Neurologic Emergencies 1 Flashcards
important part of an emergency neuro assessment
- HPI
- neuro exam
*a few minutes spent w/ pt is more effective than routine brain scans
what to do before imaging in neuro emergency
- brief bedside exam that includes:
- mental status
- eyes
- limbs
who is the glasgow coma scale not effective in?
pts with aphasia
glasgow coma scale range
-3-15
what glasgow coma scale score indicates poor prognosis?
< 9
what are the specific neurologic syndromes that should be specified in place of saying “confusion” or “altered mental status”
- delirium
- dementia
- receptive aphasia
- amnesia
- visual field deficit
- neglect
neuroanatomic localization of delirium
- bicerebral
- affects ARAS
- sleepy
neuroanatomic localization of dementia
- bicerebral
- NOT affecting ARAS
- awake
neuroanatomic localization of receptive aphasia
left temporal or parietal
neuroanatomic localization of amnesia
bithalamic or bitemporal
neuroanatomic localization of visual field deficit
parietotemporal or occipital
neuroanatomic localization of neglect
right parietal
ARAS =
- ascending reticular activating system
- consciousness center in upper brainstem
what is delirium
- syndrome of global cognitive dysfunction manifested by:
- disorientation w/ nl language fxn
- inattention
- depressed consciousness
- possible abnormal behavior, agitation or visual hallucinations
equivalent terms to delirium
- acute confusional state
- acute encephalopathy
what is the MC cause of delirium?
toxic-metabolic encephalopathy
- drugs/meds
- serum chem. abnormalities
- systemic infection or fever
what is commonly mistaken for delirium
aphasia
define aphasia
-language abnormality d/t focal brain dysfunction in dominant (usually left) hemisphere
dysnomia
difficulty naming - either can’t get word out or says incorrect word
what is the only common feature among all 7 types of aphasia?
dysnomia
two types of aphasia
- expressive (motor) aphasia
- receptive (sensory) aphasia
where are expressive (motor) aphasias?
anterior (frontal)
where are receptive (sensory) aphasias?
posterior (temporal or parietal)
expressive aphasia is associated w/ what?
- obvious deficit
- right hemiparesis (left sided brain dysfunction)
- speak less than normal
receptive aphasia is associated w/ what?
- invisible deficits
- visual field/sensory (not motor)
which type of aphasia is most often confused w/ confusion?
receptive
-speak gibberish, cannot comprehend
common causes of aphasia
- stroke
- mass lesion
aphasia
- effect on speech
- what all is normal
- where in brain
- signs
- what to check
- 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
delirium
- effect on speech
- what all is abnormal
- where in brain
- cause
- what to check
- 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
if naming if abnormal in neuro exam and expect aphasia, what do you test
- name 3 things
- follow 3-step command
- say 5 words of grammatically correct speech
- repeat sentence
what is a pt do in the language exam if they have receptive aphasia?
- 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
if pt performs language exam poorly d/t inattention or depressed consciousness what should you think?
delirium NOT aphasia
what is the spectrum of level of consciousness
- normal
- dlirium
- lethargy/drowsiness
- stupor
- coma
common cause of toxic-metabolic encephalopathy
alcohol
the ARAS that keeps us awake is located where?
upper brainstem (midbrain and upper pons), hypothalamus and basal forebrain
decreased consciousness is d/y ARAS inhibition as a result of what 2 possible things?
- brainstem lesion (focal)
- bicerebral dysfunction (diffuse)
a focal brainstem lesion is usually what?
- structural
- stroke or mass
diffuse bicerebral dysfunction is usually what?
- physiologic
- toxic - metabolic encephalopathy (drugs, infection, ETOH, etc)
what is the key to localizing depressed consciousness?
EYE MOVEMENTS !
why are eye movements key in localizing depressed consciousness?
-dorsum of upper brainstem contains both the ARAS and nuclei of CNs 3, 4 and 6
eye movements in a brainstem lesion
abnormal
eye movements in a bicerebral lesion
normal
acute bicerebral dysfunction etiologies
- toxic metabolis encephalopathy
- increased ICP
- meningeal irritation
- seizure
- b/l ischemic strokes
- hypertensive encephalopathy
- confusional migraine
what does PRES stand for
posterior reversible encephalopathy syndrome
initial toxic metabolic w/u in a pt w/ depressed consciousness / delirium
- drugs (many)
- serum chemistries (also a lot )
- serum CBC
if the initial toxic metabolic w/u is negative, what is the next step?
- ABG
- medical conditions
- toxins
- nutritional deficiencies
- sleep deprivation
- CT and MRI of brain
- lumbar puncture
define cerebral autoregulation
ability of the brain to maintain relatively constant cerebral blood flow despite changes in mean arterial pressure w/i a certain range
effect of acute BP increase on the brain
-disruption of the BBB and vasogenic edema (hypertensive encephalopathy)
effect of acute BP decrease on the brain
-cerebral ischemia and cytotoxic edema (watershed / borderzone infarction )
what type of BP changes can the brain handle?
chronic changes
what is the pathophys behind hypertensive encephalopathy (PRES)
- acute rise in BP outstrips cerebral autoregulation
- causes BBB disruption w/ resultant vasogenic edema and possible intracerebral hemorrhage
sx of hypertensive encephalopathy
- HA
- depressed consciousness
- delirium
- seizures
- possible focal deficits
if focal deficits are present during hypertensive encephalopathy, which is most common?
visual b/c edema usually occurs in occipital lobe
CT and MRI findings in hypertensive encephalopathy
- vasogenic edema in cerebral white matter (often mistaken for infarction)
- w/ or w/o ICH
- prominent posteriorly
BP values related to PRES
- 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
tx of hypertensive encephalopathy / PRES
- IV nicardipine
- start 5, then 2.5 increments
- max: 15 mg/h
- others: clevidipine, labetalol
- concurrently begin amlodipine 10 daily PO
watershed (borderzone) infarction
- usually causes cognitive deficits
- does NOT affect primary motor or sensory areas
describe what happens in watershed infarction when there is a sudden or excessive drop in BP:
- 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
anterior borderzone
- prefrontal
- causes cognitive or behavioral deficits
posterior borderzone
- temporoparieto occipital
- affects the visual association cortex and causes visual hallucinations
three possible causes of transient change in consciousness
- syncope
- seizure
- migraine
since change in consciousness is transient, what alone usually determines the syndrome?
history (need a witness)
define syncope (fainting)
transient LOC d/t hypotension
define near syncope (presyncope)
transient lightheadedness d/t hypotension
syncope etiologies
- antihypertensive agents
- volume loss
- cardiac etiologies
- neurologic etiologies
neurologic etiologies of syncope
- reflex syncope: vasovagal or situational
- autonomic neuropathy: DM, ETOH, uremia, CA
- neurodegenerative dz
- syncopal migraine: POTS
how to classify seizures
a review
- partial / focal
- simple: no change in awareness
- complex: change in awareness
- generalized (entire cortex)
- GTC
- JME
- absence
- other
simple - partial seizures
- 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
complex-partial seizures
- 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
stages of GTC (generalized tonic clonic) seizure
- tonic phase: stiff
2. clonic phase: shake
2 classifications of GTC seizure
- 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
primary GTC starts where
increased electrical activity starts simultaneously throughout cortex
secondary GTC starts where
increased electrical activity starts in focal part of cortex and spreads to thalamus then to cortex of both hemispheres
when does a seizure become an emergency?
-when in generalized status epilepticus
=recurrent GTC w/o return to baseline
=prolonged GTC
what do you NOT tx a GTC seizure with?
benzo
what is the exception of tx seizure w/ benzos
if shaking > 5 min
-lorazepam 0.1 mg / kg IV
what to give to prevent further seizures
-levetiracetam 1 g IV
or
-fosphenytoin 20 mg PE/kg IV at <150 mg PE/min
common drug toxicity that could cause generalized status epilepticus
fluoroquinolones
what meds to avoid in JME as they may worsen it
- phenytoin
- carbamazepine
- phenobarbital
HA localization to meninges - what is the range?
trigeminal n. and C2-C4
effects on the meninges that can cause HA
- stretching
- irritation
- ischemia
- sensitiziation
