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Posterior encephalopathy subsequent to cyclosporin A presenting as irreversible abulia

Makoto Nishie1, Kozo Kurahashi, Masaya Ogawa

  • 1Department of Neurology, Aomori Prefectural Central Hospital, Aomori.

Internal Medicine (Tokyo, Japan)
|August 20, 2003
PubMed

Insights

Cyclosporin A (Cys A) can cause posterior encephalopathy. Even with imaging improvements, persistent abulia may occur due to brain hypoperfusion and potential direct Cys A toxicity.

Area of Science:

  • Neuroscience
  • Immunology
  • Radiology

Background:

  • Cyclosporin A (Cys A) is an immunosuppressant drug.
  • Posterior reversible encephalopathy syndrome (PRES) is a neurological condition.
  • Cys A is known to induce PRES.

Observation:

  • A patient developed persistent abulia (a state of diminished motivation) after Cys A-induced PRES.
  • MRI showed rapid improvement in T2 and FLAIR hyperintensities.
  • Diffusion-weighted imaging revealed atypical high signal intensity at onset.

Findings:

  • Persistent abulia correlated with significant hypoperfusion in the cortex, frontal lobes, and basal ganglia, visualized by SPECT.
  • Atypical diffusion-weighted imaging findings may predict poor neurological recovery.
  • Blood-brain barrier breakdown and direct Cys A neurotoxicity are implicated.

Implications:

  • This case highlights the potential for chronic, irreversible neurological deficits following Cys A-induced PRES.
  • Early detection of atypical MRI findings and hypoperfusion is crucial for predicting outcomes.
  • Further research into Cys A's direct neurotoxic effects is warranted.

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