Neuro AC Exam Flashcards

1
Q

Difference between primary headache and secondary headache

A

Primary - not associated with any other diseases, HA is the diagnosis
Secondary - associated with or c/b other conditions, generally will not resolve until the cause has been addressed

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2
Q

Examples of primary headaches

A

tension, migraine, cluster

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3
Q

Examples of secondary headaches

A

tumor, intracranial bleeding, increased ICP, medications (nitrates), meningitis, GCA, etc.

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4
Q

What does the SNOOP pneumonic refer to

A

RED FLAGS for headaches and when you should consider a secondary cause and do a further workup
S = systemic symptoms (fever, weight loss) or secondary HA risk factors (HIV, malignancy, pregnancy, anticoagulation, marked BP increase)
N = neuro signs and symptoms (confusion, impaired alertness or consciousness. nuchal rigidity, papilledema, etc.)
O = onset (sudden, abrupt, with exercise, sexual activity, coughing, etc.)
O = onset (age older>50 or <5)
P = prior HA hx, positional, palilledema

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5
Q

Tension-type HA characteristics

A

30min - 7 days (usually 1-25h with 2+ of the following characteristics)
pressing, non-pulsatile pain
mild-moderate intensity
bilateral
notation of 0-1 of the following: nausea, photophobia, or phonophobia
F>M

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6
Q

Migraine w/o aura characteristics

A

4-72hrs with 2+ of the following
unilateral
pulsating, moderate to severe pain
aggravated by normal activity (walking)
during the HA 1+ of the following - N/V, photophobia, photophobia
F>M
positive family hx

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7
Q

migraine with aura characteristics

A

HA occurs with or after aura
focal dysfunction of cerebral cortex or brain stem causes >/= 1 aura symptoms to develop over 4min, or 2+ symptoms occur in succession
dread, anxiety, unusual fatigue, nervousness, excitement, GI upset, visual or olfactory alterations
no aura symptoms should last > 1h – if this occurs refer to neuro for seizure workup
high correlation with family hx

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8
Q

cluster type HA characteristics

A

tendency of HA to occur daily in groups or clusters
clusters usually last several weeks-months then disappear for months-years
usually occur at characteristic times (same season, same time of day, etc.)
HA location is usually behind 1 eye with a steady, intense, severe pain that lasts 15min-3h
commonly occurs with Ipsilateral autonomic sign-lacrimation, conjunctival injection, ptosis, nasal stuffiness
M>F

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9
Q

Primary HA treatment options

A

lifestyle modifications
Analgesics - NSAIDs. Tylenol - limit to 2 days/week
Rescue therapy - opioids, antiemetics **, short term use of corticosteroids
Migraine-specific meds - triptans, ergot derivatives - CAUTION in pregnancy, CV disease, uncontrolled HTN
High flow O2 for cluster HA
Control meds - Mg++ and riboflavin

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10
Q

What is the most important historical component for a stoke patient

A

time of symptom onset

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11
Q

Hospital-based care for ischemic stroke patient

A

stabilization, hx, neuro exam and stroke scale (NIHSS), finger stick, CT, ECG, metabolic panel, CBC, cardiac markers, PT/INR and PTT

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12
Q

Management of HTN in stroke

A

if a patient is a candidate for tPA - acute BP reduction should be instituted if SBP > 185 or DBP > 110
If patient is not a candidate for tPA withhold BP drugs unless SBP > 220 or DBP > 120

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13
Q

What does the NIHSS used for and what does it mean

A

NIHSS is the stroke scale
<4 = good prognosis, no tPA necessary
4-20 = ideal tPA
>20 = severe deficit, no tPA

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14
Q

Absolute contraindications for tPA for acute ischemic stroke

A

current ICH
subarachnoid hemorrhage
active internal bleeding
recent (w/in 3mo) intracranial or intraspinal surgery or serous head trauma
presence of intracranial conditions that may increase the risk of bleeding
bleeding diathesis
current severe uncontrolled HTN

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15
Q

What are the three types of intracranial bleeding

A

subarachnoid
epidural
subdural

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16
Q

Subarachnoid hemorrhage cause, s/s, and treatment

A

rapid arterial bleeding into the subarachnoid space secondary to a cerebral aneurysm or head injury
s/s - thunderclap headache**, vomiting, confusion/LOC, seizures
treatment - surgical intervention, BP control
“worst headache of my life”

17
Q

Epidural hematoma cause, s/s, and treatment

A

injury to the middle meningeal artery secondary to fracture to the temporal or parietal skull – rapid accumulation of blood beta the dura and the skull
s/s - HA, transient LOC**, unilateral fixed/dilated pupil, N/V, dizziness
Treatment - surgical intervention if significant, BP control
“usually baseball player questions”

18
Q

Subdural hematoma cause, s/s, and treatment

A

damage to bridging veins cuasing blood to accumulate under the dura
can be acute or chronic
s/s - HA, general LOC or change in mental status, seizures
treatment - surgical intervention if significant, watch and wait, anti-seizure prophylaxis (7 days, kepra)

19
Q

Subdural hematoma cause, s/s, and treatment

A

damage to bridging veins causing blood to accumulate under the dura
can be acute or chronic
s/s - HA, general LOC or change in mental status, seizures
treatment - surgical intervention if significant, watch and wait, anti-seizure prophylaxis (7 days, kepra)

20
Q

Early signs of increased ICP

A

HA, N/V, changes in mental status or LOC, changes in behavior

21
Q

Late signs of increased ICP

A

unresponsiveness, dilated pupils or nonreactive, posturing, Cushing’s triad

22
Q

What is Cushing’s triad

A

Bradycardia, widened pulse pressures, apnea

23
Q

Signs and symptoms of meningitis

A

severe HA, nuchal rigidity, high fever, altered mental status, kernig’s sign, brudzinski sign

24
Q

What is Kernig’s sign

A

patient is lying supine, pain is elicited by passive extension of the knee (this leads to increased ICP)

25
Q

What is brudzinski sign

A

Flexion at the neck causes involuntary flexion of the knee and hip

26
Q

Diagnostic testing for meningitis

A

LP as soon as diagnosis is suspected, CT scan first to r/o space-occupying lesion if: papilledema, coma, seizures, focal neuro findings

DO NOT PERFORM A LUMBAR PUNCTURE IN THE PRESENCE OF SIGNS OF INCREASED ICP OR IF THEY ARE SEIZING

27
Q

Treatment for meningitis

A

high dose parenteral antibiotics, if purulent is suspected, may need dexamethasone

28
Q

Compare and contrast spinal fluid characteristics for bacterial vs viral meningitis

A

cell count - bacterial (PMN or neutrophils present) viral (lymphocytes present)
glucose - low in bacterial (<45), normal in viral (>50)
opening pressure - high in bacterial, normal in viral

29
Q

Autonomic dysreflexia - location, cause, s/s, treatment

A

spinal cord syndrome - injury above T6
usually caused by traumatic injury
s/s - exaggerated autonomic responses - above the level of injury = diaphoresis + flushing, below the level of injury = chills + vasoconstriction, HTN, bradycardia, HA, nausea
treatment - remove stimulus, manage autonomic manifestations

30
Q

Brown-Sequard syndrome - location, cause, s/s, treatment

A

penetrating trauma to the spinal cord (anywhere) - usually hemisection injury
s/s - ipsilateral motor disturbance + proprioception, contralateral loss of pain + temp
treatment - immobilization, transfer to trauma, steroids (sometimes)

31
Q

Central cord syndrome - location, cause, s/s, treatment

A

cervical spinal cord
cause - hyperextension injury (MVA, fight)
s/s - upper and LE weakness (more deficits in upper), varying degrees of sensory loss - impaired pain, temp, light touch, position sense below the level of the injury
treatment - ICU for 24h, monitor for autonomic dysreflexia, HTN

32
Q

Most reliable testing for neuroimaging

A

CT (used most of the time), MRI used for a more thorough evaluation (infection, concussion/TBI, lesions, masses, acute stroke/TIA, dementia eval, seizures, temporal lobe epilepsy)

MRI ARE CONTRAINDICATED IN PATIENTS WITH PACEMAKERS AND METAL IMPLANTS

33
Q

First line medication of status epilepticus

A

lorazepam (benzodiazepine should be first)

34
Q

which vitamin should be priority for chronic alcohol abusers

A

vitamin B

35
Q

Characteristics of GBS & treatment

A

demyelination of peripheral nerves – paralysis usually works its way up and is self-limiting. concern for respiratory function. will eventually resolve, patients may have profound UE weakness
treatment: IVIG, plasmapheresis, lose dose heparin if hospitalized

36
Q

Myasthenia gravis characteristics & treatment

A

destruction of acetylcholinesterase
patients will have profound weakness
tx: acetylcholinesterase inhibitors, prednisone, plasmapheresis, and IVIG