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Neurology 2 > Neurologic Emergencies 1 > Flashcards

Neurologic Emergencies 1 Flashcards

1
Q

important part of an emergency neuro assessment

A
  • HPI
  • neuro exam

*a few minutes spent w/ pt is more effective than routine brain scans

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2
Q

what to do before imaging in neuro emergency

A
  • brief bedside exam that includes:
  • mental status
  • eyes
  • limbs
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3
Q

who is the glasgow coma scale not effective in?

A

pts with aphasia

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4
Q

glasgow coma scale range

A

-3-15

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5
Q

what glasgow coma scale score indicates poor prognosis?

A

< 9

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6
Q

what are the specific neurologic syndromes that should be specified in place of saying “confusion” or “altered mental status”

A
  • delirium
  • dementia
  • receptive aphasia
  • amnesia
  • visual field deficit
  • neglect
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7
Q

neuroanatomic localization of delirium

A
  • bicerebral
  • affects ARAS
  • sleepy
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8
Q

neuroanatomic localization of dementia

A
  • bicerebral
  • NOT affecting ARAS
  • awake
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9
Q

neuroanatomic localization of receptive aphasia

A

left temporal or parietal

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10
Q

neuroanatomic localization of amnesia

A

bithalamic or bitemporal

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11
Q

neuroanatomic localization of visual field deficit

A

parietotemporal or occipital

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12
Q

neuroanatomic localization of neglect

A

right parietal

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13
Q

ARAS =

A
  • ascending reticular activating system

- consciousness center in upper brainstem

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14
Q

what is delirium

A
  • syndrome of global cognitive dysfunction manifested by:
  • disorientation w/ nl language fxn
  • inattention
  • depressed consciousness
  • possible abnormal behavior, agitation or visual hallucinations
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15
Q

equivalent terms to delirium

A
  • acute confusional state

- acute encephalopathy

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16
Q

what is the MC cause of delirium?

A

toxic-metabolic encephalopathy

  • drugs/meds
  • serum chem. abnormalities
  • systemic infection or fever
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17
Q

what is commonly mistaken for delirium

A

aphasia

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18
Q

define aphasia

A

-language abnormality d/t focal brain dysfunction in dominant (usually left) hemisphere

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19
Q

dysnomia

A

difficulty naming - either can’t get word out or says incorrect word

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20
Q

what is the only common feature among all 7 types of aphasia?

A

dysnomia

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21
Q

two types of aphasia

A
  • expressive (motor) aphasia

- receptive (sensory) aphasia

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22
Q

where are expressive (motor) aphasias?

A

anterior (frontal)

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23
Q

where are receptive (sensory) aphasias?

A

posterior (temporal or parietal)

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24
Q

expressive aphasia is associated w/ what?

A
  • obvious deficit
  • right hemiparesis (left sided brain dysfunction)
  • speak less than normal
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25
Q

receptive aphasia is associated w/ what?

A
  • invisible deficits

- visual field/sensory (not motor)

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26
Q

which type of aphasia is most often confused w/ confusion?

A

receptive

-speak gibberish, cannot comprehend

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27
Q

common causes of aphasia

A
  • stroke

- mass lesion

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28
Q

aphasia

  • effect on speech
  • what all is normal
  • where in brain
  • signs
  • what to check
A
  • decreased speech d/t expressive aphasia or nonsensical speech d/t receptive aphasia
  • attention, consciousness, behavior and orientation are all normal
  • focal L brain dysfunction
  • right sided signs
  • check brain CT, MRI
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29
Q

delirium

  • effect on speech
  • what all is abnormal
  • where in brain
  • cause
  • what to check
A
  • decreased speech d/t drowsiness or nonsensical speech d/t confusion / disorientation
  • attention, consciousness, behavior and orientation all abnormal
  • diffuse brain dysfunction
  • often d/t toxic-metabolic etiology
  • check serum, CSF
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30
Q

if naming if abnormal in neuro exam and expect aphasia, what do you test

A
  • name 3 things
  • follow 3-step command
  • say 5 words of grammatically correct speech
  • repeat sentence
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31
Q

what is a pt do in the language exam if they have receptive aphasia?

A
  • pt will say incorrect words when naming
  • unable to follow 3-step command
  • will have fluent but nonsensical speech
  • may or may not be able to repeat
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32
Q

if pt performs language exam poorly d/t inattention or depressed consciousness what should you think?

A

delirium NOT aphasia

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33
Q

what is the spectrum of level of consciousness

A
  • normal
  • dlirium
  • lethargy/drowsiness
  • stupor
  • coma
34
Q

common cause of toxic-metabolic encephalopathy

A

alcohol

35
Q

the ARAS that keeps us awake is located where?

A

upper brainstem (midbrain and upper pons), hypothalamus and basal forebrain

36
Q

decreased consciousness is d/y ARAS inhibition as a result of what 2 possible things?

A
  • brainstem lesion (focal)

- bicerebral dysfunction (diffuse)

37
Q

a focal brainstem lesion is usually what?

A
  • structural

- stroke or mass

38
Q

diffuse bicerebral dysfunction is usually what?

A
  • physiologic

- toxic - metabolic encephalopathy (drugs, infection, ETOH, etc)

39
Q

what is the key to localizing depressed consciousness?

A

EYE MOVEMENTS !

40
Q

why are eye movements key in localizing depressed consciousness?

A

-dorsum of upper brainstem contains both the ARAS and nuclei of CNs 3, 4 and 6

41
Q

eye movements in a brainstem lesion

A

abnormal

42
Q

eye movements in a bicerebral lesion

A

normal

43
Q

acute bicerebral dysfunction etiologies

A
  • toxic metabolis encephalopathy
  • increased ICP
  • meningeal irritation
  • seizure
  • b/l ischemic strokes
  • hypertensive encephalopathy
  • confusional migraine
44
Q

what does PRES stand for

A

posterior reversible encephalopathy syndrome

45
Q

initial toxic metabolic w/u in a pt w/ depressed consciousness / delirium

A
  • drugs (many)
  • serum chemistries (also a lot )
  • serum CBC
46
Q

if the initial toxic metabolic w/u is negative, what is the next step?

A
  • ABG
  • medical conditions
  • toxins
  • nutritional deficiencies
  • sleep deprivation
  • CT and MRI of brain
  • lumbar puncture
47
Q

define cerebral autoregulation

A

ability of the brain to maintain relatively constant cerebral blood flow despite changes in mean arterial pressure w/i a certain range

48
Q

effect of acute BP increase on the brain

A

-disruption of the BBB and vasogenic edema (hypertensive encephalopathy)

49
Q

effect of acute BP decrease on the brain

A

-cerebral ischemia and cytotoxic edema (watershed / borderzone infarction )

50
Q

what type of BP changes can the brain handle?

A

chronic changes

51
Q

what is the pathophys behind hypertensive encephalopathy (PRES)

A
  • acute rise in BP outstrips cerebral autoregulation

- causes BBB disruption w/ resultant vasogenic edema and possible intracerebral hemorrhage

52
Q

sx of hypertensive encephalopathy

A
  • HA
  • depressed consciousness
  • delirium
  • seizures
  • possible focal deficits
53
Q

if focal deficits are present during hypertensive encephalopathy, which is most common?

A

visual b/c edema usually occurs in occipital lobe

54
Q

CT and MRI findings in hypertensive encephalopathy

A
  • vasogenic edema in cerebral white matter (often mistaken for infarction)
  • w/ or w/o ICH
  • prominent posteriorly
55
Q

BP values related to PRES

A
  • no specific value is likely to result in PRES
  • may occur at lower than expected BP value in certain cases (already had low BP, immunosuppressed, or eclampsia)
  • may NOT occur at apparently high BP value if pts premorbid bp was high
56
Q

tx of hypertensive encephalopathy / PRES

A
  • IV nicardipine
  • start 5, then 2.5 increments
  • max: 15 mg/h
  • others: clevidipine, labetalol
  • concurrently begin amlodipine 10 daily PO
57
Q

watershed (borderzone) infarction

A
  • usually causes cognitive deficits

- does NOT affect primary motor or sensory areas

58
Q

describe what happens in watershed infarction when there is a sudden or excessive drop in BP:

A
  • drop in cerebral perfusion pressure
  • insufficient blood flow to cover distal arterial territories
  • infarction of tissues b/w artery territories

*just like drop in water pressure results in death of grass b/w sprinkler zones

59
Q

anterior borderzone

A
  • prefrontal

- causes cognitive or behavioral deficits

60
Q

posterior borderzone

A
  • temporoparieto occipital

- affects the visual association cortex and causes visual hallucinations

61
Q

three possible causes of transient change in consciousness

A
  1. syncope
  2. seizure
  3. migraine
62
Q

since change in consciousness is transient, what alone usually determines the syndrome?

A

history (need a witness)

63
Q

define syncope (fainting)

A

transient LOC d/t hypotension

64
Q

define near syncope (presyncope)

A

transient lightheadedness d/t hypotension

65
Q

syncope etiologies

A
  • antihypertensive agents
  • volume loss
  • cardiac etiologies
  • neurologic etiologies
66
Q

neurologic etiologies of syncope

A
  • reflex syncope: vasovagal or situational
  • autonomic neuropathy: DM, ETOH, uremia, CA
  • neurodegenerative dz
  • syncopal migraine: POTS
67
Q

how to classify seizures

a review

A
  • partial / focal
  • simple: no change in awareness
  • complex: change in awareness
  • generalized (entire cortex)
  • GTC
  • JME
  • absence
  • other
68
Q

simple - partial seizures

A
  • increased electrical activity limited to focal part of cortex
  • sx varies based on location:
  • limb shaking, tingling, lights in vision, aphasia, deja vu
  • normal conciousness
  • postictal focal deficit
69
Q

complex-partial seizures

A
  • increased electrical activity start in focal part of cortex and spreads to part of contralateral cortex
  • aura
  • automatisms: picking, blinking, lip smacking
  • decreased consiousness
  • postictal state of delirium or confusion
70
Q

stages of GTC (generalized tonic clonic) seizure

A
  1. tonic phase: stiff

2. clonic phase: shake

71
Q

2 classifications of GTC seizure

A
  • primary: no aura or postictal deficit d/t diffuse brain dysfunction
  • secondary: starts w/ aura, ends w/ postictal focal deficit d/t focal brain lesion
72
Q

primary GTC starts where

A

increased electrical activity starts simultaneously throughout cortex

73
Q

secondary GTC starts where

A

increased electrical activity starts in focal part of cortex and spreads to thalamus then to cortex of both hemispheres

74
Q

when does a seizure become an emergency?

A

-when in generalized status epilepticus
=recurrent GTC w/o return to baseline
=prolonged GTC

75
Q

what do you NOT tx a GTC seizure with?

A

benzo

76
Q

what is the exception of tx seizure w/ benzos

A

if shaking > 5 min

-lorazepam 0.1 mg / kg IV

77
Q

what to give to prevent further seizures

A

-levetiracetam 1 g IV
or
-fosphenytoin 20 mg PE/kg IV at <150 mg PE/min

78
Q

common drug toxicity that could cause generalized status epilepticus

A

fluoroquinolones

79
Q

what meds to avoid in JME as they may worsen it

A
  • phenytoin
  • carbamazepine
  • phenobarbital
80
Q

HA localization to meninges - what is the range?

A

trigeminal n. and C2-C4

81
Q

effects on the meninges that can cause HA

A
  • stretching
  • irritation
  • ischemia
  • sensitiziation

Neurology 2 (21 decks)

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