The Daily Differential — Saturday, May 2, 2026

2 of 4

Conversion Disorders

Functional neurologic symptom disorder can mimic stroke, seizure, paralysis, blindness, or coma. The ED challenge is to identify emergencies while using...

At the Bedside

Core concept: Symptoms are real to the patient and are not intentionally produced. Diagnosis should be based on positive functional signs, not simply “normal tests.”
Common ED presentations:
Weakness/paralysis
Nonepileptic seizure-like activity
Tremor or gait disturbance
Aphonia
Sensory loss
Vision loss
Stroke mimic
First priority: rule out dangerous mimics.
Check glucose, vitals, medication/toxin exposure, pregnancy when relevant.
For acute focal deficits: stroke evaluation, NIHSS, CT/CTA as indicated.
For seizure-like activity: consider true seizure, syncope, hypoglycemia, arrhythmia, tox, CNS infection, trauma.
Positive exam clues:
Hoover sign: involuntary hip extension returns when contralateral hip flexion is tested.
Give-way/collapsing weakness with preserved protective movements.
Inconsistent sensory loss not following neuroanatomy.
Tremor that entrains to voluntary rhythm or disappears with distraction.
Functional gait: dramatic imbalance without falls/injury, improvement when distracted.
PNES clues: long duration, asynchronous movements, pelvic thrusting, side-to-side head movement, eye closure/resistance to opening, preserved awareness/recall, no postictal phase — but none are perfect.
Management approach:
Stabilize first; treat true emergencies when uncertain.
Avoid repeated painful stimuli, excessive benzodiazepines, or intubation for suspected PNES unless airway/oxygenation truly compromised.
Give a clear, validating explanation: “Your nervous system is not damaged, but it is not functioning correctly right now. This is common and treatable.”
Emphasize reversibility and outpatient follow-up.
Arrange neurology follow-up and, when available, functional neurologic disorder clinic, CBT, psychiatry/psychology, physical therapy.
Assess safety: suicidality, abuse, major stressors, inability to ambulate safely.
Disposition:
Discharge if dangerous causes reasonably excluded, patient improving/stable, safe ambulation/support, and follow-up arranged.
Admit/observe if diagnostic uncertainty remains, persistent inability to walk/care for self, recurrent events, trauma, abnormal vitals, or concerning neurologic findings.

A Classic Presentation

A 24-year-old woman presents as a stroke alert for sudden left leg weakness after an argument. Vitals and glucose are normal. CT/CTA are negative. Exam shows inconsistent weakness, normal reflexes, and a positive Hoover sign: left hip extension is weak on command but becomes strong when she flexes the right hip against resistance. The physician explains functional weakness as a reversible nervous system problem, confirms safe ambulation with assistance, and arranges neurology/physical therapy follow-up.

Study Directive

Practice Hoover sign and tremor entrainment on colleagues so you can perform them smoothly.
Build a personal script for explaining functional symptoms without blame.
Review stroke mimics and seizure mimics; make a checklist for when imaging/labs are still required.
Watch one video module of PNES vs epileptic seizure semiology and list 5 distinguishing features.

Key Medications

No medication directly treats conversion disorder in the ED. Treatment is explanation, reassurance, safety, and referral.
If true epileptic seizure/status suspected:
Lorazepam: 2–4 mg IV/IM, repeat once in 5–10 min if ongoing seizure.
Avoid escalating benzodiazepines for clear PNES without physiologic compromise.
For severe agitation requiring medication:
Haloperidol: 2.5–5 mg IM/IV, monitor QT and extrapyramidal risk.
Droperidol: 2.5–5 mg IM/IV where available; follow institutional QT monitoring policy.
For comorbid anxiety/depression, start chronic therapy only with follow-up plan; ED initiation varies.

High-Yield Pearls

Functional neurologic disorder is diagnosed by positive signs of internal inconsistency, not by accusing the patient or saying “it’s all psych.”
PNES patients can also have epilepsy; avoid anchoring when hypoxia, trauma, abnormal vitals, or prolonged unresponsiveness are present.
The explanation itself is therapeutic: real symptoms, reversible mechanism, no structural damage found, specific follow-up.

Board Question

Which exam finding most supports functional leg weakness?

AHyperreflexia and ankle clonus
BDermatomal sensory loss
CPositive Hoover sign
DBabinski sign

Reveal answer

Correct: C

Positive Hoover sign. Hoover sign demonstrates inconsistency between voluntary and automatic motor function, supporting functional weakness. Hyperreflexia, clonus, and Babinski suggest upper motor neuron disease.

Recent Literature

Review or guideline Functional neurological disorder: new subtypes and shared mechanisms
Lancet Neurol, 2022 · cited 451×

Full text · open access
Recent clinical Direct neuronal reprogramming: emerging therapeutic strategies for neurodegenerative disorders
Ann Med, 2026

Full text · open access

3 of 4

Cranial Burr Hole

Emergency burr hole placement is rare but potentially lifesaving when a patient with traumatic intracranial hemorrhage is herniating and neurosurgical...

At the Bedside

Primary scenario: rapidly deteriorating head trauma patient with suspected epidural or subdural hematoma, signs of uncal herniation, and no immediate neurosurgical access.
Herniation clues:
Declining GCS
Unilateral fixed dilated pupil
Contralateral weakness/posturing
Cushing response: hypertension, bradycardia, irregular respirations
Recurrent vomiting, severe headache, seizure
Initial trauma management:
ATLS: airway, breathing, circulation, C-spine protection.
Prevent secondary brain injury:
SpO₂ > 94%
Avoid hypotension; target SBP generally ≥100–110 mmHg depending on age/TBI protocol.
Treat hypoglycemia/hyperthermia.
Elevate head of bed 30° if not hypotensive.
Keep head midline; loosen cervical collar if venous obstruction suspected while maintaining immobilization.
Airway/ventilation:
Intubate if GCS ≤8, inability to protect airway, hypoxia, agitation preventing care, or impending herniation.
Avoid prolonged hypoxia/hypotension during RSI.
Maintain normocapnia; brief hyperventilation can be used only as a temporary bridge in active herniation.
Imaging:
If stable enough: noncontrast CT head urgently.
CT findings concerning for surgical lesion: epidural hematoma, large acute subdural, midline shift, compressed basal cisterns.
Do not delay transfer/neurosurgery for unnecessary studies.
Temporizing medical therapy:
Hyperosmolar therapy for herniation signs.
Seizure treatment/prophylaxis per trauma/neurosurgery protocol.
Reverse anticoagulation immediately.
Burr hole decision point:
Only consider if:
Patient is rapidly deteriorating/herniating,
Extra-axial hematoma is known or strongly suspected,
Neurosurgeon/OR is unavailable within a lifesaving timeframe,
Transfer delay would likely be fatal,
You have appropriate equipment/skill or remote neurosurgical guidance.
Best done with direct neurosurgical consultation by phone/video if possible.
Procedure concept:
Most emergent traumatic epidural hematomas are temporal.
Classic temporal site: approximately 2 cm superior and 2 cm anterior to the external auditory canal/tragus, avoiding the zygoma and middle meningeal artery region as directed by neurosurgery.
Incise to bone, use periosteal elevator, drill burr hole with controlled pressure, irrigate, evacuate clot if encountered, control bleeding, and prepare for definitive craniotomy.
If no clot at initial site, further holes/locations should be directed by imaging/neurosurgery.
Disposition:
Immediate neurosurgical OR/trauma center transfer even after decompression.
ICU-level care with serial neuro exams, repeat imaging, ICP-directed therapy.

A Classic Presentation

A 19-year-old man is brought in after a motorcycle crash. He was initially talking but becomes progressively obtunded. Exam shows GCS 6, right fixed dilated pupil, left-sided posturing, bradycardia, and hypertension. CT shows a large right temporal epidural hematoma with midline shift; weather prevents immediate helicopter transfer and no neurosurgeon is onsite. The ED team intubates, gives hypertonic saline, calls remote neurosurgery, administers antibiotics, and prepares for emergent temporal burr hole as a bridge to definitive neurosurgical evacuation.

Study Directive

Memorize herniation signs and the first 5 actions: airway, oxygenation, BP support, hyperosmolar therapy, neurosurgery/transfer.
Review your ED’s severe TBI and anticoagulation reversal protocols.
Locate the cranial access equipment in your department or trauma bay.
Watch a procedural video/simulation on emergency burr hole and identify the temporal landmark on a skull model.

Key Medications

3% hypertonic saline: 250 mL IV bolus commonly used; alternatively 2–5 mL/kg IV. Institutional protocols vary.
Mannitol: 0.5–1 g/kg IV over 10–20 min; avoid in hypotension or renal failure when possible.
Etomidate RSI: 0.3 mg/kg IV.
Ketamine RSI: 1–2 mg/kg IV; acceptable in TBI and may support BP.
Rocuronium: 1–1.2 mg/kg IV for RSI.
Succinylcholine: 1–1.5 mg/kg IV for RSI; avoid with hyperkalemia risk, burns/crush >24 hr, neuromuscular disease.
Levetiracetam: commonly 1,000–2,000 mg IV load for seizure prophylaxis/treatment; dosing varies by protocol and renal function.
Cefazolin: 2 g IV pre-procedure; 3 g IV if >120 kg. Broaden per open skull fracture/contamination protocol.
Lidocaine with epinephrine: 1% lidocaine with epi for local anesthesia; max lidocaine with epi generally 7 mg/kg.

High-Yield Pearls

The most important TBI intervention is preventing secondary injury: no hypoxia, no hypotension.
Hyperosmolar therapy buys time; it does not definitively treat an expanding extra-axial hematoma.
ED burr hole is not “routine procedure knowledge” — it is a rare rescue maneuver requiring neurosurgical consultation whenever possible.

Board Question

Which patient is the best candidate for an emergency ED burr hole if neurosurgery is unavailable?

AAwake patient with small traumatic subarachnoid hemorrhage and normal exam
BIntoxicated patient with normal CT head
CRapidly deteriorating trauma patient with fixed dilated pupil and CT-confirmed temporal epidural hematoma
DPatient with chronic headache and suspected brain tumor

Reveal answer

Correct: C

Rapidly deteriorating trauma patient with fixed dilated pupil and CT-confirmed temporal epidural hematoma. Emergency burr hole is a last-resort decompressive bridge for herniating patients with suspected/confirmed extra-axial hemorrhage when neurosurgical care is not immediately available. Stable patients should be transferred/managed by neurosurgery without ED burr hole.

Recent Literature

Review or guideline Burr Hole Reconstruction Techniques: A Systematic Review of Materials and Outcomes
World Neurosurg, 2025 · cited 2×

Full text · open access
Recent clinical Emergency Burr hole for an epidural hematoma: A case report
Am J Emerg Med, 2026

4 of 4

Cranial Neuropathies

Cranial nerve deficits can be benign, but they may also signal aneurysm, stroke, cavernous sinus thrombosis, meningitis, increased ICP, brainstem lesion, or...

At the Bedside

Initial approach:
ABCs, glucose, full neuro exam.
Determine: isolated single nerve vs multiple cranial nerves vs long-tract signs.
Ask about headache, trauma, diplopia, vision loss, fever, rash, tick exposure, cancer, immunosuppression, anticoagulation.
High-risk patterns requiring urgent imaging/workup:
CN III palsy with pupil involvement → posterior communicating artery aneurysm until proven otherwise.
Multiple cranial neuropathies → cavernous sinus, brainstem, meningitis, skull base, inflammatory/infiltrative disease.
CN VI palsy with headache/papilledema → increased ICP.
Facial palsy with other neuro deficits → stroke/brainstem lesion, not Bell palsy.
Painful ophthalmoplegia, fever, proptosis, chemosis → cavernous sinus thrombosis/orbital apex process.
Acute vision loss with optic nerve findings → optic neuritis, ischemic optic neuropathy, GCA, compressive lesion.
Focused localization:
CN II: visual acuity, fields, pupils, fundus; consider optic neuritis, CRAO, GCA, mass.
CN III: ptosis, “down and out,” diplopia, pupil. Pupil-involving = aneurysm emergency.
CN IV: vertical diplopia worse looking down/stairs; head tilt away from lesion.
CN V: facial sensation, corneal reflex, muscles of mastication; trigeminal neuralgia vs mass/MS/zoster.
CN VI: horizontal diplopia worse looking toward affected side; consider microvascular palsy, increased ICP, cavernous sinus.
CN VII: forehead involvement suggests peripheral palsy; forehead sparing suggests central lesion, but assess entire neuro exam.
CN VIII: hearing loss/vertigo; central signs need stroke evaluation.
CN IX/X: dysphagia, dysphonia, palate asymmetry; aspiration risk, brainstem/skull base.
CN XI/XII: shoulder shrug, tongue deviation; consider stroke, mass, neck trauma.
Testing:
CTA head/neck for suspected aneurysm, dissection, stroke vascular cause.
MRI brain/orbits with contrast for optic neuritis, brainstem, cavernous sinus, skull base, multiple neuropathies.
CT/CTV or MRV if cavernous sinus thrombosis or venous sinus thrombosis suspected.
Labs guided by concern: ESR/CRP for GCA, Lyme testing in endemic exposure, HIV/syphilis if risk, CBC/blood cultures if septic.
Slit lamp/fluorescein for facial palsy with eye symptoms or zoster ophthalmicus concern.
Condition-specific ED management:
Bell palsy: peripheral CN VII palsy, no other neuro deficits. Start steroids within 72 hr; eye protection.
Ramsay Hunt: facial palsy + ear pain/vesicles; steroids + antivirals.
CN III palsy with pupil involvement: emergent CTA/aneurysm evaluation, neurosurgery/neurointerventional consult.
Cavernous sinus thrombosis: broad-spectrum IV antibiotics, blood cultures, imaging, ENT/neuro/ophtho; anticoagulation often considered with consultants.
GCA with visual symptoms: immediate high-dose steroids; do not wait for biopsy.
Microvascular isolated CN III/IV/VI palsy: diagnosis of exclusion in older diabetic/HTN patients; still consider imaging depending on age, pain, pupil, atypical features, and local practice.
Disposition:
Admit/transfer for aneurysm concern, stroke signs, multiple cranial nerves, brainstem signs, cavernous sinus/orbital apex syndrome, meningitis, GCA visual symptoms, inability to swallow/protect airway.
Discharge possible for classic Bell palsy with eye protection/follow-up or isolated low-risk palsy after appropriate evaluation.

A Classic Presentation

A 58-year-old man with hypertension presents with sudden diplopia and severe headache. Exam shows left ptosis, the left eye is deviated down and out, and the left pupil is dilated and poorly reactive. This is a pupil-involving CN III palsy concerning for posterior communicating artery aneurysm. The ED obtains emergent CTA head/neck and consults neurosurgery/neurointerventional immediately.

Study Directive

Draw cranial nerves III, IV, and VI eye movement actions from memory.
Make a red-flag list for cranial neuropathy that mandates imaging.
Review Bell palsy vs stroke facial weakness and practice explaining eye protection.
Do 15 neuro localization questions focused on diplopia and cranial nerve palsies.

Mechanism Pearl of the Day: Many “neurologic” emergencies are localization problems: cervical artery dissection causes ischemia in vascular territories, cranial neuropathies reveal compression/inflammation at narrow anatomic corridors, and herniation from intracranial bleeding compresses CN III and brainstem pathways. Functional neurologic disorder is the counterpoint — abnormal nervous system function without structural pathway damage.

Key Medications

Bell palsy prednisone: 60 mg PO daily for 5 days, then taper over 5 days; alternative regimens exist.
Valacyclovir: 1 g PO TID x 7 days, especially severe Bell palsy or Ramsay Hunt.
Acyclovir: 400 mg PO five times daily x 7–10 days; higher dosing needed for zoster/Ramsay Hunt per reference.
Artificial tears: frequent daytime use; lubricating ointment at night + eye taping for incomplete closure.
Trigeminal neuralgia carbamazepine: start 100 mg PO BID, titrate; check interactions, CBC/LFT/sodium with follow-up.
GCA with visual symptoms: methylprednisolone 500–1,000 mg IV daily, typically x3 days then high-dose oral steroids; consult ophthalmology/rheumatology.
Cavernous sinus thrombosis empiric antibiotics: common regimen includes vancomycin plus ceftriaxone or cefepime plus metronidazole; dosing varies by renal function and institutional protocol.
Vancomycin 20–25 mg/kg IV load commonly used.
Ceftriaxone 2 g IV q12–24h depending on CNS concern.
Metronidazole 500 mg IV q8h.
Verify with local protocol/pharmacy.

High-Yield Pearls

“Pupil involved” CN III palsy is aneurysm until proven otherwise.
Bell palsy is a peripheral CN VII diagnosis: forehead weakness, no other neuro deficits, and no alternative red flags.
Multiple cranial neuropathies localize to tight spaces: cavernous sinus, orbital apex, brainstem, meninges, or skull base.

Board Question

A patient has acute ptosis, a “down and out” eye, diplopia, and a dilated pupil. What is the most important diagnosis to exclude?

ABell palsy
BPosterior communicating artery aneurysm
CVestibular neuritis
DTrigeminal neuralgia

Reveal answer

Correct: B

Posterior communicating artery aneurysm. A pupil-involving third nerve palsy suggests compressive parasympathetic fiber involvement, classically from a posterior communicating artery aneurysm. This requires emergent vascular imaging.

Recent Literature

Review or guideline Cranial Neuralgias
Continuum (Minneap Minn), 2018 · cited 11×
Recent clinical Cranial nerves involvement in craniosynostosis: a systematic review
Childs Nerv Syst, 2026

TheDaily Differential

Cervical Artery Dissection

At the Bedside

Study Directive

Recent Literature

More in Today's Issue

Conversion Disorders

Cranial Burr Hole

Cranial Neuropathies

Journal Watch

Journal Feed Weekly Wrap-Up

Podcast Picks

Severe Traumatic Brain Injury with Dr. Dana Klavansky

Ep 216 Cardiac Arrest Update: Beyond the 2025 ACLS Guidelines Part 2 – Medications, Airway, Termination and Post-ROSC Care

Pharmacology Corner

Piperacillin-Tazobactam

Norepinephrine

Case of the Day