Korean Journal of Cerebrovascular Surgery 2010;12(4):245-249.
Published online December 1, 2010.
Contrast Medium-Induced Transient Neurologic Deteriorations Following Cerebral angiography and Coil Embolization for Unruptured Aneurysm: Report of Two Cases.
Seo, Young Jun , Choi, Chang Hwa
Department of Neurosurgery, School of Medicine, Pusan National University, Busan, Korea. chwachoi@pusan.ac.kr
Cerebral angiography with contrast medium (CM) is a key method for diagnosis and interventional treatment of intracranial cerebral vascular lesions. Cerebral angiography causes few neurologic complications. There have been rare reports of complications related to disruption of the blood-brain barrier due to the administration of nonionic CM. We observed two patients with transient neurologic complications following cerebral angiography and coil embolization for unruptured aneurysm.
Key Words: Blood brain barrier disruption, Cerebral angiography complication, Contrast medium


Nonionic contrast medium (CM) is now widely used for neuroangiography. Cerebral angiography with CM is a key method for diagnosis and interventional treatment of intracranial cerebral vascular lesions. Cerebral angiography is associated with a low neurologic complication.3)4) There have been rare reports of abnormal enhancement in the cerebral cortex with transient neurologic deficits identified by non-contrast-enhanced computed tomography (CT) after cerebral angiography. These neurologic findings may be related to disruption of the blood-brain barrier (BBB) due to administration of nonionic CM.

We report on two patients with transient neurologic deficits following cerebral angiography and coil embolization for unruptured aneurysm, and review the pertinent literature.

Case 1

A 70-year-old female was referred to our clinic for evaluation of an unruptured intracranial aneurysm. On examination, the patient was neurologically free. Cerebral angiography through femoral artery was done with Optiray짋 CM (320 mg/ml; Mallinckodt Medical, St. Louis, MO, USA). The total amount of CM used was 150 ml. Angiography revealed an unruptured intracranial aneurysm in the left anterior communicating artery (A-com) and pericallosal artery (Fig. 1). After the procedure, the patient suffered a sudden onset of aphasia. Motor system examination revealed grade 1/5 right side weakness. A post-procedural non-contrast-enhanced CT scan showed cortical enhancement at the left hemisphere and right frontal lobe (Fig. 2A). Diffusion-weighted magnetic resonance imaging (MRI) did not reliably identify the acute infarction related to the procedure (Fig. 2B). Supportive care, which included hydration and steroid therapy, was applied immediately. The patient? neurologic deteriorations improved markedly within several hours after cerebral angiography. A follow-up CT scan showed no enhancement of cerebral cortex (Fig. 2C). The patient was discharged without any neurologic deficits.

Case 2

A 34-year-old male was admitted to our hospital for treatment of an unruptured intracranial aneurysm in the left petrous internal carotid artery (ICA) diagnosed by magnetic resonance angiography (MRA) (Fig. 3). The patient had a mild headache without neurologic symptoms. Cerebral angiography was done with Visipaque짋 CM (320 mg/ml; GE Healthcare AS, Nydalen, Norway). A coil embolization was applied with combined technique using two catheters and balloon (Fig. 4A). The total amount of used contrast medium was 200 ml. The aneurysm was completely packed with coils (Fig. 4B). After an uneventful endovascular treatment, the patient had a sudden onset of aphasia and mild right side motor weakness. A follow-up CT evaluation revealed focal cortical hyperattenuations in the left frontal, parietal and occipital lobes (Figs. 5A and 5B). Diffusion-weighted MRI did not detect vascular events (Fig. 5C). The patient was treated with hydration and steroid therapy. Full neurologic recovery resulted within several hours. Repeated follow-up CT images showed no hyperattenuation of cerebral cortex (Fig. 5D, E). The patient was discharged without neurologic deficits.


Cerebral angiography is important in the diagnosis and treatment of many central nervous system diseases for decades. However, it is an invasive test with potentially severe, albeit infrequent, complications. The most common complication is groin hematoma (4.2% of examinations); nausea, vomiting, and transient hypotension are common systemic complications.4) Neurologic events occur at a frequency of 0.30%-2.63%; the majority of these complications are transient neurological deteriorations such as hemiparesis, aphasia, visual symptoms, and seizure attack after cerebral angiography.3)4) Significant predictor variables associated with neurologic complications are imaging indications of subarachnoid hemorrhage, atherosclerotic cerebrovascular disease, and arteriovenous malformation.4)

Transient neurologic complications have been previously assumed to result from embolism or factors impairing cortical perfusion. But, CM-induced disruption of the BBB and direct neurotoxicity by CM may also be mechanisms of neurologic dysfuction.9) Disruption of the BBB following cerebral angiography has been reported.8)10)11) An immediate post-angiographic CT scan may show focal or diffuse hyperdensity following uneventful angiography, most likely caused by BBB disruption resulting in accumulation of CM. 5) The hyperattenuation of the cerebral cortex caused by BBB disruption disappears at the follow-up CT scan because CM is usually washed away within several hours.

The BBB is impermeable to radiographic contrast material under normal conditions. The mechanism of BBB disruption remains speculative. It has been recognized that the hyperosmolality and chemotoxicity of CM are important factors.6)7) The hypertonic solution can shrink and separate at the tight junctions by drawing water out of the endothelial cells.6) The severity of the BBB disruption is related to the ionic and chemical contents of the medium.7) Several authors have reported about the role of CM viscosity in BBB disruption. Under a condition of constant injection volume, the increased viscosity of the CM may require a compensatory increase in the duration of injection, which may contribute to its neurotoxic effects and may be related to the risk of BBB disruption.1)12) In an experimental study in rabbits, Uchiyama et al.11) reported that high iodine concentration, low temperature of the liquid and its potential relation to the variable of high viscosity, and brief injection time interval as the contributing factors to BBB disruption following intracarotid injection of CM.

BBB disruption can be identified as a transient CT finding of cortical hyperattenuation. MRI enhancement with gadolinium-diethylenetriamine pentaacetic acid has recently proved more sensitive and precise than MRI without enhancement or CT.2) But, CT scanning is performed preferentially after cerebral angiography in our hospital. If a patient has neurologic symptoms, MRI should be performed to discern cerebral ischemic events. On study reported significant relationships between the occurrence of cortical hyperattenuation on CT scan and the amount of CM used per kilogram body weight, microcatheter time, number of balloon inflations, and total time of balloon inflation.5)

In the two present cases, the patients displayed transient neurologic symptoms after cerebral angiography and endovascular treatment for unruptured aneurysms. Immediate CT images revealed diffuse or focally-increased cortical density. Diffusion-weighted MRI images showed no cerebral vascular events. After several hours, neurologic symptoms of both patients improved and follow-up CT scans revealed the disappearance of high density in the cerebral cortex. The present cases may thus be considered as transient neurologic deteriorations resulting from BBB disruption after cerebral angiography and endovascular treatment.


Cerebral angiography is useful for diagnosis and interventional treatment of intracranial cerebral vascular lesions. Although BBB disruption is rare, physicians should be aware of the possibility of this complication. Careful observation of a patient? clinical status and immediate action for diagnosis and treatment of neurologic deterioration during neurointerventinal procedure are required.


  1)    d'Avella D, Cicciarello R, Albiero F, Piscitelli G, Fiori MG, Mesiti M, et al. Effect of intracarotid injection of iopamidol on local cerebral glucose utilization in rat brain. AJNR Am J Neuroradiol 10:797-801, 1989.

  2)    De Wispelaere JF, Trigaux JP, Van Beers B, Gilliard C. Cortical and csf hyperdensity after iodinated contrast medium overdose: Ct findings. J Comput Assist Tomogr 16:998-9, 1992.

  3)    Fifi JT, Meyers PM, Lavine SD, Cox V, Silverberg L, Mangla S, et al. Complications of modern diagnostic cerebral angiography in an academic medical center. J Vasc Interv Radiol 20:442-7, 2009.

  4)    Kaufmann TJ, Huston J, 3rd, Mandrekar JN, Schleck CD, Thielen KR, Kallmes DF. Complications of diagnostic cerebral angiography: Evaluation of 19,826 consecutive patients. Radiology 243:812-9, 2007.

  5)    Ozturk A, Saatci I, Pamuk AG, Erdogan C, Akmangit I, Geyik S, et al. Focal increased cortical density in immediate postembolization ct scans of patients with intracranial aneurysms. AJNR Am J Neuroradiol 27:1866-75, 2006.

  6)    Rapoport SI, Thompson HK, Bidinger JM: Equi-osmolal opening of the blood-brain barrier in the rabbit by different contrast media. Acta Radiol Diagn (Stockh) 15:21-32, 1974.

  7)    Salvesen S, Nilsen PL, Holtermann H. Effects of calcium and magnesium ions on the systemic and local toxicities of the n-methyl-glucamine (meglumine) salt of metriozoic acid (isopaque). Acta Radiol Diagn (Stockh): Suppl 270:180+, 1967.

  8)    Shinoda J, Ajimi Y, Yamada M, Onozuka S. Cortical blindness during coil embolization of an unruptured intracranial aneurysm-case report. Neurol Med Chir (Tokyo) 44:416-9, 2004.

  9)    Shyn PB, Bell KA. Transient cortical blindness following cerebral angiography. J La State Med Soc 141:35-7, 1989.

10)    Uchiyama Y, Abe T, Hirohata M, Tanaka N, Kojima K, Nishimura H, et al. Blood brain-barrier disruption of nonionic iodinated contrast medium following coil embolization of a ruptured intracerebral aneurysm. AJNR Am J Neuroradiol 25: 1783-6, 2004.

11)    Uchiyama Y, Abe T, Tanaka N, Kojima K, Uchida M, Hirohata M, et al. Factors contributing to blood-brain barrier disruption following intracarotid injection of nonionic iodinated contrast medium for cerebral angiography: Experimental study in rabbits. Radiat Med 24:321-6, 2006.

12)    Wilson AJ, Wilcox J, Evill CA, Sage MR. The effect of contrast medium viscosity on the blood-brain barrier after intracarotid injection in the rabbit. AJNR Am J Neuroradiol 10:129-33, 1989.

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