An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
FUNCTIONAL SEIZURES
Misdiagnosing functional seizures as epilepsy exposes patients to respiratory depression, intubation, antiseizure drugs, and stigma. Missing true status epilepticus because the movements “look functional” can cause irreversible neurologic injury.
Also known aspsychogenic nonepileptic seizures · PNES · nonepileptic seizures
By the Blue Fish Med DeskAug 18, 2026 · Phoenix
0:00 / –:––AI‑generated audio
A 27-year-old woman lies on the ED stretcher, eyelids squeezed shut as her arms rhythmically tremble against the sheet. Her sister says the episode has lasted nearly 12 minutes, but the patient’s breathing remains regular and she briefly turns her head when spoken to. The monitor shows a sinus rhythm and oxygen saturation of 99%; no one has yet decided whether this is ongoing status epilepticus or something else.
— What’s your move? Read on.
Before you read
When is it dangerous to withhold treatment for possible epileptic status?
What is the ED’s therapeutic role after the event stops?
When to Think of It
Consider functional seizures with prolonged or fluctuating convulsive-appearing events, asynchronous or side-to-side movements, tightly closed eyes, preserved awareness or recall, rapid changes in motor pattern, ictal crying, and events occurring in emotionally or socially charged settings. These are clues, not standalone diagnostic proof. Video-EEG capturing a typical event without an epileptiform correlate is the diagnostic standard.
Sick or Not Sick
The key call is “Could this still be epileptic status or an immediately dangerous mimic?” Check airway, ventilation, glucose, trauma, pregnancy, toxicologic context, focal neurologic deficit, and recovery pattern before labeling the event functional.
The First Fifteen Minutes
Ongoing convulsive activity with impaired awareness and no reliable way to exclude status → midazolam 10 mg IM once (or 0.2 mg/kg IV, maximum 10 mg, if IV access); it rapidly suppresses dangerous epileptic activity while definitive assessment continues. Check a dosing reference if using nonstandard weight-based protocols.
If hypoglycemia is confirmed → dextrose 25 g IV (50 mL of D50) in an adult with severe hypoglycemia; glucose restores substrate for neuronal function. Use dextrose 10% 125–250 mL IV when peripheral extravasation risk or local protocol favors D10.
If the patient has a pulse but cannot protect the airway, has persistent hypoxemia, or has severe agitation after sedative treatment → airway positioning, suction, oxygen, and ventilation; do not administer additional sedatives solely to stop functional movements.
Once epileptic status and medical instability are unlikely → no antiseizure medication; calmly reduce stimulation, protect from injury, and avoid restraint unless necessary for immediate safety.
Definitive Care & Disposition
Obtain collateral history, review prior video-EEG and antiseizure medications, and involve neurology. A typical event should be captured on video-EEG when the diagnosis remains uncertain. Explain that the events are real, involuntary, and treatable; avoid “faking” language. Admit for persistent altered mental status, injury, pregnancy-related concern, recurrent uncertain events, suicidality, or inability to establish safe follow-up. Stable patients may be discharged with neurology and mental-health follow-up, a safety plan, and clear return precautions.
How This One Kills
The dangerous error is repeated benzodiazepine escalation for a prolonged functional event, producing respiratory failure and intubation while the underlying diagnosis remains unaddressed.
The Differential — What Else Looks Like This
Generalized convulsive status epilepticus — stereotyped tonic–clonic evolution with impaired awareness and postictal recovery; delaying therapy risks neuronal injury.
Syncope with convulsive movements — brief episode linked to standing or arrhythmia, rapid reorientation; missing cardiac syncope risks sudden death.
Hypoglycemia — low bedside glucose during symptoms; untreated neuroglycopenia can progress to coma.
Movement disorder or rigors — preserved interaction and stimulus-linked movements; mislabeling may lead to unnecessary antiseizure treatment.
The Second-Day Story
Older adults, patients with intellectual disability, and patients already receiving sedatives may have subtle shaking, staring, intermittent unresponsiveness, or unexplained post-event behavior rather than dramatic movements. Conversely, functional events may coexist with epilepsy, so a prior diagnosis of functional seizures does not make every future event functional. Repeated semiology, collateral video, glucose, medication review, and recovery trajectory are more reliable than a single visual impression.
Back to Our Patient
Back to our 27-year-old woman: she is oxygenating normally, has rhythmic but changing movements, tightly closed eyes, no lateral tongue injury, and briefly responds to her sister; bedside glucose is normal and there is no trauma. Because epileptic status cannot initially be excluded, the team protects her airway and obtains IV access, but does not repeatedly escalate medication when her breathing and examination remain stable; the movements stop with calm reassurance, and she rapidly recalls the event. Neurology reviews a prior video-EEG showing the same semiology without an epileptiform correlate, supporting functional seizures. After assessment for suicidality and a safe follow-up plan, she is discharged with neurology and psychological therapy referral.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 27-year-old woman with recurrent prolonged shaking episodes, presenting after approximately 12 minutes of bilateral arm trembling. Her sister reports preserved regular breathing and intermittent response, with no preceding fever, trauma, substance exposure, or missed antiseizure medication. She is now alert, oxygenating normally, and has no focal deficit, lateral tongue trauma, or significant injury; the movements were asynchronous with tightly closed eyelids and changed pattern several times. Glucose and ECG are normal. I’m concerned for a functional seizure, but I initially treated the event as possible status until dangerous causes were excluded; she is now stable without further sedative treatment, and I recommend neurology review, confirmation against prior video-EEG, safety assessment, and outpatient follow-up.”
Study Directive
Review three patient-recorded videos and list the semiologic clues for functional versus epileptic events.
Practice a 30-second nonstigmatizing explanation: “The events are real, involuntary, and arise from altered brain functioning rather than epileptic electrical discharges.”
Memorize the adult benzodiazepine status dose and your institution’s escalation pathway.
Write a discharge checklist including injury precautions, suicidality screening, neurology follow-up, and return precautions.
Tolchin B, Goldstein LH, Reuber M, et al. · Neurology, 2026 · PMID 41370742 · cited 14×
Provides evidence-based guidance on diagnosing and managing functional seizures, including respectful communication, avoidance of unnecessary antiseizure treatment, and referral for appropriate psychological care.
Guillain-Barré syndrome can progress from walking weakness to respiratory failure and lethal dysautonomia within hours. The neurologic examination may...
Also known asGBS · acute inflammatory demyelinating polyneuropathy · AIDP
A 46-year-old man grips the edge of the stretcher as he tries to stand, his feet numb and his legs too weak to support him. Three weeks earlier he had recovered from several days of diarrhea; today his voice sounds faint, and he says swallowing water takes concentration. His heart rate shifts from 58 to 112 while the nurse checks his blood pressure, and the next respiratory assessment has not yet been made.
Before You Read
What examination and bedside measurements determine whether this patient needs the ICU?
Which diagnostic tests are supportive but must not delay treatment?
When should immunotherapy begin?
Why It Matters
Guillain-Barré syndrome can progress from walking weakness to respiratory failure and lethal dysautonomia within hours. The neurologic examination may underestimate impending ventilatory collapse.
When to Think of It
Acute, progressive, relatively symmetric weakness—usually ascending—with paresthesias and reduced or absent reflexes, often after respiratory or gastrointestinal infection. Facial weakness, bulbar dysfunction, neuropathic pain, and autonomic instability are common. Marked asymmetry, a sensory level, brisk reflexes, or early bowel/bladder dysfunction should prompt alternative diagnoses.
Sick or Not Sick
The most important call is whether respiratory and bulbar weakness require early airway control and ICU monitoring. Measure serial forced vital capacity (FVC), negative inspiratory force (NIF), cough strength, secretion handling, single-breath count, and autonomic vital-sign variability. FVC ≤20 mL/kg, NIF weaker than approximately −30 cm H₂O, rapid decline, weak cough, bulbar dysfunction, or inability to count to 15 on one breath should trigger critical-care consultation; thresholds vary by context and should not override clinical deterioration.
The First Fifteen Minutes
Any hypoxemia, hypercapnia, inability to handle secretions, severe bulbar weakness, or rapidly declining FVC/NIF → prepare controlled intubation with ICU/anesthesia support; etomidate 0.3 mg/kg IV for induction and rocuronium 1.2 mg/kg IV for paralysis. Etomidate supports hemodynamic stability, and rocuronium avoids potassium release. Avoid succinylcholine because denervation can cause dangerous hyperkalemia.
Hypotension from dysautonomia after adequate volume assessment → norepinephrine 0.05–0.1 mcg/kg/min IV infusion, titrated to perfusion; it restores vascular tone. Autonomic responses can be exaggerated, so use an arterial line when feasible.
Severe neuropathic pain → acetaminophen 1,000 mg PO/IV every 6–8 hours, maximum 4 g/day; avoid routine opioids when respiratory weakness is evolving because they suppress ventilation. Adjust maximum acetaminophen dose in liver disease or heavy alcohol use.
Suspected GBS with progressive weakness or inability to walk independently → call neurology and ICU immediately; do not wait for lumbar puncture or electrodiagnostics before escalation.
Definitive Care & Disposition
Admit progressive or nonambulatory patients to an ICU or monitored setting with serial respiratory mechanics, telemetry, swallow evaluation, aspiration precautions, DVT prophylaxis, pressure-injury prevention, and early rehabilitation. Neurology-directed therapy is IVIG 0.4 g/kg/day IV for 5 days or plasma exchange, typically 4–6 exchanges over 1–2 weeks; they are similarly effective and should not routinely be combined. Perform lumbar puncture and electrodiagnostic testing when useful, but normal CSF early does not exclude disease. Consider MRI when a spinal cord lesion remains plausible.
How This One Kills
The fatal failure is waiting for oxygen desaturation before intubation; neuromuscular respiratory failure can produce sudden exhaustion and arrest with initially normal pulse oximetry.
The Atypical Presentation
Older adults may present with falls, unexplained inability to rise, back pain, or dysphagia rather than a textbook ascending pattern. Reflexes can be preserved early, and sensory symptoms may be mild. A normal oxygen saturation is reassuring only about oxygenation, not ventilatory reserve; serial FVC/NIF, cough, voice, and secretion handling are the signal.
Back to Our Patient
Back to our 46-year-old man: his symmetric leg weakness, absent ankle reflexes, recent diarrheal illness, facial/bulbar symptoms, and labile heart rate make GBS the leading diagnosis. His FVC is 16 mL/kg, NIF is −25 cm H₂O, and cough is weak—he is sick because respiratory reserve is failing, even though saturation remains 98%. The team calls ICU/anesthesia, performs controlled RSI with etomidate and rocuronium, and begins serial autonomic monitoring; neurology starts IVIG after airway stabilization. He is admitted to the ICU for mechanical ventilation, dysautonomia surveillance, rehabilitation planning, and complication prevention.
Patient Presentation to Attending
“This is a 46-year-old man with three days of progressive symmetric leg weakness and paresthesias after diarrheal illness three weeks ago, now with weak voice and difficulty swallowing water. He has bilateral facial weakness, absent lower-extremity reflexes, no sensory level, no back trauma, and no bowel or bladder retention. His heart rate is fluctuating from 58 to 112, FVC is 16 mL/kg, NIF is −25, and cough is weak despite normal oxygen saturation. This is Guillain-Barré syndrome with impending neuromuscular respiratory failure and dysautonomia. I recommend controlled ICU intubation, rocuronium rather than succinylcholine, continuous hemodynamic monitoring, and urgent neurology-directed IVIG or plasma exchange.”
Study Directive
Practice calculating FVC in mL/kg and interpret three sample FVC/NIF trends.
Draw a bedside comparison of GBS, myasthenic crisis, botulism, and spinal cord compression.
Review your ICU’s IVIG and plasma-exchange protocols and indications for intubation.
Key Medications
IVIG: 0.4 g/kg/day IV for 5 days. Product and institutional protocols vary; verify dosing and renal/thrombotic precautions with Lexicomp, UpToDate, or local guidance.
Norepinephrine: start 0.05–0.1 mcg/kg/min IV infusion and titrate to perfusion.
Etomidate: 0.3 mg/kg IV for RSI induction.
Rocuronium: 1.2 mg/kg IV for RSI paralysis; avoid succinylcholine.
Acetaminophen: 1,000 mg PO/IV every 6–8 hours, maximum 4 g/day in healthy adults.
Pediatric IVIG and RSI dosing are weight-based; use a pediatric protocol.
High-Yield Pearls
The “20/30/40 rule” is a warning framework, not a discharge criterion: FVC <20 mL/kg, NIF weaker than −30 cm H₂O, or maximal inspiratory pressure decline warrants urgent escalation.
Autonomic instability may alternate hypertension, hypotension, bradycardia, and tachyarrhythmia; avoid reflexively treating every number without assessing perfusion.
Albuminocytologic dissociation may be absent early; a normal early CSF does not rule out GBS.
The Mimics
Spinal cord compression — sensory level, sphincter dysfunction, or upper motor neuron signs; missing it delays urgent decompression.
Myasthenic crisis — fatigable ocular/bulbar weakness with preserved sensation and often preserved reflexes; confusing treatment pathways can delay ventilatory support.
Tick paralysis — ascending flaccid weakness with an attached tick and rapid reversal after removal; missing the exposure prolongs paralysis.
Botulism — descending paralysis, fixed/dilated pupils, autonomic and gastrointestinal symptoms; antitoxin timing is critical.
Board Question
A patient with suspected GBS has progressive bulbar weakness, a weak cough, FVC 18 mL/kg, and normal oxygen saturation. What is the best next step?
ADischarge with outpatient neurology follow-up
BWait for lumbar puncture confirmation
CElective controlled endotracheal intubation and ICU admission
DGive succinylcholine for rapid sequence intubation
Reveal answer
Correct: C
Respiratory muscle weakness and bulbar dysfunction can precede abrupt hypoventilation despite normal oxygen saturation. Succinylcholine should generally be avoided because denervation increases hyperkalemia risk.
Use this guideline to recognize and confirm GBS, monitor for respiratory failure and autonomic instability, and initiate IVIG or plasma exchange promptly while avoiding corticosteroids.
A new MS relapse can leave permanent disability, but treating infection-related pseudo-relapse with steroids can worsen the underlying infection. New focal...
A 32-year-old woman arrives holding the wall, saying her right leg has become “heavy” over four days. She has blurred vision in her left eye from a prior episode and now describes urinary urgency, but she has no fever, cough, or dysuria. The emergency physician must decide whether this is a true new inflammatory attack, a temporary worsening from an occult trigger, or an entirely different emergency.
Before You Read
How do you separate a relapse from a pseudo-relapse?
Which findings mandate MRI or admission rather than empiric outpatient treatment?
When are high-dose steroids—and plasma exchange—appropriate?
Why It Matters
A new MS relapse can leave permanent disability, but treating infection-related pseudo-relapse with steroids can worsen the underlying infection. New focal deficits may also represent stroke, cord compression, or another inflammatory disease.
When to Think of It
A relapse is a new or recurrent neurologic deficit lasting at least 24 hours, separated from a prior attack by at least 30 days, without fever or infection. Typical syndromes include unilateral optic neuritis, internuclear ophthalmoplegia, sensory symptoms, partial myelitis, diplopia, and limb weakness. Symptoms developing over hours to days favor inflammation; abrupt maximal onset favors vascular disease.
Sick or Not Sick
The key call is whether this is a disabling, atypical, or dangerous new neurologic deficit requiring admission and urgent imaging. Screen for infection, pregnancy, severe dysphagia, inability to ambulate, urinary retention, rapidly progressive weakness, altered mental status, and spinal cord or brainstem signs.
The First Fifteen Minutes
Fever, urinary symptoms, respiratory symptoms, or other relapse trigger → obtain targeted testing and cultures when indicated; do not give steroids until serious infection is reasonably assessed, because corticosteroids suppress inflammatory host defense.
Abrupt focal deficit, severe headache, altered consciousness, or atypical findings → activate stroke/neurologic imaging pathways rather than assuming relapse; reperfusion medication decisions are diagnosis- and time-dependent.
Severe, function-limiting relapse after infection is excluded → neurology consultation for methylprednisolone 1 g IV daily for 3–5 days; high-dose glucocorticoid accelerates recovery by suppressing CNS inflammation. Dose and duration vary by protocol; verify with Lexicomp, UpToDate, or institutional guidance.
Acute urinary retention → bladder scan and catheterize when clinically necessary; lidocaine 2% jelly 5–10 mL urethral may be used for comfort before catheterization, per local protocol.
Definitive Care & Disposition
MRI brain and spine with gadolinium is useful for atypical, severe, first, or diagnostically uncertain presentations. Admit for severe deficits, inability to walk or hydrate, optic neuritis with major visual loss, brainstem dysfunction, significant myelitis, or uncertain diagnosis. If a disabling relapse fails to respond to high-dose steroids, neurology may use plasma exchange, commonly 5–7 exchanges. Arrange disease-modifying therapy review; ED steroids do not substitute for long-term MS management.
How This One Kills
The classic failure is treating a UTI-associated pseudo-relapse with high-dose steroids, worsening infection while falsely concluding that MS is progressing.
The Atypical Presentation
Older patients, those on disease-modifying therapy, and those with substantial baseline disability may present with falls, fatigue, cognitive change, or worsening gait rather than a clear focal syndrome. Heat-related Uhthoff symptoms fluctuate and improve with cooling; infection-related worsening improves when the trigger resolves. Establish the baseline examination from family, prior notes, and gait function before calling every deterioration a relapse.
Back to Our Patient
Back to our 32-year-old woman: her four-day evolution, new right-leg weakness, urinary urgency, and prior optic neuritis suggest a disabling MS relapse, but the team first confirms no fever, dysuria, retention, or abrupt stroke-like onset. Examination shows right leg pyramidal weakness and an afferent pupillary defect without altered mental status; MRI demonstrates an enhancing cervical cord lesion without compression. She is admitted because gait and bladder function are impaired, receives methylprednisolone 1 g IV daily after infection assessment, and is referred for neurologic follow-up and disease-modifying therapy review.
Patient Presentation to Attending
“This is a 32-year-old woman with four days of progressive right-leg heaviness and urinary urgency, with a prior episode of left optic neuritis. She has no fever, dysuria, respiratory symptoms, abrupt onset, severe headache, or altered mental status. Examination shows right-leg pyramidal weakness and a left afferent pupillary defect, without meningismus or a clear sensory level. MRI shows an enhancing cervical cord lesion without compression. I think this is a disabling MS relapse rather than pseudo-relapse or stroke; I recommend admission, neurology consultation, high-dose IV methylprednisolone after infection screening, bladder monitoring, and review of long-term disease-modifying therapy.”
Study Directive
Create a two-column algorithm for relapse versus pseudo-relapse using fever, time course, new objective findings, and MRI enhancement.
Review MRI examples of enhancing versus chronic nonenhancing plaques.
Memorize methylprednisolone 1 g IV daily for 3–5 days and the indications for plasma exchange.
Practice a focused MS examination: visual acuity, color vision, pupils, ocular motility, strength, reflexes, sensory level, gait, and bladder assessment.
Key Medications
Methylprednisolone: 1 g IV daily for 3–5 days for severe relapse after infection is excluded. Regimens vary; check Lexicomp, UpToDate, or institutional protocol.
Prednisone taper: not routinely required after a standard high-dose IV course; if used, follow neurology protocol rather than improvising.
Acetaminophen: 1,000 mg PO/IV every 6–8 hours, maximum 4 g/day, for pain or fever; reduce maximum in liver disease or heavy alcohol use.
Pediatric relapse treatment is specialist-directed and weight-based; do not extrapolate adult dosing.
High-Yield Pearls
A relapse is a diagnosis of exclusion: infection and abrupt vascular presentations must be addressed first.
Heat- or infection-induced worsening should improve when the trigger resolves; persistent new deficits warrant relapse evaluation.
Severe optic neuritis, area postrema symptoms, or longitudinally extensive myelitis should prompt consideration of NMOSD/MOG-associated disease rather than routine MS escalation.
The Mimics
Ischemic stroke — sudden maximal deficit and vascular distribution; missing thrombolysis or thrombectomy costs salvageable brain.
Neuromyelitis optica spectrum disorder — severe optic neuritis or longitudinally extensive myelitis; MS disease-modifying therapy may be inadequate or harmful.
Pseudo-relapse — old deficits worsen with fever, infection, heat, or metabolic stress without new lesions; unnecessary steroids add risk.
Board Question
A patient with established MS develops worsening leg weakness during a febrile urinary tract infection. MRI shows no new enhancing lesion, and the weakness improves after fever resolution. What is the most likely explanation?
ANew MS relapse
BPseudo-relapse
CNeuromyelitis optica
DProgressive multifocal leukoencephalopathy
Reveal answer
Correct: B
Infection can transiently worsen prior MS deficits without new inflammatory activity. Treating the trigger is primary; high-dose steroids are not automatically indicated.
A current overview of MS diagnosis and management can help emergency clinicians distinguish true relapse from pseudo-relapse and understand when acute corticosteroid treatment and neurologic consultation are appropriate.
Acute myelopathy with bladder dysfunction is a neurologic emergency. The reversible inflammatory syndrome can look similar to epidural abscess, hematoma,...
A 39-year-old man reports a band of burning pain around his abdomen and says both legs have felt “asleep” since yesterday. This morning he could not start urinating and needed his partner’s help to stand. He has no trauma, but he remembers a recent viral illness; the team has not yet determined whether the cord is inflamed, compressed, infected, or ischemic.
Before You Read
Which examination finding most strongly localizes the problem to the spinal cord?
What imaging must happen before lumbar puncture?
When should treatment begin, and when is plasma exchange needed?
Why It Matters
Acute myelopathy with bladder dysfunction is a neurologic emergency. The reversible inflammatory syndrome can look similar to epidural abscess, hematoma, tumor, infarction, or severe disc disease—conditions with very different time-critical treatments.
When to Think of It
Subacute bilateral motor, sensory, and autonomic dysfunction developing over hours to days, often with a definable sensory level, bilateral weakness, back or radicular pain, and urinary retention. Early spinal shock can produce flaccid weakness and reduced reflexes before upper motor neuron signs emerge.
Sick or Not Sick
The one call that matters most is whether cord compression or another surgical lesion must be excluded immediately. New retention, rapidly progressive weakness, severe back pain, fever, immunosuppression, cancer, anticoagulation, or trauma demands emergent MRI and spine/neurosurgical consultation.
The First Fifteen Minutes
Suspected acute myelopathy with retention, sensory level, or progressive weakness → obtain emergent MRI of the entire spine with and without contrast when feasible, because localization and compression determine urgent therapy; do not perform lumbar puncture first.
Bladder scan showing significant retention or painful inability to void → urethral catheterization, with lidocaine 2% jelly 5–10 mL urethral for comfort per local protocol; decompression prevents overdistension and renal injury.
MRI excludes compression and inflammatory transverse myelitis remains likely → neurology-directed methylprednisolone 1 g IV daily for 3–5 days, because high-dose glucocorticoid suppresses cord inflammation. Verify regimen with Lexicomp, UpToDate, or institutional protocol.
Fever, severe back pain, or infection risk suggesting epidural abscess → obtain blood cultures before antibiotics if this will not delay treatment; begin vancomycin 20–25 mg/kg IV loading dose plus ceftriaxone 2 g IV or local broad-spectrum regimen when infection is strongly suspected. Vancomycin dosing varies with renal function and institutional monitoring—check a reference.
Definitive Care & Disposition
Admit all suspected acute transverse myelitis with objective weakness, sensory level, or bladder dysfunction. MRI, CSF cell count/protein/glucose, oligoclonal bands, infectious studies, and serum AQP4-IgG/MOG-IgG help define cause, but CSF should follow exclusion of mass effect. If severe deficits fail to improve after steroids, neurology may initiate plasma exchange, commonly 5–7 exchanges. Treat the cause—antimicrobials for infection, decompression for compression, and disease-specific immunotherapy for NMOSD/MOG or systemic autoimmune disease. Provide ICU care for high cervical involvement, respiratory weakness, or autonomic instability.
How This One Kills
The lethal miss is performing lumbar puncture—or assuming inflammation—before imaging a patient with epidural abscess or hematoma, delaying decompression while cord perfusion and neurologic function deteriorate.
The Atypical Presentation
Early transverse myelitis may lack a sensory level, and reflexes can be depressed from spinal shock. Older or immunocompromised patients may present mainly with urinary retention, falls, or back pain; fever may be absent in epidural infection. A careful pinprick comparison, sacral sensation, rectal tone, reflex trend, and bladder scan can reveal cord disease when the initial limb examination is nonspecific.
Back to Our Patient
Back to our 39-year-old man: bilateral leg symptoms, a truncal sensory band, progressive weakness, and acute urinary retention localize to the spinal cord and make him sick because neurologic function is worsening. Emergent MRI shows a longitudinally extensive intramedullary T2 lesion without epidural collection or compression; blood tests and CSF support inflammatory myelitis. After bladder decompression and neurology consultation, he begins methylprednisolone 1 g IV daily and is admitted for serial examinations, rehabilitation planning, and respiratory/autonomic monitoring. If he fails to improve, plasma exchange is added while testing for NMOSD, MOG-associated disease, infection, and systemic autoimmunity proceeds.
Patient Presentation to Attending
“This is a 39-year-old man with one day of bilateral leg numbness and weakness, a band-like abdominal burning sensation, and new urinary retention after a recent viral illness. He has no trauma, anticoagulant use, fever, severe focal back pain, or cancer history. Examination shows bilateral leg weakness with a truncal sensory level and reduced anal sensation; the bladder scan shows significant retention. Emergent MRI demonstrates a longitudinal intramedullary lesion without compression or epidural collection. This is acute inflammatory transverse myelitis, and I recommend admission, bladder decompression, urgent neurology involvement, high-dose IV methylprednisolone, and plasma exchange if he fails to improve.”
Study Directive
Draw the localization pathway from sensory level and bladder dysfunction to cord, conus, or cauda equina.
Review emergent MRI indications for epidural abscess, hematoma, compression, and inflammatory myelitis.
Memorize the sequence: MRI first, then CSF; steroids after compression is excluded; plasma exchange for severe steroid-refractory disease.
Practice distinguishing transverse myelitis from GBS using reflexes, sensory level, bladder timing, and cranial nerve involvement.
---
MECHANISM PEARL OF THE DAY: Neurologic localization determines the first lifesaving move: peripheral nerve disease threatens ventilation and autonomic control, while spinal cord disease threatens conduction and bladder function, and functional seizures require protection from iatrogenic escalation after dangerous physiology is excluded. In each case, the bedside measurement—not the label—forks management.
Methylprednisolone: 1 g IV daily for 3–5 days after compression and major infection are excluded; verify protocol-specific duration.
Vancomycin: 20–25 mg/kg IV loading dose for suspected serious spinal infection, then pharmacy-guided dosing; renal function and AUC/trough monitoring are required.
Ceftriaxone: 2 g IV every 24 hours when appropriate for suspected spinal infection; broaden based on risk factors and local antibiogram.
Lidocaine 2% jelly: 5–10 mL urethral before catheterization, per local protocol.
Pediatric steroid, antibiotic, and plasma-exchange dosing is weight-based and specialist-directed.
High-Yield Pearls
Early spinal shock can make true cord disease look like a peripheral neuropathy because reflexes may initially be absent.
Urinary retention plus a sensory level is a cord emergency until proven otherwise, even without back pain or fever.
“Transverse myelitis” is a syndrome, not an etiology; always pursue compression, infection, infarction, NMOSD/MOG, and systemic inflammation.
The Mimics
Spinal epidural abscess — fever, severe focal back pain, bacteremia risk, or rim-enhancing collection; delayed drainage causes irreversible paralysis and sepsis.
Epidural hematoma — abrupt severe pain and rapidly progressive deficit, often with anticoagulation or procedure; urgent reversal and decompression may be lifesaving.
Spinal cord infarction — sudden maximal onset with anterior spinal artery pattern; immunosuppression will not restore infarcted cord.
Cauda equina syndrome — saddle anesthesia, radicular pain, and lower motor neuron weakness without a clear thoracic sensory level; delay risks permanent bladder dysfunction.
Board Question
A patient has acute bilateral leg weakness, a T8 sensory level, and urinary retention. Before lumbar puncture, what is the most appropriate next step?
AStart oral prednisone and arrange outpatient MRI
BEmergent MRI of the spine
CLumbar puncture immediately
DElectromyography before imaging
Reveal answer
Correct: B
Acute myelopathy requires urgent imaging to exclude compression, abscess, or hematoma before lumbar puncture. CSF and electrodiagnostic studies are secondary to identifying a surgical emergency.
A practical reference for urgent MRI and CSF evaluation, exclusion of compressive and infectious mimics, and timely escalation from high-dose corticosteroids to plasma exchange in severe or refractory acute transverse myelitis.
Yesterday’s Differential
The daily puzzle — from editions past
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
A 70-year-old man presents with dyspnea. His ECG shows a markedly rightward frontal axis: leads I and aVL are dominantly negative while II, III, and aVF are dominantly positive. What’s the diagnosis, and the first move?
Check your answer
Left Posterior Fascicular Block. Treat a new right axis deviation as a prompt to exclude the dangerous causes first — get a focused history and exam for PE and TCA ingestion, and scrutinize the ECG for lateral STEMI and RVH — before you settle on LPFB, and look for accompanying RBBB signaling bifascicular block.
From the August 15 edition
Today, three days ago: Calcium Chloride. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
1 g IV of 10% calcium chloride, preferably through central line; may repeat based on ECG/hemodynamics/ionized calcium. Peripheral administration carries tissue necrosis risk with extravasation; caution in digoxin toxicity and hypercalcemia.
From the August 8 edition
A 19-year-old has nasal trauma with persistent obstruction. Examination shows a soft, fluctuant, bluish swelling of the anterior septum that is tender and does not improve with oxymetazoline. What is the best next step?
ADischarge with oral antibiotics
BCT head without contrast
CUrgent incision and drainage with ENT involvement
DDelayed closed reduction in 10–14 days
Reveal answer
Correct · C
A septal hematoma requires prompt drainage to prevent cartilage ischemia, abscess, and saddle-nose deformity. Imaging and delayed reduction do not address the time-sensitive problem.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
What should you be considering with the infant with bilious emesis? The post emDOCs Podcast – Episode 146: Pediatric Gastric and Midgut Volvulus appeared first on emDocs .
Is HFNC as effective as NIV in reducing respiratory rate and improving respiratory distress within 2 hours in ACPE? The post SPICE III Trial: Does Early Dexmedetomidine Improve Survival in Mechanically Ventilated ICU Patients? appeared first on REBEL EM - Emergency Medicine Blog .
In this episode, Sam Ashoo, MD and Dr. T.R. Eckler, MD discuss the July 2026 Emergency Medicine Practice article, Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: Diagnosis and Management in the Emergency Department . 0:17 – Intro & sponsor promo 1:09 – Episode introduction 4:03 – Definitions: SJS vs. TEN vs. "overlap" by body surface area 6:12 –...
Facial trauma is common in emergency medicine, but the biggest pitfalls are often not the fractures themselves—they're the threatened airway, vision-threatening ocular injuries, missed septal hematomas, and subtle...
Critical Care Corner
Matched to today’s topics
A critical-care reference from LITFL’s Critical Care Compendium, tied to today’s differential.
Guillain–Barré syndrome becomes an ICU disease when respiratory muscle weakness and autonomic instability demand serial vital-capacity assessment, airway planning, and close haemodynamic monitoring.
Guillain-Barré Syndrome (GBS) is the most common and most severe acute paralytic neuropathy, consisting of multiple variants with distinct clinical and pathological features
Pharmacology Corner
Two drugs for the shift
One antimicrobial and one other ED workhorse — selected daily, with sources and last-reviewed dates so every dose is cross-checkable.
Antimicrobial of the Day
Oseltamivir
Neuraminidase inhibitor antiviral
Indication
Influenza treatment, especially hospitalized, severe/progressive disease, high-risk patients, or symptom onset within 48 hours.
What’s your dose? — reveal dosing & cautions
ED Dose
75 mg PO q12h x 5 days for uncomplicated adult treatment. Severe hospitalized influenza may still receive standard dosing unless institutional guidance differs.
Renal Adjustment
CrCl 31–60: 30 mg PO q12h; CrCl 11–30: 30 mg daily; ESRD/dialysis per protocol.
Contraindications
Known hypersensitivity. Dose formulation caution in patients unable to tolerate PO/enteral therapy.
Interactions
Live attenuated influenza vaccine effectiveness may be reduced when given near antiviral therapy.
Monitoring
Nausea/vomiting, neuropsychiatric symptoms, renal function for dosing.
ED Pearl
The 48-hour window is not a hard stop for the sick patient — hospitalized or severe influenza still gets antiviral treatment even if symptoms started earlier.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Ischemia
Sgarbossa Criteria
A scoring system for diagnosing acute MI in the setting of left bundle branch block or ventricular paced rhythm — the modified version is the more sensitive bedside tool.
The Tracing
A 71-year-old man with a known left bundle branch block presents with chest pain. The old rule of 'new LBBB equals STEMI' has been retired, but ischemia in LBBB still has to be diagnosed somehow. On his ECG, lead III shows 2 mm of ST elevation in the same direction as a positive QRS — concordant ST elevation.
Original criterion 1 (5 points): concordant ST elevation ≥ 1 mm in a lead with a predominantly positive QRS
Original criterion 2 (3 points): concordant ST depression ≥ 1 mm in V1–V3
Original criterion 3 (2 points): discordant ST elevation ≥ 5 mm in a lead with predominantly negative QRS
A score of ≥ 3 has high specificity (> 90%) for acute MI but limited sensitivity
Modified (Smith) Sgarbossa replaces criterion 3 with proportional discordance: ST elevation ≥ 25% of the preceding S-wave depth — substantially more sensitive without sacrificing specificity
Pearls
In LBBB or a paced rhythm, the entire ECG already shows discordant ST changes at baseline. Sgarbossa identifies the changes that exceed what conduction delay alone would produce.
Concordance is the strongest signal. A single concordant ST elevation in any lead (criterion 1) is almost as specific as the full score.
Modified Sgarbossa is the better tool when the patient has a deep S wave and any ST elevation that would otherwise look proportionate. Use the 25% rule rather than the absolute 5 mm threshold.
Pitfalls
The old teaching of 'new LBBB equals STEMI' over-activates the cath lab. Sgarbossa is the more accurate framework — apply it.
The criteria are not very sensitive overall; a negative score does not exclude infarction. Pair the ECG with serial troponin and clinical context.
Right ventricular pacing produces an LBBB-like pattern, so Sgarbossa applies to paced rhythms too. Ask about the device interrogation if available.
At the Bedside
Apply modified Sgarbossa to any LBBB or ventricular paced rhythm with concerning chest pain. A positive score warrants STEMI activation. A negative score does not rule out MI — admit, serial troponin, and serial ECGs as the symptoms and risk profile dictate.
For educational use only. Verify ECG interpretation against the LITFL entry and your institution’s practice before clinical decision-making.
Case of the Day
From the lead · FUNCTIONAL SEIZURES
Self-Examination
Test Your Understanding
A 24-year-old patient has recurrent episodes of asynchronous shaking with tightly closed eyes, preserved oxygenation, and immediate recall. During a typical event, video-EEG shows no epileptiform activity. Which is the best next step?
AStart levetiracetam
BIntubate for refractory status epilepticus
CExplain the diagnosis empathetically and arrange neurologic and psychological follow-up
DAdminister repeated doses of lorazepam until movements stop
Reveal answer
Correct answer · C
A typical event without an epileptiform EEG correlate supports functional seizures. Antiseizure drugs and escalating benzodiazepines do not treat the underlying disorder and may cause harm.
Study Pace* 4 topics today; Issue 35 of 94 — Neurology (Week 19)Deadline · June 1, 2026