Category Archives: Neurology

Anti-platelet therapy for stroke, what’s a ED Doc to do?

As a follow up to one of my esteemed colleague’s recent quick hit on the basics of strokes, I present some findings from time spent on the stroke unit these last few weeks.  Stroke is fairly popular here in the great state of Kentucky—we supremely enjoy our fried food, cigarettes, and lack of exercise (‘Merica!).  Therefore, stroke alerts are a fairly common occurrence in the ED and we keep our neurology friends busy (aka stroke team rounded for 10 hours a day).  But not everywhere is lucky enough to have an on call neurologist present for all stroke alerts.

So you’re the ED doc and they might have a stroke. Qu’est-ce que tu vas faire*!?!

Firstly, a head CT.  This is the first branch of the decision tree.  As previously mentioned, strokes are either hemorrhagic or ischemic, and the management of each is entirely different (ie do they get tPa or not). Without regards to whether to use tPa or not, this will focus on the ischemic subtype.

And within this subtype of ischemic stroke patients who cannot receive tPa, one comes to another branch in the decision tree.  Is the patient in atrial fibrillation (afib)?  Usually this can be evident from physical exam (ie irregularly irregular pulse) and telemetry, but an EKG can be confirmatory.  The management of an ischemic stroke in afib (aka cardioembolic ischemic stroke) differs greatly from one that isn’t (aka noncardioembolic ischemic stroke).  Cardioembolic strokes requires anticoagulants (eg warfarin) while a non-cardioembolic stroke only requires anti-platelets (eg aspirin).  Once again, the following will only focus on non-cardioembolic stroke and choice of anti-platelet.

*That’s French speak for ‘What ya gonna do’

Aspirin is dece*

There is some controversy in the stroke world as to the initial choice of anti-platelet for secondary prophylaxis of non-cardioembolic ischemic strokes.  One thing most everyone can agree on though is the utility of aspirin.  Aspirin within 48 hours has shown to decrease stroke reoccurrence and improve long term outcomes in multiple trials and meta-analyses 1,2,8.

*Dece= decent in Caucasian phrasin’

So what about the other fancy anti-platelets? 

There have been a multitude of trials that one is welcome to read by following the references below but I present my personal summary for secondary prophylaxis based on what I’ve read in the trials:

– Aspirin is more effective than placebo1,2

-Aggrenox (dipyramidole+aspirin) is better than placebo3

-Plavix is better than aspirin in composite vascular endpoint (you can decide for yourself whether that’s truly better for stroke or not)7

-Aggrenox may be better than aspirin3,5

-Plavix and Aggrenox are equivalent4

– ASA+ Plavix is equivalent to plavix alone but increases risks of bad side effects (eg bleeding)6

– Ticlopidine is better than placebo9

-Ticlopidine may be better than aspirin but with increased costs, lab f/u (i.e. biweekly CBC’s the first 3 months due to risk of neutropenia), and worse side effects may decrease the cost/benefit ratio10

Blah blah too many words—Break it down, C Belch

So a patient comes in with signs of stroke.  Their CT is negative for bleed and they’re outside of the tPa window.  They’re not in afib.  What are you gonna do?  My personal guidelines based on the evidence:

–          Aggrenox or Plavix monotherapy are good initial choices for non-cardioembolic ischemic strokes and better than aspirin alone

–          Do NOT use aspirin + Plavix dual therapy for these types of strokes due to the increased risks of bleeding. Leave that combo for cardiologists.

–          Aspirin and ticlopidine are also good initial choices.  But aspirin may be less effective than Aggrenox or Plavix monotherapy and ticlopidine has a poor side effect profile and increased costs

Public Service announcement:  As always, each patient is different and requires a personalized and evidence based approach to medication choices based on side effect profile and individual patient preference.  I also reference below the American College of Chest physician’s recommendations11 —they set forth their own guidelines based on the evidence which are very similar to what is proposed above.  And if all else fails, ask your friendly neighborhood pharmacist.



  1. The International Stroke Trial (IST). Lancet. 1997 May 31; 349 (9065): 1569-81
  2. Chinese Acute Stroke Trial (CAST). Lancet 1997 Jun 7; 349 (9066): 1641-9
  3. European Stroke Prevention Study 2 (ESPS 2).  J Neurol Sci. 1996; 143(1-2): 1-13
  4. PRoFESS trial.  NEJM. 2008; 359 (12): 1238-1251
  5. European/Australasian Stroke Prevention in Reversible Ischemia Trial (ESPRIT).  Lancet. 2006; 367 (9534):  1665-1673
  6. MATCH trial.  Lancet. 2004. Jul 24-30; 364(9431):  331-7
  7. CAPRIE trial.  Lancet.  1996 Nov 16; 348(9038):  1329-39
  8. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, MI, and stroke in high risk pts.  (Antithrombotic Trialists’ Collaboration).  BMJ.  2002 Jan 12; 324 (7329):  71-86
  9. Canadian American Ticlopidine Study (CATS).  Lancet.  1989 Jun 3; 1(8649):  1215-20
  10. A randomized trial comparing ticlopidine HCL w/ asa for prevention of stroke in high risk pts.  (TASS).  NEJM.  1989 Aug 24; 321 (8):  501-7
  11. Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence based clinical practice guidelines.  Feb 2012; 141 (2_suppl)

Compiled by: Chris Belcher

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

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Strokes: the quick and dirty

2 Major Types:

1) Ischemic: blood vessel supplying the brain is obstructed by a clot

  • Embolism
  • Thrombosis 

2) Hemorrhagic: blood vessel bursts, blood leaks throughout brain #1 Risk Factor: High blood Pressure Other Risk Factors:

  • Age
  • Sex: Male
  • Ethnicity: African Americans, Mexican Americans, Hawaiians, Asian Americans
  • Smoking
  • Fat, cholesterol-rich diet
  • Overweight
  • Pregnancy
  • Birth-control Pills
  • Smoking
  • Diabetes
  • Renal problems
  • Atrial Fibrillation

Signs of Stroke

  • Sudden, severe headache
  • High blood pressure
  • Problems with vision, reflexes, walking, movement, speaking, coherence
  • Vertigo
  • “Bruit” noise when listening to carotid arteries in neck with stethoscope

Treatment Options:

  • Ischemic: Blood thinners to reduce clots: warfarin, heparin, Coumadin
  • Hemorrhagic: surgery to remove blood in brain, repair damaged blood vessels

Academic life in emergency medicine NIH stroke scale PV card. Great resource:

Click continue reading for high yield quickhits on a few specific types of stroke and brain imaging examples Continue reading

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Beating a Dead Horse: Why Ocular Ultrasound Beats Papilledema for Detecting Increased Intracranial Pressure

Our earlier article on ocular ultrasound for measuring intracranial pressure was met with a common question. Primarily, why not just use papilledema as your initial assessment for intracranial pressure? This is what we are taught in medical school. Optic nerve disc swelling equals increased intracranial pressure (ICP). End of Story. Right? Not exactly…  While optic disc swelling can indicate increased ICP, it is an inferior measure of acutely elevated ICP. And here is why…

  • It’s an indirect measure.
  • It’s a late sign of increased ICP.
  • It’s more subjective.
  • It’s not a dynamic measurement.
  • It’s not always practical.

pap vs oc us 1

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Trigeminal Neuralgia

Trigeminal Neuralgia (Facial pain, tic douloureux)

  • Pain:  Paroxysmal stabbing pain affecting one or more divisions of the trigeminal nerve
  • rarely bilateral, and never on both sides at the same time
  • may last for days or weeks and patient may remain pain free for many months after pain subsides
  • Signs and symptoms:  usually no accompanying neurological problems, sometimes blunting of pinprick over affected region
  • Triggers: speaking, brushing teeth, washing face, eating, cold wind, touching a “trigger spot”
  • Mostly affects females and patients 50+ yrs of age


  • CT or MR scan to exclude CPA lesion or demyelination

Acute Attack Treatment = Phenytoin 250 mg IV for relief for hours- 3 days

First line Agent =  Carbamazepine 100mg 1-2 times per day, with increase of 100-200mg every 3 days up to a maintenance dose of 400-800mg

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Herpes Simplex Encephalitis (HSE)

Clinical presentation of HSE in children over 3 months and adults is typically is HSV-1, acute, or subacute, and generally has non-specific signs such as:

  • Alteration of conscious (97%)
  • CSF Pleocytosis (97%)
  • Fever (90%),
  • Personality Change (85%)
  • Headache (81%)
  • Seizures(67%)
  • Vomiting (46%)

In newborns it typically presents 6-12 days after birth with general lethargy, poor feeding, and/or seizures and is HSV-2.


CSF should be taken immediately when HSE is suspected and sent for a PCR study. This is the gold standard and is sensitive 94-98% and specific 98-100%.

Lab studies are non-specific. Imaging (CT and MRI) and Electroencephalography abnormalities can take days to a week to appear on scans.

  • CSF in patient with HSE will have elevated WBC, RBC, elevated protein, and normal glucose level with lymphocytic pleocytosis
  • MRI findings if present would demonstrate temporal lobe lesions
  • Electroencephalography (EEG) has characteristic periodic high-voltage spike wave activity emanating from the temporal lobes and slow wave complexes are highly suggestive of HSE.


IV acyclovir should be started immediately , before PCR results confirm, because its toxicity is rather low and HSE prognosis is poor untreated. In adults 10-15mg/kg q8h x14-21days, 3 months-12years 20mg/kg x10 days, neonates 30mg/kg/day.

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Keeping an Eye on Intracranial Pressure: Measuring ICP Using Ocular Ultrasound

Measuring Intracranial Pressure Using Ocular Ultrasound

Measuring ICP

  • There is a caliper function on ultrasound machines that gives you precise measurements of selected structures.
  • Take your optic nerve sheath diameter (ONSD) measurement 3 mm posterior to the globe.
    • This area has the greatest contrast with surrounding tissue (more contrast = more accurate measurements).
    • Use the calipers to determine 3 mm.
  • Measure across the optic nerve sheath (not just the optic nerve).
  • Measure ONSD for both eyes and average the two measurements.

Interpreting Your Results:

  • Increased ONSD correlates with increased ICP
  • Upper limit of normal ONSD vary with age…
    • Adults: < 5 mm
    • Children > 1 yo: < 4.5 mm
    • Children < 1 yo: < 4 mm
  • ONSD 5 – 5.7 mm: may indicate ICP > 20 mmHg, especially if symptomatic
    • > 5 mm is 100% sensitive for elevated ICP
    • All patients with elevated ICP have ONSD > 5mm
  • ONSD > 5.7 mm: indicates ICP > 20 mmHg
    • > 5.7 mm is 100% specific for elevated ICP
    • Only patients with elevated ICP have ONSD > 5.7 mm
  • ONSD measurements increase with increasing ICP.
  • ONSD measurements plateau around 7.5 mm even with significantly increased ICP.
  • In severe cases, an echoluscent circle called a crescent sign may be present.
    • Crescent sign is formed by the separation of the optic nerve sheath from the optic nerve by high ICP.

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Idiopathic Intracranial Hypertension

(the diagnosis formerly known as pseudotumor cerebri)

  • Presentation = acute, subacute, chronic headache with associated blurry vision or visual loss, papilledema, pulsatile tinnitus (“whooshing sound in ears”), abducens nerve palsy, nausea, vomiting
  • Patients typically young obese women
  • ** Meds to know causing pseudotumor = vitamin A, oral contraceptives, glucocorticoids
  • ** Brain MRI = empty sella, slit like ventricles
  • ** Will have normal brain imaging with elevated CSF pressure
  • Tx = weight reduction, acetazolamide
    • Medical measure fail or visual field defects are progressive –> shunting or optic nerve sheath fenestration
    • Acetazolamide MOA = inhibits choroid plexus carbonic anhydrase –> decrease CSF production and intracranial hypertension

Dandy criteria for dx of IIH:

  1. signs/symptoms of ICP
  2. no other neuro abnormality or impaired consciousness
  3. normal CSF
  4. neuroimaging showing no etiology
  5. no other cause of intracranial hypertension apparent

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CT Imaging in Minor Head Injury

For minor head injury patients (GCS 13-15) apply the CCHR or NOC decision making tools to help you decide if a head CT is required.

Canadian CT Head Rule:

Head CT is only required in minor head injury patients with any one of the following:

High Risk Factors (for neurological intervention)

  •  GCS score <15 at 2 h after injury
  • Suspected open or depressed skull fracture
  • Any sign of basal skull fracture (haemotympanum, ‘racoon’ eyes, cerebrospinal fluid otorrhoea/rhinorrhoea, or Battle’s sign)
  • Vomiting ( > two episodes)
  • Age 65 years

Medium Risk Factors (for brain injury on CT)

  • Amnesia before impact >30 min
  • Dangerous mechanism (pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from height >3 feet or five stairs)

But the Rules Don’t Apply If:

  • GCS < 13
  •  Patient taking coumadin or had a bleeding disorder
  • Obvious open skull fracture
  • Age < 16 yo
  • Non-traumatic

MDCalc: Canadian CT Head Rule Tool

New Orleans Criteria: 

Presence of one or more of the following seven findings requires a head CT:

  • Headache
  • Vomitting
  • Age > 60 yo
  • Drug or alcohol intoxication
  • Deficits in short-term memory
  • Physical evidence of trauma above the clavicles
  • Seizure

MDCalc: New Orleans Criteria Tool

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