cervical artery dissection: quick review

CAROTID (AND VERTEBRAL) DISSECTIONS: QUICK HITS


--first consult call to Neurologists (less commonly Vascular Surgeons)


--Vascular imaging is a must, but CTA is more sensitive than MRA.  


--To catch on MRI, specific sequences are required so check with your Neurologist/Radiologist to figure out which.  


--Dissections that extend intracranially have a high incidence of forming SAH, especially when heparin is started, thus making heparin have higher mortality than anti-platelet drugs.  


--Extracranial dissections are usually treated with antiplatelet drugs and anticoagulation. 

Submitted by T. Boyd.



Reference(s): Shea et al. Carotid and Vertebral Artery Dissections in the Emergency Department. Emergency Medicine Practice.14;4. April 2012; picture

epileptic vs. non-epileptic seizure: what are the signs?

WHAT ARE THE SIGNS?

--review by Avbersek & Sisodiya in J Neurol Neurosurg Psychiatry (link below)
--looked at 34 studies
--tried to tease out what signs distinguish epileptic vs. non-epileptic seizure


WHAT DID THEY FIND?

--signs that favor psychogenic non-epileptic seizures (specificity)

• fluctuating course (96%)
• asynchronous movements (93-96%)
• pelvic thrusting (96-100%)
• side-to-side head/body movement (96-100%)
• closed eyes (74-100%)
• ictal crying (100%)
• memory recall (96%)

--signs that favor epileptic seizures (specificity)

• occurance from sleep (100%)
• post-ictal confusion (88%)
• stertorous (snoring) breathing (100%)

FYI:
--the sensitivities for all of these signs were horrible, so can't use them to rule anything out
--sometimes excluded frontal lobe partial seizures
--insufficient evidence: gradual onset, flailing/thrasing, opisthotonus, tongue biting, urinary incontinence


Reference(s): review article, picture

Spontaneous Cervical and Intracranial Arterial Dissections

(scroll to bottom for quick hits)

Background
-Arterial dissections can cause stroke in both young in old populations, and is the most common cause of stroke in the young

-Extracranial dissection is more common than intracranial dissection

-Stroke is generally caused by either diminished blood flow from intraluminal thrombus or embolized clot


Pathogenesis (stick with it)
-Dissection are believed to begin with a tear in the media of the vessel wall, leading to bleeding in the wall itself

-partially coagulated intramural blood can enter the lumen which activates platelets and
the coagulation cascade leading to intraluminal thrombus.

-Intramural blood can accumulate leading to compression of the lumen



Risk Factors
-Connective tissue and vascular disorders are thought to be main risk factors:
(e.g. Ehlers-Danlos Syndrome (type IV), Marfan Syndrome, Polycystic kidney disease, cystic medial necrosis, Fibromuscular dysplasia)

-many are caused by trauma




Diagnosis
-based on radiologic criteria taken from the Strategies Against Stroke Study for Young Adults in Japan (SASSY) using CTA or MRI/MRA

-Primary rules are based on finding an intimal flap or double lumen on Angiogram or MRI/MRA, or repeated non-specific findings associated with dissection on multiple studies.



Symptoms
-Head or neck pain

-Horner Syndrome - occurs when the sympathetic fibers on the ICA are stretched. It is usually just partial with ptosis and miosis but no anhidrosis.


Difference between Carotid and Vertebral Dissections
-Transient monocular blindness occurred only with internal carotid dissection

-Ischemic stroke is more common in vertebral dissections

-Neck pain and recent minor cervical trauma are more common in vertebral dissections

-Proportion of men and a recent infection are more common in ICA



Treatment
-Antithrombotic therapy (antiplatelet or anticoagulation) is the primary initial treatment for ischemic stroke and TIA caused by arterial dissection

-For intracranial dissection, antiplatelet therapy is often the treatment of choice

-For extracranial dissection, anticoagulation initially followed by 6 months of warfarin therapy as opposed to antiplatet therapy is often chosen

-Endovascular and surgical therapy are generally only reserved for recurrent ischemic events


BOTTOM LINE:
-arterial dissection is more common cause of stroke in the young
-extracranial (vertebral, carotid) more common than intracranial dissection
-sx: headache, neck pain, stroke-like symptoms, Horner's syndrome (for ICA)
-risk factors: connective tissue disorders, trauma
-dx: angiography, MRI/MRA
-tx: antithrombotics/anticoagulation (aspirin, heparin, coumadin, etc.); surgical/endovascular for recurrent events


Submitted by J. Grover.


Reference(s): Caplan, LR and Biousse V. “Cervicocranial Artery Dissections.” J Neuro-Opthalmol. 2004; 24:299-305. Maruyama, H et al. “Spontaneous Cervicocephalic Arterial Dissection with Headache and Neck Pain as the Only Symptom.” J Headache Pain (2012) 13: 247-253. “Spontaneous Cerebral and Cervical Artery Dissection: Treatment and Prognosis”. Uptodate.  “Spontaneous Cerebral and Cervical Artery Dissection: Clinical Features and Diagnosis”. Uptodate., picture

decision rule for subarachnoid hemorrhage?

THOSE CANADIANS ARE AT IT AGAIN:
--study by Ottawa docs, Perry et al. reviewed nicely in an AAEM/Common Sense article (see reference)
--tried to identify a set of clinical characteristics to make a decision rule for those who need SAH workup


BASIC STRUCTURE:
--1,999 patients, 130 diagnosed with SAH
--SAH diagnosis defined by +CT, xanthrochromia, or >5 x 10^6/L RBCs + aneurysm/AVM on cerebral angiography

--included:

• adults (>16 yo)
• chief complaint = headache
• GCS 15
• non-traumatic
• peak intensity of HA within 1 hr

--excluded:

• >2 wks after symptom onset
• prior SAH
• previous CT and/or LP workup
• 3 similar HA's within past six months
• papilledema/focal neuro symptom
• prior hydrocephalus or cerebral neoplasm

RULES THEY CAME UP WITH:
--all have sensitivity 100%, but specificity sucked (28-39%)

--the rules (each set works to help rule-out SAH):

• age >40, neck pain/stiffness, witnessed LOC, DBP > 100mmHg
• arrival by EMS, age>45, vomiting, DBP > 100
• arrival by EMS, age 45-55, neck pain/stiffness, SBP > 160

BOTTOM LINE:
--nice study, helps think about why we do what we do, but isolated population
--the extra H&P details (age, BP, vomiting, neck pain/stiffness, etc.) are not very specific for SAH, but together might be sensitive (reminds me of appendicitis)
--not ready for primetime just yet, but food for thought


Submitted by S. Lee.


Reference(s): AAEM/RSA review, picture

migraine headache treatment

Submitted by E. Hawkins.

Simple Partial Status Epilepticus

Submitted by E. Hawkins.

Do steroids prevent post-herpetic neuralgia in shingles?

Submitted by E. Hawkins.

nerve block for occipital neuralgia

Submitted by K. Sullivan.

Reference(s): on the slide

the blown pupil

Submitted by E. Hawkins.

vertigo and the head thrust test

QUICK RECAP:
--quick head movement toward defunct canal...
--patient loses the target, needs a "catch up" saccade to re-fixate


Submitted by. K. Sullivan.


Reference(s): bmj article

Forget about antivirals for Bell's palsy

RAGING HYPOTHETICAL:

--A guy comes in with a facial droop. You check for eyebrow raise and unequal smile and correctly identify this as a isolated peripheral VIIth nerve palsy. (Nice job not bothering the stoke fellow)

WHAT WILL YOU SEND THEM HOME WITH?

1) Eye protection

-patch to close at night and put some lacrilube in there. Artificial tears Q1 hour during the day

2) Antivirals?

-minimal extra efficacy when added to steroids vs. steroids alone, not statistically significant (looked at both valacyclovir and acyclovir)

-treating with antivirals alone was significantly worse than treating with steroid alone, and no better than placebo. (BMC Neuro 2011)

-consider adding antivirals in severe patients (only barely perceptible motion of face or complete paralysis)

3) Steroids

-Prednisolone (60 mg daily for five days, then tapered by 10 mg daily, for a total treatment length of 10 days) was studied in a large RCT.

-Patients treated with prednisolone in this RCT had a shorter return to recovery vs. those without steroid treatment.(Lancet 2008).

-An easy substitute would be Prednisone 60mg PO daily for 1 week.

10-SECOND RECAP:

--(whole) facial droop/paralysis, check eyebrows (upper face) & smile (lower face); if both involved, think 7th nerve/Bell's palsy

--eye protection/lube/tears

--antivirals not too useful, consider in severe palsy

--steroids hasten recovery; 7-10 day course prednisone.

Submitted by R. Morris.

Reference(s): Numthavaj, P. BMC Neurology 2011;  Prednisolone and valaciclovir in Bell's palsy: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet Neurol. 2008 Nov;7(11):993-1000. Epub 2008 Oct 10; image

seizure vs. syncope: is creatine kinase (CK) useful?

STUDY 1:
--37 syncope and 26 generalized tonic–clonic seizure patients
--tested serum CK and myoglobin at ED presentation and 4 hrs after the event

--no statistically significant different in myoglobin at any time
--no statistically significant different in CK at ED presentation
--CK drawn 4 hrs after the event:

• elevated in four of 37 (10.8%) patients with syncope
• elevated in nine of 26 (34.6%) patients with seizure activity
• statistically significant difference in CK between seizure and syncope groups (P<0.05)
• sensitivity 34%
• specificity 89%

STUDY 2:
--Sequential sample of 205 patients with transient loss of consciousness. The study group consisted of 96 patients who had CK measurements in the ED

--Mean (+/- SE) CK significantly higher in the seizure group (231.1 +/- 34.8 U/L vs. 70.5 +/- 5.6 U/L, p less than 0.001).
--elevated CK: sensitivity of 0.43, specificity of 0.98--elevated CK >3hrs after event: sensitivity was 0.80, specificity was 0.94


10-SECOND TAKEAWAY:
--serum CK level after seizure: not too sensitive (better after 3 hrs), pretty specific
--may be useful to confirm suspected seizure if elevated >3-4 hours s/p event


Reference(s): study 1, study 2, picture

seizure or not: is prolactin useful?

STUDY:
--200 patients with seizure-like activity, 109 ultimately diagnosed with seizure
--31% (of 200 patients) had abnormal prolactin (upper limit of normal ~30mg/dL)

--the numbers:

• sensitivity of this serum prolactin was 42%
• specificity was 82%
• positive predictive value (PPV) of 74%
• negative predictive value (NPV) of 54%
• overall accuracy of 60% in the diagnosis of seizure,
• likelihood ratio of 2.4

--their conclusion: "The measurement of serum prolactin is helpful as a confirmatory test, but not as screening test in the emergency department setting."


REVIEW ARTICLE:
--most studies used 2x baseline serum prolactin level as 'elevated'
--the numbers:

• pooled sensitivity for generalized tonic-clonic seizures (60.0%); for complex partial seizures (46.1%)
• pooled specificity was similar for both (approximately 96%)
• 2 Class II studies were consistent in showing prolactin elevation after tilt-test-induced syncope.

--their conclusion: "Elevated serum prolactin assay, when measured in the appropriate clinical setting at 10 to 20 minutes after a suspected event, is a useful adjunct for the differentiation of generalized tonic-clonic or complex partial seizure from psychogenic nonepileptic seizure among adults and older children (Level B). Serum prolactin assay does not distinguish epileptic seizures from syncope (Level B)"


META-ANALYSIS:
--usefulness of raised serum prolactin in diagnosing generalised tonic-clonic seizures (GTSC) in patients presenting to the ED after a single episode of syncope
--13 relevant studies only 3 met the criteria for evaluation

--the numbers: if a serum prolactin concentration is > 3x the baseline when taken within one hour of syncope, then...

• LR (likelihood ratio) of GTSC vs pseudoseizure = 8.92, sensitivity 0.62, specificity 0.89
• LR of GTSC vs. syncope = 4.60, sensitivity 0.71, specificity 0.85

10-SECOND TAKEAWAY:
--serum prolactin in seizure: not too useful in the ED
--generally poor sensitivity, better specificity, but only if tested early (~10-60 min s/p episode)

--so if you can draw it fast, and if its significantly elevated, it might be useful (a lot of if's), but if its low, doesn't mean it's not a seizure

--serum prolactin in seizure: not too useful in the ED

Reference(s): study, review, meta-analysis, picture

seizures and tongue lacs

QUESTION:

--my patient had some sort of 'episode', story is unclear
--does their tongue lac tell me anything? was this a seizure?


PUBMED BIOPSY (not a ton out there):
STUDY 1: "Value of tongue biting in the diagnosis of seizures"
--study of 106 patients admitted to epilepsy unit + 45 patients with syncope
--small sample size, but interesting

--8/106 seizure patients had a tongue lac: all on the side
--1/45 syncope patients had a tongue lac: at the tip.

--sensitivity of 24% and a specificity of 99% for the diagnosis of generalized tonic-clonic seizures.
--Lateral tongue biting was 100% specific to grand mal seizures.

STUDY 2: The diagnostic value of oral lacerations and incontinence during convulsive "seizures".

--84 patients on EEG
--trying to tell seizure from pseudoseizure (a.k.a. psychogenic non-epileptic seizure, or PNES)

--oral lacs: (p=0.01)

• seizure: 26% (17/66) --14 side of tongue, 1 tip of tongue, 2 cheek, 3 lip
• not a seizure: 0% (0/18)
• sensitivity 26%, specificity 100%

--Incontinence: (p = 0.09)

• seizure: 23% (15/66)
• not a seizure: 6% (1/18) --!!! (now that's commitment)
• sensitivity 23%, specificity 94%

BOTTOM LINE:
--side-of-tongue lac is near 100% specific for seizure, not very sensitive
--if the story fits, and you bit the side of your tongue and/or pissed yourself, you probably earned a seizure workup


Reference(s): tongue biting, oral lacs and incontinence, picture