What is the most likely cause of acute flaccid quadriplegia with preserved sensation, normal reflexes, and no bowel/bladder involvement in a young woman with a history of seizures?

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Functional Neurological Disorder (Conversion Disorder)

In a young woman presenting with acute flaccid quadriplegia, preserved sensation, normal reflexes, no bowel/bladder involvement, and a history of seizures, the most likely diagnosis is functional neurological disorder (conversion disorder), particularly given the dissociation between motor and sensory findings that violates neuroanatomical principles.

Why This Pattern Points to Functional Neurological Disorder

  • The preservation of reflexes with flaccid quadriplegia is neuroanatomically incompatible with organic neuromuscular disease—true flaccid paralysis from lower motor neuron, neuromuscular junction, or muscle pathology invariably produces hyporeflexia or areflexia 1, 2.

  • Normal sensation with complete motor loss does not fit any organic localization: spinal cord lesions causing quadriplegia produce sensory levels and sphincter dysfunction; peripheral neuropathies affecting motor function severely enough to cause quadriplegia would show sensory abnormalities and reflex loss 1, 3, 2.

  • The history of seizure episodes raises the possibility of psychogenic non-epileptic seizures (PNES), which frequently co-occur with other functional neurological symptoms in 10-30% of cases, particularly in young women who represent the highest-risk demographic for conversion disorders.

Critical Organic Diagnoses to Exclude First

Despite the pattern suggesting functional disorder, life-threatening organic causes must be ruled out immediately before attributing symptoms to conversion:

Guillain-Barré Syndrome (GBS)

  • GBS typically presents with ascending bilateral weakness, but reflexes are diminished or absent—not normal 1, 3, 2.
  • The pure motor variant of GBS (5-70% of cases) can spare sensation, but areflexia is a defining feature 3.
  • Normal reflexes essentially exclude GBS as the primary diagnosis 1, 2.
  • If any doubt exists, obtain nerve conduction studies immediately—do not wait, as 20% of GBS patients develop respiratory failure requiring mechanical ventilation 1, 3.

Botulism

  • Descending flaccid paralysis with preserved or normal reflexes is the hallmark of botulism 2.
  • However, botulism begins with cranial nerve palsies (ptosis, diplopia, dysarthria, dysphagia) and descends to the limbs—not ascending or simultaneous quadriplegia 2.
  • Sensory examination is completely normal in botulism, and patients remain alert and oriented 2.
  • If cranial nerve findings are present, contact CDC immediately for botulinum antitoxin 2.

Myasthenia Gravis

  • Fatigable weakness with preserved reflexes can mimic functional disorder 2.
  • However, myasthenia typically shows fluctuating weakness worsening with repetitive activity, prominent bulbar and ocular involvement, and does not cause acute complete quadriplegia 2.

Metabolic/Electrolyte Causes

  • Severe hypokalemia (K+ <2.5 mEq/L) can cause flaccid quadriplegia with preserved or diminished reflexes 4.
  • Thyrotoxic periodic paralysis presents with acute flaccid paralysis and hypokalemia, predominantly in Asian males 5, 4.
  • Check serum potassium, magnesium, phosphate, calcium, and thyroid function immediately 3, 2.
  • Hyperkalemia (>7 mEq/L) causes ascending flaccid paralysis with diminished reflexes and sensory loss—not the pattern described here 4.

Acute Spinal Cord Compression

  • Acute cord compression at C1-C2 causes flaccid quadriplegia (spinal shock) with initial areflexia, sensory level, and sphincter dysfunction 6.
  • The absence of sensory findings and sphincter involvement makes this unlikely, but obtain urgent MRI of the cervical spine with contrast to exclude compressive myelopathy 3, 2.

Diagnostic Workup Algorithm

Immediate Life-Threatening Assessment (First 30 Minutes)

  1. Assess respiratory function immediately—measure vital capacity and negative inspiratory force, as respiratory failure can develop rapidly even without dyspnea 1, 2.
  2. Monitor cardiac rhythm and blood pressure continuously to detect autonomic dysfunction 1, 3.
  3. Assess bulbar function (swallowing, cough, gag reflex) to identify aspiration risk 1, 3.

Urgent Laboratory Testing (First 2 Hours)

  1. Serum electrolytes including potassium, magnesium, phosphate, calcium 3, 2, 4.
  2. Thyroid function tests (TSH, free T4, free T3) to exclude thyrotoxic myopathy 5.
  3. Creatine kinase (CK) to assess for muscle involvement 3.
  4. Complete blood count, glucose, renal and liver function 3.

Neuroimaging (First 4 Hours)

  1. MRI of the cervical and thoracic spine with and without contrast to exclude compressive lesions, transverse myelitis, or nerve root pathology 3, 2.
  2. Brain MRI with contrast if any cranial nerve findings or altered mental status 2.

Electrodiagnostic Studies (First 24 Hours)

  1. Nerve conduction studies and EMG to evaluate for GBS, myopathy, or neuromuscular junction disorders 1, 3, 2.
  2. Repetitive nerve stimulation if myasthenia gravis is suspected 2.
  3. Normal initial studies do not exclude GBS—changes may not appear until 10-14 days after symptom onset, so repeat in 2-3 weeks if clinical suspicion persists 1, 3, 2.

Lumbar Puncture (If GBS Suspected)

  1. Perform after neuroimaging to exclude mass lesions 3.
  2. Look for albuminocytologic dissociation (elevated protein with normal cell count), though this may be absent in the first week 3, 2.
  3. Marked CSF pleocytosis should prompt reconsideration of GBS diagnosis 3.

Positive Diagnostic Features of Functional Neurological Disorder

Once organic causes are excluded, look for positive signs of functional disorder rather than relying solely on negative workup:

  • Inconsistency of examination findings over time or with distraction.
  • Hoover's sign: When the patient attempts to lift the "paralyzed" leg, there is no downward pressure from the contralateral leg (normally present as a synkinetic movement).
  • Collapsing weakness (give-way weakness) where resistance suddenly gives way during strength testing.
  • Tubular visual fields or other non-physiologic sensory findings if sensory complaints emerge.
  • La belle indifférence (inappropriate lack of concern) is present in only 20% of cases and should not be relied upon.
  • History of recent psychological stressor, trauma, or secondary gain, though absence does not exclude the diagnosis.

Management Approach

If Organic Causes Are Excluded

  1. Avoid confrontational language—do not tell the patient "it's all in your head" or "there's nothing wrong with you" 7.
  2. Provide a positive diagnosis: "Your symptoms are real and caused by a problem in how your brain is sending signals to your muscles, not damage to the muscles or nerves themselves."
  3. Neurology and psychiatry co-management is essential—functional disorders require specialized neuropsychiatric expertise.
  4. Physical therapy with gradual reactivation is the cornerstone of treatment.
  5. Cognitive-behavioral therapy (CBT) addresses underlying psychological factors.
  6. Avoid unnecessary testing or treatments that reinforce illness behavior.

If Any Doubt Remains About GBS

  1. Admit to monitored bed with capability for rapid ICU transfer 1, 3, 2.
  2. Serial vital capacity and negative inspiratory force measurements every 4-6 hours 1, 3, 2.
  3. Do not delay IVIg (0.4 g/kg/day × 5 days) if clinical suspicion is moderate to high—waiting for confirmatory testing risks respiratory failure 1, 3.

Common Pitfalls to Avoid

  • Do not diagnose functional disorder as a "diagnosis of exclusion" without positive clinical features—this leads to missed organic disease and damages the therapeutic relationship.
  • Do not assume normal reflexes exclude all organic causes—botulism and myasthenia gravis can present with preserved reflexes 2.
  • Do not dismiss the patient's symptoms as "fake" or "attention-seeking"—functional neurological disorders are involuntary and cause genuine disability.
  • Do not delay respiratory monitoring in any patient with acute quadriplegia, regardless of suspected etiology—respiratory failure can develop rapidly 1, 2.
  • Do not attribute symptoms to conversion disorder if the patient has altered mental status, fever, or autonomic instability—these indicate organic disease 2.

References

Guideline

Clinical Approach to Flaccid Quadriparesis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Approach to Acute Flaccid Paralysis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Guideline

Approach to Diagnosing and Managing Guillain-Barré Syndrome

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Research

Flaccid quadriplegia from tonsillar herniation in pneumococcal meningitis.

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia, 2000

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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