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NURS 2514 > 8 - Acute Brain Injury + Seizures > Flashcards

8 - Acute Brain Injury + Seizures Flashcards

1
Q

Romberg test

A

Test that measures your sense of balance

+ve test indicates ataxia [impaired muscle coordination]

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2
Q

PERRLA

A

Pupils equal, round, reactive to light, accomodation present

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3
Q

nystagmus

A

Nystagmus is a vision condition in which the eyes make repetitive, uncontrolled movements.

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4
Q

ICP

A

Intracranial pressure (ICP) is defined as the pressure within the craniospinal compartment, a closed system that comprises a fixed volume of neural tissue, blood, and cerebrospinal fluid (CSF).

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5
Q

epilepsy

A

group of disorders characterized by recurrent seizures

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6
Q

tonic-clonic seizure

A

most common seizure associated with epilepsy

tonic phase: characterized by generalized muscle contraction, a rigid body, + extended limbs. jaw clenches tightly and respiration stops

clonic phase: muscles contract and relaz, resulting in forceful movements of the entire body. salivation usuallly increases and incontinence is frequent

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7
Q

status epilepticus

A

recurrent or continuous seizures w/o return of consciousness is called status epilepticus

causes severe hypoxia, hypoglycemia, and acidosis, possibly resulting in brain damage

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8
Q

agnosia

A

Agnosia is the loss of the ability to recognize objects, faces, voices, or places. It’s a rare disorder involving one (or more) of the senses

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9
Q

autoregulation

A

Autoregulation is a manifestation of local blood flow regulation. It is defined as the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure.

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10
Q

Monroe-Kellie Doctrine

A

the sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two.

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11
Q

Cushing’s Triad

A

as ICP increases – the CV center of the medulla detects brain ischemia

this causes efferent signals from the vasomotor area resulting in systemic vasoconstriction

this elevates the blood pressure in an attempt to perfuse the brain

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12
Q

Decorticate Posturing

A

earns a score of 3 on the GCS

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13
Q

Decerebrate Posturing

A

earns a score of 2 on the GCS

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14
Q

seizure

A

A seizure is a burst of uncontrolled electrical activity between brain cells (also called neurons or nerve cells) that causes temporary abnormalities in muscle tone or movements (stiffness, twitching or limpness), behaviors, sensations or states of awareness

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15
Q

abscence seizure

A

generalized seizure; more common in young children

seizure usually lasts 5-10 seconds, may occur several times per day

brief loss of consciousness usually results in the child “staring into space” but can include twitches in the eyelids + lip smacking

following the seizure normal activity is resumed + no memory of the event is retained

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16
Q

EEG

A

electroencephalogram - test that detects electrical activity in your brain using electrodes attached to your scalp

can help diagnose seizure disorders, epilepsy, head injuries, etc.

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17
Q

apraxia

A

loss of skilled mvmt

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18
Q

MMSE

A

mini mental state examination

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19
Q

battle sign

A

bruise that indicates a basilar skull fracture - considered a medical emergency

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20
Q

periorbital ecchymosis

A

“raccoon eye”

associated w basilar skull fracture

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21
Q

nuchal rigidity

A

hyperextended, stiff neck

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22
Q

rhinorrhea

A

CSF leaking thru the nose

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23
Q

photophobia

A

hypersensitivity to light - not a condition; a symptom of another problem

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24
Q

generalized seizure

A

A generalized seizure occurs when the abnormal electrical activity causing a seizure begins in both halves (hemispheres) of the brain at the same time.

Generalized seizures include absence, atonic, tonic, clonic, tonic-clonic, myoclonic, and febrile seizures.

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25
Q

amnesia

A

memory loss

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26
Q

apathy

A

lack of interest, enthusiasm, or concern

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27
Q

MOCA

A

montreal cognitive assessment test for dementia

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28
Q

halo sign

A

A “halo” or “ring” sign, occurs when cerebrospinal fluid (CSF) mixes with blood on an absorbent surface. The blood forms a spot in the center and a lightly stained ring forms a halo around it.

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29
Q

diffuse axonal injury

A

Diffuse axonal injury (DAI) is a form of traumatic brain injury. It happens when the brain rapidly shifts inside the skull as an injury is occurring. The long connecting fibers in the brain called axons are sheared as the brain rapidly accelerates and decelerates inside the hard bone of the skull

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30
Q

subdural hematoma

A

A subdural hematoma (SDH) is a type of bleeding in which a collection of blood—usually associated with a traumatic brain injury—gathers between the inner layer of the dura mater and the arachnoid mater of the meninges surrounding the brain.

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31
Q

contusion

A

bruise resulting from a direct blow or impact such as a fall; type of hematoma in which an injured capillary or blood vessel leaks into the surrounding area

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32
Q

epidural hematoma

A

Epidural hematoma is when bleeding occurs between the tough outer membrane covering the brain (dura mater) and the skull. Often there is loss of consciousness following a head injury, a brief regaining of consciousness, and then loss of consciousness again.

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33
Q

Kernig’s sign

A

Kernig’s sign is one of the physically demonstrable symptoms of meningitis. Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.

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34
Q

focal seizure

A

Focal onset seizures are the most common type of seizure experienced by people with epilepsy. For short, the term focal seizure can be used. When the seizure begins in one side of the brain and the person has no loss of awareness of their surroundings during it, it is called a focal onset aware seizure.

some individuals may have a prodromal sign such as nausea or muscle twitching, while others may experience an usual sensory sensation called an aura

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35
Q

aphasia

A

Difficulty speaking

Aphasia is an impairment of language, affecting the production or comprehension of speech and the ability to read or write

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36
Q

anosognosia

A

when someone is unaware of their own mental health condition or they can’t perceive it accurately

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37
Q

ptosis

A

drooping or falling of the upper eyelid

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38
Q

ataxia

A

lack of muscle control or coordination of voluntary movements; slow to initate movements

degenerative disease of the nervous system. Many symptoms of Ataxia mimic those of being drunk, such as slurred speech, stumbling, falling, and incoordination. These symptoms are caused by damage to the cerebellum, the part of the brain that is responsible for coordinating movement.

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39
Q

List the 6 signs of high intracranial pressure

A
  1. Decreased level of consciousness
  2. Headache
  3. Projectile vomiting
  4. Dilated and fixed pupils
  5. Vital signs changes (Cushing’s Triad)
  6. decorticate + decerebrate posturing
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40
Q

define intracranial regulation

A

mechanisms or conditions that impact intracranial pressure + function

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41
Q

what are the consequences of increased CSF, blood, or brain tissue?

A

will upset the balance and can lead to cerebral edema and/or increased ICP

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42
Q

describe the breakdown of the components of the intracranial cavity

A

80% brain tissue
10% CSF
10% blood

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43
Q

what do the early signs of increased ICP originate from?

A

originate from increased pressure on the brainstem + meninges, and hypoxia to sensitive cortical neurons

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44
Q

why does a decreased LOC occur as an early manifestation of increased ICP?

A

results from pressure on the RAS. results in decreased responsiveness or arousal and hypoxia of cortical neurons leading to altered cognition

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45
Q

why do severe headaches occur as an early manifestation of increased ICP?

A

due to the stretching of the dura mater + blood vessels

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46
Q

why does vomiting occur as an early manifestation of increased ICP?

A

due to pressure on the emetic center

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47
Q

what are cheyne-stokes respirations?

A

periodic breathing or apnea alternating w increasing then decreasing tidal volume

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48
Q

why might herniation occur as a result of increased ICP>

A

increased ICP may cause the brain to become displaced within the cranium [or herniated]

49
Q

identify the 4 types of cranial herniation associated with increased ICP

A
  1. cingulate herniation
  2. central herniation
  3. uncal herniation
  4. cerebellar herniation
50
Q

what is central herniation?

A

downward pressure impairs brainstem function

51
Q

what is uncal herniation?

A

occurs when the temporal lobe is pushed under the tentorium cerebelli

oculomotor and posterior artery are frequently compressed which results in ipsilateral pupil dilation + ischemia

52
Q

what is cerebellar herniation?

A

cerabellum protrudes thru the foramen magnum - brainstem function is impaired

53
Q

what are the 3 mechanisms of brain injury?

A
  1. ischemia
  2. excitotoxicity
  3. cerebral edema
54
Q

how many minutes does it take for severe ischemia to cause irreversible neuron destruction?

A

4-6 minutes

55
Q

what is the most abundant excitatory neurotransmitter in the brain?

A

glutamate

56
Q

T or F: elevated potassium levels can predispose a pt to seizures

A

true

57
Q

Why does inhibition of the sodium potassium pump result in increased ICP?

A

Results in cerebral edema due to the accumulation of sodium + water in neurons.

58
Q

What is a supratentorial lesion?

A

lesions to the brain superior to the tentorium cerebelli - must be quite large to effect consciousness

59
Q

What is an infratentorial lesion?

A

Lesions inferior to the tentorium

Often effect consiousness, respiratory and / or circulatory function

60
Q

what is paresis?

A

contralateral weakness

61
Q

how do optic nerve lesions affect vision

A

result in blindness of the innervated eye

62
Q

how do lesions of the optic chiasm affect vision

A

lead to blindness in both eyes

63
Q

aphasia

dysphasia

A

inability to express or comprehend language

partial impairment

64
Q

expressive aphasia

A

occurs when broca’s area in L frontal lobe is damaged; results in inability to speak or write fluently

65
Q

dysarthria

A

poor articulation

66
Q

receptive aphasia

A

inability to read or understand spoken words - caused by damage to wernicke’s area in L temporal love

67
Q

global aphasia

A

combo of expressive + receptive aphasia - often results from widespread L hemisphere damage

68
Q

what is a concussion?

A

reversible interference in brain function resulting from a blow to the head

often accompanied by a LOC, headahces, and retrograde amnesia of events immediately following the blow

usually no permanent damage but multiple concussions may produce permanent neurological impairment.

post concussion symptoms can last 4-6 weeks

69
Q

what is a contrecoup injury?

A

rebound injury as the brain bounces off the opposite side of the skull [example - brain hits front of skull (direct injury), head bounces back and brain hits back of skull = contrecoup]

70
Q

what is a contusion?

A

bruising of the brain tissue resulting from rupture of small blood vessels; ICP may increase depending on the severity of the blow.

71
Q

what is a simple skull fracture?

A

break in the continuity of the bone; wound remains closed

72
Q

what is a compound skull fracture?

A

open fracture where the brain tissue is exposed to the environment; carries a high risk of infection

73
Q

what is a depressed fracture?

A

piece of bone is displaced below the level of the skull + compresses the brain

74
Q

what is a basilar skull fracture?

A

occurs at the base of the skull; often accompanied by otorrhea or rhinorrhea - risk of infectiion is increased

75
Q

define primary [direct] brain damage and provide examples

A 
•	direct injuries to the brain caused by impact
•	examples:
	concussion
	contusion
	laceration
	hemorrhage
	hypoxia
	diffuse axonal injury (shearing lesion)
76
Q

define secondary brain damage

A

• damage that results from subseq. brain swelling, intracranial hematomas, infection, ischemia, + hypoxia

77
Q

what is a hematoma?

A

collection of blood in a tissue that results from ruptured blood vessels
• can occur immediately following an injury or after some delay

78
Q

what are the 3 types of intracranial hematomas?

A

epidural, subdural, and intracerebral

79
Q

describe epidural hematomas

A

bleeding between the dura mater + bones of the cranium

80
Q

describe subdural hematomas

A

 blood accumulates w/in the potential space between the dura and the arachnoid mater
 can produce [acute] signs w/in 24 hrs after injury
 can develop slowly ~ about a week [subacute]
 or can develop weeks later [chronic]

81
Q

describe intracerebral hematomas

A

 blood accumulates w/in the cerebrum itself

 usually the result of a contusion, shearing injury, or stroke

82
Q

true or false: direct [primary] damage may cause focal injuries while secondary injuries often result in increased ICP

A

true

83
Q

describe seizures as an additional manifestation of head injuries

A

 blood + inflammation can irritate neural tissue + cause seizures

84
Q

describe cranial nerve damage as an additional manifestation of head injuries

A

 common following a basilar fracture

85
Q

describe otorrhea, ottorhagia, and rhinorrhea as an additional manifestation of head injuries

A

 CSF or blood leaking from the ear or nose; increases the risk of infection
 watch for racoon’s eyes + battle sign

86
Q

describe fever as an additional manifestation of head injuries

A

results from infection or hypothalamic impairment [temp regulator]

87
Q

T or F: RR is decreased with increased ICP

A

true

88
Q

what is bacterial meningitis?

A

• inflammation of the meninges caused by a bacterial, viral, or fungal infection, a tumor mass, or hemorrhage

89
Q

what are the 4 early manifestations of bacterial meningitis?

identify the later manifestations as well

A
  • severe headache
  • back pain
  • photophobia
  • nuchal rigidity
  • fever
  • leukocytosis
  • bacteria, protein, and WBCs in the CSF
  • petechial rash
  • kernig’s sign [resitance to extension when lying]
  • brudzinki’s sign [neck flexion results in leg flexion]
90
Q

coma

A

state of being unarousable and unresponsive to external stimuli or internal needs

91
Q

what is lock-in syndrome? what causes it?

A

condition in which the pt is aware and capable of thinking but is paralyzed and unable to communicate [scary]

results from incomplete damage to the cerebrum where brainstem function is preserved

92
Q

what happens to the pt’s body when all cortical functions are lost?

A

• when all cortical functions are lost the individual assumes a decorticate [GCS 3] / flexor posturing accompanied by Cheyne-Stokes respirations

93
Q

what is brain death?

A

irreversible loss of brain + brainstem function

94
Q

identify the 12 cranial nerves in order

A
  1. olfactory
  2. optic
  3. oculomotor
  4. trochlear
  5. trigeminal
  6. abducens
  7. facial
  8. vestibulocochlear
  9. glossopharyngeal
  10. vagus
  11. accessory
  12. hypoglossal
95
Q

how do we test for the functioning of cranial nerve 2 [optic]?

A

visual acuity test, visual field test

96
Q

describe the function of the oculomotor nerve [cranial nerve 3]

A

extraocular mvmts - the 6 cardinal positions of gaze
PERRLA
watch for nystagmus
pupil rxn to light is strictly cranial nerve 3
assess for ptosis
accomodation + convergence

97
Q

describe the function of the trochlear nerve [cranial nerve 4]

A

same function as cranial nerve 3 but does not play a role in pupillary rxn to light

98
Q

describe the function of the abducens nerve [cranial nerve 6]

A

same function as cranial nerves 3 + 4; but not responsible for pupillary rxn to light

99
Q

describe the connectin between increased ICP and cranial nerve III

A

• connection between ICP + cranial nerve III: in ICP pupils can be dilated + fixed, pressure often placed on cranial nerve III – oculomotor nerve exits at the top of the brainstem, can easily become compressed

100
Q

how do we test for the functioning of cranial nerve 5 [trigeminal]?

A

palpate temporal + masseter muscles as pt clenches teeth, push on chin to try open

touch pt face w cotton swab on forehead, cheeks, chin w eyes closed see if they feel it

101
Q

how do we test for the functioning of the facial nerve [cranial nerve 7]?

A

ask pt to smile, raise eyebrows, etc

102
Q

wht is the function of the vestibulocochlear nerve

A

hearing :)

103
Q

which reflexes are cranial nerves 9 + 10 [glossopharyngeal + vagus] responsible for? how do we assess for their functioning?

A

gag, swallow, + cough reflexes for protection against aspiration.

assess for abnormal uvula deviation. soft palate + uvula should rise midline - should consult a SLP if you’re really concerned

104
Q

describe the function of cranial nerve 11

A

spinal accessory - get pt to shrug shoulders, look for symmetry

105
Q

how to we assess for the functioning of cranial nerve 12 [hypoglossal?}

A

ask pt to stick out tongue [should be midline], move side to side, say “light, tight, dynamite”

weak tongue should be NPO

106
Q

What is the go to med for status epilepticus?

A

lorazepam

107
Q

why is lorazepam preferred over diazepam for status epilepticus?

A

bc it has a longer half life so it stays in the system longer

108
Q

asa nurse, what are the things we should take note of when a pt has a seizure?

A
  • antecedent events
  • precipitating factors
  • time it started + duration
  • postictal stags
  • vital signs
  • posturing + mvmts
109
Q

what are the goals of drug therapy w antiepileptics [also called anticonvulsants]?

A
  • control or prevent seizures while maintaining a reasonable QOL
  • minimize adverse effects and drug-induced toxicity
110
Q

identify the 5 main MOAs of antiepileptic drugs

A
  1. suppress Na influx
  2. suppress Ca influx
  3. promote K efflux
  4. antagonize glutamate
  5. potentiate GABA
111
Q

describe the pt education hilights of antiepileptic druga

A

• most antiepileptics require plasma drug level monitoring
• patient adherence is necessary: requires regular and continuous therapy
• all antiepileptic drugs should be withdrawn slowly or else rebound seizures or status epilepticus will occur
• antiepileptic drugs carry a risk for depression in pts
o monitor for anxiety, agitation, depression, and suicidal ideation
• several antiepileptic drugs decrease the effectiveness of birth control pills
• teratogenic [may cause birth defects – toxic to fetus]

112
Q

valproic acid

A

• treats all major seizure types
• moa = suppression of Na and Ca influx
• few side effects
o GI: NV – take w food
• metabolized by liver – be careful in pts w liver disease
• highly teratogenic
o take folic acid supplements if needed during pregnancy

113
Q

phenobarbitol

A
  • class = barbiturate
  • moa = potentiates the effects of GABA
  • +++ side effects
  • drowsiness ++, causes sedation
  • can cause physical dependance
  • decreases synthesis of vitamin J – monitor for bleeding
  • used for partial and generalized seizures
  • long half life
  • teratogenic
  • avoid taking with other CNS depressants [alcohol, opiates, etc]
114
Q

lorazepam

A
  • class = benzodiazepine
  • moa = potentiates the effects of GABA
  • used for status epilepticus and acute seizures
  • drowsiness ++, causes sedation
  • can cause physical dependence
  • withdraw slowly
  • avoid taking w other CNS depressants [alcohol, opiates, etc]
115
Q

keppra

A
  • moa = unknown
  • adverse effects – most common is drowsiness + weakness
  • can cause kidney injury
  • does not impact cognition or focus
  • does not interact w other drugs + does not affect birth control effectiveness
  • not teratogenic
116
Q

phenytoin

A

• hydantoin
• moa = inhibits sodium channels  suppresses aps
• plasma levels v sensitive – narrow therapeutic range
• used to treat all major forms of epilepsy
• can cause:
o nystagmus
o sedation
o ataxia
o diplopia
o cognitive impairment
o gingival hyperplasia  excessive gum growth; try to avoid giving it to children
o teratogenic
o can decrease synthesis of vit k dependent clotting factors
• when administering IV:
o can cause dysrhythmias + hypotension
o nurse should inject slowly; dilute in saline
o never mix w dextrose solutions  sugar will precipitate and destroy your vein!!!! only mix w NS
o can cause tissue damage if extravasation occurs – use a central line or large peripheral IC whenever possible
o diazepam and valproic acid can increase phenytoin levels in the blood
o carbamazepine, phenobarbital, and alcohol can reduce plasma levels of phenytoin

117
Q

topiramate

A
  • moa = potentiates the effects of gaba, blocks sodium channels, and blocks glutamate receptors
  • few sife effects
  • higher risk for suicide than any other AED
  • can cause fatigue, difficulty concentrating, weight loss, depression
  • be extra cautious if patients have kidney disease
118
Q

gabapentin

A
  • adjunctive therapy for seizures; unknown moa
  • mild to moderate side effects – drowsiness and dizziness
  • considered a v safe medication
  • v safe but takes longer to metabolize in the elderly therefore increases their susceptibility to side effects and puts them at a greater risk for falls
  • does not interact w other medications
119
Q

carbamazepine

A
  • should not be taken w grapefruit juice
  • moa = suppresses sodium channels
  • minimal effcts on cognitive function
  • BMS – monitor for leukopenia, anemia + thrombocytopenia
  • should not be administered to pts w pre-existing hematologic disorders
  • monitor CBCs
  • teratogenic

NURS 2514 (10 decks)

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