non-traumatic neurological complaints in the ED Flashcards
big question if you suspect a seizure
primary: without provocation-epliepsy
secondary: response to something
what does a post ictal state look like both in presentation and specifically with regards to chemistry panel
Disorientation, sleepy, amnesia, HA,
lactic acidosis (from the clonic muscle movements)
high PC02 metabolic acidosis
how long does a post ictal state last
Commonly lasts 30min-1hr – LOC gradually improves
grand mal seizures have been replaced by
generalized seizures
tell the store of a generalized convulsive seizure
the person experiences LOC
tonic movement followed by clonic
resolves spontaneously with post ictal state
rhythmic jerking of seizure pt
clonic phase
if they bit down they can
swallow it and swallow
what can you see that would point to a generalized seizure in a pt that has loc
stigmata of a seizure
urinary incontinence and tongue biting
generalized non-convulsant seizures
aka absense
like daydreaming
lasts seconds
formerly petit mal
simple partial seizure is now known as
focal aware seizure
three things key in focal aware seizure
awareness consciouness and memory preserved
sxs of focal aware seizures
Awareness, memory, consciousness is preserved
Uncontrolled movement, visual, auditory sx, autonomic sx’s
focal impaired awareness seizures aka
used to be a complex partial
focal impaired awareness
déjà vu,
jamais vu (You are in your house but you don’t know where you are; the familiar becomes the unfamiliar), sounds,
smell (“who is smoking a cigar right now? Nobody, we are in church”),
taste,
numbness,
automatisms,
fear/panic
Partial what is this and what are the 2 types
Limited area of brain
Sx’s match area affected
simple and complex or focal imparied and focal aware
Status Epilepticus
Seizure activity lasting > 5min
or repetitive seizures without CLEARING of mental state in between
what is the probelm with seizing for more than 5 minutes
Seizures >5min are unlikely to spontaneously resolve
Often result of secondary cause, so start looking… with status epilepticus
Electrolytes (especially: glucose (hypoglycemic), sodium, magnesium (hypomagnesemic))
Intracranial bleed, trauma
Tox, OD-until it is eliminated will not stop
status epilepticus tx
ABORT seizure before neuronal injury occurs
Benzodiazepines FIRST
THEN 2nd or 3rd line drugs (Dilantin, Phenobarb, etc)
these people are often intubated because they are not breathing
concerns with paralyzing someone
need to for intubation but can’t tell if your pt is still seizing
Most common cause of seizures in EDMost common cause of seizures in ED
Out of meds? Most common cause of seizures in ED
Hx of a seizure
have you ever had this before
if you have epilepsy is the pattern changing?
Trauma Hx?
people that see fall with abandon
Substances used?
recent illness?
LMP?
Country of origin
seizure after trauma
concern for internal bleeding in the brian
why are we worried about substance abuse with seizing
lack of alcohol can cause seizing
if you are too sick to get alcohol you need to know
why are we asking lmp in a female pt
do not want to miss pre eclampsia
PE with seizure
Post-ictal or still seizing?
ABCDE’s first
VS should improve with recovery
Tongue trauma, urinary incontinence
AND head to toe exam
what is the head to toe exam in a pt with a seizure
- Trauma
- Neuro deficit
- Infection
- Evidence other Dz
- Stigmata of EtOH
- Toxidrome
Red flags in a seizure
First seizure: Why??
Head trauma: Bleed, ICP
VS not resolving: Why??
Alcohol withdrawal (these folks are SICK – ICU admit)
Fever, infection: Need LP? Shock?
Rash: Meningitis?
Vomiting: Airway disaster, aspiration risk
Electrolytes: Which ones? Mg,
Stimulants: Bleed? CVA?
Prolonged post-ictal state: Why?
Focal neuro deficit: CVA, bleed?
Travel/Endemic area?
Neurocystercercosis
Malignancy: Mets to brain? – Often present with a first time seizure
Renal/liver Dz: Uremic or encephalopathic??
HIV: Toxo-, histo-, infection
Coumadin/Plavix: Bleed?
Pregnancy: Eclampsia
Head trauma with seizure concerns
: Bleed, ICP
Fever, infection:
LP
meningitis
if vomiting we are worried about
airway
Travel/Endemic area couplex with first seizure worry about
• Neurocystercercosis
- If history of seizures workup labs
a. D-stick on all, upreg
b. Observe, reassess
c. Safety: bedrails, etc
d. Measure drug levels
e. Alcohol, tox screen
f. Chem for electrolytes
ii. Sz causes lactic acidosis
Creatinine Kinase (CK) if prolonged down-time –> looking for rhabdomyolysis
Chem for electrolytes in a seizure where the pt has a history of seizure
If cause not obvious
- If first seizure
D-stick on all, upreg
If sz stops, pt now normal, and there is no obvious cause:
Chem panel
Magnesium, phosphorus if EtOH
EtOH, U tox
Coumadin? PT/INR
HIV test
Consider Head CT non-con
Add lumbar puncture only if fever, suspect SAH, encephalitis, etc
EEG: on admission or as outpt
what drug levels would we measure in a pt with a hx of a seizures
Dilantin, Carbamazepine, Valproic acid, Phenobarb
ii. Not: Keppra, Lamictal, etc
when would you be worried about rhabdomyolosis
why?
what would you order?
Creatinine Kinase (CK) if prolonged down-time
what would you do for a actively seizing pt
Protect pt, abort the seizure with meds
order lorazepam diazepam
When stop: suction oral blood/secretions, O2, time the event
Recheck d-stick, re-examine, cardiac monitor
what is the abortive treatment
Abortive Tx 1st line: Benzodiazepines – know 3
Lorazepam (2mg IM/IV)
Midazolam (2-5mg IM/IV),
Diazepam (5mg IV)
New Sz, now well and no Red Flags?
New Sz, now well and no Red Flags? Neurology consult to initiate EEG, tx and follow up.
etiology of febrile seizures
Rapid rise in temperature, not the number itself
Risks: hx same, family hx
want this on all children with a febrile seizure
D stick
• Search for source of fever or occult infection in children would involve getting a
CBC, Chem, UA, CXR
Blood and +/- stool culture
when would you get a CT or a LP in a kid with a seizure
No CT.
No LP if dx clear and kid looks great
When would you get a LP on a kid with seizures
when would you get a LP on a adult with seizures
recent anbx use –>LP
you’re missing whatever bug it is
kid look sick
Add lumbar puncture only if fever, suspect SAH, encephalitis, etc
if RBC are in CSF–> SAH
febrile seizure tx
for the most part febrile seizure are partial or generalized?
NOT MEDS
**
they are generalized
5 essential questions for syncope
- Ever had this before? What was the Dx?
- Really lose consciousness? Fall? Hurt yourself?
- What were you doing? Last thing you remember?
- Sick lately? Upset? EtOH, drugs?
- PMHx, Meds, Fam Hx, Soc Hx
Pseudoseizure
Psych, emotional distress • Atypical movements • Brief post-ictal period this is where you can tell • Good Soc Hx • Refer to psych, EEG outpt
say “it’s a little inconsistent with a generalized seizure post ictal”
over the age of __ we are worried about syncope
> 50yrs
how does syncope look like seizure
brief clonic activity is a thing
syncope and cardiac issues might be suspected if
Syncope w/ exertion (critical aortic stenosis) or when supine – think cardiac
Red flag hx with syncope (7)
before/after event
a. Chest pain
b. Palpitations
c. Headache
d. SOB
e. Abd pain
f. Back pain (aortic dissection)
g. Bleeding (coumadin)
have you been recently hospitalized
melena
pace maker?
important recent social/family hx as it pertains to syncope
Recent hospitalization, surgery, procedure
Fam Hx of sudden death (Thoracic aortic Dissection, PE, cardiac arrhythmias)
abnormal sxs after syncope that are of concern
Abnormal VS
• Hypotension
• Tachy-, bradycardia
• Fever
Diaphoresis • Confusion, focal deficit • Cardiac murmur • Rales, wheeze, edema • Melena (GI bleed) • Head trauma • Pregnancy • Pacemaker (issue with it itself)
main categories for the syncope ddx
cardiac intracerberal aorta GIB/anemia ectopic pregnancy pulm embolism
cardiac -three big causes of syncope
i. Arrhythmia
ii. Aortic stenosis
iii. Hypertrophic, other cardiomyopathies
intracerberal
i. Hemorrhage, SAH
ii. Ischemic stroke: rarely
common reasons people faint
a. Volume depletion – dehydration or are you bleeding from somewhere?
i. Dehydration, n/v/d
b. Medication effect
c. Drug/EtOH effect
d. Vasomotor (vasovagal)
e. Emotional event/reaction
f. Mimic – unwitnessed seizure
g. Hypoglycemia**
what are you worried about with the aorta that can cause syncope
Dissection, aneurysm, aortic stenosis
Syncope in young, healthy, completely recovered person
All get:
EKG
consider D-stick (although you really wouldn’t come back if you were hypoglycemic)
Hct +/- depending on history
Syncope in young, healthy, completely recovered person- female
All females (12-55yrs) get Upreg
what is not routine for syncope in young healthy person
CT, CBC, Chem, troponin, etc; not routine part of w/u
unless you have red flags
Other diagnostics driven by age, Hx, PE
IV hydration, O2, monitor, labs, troponin
CXR, +/-CT. Echocardiogram, Holter Monitor
c. >50yo – higher risk, more extensive work up
Young, healthy, completely recovered, stable?-syncope
Young, healthy, completely recovered, stable?
Likely benign cause. Home if stable w/ return precautions
EKG and UPT
Close follow-up, PO hydration, avoid risks
>50yo – bigger work up, home if w/u all neg, no risks
Vertigo
Sensation of motion, room spinning
is the room spinning or are you spinning inside the room
what are the two types of vertigo
Major question for us = Central or Peripheral?
- Peripheral is usually benign
- Central causes usually serious – red flag!
Hx of vertigo
- Describe what you feel
- OPQRST the sx to death
- Trauma, recent illness?
- Hearing changes, tinnitus?
- Headache, weakness?
- Associated sx’s – fever, bleeding, etc…
can you describe peripheral vertigo
onset
nystagmus is
worse with
associated sxs?
neuro deficits ?
sudden onset, intense, paroxysmal, w/ movement;
nystagmus is horizontal/torsional, fatigable; tinnitus, n/v,
+/- normal TM,
NO FOCAL NEURO deficit
BPPV -what is the cause
MOST common cause
Otolyth in the semicircular canal
Vertigo lasts seconds, positional
inflammation, after viral infection can cause this type of vertgio-ear sxs
labrynthitis
labrynthitis story
• Vertigo for days, ear/hearing sx’s
Movement exacerbates, post viral
Vestibular Neuritis:
inflammation
• Vertigo for days, no ear sx’s
• Movement worse, post viral
Story behind Meniere’s, what does it look like and what age do we see it most commonly present
40-70s
Episodic, chronic, incurable
SN hearing loss, tinnitus
central causes of vertigo
Cerebellar CVA, hemorrhage
Vertebrobasilar vascular insufficiency/CVA
Basilar artery migraine
Multiple sclerosis
Temporal lobe seizure
vertigo caused by drugs will be seen with
Drugs cause peripheral sx’s – ear sx’s predominate
nystagmus in central vertigo
Nystagmus present in all: type, direction, duration matter
peripheral vertigo presents with this type of nystagmus
horizontal and fatiguable
(bppv can be nonfatiguable_
Ptosis? w/ vertigo what are you worried about (4)
Botulism, MG, CVA, CN
what are you looking for in the ears with vertigo
Vesicles, cholesteatoma -tumor behind the eardrum, perforated TM?
Head impulse with peripheral vertigo
Abnormal (saccade) suggests peripheral
Head impulse w/ central vertigo
Normal in central causes
peripheral vertigo nystagmus
one direction: horizontal/torsional – never vertical, fast phase away from affected ear, intensity decreases w/ fixation, fatigues on repeat
what type of peripheral vertigo would NOT fatigue
BPPV may not fatigue
nystagmus beats towards or away from affected ear with peripheral vertigo
away
beats towards opposite eye
nystagmus with central vertigo
any direction (vertical, rotary), fast toward lesion, little effect with fixation/gaze direction change, does not fatigue
Test of Skew
Cover one eye, uncover, repeat. Eye position deviation when uncover, corrects.
positive test of skew indicated
b. Positive suggests central cause
Peripheral Motor Weakness differs from central how?
i. Not central nervous system
1. CVA/TIA is sudden onset, unilateral
1. Slower onset, progressive, bilateral
2. Neuromuscular junction vs. muscles
3. Respiratory compromise concerns
PE of peripheral motor weakness
- Strength testing
- DTR’s: +2 is normal
- Cranial nerves
- Sensation testing
- Cerebellar testing
Most common cause of
acute
bilateral
flaccid paralysis
v. Guillain-Barre
story of Guillain-Barre
Autoimmune, demyelinating, progressive, symmetrical
paralysis with guillain barre starts with
Ascending pattern – legs first
loss of DTR
grade 1 strength
a trace of contraction is noted in the muscle by palpating the muscle while attempting to contract
the pt may move muscles against gravity but not resistance form the examinar with the grade of strength
grade 3
the patient is able to actively move the muscle when gravity is eliminated
grade 2
the patient may move the muscle agains some resistance
grade 4
tx of guillaine barre
immunoglobulins, plasmapheresis
who gets guillane barre
- 2/3 have preceding viral illness (also Zika, etc)
a. 1/6 GB cases after Flu shot
what sxs do you see with GB
Hand paresthesia, muscle pain, may involve CN’s
what are we concerned about with GB
Dx is clinical; worry about respiratory issues, dysautonomia
Neurology consult. Admit.
Most common disorder of neuromuscular transmission
MG
MG is seen most commonly in the population
Bimodal peak: 30’s (female predominant), 80’s (male)
SXS of MG
Eye, facial, swallowing, speech muscle sx’s predominate
Bilateral or unilateral ptosis, diplopia, vision changes
Peek sign: close eyes –> can’t maintain, can see sclera
Flat expression, “lost their smile”
Gets “tired” talking, chewing fatigue, difficulty swallowing
Generalized weakness, fatigue, can’t climb stairs
DTR w/ MG
intact
botulism pt looks like
IVDU with eye sxs, facial sxs, weakness
what is the key to MG
Key: sx’s get worse with use, better with rest
Descending, DTR’s intact
ED Dx:
Tensilon (Enlon)/ edrophonium test, ice pack test (their strength comes back but when their eyes warm up their deficit comes back).
Neuro consult, Admit.
sx of botulism
Sudden, severe, symmetric, bilateral weakness – eyes, face, neck first; extremities last
Mental status, sensory intact
Infants: floppy, lethargic
tx of botulism
These pt’s are sick: recognition is key, respiratory concerns
Tx: Antitoxin, supportive care. Neuro consult. Admit
Young, female > male, autoimmune?
MS
look for monocular vision changes
need labs LP and mRI
Episodic weakness, paresthesias, disequilibrium – atypical pattern
Abrupt, progressive, bilat, proximal muscle weakness – legs usually before arms
- Can’t rise from chair, brush hair, lift, etc
May have dysphagia
Polymyositis
Must consider this Dx in anyone w/ low back pain!
Cauda Equina Syndrome
Transverse Myelitis
Spinal epidural abscess
Cauda Equina Syndrome sxs
Symptoms: Unilateral or bilateral radicular back pain with:
True leg weakness, bilat or unilateral
Bladder incontinence or retention, hesitancy
Stool incontinence, loss of anal tone
Numbness in the “saddle” and perineal distribution; genitals
Loss of or reduced lower extremity DTR’s
. Charting should reflect all of above in low back pain pt’s
“SENSORY IS INTACT in the b/l lower extremities INCLUDING the saddle region”
cause of Cauda Equina Syndrome
- Cause: mechanical compression on “horse’s tail”
a. Disc, fracture, infection, tumor
IVDU with fever + back pain, radicular sx’s
need to think about
Spinal epidural abscess
picture of transverse myelitis
Bilateral motor and sensory loss w/ radicular back pain, B/B dysfunction/incontinence, sensory changes
rapidly progressively
Low K+, Fam Hx, meds (diuretics)
Weakness local or generalized
Descending, DTR’s diminished
Hypokalemic Periodic Paralysis
Hypokalemic Periodic Paralysis triggers
Triggers: carbs, cold, exercise
Tick Paralysis looks like
- Suggestive Hx
- Ascending, DTR’s diminished
- Remove tick – resolves 24-48hrs
“Saturday Night Palsy” can’t do what
stop in the name of love
tx of “Saturday Night Palsy”
vi. Splint with wrist in extension
1. Resolves weeks to months
vii. Consider occult Fx
viii. Referral to PMD, neurologist
CN VII mononeuropathy
b. Bell’s Palsy
how do you know bells from stokre
persons forehead is involved in bells
in CVA the forehead is spared
Bell’s Palsy need a
ear exam
Diplopia can be caused by
cranial nerve palsy III, IV, VI
who gets diplopia
Idiopathic, traumatic; central: tumor, etc vs. peripheral: vascular (DM, vascullitis), cavernous sinus thrombosis
what do you need to do with pt w suspected palsy
need to isolate what is wrong (look at the chart)
3 and 6 is the most common
- Monocular or binocular? Evoke the diplopia
- Do the eyes line up on EOM’s/cover test?
- Ptosis? Pupils?
- Ptosis, “down and out” gaze, non-reactive, dilated pupil
iv. CN III – occulomotor – DM, temporal arteritis
- “head-tilt” to opposite shoulder to avoid diplopia, eye “down and away”
v. CN IV – trochlear – rare, idopathic, kids
- Lose lateral gaze, horizontal diplopia, cover affected eye – diplopia resolves
vi. CN VI – abducens – DM, increased ICP
what should you consider with palsy
: Lupus, Lyme’s, Botulism, Wenicke’s, Syphilis, Thyroid, Vit B Deficiency too
ix. Labs, CT head/face
most common location of a focal impaired awareness seizure
temporal lobe
Drug induced causes of vertigo will most likely present with
ear sxs predominate
very rare tumor that can be the cause of vertigo
cerebellar pontine angle tumor
vertigo tx
labs no necessary for peripheral
antiemetics
antihistamines
benzodiazepine
safety return precautions
epley in ED
semont at home
ENT refereal if reoccurent or hearing loss findings
central vertigo tx
w/u is necessary
MRI
UMN findings
hyper-reflexia
muscle tone: increased spastic
no fasiculations
no atrophu
babinski present
LMN findings
hyporeflexive
decreased or flaccid muscle tone
fasiculations
severe atrophy
and absent babinski
RF for transverse myelitis
Risks: Herpes MS vasculitis Lyme dz TB IVDU IMZ
polymyositis
abrupt
progressive
bilat
proximal muscle weakness
USUALLY legs before arms
polymyositis common lab finding
increase CK
increase aldalase
Anti-JO1 antibody
DYSPHAGIA
HYSPHONIA
Proximal abrupt and progressive b/l weakness
legs usually before arms
cna’t prush hair
dermatomyositis sxs
similar to polymyositis but with race to face chest and upper back in a shawl pattern
Tx for guillane Barre
immunoglobulins and plasmapharesis
age of MG pts
bimoda;
30s and 80s
what motor weakness syndromes would lead to a loss of DTRs
guillan barre- ascending
tick paralysis ascending (diminished)
hypo kalmeic paralysis (diminished) -descending
cauda equina (diminished
what would be an essential hx question to ask in a pt suspected of hypokalemic periodic paralysis
usually on diuretics
triggered by cold or carbs or exercise
