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  1. What is TBI?
    is caused by a blow to the head or violent head movement similar to what happens in a high-impact motor vehicle accident.
  2. TBI has to occure ____ not ____
    after not during birth
  3. An injury is considered a TBI when, and only when, there is....
    Evidence of total or partial functional disability or psychological impairment or both.
  4. TBI excludes
    developmental brain disorders and other neurological conditions.
  5. List examples of non-traumatic brain injuries
    • Anoxic injuries caused by reduction in oxygen.
    • Infections of the brain (meningitis and encephalitis)
    • Stroges and other vascular accidents
    • Tumors of the brain
    • Metabolic disorders
    • Toxic products.
  6. TBI can result in impairment of
    • cognitive functions
    • emotional/socia/behavioral functions
    • physical functions
    • speech/language functions and swallowing
  7. Describe the ways TBI can occur
    • Penetrating injuries: An object striking the head can break through the skull and penetrate the brain (gunshot)
    • Diffuse Axonal Injuries (DAI): Brain is stretched and twisted within the skull
    • Focal Contusions/contact injuries: A blow to the head can bur is the brain
  8. What is an open head injury vs closed head injury?
    • OHI: caused by accidents, falls abuse, assaults and surgical procedures that result in a penetrating wound to the brain (more focal)
    • CHI: caused by accidents, falls abuse, and assaults in which the membranes (meninges) surrounding the brain remain intact but damage to the brain comes from internal compression, stretching or shearing actions (more diffuse)
  9. TBI severity rating refers to...
    • the amount of acute (immediate) disruption of brain physiology or structure.
    • You derive from clinical evaluations
    • Ratings predict course of outcome. 
  10. Describe the characteristics of a Mild TBI
    • Injury to the head arising from blunt trauma or acculturation or deceleration forces that results in one or more of the following:
    •     - GCS 13-15
    •     - Loss of consciousness <20 min.
    •     - Post-traumatic amnesia + coma <1hr
    •     - Injury is NOT visible with medical imaging
    •     -Any disfunction of memory around the time of the injury
    •     -Individual appears to be "fine"
  11. 10% of individuals with MILD TBI
    experience long term consequences
  12. Mild TBI =
    does not equal mild impairment.
  13. Describe the characteristics of a Moderate TBI
    • GSC 9-12
    • LOC 20 min- 36 hours
    • COma + PTA 1-24 hours
    • Individual may sustain fractures, bruises, or bleeding of the brain (subdural hematoma)
    • Injury is visible with medical imaging
    • 1/3-1/2 of individuals will have lifetime difficulties with learning and daily activities.
  14. Describe the characteristics of a Severe TBI
    • GCS 8 or less
    • LOC> 36 hours
    • Coma + PTA longer than 24 hours
    • 80% of individuals will have lifetime disabilities
    • Long term support will be required at home, in school, and in the community and to sustain employment and independent living.
  15. At least ___ people sustain a TBI each year?
    Approximately ____ people died from a TBI
    TBI effects...
    • 1.4 million
    • 50,000
    • the entire family no just the patient.
  16. What groups are at risk for a TIB?
    • Males are about 2x as likely as females to sustain a TBI
    • Infants and children aged o-4 and adolescents aged 15-19 years are the 2 age groups at highest risk for a TBI
    • Adults aged 75 years or older have the highest rates of TBI related hospitalization and death
  17. TBI results in both primary and secondary brain injury- describe both
    • Primary injury: occurs immediately following impact and is related to instantaneous events directly caused by the blow. 
    • Secondary injury: is characterized by a cascade of biochemical, cellular and molecular events involved in the evolution of secondary damage.
  18. Describe what happens during a TBI
    • When the brain is injured, neuronal connections may be disrupted- some are stretched and some are completely torn.
    • There is evidence that new connections can be developed throughout life, and that "stretched" connections can heal
    • Broken connections cannot mend and the neurons cannot regenerate once dead.
    • When an injury occurs, the clean up process in the brain usually results in swelling around neurons, particularly around any stretched or bruised connections.
    • This swelling prevents those parts of the brain from working optimally and can last a long time up to three years following an injury
  19. Describe neuronal death
    • Impact depolarization
    • Increases in extracellular potassium and glutamate
    • Initiates excitotoxicity
    • Glutamate causes sodium dependent neuronal swelling
    • Also causes calcium influx which then in turn triggers processes that lead to mitochondrial and DNA damage and eventually cell death
  20. Describe traumatic axonal injury
    frank axonal tears and secondary axotonmy.
  21. Describe primary impact damage in CHI?
    • Biomechanical forces 
    •     -Acceleration/Deceleration (linear)-Whip lash: The brain moves back and forth inside the skull at great speeds and hits bony protuberances
    •     -Rotational acceleration (twistin): The surface of the brain can get caught and parts of the brain can twist away from other parts. 
    •     -Compression
  22. What is primary impact damage
    • CHI typically gives rise to contusions and laceration on or within the surface of the brain 
    • Lacerations: are lesion s that break the pia matter (cuts)
    • Contusions: Leave the pia mater intact (bruise)
  23. Describe acceleration and deceleration with coup and contracoup
    • After impact, the skull decelerates to a sudden halt but the brain continues to plunge forward at its accustomed velocity until it too is stopped by the frontal skull.
    • This site of initial brain impact with the skull is the coup lesion or the impact pole
    • The exact sequence of events reverses direction and the brain lags behind the skull moving in the opposite direction
    • The resulting injury at the antipope at the site directly opposite the impact pole is the countercoup.
    • The deceleration process in both directions often takes several oscillations before the brain achieves zero velocity.
  24. What is the primary damage from the acceleration and deceleration?
    Coup, contrecoup, frontal and temporal lobe crests and surface lesions of the upper boarders of the hemispheres.
  25. Describe rotational (angular) acceleration injuries
    • Brain rotates at an angle causing abrasions, lacerations and twisting/shearing forces resulting in diffuse axonal injury and hemorrhage and cranial nerve trauma
    • Most lesions occur in the deep white matter and brain stem
  26. Describe a compression injury
    • Brain matter is compressed or deformed by pressure against the skull
    • Propagation of shock waves throughout the skull and brain can also occur and may result in small intracerebral hemorrhages
  27. What is the skull-brain interface?
    • This is that it is common for contusions (bruising) to occur in cerebral regions adjacent to these skull regions where there is the greatest bone-brain interface.
    • Lacerations are often seen on the orbital frontal cortices and the tips of the frontal and temporal lobes.
  28. What is the most common neuropathological consequence?
    Damage to the hippocampus (memory) and other medial temporal lobe limbic (emotion) structures, resulting in post-traumatic memory disorder and emotional behavior changes.
  29. with the skull brain interface, the superficial bruising of ____ are frequently found in the ___  regardless of the site or direction of initial impact
    • gyral crests 
    • frontal and temporal regions
    • site or direction of initial impact.
  30. Lacerations are ..... which can lead to ....
    They usually heal and leave ....
    • hemorrhagic lesions which can lead to edema and necrosis within the brain.
    • Yellow brown atrophic scars that are easily recognized on autopsy.
  31. What are the types of primary damage associated with OHI?
    • Low velocity: Concentrated force causes fracture of the skull with debris entering the brain--destruction of tissue at the site of impact is often substantial
    • High velocity: a projectile enters the brain-causes destruction of tissue around the projectile path
    • Main areas of damage from primary involvement are surface contusion, anterior and inferior frontal and temporal damage, bilateral temporal damage, frontolimbic damage, brain stem damage, basal ganglia damage.
  32. what are impression traumas and ellipsoidal deformation that are associated with OHI?
    • Non-acceleation is a moving object that hits the head
    • Impression trauma: Meninges and cortex at site of impact are damaged as skull is deformed by a rapid blow. Negative pressure created by the rebound of skull may contribute to damage. 
    • Ellipsoidal defomation: A slow moving object with a large surface area deforms the skull from oval to circular shape--brain tissue moves outward from center resulting in stretching and tearing of central structures such as the basal ganglia.
  33. What is secondary damage with CHI?
    • Edema
    • Ischemic brain damage
    • Hemmorrhage
  34. The cranial cavity is partitioned by the ...
    • tentorium cerebelli and falx cerebri. 
    • When part of the brain is compressed by a subdural hematoma or is expanded because of a contusion, it is displaced (herniates) from one cranial compartment to another.
  35. what is edema as secondary damage?
    increase in brain volume due to an accumulation of excess water in the brain tissue. Caused by increase in permeability of capillaries allowing water to exclude out into extracellular spaces. Results in raised intra-cranial pressure (ICP)(NOT IN VENTRICLES)
  36. What is ischemic brain damage as secondary brain damage with CHI?
    Hypoperfusion (low blood supply in brain) and herniation lead to further brain damage in the form of pressure necrosis and infarction, often remote from the site of the primary injury--diaschisis.
  37. What is hemmorrhage as secondary brain damage with CHI?
    • Extracerebral: Bleeding into the meninges (epidurla, subdural, subarachnoid)
    • Epidural (or extradural): usually results from laceration from bone fracture, may develop quickly and need immediate evacuation to avoid disability
    • Subdural (veins): develop more slowly. 
    • Intracerebral: bleeding into brain tissue--associated with diffuse axonal injury.
  38. If a hemorrhage is not treated...
    • results in drowsiness, paralysis down one side of the body, compression of 3rd cranial nerve
    • compression of brain stem, herniation, fatal due to compression of vital centers in the brainstem.
  39. What is the medical management of a Tbi?
    • Evacuationof hematomas
    • control increasing ICP
    • Prevention of hypotension/hypoxia
    • maintain cerebral perfusion
  40. What are Post-traumatic complications?
    • Residual disability or new developing complication (seizure disorder) can be from impact damage or secondary processes
    • Focal injuries often leave residual focal neurological deficits such as hemiplegia, hemiparesis, hemianopsia, aphasia.
    • Cranial nerve abnormalities often arise when cranial nerves are damaged when the skull is fractured or when the brain is thrown about dying acceleration/decleration injury.
    • Post traumatic eplilepys
    • Post-traumatic vertigo
  41. What are the post-traumatic complications caused by?
    Diffuse (widespread) injury; other by focal injury
  42. What is the most severe form of diffuse damage
    chronic or persistent vegetative state- affecting 5% of head injury survivors.
  43. Post traumatic epilepsy is more probable after?
    • depressed fracture with dural tear
    • penetrating wounds
    • amnesia of > 24 hours
    • usually develops within the first 2 years post-injury
  44. Describe post traumatic vertigo
    • Dizziness/nausea
    • may last for days, weeks, or months
  45. What is the most common and most complex sequelae of HI?
    PTS-Post Traumatic Syndrome
  46. Describe PTS
    • It uses headaches, dizziness, difficulty concentrating, host of vague behavioral symptoms such as anxiety, depression, and nervous instability.
    • More common with slight trauma than serious 
    • lasts a few weeks to a few months- symptoms gradually disappear and are exacerbated by strenuous physical activity, emotional stress, and use of alcohol,
    • rest and symptomatic treatment are usually required.
  47. What are cognitive deficits following TBI?
    • Difficulty focusing and sustaining attention
    • delayed response time
    • decreased ability to organize information
    • difficulty with simultaneous processing
    • limited ability to generalize
    • rigid/concrete problem solving
    • decreased concept formation
    • altered perceptual/spatial function
    • decreased judgement
  48. What are the behavioral issues with a brain injury
    • poor self control
    • limited insight into deficits
    • lack of initiative
    • non-compliance
    • depression
    • decreased understanding of social rules
    • irritability, agitation,agression
    • low threshold for over stimulation
    • emotioanl lability
    • low frustration tolerance
  49. Describe the physical functions of TBI
    • Low energy
    • difficulty with coordination, balance, and movement
    • changes in sense of smell and taste
    • chronic pain, headaches, dizziness
    • visual or auditory changes
    • seizures
    • sleep disturbances
    • fine motor coordination
    • paralysis or spasticity
    • swallowing difficulties
  50. What are the speech/language functions?
    • Understanding language
    • expression (word-finding) 
    • abstract thought
    • speed, accuracy, and coordination of speech
    • impaired breath support for speech
  51. How do you determine the prognosis of a TBI
    • Age (younger=better)
    • GCS Motor score (higher=better)
    • Pupillary reactivity
    • Presence of epidural hematoma vs subdural hematoma on CT (less direct damage to brain, more likely to be evacuated)
    • Premorbid cognitive function
  52. What are the positive indicators of prognosis
    • GCS>9
    • PtA<24 hours
    • LOC<6hrs
    • Limited imaging findings
    • No dural penetration
    • No pupillary response abnormalities
    • No hypoxia
    • No systemic complication
  53. What are the negative indicators of Prognosis
    • GCS<9
    • PTA>24 hours
    • LOC>6hrs
    • CT/MRI findings
    • Pupillary response abnormalities
    • Hypoxia
    • Ocular Motor abnormalities
    • Secondary systemic complications
  54. REMEMBER: The severity of the injury....
    does not always equate to the functioning level of the patient.
  55. What is cognition?
    • Knowing
    • the study of the thinking mind is concerned with how we attend and gain information about the world, how that information is stored in memory by the brain and how that knowledge is used to solve problems, to think, and to formulate and use language.
  56. What is attention?
    The concentration of mental effort on sensory or mental events.
  57. What are the three components of attention?
    Arousal, vigilence, selective attention
  58. What is arousal?
    • physiological state underlying a general readiness to act or to receive and process incoming information.
    • can be hypo (coma/sleep) or hyperaroused (ptsd)
    • other forms of attention depend on optimal level of arousal 
    • orienting to sensory events.
  59. What is vigilence
    • state whereby attention is sustained over a fairly long period of time (sustained attention)
    • Maintaining attention to driving or holding a conversation
    • Selective attention depends on it
  60. What is selective attention?
    • Split attention
    • Intention:governs which actions are performed ("executive attention") 
    • Attention: Ability to select for further processing 
    • Early vs late selection
    • Controlling access to memory and awareness
  61. Attention is limited by?
    • the amount of information we can hold in our immediate attention (working memory)
    • Performing simultaneous tasks can interfere with each other in the same modality or in different modalities
  62. Describe the Bottleneck theory of attention
    • Theories that attempt to explain how people select information when some information processing stage becomes overloaded with too much information 
    • Point in information processing where only ne piece of information processed at a time (serial processing --> only one thing done at a time
  63. Describe the famous example of the bottleneck theory
    The cocktail party effect: found people were not sensitive to what they were told to ignore. played two different inputs and asked to listen to one. People were good at selecting what to listen to.
  64. Describe the capacity theories
    • Minds have limited amount of mental fuel; different tasks share the amount of mental fuel available
    • can do two tasks in parallel, if enough mental fuel available (divided attention)
    • A person has considerable control over how this limited capacity can be allocated to different activities (driving and talking)

    Thought you don't have to do serial processing.
  65. Describe the allocation of capacity
    supply and demand- when the supply of attention does not meet the demand, level of performance declines.
  66. Compare and contrast bottleneck vs capacity
    • The capacity model was proposed to supplement the bottleneck theories not replace them
    • both types of theories predict that simultaneous activities are likely to interfere with each other, but they attribute the interference to different causes.
  67. compare and contrast automatic vs controlled processes
    • automatic mental processes are those that require little or no mental effort (riding bike, tying shoes)
    • Controlled mental processes are those that require mental effort.
  68. Describ the strop test
    This is when words of colors appear and the color of the word does not match the word.
  69. What are characteristics of automatic processes?
    • Fast
    • well practiced
    • unavailable to consciousness
    • occur without intention
    • do not require mental resources
  70. What are characteristics of controlled processes.
    • Slow
    • not well practiced
    • conscious
    • require intention
    • require resources 
    • EX: obstacle course, driving in unfamiliar place
  71. What is memory?
    • Means by which we draw on our past experiences in order to use this information in the present.
    • As a process, memory refers the the dynamic mechanisms associated with retaining and retrieving information about past experience.
  72. What are the 3 operations identified in memory?
    • Encoding: during this process you transform sensory data into a form of mental representation (acquisition and consolidation)
    • Storage: you keep encoding information in memory
    • Retrieval: you pull out or use information stored in memory
  73. What are the memory subfields?
    • Decay
    • Displacement 
    • Interference
  74. Describe the sensory or immediate stage of memory
    approximatly 1 sec. Bridge between perception and memory opportunity to organize and categorize incoming info. Nothing stored here.
  75. Describe iconic memory
    • Sperling's experiments indicate the existence of a brief visual sensory memory-known as iconic memory or iconic store
    • Infromation decays rapidly (after a few hundred milliseconds) unless attention transfers items to short term-memory
    • Analogous auditory store: echoic store
  76. STM is a ...
    limited capacity store for information - place to rehearse new information from sensory buffers
  77. Items need to be rehearsed in STM...
    before entering long term memory. Probability of encoding in LTM directly related to time in STM
  78. Describe the recency effect and the primacy effect?
    • Remembering things most recently scene
    • First times scene in a list.
  79. What are serial position effects
    • Explanation from atkinson and shiffrin model:
    • Early items can be rehearsed more often (more likely to be transferred to long-term memory
    • Last items of list are still in short term memory (with no distractor task)
    • they can be read out easily from short-term memory
  80. What are the pros and cons of  modal memory model
    • Pro: provides good quantitative account of many findings
    • Con: Assumtion that all information must go through STM is probably wrong
    • Model proposes one kind of STM but evidence suggests we have multiple kinds of STM stores
  81. Describe Baddley's working memory model
    • WM contains information that can be acted on and processed
    • A unitary STM was insufficient to explain the processing and maintenance of information over short periods.
  82. How many things can be stored in short term memory
    • The STM holds 7 units-letters or words +/- two
    • Individual letters should fill each slot, whereas letters that composed words/acronyms etc. were chunked into 1 word unit. occupying only 1 slot in Stm. Chuncking is therefore greatly expands the capacity of STM
  83. Describe the phonological Loop- phonological store
    • Auditory presentation of words has direct access
    • Visual presentation only has indirect access
    • Affected by phonological similarity
  84. Articulatory process
    • converts visually presented words into inner speech that can be stored in phonological store
    • affected by word length
  85. Describe reading rate and recall
    • Reading rate seems to determine recall performance
    • Phonological loop stores 1.5-2 seconds worth of words
  86. Working memory and language differences
    • different language have different # syllables per digit
    • Therefore, recall for numbers should be differennt across languages
  87. Describe decay
    Occurs if info is not rehearsed. info processing leaves a trace with disuse these fade-use it or loose it. LTM
  88. Describe interference
    • Assumes that forgetting reflects the disruption of the memory trace by other traces w/ the degree of interference depending on the similarity of the 2 mutually interfering memory traces STM
    • Memory performance is a combination of active rehearsal and storage in STM
    • If active rehearsal is prevented by the counting-backward task, the items decay from STM
    • Interference is at a process level-counting interferes with rehearsal
    • Block necessary processes; prevent learning; erase/overwrite;exhaust resources; prevent recall
    • Performance on both tasks decreases.
  89. Storage and rehearsal processes in phonological loop are
    functionally independent. The longer the word length the lower the accuracy of recall.
  90. Describe retroactive interference and proactive interference
    • Retroactive interference: new information prevents recall of previous information e.g. overwriting a computer file
    • Proactive interference: prior learning prohibits new learning e.g. learning new cultural customes
  91. Describe long term memory
    • Permanent repository of information that has diverse amount of information-codes, abstractions, structure, etc. capacity is limitless
    • Explicit and declaritive : some level of conscious access is available-personal world knowledge
    • Implicit and nondeclarative: means no conscious access-procedural knowledge
  92. Describe declarative memory
    • available to conscious retrieval
    • can be declared (propositional)
    • Ex: what did i eat for breakfast (episodic)
    • What is the capital of spain (semantic)
    • What did I just say? (working)
  93. Describe NON-Declarative (implicit/procedural)
    • Experience-induced change in behavior
    • Cannot be declared (procedural)
    • Ex: Subliminal advertising (priming), how to ride a bicycle (skills) phobias (conditioning)
  94. Describe Episodic Memory
    info about specific events can have surprising detail-receives and stores info about temporally dated episodes or events and their relations-it is susceptible to change and loss
  95. Describe semantic (fact) memory
    permanent knowledge, memory of words, concepts, rules, abstract ideas. Subseved by cerebral cortex These differ also temporally episodic memory is more susceptible to forgetting , lost rapidly.
  96. Describe executive function
    • Cognitive control mechanism: involved in regulation of other cognitive skills (attention, working memory)
    • Complex cognitive (non-automatic) activities: Strategic planning, cognitive flexibility (disengaging and reengaging), abstract reasoning, self-monitoring, inhibiting automatic responses (not eating cake while dieting)
    • Required coordination of multiple subprocesses to organize behavior and achieve goals
    • Required to cary out activities of daily living
    • Required for complex communication: discourse, organization, appropriateness and efficient of the message
  97. Why is speech a complex motor act?
    • Disproportionate cortical sensorimotor space allotted to larynx, palate, tongue, lips
    • It recruits more motore fibers than any other motor act
    • it generates multimodal feedback probably more than any other routine behavior
    • Large #of muscles and neuromuscular events
    • Temporal precision in the range of 10 msec.
  98. What is dysarthria
    • A collective name for a group of motor speech disorders associated with disturbed muscular execution or control of the speech mechanism due to CNS and/or PNS damage 
    • Damage to nervous system pathways results in inability to send proper message from brain to the muscles involved in speech
    • May include abnormalities in strength, speed, range, tone or accuracy of speech movements. 
    • May affect respiration, phonation, resonance, articulation, and prosody.
  99. what are causes of dysarthria?
    • Cerebral palsy
    • vascular (stroke)
    • Progressive neurological disease
    • Tumor
    • Infectios diseases/toxicity
    • surgical trauma (LMN damage)
    • muscle diseases
    • Trauma
  100. Dysarthria includes...
    • several different types, each corresponding to damage to particular parts of the nervous system and presumably each having different underlying neuropathophysiology
    • Each type has different auditory perceptual characteristics which can be distinguished clinically
    • Accurate identification has implications for localization accurate description provides clues for management.
  101. What is the most common type of dysarthria in TBI?
  102. What is the incidence of dysarthria in TBI
    • Dysarthria has a large impact on communication, as well as psychological, social, academic, and occupational aspects of life following TBI
    • Dysarthria is present in approximately 1/3 of patients following TBI (excluding mild)
    • Severity of dysarthria is often associated with the severity of the cognitive deficit (not causative, probably a reflection of overall extent of brain trauma)
    • Long-term outcomes are variable and progress is slow. Prognosis for complete resolution is poor.
  103. Describe the respiratory systems role in dysarthria and TBI
    • Speech production requires airflow
    • pulmonary airstream mechanism: pushes air out of the lungs through trachea
    • Ingressive: inhalation
    • Egressive: exhalation (1:6 inhalation: exhalation during speech production)
    • Exhalation cycle needs to be extended in time for completion of utterance and modulation to reflect stress
  104. Describe the phonatory systems role in dysarthria and TBI
    • includes various muscles and structures in the larynx, and regulates the production of voice and intonational aspects of speech
    • vocal folds are brought closely together and air pressure builds up to set the vocal folds into vibration
    • Vocal folds are stretched to manipulate the frequency of vibration, controlling pitch
  105. Describe the resonatory systems role in dysarthria and TB
    • Rgulates the vibration of the airflow as it moves from the pharynx into the oral and nasal cavity
    • Manipulates the shape and size of the oral cavity for maintaining normal sound quality
    • Manipulates the vela-pharyngeal port (weather the nasal cavity is used for a resonating chamber) for determining nasality of sounds.
  106. Describe the articulatory systems role in dysarthria and TBI
    • control of the articulators within the oral cavity to manipulate the outgoing airflow
    • Major structures: lower jaw, lips, tongue (important)
    • Tongue: intrinsic muscles (fine-tuned movements) and extrinsic muscles (coarse movements- protusion, retraction, elevation, depression)
    • Muscles contract to create constrictions in the oral cavity to produce varying sounds.
  107. What are the three types of nerve fibers?
    Commissural association projection
  108. What are commissural fibers
    • connect the two cerebral hemispheres. 
    • Ex: corpus callosum
  109. What are association fibers
    • connect areas of the brain whiten the same hemisphere. Long association fibers are known as fascicle. Fasciculi are large large bundles of axons. There are three major fascicle, 
    • EX: Arcuate fasciculus
  110. What are projection fibers?
    Connect areas of the cortex with lower levels of nervous system
  111. Descrive projection fibers
    • Efferent projection fibers are motor (they carry info from the cortex)
    • Afferent fibers are sensory (they carry info to the cortex)
    • Efferent motor fibers originate in the pre-central gyrus and in the area of the frontal lobe anterior to the pre-central gyrus. They innervate cranial nerve nuclei in the brainstem or cells in the spinal cord
    • Afferent sensory projection fibers originate in sensory receptor cells and their destination in the post-central gyrus
  112. What are the four major devisions of the motor system>
    • The final common pathway (lmn)
    • The direct activation pathway (UMN or pyramidal tract)
    • the indirect activation pathway (extrapyramidal tract -direct contact with LMNs)
    • The control circuits (basal ganglia and cerebellum-no direct contact with LMNs)- Basal ganglia and cerebellum
  113. UMNs are part of the ___ and LMNs are part of the ___
    • CNS
    • PNS
  114. UMNs originate in the ____ and synapse onto the ______ in the contralateral brainstem or onto ____ in the contralateral spinal cord
    • motor cortex
    • cranial nerve nuclei (corticobulbar tract)
    • cells (corticospinal tract)
  115. The ____ and ____ are also called the pyramidal tract
    • corticobulbar tract
    • corticospinal tract
  116. cranial nerves innervate...
    pinal nerves innervate...
    • muscles of the head and neck
    • muscles of the limbs and trunk
  117. The cortical spinal tract is
    • the main pathway for nearly all voluntary muscle activity. 
    • Comprised of UMNs
    • It is a bundle of axons, which changes names as it courses from cortex to muscles 
    • This is a crossed pathway. At the level of the pyramids in the medulla, approx. 80-90 % of the fibers in the tract cross the other side of the brainstem; therefore they descend in the opposite side of the spinal cord from where they originate.
  118. The corticobulbar tract
    • is comprised of UMN 
    • originates in the motor cortex 
    • crosses to the opposite side of the brain at various levels of the brainstem 
    • innervates cranial nerve nuclei at various levels of the brainstem
    • corticobulbar projections to most cranial nerve nuclei is bilateral but corticobulbar projections to some cranial nerve nuclei is contralateral
  119. Discuss projection fibers
    • Thus, if UMNs are damaged, you get spasticity as well as not being able to initiate skilled motor movements. 
    • Spasticity: increased muscle tone. A babinski sign signals the presence of UMN damage. Reflexes are exaggerated. 
    • If LMNs are damaged, you end up with flaccid paralysis
    • Flaccidity: decreased muscle tone. Atrophy of muscles. Reflexes are diminished or absent.
  120. The type of dysarthria from TBI is dependent on...
    • type and site of lesion
    • Due to the nature of TBI, there is wide variability of presenation
  121. The most common type of dysarthria in CHI is>
    spastic, due to bilateral UMN damage resultin in reduced range and force of movement and muscle spasticity.
  122. What are the characteristics of spastic dysarthria?
    Reduced rate of speech, imprecise articulation, hyper nasality, harsh vocal quality, strain-strangled effortful phonation
  123. what type of dysarthria results from damage to the cranial nerve nuclei in the brainstem or cranial nerves themselves?
    Flaccid. (twisting, pressure from increased ICP)
  124. Describe characteristics in realtion to damage
    • CNVII: decreased strength and ROM of lower face muscles, impaired lip closing for plosives
    • CN x: decreased strength of legator muscles of soft palate hyper nasality. 
    • Phonatory incompetence: breathiness, short phrases
    • Resonatory incompetence: hypernasality, imprecise consonants
    • Phonatory prosodic incompetence: harshness, monoloudness, monopitch.
  125. Describe the cerebellar control circuit
    • imposes control on movement initiated elsewhere
    • coordinates timing and sequencing of movement
    • helps scale size of muscle actions and maintain steadiness of movement
    • major role in error control based on periphery and knowledge of action goals.
  126. Describe damage to cerebllum
    • ataxic dysarthria
    • Incoordination of speech musculature
    • slow speech movements
    • inaccurate force, range, timing.
    • imprecise consonants, distorted vowels, irregular articulatory breakdowns, prosodic errors
  127. Describe what happens with damage to the extrapyramidal system
    • basal ganglia, may result in forms of hypo or hyperkinetic dysarthria
    • Less common in TBI
  128. Describe that characteristics of hypo kinetic dysarthria
    • rigidity
    • monpitch
    • monoloudness
    • reduced stress
    • repetition of phonemes
    • rushes of speech
    • delayed response initiation
    • EX: Parkinsons disease
  129. What are the characteristics of Hyperkinetic dysarthria?
    • Unpredictable, involuntary movements
    • manifest in any or all of the respiratory, phonatory, resinatory, and articulatory aspects of speech.
    • Can be generalized or affect a small group of muscles
    • Affects prosodic aspects of speech rhythm and rate of speech.
    • May include abrupts inhalations/exhilations, momentary voice arrests and strain or strangled vocal quality. 
    • EX: huntingtons
  130. Describe dysarthria and TBI
    • Frequently involves simultaneous damage to multiple brain areas and can result in MIXED dysarthria
    • Most frequent toy of dysarthria following TBI is mixed
    • Specific deficits depend on the site and extent of damage
    • Increased severity in the mixed types, 
    • Spastic-flaccid is very common
    • Hypokinetic is not as common because it deals with basal ganglia.
  131. What are the most frequently occurring dysarthria features following a TBI?
    • Hypernasality
    • Impaired rate
    • Imprecise consonants
    • Reduced normal pitch variation 
    • reduced breath support
    • abnormal stress battern
  132. Less common dysarthria features are..
    • reduced loudness variation and prolonged intervals
    • impaired overal intelligibility.
  133. what are speech and language problems following head injury?
    • communication problems
    • Controversy about the nature of these problems especially whether the patients are aphasic or not
  134. Describe the work by Heilman, saffron and Geschwind (1971)
    • Studied 13 patients with aphasia after a CHI
    • Found 9 cases with anomic aphasia, fluent speech output, normal comprehension and repetition and verbal paraphasias and poor object naming
    • the other 4 had fluent paraphasic speech output and poor comprehension and repetition-very like classic wernickes aphasia
    • There were no Broca's or global aphasics.
  135. Describe the Groher (1977)
    • Studied the progression of language deficits over time
    • CHI average 17 days in a coma
    • Patients were assessed as soon as consciousness was reached, then reassessed every 30 days for 4 months
    • when they were acute, their gestural skills were worse than graphic skills, and those were worse then verbal than verbal skills. 
    • By the final assessment, all could make needs known and converse.
  136. What is amimia?
    A disorder of language characterized by an inability to make gestures or to understand the significance of gestures.
  137. What are the arguments against language deficits in aphasia being the same as those in TBI?
    • Some of the initial language problems may be due to post traumatic amnesia, when people are confused and don't form memories of this time
    • Language problems due to pts being confused, with a poor stm lack of understanding of the environment and disorientation. 
    • Speech can thus be irrelevant in content while still be fluent and syntactical.
  138. Why is there a controversy?
    • Due to use of nomenclature associated with aphasia to classify linguistic deficits observed in TBI -E.g. anomic and wernicke's 
    • inherent variability (level of skills are diverse across patients and this affects studies) in TBI population
    • Inconsistencies in methodological parameters used in studies
    • Relative rarity of deficits (as measured by standardized assessments)
  139. What are the 3 ways that Audry Holland described TBI to be different than stroke patients
    • TBI is diffuse brain injury with pervasive memory and cognitive deficits.
    • Rehavilitation of CHI is more interdisciplinary than that of stroke 
    • There is a big demophraphic difference. 
    • TBI has confabulations and mis-namings in addition to circumlocutions and paraphasias.
    • TIB can have a sensory deficit. 
    • Most different in pragmatics
  140. Aphasia is a disorder of ___ while TBI show a disorder of ___ thus....
    • Form
    • Use
    • there can be a problem in orientation explanations, visual attention and utilization of contextual cues as well as reasoning.
  141. What are the 3 time course patterns following injury?
    • Full language function recovered if initial injury was mild 
    • After some mild head injury expressive deficits can remain for at least 6 months post onset with anomia
    • More severe damage, with diffuse swelling and bilateral hematoma correlated with persistent expressive and receptive impairment in at least one tear post injury with residual anomia, and non-verbal and verbal deficits.
  142. What is the prognosis for TBI?
    • Most linguistic recovery occurs within the first 6 months, especially in the first 1 month
    • memory problems tend to resolve first
    • There is disagreement about the best way of predicting outcome. Some studies find a correlation between coma length and severity of linguistic problems, others do not . (NOT CONCRETE)
    • *Cognition recovery goes with language recovery.
  143. What is the assessment and TX of speech and language disorders following TBI?
    • The integrity of an individuals communication(ability to make needs known or orient self) skills subsequent to TBI is often critical in determining post injury QOL
    • The S-L deficits may impose substantial social and vocational ramifications
  144. What is the adult impact of S-L skills with TBI?
    account for social isolation, academic failure and/or vocational demotion
  145. What are the child impacts of S-L in TBI
    account for immediate communication deficits, potential for predisposition to speech and or language impediments during the formative years...Infants fail to meet milestones
  146. What are linguistic deficits with TBI
    • Despite performing largely WNL on standardized batteries, TBI patients suffer some degree of dysfunction within the language realm. 
    • These deficits, while present, are often not enough to allow criteria to stand taxonomies to be met.
  147. What types of tests are used for TBI?
    • Interpretation of ambiguous sentences
    • Inferential judgments
    • semantically constrained sentence generation tasks
    • metaphore interpretation
    • Humor
    • semantic association tasks
    • synonym/antonym generation tasks

    • All tests can measure the interplay between cognitive processes with linguistic processes
    • The interface between language and cognition that appears to be the most susceptible in TBI patients
  148. Patients with TBI have impairments in language use:
    • digressiveness (pragmatics)
    • Difficulty in self monitoring
    • -disinhibition
    • -dificultying in attending to topic
    • -disorganization
    • -difficulty in initiating speech and its converse problem-once initiated, speech is difficult to stop
    • -difficulty in changing tobik.
  149. These language impairments reflect the cognitive disfunction that may occur after TBI
    • impacting attention recall
    • organization
    • sequencing
    • retrieval impairments are frequent.
  150. Language impairments resulting from I may be called __________ rather than aphasia
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2014-03-16 18:35:46
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