NEUROIMAGING

• contrast-induced encephalopathy (CIE) is a rare neurological complication that occurs during or after the use of a contrast media in various angiographic procedures
  • such as coronary angiography, diagnostic cerebral DSA, carotid angioplasty, and EVT in acute stroke patients    (Chu, 2020)
  • it has been reported with the use of different contrast agents, but the hyperosmolar ones pose a higher risk (up to 4%)
• transient symptoms
• incidence 0.1-3%    (Chu, 2020)
• generally good prognosis, spontaneous resolution of symptoms occurs within minutes to a few days

• CIE is provoked by intraarterial administration of an iodinated contrast agent
  • not reported after intravenous administration
• the exact mechanism is not clear; probably a combination of blood-brain barrier (BBB) disruption and direct neurotoxicity from the contrast agent results in altered neuronal excitability and dysfunction   (Leong, 2012) (Yu, 2011)
  • the occipital lobes have increased BBB permeability; therefore, changes are most common here [Muruve, 1996]
• predisposing factors:
  • hypertension
  • nephropathy with reduced contrast agent clearance
  • impaired cerebral autoregulation
  • large amount of contrast agent (usually > 100 mL)
  • application into the vertebrobasilar territory (selective DSA)
  • history of stroke (the previous stroke may disrupt the BBB in the same or adjacent vascular territory, facilitating contrast leakage and causing tissue reaction and cerebral edema)

• development during the endovascular procedure or within hours following intraarterial contrast administration
• may cause the following focal symptoms or encephalopathy:
  • headache
  • cortical blindness [Studdard, 1981]
    
  • hemiparesis
  • aphasia
  • confusion
  • epileptic seizures
  • altered level of consciousness (LOC)
  • transient global amnesia (TGA)
• CIE should be suspected in acute stroke patients who exhibit clinical deterioration, contrast enhancement, and edematous changes on imaging after EVT (particularly in patients with renal impairment or a history of stroke)
• resolution typically occurs within 24 hours to a few days

• NCCT+CTA/MRI+MRA are used to rule out thromboembolism or bleeding (especially after EVT in acute stroke patients)
  
• NCCT
  • normal
  • cortical or subcortical enhancement due to contrast leakage
  • vasogenic edema with potential mass effect
• dual-energy CT may help to differentiate contrast enhancement from hemorrhage
• MRI shows cortical hyperintensities on T2, FLAIR, and DWI, but ADC is negative! (differentiation from ischemia)
• GRE or SWI can differentiate subtle hemorrhage from contrast enhancement

• hemorrhagic transformation of ischemia or recurrent thromboembolism in acute stroke patients treated with EVT
• hyperperfusion syndrome  / reperfusion syndrome
• subarachnoid hemorrhage

• hydrate with crystalloids
• provide symptomatic treatment (e.g., antiseizure medication, anxiety control, blood pressure control)
• the use of corticosteroids may have a probable effect  [Chisci, 2011]

• complete recovery usually occurs within a few days
• permanent neurological deficits are rare