the insula)
    • *Insula (a part of the cortex folded into the sylvian fissure)
    • *Subjacent white matter in the upper division of the middle-cerebral artery
  72. In non-fluent aphasia, what are the differentiating features for speech/language?
    • nofluent
    • effortful
    • slow
    • reduced phrase length
    • reduced syntactic complexity
    • awkward articulation
    • overuse of content words/nouns
    • relatively few functors and grammatical word endings.
    • Usually contains sufficient information content to communicate in daily, contextually rich situations
    • Repetition and confrontation naming moderately to severely impaired
    • Auditory comprehension relatively preserved
    • Reading and writing usually parallel auditory comprehension and verbal output (respectively)
  73. Broca's aphasia can be differenetiated by examining:
    • Speech fluency
    • Auditory comprehension
    • Confrontation naming
    • Repetition tasks
  74. For broca's aphasia, the symptoms ____ 
    Some are ___ and some have ____
    • vary
    • Some restricted to one- or two-word responses
    • Some have only a relatively mild interruption of speech fluency.
  75. What are some details about Broca's Aphasia
    • Highly aware of their problems
    • Demonstrate frustration
    • Frequently co-occurs with other communication, motor, and sensory problems
    • *Contralateral hemiparesis/hemiplegia
    • *Plan/ coordinate motor activity
    • *Mild dysarthria (muscular weakness, slowness, incoordintion
    • *Dysphagia (swallowing)
  76. Broca's Aphasia frequently...
    • Co-occurs with other communication, motor, and sensory problems.
    • Apraxia: Neurogenic phonological disorder resulting from sensorimotor impaimrent to the capacity to select, program, and/or execute in coordinated and normally timed sequences, the positioning of speech musculature for the volitional production of speech sounds.. prosodic alteration, that is, changes in speech stress, intonation, and/or rhythm, may be associated with the articulatory disruption either as a primary part of the condition or in compensation for it.
  77. Describe the location of Wernicke's Aphasia
    • Damage in temporal lobe of language dominant hemisphere (sometimes).
    • Damage confied to wernicke's area usually does not produce chronic Wernicke's aphasia. 
    • Damage confined to Wernicke's aphasia = near normal recovery after 5 months
  78. Persistent Wernicke's aphasia result of damage also in...
    the inferior parietal lobe.
  79. Subcortical damage has been ignored in the classical connectionist model but...
    can be the course of aphasia. Basal ganglia, thalamus.
  80. Wernicke's Aphasia ranges from ...
    Have difficultly with...
    • Inability to understand any spoken language to shutter-effect type comprehension where only some stimuli are unprocessed. 
    • short term (working) memory.
  81. Describe the Differentiating Features of Wernicke's or fluent aphasia
    • Verbal (semantic) paraphasias
    • Literal (phonemic) paraphasias
    • Neologisms (nonwords, jargon)
    • Empty Speech 
    • Circumlocutions
    • Logorrhea- diarrhea of the mouth.
    • Paraphasic speech (phonemic and semantic)
    • Less aware that they do not sound accurate. Mainly think that the communication error lies within the other person
    • Limited awarness of expressive deficits
    • Press of speech (logorrhea, lack of self monitoring prefer to talk during treatment instead of listen)
    • Reading comprehension difficulty
    • Writing deficits (spelling, jargon, commensurate with severity of speech disorder)
  82. What is the focus of treatment for Wernicke's
    narrow down speech
  83. Describe the Ancillary Behaviors/ consequences with Wernikes Aphasia
    • Severe Wernicke's Aphasia: Flamboyantly incomprehensible, euphoric outlook dont know anything is wrong  makes it difficult to formulate on effective intervention
    • Depression:10%-3% of stroke survivors, people with wernicke's aphasia have a lack of concern UNTIL the initiation of treatment- start to realize something is wrong
    • Friends stop coming around to visit (they dont know what to say or how to maintain a conversation, environmental problems.
  84. What is the criteria for diagnosis of conduction aphasia>
    • Fluent conversational speech (but not quite as fluent as wernicke's)
    • No significatn difficulty in comprehenesion of normal conversation
    • Significant verbal repetition disturbance (a predominant problem) more severe then Wernicke's 
    • A preponderance of phonemic paraphasias (a predominant problem)
    • Also have word finding difficulty  and error recognition
  85. This describes a person with?
    An individual who speaks with good intonation and generally understands what other says, but has trouble retreiving words. Paraphasic errors are produced which the indibidual recognizes and tries through often abortively to correct
    Although the hesitations and correction efforts might mimic nonfluent disorders, the runs of fluency, preserved melody and variety and complexity of syntactic structures found in the spontaneous speech of conduction aphasia distinguish it from Broca's aphasia and apraxia of speech.
  86. Compare and contrast Broca's and Conduction
    • Broca's: nonfluent, dysprosody, agrammatic, comprehension relatively good, repetition impaired proportionate to other verbal tanks, error recognition, probably anomic (hard tim finding words)
    • Conduction: Fluent, prosody ok, preserved grammar, comprehension relatively good, repetition disproportionately impaired, error recognition, probably anomic.
  87. Describe the anatomical debate of conduction aphasia.
    • 1. Left hemisphere supramarginal gyrus
    • 2. Contigous auditory cortex
    • 3. Arcuate fasciculus (cases conduction aphasia)
    • 4. Insula (anterior and possterior insular cortex-AIC/PIC)
    • 5. Underlying white matter of left hemisphere
  88. Describe the Disconnection model of conduction aphasia.
    • Wernicke's original hypothesis
    • Disconnection between Wernicke's and Broca's areas
    • Aruate Fasciculus (Wernicke's and Broca's areas are spared, relatively little impact on auditory comprehension and fluent speech, disconnection between those areas would result in disproportionate impairment in activities requiring the interaction of audition and production, such as verbal repetition.
  89. Describe the bimodel model of conduction aphasia.
    • Conduction aphasia results from damage along a continuum extending from Wernicke's area to Broca's area. 
    • Variability in the degree of fluency (damage in more anterior region= less fluent)
    • Damage in more posterior region = more fluent
  90. Describe Transcortical Aphasia
    • Dominant hemisphere damage
    • Central region is not impacted (but the areas in this region (brocas, wernickes, arcuate fasiculus) are isolated from each other
    • Preserved repetition.
  91. Describe transcortical motor aphasia
    • Transcortical motor aphasia 
    • similar to broca's 
    • Excetipn is they can repaeat with ease. 
    • Damage to the anterior superior frontal lobe surrounding Broca's area- not hitting Broca's directly
  92. Describe Transcortical Sensory Aphasia
    • Similar to Wernicke's aphasia
    • Exception is that repetition fine (which is nearly impossible with wernickes aphasia
    • Echolalia is a prominenet feature (repeating a question instead of answering it)
    • Lesions in the temportal occipital parietal junction (posterior to wernicke's area)
  93. Describe Transcortical Aphasia
    • Similar to global aphasia
    • Poor comprehension
    • Nonfluent, meaningless stereotypic utterances
    • Repetition OK (often compulsive)
    • Broca's area, Wernicke's area and the arcuate fasciculus not severely impacted,  but the areas around them are damaged, leaving the areas isolated.
  94. What is the Role of the Right (non-dominant) Hemisphere in Transcortical Aphasia
    • Typically the dominant (left) perisylvian area is intact
    • Research studies have indicated that the perisylvian areas (broca's and wernicke's areas) can be impacted, but repetition can still be preserved. 
    • Homologous regions of the right hemisphere may contribute to the mediation of residual aspects of repetition.
  95. Define global aphasia
    • Usually results from extensive damage to the language zones of the left hemisphere.
    • Occlusion of middle cerebral artery.
  96. what are the areas affected in global aphasia?
    • Area supplied by middle cerebral artery 
    • Temporal, frontal, parietal lobes
    • Brocas and wernickes areas
    • Basal ganaglia
  97. What are defining characteristics of aphasia?
    • Severe persisting deficits across all communicative modalities
    • Severe brocas aphasia and wernickes aphasia
    • Produce very few words (if any)
    • Usually severely apraxic (oral and limb apraxia)
    • Nonverbal problem solving deficits.
  98. All aspects of language are so severely impacted that there is no longer a distinctive pattern of preserved versus impaired components but the exceptions are...
    • Auditory comprehension of coversation about immediate personal concerns (medical problems, family members, recent personal events)
    • Unerstanding of geographical place names
  99. What are the cognitive skills intact with global aphasia?
    • Alert and aware of their surroundings. Task oriented. Socially appropriate.
    • Performance on nonverbal intelligence tasks is average or near-average.
  100. What is the prognosis of global aphasia?
    • Do not yield easily to traditional forms of treatment
    • The larger the lesion the greater its proximity to the primary language zones. 
    • The more severe the aphasia, the poorer the prognosis
    • Higher degrees of variability of performance among subtests or tasks = better prognosis.
    • often progresses to brocas aphasia
    • Some spontaneous recovery, but complete recovery is rare.
  101. What is a distinct syndrome in anomic aphasia
    Various lesion sites
    • Diverse courses
    • Main area of concern-impaired word retrieval (speech and writing)
    • Fluent
    • Grammatically correct
    • Unusual pauses
    • Circumlocution
    • Non-specific words
  102. Describe the lesions from various areas that have resulted in anomic aphasia
    • Frontal Anomia: similar to transcortical motor aphasia, severe word retrieval but when the first sound of the word is given, the word is typically retrieved. 
    • Anomia of the angular gyrus region: fluent speech but severe word retrieval, words are not retrieved nor are they recognized when presented to them. Repeat a word over and over agian
    • Anomia of the inferior temporal gyrus: Fluent speech but severe word retrieval, appropriate grammar, near normal reading writing, auditory comprehension.
    • Anomia as an expression of residual: Recovery from a more severe aphasia lading to anomic aphasia, most common means to diagnosis of anomic aphasias.
  103. what is the hallmark of anomic aphasia
    word retrieval.
  104. what is the definition of dementia?
    Dementia is a syndrome that can ve defined as the chronic, progressive deterioration of intellect, personality, memory, and communicative function resulting from central nervous system dysfunction
  105. Dementia primarily affects
    older adults
  106. According the DSM IV, an individual must exhibit
    • Impaired short-term memory
    • Impaired long-term memory
    • At least one of the following characteristics: 
    • Impaired abstract thinking
    • Personality change
    • Impaired judgment
    • Impaired constructional abilities
    • Impaired language
    • Impaired praxis
    • Impaired visual recognition
  107. Must also be
    • Insidious (gradual and progressive) in onset
    • Cognitive deficits are not due to an Axis I disorder (e.g., schizophrenia or major depressive disorder)
    • Acquired
    • Persistent
    • Affects several areas of mental function
    • Severe to the point of interfering with work, social activities, and relationships
  108. What are the principal irreversible causes of dementia
    • Alzheimer's disease
    • Pick's disease
    • Creutzfeldt-Jakob's disease 
    • Huntington's disease
    • Multiple infarctions (little strokes)
    • Kuru
    • Wilson's disease 
    • Parkinson's disease
    • Lewy body disease
    • binswanger's disease
  109. What are principal reversible causes
    • Infection
    • drug toxicity
    • vitamin deficiency
    • tumor
    • depression
    • normal pressure hydrocephalus
    • renal failre
    • congestive heart failure
    • thyroid disease
    • Hypoglycemia
  110. What are the early signs of dementia
    • memory failure
    • disorientation
    • lapses in judgment
    • difficulty with DL activities
    • Difficulty with mental tasks
    • Misplacing things
    • apathy 
    • changes in mood.
  111. The risk of developing dementia ...
    increases with age.
  112. What are the most common types of dementias and their percentages?
    • Vascular dementia 15%
    • Alzheimers disease+vascular dementia 10-15%
    • Others 15-10%
    • Alzheimer's disease 60%
  113. Cortical dementia starts where and what is the 3 types
    • Starts in cortex
    • Alzheimer's disease
    • Pick's disease
    • Primary progressive aphasia
  114. What is the prevalence of Alzheimer's Disease
    • 4 million adults in the us population
    • 5-10% of the over 65 population
    • 15-30% of the over 80 population
    • 50-70 % of all progressive dementias
    • More common in women then in men
    • Starts in hippocampus
  115. What miscroscopic changes need to be present to have Alzheimer's.
    Neuritic plaques and tangles
  116. what are neurofibrillary tangles and neuritic plaques and granulovacuolar degeneration
    • Neurofibrils are threadlike structures (cell bodies, dendrites, axons)
    • Minute areas of tissue degeneration consisting of granualr deposits and remants of neuronal processes. 
    • small fluid-filled cavities appear inside nerve cells.
  117. Describe alzheimer's disease in the early stages
    • Phonology, syntax, articulation, voice quality are well-preserved
    • Mild word retrieval problems 
    • Occasional Verbal paraphasias
    • subtle comprehension difficulties
    • adequate conversationalists.
  118. Describe alzheimer's disease in middle stages.
    • Word retrieval problems more obvious
    • Sentence fragments/ungrammatical sentences
    • Reading becomes nonfunctional except for the most familiar material
    • Conversations become difficult
    • Apathy
    • Conventions
    • Figurative language
  119. Describe Alzheimer's disease in the late stages
    • Comprehension- only familiar words and phrases
    • Speech- single words and sentence fragments (bizarre,
    • devoid of meaning)
    • Conversation- nonfunctional
    • Reading/writing- nonfunctional
  120. describe the most sever alzheimers disease brained.
    large ventricles less good area.
  121. What are the subcortical dementias?
    • Parkinsons disease
    • Huntingtons disease
    • Progressive supranuclear palsy
    • Human immunodeficiency virus encephalopathy
  122. What is the prevalence Parkinson's disease?
    • 1% of adults in the US
    • More common in men than woman
    • Usually appears between ages of 50- and 65- years old
    • Need dopamine to regulate firing of neurons, but dopamine is reduced in parkinsons and extra movemets that are uncontrollable are the result
  123. Describe the Neuropathology of Parkinsons
    • Degenerative disease affecting nuclei in the midbrain and brain stem
    • Idiopathic- unknown cause
    • Subcortical in thalamus
    • Primary symptoms:

    • Resting tremor
    • Muscle rigidity
    • Slowness of movement and difficulty initiating
    • movement
    • Impaired balance
  124. Describe Parkinsons disease in the early stages
    • First complain is weak voice
    • Speech- rate increases, rapid, stuttering like repetitions of syllables, words and phrases
    • Articulation-becomes more indistinct (slurring)
  125. Describe Parkinsons disease in the middle stages
    All other sympotms plus drooling and swallowing impairments, vocabulary and syntax are fairly well preserved
  126. Describe Parkinsons disease in the late stages
    • Drooling and swallowing impairments
    • Vocabulary and syntax deteriorate
    • Comprehension of complex verbal materials becomes difficult
    • Tasks required sustained attention and mental effort become problematic
    • Sufficient intellect to function in familiar
    • environments

    *Starts subcortical and then moves cortically*
  127. Describe Mixed Dementia
    • Vascular Dementia
    • Lewy body dementia (progressive, most common behind alzheimers, abnormal protein deposits in cell bodies. mimic parkinson's and Alzheimer's. Motoric and memory problems)
    • Frontotemporal dementia
  128. What is the prevalence of vascular dementia
    • 15-20% of dementia cases
    • Increases with age.
  129. What is the neuropathology of vascular dementia.
    • Presence of dementia
    • Evidence of cerebrovascular disease
    • Types:

    • *Multi-infarct dementia (most common)- multiple areas
    • of the brain

    • *Lacunar state
    • ****Multiple small infarcts in arteries pertaining to subcortical areas (basal
    • ganglia, thalamus, midbrain, brain stem
    • *Multiple cortical infarcts
    • ****Thrombotic/embolic occlusions of cortical arteries

    • *Binswanger’s disease
    • ***Multiple infarcts in subcortical white matter
    • *Thrombotic/embolic occlusions
    • ***Fairly uncommon
  130. What is the diagnosis for the vascular dementia
    • Memory impairment
    • Cognitive deficits cause significant impairment in social or occupational functioning and represent a significant decline from previous functioning 
    • focal neurologic signs are present plus symtoms of cv disease that is etiologically related to the disturbance 
    • Deficits do not occur during delirium
  131. Describe the cognition and communication of vascular dementia as compared to Alzheimer's disease.
    • Resemble those of patients with Alzheimer's disease: recent memory, abstract thinking, reasoning, problem solving
    • Differences: Patchy patterns of impairment, somewhat better immediate memory, tend to remain aware of disabilities (more susceptible to depression)
  132. What are other causes of dementia
    Normal pressure hydrocephalus (build up of cerebral spinal fluid and it is not absorbed as it should be. Not shunted out. Causes pressure on brain and brain reabsorbs fluid but the ventricles get enlarged and do not return to normal size.
  133. What are symptoms of pseudodementia
    Cognitive impairments, loss of appetite, difficulty sleeping, social withdrawl, apathy.
  134. What are the differences of pseudodementia and real dementia?
    • Identifiable onset with rapid symptom development with pseudodementia
    • Little effort to perform clinical test
    • Test performance is highlt variable
    • Dementia is insidious development that in the early stages try hard to prove there is nothing wrong with consisten performance.
  135. WIth Delirium a person experiences:
    • Confusion
    • disordered thinking
    • disorientation
    • agitation
    • hyperactivity
    • distractability 
    • some times delusions and hallucinations
    • Usually transient (dementia is degenerative)
    • Onset is rapid (hours to few days)
  136. What are causes of delirium
    • Medication
    • Infections
    • Metabolic disorders
    • surgery, anesthesia
    • substance withdrawl
    • kidney or liver disease
    • toxins
Card Set:
Language Final
2013-05-05 03:09:28
Language Final

Language Final
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