Last reviewed: March 2026
Contents
MDM Templates
Guillain-Barré Syndrome
Patient presents with ascending symmetric weakness and areflexia developing over days. No sharp sensory level, no bowel or bladder dysfunction, no recent trauma.
Pattern of ascending weakness with areflexia and preserved sensation is most consistent with Guillain-Barré syndrome. Not consistent with stroke (bilateral, ascending, areflexic), transverse myelitis (no sensory level, no bladder dysfunction), spinal cord compression (no sensory level, no trauma), or myasthenia gravis (no fatigable weakness, no bulbar symptoms).
Plan: Neurology consulted regarding admission, LP, and initiation of IVIG or plasmapheresis. Admit for monitoring of respiratory function.
If respiratory compromise suspected: Bedside NIF and FVC measured. NIF worse than −30 cmH2O or FVC <20 mL/kg indicates impending respiratory failure — intubate early rather than waiting for desaturation.
Transverse Myelitis
Patient presents with acute bilateral weakness, a sensory level, and bowel or bladder dysfunction. No preceding trauma. No history of IVDU or recent spinal procedure.
Presentation with weakness plus sensory level plus bladder dysfunction localizes to the spinal cord. Must consider compressive myelopathy (epidural abscess, epidural hematoma, metastatic cord compression) and vascular causes (spinal cord infarction). Emergent MRI required to differentiate — compressive causes require urgent surgical intervention.
Plan: Emergent MRI spine. Neurology and/or neurosurgery consulted. Admit.
If MRI shows no compression: Inflammatory myelopathy (transverse myelitis, neuromyelitis optica, MS) most likely. Neurology consulted regarding LP, high-dose IV steroids, and admission.
Myasthenia Gravis / Myasthenic Crisis
Patient presents with fatigable weakness, ptosis, diplopia, or bulbar symptoms (dysphagia, dysarthria). Symptoms worse with exertion and improve with rest. Sensation, reflexes, and pupils preserved.
Fatigable weakness with bulbar involvement and preserved reflexes is consistent with neuromuscular junction pathology. Not consistent with stroke (reflexes preserved, symptoms fluctuate with effort), GBS (no areflexia, no ascending pattern), or myopathy (bulbar predominant, not proximal limb predominant).
Plan: Neurology consulted regarding admission, IVIG or plasmapheresis, and pyridostigmine management. Admit.
If respiratory distress or inability to protect airway: This is myasthenic crisis. Bedside NIF and FVC measured. Intubation if NIF worse than −20 cmH2O or FVC <15 mL/kg. Avoid succinylcholine (resistant) and minimize nondepolarizing agents (exquisitely sensitive).
Central Cord Syndrome
Patient presents with neurologic deficits after cervical hyperextension injury. Upper extremity weakness greater than lower extremity weakness. No sharp sensory level, no penetrating injury.
Pattern of arm-greater-than-leg weakness after hyperextension mechanism is consistent with central cord syndrome. Not consistent with Brown-Séquard (no ipsilateral motor / contralateral sensory pattern), anterior cord syndrome (would spare posterior columns), epidural abscess (no fever, no IVDU, no recent procedure), or stroke (mechanism and pattern not consistent).
Plan: MRI cervical spine. Neurosurgery consulted. Admit. No role for steroids in acute traumatic spinal cord injury.
Clinical Education
Approach to Acute Weakness
The first question is localization: where is the lesion? Upper motor neuron (brain, spinal cord) vs lower motor neuron (peripheral nerve, NMJ, muscle). This drives the entire workup. UMN signs (hyperreflexia, spasticity, upgoing toes) point to brain or cord. LMN signs (hyporeflexia, flaccidity, fasciculations) point to peripheral nerve or NMJ.[1]
Bilateral weakness is not stroke until proven otherwise. Stroke causes unilateral deficits in the vast majority of cases. Bilateral weakness should prompt consideration of cord pathology, GBS, myasthenia, or bilateral anterior cerebral artery strokes (rare). Don’t anchor on stroke just because the patient is weak.
Always check respiratory function in neuromuscular weakness. NIF (negative inspiratory force) and FVC (forced vital capacity) are the critical numbers. By the time the patient desaturates, they’re in extremis. Intubate based on the numbers, not the pulse ox.
Localization Table
| Feature | UMN (Brain/Cord) | LMN (Nerve/NMJ/Muscle) |
| Reflexes | Hyperreflexic | Hyporeflexic or absent |
| Tone | Spastic | Flaccid |
| Babinski | Upgoing (positive) | Downgoing or absent |
| Atrophy | Late/absent | Early and prominent |
| Fasciculations | Absent | May be present |
| Sensory level | Present (cord lesion) | Stocking-glove or dermatomal |
Note: In acute cord injury, spinal shock can cause initial flaccidity and areflexia that mimics LMN lesion. The key differentiator is the sensory level and bladder dysfunction.
GBS Pearls
LP shows albuminocytologic dissociation (elevated protein, normal cell count), but CSF protein may be normal in the first week. A normal LP does not rule out GBS early in the course. If clinical suspicion is high and LP is normal, neurology should consider repeat LP or empiric treatment.[1]
The 20/30/40 rule for intubation: FVC <20 mL/kg, NIF worse than −30 cmH2O, or >30% decline in FVC from baseline. Don’t wait for hypoxia or hypercarbia. These patients crash from diaphragmatic fatigue, not from parenchymal lung disease — by the time the sat drops, they’re about to arrest.
Treatment is IVIG (0.4 g/kg/day x 5 days) or plasmapheresis. Both are equivalent. Steroids have no role and may worsen outcomes. IVIG is typically first-line because it’s easier to administer.[2]
Autonomic instability (labile BP, tachy/bradycardia, urinary retention) occurs in up to 70% and is a major cause of morbidity. These patients need telemetry.
Myasthenia Gravis Pearls
The ice test: Apply ice pack to closed eyelid for 2 minutes. Improvement of ptosis >2 mm supports myasthenia. Quick, free, bedside test with reasonable sensitivity. Useful when you’re considering MG but don’t have edrophonium readily available.[3]
Myasthenic crisis vs cholinergic crisis: Both present with weakness and respiratory failure. Myasthenic crisis = undertreated MG. Cholinergic crisis = too much pyridostigmine (look for SLUDGE symptoms: salivation, lacrimation, urination, diaphoresis). In practice, cholinergic crisis is rare with modern dosing. Assume myasthenic crisis and treat accordingly.
Medication triggers: Aminoglycosides, fluoroquinolones, beta-blockers, magnesium, and neuromuscular blockers can all precipitate crisis. Always check the med list.
Intubation considerations: Succinylcholine has unpredictable effects (patients are resistant due to reduced receptors). Use rocuronium at reduced dose (0.3-0.5 mg/kg) with sugammadex available for reversal. Or consider awake intubation if possible.
Spinal Cord Syndromes
| Syndrome | Pattern | Classic Cause |
| Central Cord | Arms > legs weakness, cape-like sensory loss | Hyperextension in elderly with stenosis |
| Anterior Cord | Motor + pain/temp loss, preserved proprioception | Aortic pathology, flexion injury |
| Brown-Séquard | Ipsilateral motor + contralateral pain/temp loss | Penetrating trauma, best prognosis |
| Posterior Cord | Loss of proprioception + vibration, preserved motor | B12 deficiency, syphilis (rare) |
| Cauda Equina | Saddle anesthesia, urinary retention, bilateral leg pain | Large midline disc herniation |
No steroids for traumatic spinal cord injury. The NASCIS trials that promoted high-dose methylprednisolone have been widely criticized and subsequent evidence (including the 2013 AOSpine guidelines) does not support their use. Steroids increase infection and GI bleeding risk without clear neurologic benefit.[1]
Disposition
Admit all acute motor weakness presentations. GBS, transverse myelitis, myasthenic crisis, and spinal cord syndromes all require inpatient monitoring, advanced imaging, and specialist consultation. There is no safe discharge pathway for new-onset acute motor weakness.
ICU: Any patient with bulbar symptoms, respiratory compromise (abnormal NIF/FVC), autonomic instability, or rapidly progressing weakness.
Floor with telemetry: Stable patients with confirmed diagnosis and no respiratory concerns, pending treatment initiation.
References
- Dubey D, Freeman M. Acute neuromuscular weakness in the emergency department. Emerg Med Clin North Am. 2021;39(1):127-141. PubMed
- Hughes RA, Swan AV, van Doorn PA. Intravenous immunoglobulin for Guillain-Barré syndrome. Cochrane Database Syst Rev. 2014;(9):CD002063. PubMed
- Benatar M. A systematic review of diagnostic studies in myasthenia gravis. Neuromuscul Disord. 2006;16(7):459-467. PubMed
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