When neurological symptoms occur after endovascular procedures in the brain, it is fundamental to distinguish this rare clinical syndrome of probable toxic origin from possible ischemic complications of the procedure.
A case of temporary nonthrombotic hemiplegia and aphasia due to neurotoxicity from angiographic contrast material?
 
  Keywords
 
 
  
   Contrast agent
  
 
 
  
   Angiography
  
 
 
  
   Cerebral angiography
  
 
 
  
   Neurological deficit
  
 
 
  
   Neurotoxicity
  
 
 
  
   Cerebral aneurysm
  
 
 
  
   Therapeutic embolization
  
 
Abstract
 We present the case of a 75-year-old woman who suddenly developed <dis>hemiplegia</dis>, <dis>aphasia</dis>, and reduced consciousness three hours after embolization of a cerebral aneurysm.
No complications occurred during embolization and the findings at end- procedure angiography were normal.
Cranial computed tomography (CT) after embolization showed hyperdensity of the cortex and sulci of the convexity; another CT examination performed four hours later showed these findings had disappeared.
Cerebral arteriography 24 h after embolization showed delayed blood flow to the parenchyma of the left hemisphere compared to the right but no vascular occlusion.
The neurological deficit lasted 72 h and resolved spontaneously and completely as suddenly as it developed.
This is one of the few cases of temporary neurological deficit related to iodinated contrast administration to be reported outside the posterior circulation (<dis>cortical blindness</dis>).
When neurological symptoms occur after endovascular procedures in the brain, it is fundamental to distinguish this rare clinical syndrome of probable toxic origin from possible ischemic complications of the procedure.
Abstract
 We present the case of a 75-year-old woman who suddenly developed hemiplegia, aphasia, and reduced consciousness three hours after embolization of a cerebral aneurysm.
No complications occurred during embolization and the findings at end- procedure angiography were normal.
Cranial computed tomography (CT) after embolization showed hyperdensity of the cortex and sulci of the convexity; another CT examination performed four hours later showed these findings had disappeared.
Cerebral arteriography 24 h after embolization showed delayed blood flow to the parenchyma of the left hemisphere compared to the right but no vascular occlusion.
The neurological deficit lasted 72 h and resolved spontaneously and completely as suddenly as it developed.
This is one of the few cases of temporary neurological deficit related to iodinated contrast administration to be reported outside the posterior circulation (cortical blindness).
When neurological symptoms occur after endovascular procedures in the brain, it is fundamental to distinguish this rare clinical syndrome of probable toxic origin from possible ischemic complications of the procedure.
When neurological symptoms occur after endovascular procedures in the brain, it is fundamental to distinguish this rare clinical syndrome of probable toxic origin from possible ischemic complications of the procedure.