What does it mean if a patient with a history of pontine stroke and locked-in syndrome, who has developed encephalopathy, has upright toes, possibly indicating a positive Babinski sign?

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Last updated: January 26, 2026View editorial policy

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Upright Toes Indicate Upper Motor Neuron Pathology (Positive Babinski Sign)

When toes are upright (great toe dorsiflexion with fanning of other toes), this represents a positive Babinski sign indicating pyramidal tract dysfunction from upper motor neuron pathology. 1 In your patient with pontine stroke and locked-in syndrome who has now developed encephalopathy, upright toes signal either progression of the original pontine lesion or a new secondary neurological complication requiring urgent investigation. 1, 2

What the Sign Means Pathophysiologically

  • The Babinski sign (upgoing toe) is always pathological in adults and indicates dysfunction of the corticospinal (pyramidal) tract anywhere from the motor cortex through the spinal cord. 1, 3

  • This sign represents loss of cortical inhibition over the primitive flexor withdrawal reflex, causing the great toe to dorsiflex instead of the normal plantar flexion response. 4

  • In pontine stroke specifically, the corticospinal tracts pass through the ventral pons, so bilateral Babinski signs would be expected from the original stroke itself. 5

Critical Distinction in Your Patient's Context

The development of encephalopathy in a patient with isolated pontine stroke is paradoxical and demands investigation for secondary complications, as consciousness should be preserved in pure pontine lesions (locked-in syndrome). 2

Most Likely Causes of New/Worsening Babinski Sign with Encephalopathy:

  • Delayed pontine swelling (4-10 days post-stroke) causing mass effect on the reticular activating system and bilateral corticospinal tract compression. 2

  • Hemorrhagic transformation of the pontine infarct with expansion. 2

  • Metabolic encephalopathy (particularly hyponatremia from SIADH, hypoglycemia, uremia, or hepatic dysfunction) can produce or unmask Babinski signs. 2, 3, 6

  • Sepsis with systemic inflammatory response affecting neurological function, especially aspiration pneumonia given bulbar dysfunction. 2

  • Medication toxicity from sedatives or anticonvulsants accumulating in altered metabolism. 2

Immediate Diagnostic Workup Required

Urgent neuroimaging is mandatory - preferably MRI brain with and without contrast to assess for: 1, 3

  • Pontine swelling or mass effect
  • Hemorrhagic transformation
  • New ischemic lesions
  • Hydrocephalus

Comprehensive metabolic evaluation: 2

  • Serum sodium (SIADH is particularly common post-stroke)
  • Bedside glucose immediately
  • Complete metabolic panel (renal and hepatic function)
  • Complete blood count and inflammatory markers
  • Arterial blood gas if acidosis suspected

Medication review for potential neurotoxicity from polypharmacy. 2

EEG monitoring if seizure activity suspected, as this is the only tool to detect subclinical seizures in encephalopathic patients. 5

Important Clinical Pitfalls

  • False negatives can occur immediately after acute stroke due to "spinal shock" where the Babinski sign may be transiently absent despite pyramidal tract damage. 1

  • The presence of encephalopathy with pontine stroke is never normal - the American Heart Association emphasizes that any deviation from alert consciousness in locked-in syndrome demands investigation for secondary causes. 2

  • Bilateral absence of cortical somatosensory evoked potentials (N20) would indicate particularly severe neuronal dysfunction, though this may be reversible if due to increased intracranial pressure from pontine swelling rather than completed infarction. 5

Management Approach

Treat the underlying cause aggressively: 2, 3

  • Correct electrolyte abnormalities (especially sodium, but avoid rapid correction to prevent central pontine myelinolysis)
  • Treat identified infections with appropriate antimicrobials
  • Discontinue or adjust offending medications
  • Consider neurosurgical consultation if imaging shows mass effect requiring decompression

Monitor for associated upper motor neuron signs: 1, 3

  • Hyperreflexia (exaggerated deep tendon reflexes)
  • Spasticity (velocity-dependent increased muscle tone)
  • Clonus (rhythmic oscillations with sustained stretch)

Maintain supportive care per stroke protocols: 5

  • Early mobilization when stable to prevent complications (pneumonia, DVT, pressure sores)
  • Swallowing assessment before oral intake given high aspiration risk with pontine lesions
  • DVT prophylaxis with pneumatic compression devices

References

Guideline

Clinical Significance of Babinski Sign and Upper Motor Neuron Lesions

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Guideline

Encephalopathy in Pontine Stroke: Causes and Mechanisms

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Guideline

Clinical Significance and Management of Babinski Sign

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

The Babinski sign: the first hundred years.

Journal of neurology, 1996

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Joseph Babinski: the phenomenon of the toes.

The Journal of emergency medicine, 1984

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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