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115 Cards in this Set
- Front
- Back
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a trauma induced alteration in mental status (confusion and amnesia lasting seconds to minutes) that may or may not involve LOC and does not have focal neurological signs is called a |
mild traumatmic brain injury |
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What duration of LOC defines severe TBI |
>12 hours |
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In addition to LOC, what other characteristics define a severe TBI |
radiographic signs of injury to brain, skull, or intracranial blood vessels |
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What 2 population groups are most at risk for severe TBI |
15-24 yeras old men OR 75 y/o men or women |
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Describe head trauma due to direct force |
direct mechanical force (coup) disrupts underlying brain tissue (parenchyma) causign cell death by necrosis, as well as inflammatory changes AS WELL AS contrecoup injury which occurs as a result of the brain hitting the opposit inner surface of the skull |
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Which part of the brain is typically injuryed by contrecoup injuries |
temporal and frontal lobes |
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Damage to the temporal and frontal lobes due to contrecoup injury generally lead to what type of deficits |
memory and personality change |
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Which type of trauma rarely leads to countercoup injuries |
frontal trauma |
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trauma to long subcortical white matter acons as well as cytoskeletal elements and fatal intracellular influx of calcium is called what |
diffuse axonal injury |
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What is the only method of imaging is able to show DAI |
diffusion tensor imaging (DTI) |
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What types of injury can result from head trauma? (5) |
direct force, diifuse axonal shearing, intracerebral bleeding, bleeding within the skull, and foregin object penetration |
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Describe the head trauma caused by intracerebral bleeding |
intraparenchymal bleeding nad diffuse cerebral edema increasing ICP which can lead to transtentorial herniation |
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innermost translucent vascualr membrane adhering to cerebral gyri |
pia mater |
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space between pia and arachnoid mater |
subarachnoid space |
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thin layer topping the gyri and capping the sulci |
arachnoid mater |
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Function of the subarachnoid space |
contain CSF |
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If a spinal tap or lumbar puncture is necessary where is the needle inserted |
subarachnoid space between lower end of spinal cord between T12 and L1 |
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What is the outermost layer of the meninges called |
dura mater |
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two infoldings of the dura mater are called what and what is their role |
falx and tentorium; support brain and house venous drainage |
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Where does the epidural space reside |
between the skull and the dura |
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What is the space between the dura and the arachnoid called |
subdural space |
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hematomas caused by head traum often occur within what spaces |
epidural and subdural |
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What doe epidural hematomas typically result from |
temporal bone fractures with concomitant middle meningeal artery lacerations |
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rapidly expanding, high pressure fresh blood clots often occuring as a result of temporal bone fractures are called what |
epidural hematomas |
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Describe transtentorial herniation |
epidural hematomas compress the brain and force it through the tentorial notch |
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What is the prognosis of epidural hematomas |
typically fatal unles surgery can immediately arrest bleeding |
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What is the lucid interval in brain injury |
a period of time during which a person with brain injury regains consciousness temporarily |
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this type of hematoma typically results from slow blleding of the bridging veins under low pressure into the the space with the same name |
subdural hematoma |
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If a subdural hematoma does not stop expanding when it hits brain, it may lead to what two possible events |
cerebral transtentorial herniation or cerebellar herniation through the foramen magnum |
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Which group of individuals are most likely to sustain acute subdural hematomas (3) |
alcoholics, people on warfarin, or the elderly |
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Initial symptoms of acute subdural hematoma |
headache,confusion, deteriorating consciousness over several hours to days and possibly focal signs and herniation |
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What shows on a CT if there is a subdural hematoma |
acute, dense blood in the subdural space |
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Define chronic subdural hematoma |
developed and persisted for weeks and extensively spread in subdural space |
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Symptoms of chronic subdural hematoma |
insidious headache, change in personality, rapid declining cognition, subtle focal physical deficits |
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Progrnosis for chronic subdural hematoma |
may spontaneously resolve or require surgery |
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Risk factors for chronic subdural hematomas in the elderly |
tendency to fall; anticoagulant use, cerebral atrophy enlarging the subdural space |
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Consequences of penetrating brain injuries (2) |
seizures; abcesses |
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What are the three neurologic functions assessed by the GCS |
eye opening, speaking, moving |
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When is the GCS useful and not so useful |
Useful: severe head injury to predict survival and sequelae NOT useful: minor head trauma and those with dementia or other neuropsychological deficits |
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If an individual has a score of 3 on the GCS after day 1, what is the prognosis |
90% fatality; never regaining consciousness |
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Do individual's in vegetative state or coma feel pain |
NO |
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How does substance abuse at the time of trauma complicate the picture of recovery from brain injury |
may have substance induced delirium comorbidly; lower pain threshold and seizures from withdrawal, or abnormal behavior due to withdrawal |
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How much more common is binge drinking in thsoe with major TBI |
18X |
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Risk factors for post-traumatic delirium (5) |
pre-existing dementia; painful injuries; adverse reactions to AED's;opioids; systemic complications (hypoxia, sepsis, fat emboli, etc) |
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3 common physical sequelae of TBI |
spasticity, ataxia, and hemiparesis |
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When does the maximum physical recovery occur as a result of TBI |
6 months |
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Frontal head trauma patients are more at risk for what sensory damage |
shearing of the filaments of olfactory nerves as they pass through the cribiform plate resulting in anosmia |
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If TBI damages hypothalamus what may result |
disruption of sleep-wake cycle causing insomnia, inattention, and inducing the need to additional medications |
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In addition to foreign bodies, what other TBI residual creates epileptic foci |
cerebral scars |
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What is the prevalence of posttraumatic epilepsy after a major TBI |
reaches 50% |
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The prevalence of posttraumatic epilepsy is greater with what type of head injury |
penetrating |
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If an individual with a major head injury has a siezure within the first week following the injury, these are called what |
provoked seizures |
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If multiple seizures occur more than 7 days after a brain injury, it is defined as |
posttraumatic epilepsy |
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Do AEDs such as phenytoin reduce the risk for post traumatic seizures |
early provoked seizures yes, but not PTE |
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What form do seizures in PTE typically take |
complex partial seizures that undergo generalization |
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How long do TBI comas typically last max? |
4 weeks |
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Describe persistent vegetative state |
eyes open, but unconscious incapable of thinking, communicating, or deliberate movement and unable to perceive pain/suffer |
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What is the DSM-V term for cognitive impairmetn as a result of TBI |
Neurocognitive disorder due to TBI |
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What does extent of cognitive deficits correlate with most |
duration of PTA including time of coma |
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Common cognitive deficits after severe TBI |
memory, apraxia, impulsivity, inattention, slowed processing speed |
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Do self reported cognitive deficits correlate better with premorbid education status, emotional stress and physical condition or with neuropsych test results |
premorbid educational status (low), emotional stress, and poor physical condition |
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True or false: With severe traumatic brain injury, the location of injury correlates well with cognitive impairments noted (with what exception) |
False with the exception of left temporal lobe injuries which routinely produce vocabulary deficits similar to anomic aphasia |
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When does recovery of motor and language skills typically reach a maximum |
6 months |
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When does intellectual recovery peak after severe brain injury |
18 months |
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What is the theory behind increased risk of AD with history of head injury |
it increases level of soluble amyloid and deposition of amyloid plaques, particularly in those with two Apo-E4 alleles |
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describe post-traumatic amnesia |
memory loss for the trauma, immediately precedng events, and newly presented information for a period of time |
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What medications have been used to assist with cognitive impairment subsequent to TBI and for what reason |
methylphenidate or other dopamine inducing medicaton: attention and memory;anticholinesterases: memory; medication for PTSD |
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What types of medication may interfere with attention and memory in recovery from TBI |
AEDs, antipsychotics, minor tranquilizers, particularly with polytherapy |
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What type of treatment is better for PTSD symptoms in trauma than medication |
exposure therapy |
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What are risk factors for post-traumatic aggression (4) |
premorbnid social functioning, substance abuse, forntal lobe injury, TBI induced depression |
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Treatment of post traumatic aggression |
antidepressants (insufficient alone), Beta blockers, AEDs with mood stablizing effects such as valproate and carbamazepine |
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personality changes often result from what areas of damage |
temporal and frontal |
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Types of personality changes often experienced with head injury |
abruptness, suspiciousness, argumentative, aggression, loquaciousness, impulsivity, hyperactivity, difficulty with executive functioning, emotional incontinence |
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Pre-injury Risk factors for posttraumatic depression |
substance abuse, premorbid depression, poor social funtioning |
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Trauma induced risk factors for posttraumatic depression |
cognitive impairment; PTE; impaired physical occupation andsocial skills |
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Posttraumatic depression is a risk factor for what other factors after head injury |
poor QOL, poor compliance, poor recovery, PTSD, aggression |
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Psychotropic medication used in depression after TBI |
SSRI, mood stabilizers, anxiolytics |
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Posttraumatic psychosis often take the form of what (3) |
delusions, paranoia, and auditory hallucinations |
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Risk factors for development of posttraumatic psychosis |
male, moderate to severe TBI, family history, long duration of unconsciousness |
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Treatmetn of posttraumatic psychosis |
atypical or typical antipsychotics with the addition of antidepressants and AEDs |
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Is GCS suitable as a guide for prognosis in children |
NO |
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Prognostic factors in childhood TBI |
severity and extent of brain damage, family SES, and psychiatric history |
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What happens if TBI occurs before growth spurts |
bones may fail to achive normal expectable size resembling spastic hemiparesis with foreshortened limbs |
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If dominant hemi injury occurs before age ____, the nondominant hemi would assume control of language |
5 |
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TBI in children to the hypothalamic pituitary axis may result in what |
endocrine disturbances leading to obesity, precocious puberty, and delayed puberty |
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Shaken baby syndrome is caused by what type of injuries |
diffuse axonal shearing, hemorrhages in brain parenchyma and subdral space and retinal hemorrhage |
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What type of injury may be the sole indicator of nonaccidental head injury in a child without external injuries |
retinal hemorrhage (which can be caused by other factors as well) |
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Residuals related to nonaccidental head injury in children |
cognitive impariment, behaviorl difficulties, learning disabilities, developmental delay, seizures, ADHD |
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trauma induced alteration in mental status with or without impairment of consciousness for less than 30 min and GCS no lower than 13 and if amnesia, it is less than 24 hours |
mild TBI including concussion |
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Most common form of minor head trauma |
concussion |
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Transient confusion shorter or longer than 15 minutes with or without loss of consciousness |
concussion |
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Describe typical confusion after a concussion |
inattention, slowed response time, disorientation, impaired memory |
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Common physical symptoms of concussion |
headache, nausea, dysarthria, impaired tandem gait, and loss of dexterity |
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Diplopia is caused by damage to which nerve |
one or both trochlear nerves (4th) |
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Injury to this with concussion may cuase vertigo when rapidly moving head or changing position |
inner ear labyrinthine system |
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if a patient has vertigo, a neurological exam may show what |
nystagmus |
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Physical deficits usually diminish within how long after concussion |
one week |
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Core Post concussive symptoms |
headache, memory impairment, insomnia lasting more than 2-3 months |
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Describe second impact syndrome |
an additional blow to the head occuring within days of the original injury leading to destrunctive and potentially fatal cerebal edema more common in children and teens |
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Sports with greatest risk of concussion (3) |
ice hockey, footbal, soccer |
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repeated episodes of blows to the head resulting in feelign dazes and leading to cognitive impariment at the level of dementia and Parkinson like physical deficits is called |
Dementia pugilistica |
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neuroimaging results in PCS |
normal on CT, MRI, neuroexam with possible minor abnormalities on EEG often due to medication effects |
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Neuropsych test results in PCS |
minor and uneven abnormalities often attributable to inattention, depression, exaggeration, lack of education, or malingering |
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Proposed etiology of PCS (3) |
diffuse axonal shearing, excitatory neurotransmitter imbalnce, and subtle cerebral contusions |
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Prolonged symptosm of PCS are just as much to do with _______ and ______ as neurological injury |
psychiatric and socioeconomic |
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Signature of PCS |
dull, generalized, endless headache worsened by movement, bending, work, alcohol (typically worse in mild head injury than mod/severe) |
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_________ used after head injury for as few as 15 days per month for three months may create chronic daily headaches |
analgesics |
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Characteristic memory impairment in PCS |
mild amnesia with inattnetion, distractibility, slowed processing, and difficulty with complex mental tasks |
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What factors may contribute to amnesia in PCS |
trauma propelled anterior poles of frontal and temporal lobes into the inner surface pof the carinal fossae; comorbid PTSD, depression, anxiety, medication, substance abuse |
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Factors that cause or exacerbate insomnia in head injury |
pain, anxiety, depression, PTSD, caffeine, alcohol, opioids, medications |
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Other noncore symptoms of PCS |
dizziness, photophonia, phonophobia, depression, anxiety, irritability, moodiness, rediced sexual desire, withdrawal |
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Percetnage of recovery in PCS |
85% |
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Time for recovery in PCS |
3 months if uncomplicated |
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Treatment of PCS |
education; reduced work load with return to work or take medical leave, treat specific symptoms, NSAIDS, analgesics, and tricyclic antidepressants for headache or antimigrain meds, avoid hyponitics, modafinil, prohibit alcohol, relaxation training, CBT, basic memory devices |
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Risk factors of incomplete recovery of PCS |
history of ADD, LD, or neurosis; low SES; job dissatisfaction; MVA as cuase of concussion; multiple symptoms with bodily pains; and comorbid psychi condition, medis, substance abuse, and PTSD |
