Prolonged unilateral vasodilatation and brain edema in fulminant hepatic failure, associated with symptomatic seizure

Joji Inamasu, Yoshiki Nakamura, Shinichiro Yamamoto, Namiko Sakamoto, Ryoichi Saito, Takashi Horiguchi, Kiyoshi Ichikizaki

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


We report prolonged unilateral vasodilatation and hemispheric brain edema in a 49-year-old man with fulminant hepatic failure (FHF). The patient presented with a tonic-clonic seizure caused by a hypertensive subcortical hemorrhage in the left parietal lobe. Serial computed tomography (CT) scans showed progressive darkening of the ipsilateral hemisphere, suggesting hemispheric cerebral infarction, but the patient did not show clinical signs of deterioration. Brain magnetic resonance angiography showed dilation of the large arteries of the left hemisphere. Evaluation of cerebral blood flow 7 days postictus with single photon emission CT revealed marked ipsilateral hyperperfusion. The darkening of the hemisphere was brain edema elicited by hyperperfusion. Brain edema was reversible, disappearing 14 days postictus. Hemispheric brain edema was caused by unilateral cerebral vasodilatation and resultant hyperperfusion. Although brain edema is a major complication in FHF patients and cerebral hyperperfusion is responsible for edema formation, CT findings of these patients almost invariably show a bilateral lesion. Unilateral vasodilatation and subsequent hemispheric hyperperfusion may be due to overproduction of vasodilators, already abundant in the brains of patients with severe hepatic failure, by seizure activity.

Original languageEnglish
Pages (from-to)157-160
Number of pages4
JournalClinical Neurology and Neurosurgery
Issue number2
Publication statusPublished - 2002
Externally publishedYes


  • Brain edema
  • Cerebral blood flow
  • Fulminant hepatic failure
  • Hyperperfusion
  • Seizure
  • Vasodilatation

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology


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