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Conference September 2020 (Neurology)

Welcome back!

Hopefully August has been kind to you. Onwards to september. September is Neurology and we will be covering some asynchronous content for you to reference. The long monthly post has had good feedback so we will keep it going.

orange and yellow dried leaves on tree
Ready for fall?

But first

The Street Medicine Fellowship is official and taking applicants!


Texas ACEP hosted a virtual meet and greet for programs to come and meet with Residency Candidates!


Thanks to Dr K. Holmes and Dr C. Holmes for putting on the Cadaver lab at UNT! It involves critical procedures and anatomy education for Residents.

Onto business

The brain by Brett Kavanaugh

Lets talk Neurology. There are quite a few board topics that are must know in terms of EM Neurology that we will cover.

Bells Palsy

Bells palsy is Cranial Nerve VII palsy unilaterally caused by Lower motor neuron involvement (1).

Treatment of Facial Paralysis
Courtesy of Sayantan Majumder

Clinical features:
– Paralysis of one half the face
– Forehead sparing (inability to wrinkle forehead)
– Inability to close eye on affected side completely or smile
– Parasympathetic involvement leads to decreased salication/lacrimation on affected side
– occurs rapidly with peak features seen <72 hrs

DDx: Ramsay hunt syndrome, Otitis media/mastoiditis, lyme disease (for boards know that bilateral Bells is characteristic although in real life not necessarily true), HIV, tumor, Guillain Barre, and of course Stroke.

Tx: Antivirals and Steroids. Prednisone 60-80mg/day x 1 wk. Acyclovir 400mg 5x/day x1wk or Valacyclovir 1000mg 3x/day x 1 wk. (4) A meta-analysis in 2009 examining use of corticosteroids alone vs. antivirals alone found that treatment with steroids was associated with a reduced risk of unfavorable recovery > treatment with antivirals alone. (3)

Other considerations:
– Risk factors for HIV, such as IV drug use or risky sexual behavior, necessitates HIV testing
– Deficits that occur over weeks to months likely represent brain tumor/mets and less likely acute Bells.
– No other signs of stroke such as extremity weakness or other sensorimotor deficits should not be present, otherwise expand workup for stroke. (2)


What constitutes a benign headache from a worrisome one? Red flags. 90% of headaches are benign. In the ED our job is not to completely diagnose the benign but make sure the other 10% are worked up and not missed. (5.6)

Red flags of headaches:
– Rapid/thunderclap onset/onset with exertion
– Immunosuppressive medication use or condition ie HIV
– Anticoagulant usage
– Malignancy history
– Hx of vasculitis or sarcoidosis
– Pregnancy or recently delivered <6 wks
– hx prior brain surgery/instrumentation/implanted device ie shunt, also including spinal device
– Any neuro deficits present

If any red flags are present – Consider at minimum non contrast HCT and possibly expansion to CTA and/or MRI. Pregnant patients may need MRI/MRV instead of NCHCT for considerations for dural venous thrombosis. (7) . Of course there is the debate between CT/CTA vs CT/LP for SAH. But we will save that for Dr Patel’s upcoming lecture.

Tx for benign headaches: Lots of debate here. lets go by the recommendations from the American Headache Society(9):
– Level B evidence: Metaclopramide, Compazine, Tripans
– Level C evidence: NSAIDS, APAP, Haldol, Droperidol, Valproate
– Level U (no evidence): Dexamethasone, Narcotics, Ergotamines, Ketamine, Magnesium
– Going beyond label vs off-label uses: IV acetaminophen, Ketamine, Mag, O2 have shown lots of promise in various clinical trials. (8)

Guillain Barre Syndrome

A demyelinating neuropathy caused by macrophages and T cells attcking peripheral neurons. From a board standpoint CMV and Campylobacter jejuni are most common causes, however HIV, Epstein Barr, other viral infections, mycoplasma pneumoniae, sarcoid, hodgkins lymphoma, and others have been implicated. (10)

DDx: also includes Myasthenia gravis, Botulism, tick paralysis, stroke, acute porphyric neuropathy, HIV, Vasculitis, Lambert Eaton syndrome, spinal shock/cord syndrome, adrenal insufficiency, organophosphate poisoning, seizure, hypokalemic periodic paralysis

Clinical presentation:
– Typically occurring 5-7 days after acute illness
– Typically ascending paralysis, starting with fine motor involving toes/fingers and ascending to entire body.
– Can be Miller Fisher Variant with descending paralysis mimicking Botulinum toxin.
– Typically diminished/absent reflexes in lower extremities and parasthesias present with diminished sensory/motor response.
– Severe cases may present with respiratory depression, autonomic dysfunction (ie urinary retention, dysrhythmias, postural hypotension), or eye movement weakness.

Workup and Tx:
– LP and CSF studies – albuminocytologic dissociation without an elevated cell count (high protein (>45) and low WBC count (<10). (11)
– LP opening pressure should be normal in GB
– Obtain a NIF (negative inspiratory force). <30 is worse prognosis with <20 indicating likely intubation needed.
– Plasmapheresis vs IVIG are mainstay of therapy. Make sure LP is done before starting IVIG as IVIG can cause aseptic meningitis findings on CSF.
– Steroids no longer considered beneficial .(10)
– No succinylcholine for RSI for suspected GB patients.

gray road beside a trees

Myasthenia Gravis

Anticholinergic receptor antibodies form in <1.5% of population typically seen age 30s-60s region. Causes Neuromuscular junction blockade and symptoms of weakness.

Clinical features:
– Ptosis, diplopia, dysarthria, dysphagia, neck extensor weakness and proximal upper extremity muscle fatigue
– Usually improved upon awakening, worsens throughout the day and in response to hot temps, prolonged muscle use, stress, infection
– If severe can progress to respiratory fatigue & distress –> “myasthenic crisis”.
– Diagnosis: Ice pack test – Place ice pack over face, if ptosis improves, likely myasthenia. Differentiate between cholinergic crisis –> cholinergic crisis has SLUDGE mnemonic – muscle fasciculations and lacrimation, salivation, etc that myasthenia does not.
– Previously gave Edrophonium or neostigmine (caused myasthenia symptoms to improve) –> caution as these can cause significant worsening in lambert eaton syndrome or cholinergic crisis leading to respiratory failure.
– EMG testing – definitive diagnosis.
– Some patients have thymus residual tissue or hyperplasia –> needs further workup.

Workup and Tx: Admit. Consult Neurology. Tx respiratory failure. Neurology will give decision for pyridostigmine or neostigmine administration. If intubating – use 1/2 doses of paralytics and sedating agents for RSI. Adjuncts for treating crisis include steroids, IVIG, plasmapheresis, azathioprine. (12)


Brain parenchyma infection or inflammation caused by several things, but most commonly HSV, HZV, EBV, CMV, west nile, dengue, rabies, arboviruses.

Clinical features:
– new onset psychiatric symptoms
– Movement disorder acute (arboviruses)
– seizure, nuchal rigidity, back pain, mental status depression, +/- fever.

DDx: Meningitis, brain abscess,lyme disease, SAH/ICH, NMS, serotonin syndrome, DT’s, anticholinergic tox, sympathomimetic tox, thyroid storm, CO2 narcosis.

Special considerations: Anti-NMDA receptor encephalitis –> young age/ female predominance. New onset bizarre behavior, dyskinesia and movement disorders, +/- dystonic features, lethargy, seizures. Needs Pediatric hospital admission, LP + CSF studies, possible starting of IVIG and steroids, Neuropsych consult. MRI brain shows +intensity in FLAIR images in cortical/subcortical regions. Ovarian teratoma must be ruled out –> patient needs pelvic US/MRI.

Workup and Tx:
– LP + CSF studies. LP will sometimes show bloody tap in acute HSV encephalitis
– MRI will show temporal increase T2 intensity in HSV/HZV
– Acyclovir 10-15mg/kg IV q8hrs, possibly gancyclovir or foscarnet for CMV, possibly Doxycycline 200mg IV for Lyme. Consider ID consult.

Multiple Sclerosis

White matter demyelinating lesions of the CNS leading to axonal injury. Something to consider in younger people with stroke-like symptoms or odd neurologic complaints that do not fit a typical stroke type pattern. (13) Suspected overall of being autoimmune in nature and seen commonly associated with thyroid disease and psoriasis. (14). MS also falls into the classification system along with NMO spectrum disorders and Transverse myelitis. Keep in mind ALS (Lou Gehrigs disease) also has some neuro deficits that appear atypical for stroke/infarction anticipated findings.

Clinical presentation:
– Optic neuritis (vision loss or ocular palsy)
– Fatigue, heat/cold intolerance, cognitive impairment, seizures, bladder dysfunction, other neurologic deficits
– no “rule out” features present in other stroke-like mimics

Workup and Tx:
– Stroke workup and evaluation is likely indicated, unless pt has known MS and Neurologist can attest to current condition/neuro status and/or recommends against stroke workup.
– if stroke ruled out –>LP with CSF studies –> will show +Oligoclonal bands and elevated Ig index.
– MRI typically shows white matter lesions
– If considered for transverse myelitis will also need spine MRIs.
– With neurology consult – can start oral or IV prednisone or prednisolone, IVIG. Typically no role for interferon therapy in the ED unless directed to do so by neurology.

The HINTS exam

Please check out this article on the HINTS exam in patients with Vertigo.

Commonly I have seen this documented as “normal” which isn’t exactly how the HINTS exam reads. It is either convincing for a peripheral cause of vertigo, not convincing for peripheral vertigo, or convincing for central cause of vertigo. Remember for central vertigo to consider vascular occlusion, cerebellar stroke or bleed, vascular dissection, or space occupying lesion. As such, there are three possible pathways for patients with vertigo: no imaging in the lowest risk (HINTS convincing for peripheral etiology). CT +/-CTA for patients with concern for infarct, bleed or dissection with central features, and in most cases followed by admission for MRI for suspected central cause. And lastly direct to MRI/MRA if available and rapid followed by admission.

Thats all for now! see you at the next conference!


  1. Eviston TJ, Croxson GR, Kennedy PGE, et al. Bell’s palsy: aetiology, clinical features, and multidisciplinary care. J Neurol Neurosurg Psychiatry. 2015;86:1356-1361.
  2. Herbert M, Swadron S, Mallon B, Lex J. Bell’s Palsy: That was then, this is now. EMRAP. 2015;15:3-4.
  3. de Almeida JR, et al. Combined corticosteroid and antiviral treatment for Bell palsy: a systemic review and meta-analysis. JAMA. 2009;302(9):985.
  4. UpToDate. Bell’s Palsy Prognosis and Treatment. March, 2014
  5. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache. Accessed July 2017.
  6. Friedman BW, Hochberg ML, Esses D, et al. Applying the international classification of headache disorders to the emergency department: an assessment of reproducibility and the frequency with which a unique diagnosis can be assigned to every acute headache presentation. Ann Emerg Med. 2007;49(4):409–419, 419 e401–409.
  7. Vinson DR. Treatment patterns of isolated benign headache in US emergency departments. Ann Emerg Med. 2002;39(3): 215–222.
  8. Long B, Koyfman A. Headache. In Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e.
  9. Orr SL, Friedman BW, Christie S, et al. Management of Adults With Acute Migraine in the Emergency Department: The American Headache Society Evidence Assessment of Parenteral Pharmacotherapies. Headache 2016;56:911-940.
  10. Ropper A.H.: The Guillain-Barre syndrome. N Engl J Med 1992; 326: pp1130-1136.
  11. Noto, A., & Marcolini, E. (2014). Select Topics in Neurocritical Care. Emergency Medicine Clinics of North America, 32(4), 927-938.
  12. Handel DA, Gaines S. Chronic Neurologic Disorders. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016.
  13. Correale J, Fiol M, Gilmore W. The risk of relapses in multiple sclerosis during systemic infections. Neurology. 2006 Aug 22;67(4):652-9
  14. Marrie RA, Reider N, Cohen J, et al. A systematic review of the incidence and prevalence of autoimmune disease in multiple sclerosis. Multiple Sclerosis. 2015 Mar; 21(3): 282–293

Image Credits
K. Holmes DO FACEP
Sayantan Majumder
Brett Kavanaugh @unsplash
Katie Mourn @unsplash

Stefan Meyering DO, FAAEM, FACEP

Dad, Academic EM Attending Physician, Fish Nerd & Backyard Mechanic | APD @ Ft Worth EM | Interests: Graduate Medical Education, Risk Management and Legal Medicine, POCUS, Free Open Access Medical Education (FOAMed), Physician Wellness

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