TY - JOUR
T1 - Prolonged unilateral vasodilatation and brain edema in fulminant hepatic failure, associated with symptomatic seizure
AU - Inamasu, Joji
AU - Nakamura, Yoshiki
AU - Yamamoto, Shinichiro
AU - Sakamoto, Namiko
AU - Saito, Ryoichi
AU - Horiguchi, Takashi
AU - Ichikizaki, Kiyoshi
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
KW - Brain edema
KW - Cerebral blood flow
KW - Fulminant hepatic failure
KW - Hyperperfusion
KW - Seizure
KW - Vasodilatation
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UR - http://www.scopus.com/inward/citedby.url?scp=0036207240&partnerID=8YFLogxK
U2 - 10.1016/S0303-8467(02)00007-0
DO - 10.1016/S0303-8467(02)00007-0
M3 - Article
C2 - 11932048
AN - SCOPUS:0036207240
VL - 104
SP - 157
EP - 160
JO - Clinical Neurology and Neurosurgery
JF - Clinical Neurology and Neurosurgery
SN - 0303-8467
IS - 2
ER -