TBI Test 1

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  1. What is the definition of TBI?
    What may it cause?
    • Insult to the brainc caused by an external force
    • Diminished or altered state of consciousness, impaired cognition, physical, behavioral, and/or emotional functioning
  2. How is a TBI different from acquired brain injury?
    Acquired includes TBI, CVA, infection, etc.
  3. What are risk factors of TBI?
    Age (infant-birth-4, adolescents, 5-19, geriatrics-65+), gender (male), military service, sports, SES (increased stress increases violence, less safe conditions), history of TBI, drug/alcohol abuse, emotinoal status, education, ethnicity, communication status, social/emotional status (kids)
  4. What are causes of TBI?
    • Falls (#1)--81% of elderly
    • MVA--most frequent cause of TBI-related deaths
    • Unintentional blunt trauma
    • Assaults, violence--firearms leading cause of TBI death
    • More in summer
  5. Describe head injuries in the geriatric population. Sex ratio? Why? What are causes? What is the prognosis? What is an indicator of recovery?
    • Sex ration approximately 1:1 b/c there are more women than men
    • Falls, mva (as pedestrian), elderly abuse/assault, suicide (3rd leading cause in elderly)
    • Poor prognosis (more vulnerable to effects)
    • More severe effects may reflect pre-injury comorbidity factors (e.g., meds, dementia, pre-existing cog-comm disorders), effects of normal aging
    • TBI severity
  6. Name 2 issues in outcomes research in tbi.
    • heterogeneity issues
    • funding issues
  7. explain the 4 components of the prognostic visual
    • injury variables (location, type, when, severity)
    • environmental influences (family support, location of accident, access to learning environment)
    • individual's pre-injury characteristics (ses, cog-comm style, emotional status, age, etc)
    • individual's reaction to injury
  8. What is primary damage?
    Secondary damage?
    Examples of secondary damage? (brief)
    • macroscopic & microscopic structural (what occurs at the time of trauma)--macro=gunshot wound, micro=with imaging; Typically irreversible damange
    • Ways brain can be damaged subsequent to primary damage; can either be prevented or reversed in many instances
    • Examples: edema, hypoxia, raised intracranial pressure, hydrocephalus, intracranial hematomas
  9. What is edema?
    How do you control?
    • Swelling, can cause pressure changes=brain damage, can squish vasculature causing a stroke
    • Treat: hyperventilation (blood vessels constrict)
    • fluid restriction (less fluid, harder to swell)
    • decrease metabolic activity (anti-seizure meds w/ tbi to avoid excessive activity); includes sedation- induce coma, hypothermia-decrease metabolic needs
    • Mannitol- inject to draw fluids
    • Bone flap/decompressive craniectomy- hole in skull to decrease swelling
  10. What is hypoxia? What is it caused by?
    What neural structures can it affect? Why are these most susceptible?
    How do you treat it?
    • lack of 02 to brain. Caused by--decreased respiration, low arterial blood pressure, increased intracranial pressure, arterial vasospasm (1 or 2 arteries constrict)
    • Affects: hippocampus, basal ganglia (motor movement and cog. functioning), watershed/borderzone areas (transcortical aphasia), cerebellum (coordination, cognition)--served by small penetrating arteries (lack of blood supply)
    • Treat: Assure adequate airway, ventilation
  11. How can intracranial pressure affect the brain? What is the treatment?
    • Pressure on neural tissue/vasculature. If goes over 20 mmHg may cause damage.
    • Treat with Richmond bolt (pressure transducer), intraventricular catheter (CSF shunt-drains), hypothermia (decrease swelling, decrease inflammatory infection)
  12. What is hydrocephalus? What is its treatment?
    • buildup of CSF on brain
    • Shunt
  13. What are intracranial hematomas? How can it be toxic? What are the types of hematomas? How do you treat them?
    • buildup of blood=blood clot/pool
    • If it has occurred within tissue, toxic to brain; if not, pressure damage
    • Epidural: forming above the dura (bleed a lot & quickly)
    • Subdural: in subdural; slower but not good
    • Subarachnoid: in subarachnoid space
    • Intracerebral hematoma: within tissue; worse because it is toxic, also bad because it is hard to reach
    • Treat by evacuation
  14. What are non-neurological complications/alterations?
    • metabolic changes (cooling down helps with swelling but affects what nutrients healthy tissues receive)
    • Electrolyte imbalances (vomiting, etc.)
    • Hyperventilation
    • Failure to maintain airway
    • orthopedic injuries (potential to throw fat clots or emboli=potential CVA)
  15. What is an open TBI? What is the primary damage? What is the secondary damage? What is open head more frequently linked to?
    • Skin, scalp, and skull are penetrated
    • Primary: Focal, @ site of opening/penetration. Can have primary damage in skull fragments as well.
    • Secondary: if BBB is broken--infections, swelling, bleeding (hematomas), increased intracerebral pressure
    • *Open head is less likely to result in unconsciousness, but more frequently linked to epilepsy
  16. What is a closed TBI? What is the primary damage?
    • Contrecoup effects (acceleration-deceleration)--damage at the site of impact AND contralateral to hit (e.g., damage on R side, also damage on L). D/t pressure changes
    • Contusions
    • Diffuse axonal shearing/injury
    • skull fractures (not open because skin and scalp are still closed)
  17. What are at risk regions for contusions? (closed TBI)
    • Inferior frontal and temporal lobes (rough, bony prominences)
    • Corpus callosum
    • Cerebral and cerebellar peduncles (lie close to stiff membrane AKA tentorial membrane)
    • Cranial nerves VI, II, VIII, I (lie at exposed area at brainstem and inferior surface of frontal lobe)
  18. What is diffuse axonal shearing/injury? What are at risk regions?
    • Myelin of axon is sheared off or torn. These are at risk because they are at the intersection of gray and white matter
    • Basal ganglia (also vulnerable for hypoxia)
    • Periventricular zone or hypothalamus (circadian rhythms)
    • Superior cerebellar peduncles
    • Fornices (connects to hippocampus for memory)
    • Corpus callosum
    • Frontal and temporal poles
  19. What are blast/polytrauma injuryes due to? What does barotrauma refer to? What does damage severity depend on?
    • D/t blast over- and/or under-pressurization
    • Barotrauma refers to damage d/t pressure changes
    • Polytrauma-blasts usually cuase trauma to several parts of body
    • Severity depends on peak pressure (how much), duration, medium (what environment?), distance (how far away from blast?), presence/type of barriers & protective gear (cannot protect from pressure changes, but can protect from debris), explosive type (pressure, released chemicals, inhaled)
  20. What are some of the primary effects/at risk regions of blasts/pressure changes? What is most susceptible to blast injuries?
    Air-fluid interfaces (e.g., eyeballs, ear structures/cochlea, lungs)--EAR is most susceptible, brain changes d/t pressure, organ damage (throw fat or air emboli leading to CVA)
  21. What are secondary effects of blast injuries?
    • Any damage d/t flying debris
    • open head injury from flying debris, eye penetration
  22. What are tertiary effects of blast injury?
    • Effects from person's body being thrown
    • Eg. blast caused structure to collapse, debris caused open head or orthopedic injury
  23. What are quarternary effects of blast injury?
    • All other possibilities (burns, excessive inhalation of gases, chemicals, dust, radiation)
    • Symptom combinations: Psychiatric consequence (PTSD), cog-comm symptoms most overlooked
  24. Name some secondary complications of TBI
    • Contractures (significant stiffening/reduction of motion @ joint, related to being comatose or unconscious for period of time)
    • Skin breakdowns (on bony prominences)
    • environmentally induced psychosis/ICU psychosis
    • seizures (long-term, seizure onset is usually 1-2 years post trauma)
    • malnutrition (as body heals, increased metabolic needs-higher intake needed)
    • heterotopic bone formation/ossification- (Bone forming in soft tissue, most common @ joints)
    • Complications of prolonged intubation/trach
    • lower extremity deep venous thrombosis (clots)
    • Sleep distrubances
  25. What is the general pattern of recovery?
    • Coma phase
    • Post-traumatic amnestic/confusion phase (PTA)
    • Rapid recovery phase
    • Long-term plateau phase (slow recovery)
  26. Recovery from TBI is extremely variable and is related to:
    • Age, site/extent/type of damage (frontal lobe has poorer prognosis; intracranial brain damage=hematomas); great extent-worse prognosis; FOCAL has better prognosis
    • Length of coma & post-traumatic amnesic/confusion
    • Premorbid and current behavioral characteristics (physical fitness)
    • Environment in which patient returns and access to learning environment
    • Initial improvement rate
    • intracranial pressure
  27. Prognosis for TBI recovery is worse if:
    • GCS <7 (<7=comatose)
    • Subdural hematomas (bleed quickly, hard to control)
    • Old age
    • Decerebrate rigidity (brainstem lesions)
    • Lack of pupillary light or oculovestibular reflexes (indicative of brainstem lesion)
    • Lack of brainstem auditory evoked response
    • Penetrating injury (open head)--Acutely open worse prognosis because of bleeding & infection
  28. Explain the theories of recovery:
    1. Resolution of temporary physiological changes
    2. Regenerative & collateral sprouting
    3. Anatomical reorganization
    4. Behavioral compensation & functional adaptation
    • 1. Other nearby arteries constrict, lessening blood supply. CON: Neurons aren't adequately supplied, causing changes; once neurons detect its okay to dilate, neurons return to normal activity; NT go into high gear w/ TBI, but return to normal activity
    • 2. Axons grow and connect with neurons that didn't previously share information; can add dendrites, axons, synapses
    • 3. Intact regions of brain take on function of damaged regions (in adults, LEAST evidence)
    • 4. e.g. if you can't do mental math, use a calculator
  29. Define coma. What are causes?
    • Minimal organized or purposeful response to external or internal environment; Decreased arousal or awareness
    • More likely if there is rotational force to BI; more DAI=more likely to lose consciousness; If reticular formation is damaged=more likely
  30. What are assessments that are viable for coma?
    • Glasgow Coma Scale, used to grade severity.
    • 3-8=severe injury
    • 9-12=moderate
    • 13-15=mild
    • Based on eye opening, best motor response, verbal response
  31. What are limitations to the GCS?
    Could have poor motor responses and eye damage due to blasts making it look like they have head injury but they don't
  32. What is the goal of neuroimaging techniques?
    ID why person is comatose (hydrocephalus, pressure, etc.); used to detect causes of coma. CT does not have good spatial imaging--may not show microscopic damage like DAI
  33. What are neurophysiological measures of coma?
    Evoked potentials (somatosensory & brainstem)--don't require response from patient
  34. What are outcomes of coma?
    • Death= 30%
    • Brain death= 2%
    • Vegetative state= 1-7%
    • PTA= 60%
  35. What are treatment issues that occur w/ coma?
    • Counseling family members (education--define coma, contractures, etc.; don't' have to be there all the time, etc.)--BE CONSISTENT
    • Pharmacotherapy (dopamine agonist to increase arousal levels)
    • Sensory/coma stimulation
    • Phsyical management (PT, OT, nursing, etc.)
    • HBOT (Hyperbaric o2 tx--limited evidnce, only worth if its applied w/in 1st 24 hours); reduce mortality w/in 1st 24 hours but no reduction in severity of disability
    • Deep brain stimulation (limited research, requires sx)
  36. Define persistent vegetative state.
    • Appear to awaken from coma, but demonstrate no meaningful interaction with external or internal environment (might see eye opening)
    • Vegetative state=return of some vegetative functions (e.g., breathing on own, sleep-wake cycles)
    • If in vegetative state for 1 month, considered persistent
  37. What are common characteristics of persistent vegetative state?
    • Emergence of eye opening (usually in response to pain)
    • Presence of abnormal motor responses (bruxism--patients chew/grind teeth w/o food in mouth); primitive reflexes (e.g., grasp)
    • Absence of communication and other sustained, reproducible, purposeful, or voluntary behaviors
  38. What is the cause of persistent vegetative state?
    Relatively intact brainstem, but diffuse profound cortical damage (cranial nerves pick up information, but no where to send it to)
  39. What is locked-in syndrome?
    Brainstem damage--inverse of vegetative state; Intact cortex, substantial brainstem damage. Don't have means to communicate/respond
  40. What is brain death?
    Criteria physician uses to evaluate patient to diagnose with brain death; closer to coma--cortical damage with brainstem damage
  41. What is the minimally conscious state (aka minimally responsive state) criteria?
    • One of the following:
    • Show can follow simple command
    • Y/N response (any modality)
    • Give any kid of intelligible verbal output
    • Show some kind of non-stereotypical movement (e.g., no bruxism)
    • Affective behavior (emotional)
  42. To show emergence of minimal conscious state the patient must do what?
    • Show reliable, consistent, interactive communication (assessed by asking y/n questions)
    • Answer at least 6 Y/N ?'s on 2 consecutive evaluations
    • Show functional object use (put items in front of them-discriminate, then show use) of at least 2 objects on 2 consecutive evaluations
  43. What is akinetic mutism?
    • Severe deficit in drive/initiation
    • Not moving or responding, but not d/t cortical or brainstem damage. Rather d/t dopaminergic pathways
    • Assessed by doing fMRI for presence/absence of cortical damage
  44. What can you use to assess patients in persistent vegetative state?
    • Sensory diagnostic (hearing, evoked response)
    • JFK Coma Recovery Scale-brief (auditory, visual, motor, oromotor/verbal function, communication scale, arousal scale)
    • Disorders of Consciousness Scale-longer (baseline observation period to look @ stereotypical movements--ADVANTAGE), control environment, great inter-rater reliability, re-test measure to capture changes x time, better @ detecting vegetative state
  45. What is outcome of persistent vegetative state?
    death, minimally conscious state, brain death. If vegetative for 1 month or longer, 50% chance of regaining consciousness within a year. After 12 months, chances of coming out of vegetative state extremely unlikely (24% after 1 year showed spontaneous recovery)
  46. How can you manage persistent vegetative state?
    • Education/counseling
    • Drug treatment (increasing arousal levels)--amphetamines, anti-depressants for vegetative and minimally conscious patients; GABA agonists--check sedation effects
    • Coma/sensory stimulation programs
    • FAST-Familiar Auditory and Sensory Training (recordings of familiar voices, tapes telling stories, play materials daily)
  47. Define post-traumatic amnesia/confusion/delerium
    • Temporary phase of generalized cognitive disturbance
    • Quantified by time of TBI until emergence of PTA (point of which they have resumed normal, continuous, day-to-day memory--orientation)
    • Period of delirium because of abnormal NT levels
  48. Memory in PTA
    • No memory of continuous, daily events (disoriented, to person, to self, marital status, etc.); Don't remember circumstances of injury or what happened after; Won't remember time in this phase of recovery
    • All attention functions
    • Visual-spatial: get lost in own room, auditory-perceptual
    • Not applying meaning to what they see/hear; doesn't make any sense; speech and comprehension impaired
  49. Behavior in PTA
    Fluctuations in PTA (may be cohesive parts of day and not in others)
    • Agitated, restless, OR inert, decreased activity
    • bizarre, impulsive, unpredictable, eating inedibles, wandering, verbally and physically aggressive, labile, delusions/hallucinations, need to be physically or chemically restrained
  50. Assessment in PTA Phase
    Possible batteries/assessments?
    • Not usually done, but if done, use brief screeners
    • GOAT (Galveston Orientation and Amnesia Test)--primarily orientation
    • Westmead PTA scale--memory items w/ orientation
    • O-Log (orientation log)- orientation only; better predictor of injury severity
    • Delirium Rating Scale-Revised (orientation, attention, hallucinations/delusions, language items)
  51. Outcome of PTA
    Length of time PTA=predictor of outcome; accounts for ⅓ of variables
  52. How to manage PTA
    • Sedation (last resort)
    • Environmental adaptations (bed)
    • Reality Orientation (doing activities designed to orient; holiday themes, etc.), also used w/ dementia
    • Education/common recommendations
  53. Name/explain motor impairments following TBI
    • Most patients show best & fastest recovery here
    • Bradykinesia (slow movements, fine motor)
    • Spasticity (excessive tension, resistant to passive & active movement)
    • Ataxia (incoordination, overshooting targets); broad-based gait, tremor (intentional, one of most common post-TBI)
    • Hemiplegia/paresis: Not as common in TBI b/c damage is more diffuse
    • Rigidity/dyskinesias: damage to basal ganglia; abnormal movements
    • Swallowing disorders
    • Motor speech disorders
    • Sleep disturbances
  54. Explain how sensation can be impaired following TBI
    • Anesthetic limb--decreased sensation of pain, temperature, vibration, proprioception
    • Stereognosis: higher level ability to identify objects by touch
  55. Are visual problems common following TBI?
    Yes, 50% of TBI patients had visual disorders but are NOT previously identified. Common in blast injuries as well.
  56. Peripheral & brainstem problems affecting vision
    • Blindness
    • Ptosis
    • Eyeball deviation
    • Diplopia
    • Blurred vision
    • Accommodation Problems (switching from various stimuli)
    • Visual vestibular problems (sensitive to movement)
  57. Occipital lobe problems following TBI
    • Visual field cuts--20-30%
    • Blindsight (patients feel like they're blind but they can see)
  58. Temporal lobe problems following TBI
    • visual agnosia (can't apply meaning to what you see but you can see)
    • To differentiate naming and visual agnosia, present stimulus in another modality
  59. Parietal lobe problems following TBI
    • Visuospatial problems (depth perception)--can confound assessments
    • Visuomotor integration problems (AAC, drawing)
    • Prosopagnosia--inability to recognize familiar faces (can be memory or visual issue, difficult to differentiate)
  60. What is Photosensitivity/photophobia?
    sensitivity to light (more common if there are other visual disturbances as well)
  61. Discuss the impact on social communication, assessment and treatment, and olfactory problems following TBI
    • Social comm: Recognizing facial cues, depth perception, etc.
    • Refer to optometrist, neuropsych, ophthalmologist
    • CN sits on frontal bony surface, susceptible to loss of smell
  62. Discuss hearing problems following TBI
    Why does the % of hearing problems drop from 60-20 w/in 6 months of injury?
    • Swelling, pressure reduced or infection is resolved
    • Conductive loss: blood pooling in middle ear, ossicles disarticulated, tympanic membrane perforation
    • Sensorineural loss: CN VIII, infection, damage to inner ear (organ of Corti) more common in blast injuries; balance issues as well=slower recovery than hearing loss
    • Tinnitus: Common in mild head injuries, blasts
    • Vertigo: More common in blast (inner ear)
    • Auditory perception/recognition problems: Auditory agnosia (can't apply meaning to sound), prosody perception, temporal processing
  63. Arousal disorder in TBI
    What is it? What structure is responsible?
    • State of readiness
    • Brainstem, reticular formation
    • Influenced by environmental stimulation, excessive or deprived; internal stimulation, stress, sleep problems
  64. Information processing speed following TBI
    • AKA bradyphenia
    • Beyond motor-sensory problems; more information=slower processing; novelty=slower
  65. Sustained attention/vigilance following TBI
    What is it?
    • Maintaing attention over time; look for time and accuracy measures during treatment 
    • Higher activation in TBI=more effort=more fatigue; vulnerable for sleep disorders
  66. Selective focused attention
    What is it?
    • Focus on one modality/stimulus; can also involve inhibition 
    • Controlled internally and/or externally
    • Problematic in distracting environments; be aware during testing
  67. What is resource allocation?
    • Allocating certain amounts of attention to certain tasks
    • Ignoring information on one side; more severe in RH damage; neglect is side contralateral to lesion--negative prognostic indicator
  68. What is working memory? What are the components?
    • holding information for LTM while manipulating; allows conscious information processing and storage; capacity is limited
    • Components are temporary storage buffers (phonological loops, visuospatial sketchpad), executive component 
    • Executive control=dorsolateral frontal lobes
    • Articulatory loop: Broca's area
    • Visuospatial sketchpad: Right side
  69. What is encoding?
    Constructing an internal representation of an event (visual imagery, chunking, associations)
  70. What is strategic learning?
    Extracting pertinent details to combine and form abstract gist
  71. What is retrieving?
    transferring information from long-term storage to consciousness
  72. Declarative memory is a type of ___ term memory. There are 2 major types ___ and ___. The latter has 2 subtypes. There is also another type that is debated on, this is ____ memory.
    • long-term
    • semantic (remembering facts, context independent; LH), episodic (personal, eventful memory; context dependent; RH)
    • Prospective memory: remembering what you need to do in the future; time based or event-based
    • Recency discrimination: Knowing how long ago something happened
    • Lexical memory
  73. What structure is important for storing LTM?
    Hippocampus/medial temporal lobe
  74. What is procedural memory? What structures are responsible?
    • Habits, procedures, routines
    • Can access by doing the procedure/routine
    • Basal ganglia and cerebellum
  75. Why type of memory is most compromised in TBI?
    What other kinds of memory issues occur following TBI?
    What is retrograde amnesia?
    Anterograde amnesia?
    • Episodic
    • Prospective memory
    • Metamemory (being aware of accuracy of memories--frontal lobe damage)
    • Confabulations
    • Orientation to time is last to recover b/c it is always updating
    • Difficulty recalling information BEFORE TBI; most recently stored information is most vulnerable
    • Difficulty recalling information AFTER TBI
  76. What is the definition of executive function?
    • Cognitive abilities that encompass the generation, selection, planning, & regulation of responses that are goal-directed and adaptive
    • Multidimension construct
    • Frontal lobes and other neural circuits
  77. What are specific functions of EF?
    Planning, organizing, sequencing, self-monitoring/awareness, reasoning, goal-setting/selecting, initiation behaviors, inhibiting, flexible problem solving
  78. What is EF critical to?
    Social success, academic success, vocation success, community reintegration, rehab/education success, independent living
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TBI Test 1
tbi test
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